The Intensive Care Manual - part 2 ppt

TABLE 2–3 Complications of Central Venous CannulationHematoma Microshock Pneumothorax Hemothorax Chylothorax: Left internal jugular LIJ approach Arterial puncture from cannulation Subcut

left ventricle and, therefore, implies contractility information, and the rate ofdownstroke in the arterial waveform allows inferences regarding systemic vascu-lar resistance.

The blood pressure measured by an intra-arterial cannula depends to someextent on the properties of the vessel cannulated The arterial pressure waveform

is susceptible to artifacts, such as catheter whip and damping, which influencethe validity of the pressure data Catheter whip, or systolic amplification, occurswhen arterial pressure waves are reflected back to the catheter tip from points ofconstriction, branching, or noncompliant arterial walls Reflection of pressurewaves off arterial walls can distort pressure waveforms, causing overreading ofsystolic pressure Peripheral catheters are more susceptible to systolic amplifica-tion because the velocity of blood flow increases gradually as the blood pulsemoves peripherally, since the walls of the large arteries are more compliant andabsorb energy The systolic pressure increases and the systolic wave narrows pro-gressively as the arterial pressure wave is measured more peripherally, and sys-tolic amplification of the waveform increases as the compliance of the arteriesdecreases peripherally

Spontaneous oscillation is a characteristic of fluid-filled transducer systems.The resonant frequency of a transducer system is the inherent oscillation fre-quency produced by a pressure signal introduced into the system Mechanicaltransducers absorb some of the energy of the systems they monitor and release ofsome of this energy This causes a vibration to occur at the natural resonance fre-quency specific to the system

Damping is the tendency for the vibration, or oscillation, to stop and is a tion of compliance, air, tube length, tube coiling, connections in the tubing, andstopcocks Air in the form of bubbles in the flush solution is very compressible andabsorbs a great deal of energy, resulting in significant damping Excessive dampingresults in an underestimation of the systolic blood pressure and an overestimation

func-of the diastolic blood pressure, whereas the opposite is true for underdamped tems Mean pressure is only minimally affected by damping The resonant fre-quency can be quantitatively determined using the “flush formula,”6in which thefrequency (in hertz) equals the paper speed (in millimeters per second) divided bythe distance (in millimeters) between oscillation waves The more closely matched

sys-a pressure signsys-al is to the resonsys-ant frequency of the system, the gresys-ater the hood of signal amplification, which defines the underdamped system An underin-flated pressure bag causes an artifactual drop in the blood pressure reading Atransducer that has fallen to the floor causes the displayed blood pressure to begreatly elevated

likeli-Pulse Oximetry

The adjunctive use of pulse oximetry in CCUs has added an additional level of itoring, which allows the saturation of arterial blood to be measured directly usingthe law of Beer-Lambert and the principle of reflectance spectrophotometry

mon-The mandated use of pulse oximetry during anesthesia has greatly improvedanesthesia safety; ideally therefore, pulse oximeters should be used on all criti-cally ill patients However, pulse oximetry alone is not considered an appropriateearly warning of apnea, because significant desaturation may not occur for 15minutes or more in patients with a normal functional residual capacity who arebreathing pure oxygen Furthermore, the pulse oximeter does not indicate theadequacy of ventilation Clinically detectable cyanosis does not occur until theoxygen saturation of arterial blood reaches 80% or less.

Oxyhemoglobin reflects more red light than does reduced hemoglobin,whereas both hemoglobins reflect infrared light identically Adult blood usuallycontains four types of hemoglobin: oxyhemoglobin (HbO2), methemoglobin(MetHb), reduced hemoglobin (Hb), and carboxyhemoglobin (HbCO2) How-ever, except in pathologic conditions, methemoglobin and carboxyhemoglobinoccur only in very low concentrations

Pulse oximeters emit light only at only two wavelengths, 660 nm (red light)and 940 nm (near-infrared light) Reduced hemoglobin absorbs approximately

10 times more light, at a wavelength of 660 nm, than does oxyhemoglobin; at awavelength of 940 nm, the absorption coefficient of oxyhemoglobin is greaterthan that of reduced hemoglobin Signal processing based on a calibration curvedetermines the saturation of the arterial blood as it pulses past the probe Thepulse oximeter has substantially affected the use of ABG analysis for the determi-nation of oxygenation saturation alone

The SaO2displayed by the pulse oximeter is correctly referred to as the SpO2,

to differentiate it from the SaO2obtained by ABG analysis and is represented bythe following equation:

Where

SpO2is Saturation of Hb with 02measured by pulse oximetry

HbO2 is oxyhemoglobin concentration in blood

HbO2+ Hb is total hemoglobin concentratin in blood

Using the oxyhemoglobin dissociation curve, an SpO2of 90% corresponds to a

PaO2of approximately 60 mm Hg and an SpO2of 75%, to a PaO2of 40 mm Hg.The SpO2measured by pulse oximetry can be expected to be within 2% of thevalue for hemoglobin saturation of blood measured by a co-oximeter Anemiadoes not interfere with the accuracy of the SpO2as long as the hematocrit remainsabove 15% The heart rate on the oximeter must correlate with the true heart ratefor the SpO2to be considered accurate The SpO2is falsely elevated in the presence

of carboxyhemoglobinemia and the SpO2 falsely reads 85% when significantmethemoglobinemia is present

Methemoglobinemia may occur more frequently in septic critically ill patientsthan previously recognized, since methemoglobin is generated in the presence ofnitrites, which are a by-product of the nitric oxide pathway In addition, since thepulse oximeter requires pulsatile flow, placement of the probe on the index finger

or thumb of a patient with a radial arterial cannula serves as an early warning ofischemia in the radial artery distribution The accuracy of the pulse oximeter isgreatly reduced when the arterial oxygen saturation falls below 75%

CENTRAL VENOUS CATHETERIZATION

The central veins are the major veins that drain directly into the right heart cations for central venous cannulation include a need for both access and moni-toring (Table 2–2) The approaches to the central circulation can be classified onthe basis of whether the inferior or superior vena cava is used Venous air em-bolism is a possibility whenever the venous system is opened to atmosphericpressure above the level of the right atrium, or phlebostatic axis Inadvertent en-trainment of air through a 14-gauge catheter can occur at a rate of 90 mL/sec andproduce a fatal air embolism in less than 1 second Air embolism is most likely tooccur during hypovolemia and spontaneous respiration when the hydrostaticpressure in the right side of the heart falls significantly below atmospheric pres-sure during early inspiration The probability of air embolism is diminished, butnot eliminated, by placing the patient in Trendelenburg’s (head down) positionfor superior vena cava (SVC) cannulation and reverse Trendelenburg’s (head up)

Indi-TABLE 2–2 Indications for Central Venous Cannulation

Access for rapid infusion of fluid

Long-term access required

Monitoring of cardiac function

Temporary transvenous pacing wire placement

Aspiration of air emboli

Jugular venous bulb monitoring

position for femoral inferior vena cava (IVC) cannulation Venous air embolism

is best treated by aspiration of the air from the heart, but immediate temporizingmeasures include placing the patient in the left lateral decubitus Trendelenburg’sposition, increasing preload cautiously, and using aggressive inotropic support.Embolization of catheter fragments or the guide wire most often indicate seriousdeviation from proper technique Difficulty in obtaining successful venipuncture

is most often the result of poor anatomic landmarks, previous phlebitis orthrombosis, or distortion of anatomy by surgery or trauma The complications ofcentral venous cannulation are many, including those based in the patient’sanatomic variability, inadvertent complications despite maintaining the standard

of care, a breach in technique, and operator inexperience Complications of tral vein cannulation are listed in Table 2–3

cen-Approaches to the Central Venous CirculationINFERIOR VENA CAVAL ACCESS The IVC is accessed via the femoral vein,

which lies medial to the palpable femoral artery and below the inguinal ligament

in the femoral triangle (Figure 2–1) Radiographic confirmation of subsequentcatheter placement is not necessary The primary advantage to the femoral ve-nous access site is the relatively low rate of insertion-related complications, mak-ing it a good choice for emergent high-volume infusion However, higher rates ofcatheter infection have been reported at this site, especially when the catheter isbeing used for total parenteral nutrition, and higher rates of deep venous throm-bosis (DVT), especially in trauma patients, may outweigh the potential advan-tages During cardiopulmonary resuscitation, thoracic compressions mayincrease inferior vena caval pressure, prolonging the circulation time of drugs tothe heart The femoral vein should not be cannulated for volume infusion intrauma patients if abdominal or pelvic venous injury or hepatic trauma is sus-pected or if surgical clamping of the IVC is anticipated In the presence of known

or suspected DVT, the femoral approach should be used with great caution, sinceinstrumentation of the vein may dislodge thrombi proximally The occurrence ofDVT after prolonged instrumentation of the femoral venous system, especially inpatients who are immobile as a result of trauma or who are in hypercoagulablestates, is another consideration before planning femoral vein access

SUPERIOR VENA CAVAL ACCESS The SVC is accessed directly via the

subcla-vian, internal jugular, or external jugular veins (Figure 2–2) and indirectly via theantecubital veins The proximity of these veins to major arteries in the neck andthorax and the possibility of pneumothorax reflect the more common complica-tions of these approaches

Since the catheters and guide wires are of sufficient length to reach the rightatrium and ventricle, arrhythmias caused by mechanical stimulation of the heartare common Transient ectopy is very common and need not be treated How-ever, the ability to immediately recognize and treat ventricular tachyarrhythmias

TABLE 2–3 Complications of Central Venous Cannulation

Hematoma

Microshock

Pneumothorax

Hemothorax

Chylothorax: Left internal jugular (LIJ) approach

Arterial puncture from cannulation

Subcutaneous infiltration: proximal port

• Pulmonary artery rupture

is necessary; therefore, continuous monitoring of the electrocardiogram (ECG)during central venous access is highly recommended.

The tip of central venous catheters should lie in the SVC and not in the rightatrium, where the catheter tip can perforate or erode into the pericardium, or in theright ventricle, where stimulation of conduction pathways can lead to paroxysmalarrhythmias and conduction block Perforation of the SVC and right atrium haveresulted in mortality rates that approach 70% and 100%, respectively

SUBCLAVIAN VEIN CANNULATION The subclavian vein is the preferred site

for central venous cannulation (Figure 2–2), since it is a large vein with relatively

FIGURE 2–1 Anatomy of the femoral triangle The femoral vein is the most medial

neurovas-cular structure within the femoral triangle The palpable landmark is the femoral artery The base of the inverted triangle is the inguinal ligament; the vastus intermedius (laterally) and the adductor longus (medially) are the muscular boundaries The femoral nerve lies laterally and must be avoided The arrow represents the direction of flow in the femoral vein.

constant anatomy and is the vein most likely to be patent, even during profoundhypovolemia since the vein is tethered to the surrounding dense connective tis-sue The subclavian vein crosses under the clavicle, medial to the midclavicularline The vein is most often entered at the junction of the outer one-third andmedial two-thirds of the clavicle, with the needle parallel to the clavicle and di-rected at the sternal notch The subclavian vein is the direct continuation of theaxillary vein as it passes over the first rib and under the clavicle The veins runanterior to the anterior scalene muscle, which separates the vein from the subcla-vian artery and pleura The subclavian vein and internal jugular veins join at thethoracic inlet to form the brachiocephalic vein, which drains directly into theSVC The left side is somewhat preferable for right heart catheterization becausethe angulation from the right subclavian vein into the right side of the heart ismore acute In experienced hands, the incidence of pneumothorax is no greaterwith the subclavian approach than it is with the internal jugular approach.

INTERNAL JUGULAR VEIN CANNULATION The internal jugular vein passes

under the clavicular (lateral) head of the sternocleidomastoid muscle as the mostlateral structure in the carotid sheath Since the internal jugular vein lies poste-rior to the muscle belly, it can be accessed from either a medial (anterior) ap-proach or a lateral (posterior) approach (Figure 2–2) The use of portableultrasonography to guide internal jugular vein cannulation is becoming increas-

FIGURE 2–2 Anatomical landmarks for superior vena cava access The internal jugular vein

lies under the lateral head (clavicular) of the sternocleidomastoid (SCM) muscle and can be approached anteriorly (a) or posteriorly (b) The vulnerable structures include the carotid artery, brachial plexus cords, the dome of the pleura, and on the left side, the thoracic duct A superior approach to the subclavian artery is possible in the base of the anterior cervical trian- gle (c) The subclavian vein passes under the medial aspect of the clavicle and can be accessed there (d); see text.

ingly common and has obvious benefits in those patients in whom the palpation

of anatomic landmarks is not possible

The risk of inadvertent carotid artery puncture is always present and is slightlyhigher with the anterior approach and during periods of hypotension Carotidpuncture with a small-gauge needle carries a low risk of morbidity; hematomaand plaque embolization are relatively rare Cannulation of the internal carotidartery with a large-bore catheter may provoke serious hemorrhage and may re-quire emergent vascular surgery consultation A foreign body in the carotidartery carries a high risk of embolic (e.g., air, clot) cerebrovascular complication:definitive therapy must not be delayed The left internal jugular approach carries

a risk of injury to the thoracic duct and resulting chylothorax The indirect vantages of jugular venous cannulation include limited neck mobility and patientdiscomfort, proximity to oral and tracheostomal secretions, and overgrowth ofthe insertion site by facial hair in males, predisposing these catheters to contami-nation and infection

disad-EXTERNAL JUGULAR VEIN CANNULATION The external jugular vein is an

alternative jugular approach to the central venous system The advantages of ternal jugular cannulation are a low risk of pneumothorax, minimal risk ofcarotid artery puncture, and easy control of bleeding However, these advantagesare outweighed by the difficulty in accessing the highly mobile and collapsiblevein, in anchoring catheters, in passing the guide wire and catheter through a ve-nous valve (which may be made incompetent after catheterization), and the risk

ex-of venous injury at the acutely angled junction ex-of the internal and external lar veins The external jugular approach is not recommended for routine criticalcare central venous access

jugu-PERIPHERALLY INSERTED CENTRAL CATHETERS A reasonable alternative

to direct access to major veins is the use of a peripherally inserted central catheter(PICC) or long-arm central catheter; however, these are more applicable for pa-tients who need long-term care than patients in the CCU These catheters areinserted into the brachial or cephalic veins in the antecubital area and thenthreaded into the SVC, where the proper position is confirmed either radio-graphically or electrocardiographically Anesthesiologists routinely place speciallong-arm central catheters, which have multiple aspiration ports, in patients forneurosurgical procedures to facilitate aspiration of air embolism, to monitor cen-tral venous pressure (CVP), and to administer some medications The PICCcatheter is used mainly for long-term antibiotic or chemotherapy administration

Central Venous Pressure Monitoring

CVP can be transduced at any point in the central venous system, includingthe IVC; however, the reliability and validity of the IVC is affected by intra-abdominal pathology The phlebostatic axis is at the level of the tricuspid valve

or right atrium in a supine patient; this is where intravascular pressure reacheszero and is independent of body habitus Although changes in posture can be ex-pected to affect the reference pressure at the phlebostatic axis by less than 1 mm

Hg, the CVP is a less accurate indicator of filling pressures when it is measured

in the lateral or upright position, because of venous pooling The CVP is mostoften used as an approximation of preload and reflects a balance between venousreturn and right-sided cardiac output Under normal conditions, the right side ofthe heart is composed of a thin wall of myocardium and is more compliant thanthe more muscular left side of the heart Since CVP measures intravascular pres-sure and not transmural pressure, which is the actual determinant of ventricularpreload, its validity as an index of preload is influenced by pulmonary variables,such as intrathoracic pressure, and by cardiac variables, such as cardiac compli-ance

Central filling pressures, such as the CVP, pulmonary artery wedge pressure(PAWP), and pulmonary capillary wedge pressure (PCWP), are measured

at end-expiration, when the relative intrathoracic pressure is zero (i.e., it equalsatmospheric pressure), and therefore intravascular pressure equals transmuralpressure High levels of positive pressure ventilation, which affect the CVP,should never be discontinued to determine a “more accurate” CVP In instanceswhere the CVP is thought to be falsely elevated by intrathoracic pressure, an al-ternative form of preload assessment should be considered or esophagealmanometry should be used to estimate transthoracic pressure The transthoracicpressure can then be subtracted from the CVP to provide a better estimate ofpreload

Graphic depiction of the CVP (also the PCWP and left atrial pressure)

wave-forms consists of three positive wave deflections (a, c, and v) and two descents (x and y) (Figure 2–3) The a wave is the increase in venous pressure that is gen- erated by atrial contraction The c wave occurs when the atrioventricular valve

(tricuspid or mitral) is displaced into the atrium during isovolumetric

ventricu-lar contraction The v wave reflects the increase in atrial pressure that occurs as

venous return begins to fill the atrium during isovolumetric relaxation, while the

atrioventricular valves are still closed The x descent corresponds to ventricular

ejection, as the emptying ventricle draws down on the floor of the atrium and

de-creases the CVP The y descent occurs as the atrioventricular valve opens and

blood enters the ventricle during ventricular diastole

The importance of these waveforms lies in their ability to reflect on

patho-physiologic processes Absence of the a wave occurs in atrial fibrillation, in which case the x descent may also be absent Amplified, or “cannon,” a waves occur in the presence of stenosis of the atrioventricular (mitral) wave Both the x and y

descents are exaggerated in the presence of constrictive pericarditis, whereas

car-diac tamponade magnifies the x descent and abolishes the y descent

In the presence of atrioventricular valve incompetency, free transduction ofventricular pressure during ventricular contraction generates large “cannon” Vwaves that are pathognomonic for regurgitant flow, especially mitral regurgita-

tion In the case of the CVP, pulmonary hypertension increases right ventricular

afterload, decreases right ventricular compliance, and accentuates the v

wave-form depicted on the monitor

PULMONARY ARTERY CATHETER

The pulmonary artery catheter (PAC), or Swan-Ganz catheter, provides a moreaccurate measure of left ventricular preload; however, it also is subject to opera-tor bias and misinterpretation.7,8The pulmonary artery catheter was originallyintroduced in 1970 by Swan and Ganz, whose names are still attached to thecatheter today The importance of basing clinical interventions on judicious in-terpretation of the data obtained from the PAC cannot be overemphasized.9,10Although the discipline of critical care medicine is to a large extent rooted in use

of the PAC, recent suggestions that the use of the PAC in clinical medicine is sociated with increased morbidity and mortality may reflect, in large part, deci-sions made on the basis of inaccurate data alone, without sufficient consideration

as-of the underlying physiologic principles

FIGURE 2–3 The CVP wave form as it relates to the electrocardiogram (see text).

Pulmonary Artery Catheter Placement

The PAC is passed into the central venous circulation through an introducercatheter, or cordis, and is then passed sequentially through the great veins, theright atrium, right ventricle, pulmonary outflow tract, and into a pulmonaryartery A 1.5-mL silastic balloon allows catheter placement to be flow-directed,because the balloon tip of the catheter, inflated during catheter passage, facilitatesplacement in the pulmonary outflow tract Fluoroscopic assistance during place-ment may be indicated if a transvenous pacemaker has been placed recently, se-lective pulmonary artery catheterization is necessary, or anatomic abnormalities,such as Eisenmenger’s complex, exist

Catheterization of the right side of the heart carries the additional risks of rhythmias, intravascular coiling and knotting, and vascular perforation Con-tinuous waveform analysis of the pressures transduced at the PAC tip allowssubjective assessment of the location of the catheter tip Progression of thecatheter tip through the right side of the heart must be monitored by transducedwaveform analysis (Figure 2–4)

ar-Since the placement of the catheter is flow-directed, advancement of the catheterincrementally with each heartbeat facilitates appropriate passage Catheter ad-vancement without concomitant waveform progression strongly correlates withplacement in the IVC or coiling within the right heart chambers When the catheter

FIGURE 2–4 Waveform analysis during pulmonary artery catheterization The pressures

transduced sequentially include the superior vena cava (SVC) and right atrium (RA) which are typical CVP readings Entry into the right ventricle (RV) is marked by a rise in the systolic component The characteristic rise in diastolic pressure signals entry into the pulmonary artery (PA) With the balloon inflated, ‘wedge’ positioning of the balloon tip is signaled by a flattening of the PA waveform Deflation of the pulmonary artery balloon in the wedge posi- tion should be accompanied by a return to the PA waveform, as blood flow resumes past the catheter tip.

reaches the distal pulmonary artery, the diastolic pressure characteristically rises.Further advancement of the catheter causes the waveform to flatten and signifiesthat the “wedge” position has been reached; at this point, the balloon occludes theflow of blood past the catheter tip “Pseudo-wedging” may occur if the catheter iscaught underneath the pulmonary valve or trabeculae or between papillary muscles.

In this case, waveform flattening occurs prior to pulmonary artery waveform tification Deflation and reinflation of the balloon is critical, since distal migration

iden-of the catheter tip occurs frequently If slow inflation iden-of the balloon results in a tinued rise of the transduced pressure to high levels, the catheter tip is either “over-wedged” in the pulmonary capillary, which carries a high risk of pulmonary arteryrupture, or the balloon has herniated past the tip of the catheter, where pressuretransduction occurs Suspicion of “overwedging” requires that inflation attempts

con-be immediately abandoned, the catheter withdrawn a short distance into the monary artery, and the wedge position re-ascertained by slow re-advancement ofthe catheter

pul-The Physiology and Analysis of Pulmonary Catheter DataPULMONARY CAPILLARY WEDGE PRESSURE AND CARDIAC FUNCTION

The pressure determined from this “wedge” waveform at end-expiration is thePCWP, and may be used as an index of left atrial pressure, and by further extrap-olation, the left ventricular end-diastolic pressure However, true left ventricularpreload is actually ventricular wall tension caused by ventricular end-diastolicfilling volume, which stretches myocardial sarcomeres

The relationship of ventricular performance to isometric preload is Starling’slaw of the heart, and the resulting graphic depiction of this relationship is re-ferred to as a Starling curve (Figure 2–5) Interpretation of the data obtainedfrom use of the PAC is based on the Starling curve and is the foundation for car-diovascular critical care

A fundamental concept of cardiac physiology is that optimal preload develops

a tension on the muscle, which causes the overlap of actin and myosin in themyocyte to approximate 2.2 µm Otherwise, and more practically stated, optimalpreload is that precontraction load, or tension, that optimizes ventricular perfor-mance In graphic terms, optimal preload is the volume that produces ventriculardistension nearing the apex of the Starling curve, maximally increasing cardiaccontractile function Overdistention of the sarcomeres beyond 3.0 µm causes adecrease in contractile performance and a negative slope in the Starling curve.Since the pulmonary artery catheter measures pressure, the corresponding vol-ume preload can be inferred only if compliance remains constant during the pe-riod of measurement (i.e., compliance = volume/ pressure)

The pulmonary artery catheter has as its greatest utility the ability to depict amathematical and graphic relationship between cardiac filling pressure and car-diac performance Data is most reliable when it is directly measured, and mathe-matical manipulation sequentially introduces error The use of indexed values,

standardized to body surface area (i.e., cardiac index = cardiac output/body face area) facilitates the comparison of hemodynamic variables among patients.However, if the data is used primarily to predict trends over time, indexing pro-vides little added benefit.

sur-The principle on which the use of the PCWP as a measurement of left ular preload rests on is the assumption that inflation of the balloon in the wedgeposition within the pulmonary artery obstructs blood flow around the cathetertip and creates a static column of blood that is contiguous to the left atrium and,

ventric-at end diastole before mitral valve closure, with the left ventricular end-diastolicpressure Since catheter placement is flow-directed, the balloon usually carriesthe PAC tip to zone 2 of West, where the hydrostatic pressure in the pulmonaryartery (Ppa) exceeds alveolar (PA) pressure, which exceeds pulmonary venous(Ppv) pressure (Ppa> PA> Ppv), or to zone 3 of West, where Ppa> Ppv> PA(Figure2–6) Since the mean airway pressure in zones 1 and 2 is intermittently greaterthan pulmonary venous pressure, collapse of the vasculature causes inability totransduce accurate intravascular pressure The reliability of the PCWP is greatest

FIGURE 2–5 Curvilinear depiction of Starlings law of the heart: The Starling curve relates

preload (CVP, PCWP, LVEDP, or LVEDV) to cardiac function (EF, SV, CO) and forms the basis of cardiovascular critical care since both dependent and independent variables can be tracked using a PAC The incremental increases in preload (a, b, c) are accompanied by corre- sponding increases in cardiac function (A, B, C) Therapeutic interventions can change the variables Diuresis decreases preload (1), inotropes increase cardiac function at any given fill- ing pressure (2), and the use of beta or calcium channel blockers can inhibit contractility and move the patient’s cardiac function between curves I and II.

when the catheter tip is in zone 3 or 4, since only in these zones is there a ual column of uninterrupted blood between the catheter tip and the left atrium.High mean airway pressure and hypovolemia are the most common causes ofrelatively decreased zones 3 and 4 of the lung.

contin-The risks and difficulties inherent in repeated efforts at repositioning guided

by lateral chest radiographs is not practical, cost-effective, or safe Instead, thecatheter is assumed to be in zone 3 or 4, unless there is a marked transduction ofpulmonary pressures on the pulmonary artery and PCWP waveforms

Airway PEEP increases the proportion of zones 1 and 2 relative to zone 3 cause of alveolar recruitment The probability that the catheter tip lies in zone 3

be-or 4 is higher if a change in PCWP is less than half the incremental change inPEEP, and if the pulmonary artery diastolic (PAD) pressure is slightly higherthan the PCWP The true PCWP may be approximated using the formula:

PCWP = PCWP − 0.5(PEEP − 10)

FIGURE 2–6 West zones of the lung West zones relate ventilation and perfusion Flow is

greatest in dependent zones, partially governed by gravity Ventilation/perfusion ratio is greatest toward the apex of the lung In order to best reflect cardiac function, the tip of the PAC should lie in zone 3 or 4.

PCWPMis the measured PCWP at any level of PEEPBecause the PCWP, analogous to the CVP, reflects a balance between blood re-turn to the left side of the heart and the ejection of blood in the left ventricle by car-diac pumping function, it is not in itself an absolute Elevated PCWP may indicateeither fluid overload or decreased cardiac contractility The PCWP does not reflectthe volume of extracellular fluid During myocardial ischemia, decreased ventricu-lar compliance and impaired contractility reduce the ability of the left side of theheart to maintain an effective forward flow of blood, which is reflected in decreasedstroke volume and ejection fraction, causing the measured PCWP to become ele-vated at any given preload The appropriate therapeutic intervention at this time,active decrease of preload or active increase in contractility, requires both moredata regarding cardiac output and previous training and experience The accuracy

of the PCWP as an indicator of left ventricular end-diastolic pressure (LVEDP) iscompromised in a number of pathophysiologic conditions in addition to the car-diopulmonary interactions described earlier.11Mitral stenosis results in left atrialend-diastolic pressure and PCWP that are higher than LVEDP, an artifact caused

by impaired left atrial ejection The presence of “cannon” v waves on the pressure

tracing can aid diagnosis of this condition

Large atrial masses, such as myxomas or mural thrombi, may falsely increaseatrial pressures by decreasing atrial compliance and falsely elevate the PCWP Inaortic regurgitation, the PCWP underestimates the LVEDP because the mitral valvecloses before left ventricular filling is completed Regurgitant flow across the aorticvalve continues to increase LVEDP and cannot be measured unless the mitral valvehas also become incompetent The CVP is always lower than the PCWP, exceptwhen pulmonary vascular resistance is substantially elevated, in which case CVP ishigher than PCWP, or in the case of tamponade, in which the two pressures areequal Pericardial tamponade restricts the filling of all cardiac chambers and results

in the pathognomonic condition known as “equalization of pressures,” in whichCVP, mean pulmonary artery pressure, and PCWP are equal The PCWP and thepulmonary artery diastolic pressure are usually similar if the heart rate is less than

90 beats per minute

PULMONARY CAPILLARY WEDGE PRESSURE AND ADULT RESPIRATORY DISTRESS SYNDROME The PCWP is a useful guide to both pulmonary capillary

filtration pressure and left ventricular filling pressure The determination of thePCWP is often emphasized as a diagnostic tool in the differentiation of cardio-genic and noncardiogenic pulmonary edema The diagnosis of ARDS rests on thePCWP determination; however, patients with ARDS are usually receiving venti-lation using PEEP The relationship of actual and measured PEEP has been dis-cussed in the preceding section Pulmonary capillary transmembrane fluid flux isdescribed by Starling’s law, which defines the equilibrium between hydrostaticand osmotic forces across a capillary membrane:

F = [(Pi− Po) − (COPi− COPo)]× KWhere

F is transmembrane fluid flux

Piis hydrostatic pressure within artery

POis hydrostatic pressure outside the capillary

COPiis intravascular oncotic pressure

COPois extravascular oncotic pressure

K is the filtration coefficient

or

Pcap= PCWP + 0.4 (Pa− PCWP)Where

Pcapis pulmonary capillary filtration pressure

Pais pulmonary artery pressure

Elevation of the pulmonary capillary hydrostatic pressure in the presence ofleft ventricular failure favors transudation of fluid across the basement mem-brane and into the alveoli When the volume of fluid overcomes the maximallymphatic clearance, pulmonary edema occurs, manifested by a widening of thealveolar-arterial oxygen gradient and decreased lung compliance Since a greatmany other factors can produce an identical picture (e.g., inflammation, highlevels of negative alveolar pressure, hypoalbuminemia), the PCWP aids the dif-ferential diagnosis Low or normal levels of PCWP in the presence of clinicallydetermined pulmonary edema is a major criterion for the diagnosis of ARDS

CARDIAC OUTPUT MEASURED BY THERMODILUTION In addition to

in-tracardiac pressure measurements, the PAC also enables the measurement of diac output by thermodilution.12A thermistor at the tip of the PAC continuallymeasures the temperature of the blood in the pulmonary artery as it flows pastthe catheter tip Injection of a known quantity of fluid at a known temperatureinto the right atrium allows the change in the temperature of the mixed blood as

car-it flows past the thermistor to be plotted as a function of time, as shown in Figure2–7 The differentiated rate of change (dT/dt) is proportional and the integratedarea under the curve is inversely proportional to the cardiac output Thermodilu-tion is a modification of an indirect indicator dye (indocyanine green) dilutiontechnique in which the flow is equal to the amount of dye injected divided by theintegral of the instantaneous concentration of dye in sampled arterial blood overtime The determination of cardiac output using the Fick equation predates thePAC but nonetheless requires right heart catheterization The Fick equation is:

CO is cardiac output

VO2 is whole body O2 consumption

CaO2 is content of O2in arterial blood

CvO2 is content of O2in venous bloodThis equation is now most commonly used as a method of calculating V˙O2whenthe cardiac output is measured directly, using the PAC Thermodilution cardiacoutput determination is the currently accepted standard of practice and addsgreatly to the utility of the PAC Although room temperature injectates are reliable

in most patients, the signal-to-noise ratio is more favorable with cold injectates, pecially in patients with low body temperature or low cardiac output Variation ofthe cardiac output with phases of the respiratory cycle suggest that either measure-ments be timed to coincide with the same respiratory phase or an average value beused to predict trends In clinical situations, trends which occur over time duringthe care of a patient are always more valuable than absolute numerical values

O2 O2

˙

2

FIGURE 2–7 Thermodilution cardiac output curves The curves represent a change in

tem-perature detected by the thermistor at the PAC tip as a mixed injectate of known temtem-perature flows past The curve with the greatest change in temperature (dT) per unit of time has the lower area under the curve but has the greatest cardiac output associated with it (A and B) Curve C depicts a thermodilution curve as sensed by a rapid response thermistor capable of determining end–diastolic volume (EDV) and subsequent volume changes (ESV) as the right ventricle empties The ejection fraction (EF) is the EDV-ESV, which is the stroke volume SV, divided by EDV.

The thermodilution cardiac output as determined by the PAC is subject to tifactual inaccuracies based on the method used Since the determination of car-diac output is directly based on the temperature change sensed by the thermistor

ar-at the car-atheter tip, smaller changes in temperar-ature produce a falsely elevar-ated level

of cardiac output Smaller temperature changes, which artifactually elevate thederived cardiac output, can occur with the use of less injectate than necessary orwarmer-than-measured injectate (after a long wait at room temperature beforeinjection of cold saline) and in the presence of right-to-left cardiac shunts Onthe other hand, the most common cause of artifactually decreased cardiac output

is tricuspid regurgitation, which allows a prolonged mixing time of blood and jectate, resulting in prolonged transit time in the right side of the heart and a de-crease of the temperature change with time A rate of injection that is too slowalso gives a falsely low value for cardiac output Left-to-right shunts may makethermodilution cardiac output unmeasurable Finally, rapid infusion of fluidsmay dilute the injectate and also render the cardiac output measurement inaccu-rate

in-DERIVED CARDIAC INDEXES Cardiac performance interpretation must be

based on the fundamentals of cardiac physiology The amount of blood ejectedfrom each ventricle per heartbeat is the stroke volume (SV) The output of theleft ventricle per unit time is the cardiac output (CO) CO can also be expressed

as a function of heart rate and stroke volume:

CO (L/min) = HR (beats/min) × SV (mL/beat)Where

Mathematically, vascular resistance on the pulmonary and systemic tions can be expressed as derivatives of Ohm’s law, which states that current iselectromotive force divided by resistance, or flow equals pressure divided by re-sistance Rearrangement to solve for vascular resistance produces:

circula-Where

MAP is mean arterial pressureCVP is central venous pressure

CO is cardiac outputAlternatively, ventricular afterload can be expressed as the myocardial walltension during ejection as defined by the Laplace equation Note that the CO andvascular resistances are thus mathematically inversely proportional CO is mea-sured and vascular resistance is calculated, lending greater credence to the treat-ment of CO A more direct estimate of aortic resistance is based on therelationship:

Where

R (aortic) is aortic resistance

SV is stroke volumeNote that the Poiseuille-Hagen formula suggests that resistance is also indi-rectly influenced by viscosity (hematocrit) Furthermore, patients with arteriove-nous shunting typically have decreased baseline SVR Further manipulation ofmeasured data can potentially increase the inferences possible PAC monitoring;however, these manipulations must be interpreted with caution The data which

is directly obtained from the PAC (i.e., CVP, PCWP, CO, SvO2)can be combinedwith ECG information and manipulated mathematically to derive additional in-dexes of hemodynamic function (Table 2–4) Note however, that since informa-tion that is directly measured, such as the CO, has greater validity than derivedindices, such as SVR, the former should carry more weight in management deci-sions

ASSESSMENT OF CARDIAC PHARMACOLOGIC INTERVENTION The PAC is

the gold standard for the clinical assessment of the physiologic response of the

R (aortic) =arterial pulse pressure

Cardiac index (CI) 2.8–4.2 L/min/m 2

resistance (SVR)

resistance (PVR)

Left ventricular stroke

work index (LVSWI) LVSWI (g-m per beat per m 2 ) = 0.0136 [MAP (mm Hg) − PCWP (mm Hg)] SI 45–60

(mL per beat per m 2 )

mean pulmonary artery pressure; PCNP, pulmonary capillary wedge pressure.

critically ill patient to therapeutic intervention (Figure 2–5) Because of thismode of assessment, pharmacologic intervention that affects cardiac perfor-mance can be specifically, and often selectively, directed at preload, chronotropy,inotropy, or afterload.

Preload is increased by the administration of fluids that replenish or expandintravascular volume, such as blood products, colloids, or crystalloid (Figure

2–5a,b,c) Effective decreases in preload can be accomplished relatively by

veno-dilating agents, such as low-dose nitrates or morphine, or definitively through

diuresis (Figure 2–5, arrow 1) Chronotropy can be increased by vagolytic agents,

such as atropine sulfate or related compounds, indirect and direct pathomimetic agents, or artificial electrical pacing Indirect sympathomimeticagents are those compounds, such as ephedrine, which trigger the release of epi-nephrine from sympathetic nerve terminals, and direct sympathomimetic agentsare the epinephrine analogs, such as isoproterenol, which acts directly on the

sym-β1-receptors to increase heart rate Heart rate is also indirectly regulated by thecarotid baroreceptors and possibly also by atrial stretch receptors (Bainbridge re-

flex) Inotropy can be decreased (Figure 2–5, arrow 3) indirectly through the

blockade of β1-receptors or calcium antagonists and directly through depression

of excitation-contraction coupling at the subcellular level Recently, the cation and demonstration of physiologically active myocardial β3-receptors13thatexert negative effects on the inotropic state of the human heart have opened anew and exciting potential avenue of therapeutics based on the selective stimula-tion and blockade of this receptor Inotropy can likewise be augmented (Figure

identifi-2–5, arrow 2) with indirect and direct β1-receptor stimulation by means ofsympathomimetic agents, with inhibition of the membrane-based transtubularsodium-potassium ATPase pump by means of digitalis glycosides (which in-crease calcium flux into the myocytes), with manipulation of the serum-ionizedcalcium concentration relative to intracellular calcium concentration by means

of administration of intravenous calcium salts, and by means of the inhibitors ofphosphodiesterase (PDE), such as aminophylline, and specifically the inhibition

of PDE-3 by amrinone and milrinone Afterload can be increased by the ized stimulation of sympathetic tone, administration of vasopressin, or by selec-tive activation of α1-receptors, which precipitate vasoconstriction Cold-inducedvasoconstriction and increased cardiac afterload are an often-unrecognized cause

general-of increased cardiac workload and therefore a potential cause general-of cardiac ischemia.However, afterload can be decreased pharmacologically by activators of the nitricoxide pathway, such as sodium nitroprusside; calcium channel blocking agents,such as nicardipine; direct smooth-muscle dilators, such as hydralazine; in-hibitors of angiotensin-converting enzyme (ACE), such as captopril; or indirectsympathectomy, affecting central sympathetic outflow

ASSESSMENT OF CARDIOPULMONARY INTERACTION Cardiac and

pul-monary function are highly interdependent, and changes in pleural and trathoracic pressure, oxygenation, and ventilation exert important effects onpulmonary blood flow and left-sided CO.14During spontaneous ventilation, the