Summary:

• Cardiogenic shock begins with an initial myocardial insult that reduces cardiac output and stroke volume, causing hypotension, reduced coronary perfusion, ischemia, and progressive cardiac dysfunction. Concurrently, LV filling pressures rise, pulmonary edema develops, hypoxia worsens ischemia, and a systemic inflammatory response with vasodilation further reduces SVR. The result is an expanding spiral of dysfunction and death unless multiple points are addressed.

• SCAI stages (A–E) standardize description and correlate with rising in-hospital mortality from patients at risk to those in extremis. Etiologies include acute myocardial infarction (including mechanical complications), myocarditis, stress-induced or toxin-mediated cardiomyopathy, acute on chronic heart failure, valvular disease, RV-predominant causes (e.g., PE, pulmonary hypertension), tamponade, and postcardiotomy.

• The golden hour requires simultaneous resuscitation, investigations, reversal of the primary cause, and triage. Norepinephrine is first-line; vasopressin and epinephrine are added as needed. Inotropes (dobutamine; milrinone for elevated PA pressures/RV shock) support contractility. Higher cumulative vasoactive use correlates with higher mortality.

• PA catheter data in cardiac ICUs show lower in-hospital mortality by guiding decisions, including temporary mechanical circulatory support selection. A multidisciplinary cardiogenic shock team improves outcomes, especially in heart failure–related shock.

• Prognosis depends on severity and trajectory, patient factors (age, frailty, comorbidities, neurologic injury), exit strategy (recovery, LVAD, transplant, palliation), and phenotype. Long-term issues include cognitive dysfunction, persistent organ impairment, psychological burden, reduced mobility, and social impact.

1. Pathophysiology

• Initial myocardial insult → ↓ cardiac output/stroke volume → hypotension → ↓ coronary perfusion → ischemia → more myocardial depression

• ↑ LV filling pressures → pulmonary edema → hypoxia → worsened ischemia → progressive dysfunction

• Systemic response: nitric oxide/cytokines, bleeding/transfusions, vasodilation → ↓ SVR

• Peripheral hypoperfusion → vasoconstriction and fluid retention

2. Staging (SCAI A–E)

• A: at risk; initiation (AMI or stunning) with reduced contractility/stroke volume

• B: beginning shock; tachycardia, vasoconstriction, fluid retention; maladaptive consequences

• C: classic shock; hypoperfusion and early end-organ dysfunction

• D: deteriorating; severe hypoperfusion with vasoplegia and refractory shock

• E: extremis; imminent circulatory collapse/cardiac arrest

• Importance: standardized communication, research, and rising in-hospital mortality across stages

3. Etiologies and Types

• Acute myocardial infarction (including mechanical complications)

• Myocarditis; stress-induced and toxin-mediated cardiomyopathy

• Acute on chronic heart failure progression

• Valvular dysfunction (acute or progressive)

• RV-predominant: acute PE, pulmonary hypertension exacerbation

• Tamponade; postcardiotomy

4. Initial Assessment and Golden Hour

• Resuscitate: ventilation/respiration; vasoconstrictors; inotropes; assess end-organ function

• Investigate: ECG, focused ultrasound, chest X-ray/CT, coronary angiography as indicated

• Reverse primary cause: PCI, thrombolysis for PE, pericardial drainage, structural interventions

• Triage: arterial line; consider PA catheter; evaluate for temporary mechanical circulatory support; ICU care; transfer to hub if needed; assess candidacy for durable LVAD or transplant

5. Vasoactive and Inotropic Therapy

• First-line vasopressor: norepinephrine (α with some β, inotropy)

• Add vasopressin for severe vasoplegia or mixed shock; epinephrine second line

• Inotropes: dobutamine for depressed LV; milrinone for elevated PA pressures/RV shock (can use with beta-blocker)

• Higher vasoactive medication use within 24 hours → higher in-hospital mortality across stages and etiologies

6. PA Catheter and Hemodynamics

• Use in cardiac ICU with mechanical circulatory support availability → lower in-hospital mortality

• Guides device selection; suggested unless absolute contraindications

• Key metrics: cardiac output/index; cardiac power output/index; SVR; RA/CVP; CVP:PCWP; PAPI; RV stroke work index; TPG; PVR

• Thresholds: low cardiac power output (severe LV); low PAPI (severe RV); elevated TPG after decongestion (pulmonary hypertension not purely left-sided)

7. Shock Team and Workflow

• Multidisciplinary team (heart failure, interventional, surgery, ICU, nursing, pharmacy, rehab, nephrology, ID)

• Presence of a shock team reduces mortality, especially in heart failure–related cardiogenic shock

• Follow pragmatic algorithm: early staging, early PA catheter, early transfer, early temporary mechanical support, defined exit strategy

8. Prognosis and Trajectory

• Three-axis model: severity/trajectory and metabolic derangement; patient factors (age, frailty, comorbidities, neurologic injury) and reversibility; exit strategy (recovery/LVAD/transplant/palliation) and phenotype (LV, RV, biventricular, vasodilation, congestion, respiratory failure)

• Post-ICU considerations: cognitive dysfunction, persistent organ dysfunction (oxygen/dialysis), psychological burden/PTSD, reduced mobility, family/social impact

9. Key Points

1. Cardiogenic shock is an expanding spiral requiring multi-point intervention

2. Higher SCAI stage and higher vasoactive use → higher in-hospital mortality

3. Etiologies extend beyond acute myocardial infarction

4. Golden hour: simultaneous resuscitation, investigation, reversal, and triage

5. PA catheter–guided care and a shock team improve outcomes

6. Always define and pursue an exit strategy