Cardiogenic shock is inadequate tissue perfusion from cardiac dysfunction. A seemingly adequate blood pressure does not exclude low-output shock. Identify the cause and ventricular phenotype while resuscitation proceeds.
1

Read four domains together

DomainBedside questions
PerfusionMentation, skin temperature, capillary refill, urine output, lactate trend and renal/hepatic injury. Does support improve organ function?
Pressure and flowBlood pressure, pulse pressure, rhythm, cardiac output and response to treatment. A higher MAP alone can conceal persistently poor flow.
CongestionJVP, edema, lung ultrasound, oxygen requirement and LV/RV filling. A congested patient can still have inadequate forward output.
Cause and trajectoryAcute MI, acute-on-chronic HF, myocarditis, arrhythmia, valve/mechanical disease or mixed vasoplegia. Record the direction of change and support needed.

Classify severity serially rather than treating a single lactate or cardiac-index value as the whole syndrome.

2

SCAI stage is a common language

StageWorking interpretation
A · At riskRisk factors for shock without current shock.
B · BeginningHemodynamic instability without hypoperfusion.
C · ClassicHypoperfusion requiring an intervention beyond simple volume replacement.
D · DeterioratingInitial support is insufficient and escalation is needed.
E · ExtremisCirculatory collapse or imminent collapse despite intensive resuscitation.

Document the arrest context and neurologic uncertainty separately. Stage describes severity and treatment response, not automatic device eligibility or an individual prognosis.

First handoff: cause, stage and trajectory, LV/RV pattern, congestion, lactate/organ trend, current support, reversible lesion and the next reassessment time.
1 · Find the causeECG, echocardiography and focused clinical assessment.
2 · Measure the responsePerfusion, pressure, urine output, lactate and support burden.
3 · Resolve uncertaintyInvasive hemodynamics when the result changes treatment.

Early echo should look for LV and RV dysfunction, tamponade, acute severe valve disease and post-MI mechanical complications. Coronary evaluation and definitive treatment of a reversible cause should not be delayed by a search for a perfect hemodynamic profile.

1

Pressure and flow must tell the same story

PhenotypeInterpretation and reassessment
LV dominantPulmonary congestion and impaired systemic flow. Reassess afterload, ischemia, valve lesions and LV unloading needs.
RV dominantHigh right-sided pressure with limited LV filling. Assess RV ischemia, pulmonary vascular load, ventilation, rhythm and septal interaction.
BiventricularBoth filling-pressure compartments and organ perfusion are abnormal. An isolated LV device may not correct the whole circulation.
Mixed shockLow output with vasodilation, infection or post-arrest inflammation. Address both cardiac performance and vascular tone.
UnderfilledConfirm that low filling is real before fluid. Reassess after small, monitored interventions rather than giving blind volume into congestion.
2

Use calculated indices as context

CPO = MAP × cardiac output / 451 in watts. It combines pressure and flow. PAPi = (PA systolic − PA diastolic pressure) / right atrial pressure. It is affected by loading conditions, pulmonary vascular disease, ventilation and measurement technique.

No single PAPi value chooses an LV, RV or biventricular device. Pair invasive data with imaging, the cause, vascular anatomy, oxygenation, device risks and an achievable exit strategy.

Repeat questionable waveforms and reconcile measured output with oxygen saturations and the bedside examination. Use the hemodynamics guide for acquisition and waveform interpretation.

Stabilize perfusion while treating the cause. Use the least vasoactive and mechanical support that achieves the intended physiologic goal, then reassess for benefit and harm.
1

Vasoactive treatment has trade-offs

When a vasopressor is needed, norepinephrine is commonly favored over dopamine and often over epinephrine because of arrhythmia and metabolic concerns. Add an inotrope selectively for persistent low output after pressure and filling assessment. Dobutamine and milrinone have different kinetic, renal and vascular effects.

2

Trials answer different clinical questions

EvidenceFinding and boundary
CULPRIT-SHOCKIn AMI shock with multivessel disease, initial culprit-only PCI reduced the composite of death or renal-replacement therapy compared with immediate multivessel PCI. This does not mean ignoring later nonculprit disease.
IABP-SHOCK IIRoutine IABP did not reduce mortality in AMI shock treated with early revascularization. This does not settle every bridge or mechanical-complication use.
DanGer-ShockSelected STEMI-shock patients had lower 180-day mortality with a microaxial flow pump, with more adverse events. Selection and exclusions matter. Do not generalize to all shock, severe RV failure or comatose arrest.
ECLS-SHOCK / ECMO-CSRoutine early VA-ECMO strategies did not establish a broad survival advantage and introduce substantial complication burden. Rescue decisions remain individualized.
3

Device choice follows the failed function

Decide whether the unmet need is LV support, RV support, biventricular support, oxygenation or a bridge through a reversible lesion. Document bleeding, limb ischemia, stroke, hemolysis, infection and ventricular-loading risks before and during support.

Related guides: Impella, VA-ECMO, RV/BiV support and IABP.

1

Escalate before the window closes

Worsening perfusion, rising support needs, persistent lactate elevation, new organ injury or uncertainty about the phenotype should trigger multidisciplinary reassessment and consideration of transfer to a capable center. A serial SCAI stage makes deterioration visible.

ReassessmentDecision to record
Has the cause been treated?Revascularization, rhythm control, correction of a valve/mechanical lesion or disease-specific treatment.
Is support achieving its goal?Perfusion and organ recovery, ventricular unloading, oxygenation and reduced vasoactive need.
Is treatment creating harm?Bleeding, hemolysis, limb/mesenteric ischemia, neurologic injury, infection or worsening ventricular distension.
Is the exit still feasible?Recovery and weaning, durable LVAD, transplantation, another temporary configuration or a goal-concordant limit.
1 · RecoveryDefine objective readiness and supervised weaning.
2 · Durable therapyAssess candidacy before irreversible injury.
3 · Time-limited trialName the milestone, review date and stopping conditions.

For prolonged support dependence, integrate hemodynamics, end-organ reversibility, neurologic information, frailty, RV reserve and patient goals. A device buys time but does not itself establish candidacy.

2

Communication is part of treatment

Use one coordinated plan with named clinical responsibility. Explain uncertainty and the next decision to the patient and family. Palliative care can support symptoms and decision-making alongside recovery, transplant or device treatment.

Daily exit statement: intended bridge ___, evidence of recovery ___, unresolved organ/neurologic question ___, candidate constraints ___, next trial or review ___, patient priorities ___.