- Approach to the deteriorating post-MI patient
- Retroperitoneal hematoma
- Post-MI pericarditis
- Mechanical complications
- Questions & discussion
approach to deteriorating post-MI patient
- Certain complications tend to occur within 1-2 weeks after MI (mostly STEMI).
- Most common scenario: patient is improving after MI and then deteriorates.
- Occasionally, patients may have a silent MI and present with one of these post-MI complications.
- PCI has reduced mechanical complications, but these still occur (especially in the absence of successful revascularization).
common causes for delayed deterioration s/p MI
- Reinfarction (e.g. in-stent thrombosis)
- Ventricular free wall rupture
- Ventricular septal defect (VSD)
- Mitral valve chordae tendinae rupture
- Post-MI Pericarditis (Post-cardiac injury syndrome)
- Hemorrhage (e.g. retroperitoneal hemorrhage)
- Medication effect (e.g. beta-blockers, ACE-inhibitors, diuretics)
- Other complications
- Aortic dissection
- Pulmonary embolism
- Ventilator-associated pneumonia
- Line infection
investigation of delayed deterioration
- Review any recent interventions (e.g. medications, procedures).
- EKG (new ischemia?).
- ? new murmur (mitral regurgitation, VSD)
- ? pericardial friction rub
- ? 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 (pump failure/MI/beta-blockers)
- ? evidence of VSD (color doppler shows flow across septum)
- ? hypovolemia (hemorrhage, over-diuresis)
- ? RV dilation (RV infarction, PE, VSD)
- One of the most common complications (~1/200 procedures).
- Only occurs with femoral access (not radial access, #RadialFirst).
- Usually occurs very early following catheterization.
- Severe hemorrhage manifests with hypotension/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)
- Bleeding elsewhere (e.g. gastrointestinal bleed due to anticoagulation)
- Vasovagal reaction
- Other causes of shock (see the shock chapter)
- CT angiogram – the study should be specifically protocoled to evaluate for active extravasation.
- Performing a non-angiogram CT scan has little or no value (because mere identification of the hemorrhage isn't very helpful (28707444).
- (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 in heparin infusion). For hemorrhagic shock, anticoagulation reversal may be considered.
- (2) Interventional management
- Definitive control can generally be achieved by interventional radiology. Techniques will vary depending on the nature of the bleed, but may include coil embolization or placement of a covered stent.
- Indications for intervention may include clinical course (e.g. hemorrhagic shock) and/or imaging findings seen on CT scan (e.g. active extravasation). With conservative therapy, most bleeds will tamponade eventually.
- (3) Vascular surgery?
- Theoretically a third-line treatment if all else fails.
Also known as Dressler's Syndrome, or post-cardiac injury syndrome (although these terms include other causes such as post-CABG pericarditis).
- Occurs between one week to three months after MI.
- Chest pain, typically pleuritic (different in quality from original ischemic pain).
- Radiation to trapezius ridge supports pericarditis.
- May improve with leaning forward.
- Fever often seen.
- Tamponade is rare.
- Auscultation may reveal pericardial friction rub.
- EKG: may cause ST elevation.
- Echocardiogram: may see pericardial effusions (although these may also occur in the absence of pericarditis).
- CXR: pleural effusion and pneumonitis may be seen.
- Labs: leukocytosis may occur.
- Ventricular free wall rupture (may be suggested by pericardial effusion >10 mm).
- Pulmonary embolism.
- First line therapy is high-dose aspirin (e.g. 750-1000 mg Q6-8 hours). A proton pump inhibitor should be given to prevent gastric ulceration.
- If the effusion is >1cm large or enlarging, may consider discontinuation of anticoagulation (to reduce the risk of hemorrhagic pericarditis).
- Recurrent ischemic symptoms (e.g. anginal chest pain).
- In-stent thrombosis may cause severe transmural infarction.
- Prior infarction with other aggravating factor (e.g. anemia, hemorrhage).
- Pulmonary embolism.
- 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 new wall motion abnormality.
- Key is comparison to the last EKG and echocardiogram obtained (some patients may have persistent ST elevation, in which case this probably doesn't represent re-infarction)
- (a) In-stent thrombosis requires immediate repeat PCI.
- (b) NSTEMI may be treated in the usual fashion (e.g. beta-blocker to reduce myocardial oxygen demand, possibly nitroglycerine).
mitral valve chordae tendinae rupture
- Rare, usually occurs within a week of MI.
- Typically occurs with inferior or posterior MI, affecting the posterio-medial valve leaflet (figure above).
- Can occur with relatively small infarctions in about half of cases (e.g. NSTEMI).
- Dyspnea, respiratory failure due to pulmonary edema.
- 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.
- 😳Pearl: Whenever a patient with heart failure is encountered with normal ejection fraction, be sure to investigate valvular function with color doppler.
- Chest ultrasound and/or chest X-ray shows cardiogenic pulmonary edema.
- Echocardiography generally shows mitral regurgitation with flail leaflet. However, this can be missed if there is a narrow and eccentric regurgitant jet.
- (On ascultation, murmur may be unimpressive or absent due to rapid pressure equalization.)
- Ventricular septal defect can present in a similar fashion.
- Mild mitral regurgitation is common following MI (e.g. due to papillary muscle dysfunction, but not rupture).
- Temporary stabilization
- Afterload reduction (often with high-dose nitroglycerine) reduces regurgitation.
- 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.
— J. Christian Fox (@jchristianfox) May 23, 2017
— Lars Mølgaard Saxhaug (@LMSaxhaug) March 7, 2018
ventricular septal defect (VSD)
- Rare, typically within the first week post-MI.
- Often a large anterior infarct, but the rate may be similar among either anterior or inferior MIs.
- Sudden hemodynamic deterioration.
- Dyspnea (although not usually pulmonary edema).
- Recurrent anginal chest pain (due to myocardial strain).
- Auscultation: new holosystolic harsh murmur might be heard.
- RV volume overload (dilation).
- Doppler echo may show flow across ventricle.
- Agitated saline may show negative contrast in the RV.
- Presentation most similar to papillary muscle rupture.
- Hemodynamic deterioration with RV dilation may mimic PE.
- Vasodilator (e.g. nitroglycerine) may favor blood flow to body (rather than RV).
- Inotropic support often needed.
- Intra-aortic balloon pump may be considered, but shouldn't delay surgery.
- Even small VSDs should be repaired (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, trans-catheter closure may be used to stabilize the patient as a bridge to definitive surgical repair.
Here’s the CFD of the post-infarct VSD. Note the serpiginous course of the rupture- pretty common.
Also common: this was 4d after late presenting STEMI – no PCI. pic.twitter.com/n7e9RxosWQ
— V.L.Sorrell, MD (@VLSorrellImages) March 27, 2018
65 yr old with chest pain 1 week ago. BP 80/60, p90. Able to lie flat but crackles in chest. Angiogram in next tweet. Any suggestions on what to do and when to do it? @angioplastyorg @mmamas1973 @nolanjimradial pic.twitter.com/SkU42NoIdJ
— Richard Bogle (@richardbogle) November 28, 2017
Patient was referred to surgeons and did an echo on way to the OR ⤵️ pic.twitter.com/nBcRb0UpXY
— Jedicath (@jedicath) December 17, 2017
VSD caused by a complication of MI pic.twitter.com/Zif2WxCyHd
— Echocardiography (@EchoCases) August 26, 2018
— Ivan Stankovic, MD, PhD (@Ivan_Echocardio) June 12, 2018
The above tweet is an Atrial septal defect (ASD), not a VSD, but it illustrates the concept of negative contrast.
ventricular free wall rupture
ventricular free wall rupture
- Rare, typically large anterior MI with occluded LAD.
- Generally within first 1-2 weeks.
- Risk factors include: single-vessel transmural infarction, late or incomplete reperfusion.
- Sudden rupture: tamponade, PEA.
- Incomplete or subacute rupture: chest pain, 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 or aortic dissection may also cause pericardial effusion.
- In tamponade, pericardiocentesis may be used as bridge to surgery.
- Hemodynamic optimization (e.g. fluid, inotropes).
- Emergent surgical repair is required.
LV pseudo-aneurysm formation
- 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.
atrial fibrillation & atrial flutter
- May represent recurrence of pre-existing paroxysmal AF, or new-onset AF.
- Risk factors include:
- History of atrial fibrillation.
- Congestive heart failure, LV dysfunction.
- Similar to atrial fibrillation in general.
- If AF appears to trigger hemodynamic instability or ischemia, consider DC 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 preferrable to diltiazem).
non-sustained ventricular tachycardia
- Definition: Wide-complex tachycardia lasting <30 seconds, terminating spontaneously, and not causing hemodynamic collapse.
- 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) & 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).
sustained monomorphic VT
- Sustained monomorphic VT is defined as ventricular tachycardia which lasts >30 seconds or causes hemodynamic collapse.
- 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 > 4 mM).
- Avoid beta-agonists wherever possible (e.g. dobutamine, epinephrine). Beta-blockers should be considered if hemodynamics will tolerate them.
- 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 anti-arrhythmic therapy and perhaps from an implanted cardioverter-defibrillator (ICD). Electrophysiology consultation is indicated to sort this out.
polymorphic VT with normal QT interval (this isn't Torsades!)
- 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 (Torsades de pointes)
- Not 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 Torsades de pointes (e.g. stop offensive medications, provide magnesium infusion).
heart block s/p MI
- See the chapter on bradycardia.
heart block due to inferior MI
- 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).
- 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
- Generally located below the AV node.
- Reflects diffuse necrosis resulting from a very proximal occlusion.
- Clinical presentation
- May develop abruptly, or can be preceded with RBBB with either LAFB or LPFB (bi-fascicular block).
- Often causes (or associated with) instability.
- 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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questions & discussion
To keep this page small and fast, questions & discussion about this post can be found on another page here.
- 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 tendinae (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.