Cardiogenic Shock

Definition, etiology, pathogenesisTop

Cardiogenic shock is shock due to dysfunction of the heart (see Acute Heart Failure) that leads to reduced cardiac output. Causes:

1) Myocardial injury: Acute systolic heart failure caused by acute coronary syndrome (ACS) (most commonly myocardial infarction [MI], usually ST-elevation myocardial infarction with a left ventricular [LV] function decrease >40%) and its complications (acute mitral insufficiency, free wall rupture, ventricular septal defect), myocarditis, cardiac injury (trauma), cardiomyopathies, exacerbation of or end-stage chronic heart failure.

2) Cardiac arrhythmias: Bradycardia, tachyarrhythmias (particularly ventricular tachycardia and atrial fibrillation).

3) Acute valvular heart disease (acute mitral or aortic regurgitation), prosthetic valve dysfunction.

 4) Pericardial tamponade (also classified as obstructive shock) should be considered in patients with symptoms suggestive of pericarditis or heart failure, sinus tachycardia, and relatively clear lungs.

 5) Pulmonary embolism (also could be classified as obstructive shock) can rarely present with cardiogenic shock but clinically may be difficult to distinguish from other forms of cardiogenic shock.

Traditionally, the term “cardiogenic shock” has denoted a shock caused by impaired cardiac output (pump function that may be related to contractility or the ability for the heart to fill).

The current classification of the severity of cardiogenic shock is based on the Society of Cardiovascular Angiography and Interventions (SCAI) classification anchored on clinical findings. This scale has been validated and correlates with in-hospital mortality: Table 3.17-1.

Clinical features and diagnosisTop

Symptoms of shock and of the underlying disease.

Diagnostic Tests

See Shock; see Acute Heart Failure.

TreatmentTop

Use of the following methods of treatment depends on the specific underlying pathophysiology.

1. Patients need to be in a setting where airway, breathing, and circulation (ABC) can be continually monitored and addressed. Reliable IV access (including central venous access) and invasive blood pressure monitoring when available (arterial line) are critical, as these patients can deteriorate rapidly, needing timely resuscitative measures.

2. Depending on availability, consider early transfer to a center with advanced support including “shock team” management, depending on the patient’s age and comorbidities.

3. Discontinue beta-blockers, angiotensin-converting enzyme inhibitors (ACEIs), and other drugs that may lower blood pressure unless used specifically to counteract the mechanism of shock (eg, a beta-blocker in a patient with mitral stenosis and very rapid atrial fibrillation).

4. In case of ventricular tachycardia (or other supraventricular tachycardia causing shock), perform cardioversion. If the patient has atrial fibrillation or atrial flutter, consider cardioversion if the arrhythmia is thought to be contributing to shock (eg, in the setting of aortic stenosis or if the arrhythmia is an acute change). Consider subsequent administration of medications to prevent or treat arrhythmia recurrence (see Cardiac Arrhythmias).

5. In patients with bradycardia, consider atropine, chronotropic agents (eg, epinephrine 2-10 microg/min in a continuous IV infusion; alternatively isoproterenol [INN isoprenaline] 5 microg/min or dopamine), or cardiac pacing (see Cardiac Arrest).

6. In patients without symptoms of volume overload and pulmonary congestion, initiate fluid resuscitation to achieve optimal LV filling (this is particularly important in right ventricular dysfunction). Start with 250 mL of a crystalloid over 10 to 15 minutes, continue fluid resuscitation, and make adjustments based on response to treatment and appearance of volume overload. In patients with volume overload (pulmonary congestion) and patients without volume overload who do not respond to fluid therapy, consider one of treatment interventions discussed below.

7. In patients with documented myocardial dysfunction, an inotropic agent may be beneficial. For most patients, starting with norepinephrine is reasonableEvidence 1Strong recommendation (benefits clearly outweigh downsides; right action for all or almost all patients). Moderate Quality of Evidence (moderate confidence that we know true effects of the intervention). Quality of Evidence lowered due to indirectness to other pressors. De Backer D, Aldecoa C, Njimi H, Vincent JL. Dopamine versus norepinephrine in the treatment of septic shock: a meta-analysis*. Crit Care Med. 2012 Mar;40(3):725-30. doi: 10.1097/CCM.0b013e31823778ee. PubMed PMID: 22036860. Levy B, Perez P, Perny J, Thivilier C, Gerard A. Comparison of norepinephrine-dobutamine to epinephrine for hemodynamics, lactate metabolism, and organ function variables in cardiogenic shock. A prospective, randomized pilot study. Crit Care Med. 2011 Mar;39(3):450-5. doi: 10.1097/CCM.0b013e3181ffe0eb. PubMed PMID: 21037469. De Backer D, Biston P, Devriendt J, et al; SOAP II Investigators. Comparison of dopamine and norepinephrine in the treatment of shock. N Engl J Med. 2010 Mar 4;362(9):779-89. doi: 10.1056/NEJMoa0907118. PubMed PMID: 20200382. as its pharmacologic effects include not only vasoconstriction but also some inotropy (via beta2 stimulation). In patients with ongoing signs of shock despite initial therapy, milrinone or dobutamine can be administered via a continuous IV infusion (no difference in patient outcomes between those two agents).Evidence 2Moderate Quality of Evidence (moderate confidence that we know true effects of the intervention). Quality of Evidence lowered due to imprecision. Mathew R, Di Santo P, Jung RG, et al. Milrinone as Compared with Dobutamine in the Treatment of Cardiogenic Shock. N Engl J Med. 2021;385(6):516-525. doi:10.1056/NEJMoa2026845 In case of unsatisfactory response or issues with significant arrhythmias, consider enoximone or levosimendan (all of these drugs may have serious adverse effects and their use is controversial).

8. In patients with pulmonary congestion in whom blood pressure has been raised to a physiologically adequate level (usually at least 90 mm Hg) without catecholamine support, you may consider a loop diuretic (see Acute Heart Failure). In patients in whom diuretic treatment is ineffective, consider ultrafiltration. In patients with renal failure consider hemodialysis.

9. In patients with pulmonary congestion and systolic blood pressure >110 mm Hg, consider a vasodilator, usually nitroglycerin or nitroprusside (dosage: see Acute Heart Failure; these should not be used in isolated right ventricular failure).

10. Treatment of the underlying condition. In the case of ACS, refer the patient for urgent invasive revascularization (see Acute Coronary Syndromes). In the case of mechanical complications of MI, acute valvular disease, or prosthetic valve dysfunction, refer the patient for cardiac surgery.

11. In patients with refractory cardiogenic shock (persisting despite medical support), specialized centers may consider intra-aortic counterpulsation (after excluding contraindications: aortic regurgitation and aortic dissection) or short-term mechanical circulatory support, depending on the patient’s age, comorbidities, and neurologic function (see Mechanical Circulatory Support).

12. Other management steps (including oxygen therapy): As in other forms of shock.

TablesTop