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Ebook Neurocritical care board review: Part 2

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II
General Critical Care:
Pathology, Pathophysiology,
and Therapy

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15
Cardiovascular Physiology
David J. Powner
QUESTIONS

1. The four determinants of cardiac output include:
A. Diastolic time
B. Heart rate
C. Systolic time interval
D. Arterial pulse–pressure variation
E. All of the above
F. None of the above
2. Complete the following equation:
Pressure = ______ × Resistance
A. Afterload
B. Volume


C. Flow
D. Heart rate
E. Impedance

ANSWERS TO THIS SECTION CAN BE FOUND ON PAGE 209

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GENERAL CRITICAL CARE: PATHOLOGY, PATHOPHYSIOLOGY, AND THERAPY

3. The components of the equation for oxygen content of blood (mL O2/100 mL blood)
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 coefficient of oxygen in blood
4. The partial pressure or percent hemoglobin saturation of oxygen in blood drawn slowly
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
5. To compare cardiovascular parameters among patients and to normalize values, measurements 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
6. The ejection fraction measured by echocardiography primarily evaluates:
A. Myocardial contractility
B. Valvular incompetence or stenosis
C. Cardiac output
D. Venous preload
E. Vascular resistance
7. The thermodilution method of cardiac output measurement by iced-saline injection utilizes 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
8. The normal partial pressure of oxygen in a properly collected mixed venous blood
sample is:
A. 40 mmHg
B. 65 to 70 mmHg
C. 100 mmHg
D. 65% to 70%
E. None of the above

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CARDIOVASCULAR PHYSIOLOGY: Questions

9. Anatomic mixing of venous blood from the superior and inferior venae cavae occurs in
the:
A. Right atrium
B. Pulmonary artery
C. Left atrium
D. Pulmonary veins
E. None of the above
10. The pulmonary artery “wedge” or occlusion pressure is intended to reflect and direct
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
11. Which cardiac variable listed here increases in proportion to preload?
A. Left ventricular (LV) systolic filling
B. Mitral stenosis
C. Left atrial dp/dt during atrial fibrillation
D. Contractility
E. Right atrial systole during atrial fibrillation
12. Although “shunt” has been discussed throughout sections about the lung, the actual
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 flow, that is, shunt flow/total flow.
Stated another way, it is the percentage of cardiac output that does not effectively participate 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
13. The arterial pulse pressure variation is used by some cardiac output monitoring devices
to suggest that the patient will benefit 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

14. Arterial pressure waveform analysis is used by several commercially available devices
to measure cardiac output. These devices calculate the cardiac output after using arterial
waveform analysis to define:
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 first 0.04 seconds of the arterial pressure during systole
E. The area under the curve of the diastolic relaxation waveform
15. The oxygen saturation in blood drawn from a thoracic central venous catheter has been

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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15
ANSWERS

1. The answer is B. The four determinants of cardiac output are preload, afterload, heart
rate, and contractility. Heart rate is a straightforward measurement, except when myocardial efficiency is altered by various dysrhythmias.
i. Afterload (or more properly, impedance) is usually evaluated by the equation for systemic 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
is calculated as:
LVSWI = 0.0136 (MAP – PCWP) × SVI

where PCWP, pulmonary capillary wedge (occluded) pressure; SVI, stroke volume
index (CI/heart rate) (Normal: 40–60 g·m/m2)
iii. Preload is the volume of blood returning to the heart (usually per minute), best measured as the left ventricular end-diastolic volume (LVEDV). This volume has traditionally been represented by a pressure, variously available as the pulmonary artery
occlusion (wedge) pressure, which corresponds to the left atrial pressure that represents LV end-diastolic pressure (LVEDP). Another clinical estimate has been the
pulmonary artery diastolic pressure when any of the preceding pressures are unavailable. As a function of physiology, for a pressure to represent a volume, especially as

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a trended variable overtime, their relationship, that is, ΔP representing a ΔV, must
be constant. This relationship, ΔV/ΔP, defines 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 during mechanical ventilation may make interpretation of these pressures more difficult.
Therefore, defining preload remains difficult because of the imprecise methodology
used to measure it (1,2).
2. The answer is C. This is a fundamental equation in many aspects of physiology and is
modified for cardiovascular issues as:
Blood pressure = Cardiac output × Systemic vascular resistance
As a flow 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.
3. The answer is E. The oxygen content of arterial blood in mL O2/100 mL blood is determined 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 coefficient 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 residual 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; normal 40 mmHg), blood Hgb, and Hgb saturation (SvO2; normal 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


Therefore, it is possible and clinically important to compare oxygen supply to oxygen
consumed by the entire body. Organ-specific demand/supply relationships would be
important, but are unavailable unless the specific 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 provides 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 flow 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 concentration 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 specialized 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).
4. The answer is B. 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.
5. The answer is E. The “indexing” of many parameters allows a normal value for that
parameter to be determined among patients with differing body configurations. 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, or
BSA = 0.007184 × Weight0.425 × Height0.725
6. The answer is A. 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 reflects work done
by the left ventricle to overcome outflow impedance. Contractility is difficult 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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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).
7. The answer is C. The traditional thermodilution method of measuring cardiac output
has evolved from Stewart’s original work in the 1890s to the traditional method of injecting iced or room temperature saline into the pulmonary artery. This injection of a known
quantity of injectate at a known temperature into a flowing 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, specific heats of injectate and blood (constants); Kcal, calibration constant; Si and Sb, specific gravity of injectate and blood
(constants); Kcor, temperature loss constant; Tb and Ti, baseline blood and injectate temperatures; integral term, area under thermal curve of temperature change versus time.
Continuous cardiac output pulmonary artery catheters (PACs) use similar changes in pulmonary blood temperature, but instead generate a burst of heat (not cold) into the bloodstream, and the change in blood temperature is sensed along a thermistor filament within
the catheter.
8. The answer is A. See Answer 3 for a more complete discussion. Abnormal PvO2, either
below or above normal, will help evaluate the predominant abnormality in cardiovascular 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 reflection of the oxyhemoglobin dissociation curve.
The “30–60-90” guideline is a useful rule of thumb describing Hgb-association parameters: 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.
9. The answer is E. Streaming of blood from the superior and inferior venae cavae into the
relatively small right atrium does not achieve full mixing. Mixing occurs in the right ventricle (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 possible, 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

be a linear (straight-line) relationship between the two variables of pressure and volume.
The relationship between left ventricular end-diastolic volume (LVEDV) and LV enddiastolic pressure (LVEDP) reflects LV compliance (ΔV/ΔP). Therefore, LV compliance
must be constant (and normal) if LVEDP (or its surrogate, the PA wedge pressure) is to
accurately reflect 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 conditions 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 influence on treatment.
11. The answer is D. Starling, using Howell and Donaldson’s IV fluid venous reservoir to
simulate venous return, showed the heart’s ability to increase its output as venous preload 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 capillary oxygen content of an idealized “perfect” alveolus adjacent to a “perfect” capillary. 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
compares 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 failure (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 quantifies 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”
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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 systolic pressure variabilities. When the calculated arterial pulse pressure variability reaches
a particular magnitude (10%–13%), the manufacturer recommends rapid fluid administration 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 reflects that contractility. Therefore, SV is proportional to
the force of systolic contraction as assessed by the arterial waveform. This contractile force
is also influenced 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)/Z
where 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 pulmonary 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 defined.

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, rightheart chambers, and pulmonary vessels of healthy subjects. J Lab Clin Med. 1957;50(1):
93–106.

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CARDIOVASCULAR PHYSIOLOGY: Answers

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 filling—assessment by automated segmentation of routine 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 fluid 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 define fluid 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.

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16
Cardiovascular Diseases
Jean Onwuchekwa Ekwenibe, Francisco Fuentes,
Siddharth Mukerji, Husnu Evren Kaynak,
Nicoleta Daraban, Charles Hebenstreit, and
Ketan Koranne
QUESTIONS

1. The FDA-approved dosage for dabigatran etexilate in patients with renal insufficiency is:
A. 150 mg orally twice daily
B. 110 mg orally twice daily
C. 75 mg orally twice daily
D. 150 mg orally once daily
2. A patient presents with right-sided weakness and aphasia. On subsequent workup, he
is found to have a dissection of the ascending thoracic aorta, which is extending into the
great arteries of the neck. What is the first 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

ANSWERS TO THIS SECTION CAN BE FOUND ON PAGE 226

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GENERAL CRITICAL CARE: PATHOLOGY, PATHOPHYSIOLOGY, AND THERAPY

3. A 57-year-old man is admitted for progressive shortness of breath, chest pain, and palpitations. 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)
D. Aortic coarctation

200

200

180


180

160

160

140

140

120

120

100

100

80

80

60

60

40

40


20

20

PVC

0

0
9:25:33 AM

9:25:34 AM

9:25:35 AM

9:25:36 AM

9:25:37 AM

4. A 48-year-old man with a history of hypertension and end-stage renal disease on peritoneal 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 confirms 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?
A. Subcutaneous enoxaparin
B. Subcutaneous unfractionated heparin
C. Subcutaneous fondaparinux
D. Oral warfarin


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CARDIOVASCULAR DISEASES: Questions

5. A 58-year-old woman who suffers from a significant
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 ventilation, and IVs are placed for fluid 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 completed, 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?
A. Aspiration pneumonia
B. Septic shock
C. Subarachnoid hemorrhage (SAH)
D. Decompensated congestive HF
6. A 55-year-old man with chronic arterial hypertension for 16 years presented with sudden
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 findings
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
7. The commonly occurring ECG changes noted in patients with an subarachnoid hemorrhage (SAH) include all of the following except:
A. ST-segment elevation
B. ST-segment depression
C. QTc interval prolongation
D. PR segment prolongation

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8. A patient with a history of smoking and hypertension presents with an ischemic stroke.
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 profile optimization
D. Blood pressure (BP) management
9. The following parameters are obtained after performing a cardiac catheterization on a
38-year-old woman who presents with shortness of breath: Ao saturation, 97%; PA saturation, 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
10. A 72-year-old man with a history of type II diabetes mellitus and hypertension presents with
hypoxia and right-sided weakness. Spiral CT scan
of the chest reveals bilateral segmental pulmonary emboli, and MRI of the brain demonstrates a
left middle cerebral artery occlusion. Echocardiography reveals a large thrombus partially crossing
a patent foramen ovale (PFO). Which of the following 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

11. All of the following are associated with neurogenic pulmonary edema (NPE) except:
A. Presence of a CNS insult such as an subarachnoid hemorrhage (SAH), seizure, or cerebrovascular 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

12. A 55-year-old woman presented to the ED complaining of worsening occipital headache
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 nonspecific ST-T wave abnormalities in the lateral leads. CT scan of the head without contrast
revealed diffuse bilateral white matter changes consistent with hypertensive encephalopathy. 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 spontaneously 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
nifedipine
13. Tall R wave on 12-lead ECG is noted in all the following conditions except:
A. Duchenne muscular dystrophy
B. Friedreich’s ataxia
C. Limb girdle muscular dystrophy
D. Facioscapulohumeral muscular dystrophy
14. What is the most important laboratory test for diagnosing acute pericarditis?
A. 2D echocardiogram

B. ECG
C. Chest x-ray (CXR)
D. Cardiac enzymes
15. Which of the following statements does not apply to catheter-based reperfusion therapy
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
16. A 34-year-old woman with melanoma is admitted for mental status changes and is found
to have multiple brain metastases. Restaging is performed and incidentally reveals
multiple bilateral subsegmental pulmonary emboli. Physical examination is remarkable 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 filter placement alone
B. Inferior vena cava filter placement and thrombolytic therapy
C. Dabigatran
D. Systemic anticoagulation and systemic thrombolytic therapy
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17. Sleep-disordered breathing is common in patients with heart failure (HF).
A. True
B. False
18. A 72-year-old man with a history of hypertension, diabetes mellitus, and hyperlipidemia presented to the ED 10 hours after sudden onset of
right arm and right leg weakness. His mental status 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 pressure (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 examination. Laboratory studies were normal. CT scan
of head without contrast showed no evidence of
acute hemorrhage. MRI of the brain without contrast demonstrated the finding 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
decreases
19. Idebenone is indicated in patients with Friedreich’s ataxia because:
A. It decreases overall left ventricular mass
B. It increases markers of oxidative damage, thus acting as a prognostic indicator for progression of disease
C. It has no direct effect on left ventricular function
D. All of the above
20. What is the most sensitive physical finding that suggests cardiac tamponade?
A. Systemic arterial hypotension
B. Elevated jugular venous pressure
C. Pulsus paradoxus
D. Tachycardia
21. Which of the following cardiac biomarkers will provide information about prognosis and

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

22. A 49-year-old woman with multiple sclerosis is being treated for acute pulmonary thromboembolism 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
23. A healthy 40-year-old man with no medical history travels to east Africa to join a hiking
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 difficulty breathing, headache, 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 beneficial in improving the

patient’s symptoms immediately except:
A. Nifedipine
B. Lasix
C. Supplemental oxygen
D. Hyperbaric treatment
E. Acetazolamide
24. A 60-year-old woman with a history of hypertension, diabetes mellitus, and hyperlipidemia 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 cranial nerve deficits. 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
25. According to current guidelines, in patients with cardiovascular implantable electric
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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26. What is the most common form of pericardial infection?
A. Viral infection
B. Tuberculosis
C. Bacterial infection
D. Fungal infection
27. All the following situations are absolute contraindications to fibrinolytic therapy in acute
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. Significant closed head or facial trauma within 3 months
28. Cardiogenic shock is defined by the presence of all of the following except:
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
29. In patients being evaluated for cardiac resynchronization therapy, in addition to HF
symptoms, the QRS duration on surface ECG should be at least:
A. 100 milliseconds
B. 110 milliseconds
C. 115 milliseconds
D. 120 milliseconds
30. What is the leading cause of cardiac tamponade in developed countries?
A. Viral pericarditis
B. Malignant pericardial effusion

C. Radiation-induced pericardial disease
D. Post-myocardial infarction (MI) pericarditis
31. A 58-year-old man is admitted to the coronary care unit after a diagnosis of inferior myocardial 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
B. Tricuspid regurgitation
C. Ventricular septal defect
D. Aortic stenosis
E. Ruptured posterior papillary muscle

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CARDIOVASCULAR DISEASES: Questions

32. The following have been documented as adverse effects in more than 1% of patients taking amiodarone except:
A. Peripheral neuropathy
B. Photosensitivity
C. Worsening of ejection fraction (EF) by less than 5%
D. Halo vision
33. Ventricular tachycardia (VT) ablation should be considered in all of the following scenarios 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 VT
34. The gold standard for diagnosis of neurocardiogenic syncope is:
A. Tilt-table testing
B. Implantable loop recorder
C. Electrophysiological study
D. None of the above

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16
ANSWERS

1. The answer is C. Dabigatran etexilate is a prodrug that is rapidly converted to the active
direct thrombin (factor IIa) inhibitor dabigatran. This conversion is independent of cytochrome 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 nonvalvular AF. There was no difference in mortality with dabigatran compared to warfarin.
Dabigatran appeared to be noninferior to warfarin with respect to the primary efficacy
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 insufficiency (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).
2. The answer is C. Medical management of BP and heart rate is the first step in management 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 angiotensinconverting enzyme inhibitors and/or other vasodilators should be administered intravenously to further reduce BP while maintaining adequate end-organ perfusion. Betablockers 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 anatomic location (ascending vs. descending) as soon as the diagnosis is made or highly
suspected (2).

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CARDIOVASCULAR DISEASES: Answers

3. The answer is C. The following tracing demonstrates a premature ventricular complex
(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 signifies dynamic outflow tract
obstruction. In aortic stenosis and fixed 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).
4. The answer is B. Although subcutaneous enoxaparin can be dose adjusted for glomerular filtration rates less than 30, its longer half-life compared with unfractionated heparin 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 contraindicated in renal failure. Oral warfarin cannot be used alone in initial management of
pulmonary embolism (4).
5. The answer is D. The distinction between cardiogenic and noncardiogenic pulmonary
edema can be difficult to determine; however, the diagnosis is important because treatment is guided by the underlying pathophysiology. Cardiogenic pulmonary edema occurs
as a result of an increase in pulmonary capillary hydrostatic pressure, which causes fluid
extravasation into the interstitial space due to changes in oncotic pressure. Noncardiogenic
pulmonary edema, in contrast, is a result of increased alveolar–capillary membrane permeability 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 reflects
filling 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).
6. The answer is C. This patient presents with hypertensive emergency. The CTA of the
chest on page 219 demonstrates a descending aortic dissection. The appropriate management 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 dissection, the BP should be reduced rapidly (6).
7. The answer is D. ECG changes associated with an SAH primarily reflect repolarization
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 influence 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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