Cardiogenic Shock

Definition 

• Impairment of cardiac output due to primary cardiac disorder that results in end-organ hypoperfusion and hypoxia

Etiology

• Cardiomyopathic: acute myocardial infarction with LV dysfunction (most common cause), exacerbation of heart failure, pHTN exacerbation, myocarditis, myocardial contusion, druginduced cardiac injury 
• Arrhythmogenic: sustained atrial and ventricular tachyarrhythmias (ex: sustained VT) and bradyarrhythmias (ex: complete heart block) 
• Mechanical: severe valvular insufficiency, acute valvular defects, ventricular septal wall defect or rupture of intraventricular septum, ruptured ventricular wall aneurysm, atrial myxoma, retrograde dissection of ascending aorta

Presentation and Diagnostic Criteria 

• Severe systemic hypotension: SBP < 90 mmHg for > 30 minutes OR MAP < 60 mmHg for > 30 mins OR mean BP 30 mmHg lower than baseline OR requirement of vasopressors to maintain SBP > 90/MAP > 60 
• Signs of end-organ hypoperfusion: cool extremities, oliguria, AMS, and/or lactate > 2.0 
• Echocardiographic evidence of cardiac dysfunction - Respiratory distress due to pulmonary congestion, elevated JVP, peripheral edema 
• Pulmonary artery catheterization findings: PCWP > 15mmHg, CI <1.8 L/min/m2 without hemodynamic support or <2.2 L/min/m2 with support, SVR > 1400 dynes*sec/cm5 , SvO2 < 65%

SCAI Classification for Cardiogenic Shock

Provides standardized framework for categorizing shock severity with each progressive stage correlating with higher mortality 

• Stage A: “At Risk” for cardiogenic shock but without clinical evidence of shock 
• Stage B: “Beginning” Shock - Hypotension or tachycardia without hypoperfusion 
• Stage C: “Classic” Cardiogenic Shock - hypotension and hypoperfusion (lactate > 2) 
• Stage D: “Deteriorating” Shock - initial interventions have failed to restore stability and adequate perfusion 
• Stage E: “Extremis” - highly unstable patient often with cardiovascular collapse

Evaluation 

• CBC, CMP, BNP/NT-pro-BNP, troponin, lactate, VBG, EKG, CXR 
• Echocardiogram to assess ventricular and valvular function 
• LHC if concern for ischemic cause (see ACS) 
• Continuous hemodynamic monitoring via Swan-Ganz - no benefit for general shock but does improve in-hospital mortality for those with cardiogenic shock 
  • Swan-Ganz Hemodynamic Profile / Swan Sheets: 
    • While rotating in the CCU, the “Swan Sheet” will be provided. You will update the Swan Sheet Q4H for patients with active Swan-Ganz/PA catheters. An equation is built into the spreadsheet to compute the hemodynamic profile, but you will need to make sure to input patient specific height and weight metrics in top right corner of the sheet. This sheet provides hemodynamics/filling pressure information that also correlates with timing of MVO2 lab draw by nursing staff. 
    • See Right Heart Cath section for interpreting Swan-Ganz/PA catheter profiles 
    • Utilizing PAC hemodynamic profile to determine phenotype of cardiogenic shock: 
      • LV-dominant Shock: PCWP > 15, normal RAP, PAPi >1.0 
      • RV-dominant Shock: RAP >15, PCWP <15, RAP/PCWP ratio > 0.6 
      • Bi-V-dominant Shock: RAP >15, PCWP >15, PAPi <1.0

Management

• Medical Management – primary goal is to mitigate congestion, optimize cardiac output, and enhance perfusion to vital organs 
  • Volume Optimization: IV diuresis (hypotension IMPROVES with diuresis in cardiogenic shock) 
  • Vasopressor Therapy: norepinephrine is preferred first line for hypotensive cardiogenic shock due to fewer arrhythmic events and mortality compared to dopamine; alternatives include vasopressin, phenylephrine, and dopamine 
  • Inotropic Therapy: 
    • Inodilators to increase contractility and decrease afterload - Dobutamine (B1 and B2 receptor agonist) or milrinone (PDE-3 inhibitor) 
    • Inoconstrictors to increase contractility and increase afterload – norepinephrine (alpha-1 > B1 > B2), epinephrine (B1 > alpha-1 = B2), dobutamine (D1 > B1 > alpha-1) 
  • Afterload Reduction: IV nitroglycerine, IV nitroprusside may be considered in normotensive cardiogenic shock with increased SVR 
• Mechanical Circulatory Support (MCS) - reasonable when end-organ function cannot be maintained by pharmacologic means. Goal is to promote ventricular unloading, restore systemic perfusion and serve as bridge to recovery, durable MCS, or transplantation. 
  • Indications: refractory hypoperfusion/hypotension despite vasopressors, persistently low CI (<2.0 L/min/m2), RV failure refractory to medical therapy, biventricular failure, concurrent respiratory failure, cardiac arrest with ongoing shock

Types of MCS:

Contraindications to MCS

• Absolute contraindications: irreversible cardiac failure without an exit strategy (transplant or durable LVAD) and concomitant irreversible noncardiac organ failure 
• Severe aortic regurgitation/stenosis, intracardiac shunt, mechanical aortic valve, severe RV dysfunction, LA or ventricular thrombus, aortic dissection, severe peripheral arterial disease/inability to achieve adequate vascular access, uncontrolled sepsis, disseminated malignancy, severe coagulopathy or bleeding diathesis

Daily Management of MCS Devices

• Daily CXR (IABP) / limited TTE (Impella) to ensure correct position of device 
• Monitor for hematoma at device site 
• Distal pulses check to monitor for limb ischemia 
• Anticoagulation - based on device (www.vumc.org/department-pharmacy/vuh-adultanticoagulation- stewardship-committee-resources) 
• Impella: Daily hemolysis labs (Hgb, PT/INR, PTT, LFTs, LDH, Haptoglobin) and monitoring of urine color 
• IABP: Ensure that the balloon inflation and deflation are synchronized with the cardiac cycle - Inflation should occur at the onset of diastole (middle of the T-wave on ECG) and deflation at the onset of systole (peak of the R-wave on ECG)