What is the target mean arterial pressure (MAP) in cardiogenic shock?

Target Mean Arterial Pressure in Cardiogenic Shock

Primary MAP Target

In cardiogenic shock, target a minimum MAP of ≥65 mmHg initially, but aim for ≥70 mmHg based on emerging evidence showing improved outcomes at higher pressures in this specific population. 1, 2

The standard 65 mmHg threshold represents the critical point below which organ autoregulation fails and tissue perfusion becomes linearly dependent on arterial pressure across all shock states. 3 However, cardiogenic shock differs fundamentally from distributive shock in its pathophysiology—the problem is inadequate cardiac output rather than vasodilation—which may necessitate higher perfusion pressures to maintain adequate organ blood flow. 4

Evidence Supporting Higher MAP Targets in Cardiogenic Shock

• A post-hoc analysis of the DOREMI trial demonstrated that patients achieving MAP ≥70 mmHg had significantly lower mortality (28.9%) compared to those with MAP <70 mmHg (57.8%), with an adjusted relative risk of 0.56 (95% CI 0.40-0.79, P <0.01). 2

• The composite outcome of death, cardiac arrest, need for mechanical support, myocardial infarction, stroke, or renal replacement therapy occurred in 42.2% of high MAP patients versus 67.6% of low MAP patients (adjusted RR 0.70, P = 0.01). 2

• A 2025 narrative review examining cardiovascular disease populations concluded that higher MAPs are associated with improved outcomes in cardiogenic shock, though the authors acknowledge the retrospective nature limits causal inference. 4

• The American College of Cardiology specifically suggests targeting MAP ≥70 mmHg in cardiogenic shock may improve outcomes, extrapolating from septic shock data where chronic hypertensive patients benefited from higher targets. 1

Practical Management Algorithm

Initial Stabilization

• Achieve MAP ≥65 mmHg immediately using norepinephrine as first-line vasopressor (start at 0.02–0.05 µg/kg/min). 5, 1
• Ensure adequate preload with judicious fluid administration—avoid excessive crystalloid that may worsen pulmonary edema in the setting of left ventricular dysfunction. 5

Target Optimization

• Once MAP ≥65 mmHg is achieved, titrate vasopressors to reach MAP ≥70 mmHg as the therapeutic goal in cardiogenic shock. 1, 2
• Use the lowest necessary vasopressor dose to minimize arrhythmia risk and myocardial oxygen demand. 1

Escalation Strategy

• If norepinephrine reaches 0.1–0.25 µg/kg/min without achieving target MAP, add vasopressin 0.03 units/min (do not exceed 0.03–0.04 units/min). 5
• Consider adding dobutamine 2.5–20 µg/kg/min if myocardial dysfunction persists despite adequate MAP, to augment cardiac output rather than relying solely on vasoconstriction. 5
• For refractory shock after ≥4 hours of high-dose vasopressors, add hydrocortisone 50 mg IV every 6 hours. 5

Monitoring Beyond MAP

MAP alone is insufficient to assess tissue perfusion adequacy in cardiogenic shock. 3 Concurrently monitor:

• Lactate clearance (measure every 2–4 hours, aim for normalization). 3, 5
• Urine output ≥0.5 mL/kg/h as a renal perfusion surrogate. 3, 5
• Mental status to assess cerebral perfusion. 3, 5
• Capillary refill ≤2 seconds and skin temperature for peripheral perfusion. 3, 5
• Mixed or central venous oxygen saturation to gauge global oxygen delivery. 3

Critical Caveats and Pitfalls

• Do not delay vasopressor initiation while pursuing aggressive fluid resuscitation in profound hypotension (SBP <70 mmHg or DBP ≤40 mmHg)—start norepinephrine emergently while fluid resuscitation continues. 5

• Avoid excessive vasopressor escalation beyond what is needed to achieve MAP 70 mmHg, as targeting MAP 85 mmHg in septic shock trials resulted in significantly higher arrhythmia rates without mortality benefit. 6, 1 This risk is particularly relevant in cardiogenic shock where myocardial irritability is already elevated.

• Recognize that elevated systemic vascular resistance can maintain normal MAP despite critically low cardiac output ("cold shock" physiology)—assess stroke volume index and cardiac output, not just MAP. 3 A normal MAP with poor peripheral perfusion (cool extremities, prolonged capillary refill, narrow pulse pressure) indicates inadequate tissue perfusion despite adequate pressure.

• In post-CABG cardiogenic shock specifically, optimize coronary perfusion pressure by maintaining adequate MAP while minimizing myocardial oxygen demand—this requires balancing vasopressor support against the risk of increased afterload. 1

• Central venous catheter placement is strongly preferred for norepinephrine infusion to minimize extravasation risk, though large-bore peripheral access is acceptable temporarily to avoid treatment delays. 5

Strength of Evidence

The recommendation for MAP ≥70 mmHg in cardiogenic shock is based on high-quality post-hoc analysis of a randomized trial 2, supported by guideline society suggestions 1 and narrative review 4. While the DOREMI trial was not designed to test MAP targets as a primary endpoint, the magnitude of mortality difference (28.9% vs 57.8%) and the adjusted analysis controlling for confounders provide compelling evidence. The baseline 65 mmHg threshold derives from strong guideline recommendations across all shock states 6, 3, making it the minimum acceptable target while higher pressures are pursued in cardiogenic shock specifically.