The Sick MI Patient

Author: Max Hockstein, MD (@MaxHockstein, EM Resident Physician, UTSW / Parkland Memorial Hospital) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Brit Long, MD (@long_brit, EM Chief Resident at SAUSHEC, USAF)

As usual, you’re minding your own business when a nurse comes up to you and says “Hey, Mr. Badhart in room 5 looks appalling – he’s dyspneic, hypotensive to the 60’s, and has ST elevations, and may or may not have just gone into V-Tach.”

Sequelae of an acute MI can be divided into two broad categories: electrical and mechanical consequences (or, as Occam’s razor is occasionally dull, both electrical and mechanical problems may occur together).

Electrical Problems:

The origin of the arrhythmia depends on the vascular territory of the acute infarct. After MIs, scars can develop which serve as foci for macroreentrant arrhythmias. One of the goals of reperfusion is to prevent myocardial scars.

Right Coronary Artery: The RCA supplies conduction tissue proximal to (and including) the bundle of His, which has dual blood supply. RCA lesions, if affecting nodal branches, will present as sinus bradycardia or high degree AV block which frequently resolve once revascularization has occurred. Caution should be applied to use of chronotropes and inotropes as they may increase myocardial oxygen demand (ex: isoproterenol). Consider transcutaneous (or transvenous) pacing as a temporizing measure.

Left Anterior Descending: The LAD supplies conduction tissue distal to (and including) bundle of His. LAD lesions, known as “widow makers,” may present with ventricular arrhythmias (VF, VT). VF/VT arrests should be treated with standard ACLS protocol. In the patient who presents with cardiogenic shock (see later) and develops malignant ventricular arrhythmias, most other antiarrhythmics other than amiodarone will suppress myocardial contractility and should be avoided. Prophylactic lidocaine given in MI may increase rates of asystole.

Shout-out to Accelerated Idioventricular Rhythm (AIVR, aka ventricular escape): it’s the most common arrhythmia seen after reperfusion is achieved. The old terminology for this pattern is “slow VT” as it is wide-complex and regular. AIVR is transient and should not be treated with antiarrhythmics.

  • Related factoid: Ever wonder why patients will frequently have an idioventricular rhythm after cardiac arrest? This rhythm originates from the Purkinje fibers which, interestingly, don’t rely on coronary artery blood supply – they rely on cavitary (blood in the cavity of the ventricles) for their oxygen supply.

Mechanical Problems:

Myocardial ischemia/infarction can lead to progressive LV dysfunction and subsequently the bad mama jama that is cardiogenic shock (see detailed write-up here: In theory, the incidence of cardiogenic shock should be decreasing[1] because we’re getting better at identifying STEMIs and those patients are getting revascularized sooner. Additionally, cardiogenic shock may not declare itself in the ED – half of the patients who develop cardiogenic shock do so within the first day and the second half in the week following the insult. The 30-day mortality for cardiogenic shock has been quoted anywhere from 50-74% – that’s approximately 20 times that of a run-of-the-mill STEMI![2]

The definition of cardiogenic shock relies solely on nerdy hemodynamic parameters: a cardiac index < 1.8 L/min/meter2 and high ventricular filling pressures. Though an independent predictor of mortality, do not rely on the ejection fraction to diagnose cardiogenic shock – it may deceptively be normal or high. Given that these variables will likely be unavailable in the ED, evidence of LV dysfunction, myocardial ischemia, and hypotension are sufficient to initiate treatment for cardiogenic shock in the ED. There are three standard treatment modalities for the treatment of the hemodynamically unfortunate cardiogenic shock patients.

  • Cath ‘em sooner rather than later. The SHOCK trial[3] showed that MIs complicated by cardiogenic shock had a lower mortality rate at six months if early PCI (angioplasty) was performed over medical therapy (medications and hoping they don’t code). Until the patient can have the lesion(s) repaired, routine antithrombotic therapy (ex: aspirin) for MI should be initiated[4].
  • Pharmacologic agents (inotropes and vasopressors) should only address the immediate hemodynamic concerns caused by systolic dysfunction as treatment of the diastolic failure (nitrates, diuresis) component would risk exacerbating the hypotension. Hypotension due to cardiogenic shock is not responsive to aggressive volume resuscitation and may be potentially injurious to a failing LV. In contrast, cardiogenic shock due to RV failure may be initially addressed with repletion of preload. In the setting of isolated acute RV failure consider pulmonary embolism as the primary cause.
    • For moderate hypotension (70<SBP<100), the AHA recommends[5] higher-dose (where alpha agonism is most significant) dopamine (>15 mcg/kg/min).
    • Profound hypotension (SBP<70) should be treated with norepinephrine (2-10 mcg/min).
    • Dobutamine (2-20 mcg/kg/min) may also be used as an adjunct.
    • Milrinone (0.375 – 0.75 mcg/kg/min) should be used with caution in hypotensive patients because of its peripheral vasodilatory properties and long half-life.
  • Of note, Annals of Intensive Care recommends norepinephrine as the first line vasopressor with a goal MAP of 65 mg Hg. Dobutamine can be added to norepinephrine for additional inotropic support.
  • Intra-aortic balloon pumps have been used for decades to treat cardiogenic shock. Interestingly, the IABP-SHOCK[7] studies (RCT’s) demonstrated that IABPs confer no long-term mortality benefit. There is no data to support the use of Swann-Ganz catheters in the ED despite much of the evidence surrounding the treatment of cardiogenic shock coming from PA catheter readings.

There are three emergent impending structural disasters that follow MIs the EP should be familiar with: free wall rupture, interventricular septal rupture, and acute mitral insufficiency. All may be diagnosed with a bedside cardiac ultrasound and mandate early involvement of the cardiology team.

Free wall rupture: Occurs in the first five to fourteen days post MI. Free wall rupture is more likely to occur in areas with less collateral blood supply and with transmural infarctions. Infarction leads to necrosis and subsequent weakening of myocardial walls. Subsequently, high pressure in the ventricle perforates the weakest point of the wall resulting in massive hemopericardium, tamponade, RV failure, PEA, and death.

  • Pericardiocentesis will reveal frank blood.
  • Subacute ruptures (slit-like defects that have been thrombosed) may present less dramatically.
  • Survival depends on prompt surgical intervention but standard therapy for cardiogenic shock (see above) still applies.

Interventricular septum rupture (IVS): Occurs in the first one to fourteen days post MI. Presents with a horrific triad:

  • A new holosystolic murmur (left to right shunt)
  • Hypotension
  • Biventricular failure (more often right than left)

In general, the top of the septum ruptures if it’s a left-sided coronary occlusion and the bottom of the septum ruptures if it’s a right-sided coronary occlusion. If the patient presents in cardiogenic shock, standard CS treatment applies. If the patient with a septal rupture is hemodynamically reasonable (i.e. not hypotensive and displaying frog-heart physiology) consider agents to reduce shunt physiology (afterload reduction, diuretics) to relieve the RV failure. Timing of operative repair (vs. repair in the cath lab) of septal ruptures remains controversial.

Acute mitral regurgitation: Occurs two to seven days post MI. A papillary muscle rupture occurs when the papillary muscle infarcts its connection with the chordae tendinae (which then connect to mitral leaflets) resulting in mitral valve insufficiency. This will present with:

  • A new holosystolic murmur
  • Hypotension
  • Pulmonary edema

On initial presentation, it may be clinically indistinguishable from an IVS. Dissimilar to IVS, however, the mainstay of treatment is emergent surgical intervention. For the increasingly symptomatic patients with AMR, consider afterload reduction (nitrates, IABP) to increase forward flow.

The Punchline – Three mainstays of treatment for cardiogenic shock:

  1. Revascularize early
  2. Inotropic support
  3. Aortic counterpulsation



[1] Circulation. 2009 Mar 10;119(9):1211-9. doi: 10.1161/CIRCULATIONAHA.108.814947. Epub 2009 Feb 23.

[2] J Am Coll Cardiol. 2010 Jul 20;56(4):254-63. doi: 10.1016/j.jacc.2010.05.008.

[3] N Engl J Med 1999; 341:625-634 August 26, 1999DOI: 10.1056/NEJM199908263410901

[4] Circulation.2008; 117: 686-697doi: 10.1161/CIRCULATIONAHA.106.613596

[5] Circulation.2008; 118: 1047-1056 doi: 10.1161/CIRCULATIONAHA.107.728840

[6] Annals of Intensive Care. 2015; 5:17 doi: 10.1186/s13613-015-0052-1

[7] Cochrane Database Syst Rev. 2015 Mar 27;3:CD007398. doi: 10.1002/14651858.CD007398.pub3.


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