CONTENTS
- Approach to the deteriorating post-MI patient
- Re-infarction
- Post-MI pericarditis
- Bleeding & clotting:
- Mechanical complications
- Tachyarrhythmia
- Bradyarrhythmia
- Podcast
- Questions & discussion
- Pitfalls
differential diagnosis for deterioration s/p MI
- Reinfarction (e.g., in-stent thrombosis).📖
- Rupture:
- Post-MI Pericarditis (Post-cardiac injury syndrome).📖
- Hemorrhage (e.g., retroperitoneal hemorrhage 📖).
- Medication effect (e.g., beta-blockers, ACE-inhibitors, diuretics).
- Arrhythmia.
- Other complications:
- Pneumothorax.
- Aortic dissection.
- Pulmonary embolism.
- Infection (e.g., ventilator-associated pneumonia, line infection).
investigation of delayed deterioration
- Review any recent interventions (e.g., medications, procedures).
- EKG (new ischemia?).
- Auscultation:
- ? New murmur (mitral regurgitation, VSD).
- ? Pericardial friction rub.
- Echocardiogram:
- ? Pericardial effusion (pericarditis, ventricular wall rupture).
- ? New mitral regurgitation.
- ? New aortic regurgitation (may suggest aortic dissection).
- ? Fall in ejection fraction or new wall motion abnormality (reinfarction, excess beta-blockers).
- ? Evidence of VSD (color doppler shows flow across septum).
- ? Hypovolemia (hemorrhage, over-diuresis).
- ? RV dilation (RV infarction, PE, VSD).
presentation
- Recurrent ischemic symptoms (e.g., anginal chest pain).
- In-stent thrombosis may cause severe transmural infarction.
differential diagnosis
- Type-II MI due to another aggravating factor (e.g., anemia, hemorrhage).
- Pericarditis.
- Pulmonary embolism.
diagnostic tests
- EKG may show new ischemic changes.
- Troponin may re-elevate, but this is often difficult to discern in the context of previously elevated troponin values.
- Echocardiography may reveal a new wall motion abnormality.
- The key is comparison to the last EKG and echocardiogram obtained:
- Some patients with poor reperfusion following their initial MI will have have persistent ST elevation (which may eventually evolve into an LV-aneurysm pattern on the EKG). This pattern of persistent ST elevation doesn't represent represent re-infarction.
treatment
- (a) In-stent thrombosis requires immediate repeat PCI.
- (b) Type-II MI may be treated in the usual fashion (e.g., beta-blocker to reduce myocardial oxygen demand, possibly nitroglycerine).
early infarct-related pericarditis
- Occurs within the first 4 days after MI (due to transmural necrosis that directly causes pericardial inflammation).
- Diagnosis: Diagnostic criteria are the same as for late pericarditis (listed below).
- Treatment:
- This is mostly transient and self-limiting.
- Treatment may include aspirin 500 mg q8-12 hours.
- Therapy beyond 5-7 days usually isn't required. (ESC 2023, 37622654)
late pericarditis, aka post-cardiac injury (Dressler) syndrome
This may solely include pericarditis, or it may involve a combination of pericarditis plus pleural effusions (pleuropericarditis).
epidemiology
- Rare.
- Occurs between one week to three months after MI (most frequently after 1-2 weeks).(ESC 2023, 37622654)
presentation
- Chest pain, typically pleuritic (different in quality from original ischemic pain).
- Radiation to trapezius ridge supports pericarditis.
- May improve with leaning forward.
- Fever is often seen.
- Tamponade is rare.
diagnostic tests
- Auscultation may reveal pericardial friction rub.
- EKG may reveal diffuse ST elevation.
- Echocardiogram may reveal pericardial effusions (although these may also occur in the absence of pericarditis).
- CXR may reveal pleural effusion and pneumonitis.
- Lab evaluation may show leukocytosis (which is neither sensitive nor specific).
diagnostic criteria for pericarditis
- Two of the following support the diagnosis of pericarditis: (ESC 2023, 37622654)
- Pleuritic chest pain (>80%).
- Pericardial friction rub (>60%).
- Suggestive EKG changes.
- New or worsening pericardial effusion (>70%).
differential diagnosis
- Re-infarction.
- Ventricular free wall rupture (may be suggested by pericardial effusion >1 cm).
- Pulmonary embolism.
treatment
- First line therapy is high-dose aspirin:
- 500-1000 mg every 6-8 hours, until symptomatic improvement.
- Then taper by 250-500 mg every two weeks. (ESC 2023, 37622654)
- A proton pump inhibitor should be given to prevent gastric ulceration.
- Colchicine:
- Pericardial effusion isn't a contraindication to the use of antithrombotics and/or anticoagulants if these are otherwise indicated. (ESC 2023, 37622654)
epidemiology
- One of the most common complications (~1/200 procedures).
- Only occurs with femoral access (#RadialFirst).
- Usually occurs very early following catheterization.
presentation
- Severe hemorrhage manifests with hypotension and/or shock.
- Pain may occur in the abdomen, back, or flank. Tenderness or fullness may be noted.
- Less severe hematoma may present in a delayed fashion, with falling hemoglobin and hematoma tracking over abdomen/flank.
- Can present as jaundice and abnormal liver function tests (elevated lactate dehydrogenase, AST, and unconjugated bilirubin)
differential diagnosis
- Bleeding elsewhere (e.g., gastrointestinal bleed due to anticoagulation).
- Vasovagal reaction.
- Other causes of shock. 📖
diagnostic tests
- CT angiogram – the study should be specifically protocoled to evaluate for active extravasation.
- Performing a non-angiogram CT scan has little or no value. Merely identifying the hemorrhage isn't helpful, as this doesn't guide the next step in management. (28707444)
treatment
- (1) Supportive measures should be instituted without delay:
- PRBC transfusion (type & cross-match, stay 2-4 units ahead).
- Interruption of anticoagulation (e.g., if patient on a heparin infusion). For hemorrhagic shock, anticoagulation reversal may be considered (although this must be weighed against the risk of coronary stent thrombosis).
- (2) Interventional management:
- Definitive control can generally be achieved by interventional radiology or interventional cardiology. Techniques will vary depending on the nature of the bleed, but may include coil embolization or placement of a covered stent.
- Perhaps the most important indication for intervention is ongoing extravasation of blood seen on CT scan.
- Most patients don't require interventional therapy. Rather, with conservative management most bleeds will tamponade eventually.
- (3) Vascular surgery?
- Theoretically this is a third-line treatment, if all else fails.
epidemiology
- Most likely following anterior occlusive MI (with incidence of ~10%).
- Incidence increases over the first two weeks following MI. (ESC 2023, 37622654)
diagnosis
- Echocardiography is the front-line screening test. However, echocardiography may be equivocal.
- Cardiac MRI is the definitive gold-standard test. Cardiac MRI should be utilized if echocardiography yields unclear results. (ESC 2023, 37622654)
treatment
- Anticoagulation is indicated (e.g., heparin infusion initially with transition to chronic oral anticoagulation).
- The duration of therapy may typically range from 3-6 months. Repeat imaging is important to ensure resolution. (ESC 2023, 37622654)
epidemiology
- Rare, usually occurs within a week of MI.
- Typically occurs with inferior or posterior MI, affecting the posteromedial valve leaflet (figure above).
- Can occur with relatively small infarctions in about half of cases (e.g. NSTEMI).
presentation
- Dyspnea, respiratory failure due to pulmonary edema.
- Hypotension/shock.
- The initial MI may be mild, so patients may present initially with ruptured papillary muscle.
- In this presentation, the initial findings are often those of acute heart failure.
- 💡 Whenever a patient with heart failure is encountered with normal ejection fraction, be sure to investigate valvular function with color doppler.
diagnostic tests
- Chest ultrasound and/or chest X-ray shows cardiogenic pulmonary edema. Dysfunction of the posterior mitral valve leaflet may cause asymmetric pulmonary edema, which predominantly involves the right upper lobe.
- Echocardiography generally shows mitral regurgitation with a flail leaflet. However, this can be missed if there is a narrow and eccentric regurgitant jet. Transthoracic echocardiography only has a sensitivity of ~80%, so transesophageal echocardiography may be needed.(30987913)
- (On auscultation, the murmur may be unimpressive or absent due to rapid pressure equalization between the left ventricle and left atrium.)
differential diagnosis
- Ventricular septal defect can present in a similar fashion.
- Causes of acute mitral regurgitation after MI:
- (1) Rupture of chordae tendineae.
- (2) Papillary muscle dysfunction is common following MI (usually due to inferior MI).
- (3) Mitral valve annulus dilation, due to dilation of the left ventricle.
treatment
- Temporary stabilization
- Afterload reduction (often with high-dose nitroglycerine) reduces regurgitation. However, in patients with profound hypotension, norepinephrine may be required to maintain a minimal blood pressure consistent with life.
- Inotrope may be required.
- Intra-aortic balloon pump may be considered (but shouldn't delay surgery).
- Emergent surgery is required.
- If the patient hasn't been revascularized, this surgery should be a combined CABG plus mitral valve repair/replacement.
epidemiology
- Rare, typically within the first week post-MI.
- Often follows a large anterior infarct, but the rate may be similar among either anterior or inferior MIs.
presentation
- Dyspnea that may be accompanied by cardiogenic pulmonary edema.
- Sudden hemodynamic deterioration.
- Recurrent anginal chest pain (due to myocardial strain).
diagnostic tests
- Auscultation: New holosystolic harsh murmur might be heard.
- Echocardiogram:
- RV volume overload (dilation).
- Doppler echo may show flow across ventricle.
differential diagnosis
- Presentation most similar to papillary muscle rupture.
- Hemodynamic deterioration with RV dilation may mimic PE.
treatment
- Stabilization
- Afterload reduction with a systemic vasodilator (e.g., nitroglycerine) may favor blood flow from the left ventricle to the aorta (instead of refluxing into the right ventricle) – if the systemic blood pressure is high enough to tolerate this. Alternatively, for patients with profound hypotension, norepinephrine may be required to achieve a blood pressure compatible with life.
- Inotropic support often needed.
- Intra-aortic balloon pump may be considered, but shouldn't delay surgery.
- Cardiogenic pulmonary edema may be stabilized temporarily with noninvasive ventilation. Caution is required with intubation, as this may precipitate cardiovascular collapse.
- Repair:
- Even small VSDs should be repaired (they may suddenly enlarge). Historical series suggest a mortality of ~95% without surgery. (10618300)
- Surgery is generally preferred, but transcatheter closure is another option. In some cases, transcatheter closure may be used to stabilize the patient as a bridge to definitive surgical repair.
ventricular free wall rupture
- Epidemiology
- Rare, typically large anterior MI with an occluded LAD (although LCX causes 40% of ruptures and RCA occlusion causes 18%).(30987913)
- Generally within first 1-2 weeks.
- Risk factors include: single-vessel transmural infarction, late or incomplete reperfusion.
- Presentation
- Sudden rupture: Tamponade, cardiac arrest due to pulseless electrical activity.
- Incomplete or subacute rupture: Chest pain, dyspnea, vomiting, fluctuating hemodynamic instability.
- Diagnostics: EKG
- May see variety of findings (e.g., recurrent ST elevation or depression, new Q-waves).
- Overall, this may be misleading (potentially pointing towards re-infarction).
- Diagnostics: Echocardiography
- Pericardial effusion is sensitive, but nonspecific. Presence of internal echoes or echogenic masses (clot) within pericardial effusion increases specificity.
- Contrast echocardiography may show extravasation of contrast material into the pericardium.
- Additional diagnostic features similar to other causes of tamponade.📖
- Differential diagnosis
- Post-MI pericarditis may cause a pericardial effusion.
- Aortic dissection may cause hemorrhagic tamponade.
- Treatment
- In tamponade, pericardiocentesis may be used as bridge to surgery. However, there is also a risk that pericardiocentesis could increase blood pressure and the pressure gradient across the myocardium, causing the wall rupture to extend further.(30987913)
- Hemodynamic optimization (e.g., fluid, inotropes).
- Emergent surgical repair is required.
LV pseudoaneurysm formation
- This is essentially a contained rupture of the LV (clot and pericardium seal off the rupture).
- Diagnosis is based on echocardiography (compared to a true aneurysm, the neck is generally narrower).
- Don't be misled by the “aneurysm” verbiage – this is extremely dangerous.
- Treatment: overall, similar to the management of a subacute myocardial rupture. Stabilize the patient and consult cardiothoracic surgery.
epidemiology
- May represent recurrence of pre-existing paroxysmal AF, or new-onset AF.
- Risk factors include:
- History of atrial fibrillation.
- Congestive heart failure, LV dysfunction.
treatment
- Management is similar to atrial fibrillation in general.📖
- If AF appears to trigger hemodynamic instability or ischemia, consider electrical cardioversion.
- For new-onset AF in the context of MI, this could tip the balance a bit towards considering rhythm control (as opposed to rate control). With resolution of transient instability due to MI, hopefully sinus rhythm could be sustained.
- Beta-blockade may be useful if hemodynamically tolerated (and would generally be preferable to diltiazem).
non-sustained ventricular tachycardia
- Definition: Wide-complex tachycardia lasting <30 seconds, terminating spontaneously, and not causing hemodynamic collapse.
- Treatment:
- Generally this should not be treated (specifically, this is not an indication for anti-arrhythmic therapy such as amiodarone).
- It is reasonable to check electrolytes (especially magnesium & potassium) and EKG to look for any underlying causes that may warrant therapy.
- If the patient is hypertensive, treatment with a beta-blocker may be considered (especially if this would otherwise be a consideration). See the section on beta-blockade s/p MI here.📖
sustained monomorphic VT
- Definition
- Sustained monomorphic VT is defined as ventricular tachycardia which lasts >30 seconds or causes hemodynamic collapse.
- Diagnosis
- When in doubt, wide-complex tachycardia in the context of MI should be treated as VT.
- Note that if the rate is low (<100 b/m) this may represent accelerated idioventricular rhythm (AIVR) – which is typically a benign arrhythmia associated with reperfusion.
- Treatment: Initial considerations
- Initial management is based on ACLS algorithms (DC Cardioversion for unstable patients versus amiodarone for hemodynamically stable patients). Following conversion to sinus rhythm, patients will often be treated with an amiodarone infusion to prevent recurrence. Lidocaine 💊 may be used as a second-line anti-arrhythmic (with typical dosing including a bolus of ~100 mg followed by 1-4 mg/min infusion).
- Ischemia should be considered as a potential underlying cause, and treated if appropriate (e.g., with percutaneous coronary intervention).
- Electrolyte abnormalities should be corrected (e.g. target Mg >2 mg/dL and K >3.5 mM).
- Avoid beta-agonists wherever possible (e.g., dobutamine, epinephrine). Beta-blockers should be considered if hemodynamics will tolerate them (noting that beta-blockers are supported by the most robust evidence to reduce post-MI ventricular arrhythmias).📖
- Treat conditions which may be increasing sympathetic tone (e.g., pain or anxiety). This is an especially important consideration among patients who are intubated and may be unable to report these problems.
- For recurrent arrhythmias refractory to therapy, see the chapter on VT storm.📖
- Treatment: Longer term considerations
- Early VT may not require ongoing antiarrhythmic therapy (especially if the patient can be successfully revascularized).
- VT which occurs later in the patient's course (e.g., >48 hours) and/or after revascularization raises concern about the presence of myocardial scar tissue. These patients may benefit from longer periods of antiarrhythmic therapy and perhaps from an implanted cardioverter-defibrillator (ICD). Electrophysiology consultation can help sort this out.
polymorphic VT with normal QT interval (this isn't Torsades!)
- This seems to reflect myocardial ischemia.
- Optimal treatment may be reperfusion (this is potentially an indication for PCI).
- Anti-arrhythmic therapies may be similar to monomorphic VT (see above).
polymorphic VT with prolonged QT interval (torsade de pointes)
- This isn't particularly common in MI patients, but may be caused by various medications (e.g., sotalol or dofetilide).
- Treatment is the same as for non-MI torsade de pointes (e.g. stop offensive medications, provide magnesium infusion). 📖
immediate management
- See the chapter on bradycardia.📖
heart block due to inferior MI
- Anatomy
- Generally due to lesion within the AV node.
- Clinical presentation
- Patients often have a junctional escape rhythm (narrow-complex, with heart rate 40-60 b/m).
- Usually transient (resolving within a week).
- Treatment
- May respond to atropine if occurring early in course of MI (within the first ~6 hours, patients may have bradycardia due to excess vagal tone)
- Can generally be managed conservatively (without transvenous wire insertion).
heart block due to anterior MI
- Anatomy
- Generally located below the AV node.
- Reflects diffuse myocardial necrosis resulting from a very proximal occlusion.
- Clinical presentation
- May develop abruptly, or can be preceded with RBBB with either LAFB or LPFB (bifascicular block).
- Often causes instability (or associated with instability).
- Treatment
- Indications to consider transvenous pacing may include:
- (a) Mobitz II or higher grade block.
- (b) New bundle-branch block (especially LBBB).
- (c) Bifascicular block (RBBB plus either LAHB or LPFB).
- Indications to consider transvenous pacing may include:
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- For suspected retroperitoneal hemorrhage, obtain a stat CT angiogram (make sure the study is protocoled as an angiogram).
- For decompensation after myocardial infarction, echocardiogram is critical to evaluate for a diverse range of complications.
- Some patients may present to the hospital with heart failure due to a ruptured chordae tendineae (following a silent or mildly symptomatic myocardial infarction). For patients with heart failure and a normal appearing ventricle, look carefully for a small eccentric regurgitant jet from the mitral valve.
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References
- 10618300 Crenshaw BS, Granger CB, Birnbaum Y, Pieper KS, Morris DC, Kleiman NS, Vahanian A, Califf RM, Topol EJ. Risk factors, angiographic patterns, and outcomes in patients with ventricular septal defect complicating acute myocardial infarction. GUSTO-I (Global Utilization of Streptokinase and TPA for Occluded Coronary Arteries) Trial Investigators. Circulation. 2000 Jan 4-11;101(1):27-32. doi: 10.1161/01.cir.101.1.27 [PubMed]
- 26295381 Bajaj A, Sethi A, Rathor P, Suppogu N, Sethi A. Acute Complications of Myocardial Infarction in the Current Era: Diagnosis and Management. J Investig Med. 2015 Oct;63(7):844-55. doi: 10.1097/JIM.0000000000000232 [PubMed]
- 28707444 Safian RD. Current approaches to retroperitoneal hemorrhage: Too little, too late. Catheter Cardiovasc Interv. 2017 Jul;90(1):112-113. doi: 10.1002/ccd.27168 [PubMed]
- 30987913 Montrief T, Davis WT, Koyfman A, Long B. Mechanical, inflammatory, and embolic complications of myocardial infarction: An emergency medicine review. Am J Emerg Med. 2019 Jun;37(6):1175-1183. doi: 10.1016/j.ajem.2019.04.003 [PubMed]
- 37622654 Byrne RA, Rossello X, Coughlan JJ, Barbato E, Berry C, Chieffo A, Claeys MJ, Dan GA, Dweck MR, Galbraith M, Gilard M, Hinterbuchner L, Jankowska EA, Jüni P, Kimura T, Kunadian V, Leosdottir M, Lorusso R, Pedretti RFE, Rigopoulos AG, Rubini Gimenez M, Thiele H, Vranckx P, Wassmann S, Wenger NK, Ibanez B; ESC Scientific Document Group. 2023 ESC Guidelines for the management of acute coronary syndromes. Eur Heart J. 2023 Oct 12;44(38):3720-3826. doi: 10.1093/eurheartj/ehad191 [PubMed]