16. C. Chronic hypertensive patients show wide fluctuations in blood pressure on

induction (hypotension) and intubation (hypertension). Duration of laryngoscopy <15

seconds has been shown to prevent this hypertensive response to intubation.

Intubation performed under deep anesthesia is also shown not to produce significant

rise in blood pressure. But this comes at the price of hypotension. There are several

techniques that can be used to prevent sudden spikes in blood pressure on intubation.

Topical airway anesthesia, β-blockers like esmolol 0.3 to 1.5 mg/kg, short-acting

opioids like fentanyl 2.5 to 5 μg/kg, intravenous preservative-free lidocaine at 1.5

mg/kg have all been shown to be effective in attenuating the hypertensive response.

17. B. Direct α1 agonists like phenylephrine are preferable to indirect

sympathomimetics like ephedrine to treat hypotension, following induction in patients

with uncontrolled hypertension preoperatively. Catecholamines—both endogenous

and exogenous—can produce exaggerated hypertensive response in these patients.

We can start with small doses of phenylephrine, for example, 25 to 50 μg, provided

the heart rate is not too low. If the heart rate is low, small doses of ephedrine (5–10

mg) or even epinephrine (2–5 μg) may be used. In patients who are on angiotensinreceptor blocker preoperatively, the refractory hypotension may respond only to

vasopressin. Avoiding high heart rates and prolonged hypertension has been shown to

decrease cardiovascular morbidity.

18. C. Coronary vasodilation potential of dihydropyridines (nifedipine, nicardipine,

nimodipine) is much greater than those by verapamil and diltiazem. They even

exceed nitrates in their vasodilatory potential. β-Blockers however have no

vasodilatory action on coronary blood vessels.

19. D. CCBs have significant anesthetic implications. Both depolarizing and

nondepolarizing neuromuscular-blocking agents are potentiated by CCBs. CCBs also

potentiate the circulatory effects of volatile agents and may cause more hypotension.

Both verapamil and diltiazem can potentiate cardiac depression and inhibit

conduction in the AV node caused by volatile anesthetics. Verapamil may also

modestly decrease anesthetic requirements. Dihydropyridine derivatives potentiate

systemic vasodilation under anesthesia.

20. C. Cardioselectivity of agents like metoprolol is dose-dependent (β1

-receptorspecific). Even the β1

-receptor-specific agents can have some β2

-blocking action at

higher doses. β-Blockers with intrinsic sympathomimetic activity, like acebutolol,

provide a unique advantage in patients with bronchospastic airway disease.

21. C. Prolonged QT interval (QTc >0.44 second) can be caused by myocardial

ischemia, drug toxicity (antiarrhythmic agents, antidepressants, or phenothiazines),

electrolyte abnormalities (hypokalemia or hypomagnesemia), autonomic dysfunction,

mitral-valve prolapse, or, less commonly, a congenital abnormality. Prolonged QT

interval predisposes patients to ventricular arrhythmias, particularly polymorphicventricular tachycardia, also known as torsade de pointes or twisting points, which

can lead to ventricular fibrillation. Prolonged QT interval is due to nonuniform

prolongation of ventricular repolarization. This predisposes patients to reentry

phenomena and results in ventricular tachycardia or fibrillation. Elective surgery

should be postponed until drug toxicity and electrolyte imbalances are excluded.

Polymorphic tachyarrhythmias with a long QT interval are usually treated with

intravenous magnesium or by pacing. This is because they do not respond to

conventional antiarrhythmics. Patients with congenital prolongation generally respond

to β-adrenergic blocking agents. Left-stellate-ganglion blockade has also been tried

and has some success in these patients suggesting that this may be due to an

autonomic imbalance.

22. D. Severe multivessel disease can be detected using exercise EKG if the patient

(develops)

• Cannot attain a maximum HR >70% of predicted

• Dysrhythmias at a lower HR

• Sustained fall in systolic blood pressure during exercise (>10 mm Hg)

• ST depression >2 mm, either horizontal or down sloping

• ST depression at a very low workload

• ST depression sustained even after the exercise is >5 min

23. D. Surgical electrocautery interference with AICDs and pacemaker devices are

well known. The old adage of “put a magnet on it” is based on the fact that

antitachycardia function in some (older) pacemakers was turned off by the

application of a magnet. However, this is not true for most of the newer AICDs.

Ideally, the manufacturer’s representative or cardiology should be contacted to find

out if the device could be reprogrammed to have the antitachycardia function off

prior to the surgery. This is in addition to confirming that the pacemaker was

interrogated for functionality within the last year and AICD was interrogated in the

last 6 months.

Electrosurgical interference can be caused by the device interpreting the current as

ventricular fibrillation and firing, interfering with its pacemaker capability, resetting

of the device to backup mode. Some AICDs are programmed with a rate-responsive

function, and this may be activated by a cautery device.

If there is no time to reprogram the device prior to surgery, use of a bipolar cautery,

placement of electrical return pad far away from the device, using electrocautery in

small bursts are some methods to decrease such an interference. In addition, all such

patients should have transcutaneous pads on and a defibrillator/pacer should be

available in the room. Every effort should be made to reprogram the device to its

original setting prior to discharge of the patient from the postanesthesia care unit.

24. A. The sensitivity of the intraoperative/perioperative ECG in detecting ischemia is

directly proportional to the number of leads monitored. V5 is the most useful lead. In

order of decreasing sensitivity, V5 is followed by V4, II, V2, and V3 leads. Usually

two leads are monitored simultaneously in perioperative period. Leads II and V5 are

the two most commonly used leads. Lead II helps to detect arrhythmias and inferiorwall ischemia, while lead V5 is useful for detecting lateral-wall ischemia. Modified

V5 lead is very useful when only one channel can be monitored (three leads applied

with left-arm lead at V5 position and monitoring lead I). Posterior wall can be

monitored using an esophageal lead.

25. A. It is a common practice to cool the body to a core body temperature of 20 to

32°C following CPB start. However, it is not always required. This is based on the

principle that metabolic oxygen requirements can be halved with each reduction of

10°C in body temperature. This temperature is brought back to acceptable levels

(where arrhythmias are lower) at the end of CPB—a phase called rewarming. Some

procedures need a complete circulatory standstill—called circulatory arrest—and

deep hypothermia is employed for such procedures—cooling to 15 to 18°C allows an

arrest time of around 60 minutes.

26. B. The adverse effects of hypothermia are arrhythmias, platelet dysfunction,

coagulopathy, decreased systolic function of myocardium, and reduction in serumionized calcium due to citrate toxicity.

27. A. Coronary perfusion pressure is determined by the difference between the

arterial diastolic pressure and the left-ventricular end diastolic pressure. The left

ventricle is perfused during diastole, while the right ventricle is perfused both during

diastole and systole. An increase in heart rate reduces coronary perfusion because of

a shorter diastole. Normal coronary blood flow at rest is about 250 mL/min.

28. C. Transgastric mid-papillary (midshort axis) view provides a snapshot of all the

different blood vessels supplying the heart (Fig 11-2).

Figure 11-2. Reused with permission from Shanewise JS, Shin JJ, Vezina DP, et al. Comprehensive and abbreviated

intraoperative TEE examination. In: Savage RM, Aronson S, Shernan SK, eds. Comprehensive Textbook of

Perioperative Transesophageal Echocardiography. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins;

2011: 86.

29. D. Pure high-dose opioid anesthesia (e.g., fentanyl 50–100 μg/kg or sufentanil 15–

25 μg/kg) has fallen out of vogue in cardiac anesthesia practice. It was useful at a

time in anesthesia when the only inhaled agents available produced unacceptable

myocardial depression. The main disadvantages of high-dose opioid technique

include prolonged postoperative respiratory depression (early extubation is becoming

a very common trend in coronary artery bypass grafting surgeries), high incidence of

patient awareness/recall, exaggerated hypertensive response to stimulation like

sternotomy in a patient with good left-ventricular function, bradycardia, chest-wall

rigidity, postoperative ileus, and impaired immunity.

30. A. A progressive decline in cardiac output is sometimes seen after the chest is

opened. This is attributed to the loss of negative intrathoracic pressure and decreased

preload. Hence a IV fluid bolus may help. Factors potentiating such a response

include deep anesthesia and preoperative angiotensin-receptor-blockade use. Another

common response seen during sternal retraction and pericardiectomy is bradycardia

and hypotension due to exaggerated vagal response. This is potentiated by hypoxia,

β-blockers, and calcium channel blockers.

31. C. Aprotinin, an inhibitor of serine proteases, such as plasmin, kallikrein, and

trypsin, also helps to preserve platelet aggregation and adhesiveness. It has been

shown to decrease blood loss and transfusion requirements and should be considered

in redo surgeries, Jehovah’s witnesses, recent administration of glycoprotein IIb/IIIa

inhibitors (abciximab [ReoPro], eptifibatide [Integrilin], or tirofiban [Aggrastat],

patients with coagulopathies, and patients with long pump runs. However, repeat

exposure to aprotinin has been shown to cause allergic reactions, which may include

anaphylaxis. Patients on a combination of aspirin and ADP-receptor antagonist are at

high risk of bleeding and may benefit from aprotinin.

32. A. The events occurring in sequence after heparinization are aortic cannulation

followed by venous cannulation. Venous cannulation usually causes hemodynamic

changes, and we have an access to provide rapid infusion through the aortic cannula

if necessary. Venous cannulation also frequently precipitates arrhythmias. Premature

atrial contractions and transient bursts of a supraventricular tachycardia are common.

Sustained arrhythmias must be treated pharmacologically, electrically, or by

immediate anticoagulation and initiation of bypass depending on the amount of

hemodynamic compromise. Sometimes, stopping the surgical stimulus is all that is

needed. Superior vena cava syndrome can be caused by a malpositioned venous

cannulas can be interfering with venous drainage from the head and neck.

33. B. After initiation of CPB, pump flow is gradually increased to 2 to 2.5 L/min/m2

and MAPs are monitored. It is common to see an initial fall in BP. Initial mean

systemic arterial (radial) pressures of 30 to 40 mm Hg are not unusual. Abrupt

hemodilution, which reduces blood viscosity and effectively lowers systemic

vascular resistance (SVR), may be responsible for this drop. The effect is partially

compensated by subsequent hypothermia, which tends to raise blood viscosity again.

A disastrous scenario is a persistent and excessive decrease in MAP (<30 mm Hg);

transesophageal echocardiograph evaluation is very useful in such a situation to look

for unrecognized aortic dissection. If dissection is present, CPB must be temporarily

stopped until the aorta is recannulated distally to prevent further extension of a

dissection flap with grave consequences. Poor venous return, pump malfunction, or

pressure-transducer error may all cause hypotension. Aortic cannula misdirected

toward the innominate artery may be a cause for false hypertension when right radial

artery is used for monitoring.

The relationship between pump flow, SVR, and mean systemic arterial blood

pressure may be conceptualized as follows:

MAP = Pump flow × SVR

With a constant SVR, MAP is proportional to pump flow. Similarly, at any given

pump flow, MAP is proportional to SVR. Pump flows of 2 to 2.5 L/min/m2

(50–60

mL/kg/min) and mean arterial pressures between 50 and 80 mm Hg are commonly

used. Flow requirements are generally lower during deep hypothermia (20–25°C), as

mean blood pressures as low as 30 mm Hg may still provide adequate cerebral blood

flow. SVR can be increased with α agonists like phenylephrine.

High systemic arterial pressures (>150 mm Hg) are also deleterious because they

promote aortic dissection or a cerebrovascular accident in addition to increasing the

surgical bleeding. Hypertension is said to exist on pump when MAPs exceed 100 mm

Hg, and this is treated by decreasing pump flow or deepening anesthesia using

isoflurane at the oxygenator inflow gas. Sometimes, a hypertension is refractory to

these maneuvers or, if pump flow is already low, may necessitate a vasodilator like

nitroprusside.

34. 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