Cardiogenic Shock

Defined loosely as a shock state from a primary cardiac cause. Generally patients will present with hypotension, peripheral hyperperfusion, and evidence of end-organ ischemia, which is unresponsive to fluid resuscitation. High mortality rates (40-60%) depending on the severity and cause.

Etiology of CS

1. Acute MI (most common)
   1. LV dysfunction
   2. septal rupture
   3. Papillary muscle rupture
   4. Free wall rupture
2. Arrhythmias
3. Myocarditis
4. End-stage cardiomyopathy
5. Stress cardiomyopathy
6. Cardiac tampondade
7. Arrhythmia
8. Critical valvular disease
9. Myocardial contusion
10. RV failure
    1. AMI
    2. Decompensated cor pulmonale
11. Severe sepsis, metabolic derangement

Epidemiology

CS occurs in 5-10% of AMI, and is more common with STEMI than NSTEMI.

Pathophysiology

Complex but essentially:

• Profoundly depressed myocardial contractility
• Spiral of reduced cardiac output, hypotension, and ongoing myocardial ischemia. This leads to a death spiral of hypoperfusion which can also be accompanied by deranged circulatory compensation (microvascular dysfunction, hypersympathomimetic state, lactic acidosis, mitochondrial dysfunction)

Timing of CS

CS is generally present at admission or develops within the first day post-AMI. Later development of CS can be due to reinfarction, infarct expansion or mechanical complications.

Evaluation

• Swan-Ganz: The ESCAPE RCT has examined this intervention - no improvement in mortality with the routine use of PAC in CS. PACs can confirm and further delineate the pathophysiology of CS in complex/uncertain cases, and tailor therapy.
• Cardiac cath/angiography is immediately indicated in all patients with CS complicating MI.

Management of CS

General Measures

1. Maintain adequate systemic and coronary perfusion pressures: SBP ~90 or MAP ~65 mm Hg.
2. Moderate glucose control.
3. Consider ventilatory support for correction of hypoxemia, acidosis, work of breathing.
4. Treat arrhythmias (brady, tachys)

Acute MI

1. Reperfusion-revascularization: This is the only EBM-based strategy for mortality reduction in CS from AMI.
   1. SHOCK trial: NNT = 6 for early revascularization (PCI/CABG) vs optimal medical therapy for LV failure in the setting of STEMI. 86% of both groups received IABP.
   2. CULPRIT-SHOCK trial: culprit-lesion only PCI ± possible staged revascularization reduced MACE/RRT in comparison to immediate multivessel PCI.

Vasopressors and Inotropes

Vasoactive medications are often used in the management of patients with CS and all have important disadvantages, including increase in myocardial O2 consumption, afterload, lethal arrhythmias, and possible myocardial cell death. No vasopressor has been demonstrated to change outcome in large clinical trials.

1. Norepinephrine is a reasonable first line vasopressor based on several RCTs
   1. SOAP II: NE > dopamine in the treatment of CS, and may have less incidence of arrhythmias
   2. OptimaCC: NE > Epinephrine in the treatment of CS from AMI, with lower incidence of refractory shock.
2. Either dobutamine or milrinone are reasonable inodilators in addition to vasopressors per the recent DOREMI trial. See Inotropes for more information.

Mechanical Circulatory Support

Intra-aortic balloon pump

IABP (intra-aortic balloon pump) is the most commonly used MCS device. It is inserted into the femoral artery and provides massive hemodynamic support. In the IABP-SHOCK II trial, routine IABP use in conjunction with early revascularization (PCI dominant) did NOT reduce 30d or 12m mortality. There was also no benefit on secondary endpoints of lactate, pressor doses, renal function, critical illness scores. Therefore, IABP is no longer routinely recommended for CS with LV failure.

Active MCS

• These support the RV, LV, or both and can be placed percutaneously or surgically.
• Percutaneous MCS such as the TandemHeart, Impella, and VA-ECMO have been used in refractory CS and also as a first-line treatment, but the appropriate role of such interventions is unclear at this time and no clear positive impact on clinical outcomes has been demonstrated.

ECLS

Interventions such as VA-ECMO can also be considered in refractory/severe cases as a bridge to definitive treatment.

The recent ECMO-CS (2023) RCT examined immediate VA-ECMO vs an initially conservative strategy in patients with rapidly deteriorating or severe CS. In this study of 117 patients, there was no difference in a composite outcome of all-cause mortality, resuscitated cardiac arrest, or other MCS at 30d. Therefore, early VA-ECMO does not improve relevant outcomes in severe/progressive CS.

Specific Situations

1. Acute MR - confirmed by echocardiography. Management: afterload reduction with IABO, vasodilators to reduce pulmonary edema. Definitively, these patients need surgery or interventional treatment.
2. Ventricular septal rupture - can occur 2 weeks after infarction. Leads to severe L to R shunting. Management: immediate surgical VSR closure, may need IABP as a bridge to surgery.
3. Free wall rupture ± tamponade: most likely to occur in the first week, and typically leads to PEA arrest. Definitive surgical repair is required.

References

1. Harrisons Internal Medicine - Ch 298 Cardiogenic Shock