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Ebook Neurocritical care board review: Part 2

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(BQ) Part 2 book Neurocritical care board review has contents: Cardiovascular physiology, cardiovascular diseases, pulmonary physiology and fundamentals of mechanical ventilation, respiratory diseases, renal diseases, infectious diseases,.... and other contents.

Trang 1

General Critical Care:

Pathology, Pathophysiology,

and Therapy

II

Trang 3

C Systolic time interval

D Arterial pulse–pressure variation

E All of the above

F None of the above

Complete the following equation:

Trang 4

GENERAL CRITICAL CARE: PATHOLOGY, PATHOPHYSIOLOGY, AND THERAPY

206

The components of the equation for oxygen content of blood (mL O

include:

A Partial pressure of O2 in central venous blood

B Oxygen saturation in blood drawn slowly from a pulmonary artery catheter (PAC)

C Cardiac output

D Partial pressure of CO2 in arterial blood

E Solubility coeffi cient of oxygen in blood

The partial pressure or percent hemoglobin saturation of oxygen in blood drawn slowly

4

from a pulmonary artery catheter (PAC) is intended to evaluate:

A Oxygen consumption by lung tissue

B Relationship of oxygen delivered versus consumed by all body tissues

C Oxygen absorption across the alveolar–capillary membrane

D Oxygen transport (mL O2/minute)

E None of the above

To compare cardiovascular parameters among patients and to normalize values,

measure-5

ments may be “indexed” by dividing the measured value by:

A Body mass index

B Body weight

C Creatinine-height index

D Cardiac output

E None of the above

The ejection fraction measured by echocardiography primarily evaluates:

lizes all variables listed here except:

A Temperature of the pulmonary artery blood

B Distance between the injection port and the thermistor

C Transpulmonary gas temperature

D Volume of saline injected

The normal partial pressure of oxygen in a properly collected mixed venous blood

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CARDIOVASCULAR PHYSIOLOGY: Questions

E None of the above

The pulmonary artery “wedge” or occlusion pressure is intended to refl ect and direct

10

therapy as a surrogate of:

A The ejection fraction

B Left ventricular end-diastolic volume (LVEDV)

C Right ventricular end-diastolic pressure

D Afterload

E None of the above

Which cardiac variable listed here increases in proportion to preload?

E Right atrial systole during atrial fi brillation

Although “shunt” has been discussed throughout sections about the lung, the actual

12

evaluation is measured as the QS/QT or ratio of the blood “shunted” around the lung as

a fraction (or percentage) of the total cardiac output fl ow, that is, shunt fl ow/total fl ow

Stated another way, it is the percentage of cardiac output that does not effectively

par-ticipate in full oxygenation, acting as though it has never been to the lung The complex

formula for this important ratio is QS/QT = (CcO2 − CaO2)/(CcO2 − CvO2) A pulmonary

artery catheter (PAC) is required to measure what variable needed in this formula?

A CcO2

B CaO2

C Cardiac output

D CvO2

E None because a PAC is not needed

The arterial pulse pressure variation is used by some cardiac output monitoring devices

13

to suggest that the patient will benefi t from what intervention?

A Preload augmentation

B Afterload reduction

C Vasopressor (e.g., norepinephrine) administration

D Inotropic (e.g., dopamine) support

E Resumption of normal sinus rhythm

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GENERAL CRITICAL CARE: PATHOLOGY, PATHOPHYSIOLOGY, AND THERAPY

208

Arterial pressure waveform analysis is used by several commercially available devices

14

to measure cardiac output These devices calculate the cardiac output after using arterial

waveform analysis to defi ne:

A The dp/dt of left ventricular (LV) diastole

B LV ejection time (speed)

C Stroke volume (SV)

D First derivative of the rate of rise of the fi rst 0.04 seconds of the arterial pressure

dur-ing systole

E The area under the curve of the diastolic relaxation waveform

The oxygen saturation in blood drawn from a thoracic central venous catheter has been

15

suggested as a clinically satisfactory replacement for what hemodynamic parameter?

A Oxygen-carrying capacity of pulmonary blood

B Oxygen content of arterial blood

C Arteriovenous O2 difference

D Oxygen transport into the systemic circulation

E None of the above

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ANSWERS

The answer is B.

rate, and contractility Heart rate is a straightforward measurement, except when

myocar-dial effi ciency is altered by various dysrhythmias

i Afterload (or more properly, impedance) is usually evaluated by the equation for

sys-temic vascular resistance index (SVRI):

SVRI = 80 (MAP − CVP)/CI where MAP, mean arterial pressure; CVP, central venous pressure; CI, cardiac index

(cardiac output/body surface area [BSA]) (Normal: 1,600–2,400 dyne·second·m2/cm5)

ii Contractility is usually measured in the ICU as the ejection fraction obtained by

echocardiography Other measures, such as the dp/dt (rate of rise of left ventricular (LV) pressure) during initial LV systole, may be more accurate, but are not available

at bedside Another estimate of contractility is LV stroke work index (LVSWI) as work done during systole This parameter requires a pulmonary artery catheter (PAC) and

tradi-pu lmonary artery diastolic pressure when any of the preceding pressures are able As a function of physiology, for a pressure to represent a volume, especially as

unavail-15

Trang 8

GENERAL CRITICAL CARE: PATHOLOGY, PATHOPHYSIOLOGY, AND THERAPY

210

a trended variable overtime, their relationship, that is, ΔP representing a ΔV, must

be constant This relationship, ΔV/ΔP, defi nes LV compliance, which is not constant, particularly during sepsis, hypertension, or coronary artery–induced myocardial dysfunction In addition, changes in thoracic pressure that affect venous return dur-ing mechanical ventilation may make interpretation of these pressures more diffi cult

Therefore, defi ning preload remains diffi cult because of the imprecise methodology used to measure it (1,2)

The answer is C

modifi ed for cardiovascular issues as:

Blood pressure = Cardiac output × Systemic vascular resistance

As a fl ow variable, the units of cardiac output are L/minute These relationships highlight

the interdependency of cardiac output and changes in vascular constriction to maintain

blood pressure In clinical therapy, of course, one must treat one of the determinants of

cardiac output (Answer 1) to affect change in cardiac output

The answer is E.

deter-mined by the equation:

CaO2 = (Hgb × 1.37 × SaO2) + (PaO2 × 003)where Hgb, hemoglobin in g/dL; SaO2, the % Hgb saturation at the given FIO2; 003, the

solubility coeffi cient of oxygen in blood (Normal: 18 to 20 mL O2/dL)

Oxygen delivery (transport) (VDO2 or DO2) extends the O2 content in mL/100 mL blood

to the oxygen carried forward to tissues by the cardiac output (L/minute):

DO2 = CaO2 × CO × 10 (Normal: 900–1,100 mL O2/L/minute)

As oxygen is delivered to body tissues, some is consumed and some enters the venous

circulation to return via the superior and inferior venae cavae to the right atrium These

caval streams of blood do not mix fully until both enter the right ventricle, and the

resid-ual venous oxygen enters the pulmonary artery as the mixed venous oxygen Sampling of

the mixed venous blood by aspirating from a PAC allows calculation of the mixed venous

content of oxygen (CvO2), from measurement of the partial pressure of O2 (PvO2;

nor-mal 40 mmHg), blood Hgb, and Hgb saturation (SvO2; nornor-mal 0.66–0.74) from a mixed

venous blood gas:

CvO2 = (Hgb × 1.37 × SvO2) + (PvO2 × 003) (Normal: ~15 mL/dL)The amount of oxygen consumed (VO2) by all tissues is the difference between what

was delivered and what remained in the circulation within mixed venous blood The

a-vDO2:

a-vDO2 = CaO2 − CvO2 (Normal: 3.6–5.0 mL/dL)

When adjusted by the cardiac output to calculate consumption for the whole body:

VO2 = (CaO2 – CvO2) × CO × 10 (Normal: 200–300 mL/minute)All of the preceding values can be indexed by dividing the parameter by the patient’s BSA,

providing the ability to compare patients of different body habitus Clinically, oxygen

delivery index (DO2I) and oxygen consumption index (VO2I) may be compared: Normal

DO2I is 530 to 600 mL/minute/m2; VO2I is 110 to 160 mL/minute/m2

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CARDIOVASCULAR PHYSIOLOGY: Answers

211

Therefore, it is possible and clinically important to compare oxygen supply to oxygen

consumed by the entire body Organ-specifi c demand/supply relationships would be

important, but are unavailable unless the specifi c arteries to and veins from individual

organs are cannulated Because of the unique isolated anatomy of the brain, its supply

and consumption have been explored using arterial oxygen delivery and venous return

obtained from the jugular vein

Another variable derived from this information is the oxygen extraction ratio that

pro-vides perspective on the fraction or percentage of oxygen delivered that is used by the

body during normal or stressed metabolism Oxygen extraction may be increased during

hypoperfusion to compensate for reduced delivery Extraction may appear to be reduced

by anatomic arteriovenous connections such as in liver disease or may actually be reduced

when mitochondrial oxygen uptake is inhibited in sepsis or cyanide poisoning

O2 extraction = VO2/DO2 (Normal: 0.22–0.28)

As cardiac output falls, the slower fl ow through tissue capillaries, and perhaps increased

O2 extraction within that tissue bed, removes maximal amounts of arterial oxygen, thereby

reducing the amount of venous oxygen that returns to the circulation This, of course,

decreases the CvO2 and its components, PvO2 and SvO2, assuming hemoglobin

concen-tration remains constant Because the PvO2 is diminished by the O2 solubility factor, the

SvO2 has become the commonly used surrogate for the CvO2 in monitoring the mixed

venous:arterial O2 relationship Continuous monitoring of SvO2 is available via

special-ized PACs, allowing abnormalities to be trended

During clinical conditions (e.g., sepsis) that reduce oxygen uptake by mitochondria, more

O2 remains in the venous blood, and mixed venous content and SvO2 rise Similarly, in

patients with therapeutic or pathophysiological arteriovenous shunts, venous O2 and

SvO2 rise (3)

The answer is B

4 See Answer 3 for a full explanation of the value of monitoring the SvO2

Mixed venous samples are processed via a blood gas analyzer as an arterial specimen

Care must be taken that blood is not drawn too quickly from the PAC, because oxygenated

blood may be pulled backward through the capillary and cause an erroneous elevation in

the PvO2 from which the SvO2 is abstracted

The answer is E

parameter to be determined among patients with differing body confi gurations Body

surface area (BSA) is most easily available from a Dubois body surface chart but can be

calculated from complex equations (2,3):

BSA (m2) = [√ Height (cm) × Weight (kg)]/3,600, orBSA = 0.007184 × Weight0.425 × Height0.725

The answer is A.

6 Contractility is one of the four determinants of cardiac output LV stroke

work (see Answer 3) has been used as an estimate of contractility and refl ects work done

by the left ventricle to overcome outfl ow impedance Contractility is diffi cult to quantify

in the ICU setting because of its interdependence with preload, afterload, and heart rate

The ejection fraction (Normal: >55%–60%) obtained by echocardiography is most often

used clinically

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GENERAL CRITICAL CARE: PATHOLOGY, PATHOPHYSIOLOGY, AND THERAPY

212

Contractility is abnormal in several neurological conditions associated with large amounts

of catecholamine release from the brain “Myocardial stunning,” evidenced by decreased

contractility, is documented in subarachnoid hemorrhage and particularly during the

evolution of brain death in some patients This pattern appears similar to the Takotsubo

cardiomyopathy documented in patients with pheochromocytoma and other syndromes

associated with high catecholamine release (4)

The answer is C

has evolved from Stewart’s original work in the 1890s to the traditional method of

inject-ing iced or room temperature saline into the pulmonary artery This injection of a known

quantity of injectate at a known temperature into a fl owing bloodstream also of known

temperature induces a temporary temperature change in the pulmonary artery blood as it

passes a temperature sensor (thermistor) a known distance from the site of injection The

Stewart-Hamilton equation (2) to determine the cardiac output from this thermodilution

method is:

CO = [60 × Vi × Ci × Si × Kcal × Kcor × (Tb − Ti)]/[Cb × Sb × ∫ΔTb(t)dt]

where Vi, injectate volume (mL); Ci and Cb, specifi c heats of injectate and blood

(con-stants); Kcal, calibration constant; Si and Sb, specifi c gravity of injectate and blood

( constants); Kcor, temperature loss constant; Tb and Ti, baseline blood and injectate

tem-peratures; integral term, area under thermal curve of temperature change versus time

Continuous cardiac output pulmonary artery catheters (PACs) use similar changes in

pul-monary blood temperature, but instead generate a burst of heat (not cold) into the

blood-stream, and the change in blood temperature is sensed along a thermistor fi lament within

the catheter

The answer is A

below or above normal, will help evaluate the predominant abnormality in

cardiovascu-lar performance or oxygen debt (when O2 delivery does not meet need) It is helpful to

note the PvO2, although the SvO2 is used more extensively Because blood gas analyzers

do not directly measure the SaO2 or SvO2, as does an oximeter or cooximeter, it is useful

to ensure that the saturation (venous or arterial) presented by the blood gas analyzer is

consistent with the measured PaO2 or PvO2 The extrapolation from partial pressure to

saturation is, of course, a refl ection of the oxyhemoglobin dissociation curve

The “30–60-90” guideline is a useful rule of thumb describing Hgb-association

param-eters: At a PaO2 or PvO2 of 30 mmHg, there is 60% Hgb saturation, and at PaO2 or PvO2 of

60 mmHg, Hgb is 90% saturated

The answer is E

relatively small right atrium does not achieve full mixing Mixing occurs in the right

ven-tricle (5)

10 The answer is B As discussed in Answer 1, the intention of the pulmonary artery (PA)

wedge (or PA-occlusion pressure [PAoP]) is to evaluate cardiac preload, a volume, not

pressure, measurement Although a direct conversion of pressure to volume is not

pos-sible, the relationship between the two could be useful as a relative trend in their values

over time as therapy changes However, to be useful even as a trended value, there must

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CARDIOVASCULAR PHYSIOLOGY: Answers

213

be a linear (straight-line) relationship between the two variables of pressure and volume

The relationship between left ventricular diastolic volume (LVEDV) and LV

end-diastolic pressure (LVEDP) refl ects LV compliance (ΔV/ΔP) Therefore, LV compliance

must be constant (and normal) if LVEDP (or its surrogate, the PA wedge pressure) is to

accurately refl ect LVEDV or its trend LV compliance is not constant and may change over

short periods of time

This concept also introduces the potential for abnormal diastolic relaxation (distension)

of the left ventricle, as it alters LV compliance characteristics Coronary artery disease,

hypertension, diabetes, some forms of cardiomyopathy, and sepsis are examples of

con-ditions that decrease LV diastolic relaxation and cause the LV myocardium to become

more stiff This change in diastolic compliance also may reduce venous return, as LVEDV,

and/or alter the wedge reading A smaller volume in the stiffer left ventricle may be

represented by an elevated wedge pressure, a false measurement of LVEDV (3,6,7) The

prevalence among ICU patients of those conditions that might alter LV compliance makes

this an important clinical consideration in trying to interpret wedge measurements and

their infl uence on treatment

11 The answer is D Starling, using Howell and Donaldson’s venous reservoir to

simulate venous return, showed the heart’s ability to increase its output as venous

pre-load increased, “up to the limit of its capacity” (8)

12 The answer is D The CvO2 represents the mixed venous specimen returned to the heart

after tissues have removed oxygen from the arterial blood delivered to them (VDO2) The

mixed venous specimen is obtained distal to mixing in the right ventricle from pulmonary

artery blood through the pulmonary artery (PA) catheter The CcO2 represents the

capil-lary oxygen content of an idealized “perfect” alveolus adjacent to a “perfect” capilcapil-lary This

value, of course, is not measurable, but utilizes the PAO2 in the standard content equation:

CcO2 = (Hgb × 1.37 × SPAO2) + (0.003 × PAO2)where (as discussed in Chapter 17, Answer 18) the PA (short form) equation is PAO2 =

PIO2 − (1.25 × PaCO2), where PIO2 = (Pb − 47) × FIO2

The shunt equation is similar to the Bohr equation (Chapter 17, Answer 17) in that it

co mpares lung failure in the numerator to lung potential in the denominator In the

numerator, the CcO2 represents the ideal transfer of oxygen from the perfect alveolus to

the perfect capillary, whereas the actual accomplishment of that transfer is represented by

the CaO2 The difference between them shows the failure of that perfect opportunity The

denominator highlights the optimal opportunity to add oxygen to the blood delivered

to the lung from the mixed venous circulation Therefore, the shunt equation relates

fail-ure (numerator) to ideal opportunity (denominator) as a fraction or percentage Normal

shunt (QS/QT) is up to 0.08 or 8% This equation utilizes oxygen as an indicator gas and

informs the clinician as to what portion of the cardiac output perfused the lung but failed

to maximally gain oxygen This equation quantifi es the magnitude of the V/Q mismatch

(shunt effect) as the primary cause of hypoxemia

13 The answer is A Variability in the arterial pulse pressure (systolic–diastolic pressures),

stroke volume (SV), systolic pressure, and preload are caused by cyclic variation in

intrathoracic pressure during mechanical ventilation Several “minimally invasive”

IV fl uid

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GENERAL CRITICAL CARE: PATHOLOGY, PATHOPHYSIOLOGY, AND THERAPY

214

devices (e.g., FloTrac and LIDCO) derive cardiac output from arterial pressure waveform

contour and power analysis, and include an analysis of the pulse pressure, SV, and

sys-tolic pressure variabilities When the calculated arterial pulse pressure variability reaches

a particular magnitude (10%–13%), the manufacturer recommends rapid fl uid

adminis-tration to improve cardiovascular instability (9,10)

14 The answer is C Characteristics of the arterial pressure waveform are used to derive

SV Cardiac output is then calculated from CO = SV × heart rate Heart rate is separately

measured The strength of myocardial systole depends on the preload (see Answer 11),

and the systolic arterial pressure refl ects that contractility Therefore, SV is proportional to

the force of systolic contraction as assessed by the arterial waveform This contractile force

is also infl uenced by the impedance of the aorta and larger arterial vessels The devices

(e.g., FloTrac, LIDCO, and others) that utilize this technology and proprietary algorithms

calculate CO from the equation:

SV = (∫dp/dt)/Zwhere Z, aortic impedance; ∫dp/dt, integral of changing pressure over time during

systole

Correlation with thermodilution methods for CO measurement is 0.88 to 0.91, but data

are controversial among some patient groups wherein algorithms used in the devices

may apply less well (9–12)

15 The answer is E Substitution of the percentage oxygen saturation from central venous

blood (ScvO2) for the true mixed venous blood oxygen saturation (SvO2) from the

pul-monary artery was initially proposed within the treatment protocol for septic patients in

the emergency department (13) Review of this utilization among several patient groups

with other diagnoses shows a variable correlation between the two measures (14–16)

Proponents of the substitution suggest that an ScvO2 above 70% indicates that ongoing

treatment is safe and likely meets tissue oxygen delivery needs Utilization of the ScvO2

during titrated neurocritical care, however, remains poorly defi ned

References

1 Oren-Grinberg A, Lerner AB, Talmor D Echocardiography in the intensive care unit

In: Irwin RS, Rippe JM, eds Intensive Care Medicine 6th ed Philadelphia, PA: Wolters

Kluwer/ Lippincott Williams & Wilkins; 2008:289–302

2 Kruse JA Hemodynamic monitoring In: Kruse JA, Fink MP, Carlson RW, eds Saunders

Manual of Critical Care Philadelphia, PA: Saunders; 2003:774–777.

3 Cheatham ML, Block EFJ, Promes JT, et al Shock: an overview In: Irwin RS, Rippe JM, eds

Intensive Care Medicine 6th ed Philadelphia, PA: Wolters Kluwer/Lippincott Williams &

Wilkins; 2008:1831–1842

4 Nykamp D, Titak JA Takotsubo cardiomyopathy, or broken-heart syndrome Ann

Pharmacother 2010;44(3):590–593.

5 Barratt-Boyes BG, Wood EH The oxygen saturation of blood in the venae cavae,

right-heart chambers, and pulmonary vessels of healthy subjects J Lab Clin Med 1957;50(1):

93–106

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CARDIOVASCULAR PHYSIOLOGY: Answers

215

6 Ogunyankin KO Assessment of left ventricular diastolic function: the power, possibilities,

and pitfalls of echocardiographic imaging techniques Can J Cardiol 2011;27(3):311–318.

7 Mendoza DD, Codella NC, Wang Y, et al Impact of diastolic dysfunction severity on

global left ventricular volumetric fi lling—assessment by automated segmentation of

rou-tine cine cardiovascular magnetic resonance J Cardiovasc Magn Reson 2010;12:46.

8 Starling EH The Linacre lecture on the law of the heart given at Cambridge 1915 London:

Longmans Green; 1918

9 Powner DJ, Hergenroeder GW Measurement of cardiac output during adult donor care

Prog Transplant 2011;21(2):144–50; quiz 151.

10 Marik PE, Cavallazzi R, Vasu T, Hirani A Dynamic changes in arterial waveform derived

variables and fl uid responsiveness in mechanically ventilated patients: a systematic

review of the literature Crit Care Med 2009;37(9):2642–2647.

11 de Waal EE, Wappler F, Buhre WF Cardiac output monitoring Curr Opin Anaesthesiol

2009;22(1):71–77

12 Cecconi M, Dawson D, Casaretti R, Grounds RM, Rhodes A A prospective study of the

accuracy and precision of continuous cardiac output monitoring devices as compared to

intermittent thermodilution Minerva Anestesiol 2010;76(12):1010–1017.

13 Rivers E, Nguyen B, Havstad S, et al Early goal-directed therapy in the treatment of

severe sepsis and septic shock N Engl J Med 2001;345(19):1368–1377.

14 Powner DJ, Doshi PB Central venous oxygen saturation monitoring: role in adult donor

care? Prog Transplant 2010;20(4):401–5; quiz 406.

15 Giraud R, Siegenthaler N, Gayet-Ageron A, Combescure C, Romand JA, Bendjelid K

ScvO(2) as a marker to defi ne fl uid responsiveness J Trauma 2011;70(4):802–807.

16 Ho KM, Harding R, Chamberlain J, Bulsara M A comparison of central and mixed venous

oxygen saturation in circulatory failure J Cardiothorac Vasc Anesth 2010;24(3):434–439.

Trang 15

ANSWERS TO THIS SECTION CAN BE FOUND ON PAGE 226

Cardiovascular Diseases

Jean Onwuchekwa Ekwenibe, Francisco Fuentes,

Siddharth Mukerji, Husnu Evren Kaynak, Nicoleta Daraban, Charles Hebenstreit, and

Ketan Koranne

QUESTIONS

The FDA-approved dosage for dabigatran etexilate in patients with renal insuffi ciency is:

1

A 150 mg orally twice daily

B 110 mg orally twice daily

C 75 mg orally twice daily

D 150 mg orally once daily

A patient presents with right-sided weakness and aphasia On subsequent workup, he

2

is found to have a dissection of the ascending thoracic aorta, which is extending into the

great arteries of the neck What is the fi rst step in management of this patient?

A Immediate surgery for repair of the aortic dissection

B Chest x-ray (CXR)

C Medical management of BP and heart rate (HR)

D Cardiac enzymes

16

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GENERAL CRITICAL CARE: PATHOLOGY, PATHOPHYSIOLOGY, AND THERAPY

218

A 48-year-old man with a history of hypertension and end-stage renal disease on

perito-4

neal dialysis is hospitalized for acute onset ischemic stroke Because onset of his symptoms

occurred 10 hours prior to presentation in the ED, he is treated conservatively with oral

aspirin On the third day of admission, he develops acute onset shortness of breath, and

a ventilation/perfusion (V/Q) scan confi rms a segmental pulmonary thromboembolus

He loses peripheral intravenous access, and attempts to reestablish it are unsuccessful

Peripheral blood draws are still possible What method of anticoagulation is preferable to

begin treatment for the pulmonary thromboembolism?

tions During his hospital course, he undergoes a diagnostic cardiac catheterization and

his hemodynamic tracings are shown below What is the most likely diagnosis for this

patient?

A Valvular aortic stenosis

B Supravalvular aortic stenosis

C Hypertrophic obstructive cardiomyopathy (HOCM)

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CARDIOVASCULAR DISEASES: Questions

219

A 58-year-old woman who suffers from a signifi cant

5

history of alcohol and substance abuse is admitted

to the ICU after she is discovered obtunded on the

street by police She is profoundly hypotensive

and hypoxic She is intubated for mechanical

ven-tilation, and IVs are placed for fl uid resuscitation

Initial serum chemistries are sent to the laboratory

and an ECG and chest x-ray (CXR) are completed

Her CXR is shown here A Swan–Ganz catheter

is placed to further assess her volume status, and

reveals a pulmonary capillary wedge pressure

(PCWP) of 10 An echocardiogram is also

com-pleted, and the results are still pending Which of

the following diagnoses is the least likely to be the

cause of the patient’s pulmonary edema?

onset of severe crushing, substernal chest pain radiating to the back Physical examination

demonstrated a BP of 200/130 mmHg, with a heart rate of 84 beats/minute Pulmonary

and cardiac examination revealed

no abnormalities Electrocardiogram

(ECG) showed no acute ST-T wave

changes, and cardiac enzymes were

negative Computed tomography

angiography (CTA) of the chest was

performed and revealed the fi ndings

shown here Which of the following is

the best approach for managing this

patient’s BP?

A Nicardipine infusion to reduce

the BP to a goal of 170/110 mmHg

over 3 to 6 hours

B Nicardipine infusion to reduce the BP immediately below 105 mmHg

C IV labetalol to rapidly reduce the SBP below 105 mmHg

D IV labetalol to reduce the BP to a goal of 170/100 mmHg over 3 to 6 hours

The commonly occurring ECG changes noted in patients with an subarachnoid

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GENERAL CRITICAL CARE: PATHOLOGY, PATHOPHYSIOLOGY, AND THERAPY

220

A patient with a history of smoking and hypertension presents with an ischemic stroke

8

During the stroke workup, he is incidentally found to have a 5.7-cm ascending aortic

aneurysm What is the next step in management of his aortic disease?

A Surgical consultation for aneurysm repair

B Smoking cessation

C Lipid profi le optimization

D Blood pressure (BP) management

The following parameters are obtained after performing a cardiac catheterization on a

9

38-year-old woman who presents with shortness of breath: Ao saturation, 97%; PA

satu-ration, 71%; hemoglobin, 14 g/dL; body surface area (BSA), 1.68 m2 What is the cardiac

output of this patient using the Fick formula?

A 3.5 L/minute

B 4.2 L/minute

C 2 L/minute

D 3.9 L/minute

E Cannot be calculated with the given data

A 72-year-old man with a history of type II

dia-10

betes mellitus and hypertension presents with

hypoxia and right-sided weakness Spiral CT scan

of the chest reveals bilateral segmental

pulmo-nary emboli, and MRI of the brain demonstrates a

left middle cerebral artery occlusion

Echocardio-graphy reveals a large thrombus partially crossing

a patent foramen ovale (PFO) Which of the

follow-ing is not a risk factor traditionally associated with

paradoxical embolization?

A Large size of PFO

B Presence of atrial septal aneurysm

C Prominent eustachian valve

D Mitral valve stenosis

All of the following are associated with neurogenic pulmonary edema (NPE)

A Presence of a CNS insult such as an subarachnoid hemorrhage (SAH), seizure, or

cere-brovascular accident (CVA)

B Decreased pulmonary capillary permeability

C Normal left ventricular systolic function

D Increased sympathetic response after a central nervous system (CNS) event

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CARDIOVASCULAR DISEASES: Questions

221

A 55-year-old woman presented to the ED complaining of worsening occipital headache

12

and confusion She was oriented to person but not to place or time On arrival, her BP

was 220/135 mmHg On physical examination, she was confused Papilledema was seen

on fundoscopic examination Laboratory studies demonstrated an elevated creatinine of

2.3 mg/dL ECG revealed left ventricular hypertrophy by voltage criteria and

nonspe-cifi c ST-T wave abnormalities in the lateral leads CT scan of the head without contrast

revealed diffuse bilateral white matter changes consistent with hypertensive

encephal-opathy Which of the following is the best next step in management?

A Reduction of the BP to 190/100 over 1 hour using nicardipine infusion

B Watchful observation over next 2 hours to determine whether the BP will

spontane-ously decrease

C Rapid reduction in the BP to 160/100 using IV labetalol

D Gradual reduction of BP over 24 to 48 hours using oral captopril and long-acting

nifedipineTall R wave on 12-lead ECG is noted in all the following conditions

A Duchenne muscular dystrophy

B Friedreich’s ataxia

C Limb girdle muscular dystrophy

D Facioscapulohumeral muscular dystrophy

What is the most important laboratory test for diagnosing acute pericarditis?

in acute myocardial infarction (MI) when performed by experienced operators?

A Primary stenting compared with angioplasty reduces mortality and recurrent

infarction

B Primary angioplasty results in lower stroke rates than thrombolysis

C Stenting in patients with an acute MI decreases the need for subsequent target vessel

revascularization

D Primary angioplasty results in higher coronary artery patency rates than thrombolysis

E Primary angioplasty results in lower mortality than thrombolysis

A 34-year-old woman with melanoma is admitted for mental status changes and is found

16

to have multiple brain metastases Restaging is performed and incidentally reveals

multiple bilateral subsegmental pulmonary emboli Physical examination is

remark-able for left lower extremity pitting edema, and doppler ultrasound reveals a partially

occlusive popliteal deep venous thrombosis What is the best treatment for her venous

thromboembolic disease?

A Inferior vena cava fi lter placement alone

B Inferior vena cava fi lter placement and thrombolytic therapy

C Dabigatran

D Systemic anticoagulation and systemic thrombolytic therapy

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GENERAL CRITICAL CARE: PATHOLOGY, PATHOPHYSIOLOGY, AND THERAPY

sion, diabetes mellitus, and hyperlipidemia

pre-sented to the ED 10 hours after sudden onset of

right arm and right leg weakness His mental

sta-tus was intact, and he was alert and oriented to

time, place, and person His BP on presentation

was 210/130 mmHg with a mean arterial

pres-sure (MAP) of 157 mmHg Physical examination

demonstrated 2/5 strength in the right upper and

lower extremities and 5/5 strength on the left side

No papilledema was seen on fundoscopic

exami-nation Laboratory studies were normal CT scan

of head without contrast showed no evidence of

acute hemorrhage MRI of the brain without

con-trast demonstrated the fi nding shown here Which

of the following is the best next step in managing

this patient’s hypertension?

A Gradual reduction of MAP by 15% to 20% over 3 hours

B Rapid reduction of BP to less than 185/110 mmHg

C Gradual reduction of MAP by 15% to 20% over 24 hours

D Watchful observation over 2 to 3 hours to determine whether the BP spontaneously

decreasesIdebenone is indicated in patients with Friedreich’s ataxia because:

19

A It decreases overall left ventricular mass

B It increases markers of oxidative damage, thus acting as a prognostic indicator for

pro-gression of disease

C It has no direct effect on left ventricular function

D All of the above

What is the most sensitive physical fi nding that suggests cardiac tamponade?

20

A Systemic arterial hypotension

B Elevated jugular venous pressure

C Pulsus paradoxus

D Tachycardia

Which of the following cardiac biomarkers will provide information about prognosis and

21

help in determining the patient’s possible infarct size?

A Creatinine kinase-MB fraction (CK-MB)

B Myoglobin

C Cardiac troponin T (cTnT)

D B-natriuretic peptide (BNP)

E Matrix metalloproteinase (MMP)

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CARDIOVASCULAR DISEASES: Questions

223

A 49-year-old woman with multiple sclerosis is being treated for acute pulmonary

throm-22

boembolism with IV heparin and warfarin She has a previous history of prophylactic

heparin use while inpatient One day after initiation of therapy, her platelet count has

fallen from 230,000 to 45,000 Physical examination reveals dusky areas on several digits

as well as edema in the left arm and hand, which was not seen previously What is the

next immediate step in management?

A Discontinuation of heparin, administration of vitamin K and argatroban

B Discontinuation of heparin, administration of bivalirudin

C Discontinuation of heparin, administration of enoxaparin

D Discontinuation of heparin, continued administration of warfarin to goal INR 2.0

to 3.0

A healthy 40-year-old man with no medical history travels to east Africa to join a hiking

23

expedition to trek to the top of Mount Kilimanjaro The group ascends to 3,500 meters

in 2 days On the third day of the expedition, he experiences diffi culty breathing,

head-ache, cough with pink frothy sputum, chest tightness, and congestion One of the guides

decides that it is no longer safe for him to continue the climb so together they begin their

descent down the mountain All of the following therapies are benefi cial in improving the

patient’s symptoms immediately except:

emia presented to the clinic with the complaint of pressure-like headache Her BP was

noted to be 180/120 mmHg She did not have any altered mental status and denied chest

pain or shortness of breath Neurological examination revealed no motor, sensory, or

cra-nial nerve defi cits No papilledema was seen on fundoscopic examination Which of the

following is the most appropriate approach in managing this patient’s hypertension?

A Oral short-acting antihypertensives under observation

B Reduction of BP to 155/100 mmHg over 3 to 6 hours using nicardipine infusion

C Rapid reduction of SBP to less than 100 mmHg using IV labetalol

D Reduction of BP to 155/100 mmHg over 24 hours using nicardipine infusion

According to current guidelines, in patients with cardiovascular implantable electric

25

devices (CIEDs) needing transcutaneous electrical nerve stimulation (TENS), the correct

statement is:

A TENS units can now be safely used in all patients with devices implanted after 2009

B Use of TENS units is not recommended because of possible electromagnetic

interference

C TENS units can be safely used in all patients except in the area of the thoracic spine

D TENS units can be safely used in all patients if the frequency utilized is less than

30 Hz

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GENERAL CRITICAL CARE: PATHOLOGY, PATHOPHYSIOLOGY, AND THERAPY

myocardial infarction (MI) except:

A Suspected aortic dissection

B Any prior intracranial hemorrhage

C Known malignant intracranial neoplasm (primary or metastatic)

D Severe uncontrolled hypertension on presentation (SBP > 180 mmHg or diastolic

blood pressure [DBP] > 110 mmHg)

E Signifi cant closed head or facial trauma within 3 months

Cardiogenic shock is defi ned by the presence of all of the following

A SBP < 80 mmHg for more than 30 minutes

B Decreased cardiac output resulting in decreased tissue perfusion

C Pulmonary arterial wedge pressure greater than 15 mmHg

D Cardiac index greater than 1.8 L/minute/m2

In patients being evaluated for cardiac resynchronization therapy, in addition to HF

B Malignant pericardial effusion

C Radiation-induced pericardial disease

D Post-myocardial infarction (MI) pericarditis

A 58-year-old man is admitted to the coronary care unit after a diagnosis of inferior

myo-31

cardial infarction (MI) The patient did not receive any thrombolytic or catheter-based

reperfusion therapy because he was not in the window for reperfusion The initial ECG

showed 1-mm ST elevation with ST depressions and pathologic Q waves in II, III, and

aVF Twenty-four hours after admission, the patient develops mild dyspnea and the chest

x-ray (CXR) shows pulmonary vascular redistribution A faint late systolic murmur is

heard at the apex What is the probable cause of the murmur?

A Infarcted posterior papillary muscle

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CARDIOVASCULAR DISEASES: Questions

Ventricular tachycardia (VT) ablation should be considered in

sce-narios except:

A A 23-year-old man with no evidence of structural heart disease and frequent episodes

of syncope related to VT

B A 67-year-old woman with coronary artery disease (CAD) and depressed systolic

function on optimal medical therapy with persistent VT

C A 56-year-old man on dofetilide therapy with recurrent episodes of VT

D A 47-year-old man with prior history of CAD, no evidence of systolic dysfunction, and

stage I prostate cancer with frequent episodes of symptomatic VTThe gold standard for diagnosis of neurocardiogenic syncope is:

Trang 24

ANSWERS

The answer is C.

1 Dabigatran etexilate is a prodrug that is rapidly converted to the active

direct thrombin (factor IIa) inhibitor dabigatran This conversion is independent of

cyto-chrome P-450, making drug–drug interactions less likely It is predominantly excreted via

a renal pathway Dabigatran was recently evaluated in a large, open-label, randomized

trial (RE-LY) in which it was compared with warfarin in 18,113 patients with

nonval-vular AF There was no difference in mortality with dabigatran compared to warfarin

Dabigatran appeared to be noninferior to warfarin with respect to the primary effi cacy

outcome of stroke or systemic embolism A dose of 150 mg twice daily was approved for

patients with a creatinine clearance more than 30 mL/minute, whereas in patients with

severe renal insuffi ciency (creatinine clearance 15–30 mL/minute) the approved dose is

75 mg twice daily The 110 mg twice-daily dose used in the RE-LY trial did not receive

FDA approval (1)

The answer is C.

manage-ment of aortic dissection In the absence of contraindications, IV β blockade should be

initiated and titrated to a target heart rate of 60 beats/minute or less In patients with

clear contraindications to β blockade, nondihydropyridine calcium channel–blocking

agents should be used as an alternative for rate control If the SBP remains greater than

120 mmHg after adequate heart rate control has been obtained, then

angiotensin-converting enzyme inhibitors and/or other vasodilators should be administered

intra-venously to further reduce BP while maintaining adequate end-organ perfusion

Beta-blockers should be used cautiously in the setting of acute aortic regurgitation because

they will block the compensatory tachycardia Urgent surgical consultation should be

obtained for all patients diagnosed with thoracic aortic dissection regardless of the

ana-tomic location (ascending vs descending) as soon as the diagnosis is made or highly

suspected (2)

16

Trang 25

CARDIOVASCULAR DISEASES: Answers

227

The answer is C.

(PVC), and during the beat following the PVC, there is an increase in the gradient between

the left ventricle and the aorta, as well as a decrease in the aortic systolic pressure This is

called the Brockenbrough–Braunwald–Morrow sign and signifi es dynamic outfl ow tract

obstruction In aortic stenosis and fi xed obstruction, in the beat following the PVC, there

is an increase in the aortic pressure, whereas in dynamic obstruction, there is a decrease in

the aortic pressure and an increase in the left ventricular pressure This is seen in HOCM

and can be observed during physical examination as well (3)

The answer is B.

glomeru-lar fi ltration rates less than 30, its longer half-life compared with unfractionated

hepa-rin presents an increased risk for bleeding complications in renal failure Subcutaneous

unfractionated heparin can be monitored by activated partial thromboplastin time (aPTT)

in a similar fashion to intravenous administration Subcutaneous fondaparinux is

con-traindicated in renal failure Oral warfarin cannot be used alone in initial management of

pulmonary embolism (4)

The answer is D.

edema can be diffi cult to determine; however, the diagnosis is important because

treat-ment is guided by the underlying pathophysiology Cardiogenic pulmonary edema occurs

as a result of an increase in pulmonary capillary hydrostatic pressure, which causes fl uid

extravasation into the interstitial space due to changes in oncotic pressure Noncardiogenic

pulmonary edema, in contrast, is a result of increased alveolar–capillary membrane

per-meability seen in disease states such as acute respiratory distress syndrome A Swan–Ganz

catheter can be helpful in distinguishing between the two entities The PCWP refl ects

fi lling pressures on the left side of the heart and indirectly intravascular volume status

Since the PCWP is normal in this patient, decompensated congestive HF is the least likely

etiology The remaining choices are examples of noncardiogenic pulmonary edema and

therefore could be present in the patient (5)

The answer is C.

chest on page 219 demonstrates a descending aortic dissection The appropriate

manage-ment goal for BP in aortic dissection is to rapidly reduce the SBP below 105 mmHg Either

intravenous labetalol or a combination of esmolol and nicardipine are the drugs of choice

Beta-blockers help to control the heart rate and reduce the shearing stress on the aorta,

and therefore should be used Nicardipine infusion alone is not the appropriate choice, as

it increases the shearing stress on the aorta Intravenous labetalol aiming at 15% to 25%

reduction in BP would be appropriate in neurological emergencies, but in aortic

dissec-tion, the BP should be reduced rapidly (6)

The answer is D.

abnormalities involving the ST segment, T wave, U wave, and QTc interval Because of the

combination of ST-segment elevation or depression and abnormal T-wave morphology,

myocardial ischemia or infarction is often suspected in patients with SAH Arrhythmias

are a relatively common occurrence as well Factors that may infl uence the development

of arrhythmias in patients with SAH include cerebral vasospasm, hypoxia, electrolyte

imbalance, and sudden increase in intracranial pressure triggering a sympathetic or vagal

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GENERAL CRITICAL CARE: PATHOLOGY, PATHOPHYSIOLOGY, AND THERAPY

228

discharge due to compression of brain structures Another well-recognized entity is the

T-wave abnormality The pattern of broad, slurred, inverted T waves associated with long

QTc intervals is commonly termed cerebral, neurogenic, or giant T waves The results have

indicated that ECG abnormalities are not a signifi cant predictor of mortality To date,

patients’ outcomes have not been studied in a prospective investigation that includes

a large sample size Whether the observed ECG changes are transient or permanent is

unclear (7)

The answer is A.

with an ascending aortic or aortic sinus of Valsalva diameter of 5.5 cm or greater

Patients with an aneurysm growth rate of more than 0.5 cm/year in the aorta that is

less than 5.5 cm in diameter should also be considered for surgery Stringent control of

hypertension, lipid profi le optimization, smoking cessation, and other atherosclerosis

risk-reduction measures should be instituted for patients with small aneurysms not

requiring surgery, as well as for patients who are not considered surgical or stent graft

candidates (2)

The answer is B.

demon-strated here:

[O2 consumption (mL/minute)]/[(AVO2 difference (mL O2/100 mL of blood) × 10)]

The oxygen consumption can be taken as 125 mL/minute/m2 in women, 110 mL/minute/

m2 in the elderly, and 140 mL/minute/m2 in men Since the patient’s BSA is 1.68 m2, the

total oxygen consumption is 210 mL/minute

O2 consumption: 125 mL/minute/m2 × 1.68 m2 = 210 mL/minute

The AVO2 difference is the amount of oxygen taken up by the tissues in muscle It is

the arterial oxygen content minus mixed venous oxygen content multiplied by 1.36 (this

number represents the fact that each gram of hemoglobin can carry 1.36 mL of O2) and by

the hemoglobin concentration

AVO2 difference: (AO2 − VO2) × 1.36 × hemoglobin

AVO2 difference: (0.97 − 0.71) × 1.36 × 14 = 4.95 mL O2/100 mL of blood

Placing all of the numbers back into the original formula:

Cardiac output (CO) = 210/(4.95 × 10) = 4.24 L/minute (8)

10 The answer is D Risk factors thought to be associated with increased risk of paradoxical

embolism include a large PFO, atrial septal aneurysm, prominent eustachian valve, and

conditions that cause elevated right atrial pressure, such as pulmonary embolism or

tri-cuspid regurgitation Conditions causing increased left atrial pressure are more likely to

decrease shunting across the PFO and decrease risk of paradoxical embolism (9)

11 The answer is B Several CNS insults can be complicated by the development of acute

pulmonary edema This occurrence has been termed neurogenic pulmonary edema (NPE)

and is not fully understood NPE is a form of noncardiogenic pulmonary edema, and

these patients are often found to have normal left ventricular systolic function CNS

insults associated with NPE include SAH, seizures, brain tumors, and CVAs Two main

theories about the mechanism of NPE are postulated in the literature: (a) the presence of

increased permeability of the pulmonary capillaries causing exudative edema and (b) a

Trang 27

CARDIOVASCULAR DISEASES: Answers

229

sympathetic discharge after a CNS event that produces hydrostatic edema Treatment for

NPE is supportive (10,11)

12 The answer is A Hypertensive emergencies are characterized by severe elevations in

BP (>180/120 mmHg) complicated by evidence of impending or progressive end organ

dysfunction Hypertensive encephalopathy is one such example The initial goal of

ther-apy in hypertensive emergencies is to reduce the mean arterial BP by 15% to 25% over

1 to 2 hours Rapid reduction in BP may precipitate renal, cerebral, or coronary ischemia

These patients must be managed in the ICU using IV antihypertensives for appropriate

titration of BP, and therefore use of oral antihypertensives is inappropriate (12)

13 The answer is D ECG abnormalities can be noted in up to 90% of patients with Becker

and Duchenne muscular dystrophy Tall R waves and an increased RS amplitude in V1

with deep narrow Q waves in the left precordial leads, are a characteristic ECG

pat-tern of the posterolateral left ventricular involvement Incomplete right bundle branch

block may also be noted, suggesting right ventricular involvement in these patients

Friedreich’s ataxia is commonly associated with concentric hypertrophic

cardiomyopa-thy and, at times, asymmetric septal hypertrophy Up to 95% of these patients manifest

ECG abnormalities Surprisingly, ECG manifestations do not always include left

ven-tricular hypertrophy, although echo demonstrates this Widespread T-wave

abnormali-ties are noted with tall R waves in all leads Limb-girdle muscular dystrophy is a

sarco-glycanopathy and is associated with cardiomyopathy ECG changes are consistent with

those seen in Becker and Duchenne muscular dystrophy Cardiac involvement is rare in

facioscapulohumeral muscular dystrophy Specifi c cardiac monitoring or treatment has

not yet been described (13)

14 The answer is B ECG is the most important laboratory test for diagnosing acute

peri-carditis A diagnosis of acute pericarditis should be reserved for patients with an audible

pericardial friction rub or chest pain with typical ECG fi ndings The classic presentation is

diffuse, concave upward ST-segment elevation and PR segment depression The

distinc-tion between acute pericarditis and transmural ischemia is usually not diffi cult because

of more extensive lead involvement in acute pericarditis and the presence of reciprocal

ST-segment depression in acute ischemia An echocardiogram and CXR would be useful

in identifying a pericardial effusion or other causes of chest pain, but have otherwise no

role in diagnosing pericarditis A signifi cant fraction of patients with pericarditis have

elevated creatinine kinase-MB fraction or troponin I values, which suggests concomitant

myocarditis (14)

15 The answer is A Primary angioplasty in patients with an acute MI, when performed by

experienced operators, has shown in large registries and randomized trials to result in

higher patency rates (93%–98% vs 54%) and lower 30-day mortality rates (5% vs 7%)

than thrombolytic therapy An additional advantage of primary angioplasty over

throm-bolysis is a signifi cant reduction in bleeding complications and strokes The

superior-ity of primary angioplasty to thrombolytic therapy is particularly evident in higher-risk

patients such as diabetics and the elderly The use of primary stenting versus primary

angioplasty does not result in a mortality advantage, but correlates well with a reduced

need for subsequent target vessel revascularization A meta-analysis of trials comparing

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GENERAL CRITICAL CARE: PATHOLOGY, PATHOPHYSIOLOGY, AND THERAPY

230

primary stenting with angioplasty found little difference in the rates of death (3.7% vs

3.6%) or recurrent MI (2.1% vs 2.9%) (15)

16 The answer is A Certain high-risk intracranial carcinomas such as melanoma, renal

cell cancer, thyroid cancer, and choriocarcinoma are strict contraindications to

sys-temic anticoagulation and syssys-temic thrombolysis Inferior vena cava fi lter placement is

indicated for treatment of pulmonary embolism when anticoagulation is not possible;

although anticoagulation in some cases is controversial and should be started once a

reversible contraindication has resolved (16)

17 The answer is A Cheyne–Stokes breathing is a central sleep apnea that is common in

patients with congestive HF and is seen in approximately 40% of patients Obstructive

sleep apnea is seen in 10% of patients These patients have an increased risk of mortality

and cardiac transplantation Central sleep apneas cause neurohumoral activation

(espe-cially norepinephrine), and this results in elevations in nocturnal BP and heart rate (17)

18 The answer is D This patient presented with an acute ischemic stroke MRI

demon-strates a left subcortical ischemic infarct In such patients, perfusion pressure distal to

the obstructed vessel is low, and compensatory vasodilation occurs to maintain adequate

blood fl ow A high systemic pressure is required to maintain blood fl ow in these dilated

vessels Therefore, in patients with ischemic stroke, BP should be carefully observed for

1 to 2 hours to see whether it will spontaneously decrease A persistent elevation in MAP

above 130 mmHg or SBP above 220 mmHg should be carefully treated with an aim to

lower the MAP by 15% to 20% Rapid reduction in BP may compromise the cerebral

per-fusion and worsen ischemia (18)

19 The answer is A Idebenone is a free-radical scavenger from the quinone family that is

also a synthetic analogue of Coenzyme Q10 It has been studied in an unblinded,

noncon-trolled trial and reportedly decreases the left ventricular mass in patients with Friedreich’s

ataxia signifi cantly However, no characteristics were identifi ed that separated responders

from nonresponders It is currently being studied in patients with Duchenne muscular

dystrophy and Alzheimer disease In patients with low ejection fraction (EF), an

improve-ment was noted after initiation of idebenone therapy It decreases markers of oxidative

damage, without a clear improvement in neurological outcome Thus, it reduces the rate

of cardiac function deterioration without actually halting the progression of ataxia (19)

20 The answer is C Pulsus paradoxus is the most sensitive, although not specifi c,

physi-cal fi nding that suggests cardiac tamponade Pulsus paradoxus represents a decrease in

the systolic arterial pressure of more than 10 mmHg with inspiration Systemic arterial

hypotension, elevated jugular venous pressure, and tachycardia are physical fi ndings

associated with cardiac tamponade, but are neither sensitive nor specifi c (20)

21 The answer is C Data support the use of cardiac biomarkers to estimate prognosis and

infarct size The GUSTO-III trial of over 12,000 patients showed that 16% of patients with

an elevated cardiac TnT had died within 30 days compared with 6% of those without

an enzyme leak A recent meta-analysis of patients with non-ST-segment elevation

myo-cardial infarction (STEMI) suggested that patients with elevated cardiac troponins had a

Trang 29

CARDIOVASCULAR DISEASES: Answers

231

greater than 3-fold increase of death compared with those with a normal value Troponins

are more specifi c to cardiac muscle, whereas CK-MB can rise in skeletal muscle damage

as well One-third of patients with acute myocardial infarction (MI) have an elevated cTn

despite a normal CK-MB Myoglobin, although fast in detecting damage, is not sensitive

BNP and MMP are newer markers correlating with muscle damage and plaque rupture,

but will need further studies for determining their effects on prognosis (21)

22 The answer is A Onset of heparin-induced thrombocytopenia (HIT) is typically within

24 hours of heparin administration when there is a history of previous heparin exposure,

but is otherwise seen in 5 to 14 days when there is no history of previous heparin

expo-sure Current recommendations from the American College of Chest Physicians (ACCP)

for HIT include discontinuation of heparin, avoidance of low-molecular-weight heparin,

and immediate initiation of an alternative parenteral anticoagulant such as bivalirudin

or argatroban When warfarin has been coadministered with heparin, the ACCP

recom-mends administration of vitamin K to prevent potential venous limb gangrene associated

with protein C defi ciency (22)

23 The answer is B The patient is suffering from high-altitude pulmonary edema (HAPE),

which is a form of noncardiogenic pulmonary edema HAPE can result from a rapid

ascension in altitude without proper acclimatization The mainstay of treatment is descent

for anything other than mild symptoms Oxygen is life saving and should be given at

4 L/minute for 4 to 6 hours In addition to oxygen, nifedipine, acetazolamide, and portable

hyperbaric chambers are all benefi cial therapies Nifedipine is thought to work by

dilat-ing the pulmonary vasculature, reducdilat-ing hydrostatic pressures and subsequent edema in

the lungs Acetazolamide is shown to accelerate acclimatization and acts as a stimulant to

induce breathing Portable hyperbaric chambers are widely used among climbing

expe-ditions and quickly fl ush carbon dioxide from the system Diuretics are not advised, or

should be used with substantial caution in patients with HAPE since many are already

depleted intravascularly and can clinically deteriorate (23,24)

24 The answer is A This patient has hypertensive urgency Hypertensive urgency is severe

elevation of BP (>180/120 mmHg) without any evidence of end organ damage This

patient’s only symptom is headache; there is no evidence of papilledema and no evidence

of cardiac, neurological, or renal complications In general, hypertensive urgency can be

managed using oral antihypertensive agents in an observation setting or outpatient

set-ting with close follow-up Excessive and rapid reduction in BP should be avoided to

pre-vent hypotension and compromising the cerebral perfusion (25,26)

25 The answer is B TENS is the use of electric current produced by a device to stimulate the

nerves for therapeutic purposes It covers the complete range of transcutaneously applied

currents used for nerve excitation, although more specifi cally the unit encompasses a

stimulator that produces pulses to treat pain It is usually connected to the skin using two

or more electrodes A typical battery-operated TENS unit is able to modulate pulse width,

frequency, and intensity Generally TENS is applied at high frequency (>50 Hz) with an

intensity below motor contraction (sensory intensity) or at low frequency (<10 Hz) with

an intensity that produces motor contraction According to the Heart Rhythm Society

(HRS)/American Society of Anesthesiologists (ASA) Expert Consensus Statement on the

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GENERAL CRITICAL CARE: PATHOLOGY, PATHOPHYSIOLOGY, AND THERAPY

232

Perioperative Management of Patients with Implantable Defi brillators, Pacemakers and

Arrhythmia Monitors: Facilities and Patient Management, the use of TENS units is not

recommended in patients with CIEDs TENS can interfere with pacemaker and

implant-able cardioverter-defi brillator (ICD) function Adverse responses include inhibition of

pacing (or triggering noise reversion mode) and inappropriate ICD therapy due to

mis-interpreted electrical noise The transcutaneous impulses could also be mismis-interpreted as

inappropriate supraventricular arrhythmia in atrial tachycardia devices High-frequency

stimulation (>30 Hz) should be maintained at all times TENS units should be avoided

in the thoracic spine, cervical spine, shoulder, upper lumbar, and chest areas because of

the proximity of the ICD or pacemaker (PM) and lead system These recommendations

generally extend to spinal cord stimulators as well (27)

26 The answer is A Viral pericarditis is the most common cause of pericardial

infec-tion Echoviruses and coxsackie viruses are most often involved The most defi nitive

way to diagnose viral pericarditis is by detection of DNA by polymeras chain reaction

(PCR) or in situ hybridization in pericardial fl uid or tissue This is rarely necessary, as

it will not change prognosis or course of treatment Tuberculous pericarditis remains

a major problem in the developing world and in immunocompromised patients

Bacterial pericarditis is usually caused by direct extension from empyema and

pneu-monia Hematogenous spread during bacteremia and contiguous spread after thoracic

surgery or trauma are also important Fungal infections can rarely cause pericarditis

Histoplasmosis is the most common cause in endemic areas Immunocompromised

patients are at increased risk (28)

27 The answer is D Severe uncontrolled hypertension on presentation (SBP > 180 mmHg

or DBP > 110 mmHg) is a relative contraindication for fi brinolytic therapy; however, it

could be an absolute contraindication in low-risk patients with MI Lowering the BP to

levels less than 180/110 mmHg will enable the physician to administer fi brinolytic

ther-apy, but catheter-based reperfusion methods would be preferred if available All the other

choices are absolute contraindications to fi brinolytic therapy, and in addition to those

mentioned previously, known structural vascular lesion (e.g., V malformation), ischemic

stroke within 3 months except acute ischemic stroke within 3 hours, active bleeding, or

bleeding diathesis are also contraindications to fi brinolytic therapy (29)

28 The answer is D Cardiogenic shock results in a low cardiac index The cardiac index is

used to measure the cardiac output, or the amount of blood pumped out of the left

ventri-cle each minute In cardiogenic shock, the cardiac index (CI) is less than 1.8 L/minute/m2

The cardiac index is derived by dividing the patient’s CO by the patient’s body surface

area (BSA)

CI = CO/BSA

CO is calculated by multiplying the patient’s stroke volume (SV) by the heart rate (HR)

Therefore, we can insert these entities into the previous equation

CI = (SV × HR)/BSA

Normal values for the cardiac index range from 2.6 to 4.2 L/minute/m2 The remaining

answer choices all defi ne the presence of cardiac shock and provide clinical clues that the

patient is unstable and needs additional hemodynamic support (30)

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CARDIOVASCULAR DISEASES: Answers

233

29 The answer is D Approximately 15% to 30% of all patients with HF and moderate to

severe symptoms have inter- and intraventricular conduction delays with QRS duration

greater than 120 milliseconds This results in mechanical dyssynchrony of right and left

ventricular contractions Furthermore, prolonged conduction has been associated with

adverse outcomes In a large study conducted in Italy involving more than 5,500 patients,

a left bundle branch block (LBBB) was associated with an increased 1-year mortality

from any cause (hazard ratio, 1.70; 95% confi dence interval, 1.41–2.05) LBBB was also

associated with an increased 1-year mortality rate from sudden death (hazard ratio, 1.58;

95% confi dence interval, 1.21–2.06) Multivariate analysis showed that this increased risk

of death due to LBBB was still signifi cant even after adjusting for age, underlying

car-diac disease, other indicators of HF severity, and prescription of angiotensin- converting

enzyme inhibitors and β-blockers A substudy analysis from the vesnarinone study

(VEST) assessed the relationship between QRS duration and mortality In this analysis,

3,654 resting, baseline ECGs of patients with NYHA Class II to IV HF were digitally

scanned Age, creatinine, LV ejection fraction (LVEF), heart rate, and QRS duration were

found to be independent predictors of mortality (p < 0001) Patients with wider QRS

durations (>200 milliseconds) had a 5 times greater risk of death than those with narrow

QRS durations (<90 milliseconds) On the basis of this fi nding, the authors concluded

that the resting ECG is a powerful, accessible, and inexpensive marker of prognosis in

dilated cardiomyopathy (31)

30 The answer is B Malignant pericardial disease is the most common cause of cardiac

tamponade in developed countries Lung carcinoma is the most common, accounting for

about 40% of malignant effusions; breast carcinoma and lymphomas are responsible for

about another 40% In most cancer patients with effusions, it is important that metastatic

involvement of the pericardium be confi rmed by identifi cation of malignant cells or tumor

markers in pericardial fl uid (32,33)

31 The answer is A The posterior papillary muscle is more susceptible to ischemia

than the anterior papillary muscle because of the nature of vascularization The

pos-terior muscle has one blood supply (pospos-terior descending branch of the right

coro-nary artery), whereas the anterior papillary muscle has dual blood supply (diagonal

branches of the left anterior descending artery and marginal branches of the

circum-fl ex artery) The clinical picture in Question 31 does not fi t a ruptured papillary muscle

scenario because the ruptured papillary muscle would cause a graver situation

result-ing in pulmonary edema Ventricular septal defect is also a mechanical complication

of MI; however, the physical examination fi ndings are not compatible, and a sternal

holosystolic murmur would be heard Tricuspid regurgitation and aortic stenosis are

not complications of MI (34)

32 The answer is C Amiodarone is a complex pharmacological agent with multiple adverse

effects on multiple organ systems Owing to its prolonged half-life (~100 days), organ

tox-icity is potentially more severe and more diffi cult to manage The more common effects

include a decrease in the diffusing capacity of the lung for carbon monoxide (DLCo),

interstitial pneumonitis, thyroid abnormalities, and photophobia, which can be seen in

15% to 60% of patients Neurological effects are typically dose dependent These include

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GENERAL CRITICAL CARE: PATHOLOGY, PATHOPHYSIOLOGY, AND THERAPY

234

ataxia, tremors, neuropathy, and paresthesias, with an incidence of 3% to 30% Adjusting

the dose results in resolution of symptoms Skin effects include photosensitivity and

dis-coloration, which may occur in 75% of patients These can be managed with reassurance

and sun block Ocular effects such as halo vision and optic neuritis can be noted in up

to 5% of cases, with incidence of photophobia being as high as 80% Reassurance is

rec-ommended, although the medication needs to be discontinued if optic neuritis occurs

Adverse cardiac reactions are uncommon Although prolongation of QT is expected,

tosades de pointes is noted in less than 1% of patients Ventricular systolic function is

not compromised (35)

33 The answer is C Selection of catheter ablation for an individual patient should

con-sider risks and benefi ts that are determined by patient characteristics, as well as the

availability of appropriate facilities with technical expertise In patients with

struc-tural heart disease, episodes of sustained VT are a marker for increased mortality; with

reduced quality of life in patients who have implanted defi brillators and structural

heart disease Antiarrhythmic medications can reduce the frequency of implantable

cardioverter-defi brillator (ICD) therapies, but have disappointing effi cacy and side

effects In the past, ablation was often not considered until pharmacological options

had been exhausted, often after the patient had suffered substantial morbidity from

recurrent episodes of VT and ICD shocks However, since the release of data of the

SMASH-VT trial, the general approach is changing Contraindications to this

proce-dure include:

i Presence of a mobile ventricular thrombus (epicardial ablation may be considered)

ii Asymptomatic premature ventricular complex (PVC) and/or nonsustained VT that

are not suspected of causing or contributing to ventricular dysfunctioniii VT due to transient, reversible causes, such as acute ischemia, hyperkalemia, or drug-

induced torsade de pointes (TdP) In our patient, it is imperative to rule out induced TdP before considering ablation (36)

drug-34 The answer is D Neurocardiogenic (vasovagal) syncope is the most common of a

group of refl ex (neurally mediated) syncopes, characterized by a sudden failure of the

autonomic nervous system to maintain blood pressure (BP) and sometimes heart rate

at a level suffi cient to maintain cerebral perfusion and consciousness A detailed

his-tory and physical examination are central to the diagnosis In the absence of another

identifi able cause, a compatible history is often suffi cient to make the diagnosis of

neu-rocardiogenic syncope Further testing is warranted if the diagnosis remains

uncer-tain Tilt-table testing is used to aid in the diagnosis Specifi city is about 90%, with

uncertain sensitivity Moreover, the reproducibility of the test (over time) is lower for

an initially positive response, making this test not completely reliable Implantable

loop recorders are small recording devices that are placed in a subcutaneous pocket

and can store about 45 minutes of retrospective ECG recording A diagnostic yield

of 25% to 40% has been reported with the use of the device during a period of 8 to

10 months The diagnostic effi cacy of EPS to determine the cause of syncope is highly

dependent on the degree of suspicion for the abnormality Positive results occurred

predominantly in patients with structural heart disease, as in heart failure (HF) There

is no gold standard for the diagnosis (37)

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CARDIOVASCULAR DISEASES: Answers

235

References

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the management of patients with atrial fi brillation (update on dabigatran) A report of the

American College of Cardiology Foundation/American Heart Association Task Force on

Practice Guidelines Heart Rhythm 2011;8(3):e1–e8.

2 Hiratzka LF, Bakris GL, Beckman JA, et al 2010 ACCF/AHA guidelines for the diagnosis

and management of patients with thoracic aortic disease: executive summary Circulation

2010;121:1544–1579

3 Libby P, Bonow RO, Mann DL, et al Braunwald’s Heart Disease: A Textbook of Cardiovascular

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12 Adams HP Jr, del Zoppo G, Alberts MJ, et al Guidelines for the early management of

adults with ischemic stroke: a guideline from the American Heart Association/American

Stroke Association Stroke Council, Clinical Cardiology Council, Cardiovascular

Radiology and Intervention Council, and the Atherosclerotic Peripheral Vascular

Disease and Quality of Care Outcomes in Research Interdisciplinary Working Groups:

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educa-tional tool for neurologists Circulation 2007;115(20):e478–e534.

13 Libby P, Bonow RO, Mann DL, et al Braunwald’s Heart Disease: A Textbook of Cardiovascular

Medicine 8th ed Philadelphia, PA: Saunders/Elsevier; 2008:2135–2142.

14 Lange RA, Hillis LD Clinical practice Acute pericarditis N Engl J Med 2004;

351(21):2195–2202

15 Libby P, Bonow RO, Mann DL, et al Braunwald’s Heart Disease: A Textbook of Cardiovascular

Medicine 8th ed Philadelphia, PA: Saunders/Elsevier; 2008:1301–1303, 1308.

16 Alvarado G, Noor R, Bassett R, et al Risk of intracranial hemorrhage with anticoagulation

therapy in melanoma patients with brain metastases Melanoma Res 2012;22:310–315.

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GENERAL CRITICAL CARE: PATHOLOGY, PATHOPHYSIOLOGY, AND THERAPY

236

17 Libby P, Bonow RO, Mann DL, et al Braunwald’s Heart Disease: A Textbook of Cardiovascular

Medicine 8th ed Philadelphia, PA: Saunders/Elsevier; 2008:1917–1918.

18 Lisk DR, Grotta JC, Lamki LM, et al Should hypertension be treated after acute stroke?

a randomized controlled trial using single photon emission computed tomography Arch

Neurol 1993;50:855–862.

19 Libby P, Bonow RO, Mann DL, et al Braunwald’s Heart Disease: A Textbook of Cardiovascular

Medicine 8th ed Philadelphia, PA: Saunders/Elsevier; 2008:2146–2147.

20 Libby P, Bonow RO, Mann DL, et al Braunwald’s Heart Disease: A Textbook of Cardiovascular

Medicine 8th ed Philadelphia, PA: Saunders/Elsevier; 2008:1835–1838.

21 Murphy JG, Lloyd MA Mayo Clinic Cardiology: Concise Textbook 3rd ed Boca Raton, FL:

Informa Healthcare; 2006:776

22 Kearon C, Kahn SR, Agnelli G, Goldhaber S, Raskob GE, Comerota AJ Antithrombotic

therapy for venous thromboembolic disease: American College of Chest Physicians

Evidence-based clinical practice guidelines (8th edition) Chest 2008;133(6 Suppl):

25 Lipsitz LA, Gagnon M, Vyas M, et al Antihypertensive therapy increases cerebral

blood fl ow and carotid distensibility in hypertensive elderly subjects Hypertension

2005;45(2):216–221

26 Bertel O, Marx BE, Conen D Effects of antihypertensive treatment on cerebral perfusion

Am J Med 1987;82(3B):29–36.

27 Crossley GH, Poole JE, Rozner MA, et al The Heart Rhythm Society (HRS)/American

Society of Anesthesiologists (ASA) Expert Consensus Statement on the perioperative

management of patients with implantable defi brillators, pacemakers and arrhythmia

monitors: facilities and patient management this document was developed as a joint

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American Heart Association (AHA), and the Society of Thoracic Surgeons (STS) Heart

Rhythm 2011;8(7):1114–1154.

28 Libby P, Bonow RO, Mann DL, et al Braunwald’s Heart Disease: A Textbook of Cardiovascular

Medicine 8th ed Philadelphia, PA: Saunders/Elsevier; 2008: 1846–1848.

29 Willerson J, Cohn JN, Wellens HJJ, Holmes DR Textbook of Cardiovascular Medicine

3rd ed London, United Kingdom: Springer Verlag; 2007: 966

30 Libby P, Bonow RO, Mann DL, et al Braunwald’s Heart Disease: A Textbook of Cardiovascular

Medicine 8th ed Philadelphia, PA: Saunders/Elsevier; 2008: 1269.

31 Saxon LA, DeMarco T, Prystowsky EN, et al Effects of long-term biventricular

stimu-lation for rsynchronization on ehocardiographic measures of remodeling Circustimu-lation

2002;105:1304–1310

32 Little WC, Freeman GL Pericardial disease Circulation 2006;113(12):1622–1632.

33 Spodick DM Acute cardiac tamponade N Engl J Med 2003;349:684.

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myocardial infarction Coron Artery Dis 2002;13(6):337–344.

35 Goldschlager N, Epstein AE, Naccarelli GV, et al A practical guide for clinicians who treat

patients with amiodarone: 2007 Heart Rhythm 2007;4(9):1250–1259.

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CARDIOVASCULAR DISEASES: Answers

237

36 Aliot EM, Stevenson WG, Almendral-Garrote JM, et al EHRA/HRS Expert Consensus

on Catheter Ablation of Ventricular Arrhythmias: developed in a partnership with the

European Heart Rhythm Association (EHRA), a registered branch of the European

Society of Cardiology (ESC), and the Heart Rhythm Society (HRS); in collaboration with

the American College of Cardiology (ACC) and the American Heart Association (AHA)

Heart Rhythm 2009;6(6):886–933.

37 Libby P, Bonow RO, Mann DL, et al Braunwald’s Heart Disease: A Textbook of Cardiovascular

Medicine 8th ed Philadelphia, PA: Saunders/Elsevier; 2008: 977–983.

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ANSWERS TO THIS SECTION CAN BE FOUND ON PAGE 249

Pulmonary Physiology and

Fundamentals of Mechanical Ventilation

David J Powner

QUESTIONS

The respiratory center sensitive to CO

Chemo-receptors sensitive to hypoxemia (PaO2 < about 60 torr) and its effect on hydrogen

ion sensitivity are located in the:

A Carotid and aortic bodies

B Pulmonary artery oxygen sensors at the fi rst division of the main pulmonary artery

C Oxygen sensory center(s) in the medial and lateral dorsal brainstem

D Left ventricular sensor(s) associated with pro-brain natriuretic peptide release sites

E Neurofi brillary bodies at bifurcation of femoral arteries from the aorta

17

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GENERAL CRITICAL CARE: PATHOLOGY, PATHOPHYSIOLOGY, AND THERAPY

240

As the spontaneously breathing patient initiates inspiration, the subambient pleural

pres-2

sure is transmitted through the open airways, overcomes the inertia of atmospheric gas

molecules and initiates the inspiratory gas fl ow into the patient This fl ow is another

mea-sure of parenchymal “distensibility” and is proportional to the amount of subambient

pressure created by the muscles of inspiration This measure, Δfl ow ÷ Δpressure, is:

A Pulmonary conductance

B Pulmonary resistance

C Pulmonary compliance

D Airway fl ow capacitance

E Flow-gated airway distension

At the end of inspiration gas fl ow into the lung stops, turbulence subsides and a tidal

3

volume has been delivered The tidal volume is also proportional to the transpulmonary

inspiratory pressure created by the patient during spontaneous inhalation or by the

ven-tilator during mechanical infl ation, that is, Δvolume ÷ Δpressure This relationship is

known as:

A Pulmonary conductance

B Pulmonary resistance

C Pulmonary compliance

D Functional residual capacity (FRC)

E Airway volume capacity

The tidal volume produced at the end of inspiration has distended airways and lung units

4

As the muscles of inspiration relax, a recoil force is created that initiates and maintains an

outward fl ow of gas, which is proportional to the amount of distension created by the tidal

inhalation The relationship is known as:

loss The relative humidity of inhaled gas is increased to 100% at body temperature and

atmospheric pressure In which anatomic area is this important respiratory function

pre-dominately accomplished?

A Distal airways beyond the terminal bronchiole

B Respiratory bronchioles

C Nose and trachea

D Segmental bronchi beyond division two airways

E All of the above

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PULMONARY PHYSIOLOGY AND MECHANICAL VENTILATION: Questions

241

The so-called “bulk” fl ow of gas responding to changes in pleural pressure occurs through

6

the terminal bronchiole (16th of the 23 normal airway divisions) Distal to the terminal

bronchiole, gas-in-gas migration carries oxygen to the alveolo-capillary membrane (ACM)

and CO2 from it Which statement describes this gas-in-gas diffusion correctly?

A Oxygen diffuses more quickly than CO2 but dissolves more slowly in the ACM

B Oxygen diffuses more slowly than CO2 and dissolves more slowly in the ACM

C Oxygen diffuses more quickly than CO2 and dissolves more quickly in the ACM

D Both gases diffuse and dissolve equally

The primary determinant of the normal distribution of blood perfusion in the lung is:

E Pulmonary vascular resistance

John West, MD, has described three lung zones that characterize normal and potentially

8

abnormal ventilation and perfusion relationships West’s zone 1 is abnormal, may

pro-duce increased dead space or erroneous interpretations of pulmonary artery occlusion

pressure measurements, and is characterized by:

A Airway pressure > venous capillary pressure > arteriolar capillary pressure

B Venous capillary pressure > arteriolar capillary pressure > airway pressure

C Arteriolar capillary pressure > venous pressure > airway pressure

D Left atrial pressure > “wedge” pressure > bronchial airway pressure

E Airway pressure > arteriolar capillary pressure > venous capillary pressure

Dalton’s Law reminds us that the sum of the partial pressures of gases in the airway must

lungs and may lead to microatelectasis throughout poorly ventilated lung units Nitrogen

washout normally occurs in about:

A An hour

B 8 minutes

C 15 to 20 minutes

D 24 hours

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GENERAL CRITICAL CARE: PATHOLOGY, PATHOPHYSIOLOGY, AND THERAPY

242

As gas fl ows into and out of the lung, impedance forces in the form of mucus, bifurcations

11

in the airways, bronchoconstriction, and so on are encountered that are proportional to

the gas fl ow (ΔP ÷ Δfl ow) This measures:

A Pulmonary compliance

B Pulmonary elastance

C Pulmonary resistance

D Pulmonary conductance

The equation: Vg = (A) (

(where A is the cross-sectional area of open alveoli, ΔP the pressure gradient for gas, L is

the length of pathway, and viscos is the viscosity of pathway), describes what respiratory

function?

A Transcapillary blood fl ow from pulmonary arteriole to pulmonary venule

B Gas fl ow along airways distal to the terminal bronchioles

C Oxygen delivery to peripheral tissue beds

D Oxygen content in the blood

E Gas diffusion across the alveolo-capillary membrane (ACM)

A pulmonary ventilation:perfusion (V/Q) mismatch described as a “shunt” or “shunt

13

effect” describes a preponderance of lung units in which:

A Dead space (VD/VT) to tidal volume ratio is increased

B Airway ventilation is greater than capillary perfusion

C Capillary perfusion exceeds airway ventilation

D Carbon dioxide retention occurs

E Pulmonary edema occurs

The primary determinants of CO

equation, which includes:

A Transpulmonary pressure gradient

B Inspiratory force (negative pressure generated by patient)

C Zones of V/Q shunting

D Functional residual capacity (FRC)

E Zones of dead space effect

During mechanical ventilation, the primary determinant(s) of oxygenation is/are:

15

A Fraction of inspired oxygen (FIO2)

B Positive end-expiratory airway pressure (PEEP)

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