Ebook Surgical review an integrated basic and clinical science study: Part 2

(BQ) Part 2 book Surgical review an integrated basic and clinical science study presents the following contents: Cardiovascular and respiratory systems, trauma, surgical subspecialties.

S E C T I O N

Cardiovascular and Respiratory Systems

K E Y P O I N T S

• On taking initial breaths the neonatal pulmonary vascular

resistance drops, pressure in the left atria exceeds that inthe right atria, and spontaneous closure of the foramenovale occurs

• The anterior leaflet of the mitral valve is in proximity to the

aortic valve

• The coronary arteries are the first branches of the aorta

• Cardiac cells can maintain prolonged action potentials,

con-duct from cell to cell via gap junctions, and self-generate

• Coronary perfusion occurs during diastole

• The major resistance to blood flow occurs at the level ofpenetrating arteries

• Myocardial oxygen demand is dependent on myocardialoxygen tension

• VSD is the most common congenital heart defect

• New onset murmur following a myocardial infarction maysignify either a postinfarction VSD or papillary musclerupture

• Type A dissections require emergent operation, while type

B dissections are managed conservatively

roper function of the cardiovascular system is essential tonormal homeostasis Alterations in the cardiovascular sys-tem’s ability to supply oxygen- and nutrient-rich blood re-sult in multiple organ dysfunction The heart is a complex pump

with many intricate components A thorough understanding of

nor-mal cardiovascular physiology allows for an intricate understanding

of cardiovascular disease processes Normal cardiovascular

physiol-ogy as well as disease processes will be discussed in detail

CARDIOVASCULAR PHYSIOLOGY

Fetal Circulation

Oxygenated blood from the placenta is brought to the fetus via the

umbilical vein Roughly half of the blood from the placenta passes

through hepatic sinusoids, while the remainder bypasses hepatic

circulation flowing directly into the inferior vena cava (IVC) via the

ductus venosus In the IVC, oxygenated placental blood mixes with

deoxygenated venous blood from the lower extremities before

en-tering the right atrium Once in the right atrium, the majority of

blood passes directly to the left atrium via the foramen ovale,

thereby bypassing the pulmonary circulation Left atrial blood

mixes with the small amount of deoxygenated blood in the fetal

pulmonary circulation before entering the left ventricle and

ulti-mately the ascending aorta

A small portion of right atrial blood mixes with superior vena

caval (SVC) blood from the head and upper extremities as well as

coronary sinus blood and passes into the right ventricle (5% to

10% of total cardiac output) Since there is very high pulmonary

vascular resistance (PVR) in the fetus, the majority of right

ventric-ular blood enters the pulmonary artery (PA) and is shunted to the

descending aorta via a patent ductus arteriosus (PDA) Roughly

P half of the descending aortic blood passes into paired umbilical ar-teries and is returned to the placenta These two fetal shunts, a

patent foramen ovale (PFO) and PDA, allow many neonates bornwith cyanotic congenital heart disease to survive Figure 19.1 illus-trates the fetal circulation

At birth, as the placental circulation is no longer present andthe neonatal lungs are expanded, the PVR is greatly reduced Thisallows increased pulmonary blood flow With increased pulmonaryblood flow, left atrial pressure is greater than right atrial pressure.This allows closure of the foramen ovale by the septum primumpressed against the septum secundum During the first days of life,this closure is reversible When an infant cries, an increase in pul-monary pressure with a right to left shunt through the foramenovale may be present This is manifested as cyanosis in newborns.Closure of the ductus arteriosus results from the release ofbradykinin, which mediates contraction of the muscular ductuswall Functional closure of the ductus typically occurs within thefirst 15 hours after birth, and anatomic closure occurs by day 12 ofparturition Prior to birth, locally produced prostaglandins main-tain patency of the ductus The fibrotic, atrophied remnant of theductus arteriosus is referred to as the ligamentum arteriosum

Anatomy

The human cardiovascular system is composed of the systemic culatory system, pulmonary circulation, and heart at the center ofthe circulatory system The heart is situated obliquely within thepericardial sac, with one third situated to the right of the medianplane and two thirds to the left The right ventricle abuts the ster-nocostal surface and forms the anterior surface of the heart Theright side of the heart receives deoxygenated systemic blood via the

cir-19

C H A P T E R

Cardiovascular Disease and Cardiac Surgery

PAVAN ATLURI AND Y JOSEPH WOO

superior and IVC as well as deoxygenated blood from the coronary

circulation via the coronary sinus The right heart then pumps this

blood through the low-pressure, high-flow pulmonary arteries

Once the blood has circulated through the pulmonary circulation,

it is returned to the left atrium via four posteriorly situated

pul-monary veins (two superior and two inferior pulpul-monary veins)

Blood from the left heart is ejected from the left ventricle into the

systemic circulation via the aorta

Valvular Anatomy

The mammalian heart is composed of four one-way valves Two

atrioventicular valves (mitral and tricuspid) provide unidirectional

diastolic flow from the atria to the ventricles and allow a systolic

pres-sure gradient between the atria and ventricles The semilunar valves

(aortic and pulmonary) allow systolic flow and maintain a diastolic

pressure gradient between the ventricles and outflow circulations

The tricuspid and mitral valves are fibrous endocardium–lined

valves The tricuspid valve separates the right atrium from the right

ventricle and consists of a large anterior leaflet attached to the

ante-rior wall of the heart, a posteante-rior leaflet at the right margin, and a

septal leaflet attached to the septum Three chordae tendinae are

attached to the free surface of the leaflets and to the papillary muscles

at the right ventricular base This apparatus prevents prolapse of the

tricuspid valve leaflets into the right atrium during systole The tral valve, located at the orifice of the left ventricle, consists of a largeanterior leaflet in continuity with the posterior wall of the aorta and

mi-a smmi-aller posterior lemi-aflet The mi-anterior lemi-aflet of the mitrmi-al vmi-alve isanatomically in proximity to the aortic valve Chordae tendineae(Fig 19.2) secure the leaflets to the anterior and posterior papillarymuscles and ensure coaptation of the valve leaflets during systole.The aortic and pulmonic valves are situated at the outflow of theleft and right ventricles, respectively The aortic valve is a trileafletvalve These leaflets are named according to the origin of the coro-nary arteries, namely the right coronary, left coronary, and noncoro-nary leaflets (Fig 19.3) Similarly, the pulmonic valve is a trileafletvalve with a right, left, and noncoronary leaflet

Coronary Anatomy

The coronary circulation (Fig 19.4) supplies oxygen-rich blood tothe myocardium and epicardium The endocardium is in continu-ous contact with intracardiac blood and does not require addi-tional blood flow The right and left coronary arteries of the heartarise just superior to the aortic valve in the coronary sinuses and arethe first branches of the aorta

The right coronary artery arises from the anterior (right) sinus

of Valsalva in the aorta and runs along the atrioventricular (AV)

266 Section IV • Cardiovascular and Respiratory Systems

FIGURE 19.1 Diagram of the human circulation

before birth Arrows indicate the direction of blood

flow Note where oxygenated blood mixed with

deoxy-genated blood: in the liver (I), in the inferior vena

cava (II), in the right atrium (III), in the left atrium

(IV), and at the entrance of the ductus arteriosus into

the descending aorta (V) (From Sadler TW Langman’s

Medical Embryology 7th ed Baltimore: Williams &

Wilkins; 1995:225, with permission.)

coronary arteries supply the posterior descending artery, branches

to the septum, and AV node (Fig 19.5)

The left coronary artery arises from the left sinus of Valsalva and

passes between the left auricle (atrial appendage) and pulmonarytrunk toward the anterior AV groove In 40% of the patients, the SAbranch arises from the left coronary artery The left coronary artery

divides at the AV groove to give off the left anterior descending artery (LAD) and circumflex coronary artery (Fig 19.5) The LAD passes an-

teriorly along the interventricular groove to the apex and providesseptal branches that supply the anterior two thirds of the interven-tricular septum and diagonals that supply the anterior-lateral wall ofthe left ventricle The circumflex coronary artery follows the AVgroove around the left border of the heart to the posterior surface ofthe heart and provides marginal branches (i.e., obtuse marginal) thatsupply the posterior left ventricle In 10% of the population, the cir-cumflex coronary artery ends in the posterior descending artery, pro-viding blood flow to the posterior one third of the interventricularseptum and AV node, defining a left-side dominant circulation.The venous drainage of the heart is via veins that drain into thecoronary sinus as well as into smaller venae cordis minimae and an-terior cardiac veins that drain into the right atrium The coronarysinus is a large vein that receives coronary venous blood from theleft (great cardiac, left marginal, and left posterior ventricularveins) and right (middle and small cardiac veins) side veins It runs

in the posterior AV groove

Electrophysiology

As with any striated muscle, cardiac muscle contraction is initiated

by action potentials (rapid voltage changes of the cell membrane).Certain cells within the cardiac muscle are capable of acting as thepacemaker and spontaneously initiate action potentials The actionpotentials of cardiac muscle are special in that they can self-generate,conduct from cell to cell via gap junctions, and are long in duration.Action potentials of the myocardium can be classified as either

fast action potentials or slow action potentials Fast action potentials

occur in normal myocardium of atria, ventricle, bundle of His, and

Purkinje fibers Slow action potentials are seen in the pacemaker

cells of the SA and AV nodes As seen in Figure 19.6 (solid line), fastaction potentials are characterized by a rapid depolarization (phaseChapter 19 • Cardiovascular Disease and Cardiac Surgery 267

Left coronarycusp

Left coronaryartery

Anterior mitralleaflet

Right coronarycusp

Right coronaryartery

Bundle

of HisNoncoronary

cusp

FIGURE 19.2 Chordae tendineae tether the leaflets of the mitral and

tricuspid valves, allowing precise coaptation during systole (From

Chitwood WR Jr Mitral valve repair: ischemic In: Kaiser LR, Kron

IL, Spray TL, eds Mastery of Cardiothoracic Surgery Philadelphia:

Lippincott–Raven Publishers; 1998:312, with permission.)

FIGURE 19.3 Normal aortic valve from a

surgeon’s point of view (From Damiano RJ.Aortic valve replacement: prosthesis In:

Kaiser LR, Kron IL, Spray TL, eds Mastery

of Cardiothoracic Surgery Philadelphia:

Lippincott–Raven Publishers; 1998:362, withpermission.)

(coronary) groove In about 60% of the population, the right

coro-nary artery gives off a sinoatrial (SA) branch near its origin to

sup-ply the SA node It traverses posteriorly toward the apex of the

heart and gives off a right marginal artery, which supplies the right

ventricle After giving off this branch it continues in the posterior

interventricular groove In roughly 85% of patients, the posterior

descending artery arises from the right coronary artery and defines a

right-side dominant circulation In approximately 5% of patients, a

balanced pattern exists in which the right coronary and circumflex

268 Section IV • Cardiovascular and Respiratory Systems

A

B

Right

FIGURE 19.4 Anatomy of the coronary arteries and

cardiac veins.A Anterior view The origin of the left

main coronary artery is left lateral and somewhat

pos-terior with respect to the aorta; it courses behind the

pulmonary artery and then divides into the left anterior

descending and circumflex coronary arteries The

ori-gin of the right coronary artery is almost directly

ante-rior, and it runs in the atrioventricular groove

B Posterior view The great, middle, and small cardiac

veins come together at the level of the coronary sinus,

which lies in the left inferior atrioventricular groove

and empties into the right atrium (From Greenfield LJ,

Mulholland MW, Oldham KT, et al Surgery: Scientific

Principles and Practice 3rd ed Philadelphia: Lippincott

Williams & Wilkins; 2001:1487, with permission.)

0—transient increase in Na⫹conductance), partial repolarization

(phase 1—outward movement of K⫹), a plateau (phase 2—inward

Ca2⫹), membrane repolarization (phase 3—decreased Ca2⫹

con-ductance and increased K⫹conductance), and a resting membrane

potential (phase 4—equal inward and outward currents) In

con-trast, slow action potentials demonstrate a slower depolarization

phase (phase 0), and shorter plateau and repolarization (phase 3) to

an unstable slow depolarization resting phase (phase 4) The

alter-ations in the membrane potential are a factor of a cell membrane’s

permeability to particular ions (Na⫹, K⫹, Ca2⫹) and the resulting

gradients that exists

During an action potential, cardiac myocytes are in an effective

refractory period (ERP) and cannot be stimulated by another

ac-tion potential This occurs during phases 1 and 2, and at the

begin-ning of phase 3 Shortly after this period is a relative refractory

period (RRP, late phase 3), during which a supranormal action

potential is needed for excitation Immediately after the action

po-tential, before return to a normal resting state (phase 4), is the

supranormal period during which the cells are hyperexcitable and

require a lower than normal action potential for stimulation

Once an action potential arises, it is conducted across the cellmembrane to adjacent cells via gap junctions The speed of trans-mission of the action potential is determined by a combination ofcell size and rate of depolarization The smaller cells of the pace-maker cells demonstrate a slower conduction velocity than thelarger Purkinje cells Similarly, the slow response of the pacemakercells mediates a slower conduction velocity when compared withthe fast response of ventricular myocardial cells

SA nodal cells demonstrate the most rapid spontaneous larization and hence act as the pacemaker under routine condi-tions This tissue lies within the wall of the right atrium at thejunction of the right atrium and SVC Once the action potential isinitiated in the SA node, it is propagated via the atria to the AVnode The AV node is located in the interatrial septum above thetricuspid valve near the coronary sinus In pathologic conditionswith SA nodal discontinuity, the AV node can act as a pacemaker.The AV node protects the ventricle from excess stimulation in thecase of increased atrial rates, allowing the ventricle adequatediastolic filling From the AV node, the action potential is sent tothe ventricle via the bundle of His The bundle of His splits into

depo-Chapter 19 • Cardiovascular Disease and Cardiac Surgery 269

FIGURE 19.5 Coronary anatomy: RCA, right coronary artery; PDA, posterior descending artery; LAD, left

anterior descending artery; OM, obtuse marginal artery (From P Atluri, YJ Woo The cardiovascular system In: A

Atluri, GC Karakousic, PM Porrett et al., eds The Surgical Review 2nd ed Philadelphia: Lippincott Williams &

Wilkins; 2005, with permission.)

Na+efflux

K+influx

right and left bundle branches and ultimately into Purkinje fibers,

which conduct to the subendocardial surfaces (Fig 19.7)

The autonomic nervous system (sympathetic and

parasympa-thetic nervous systems) innervates the SA node and controls heart

rate by modifying SA nodal activity The sympathetic nervous system

increases heart rate by increasing the rate of depolarization In

contrast, the parasympathetic nervous system increases potassium

conductance, increases the magnitude of hyperpolarization, slowsdown the rate of spontaneous depolarization, decreases the rate ofclosure of potassium channels, and slows down the heart rate In ad-dition to increasing heart rate (positive chronotropic effect), thesympathetic nervous system increases the rate of conduction of ac-tion potentials through the conduction system The parasympatheticnervous system, in contrast, acts to slow down conduction

FIGURE 19.6 Schematic fast action potential

of human ventricular myocardium (solid) with

electrolyte movements, refractory periods (see

text) and force generated (dashed line) The five

phases of fast cardiac action potential are

indi-cated as numbers Phase 4: the resting

mem-brane potential Potassium conductance is high

and sodium conductance is low Phase 0:

Up-stroke of the action potential due to membranedepolarization An increase in sodium conduc-tance due to the opening of voltage dependentfast sodium channels causes depolarization.There is a simultaneous decrease in potassium

conductance Phase 1: Period of partial

repolar-ization due to a dramatic decrease in sodiumconductance and a brief increase in chloride

conductance Phase 2: Plateau phase during

which changes in potassium efflux tance decrease and then plateaus) is matched

(conduc-by calcium influx (conductance increases and

then plateaus) Phase 3: Membrane

repolariza-tion phase due to an increase in potassiumefflux (increase potassium conductance) and adecrease in calcium influx (decreased calciumconductance) (From P Atluri, YJ Woo Thecardiovascular system In: A Atluri, GC

Karakousic, PM Porrett et al., eds The Surgical Review 2nd ed Philadelphia: Lippincott

Williams & Wilkins; 2005, with permission.)

The electrical activity of the heart can be interpreted

utiliz-ing an electrocardiogram (ECG) The normal ECG demonstrates

P waves and QRS complexes, which represent atrial and ventricular

depolarization, respectively Ventricular repolarization is

demon-strated by the T wave.

Circulatory Physiology

As previously stated, the cardiovascular system is composed of

the pulmonary circulation to provide perfusion to the lung

parenchyma and the systemic circulation to provide systemic

per-fusion (and a very small degree of pulmonary circulation via the

bronchial vessels) The pulmonary circuit is a low-pressure (mean

PA pressure of 15 mm Hg), high-flow system As compared to the

systemic circulation, the pulmonary vessels contain very little

smooth muscle and are much shorter This results in highly

compli-ant (compliance [mL/mm Hg] ⫽ volume [mL]/pressure [mm Hg];

inversely proportional to elastance), low-resistance vessels It

should be remembered that the pulmonary circulation must be

capable of handling the same volume as the systemic circulation, as

right heart output is equal to left heart output

The pulmonary circulation is capable of handling increased

cardiac output as seen with exercise by both recruiting additional

pulmonary capillaries that are not normally utilized as well as

dis-tending the pulmonary vessels PVR is able to decrease with

in-creasing cardiac output because of these two mechanisms This

drop in resistance maintains low PA pressures, thereby preventing

pulmonary edema and decreasing right heart cardiac work Other

regulators of pulmonary blood flow are lung volume, hypoxia

(which causes pulmonary vasoconstriction), and hypercapnea

(which results in pulmonary vasodilation)

In contrast to the pulmonary circuit, the systemic circulation

operates at a high pressure, with high resistance to blood flow The

flow of blood is from the left heart (left ventricle) to the aorta

From the aorta, blood flows down a pressure gradient through

var-ious branches to arterioles and capillary beds The large and small

arteries are thick-walled vessels with extensive elastic tissue and

smooth muscle They are under high pressure but offer little tance to blood flow Resistance can be calculated using the follow-ing equation derived from the work of Jean Leonard MariePoiseuille on flow mechanics:

resis-Resistance ⫽ 8(viscosity of blood) (length of vessel)

⌸(radius of blood vessel)4

Aortic and arterial elasticity maintains perfusion during the

diastolic/filling phase of left ventricular cycling Arterioles, the

short, terminal branches of the arteries, are the principal resistancevessels of the systemic circulation They comprise a large percent-age of vascular smooth muscle innervated by the autonomic ner-vous system within the vessel wall that can constrict and impedethe flow of blood Arterioles provide the largest pressure drop in thecirculation Arteriolar resistance is regulated by the autonomicnervous system

As arterial structures progressively branch from the aorta mately to the capillary bed, the cross-sectional area of the vascularbed continues to increase On the outflow side of the capillary bed,the cross-sectional area decreases as capillaries drain into venulesthat merge into small veins, large veins, and ultimately the venacava The velocity of blood flow is directly proportional to volume

ulti-of blood flow and inversely proportional to cross-sectional area.Velocity of blood flow (cm/sec) ⫽ Flow (cm3/sec)/cross-sectional

area (cm2)

As illustrated in Figure 19.8, there is a decrease in the velocity

of blood flow as the cross-sectional area of the vascular bed creases This is ideal at the capillary level (high surface area, lowvelocity), where a high contact surface area and low velocity pro-vide for optimal exchange of metabolic products at a cellular level

in-Cardiac Mechanics

The heart is a biomechanical pump The mechanical force ated by the heart is utilized to eject blood from the heart to eitherthe pulmonary or systemic circulations providing perfusion to endorgans There must be synchrony of the cardiac myocytes, valves,

gener-270 Section IV • Cardiovascular and Respiratory Systems

Rightatrium

Leftatrium

AV node

Tricuspid valve

Right ventricleSeptumLeft ventricle

Purkinje fibers

Bundle of HisLeft bundle branch

Right bundle branch

FIGURE 19.7 Structure of conduction system of

the heart (From Johnson LR Essential Medical

Physiology 2nd ed Philadelphia: Lippincott–Raven;

1998:166, with permission.)

and four chambers of the heart for maximum efficiency The heart

is in a constant state of flux to ensure that adequate end organ

per-fusion is achieved The primary variables that alter cardiac function

are preload, afterload, and autonomic nervous system stimulation

A proper understanding of these forces is a prerequisite to an

ade-quate understanding of cardiac mechanics

The left and right ventricles function in a cyclical manner

Contraction and ejection of blood occurs during systole Myocardial

perfusion as well as filling of the ventricles occurs during the

relax-ation phase known as diastole To simplify the discussion all

refer-ences to ventricular function will focus on left ventricular mechanics

The left ventricular intracavitary volume and pressure at end

di-astole (immediately prior to contraction) determine the preload of

the heart There are several factors that affect preload Increasing

ve-nous return increases preload, while fibrotic, hypertrophied, and

aging hearts become increasingly stiff and limit left ventricular filling

and preload As described earlier, relaxation is an energy-dependent

process (calcium-ATPase), which is augmented by adrenergic

stimu-lation, but is impaired in ischemia, hypothyroidism, and congestive

heart failure—all conditions that limit preload

The afterload of a muscle is the pressure against which it must

contract For the left ventricle, this is equivalent to the aortic

pres-sure against which it must eject blood during systole Afterload for

the right ventricle is equal to the PA pressure The greater the

after-load, the greater the potential energy the heart must generate to

provide adequate ejection into the aorta, and subsequently the

greater the cardiac work (described in the following text) Maximal

velocity of contraction is achieved when afterload is minimal

Within normal physiologic ranges, the heart is able to

accom-modate a broad range of end-diastolic volume by altering

contrac-tility This dynamic activity is described by the Frank–Starling

relationship, which describes the interplay between ventricular

filling and contractility With increased ventricular filling the

sar-comeres are stretched to an optimal length, thereby facilitating

increased contractility Adrenergic stimulation can further increase

contractility (inotropy) of the heart, thereby increasing the stroke

volume (volume of blood ejected from the heart with each beat)

Parasympathetic innervation decreases inotropy Additionally,

right atrial stretch leads to an increase in heart rate with subsequentincrease in cardiac output

Cardiac output (l/min) ⫽ stroke volume (l/beat)

⫻ heart rate (beats/min)The cardiac cycle, as well as the interplay between preload andafterload on stroke volume, can best be described usingpressure–volume loops (Fig 19.9) These pressure–volume loops areconstructed by combining systolic and diastolic pressure curves Thediastolic component (dotted line) is determined by diastolic filling(preload) The shape of the loop is determined by both contractilityand the afterload against which the ventricle must contract The car-diac cycle begins at end diastole when the left ventricle is filled withleft atrial blood and the cardiac muscle is relaxed On excitation themuscle begins to contract and generate force against closed valves(isovolumetric contraction) Once the pressure in the left ventricleexceeds aortic pressure, the blood is ejected into circulation duringsystole This volume ejected is the stroke volume (depicted by thewidth of the pressure–volume loop) The remaining volume at theend of contraction is the end-systolic volume At the end of contrac-tion the ventricle begins to relax (isovolumetric relaxation) and theaortic valve closes as the pressure in the aorta exceeds that of the leftventricle With a drop in left ventricular pressure the mitral valveopens and left atrial blood begins to fill the left ventricle during di-astole It should be noted that in the ideal system following passiveflow of atrial blood, atrial contraction near the end of diastole opti-

mizes filling of the left ventricle (atrial kick), thereby optimizing the

Frank–Starling relationship Loss of this end-diastolic atrial tion as in atrial fibrillation in a heart with ventricular hypertrophycan have adverse systemic hemodynamic consequences

contrac-There are several factors that affect the pressure–volume loops.Increased preload increases end-diastolic volume and stroke volume.Increased afterload increases pressure that is required to be generatedduring isovolumetric contraction to eject blood and decreases thestroke volume Increased contractility, as with adrenergic stimula-tion, increases stroke volume and decreases end-systolic volume Theability of a hypertrophic heart to increase stroke volume is severelylimited by its decreased diastolic compliance, limiting preload

Chapter 19 • Cardiovascular Disease and Cardiac Surgery 271

large arteries,small arteries

FIGURE 19.8 Pressure, area, and velocity

rela-tionship across the systemic circulation (From

Kreisel D, Krupnick AS, Kaiser LR, eds The gical Review 1st ed Philadelphia: Lippincott

Sur-Williams & Wilkins; 2001:308, with permission.)

Oxygen utilization by the heart is twofold A small amount of

oxygen is utilized for cellular homeostasis and a large amount is

uti-lized during contraction Changes in myocardial oxygen

consump-tion are directly related to the work of the heart and changes in

contractility Cardiac work can be quantified as stroke work, or work

that the heart performs with each beat (stroke work ⫽ aortic

pres-sure ⫻ stroke volume) The minute work of the heart is equal to the

product of heart rate times the stroke volume multiplied by the

aor-tic pressure (or cardiac output ⫻ aortic pressure), so an increase in

any of these three variables will increase cardiac work and ultimately

increase myocardial oxygen consumption and demand

The major determinant of oxygen demand is myocardial wall

tension Tension in the wall of the ventricle is determined by both

the pressure in the ventricle and the geometry of the ventricle The

normal left ventricle is a pressurized irregularly shaped chamber If

we were to consider the ventricle as a cylinder then the law of

Laplace states that wall tension is proportional to internal pressure

times the radius Increasing the wall thickness decreases the wall

tension by distributing the internal pressure over a greater number

of muscle fibers In other words, wall tension equals pressure times

radius divided by wall thickness Altering the geometrical

configu-ration of the ventricle (as with cardiomyopathy), increasing the

ra-dius, decreasing the wall thickness, and increasing ventricular

pressure all increase wall tension and myocardial oxygen demand

Changing the geometry of the ventricle requires extra energy

con-sumption to realign the myocytes prior to each systolic contraction

As stated previously, cardiac output is equal to the product of

stroke volume multiplied by the heart rate A clinically feasible

means of calculating cardiac output is to utilize the Fick equation:

Dye dilution and thermal dilution of heat are other clinically

utilized methods of calculating cardiac output Given the varying

sizes of patients (varying body surface area), simply calculating a

cardiac output may not provide enough information regarding

cardiac function and adequate systemic perfusion The calculated

parameter of cardiac index factors in patient size and expresses

Cardiac output = Total body oxygen consumption

3O2] arterial blood - [O2] venous blood

cardiac output per square meter of surface area, thereby ing the variable of patient size (cardiac index ⫽ cardiac output/body surface area) A cardiac index greater than 2 L/min/m2isaccepted as adequate Figure 19.10 demonstrates the mechanicaland electrical events during the various phases of the cardiac cycle(Table 19.1)

eliminat-Coronary Physiology

Coronary blood flow follows the major vessels into smaller trating arteries, which provide the majority of the resistance toblood flow There is a dense capillary network by which the exten-sive metabolic demands of the heart can be provided At rest coro-nary blood flow is approximately 1 mL/g of myocardium, but withdemand this flow is capable of increasing nearly fourfold The in-crease in blood flow is accomplished with a combination of localvasodilatation of the penetrating arteries as well as recruitment ofvessels that are collapsed at rest Since nearly 70% of the oxygen isderived from delivered coronary blood, there exists a very tight reg-ulatory system to ensure adequate perfusion of the myocardium.The myocardial tissue functions most optimally under aerobic con-ditions and is capable of sustaining only a few minutes of anaerobicactivity

pene-Coronary perfusion is accomplished during the relaxing stolic phase During systole the compressive forces within the myo-cardial wall are powerful enough to collapse the penetratingvessels and prevent myocardial perfusion Therefore, increasingheart rate will not only increase myocardial oxygen demand butalso decrease myocardial perfusion Regulation of coronary bloodflow is accomplished by a combination of the autonomic nervoussystem, metabolic vascular mediators, and vascular endothelium–mediated vasodilatation There are a combination of ␣- and

dia-␤-receptors on the conductance vessels, which regulate nervous

system–mediated vasoconstriction and vasodilatation, respectively

Adenosine is produced by cardiac myocytes in response to ischemia

and is the primary metabolic vascular mediator It acts locally onvascular smooth muscle to cause vasodilatation The vascular en-dothelium is capable of releasing both vasodilatory and vasocon-stricting mediators

272 Section IV • Cardiovascular and Respiratory Systems

end-Systole

Diastolic filling

Stroke volumeIntraventricular volume (mL)

FIGURE 19.9 Pressure–volume loop

of one cardiac cycle (From Mohrman

DE, Heller LJ Cardiovascular

Physiol-ogy 3rd ed New York: McGraw-Hill;

1991:54, with permission.)

CARDIOVASCULAR PATHOPHYSIOLOGY Congenital Heart Disease

Atrial Septal Defect

Atrial septal defects (ASDs) account for 10% to 15% of cardiacanomalies Additionally, these are the most common congenitalconditions encountered in adults ASDs may occur in associationwith other complex congenital heart and genetic defects includingDown, Turner, Marfan, and Ehlers–Danlos syndromes

A defect in formation of the septum primum results in tium secundum–type ASD (Fig 19.11) Ostium primum–typeASDs are a result of malformation of the AV canal Other lesscommon types of ASDs include sinus venosus–type ASD (defect

os-at the level of the SVC and IVC) and coronary sinus ASD (defect

in the wall between coronary sinus and left atrium) Roughly 20%

of adults have a PFO, which is clinically inconsequential as itremains closed due to higher left atrial pressure compared withright atrial pressures But, with high right-sided pressures theforamen ovale may become patent causing right to left shunting

Ventricularvolume

Heart sounds

Atrialpressure

Ventricularpressure

Aorticpressure

dur-ing a sdur-ingle cardiac cycle The seven phases are denoted

by letters as follows:(A) atrial systole, (B)

isovolumet-ric ventisovolumet-ricular contraction, (C) rapid ventricular

ejection,(D) reduced ventricular ejection, (E)

isovolu-metric ventricular relaxation,(F) rapid ventricular

fill-ing, and (G) reduced ventricular filling (From Johnson

LR Essential Medical Physiology 2nd ed Philadelphia:

Lippincott–Raven; 1998:190, with permission.)

Normal hemodynamic parameters.

Cardiac output 4.0–8.0 L/min

Cardiac index 2.5–4.5 L/min/m2

Systemic blood pressure 100–130/60–90 mm Hg

Mean arterial pressure (MAP) 70–105 mm Hg

Right atria/central venous pressure 2–10 mm Hg

Right ventricular pressure 15–30/0–18 mm Hg

Pulmonary artery pressure 15–30/6–12 mm Hg

Pulmonary capillary wedge pressure 5–12 mm Hg

Systemic vascular resistance (SVR) 700–1,600 dynes/sec/cm2

Pulmonary vascular resistance 20–130 dynes/sec/cm2

mm Hg, millimeters of mercury; L/min, liters/minute; m, meter, cm,

centimeter; sec, second

T A B L E 1 9 1

Often patients remain asymptomatic Symptomatic patients

present with signs of heart failure, exercise intolerance, or

arrhythmias Echocardiography is usually diagnostic Many small

ASDs in children will close spontaneously and should be

moni-tored All symptomatic and large/significant ASDs should be closed

by either percutaneous or surgical means Prior to closure it is

critical to measure PVR by cardiac catheterization Elevated PVR

(⬎8 woods units) is a contraindication to closure

Ventricular Septal Defect

Ventricular septal defects (VSDs) account for roughly 25% of

con-genital heart defects VSDs can either occur singly or in

combina-tion One half of patients with VSDs will also have another cardiac

anomaly, and should therefore undergo thorough evaluation VSDs

are defined on the basis of their location in the ventricular septum,

i.e., outlet, septal, conoventricular, anterior muscular,

midmuscu-lar, apical muscumidmuscu-lar, and inlet septal (Fig 19.12)

Hemodynami-cally, VSDs result in left to right shunting of blood, thereby

resulting in elevated PVR and left atrial and ventricular overload

With long-standing left to right shunting there is medial

hypertro-phy of the pulmonary vasculature and an increase in PA pressures

Over time as the PVR increases, volume overload on the left heartdecreases and eventually there is a reversal of flow through the VSD.With right to left shunting there is a worsening cyanosis that en-sues, referred to as Eisenmenger syndrome Once a diagnosis ofEisenmenger syndrome has been made, operative repair is con-traindicated, given the high risk of right heart failure With an intra-cardiac defect, a functioning right ventricle, and failing lungssecondary to elevated PVR, bilateral lung transplantion and intracar-diac repair may be the only option In the presence of a failing rightventricle the only option would be a heart–lung transplant of whichonly few are done currently because of the scarcity of donors.VSDs can be diagnosed by echocardiography Early surgical re-pair is indicated for children with large VSDs with a pulmonary

blood flow (Qp)–systemic blood flow (Qs) ratio greater than 2.Moderate-sized defects are often monitored until childhood

Patent Ductus Arteriosus

PDA results from failure of closure of the ductus arteriosus, which sults in blood being shunted from the proximal descending thoracicaorta to the PA bifurcation PDAs take up to 3 months after birth toclose, and are therefore not considered pathologic until after this age.The male–female ratio is 1:2 Failure of closure after 3 months isthought to be secondary to immaturity of the medial muscular layer

re-As with VSDs, left to right shunting of blood occurs, resulting

in increased pulmonary blood flow and left atrial and ventricularoverload On auscultation a classic “machinelike” murmur is heard.Closure of the PDA can be attempted by pharmacologic means innewborns with inhibition of prostaglandins utilizing agents such asindomethacin PDAs that fail to close may be amenable to percuta-neous embolization utilizing coils In infants if operative closure isrequired, these defects can often be approached thoracoscopically

or via a small left thoracotomy

Tetralogy of Fallot

Tetralogy of Fallot (TOF) results from an anterior malalignment ofthe infundibular septum Classically this malformation results in aVSD, overriding aortic valve, right ventricular outflow obstruction,and resultant right ventricular hypertrophy (Fig 19.13) With the ad-dition of an ASD, the condition is referred to as pentalogy of Fallot.Twenty-five percent of TOF patients have a right-sided aorta, and inaddition, anomalies in the coronary circulation may also exist.The extent of the cyanosis depends on the severity of the tetral-ogy In severe cases, increased cyanosis can occur with agitation orcrying Older children often learn to squat to relieve cyanotic spells.Physical examination reveals a systolic murmur over the left heart

274 Section IV • Cardiovascular and Respiratory Systems

C

FIGURE 19.11 Normal atrial septum

for-mation (A) and ostium secundum–type atrial

septal defect caused by excessive resorption of

the septum primum (B, C) (From Sadler

TW Langman’s Medical Embryology 5th ed.

Baltimore: Williams & Wilkins; 1985, with

permission.)

FIGURE 19.12 Major types of ventricular septal defects categorized

by anatomic location (From Kaiser LR, Kron IL, Spray TL, eds Mastery

of Cardiothoracic Surgery Philadelphia: Lippincott–Raven Publishers;

1998, with permission.)

border and an accentuated second aortic heart sound Chest

roentgenogram often demonstrates a boot-shaped heart

Conser-vative therapy includes a knee to chest position, supplemental

oxy-gen, volume expansion, and sedation Symptomatic infants should

undergo immediate repair with elective repair done at 1 year of age

for asymptomatic patients

Tricuspid Atresia

Tricuspid atresia results from a lack of communication between the

right atrium and ventricle Associated anomalies include an ASD,

enlarged mitral valve and left ventricle, and right ventricular

hy-poplasia As with other congenital cardiac anomalies,

echocardiog-raphy secures the diagnosis and nicely demonstrates the anatomic

abnormalites These patients require surgical correction to increase

systemic oxygen saturation and avoid the development of heart

failure Surgical repair requires a Fontan procedure, an operation

that results in the systemic venous return being connected directly

to the PA, resulting in increased pulmonary blood flow, a decreased

right to left shunt, and decreased volume overload of the left heart

Transposition of the Great Vessels

Transposition of the great vessels (TGAs) occurs when the aorta

arises from the anatomic right ventricle and the PA arises from the

anatomic left ventricle (Fig 19.14) TGA accounts for 8% to 10%

of all congenital heart defects Associated cardiac anomalies can

include ASD, VSD, PDA, left ventricular outflow obstruction,

ab-normal coronary branching, or PFO Normal physiologic closure

of the ductus arteriosus can result in profound cyanosis In the

case of complete TGA, survival depends on early recognition and

the presence of a right to left shunt in the form of a PDA or ASD A

closing ductus arteriosus can be maintained patent with infusion

of prostaglandin E1to enhance the requisite left to right shunting,

thereby providing temporary palliation Alternatively, an ASD can

be created percutaneously with a balloon septoplasty

Diagnosis is confirmed by echocardiography On physical

ex-amination a systolic murmur and loud single heart sound can be

appreciated Chest roentgenogram reveals an oval or egg-shaped

heart, narrow superior mediastinum, and increased pulmonary

vascular markings An arterial switch procedure in which the great

vessels are transposed to their appropriate anatomic positions is thedefinitive operation for this anomaly

Coarctation of the Aorta

Coarctation of the aorta is characterized by a focal narrowing of thethoracic aorta, most frequently just distal to the origin of the leftsubclavian artery usually near the ductus arteriosus Coarctationaccounts for 5% to 8% of all congenital heart defects Associatedanomalies include PDA, VSD, bicuspid aortic valve, subaortic ob-struction, and mitral valve anomalies

Coarctation has historically been categorized as either infantile

or adult In infantile coarctation, the aortic obstruction is mostoften preductal and leads to separation of the left ventricular flowdirected to the head and arms from the PA flow directed to the lowerbody This type of coarctation results in early left ventricular failureand death if not surgically corrected The more common adult type

of coarctation is postductal and leads to proximal hypertension andeventual congestive heart failure over time, although patients mayremain asymptomatic and appear healthy well into adulthood.Physical findings of absent femoral pulses with poor distal per-fusion should warrant a workup for coarctation of the aorta Find-ings on physical examination include upper extremity systolichypertension and a pressure differential between the left and rightupper extremity, absent or decreased lower extremity pulses, promi-nent pulsations at the sternal notch, and a systolic heart murmurover the left sternal border that may be transmitted to the back Chestroentgenograms may reveal rib notching by the age of 10 years sec-ondary to enlarged intercostal artery collateral circulation Other ra-diologic findings include an indentation over the left border of theheart at the site of coarctation, which results in the classic “3” sign

In severe cases of aortic coarctation lower extremity blood flow

is entirely dependent on a PDA With spontaneous ductal closure,abdominal and lower extremity ischemia will ensue and prostag-landin E1infusion to maintain patency of the ductus arteriosusmay be required Severe cases require immediate operative repair,whereas asymptomatic cases can be repaired on an elective basis.Repair entails an end-to-end repair, bypass from the enlarged sub-clavian artery to the descending aorta, prosthetic flap with a syn-thetic graft, or subclavian flap aortoplasty

Chapter 19 • Cardiovascular Disease and Cardiac Surgery 275

FIGURE 19.13 Tetralogy of Fallot: schematic drawing (From Sadler

TW Langman’s Medical Embryology 5th ed Baltimore: Williams &

Wilkins; 1985, with permission.) FIGURE 19.14 Transposition of the great vessels: schematic drawing.

(From Sadler TW Langman’s Medical Embryology 5th ed Baltimore:

Williams & Wilkins; 1985, with permission.)

arteriosus

Pulmonaryartery

Total Anomolous Pulmonary Venous Connection

Total anomalous pulmonary venous connection (TAPVC) is a

con-dition in which there is abnormal drainage of the pulmonary veins

into the right atrium The presence of either a PFO or ASD is

re-quired to maintain blood flow to the left heart and thus the

sys-temic circulation Severity of symptoms depends on whether there

is obstructed or nonobstructed TAPVC With obstructed TAPVC,

the obstruction causes pulmonary hypertension, decreased venous

return, low cardiac output, venous congestion, and acidosis

Ob-structed TAPVC is a surgical emergency UnobOb-structed cases

pres-ent similar to that of an ASD Operative repair is recommended for

unobstructed TAPVC once diagnosed to prevent pulmonary

hyper-tension and minimize mortality Up to 80% of infants with TAPVC

will die by 1 year of age if the condition is not surgically repaired

Hypoplastic Left Heart Disease

Hypoplastic left heart syndrome (HLHS) accounts for 7% of

con-genital cardiac anomalies and 25% of deaths within the first week

of life HLHS is a complex anomaly with aortic and aortic valve

hy-poplasia, mitral valve stenosis, and a hypoplastic left ventricle A

PDA is essential for survival of the neonate and mandates infusion

of prostaglandin E1 Systemic blood flow is dependent on the

paral-lel circulation that exists from the right ventricle to the systemic

cir-culation via the PDA Once the lungs expand and the PVR drops,

blood flow preferentially flows to the pulmonary circulation To

balance pulmonary and systemic circulations, PVR should be

con-trolled by adjusting ventilation, hematocrit should be increased,

and SVR should be altered pharmacologically

Newborns typically present within the first 48 hours of life

with tachypnea and cyanosis Echocardiography is almost

univer-sally diagnostic Initial management includes prostaglandin E1

in-fusion and pharmacologic balancing of the systemic and

pulmonary circulations Operative repair is carried out in three

stages The first operation, the Norwood procedure, involves

con-nection of the diminutive aorta to the proximal PA; at the same

time a graft is placed between the innominate artery and

pul-monary trunk The second stage, performed at 3 to 10 months of

age, comprises a hemi-Fontan procedure whereby SVC blood is

directed exclusively into the PA The final stage, performed at 18 to

24 months, involves redirection of the IVC and SVC blood flow into

the pulmonary circulation, the Fontan procedure Some centers

prefer to immediately list these neonates for heart transplantationsand reserve the three-stage procedure if a donor cannot be found

Acquired Heart Disease

Cardiovascular disease is the number one killer, accounting for37.3% of all deaths in the United States The 2007 American HeartAssociation Heart Disease and Stroke Update estimates that thereare 15.8 million Americans suffering from coronary heart diseaseand 5.2 million suffering from heart failure With an increasingprevalence of diabetes, obesity, and a sedentary lifestyle the inci-dence of cardiovascular disease is expected to increase dramatically

Coronary Artery Disease

Coronary artery disease (CAD) is the leading cause of mortality inthe United States Similar to peripheral vascular disease, CAD is due

to luminal narrowing with a resultant decrease in blood flow ary to progressive atherosclerotic disease Risk factors for atheroscle-rotic disease include hypertension, diabetes, hypercholesterolemia,smoking, sedentary lifestyle, and family history Men are at higherrisk than women for developing premature coronary artery, but aftermenopause, the risk is equivalent Patients with CAD can presentwith a spectrum of signs and symptoms ranging from asymptomatic

second-to chronic severe angina, depending on the extent of disease and gree of luminal narrowing Diabetic patients often have no symp-toms until a major cardiovascular event ensues The CanadianCardiovascular Society Functional Classification has been developed

de-to classify anginal sympde-toms related de-to CAD (Table 19.2) A secondsimilar grading system for heart failure is the New York Heart Associ-ation Heart Failure Functional Classification, which is a subjectiveclassification system (Table 19.3) Asymptomatic patients may pres-ent with myocardial infarction (MI) or even sudden death related tomalignant arrhythmias Roughly one half of all fatal heart attacksoccur in previously asymptomatic individuals

Over 10% of patients undergoing noncardiac surgical dures in the United States are estimated to be at risk for CAD Morethan 15% of these patients suffer from cardiovascular complications

proce-in the postoperative period This risk is even greater proce-in patients withperipheral vascular disease It is critical to appropriately identifypatients at risk for CAD and evaluate them for critical disease.Diagnostic studies traditionally utilized to identify patients at risk for CAD have included stress echocardiography, stress

276 Section IV • Cardiovascular and Respiratory Systems

Canadian Cardiovascular Society functional classification.

Class I Ordinary physical activity does not cause angina Angina may occur with strenuous

or prolonged exertion

Class II Slight limitation of ordinary activity Angina may occur with walking or climbing

stairs rapidly, walking uphill, walking or stair climbing after meals or in the cold, inthe wind, or under emotional stress, or walking more than two blocks on the level orclimbing more than one flight of stairs under normal conditions at a normal pace

Class III Marked limitation of ordinary physical activity Angina may occur after walking one

or two blocks on level ground or climbing one flight of stairs under normalconditions at a normal place

Class IV Inability to carry out any physical activity without anginal discomfort; angina may

be present at rest

From Braunwald E The history In: Braunwald E, ed Heart Disease: A Textbook of Cardiovascular Medicine.

5th ed Philadelphia: WB Saunders; 1997:1–14, with permission

T A B L E 1 9 2

electrocardiography and thallium tests, and intravenous

dipyri-damole thallium-201 or technetium-99m scintigraphy (DTS)

Newer modalities, including high-resolution cardiac computed

to-mography and magnetic resonance imaging, are gaining popularity

and may soon become accepted as routine screening studies DTS is

the best initial preoperative noninvasive screening test As compared

with exercise stress tests, DTS can be performed on patients who are

unable to perform the exercise portion of the study In DTS, a

find-ing of reversible defects followfind-ing infusion of the radiotracer at

stress when compared with resting images reflects reversible defects

and viable myocardium, whereas a nonreversible defect signifies

that the defect is fixed likely resulting from scar and thus neither

amenable nor responsive to revascularization Results obtained by

either thallium or technetium scintigraphy are 90% sensitive and

75% specific The findings of CAD on DTS warrants a coronary

angiogram to define any coronary lesions and appropriate therapy

either in the form of coronary artery bypass grafting (CABG) or a

percutaneous coronary intervention (PCI) to enhance myocardial

perfusion Coronary revascularization is generally performed to

al-leviate increasing anginal symptoms, preserve at-risk myocardium,

and prevent MI and damage Noncritical coronary lesions can often

be managed medically until progression of disease ensues

On the basis of the large body of literature comparing medical

therapy, PCI, and CABG, the American College of Cardiology and

the American Heart Association have established guidelines for

sur-gical revascularization These in-depth criteria are beyond the scope

of this chapter The general guidelines include left main stenosis,

dis-ease in three or more vessels, proximal LAD stenosis, and failure of

PCI Diabetic patients have been shown to fare better with CABG as

compared to PCI In general, CABG is not performed on vessels with

lesions less than 70% because of decreased patency rates related to

outflow obstruction from competitive flow in the native circulation

The long-term benefits of CABG are primarily related to patency

of the conduit Vein grafts develop intimal hyperplasia that limits

long-term patency to 50% to 60% at 10 years In contrast, the

inter-nal mammary artery (IMA) has been reported to have patency rates

upwards of 95% as far out as 20 years following operation

Statisti-cally significant improvements in patient survival have been

demon-strated in patients receiving an IMA to LAD bypass (Fig 19.15)

Alternatives to Traditional Coronary Artery Bypass Grafting

CABG accounted for 427,000 operative procedures in 2004 CABG

has traditionally been performed with the assistance of the

cardiopulmonary bypass (CPB) circuit with an arrested heart This

allows for a still operative field and optimal circulatory management.The CPB circuit is utilized to isolate the cardiopulmonary system andthereby provide optimal, blood-free operative exposure for cardio-vascular surgery The CPB circuit must perform the functions of thecardiovascular system It must oxygenate blood, remove carbon diox-ide, and provide adequate perfusion to end organs The cardiovascu-lar surgeon can utilize either total or partial CPB During total CPB,the venous return of the heart is circulated through the CPB circuit

in its entirety, whereas during partial CPB, a fraction of the blood isallowed to circulate to the right ventricle and pulmonary circulation.The basic components of the CPB circuit include the venousreservoir, oxygenator, heat exchanger, and pump The venous reser-voir stores systemic venous return The oxygenator both adds oxy-gen and removes carbon dioxide from the blood Thermoregulation

of blood is controlled by the heat exchanger Blood is returned to thesystemic circulation via the ascending aorta or femoral artery bythe pump The pump can either be a kinetic centrifugal pump or themore common electric motor driven, load-independent rollerpump It is important to note, however, that CPB activates the com-plement cascade, triggers release of pro-inflammatory cytokines,

Chapter 19 • Cardiovascular Disease and Cardiac Surgery 277

New York Heart Association heart failure functional classification.

Class I Patients with cardiac disease but without resulting limitation of physical activity

Class II Patients with cardiac disease resulting in slight limitation of physical activity Ordinary

physical activity causes fatigue, palpitations, dyspnea, or angina No symptoms at rest

Class III Patients with cardiac disease resulting in marked limitation of physical activity Less

than ordinary physical activity results in fatigue, palpitations, dyspnea, or angina Nosymptoms at rest

Class IV Patients with cardiac disease who are unable to carry on any physical activity without

discomfort Symptoms of cardiac insufficiency or angina may be present even at rest

Any physical activity increases discomfort

From Braunwald E The history In: Braunwald E, ed Heart Disease: A Textbook of Cardiovascular Medicine.

5th ed Philadelphia: WB Saunders; 1997:1–14, with permission

T A B L E 1 9 3

FIGURE 19.15 Coronary artery bypass grafting performed for

ather-osclerotic coronary artery disease

upregulates inflammatory mediators (IL-1, TNF-␣, IL-6, IL-8, IL-10),

initiates the systemic inflammatory response syndrome (SIRS),

stimulates oxygen-free radical generation, and increases oxidative

stress To minimize these systemic manifestations a renewed interest

in beating heart surgery has arisen

Off-pump coronary artery bypass grafting (OPCAB) is

per-formed on a beating heart with the use of stabilization devices to

minimize motion at the site of anastomoses Blood flow to the

af-fected myocardium can be sustained with the use of an intraluminal

shunt, which additionally minimizes blood in the operative field

Al-ternatively, silastic tapes can be utilized as a tourniquet for proximal

and/or distal control The most critical vessels that supply the

great-est amount of myocardium at risk are traditionally grafted first, i.e.,

LAD, to maximize perfusion to the heart throughout the case

Ran-domized, controlled trials have demonstrated significantly lower

transfusion requirements, decreased systemic inflammation, shorter

hospital stay, and decreased cost Trends toward lower renal

compli-cations have been observed Circulatory management is much more

difficult in OPCAB and requires very close communication between

the surgeon and the anesthesiologist OPCAB is associated with a

sig-nificant learning curve and is therefore performed at the discretion

of the surgeon based on experience Heart failure, hemodynamic

in-stability, severe left ventricular dysfunction, cardiomyopathy,

fre-quent arrhythmias, and emergent operations were once absolute

contraindications for OPCAB, but are now relative contraindications

based on surgeon experience and preference

The rapid development of minimally invasive techniques in

gy-necologic, urologic, and general surgery has stimulated an interest in

revascularizing myocardium utilizing smaller incisions Initially this

consisted of performing beating heart revascularization through

small partial sternotomies or anterolateral thoracotomies, depending

on the target vessels of interest This approach was originally termed

minimally invasive direct coronary artery bypass (MIDCAB) Often

these incisions can be limited to between 8 and 10 cm and yield

ex-cellent cosmetic results MIDCAB is amenable to single- as well as

multivessel coronary disease However, it is most ideally suited for an

isolated left internal mammary artery (LIMA) to LAD anastomosis

Clinical trials have demonstrated excellent patency and rapid

recov-ery following MIDCAB

The development of robotic technology has further advanced

minimally invasive techniques in cardiac surgery Robotic

plat-forms provide 3-D vision, magnification, miniature instruments,

elimination of tremor, and mobility through multiple degrees of

movement, thereby allowing very precise and controlled motion

(Fig 19.16) Several investigators have demonstrated feasibility of

performing precise coronary anastomoses with the robotic

plat-form Randomized clinical trials of robotically assisted totally

en-doscopic coronary artery bypass grafting (TECAB) performed

using CPB with peripheral cannulation have demonstrated TECAB

to be a safe procedure with angiographic patency, mortality, and

morbidity equivalent to standard CABG procedures Further

ad-vances in technology, surgical expertise, and reduced cost will be

required before TECAB can become widespread

Myocardial Infarction

The American Heart Association estimates that 700,000 Americans

will have a heart attack, 500,000 will have a recurrent attack, and an

additional 175,000 will have a silent heart attack About 38% of

patients suffering an MI will die the ensuing year Roughly every

60 seconds an American will die from a heart attack Advances inmedical management and interventions for MI have reduced themortality from acute MI by 24% since 1989 The goal of therapy is

to rapidly salvage as much myocardium as is feasible Loss of morethan 40% of functional left ventricular mass often results in cardio-genic shock Reperfusion of myocardium 40 minutes after onset ofacute ischemia results in salvage of 60% to 70% of affected my-ocardium, while as little as 3 hours following ischemia only 10% ofmyocardium can be salvaged

Medical management of MI necessitates rapid intervention.Treatment should include decreasing myocardial oxygen demand,increasing arterial oxygen delivery, maintaining perfusion, and pro-tecting the threatened myocardium Early reperfusion should bethe goal Depending on the expertise of a given medical facilitythrombolytics or angioplasty can be utilized Thrombolytic therapy

is easy to perform in most community settings by trained healthcare professionals Since time to reperfusion is essential, this isoften the strategy utilized in facilities lacking cardiac catheteriza-tion laboratories If feasible, the preferred approach to myocardialsalvage is rapid evaluation and transfer to a cardiac catheterizationlab for PCI with the potential for emergent CABG in the event ofleft main CAD or if the lesions are not revascularizable by PCI.Vasopressors and inotropic agents are the first-line therapy forcardiogenic shock Maintenance of optimal filling pressures is es-sential and may require insertion of a PA catheter to optimize man-agement Ventilatory support and/or diuresis may be necessary tomaintain proper oxygenation in the setting of acute cardiogenicpulmonary edema While medical management is essential, earlyrevascularization with either PCI or CABG is critical and has beenshown to significantly improve long-term survival

Complications of Myocardial Infarction

A number of structural sequelae may ensue in the early- or postinfarction period, which require prompt surgical intervention.These complications include VSD, ventricular free wall rupture, leftventricular aneurysm, and ischemic mitral regurgitation (MR).Early recognition and treatment of these complications is critical tomaximizing survival Overall these postinfarction complicationsare responsible for 20% of deaths following MI

late-278 Section IV • Cardiovascular and Respiratory Systems

FIGURE 19.16 The da Vinci robotic telemanipulation system A The

operative console at which the surgeon is seated.B The instrument

cart with two instrument arms and a camera arm that stands next tothe operating room table (From From Kaiser LR, Kron IL, Spray TL,

eds Mastery of Cardiothoracic Surgery 2nd ed Philadelphia:

Lippincott–Raven Publishers; 2007, with permission.)

Ventricular Septal Defect

Postinfarction VSDs complicate 1% to 2% of MIs, accounting for

5% of deaths following an MI Roughly 60% of postinfarction VSDs

occur in the anteroapical septum as a result of a full-thickness

ante-rior wall MI secondary to an LAD occlusion with limited collateral

vessel formation The remainder of patients have posterior septal

VSDs resulting from occlusion of either a dominant right or

cir-cumflex coronary artery Postinfarction VSDs occur most frequently

2 to 4 days following an acute MI, but can occur between a few

hours and a few weeks following infarction The VSD may be a

sim-ple rupture or may develop a serpigenous dissection tract

Typically, patients present with a new-onset harsh holosystolic

murmur that radiates to the axilla and is often associated with chest

pain and a thrill The gold standard for diagnosis of a postinfarction

VSD is a right heart catheterization with a greater than 9% “step-up”

in oxygen saturation between the right atrium and PA Color flow

Doppler echocardiography is also a good diagnostic modality for

VSD Once diagnosed, immediate placement of an intra-aortic

bal-loon pump (IABP) and early surgical intervention are necessary

Pre-operative management centers on reducing systemic vascular

resistance while maintaining cardiac output and systemic perfusion

Without an operation this condition is almost universally fatal, with

7% survival at 1 year if left untreated Patients in cardiogenic shock

should be immediately taken to the operating room Operative repair

depends on the location of the defect, but in general involves

endocar-dial patch repair with possible exclusion of the infracted myocardium

Ventricular Free Wall Rupture

Postinfarction ventricular free wall rupture is more frequent thanVSDs, occurring in 11% of patients following an acute MI Ventric-ular rupture and cardiogenic shock are the leading causes of mor-tality following an MI Postinfarction ventricular free wall rupture

is more common in elderly women suffering their first MI In thepresent era, ruptures occur most frequently in hypertensive pa-tients within 5 days of infarction Rupture can affect the anterior,lateral, and posterior walls LV ruptures are divided into three cate-gories: acute, subacute, and chronic Acute ruptures result in sud-den chest pain, profound shock, electromechanical dissociation,and rapid death Subacute rupture is characterized by a smaller de-fect that may be sealed by clot or fibrinous pericardial adhesions.They usually present with signs of tamponade and cardiogenicshock and may remain stable for several hours or days prior to in-tervention A chronic rupture presents as a false aneurysm of theleft ventricle with adhesions containing the aneurysm Diagnosis ofrupture is best made with echocardiography Operative repair in-volves mattress closure of the defect buttressed with Teflon felt or aDacron patch

Left Ventricular Aneurysm

Left ventricular aneurysms affect between 10% and 35% of patientsfollowing an MI (Fig 19.17) Aneurysm formation occurs in 50% ofpatients by 48 hours following an MI Aneurysm formation isChapter 19 • Cardiovascular Disease and Cardiac Surgery 279

FIGURE 19.17 The pathophysiology of LV aneurysm formation A Area of infarction B True aneurysm.

C False aneurysm (From Kaiser LR, Kron IL, Spray TL, eds Mastery of Cardiothoracic Surgery Philadelphia:

Lippincott–Raven Publishers; 1998, with permission.)

thought to occur as a result of early infarct expansion and late

remodeling of the aneurysmal wall with scar Asymptomatic

pa-tients have an excellent prognosis following aneurysm formation

with a 90% 10-year survival Symptomatic patients have a much

poorer prognosis Angina related to underlying CAD and dyspnea

are the most common presenting symptoms Diagnosis can be made

using multiple diagnostic modalities ECGs frequently demonstrate

Q waves with persistent ST elevation Chest radiographs may

demonstrate LV enlargement (Fig 19.18) Echocardiography can

often detect a paradoxical bulge during systole of the aneurysm The

gold standard for diagnosis remains left ventriculography There are

no absolute indications for operative repair Symptomatic patients

with angina, congestive heart failure (CHF), or arrhythmias appear

to do better following repair Surgical intervention involves either

simple plication of the aneurysm, linear closure, or closure with a

Dacron patch In the absence of thrombus there is a low

throm-boembolic risk, 0.35%/patient-year, and therefore anticoagulation is

not required In the setting of large LV thrombus or diminished left

ventricular function long-term anticoagulation is recommended

Ischemic Mitral Regurgitation

MI or papillary muscle ischemia results in ischemic MR By

defini-tion the leaflets and subvalvular apparatus are normal in ischemic

MR The disease is a manifestation of postischemic myocardial

re-modeling The presentation may be acute and immediately

life-threatening or may present in a chronic fashion with an insidious

onset of heart failure The incidence of ischemic MR is between

17% and 55% following an MI, with up to 18% of patients having

evidence of MR within 6 hours of the onset of ischemia In many

patients, however, the MR is mild and may be transient and

im-prove over time The development of ischemic MR is dependent on

transmural involvement, location, and extent of infarction or

re-sultant papillary muscle ischemia, with posteroinferior MIs having

the highest likelihood of MR secondary to papillary muscle function Ruptured papillary muscles can lead to life-threateningacute MR, with the posterior papillary muscle involved three to sixtimes more commonly than the anterior Complete rupture usuallyoccurs within the first 7 days after MI but may be delayed by up to

dys-3 months The presentation of acute MR represents only 1% to 2%

of all cases of ischemic MR A murmur may be absent followingpapillary muscle rupture given the rapid equalization of pressurebetween the left atrium and ventricle Rapid diagnosis is essential tosurvival Patients usually present with acute chest pain and short-ness of breath and typically have a loud apical holosystolic murmurthat radiates to the left axilla Transesophageal echocardiography isthe diagnostic tool of choice and can document the degree of MR,wall motion abnormalities, and papillary muscle function Medicaltherapy includes afterload reduction with vasodilators and/or in-sertion of an IABP, although these patients often suffer from severecardiogenic shock that is unresponsive to either inotropic support

or therapy with an IABP Mitral valve replacement is associatedwith 10% to 40% mortality depending on comorbidities The natu-ral history of untreated papillary muscle rupture is death within 3

to 4 days, although patients with partial rupture may survive forweeks For patients with chronic ischemic MR, indications for op-eration include symptomatic coronary disease, severe MR (3⫹ or

4⫹), or significant LV dysfunction secondary to MR Surgical vention consists of either valve replacement or repair with potentialCABG for severe CAD

inter-Valvular Heart Disease

Aortic Stenosis

The majority of aortic stenosis (AS) within the United States is aresult of either degenerative or congenital AS, with rheumatic ASrepresenting a small subset Age-related degenerative AS is second-ary to protein and lipid infiltration of the aortic valve leaflet withsubsequent cellular infiltration and ultimately calcification Thisresults in increased valve stiffness and increasing valvular obstruc-tion Risk factors for calcific AS are the traditional risk factors foratherosclerosis, including hypertension, hypercholesterolemia, dia-betes, and smoking Calcified bicuspid AS is the most commonform of congenital aortic valve disease, with an incidence of 0.9%

to 2.0% of the general population The bicuspid structure of thevalve results in turbulent flow, which disrupts the valve resulting infibrosis and calcification Clinically evident stenosis is present bythe age of 50 to 60 Calcifications of bicuspid aortic valves occurmore commonly at the commisures and often extend to the valveannulus Rheumatic AS results in fusion of the aortic valve leafletsand subsequent narrowing of the outflow tract

Physiologically, as the valve area narrows, the left ventricle pertrophies (with resultant decreasing diastolic compliance) togenerate increased pressures for ventricular ejection, thereby main-taining cardiac output Over time, the left ventricle is no longer able

hy-to compensate for progressively decreasing valve area and ally begins to dilate, resulting in decreased cardiac output, in-creased pulmonary pressures, and heart failure Patients oftenremain asymptomatic until they develop one or more classic symp-toms associated with AS: syncope, angina, dyspnea/congestive heartfailure Most patients will become symptomatic at aortic valve areas

eventu-of 1.0 cm2(normal, 2.5 to 3.5 cm2; mild AS,⬎1.5 cm2; moderate

AS, 1.0 to 1.5 cm2; severe AS,⬍1.0 cm2; and critical AS,⬍0.7 cm2)

280 Section IV • Cardiovascular and Respiratory Systems

FIGURE 19.18 Chest radiograph demonstrating large ventricular

aneurysm (From Kaiser LR, Kron IL, Spray TL, eds Mastery of

Cardio-thoracic Surgery Philadelphia: Lippincott–Raven Publishers; 1998, with

permission.)

A weak arterial pulse that rises slowly (“parvus and tardus”) is

indicative of AS On auscultation a harsh systolic aortic murmur

and loud S4signifying the vigorous atrial contraction against the

noncompliant left ventricle are audible ECG is consistent with left

ventricular and atrial hypertrophy Echocardiography is helpful in

visualizing the aortic valve and measuring aortic valve area Cardiac

catheterization is required to assess pressure gradients and flow

across the aortic valve Indications for valve replacement are

symp-tomatic patients or asympsymp-tomatic patients with a valve area less

than 1.0 to 0.7 cm2depending on the clinical scenario AS patients

have increased risk of myocardial ischemia related to LV

hypertro-phy and are therefore at increased risk of sudden death (Fig 19.19)

Aortic Regurgitation

Aortic regurgitation/aortic insufficiency (AI) results from

inade-quate coaptation of the valve leaflets Inadeinade-quate coaptation allows

ejected blood to return to the LV during diastole, thereby increasing

diastolic stress and resulting in concentric LV hypertrophy Etiology

of AI includes rheumatic heart disease, dilatation of the aortic root,

aortic dissection, infective endocarditis, myxomatous

degenera-tion, bicuspid aortic valve, rheumatoid arthritis, and systemic lupus

erythematosus With acute AI the LV is unable to dilate to

accom-modate the large regurgitant flows, leading to a low cardiac output

state with elevated heart rate and diastolic ventricular pressures

Physical findings with AI vary depending on the duration of

symptoms For example, in acute AI the pulse pressure is not

widened, resulting in a lack of clinical symptoms A classic

“water-hammer pulse” is present with chronic AI Auscultation reveals a

prominent S3 and other symptoms of heart failure, including rales

Most patients with chronic AI remain asymptomatic for years

until there is an increase in the size of the regurgitant orifice

lead-ing to the onset of symptoms and heart failure The onset of

symp-toms is associated with nearly 60% to 70% of regurgitant stroke

volume to the left ventricle Echocardiography is the most helpful

diagnostic modality, since it allows for measurement of the

regur-gitant jet and left ventricular geometry and function

Asympto-matic patients may be followed with close observation and serial

echocardiograms until they experience symptoms or non-invasive

modalities demonstrate LV dilatation Patients with acute AI and

those with chronic disease and symptoms should undergo valve

replacement

Idiopathic Hypertrophic Subaortic Stenosis

Idiopathic hypertrophic subaortic stenosis (IHSS) is an cal, obstructive hypertrophic cardiomyopathy in which there isanatomic and physiologic obstruction of the left ventricular out-flow tract Pathologically, IHSS results in marked thickening of themiddle and upper ventricular septum Histologic examination re-veals an atypical whorled configuration of myocytes and connec-tive tissue elements described as myocardial disarray

asymmetri-Left ventricular outflow obstruction is dynamic, increasingwith decreased ventricular volume and the use of inotropes Pa-tients with IHSS can be asymptomatic or present with symptoms ofleft ventricular outflow tract obstruction (dyspnea, angina) or evensudden death On physical examination, a systolic murmur can beheard over the left sternal border ECG and chest radiographsdemonstrate LV hypertrophy Echocardiograms display variouspatterns of hypertrophy and mitral valve function Cardiaccatheterization provide pullback gradient measurements across theoutflow tract as well as coronary arteriograms

Usually, symptomatic patients can be treated nonsurgicallywith ␤-blockers and calcium channel blockers Operation is re-

served for patients with severe symptoms and resting or tive gradients despite maximal medical therapy Operativeintervention is also indicated in patients who have survived suddendeath episodes and have significant resting or provocative gradi-ents Surgical treatment of IHSS may involve left ventricular my-otomy and myomectomy or, in certain cases, elimination of systolicanterior motion of the mitral valve by mitral valve replacement orAlfieri repair of the mitral valve Modern innovations also includealcohol ablation of the hypertrophic septum by injection into thefirst septal perforator using percutaneous techniques and synchro-nized AV pacing to reduce dynamic outflow obstruction

provoca-Mitral Stenosis

Rheumatic heart disease is the most common cause of mitral sis (MS) In the United States and other developed countries, the in-cidence of MS has decreased dramatically Pathologic changesinclude commissural fusion, leaflet fibrosis, and chordal fusion andshortening With progression of disease and narrowing of the valvearea chronic pulmonary venous obstruction ensues with elevations

steno-of left atrial pressures, pulmonary hypertension, right ventricularenlargement, and congestive heart failure Classically, patients pres-ent with dypsnea (initially on exertion but eventually even at rest),orthopnea, paroxysmal nocturnal dyspnea, and fatigue Systemicthromboembolism may be the presenting symptom and occurs in

up to 20% of patients Auscultory findings include a presystolicmurmur, opening snap, and diastolic rumble Chest radiographyoften reveals left atrial enlargement and pulmonary congestion.Echocardiography is the primary means for assessing mitral valveanatomy and flow dynamics Symptomatic patients often have mi-tral valve areas of 1.5 to 2.0 cm2(normal, 4.0 to 6.0 cm2), whereasvalve areas of 1.0 cm2or less are associated with severe symptoms.Surgery is indicated for patients with hemodynamically significantvalve obstruction and New York Heart Association (NYHA) class III

to IV symptoms, onset of atrial fibrillation regardless of symptoms,increasing pulmonary hypertension, episodes of systemic emboliza-tion, or infective endocarditis Operative intervention consists ofmitral valve replacement (Fig 19.20) The choice of a mechanical ortissue valve depends on the age of the patient, the probability of

Chapter 19 • Cardiovascular Disease and Cardiac Surgery 281

FIGURE 19.19 The natural history of medically treated aortic

steno-sis (From Kaiser LR, Kron IL, Spray TL, eds Mastery of Cardiothoracic

Surgery 2nd ed Philadelphia: Lippincott–Raven Publishers; 2007, with

permission.)

long-term survival, and risks/desire of anticoagulation Mechanical

valves have good long-term durability but require life-long

antico-agulation Tissue valves often last between 10 and 14 years and

re-quire redo cardiac surgery and valve replacement at that point

Mitral Regurgitation

Mitral valve competence depends on the coordinated function of

the annulus, leaflets, chordae tendineae, papillary muscles, left

atrium, and left ventricle Dysfunction of any of these components

can result in MR The most common etiology of MR is

myxoma-tous degeneration Other causes include ischemic heart disease,

di-lated cardiomyopathy, rheumatic heart disease, mitral annular

calcification (MAC), endocarditis, chordal rupture, and collagen

vascular disorders

Clinically, left atrial pressures are elevated secondary to

regur-gitant blood flow Progressive disease results in pulmonary venous

obstruction, pulmonary hypertension, and right heart failure

Ad-ditionally, the left ventricle is chronically subjected to volume

over-load, resulting in left ventricular dilatation and left heart failure

Patients may remain asymptomatic for years until the heart is no

longer able to compensate Symptoms occur when the regurgitant

volume approaches 50% and can include dyspnea, weakness,

fa-tigue, and palpitations Physical examination reveals an apical

pan-systolic murmur and S3 gallop Patients often will have atrial

fibrillation secondary to atrial dilatation Operative intervention is

recommended for symptomatic patients with compromise of their

lifestyle and for asymptomatic patients with progression of

pul-monary hypertension, atrial fibrillation, or LV dilatation Any

pa-tient with acute MR should undergo an urgent operation The type

of operation performed is dependent on surgical expertise and

patient comorbidities Operative strategies include complex mitral

valve repair, replacement, and, in rare cases, commissurotomy(Figs 19.21 and 19.22)

Tricuspid and Pulmonic Valves

Tricuspid regurgitation commonly occurs in the setting of heartfailure with annular dilatation Rheumatic heart disease can affectthe tricuspid valve, thereby leading to tricuspid stenosis and/or re-gurgitation Acquired pulmonary valve disease is rare, althoughrheumatic involvement can occur Valve fibrosis secondary to carci-noid syndrome most commonly affects right-sided valves

Infective Endocarditis

Infection of the heart most commonly affects the valves ing factors for development of infective endocarditis include previ-ous congenital or acquired cardiac lesions, immunocompromisedstatus, IV catheters, and IV drug abuse Gram-positive organisms

Predispos-are the most common cause of bacterial endocarditis (i.e., coccus viridans, Staphylococcus aureus, and Staphylococcus epider- mis), although gram-negative bacteria, fungi, and viruses can also

Strepto-result in endocarditis

Classic presenting symptoms of endocarditis include fever,weakness, night sweats, and anorexia Physical examination com-monly reveals a cardiac murmur, splinter hemorrhages, Osler nodes,Janeway lesions, and Roth spots Persistent bacteremia results in pos-itive blood cultures in 85% to 95% Echocardiography, eithertransthoracic or transesophageal, can provide visualization of result-ant valvular vegetations Medical management with appropriate IVantibiotics is the treatment of choice and is often successful in clear-ing the bacteremia and vegetation Valve replacement is reserved forprosthetic valve endocarditis, failure of medical management, life-threatening emboli, severe valvular insufficiency or obstruction, andcongestive heart failure Localized mitral valve endocarditis can occa-sionally be treated with partial leaflet resection and valve repair

Heart Failure

Heart failure is a major global health concern It is estimated thatthere are 5 million cases of congestive heart failure in the UnitedStates alone, with 550,000 new cases diagnosed each year The majorcause of heart failure is ischemia, with idiopathic dilated cardiomy-opathy being the second leading cause The majority of these pa-tients are medically managed with angiotensin-converting enzyme(ACE) inhibitors,␤-blockers, and diuresis to optimize preload, af-

terload, and contractility Medical management has been shown tohave beneficial effects on ventricular remodeling Percutaneous andsurgical interventions allow optimization of myocardial function byrevascularization, mitral valve repair, resynchronization therapywith biventricular pacemakers, myocardial reconstruction, and pas-sive ventricular restraint devices Mechanical ventricular restraintsand surgical resections have attempted to restore myocardial effi-ciency and function by restoring ventricular geometry and prevent-ing the progression of adverse ventricular remodeling One suchmechanical ventricular restraint is the Acorn Cardiac Support De-vice This polyester mesh fabric cradle maintains ventricular confor-mation, reduces dilatation, and diminishes wall stress Surgicalresections, such as the Dor procedure, have attempted to restoreventricular geometry and resect nonviable myocardium that hin-ders normal, efficient myocardial contractility Multiple studies havereported variable success from improvements in left ventricularfunction and geometry following these reconstructive procedures

282 Section IV • Cardiovascular and Respiratory Systems

FIGURE 19.20 Conventional mitral valve replacement with complete

excision of the leaftlets and the entire subvalvular apparatus The mitral

prosthesis is implanted using a series of horizontal mattress sutures

(From Kaiser LR, Kron IL, Spray TL, eds Mastery of Cardiothoracic

Surgery 2nd ed Philadelphia: Lippincott–Raven Publishers; 2007, with

permission.)

right atria, aorta, and PA (Fig 19.23) Newer techniques utilize caval anastomosis (SVC and IVC, left atrium, aortic, and PA anasto-mosis) in an attempt to diminish tricuspid regurgitation and theneed for pacemakers (Fig 19.24) Long-term survival is institutionspecific, but can approach 90% at 1 year and 85% at 5 years Long-term graft failure is most often secondary to accelerated coronaryartery atherosclerotic disease.

bi-Chapter 19 • Cardiovascular Disease and Cardiac Surgery 283

C

FIGURE 19.21 Technique of mitral ring annuloplasty A Placement of

annular sutures.B Placement of sutures on the annular ring prosthesis.

C Completed ring annuloplasty (From Kaiser LR, Kron IL, Spray TL, eds.

Mastery of Cardiothoracic Surgery Philadelphia: Lippincott–Raven

Publish-ers; 1998, with permission.)

FIGURE 19.22 Quadrangular resection of the

posterior mitral valve leaflet and mitral valveannuloplasty for mitral valve prolapse The freeedges of the resected margin are reapproxi-mated in the midline and the posterior valve issutured to the annulus (From Kaiser LR, Kron

IL, Spray TL, eds Mastery of Cardiothoracic Surgery Philadelphia: Lippincott–Raven Pub-

lishers; 1998, with permission.)

Orthotopic heart transplant remains the gold standard and

de-finitive therapy for end-stage heart failure Unfortunately, access to

heart transplantation is limited by the shortage of available donor

hearts, with only about 2,400 heart donors annually Therefore,

careful selection criteria and rational allocation of the organs have

been developed Traditionally heart transplants were performed in

a biatrial fashion with anastomoses performed between left and

Given the limited number of donor hearts available for

trans-plantation, a great deal of interest has developed in mechanical

as-sist devices and totally artificial hearts At present, mechanical

cardiac assistance can be utilized either as a bridge to

transplanta-tion or as destinatransplanta-tion therapy The longevity of mechanical devices

is currently limited, thereby necessitating the need for either device

replacement, transplantation, or end-of-life decisions

Cardiac Neoplasms

Neoplasms of the heart are either primary cardiac tumors or

metastatic tumors Seventy-five percent of primary cardiac tumors

are benign with the half of these being myxomas, while 75% of

ma-lignant primary cardiac tumors are sarcomas Cardiac myxomas

occur roughly twice as frequently in women than in men, with a

peak incidence between the third and sixth decades of life

Seventy-five percent of myxomas occur in the left atrium, with 5%

demon-strating an autosomal dominant pattern of inheritance

Atrial myxomas generally arise from the interatrial septum, but

have been demonstrated to arise from heart valves and vasculature

They appear as round, smooth tumors with a lobulated surface

Most of these lesions are asymptomatic and are incidentally

discov-ered by echocardiography or computed tomography Symptoms

can include malaise, valve orifice obstruction, or embolism

Myxomas should be resected once discovered Newer minimally vasive approaches have allowed for resection with small incisionsand rapid recovery (Fig 19.25)

in-Primary malignant tumors of the heart include angiosarcoma,malignant fibrous histiocytoma, and rhabdomyosarcoma Theseaggressive tumors grow rapidly and invade surrounding structures.Metastatic lesions are present in 80% of all cases The long-termprognosis is poor with median survival less than 1 year followingresection Primary malignancies that can metastasize to the heartinclude bronchogenic carcinoma, melanoma, leukemia, lym-phoma, and carcinoma of the breast

284 Section IV • Cardiovascular and Respiratory Systems

FIGURE 19.23 Orthotopic implantation of a cardiac allograft The

aortic anastamosis is being completed (From Kaiser LR, Kron IL,

Spray TL, eds Mastery of Cardiothoracic Surgery Philadelphia:

Lippincott–Raven Publishers; 1998, with permission.)

FIGURE 19.24 Bicaval orthotopic heart transplant starts with the left

atrial anastomosis (From Kaiser LR, Kron IL, Spray TL, eds Mastery of Cardiothoracic Surgery 2nd ed Philadelphia: Lippincott–Raven Pub-

lishers; 2007, with permission.)

FIGURE 19.25 Gross pathologic appearance of this myxoma, which

consists of large, mottled-tan hemorrhagic tissue, somewhat gelatinousand myxoid, measuring 6 cm in maximal dimension (From Kaiser LR,

Kron IL, Spray TL, eds Mastery of Cardiothoracic Surgery 2nd ed.

Philadelphia: Lippincott–Raven Publishers; 2007, with permission.)

Thoracic Aortic Disease

Aortic Dissection

Aortic dissection occurs three times as frequently as rupture of the

abdominal aorta Up to 40% of patients suffering from an acute

aor-tic dissection die immediately Fifty percent of patients with an acute

type A dissection die within 48 hours There are roughly 2,000 new

cases of aortic dissection diagnosed in the United States annually

Aortic dissections arise from an intimal disruption that permits

blood to form a plane of separation within the media of the aortic

wall, creating a false lumen Patients with connective tissue disorders,

i.e., Marfan disease, undergo cystic medial necrosis related to a tissue

factor defect as the inciting event for dissection Iatrogenic causes,

i.e., catheterization and cannulation, are also potential causes of

aor-tic dissection Dissection of the aorta has been linked to bicuspid

aortic valve, hypertension, and AS Dissections are classified as either

acute (⬍2 weeks) or chronic (⬎2 weeks) By the Stanford

classifica-tion system type A dissecclassifica-tions involve the ascending aorta and

classi-cally propagate to the arch and descending aorta, whereas type B

dissections involve only the descending aorta (Fig 19.26) Type A

dissections are usually located in the right anterior aspect of the aortafrom which they extend to involve the ascending aorta, arch, and de-scending aorta Retrograde propagation can also occur whereby thecoronary ostia are involved, resulting in myocardial ischemia and in-farction Type B dissections begin distal to the left subclavian arteryorigin and involve the descending thoracic and abdominal aorta.Aortic dissection should always be considered in patients withsevere, unrelenting chest or back pain that is described as ripping ortearing Pain is usually mid-sternal for ascending dissections andmid-back for descending dissections Findings may also includesigns of malperfusion to the brain, viscera, limbs, or heart Perfusion

to end organs will be maintained as long as flow to the major lature remains patent through a true (native) or false (new, artificial)lumen Malperfusion will occur with occlusion of aortic branchessecondary to dissection Hypotension and tachycardia can be signs

vascu-of free rupture, pericardial tamponade, acute aortic insufficiency, ormyocardial ischemia and should be immediately investigated.ECG findings consistent with acute ischemia will be present ifthe dissection involves the coronary ostia with resultant limitation

of coronary perfusion The classic finding of a widened tinum by chest x-ray should prompt further investigation, but thisfinding is not necessarily always present Diagnosis is established byeither high-resolution computed tomography or transesophagealechocardiography Magnetic resonance imaging, intravascular ul-trasound, and aortography are second-line modalities for diagno-sis Initial management involves tight blood pressure control withthe goal of minimizing the change in pressure over the change intime (⌬P/⌬t) thereby reducing aortic wall stress Acute type A dis-sections mandate immediate operative treatment given the highrate of mortality Acute type B dissections are initially treated med-ically with control of hypertension unless there is evidence of aorticrupture into the left chest or severe major organ or limb ischemiafrom aortic branch obstruction

medis-The indications for surgical repair of chronic dissections differ.Type A dissections that are not recognized acutely are repaired toprevent late development of aortic insufficiency and congestive heartfailure or aneurysmal dilation of the ascending aorta exceeding 5 cm.Chronic type B dissections are repaired for aneurysmal dilation ofthe descending aorta greater than 6 cm or end-organ malperfusion.The goal of surgical repair is to replace the segment of aortacontaining the intimal tear with a prosthetic graft while maintain-ing or restoring perfusion of the heart, carotid and subclavian ar-teries, spine, and lower body In acute type A dissections, aorticreplacement is limited to the ascending aorta and proximal aorticarch, even when the dissection extends distally This procedure ef-fectively eliminates the causes of death related to type A dissectionwithout exposing the patient to the morbidity of replacement ofthe entire aorta Lifetime follow-up with serial cross-sectional im-aging is necessary to identify and follow the development ofaneurysmal dilation of the remaining dissected aorta

Thoracic Aortic Aneurysm

Aneurysm is defined as dilatation of a vessel by 50% or more of thenormal diameter Patients with connective tissue disorders and in-herent vascular wall abnormalities have a greatly increased predis-position to aneurysm formation The incidence of thoracic aorticaneurysms are estimated to be roughly 5.9/100,000 person-years.Risk of rupture is directly proportional to the size of the aneurysm.For the scope of this discussion, thoracic aneurysms will be

Chapter 19 • Cardiovascular Disease and Cardiac Surgery 285

Intimaltear

Intimal tear

FIGURE 19.26 The Stanford classification of aortic dissections (From

Kaiser LR, Kron IL, Spray TL, eds Mastery of Cardiothoracic Surgery.

Philadelphia: Lippincott–Raven Publishers; 1998, with permission.)

286 Section IV • Cardiovascular and Respiratory Systems

Left subclavian artery

Crawford I Aorta

Celiac artery Diaphragm Renal artery Superior mesenteric artery

A

Left subclavian artery

Crawford II Aorta

Celiac artery Diaphragm Renal artery

Superior mesenteric artery

B

Left subclavian artery

Crawford III Aorta

Celiac artery Diaphragm Renal artery Superior mesenteric artery

C

Left subclavian artery

Crawford IV Aorta

Celiac artery Diaphragm Renal artery Superior mesenteric artery

D FIGURE 19.27 Crawford classification of thoracoabdominal aneurysms (From Kaiser LR, Kron IL, Spray TL,

eds Mastery of Cardiothoracic Surgery Philadelphia: Lippincott–Raven Publishers; 1998, with permission.)

Chapter 19 • Cardiovascular Disease and Cardiac Surgery 287

classified as ascending aortic aneurysms, aortic arch aneurysms, or

descending thoracic and thoracoabdominal aneurysms

Ascending aortic aneurysms are most often asymptomatic but

occasionally can present with chest pain These aneurysms are often

found incidentally On physical examination a clinician may detect a

diastolic murmur or widened pulse pressure that indicates aortic

in-sufficiency secondary to dilatation of the aortic root A chest x-ray

may reveal a widened mediastinum, thereby raising concern for an

ascending aortic aneurysm or dissection Concern of an aneurysm

warrants further diagnostic workup Classically, this consisted of an

aortogram to define the aneurysm and relation of the great vessels

This has now been replaced by high-resolution helical CT with

con-trast, MRI, or transesophageal echocardiography CT is the imaging

study of choice given its ability to evaluate the entire aorta,

dissec-tions, and mural thrombus Unfortunately, CT is contraindicated in

patients with renal insufficiency Emergent repair is indicated with

rupture, impending rupture, or concomitant dissection

Sympto-matic aneurysms, valvular dysfunction, an aortic diameter greater

than 5 cm, or growth greater than 1 cm/y warrant elective repair

There are many choices for repair including simple tube-graft

re-placement, composite valve-graft conduit, or valve-sparing

opera-tions with or without aortic root replacement Smaller aneurysms

should be closely monitored for progression of disease

Aortic arch aneurysms have a pathophysiology similar to that of

isolated ascending aortic aneurysms However, involvement of the

aortic arch branch vessels carries an increasingly greater risk with

operative repair Therefore, elective repair for arch aneurysms is

re-served for patients with aortic diameters greater than 6 cm, saccular

aneurysms, or asymmetric aneurysms Repair of arch aneurysms

re-quires a period of deep hypothermic circulatory arrest, in which the

core body temperature is cooled to 10oC and circulatory flow is

tem-porarily arrested to allow repair The procedure involves resection of

the aneurismal aorta, leaving behind a patch(es) containing the arch

vessels, and replacement of the diseased vessel with a synthetic graft

to which the arch vessels are incorporated Cerebral protection is

achieved either by isolated hypothermia alone or by antegrade

and/or retrograde perfusion of cold blood

Thoracoabdominal aneurysms are traditionally classified

ac-cording to the Crawford Classification System By this system type I

aneurysms are isolated to the thoracic aorta, and type II–IV involve

varying portions of the thoracic and abdominal aorta (Fig 19.27)

As compared to ascending aortic aneurysms, roughly 50% of

pa-tients are symptomatic at the time of diagnosis of

thoracoabdomi-nal aneurysms Diagnosis can be made with CT, MRI, or rarely

aortogram Repair of thoracoabdominal aneurysms carries a high

morbidity, and for this reason surgical intervention is reserved for

aneurysms greater than 6 cm All symptomatic aneurysms should be

repaired, regardless of size Thoracoabdominal aneurysms are

tradi-tionally repaired utilizing a prosthetic tube graft Circulatory

man-agement consists of partial CPB (left atrium to femoral artery) or a

shunt to provide blood flow to the viscera and lower extremities

during cross-clamping and repair The major morbidity associated

with this procedure is spinal cord ischemia resulting in paralysis In

addition, pulmonary insufficiency is also commonly seen following

this procedure The clamp and sew technique, the original repair

strategy, was associated with a high rate of spinal cord ischemia To

minimize spinal cord ischemia all large intercostal arteries should

be preserved to maximize perfusion to the spinal cord

Intraopera-tive management includes utilization of a lumbar drain to maximize

perfusion pressure to the spinal cord Postoperatively, perfusion

pressure should be maintained by increasing mean arterial pressureand decreasing spinal cord pressure

Endovascular Repair of Aortic Aneurysms

Endovascular repair of thoracic aortic aneurysms is a direct ment of endovascular technology for repairing infrarenal AAA Thusfar, endovascular stent grafts are utilized for repair of thoracic aorticaneurysms that are distal to the left subclavian artery and proximal tothe visceral segment (Fig 19.28) As with open repair, there is a highincidence of spinal cord ischemia and paralysis, which mandatesclose postoperative monitoring, with or without a spinal drain In thehigh-risk patients, morbidity and mortality are markedly improvedfollowing endovascular thoracic aortic repair as compared with tra-ditional open repair Additionally, endovascular stent grafts havebeen used in the setting of isolated type B dissections and in combi-nation with type A dissections to stent the descending thoracic aorta.Thus far, this modality is limited to segments of aorta without criticalbranches Strategies to overcome this shortcoming have involvedperforming bypass procedures to allow for coverage of the orifice of adesired vessel (i.e., left carotid to subclavian artery bypass; bypassgrafts to visceral vessels, also known as debranching) Newer experi-mental technologies are attempting to utilize fenestrated endografts

develop-to incorporate segments of aorta involving either the arch vessels orvisceral and renal arteries

CARDIOVASCULAR DEVICES Intra-Aortic Balloon Pumps

A failing heart can benefit from both decreased myocardial work aswell as increased perfusion An IABP can help satisfy these needs(Fig 19.29) The IABP is positioned in the descending thoracicaorta just below the left subclavian artery takeoff The IABP istimed to inflate during diastole This allows for increased retro-grade flow of aortic blood through the coronary ostia, enhancing

FIGURE 19.28 A CT angiogram demonstrating a thoracoabdominal aortic aneurysm, preoperative B CT angiogram following placement

of a thoracic endovascular stent graft, demonstrating successful sion of the aneurysm

exclu-coronary perfusion During systole the IABP deflates, allowing

in-creased empty space This allows a decrease in afterload and

thereby a decrease in myocardial work This results in a diminished

myocardial oxygen demand and consumption IABP utilization can

provide significant myocardial support when utilized properly

Un-fortunately, IABP utilization can carry significant risk, namely,

ex-acerbation of aortic insufficiency, lower extremity malperfusion,

aortic dissection, or embolic disease IABP is good treatment for

288 Section IV • Cardiovascular and Respiratory Systems

FIGURE 19.30 Intraoperative picture

fol-lowing placement of both left (LVAD) and

right ventricular assist devices (RVAD)

(Thoratec paracorporealventricular assist

devices) Arrows indicate in- and outflow

cannulas

left heart dysfunction but unfortunately affords little benefit intreating isolated right ventricular failure

Mechanical Ventricular Assistance

Mechanical ventricular assistance has developed over the past eral years to serve as either a bridge to transplantation or as long-term destination therapy to prolong survival of patients inclinically significant heart failure The Randomized Evaluation ofMechanical Assistance of the Treatment of Congestive Heart Fail-ure (REMATCH) study demonstrated a significant improvement in2-year survival with implantation of a left ventricular assist device(LVAD) as destination therapy when compared to medical manage-ment alone Early ventricular assist devices (VADs) were pulsatileflow systems that mimicked the ejection of blood witnessed withthe human heart Newer and smaller devices have utilized continu-ous flow by either axial or centrifugal rotors to generate non-pulsatile flow There is significant debate over whether pulsatility

sev-is superior to continuous nonpulsatile flow While VADs provideassistance and flow in addition to the mechanical activity of theheart, implantable total artificial hearts replace an existing heartwith a mechanical device, which provides the entirety of inotropicactivity (Fig 19.30)

FIGURE 19.29 Snapshot of electronic display from an intra-aortic

balloon pump set to augment blood flow on every other cardiac cycle

(1:2 augmentation)

SUGGESTEDREADINGS

Cohn LH, ed Cardiac Surgery in the Adult 3rd ed New York:

McGraw-Hill; 2008

Kaiser LR, Kron IL, Spray TL, eds Mastery of Cardiothoracic Surgery.

2nd ed Philadelphia: Lippincott Williams & Wilkins; 2008

Sellke FW, del Nido PJ, Swanson SJ, eds Sabiston & Spencer Sugery

of the Chest 7th ed Philadelphia: Elsevier WB Saunders; 2005.

• Atherosclerosis is responsible for the vast majority of

vascular diseases Nonmodifiable risk factors include vanced age, family history, and genetic disorders Modifi-able risk factors include hyperlipidemia, hypertension,diabetes mellitus, smoking, and obesity

ad-• Stroke resulting from cerebrovascular disease is the third

leading cause of death in the United States Diagnosis ofcarotid artery disease is best accomplished with a combi-nation of duplex ultrasonography and magnetic resonanceangiography Carotid endarterectomy is of proven benefit

in patients with symptomatic carotid stenosis and selectpatients with asymptomatic stenosis Endovascular therapywith angioplasty and stenting is emerging as valid option

in high-risk patients

• Arterial occlusive disease can affect any portion of the

arte-rial vascular tree, but is most common in the aortoiliac,femoropopliteal, and tibioperoneal circulations Initial treat-ment is conservative, though revascularization is indicatedfor patients with crippling claudication or critical limb is-chemia Bypass grafting is the traditional option, though en-dovascular angioplasty with or without stenting is rapidlyemerging as a viable alternative Acute limb ischemia is lifethreatening, and revascularization should be undertakenpromptly

• Aneurysms of the aorta, iliac arteries, visceral arteries, and

peripheral arteries remain a major cause of morbidity andmortality The majority of these aneurysms are caused by

atherosclerosis The main risks are bleeding and death due

to rupture or acute ischemia due to embolization orthrombosis The diagnosis and treatment of aneurysms ineach of these locations is unique Endovascular aneurysmrepair is rapidly changing the practice of vascular surgery

• Renal artery stenosis accounts for 5% to 10% of all cases ofhypertension These lesions can result from atherosclerosis

or fibromuscular dysplasia Revascularization can typically beaccomplished with endovascular angioplasty and stenting,though ostial lesions may require bypass or endarterectomy

• TOS can cause neurologic, arterial, or venous symptoms bycompression of the brachial plexus, subclavian artery, orsubclavian vein Neurologic TOS should be approachedcautiously, as symptoms may not improve after surgery.Arterial and venous symptoms from TOS should promptsurgical resection of the compressing structure (either acervical rib or a hypertrophied scalene muscle)

• Diagnosis of acute or chronic mesenteric ischemia requires

a high degree of suspicion, and early intervention can belifesaving Surgical treatment involves resection of nonviablebowel and revascularization of the remaining intestine

• DVT is common in surgical patients but can usually beavoided by appropriate prophylactic measures (sequentialcompression devices, subcutaneous heparin) Treatment in-volves anticoagulation and close monitoring for complica-tions When anticoagulation fails or is contraindicated,insertion of an inferior vena cava filter dramatically decreasesthe incidence of pulmonary embolism Venous insufficiencymay result from severe DVTs or inadequate anticoagulation

ascular diseases are epidemic in the western world andaccount for more morbidity and mortality than any othercategory of human disease By far the most common cause ofvascular disease is atherosclerosis, though many other vascular disor-

ders cause significant human disease This chapter will discuss

vascu-lar anatomy, the pathogenesis of atherosclerosis, atherosclerotic

vascular diseases and their management, and other vascular

pathol-ogy relevant to surgical practice

VASCULAR ANATOMY

All blood vessel walls consist of three layers: the tunica intima,

tu-nica media, and tutu-nica adventitia (Fig 20.1) Arteries have thicker

walls and a higher wall thickness-to-lumen diameter ratio than

V veins Arteries are a high-pressure, low-volume system, while theconverse is true of veins

The tunica intima lines the luminal surface of the vessel wall and is composed of a thin layer of endothelial cells overlyingsubendothelial connective tissue Through the release of vasoactivemediators, anti-inflammatory cytokines, and antithrombotic agents,endothelial cells modulate vascular tone and blood flow and play anintegral role in hemostasis, coagulation, and inflammation The tu-nica media layer is the muscular layer of the vessel wall comprisingsmooth muscle cells It is separated from the tunica intima by the in-ternal elastic lamina, which is well developed to withstand the higherpressure in the arterial system The media is demarcated from theadventitial layer by the external elastic lamina The tunica adventitia

is a collection of adipose and other supportive connective tissue The

290 Section IV • Cardiovascular and Respiratory Systems

vaso vasorum, a collection of feeding vessels only present in large

ves-sels, is contained in the adventitia and functions as the blood supply

of the vessel wall

Arteries are classified as elastic, distributing, or small Elastic

arteries are the largest and consist of the aorta and its largest

branches, such as the brachiocephalic, common carotid, and

com-mon iliac arteries Distributing arteries are the second largest and

are exemplified by the coronary, renal, and hepatic arteries The

small arteries are contained within the substance of organs and

tis-sues Arterioles are the smallest arteries and their primary function

is to control tissue blood flow and systemic arterial pressure

Capil-laries are the smallest vessels, typically about the diameter of a

sin-gle red blood cell In tissues, they are the primary site for exchange

of oxygen, nutrients, and waste

Lymphatics are small, thin walled structures with an

endothe-lial lining These channels function as conduits, which carry

extra-cellular fluids centrally away from tissues for processing in the

lymph nodes and eventual return to the vascular system

RISK FACTORS FOR ATHEROSCLEROSIS

Risk factors for atherosclerosis can be classified as nonmodifiable

and modifiable Age, gender, family history, and genetic

predisposi-tions are nonmodifiable risk factors Modifiable risk factors are

de-scribed as follows:

Hyperlipidemia

Hypercholesterolemia is a major risk factor for atherosclerosis Of

particular importance is the level of low-density cholesterol, or

low-density lipoproteins (LDLs) LDLs undergo oxidative

modifi-cation in the bloodstream The oxidized end products (oxLDL)

then function as inflammatory mediators oxLDL induces adhesion

molecule expression by endothelial cells and is a potent

macrophage chemokine, promoting its migration into the tunica

intima High-density cholesterol, or high-density lipoproteins

(HDLs), another component of the total cholesterol level, also plays

a key role HDL exerts a protective effect against atherosclerosis

be-cause HDL is involved in transporting cholesterol away from the

periphery to the liver for processing and excretion

Hypertension

Hypertension promotes atherogenesis via multiple pathways First,

chronic elevation of blood pressure causes endothelial damage, which

incites atherogenic inflammatory pathways Second, patients with

hypertension have elevated levels of angiotensin II (AT II), a potentvasoconstrictor AT II promotes the production of superoxide anions

by endothelial cells and vascular smooth muscle cells Additionally,

AT II induces the secretion of proinflammatory cytokines fromsmooth muscle cells These two mechanisms function synergistically

to cause endothelial injury and promote the ensuing inflammatoryresponse, leading to atherosclerotic plaque development

Diabetes Mellitus

Diabetes is associated with a twofold increase in myocardial tion and an 8- to 15-fold increase in gangrene of the lower extremi-ties Diabetic patients have impaired vasodilation due to dysfunction

infarc-of endothelial nitric oxide synthase and increased production infarc-of dothelin-1, a potent vasoconstrictor Platelet hyperactivity due to anincreased number of glycoprotein IIb–IIIa receptors also contributes

en-to decreased microvascular blood flow Additionally, hyperglycemiaresults in the formation of reactive oxygen species and advanced gly-cation endproducts (AGEs), which promote inflammatory pathways

Smoking

Smoking a pack or more of cigarettes per day increases the deathrate from ischemic heart disease by up to 200% Cessation of smok-ing approximately halves this increased risk

CEREBROVASCULAR DISEASE

Stroke is the third leading cause of death in the United States behindheart disease and cancer Ischemic strokes occur most commonly inthe distribution of the carotid arteries, which carry approximately

FIGURE 20.1 Structure of the vascular wall (From Robbins SL.

Pathologic Basis of Disease 6th ed Philadelphia: WB Saunders;

1999:494, with permission.)

Chapter 20 • Vascular Disease and Vascular Surgery 291

85% of the blood flow to the brain Ischemic events, classified on the

basis of their duration, are separated into transient ischemic attacks

(TIAs;⬍24 hours), reversible ischemic neurologic deficits (RINDs;

24 hours to 3 days), and completed strokes (longer than 3 days)

Pathophysiology

Carotid artery disease, except that related to trauma, almost always

occurs as a result of atherosclerosis Cerebral ischemia occurs most

commonly due to embolization rather than thrombosis The most

common source of emboli is the internal carotid artery, followed by

cardiac emboli Ischemia can also occur as a result of a low-flow

state through a severely stenotic lesion

Risk Factors

Previously described risk factors for atherosclerosis, such as

hyper-lipidemia, smoking, diabetes, and hypertension also contribute to

the development of carotid stenosis

Diagnosis

A detailed history and physical examination will often point toward

carotid stenosis Presence of multiple risk factors or a reported

his-tory of TIAs, RINDs, stroke, or amaurosis fugax should raise the

level of suspicion The only objective physical finding may be a

carotid bruit The North American Symptomatic Carotid

En-darterectomy Trial (NASCET) found that carotid bruit is only 63%

sensitive and 61% specific for high-grade carotid stenosis

Contrast angiography is the criterion standard test for carotid

stenosis It allows for visualization of the entire carotid artery

circu-lation as well as the vertebrobasilar circucircu-lations In addition it

pro-vides detailed information about plaque structure, ulceration, and

dissection This invasive test historically carries a 4% risk of

neuro-logic complications and a 1% risk of major stroke or death Use of

contrast dye also limits the use of this modality in patients with

renal insufficiency and/or severe iodine allergy

FIGURE 20.2 Plaque in atherosclerosis (From

Benditt EP, Schwartz SM Blood vessels In: Rubin

E, Farber JL, eds Pathology 2nd ed Philadelphia:

J.B Lippincott; 1994:472, with permission.)

The most commonly used test is carotid artery duplex sonography (CDUS) Duplex ultrasonography estimates the degree

ultra-of stenosis on the basis ultra-of flow velocity While CDUS is an excellenttest for extracranial carotid stenosis due to high sensitivity and speci-ficity, it does have limitations It is not as precise with stenoses greaterthan 50% and cannot reliably distinguish very high-grade stenosesfrom occlusions Additionally, CDUS cannot be used to evaluate in-tracranial portions of the carotid artery system Finally, performance

of the test requires experience, and is therefore operator dependent.MRA and computed tomographic angiography (CTA) are beingused more frequently to diagnose carotid stenoses Advantages ofthese tests include high-fidelity image generation and the capability

to visualize the entire carotid circulation However, evidence showsthat CT contrast dye, and more recently gadolinium used for MRA,may have deleterious effects in patients with renal insufficiency Ad-ditionally, MRA cannot be used in patients with metallic implantsand is not advisable in critically ill or claustrophobic patients

We recommend CDUS as a screening test and MRA as a matory adjunct to evaluate patients for carotid artery stenosis Un-less a percutaneous intervention is planned, angiography should bereserved for cases of complex or equivocal findings

confir-Treatment

Prevention is the best therapy Elimination or treatment of able risk factors can significantly decrease the incidence and pro-gression of carotid stenosis Multiple large prospective clinical trialshave demonstrated a significant reduction in the incidence ofstroke with CEA as opposed to medical therapy in patients withsymptomatic carotid stenosis and select patients with asympto-matic carotid stenosis

Shoulder

Lipid-ladenmacrophageElastic media

292 Section IV • Cardiovascular and Respiratory Systems

Neurology guidelines on CEA suggest that a low dose of 81 to 325

mg daily be used prior to and after CEA As outlined in the

follow-ing sections, medical therapy is reserved for those with (a)

sympto-matic disease and less than 50% stenosis, (b) asymptosympto-matic disease

and less than 60% stenosis, and (c) patients whose risk of surgical

complications outweighs the potential benefits of CEA

Patient Selection

For symptomatic patients, stenosis greater than 70% should prompt

CEA Symptomatic patients with stenoses from 50% to 69% have an

approximately 5% annual risk reduction with CEA Because their risk

is less than those with higher-grade stenoses, these patients should be

considered for CEA if they are low-risk surgical candidates

For asymptomatic patients with a surgical complication risk less

than 3% (low risk), those with greater than 60% stenosis should be

considered for CEA In asymptomatic patients with 3% to 5% surgical

risk, there is no proven benefit to performing CEA, however, it is

ac-ceptable to perform CEA in patients with greater than 75% stenosis

Urgent/emergent CEA (within 2 weeks) should be performed

for patients with severe stenosis and recent or crescendo symptoms

The traditional recommendation was to wait 4 to 6 weeks after a

completed stroke to perform CEA; however, this recommendation

is not supported by high-level evidence

Surgical Therapy

CEA can be performed under local anesthesia with frequent

neurologic checks or under general anesthesia using continuous

electroencephalographic (EEG) monitoring If the neurologic

examination or EEG changes after clamping of the artery, a

tempo-rary shunt should be used to provide continuous ipsilateral blood

flow while the artery is clamped If general anesthesia is used

with-out EEG monitoring, a shunt should be used if the internal carotid

artery stump pressure is less than 50 mm Hg

Complications

The most dreaded complication of CEA is stroke This can be

avoided with meticulous intraoperative technique and prompt

re-exploration if the patient develops an acute postoperative neurologic

deficit Myocardial infarction is a common complication in patients

undergoing CEA due to the clustering of atherosclerotic diseases in

this population Postoperative hypertension is due to manipulation

of the carotid body and occurs in 20% of patients Hypertension puts

this population of patients at particularly high risk of intracranial

hemorrhage due to vasoplegia induced by a longstanding low-flow

state preoperatively Therefore, postoperative hypertension and/or

headache should be aggressively treated with an intravenous infusion

of a vasodilator such as nicardipine or nitroprusside Cranial nerve

injury is another complication of CEA The vagus nerve (CN X) is

the nerve most commonly traumatized during CEA This injury is

due to inadvertent clamping or stretching of the nerve and results in

hoarseness and increased risk of postoperative aspiration Injury to

the hypoglossal nerve (CN XII) results in tongue deviation to the side

of the injury, as well as speech and mastication difficulties This often

occurs due to retraction and is temporary

Endovascular Therapy

Percutaneous angioplasty with stenting has become an option in

the treatment algorithm for carotid stenosis Because of a steep

procedural learning curve and evolving device technology, plasty and stenting is currently only an option for patients at highrisk for surgical complications, though this is likely to change in thenear future Currently the ideal candidate for carotid stenting is thepatient with severe recurrent stenosis following previous CEA

angio-ARTERIAL OCCLUSIVE DISEASE

Arterial occlusive disease affects roughly 5% of the population 55

to 74 years of age It can affect the upper extremity, the aortoiliaccirculation, the viscera, and the lower extremity Occlusive arterialdisease in these areas is primarily related to atherosclerosis Thissection will discuss occlusive disease related to the lower extremi-ties, including aortoiliac occlusive disease Upper extremity and vis-ceral occlusive diseases will be discussed elsewhere in this chapter.Peripheral arterial disease (PAD) can be subclassified into acuteischemia and chronic ischemia, with differing principles of man-agement The main tenet of ischemic diseases, however, applies toboth acute and chronic ischemia: the highest likelihood of limb sal-vage is achieved by maximizing proximal inflow and distal outflow

Acute Lower Extremity Ischemia

The etiology of acute lower extremity ischemia is either embolism of aclot or plaque from a proximal source or local development of throm-bus, both of which occlude blood flow to the distal portion of the ex-tremity The Thrombolysis or Peripheral Artery Surgery (TOPAS)trial established that local thrombus is causative in 85% of cases.Outcome is directly related to the degree of ischemia Left un-treated, patients commonly progress to limb loss and potentiallydeath The amputation rate is clearly linked to the time betweenonset of acute limb ischemia and intervention; therefore, treatmentshould be initiated as quickly as possible

Diagnosis

Patients with acute ischemia will manifest the “six P’s,” which includepain, pallor, paresthesias, pulselessness, poikilothermia, and paraly-sis, in some variation The most common presenting symptom ispain Paralysis is a late finding and is indicative of advanced ischemia.Systemic effects of tissue necrosis include acidosis, hyperkalemia,myoglobinuria, renal failure, sepsis, and death Diagnostic tests such

as arterial duplex ultrasonography or noninvasive angiography (CTA

or MRA) may be helpful; however, these tests take valuable time toobtain, and it is likely wiser to proceed directly to arteriography anddefinitive management to maximize the likelihood of limb salvage

Management

Systemic anticoagulation with heparin should be instituted diately when a diagnosis of acute ischemia is made This preventsclot propagation to the distal circulation and decreases morbidityand mortality The first step in diagnosis and intervention is arteri-ography Figure 20.3 outlines the treatment algorithm for acutelimb ischemia

imme-Complications

The development of most complications is related to the duration

of ischemia Compartment syndrome arises in approximately 2%

Chapter 20 • Vascular Disease and Vascular Surgery 293

of patients and is due to reperfusion injury following

revasculariza-tion This syndrome is characterized by pain with passive stretch of

the muscles and increased compartment pressures (⬎20 to 30 mm

Hg) Diagnosis is made by history, physical examination, and a high

index of suspicion Four-compartment fasciotomy of the leg

should be performed if there is any concern of compartment

syn-drome It is worth noting that the extent of reperfusion injury is

less when flow is gradually restored to the extremity, as in

catheter-directed thrombolysis

Other complications are those associated with thrombolysis

and include minor catheter-related bleeding (10% to 15%),

bleed-ing requirbleed-ing transfusion (5%), and hemorrhagic stroke (1%)

Chronic Lower Extremity Ischemia

Chronic ischemia of the lower extremity most commonly results

from occlusive atherosclerotic lesions of the aortoiliac,

femo-ropopliteal, or infrapopliteal vascular systems Most patients are

asymptomatic despite having physical signs of chronic ischemia

The most common symptoms are intermittent claudication, rest

pain, ischemic ulcers, and frank gangrene In general, claudication

alone is rarely limb threatening In contrast, rest pain and ischemic

ulcers usually lead to limb loss if left untreated

Diagnosis

History and Physical Examination

A careful history and a detailed physical examination will often

raise the level of suspicion and indicate the need for diagnostic

test-ing or treatment Many patients will report underlytest-ing medical

dis-ease including heart disdis-ease, diabetes, kidney disdis-ease, and

hypertension Advanced age, male gender, and family history may

also be noted Physical examination may reveal diminished eral pulses, hair loss, skin atrophy, nail hypertrophy, elevation pal-lor, and dependent rubor

periph-Intermittent claudication is typically the initial symptom.Claudication is defined as extremity discomfort, pain, or weaknessconsistently produced by exercise and promptly relieved by rest.Symptoms generally occur one level below the area of disease.Therefore, buttock claudication can likely be attributed to an aortic

or common iliac lesion, while midthigh claudication is commonlyassociated with an external iliac lesion Likewise, calf pain is mostlikely due to a common femoral or superficial femoral artery (SFA)occlusion Finally, an occlusion in the distal SFA or popliteal arteryoften results in foot claudication

Claudication can be caused by nonvascular conditions, and thediagnoses should be considered by the vascular surgeon Neuro-genic leg pain caused by spinal stenosis, nerve compression, or dia-betic neuropathy is the most common conflicting diagnosis It isworth noting that vascular and nonvascular diseases can coexist,which mandates that the vascular surgeon identify and treat vascu-lar claudication, even in the presence of another condition.Ischemic rest pain indicates that the arterial blood supply is in-sufficient to meet the metabolic demands of the resting tissue Itusually affects the forefoot and toes, but when pain is felt moreproximally, distal areas are usually not spared The pain is aggra-vated by elevation of the extremity and diminished or relieved bydependency Therefore, pain commonly occurs while the patient isreclining or sleeping

Ischemic ulcers usually result from minor traumatic injuries,which fail to heal because of lack of adequate blood supply Theyare most common in areas of focal pressure on the foot and areusually dry and punctate Conversely, the ulcers of venous insuffi-ciency are usually located superior to the medial malleolus, and are

FIGURE 20.3 Treatment algorithm for acute limb ischemia.

294 Section IV • Cardiovascular and Respiratory Systems

often moist, superficial, and diffuse Venous ulcers are also

associ-ated with hemosiderin skin pigmentation and venous varicosities

It should be noted that arterial occlusive disease and venous

insuf-ficiency can coexist

Gangrene is characterized by cyanotic, anesthetic tissue

associ-ated with necrosis due to inability of the arterial blood supply to

meet minimal metabolic requirements Gangrene can be classified

as dry or wet Dry gangrene is more common in patients with

ath-erosclerotic disease and frequently results from embolization to the

toes or forefoot Elective amputation is required Wet gangrene is

more common in diabetic patients who sustain unrecognized

trauma to the foot The severe infection present in wet gangrene

makes it a true surgical emergency that mandates either complete

debridement of infected, nonviable tissue, or guillotine

amputa-tion Guillotine amputation may be revised to a formal amputation

once the infection has been controlled

The blue toe syndrome refers to the sudden development of

cool, painful, cyanotic toe(s) or forefoot This develops as a result of

embolic occlusion of digital arteries with atherothrombotic

material from a proximal source The affected digit(s) may require

amputation, and because these episodes tend to increase in

fre-quency and severity, localizing and eradicating the embolic source

is indicated

Diagnostic Testing

Patients with suspected arterial occlusive disease should undergo

noninvasive testing to establish the diagnosis, quantify the severity

of the disease, and localize the level of occlusion(s) Three simple

tests include the measurement of segmental systolic blood

pres-sures, the ankle-brachial index (ABI), and pulse volume recordings

(PVRs) (Fig 20.4) Normally, Doppler segmental pressures increase

20 mm Hg from the brachial artery to the proximal femoral artery

Any change less than a 20 mm Hg increase indicates significant

aor-toiliac disease Pressures are then measured segmentally at the

proximal and distal thighs, and the proximal and distal calves A

pressure drop of more than 30 mm Hg signifies a significant

ob-struction between two levels

The ABI is the ratio of the ankle blood pressure to the brachial

blood pressure An ABI greater than 1.0 is considered normal An

ABI from 0.5 to 0.84 is usually accompanied by claudication, while

an ABI less than 0.5 is often associated with critical ischemia (i.e.,

rest pain, tissue loss, gangrene) In cases where the arteries are

sig-nificantly calcified and therefore noncompressible, noninvasive

pressure measurements may be artificially elevated In this case,

PVRs can still accurately diagnose and localize arterial stenoses

PVRs are recorded with plethysmographic waveforms derived from

calibrated cuffs placed at the proximal and distal thigh, calf, ankle,

metatarsals, and toes The cuffs measure the pressure waveform of

each pulse, and the volume is calculated as the area under the curve

Duplex imaging can be a useful tool in determining the tion and severity of arterial obstruction However, the time, equip-ment, and experience required to perform a complete screening ofthe lower extremity vessels make its use impractical Therefore itsuse is primarily limited to surveillance of specific arterial segmentsand bypass grafts

loca-MRA and CTA are increasingly used to image significant sions identified by the previously mentioned tests However, con-trast angiography remains the gold standard for the evaluation oflower extremity ischemia A complete study of the abdominalaorta, iliac, femoral, popliteal, and runoff vessels is performed bilat-erally since atherosclerotic disease commonly occurs at any of thesesites Angiography is reserved for patients who are expected to un-dergo intervention or revascularization

occlu-Management

Initial management is medical and consists of antiplatelet therapyand risk factor modification, including smoking cessation, weightloss, and statin therapy for hypercholesterolemia In addition,

30 minutes of daily exercise, most commonly walking, is essential.This regimen promotes the development of a robust collateral cir-culation, which supplies blood to the areas distal to significantstenoses

Revascularization is reserved for patients with critical limb chemia, exemplified by incapacitating claudication, rest pain, andtissue loss Endovascular intervention, though historically lessdurable than open surgical procedures, provides acceptable long-term patency rates with very low morbidity and mortality

is-Aortoiliac Occlusive Disease

Endovascular therapy provides excellent long-term patency withvery low mortality in aortoiliac occlusive disease For singlestenoses of the common iliac artery (CIA) or external iliac artery(EIA), shorter than 3 cm, endovascular therapy is the preferredmodality It is also reasonable to employ endovascular therapy for(a) a single stenosis in the CIA between 3 and 10 cm in length,(b) two isolated stenoses in the CIA/EIA less than 5 cm, or (c) a sin-gle CIA occlusion Angioplasty alone often produces an adequateresult, and stenting can be used in cases of residual stenosis, dissec-tion, or lesions with high embolic risk

Surgical revascularization is the method of choice for morecomplex lesions Aortobifemoral bypass grafting with a Dacrongraft has 88% patency at 5 years However, the morbidity and mor-tality of aortic surgery is significant In patients with a hostile ab-domen or high surgical risk, who cannot be revascularized with anendovascular approach, axillobifemoral bypass grafting (or itsequivalent) is the approach of choice Unfortunately, the patency ofthese grafts is less than that of the aortobifemoral graft For patientswith unilateral iliac disease not amenable to endovascular therapy,unilateral aortofemoral grafting yields the best results, though afemoral–femoral crossover graft is an option, which minimizespostoperative morbidity and mortality

Femoropopliteal Disease

Endovascular therapy for infrainguinal disease as compared to toiliac disease has the following characteristics: (a) the patency ratesare lower, though acceptable, (b) no more than two focal stenosesless than 3 cm in length should be treated, and (c) the role of pri-mary stenting is unclear, though angioplasty remains well accepted

FIGURE 20.4 Normal and abnormal pulse volume recordings at ankle

level (From Rutherford RB Vascular Surgery 4th ed Philadelphia:

WB Saunders; 1995:86, with permission.)

Chapter 20 • Vascular Disease and Vascular Surgery 295

Bypass grafting is indicated when endovascular therapy is

inappro-priate or inadequate When grafting to a target above the knee, vein

grafts have only slightly higher patency than polytetrafluoroethylene

(PTFE) grafts, however, vein grafts are far superior to PTFE for

below-knee targets Recently, percutaneous stent grafting to the

suprageniculate popliteal has demonstrated highly favorable results

Tibial Disease

The role of angioplasty and stenting for infrapopliteal disease

re-mains controversial and is reserved for patients in whom

revascu-larization is otherwise not possible Bypasses to the distal

circulation are typically performed only for limb salvage due to

poorer success rates with these grafts A femoral-distal bypass is the

option of choice because it provides the best inflow Autologous

vein has an approximately 50% patency rate at 4 years, while PTFE

has only 12% patency

Postoperative Graft Surveillance

Bypass grafts fail at three common time point: early (⬍30 days),

in-termediate (30 days to 2 years), and late (⬎2 years) Early failure

must be assumed related to a technical or judgment error, though

infection and hypercoagulability are also possible Intermediate

failure is most often caused by neointimal hyperplasia within a vein

graft or at anastomotic sites Late failure is caused by natural

pro-gression of atherosclerotic disease Meticulous postoperative

sur-veillance of bypass grafts can significantly increase long-term

success A typical surveillance protocol includes duplex

ultrasonog-raphy of the graft as well as ABI measurements Examinations

should be performed perioperatively, at 6 weeks, and then at

3-month intervals for 2 years and every 6 months thereafter

Complications

Morbidity and mortality of intervention for chronic lower

extrem-ity ischemia fits into two categories: those related to concomitant

systemic illnesses and those related to surgery Myocardial

infarc-tion and renal failure are common examples of the first category

Surgical complications include pseudoaneurysm resulting from

ar-terial puncture, compartment syndrome, and graft infection All of

these must be treated promptly and aggressively

ANEURYSMAL VASCULAR DISEASE

Aneurysms of the aorta, iliac arteries, visceral arteries, and

periph-eral arteries remain a major cause of morbidity and mortality

Ath-erosclerosis is the major cause of aneurysmal disease in all locations

except for the ascending aorta, where cystic medial necrosis

ac-counts for the majority of aneurysms Less common causes of

aneurysms include dissection and, in the past, syphilis

Abdominal Aortic Aneurysms

Risk factors for abdominal aortic aneurysm (AAA) include male

gender, hypertension, smoking, advanced age, family history, and

presence of other atherosclerotic or aneurysmal diseases By far

the greatest risk of an untreated AAA is death due to rupture Risk

of rupture increases significantly with the size of the aneurysm

because of the exponential increase in wall stress with increased

radius

Diagnosis

AAAs are usually asymptomatic The presence of symptoms fies impending or active rupture and should lead to urgent inter-vention Typical signs and symptoms include abdominal or backpain and peripheral embolization Rupture of an AAA presents assevere abdominal or back pain with associated hypotension, tachy-cardia, and shock If an AAA ruptures into the inferior vena cava,high output cardiac failure develops with tachycardia and lower ex-tremity edema Finally, AAAs may rupture into the third or fourthportion of the duodenum, producing exsanguinating gastrointesti-nal hemorrhage Physical examination may reveal a pulsatile ab-dominal mass, but is unreliable as it is very insensitive

signi-It is worth noting that ruptured aneurysms must be contained

by the retroperitoneum if the patient is to have a chance at survival.Aneurysms, which rupture into the peritoneal cavity, are uniformlyfatal because the entire blood volume rapidly accumulates in theperitoneal space

AAAs are often diagnosed accidentally by ultrasonography orabdominal CT scan ordered for an unrelated reason Ultrasonogra-phy, CT scan of the abdomen and pelvis, and MRA are all 100%sensitive in the detection of AAA Because of its low cost, ultra-sound is used for surveillance as well as screening purposes In re-cent years the value of screening the population deemed to be athigh risk for the development of AAA has been recognized, and ul-trasound screening now is covered by Medicare CT angiography isthe diagnostic test of choice (Fig 20.5) It is useful in planning op-erative repair because it details the size, extent, and relation to therenal arteries of the aneurysm Multiplanar analysis and 3-D recon-struction can also be used to provide the additional level of detailrequired for planning endovascular stent graft repair

Patient Selection

Large randomized prospective trials in both the United Kingdomand United States indicate that there is no survival advantage to op-erating on AAAs up to 4.5 cm in diameter Once the aneurysm hasreached a size of 4.5 to 5.5 cm, operative repair should be strongly

FIGURE 20.5 Abdominal computerized tomographic scan

demon-strating abdominal aortic aneurysm with mural thrombus (FromGoldstone J Abdominal aortic aneurysms In: Greenfield LJ, Mulholland

MW, Oldham KT, et al., eds Surgery: Scientific Principles and Practice.

1st ed Philadelphia: J.B Lippincott; 1993:1715, with permission.)

296 Section IV • Cardiovascular and Respiratory Systems

considered The decision to operate involves many variables

includ-ing size, recent expansion, operative risk, medical comorbidities,

age, life expectancy, and family history of rupture In the case of a

ruptured aneurysm, the only chance at survival is to proceed

im-mediately with surgical repair

Open Surgical Repair

Conventional AAA repair consists of a retroperitoneal approach

through the left flank or a transabdominal, transperitoneal approach

via a midline incision Juxtarenal and suprarenal aneurysms are best

approached through the left retroperitoneal space Upon clamping of

the aorta proximally, the aneurysm sac is entered, and bleeding

lum-bar arteries are ligated A prosthetic graft is sewn proximally and

dis-tally to normal aorta In the presence of significant iliac artery

disease, a bifurcated graft can be sewn to either the iliac arteries or

the common femoral arteries The aneurysm sac is closed over the

graft in an attempt to lessen the risk of aortoenteric fistulization from

erosion of the duodenal wall by friction from the prosthetic graft

In the presence of a ruptured or inflammatory aneurysm, the

aorta must be controlled at the supraceliac level before the

in-frarenal aorta is exposed Once control of the aneurysmal segment

of the aorta is established, the supraceliac clamp should be moved

as caudally as possible ideally to an infrarenal location

Some special anatomic considerations apply to AAA repair

Prior to aortic cross clamping, the left renal vein must be identified

and protected to avoid injury With regard to pelvic outflow, if the

inferior mesenteric artery (IMA) is to be sacrificed, then at least

one hypogastric (internal iliac) artery must have good flow to

pre-vent colon ischemia and vasculogenic impotence If both

hypogas-tric arteries are sacrificed secondary to aneurysmal disease, the

patent IMA should be reimplanted into the aorta

Endovascular Abdominal Aortic Aneurysm Repair

EVAR was introduced by Parodi in 1991 and two stent graft devices

obtained U.S FDA approval in 2000 (Fig 20.6) Multiple studies

have shown that EVAR can be accomplished with shorter hospital

stay and decreased morbidity compared with open repair

Mortal-ity rates between the two approaches are similar Stent grafting was

initially reserved for patients who presented a prohibitive risk for

open repair; however, as the technology has gained acceptance and

long-term durability of the devices has been established, stent

grafts are being offered to standard risk patients

The key anatomic factors, which determine eligibility for

EVAR, are the size and location of the aneurysm neck (especially its

proximity to the renal arteries), the degree of tortuosity of the

aorta, and the size and shape of the access vessels (the femoral or

iliac arteries) An adequate neck length (usually 15 mm) is

neces-sary to ensure proper fixation of the device without compromising

flow to the renal arteries

Complications

The most common early complications following conventional open

AAA repair are paralytic ileus, coronary ischemia, cardiac

arrhyth-mias, renal dysfunction, and pneumonia Less common early

compli-cations include ischemic colitis, impotence, paralysis, graft infection,

and pseudoaneurysm Late complications include incisional hernia,

pseudoaneurysm development, atherosclerotic graft occlusion, graft

thrombosis, and aortoenteric fistula It should be noted that the

complication rate following repair of ruptured aneurysms is cantly higher in all categories

signifi-Endovascular aneurysm repair, despite having a lower rate ofoverall morbidity, has its own set of unique complications Device-related complications include kinking, occlusion, thrombosis, and en-doleak Most concerning of these is the development of an endoleak,because this implies that the aneurysm sac is still filling with blood atarterial pressure, and therefore the risk of rupture has not been elimi-nated Figure 20.7 details the types of endoleaks Non-device-relatedcomplications include dissection or thrombosis of the access vessels,contrast-induced nephropathy, and wound complications

Visceral Aneurysms

Aneurysmal disease also occurs in the renal, hepatic, and splenic teries; however, these aneurysms are usually not of atheroscleroticetiology and tend to occur in younger patients Renal and hepaticaneurysms should be repaired when discovered because of theirhigh risk of rupture Splenic artery aneurysms have a lesser risk ofrupture and can be closely monitored, although there are excep-tions to this rule Splenic aneurysms in pregnant women (orwomen who may become pregnant) and those larger than 2 cm indiameter have a higher risk of rupture and should be repaired

ar-FIGURE 20.6 Zenith stent graft for treatment of endovascular repair

of abdominal aortic aneurysms (AAAs) Note the barbs for suprarenalaorta fixation (From MA Moise, RM Fairman Vascular disease andvascular surgery In: A Atluri, GC Karakousic, PM Porrett et al., eds

The Surgical Review 2nd ed Philadelphia: Lippincott Williams &

Wilkins; 2005, with permission.)

Chapter 20 • Vascular Disease and Vascular Surgery 297

Renal, hepatic, and splenic aneurysms are typically treated with

exclusion and bypass grafting Proximal aneurysms of the hepatic

and splenic arteries, however, can be simply excluded because of

the rich collateral blood supply around these vessels Endovascular

coil embolization is useful in the treatment of saccular aneurysms,

and covered stent grafts may also be utilized to repair fusiform

aneurysms of these vessels

Peripheral Aneurysms

Aneurysms of the iliac, femoral, and popliteal arteries are common

in patients with atherosclerotic diseases The primary risk of an

iliac aneurysm is rupture, while femoral and popliteal aneurysms

have a tendency to thrombose or embolize Each of these

aneurysms is strongly correlated with the presence of significant

aneurysmal disease in other arteries, therefore additional testing is

warranted to search for other aneurysms

Iliac artery aneurysms should be repaired if they are

sympto-matic, larger than 3 cm, or mycotic Repair is accomplished with

either a covered stent or a bypass graft with exclusion of the

aneurysm Femoral artery aneurysms should be repaired if they are

symptomatic, larger than 2.5 cm, or mycotic Repair is carried outwith exclusion of the aneurysm and bypass graft Popliteal arteryaneurysms are repaired if they are symptomatic, larger than 2 cm,

or mycotic Treatment is with exclusion and bypass grafting, though recently stent grafting has gained support, especially inhigh-risk patients

al-Pseudoaneurysms

Pseudoaneurysms occur when arterial blood fills a cavity that isnot enclosed by all three layers of the vessel wall This most com-monly occurs in the femoral artery after puncture for a percuta-neous procedure but can also occur at vascular suture lines Smallpseudoaneurysms associated with puncture of the vessel can re-solve spontaneously, but larger pseudoaneurysms and those pres-ent at surgical suture lines require intervention to avoid rupture.For pseudoaneurysms resulting from percutaneous puncture,treatment consists of either duplex-guided compression or throm-bin injection Operation is necessary for pseudoaneurysms associ-ated with bypass grafts, as there is often a defect in the graft at thesuture line

FIGURE 20.7 Graphic representation of the four

types of endoleaks (A) Type I endoleaks result

from an inadequate seal between the graft and thelanding zones These can be divided into IA (proxi-mal) and IB (distal).(B) Type II endoleaks result

from collateral flow into the aneurysm sac

(C) Type III endoleaks occur when graft

compo-nents are inadequately sealed to each other (IIIA),

or when a hole in the graft develops (IIIB)

(D) Type IV endoleaks result from porosity of the

graft fabric and are usually self-limited

298 Section IV • Cardiovascular and Respiratory Systems

RENAL ARTERY STENOSIS

Renovascular hypertension accounts for approximately 5% to 10%

of all cases of hypertension Stenotic lesions in the renal arteries

re-sult from atherosclerosis in 70% of cases and fibromuscular

dyspla-sia in the remainder Atherosclerotic lesions usually occur in older

patients with systemic atherosclerotic disease and are more

com-mon on the left side Fibromuscular dysplasia occurs most often in

younger women and is either bilateral or has a predilection for

right-sided disease Renovascular hypertension is mediated by the

rennin–angiotensin–aldosterone system

Diagnostic tests include captopril renal flow scanning, duplex

ultrasonography, MRI, and arteriography The most commonly

performed confirmatory test is the renal vein renin assay This test

measures renin activity in the renal vein and compares it to

sys-temic renin activity in the case of bilateral renal artery stenosis In

the presence of unilateral renal artery stenosis, the renal vein renin

activity on the affected side is compared with the renal vein renin

activity on the normal side

Renal artery revascularization is indicated in the presence of

renovascular hypertension or ischemic nephropathy In most

in-stances, adequate revascularization can be accomplished with

per-cutaneous transluminal angioplasty and stenting, though ostial

lesions tend to respond less well than distal lesions

UPPER EXTREMITY VASCULAR DISEASE

Clinically evident upper extremity arterial occlusive disease is relatively

uncommon Most lesions are proximal and have adequate

collateral-ization, leaving the majority of patients asymptomatic The most

commonly affected vessel is the subclavian artery Subclavian steal

syndrome occurs in the presence of a proximal stenosis or occlusion of

the subclavian artery The delivery of arterial blood to the ipsilateral

extremity thus depends on reversed flow through the ipsilateral

verte-bral artery via the Circle of Willis Strenuous activity of the affected

upper extremity may result in ischemic pain in the extremity referred

to as subclavian steal syndrome With an increased demand for blood,

the exercising extremity “steals” blood from the ipsilateral

brobasilar circulation, resulting in neurologic symptoms of

verte-brobasilar insufficiency (i.e., syncope) Revascularization is indicated

for symptomatic stenoses and is accomplished with either

percuta-neous transluminal angioplasty or carotid to subclavian artery bypass

Thoracic Outlet Syndrome

Thoracic outlet syndrome (TOS) describes a constellation of vascular

and/or neurologic symptoms, often without any physical findings and

most commonly without an anatomic correlate It usually occurs in

younger patients and is caused by compression of the subclavian

ar-tery, vein, or branches of the brachial plexus Patients complain of

weakness, numbness, paresthesias, pain, and swelling of the extremity

Anatomy

The brachial plexus and subclavian artery pass through the narrow

triangle formed by the anterior scalene muscle, the middle scalene

muscle, and the first rib (the scalene triangle) The subclavian vein

also passes over the first rib, but lies anterior to the anterior scalene

muscle Presence of an anomalous cervical rib or hypertrophy of

the anterior scalene muscle can cause compression of the brachial

plexus, subclavian artery, and/or subclavian vein

Neurologic Symptoms

The symptoms and signs caused by irritation and seemingly pression of the brachial plexus are far more common than symp-toms attributable to the subclavian artery or vein Complaintsinclude weakness, numbness, paresthesias, and pain; however, theremay be no objective findings on neurologic examination Pain isdescribed in the subscapular, scapular, and cervical regions, whileparesthesias and numbness typically occur in the hand and medialforearm (ulnar distribution) Elevation of the arm will often exac-erbate symptoms Physical findings are uncommon but may in-clude weakness and atrophy of the triceps muscle, the intrinsicmuscles of the hand, and the wrist flexors

com-Diagnosis is difficult due to a lack of objective findings and isoften based on history, physical examination, and exclusion of otherconditions Chest and cervical spine x-rays can demonstrate the pres-ence of a cervical rib but this is found only in the occasional patient,and EMG may be helpful in diagnosing a subtle neurologic defect.The mainstay of treatment is conservative, with exercise andphysical and occupational therapy providing symptomatic relief.Surgical treatment of neurologic TOS should be reserved for refrac-tory cases because major neurovascular complications are not un-common It is critical that this operation be performed by a surgeonexperienced in the management of TOS as outcomes are markedlyimproved First rib resection may be performed via a transaxillaryapproach, or a supraclavicular approach can be used to perform an-terior and middle scalenectomies with or without first rib resection

Vascular Symptoms

Subclavian artery compression usually results from hypertrophy ofthe anterior scalene muscle in athletes but may also be caused bythe presence of a cervical rib Ischemic symptoms may be exacer-bated by maximal abduction of the arm Surgical intervention is in-dicated for arterial compressive symptoms resulting from TOS andinvolves release of the scalene muscles and resection of bony abnor-malities Embolizing lesions and aneurysms require resection andinterposition grafting In the presence of acute ischemia, immedi-ate anticoagulation should be followed with thrombectomy, anddefinitive repair can be accomplished at a later time

Compression of the subclavian vein in TOS usually presents aseffort-induced thrombosis (Paget–von Schrötter disease) Com-mon in young men with a history of strenuous upper extremity ac-tivity, it presents as painful swelling of the affected arm Diagnosis

is made with venous duplex studies and venography Initial ment is directed at recanalizing the subclavian vein and consists ofthrombolytics and anticoagulation Assuming that the subclavianvein is reopened with medical therapy, surgical therapy to relievethe compression should follow If the thrombosis does not respond

treat-to medical therapy alone, decompression should be performed lier, and angioplasty may be required as an adjunct

ear-MESENTERIC ISCHEMIA

Mesenteric ischemic syndromes can be divided into acute and chronic.Acute syndromes can be further classified as embolic, thrombotic,nonocclusive, and venous Chronic mesenteric ischemia is caused byatherosclerosis, or rarely, median arcuate ligament syndrome

Acute embolic occlusion, responsible for 50% of acute mesenteric

ischemia, usually affects the superior mesenteric artery (SMA), and

Chapter 20 • Vascular Disease and Vascular Surgery 299

the embolus is typically from a cardiac source The most common

site for an embolus to lodge is at the origin of the middle colic

ar-tery, distal to the first jejunal branches Thus, the most proximal

small bowel is typically spared It is extremely important to make

the diagnosis and intervene rapidly, as patients who progress to the

point of peritonitis usually have irreversible damage that is

associ-ated with a high incidence of mortality

Early diagnosis depends greatly on a high degree of suspicion,

because the classic finding is “pain out of proportion to physical

ex-amination.” Common symptoms include sudden onset of

perium-bilical pain, diarrhea, vomiting, and gastrointestinal (GI) bleeding

If the diagnosis is suspected before the onset of peritoneal signs,

mesenteric angiography is the diagnostic procedure of choice If an

embolism is present, laparotomy should be performed immediately,

with embolectomy of the SMA and resection of nonviable bowel

Acute thrombotic occlusion is the cause of acute mesenteric

is-chemia in about 25% of cases The presenting symptoms are

simi-lar to those of embolic occlusion; however, angiography is likely to

show an occlusion at or near the ostium of the SMA without

spar-ing the jejunal vessels Once the diagnosis is made, laparotomy is

performed immediately to resect infarcted bowel and revascularize

the remaining intestine

Nonocclusive mesenteric ischemia accounts for 20% of acute

mesenteric ischemia This occurs almost exclusively in critically ill

patients with severely diminished cardiac output and

correspon-ding splanchnic vasospasm The primary symptom is vague

ab-dominal pain, though tube feeding intolerance, distension,

leukocytosis, and metabolic acidosis may also be present

Angiogra-phy shows a patent vascular tree with nonvisualized mesenteric

arcades (“pruning”) Treatment includes directed injection of

va-sodilators such as papaverine into the mesenteric vessels in

con-junction with aggressive treatment of the underlying disorder

Mesenteric venous thrombosis accounts for the remaining 5% of

acute mesenteric ischemia It primarily affects younger patients,

most of whom will have an underlying hypercoagulability disorder

Thrombosis usually develops initially in distal vessels and then

propagates to the larger veins The most common complaint is

dif-fuse abdominal pain, but some patients have vomiting, diarrhea,

and GI bleeding as well Peritonitis is rare CT scan reveals marked

bowel wall edema, mesenteric thickening, ascites, and an enlarged

superior mesenteric vein with a central lucency suggestive of

thrombus The patient should be followed closely for peritonitis, as

medical therapy with fluid resuscitation, bowel rest, antibiotics, and

anticoagulation is usually curative

Chronic mesenteric ischemia occurs primarily because of

ather-osclerotic disease at the ostia of the visceral vessels Because of the

rich collateral supply of the intestine, symptomatic chronic

mesen-teric ischemia usually does not occur until multiple vessels are

se-verely stenosed The classic symptom is postprandial pain, which is

severe enough to deter the patient from eating, resulting in

signifi-cant weight loss Diagnosis is made with angiography

Revascular-ization should occur promptly, as this population is at high risk for

acute thrombosis Revascularization is accomplished with either

PTA with or without stenting, bypass, or endarterectomy

NONATHEROSCLEROTIC VASCULAR DISEASE

Nonatherosclerotic diseases affecting the vascular system comprise

a broad and varied spectrum of diseases, most of which are beyond

the scope of this review, though a few deserve mention here

Fibromuscular dysplasia, previously mentioned in the setting of

renal vascular hypertension, encompasses multiple subtypes, themost common of which is called medial fibrodysplasia (80% to90%) In this type, degeneration of the media causes fibrous con-strictions alternating with aneurysmal dilatation creating a “string

of beads” appearance on angiography Fibromuscular dysplasia isseen most commonly in young women and affects the renal arteriesmost often, followed by the carotid and iliac arteries

Buerger disease (thromboangiitis obliterans) is a severe,

progres-sive, nonatherosclerotic arterial occlusive disease The typical tient is a young male smoker of Eastern European, Mediterranean,

pa-or Asian descent Symptoms begin with lower extremity tion and rapidly progress to rest pain and ischemic ulceration Oc-casionally, the upper extremity is also affected by Raynaudphenomenon, with cyanosis or gangrene of the digits Angiographyshows (a) absence of atherosclerotic disease, (b) severe occlusivedisease of small vessels, and (c) “corkscrew” collaterals along thecourse of the occluded vessels Absolute cessation of smoking re-sults in disease remission in most patients, and exercise therapy todevelop collaterals is essential Other therapies used with some suc-cess include vasodilators, antiplatelet agents, and even sympathec-tomy (loss of vascular tone produces vasodilation)

claudica-Autoimmune vasculitides: Takayasu arteritis and temporal tis, both classified as forms of giant cell arteritis, deserve mention in

arteri-that they occasionally require intervention by a vascular surgeon

Takayasu disease causes stenotic or occlusive lesions, and

occasion-ally aneurysms, of the aorta and its major branches It occurs rily in women younger than 35 years The mainstay of treatment isimmunosuppression with glucocorticoids; chemotherapy is usedwhen recurrences present during steroid therapy One quarter of pa-tients are unresponsive to medical therapy Those who require surgi-cal intervention respond best to open vascular bypass, thoughangioplasty and stenting may have a role in renal artery lesions

prima-Temporal arteritis affects women more commonly than men

and usually occurs in patients older than 50 years The most monly affected vessels are the temporal, occipital, subclavian, andaxillary arteries Besides constitutional symptoms, many patientspresent with visual deficits Diagnosis is established by temporal ar-tery biopsy Corticosteroids are the treatment of choice

com-Popliteal entrapment syndrome is a rare disease, which typically

affects young adults In this disorder, the popliteal artery deviatesaround the medial head of the gastrocnemius muscle Most pa-tients present with mild claudication; physical examination may re-veal loss of distal pulses with plantar flexion of the foot Treatmentinvolves surgical resection of the medial head of the gastrocnemiusmuscle, though arterial reconstruction may be necessary

VENOUS DISEASES

Deep venous thrombosis (DVT) is a common problem in surgical

patients and can cause serious short- and long-term morbidity andmortality Risk factors for DVT include age greater than 40 years,obesity, malignancy, prolonged immobilization, surgery, trauma,pregnancy, and hypercoagulability DVT prophylaxis is a controver-sial and evolving topic; however, it is known that pneumatic com-pression stockings, subcutaneous doses of either unfractionated orlow–molecular weight heparin, and early mobility decrease the rate

of DVT when applied both pre- and postoperatively

The most common presentation of DVT is unilateral swelling

of an extremity, though clinical diagnosis is difficult Occasionally,

300 Section IV • Cardiovascular and Respiratory Systems

in the case of iliofemoral venous thrombosis, massive swelling,

pain, and cyanosis develop This is referred to as phlegmasia cerulea

dolens (swollen, blue, painful) If this condition progresses and

ar-terial supply to the extremity is compromised because of swelling,

phlegmasia alba dolens (swollen, white, painful) develops In severe

cases, gangrene can develop

The most feared acute complication of DVT is pulmonary

em-bolism Seventy percent of pulmonary emboli arise from DVTs in

the pelvic and deep veins of the lower extremities The upper

ex-tremity, the calf, and the superficial venous system are rare sources

of pulmonary emboli The late complication of a lower extremity

DVT is chronic venous insufficiency, which results from residual

obstruction and valvular incompetence

Venography is the gold standard for diagnosis of venous

thrombosis, but it is rarely used because of its invasiveness and the

need for IV contrast Duplex ultrasonography has excellent

sensi-tivity and specificity and is inexpensive and easy to obtain

The mainstay of treatment for DVT is anticoagulation with

he-parin, followed by warfarin Low–molecular weight hehe-parin, given

subcutaneously twice daily, is now an accepted alternative to

intra-venous heparin For a first occurrence of DVT, anticoagulation

should continue for 6 months For a second DVT, treatment is

ex-tended to 1 year For patients who develop pulmonary embolism or

a third DVT, lifelong anticoagulation is recommended Placement

of an inferior vena cava filter (IVC filter) should be considered for

patients who have a contraindication to anticoagulation or develop

pulmonary embolism or recurrent DVT despite therapeutic

antico-agulation Thrombolytic therapy for DVT is controversial and is

usually reserved for iliofemoral thromboses where phlegmasia

cerulean dolens or phlegmasia alba dolens is present

Venous insufficiency is primarily a disease of the lower

extremi-ties that results from insufficiency of venous valves Because the

vertical fluid column in the vein is longer, the venous pressure at

the bottom of the column is increased This results in progressive

dilation of the vein and worsening valvular incompetency Fluid

translocation into the soft tissue results in edema The skin

devel-ops brown discoloration due to hemosiderin deposition in the

tis-sues, and venous stasis ulcers develop in severe cases These ulcers

have a classic location superior to the medial malleolus, and they

are superficial, wet, and diffuse Most patients with varicose veins

and/or venous insufficiency do not require surgery Treatment with

compression stockings and frequent ambulation result in

resolu-tion of edema, skin changes, and ulceraresolu-tion in 90% of patients

Pa-tients unresponsive to conservative therapy may require greater

saphenous vein stripping or sclerotherapy

LYMPHATIC DISEASES

Lymphedema is caused by obstruction or interruption of

lym-phatic channels or lymph nodes, leading to accumulation of

lymph fluid in the soft tissues Congenital lymphedema is a rare

inherited condition caused by absence or malformation of

lym-phatic vessels Secondary lymphedema, far more common, is

caused by obstruction of lymphatics or lymph nodes Worldwide,

the most common cause of secondary lymphedema is filariasis, a

parasitic infection, which obstructs lymphatic channels In oped countries, the most common cause is malignancy, thoughlymphedema can also result from radiation, infection, or lym-phadenectomy Complications of lymphedema include cellulitis,fibrosis, and neoplasia

devel-Treatment of lymphedema is initially conservative and consists oflimb elevation, compression bandaging, exercise therapy, and meticu-lous skin care Pharmacologic therapy with benzopyrones hasemerged as a potential adjunct to conservative, mechanically basedtherapies Benzopyrones increase the number of macrophages,thereby enhancing proteolysis and resulting in removal of proteinand edema However, benzopyrones are not FDA approved in theUnited States

ARTERIOVENOUS ACCESS

With the number of patients affected by end-stage renal disease(ESRD) increasing, surgeons must be familiar with the various op-tions for hemodialysis access AV access options can be classified astemporary or permanent

Percutaneous catheters, usually considered a temporary tion, are typically used in patients who need urgent dialysis or whohave exhausted all options for permanent surgical access Theselarge, double-lumen catheters are usually placed in the internaljugular, subclavian, or femoral veins Catheters should be removedfrom the femoral veins as soon as possible due to the high risk ofinfection If more than a brief period of dialysis is anticipated, apercutaneous cuffed, tunneled catheter should be placed as this sig-nificantly decreases the risk of infection Catheter placement in thesubclavian vein results in a high rate of vein thrombosis and steno-sis, making the internal jugular vein the ideal target vessel.The basic tenets of permanent AV access are as follows: (a) na-tive fistulas are preferable to prosthetic grafts; (b) distal sites should

solu-be used solu-before proximal sites; (c) the nondominant extremityshould be used whenever possible; and (d) an access site should not

be abandoned until reasonable efforts at revision have been hausted

ex-In order of preference, AV fistula options include the cephalic fistula (Brescia–Cimino), brachiocephalic fistula, andbasilic vein transposition AV graft options include looped forearmgrafts, upper arm grafts, and lower extremity or chest wall grafts

• Definitions of pulmonary function tests

❍ TV (tidal volume): The amount of air inspired or expiredduring normal breathing

❍ FRC: The amount of air contained in the lungs after mal expiration

nor-❍ VC: The amount of air exhaled following maximal ration and forced expiration

inspi-❍ RV: The amount of air remaining in the lungs after imal expiration

max-❍ FEV1: The volume of air exhaled in 1 second with amaximum expiratory effort

• Criteria for operative risk for pulmonary resection

❍ V/Qmismatch: physiologic dead space versus shunt

• Tension pneumothorax causes hypotension and possiblesudden death by mediastinal shifting resulting in compres-sion of the vena cava, decreased venous return, and de-creased cardiac output

• Presence of a new solitary nodule in a patient with asmoking history must be assumed to be a lung canceruntil proven otherwise

• Lung cancer most common cause of cancer-related deaths

in both men and women, adenocarcinoma most common

• Surgical resection is the mainstay of therapy for stage I andstage II NSCLCs

• Mortality of pneumonectomy: 5% to 10%

• Mortality of lobectomy: less than 2%

• Signs of inoperability in lung cancer are bloody pleural fusion, Horner syndrome, vocal cord paralysis, SVC syn-drome, distant metastases

ef-• Resection of the thymus in myasthenia gravis improvessymptoms in over 80%

RESPIRATORY PHYSIOLOGY

The purpose of respiration, the process of inhalation and exhalation

of air, is to transfer atmospheric oxygen to erythrocytes and dispose

of carbon dioxide enabling humans to undergo aerobic metabolism,

the end result of which is the production of ATP This exchange of

gases occurs in the lung and consists of three components

Ventila-tion is the process by which atmospheric air reaches the alveoli The

alveolar-pulmonary capillary membrane is the anatomic site of gas

exchange referred to as the blood–gas interface The process whereby

blood passes through this interface is referred to as perfusion Each of

these components is essential to respiration; thus, it is important to

understand the physiology in detail to be able to intervene

appropri-ately in the setting of respiratory pathology

Air Movement

Airways

Air passes through the upper airways consisting of the pharynx and

larynx to reach the tracheobronchial tree, a system of successively

branching tubes that decrease in diameter but increase in total

cross-sectional area with each division The trachea extends from C6 or C7

to T4 or T5 and connects the larynx to the right and left main bronchi.

The right main bronchus gives rise to the upper lobar bronchus andthe bronchus intermedius, which subsequently splits into the middleand lower lobar bronchi On the left, the main bronchus bifurcates di-rectly to give rise to the upper and lower bronchi Segmental bronchicontinue to divide until they reach the most distal airways, which are

called the terminal bronchioles These first 16 divisions of the bronchial tree, also known as the conducting zone of the lung, are responsible

only for gas transport These airways, along with the pharynx, larynx,

and trachea, constitute the anatomic dead space because gas exchange does not occur within them The acinus is the respiratory unit of the

lung and consists of approximately the last seven divisions of the way The 17th to 19th generations consist of the respiratory bronchi-oles, from which the first alveoli emerge This region is termed the

air-transitional zone of the lung Subsequent generations are lined with alveolar ducts and sacs and are known collectively as the respiratory zone whose primary function is gas exchange (Fig 21.1).

The airways of the conducting zone are lined with ciliated ithelium interspersed with mucus-secreting goblet cells (Fig 21.2).The mucociliary apparatus carries particles in the tracheobronchial

ep-302 Section IV • Cardiovascular and Respiratory Systems

tree to the pharynx, where they are either swallowed or rated Smokers demonstrate abnormalities in both mucousproduction and ciliary motility that cause difficulties with secretionclearance, and following pulmonary surgery, there is transient dys-function of the mucociliary apparatus, which predisposes these pa-tients to postoperative atelectasis and/or pneumonia

expecto-The anatomic structure of the bronchi and bronchioles differs atvarious levels of the tracheobronchial tree The trachea and first threegenerations of the conducting zone contain cartilage as part of theirstructure The trachea is buttressed with C-shaped cartilaginousrings anterolaterally that prevent airway collapse when significant in-trathoracic pressure is generated such as during forced expiration.The amount of cartilage in the airways decreases as the conductingzone transitions into the respiratory zone, where the presence of car-tilage would hinder gas exchange Cartilaginous plates support thebronchi, while bronchioles and alveoli are completely devoid of car-tilage, rendering them more susceptible to collapse

Mechanics of Ventilation

Air movement, and inhalation in particular, is the result of a sure gradient between the thoracic cavity and the atmosphere Thisgradient is established by the muscles of respiration, increasing thevolume of the pleural spaces, which results in a negative intratho-

pres-racic pressure with respect to the atmosphere The diaphragm, the

principal muscle involved, flattens as it contracts, increasing thecraniocaudal dimension of the pleural spaces (Fig 21.3) In addi-tion, at times when the movement of larger volumes of air is

needed such as in exercise, the external intercostal muscles contract,

pulling the rib cage upward and outward increasing the terior (AP) and lateral dimensions In times of forced inspiration,the scalene and sternocleidomastoid muscles, referred to as the

1

234

17181920212223

T-3T-2T-1T

FIGURE 21.1 Lung zones BR, bronchi; BL, bronchioles; TBL,

termi-nal bronchioles; RBL, respiratory bronchioles; AD, alveolar ducts; AS,

alveolar sacs (From Weibel ER Morphometry of the Human Lung.

Berlin: Springer-Verlag; 1963:111, with permission.)

FIGURE 21.2 Respiratory tract epithelium in bronchus, bronchiolus, and alveolus EP, epithelium; BM, basement

mem-brane; SM, smooth muscle; FC, fibrocartilage (From Weibel ER, Taylor CR Design and structure of the human lung In:

Fishman AP, ed Pulmonary Diseases and Disorders Vol 1 2nd ed New York: McGraw-Hill; 1988:14, with permission.)