01Approach to the Critical Patient/attcp63

Immediate recognition and stabilization

›SUSPECT CS mnemonic triggers (2025 ACC Expert Consensus)

›SBP <90 mmHg or MAP <65 mmHg for >30 minutes

›Or >30 mmHg drop from baseline requiring vasoactive support

›Normotensive CS possible with end-organ hypoperfusion despite SBP >90 mmHg

›Cold, mottled, or cyanotic extremities

›Capillary refill >2 seconds

›Livedo reticularis

›Altered mentation

›Confusion, agitation, or obtundation

›Decreased GCS

›Oliguria <30 mL/h (<0.5 mL/kg/h)

›Foley catheter immediately for hourly monitoring

›Lactate >2 mmol/L

›Worsening metabolic acidosis pH <7.2

›Airway and breathing priorities

›Oxygenation failure requiring escalation

›High-flow oxygen initially; titrate to SpO2 >=94%

›Intubation if respiratory failure or airway unprotected

›If intubation required, anticipate hemodynamic deterioration

›Minimize sedation doses (ketamine preferred for induction in hypotension)

›Avoid excessive PEEP (reduces preload)

›Avoid NIV as primary strategy in cardiogenic pulmonary edema with shock

›Hemodynamic monitoring targets

›Arterial line placement for continuous BP monitoring

›Essential for vasopressor titration

›Avoids cuff inaccuracy in shock

›Central venous catheter for vasopressor and CVP monitoring

›Large-bore peripheral access if central line not yet secured

›Target MAP >65 mmHg

›Higher targets (>70 mmHg) may be needed in chronic hypertension

›Serial lactate every 1-2 hours until clearance trend established

Key decision points and escalation triggers

›SCAI staging guides escalation (A to E)

›Stage C (classic CS): hypotension plus hypoperfusion, cold and oliguric

›Initiate vasopressors and inotropes

›Emergent cardiology consultation

›Stage D (deteriorating): worsening despite initial therapy

›Mechanical circulatory support (MCS) activation

›Transfer to Level 1 CS center if not already there

›Stage E (extremis): cardiac arrest, refractory VT/VF, PEA

›VA-ECMO consideration if appropriate candidate

›Shock team activation immediately

›Cause-specific emergent intervention triggers

›STEMI with CS: emergent coronary angiography and culprit-vessel PCI

›Class I recommendation; only RCT-proven mortality benefit

›Culprit-only PCI preferred per CULPRIT-SHOCK trial

›New harsh systolic murmur: mechanical complication

›VSD, papillary muscle rupture, or free wall rupture

›Emergent surgical consultation

›Muffled heart sounds and pulsus paradoxus: tamponade

›Emergent pericardiocentesis

›Massive PE with CS: systemic thrombolysis or catheter-directed therapy

›Shock team activation (Class 2a recommendation)

›Interventional cardiology, cardiac surgery, advanced HF, critical care

›Early multidisciplinary approach associated with improved outcomes

›Standardized protocol reduces time to MCS if needed

Volume management

›Cautious fluid approach

›Most CS patients are euvolemic or volume-overloaded

›Avoid empiric large-volume resuscitation unlike septic shock

›Small fluid challenge 250 mL only if signs of hypovolemia present

›IVC ultrasound and clinical assessment before fluid

›Flat IVC suggests hypovolemia; plethoric IVC suggests overload

›If pulmonary edema present, diuresis not fluid resuscitation

›IV furosemide 40-80 mg IV bolus; titrate to urine output

02History/hx60

Presenting symptoms

›Cardiovascular symptoms

›Chest pain or pressure

›Onset, duration, radiation to arm or jaw

›Prior episodes or known CAD

›Palpitations

›Rapid, irregular, or slow rhythm symptoms

›Syncope or near-syncope

›Dyspnea

›Acute onset vs progressive worsening

›Orthopnea and paroxysmal nocturnal dyspnea

›Hypoperfusion symptoms

›Altered mentation

›Confusion, lethargy, or agitation

›Decreased urine output

›Patient or nursing-reported oliguria

›GI symptoms reflecting mesenteric hypoperfusion

›Nausea, vomiting, abdominal pain

›Early satiety, anorexia

Temporal pattern and precipitants

›Onset and progression

›Shock at presentation vs delayed onset

›Median ~6 hours post-AMI in SHOCK registry

›Insidious vs rapid deterioration

›Preceding ACS symptoms

›Hours to days of angina before hemodynamic collapse

›Recent triggers

›Medication nonadherence (common precipitant of HF-CS)

03Physical Exam/exam49

Vital signs

›Hemodynamic snapshot

›SBP <90 mmHg or MAP <65 mmHg defining threshold

›Or >30 mmHg drop from baseline

›Narrow pulse pressure (<25% of SBP) indicating low cardiac output

›Heart rate

›Tachycardia >100 bpm (compensatory)

›Bradycardia suggests high-grade AV block (inferior MI/RV involvement)

›Respiratory rate and oxygen saturation

›Tachypnea and hypoxemia indicating pulmonary edema

Perfusion and volume assessment

›Peripheral perfusion signs

›Extremity temperature and color

›Cold, clammy, mottled, or cyanotic

›Livedo reticularis in severe shock

›Capillary refill time

›>2 seconds indicates impaired perfusion

›Pulse character

›Weak or absent peripheral pulses

›Pulsus alternans in severe LV dysfunction

›Volume status signs

›Jugular venous pressure elevation

›RV failure, biventricular failure, or tamponade

›Kussmaul sign suggests RV infarct or tamponade

›Peripheral edema (chronic HF)

›Pulmonary edema signs

›Bilateral basilar crackles or rales

›May be absent in isolated RV failure

04Differential Diagnosis/ddx39

Life-threatening shock mimics

›Septic shock

›ICD-10 A41.9

›Warm extremities (early), fever, leukocytosis, low SVR

›May coexist as mixed shock (highest mortality subset, 48%)

›PA catheter differentiates: CS shows low CI and high SVR; sepsis shows high CI and low SVR

›Obstructive shock

›Massive PE (ICD-10 I26.01)

›RV strain pattern on ECG, pleuritic chest pain

›CT-PA or POCUS RV dilation

›Cardiac tamponade (ICD-10 I31.9)

›Beck triad: hypotension, JVP elevation, muffled sounds

›POCUS effusion with chamber collapse

›Tension pneumothorax

›Absent breath sounds, tracheal deviation

›Hypovolemic shock

›ICD-10 R57.1

›Hemorrhage, dehydration; low CVP, flat IVC on ultrasound

CS subtypes and mechanical complications

›AMI-CS

›ICD-10 I21.A9, I21.0, I21.4

›Most commonly LAD-territory STEMI

›~30% of contemporary CS cases

›30-day mortality ~40%

›HF-CS (decompensated heart failure)

›ICD-10 I50.9

›Most common etiology (~46% of CS)

›Acute-on-chronic or de novo

05Laboratory Tests/lt47

Perfusion and organ function markers

›Lactate (arterial or venous)

›>2 mmol/L indicates tissue hypoperfusion

›Serial trending essential for treatment response

›Lactate clearance target >10% per hour

›>4 mmol/L associated with very high mortality

›Comprehensive metabolic panel

›Creatinine (>=2x ULN indicates shock kidney)

›BUN, electrolytes, glucose

›Hyponatremia portends worse prognosis

›Hepatic panel

›ALT >200 U/L or >3x ULN indicates shock liver

›Bilirubin elevation in hepatic hypoperfusion

›Central venous oxygen saturation (ScvO2)

›Low in CS (increased O2 extraction to compensate for low delivery)

›ScvO2 <65% consistent with CS hemodynamic profile

›Helps distinguish from septic shock (ScvO2 high or normal)

Cardiac biomarkers

›High-sensitivity troponin

›Elevated in AMI-CS; serial values for delta assessment

›Magnitude correlates with infarct size

›Also elevated in myocarditis and demand ischemia

›BNP or NT-proBNP

›Elevated in HF-related CS

›Severity of CS correlates with degree of elevation

›Serial values guide diuresis response

›Cardiac Power Output (CPO) via PA catheter

›CPO = (CO x MAP) / 451

06Diagnostic Tests/dt82

Scoring Systems

›SCAI Shock Classification (A to E)

›Standardized severity staging system

›Stage A: At risk (large MI, known HF); normotensive, normal perfusion

›Stage B: Beginning/pre-shock; hypotension without hypoperfusion markers

›Stage C: Classic CS; hypotension plus hypoperfusion

›Stage D: Deteriorating; worsening despite initial interventions

›Stage E: Extremis; cardiac arrest, refractory VT/VF, PEA

›Higher stages correlate with higher in-hospital mortality

›Stage C ~30%, Stage D ~40-50%, Stage E >60%

›Cardiac Power Output (CPO)

›CPO = (CO x MAP) / 451

›<0.6 W indicates severe CS; strongest hemodynamic mortality predictor

›Used to guide MCS device selection and escalation

›PAPi (Pulmonary Artery Pulsatility Index)

›PAPi = (PASP - PADP) / CVP

›<1.0 suggests RV dominant shock

›Guides RV-specific MCS device selection (Impella RP, RVAD)

›IABP-SHOCK II Risk Score

›Clinical risk model for AMI-CS

›Variables: age, glucose, creatinine, TIMI flow, lactate, prior resuscitation

›Stratifies low, intermediate, and high mortality risk

›Shock Index

›HR / SBP

›>1.0 is concerning for hemodynamic compromise

›Simple bedside screening tool

MRI

›Cardiac MRI role in CS

›Not a first-line investigation in acute CS

›Hemodynamic instability and monitoring equipment are absolute barriers

›Access, time, and patient tolerance are limiting factors

›Post-stabilization or subacute phase indications

›Myocarditis characterization (T2 edema, late gadolinium enhancement)

›Takotsubo vs myocarditis differentiation

›Viability assessment post-AMI before revascularization decisions

›Contraindications

›Unstable patient requiring continuous monitoring

›MCS devices (Impella, IABP) not MRI-compatible

›Non-MRI-compatible ICDs or pacemakers

CT

›CT coronary angiography

›Not preferred in AMI-CS (invasive angiography preferred for simultaneous PCI)

›May be considered if pre-test probability of CAD is intermediate

›Radiation and contrast limitations apply

›CT pulmonary angiography

›Indicated when massive PE is in differential diagnosis

›Sensitivity ~95%, specificity ~98% for PE

›RV-to-LV ratio >0.9 on CT indicates hemodynamically significant PE

›Risk-benefit in hemodynamically unstable patient

›POCUS may be faster and safer initial step

›CT aorta

›Indicated when aortic dissection suspected

›Aortic dissection may cause CS via coronary involvement (Type A)

›Sensitivity and specificity >98% for dissection

›Contrast and renal function considerations

›CT chest without contrast

›Pulmonary edema and cardiomegaly confirmation

›Pneumonia or effusion as precipitant

›Pneumothorax exclusion if post-procedure

Ultrasound

›Bedside echocardiography/POCUS (mandatory in all suspected CS)

›LV function assessment

›Global systolic dysfunction (low EF) vs regional wall motion abnormality

›Estimated EF guides inotrope vs vasopressor emphasis

›RV function assessment

›RV dilation, RV/LV ratio >0.9 suggests RV failure or PE

›Septal flattening (D-sign) in RV pressure overload

›Valvular pathology

›Severe MR (papillary muscle dysfunction or rupture)

›VSD visualization with color Doppler

›Aortic stenosis or regurgitation contributing

›Pericardial effusion

›Tamponade physiology: chamber collapse, IVC plethora, respiratory variation

›IVC assessment

›Plethoric non-collapsing IVC suggests RV overload or tamponade

›Collapsible IVC may indicate relative hypovolemia

›Lung ultrasound

›B-lines (comet tails)

›Bilateral diffuse B-lines indicate cardiogenic pulmonary edema

›More sensitive than CXR for interstitial edema

›Pleural effusion identification

›Guides thoracentesis when infection precipitant suspected

›Transesophageal echocardiography (TEE)

›When TTE images are inadequate

›Mechanical complications suspected but not visualized on TTE

›Intraoperative guidance for mechanical complication repair

07Disposition/dispo27

Immediate disposition

›All CS patients require ICU admission

›Cardiovascular-specific ICU preferred

›Expertise in MCS management and invasive hemodynamics

›Never an observation-level or step-down diagnosis

›ED resuscitation bay until ICU bed available

›Continuous monitoring mandatory during transfer

Transfer criteria

›Transfer to Level 1 CS center

›CS refractory to initial pharmacologic therapy at Level 2/3 center

›Level 1 centers have tMCS capabilities (Impella, VA-ECMO, RVAD)

›Advanced HF program (durable LVAD, transplant evaluation)

›Transfer timing

›Stabilize on vasopressors/inotropes before transport

›IABP may be placed as bridge to transfer

›Communication with receiving center

›Cath lab activation and shock team pre-notification

Specialist consultation triggers

›Interventional cardiology

›AMI-CS with STEMI or high clinical suspicion for ACS

›Cath lab activation immediately

›Cardiac surgery

›Mechanical complications (VSD, free wall rupture, papillary muscle rupture)

›Postcardiotomy CS

›Advanced heart failure team

›Durable LVAD or cardiac transplant evaluation

›Acute bridge decisions

›Palliative care

08Treatment/t98

Vasopressor therapy

›Norepinephrine (first-line vasopressor)

›Dose 0.05-1 mcg/kg/min IV infusion

›Start at 0.05-0.1 mcg/kg/min; titrate to MAP >65 mmHg

›Lower arrhythmia risk than dopamine (SOAP II trial)

›Preferred over dopamine in CS (Class 2a recommendation)

›Monitoring

›Continuous arterial line

›Heart rate and arrhythmia surveillance

›Vasopressin

›Dose 0.01-0.04 units/min fixed dose

›Useful in tachycardic patients or pulmonary hypertension

›Norepinephrine-sparing effect; limited CS-specific trial data

›Dopamine (alternative only)

›Dose 5-20 mcg/kg/min

›Associated with more tachyarrhythmias than norepinephrine

›Consider only if bradycardia is contributing to CS

›Avoid phenylephrine as sole agent

›Causes reflex bradycardia and reduces cardiac output

›Strongly discouraged in CS

Inotropic therapy

›Dobutamine (most commonly used inodilator)

›Dose 2-20 mcg/kg/min IV infusion

›Titrate to clinical response (urine output, lactate clearance, MAP)

›Risk of hypotension if used without vasopressor support

›Risk of arrhythmia with higher doses

›Dose equivalence with milrinone (DOREMI trial: no significant difference in outcomes)

›Class 2b recommendation for inotrope use in CS

›Milrinone (PDE-3 inhibitor alternative)

›Dose 0.375-0.75 mcg/kg/min IV infusion (no loading bolus in CS)

›Use cautiously in renal dysfunction (renally cleared, long half-life)

›May cause more hypotension than dobutamine

›Preferred by some in post-cardiac surgery or RV failure context

›Epinephrine (use with caution)

›Dose 0.01-0.5 mcg/kg/min

›OPTIMA-CC trial terminated early due to higher refractory shock (37% vs 7%)

›Higher rate of lactic acidosis masking true resuscitation response

›Reserve for refractory CS or bridge to MCS

›Minimize catecholamine doses to lowest effective

›Reduces myocardial O2 demand and arrhythmia risk

›Wean as hemodynamics allow (de-escalation protocol)

Congestion management

›IV loop diuretics

›Furosemide 40-80 mg IV bolus; repeat or infuse as needed

›Target urine output 0.5-1 mL/kg/h

›Monitor electrolytes (K+, Mg2+) with aggressive diuresis

›Thiazide augmentation for loop-diuretic resistance

›Metolazone 2.5-5 mg PO 30 minutes before furosemide

›Renal replacement therapy

›Refractory fluid overload with oliguria

›CRRT preferred in hemodynamically unstable patients

Cause-specific treatment

›AMI-CS: emergent PCI

›Culprit-only PCI preferred (CULPRIT-SHOCK trial)

›Immediate multivessel PCI associated with worse 30-day mortality and renal failure

›Class I recommendation; only therapy with RCT-proven mortality benefit

›Timing: <120 minutes from first medical contact for STEMI-CS

›Mechanical complications

›VSD: emergent surgical repair; bridge with IABP and inotropes

›Catheter-based closure devices in selected cases

›Papillary muscle rupture with severe MR: emergent mitral valve surgery

›Free wall rupture: emergent surgical repair; pericardiocentesis if tamponade bridge

›Arrhythmia-driven CS

›Cardioversion for sustained VT/VF

›Temporary transvenous pacing for high-grade AV block

›Antiarrhythmics (amiodarone 150 mg IV bolus then 1 mg/min infusion) for VT storm

›Tamponade: emergent pericardiocentesis

›Ultrasound-guided preferred

›Surgical drainage if recurrent or loculated

Mechanical circulatory support (MCS)

›Indication: pharmacologic support inadequate (Class 2a)

›Device selection based on ventricular phenotype and shock severity

›LV-dominant CS: Impella CP or 5.5

›RV-dominant CS: Impella RP or temporary RVAD

›Biventricular CS or cardiac arrest: VA-ECMO

›IABP (intra-aortic balloon pump)

›Limited evidence in AMI-CS (IABP-SHOCK II: no mortality benefit)

›May be considered in non-AMI CS or as bridge to transfer

›Reduces LV afterload and improves coronary perfusion

›Impella (percutaneous LV assist device)

›DanGer Shock trial: mortality benefit in selected LV-dominant AMI-CS patients

›Improves CI and reduces PCWP

›Access site complications and hemolysis require monitoring

›VA-ECMO

›Most potent device; provides full cardiopulmonary bypass

›No survival benefit with routine use in AMI-CS (patient-level meta-analysis of 4 RCTs)

›LV distension risk (increased afterload); may require LV venting

›Bridge strategy in refractory shock or cardiac arrest

›Absolute contraindications to temporary MCS

›Irreversible cardiac failure without exit strategy

›No bridge to transplant, LVAD, or recovery possible

›Irreversible non-cardiac organ failure

›Severe anoxic brain injury, terminal illness

Adjunct and anticoagulation

›Anticoagulation during MCS

›UFH infusion for Impella or VA-ECMO

›Target ACT 160-180 seconds for Impella

›Target ACT 180-220 seconds for VA-ECMO

›Antiplatelet therapy in AMI-CS

›Aspirin 325 mg loading dose (chewed) if no contraindication

›P2Y12 inhibitor (ticagrelor or prasugrel) after PCI when hemostasis adequate

›Glycemic control

›Target glucose 7.8-10 mmol/L

›Insulin infusion in ICU for persistent hyperglycemia

09Special Populations/sp78

Pregnancy

›Unique CS etiologies in pregnancy

›Peripartum cardiomyopathy (PPCM)

›Occurs in final month of pregnancy to 5 months postpartum

›LVEF typically <45%; frequently recovers with treatment

›Bromocriptine therapy may be considered postpartum (inhibits prolactin)

›Amniotic fluid embolism

›Sudden cardiovascular collapse during labor or delivery

›Acute DIC common co-occurrence

›Acute MI in pregnancy

›Coronary artery dissection more common than atherosclerotic AMI

›Hemodynamic considerations

›Normal pregnancy: increased plasma volume, lower SVR, higher CO

›BP thresholds for CS differ from non-pregnant

›Aortocaval compression in supine position: left lateral tilt

›Vasopressors

›Norepinephrine is first-line in pregnancy

›Phenylephrine used cautiously (may reduce uteroplacental flow)

›Inotropes

›Dobutamine: limited data; use if hemodynamically required

›Milrinone: limited pregnancy data; use only if no alternative

›Fetal and obstetric considerations

›Fetal monitoring when viable gestation (>=24 weeks)

›Obstetric and maternal-fetal medicine consultation

›Delivery timing decision in maternal hemodynamic compromise

›Medications: avoid ACE inhibitors (teratogenic)

›Beta-blockers generally acceptable

›Imaging

›Echocardiography is first-line (no radiation)

›CXR with abdominal shielding when needed

›CT-PA with fetal radiation counseling if massive PE suspected

Geriatric

›Epidemiology and baseline differences

›CS complicates >10% of AMI in patients >75 years

›Frailty present in 71% of AMI-CS patients (registry data)

›Higher baseline comorbidity burden (CKD, DM, PVD)

›Higher in-hospital mortality and worse functional outcomes

›Clinical presentation differences

›Atypical presentation common

›Dyspnea and altered mentation without classic chest pain

›Silent MI more frequent

›Reduced physiologic reserve

›Narrower therapeutic window for vasopressors and inotropes

›Treatment modifications

›Vasopressor and inotrope dosing

›Start at lower end of dose range; titrate cautiously

›Greater arrhythmia risk at higher doses

›Renal dosing adjustments

›Milrinone: reduce dose or avoid in severe CKD (GFR <30 mL/min)

›Contrast volume limitation for angiography

›MCS considerations

›Peripheral vascular disease may limit femoral access (Impella, VA-ECMO)

›Higher MCS complication rates in elderly (bleeding, limb ischemia)

›Goals of care

›Early goals of care discussion given high mortality

›Advance directives and family involvement

›Palliative care consultation for refractory shock in frail patients

Pediatrics

›Etiology differences from adults

›Congenital heart disease is leading cause

›Structural defects with outflow obstruction or shunt

›Post-cardiac surgery CS in neonates and infants

›Myocarditis

›Viral etiology most common (enterovirus, adenovirus)

›Acute fulminant myocarditis may require VA-ECMO bridge

›Kawasaki disease with coronary artery aneurysm and AMI

›Arrhythmia-induced cardiomyopathy (persistent SVT, complete AV block)

›Hemodynamic definitions differ by age

›Age-appropriate BP thresholds for hypotension

›Neonate: SBP <60 mmHg; infant: SBP <70 mmHg; child: SBP <70 + (2 x age in years) mmHg

›Heart rate targets also age-dependent

›Weight-based dosing

›Norepinephrine 0.05-2 mcg/kg/min; titrate to MAP for age

›Dobutamine 2-20 mcg/kg/min

›Milrinone 0.25-0.75 mcg/kg/min (load 50 mcg/kg over 10-60 min if tolerated)

›Epinephrine 0.05-1 mcg/kg/min for refractory CS

›MCS in pediatrics

›VA-ECMO is the primary bridge device in pediatric CS

›Size-appropriate cannulae; specialized perfusionist required

›Berlin Heart EXCOR VAD for older children as bridge to transplant

›Pediatric cardiology and cardiac surgery essential from the outset

10Background/b59

Epidemiology

›Incidence and etiology distribution

›~10% of AMI cases are complicated by CS

›AMI-CS accounts for ~30% of contemporary CS cases (declining relative frequency)

›HF-CS now most common (~46% of cases)

›Other etiologies: secondary CS (arrhythmias, valvular, pericardial), postcardiotomy CS

›Mixed-etiology CS (cardiogenic plus distributive) carries highest mortality (~48%)

›Mortality data

›30-day mortality AMI-CS: ~40%

›1-year mortality approaches 50% for AMI-CS

›In-hospital mortality: 25% (acute-on-chronic HF) to 48% (mixed CS)

›Short-term mortality exceeds 30-50% despite contemporary therapy

›Median onset post-AMI is ~6 hours (SHOCK registry)

›Patient characteristics

›Older age (>75 years), frailty, diabetes, multivessel CAD

›Female sex associated with higher AMI-CS rate

›Elevated admission glucose predicts CS risk even in non-diabetics

Pathophysiology

›Primary pump failure cascade

›Myocardial injury reduces stroke volume and cardiac output

›Compensatory tachycardia and vasoconstriction maintain BP initially

›Elevated PCWP causes pulmonary edema as LV fills against impaired function

›End-organ hypoperfusion activates neurohormonal cascades

›RAAS and sympathetic activation worsen vasoconstriction

›Vicious cycle: myocardial ischemia from hypotension worsens pump failure

›Hemodynamic profile

›Low cardiac index (CI <=2.2 L/min/m2)

›Elevated PCWP (>15 mmHg) indicating pulmonary venous congestion

11Patient Discharge Instructions/pdi35

copy discharge instructions

›Cardiogenic shock recovery — home instructions

›Take all medications exactly as prescribed

›Do not stop heart medications without calling your doctor

›Bring medication list to all follow-up appointments

›Daily weight monitoring

›Weigh every morning after using the washroom, before eating

›Call your doctor if weight increases >1 kg (2 lbs) in one day or >2 kg (4 lbs) in one week

›Fluid and sodium restriction

›Follow the fluid limit your doctor gives you (often 1.5-2 litres per day)

›Reduce salt intake; avoid adding salt to food

›Activity restrictions

›Gradually increase activity as guided by your care team

›No strenuous exercise without medical clearance

›Cardiac rehabilitation referral if provided

›Return to emergency immediately if

›Chest pain or pressure

›Sudden severe shortness of breath

›Rapid weight gain (>1 kg in 24 hours)

›Legs or ankles swelling suddenly or worsening

›Confusion, dizziness, or fainting

›Decreased urine output or no urine for several hours

›Palpitations or very fast or irregular heartbeat

›Blue or grey lips or fingertips

›Follow-up appointments

›Cardiology follow-up within 1-2 weeks of discharge

›Repeat echocardiogram at 4-6 weeks to reassess LVEF

›If EF remains <=35% after 40 days post-MI, ICD evaluation required

12References/r27

Guidelines and key sources

›ACC/AHA guidelines and expert consensus

›2025 ACC Expert Consensus Statement on Cardiogenic Shock (Sinha SS et al., JACC 2025)

›Introduced SUSPECT CS mnemonic and updated shock team activation recommendations

›AHA Scientific Statement on Contemporary Management of Cardiogenic Shock (van Diepen S et al., Circulation 2017)

›AHA Scientific Statement on Invasive Management of AMI Complicated by CS (Henry TD et al., Circulation 2021)

›AHA Scientific Statement on Escalating and De-Escalating tMCS (Geller BJ et al., Circulation 2022)

›2022 AHA/ACC/HFSA Guideline for Management of Heart Failure (Heidenreich PA et al., JACC 2022)

›Landmark trials

›SHOCK trial: early revascularization vs initial stabilization in AMI-CS

›53% multivessel CAD prevalence; revascularization benefit at 6 months

›CULPRIT-SHOCK trial: culprit-only PCI superior to multivessel PCI in AMI-CS

›Reduced 30-day mortality and renal replacement therapy requirement

›IABP-SHOCK II: IABP did not reduce 30-day mortality in AMI-CS

›DanGer Shock trial: Impella CP improved survival in selected LV-dominant AMI-CS

›DOREMI trial: milrinone vs dobutamine; no significant difference in outcomes

›SOAP II trial: norepinephrine superior to dopamine (lower arrhythmia rate)

›OPTIMA-CC trial: epinephrine vs norepinephrine; terminated early due to higher refractory shock with epinephrine

›Key reviews

›Jentzer JC et al. Advances in the Management of Cardiogenic Shock. Crit Care Med 2023

›Thiele H, Hassager C. Cardiogenic Shock. NEJM 2026

›Lüsebrink E et al. Cardiogenic Shock. Lancet 2024

›Samsky MD et al. Cardiogenic Shock After AMI: A Review. JAMA 2021

›Narang N et al. Management of HF-Related CS. JACC Heart Fail 2023

›SCAI staging system

›SCAI Shock Classification Stages A-E

›Baran DA et al. SCAI Clinical Expert Consensus Statement on the Classification of CS. Catheter Cardiovasc Interv 2019

›Updated 2022 with mortality correlation data

Evidence & Review

Evidence & Review