18 Question 18. A 68-year-old man presents with chest pain. He is dizzy and weak. Blood pressure is 80/55 and pulse is 55 bpm. JVP is 5 cmH2O and lungs are clear. ECG shows sinus rhythm with 2:1 AV block and a ventricular rate of 55 bpm, along with inferior ST elevation. What is the immediate next step?IV fluidsIV fluids + dopamineIV fluids + atropineAtropine + transvenous pacing + IV fluidsPrimary PCIIABP followed by primary PCI
19 Question 19. The patient in Question 19 receives atropine and a fluid bolus. AV conduction improves and heart rate is 100 bpm. He remains hypotensive and dizzy. Peripheral O2 saturation is 94% on ambient air. No murmur or thrill is present. What is the most likely diagnosis?RV MI shockMechanical complication (papillary muscle rupture or ventricular septal rupture)LV shock from an isolated inferior MILV shock from inferior MI extending to the lateral wall or inferior MI associated with an old anterior MI
20 Question 20. The patient in Question 19 now has a JVP of 11 cmH2O. What is the next step?NorepinephrineAdminister another 500 ml IV fluid bolus. If he remains hypotensive, add norepinephrinePrimary PCIIABP followed by primary PCIA+CB+CA+D
21 Question 21. With the administration of more fluids, the patient in Question 19 now develops arterial desaturation (85%), which is mini- mally responsive to supplemental O2. His lungs are still clear and no murmur is heard. What is the most likely cause?Ventricular septal rupturePatent foramen ovaleSevere MRLV failure
22 Question 22. A 67-year-old woman had severe nausea 2 days ago. This was followed by dyspnea and cough. On presentation, she is hypotensive (90/45 mmHg) and has respiratory distress with lung crackles and orthopnea. A holosystolic mumur is heard with S3 and without a thrill. ECG shows lateral ST elevation of 1 mm in leads I and aVL. She later develops fever. What is the most likely diagnosis?Cardiogenic shock from extensive infarctionRV shockPosterior papillary muscle ruptureAnterior papillary muscle ruptureSeptic shockC + ED + E
23 Answers 1. E. The patient has an expected DTB>120 min, which justifies thrombolysis. This is even more paramount when the patient is presenting within 3 hours, or has high risk features: anterior STEMI, tachycardia>100 bpm, SBP<100, Killip≥ 2 (crackles). The current standard of care for every STEMI patient receiving thrombolysis is to immediately transfer for rescue PCI (if thrombolysis fails) or for systematic coronary angiography and PCI 3-24 hours later (even if thrombolysis succeeds, the so called pharmacoinvasive strategy).
24 Answers 2. C. This is a patient presenting with Q-wave MI >24 hours after MI onset without residual angina. Stress test may be performed and followed by angiography ± revascularization in the presence of severe residual ischemia in the infarcted territory. Alternatively, angiography may be performed first (class II): (i) if left main or three-vessel CAD is found, CABG may be considered on a non-urgent basis (>3–7 days after MI); (ii) if the culprit is not totally occluded, PCI may be performed (class IIb); (iii) if the culprit is totally occluded, PCI should not be immediately performed. In the latter case, stress testing should be performed and the patient brought back for PCI if severe ischemia is present. Viability is different from ischemia. It is important to document that the wall is ischemic with stress, not just viable. A moderate viability without documented ischemia is not a clear indication to revascularize. Ischemia is documented clinically (angina), by ECG (ST depression), or by reduction of nuclear uptake at stress.
25 Answers 3. B. This patient has a combination of four features (elderly small woman with HTN). The combination predicts >4% risk of intracranial hemorrhage with fibrinolytics.
26 Answers 4. D. Thrombolysis improved survival in the medically treated arm of the SHOCK trial and in all arms of the SHOCK registry. The insertion of IABP was part of the protocol of the SHOCK trial and was associated with better outcomes in the SHOCK registry (although recent data question its benefit).
27 Answers 5. A or D. In the SHOCK trial, patients with complex multivessel CAD more frequently underwent CABG than PCI. CABG was associated with the same survival as PCI, despite the higher prevalence of extensive CAD.PCI is reasonable at institutions where CABG cannot be promptly performed, which is commonly the case. Culprit-only PCI is performed; multivessel acute PCI is not advised in cardiogenic shock (CULPRIT SHOCK trial).
28 Answers 6. B. The presentation is consistent with free wall rupture. Stent thrombosis is a second possibility. Echocardiography is immedi- ately followed by pericardiocentesis and surgical correction if the diagnosis of myocardial rupture/tamponade is confirmed.
29 Answers 7. C. A moderate pericardial effusion is concerning for a sealed cardiac rupture (in at least 8% of the cases) and warrants further observation and MRI if possible. Late NSVT, while carrying a worse prognosis, does not, per se, change management and does not dictate earlier ICD or Lifevest placement.
30 Answers 8. D. Non-culprit lesions are revascularized even in the absence of angina. They are revascularized before discharge or within 45 days, as per COMPLETE trial; pre-discharge PCI is preferred in patients with critical disease or angina at mild exertion. Non-critical lesions may improve on subsequent angiograms as the vasospastic component improves (J Am Coll Cardiol 2002; 40: 911–16); thus, before elective revascularization of these lesions in asymptomatic patients, the lesion is reassessed on repeat angiography and non-culprit FFR may be performed.
31 Answers 9. C. In anterior MI, AV block indicates extensive anterior infarction. The patient likely has multivessel disease preventing collateral supply to the left bundle. In the pre-reperfusion era, the mortality of complete AV block in anterior MI was ≥50%. Also, a shock that persists with pacing (Killip IV) portends a mortality of ≥50%.
32 Answers 10. B. Cardiogenic shock or massive HF qualifies for emergent reperfusion regardless of the time of presentation, as long as it is not purely secondary to bradyarrhythmia (a purely bradycardic shock was excluded from the SHOCK trial). Massive HF is defined as Killip class III, i.e., massive pulmonary edema frequently requiring mechanical ventilation. Since the patient’s shock resolved with pacing and since she does not have massive HF, there is no indication for emergent PCI >24 hours after the infarct. However, persistent severe HF qualifies for coronary angiography after diuresis and stabilization (non-urgently, e.g., after 24 hours of diuresis), and may benefit from late revascularization. A persistent severe HF prevents the patient from receiving stress testing and was an exclusion criterion from the negative OAT trial of late post-STEMI PCI. Conversely, a patient who stabilizes and becomes ambulatory without severe HF qualifies for risk stratification with stress testing, in which case PCI is only performed for severe ischemia.
33 Answers 11. B. STEMI may be over 12–24 hours old, at a stage where ST-segment elevation is resolving but has not fully resolved yet (close to phase 3). Alternatively, STEMI may be more recent with ongoing or resolving ischemia. This patient does not qualify for fibrinolytics, as ST elevation is <1 mm and the occlusion duration is questionable, but qualifies for primary PCI if the discomfort is ongoing, or if the dis- comfort occurred within the last 24 hours, even if it is not ongoing.
34 Answers 12. B. The ECG shows persistent ST elevation in leads V1–V4. ST elevation is barely 2 mm, but the morphology is typical of STEMI (terminal T inversion, reciprocal ST depression in I–aVL, and lack of alternative explanation of the mild ST elevation in V1–V3, i.e., no LVH/ LBBB). Even if chest pain resolves, a persistent ST elevation along with a presentation <12 hours qualifies the patient for primary PCI or thrombolysis.
35 Answers 13. A. The ECG shows subtle signs of inferior, lateral, and posterior ST elevation injury. In fact, the isolated ST depression in leads V1–V3 implies posterior ST elevation. The ST segment is minimally elevated in the inferior leads and in leads V5 and V6 (~0.5 mm), but has a strikingly convex morphology with a wide hyperacute T wave, particularly evident on the aberrant beat. Also, reciprocal ST depression is seen in lead aVL. All this confirms that the ECG, while subtle, is definitely consistent with ST elevation injury. Being <1 mm, thrombolysis is not justified.