Lippincott's Anesthesia Review: 1001 Questions and Answers
Chapter 11. Cardiovascular Anesthesia
Deppu Ushakumari and Ashish Sinha
1. Which of the following is responsible for the plateau phase of cardiac action potential?
A. Slow movement of potassium out of the cell
B. Slow movement of calcium into the cell
C. Slow movement of calcium out of the cell
D. Both A and C
2. A 2-year-old boy is induced with halothane-inhalation induction. The patient suddenly gets bradycardic, and you decide to administer atropine 0.4 mg intravenously. Immediately thereafter, you notice that the patient is having a junctional tachycardia. Which of the following most accurately describes the sequence of events?
A. Sinoatrial (SA) node suppression by halothane followed by anticholinergic action of atropine
B. Atrioventricular (AV) node suppression by halothane followed by anticholinergic action of atropine
C. SA node and AV node suppression by halothane followed by anticholinergic action of atropine
D. SA node and AV node suppression by halothane followed by paroxysmal tachycardic action of atropine
3. Significant intravenous absorption/inadvertent intravenous injection of bupivacaine can cause profound bradycardia and sinus node arrest. Which of the following best describes the mechanism of cardiac toxicity of bupivacaine?
A. Bupivacaine binds inactivated fast sodium channels and dissociates from them slowly
B. Bupivacaine binds activated fast sodium channels and dissociates from them slowly
C. Bupivacaine binds inactivated slow sodium channels and dissociates from them slowly
D. Bupivacaine binds activated slow sodium channels and dissociates from them slowly
4. The mechanisms of depression of cardiac contractility by volatile anesthetics include all the following, except
A. They decrease the entry of calcium into cells during depolarization
B. They affect only L-type calcium channels
C. They alter kinetics of calcium release
D. They decrease the sensitivity of contractile proteins to calcium
5. The mechanism of “x” descent (descent between C and V waves) in the following right atrial tracing (Fig 11-1) is
A. Downward movement of the atrioventricular (AV) valve cusps after ventricular contraction
B. Pulling down of the atrium by ventricular contraction
C. Relaxation of atrium after atrial systole
D. Decline in atrial pressure as the AV valves open
6. A 38-year-old healthy male volunteer is undergoing cardiac function tests as part of a physiology experiment. His vital signs are HR = 62 bpm, BP = 124/74 mm Hg, respiratory rate = 12 breaths/min, SpO2 = 100% on room air, and Hb = 14 g/dL. Which of the following is the best determination of the adequacy of his cardiac output?
A. Cardiac index 4.0 L/min/m2
B. Cardiac output 8.1 L/min by thermodilution technique
C. Cardiac output 8.1 L/min by Fick method
D. SvO2 of 75% from a pulmonary artery (PA) catheter
7. Which of the following patients will be affected the most from loss of atrial contribution to preload?
A. A 65-year-old patient with severe aortic regurgitation who went into recent onset atrial fibrillation
B. A 35-year-old patient with mitral-valve area of 1.0 cm2 who went into recent onset atrial fibrillation
C. An 80-year-old patient with severe aortic stenosis who went into recent onset atrial fibrillation
D. A 55-year-old patient with acute right-ventricular myocardial infarction
8. Which of the following formulae explains the hypertrophy of heart in response to pressure or volume loads (P, intraventricular pressure; R, ventricular radius; t, wall thickness; T, circumferential stress)?
A. P = 2Tt/R
B. T = 2P/Rt
C. T = 2R/Pt
D. PT = Rt
9. Dose of heparin (U/kg) administered for cardiopulmonary bypass is (approximately)
A. 100 to 200
B. 200 to 300
C. 300 to 400
D. 400 to 500
10. The sinoatrial and the atrioventricular (AV) nodes are supplied in majority of the individuals by
A. Left anterior descending artery
B. Right coronary artery
C. Circumflex artery
D. Posterior descending artery
11. Baroreceptor reflex is ineffective for long-term blood pressure (BP) control because
A. Renin angiotensin aldosterone system takes over the control
B. Renal regulation of BP is more powerful
C. Of adaptation to changes in BP over 1 to 2 days
D. All of the above
12. Which of the following portions of myocardium has a dual blood supply?
A. Bundle of His
B. Atrioventricular node
C. Posterior papillary muscle
D. Sinoatrial node
13. Which of the following types of myocardial work needs the highest oxygen requirement?
A. Electrical activity
B. Volume work
C. Pressure work
D. Basal requirement
14. Which of the following inhalational agents causes the least coronary vasodilation?
15. Which of the following surgeries carries the highest cardiovascular risk?
A. Emergency appendectomy
B. Carotid endarterectomy
C. Femoral–popliteal bypass surgery
D. Inguinal hernia repair
16. A 67-year-old patient with uncontrolled hypertension presents for an elective dialysis access creation. Which of the following techniques is not suited for attenuating the hypertensive response to intubation?
A. Administering 3 μg/kg of fentanyl intravenously
B. Administering topical airway anesthesia
C. Administering lidocaine 0.5 mg/kg intravenously
D. Administering esmolol 1 mg/kg intravenously
17. The patient mentioned above develops severe hypotension immediately after intubation. Which of the following agents is most suited to bring the blood pressure back to normal values?
18. Which of the following antianginal agents has the highest coronary vasodilating potential?
19. Which of the following statements about calcium channel blockers (CCBs) is not true?
A. CCBs potentiate both depolarizing and nondepolarizing neuromuscular blockers
B. CCBs potentiate the circulatory effects of volatile anesthetic agents
C. Verapamil may decrease anesthetic requirements
D. Verapamil has no effect on cardiac contractility; it acts only on the atrioventricular (AV) node
20. Which of the following β-blockers is most suited for a patient with bronchospastic disease?
21. A 24-year-old female patient with a preoperative QTc interval of 550 ms is undergoing breast surgery under general anesthesia. Droperidol is administered to the patient for prevention of postoperative nausea, following which the patient goes into polymorphic-ventricular tachycardia. Which of the following drugs/therapies is best for the patient at this point?
22. Which of the following factors is not associated with severe multivessel disease during exercise electrocardiography?
A. Sustained decrease (≥10 mm Hg) in systolic blood pressure during exercise
B. Failure to reach a maximum heart rate greater than 70% of predicted
C. Persistence of ST-segment depression after exercising for 5 minutes or longer
D. A 1-mm upsloping of ST segment
23. Surgical electrocautery may cause a problem with an automated implantable cardioverter defibrillator (AICD) by all the following mechanisms, except
A. AICD interpreting a cautery current as ventricular fibrillation
B. Inhibition of pacemaker function due to cautery artifact
C. Increased pacing rate due to activation of a rate-responsive sensor
D. Cautery current generating too much heat at the location of AICD and causing burns
24. Which of the following ECG leads is most sensitive to detect an anterior-wall myocardial ischemia?
25. Which of the following is not true about systemic hypothermia during cardiopulmonary bypass (CPB)?
A. Intentional hypothermia is always used following the initiation of CPB
B. Core body temperature is usually reduced to 20 to 32°C
C. Metabolic oxygen requirements are usually halved for every of 10°C reduction in temperature
D. Profound hypothermia to temperatures of 15 to 18°C allows total circulatory arrest for up to 60 minutes
26. Adverse effects of hypothermia include all the following, except
A. Platelet dysfunction
B. Irreversible coagulopathy
C. Potentiation of citrate toxicity
D. Depression of myocardial contractility
27. Coronary perfusion pressure is
A. Arterial diastolic pressure
left-ventricular end diastolic pressure
B. Arterial diastolic pressure
left-ventricular end systolic pressure
C. Arterial systolic pressure
left-ventricular end diastolic pressure
D. Arterial systolic pressure
left-ventricular end systolic pressure
28. Which of the following views of transesophageal echocardiograph (TEE) is most suited to visualize blood supply of all the segments of the heart?
A. Midesophageal fourth-chamber view
B. Midesophageal second-chamber view
C. Transgastric midshort axis view
D. Midesophageal third-chamber view
29. Disadvantages of high-dose opioid induction include all the following, except
A. Prolonged postoperative respiratory depression
B. High incidence of recall during surgery
C. Possible impairment of immune response
D. Myocardial depression
30. A 66-year-old male is undergoing coronary artery bypass grafting (CABG). After the chest is opened, a progressive decline in cardiac output is noticed. The most accurate statement regarding the change is
A. It is normal in deeply anesthetized patients
B. Intravenous fluid administration will not help correct this change
C. It implies imminent risk of death, and you should ask for blood to be transfused
D. It is caused by surgeon lifting the heart, especially if it is not accompanied by a drop in blood pressure
31. Aprotinin therapy should be considered for all of the following patients, except
A. Jehovah witnesses
B. Redo surgeries
C. Patients who had prior exposure to aprotinin
D. Patients on combined clopidogrel (Plavix) and aspirin therapy
32. Which of the following statements is false regarding placement of venous cannulas for cardiopulmonary bypass (CPB)?
A. Venous cannulas are inserted before aortic cannula placement
B. Venous cannula insertion frequently precipitates atrial or ventricular arrhythmias
C. Venous cannulas can impede venous return to the heart
D. Venous cannulas can cause superior vena cava syndrome
33. Following initiation of cardiopulmonary bypass (CPB) for aortic valve replacement, you notice the mean arterial pressure (MAP) consistently above 100 mm Hg. The most appropriate next step is
A. It is normal, and no action is needed
B. Pump flow should be decreased to decrease the blood pressure
C. It is usually caused by an air lock in the arterial cannula
D. Administer midazolam to prevent awareness
34. Which of the following is not an indication of low flow rates under cardiopulmonary bypass (CPB)?
A. SvO2 >80%
B. Progressive metabolic alkalosis
C. Low urine output
D. Hypoxemia noticed on an in-line venous oxygen saturation monitor
35. Discontinuing ventilation prematurely before full flow is achieved on cardiopulmonary bypass (CPB) causes
A. A right-to-left shunt leading to hypoxemia
B. Increased dead space
C. Helps to increase venous return via the venous outflow cannula
D. Aids the surgeon to visualize and cannulate the coronary sinus
36. Which of the following is the most sensitive to detect air bubbles at the termination of cardiopulmonary bypass (CPB)?
A. Transesophageal echocardiography (TEE)
B. Doppler ultrasonography
C. Manual visualization
D. Epiaortic echocardiography
37. Sweating during the rewarming phase of termination of cardiopulmonary bypass (CPB)
A. Implies light anesthesia
B. Is a hypothalamic response to perfusion with blood that is often at 39°C
C. Necessitates cooling the operating room
D. Can be prevented by using a forced air-warming device during the surgery
38. Use of corrected gas tensions during hypothermia
A. Is called pH-stat management
B. Preserves cerebral autoregulation
C. Improves myocardial preservation
D. Is done by adding sodium bicarbonate to the venous reservoir
39. Infusion of nitroglycerin at the termination of cardiopulmonary bypass (CPB)
A. Dilates the coronary vessels and helps improve coronary flow
B. Speeds the rewarming process and decreases large temperature gradients
C. Is an old technique that produces unnecessary hemodynamic changes
D. Improves renal blood flow
40. General guidelines for separation from cardiopulmonary bypass (CPB) include all the following, except
A. Core body temperature of at least 34°C
B. Stable heart rhythm or pacer rhythm
C. Heart rate around 80 to 100 bpm
D. Adequate ventilation with 100% O2
41. Timing of inflation of an intra-aortic balloon pump (IABP) should be
A. Just before the dicrotic notch
B. Just after the dicrotic notch
C. As soon as the downward slope of aortic pulse begins
D. Synchronized with the rise of aortic pulse
42. A 68-year-old patient with an infected prosthetic aortic valve underwent a valve replacement. Post–cardiopulmonary bypass (CPB), his central venous pressure (CVP), pulmonary capillary wedge pressure (PCWP), and systemic vascular resistance (SVR) are low, while the cardiac output (CO) is high. The next step in management of this patient is
A. Adding an inotrope
B. Adding intra-aortic balloon pump (IABP)
C. Adding a pulmonary vasodilator
D. Increasing the hematocrit
43. After neutralizing heparin, which of the following is the fate of the heparin–protamine reaction product?
A. The only product remaining will be water since it is an acid–base reaction
B. It is removed by the reticuloendothelial system
C. It is removed by the kidneys
D. It is excreted unchanged via gastrointestinal (GI) tract
44. Heparin rebound after termination of cardiopulmonary bypass (CPB) is due to
A. Redistribution of protamine to peripheral compartments
B. Redistribution of heparin to central compartment
C. Both A and B are true
D. Both A and B are false; it is due to inadequate protamine dosing
45. DDAVP (desmopressin) administration can increase the activity of all the following factors, except
A. Factor VII
B. Factor VIII
C. Factor XII
D. von Willebrand factor
46. In the first few postoperative hours after an open heart surgery, the emphasis is on
A. Monitoring for excessive postoperative bleeding
B. Maintaining adequate urine output
C. Trying for an early extubation
D. Maintaining euthermia
47. Inhaled nitric oxide (NO) at 60 ppm has all of the following effects, except
A. Drop in systemic vascular resistance (SVR)
B. Drop in pulmonary vascular resistance (PVR)
C. Improvement in cardiac output
D. Better right coronary perfusion
48. Donor–recipient compatibility in cardiac transplantation is based on all, except
A. Heart size
B. ABO blood–group typing
C. Cytomegalovirus serology
D. Tissue crossmatching
49. The central venous pressure (CVP) waveform in cardiac tamponade is characterized by
A. Abolition of X descent
B. Abolition of Y descent
C. CV waveform
D. Tall C waves
50. In constrictive pericarditis,
A. Increased diastolic filling does not occur, in contrast to acute tamponade
B. The Y descent is absent in CVP waveform
C. Pulsus paradoxus is uncommon
D. Diffuse T-wave abnormalities are a rare sign
51. A 25-year-old male with a family history of sudden cardiac deaths is undergoing a laparoscopic appendectomy. Immediately after induction and intubation, you notice a heart rate of 120 bpm and blood pressure of 60/40 mm Hg, with a normal capnogram. You suspect the patient has idiopathic hypertrophic subaortic stenosis. Which of the following maneuvers is most likely to help this patient’s hemodynamics?
A. Lowering the head end of the bed and administering 10 mg of ephedrine IV
B. Administering a bolus of 1 L of normal saline and esmolol 10 mg IV
C. Administering verapamil 5 mg IV immediately
D. Administering a bolus of normal saline and phenylephrine 100 μg IV
52. Pulmonary capillary wedge pressure (PCWP) does not correspond to the left-ventricular end diastolic pressure (LVEDP) in all of the following situations, except
A. Mitral stenosis
B. Tricuspid regurgitation
C. Very high positive end–expiratory pressure (PEEP)
D. Left-atrial myxoma
53. Normal mixed venous oxygen tension is ______ (mm Hg):
54. The only clinically proven method to reduce the risk of perioperative myocardial infarction (MI) and associated death is
A. Perioperative β-blocker therapy
B. Perioperative clonidine therapy
C. Both A and B
D. Use of esmolol boluses intraoperatively to keep the heart rate <80 bpm
55. Which of the following statements is false regarding perioperative myocardial infarction (MI)?
A. Most perioperative MIs occur in the first 48 to 72 hours postoperatively
B. A 1-minute episode of 1-mm ST-segment elevation or depression on the ECG increases the risk for cardiac events by 10-fold
C. Perioperative risk reduction with β-blockers and clonidine is inferior to risk stratification with invasive testing, angioplasty, and coronary artery bypass grafting (CABG)
D. Tachycardia (>105 bpm) for 5 minutes in the postoperative period can increase the risk of death by 10-fold
56. Which of the following is the most effective means of predicting a perioperative cardiac event?
A. Echocardiography wall-motion abnormalities
B. Echocardiography ejection fraction
C. Dipyridamole–thallium scintigraphy
D. Careful preoperative evaluation
57. Which of the following is most effective method of preventing the hemodynamic changes associated with intubation?
A. Brief laryngoscopy (<15 seconds)
B. Esmolol 1 mg/kg IV before intubation
C. Lidocaine 2 mg/kg before intubation
D. Deepen the anesthesia with propofol 1 mg/kg
58. Which of the following events is not likely to adversely affect hemodynamics in a patient with mitral-valve prolapse?
A. Sympathetic stimulation
B. Decreased systemic vascular resistance
C. Head-up position of the patient
D. Increased pulmonary vascular resistance
59. Anesthetic considerations in a patient with mitral regurgitation include all the following, except
A. Avoid sudden decreases in heart rate
B. Avoid sudden decreases in systemic vascular resistance (SVR)
C. Minimize drug-induced myocardial depression
D. Monitor the magnitude of the C wave of CVP as a reflection of mitral-regurgitant flow
60. Treatment of patients with prolonged QT interval include all, except
B. Right stellate ganglion block
C. Avoidance of drugs that prolong the QT interval
D. Availability of electrical cardioversion while the patients are undergoing surgical procedures
61. Anesthetic considerations in patients with aortic stenosis include all, except
A. Intra-arterial blood pressure monitoring
B. Prophylactic administration of intravenous vasoconstrictor phenylephrine
C. Avoidance of extreme bradycardia or tachycardia
D. Avoidance of sudden increases in systemic vascular resistance (SVR)
62. Ventricular premature beats (VPCs) can be treated with lidocaine (1–2 mg/kg IV) when they
A. Are frequent (more than six premature beats/min)
B. Are multifocal
C. Take place during the ascending limb of the T wave (R-on-T phenomenon)
D. All of the above
63. Which of the following drugs needs not be avoided in the anesthetic management of a patient with Wolff–Parkinson–White (WPW) syndrome?
64. Which of the following statements is false regarding management of a patient with an automated implantable cardioverter defibrillator (AICD)?
A. The “magnet mode” is always safe
B. The ground plate should be placed as far as possible from the pulse generator
C. Bipolar electrocautery may be used over unipolar electrocautery to reduce interference between electrosurgical cautery and the pacemaker
D. The magnet mode may produce asynchronous pacing at 99 bpm
65. Cardiac tamponade is characterized by
A. Increase in diastolic filling of the ventricles
B. Decrease in stroke volume
C. Increase in systemic blood pressure due to increased intrapericardial pressure from accumulation of fluid in the pericardial space
D. Systolic dysfunction, and not diastolic dysfunction, is the primary problem
66. An 81-year-old patient with a history of moderate aortic regurgitation is undergoing a coronary artery bypass grafting (CABG). The surgeon decides not to vent the left ventricle. You think this is a wrong decision, and your arguments include all the following, except
A. Venting can be done through a drain placed from the right superior pulmonary vein into the left ventricle
B. Venting can be done through a pulmonary venous drain
C. Retrograde flow through the aortic valve could cause left-ventricular distension
D. Venting done by aspirating from the antegrade cardioplegia line placed in the proximal ascending aorta will not be helpful
67. Centrifugal pumps are superior to roller pumps because of all, except
A. They are less traumatic to blood cells
B. They do not pump air bubbles secondary to air being less dense than blood
C. They are afterload-dependent, and avoid the risk of line rupture with clamping of the arterial inflow circuit
D. Roller pumps compress the fluid-filled tubing between the roller and curved metal back plate and hence avoid air
68. During cardiopulmonary bypass (CPB), the nasopharyngeal temperature is 28°C, the hematocrit is 20%, the temperature corrected PaCO2 is 50 mm Hg, and the uncorrected PaCO2 is 60 mm Hg. The most appropriate management is to
A. Administer additional opioid
B. Administer packed red blood cells to increase hematocrit to 25%
C. Further decrease the patient’s temperature
D. Increase fresh-gas flow to the oxygenator
69. Two days after coronary artery bypass grafting, a 62-year-old man remains sedated, endotracheally intubated, and mechanically ventilated. Over the next 3 hours, PaO2 decreases from 90 to 70 mm Hg at an FIO2 of 0.7, peak inspiratory pressure measured proximally in the ventilator circuit increases from 40 to 66 cm H2O, and plateau pressure remains unchanged at 30 cm H2O. Which of the following is the most likely case of these changes?
A. Adult respiratory distress syndrome (ARDS)
B. Bronchial mucus plugging
C. Left-ventricular failure
D. Tension pneumothorax
70. Regarding the maintenance of blood pressure during cardiopulmonary bypass (CPB), which of the following is false?
A. Lower blood pressures may reduce cerebral blood flow and reduce emboli load to the brain, while higher pressures may improve cerebral blood flow but cause more emboli
B. Pressures less than 40 mm Hg are avoided if possible in adults
C. Pressures higher than 90 mm Hg are used during rewarming
D. Pressures up to 90 mm Hg may be used in patients with cerebral vascular disease
71. During total cardiopulmonary bypass, metabolic acidosis and decreasing mixed venous oxygen saturation are noted. The most likely cause is
D. Light anesthesia
72. While monitoring coronary sinus pressure during retrograde cardioplegia,
A. If the pressure at the distal tip of the coronary sinus catheter during cardioplegia administration at 200 mL/min is equal to central venous pressure, the catheter is not in the coronary sinus but is most likely in the pulmonary artery
B. If the pressure is very high (>100 mm Hg), the coronary sinus catheter is in the left ventricle
C. If the pressure in the coronary sinus catheter is 40 to 60 mm Hg during a 200-mL/min infusion, the catheter is correctly positioned
D. If the catheter is placed too distally, delivery of cardioplegia to the left ventricle will be compromised and result in left-ventricular dysfunction
73. The electromechanically quiet heart at 22°C consumes oxygen at a rate of
A. 2 mL/100 g/min
B. 8 mL/100 g/min
C. 0.3 mL/100 g/min
D. 0.1 mL/100 g/min
74. Additional supplemental anesthetics and muscle relaxants should be administered
A. At institution of cardiopulmonary bypass (CPB)
B. At rewarming
C. Both A and B
D. In the early period after conclusion of CPB
75. The most common hemodynamic abnormality after cardiopulmonary bypass (CPB) is
A. Low cardiac output
B. Low systemic vascular resistance (SVR)
C. High pulmonary vascular resistance
D. Low heart rate
76. A 57-year-old male is undergoing coronary artery bypass grafting (left internal mammary artery to left anterior descending artery). After termination of cardiopulmonary bypass (CPB), you notice a prominent V wave in the pulmonary artery occlusion pressure (PAOP) tracing. The most likely reason for the finding is
A. Left-ventricular dysfunction
B. Right-ventricular dysfunction
C. Cardiac tamponade
D. Posterior papillary muscle dysfunction
CHAPTER 11 ANSWERS
1. B. The normal ventricular cell–resting membrane potential is −80 to −90 mV. Na–K ATPase bound to the membrane is responsible for concentrating K+ intracellularly and in exchange for Na and maintaining this resting-membrane potential. Action potential (depolarization) occurs when cell membrane becomes less negative and crosses a threshold value. This depolarization raises the membrane potential of the myocardial cell, sometimes as high as +20 mv. The cardiac action potential is slightly different from neuronal action potential in that it has a characteristic spike and plateau appearance. The spike portion of this action potential is produced by opening of fast sodium channels along with a decreased permeability to potassium and the plateau portion (0.2–0.3 seconds) is due to opening of slower calcium channels. After depolarization, the sodium and calcium channels close and the membrane permeability to potassium is restored. This restores the resting-membrane potential to its baseline. Spontaneously depolarizing cells, responsible for the myocardial rhythm, do so primarily by intrinsic slow leakage of calcium into cells aided by leaky Na channels moving Na+ in (Table 11-1).
ACTION POTENTIAL PHASE
NET ION MOVEMENT
Na+ in (relative impermeability to K+)
Early rapid repolarization
K+ out (increased permeability to K+ transiently)
Plateau (a part of repolarization)
K+ out of cells
Na+ in and K+ out
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 T- and 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.
cusps bulging into the right atrium
atrial relaxation during ventricular systole
venous filling of the right atrium
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.
MYOCARDIAL OXYGEN SUPPLY
MYOCARDIAL OXYGEN DEMAND
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%)
Head and neck surgery
Intraperitoneal and intrathoracic surgery
Low (reported cardiac risk generally less than 1%)
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 angiotensin-receptor 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-receptor-specific). 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 polymorphic-ventricular 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 inferior-wall 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 serum-ionized 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 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 right-to-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 ventricular-assist 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 left-ventricular 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 PvO2is 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%.
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 β-adrenergic 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 afterload-dependent, 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.
71. B. A mixed venous PO2 lower than 30 mm Hg associated with metabolic acidosis suggests inadequate tissue perfusion. Temperature correction of PaCO2 and pH is probably not necessary. Urine output may serve as a guide to the adequacy of renal perfusion, with an output of 0.5 to 1 mL/kg/hr, indicating adequate renal perfusion.
72. C. Monitoring of coronary sinus pressures during retrograde administration is used to assess proper catheter placement. The anatomical location of coronary sinus ostia makes it very difficult for proper visualization by the surgeon. A properly placed coronary sinus catheter will have pressure of 40 to 60 mm Hg during a 200-mL/min infusion. If the pressure at the distal tip of the coronary sinus catheter during cardioplegia administration at 200 mL/min is equal to central venous pressure, the catheter is not in the coronary sinus but is most likely in the right atrium or in the superior vena cava. Being up against a wall produces a very high (>100 mm Hg) pressure. Positioning of the coronary sinus catheter should be checked with transesophageal echocardiography and manual feel by the surgeon. If the catheter is too deep, cardioplegia to the right ventricle will be compromised, resulting in poor right-ventricular protection.
73. C. At 30°C, the heart muscle consumes oxygen at a rate of 8 to 10 mL/100 g/min, provided it is normally contracting. Oxygen consumption in the fibrillating ventricle at 22°C is 2 mL/100 g/min. The electromechanically quiet heart at 22°C consumes oxygen at a rate of 0.3 mL/100 g/min.
74. A. The extra volume of crystalloid used in priming the CPB circuit may produce a sudden dilution of circulating drug concentrations. This creates a high chance of patient recall/ movement. Supplemental anesthetics, such as benzodiazepines or opioids, and an additional dose of nondepolarizing muscle relaxant, may be administered prophylactically. Volatile anesthetics delivered using vaporizers incorporated into the CPB circuit have largely negated this problem along with the use of BIS monitors. The effect of hemodilution on drug concentrations is likely to be offset by a decreased need for drugs during hypothermia. On the contrary, anesthetic requirements seem to be minimal if the patient was adequately rearmed at the conclusion of CPB. Therefore, additional anesthesia is not routinely required during rewarming at the termination of CPB.
75. B. Low SVR is a very common hemodynamic abnormality after CPB. This makes weaning from CPB very difficult. SVR is usually calculated using the formula mean arterial pressure (mm Hg) − central venous pressure (mm Hg)/pump flow (L/mi) × 80.
SVR should be between 1,200 and 1,400 prior to CPB separation. The units of SVR are dyn s/cm5. SVR can be normalized with a vasoconstrictor prior to weaning from CPB. By this, we are attempting to match the vascular input impedance to the cardiac output impedance and optimizing energy transfer.
76. D. Acute mitral regurgitation (MR) post–CPB is often noticed as a prominent V wave in PAOP tracing. If there is a transesophageal echocardiograph (TEE) in place, we may be able to see a wide MR jet, with observation of an echogenic mass attached to the mitral valve or when a mobile mass is seen to prolapse into the left atrium during systole and to move back into the left ventricle during diastole. The posterior papillary muscle, along with the posterior wall, is entirely perfused either by the right coronary artery (RCA) or by the third obtuse marginal branch, usually by a single artery unlike the anterior, which derives its blood supply from two arteries. It is usually a complication of acute mitral infarction but maybe seen at the end of CPB due to inadequate myocardial protection (warm blood in the adjacent descending aorta providing inadequate protection) during CPB or air entry into the RCA. Acute MR due to volume overload from excessive fluid administration is usually a central MR as evidenced in TEE with a distended ventricle and can be managed by decreasing the preload.