E Editorial
Noninvasive Hemodynamic Monitoring: Can We Have It All? Maxime Cannesson, MD, PhD,* and Michael Pinsky, MD, CM, Dr hc, MCCM, FCCP†
T
he initial promise of functional hemodynamic monitoring1 was to advise the bedside clinician in either the operating room or acute care environment whether his or her patient was volume responsive. The point, of course, was to guide therapy for the hypotensive patient requiring increased cardiac output. If the patient would respond to volume, then resuscitation should start with fluids. To that end we2–4 and others5,6 showed that threshold values of arterial pulse pressure variation (PPV) during positive pressure accurately separated volume responders from nonresponders. Subsequently, stroke volume variation (SVV) estimated from esophageal Doppler7 or derived from arterial waveform analysis8 also proved predictive of volume responsiveness. With greater scrutiny, it became clear that these robust measures were limited to patients on mechanical ventilation with tidal volumes of 8 mL/kg or greater9 (although they still remain predictive of fluid responsiveness when >13% in this setting), and that they could not predict fluid responsiveness accurately in conditions such as increased intraabdominal pressure,10 atrial fibrillation,11 and acute cor pulmonale. In addition, it was recently identified that when PPV is between 8% and 13% (“gray zone”), other tests should be used to aid the bedside clinician in defining volume responsiveness.3 Two recent developments simplify these issues. First, one may use the magnitude of the PPV or SVV as a surrogate for cardiac reserve. If a patient has a good cardiac reserve, then the SVV or PPV will be higher. The inverse is also true. If a patient has poor cardiac reserve, then SVV and PPV will be lower. This is expected, of course, because the Starling mechanism is the underlying physiology responsible for PPV and SVV. Maas et al.12 demonstrated that postoperative cardiac surgery patients given norepinephrine to increase mean arterial pressure by 20 mm Hg also increased their cardiac output if their initial SVV was >12%. Thus,
From the *Department of Anesthesiology & Perioperative Care, University of California Irvine, Orange, California; and †Department of Critical Care Medicine, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania. Accepted for publication July 22, 2014. Funding: N/A. Conflict of Interest: See Disclosures at the end of the article. Reprints will not be available from the authors. Address correspondence to Maxime Cannesson, MD, PhD, Department of Anesthesiology & Perioperative Care, University of California Irvine, 101 S City Dr., Orange, CA 92868. Address e-mail to [email protected]. Copyright © 2014 International Anesthesia Research Society DOI: 10.1213/ANE.0000000000000439
10 www.anesthesia-analgesia.org
one may use PPV and SVV as functional parameters of cardiac reserve. Second, although the absolute values of PPV and SVV may be altered by tidal volume and other disease states, as listed above, the dynamic relationship between changes in stroke volume and arterial pulse pressure is independent of these limitations. As quantified by the ratio of PPV to SVV and approximate dynamic arterial elastance, PPV/SVV appears to define central arterial tone. Monge Garcia et al. demonstrated that hypotensive but volumeresponsive septic patients had a variable blood pressure response to fluid resuscitation that was dependent on PPV/ SVV or dynamic arterial elastance. A dynamic arterial elastance
Noninvasive Hemodynamic Monitoring: Can We Have It All? Maxime Cannesson, MD, PhD,* and Michael Pinsky, MD, CM, Dr hc, MCCM, FCCP†
T
he initial promise of functional hemodynamic monitoring1 was to advise the bedside clinician in either the operating room or acute care environment whether his or her patient was volume responsive. The point, of course, was to guide therapy for the hypotensive patient requiring increased cardiac output. If the patient would respond to volume, then resuscitation should start with fluids. To that end we2–4 and others5,6 showed that threshold values of arterial pulse pressure variation (PPV) during positive pressure accurately separated volume responders from nonresponders. Subsequently, stroke volume variation (SVV) estimated from esophageal Doppler7 or derived from arterial waveform analysis8 also proved predictive of volume responsiveness. With greater scrutiny, it became clear that these robust measures were limited to patients on mechanical ventilation with tidal volumes of 8 mL/kg or greater9 (although they still remain predictive of fluid responsiveness when >13% in this setting), and that they could not predict fluid responsiveness accurately in conditions such as increased intraabdominal pressure,10 atrial fibrillation,11 and acute cor pulmonale. In addition, it was recently identified that when PPV is between 8% and 13% (“gray zone”), other tests should be used to aid the bedside clinician in defining volume responsiveness.3 Two recent developments simplify these issues. First, one may use the magnitude of the PPV or SVV as a surrogate for cardiac reserve. If a patient has a good cardiac reserve, then the SVV or PPV will be higher. The inverse is also true. If a patient has poor cardiac reserve, then SVV and PPV will be lower. This is expected, of course, because the Starling mechanism is the underlying physiology responsible for PPV and SVV. Maas et al.12 demonstrated that postoperative cardiac surgery patients given norepinephrine to increase mean arterial pressure by 20 mm Hg also increased their cardiac output if their initial SVV was >12%. Thus,
From the *Department of Anesthesiology & Perioperative Care, University of California Irvine, Orange, California; and †Department of Critical Care Medicine, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania. Accepted for publication July 22, 2014. Funding: N/A. Conflict of Interest: See Disclosures at the end of the article. Reprints will not be available from the authors. Address correspondence to Maxime Cannesson, MD, PhD, Department of Anesthesiology & Perioperative Care, University of California Irvine, 101 S City Dr., Orange, CA 92868. Address e-mail to [email protected]. Copyright © 2014 International Anesthesia Research Society DOI: 10.1213/ANE.0000000000000439
10 www.anesthesia-analgesia.org
one may use PPV and SVV as functional parameters of cardiac reserve. Second, although the absolute values of PPV and SVV may be altered by tidal volume and other disease states, as listed above, the dynamic relationship between changes in stroke volume and arterial pulse pressure is independent of these limitations. As quantified by the ratio of PPV to SVV and approximate dynamic arterial elastance, PPV/SVV appears to define central arterial tone. Monge Garcia et al. demonstrated that hypotensive but volumeresponsive septic patients had a variable blood pressure response to fluid resuscitation that was dependent on PPV/ SVV or dynamic arterial elastance. A dynamic arterial elastance
