Hemodynamic monitoring can identify cardiovascular insufficiency and facilitate optimal treatment of the critically ill. Advanced techniques help sort through various causes of hemodynamic instability and enable tailored interventions.
We focus on techniques applicable in the ED: blood pressure monitoring, central venous pressure (CVP) monitoring, cardiac output (CO) monitoring, and blood oxygenation and lactate monitoring (Table 32-1). In practice, it is best to use more than one approach and monitor therapeutic responses.1
TABLE 32-1Hemodynamic Variables Obtainable in the ED ||Download (.pdf) TABLE 32-1 Hemodynamic Variables Obtainable in the ED
|Hemodynamic Variable ||Method of Measurement |
|Blood pressure, mm Hg ||Sphygmomanometry, oscillometry, intra-arterial catheterization |
|Central venous pressure, mm Hg ||Jugular venous pulsation, ultrasonography |
|Cardiac output, L/min ||Transthoracic echocardiography, pulse contour analysis |
|Central venous oxygen saturation, % ||Central venous catheterization for venous blood sampling |
|Lactate, mmol/L ||Blood sampling |
Blood pressure is the force exerted by circulating blood through a blood vessel. Assessing arterial pressure is important, as hypotension implies tissue hypoperfusion. Hypotension is always pathologic and reflects a failure of normal circulatory homeostatic mechanisms. Shock is a state of organ hypoperfusion; while often present with hypotension, it can occur in the setting of normotension. For example, a patient in cardiogenic or hypovolemic shock may remain normotensive because of a marked increase in vascular resistance.
Arterial pressure is the input pressure for organ perfusion and is a function of peripheral vascular resistance and blood flow. Mean arterial pressure (MAP) is measured directly by indwelling catheter or estimated (see below). Organ perfusion pressure often becomes compromised as MAP decreases below 65 mm Hg.2,3
Optimal MAP varies depending on the underlying cause of hemodynamic instability. In septic shock, many target a minimum MAP of 65 mm Hg,4 and increasing MAP beyond 65 mm Hg with fluids and vasopressors increases oxygen delivery but does not improve mortality.5 However, aiming for a higher MAP (75 to 85 mm Hg) may reduce kidney injury in patients with chronic hypertension.3,6
Debate exists regarding whether MAP or systolic blood pressure is a better target in trauma patients. In patients with hemorrhagic shock, recommendations seek a systolic blood pressure of 80 to 90 mm Hg until major bleeding stops. This concept, called permissive hypotension, decreases complications and improves outcomes in trauma patients in the preoperative period.7-9 The Brain Trauma Foundation recommends maintaining a systolic blood pressure greater than 110 mm Hg for patients with traumatic brain injury, with a minimum systolic blood pressure of 100 mm Hg for patients between the ages of 50 to 69 years.10 For patients in hemorrhagic shock with concomitant severe traumatic brain injury, maintain a MAP greater than 80 mm Hg.11