2. A. Halothane and isoflurane depress SA node automaticity and make AV node

refractory. By giving an anticholinergic, we stimulated the conduction system of the

heart, but SA and AV nodes have been suppressed by the inhalational agent. So the

next tissue in the conducting pathway (junctional pacemakers) takes over and

produces junctional rhythm. While the depression of SA and AV nodes by

inhalational agents is well known, the effect of inhalational agents on Purkinje fibers

and ventricular myocardium is unpredictable with reports of both arrhythmia-inducing

and antiarrhythmic effects. Arrhythmogenicity by inhalational agents is due to

potentiation of action of catecholamines, and the direct depression of calcium

channels renders some antiarrhythmic effect. Opioids depress cardiac conduction,

increase AV node refractoriness, and prolong the duration of Purkinje fiber–action

potential.

3. A. The therapeutic effects of low concentrations of lidocaine turn toxic at higher

concentrations—they bind to fast Na channels and depress conduction. If we increase

the concentration further, they depress the automaticity of heart by its effect on

sinoatrial node. This is very different from the more potent local anesthetics like

bupivacaine and ropivacaine, which cause toxicity by its effect on Purkinje fibers

and ventricular muscle. Bupivacaine binds inactivated fast sodium channels and

dissociates from them slowly. Its effects can be sinus bradycardia, sinus node arrest,

or malignant ventricular arrhythmia.

4. B. All anesthetic agents can depress cardiac contractility. This occurs by

alterations in the intracellular concentration of calcium as follows:

Inhalational agents: decreasing the entry of calcium into cells by affecting both Tand L-type calcium channels, altering the kinetics of calcium release and uptake into

the sarcoplasmic reticulum, and decreasing the sensitivity of contractile proteins to

calcium. These effects are more apparent with halothane than with modern

inhalational agents like isoflurane, sevoflurane, and desflurane. Factors that can

worsen this cardiac depression include hypocalcemia, α-adrenergic blockade, and

calcium channel blockers.

Nitrous oxide: reduces the intracellular calcium concentration (dose-dependent).

Intravenous-induction agent ketamine: agent with no significant myocardial

depression, except in critically ill patients with depleted catecholamines, where it

acts as a direct myocardial depressant.

Local anesthetic agents: reduce calcium influx and release in a dose-dependent

fashion. Bupivacaine, tetracaine, and ropivacaine cause greater depression than

lidocaine and chloroprocaine.

5. C. The CVP waveform consists of three positive waveforms called a, c, and v and

two negative slopes called the x and y depressions.

a wave atrial contraction

c wave cusps bulging into the right atrium

xdescent atrial relaxation during ventricular systole

v wave venous filling of the right atrium

y descent atrial emptying when tricuspid valve opens

6. D. Ventricular systolic function is documented most commonly as cardiac output

or ejection fraction. Cardiac output is defined as the volume of blood pumped by the

heart per minute. Normally, the right and left ventricles have the same output. CO =

SV × HR, where CO is the cardiac output, SV is the stroke volume (the volume

pumped per contraction), and HR is heart rate. Variations in body size can lead to

ambiguity if we just use cardiac output as a measure. This can be avoided by using

cardiac index: CI = CO/BSA, where CI is the cardiac index and BSA is the total

body surface area. BSA is usually obtained from nomograms based on height and

weight. Normal CI is 2.5 to 4.2 L/min/m2

. As you can see, there is a wide range for

CI and the patient should have a gross ventricular impairment prior to it being evident

on CI. Mixed venous oxygen saturation is ideally obtained from a PA catheter. A

better estimate of ventricular performance can be obtained if we subject the

ventricles to some stress like exercise. This will reveal underlying inability of the

heart to deliver adequate oxygen to the tissues and can be noted as a falling mixed

venous oxygen saturation. Inadequate tissue perfusion relative to demand is causing

the drop in mixed venous saturation. Thus, in the absence of hypoxia or severe

anemia, measurement of mixed venous oxygen tension (or saturation) is the best

determination of the adequacy of cardiac output.

7. C. Ventricular filling is influenced by both heart rate and rhythm. Since the time

spent in diastole is higher than the time spent in systole, any increase in heart rate has

more effect on the diastolic filling time more than the systolic ejection time. At very

high heart rates (>120 bpm) in adults, the left-ventricular filling is significantly

impaired by the sheer decrease in duration of diastole. In addition, atrial contraction

(kick) contributes about 20% to 30% of the ventricular filling in a normal heart. Any

condition that affects the atrial contraction, like atrial fibrillation/flutter, or alters the

timing of atrial kick, will negate this contribution and can have significant

hemodynamic consequences in some patients. The atrial contribution to ventricular

filling is more important in patients with reduced ventricular compliance who depend

on active filling with atrial contraction than passive filling of the ventricle for

adequate preload.

8. A. Afterload is the force against which ventricle is pushing the blood out. It can be

denoted by the ventricular-wall tension during systole or impedance of the arterial

tree. Ventricular-wall tension can be calculated by Laplace law:

Circumferential stress = intraventricular pressure × ventricular radius/2 × wall thickness

This relationship is applicable to spherical structures, but can be applied to left

ventricle as well, which is a prolapsed ellipsoid. Any increase in ventricular radius

as in a dilation increases the wall tension. However, any increase in thickness

(hypertrophy) decreases the wall tension. This is a protective mechanism seen in

patients with long-standing hypertension or aortic stenosis in an attempt to decrease

the wall tension.

9. C. Recommended dose of heparin before initiation of cardiopulmonary bypass is

300 to 400 U/kg. The dose is given to achieve an activated clotting time of 400 to

450 seconds.

10. B. The SA node is supplied by the right coronary artery in 60% of individuals, and

by the left anterior descending artery in 40% of the individuals. The AV node is

supplied by the right coronary artery in 85% of individuals, and by the circumflex

artery in 15% of individuals.

11. C. Baroreceptors have an important role in acute regulation of blood pressure.

They are located at the bifurcation of the common carotid and in the aortic arch.

These receptors sense an increase in blood pressure and enhance the vagal tone,

thereby inhibiting systemic vasoconstriction. This is called the baroreceptor reflex.

The afferent pathway for the baroreceptor reflex is via a branch of the

glossopharyngeal nerve, sometimes called the Hering nerve. The afferent pathway for

baroreceptor reflex from the aortic receptors travels along the vagus nerve. Changes

in blood pressure caused by acute events like change in posture are minimized

primarily by the carotid baroreceptor between mean arterial pressures of 80 and 160

mm Hg. However, readaptation to changes in acute blood pressure occurs over the

course of 1 to 2 days, making this reflex ineffective for long-term blood pressure

control. All volatile anesthetics depress the normal baroreceptor response, less so

with isoflurane and desflurane.

12. A. The bundle of His is the only part of the cardiac conducting system, which has

a dual blood supply derived from the posterior descending artery (PDA) and the left

anterior descending (LAD) artery. Blood supply to the heart is from the right and left

coronary arteries. The right coronary artery (RCA) normally supplies the right atrium,

most of the right ventricle, and the inferior wall of the left ventricle. In 85% of

persons, the PDA, which supplies part of the interventricular septum and inferior

wall, arises from the RCA, and these people are said to have a right-dominant

circulation. In the remaining 15% of persons, the PDA arises from the left coronary

artery and is appropriately labeled left-dominant circulation.

The left coronary artery normally supplies the left atrium and most of the

interventricular septum and left ventricle. The left main coronary artery divides into

the LAD artery and the circumflex (CX) artery. The LAD artery supplies the septum

and anterior left-ventricular wall, and the CX artery supplies the lateral wall.

13. C. Autoregulatory nature of the myocardium makes the myocardial oxygen

demand an important determinant of myocardial blood flow. Pressure work uses most

of the oxygen, 65%, followed by basal requirements = 205, volume work = 15%,

with only 1% of the supplied oxygen being used for electrical activity. The

myocardium also has a very high extraction ratio. It extracts 65% of the oxygen in

arterial blood, compared with 25% in most other tissues. Coronary sinus oxygen

saturation is usually 30%. Hence, any drop in myocardial oxygen supply is

deleterious, as it cannot compensate for reduction in flow by increasing oxygen

extraction. Factors influencing the supply and demand are listed in Table 11-2.

Table 11-2

MYOCARDIAL OXYGEN SUPPLY MYOCARDIAL OXYGEN DEMAND

Heart rate

Diastolic time

Aortic diastolic blood pressure

Coronary perfusion pressure

Ventricular end diastolic pressure

Arterial oxygen content and tension

Hemoglobin concentration

Coronary vessel diameter

Basal requirements

Heart rate

Wall tension

Preload

Afterload

Contractility

14. D. Halogenated anesthetic agents are inherent vasodilators. Their effect on

coronary blood flow is variable and depends on an interplay between their effect on

blood pressure, metabolic oxygen requirements of the myocardium, and their direct

vasodilating properties. Although the mechanism is not clear, it may involve

activation of ATP-sensitive K

+ channels and stimulation of adenosine (A1

) receptors.

Halothane and isoflurane stand apart, as halothane primarily affects large coronary

vessels and isoflurane affects mostly smaller vessels. Dose-dependent abolition of

autoregulation may be greatest with isoflurane. Autonomically mediated vasodilation

is significant for desflurane. Sevoflurane appears to lack coronary vasodilating

properties.

15. C. According to ACC/AHA guidelines for noncardiac surgery in cardiac patients,

Surgeries can be classified into high, intermediate, and low risk with high-risk

surgeries having >5% risk and low-risk surgeries having <1% risk (Table 11-3).

Table 11-3 Cardiac Risk Stratification for Noncardiac Surgical Procedures.

High (reported cardiac risk often greater than 5%)

Emergent major operations, particularly in the elderly

Aortic and other major vascular surgery

Peripheral vascular surgery

Anticipated prolonged surgical procedures associated with large fluid shifts and/or blood loss

Intermediate (reported cardiac risk generally less than 5%)

Carotid endarterectomy

Head and neck surgery

Intraperitoneal and intrathoracic surgery

Orthopedic surgery

Prostate surgery

Low(reported cardiac risk generally less than 1%)

Endoscopic procedures

Superficial procedure

Cataract surgery

Breast surgery