Cardiac Anatomy and Physiology Review Practice Questions

31 multiple-choice questions on Cardiac anatomy and physiology review for paramedic and EMT students, from Chapter 18 (Cardiovascular Emergencies). Read each question, pick your answer, then tap Show answer to check it and read the explanation.

31 practice questions

1. In most patients, which coronary artery supplies the sinoatrial (SA) and atrioventricular (AV) nodes?

   1. A. Left anterior descending artery
   2. B. Right coronary artery
   3. C. Left circumflex artery
   4. D. Left main coronary artery
   Show answer

   Answer: B. Right coronary artery

   In most people the right coronary artery supplies the SA node and the AV node. This is why inferior MIs from RCA occlusion often produce bradycardia and AV blocks.

2. A 70-year-old with long-standing hypertension has an extra, low-pitched heart sound just before S1. What does this sound most likely reflect?

   1. A. Blood rushing into an overfilled, dilated ventricle
   2. B. The atria contracting into a stiff ventricle
   3. C. Normal closure of the aortic and pulmonic valves
   4. D. Friction between inflamed layers of pericardium
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   Answer: B. The atria contracting into a stiff ventricle

   An S4 occurs late in diastole when the atrium contracts against a stiff, noncompliant ventricle, as with hypertensive hypertrophy or ischemia. An S3, early in diastole, reflects rapid filling of an overfilled, dilated ventricle in heart failure. Closure of the aortic and pulmonic valves makes the normal S2, and a pericardial rub is a scratchy sound rather than an extra heart sound.

3. Why does a dilated, thin-walled failing left ventricle need more oxygen to generate a normal pressure than a normal-sized ventricle does?

   1. A. Its walls are much thicker than a normal ventricle's
   2. B. Wall tension rises as the chamber radius grows
   3. C. Its coronary flow is higher than normal
   4. D. It ejects more blood with each beat
   Show answer

   Answer: B. Wall tension rises as the chamber radius grows

   By the law of Laplace, the wall tension needed to produce a given pressure rises with the radius of the chamber, so a dilated ventricle must work harder and use more oxygen. A dilated failing ventricle has thin, not thick, walls. Its coronary flow is not higher than normal, and a failing ventricle ejects less blood per beat, not more.

4. During exercise, how does the heart mainly meet its own higher demand for oxygen?

   1. A. By extracting more oxygen from its blood
   2. B. By switching to anaerobic metabolism
   3. C. By slowing its rate to save oxygen
   4. D. By raising coronary blood flow
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   Answer: D. By raising coronary blood flow

   The heart already extracts about 70% to 75% of the oxygen in coronary blood at rest, so it can only meet a higher demand by increasing coronary flow. That is why a fixed narrowing causes ischemia during exertion. Extraction has little room to rise, the heart cannot run on anaerobic metabolism for long, and its rate rises rather than slows during exercise.

5. Why is the inner (subendocardial) layer of the left ventricle usually the first to become ischemic when coronary flow falls?

   1. A. It draws its blood supply from the coronary sinus
   2. B. It is squeezed hardest during systole
   3. C. It lies farthest from the ventricle cavity
   4. D. It contracts less than the outer layer
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   Answer: B. It is squeezed hardest during systole

   Coronary arteries run on the outer surface and send branches inward, and the subendocardium is compressed most by the high pressure inside the ventricle during systole, so it is perfused mainly in diastole. This is why early ischemia often shows as ST depression. The coronary sinus is a vein that drains the heart rather than supplying it, the subendocardium lies closest to (not farthest from) the cavity, and it does not contract less than the outer layer.

6. A patient in cardiogenic shock has a BP of 82/40 and severe pulmonary edema. Why is blood flow to his left ventricular muscle especially poor?

   1. A. Low diastolic pressure and high LV filling pressure
   2. B. A fast heart rate that lengthens the time in diastole
   3. C. Pulmonary edema that dilates the coronaries
   4. D. Low afterload that diverts flow to the skin
   Show answer

   Answer: A. Low diastolic pressure and high LV filling pressure

   Coronary perfusion pressure is roughly aortic diastolic pressure minus left ventricular end-diastolic pressure. A diastolic pressure of 40 combined with the high filling pressure that causes pulmonary edema leaves very little driving pressure, which worsens ischemia and pump failure. A fast rate shortens diastole rather than lengthening it, pulmonary edema does not dilate the coronaries, and in cardiogenic shock vasoconstriction diverts flow away from the skin, not toward it.

7. Sympathetic stimulation speeds the SA node mainly by:

   1. A. Lengthening the conduction delay in the AV node
   2. B. Blocking calcium entry into its cells
   3. C. Raising its threshold for firing
   4. D. Steepening its spontaneous depolarization
   Show answer

   Answer: D. Steepening its spontaneous depolarization

   Pacemaker cells drift toward threshold on their own during phase 4. Norepinephrine acting on beta-1 receptors makes that drift steeper, so threshold is reached sooner and the rate rises. Sympathetic input shortens, not lengthens, the AV nodal delay. Blocking calcium entry (as calcium channel blockers do) and raising the threshold would both slow the rate.

8. A PVC falls on the peak of the preceding T wave. Why does this timing raise the risk of ventricular fibrillation?

   1. A. It lands in the absolute refractory period
   2. B. It blocks the next impulse from the SA node
   3. C. It lands in the relative refractory period
   4. D. It arrives before the atria depolarize
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   Answer: C. It lands in the relative refractory period

   Near the peak of the T wave, some ventricular cells have recovered and others have not (the relative, or vulnerable, period), so a stimulus there can conduct unevenly and start reentry and VF. During the absolute refractory period no stimulus can cause depolarization at all. Blocking a sinus impulse and arriving before atrial depolarization do not explain the risk of VF.

9. A hypoxic COPD patient on the monitor develops frequent PVCs that fade once his SpO2 improves. What best explains the PVCs?

   1. A. Hypoxia made ventricular cells more irritable
   2. B. Hypoxia caused a long pause in the SA node's firing
   3. C. The oxygen therapy blocked the AV node
   4. D. They were escape beats from a heart block
   Show answer

   Answer: A. Hypoxia made ventricular cells more irritable

   Hypoxia, ischemia, catecholamines and electrolyte problems increase the automaticity of ventricular cells, producing PVCs; correcting the cause usually settles them, which is better than suppressing them with drugs. The sinus node did not stop, since the PVCs were premature beats in an otherwise running rhythm. Oxygen does not block the AV node, and escape beats come late after a pause rather than early.

10. A dyspneic patient's hospital discharge papers show a markedly high BNP level. What does this hormone mainly reflect?

    1. A. Injury to the kidney tubules
    2. B. Rupture of a coronary plaque
    3. C. A stress-related spike in glucose
    4. D. Stretch of the ventricular walls
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    Answer: D. Stretch of the ventricular walls

    B-type natriuretic peptide is released by ventricular muscle when it is stretched by high volume or pressure, so a high level supports heart failure as a cause of dyspnea. It promotes sodium and water loss and vasodilation, partly offsetting RAAS. Kidney tubule injury, plaque rupture (troponin is the marker of myocardial injury) and stress hyperglycemia are not what BNP measures, although kidney failure can raise BNP by reducing its clearance.

11. A 60-year-old has a BP of 168/42, bounding pulses, and a soft murmur heard after S2. Which valve problem best explains the wide pulse pressure?

    1. A. Aortic stenosis
    2. B. Mitral stenosis
    3. C. Aortic regurgitation
    4. D. Tricuspid regurgitation
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    Answer: C. Aortic regurgitation

    In chronic aortic regurgitation the ventricle ejects a large stroke volume (high systolic pressure) and blood leaks back into the ventricle in diastole (low diastolic pressure), giving a wide pulse pressure, bounding pulses and a diastolic murmur. Aortic stenosis narrows the pulse pressure and causes a systolic murmur with a weak, slow-rising pulse. Mitral stenosis and tricuspid regurgitation do not produce a wide arterial pulse pressure.

12. A patient with a hemoglobin of 6 g/dL from slow GI bleeding has a resting heart rate of 118 and bounding pulses. What best explains the tachycardia?

    1. A. Anemia slows conduction through the AV node
    2. B. Low hemoglobin raises systemic vascular resistance
    3. C. The heart raises output to deliver enough oxygen
    4. D. Iron deficiency directly irritates the SA node
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    Answer: C. The heart raises output to deliver enough oxygen

    Each liter of blood carries less oxygen in severe anemia, so the body raises cardiac output (faster rate, larger stroke volume, lower vascular resistance) to keep oxygen delivery up. That high-output state also raises myocardial oxygen demand and can provoke angina. Anemia does not slow AV conduction, it lowers rather than raises vascular resistance, and iron deficiency does not directly irritate the SA node.

13. A patient with an acute inferior MI has a heart rate of 44 and a BP of 82/50 with warm, dry skin. Which mechanism best explains these findings?

    1. A. Major internal blood loss from a ruptured coronary plaque
    2. B. A sympathetic surge caused by the chest pain
    3. C. A vagal reflex triggered by the injured inferior wall
    4. D. Calcium overload that has stunned the SA node
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    Answer: C. A vagal reflex triggered by the injured inferior wall

    Ischemia of the inferior and posterior wall can stimulate receptors that trigger a vagal reflex (the Bezold-Jarisch reflex), causing bradycardia, vasodilation and hypotension with warm skin. It often responds to atropine and fluid. A ruptured plaque does not bleed outward, a sympathetic surge would cause tachycardia and cool, pale skin, and calcium overload of the SA node is not the mechanism.

14. Why can 150 mL of blood that collects in the pericardium within minutes cause tamponade, while 1 liter of fluid that builds up over months may not?

    1. A. Blood is much heavier than other pericardial fluid
    2. B. Slow effusions drain into the coronary sinus
    3. C. Rapid bleeding raises the heart rate too much
    4. D. The pericardium stretches only when filled slowly
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    Answer: D. The pericardium stretches only when filled slowly

    The fibrous pericardium is stiff over short periods, so even a small, rapid collection raises pericardial pressure enough to block filling of the heart; given months, it gradually stretches to hold large volumes at lower pressure. The weight of blood, drainage into the coronary sinus and the heart rate do not explain this difference.

15. Phase 0 of the ventricular myocardial action potential is caused primarily by:

    1. A. Slow calcium influx
    2. B. Potassium efflux
    3. C. Rapid sodium influx
    4. D. Chloride influx
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    Answer: C. Rapid sodium influx

    Phase 0 is rapid depolarization caused by fast sodium channels opening. The plateau (phase 2) is maintained by calcium influx, and repolarization (phase 3) by potassium efflux.

16. Unlike skeletal muscle, heart muscle cannot be held in a sustained contraction by rapid stimulation. Why?

    1. A. It has no calcium stores inside its cells
    2. B. It has no gap junctions between its cells
    3. C. Its contractions are triggered by vagal nerve impulses
    4. D. Its long refractory period lasts through contraction
    Show answer

    Answer: D. Its long refractory period lasts through contraction

    The cardiac action potential has a long plateau, so the refractory period lasts almost as long as the contraction; the muscle must relax before it can respond again, which lets the ventricles fill. Cardiac cells do store calcium in the sarcoplasmic reticulum, they are linked by gap junctions, and contraction is triggered by the conduction system, not by vagal input.

17. Why is the measured QT interval corrected for heart rate (QTc) before deciding whether it is prolonged?

    1. A. The QT normally lengthens as the heart rate rises
    2. B. Heart rate changes the height of the T wave
    3. C. The QT normally shortens as the heart rate rises
    4. D. Correction removes muscle artifact from the QT
    Show answer

    Answer: C. The QT normally shortens as the heart rate rises

    Repolarization speeds up at faster rates, so the raw QT shortens as the rate rises and lengthens as it slows; formulas such as Bazett (QT divided by the square root of the R-R interval) adjust for this. The QT does not lengthen with faster rates. T-wave height and muscle artifact are not what the correction addresses.

18. A patient with known mitral stenosis develops atrial fibrillation at 150/min and sudden pulmonary edema. Why did the fast rate cause the edema?

    1. A. The valve opened wider at the faster rate
    2. B. Less diastolic time to fill across the narrow valve
    3. C. Atrial fibrillation lowered the left atrial pressure
    4. D. The right ventricle pumped less blood forward
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    Answer: B. Less diastolic time to fill across the narrow valve

    With a narrowed mitral valve, the left ventricle fills slowly and depends on a long diastole and the atrial kick. A rapid rate shortens diastole and AF removes the kick, so left atrial pressure rises and fluid backs into the lungs; rate control helps. The valve does not open wider at fast rates, AF raises rather than lowers left atrial pressure, and reduced right-sided output would lessen, not cause, pulmonary congestion.

19. Why can a large pulmonary embolism cause sudden right heart failure, while pulmonary pressure that rises over years is often tolerated?

    1. A. The RV wall is thicker than the left ventricle's
    2. B. Emboli usually block the right coronary artery
    3. C. The pulmonic valve closes off after a large clot lodges
    4. D. A thin RV cannot adapt to a sudden rise in afterload
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    Answer: D. A thin RV cannot adapt to a sudden rise in afterload

    The right ventricle is a thin-walled, low-pressure pump. Given time it can hypertrophy, but a sudden large rise in pulmonary resistance makes it dilate and fail within minutes. Its wall is thinner, not thicker, than the left ventricle's. Venous emboli lodge in the pulmonary arteries, not the coronary arteries, and the pulmonic valve does not close off.

20. Sudden occlusion of the left main coronary artery is especially dangerous because this artery:

    1. A. Supplies most of the right ventricular wall
    2. B. Is the sole supply of the SA node
    3. C. Drains blood into the coronary sinus
    4. D. Feeds both the LAD and the circumflex
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    Answer: D. Feeds both the LAD and the circumflex

    The left main divides into the LAD and the circumflex, so its occlusion threatens most of the left ventricle and often causes shock or sudden death; ST elevation in aVR with widespread ST depression can be a clue. It does not supply the right ventricle, which is mainly fed by the right coronary. The SA node is usually supplied by the right coronary, and arteries do not drain into the coronary sinus, which collects venous blood.

21. In a healthy person sitting at 45 degrees, the jugular venous pulsation falls slightly with each breath in. Why?

    1. A. The tricuspid valve closes during inspiration
    2. B. Inspiration raises the pressure in the right atrium
    3. C. The neck muscles compress the jugular vein
    4. D. Negative chest pressure draws blood into the thorax
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    Answer: D. Negative chest pressure draws blood into the thorax

    Inspiration lowers pressure inside the chest, pulling venous blood into the right heart, so the neck veins normally fall. A rise in neck veins on inspiration (Kussmaul sign) is abnormal and suggests that the right heart cannot accept the extra return. The tricuspid valve does not close with breathing, right atrial pressure falls rather than rises, and neck muscles do not explain the normal fall.

22. An older patient's run of SVT suddenly stops, and the monitor shows a 4-second pause before sinus beats return. What best explains the pause?

    1. A. The AV node was permanently damaged
    2. B. The fast rhythm suppressed a diseased SA node
    3. C. The SVT caused a new left bundle branch block
    4. D. Potassium rose during the fast rhythm
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    Answer: B. The fast rhythm suppressed a diseased SA node

    A fast rhythm overdrives and suppresses the pacemaker cells below it; a healthy sinus node recovers quickly, but a diseased one (sick sinus syndrome, tachy-brady pattern) may take seconds, causing dizziness or syncope. Permanent AV nodal damage, a new bundle branch block and a rise in potassium do not explain a pause in sinus activity right after the tachycardia ends.

23. A patient had weeks of untreated atrial fibrillation at 140/min and developed heart failure with a low ejection fraction, which recovered after the rate was controlled. What is the best term for this?

    1. A. Stress-induced (takotsubo) cardiomyopathy
    2. B. Hypertrophic cardiomyopathy
    3. C. Tachycardia-induced cardiomyopathy
    4. D. Peripartum cardiomyopathy
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    Answer: C. Tachycardia-induced cardiomyopathy

    A persistently fast rate over weeks can weaken the ventricle; controlling the rate or rhythm often restores function, which is why long-standing rapid AF is not ignored. Takotsubo follows a sudden emotional or physical stress, hypertrophic cardiomyopathy is an inherited thickening of the muscle, and peripartum cardiomyopathy occurs late in pregnancy or after delivery.

24. A patient with pericarditis has sharp chest pain that spreads to the ridge of his left trapezius muscle. What explains the pain at this site?

    1. A. The vagus nerve supplies the trapezius muscle
    2. B. The phrenic nerve carries pain from the pericardium
    3. C. Inflamed pericardium spreads into that muscle
    4. D. The left coronary artery also feeds the trapezius muscle
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    Answer: B. The phrenic nerve carries pain from the pericardium

    The phrenic nerve supplies the pericardium and enters the spinal cord at C3 to C5, the same levels that carry sensation from the trapezius ridge, so the pain is referred there; this pattern favors pericarditis over ischemia. The vagus nerve does not supply the trapezius, the inflammation does not spread into the muscle, and the coronary arteries do not supply it.

25. Why can lowering a long-standing hypertensive patient's BP to normal within minutes cause a stroke?

    1. A. A normal pressure bursts the weakened cerebral vessels
    2. B. Rapid lowering raises intracranial pressure
    3. C. Antihypertensive drugs clot the carotid arteries
    4. D. Brain autoregulation has shifted to higher pressures
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    Answer: D. Brain autoregulation has shifted to higher pressures

    With chronic hypertension, the range over which the brain keeps its blood flow steady shifts upward, so a pressure that is normal for others can underperfuse this patient's brain, heart and kidneys; that is why most hypertensive emergencies are lowered gradually. A lower pressure does not burst vessels, rapid lowering does not raise intracranial pressure, and antihypertensives do not clot the carotids.

26. A 72-year-old on metoprolol is hypotensive from a GI bleed but has a heart rate of 64. What best explains the lack of tachycardia?

    1. A. The bleed is too small to cause shock
    2. B. Low blood pressure slows the SA node directly
    3. C. Beta-1 blockade blunts the rate response
    4. D. Beta-2 blockade lowers the heart rate
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    Answer: C. Beta-1 blockade blunts the rate response

    Beta-blockers block the sympathetic beta-1 response that normally raises heart rate in shock. A normal heart rate in a patient on these drugs does not rule out significant hypovolemia. The rate effect comes from beta-1 receptors in the heart, not beta-2, hypotension normally speeds the SA node through the baroreflex, and the bleed is not small just because the rate is normal.

27. In atrial fibrillation the atria fire at 400 or more times a minute, yet the ventricular rate is usually below about 200. Why?

    1. A. The AV node blocks many of the atrial impulses
    2. B. The ventricles cannot beat faster than 100
    3. C. The SA node overrides the atrial impulses
    4. D. The Purkinje fibers filter out most of the impulses
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    Answer: A. The AV node blocks many of the atrial impulses

    The AV node conducts slowly and stays refractory after each beat, so it filters out most fibrillatory impulses. An accessory pathway (as in WPW) bypasses this filter, which is why pre-excited AF can reach 250 to 300 and degenerate into VF. Ventricles can beat much faster than 100, the SA node is not in control during AF, and Purkinje fibers are not the filter.

28. Why does a beat that starts in the ventricular muscle produce a wide QRS complex?

    1. A. It travels down both bundle branches together
    2. B. It spreads cell to cell instead of via Purkinje fibers
    3. C. It is first delayed within the AV node
    4. D. It has to depolarize both of the atria before the ventricles
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    Answer: B. It spreads cell to cell instead of via Purkinje fibers

    A normal impulse reaches the ventricles through the fast bundle branches and Purkinje network, giving a narrow QRS. An ectopic ventricular beat spreads slowly from muscle cell to muscle cell, so the QRS is wide and bizarre. Travel down both bundle branches is normal conduction, the AV node delay comes before the QRS, and the atria are not depolarized first.

29. An 80-year-old at rest has a regular, narrow-complex rhythm at 180/min with no visible P waves. Why is sinus tachycardia unlikely?

    1. A. Sinus tachycardia starts and ends abruptly, not gradually
    2. B. Sinus tachycardia tops out near 150/min
    3. C. Her maximum sinus rate is about 220 minus her age
    4. D. Sinus tachycardia is irregular above 150/min
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    Answer: C. Her maximum sinus rate is about 220 minus her age

    A useful rule is that the sinus node rarely exceeds about 220 minus age, so 180/min at rest in an 80-year-old (whose maximum is about 140) points to SVT or atrial flutter rather than sinus tachycardia. Sinus tachycardia speeds up and slows down gradually rather than abruptly, it can exceed 150/min in younger people, and it remains regular at high rates.

30. When a cardiologist says a patient has a right-dominant coronary circulation, what does this mean?

    1. A. The right coronary carries more blood flow than the left main
    2. B. The right ventricle is thicker than the left one
    3. C. The right coronary supplies the entire septum
    4. D. The right coronary gives rise to the posterior descending
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    Answer: D. The right coronary gives rise to the posterior descending

    Coronary dominance is defined by which artery gives rise to the posterior descending artery, which supplies the inferior wall and back of the septum. Most people are right dominant, which is why most inferior MIs come from the right coronary; in left-dominant people it comes from the circumflex. The right coronary does not carry more flow than the left main, the left ventricle remains thicker, and the LAD supplies most of the septum.

31. Which electrolyte is most directly responsible for linking electrical excitation to myocardial contraction?

    1. A. Sodium
    2. B. Chloride
    3. C. Magnesium
    4. D. Calcium
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    Answer: D. Calcium

    Calcium entering the cell and released from the sarcoplasmic reticulum binds the contractile proteins and triggers contraction (excitation-contraction coupling). Sodium drives depolarization but not contraction itself.