Intraoperatively, strict hemodynamic control using an intra-arterial catheter and

prompt pharmacologic intervention or fluid infusion to treat physiologic

hemodynamic alterations from the normal range may decrease the risk of

perioperative cardiac morbidity in high-risk patients.

55. C. Perioperative risk-reduction therapy with medications is superior to risk

stratification with invasive testing, angioplasty, and CABG. β-Blockers, clonidine,

statin, and aspirin have all been used for this. A single 1-minute episode of

myocardial ischemia detected by 1-mm ST-segment elevation or depression

increases the risk of cardiac events 10-fold and the risk for death 2-fold. Tachycardia

for 5 minutes above 120 bpm in the postoperative period can increase the risk of

mortality 10 times. The incidence of perioperative myocardial reinfarction does not

stabilize at 5% to 6% until 6 months after the prior myocardial infarction. Thus,

elective surgery, especially thoracic and upper abdominal, or other major procedures

used to be delayed for a period of 2 to 6 months after a myocardial infarction.

However, recently this has reduced to 6 to 8 weeks following the ACC/AHA

guidelines. Perioperative myocardial reinfarctions occur most frequently in the first

48 to 72 hours postoperatively. However, the risk of myocardial infarction remains

increased for several months after surgery.

56. D. Careful preoperative evaluation is the most effective method of predicting a

perioperative cardiac event. Risk stratification based on preoperative history and

physical examination followed by some series of tests (if deemed necessary) predicts

perioperative cardiac morbidity and mortality risk. Invasive testing adds little

information, which can be used to produce a change in outcome. The risks of

interventional procedures like angiography and an intracoronary stent or even

coronary artery bypass graft (CABG) surgery adds to the already-existing risk of the

proposed surgical procedure and does not reduce total risk. The combined risk of

two procedures exceeds that of the original operation. The American College of

Cardiology (ACC) and American Heart Association (AHA) have developed a

protocol entitled ACC/AHA Guideline Perioperative Cardiovascular Evaluation for

Noncardiac Surgery. The ACC/AHA guidelines have not been shown to actually

reduce perioperative risk. Perioperative medical optimization of the patient with βadrenergic blockers, clonidine, statins, and aspirin may be superior to invasive

approach with angioplasty and/or CABG.

57. A. Deep anesthesia and brief duration of direct laryngoscopy (<15 seconds) is

important in minimizing the hemodynamic changes associated with intubation. If you

anticipate a longer intubation or if the patient has uncontrolled hypertension

preoperatively, addition of other drugs should be considered. Lidocaine can be given

IV (1.5 mg/kg IV) or topically (2 mg/kg) on the airway. Other pharmacologic options

include esmolol 0.5 mg/kg and fentanyl 2 to 5 μg/kg. However, brief duration of

laryngoscopy seems to be the most effective method in avoiding the sympathetic

response to intubation.

58. D. Barlow syndrome, as it is sometimes called, refers to mitral valve. It is an

abnormality of the mitral-valve structure (suspected to be myxomatous in origin) that

permits prolapse of the mitral valve into the left atrium during left-ventricular

systole. Any condition that increases cardiac emptying can accentuate this prolapse:

(1) sympathetic nervous system stimulation, (2) decreased systemic vascular

resistance, and (3) performance of surgery with patients in the head-up or sitting

position all of these conditions predispose to increased cardiac emptying. Adequate

preload and a sudden prolonged decrease in systemic vascular resistance must be

avoided during induction of anesthesia in these patients to prevent the worsening of

prolapse.

59. D. Anesthetic considerations in patients with regurgitant lesions:

• Keep the heart rate high—decreases the duration of systole

• Keep SVR high

• Avoid decrease in myocardial contractility

• V wave is a reflection of mitral-regurgitant flow

60. B. QTc >440 ms in EKG is considered a predisposing factor for ventricular

dysrhythmias, syncope, and sudden death due to delayed repolarization. Common

congenital syndromes associated with these conditions are Jervell and Lange-Nielsen

syndrome (with deafness) and Romano Ward syndrome (no deafness). Any condition

that increases the heart rate predisposes these patients to arrhythmias—avoidance of

sympathetic stimulation during anesthetic induction is vital. Care should also be

taken to avoid the drugs that prolong the QT interval like phenothiazines. If the

patient is hemodynamically stable, these patients can be treated with β-blockers.

Unstable ventricular arrhythmias need electrical cardioversion. Left-stellate ganglion

block has been shown to have some therapeutic benefit, suggesting an autonomic

nervous system imbalance as possible etiology for this syndrome.

61. D. Anesthetic considerations in patients with aortic stenosis:

• Maintaining a high SVR

• Optimal preload

• Avoiding extreme fluctuations in HR (60–80 bpm is ideal)

• Avoiding arrhythmias

• Rapid availability of α agonists to counter the drop in SVR with induction

• Accurate BP measurements preferably with an intra-arterial catheter

62. D. VPCs are recognized on the ECG by (1) premature occurrence, (2) the absence

of a P wave preceding the QRS complex, (3) a wide and often bizarre QRS complex,

(4) an inverted T wave, and (5) a compensatory pause that follows the premature

beat. The primary goal with VPCs should be to identify any underlying cause

(myocardial ischemia, arterial hypoxemia, hypercarbia, hypertension, hypokalemia,

mechanical irritation of the ventricles) if possible and correct it. VPCs can be treated

with lidocaine (1 to 2 mg/kg IV) when they (1) are frequent (more than six premature

beats/min), (2) are multifocal, (3) occur in salvos of three or more, or (4) take place

during the ascending limb of the T wave (R-on-T phenomenon) that corresponds to

the relative refractory period of the ventricle.

63. C. WPW syndrome is characterized by a short PR interval (less than 120 ms), a

wide QRS complex, and δ wave in EKG. The short PR interval is due to conduction

along the bundle of Kent, which does not have a physiologic delay like conduction

across the atrioventricular node. The composite of cardiac impulses conducted by

normal and accessory pathways is the reason for δ wave and wide QRS complex.

WPW is the most common preexcitation syndrome, with an incidence of

approximately 0.3% of the general population. Atrial arrhythmias like paroxysmal

atrial tachycardia (most frequent) and supraventricular may lead to hemodynamic

collapse in patients with WPW syndrome.

Anesthetic management in the presence of a preexcitation syndrome is to avoid

increase in sympathetic nervous system activity events (anxiety) or drugs

(anticholinergics, ketamine, pancuronium) that might predispose to

tachydysrhythmias. All cardiac antidysrhythmic drugs should be continued

throughout the perioperative period.

Ketamine with its sympathomimetic property will be a poor choice for induction.

Intravenous β-blockers (atenolol, metoprolol, propranolol, or esmolol) can be used to

avoid tachycardia during induction of anesthesia. Histamine-releasing agents like

mivacurium/atracurium are also preferably avoided. In case of a sudden onset of

tachycardia, adenosine or procainamide will be a good choice to treat the arrhythmia.

Digitalis and verapamil may decrease the refractory period of accessory pathways

responsible for atrial fibrillation, resulting in an increase in ventricular response rate

during this dysrhythmia and should be avoided.

64. A. The magnet mode of many implanted devices, especially the newer AICDs, is

now programmable and does not always default to asynchronous pacing. Hence, it

should not be considered “safe.” The specific magnet mode for a patient’s device

should be identified by interrogation prior to surgical procedures as some magnet

modes change with device state or are programmable. Electrosurgical cautery is

interpreted as spontaneous cardiac activity by the artificial cardiac pacemaker when

the ground plate for electrocautery is placed too near the pulse generator or with use

of a unipolar cautery. For this reason, the electrical return plate (wrongly called

ground plate) should be placed as far as possible from the pulse generator. Other

techniques to improve safety include using a bipolar cautery, and placement of

external pads prior to the beginning of the case.

Magnet mode for many pacemakers (not AICDs) is asynchronous at 99 bpm.

However, in some devices, the magnet mode shifts to asynchronous at 50 bpm at the

end of battery life. Asynchronous pacing at such a low heart rate with the sensing

function off may lead to R-on-T phenomenon if the patient has a spontaneous heart

rate above 50 bpm.

65. B. Cardiac tamponade is characterized by (1) decreases in diastolic filling of the

ventricles, (2) decreases in stroke volume, and (3) decreases in systemic blood

pressure due to increased intrapericardial pressure from accumulation of fluid in the

pericardial space. Inadequate ventricular filling leads to a decreased stroke volume,

which in turn results in activation of the sympathetic nervous system (tachycardia,

vasoconstriction) in attempts to maintain the cardiac output. These patients need to

be kept “full and fast” as the right-sided filling occurs only when central venous

pressure exceeds the right-ventricular end diastolic pressure.

66. D. If the aortic valve is not competent, the regurgitant flow from the aorta will

keep distending the left ventricle, impairing perfusion and myocardial preservation.

This can be avoided (1) by a drain placed from the right superior pulmonary vein into

the left ventricle, (2) by aspirating from the antegrade cardioplegia line placed in the

proximal ascending aorta, or (3) via a pulmonary venous drain. The goal is to keep

the ventricle from overdistention when it is not pumping. Venting of blood returning

via the Thebesian or bronchial veins may also be necessary.

67. D. The bypass pump serves to pump the oxygenated blood back to the arterial

side of the patient. They are of two types: centrifugal and roller pump. The

centrifugal pump has three disks rotating at 3,000 to 4,000 rpm that use blood

viscosity to pump blood. Centrifugal pumps are less traumatic to blood cells, do not

pump air bubbles secondary to air being less dense than blood, and are afterloaddependent, avoiding the risk of line rupture with clamping of the arterial inflow

circuit. Roller pumps generate flow by compression of fluid-filled tubing between the

roller and curved metal back plate and can pump air. Because of their mechanism,

they can cause tube rupture with arterial inflow clamping. The flow is determined by

a dial on the cardiopulmonary bypass machine, and usual flows for normothermia or

mild hypothermia aim for a cardiac index between 2 and 4 L/min/m2

.

68. D. In the clinical scenario described, the patient has an increased CO2

in the blood

(irrespective of temperature correction).

PaCO2

is a balance of CO2 production and removal. If removal exceeds production,

PaCO2 decreases. If production exceeds removal, PaCO2

increases. The resulting

PaCO2

is expressed by the alveolar CO2 equation:

PaCO2 = k. VCO2

/VA

In the equation, k is a constant (0.863) that corrects units, VCO2

is carbon dioxide

production, and VA is alveolar ventilation. Since the patient is on cardiopulmonary

bypass, increasing the fresh-gas flow to the oxygenator will wash out more CO2

.

None of the other options has any role in CO2 production or elimination during

cardiopulmonary bypass.

69. B. This patient has a drop in PaO2 from 90 to 70 mm Hg despite having a FIO2 of

70. Along with the relative hypoxemia, he also developed an increase in peak

inspiratory pressure with no change in plateau pressure. The lack of change in

plateau pressure rules out any intrinsic change in the lung compliance. Both ARDS

and left-ventricular failure (pulmonary edema) will result in a change in lung

compliance. The clinical scenario described can result from both tension

pneumothorax and bronchial mucous plugging. But the fact that it occurred after 2

days of mechanical ventilation and without any change in the hemodynamic status

makes bronchial mucous plugging the most likely cause.

70. C. The drop in mean arterial pressure at the beginning of CPB is caused by a

sharp decrease in systemic vascular resistance caused by the drop in hematocrit

caused by the priming solution on pump. This drop in blood pressure along with

decreased hematocrit may cause a drop in tissue oxygen delivery. This is very

important for tissues with high oxygen consumption like myocardium and brain. Use

of α agonists to keep the mean arterial pressure may aid the cerebral perfusion. The

correct blood pressure during bypass is often decided based on the patient’s

coexisting conditions, carotid stenosis, etc. Lower pressures may reduce cerebral

blood flow and emboli load to the brain. Higher pressures may improve cerebral

blood flow and reduce watershed infarction but higher pressures come from higher

flows and more emboli per unit time. Pressures less than 40 mm Hg are avoided if

possible in adults. Pressures higher than 60 mm Hg are used during rewarming.

Pressures up to 80 to 90 mm Hg may be used in patients with cerebral vascular

disease.