Cardiac Lipp Flashcards
- 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
- 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).
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
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.
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
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.
- 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
- 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 adirect 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.
- 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 cuspsafter 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
C.
○ The CVP waveform consists of three positive waveforms called a, c, and v and two negative slopes called the x and y depressions.
• a wave atrial contraction
• c wave cusps bulging into the right atrium
• x descent atrial relaxation during ventricular systole
• v wave venous filling of the right atrium
• y descent atrial emptying when tricuspid valve opens
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, Sp O 2 = 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/m 2
B. Cardiac output 8.1 L/min by thermodilution technique
C. Cardiac output 8.1 L/min by Fick method
D. Sv O 2 of 75% from a pulmonary artery (PA) catheter
- 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/m 2 .
• 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.
- 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 cm 2 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
- 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.
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
- 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.
- 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
- 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.
- The sinoatrial and the atrioventricular (AV) nodes aresupplied in majority of the individuals by
A. Left anterior descending artery
B. Right coronary artery
C. Circumflex artery
D. Posterior descending artery
- 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.
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
- 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.
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
- 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.
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
- 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.
Which of the following inhalational agents causes the least coronary vasodilation?
A. Halothane
B. Isoflurane
C. Desflurane
D. Sevoflurane
- 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 (A 1 ) 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.
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
C.
○ According to ACC/AHA guidelines for noncardiac surgery in cardiac patients, Surgeries can be classified into high, intermediate, and low risk with high-risk surgeries having >5% risk and low-risk surgeries having <1% risk (Table 11-3).
○ Table 11-3 Cardiac Risk Stratification for Noncardiac Surgical Procedures.
☆ High (reported cardiac risk often greater than 5%)
• Emergent major operations, particularly in the elderly Aortic and other major vascular surgery Peripheral vascular surgery
• Anticipated prolonged surgical procedures associated with large fluid shifts and/or blood loss
☆ Intermediate (reported cardiac risk generally less than 5%)
• Carotid endarterectomy
• Head and neck surgery
• Intraperitoneal and intrathoracic surgery
• Orthopedic surgery
• Prostate surgery
☆ Low (reported cardiac risk generally less than 1%)
• Endoscopic procedures
• Superficial procedure
• Cataract surgery
• Breast surgery
- 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
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.
The patient mentioned abovedevelops severe hypotension immediately after intubation. Which of the following agents is most suited to bring the blood pressure back to normal values?
A. Ephedrine
B. Phenylephrine
C. Epinephrine
D. Dopamine
- B.
○ Direct α 1 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.
Which of the following antianginal agents has the highest coronary vasodilating potential?
A. Nitrates
B. Verapamil
C. Dihydropyridines
D. β-Blockers
- 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.
- 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
- 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.
- Which of the following β-blockers is most suited for a patient with bronchospastic disease?
A. Propranolol
B. Metoprolol
C. Acebutolol
D. Bisoprolol
C.
○ Cardioselectivity of agents like metoprolol is dose-dependent B1-receptor-specific).
○ Even the β 1 -receptor-specific agents can have some β 2 -blocking action at higher doses.
○ β-Blockers with intrinsic sympathomimetic activity, like acebutolol, provide a unique advantage in patients with bronchospastic airway disease.
- 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?
A. Amiodarone
B. Lidocaine
C. Pacing
D. Diltiazem
- 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.
- 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
- 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
- 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
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.
- Which of the following ECG leads is most sensitive to detect an anterior-wall myocardial ischemia?
A. V5
B. V4
C. II
D. V2
- 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.
- 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
- 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 no 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.
- 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
- 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.
- 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
- 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.
- 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
- C. Transgastric mid-papillary (midshort axis) view provides a snapshot of all the different blood vessels supplying the heart
- 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
- 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.
- 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
- 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.