Cardiogenic Shock
Definition:
Cardiogenic shock (CS) is defined as a low cardiac output state that results in end-organ hypoperfusion/hypoxia and ultimately multisystem organ failure. Various trial studies have developed clinical criteria to define CS, most common including: SBP<90 mm Hg for >/= 30 min, or support to maintain SBP>/=90 AND end-organ hypoperfusion (i.e. urine output<30cc/kg/hr, elevated Cr, cool/mottled extremities, altered mental status, Lactate >2.0) AND pulmonary congestion AND CI </=2.2 AND PCWP >/= 15 mmHg.
Etiologies:
Possible causes leading to cardiogenic shock are extensive. The most common etiology is acute myocardial infarction with left ventricular dysfunction. Other less common, but possible causes, include acute on chronic systolic heart failure with severely reduced LVEF, acute valvular dysfunction (severe MR, AR, AS, etc.), papillary muscle rupture, VSD, free wall rupture, cardiac tamponade, acute myocarditis, severe bradycardia, tension pneumothorax, pulmonary embolism, aortic dissection, hypo/er-thyroidism, or peripartum cardiomyopathy. Post-cardiotomy cardiogenic shock is another possible etiology, and seen in about 2-6% of open heart surgical patients. A common reason for this particular complication is insufficient intra-operative cardioprotection (i.e. hypothermia / high-potassium cardioplegia) that results in myocardial stunning and difficulty coming off CPB.
Pathophysiology of MI-induced Cardiogenic Shock:
In myocardial ischemia-associated CS, myocardial depression following ischemic insult results in reduced contractility, a low cardiac output state, and hypotension, which further reduces coronary artery perfusion, leading to cascade of multi-organ system collapse. In response to injury and hypoperfusion, the peripheral vasculature vasoconstricts, raising SVR to perfuse vital organs, such as the heart, kidneys, brain, etc. In order for this response to occur, the body releases catecholamines (epinephrine, norepinephrine), as well as neurohormones (vasopressin, angiotensin II, etc.) that result in peripheral vasoconstriction and fluid retention. These defensive strategies increase the workload on the heart by providing added ionotropy/chronotropy, creating a higher afterload for the heart to overcome, and likewise increasing pulmonary vascular congestion.
LV ischemia/dysfunction is the most common presentation of cardiogenic shock.
With RV ischemia and dysfunction, right-sided filling pressures are elevated, thus leading to an over-filled right heart that pushes into the interventricular septum toward the left side. This can ultimately lead to elevated left-atrial filling pressures, but reduced LVEF since the cavity size is smaller, and systolic function becomes impaired.
Typical findings in RV failure are relatively higher LVEF and CVPs and relatively lower PA systolic pressures in comparison to LV failure. Both RV and LV failure will likely involve drop in cardiac indices and elevated PCWP, as the left ventricular end-diastolic pressure is affected by both right and left-sided failure.
Signs/Symptoms:
Common signs of CS include delirium/altered mental status, tachycardia, hypotension, cool/clammy skin, oliguria, dyspnea, and narrow pulse pressure.
Invasive Monitoring:
Placement of a central line (for vasopressor/ionotrope infusion), PA catheter (for mixed venous, SvO2, monitoring response to interventions), Arterial line (continuous arterial blood pressure monitoring) should be considered.
Diagnosis:
Diagnosis of cardiogenic shock can be made through evaluating labs [ABG (assess oxygenation, lactate, metabolic derangements), CBC (evaluate WBC for infection, H/H for anemia), BMP (renal function, K+ levels), LFTs/Coags (evaluate for hepatic shock)]; EKG (ischemia?), CXR (signs of dissection, tamponade, pulmonary edema, ETT/central line/swan ganz placement), TTE/TEE (evaluate LVEF, valvular pathology, signs of VSD, pericardial tamponade)
Treatment:
Treatment options for these patients is dependent upon the clinical picture. In the event of ACS, early PCI or emergent surgical intervention for CABG (in multi-vessel disease) are recommended. Early antithrombotic therapy (ASA/Plavix, heparin gtt) in the event of myocardial infarct is also indispensable.
Other hemodynamic stabilizing measures that are important to consider include: intubation and mechanical ventilation, which assists in improving oxygenation and cardiac function via decreasing preload, afterload, and metabolic demand. Placement of a central line, PA catheter, and arterial line for initiation of vasopressors/ionotropes for monitoring of clinical response to interventions. Foley catheter insertion for accurate hourly intake/output. Lastly, evaluation for possible mechanical circulatory support, IABP/Impella/VA-ECMO/VAD.
Vasopressor considerations include Norepinephrine (Levophed), Vasopressin (for refractory shock), and/or Dopamine (typically reserved for bradycardic patients, as it is highly arrhythmogenic).
Of note, adding an ionotropic agent (Dobutamine, Milrinone, Epinephrine) in myocardial ischemia should ideally be considered after revascularization via PCI/CABG, as these medications increase the workload of the already compromised heart.
Below is a fantastic table from one of the referenced articles that depicts possible treatment options in the various etiologies of cardiogenic shock, as not all cardiogenic shock is treated the same.
References:
1. Menon, V., & Hochman, J. S. (2002). Management Of Cardiogenic Shock Complicating Acute Myocardial Infarction. Heart,88(5), 531-537. doi:10.1136/heart.88.5.531
2. Reynolds, H. R., & Hochman, J. S. (2008). Cardiogenic Shock: Current Concepts and Improving Outcomes. Circulation,117(5), 686-697. doi:10.1161/circulationaha.106.613596
3. Van Diepen, S., MD, & Katz, J. N., MD. (2017). Contemporary Management of Cardiogenic Shock. Circulation,136, 232-268. doi:10.1161/CIR.0000000000000525
