Cardiovascular System Basics
Q: What is the normal adult cardiac output (CO) range at rest?
A: 4–8 L/min
Rationale: CO = HR × SV; typical resting values yield ~4–8 L/min.
Q: Which organ initiates renin release to help regulate blood pressure?
A: Kidney (juxtaglomerular cells)
Rationale: RAAS activation raises BP via angiotensin II and aldosterone.
Q: In general, how do volatile anesthetics affect SVR?
A: They decrease SVR (vasodilation)
Rationale: Smooth muscle relaxation → reduced afterload.
Q: Which commonly used IV induction agent most predictably causes hypotension?
A: Propofol
Rationale: Venodilation + arterial dilation → ↓ preload/afterload.
Q: Immediately after induction, BP falls from 120/70 to 80/45. What is the most appropriate first step?
A: Reduce anesthetic depth and give a 250–500 mL crystalloid bolus (while verifying measurement and assessing airway/ventilation).
Rationale: Address common vasodilation/relative hypovolemia before escalating meds.
Q: Name the valve between the left atrium and left ventricle.
A: Mitral (bicuspid) valve
Rationale: Prevents backflow from LV to LA during systole.
Which hormone directly promotes water reabsorption to affect BP? →
Vasopressin (ADH);
Rationale: Acts on V2 receptors in kidneys.
Q: Which anesthetic technique is most associated with bradycardia due to sympathetic blockade of cardiac accelerators?
A: High neuraxial (spinal/epidural) block affecting T1–T4
Rationale: Blocks sympathetic fibers to the heart → bradycardia.
What are the two serum markers of cardiac infarction?
A: Cardiac troponin I and creatine kinase MB (CK-MB)
Rationale: Troponin is cardiac specific regulatory protein in muscle class that controls interactions between skeletal and cardiac muscle.
Q: During spinal anesthesia, the patient’s BP drops significantly. Which vasopressor is commonly used first-line?
A: Phenylephrine (consider ephedrine if bradycardic)
Rationale: Phenylephrine raises SVR; ephedrine adds β effect for low HR.
Q: Which cardiac conduction structure typically initiates the heartbeat?
A: Sinoatrial (SA) node
Rationale: The primary pacemaker, ~60–100 bpm intrinsic rate.
Q: Name two key electrolytes essential for normal cardiac action potentials.
A: Potassium (K+) and Calcium (Ca2+)
Rationale: K+ repolarization; Ca2+ plateau/contraction (Na+ also critical for depolarization).
Q: Why can positive-pressure ventilation (PPV) reduce venous return?.
A: Increased intrathoracic pressure compresses venous structures → ↓ preload
Rationale: Less venous return → ↓ CO
Q: What are propofol’s effects on preload and afterload?
A: Decreases both (venodilation and arterial vasodilation)
Rationale: Reduces venous return and systemic resistance.
Q: A patient with CAD needs a hemodynamically stable induction. Which agent is preferred?
A: Etomidate
Rationale: Minimal changes in HR/BP—useful in limited cardiac reserve.
Q: Define afterload. →
Resistance the LV must overcome to eject blood (closely related to SVR/aortic impedance).
Q: Which cranial nerve provides parasympathetic input that slows heart rate?A: Vagus nerve (CN X)Rationale: Increases AV nodal refractoriness and slows SA node firing.
A: Vagus nerve (CN X)
Rationale: Increases AV nodal refractoriness and slows SA node firing.
Q: What is the typical effect of modern volatile agents on myocardial contractility?
A: Dose-dependent depression of contractility
Rationale: Decreased Ca2+ availability/handling → reduced inotropy.
: Which neuromuscular blocker is known to cause tachycardia due to vagolytic properties?
A: Pancuronium
Rationale: Blocks muscarinic receptors → ↑ HR.
Q: Post-op patient develops a new ventricular ectopy. Which electrolyte imbalance should you suspect first?
A: Hypokalemia (also consider hypomagnesemia)
Rationale: Low K+ predisposes to arrhythmias.
: State the Frank–Starling principle of the heart.
A: Increased preload (end-diastolic fiber stretch) → increased stroke volume up to an optimal point.
Rationale: Sarcomere length affects contractile force; excessive stretch impairs function.
Q: Briefly describe how baroreceptors help maintain hemodynamic stability.
A: Stretch receptors (carotid sinus/aortic arch) sense BP changes and modulate autonomic outflow to keep BP near set point.
Rationale: Rapid feedback loop adjusting HR, SVR, and contractility.
Q: Explain the primary mechanism of hypotension during spinal anesthesia.
A: Sympathetic blockade → vasodilation & venous pooling → ↓ preload/afterload → hypotension
Rationale: The extent depends on block level, patient volume status.
Q: Summarize how perioperative beta-blockade interacts with anesthetic agents.
A: Blunts sympathetic responses (↓ HR/contractility), reduces ischemia/arrhythmias, but may increase risk of bradycardia/hypotension—dose titration and readiness to treat are essential.
Rationale: Maintain coronary perfusion while avoiding excessive hemodynamic depression.
Q: What is the rationale for using vasopressors during anesthesia-induced hypotension?
A: Restore SVR and perfusion pressure to maintain organ/coronary perfusion when vasodilation or myocardial depression lowers BP
Rationale: Temporizes while optimizing volume and anesthetic depth.