ANCC Cardiac Vascular Nursing 2 — Questions and Answers
Question 1: A patient develops ventricular fibrillation (VF) on a cardiac monitor and the nurse is alone at the bedside. What is the correct first action?
- Call rapid response team and wait for assistance
- Confirm pulselessness, call for help and crash cart, then begin CPR immediately (Correct answer)
- Apply synchronized cardioversion at 200 joules
- Administer amiodarone 300 mg IV push first
Correct answer: Confirm pulselessness, call for help and crash cart, then begin CPR immediately
For witnessed VF with confirmed pulselessness: call for help and crash cart, then immediately begin high-quality CPR. Every minute without defibrillation decreases survival by 7-10%.
ACLS VF/pVT algorithm: confirm unresponsiveness and pulselessness; activate emergency response and call for crash cart; begin CPR immediately; defibrillate as soon as available (200 J biphasic or 360 J monophasic, unsynchronized); resume CPR 2 minutes after each shock; epinephrine 1 mg IV/IO every 3-5 minutes; after third shock amiodarone 300 mg or lidocaine 1-1.5 mg/kg. Synchronized cardioversion is NEVER used for VF as there is no organized R wave to synchronize to.
Question 2: A patient with PAD reports cramping calf pain after walking two blocks that reliably resolves with rest. This symptom pattern is called:
- Rest pain
- Critical limb ischemia
- Intermittent claudication (Correct answer)
- Deep vein thrombosis
Correct answer: Intermittent claudication
Intermittent claudication is reproducible ischemic muscle pain during exercise that reliably resolves with rest, resulting from inadequate arterial flow to meet muscle oxygen demands during exertion.
Intermittent claudication: reproducible cramping in muscles distal to arterial stenosis during exercise, relieved by rest within 1-5 minutes. Location correlates with disease: calf = superficial femoral or popliteal artery; thigh and buttock = iliac artery disease (Leriche syndrome if bilateral with impotence). ABI at rest typically 0.5-0.8. Rest pain (ABI below 0.4) and critical limb ischemia (rest pain plus ischemic ulcers or gangrene) represent more advanced disease. Management: supervised exercise, smoking cessation, antiplatelet therapy, statins, cilostazol.
Question 3: A patient is preparing for permanent pacemaker insertion. Which finding is most important to communicate to the proceduralist?
- The patient took aspirin 81 mg this morning
- The left subclavian vein was used for a previous central line (Correct answer)
- Blood pressure is 138/82 mmHg
- The patient reports mild anxiety about the procedure
Correct answer: The left subclavian vein was used for a previous central line
Previous subclavian vein use may have caused stenosis or occlusion, preventing pacemaker lead placement via that route. The proceduralist needs this information to plan venous access.
Pacemaker leads are placed via subclavian, axillary, or cephalic vein. Critical history: previous central venous access especially subclavian or axillary risking stenosis or occlusion (may require venogram or contralateral approach); PICC or port history; prior pacemaker or ICD with leads already present; dialysis AV fistula or graft on same side (contraindication for ipsilateral pacemaker). Blood pressure of 138/82 is not a contraindication. Anxiety is managed with anxiolytics per order.
Question 4: Which ECG finding is consistent with left ventricular hypertrophy (LVH)?
- ST elevation in leads II, III, and aVF
- S wave in V1 + R wave in V5 or V6 at or above 35 mm (Sokolow-Lyon criteria) (Correct answer)
- Delta wave and shortened PR interval
- Sawtooth baseline at 300 bpm in leads II, III, aVF
Correct answer: S wave in V1 + R wave in V5 or V6 at or above 35 mm (Sokolow-Lyon criteria)
The Sokolow-Lyon criteria for LVH: S wave depth in V1 plus the tallest R wave in V5 or V6 at or above 35 mm. LVH reflects increased myocardial mass from hypertension or aortic stenosis.
ECG criteria for LVH: Sokolow-Lyon (SV1 + RV5 or RV6 at or above 35 mm, sensitivity approximately 50%, specificity approximately 95%); Cornell voltage (RaVL + SV3 above 28 mm in men or above 20 mm in women); RaVL at or above 12 mm. LVH strain pattern: ST depression and T-wave inversion in lateral leads (I, aVL, V5-V6). Causes: hypertension, aortic stenosis, aortic or mitral regurgitation. ST elevation in II/III/aVF = inferior STEMI. Delta wave + short PR = Wolff-Parkinson-White. Sawtooth baseline = atrial flutter.
Question 5: A patient on IV heparin for DVT develops platelet count drop from 210,000 to 62,000/uL on day 7 and has a new arterial clot in the left arm. Which condition is suggested?
- Heparin-associated thrombocytopenia Type I (benign)
- Heparin-induced thrombocytopenia Type II (HIT) with thrombosis (HITT) (Correct answer)
- Disseminated intravascular coagulation (DIC)
- Idiopathic immune thrombocytopenic purpura (ITP)
Correct answer: Heparin-induced thrombocytopenia Type II (HIT) with thrombosis (HITT)
HIT Type II presents with platelet count drop greater than 50% on days 5-10 of heparin therapy plus paradoxical thrombosis. When combined with thrombosis it is called HITT.
HIT Type II: immune-mediated platelet activation by antibodies against PF4/heparin complex. Key features: platelet count drop greater than 50% from baseline on days 5-14; paradoxical thrombosis (HIT is prothrombotic, not a bleeding disorder); thrombosis in unusual arterial and venous locations. Use 4T score (Thrombocytopenia, Timing, Thrombosis, no oTher cause). Management: IMMEDIATELY stop ALL heparin including flushes, LMWH, heparin-coated catheters; start non-heparin anticoagulant (argatroban, bivalirudin, fondaparinux); do NOT transfuse platelets; do NOT start warfarin until platelets exceed 150,000.
Question 6: A patient on clopidogrel and aspirin for unstable angina — which factor most significantly reduces clopidogrel effectiveness?
- Concurrent use of atorvastatin
- CYP2C19 poor metabolizer genetic variant (Correct answer)
- Taking clopidogrel with food
- History of peptic ulcer treated with ranitidine
Correct answer: CYP2C19 poor metabolizer genetic variant
Clopidogrel is a prodrug requiring activation by CYP2C19. Poor metabolizers with loss-of-function alleles have significantly reduced active metabolite levels and diminished platelet inhibition.
Clopidogrel mechanism: prodrug converted by hepatic CYP2C19 to active thiol metabolite that irreversibly blocks platelet P2Y12 receptors. CYP2C19 poor metabolizers (loss-of-function alleles *2, *3): reduced active metabolite, reduced platelet inhibition, increased risk of MI and stent thrombosis (TRITON-TIMI 38). FDA black box warning. Consider alternatives: prasugrel or ticagrelor which do not require CYP2C19 activation. Omeprazole and esomeprazole significantly inhibit CYP2C19 and reduce clopidogrel effectiveness; ranitidine (H2 blocker) has less interaction. Atorvastatin has minimal clinically significant effect. Food has minimal effect on absorption.
A patient develops ventricular fibrillation (VF) on a cardiac monitor and the nurse is alone at the bedside.
What is the correct first action?