Cardiogenic Shock

Cardiogenic shock occurs when there is insufficient perfusion to meet the metabolic demands of tissue due to cardiac dysfunction. Data suggests that cardiogenic shock has complicated 5% to 8% of STEMI cases and 2.5% of non-STEMI cases yearly. This amounts to approximately 40,000 to 50,000 cases per year.

The basic pathophysiology stems from the consequences of systolic and diastolic dysfunction. As a result of systolic impairment, cardiac output and stroke volume fall which produces decreased systemic perfusion and decreased coronary perfusion pressure. In response to this shock state, reflex release of catecholamines constrict peripheral arterioles to maintain perfusion of tissue. The benefit of a slight improvement in perfusion pressure is done at the expense of an increase in systemic vascular resistance which further exacerbates myocardial dysfunction. On the other side, diastolic dysfunction leads to elevated left ventricle end diastolic pressure, pulmonary congestion, worsening hypoxemia and an exacerbation of ischemia. Taken together, the process produces a downward spiral of progressive myocardial dysfunction and increasingly poor tissue perfusion.

MI with left ventricular dysfunction is the most common cause of cardiogenic shock. Other causes include cardiomyopathies, valvular obstruction, aortic dissection, pericarditis or cardiac tamponade.

Pertinent signs include:

• Cold, clammy skin due to vasoconstriction and tissue hypoperfusion

• Falling systolic blood pressure

• Weak, thready pulse

• Signs of heart failure such as pulmonary edema, jugular venous distention, bilateral lower ext swelling

Consider the following to aid in a diagnosis:

• EKG: Use this to establish evidence of an MI, dysrhythmia or cardiomyopathy

• Echocardiogram: signs of valvular dysfunction, obstructed outflow tract or cardiac tamponade

• Laboratory cardiac markers (CKMB, troponin): indicate cardiac injury

• Lactate: marker of tissue hypoperfusion

Airway management and circulatory stabilization are key priorities in the early management of cardiogenic shock.

1. Ensure patient is connected to monitor with two large bore IVs.

2. In setting of cardiogenic shock secondary to ischemia, every attempt should be made to ensure early revascularization. Percutaneous coronary intervention is preferred if available. If not readily available, and a transfer is not feasible, then fibrinolysis can be pursued.

3. AVOID: beta blockers in cardiogenic shock. Use morphine and nitroglycerin with caution in the setting of right ventricular ischemia.

4. Consider a fluid challenge in the setting of hypotension without evidence of pulmonary congestion.

5. Pressors: There are several options to consider if pressors become necessary.         

• Norepinephrine is an excellent choice because it is a vasopressor and provides positive inotropy. Dose: 2 micrograms/min and titrate up.

• Dobutamine is the usual choice in cardiogenic shock because it provides excellent inotropy. However, it may cause peripheral vasodilation. Dose: 2.5 to 20 micrograms/kg/min.

• Dopamine can be used alongside dobutamine in the event of peripheral vasodilation. Dose: 2.5 to 20 micrograms/kg/min.  

• Milrinone can be used for positive inotropy. Dose: loading dose of 50 micrograms/kg IV followed by drip of 0.5 microgram/kg/min.

     6.   If there is severe cardiogenic shock, an intraaortic balloon pump may be considered to  

           augment forward flow. This is a temporizing measure. Consult cardiology to coordinate   

           this decision.

1. Circulation: http://circ.ahajournals.org/content/117/5/686

2. Tintinalli’s 7th edition

3. Wikipedia: https://en.wikipedia.org/wiki/Cardiogenic_shock