B. Monitoring during CPB is usually done by the perfusionists. They monitor the

pump flow rate, venous reservoir level, arterial inflow line pressure, blood (perfusate

and venous) and myocardial temperatures, and in-line (arterial and venous) oxygen

saturations. In-line pH, CO2

tension, and oxygen-tension sensors are also available in

newer bypass machines. But most machines do not provide a glucose monitor, and

hypoglycemia is still a threat. Blood gas tensions and pH are confirmed by direct

measurements periodically—30 minute-intervals. Inadequate tissue perfusion caused

by inadequate flow rates is evidenced by low venous oxygen saturations (<70%),

progressive metabolic acidosis, or low urinary output, provided there is no

hypoxemia.

During bypass, arterial inflow line pressure is almost always higher than the

systemic arterial pressure recorded from a radial artery or even an aortic catheter,

caused by the pressure drop across the arterial filter, the arterial tubing, and the

narrow opening of the aortic cannula.

35. A. Before discontinuing ventilation after initiation of CPB, it is a good practice to

confirm whether full flow has been attained with the perfusionist. Discontinuing

ventilation prematurely causes any remaining pulmonary blood flow to act as a rightto-left shunt, which can promote hypoxemia. The extent of hypoxemia depends on the

relative ratio of remaining pulmonary blood flow to pump flow. Once the heart stops

ejecting blood, ventilation can be discontinued. Following institution of full CPB,

ventricular ejection may continue for a brief period of time.

36. D. Epiaortic echocardiography is the most sensitive and specific technique to

detect air bubbles at the termination of CPB. De-airing is facilitated by head-down

position, and venting before and during initial cardiac ejection, in addition to filling

up the heart with vent in place. TEE is very useful in detecting pockets of air,

especially within the left ventricle. But the risk of atheromatous emboli still persists

and is worse in cases where aorta was manipulated extensively, cross-clamped

numerous times and in percutaneous transcatheter aortic valve replacements. Newer

devices with baskets to catch such emboli have proven to be very useful.

37. B. Sweating during rewarming is a hypothalamic response to perfusion with blood,

which is often at 39°C. It is important to remember to administer anesthetic agents,

and sometimes additional muscle relaxants, during the rewarming phase. The

incidence of awareness/recall is high during rewarming because the inhalational agent

delivered via the oxygenator is turned off just prior to termination of CPB to avoid

residual myocardial depression.

38. A. pH-stat management refers to the practice of temperature-correcting gas

tensions by adding CO2 and maintaining a “normal” CO2

tension of 40 mm Hg and a

pH of 7.40 during hypothermia. α-Stat management, on the other hand, refers to the

use of uncorrected gas tensions during hypothermia. This does not require addition of

CO2 and has been shown to preserve cerebral autoregulation and improve

myocardial preservation. At physiologic pH, the histidine residues of intracellular

proteins play a major role in maintaining electrical neutrality. pH-stat management is

commonly used in pediatric cardiac surgery, but α-stat is more commonly used in

adult cardiac surgery.

39. B. Rapid rewarming can release gas bubbles that were dissolved rapidly back into

the blood stream. It also results in large temperature gradients between well-perfused

organs and peripheral vasoconstricted tissues. The body equilibrates this gradient

following separation from CPB, and patient may become hypothermic again. Methods

used to speed the rewarming process include infusion of a vasodilator drug

(nitroprusside or nitroglycerin) and allowing some pulsatile flow (ventricular

ejection).

40. A. Separation from CPB can be guided by a mnemonic:

A = Airway—oxygenation and ventilation with 100% oxygen

B = Blood gas—correct electrolyte abnormalities/hemoglobin

C = Coagulation—reverse heparin with protamine

D = Dysrhythmias—sinus rhythm is good; pacing needed sometimes (80–100 bpm)

E = Epinephrine—inotropes/vasopressors used as needed. Epinephrine may increase

myocardial O2 need

F = Fluids—for rapid volume resuscitation

G = Good contractility by direct visualization/transesophageal echocardiogram

H = Hypothermia is avoided; >37°C is aimed

I = Invasive monitors recalibrated

41. B. IABP is sometimes used to facilitate weaning the patient off cardiopulmonary

bypass. This provides a systolic augmentation of blood pressure in addition to

improving myocardial oxygen supply during diastole. Timing and location of an

IABP are critical for optimal functioning. Ideal inflation of the balloon should be just

after the dicrotic notch (closure of aortic valve). Inflation while the aortic valve is

still open can increase afterload, worsen aortic regurgitation and left-ventricular (LV)

volume. Inflation too late in the diastolic phase will reduce diastolic augmentation

and myocardial supply. Similarly, the deflation should be timed just prior to LV

ejection to produce an optimal reduction in afterload. Timing is usually synchronized

with EKG/arterial pulse. The location of the tip of the IABP should be just distal to

the takeoff of the left-subclavian artery, usually confirmed with transesophageal

echocardiograph/fluoroscopy.

42. D. This patient has a low CVP, PCWP suggestive of low-filling pressures,

indicating that he is hypovolemic. But the rest of the clinical picture of low SVR and

high CO is strongly suggestive of a hyperdynamic circulatory state (vasodilated).

The treatment in such a scenario will be to increase the hematocrit. If the patient had

a decreased cardiac output, the treatment would be to administer

volume/crystalloids. Left-heart failure (LHF) will have a high PCWP and pulmonary

artery pressure. Right-heart failure (RHF) will have a high CVP and normal or low

PCWP. Both LHF and RHF will have low CO.

43. B. Protamine binds and effectively inactivates heparin because the positive charge

of protamine neutralizes the negative charge of heparin. Timing of protamine

administration should be determined by close communication with the surgeon. Too

early administration may lead to clot formation in the cardiopulmonary bypass

circuit. The electrically neutral heparin–protamine complexes are removed by the

reticuloendothelial system. Protamine dosing is based on the amount of heparin

initially required to produce the desired activated clotting time; protamine is then

given in a ratio of 1 to 1.3 mg per 100 U of heparin. Another approach calculates the

protamine dose based on the heparin dose–response curve and the estimation of

heparin concentration using special monitors (Hepcon).

44. C. The activated clotting time should return to baseline following reversal of

heparin with protamine; sometimes, additional doses of protamine (25–50 mg) may

be necessary. Coagulopathy often follows long bypass periods (>2 hours) and is due

to multifactorial causes: surgical bleeding sites, inadequate reversal of heparin,

reheparinization, thrombocytopenia, platelet dysfunction, hypothermia, preoperative

coagulation defects, or newly acquired defects may be responsible. Reheparinization

(heparin rebound) after apparent adequate reversal is due to a relative heparin–

protamine concentration mismatch and can be caused by a redistribution either of

protamine to peripheral compartments or of peripherally bound heparin to the central

compartment. Hypothermia (<35°C) often exacerbates such bleeding problems.

45. A. DDAVP, 0.3 μg/kg (intravenously over 20 minutes), can increase the activity

of factors VIII and XII and the von Willebrand factor. DDAVP facilitates their

release from the vascular endothelium. Hence, a second dose is usually not effective.

DDAVP is very useful in reversing qualitative platelet defects, but is not

recommended for routine use.

46. A. Immediately following cardiac surgery, the emphasis is on maintaining

hemodynamic stability and monitoring for excessive perioperative bleeding. Sedation

using propofol/fentanyl/titrated doses of morphine/dexmedetomidine is used in

different institutions to ensure a calm, comfortable patient. Chest-tube drainage more

than 10 mL/kg/hour in the first 2 hours often raises a red flag and prompts

coagulation studies and sometimes require chest reexploration. A very deadly site

for postoperative monitoring is into the pericardium causing cardiac tamponade. This

is usually signaled by equalization of diastolic pressures and hemodynamic

compromise and needs immediate surgical intervention. After the first 2 hours, any

drainage from chest tube >100 mL/hour should be closely observed.

47. A. NO is a potent vasodilator, which can be given as inhaled nitric oxide, which

circumvents the unwanted side effect of decreased SVR and systemic blood

pressure, at the same time retaining the therapeutic potential of decreasing pulmonary

hypertension. Inodilators like dopamine and milrinone may help in situations with

right-ventricular (RV) failure secondary to pulmonary hypertension. Vasodilators like

nitroglycerin will also decrease the PVR, but they produce drop in systemic blood

pressure. Inhaled prostaglandin E1

(PGE1

) is also very specific in decreasing PVR

without affecting SVR. Advanced RV failure may necessitate a RV–assist device or

an intra-aortic balloon pump, which works by increasing the perfusion to the right

side of the heart. Inhaled NO at 10 to 60 ppm and PGE1 at 0.01 to 0.2 μg/kg/min are

very effective pulmonary vasodilators.

48. D. End-stage heart disease patients have an option to get a destination ventricularassist device therapy or get a cardiac transplantation. Their position in the transplant

list is higher if they are unlikely to survive the next 6 to 12 months. Survival rates

after cardiac transplantation are usually high at a 5-year survival rate of 60% to 90%.

High pulmonary vascular resistance >6 to 8 Wood units (1 Wood unit = 80

dyn[middot]s/cm5

) is a predictor of right-ventricular failure, which has a high early

postoperative mortality. Hence, irreversible pulmonary vascular disease is

considered a contraindication to orthotopic cardiac transplantation. They still qualify

for a combined heart–lung transplantation, which is allocated from a separate list.

Size, ABO blood–group typing, and cytomegalovirus serology are used for donor–

recipient compatibility testing. However, tissue crossmatching is generally not

performed. Donor organs from patients with hepatitis B or C or HIV infection are

excluded.

49. B. The CVP waveform is characteristic in cardiac tamponade. Cardiac tamponade

is characterized by equalization of diastolic pressures throughout the heart: LAP =

RAP = LVEDP = RVEDP. This produces a reduced stroke volume and high central

venous pressure. The external compression on the collapsible chambers prevents

emptying, and these patients compensate by having tachycardia and an increase in

contractility. However, in the presence of impaired emptying, the contribution from

stroke volume is very limited. This is particularly important to the anesthesiologist

while inducing general anesthesia in such patients. They do not tolerate the switch

from negative-pressure to positive-pressure breathing. Characteristic CVP waveform

in cardiac tamponade is described as impairment of both diastolic filling and atrial

emptying abolishes the y descent; the x descent (systolic-atrial filling) is normal or

even accentuated. Arterial vasoconstriction (increased systemic vascular resistance)

supports systemic blood pressure, whereas venoconstriction augments the venous

return to the heart.

50. C. Constrictive pericarditis is characterized by a stiff pericardium that limits

diastolic filling of the heart. Pathophysiology consists of a thickened, fibrotic, and

often calcified pericardium secondary to acute or recurrent pericarditis. The adherent

parietal pericardium allows the heart to fill only to a fixed volume. Filling during

early diastole is typically accentuated and manifested by a prominent y descent on

the CVP waveform. This is in contrast to cardiac tamponade, which causes a filling

defect. This pathophysiology is responsible for Kussmaul sign—paradoxical rise in

venous pressure during inspiration. Chest X-ray may show some pericardial

calcifications, and EKG may show atrial fibrillation, conduction blocks, low QRS

voltage, and diffuse T-wave abnormalities. Clinical signs include raised jugular

venous pressure, hepatomegaly, ascites, and abnormal liver function.

51. D. The goal during management of anesthesia for patients with hypertrophic

cardiomyopathy is to decrease the pressure gradient across the left-ventricular

outflow obstruction. Decreases in myocardial contractility and increases in preload

(ventricular volume) and afterload will decrease the magnitude of left-ventricular

outflow obstruction. Intraoperative hypotension is generally treated with intravenous

fluids or an α agonist such as phenylephrine. Drugs with β-agonist activity are not

likely to be used to treat hypotension because any increase in cardiac contractility or

heart rate could increase left-ventricular outflow obstruction. When hypertension

occurs, an increased delivered concentration of isoflurane or sevoflurane can be

used. Vasodilators, such as nitroprusside or nitroglycerin, should be used with

caution because decreases in systemic vascular resistance can increase leftventricular outflow obstruction.

52. B. PCWP is an indirect measure of LVEDP, with many false positives and

negatives:

PCWP > LVEDP

• PEEP/positive-pressure ventilation

• Increased intrathoracic pressure

• Left-atrial pathology—myxoma

• Mitral-valve pathology—stenosis/regurgitation

• Pulmonary hypertension

• Chronic obstructive pulmonary disease

LVEDP > PCWP

• LVEDP >25 mm Hg

• Premature mitral-valve closure (usually an aortic regurgitation jet causing this)

• Left-ventricular diastolic dysfunction (left-ventricular hypertrophy/ischemia)

53. B. Mixed venous oxygen tension refers to the oxygen tension in a venous sample

with blood mixed from both inferior vena cava and superior vena cava. Ideally, this

sample is drawn from the tip of a pulmonary artery catheter. It is a good measure of

tissue oxygen supply relative to its demand. A reduction in delivery (decreased

cardiac output) or an increase in consumption (increased BMR) can both cause a

reduction in PvO2

. Normal PvO2

is about 40 mm Hg, with a saturation of 75%.

54. C. Site of previous MI, history of coronary artery bypass grafting, site of

procedure for procedures <3 hour, and type of anesthesia used (general anesthesia

vs. regional) have no influence on perioperative myocardial reinfarction.

Only three pharmacologic measures have been proven to produce a decrease in

cardiovascular morbidity and mortality: β-blockers, clonidine, and statins. β-Blockers

started 7 to 30 days prior to surgery and continued for 30 days postoperatively

reduce the risk of cardiac morbidity (MI or cardiac death) by 90%. If started just

prior to surgery and continued for 7 days, it will still confer a reduction in mortality

risk by 50%. Perioperative clonidine administration reduces the 30-day and 2-year

mortality risks. Statin therapy with fluvastatin for 30 days before and after surgery, in

addition to β-blockade, reduces risk of MI and death by an additional 50%.