CCRN Cardiovascular Practice Test

25 practice questions

Choose an answer, then check it under Show answer.

1. Question 1 of 25Medium

   A patient with unstable angina is receiving an intravenous infusion of eptifibatide along with unfractionated heparin. A complete blood count drawn 4 hours after initiating the infusion shows the platelet count has fallen from a baseline of 210,000/mcL to 18,000/mcL. There is no visible bleeding. Which action is the priority nursing intervention?

   1. AA. Immediately stop the eptifibatide infusion and notify the provider
   2. BB. Decrease the eptifibatide infusion rate by half and recheck platelets
   3. CC. Infuse two units of pooled platelets immediately
   4. DD. Administer protamine sulfate to reverse anticoagulation
   Show answer to question 1

   Answer: A. Immediately stop the eptifibatide infusion and notify the provider

   Glycoprotein IIb/IIIa inhibitors such as eptifibatide can trigger acute, profound immune-mediated thrombocytopenia within hours of initiation, necessitating the immediate cessation of the drug. Decreasing the rate or continuing the drug risks catastrophic bleeding, while platelet transfusions are generally reserved for active severe bleeding because transfused platelets will also be targeted by the drug-dependent antibodies. Protamine sulfate reverses heparin rather than the glycoprotein IIb/IIIa inhibitor.

2. Question 2 of 25Easy

   Before starting a prescribed clevidipine infusion for severe hypertension, the nurse reviews the patient's history. Which finding is a contraindication to this drug?

   1. AA. History of severe persistent asthma
   2. BB. Resting heart rate of 58/min
   3. CC. Allergy to shellfish
   4. DD. Allergy to soybeans or eggs
   Show answer to question 2

   Answer: D. Allergy to soybeans or eggs

   Clevidipine is an IV dihydropyridine calcium channel blocker supplied in a lipid emulsion that contains soybean oil and egg yolk phospholipids, so allergy to soy or egg products is a contraindication. Defective lipid metabolism and severe aortic stenosis are also contraindications.

   Why the other options are wrong

   • AAsthma is a concern with nonselective beta-blockers such as labetalol, not with clevidipine.
   • BClevidipine does not slow the sinus rate, and reflex tachycardia is more typical than bradycardia.
   • CShellfish allergy is unrelated to clevidipine and does not predict a reaction to its lipid emulsion.

3. Question 3 of 25Medium

   A 68-year-old man arrives with an anterior STEMI and cardiogenic shock: blood pressure 78/50 mm Hg, cool mottled skin, lactate 5.8 mmol/L and crackles in both lung bases. Which intervention offers the greatest survival benefit?

   1. AA. Routine insertion of an intra-aortic balloon pump
   2. BB. Emergency revascularization of the culprit artery
   3. CC. A 2 L crystalloid bolus to raise the blood pressure
   4. DD. High-dose IV loop diuretic to clear the lung crackles
   Show answer to question 3

   Answer: B. Emergency revascularization of the culprit artery

   Early revascularization of the infarct-related artery, usually by primary PCI, is the intervention shown to improve survival in cardiogenic shock caused by acute myocardial infarction. Vasopressors, inotropes and selected mechanical support stabilize the patient around that procedure.

   Why the other options are wrong

   • ARoutine balloon pump use did not improve survival in infarct-related cardiogenic shock, so it is reserved for selected patients.
   • CA large fluid bolus can worsen pulmonary congestion in a failing left ventricle that is already causing crackles.
   • DAggressive diuresis during hypotensive shock can lower preload and perfusion further and does not open the occluded artery.

4. Question 4 of 25Hard

   A 66-year-old man has had crushing chest pressure for 40 minutes. His 12-lead ECG shows 2 mm of horizontal ST depression in leads V1 to V3 with tall R waves and upright T waves in those leads, and no ST elevation in any standard lead. Which action should the nurse anticipate next?

   1. AA. Repeat the standard 12-lead ECG in 24 hours
   2. BB. Obtain right-sided leads, including V4R, to look for ST elevation
   3. CC. Obtain posterior leads V7 to V9 to look for ST elevation
   4. DD. Start a heparin infusion and plan catheterization within 72 hours
   Show answer to question 4

   Answer: C. Obtain posterior leads V7 to V9 to look for ST elevation

   ST depression in V1 to V3 with tall R waves can be the mirror image of a posterior wall STEMI, which the standard 12 leads do not view directly. ST elevation in posterior leads V7 to V9 confirms the diagnosis, and the patient then needs emergency reperfusion like any other STEMI.

   Why the other options are wrong

   • AOngoing ischemic pain with a suggestive pattern calls for additional leads and serial tracings within minutes, not a wait of a full day.
   • BRight-sided leads look for right ventricular infarction, which accompanies inferior ST elevation rather than isolated ST depression in V1 to V3.
   • DTreating this pattern as NSTE-ACS with delayed catheterization could miss an evolving posterior STEMI that needs emergency reperfusion.

5. Question 5 of 25Medium

   A 64-year-old patient who underwent percutaneous coronary intervention via the right common femoral artery 4 hours ago reports worsening lower back and right flank pain. The patient appears pale and diaphoretic. Vital signs are BP 84/48 mm Hg, HR 118/min, and SpO2 97% on room air. The femoral puncture site dressing is dry, intact, and without a palpable hematoma. What is the priority nursing action?

   1. AA. Administer a rapid IV crystalloid fluid bolus
   2. BB. Administer ordered IV hydromorphone for pain
   3. CC. Place a pneumatic compression device over the groin
   4. DD. Obtain an immediate right hip radiograph
   Show answer to question 5

   Answer: A. Administer a rapid IV crystalloid fluid bolus

   The sudden development of flank or back pain accompanied by hypotension and tachycardia following femoral artery catheterization is highly suspicious for retroperitoneal hemorrhage, even without external bleeding or a palpable hematoma. Immediate volume expansion with isotonic crystalloids is the critical initial nursing priority to maintain organ perfusion while preparing for diagnostic computed tomography and surgical or interventional vascular management. External pressure over the puncture site will not arrest retroperitoneal bleeding originating proximal to the inguinal ligament.

6. Question 6 of 25Easy

   A patient with a temporary transvenous pacemaker in VVI mode has an intrinsic heart rate of 78 beats/min. The cardiac monitor displays regular pacing spikes at the set rate of 70 beats/min occurring intermittently across the native rhythm, including some spikes landing on the ST segment and T wave. Which pacemaker malfunction is present?

   1. AA. Undersensing
   2. BB. Oversensing
   3. CC. Output failure
   4. DD. Failure to capture
   Show answer to question 6

   Answer: A. Undersensing

   Undersensing occurs when the pacemaker fails to recognize the patient's intrinsic cardiac activity, resulting in pacing spikes firing inappropriately into native complexes and risking lethal dysrhythmias via the R-on-T phenomenon. Oversensing would cause inappropriate inhibition and a lack of pacing spikes. Failure to capture occurs when delivered spikes fail to generate a myocardial depolarization, and output failure presents as an absence of spikes despite a rate below the programmed threshold.

7. Question 7 of 25Easy

   A patient with unstable atrial flutter and a heart rate of 168 beats/min is prepared for emergent synchronized cardioversion. What is the physiological rationale for ensuring the synchronization mode is activated prior to shock delivery?

   1. AA. To stimulate the sinoatrial node during the relative refractory phase of the cardiac cycle
   2. BB. To deliver energy coincident with the QRS complex to prevent the R-on-T phenomenon
   3. CC. To discharge energy during the ST segment when myocardial cell membranes are depolarized
   4. DD. To time energy release during the peak of the T wave to maximize refractory repolarization
   Show answer to question 7

   Answer: B. To deliver energy coincident with the QRS complex to prevent the R-on-T phenomenon

   Synchronized cardioversion delivers electrical energy coincident with the R wave of the QRS complex to avoid shocking during the vulnerable relative refractory period of ventricular repolarization (the peak or downslope of the T wave). Discharging energy during the T wave can precipitate the R-on-T phenomenon, leading to ventricular fibrillation. Shocking during the peak of the T wave is the exact hazard synchronization is engineered to avoid.

8. Question 8 of 25Hard

   A patient with an extensive right ventricular infarction remains in shock with a blood pressure of 80/44 mm Hg despite receiving 2.5 liters of IV isotonic crystalloid over the past two hours. Repeat hemodynamics show a central venous pressure of 20 mm Hg, pulmonary artery occlusion pressure of 13 mm Hg, and a cardiac index of 1.6 L/min/m2. Which pharmacological intervention is most appropriate next?

   1. AA. Administer an additional 1-liter crystalloid bolus
   2. BB. Initiate an IV phenylephrine continuous infusion
   3. CC. Administer IV furosemide to reduce preload
   4. DD. Initiate an IV dobutamine infusion
   Show answer to question 8

   Answer: D. Initiate an IV dobutamine infusion

   When right ventricular infarction is refractory to volume loading and central venous pressure reaches elevated levels (typically 15 to 20 mm Hg), further fluid boluses cause right ventricular overdistention, shift the interventricular septum into the left ventricle, and further compromise left ventricular filling. An inotrope such as dobutamine is the therapy of choice to augment right ventricular contractility and restore cardiac output. Phenylephrine provides pure alpha-1 vasoconstriction without inotropic support, which increases right ventricular afterload and exacerbates failure.

9. Question 9 of 25Easy

   Fibrinolytic therapy is planned for a patient with STEMI because timely primary PCI is not available. Which finding in the patient's history is an absolute contraindication to fibrinolysis?

   1. AA. Warfarin therapy with an INR of 2.1
   2. BB. Blood pressure of 168/96 mm Hg on arrival
   3. CC. Menstrual bleeding that began yesterday
   4. DD. Hemorrhagic stroke 5 years ago
   Show answer to question 9

   Answer: D. Hemorrhagic stroke 5 years ago

   Any prior intracranial hemorrhage is an absolute contraindication to fibrinolytic therapy, no matter how long ago it occurred, because the risk of new intracranial bleeding is too high. Transfer for primary PCI becomes the reperfusion option.

   Why the other options are wrong

   • ACurrent oral anticoagulant therapy is a relative contraindication that requires weighing bleeding risk against benefit, not an absolute bar.
   • BOnly a pressure above about 180/110 mm Hg on presentation counts as a relative contraindication, and 168/96 mm Hg is below it.
   • CMenstruation is specifically excluded from the active bleeding contraindication to fibrinolysis.

10. Question 10 of 25Easy

    A patient with a left radial arterial catheter is repositioned from supine to a 45-degree head-of-bed elevation. The arterial pressure transducer remains secured to the bed frame, which elevates the transducer 10 cm above the phlebostatic axis. How will this change affect the displayed arterial blood pressure readings?

    1. AA. Both systolic and diastolic readings will be falsely increased
    2. BB. Both systolic and diastolic readings will be falsely decreased
    3. CC. The mean arterial pressure will remain unchanged despite the position change
    4. DD. The systolic reading will decrease while the diastolic reading increases
    Show answer to question 10

    Answer: B. Both systolic and diastolic readings will be falsely decreased

    When an arterial transducer is positioned higher than the reference level (phlebostatic axis), the hydrostatic pressure exerted on the transducer decreases, producing falsely low systolic, diastolic, and mean arterial pressure measurements. For every inch (2.54 cm) the transducer is placed above the reference axis, the pressure drops by approximately 1.86 mm Hg (roughly 7.4 mm Hg for 10 cm). Placing the transducer below the phlebostatic axis causes falsely elevated readings.

11. Question 11 of 25Hard

    A patient in cardiogenic shock has a mean arterial pressure of 62 mm Hg, a heart rate of 105 beats/min, and a cardiac output of 3.2 L/min measured by thermodilution. What is the patient's calculated cardiac power output (CPO), and what does this value signify?

    1. AA. 1.98 W, indicating supranormal cardiac performance requiring inotropic weaning
    2. BB. 0.44 W, indicating severe hemodynamic compromise and high mortality risk
    3. CC. 0.88 W, indicating adequate ventricular work despite borderline mean arterial pressure
    4. DD. 1.25 W, indicating hyperdynamic compensation requiring immediate vasodilation
    Show answer to question 11

    Answer: B. 0.44 W, indicating severe hemodynamic compromise and high mortality risk

    Cardiac power output is calculated as (mean arterial pressure multiplied by cardiac output) divided by 451, which in this case equals (62 multiplied by 3.2) divided by 451, yielding 0.44 W. A cardiac power output below 0.6 W is a validated predictor of severe pump failure and high in-hospital mortality in cardiogenic shock. Values approaching or exceeding 1.0 W reflect normal to high cardiac work, which does not match this patient's calculated profile.

12. Question 12 of 25Hard

    A 63-year-old man admitted with an anterior wall MI develops a rhythm with regular P waves at 84/min, a constant PR interval of 0.18 seconds in conducted beats, and intermittent P waves that are not followed by a QRS complex. The QRS measures 0.14 seconds. He is alert without symptoms, and his BP is 114/72 mm Hg. Which action should the nurse take first?

    1. AA. Apply transcutaneous pacing pads and keep the pacer ready
    2. BB. Give atropine now to prevent progression of the block
    3. CC. Continue routine monitoring, since he has no symptoms
    4. DD. Give his scheduled oral beta-blocker to reduce oxygen demand
    Show answer to question 12

    Answer: A. Apply transcutaneous pacing pads and keep the pacer ready

    A constant PR interval with intermittently nonconducted P waves and a wide QRS is second-degree AV block type II (Mobitz II). The block is usually below the AV node and can progress suddenly to complete heart block, especially with an anterior MI, so pacing pads are applied now and transvenous pacing is anticipated.

    Why the other options are wrong

    • BAtropine acts on the AV node, often fails in infranodal block, may worsen the conduction ratio, and is not indicated without symptoms.
    • CMobitz II can abruptly become complete heart block with a slow escape rhythm, so waiting for symptoms is unsafe.
    • DA beta-blocker further slows AV conduction and could precipitate complete heart block.

13. Question 13 of 25Medium

    During balloon angioplasty and stent deployment for severe right internal carotid artery stenosis, the patient abruptly develops sinus bradycardia at 34 beats/min and a blood pressure of 72/40 mm Hg. The patient is awake but reports feeling lightheaded. Which underlying mechanism best explains this hemodynamic response?

    1. AA. Compression of the stellate ganglion reducing cardiac sympathetic tone
    2. BB. Stretching of the carotid sinus baroreceptors triggering excessive parasympathetic outflow
    3. CC. Acute embolization of atherosclerotic debris into the vertebrobasilar circulation
    4. DD. Anaphylactoid reaction to the intra-arterial iodinated contrast media
    Show answer to question 13

    Answer: B. Stretching of the carotid sinus baroreceptors triggering excessive parasympathetic outflow

    Balloon inflation and stent expansion in the proximal internal carotid artery exert direct mechanical pressure on the carotid sinus baroreceptors, triggering the glossopharyngeal nerve (Hering nerve) to activate medullary vagal centers, resulting in abrupt bradycardia and hypotension. Atherosclerotic embolization into the posterior circulation would cause neurological deficits such as ataxia or cranial nerve signs rather than isolated transient vagal-mediated bradycardia.

14. Question 14 of 25Medium

    Four hours after cardiopulmonary bypass, a patient remains hypotensive despite receiving 2,000 mL of crystalloid and 2 units of packed red blood cells. Pulmonary artery catheter data reveal: blood pressure 82/44 mmHg (mean arterial pressure 57 mmHg), heart rate 98 beats/min, cardiac index 3.9 L/min/m², central venous pressure 7 mmHg, pulmonary artery occlusion pressure 9 mmHg, and systemic vascular resistance 480 dynes·sec/cm⁵. Which complication best accounts for these findings?

    1. AA. Right ventricular failure
    2. BB. Acute cardiogenic shock
    3. CC. Cardiac tamponade
    4. DD. Vasoplegic syndrome
    Show answer to question 14

    Answer: D. Vasoplegic syndrome

    Vasoplegic syndrome is a distributive shock state common after cardiopulmonary bypass, characterized by severe hypotension, low systemic vascular resistance (under 800 dynes·sec/cm⁵), and a normal or elevated cardiac index (greater than 2.5 L/min/m²). In contrast, cardiogenic shock and cardiac tamponade present with a depressed cardiac index, elevated filling pressures, and a compensatory rise in systemic vascular resistance. Right ventricular failure typically presents with disproportionately high central venous pressure and low cardiac output.

15. Question 15 of 25Medium

    A patient with a confirmed acute Stanford Type B aortic dissection is admitted to the intensive care unit with a heart rate of 108 beats/min and a blood pressure of 194/102 mm Hg. The physician prescribes intravenous esmolol and intravenous sodium nitroprusside. Which action should the nurse implement first?

    1. AA. Titrate both infusions concurrently to reduce the systolic blood pressure below 90 mm Hg within fifteen minutes
    2. BB. Initiate the sodium nitroprusside infusion first to promptly lower the dangerously high systolic pressure
    3. CC. Initiate the esmolol infusion to decrease aortic wall shear stress before starting the vasodilator
    4. DD. Administer an intravenous hydralazine bolus to reduce systemic vascular resistance before infusion therapy
    Show answer to question 15

    Answer: C. Initiate the esmolol infusion to decrease aortic wall shear stress before starting the vasodilator

    Initial medical management of acute aortic dissection requires beta blockade prior to vasodilator administration to decrease heart rate and ventricular ejection force (dP/dt), which reduces shear stress on the dissected aortic wall. Administering a vasodilator such as sodium nitroprusside first causes reflex tachycardia and increased inotropy, which can propagate the false lumen and precipitate aortic rupture. Target systolic blood pressure is typically 100 to 120 mm Hg, not below 90 mm Hg.

16. Question 16 of 25Medium

    A 77-year-old woman is 4 days after a first, large anterior myocardial infarction that was not reperfused. She reports sudden severe chest pain, becomes hypotensive and confused, and her neck veins distend. Within minutes the monitor shows sinus rhythm at 94/min, but she has no palpable pulse. Which complication should the nurse suspect?

    1. AA. Left ventricular free wall rupture with tamponade
    2. BB. Ventricular septal rupture with left-to-right shunt
    3. CC. Recurrent infarction with ventricular fibrillation
    4. DD. Dressler syndrome with a pericardial effusion
    Show answer to question 16

    Answer: A. Left ventricular free wall rupture with tamponade

    Sudden chest pain, hypotension and jugular venous distension progressing to pulseless electrical activity days after a first transmural infarction suggest free wall rupture with hemopericardium and tamponade. The nurse starts CPR and calls for help while the team prepares for emergency pericardiocentesis and surgery.

    Why the other options are wrong

    • BSeptal rupture usually presents with a new harsh murmur and progressive shock rather than abrupt pulseless electrical activity.
    • CVentricular fibrillation appears as a chaotic waveform on the monitor, not an organized sinus rhythm without a pulse.
    • DDressler syndrome is an immune-mediated pericarditis that develops weeks after infarction and seldom causes sudden collapse.

17. Question 17 of 25Hard

    A 27-year-old man with known Wolff-Parkinson-White syndrome reports palpitations. The monitor shows an irregularly irregular rhythm at 220 to 280/min with wide QRS complexes that vary in shape from beat to beat. He is alert, and his BP is 110/68 mm Hg. Which medication does the nurse anticipate?

    1. AA. Diltiazem IV
    2. BB. Procainamide IV
    3. CC. Adenosine IV
    4. DD. Digoxin IV
    Show answer to question 17

    Answer: B. Procainamide IV

    This is pre-excited atrial fibrillation conducting over the accessory pathway. Drugs that block the AV node can increase conduction down the pathway and precipitate ventricular fibrillation, so a stable patient receives a drug that slows pathway conduction, such as IV procainamide, and an unstable patient receives synchronized cardioversion.

    Why the other options are wrong

    • ADiltiazem blocks the AV node, which can increase conduction over the accessory pathway and trigger ventricular fibrillation.
    • CAdenosine blocks the AV node, does not convert atrial fibrillation, and can accelerate the ventricular response through the pathway.
    • DDigoxin slows the AV node and shortens the accessory pathway refractory period, which can dangerously raise the ventricular rate.

18. Question 18 of 25Medium

    A patient with a stable, regular narrow-complex tachycardia has not converted with a modified Valsalva maneuver, and the provider orders adenosine. Which administration technique is correct?

    1. AA. Rapid push at a proximal IV site, then a rapid saline flush
    2. BB. Slow IV push over 2 minutes, followed by a slow saline flush
    3. CC. Diluted in 50 mL of saline and infused over 10 to 15 minutes
    4. DD. Rapid push into a hand vein, with no flush given afterward
    Show answer to question 18

    Answer: A. Rapid push at a proximal IV site, then a rapid saline flush

    Adenosine is cleared from the blood within seconds, so it must reach the AV node as a concentrated bolus: a rapid IV push through a proximal site such as an antecubital vein, followed immediately by a rapid saline flush, while the ECG is recorded continuously.

    Why the other options are wrong

    • BA slow push lets the drug be metabolized before it reaches the heart, so it is unlikely to interrupt the reentrant circuit.
    • CAn infusion over several minutes cannot produce the brief high concentration at the AV node needed to stop the tachycardia.
    • DWithout a flush, much of the dose stays in the distal vein and is degraded before it reaches the heart.

19. Question 19 of 25Medium

    A 79-year-old woman with atrial fibrillation who does not take an anticoagulant reports sudden severe pain in her left leg that began 1 hour ago. The leg is pale and cool below the knee, pedal pulses are absent by Doppler, and sensation in the foot is reduced. An IV heparin infusion and an emergent vascular surgery consult are ordered. How should the nurse position the affected leg?

    1. AA. Elevated on two pillows above heart level
    2. BB. Elevated with an elastic compression wrap
    3. CC. Flat or slightly dependent, lower than the heart
    4. DD. Flexed at the knee over a pillow for comfort
    Show answer to question 19

    Answer: C. Flat or slightly dependent, lower than the heart

    In acute arterial occlusion, keeping the limb level or slightly dependent lets gravity help whatever arterial inflow remains while revascularization is arranged. The limb is also protected from pressure, heat and cold.

    Why the other options are wrong

    • AElevation lowers arterial perfusion pressure in the foot and worsens ischemia.
    • BCompression further limits blood flow to an ischemic limb; it is used for venous, not arterial, problems.
    • DKnee flexion over a pillow can compress the popliteal vessels and further reduce flow to the lower leg.

20. Question 20 of 25Easy

    When timing an intra-aortic balloon pump from the arterial pressure waveform, at which point should balloon inflation begin?

    1. AA. At the peak of the systolic upstroke
    2. BB. Just before the next systolic upstroke
    3. CC. At the start of the QRS complex
    4. DD. At the dicrotic notch after systole
    Show answer to question 20

    Answer: D. At the dicrotic notch after systole

    Inflation is timed to the dicrotic notch, which marks aortic valve closure and the start of diastole, so the balloon raises diastolic pressure and coronary perfusion. Deflation is timed just before the aortic valve opens, which lowers afterload for the next ejection.

    Why the other options are wrong

    • AInflating at peak systole would oppose ejection, raise afterload and myocardial oxygen demand, and could cause aortic regurgitation.
    • BThe point just before the systolic upstroke is the deflation target, not the inflation point.
    • CThe QRS complex marks the onset of ventricular systole, when the balloon should already be deflated.

21. Question 21 of 25Medium

    A 67-year-old woman developed chest pain and anterior ST elevation hours after learning of her son's death. Coronary angiography shows no obstructive coronary disease, and ventriculography shows apical ballooning with a hyperkinetic base. She asks whether her heart will stay damaged. Which response by the nurse is most accurate?

    1. AA. "The weakened muscle is permanent scar, so a transplant evaluation is needed."
    2. BB. "A blocked artery is the cause and will need a stent before discharge."
    3. CC. "Heart function usually returns to normal within days to weeks."
    4. DD. "A viral infection is the cause and will need a heart muscle biopsy."
    Show answer to question 21

    Answer: C. "Heart function usually returns to normal within days to weeks."

    Stress (takotsubo) cardiomyopathy is a transient left ventricular dysfunction, often triggered by emotional or physical stress, that mimics an acute MI but occurs without obstructive coronary disease. Wall motion usually recovers within days to weeks, although heart failure, outflow obstruction and dysrhythmias can occur in the acute phase.

    Why the other options are wrong

    • AThe dysfunction in stress cardiomyopathy is usually reversible, so transplant evaluation is not expected.
    • BAngiography showed no obstructive coronary disease, so there is no blocked artery to stent.
    • DApical ballooning after an emotional trigger with normal coronaries fits stress cardiomyopathy rather than a myocarditis that needs biopsy.

22. Question 22 of 25Hard

    Three days after an inferior myocardial infarction, a 71-year-old man suddenly develops severe dyspnea, pink frothy sputum and an SpO2 of 84%. A new systolic murmur is heard best at the apex and radiates to the axilla, and the pulmonary artery occlusion pressure tracing shows tall v waves. Which complication is most likely?

    1. AA. Ventricular septal rupture
    2. BB. Left ventricular free wall rupture
    3. CC. Papillary muscle rupture
    4. DD. Right ventricular infarction
    Show answer to question 22

    Answer: C. Papillary muscle rupture

    Papillary muscle rupture causes acute severe mitral regurgitation, with sudden pulmonary edema, a new apical systolic murmur that radiates to the axilla and may be soft because left atrial pressure rises quickly, and tall v waves as blood regurgitates into a small, noncompliant left atrium. The posteromedial papillary muscle, which usually has a single blood supply, is the one most often affected after inferior infarction.

    Why the other options are wrong

    • ASeptal rupture causes a harsh holosystolic murmur best heard at the left lower sternal border, often with a palpable thrill.
    • BFree wall rupture usually causes abrupt tamponade and pulseless electrical activity rather than a new murmur with pulmonary edema.
    • DRight ventricular infarction causes hypotension with clear lungs and distended neck veins, not acute pulmonary edema with a new murmur.

23. Question 23 of 25Easy

    CT angiography shows an acute aortic dissection that involves the ascending aorta. Which treatment should the nurse prepare the patient for?

    1. AA. Medical therapy with repeat imaging in 1 week
    2. BB. Systemic fibrinolytic therapy to restore blood flow
    3. CC. Elective aortic repair after weeks of blood pressure control
    4. DD. Emergency open surgical repair in the operating room
    Show answer to question 23

    Answer: D. Emergency open surgical repair in the operating room

    Dissection involving the ascending aorta (Stanford type A) carries a high early risk of rupture, tamponade, acute aortic regurgitation and coronary occlusion, so emergency open surgical repair is indicated while heart rate and blood pressure are controlled medically. Uncomplicated dissection confined to the descending aorta is usually managed medically.

    Why the other options are wrong

    • AMedical therapy without surgery is the usual approach for uncomplicated descending dissection, not for ascending involvement.
    • BFibrinolytics are contraindicated in aortic dissection because they can cause catastrophic bleeding.
    • CDelaying repair of an ascending dissection exposes the patient to a high early risk of death.

24. Question 24 of 25Hard

    A 69-year-old man has atrial fibrillation of unknown duration. On oral metoprolol his ventricular rate is 84/min, his BP is 128/76 mm Hg, and he has no symptoms at rest. He has not been taking an anticoagulant. The team plans elective cardioversion before discharge. Which step does the nurse anticipate before cardioversion?

    1. AA. Cardioversion today, with anticoagulation started afterward
    2. BB. Holding metoprolol for 24 hours to reassess the atrial rhythm
    3. CC. Anticoagulation and a TEE to rule out left atrial thrombus
    4. DD. An adenosine IV push to confirm the rhythm before the shock
    Show answer to question 24

    Answer: C. Anticoagulation and a TEE to rule out left atrial thrombus

    Atrial fibrillation lasting 48 hours or more, or of unknown duration, can leave thrombus in the left atrial appendage that cardioversion may dislodge. Before elective cardioversion the patient needs either at least 3 weeks of therapeutic anticoagulation or anticoagulation plus a transesophageal echocardiogram (TEE) showing no thrombus, and anticoagulation continues for at least 4 weeks afterward.

    Why the other options are wrong

    • AStarting anticoagulation only after the shock leaves an existing atrial thrombus free to embolize when sinus rhythm returns.
    • BStopping the beta-blocker lets the ventricular rate rise and does nothing to reduce the risk of stroke with cardioversion.
    • DThe rhythm is already known to be atrial fibrillation, and adenosine neither treats it nor lowers the risk of embolism.

25. Question 25 of 25Medium

    A 58-year-old man arrives in the unit with a pneumatic compression band on his right wrist following a transradial coronary angiogram. While monitoring the access site, the nurse notes the patient's right thumb is pale, cool to the touch, and has a capillary refill time of 5 seconds. A pulse oximetry probe on the right thumb shows a loss of waveform. Which intervention should the nurse perform immediately?

    1. AA. Remove 1 to 2 mL of air from the band until the thumb waveform returns
    2. BB. Inject subcutaneous lidocaine near the radial artery to relieve vascular spasm
    3. CC. Apply a warm compress directly over the radial access site and reassess in 30 minutes
    4. DD. Release all air from the compression band and apply manual direct pressure over the site
    Show answer to question 25

    Answer: A. Remove 1 to 2 mL of air from the band until the thumb waveform returns

    Patent hemostasis is the standard of care for transradial access, maintaining radial artery patency while preventing bleeding. Pale, cool digits and a loss of thumb pulse oximetry waveform indicate severe arterial compromise, requiring immediate stepwise deflation (withdrawing 1 to 2 mL of air) until thumb perfusion and the plethysmographic waveform return while maintaining hemostasis. Deflating the band completely risks massive rebleeding and hematoma formation, whereas warm compresses delay urgent restoration of blood flow.

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