Cardiogenic shock (CS) is a state of critical end-organ hypoperfusion resulting from cardiac dysfunction, with short-term mortality exceeding 30–50% despite contemporary therapy. [1-2] The 2025 ACC Expert Consensus Statement uses the mnemonic "SUSPECT CS" to aid early recognition. [3] The SCAI staging system (A–E) classifies severity and guides escalation. [4]
The following figure illustrates the diverse etiologies of cardiogenic shock, including AMI-related, heart failure-related, secondary nonmyocardial, and postcardiotomy causes:
1. History
- Chest pain/pressure — timing, onset, radiation, prior episodes; relationship to exertion or rest
- Dyspnea — acute onset, orthopnea, paroxysmal nocturnal dyspnea, exercise tolerance at baseline
- Altered mentation — confusion, lethargy, syncope/near-syncope
- GI symptoms — nausea, vomiting, abdominal pain, early satiety (reflect mesenteric hypoperfusion) [3]
- Decreased urine output — patient or nursing report of oliguria
- Timing and triggers — preceding ACS symptoms, recent cardiac surgery, medication nonadherence, infection, arrhythmia
- Progression — rapid vs insidious; shock at presentation vs delayed onset (median ~6 hours post-AMI in the SHOCK registry) [5]
- Important negatives — fever/chills (sepsis), trauma, hemorrhage, recent procedures, drug ingestion
2. Alarm Features
- SBP <90 mmHg (or MAP <65 mmHg) for >30 minutes, or >30 mmHg drop from baseline [3]
- Narrow pulse pressure (<25% of SBP) — indicates reduced cardiac output [3][5]
- Altered mental status, cold/mottled/cyanotic extremities, prolonged capillary refill >2 seconds [3]
- Oliguria <30 mL/h (<0.5 mL/kg/h) [3]
- Lactate >2 mmol/L, worsening metabolic acidosis (pH <7.2) [2-3]
- Signs of mechanical complication — new harsh systolic murmur (VSD, papillary muscle rupture), muffled heart sounds/pulsus paradoxus (tamponade) [6]
- Refractory arrhythmias — recurrent VT/VF, PEA (SCAI Stage E) [7]
- Escalating vasopressor requirements — signals transition from SCAI C → D [7]
3. Medications
Vasopressors
- Norepinephrine — first-line vasopressor for most CS patients; 0.05–1 μg/kg/min. Lower arrhythmia risk than dopamine (SOAP II trial) [2-4]
- Dopamine — alternative if bradycardia contributes; associated with more tachyarrhythmias [2][5]
- Epinephrine — use with caution; OPTIMA-CC trial terminated early due to higher refractory shock (37% vs 7%) [4]
- Vasopressin — may be useful in tachycardic patients or pulmonary hypertension; limited CS-specific data [8]
- Phenylephrine — strongly discouraged as sole agent in CS (reflex bradycardia, reduced CO) [3]
Inotropes
- Dobutamine — most commonly used inodilator; 2–20 μg/kg/min [3][5]
- Milrinone — PDE-3 inhibitor; no difference vs dobutamine in DOREMI trial; use cautiously in renal dysfunction (renally cleared, long half-life) [3-5]
Contraindicated/Caution
- Avoid beta-blockers, calcium channel blockers (non-DHP), and other negative inotropes in acute CS
- Minimize catecholamine doses to lowest effective dose to reduce myocardial oxygen demand and arrhythmia risk [4]
- Inodilators (dobutamine, milrinone) may worsen hypotension if used without vasopressor support
Congestion management: IV loop diuretics ± thiazide augmentation; renal replacement therapy if refractory [3]
4. Diet
- NPO initially — anticipate potential intubation, catheterization, or surgical intervention
- Fluid management is critical — avoid empiric large-volume resuscitation; cautious volume assessment (unlike septic shock, most CS patients are euvolemic or volume-overloaded) [7][9]
- Sodium and fluid restriction once stabilized in HF-related CS
- Nutritional support in prolonged ICU stays per standard critical care protocols
5. Review of Systems
- Cardiovascular — chest pain, palpitations, syncope, leg swelling, prior HF symptoms
- Pulmonary — dyspnea, orthopnea, PND, cough with pink frothy sputum
- Neurologic — confusion, altered mentation, focal deficits (embolic event)
- Renal — decreased urine output, dark urine
- GI — nausea, vomiting, abdominal pain, anorexia (mesenteric ischemia) [3]
- Extremities — cold hands/feet, color changes, pain (limb ischemia if MCS in place)
- Hematologic — bleeding, bruising (coagulopathy, DIC in advanced shock)
6. Collateral History and Family History
- Medication adherence — particularly in chronic HF patients (common precipitant of HF-CS) [6]
- Prior cardiac history — known EF, prior MI, prior interventions (PCI, CABG, valve surgery)
- Substance use — cocaine, methamphetamine (can cause acute MI or cardiomyopathy)
- Recent illness — viral prodrome (myocarditis), peripartum status
- Family history — premature CAD, cardiomyopathy (HCM, DCM), sudden cardiac death
- Goals of care/advance directives — critical to establish early given high mortality [9]
7. Risk Factors
- AMI-CS: Large anterior STEMI (LAD/left main), multivessel CAD (53% had 3-vessel disease in SHOCK trial), delayed reperfusion, older age, diabetes, prior MI, female sex [5][10]
- HF-CS: Chronic HF with reduced EF, medication nonadherence, acute-on-chronic decompensation, de novo cardiomyopathy [4][9]
- General: Advanced age (>75 years — CS in >10% of AMI patients), frailty (71% of AMI-CS patients), renal dysfunction, prior cardiac surgery [2][9]
- Comorbidities: Diabetes, hypertension, peripheral vascular disease, chronic kidney disease
- Elevated admission glucose (even in non-diabetics) is associated with increased CS risk [11]
8. Differential Diagnosis
- Septic shock — warm extremities (early), fever, leukocytosis, low SVR; may coexist as "mixed shock" [2]
- Hypovolemic shock — hemorrhage, dehydration; low CVP, flat IVC on ultrasound
- Obstructive shock — massive PE, tension pneumothorax, cardiac tamponade (may overlap with CS)
- Distributive shock — anaphylaxis, adrenal crisis, neurogenic shock
- Mixed shock — cardiogenic + septic or other etiology; common and associated with highest mortality (48%) [2]
- Mechanical complications of MI — VSD, free wall rupture, papillary muscle rupture (distinguish from primary pump failure) [6]
- Aortic dissection — may mimic or cause CS; chest x-ray, CT angiography
- Takotsubo cardiomyopathy — apical ballooning, often post-emotional/physical stress
Hemodynamic profiling via PA catheter helps distinguish: CS shows low CI (≤2.2), high PCWP (>15 mmHg), high SVR vs septic shock (high CI, low SVR) [2][7]
9. Past Medical History
- Prior MI, PCI, CABG, valve surgery
- Known cardiomyopathy and baseline LVEF
- Chronic HF (NYHA class, prior hospitalizations, ICD/CRT)
- Cardiac arrest history
- Peripheral vascular disease (impacts MCS access site selection)
- Chronic kidney disease (affects milrinone clearance, contrast decisions)
- Prior cardiac surgery (impacts postcardiotomy CS risk)
10. Physical Exam
Vital signs
- Hypotension: SBP <90 mmHg or MAP <65 mmHg [2-3]
- Tachycardia: HR >100 bpm (compensatory); bradycardia may indicate high-grade AV block
- Narrow pulse pressure (<25% of SBP) [3][5]
- Tachypnea, hypoxemia
Focused exam
- General: Diaphoretic, ashen, anxious, altered mentation
- Neck: Elevated JVP (RV failure, biventricular failure, tamponade); Kussmaul sign (RV infarct, tamponade)
- Lungs: Rales/crackles (pulmonary edema); may be clear in isolated RV failure
- Heart: S3 gallop, new murmur (MR from papillary muscle dysfunction, VSD), muffled sounds (tamponade)
- Abdomen: Hepatomegaly, pulsatile liver (tricuspid regurgitation), ascites
- Extremities: Cold, clammy, mottled, livedo reticularis, weak/absent pulses, capillary refill >2 seconds [3][5]
- Urine output: Foley catheter — monitor hourly; <30 mL/h is concerning [3]
11. Lab Studies
Immediate
- Lactate (arterial or venous) — >2 mmol/L indicates hypoperfusion; serial trending is essential [2-3]
- High-sensitivity troponin — assess for myocardial injury/infarction [3]
- BNP/NT-proBNP — elevated in HF-related CS [3][7]
- Comprehensive metabolic panel — creatinine (≥2× ULN), BUN, electrolytes, glucose
- Hepatic panel — ALT >200 U/L or >3× ULN indicates shock liver [3]
- ABG/VBG — pH <7.2, metabolic acidosis [3]
- CBC — anemia (worsens O₂ delivery), thrombocytopenia (DIC, MCS-related)
- Coagulation studies — PT/INR, fibrinogen (DIC screening)
- Central venous oxygen saturation (ScvO₂) — low in CS (increased extraction) [3]
Monitoring
- Serial lactate clearance as a marker of treatment response [9][12]
- Serial renal and hepatic function
- Serum sodium (hyponatremia portends worse prognosis)
12. Imaging
First-line
- Bedside echocardiography/POCUS — mandatory in all suspected CS; assess biventricular function, wall motion abnormalities, valvular pathology, pericardial effusion, mechanical complications [3][5-6]
- Chest x-ray — pulmonary edema, cardiomegaly, device positioning, rule out pneumothorax/aortic dissection [6]
Additional
- CT angiography — if PE or aortic dissection suspected
- Coronary angiography — urgent/emergent if AMI suspected (ST elevation or high clinical suspicion) [3][5]
- Transesophageal echocardiography — when TTE images are inadequate or mechanical complication suspected [6]
When imaging is unnecessary: Routine CT chest is not needed if echocardiography and clinical picture are diagnostic
13. Special Tests
Scoring systems
- SCAI Shock Classification (A–E) — standardized severity staging; higher stages correlate with higher mortality [4]
- CLIP Score (cystatin C, lactate, IL-6, BNP) — predicts 30-day mortality in AMI-CS; C-statistic 0.82 [5]
- IABP-SHOCK II risk score — clinical risk model for AMI-CS
- Cardiac Power Output (CPO) = (CO × MAP)/451; <0.6 W indicates severe CS [7]
- Shock Index = HR/SBP; >1.0 is concerning [7]
- PAPi (Pulmonary Artery Pulsatility Index) = (PASP − PADP)/CVP; <1.0 suggests RV shock [7]
Invasive hemodynamics
- Pulmonary artery catheter — may be considered (Class 2b) to define hemodynamic subsets (LV vs RV vs BiV), guide therapy, and assess response [2][7]
- Key parameters: CI, PCWP, CVP, SVR, CPO, PAPi
Point-of-care
- Bedside ultrasound (IVC assessment, lung B-lines, cardiac function)
- Point-of-care lactate
The SCAI staging system is shown in the following figure:
14. ECG
Every patient with suspected CS should have a 12-lead ECG performed immediately. [3]
- ST-segment elevation — STEMI requiring emergent catheterization/revascularization [3]
- ST depression, T-wave inversions — NSTEMI, ongoing ischemia
- New LBBB — may represent acute MI equivalent
- Sinus tachycardia — most common rhythm in CS
- Bradyarrhythmias — high-grade AV block (especially inferior MI with RV involvement)
- Ventricular tachycardia/fibrillation — SCAI Stage E [7]
- Low voltage — consider tamponade, large effusion
- RV strain pattern (S1Q3T3, right axis, RV strain in V1–V4) — massive PE
- Diffuse ST elevation with PR depression — myocarditis/pericarditis
- QTc prolongation — monitor during inotrope/vasopressor use
15. Assessment
Definition: CS is a cardiac disorder resulting in both clinical and biochemical evidence of sustained tissue hypoperfusion, defined by SBP <90 mmHg for >30 minutes (or need for vasoactive support) plus end-organ hypoperfusion. [2][4]
Severity stratification per SCAI stages: [4][7]
- Stage A — At risk (e.g., large MI, known HF); normotensive, normal perfusion
- Stage B — Beginning/pre-shock; hypotension without hypoperfusion
- Stage C — Classic CS; hypotension + hypoperfusion (cold, oliguric, elevated lactate)
- Stage D — Deteriorating; worsening despite initial interventions
- Stage E — Extremis; cardiac arrest, refractory VT/VF, PEA
Etiologic classification: [2-4]
- AMI-CS (~30% of contemporary cases)
- HF-CS (~46%, now the most common)
- Secondary CS (arrhythmias, valvular, pericardial)
- Postcardiotomy CS
Mortality: 30-day mortality ~40% for AMI-CS; in-hospital mortality ranges from 25% (acute-on-chronic HF) to 48% (mixed-cause CS) [2][5]
Normotensive CS — end-organ hypoperfusion despite SBP >90 mmHg; associated with increased mortality and must not be missed [2][5]
16. Treatment Plan
Initial stabilization (ED/ICU)
- ABCs — secure airway if respiratory failure; avoid excessive positive pressure ventilation (reduces preload)
- IV access — large-bore peripheral + central venous catheter; arterial line for continuous BP monitoring
- Cautious volume assessment — small fluid bolus (250 mL) only if no signs of congestion; avoid large-volume resuscitation [7][9]
Pharmacotherapy
- Norepinephrine 0.05–1 μg/kg/min as first-line vasopressor; target MAP >65 mmHg [2-4][14]
- Add dobutamine (2–20 μg/kg/min) or milrinone if persistent hypoperfusion despite adequate MAP [3][5]
- Titrate to lowest effective dose; monitor for arrhythmias and worsening ischemia [4][15]
- Diuretics for congestive phenotype [3]
Cause-specific treatment
- AMI-CS: Emergent coronary angiography and culprit-vessel PCI (Class I recommendation; only therapy with RCT-proven mortality benefit). Culprit-only PCI preferred over immediate multivessel PCI per CULPRIT-SHOCK trial [5]
- Mechanical complications: Emergent surgical consultation (VSD repair, mitral valve surgery, free wall rupture)
- Arrhythmia-driven: Cardioversion, antiarrhythmics, temporary pacing
- Tamponade: Emergent pericardiocentesis
- Massive PE: Systemic thrombolysis, catheter-directed therapy, or surgical embolectomy
Mechanical circulatory support (MCS)
- Indicated when pharmacologic support is inadequate (Class 2a) [7]
- Device selection based on ventricular phenotype (LV vs RV vs BiV) and shock severity [3][16-17]
- IABP — limited evidence in AMI-CS (IABP-SHOCK II showed no mortality benefit); may be considered in non-AMI CS [4]
- Impella — percutaneous LV support; DanGer Shock trial showed benefit in selected LV-dominant AMI-CS patients [2]
- VA-ECMO — most potent device; no survival benefit with routine use in AMI-CS per patient-level meta-analysis of 4 RCTs; may be useful as bridge strategy [4]
- Absolute contraindications to tMCS: Irreversible cardiac failure without exit strategy, irreversible noncardiac organ failure (severe anoxic brain injury, terminal illness) [18]
The following figure summarizes pharmacologic and mechanical support strategies:
Multidisciplinary shock team activation is recommended (Class 2a) [7][12]
17. Disposition
- All patients with CS require ICU admission — preferably a cardiovascular-specific ICU [9]
- Transfer criteria: Patients at Level 2/3 CS centers who are refractory to initial pharmacologic therapy should be transferred to a Level 1 CS center with tMCS and advanced HF capabilities [3][7]
- Shock team activation should occur early, including interventional cardiology, cardiac surgery, advanced HF, and critical care [7][12]
- Observation is not appropriate — CS is never an observation-level diagnosis
- Specialist consultation triggers: Interventional cardiology (AMI), cardiac surgery (mechanical complications, CABG candidacy), advanced HF (durable LVAD/transplant evaluation), palliative care (goals of care in refractory shock) [9][18]
18. Follow Up / Return Precautions
For survivors of CS
- Close cardiology follow-up within 1–2 weeks of discharge
- Reassess LVEF at 4–6 weeks (potential for recovery)
- Optimize guideline-directed medical therapy for HF (ACEi/ARNi, beta-blocker, MRA, SGLT2i) as tolerated
- Cardiac rehabilitation referral
- ICD evaluation if EF remains ≤35% after ≥40 days post-MI or ≥3 months of optimal medical therapy
- Assess for advanced HF therapies (LVAD, transplant) if no recovery
Return precautions (patient counseling)
- Return immediately for recurrent chest pain, worsening dyspnea, syncope, palpitations, decreased urine output, or confusion
- Daily weight monitoring; report weight gain >2–3 lbs in 24 hours
- Strict medication adherence; do not stop cardiac medications without physician guidance
Expected course: Recovery is variable; some patients recover ventricular function (especially myocarditis, Takotsubo), while others progress to advanced HF requiring durable MCS or transplant. Overall 1-year mortality approaches 50% for AMI-CS. [5]
References
1. Advances in the Management of Cardiogenic Shock. — Jentzer JC, Pöss J, Schaubroeck H, et al. Critical Care Medicine. 2023.
2. Cardiogenic Shock. — Thiele H, Hassager C. The New England Journal of Medicine. 2026.
3. 2025 Concise Clinical Guidance: An ACC Expert Consensus Statement on the Evaluation and Management of Cardiogenic Shock: A Report of the American College of Cardiology Solution Set Oversight Committee. — Sinha SS, Morrow DA, Kapur NK, Kataria R, Roswell RO. Journal of the American College of Cardiology. 2025.
4. Cardiogenic Shock. — Lüsebrink E, Binzenhöfer L, Adamo M, et al. Lancet. 2024.
5. Cardiogenic Shock After Acute Myocardial Infarction: A Review. — Samsky MD, Morrow DA, Proudfoot AG, et al. The Journal of the American Medical Association. 2021.
6. Contemporary Management of Cardiogenic Shock: A Scientific Statement From the American Heart Association. — van Diepen S, Katz JN, Albert NM, et al. Circulation. 2017.
7. 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. — Heidenreich PA, Bozkurt B, Aguilar D, et al. Journal of the American College of Cardiology. 2022.
8. The Medical Treatment of Cardiogenic Shock: Cardiovascular Drugs. — De Backer D, Arias Ortiz J, Levy B. Current Opinion in Critical Care. 2021.
9. Cardiogenic Shock in Older Adults: A Focus on Age-Associated Risks and Approach to Management: A Scientific Statement From the American Heart Association. — Blumer V, Kanwar MK, Barnett CF, et al. Circulation. 2024.
10. Acute Myocardial Infarction in Women: A Scientific Statement From the American Heart Association. — Mehta LS, Beckie TM, DeVon HA, et al. Circulation. 2016.
11. Elevated random glucose levels at admission are associated with all‐cause mortality and cardiogenic shock during hospitalisation in patients with acute myocardial infarction and without diabetes: A retrospective cohort study. — Yuan Y, Tao J, Shen X, et al. Diabetes/Metabolism Research and Reviews. 2023.
12. Current Perspectives in Cardiogenic Shock. — Es-Saad O, Ng W, Messina A, Chew MS. Journal of Critical Care. 2026.
13. Cardiogenic Shock. — Koji Takeda, Lucas Witer, and Hiroo Takayama Transplantation and Mechanical Support for End‐Stage Heart and Lung Disease. 2023.
14. Invasive Management of Acute Myocardial Infarction Complicated by Cardiogenic Shock: A Scientific Statement From the American Heart Association. — Henry TD, Tomey MI, Tamis-Holland JE, et al. Circulation. 2021.
15. Prevention of Complications in the Cardiac Intensive Care Unit: A Scientific Statement From the American Heart Association. — Fordyce CB, Katz JN, Alviar CL, et al. Circulation. 2020.
16. Management of Heart Failure-Related Cardiogenic Shock: Practical Guidance for Clinicians. — Narang N, Blumer V, Jumean MF, et al. JACC. Heart Failure. 2023.
17. A Standardized and Comprehensive Approach to the Management of Cardiogenic Shock. — Tehrani BN, Truesdell AG, Psotka MA, et al. JACC. Heart Failure. 2020.
18. Escalating and De-Escalating Temporary Mechanical Circulatory Support in Cardiogenic Shock: A Scientific Statement From the American Heart Association. — Geller BJ, Sinha SS, Kapur NK, et al. Circulation. 2022.