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Chapter 40. Hemodynamic Monitoring

Seth Manoach, MD, CHCQM; Jean Charchaflieh, MD, DrPH, FCCM, FCCP

  • Invasive hemodynamic monitoring relies on insertion of catheters into:
    • Systemic arteries: arterial catheter (A-line)
    • Central veins: central venous catheter (CVC)
    • The pulmonary artery: pulmonary artery catheter (PAC)
  • These catheters allow clinicians to:
    • Visualize waveforms and measure pressures to perform continuous assessment of cardiac function
    • Measure or derive cardiac output (CO) and other key hemodynamic variables
    • Sample and analyze oxygenation of systemic arterial (SaO2), central venous (ScvO2), or mixed venous (pulmonary arterial) (SvO2) blood from the catheters
    • Use this information to make diagnoses and guide treatment (Tables 40-1 and 40-2)
  • The A-line measures systemic systolic (SBP) and diastolic (DBP) blood pressure:
    • Clinicians can use this to calculate perfusion pressures (cerebral, cardiac, and spinal cord)
    • ABG, electrolytes, Hb, and lactate measurements from the A-line provide downstream or tissue bed perfusion indices and may help pinpoint “upstream” (e.g., cardiopulmonary or vascular) causes of ↓ oxygen delivery (DO2)
    • The A-line can also assess volume status and volume responsiveness:
      • Patients must be sedated and/or pharmacologically paralyzed so they are synchronous with mechanical positive pressure ventilation with Vt ≥8 mL/kg. They must also be in sinus rhythm:
        • Positive pressure ventilation causes ↓ right heart filling during inspiration, when intrathoracic pressures ↑, and ↑ filling during expiration
        • Blood typically crosses the pulmonary vascular bed during half a respiratory cycle; thus, LV preload ↑ during inspiration, and vice versa. The timing can change depending on HR and RR
        • This causes respiratory pulse pressure variation (ΔPP) in patients on the ascending part of the Starling curve
        • Patients on the flat portion of the Starling curve (e.g., exacerbations of congestive heart failure, acute renal failure and volume overload, hypothermia) are preload insensitive and volume repleted or overloaded. Stroke volume (SV) will not significantly change in these patients
        • ΔPP >11–13% predicts relative hypovolemia and volume responsiveness
        • With severe intravascular volume depletion clinicians may observe gross ΔPP on the A-line tracing. Such patients may have significant ΔPP even when Vt <8 cm3/kg or during spontaneous respiration (Figure 40-1)
        • In spontaneous respiration, the respiratory RV–LV filling cycle and ΔPP is reversed, as inspiration causes a negative intrathoracic pressure and increases venous return and RV filling
    • Some proprietary monitoring systems use ΔPP and complex age-adjusted analysis of A-line waveform to estimate CO
    • New noninvasive systems use analogous respiratory cycle–based changes in the pulse oximetry waveform to predict volume responsiveness and estimate CO
  • The CVC:
    • Measures CVP, which is ≈RAP:
      • Normal values for CVP are from 6 to 8, but rise with mechanical ventilation and PEEP
      • In patients with tricuspid regurgitation, primary right heart failure, or pulmonary hypertension this value may rise
      • In general, low single-digit CVP values predict hypovolemia more accurately than elevated values predict volume overload
    • Can be used to measure ScvO2 (central venous):
      • ScvO2 is typically ≈5% higher than ...

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