Understanding the Paradox: Normal MAP with Low Stroke Volume Index
Blood pressure (MAP) does not necessarily reflect cardiac output or adequate tissue perfusion—you can have "excellent" MAP while simultaneously having critically low stroke volume index (SVI) because elevated systemic vascular resistance (SVR) is compensating to maintain pressure despite poor flow. 1, 2
The Fundamental Hemodynamic Relationship
The key to understanding this apparent contradiction lies in the basic equation of perfusion pressure:
- MAP = Cardiac Output (CO) × Systemic Vascular Resistance (SVR) 1
- Since CO = Heart Rate × Stroke Volume, a critically low SVI can still produce normal or elevated MAP if SVR is sufficiently elevated 1
- Blood flow (Q) correlates directly with perfusion pressure but inversely with vascular resistance 1
The Clinical Scenario: "Cold Shock" Physiology
This represents classic high-resistance, low-output shock (often called "cold shock"):
- When ventricular function is reduced or stroke volume falls (from endotoxin-induced cardiac dysfunction, hypovolemia, or other causes), the body's compensatory response is to vasoconstrict aggressively to maintain blood pressure 1
- If the elevation in vascular resistance is marked, the reduction in blood flow results in shock despite normal blood pressure 1
- This is clinically identified by: absent or weak distal pulses, cool extremities, prolonged capillary refill, and narrow pulse pressure with relatively increased diastolic blood pressure 1
Why MAP Alone is Misleading
- A cardiac index between 3.3 and 6.0 L/min/m² is associated with best outcomes in septic shock patients, compared to patients without septic shock for whom a CI above 2.0 L/min/m² is sufficient 1
- The presence of normal blood pressure with high vascular resistance means that cardiac output is reduced 1
- Multiple studies demonstrate poor agreement between physician-assessed hemodynamics based on blood pressure alone and objective measurements of cardiac index and SVR 3
- In septic shock patients, changes in MAP do not reliably track changes in cardiac index after fluid challenge, with no significant correlation between the two 4
Clinical Assessment Beyond MAP
Your "excellent systemic perfusion" assessment based on MAP and shock index is incomplete. You must evaluate:
- Lactate clearance (most important marker of tissue perfusion adequacy) 2
- Urine output (goal >0.5 mL/kg/h; kidney receives second-highest blood flow relative to mass) 2
- Mental status (cerebral perfusion indicator) 2
- Skin perfusion and capillary refill (peripheral perfusion marker) 1, 2
- Mixed or central venous oxygen saturation 2
- Pulse pressure (narrow PP suggests high SVR/low stroke volume state) 1
The Therapeutic Implication
The effective approach for patients with low SVI and elevated SVR despite normal MAP is vasodilator therapy with additional volume loading as vascular capacity is expanded 1:
- Vasodilator therapy reduces afterload and increases vascular capacitance 1
- This shifts the venous compliance curve so more volume can exist in the ventricles at lower pressure 1
- Giving volume to restore filling pressure results in a net increase in end-diastolic volume (preload) and higher cardiac output at the same or lower filling pressures 1
- Effective use of this approach results in decreased heart rate and improved perfusion 1
Common Pitfall to Avoid
Do not equate adequate MAP with adequate perfusion—this is the most dangerous assumption in shock management 1, 2, 4. A patient can have MAP of 75 mmHg (above the 65 mmHg target) while having:
- Critically low cardiac output 1
- Elevated lactate indicating tissue hypoperfusion 2
- Oliguria from inadequate renal blood flow 2
- Cool extremities and prolonged capillary refill 1
In this scenario, the patient needs afterload reduction and volume expansion, not continued vasopressor support or reassurance that perfusion is "excellent" 1.