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AHA Cardiogenic Shock Spoon Feed

October 5, 2017

Written by Thomas Davis, MD.

Spoon Feed
This 50 page AHA guideline is very concisely but completely summarized right here.  Save some time and get the pearls.  Table 5 is fantastic, and this article is available in free full text (see Source below), so take advantage and look at this.

Shocking developments
1.  ACS is by far the most common cause of cardiogenic shock accounting for 80+% of cases.

  • Fibrinolysis does not affect mortality for STEMI patients with cardiogenic shock. Going to the cath lab does. Therefore, if a patient is in cardiogenic shock, get him to the cath lab regardless of time delay from MI onset.
  • Mechanical complications (papillary muscle rupture, ventricular septal defect, free wall rupture) were historically thought to be late complications. However, these most frequently present within 24 hours of hospitalization.

2.  Decompensation of chronic heart failure is the second most common cause of cardiogenic shock.

3.  Other less common causes that we may see in the ED include:

  • Myocarditis – Paradoxically, the sickest patients on presentation tend to do best. Only 50% will have elevated troponin. So be on the lookout for other clues, such as arrhythmia (e.g. unexplained sinus tach) or clinical signs of heart failure.
  • Stress induced AKA takotsubo – These patients usually recover. However, risk for in-hospital complications is as high as in those admitted for ACS.
  • Advanced valvular disease or prosthetic valve dysfunction
  • Hyper- or hypo- thyroidism
  • Pregnancy related complications:
    • Peripartum cardiomyopathy
    • Spontaneous coronary artery dissection – Accounts for up to 25% of cases of ACS among women < 50 years old. Though classically thought to be seen in young women, a recent study shows 62% of cases of SCAD were in post-menopausal women. They present as STEMI or NSTEMI.

4.  Hemodynamic goals

  • Admittedly there is no clear preference for MAP or SBP goals since the data are extrapolated from non-cardiogenic shock populations.
  • There is a theoretical sweet spot where MAP/SBP is neither too low nor too high. Trend signs of end organ function to find the right goal for the individual patient: urine output, creatinine, LFTs, mental status, lactate, etc.

5.  Vasopressors and inotropes

  • Again, evidence is limited but norepinephrine is thought to be the preferred starting agent for most situations, given its lower risk for arrhythmias. The AHA acknowledges the mortality benefit in the cardiogenic shock subgroup of the SOAP II trial but expresses concern regarding the study’s vague definition of cardiogenic shock and the likely heterogeneous subtypes of cardiogenic shock included in this trial.
  • There are some situations where you should consider additional or different approaches (see Table 5 for complete list):
    • Aortic stenosis: This is afterload dependent shock. Start with phenylephrine or vasopressin.
    • Mitral stenosis: This is preload dependent shock. Goals are to slow the heart rate (esmolol), improve AV synchrony (amiodarone), and avoid chronotropic agents (therefore use phenylephrine or vasopressin).
    • Aortic regurgitation: Increasing the heart rate may shorten diastolic filling time and decrease LVEDP. Therefore, consider dopamine or temporary pacing.
    • RV shock: Goals include maintaining pre-load (fluid boluses), lowering RV afterload aka PVR (inhaled pulmonary vasodilators), treating bradycardia, and maintaining AV synchrony. Vasopressin may raise SVR and have neutral effect on PVR.
    • Normotensive shock: If SBP > 90 mmHg but with signs of peripheral hypoperfusion, inotropy may be a reasonable first move.
    • Pericardial tamponade: Fluid boluses to help pre-load dependent state.

6.  Mechanical Ventilation

  • No known preferred mode in cardiogenic shock.
  • PEEP can help you or hurt you. PEEP improves oxygenation, shifts fluid out of the alveoli in pulmonary edema, and decreases LV afterload. However, PEEP also drops preload and increases RV afterload.
  • Avoid hyperoxia and hypoxemia.

7.  Devices, tools and widgets

  • ECMO is best for reversible causes like myocarditis.
  • Data on use of intra-aortic balloon pumps in MI-associated cardiogenic shock have been disappointing. As a result, IABP is being used less often.
  • Similarly, pulmonary artery catheters are only used selectively when the cause of shock is unclear or when patients are unresponsive to initial management.

Contemporary Management of Cardiogenic Shock: A Scientific Statement From the American Heart Association.  Circulation. 2017 Sep 18. pii: CIR.0000000000000525. doi: 10.1161/CIR.0000000000000525. [Epub ahead of print]

Another Spoonful
Phenotypes: The AHA describes three phenotypes all sharing in common decreased cardiac index.

  • Cold (increased ­SVR) and wet (­increased PCWP): This is classic cardiogenic shock and is seen in 2/3 of cases of MI-associated cardiogenic shock.
  • Cold and dry (decreased PCWP): This is classically a diuretic responsive HF patient with subacute decompensation. However, up to 28% of MI-associated cardiogenic shock may have this presentation.
  • Warm (decreased SVR) and wet: Though less common, MI patients may experience a SIRS response causing a vasodilatory cardiogenic shock. They have higher risk for in-hospital sepsis and mortality.

Peer reviewed by Clay Smith, MD.

What are your thoughts?