323. Beyond the Boards: Complications of Acute Myocardial Infarction with Dr. Jeffrey Geske

CardioNerds co-founder Dr. Amit Goyal and episode leads Dr. Jaya Kanduri (FIT Ambassador from Cornell University) and Dr. Jenna Skowronski (FIT Ambassador from UPMC) discuss Complications of acute myocardial infarction with expert faculty Dr. Jeffrey Geske. They discuss various complications of acute MI such as cardiogenic shock, bradyarrythmias, left ventricular outflow tract obstruction, ruptures (papillary muscle rupture, VSD, free wall rupture), and more. Show notes were drafted by Dr. Jaya Kanduri. Audio editing by CardioNerds Academy Intern, student doctor Tina Reddy.

The CardioNerds Beyond the Boards Series was inspired by the Mayo Clinic Cardiovascular Board Review Course and designed in collaboration with the course directors Dr. Amy Pollak, Dr. Jeffrey Geske, and Dr. Michael Cullen.

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323. Beyond the Boards - Complications of Acute Myocardial Infarction with Dr. Jeffrey Geske

Pearls and Quotes – Complications of Acute Myocardial Infarction

  1. Sinus tachycardia is a “harbinger of doom”!
  2. The triad for RV infarction includes hypotension, elevated JVP, and clear lungs. These patients are preload dependent and may need fluid resuscitation despite having an elevated JVP.
  3. Bradyarrythmias in inferior MIs are frequently vagally mediated. The focus should be on medical management before committing to a temporary transvenous pacemaker, such as reperfusion, maintaining RV preload and inotropy, avoiding hypoxia, and considering RV-specific mechanical circulator support (MCS).
  4. Worsening hypotension with inotropic agents (e.g., dobutamine, epinephrine, dopamine, norepinephrine) after a large anterior-apical MI should raise suspicion for dynamic left ventricular outflow tract obstruction due to compensatory hyperdynamic basal segments.
  5. The myocardium after a late presentation MI is as “mushy as mashed potatoes”! Need to look out for papillary muscle rupture, VSD, and free wall rupture as potential complications. Papillary muscle rupture can occur with non-transmural infarcts, and often presents with flash pulmonary edema. VSDs will have a harsh systolic murmur and are less likely to present with pulmonary congestion. Free wall rupture can present as a PEA arrest. All of these complications require urgent confirmation on imaging and early involvement of surgical teams.

Notes – Complications of Acute Myocardial Infarction

How should we approach cardiogenic shock (CS) in acute myocardial infarction (AMI)?

  • Only 10% of AMI patients present with CS, but CS accounts for up to 70-80% of mortality associated with AMI, usually due to extensive LV infarction with ensuing pump failure.
  • Physical exam
    • Sinus tachycardia is considered a “harbinger of doom”, when the body compensates for low cardiac output by ramping up the heart rate
    • The presence of sinus tachycardia and low pulse and/or blood pressure in a patient with a large anterior MI should raise suspicion for cardiogenic shock
    • Be wary of giving IV beta blockers in this situation as negative inotropes can precipitate cardiogenic shock (Commit Trial)
    • When interpreting a patient’s blood pressure in the acute setting, it is helpful to know their baseline blood pressure and if they have a significant history of hypertension.
  • Patients <75 years of age with CS have improved survival at 6 months and at 1 year with early revascularization (SHOCK trial)
  • Mechanical circulatory support
    • Intra-aortic balloon pump (IABP)
      • No mortality benefit with IABP use in CS at 30 days and at 1 year (IABP-SHOCK II trial)
      • ACC/AHA guidelines give IABP a class IIa recommendation for medically refractory AMI-CS in the USA, whereas the ESC guidelines give it a class III recommendation.
    • Percutaneous left ventricular assist device (Impella)
      • No difference in mortality between IABP or Impella use after 30 days or 6 months (IMPRESS trial)
      • However, observational data like the Detroit & VAD registries show improvement in survival with Impella use in AMI-CS with the cost of excess complications (vascular injury, bleeding, etc)
      • Upcoming trials (DanGer Shock and Recover IV) will hopefully have more promising data supporting the use of Impella in AMI-CS
    • In the setting of discrepant guidelines, the decision for MCS should be multidisciplinary and based on clinical expertise.  
  • For more on AMI-CS, enjoy CardioNerds #223. CCC: Approach to Acute Myocardial Infarction Cardiogenic Shock with Dr. Venu Menon

How does RV infarction present?

  • Physical exam
    • RV infarct triad: hypotension, elevated JVP, clear lungs
    • Hypotension precipitated by nitroglycerin administration highlights the preload dependent state of an infarcted RV
    • GI symptoms (nausea and emesis) are common
    • Patients may actually need fluids despite an elevated JVP because of an underfilled left ventricle
  • EKG
    • Consider a right sided leads (ST elevation in V1 and V4R are the most sensitive EKG markers of RV injury), but this should not delay emergent coronary angiography +/- PCI if suspicion for AMI is high
  • Rhythm
    • AV synchrony plays an important role in RV infarct given the dependence on preload
    • If a patient loses AV synchrony due to heart block or atrial fibrillation, they can become more unstable due to a further drop in RV preload and overall cardiac output
    • However, bradyarrythmias in inferior MIs are frequently vagally mediated, and therefore temporary
    • Strategy for management of an inferior MI with RV infarct should be to optimize all other aspects hemodynamically before placing a temporary transvenous pacemaker (risk of RV perforation)
      • Prompt reperfusion
      • Maintain RV preload
      • Inotropes
      • Avoid hypoxia (potent pulmonary vasoconstriction, can increase RV afterload)
      • MCS providing RV support (Protek-Duo, RP Impella, VA-ECMO)
  • For more on RV-predominant cardiogenic shock, enjoy CardioNerds #239. CCC: Approach to RV Predominant Cardiogenic Shock with Dr. Ryan Tedford

How does LVOT obstruction in a large anterior MI present?

  • Hypotension with dobutamine or norepinephrine in a patient with an anterior MI and apical infarct, should raise suspicion for dynamic left ventricular outflow tract obstruction due to compensatory hyperdynamic basal walls
  • Echocardiography is invaluable for diagnosis!
  • Management
    • Prompt reperfusion
    • IV fluids (preload dependent)
    • Beta blockers (eg: esmolol quick on, quick off)
    • Phenylephrine (can improve BP by increasing afterload)
    • Avoid positive inotropes (e.g., norepinephrine, epinephrine, dopamine, dobutamine, milrinone)
    • Avoid IABP

What are the different types of ruptures which may complicate a late-presentating MI?

  • Papillary muscle rupture
    • Posteromedial papillary more likely to be affected due to single coronary blood supply
    • Papillary muscles are subendocardial so rupture can occur with non-transmural infarcts
    • Presents with acute dyspnea from flash pulmonary edema and hypotension from drop in cardiac output
    • Exam with new systolic murmur which may not be audible due to rapid equalization of pressures. For the same reason, Doppler may also underestimate the degree of MR.
    • V wave from mitral regurgitation
  • Ventricular septal rupture
    • Risk factors: advanced age, female sex, first MI with lack of coronary collaterals
    • Presents with hypotension, chest discomfort, dyspnea
    • Exam with harsh systolic murmur with palpable thrill; pulmonary congestion is unusual unusual
    • V wave from increased flow through the pulmonary circuit (but not high enough to cause flash pulmonary edema)
    • Step up in RV saturation during right heart catheterization
    • Inferobasal VSD with RCA infarcts (near the valves and conduction tissue and with more serpentine lesions, leading to worse outcomes)
    • Apical VSD with LAD infarcts (can miss on TTE)
  • Free wall rupture
    • Risk factors: advanced age, female sex, first MI with lack of coronary collaterals
    • Partial rupture may present as a vagal event that heralds the initial tear; TTE with new pericardial effusion should raise suspicion of an incomplete rupture
    • Full rupture can present as PEA arrest with abysmally low survival
    • May partially heal as a pseudo-aneurysm

How do we manage rupture complications?

  • For any of the three rupture scenarios (VSR, papillary muscle rupture, or free wall rupture), time is of the essence to confirm the site of rupture and to get the surgical team involved
  • Can have abrupt, unexpected, unpredictable progression so need to bring in surgical expertise early
  • Papillary muscle rupture will need mitral valve replacement
  • For VSR closure, can pursue surgical versus percutaneous options depending on anatomical features of the lesion and patient characteristics
    • Intervention is more challenging in inferobasal VSRs with higher operative mortality, but also less amenable to percutaneous closure (less likely to have appropriate rims for closure)
    • If poor operative candidacy, more likely to opt for percutaneous options
    • If size of defect large, would more likely lean towards surgery
  • Can consider bridging with MCS if patient in CS (eg: IABP, Impella) as long as this will not delay the surgical intervention


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