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A Case for Echocardiography for Assessing Hemodynamic Instability

Hemodynamic instability refers to global or regional perfusion that is inadequate to support normal organ function. Numerous hemodynamic parameters (heart rate, blood pressure, central venous pressure, pulmonary artery pressure, pulmonary artery occlusion pressure, and cardiac output) can be monitored and controlled, and abnormalities in any of them parameters may indicate hemodynamic instability.

James Bailey, MD, PhD
Associate Professor in the Department of Anesthesiology, Cardiac Anesthesia and Critical Care Medicine Division, Emory University School of Medicine, Atlanta, Georgia, USA

Published by permission of GASNet Inc. © 2003

Scope of the problem: Why is hemodynamic instability important?

The term “hemodynamic instability” is most commonly associated with an abnormal or unstable blood pressure, especially hypotension. Here, hemodynamic instability will be defined more broadly as global or regional perfusion that is not adequate to support normal organ function. This definition recognizes the obligation to insure adequate organ perfusion during the perioperative period.

Numerous hemodynamic parameters (heart rate, blood pressure, central venous pressure, pulmonary artery pressure, pulmonary artery occlusion pressure, and cardiac output) can be monitored and controlled. Abnormalities of any of these parameters may indicate hemodynamic instability, and control of any of these variables may restore adequate organ perfusion. However, the two variables that most directly reflect organ perfusion are blood pressure and indices of global perfusion, such as cardiac output or mixed-venous hemoglobin oxygen saturation (SvO₂).

Due to limits on coronary and cerebral autoregulation, hypotension may compromise adequate perfusion of the brain and heart. Animal studies have demonstrated that blood pressure is the primary determinant of cerebral and coronary blood flow when the limits of autoregulation are exceeded. However, studies relating hypotension to outcome have shown mixed results 1-6. Therefore, the clinician can only conclude that there are blood pressure thresholds below which coronary and cerebral ischemia may occur, that these are probably more stringent in individuals with fixed vascular stenoses, and that they may vary greatly among individuals.

For the same reasons that there are mixed data relating hypotension to outcome, it has been difficult to design studies relating outcome to decreased cardiac output or SvO₂ 7-17. Overall the evidence indicates that maintaining adequate global perfusion contributes to improved outcome. The difficulty is that the definition of “good” is unclear. Supranormal oxygen delivery (a cardiac index roughly greater than 4.5 L.min/m2) has not been widely accepted. A reasonable goal would be a cardiac index of 2.5-3 L/min/m² or greater in conjunction with an SvO₂ greater than 65-70% and a lactate level lower than 2-3 mM/l.

Who is at risk?

It is important for the anesthesiologist to understand the risk to the patient from pre-existing conditions or the surgical procedure to plan perioperative patient management. However, even healthy patients undergoing minor procedures may manifest hemodynamic instability due to anesthesia itself. Often, anesthesiologists are better prepared to manage the anticipated hemodynamic instability in a patient with significant cardiovascular disease undergoing major surgery than they are in a relatively healthy patient undergoing outpatient surgery.

Recognizing hemodynamic instability

A key concept necessary for understanding hemodynamic instability is the simple equation relating blood pressure and cardiac output:


(where MAP is mean arterial systemic blood pressure, SVR is systemic vascular resistance, CO is cardiac output, and CVP is central venous pressure). This equation warns us that a normal blood pressure does not guarantee an adequate cardiac output. Recognition of hemodynamic instability requires monitoring of both blood pressure and global perfusion.

While hypotension is probably the most commonly recognized manifestation of hemodynamic instability it is not the most common problem. An adequate blood pressure may insure coronary and cerebral perfusion 18,19; however, it does not insure renal and mesenteric perfusion, which cannot be measured directly. It is best to assume that appropriate “global” perfusion (i.e., cardiac output or SvO₂) will increase the chance that the kidneys and mesentery are also adequately perfused. There is ample evidence that maintaining blood pressure in the presence of inadequate cardiac output by excessive vasoconstriction of efferent glomerular arterioles is deleterious to renal function 20. Mesenteric circulation is even more sensitive to excessive vasoconstriction 21 and the global cardiac output needed to insure mesenteric and renal perfusion is unclear. However, cardiac indices lower than normal values must be viewed as suspect. In addition, it is most prudent to look at multiple indicators of adequate perfusion, such as cardiac output, SvO₂, and lactate concentrations.


Blood pressure

While noninvasive blood pressure monitoring may be quite accurate, if the patient is hemodynamically unstable it is important to monitor blood pressure invasively on a beat-to-beat basis. The most common catheterization site is the radial artery, although femoral, brachial and axillary arteries have also been used. The monitoring system must be appropriately zeroed and calibrated. It is often helpful to utilize both invasive and noninvasive monitoring in order to have both beat-to-beat monitoring and an independent measure of the accuracy of the invasive system. There may be discrepancies between peripherally measured blood pressure and central aortic pressures (aortic systolic lower than radial). However, in two important situations — immediately after cardiopulmonary bypass and in septic patients — the systolic blood pressure measured from the radial arterial catheter may be misleadingly low (22).

Finally, one should note that any system of monitoring actually gives the clinicians three blood pressures — diastolic, mean and systolic. Of these, the mean is least likely to be affected by monitoring artifacts and (with the exception of diastolic pressure and coronary perfusion) is the measure most directly correlated with organ perfusion. Systolic pressure often gets the most attention, but is often the least informative.

Cardiac output

While invasive monitoring of blood pressure is relatively common in surgical patients who are at higher risk for hemodynamic instability, cardiac output monitoring is less common. Clinical recognition of low cardiac output syndrome in the absence of hypotension can be difficult (23, 24). The mainstay for cardiac output measurement has been the pulmonary artery catheter, which allows measurement of cardiac output using the thermodilution technique, and which simultaneously allows measurement of central venous pressure, pulmonary artery pressure, and pulmonary artery occlusion pressure. Recent advances in applications of the thermodilution principle now allow for continuous cardiac output measurements. Furthermore, mixed venous blood samples can be drawn and mixed venous hemoglobin oxygen saturation can be monitored, either intermittently or continuously, using fiberoptic technology.

Given these capabilities, it is no surprise that the pulmonary artery catheter has been a mainstay of hemodynamic monitoring. However, its use is not without controversy. No definitive study has demonstrated that use of the pulmonary artery catheter improves outcome, rather two retrospective studies have suggested that mortality is increased by use of pulmonary artery catheters (25,26). The conclusion, if not readily accepted, must be taken seriously and has promoted interest in alternative methods of measuring cardiac output.

Promising technology has been introduced, including Fick measurement of cardiac output using CO₂ rebreathing, Doppler echocardiographic measurement of descending aortic flow, pulse contour analysis and thermodilution using femoral arterial temperature sensing and lithium dilution (27-29). While these new technologies have not yet been extensively validated, early studies indicate that each may provide accurate estimations of cardiac output, although there are caveats in their use (30).

Mixed-venous hemoglobin oxygen saturation (SvO₂)

One of the pitfalls of monitoring cardiac output is that the definition of an “adequate” cardiac index is unclear. While normal cardiac index is, in general, greater than 2.5 L/min/m2, this is only a very rough guide to appropriate values of cardiac output. Consideration of venous hemoglobin oxygen saturation is a logical means of assessing the adequacy of cardiac output. From the Fick principle, we know that if delivery of oxygen is inadequate SvO₂ will decrease unless there is a concomitant decrease in oxygen consumption. Oxygen delivery depends on hemoglobin concentration, arterial oxygenation, and cardiac output. If hemoglobin saturation, and arterial oxygenation are essentially normal (or remain unchanged) then a low (or decreasing) SvO₂ (< 65-70%) indicates that cardiac output is inadequate for oxygen consumption.

In general, measurement of true mixed-venous hemoglobin oxygen saturation requires a sample from the pulmonary artery, and hence a pulmonary artery catheter. However, a simple central venous hemoglobin oxygen saturation may track the true SVO₂ and direct therapy for septic patients (17). It appears that this approach to monitoring the adequacy of cardiac output merits consideration in other clinical scenarios, especially as it avoids the necessity of a pulmonary artery catheter.


When hemodynamic instability has been recognized — as either hypotension or low cardiac output syndrome — treatment may be greatly facilitated by echocardiography providing a quick and accurate assessment of preload and contractility (31). Preload refers to the stretch of the myocardial fiber and is best estimated by left-ventricular end-diastolic volume (LVEDV). Echocardiography provides cardiac dimensions, not pressures, and, unlike those obtained using the pulmonary artery catheter, echocardiographic measures of preload correlate well with LVEDV (32-34). In addition, echocardiography can estimate ejection fraction, a useful measure of contractility (33, 34).

Also, besides providing good estimates of the two most important determinants of cardiac output (preload and contractility), echocardiography assesses valve function, regional wall motion abnormalities, sources of emboli, pericardial constraints to normal hemodynamics (e.g., tamponade, constrictive pericarditis), as well as allowing the clinician to distinguish right from left heart performance. For these reasons, echocardiography is highly recommended whenever there is hemodynamic instability of unknown etiology or that is not readily corrected by standard therapy.


  1. Slogoff, S. and Keats, A.S. Does perioperative myocardial ischemia lead to postoperative myocardial infarction. Anesthesiology 62, 107 (1985).
  2. Smith, R.C. et al. Postoperative myocardial ischemia in patients undergoing coronary artery bypass graft surgery. Anesthesiology 74, 464 (1991).
  3. Reed, D.L. et al. Intraoperative predicators of mortality, stroke, and myocardial infarction after coronary artery bypass surgery. Anesth Analg 89, 814 (1999).
  4. Jain, U. et al. Electrocardiographic and hemodynamic change and their association with myocardial infarction during coronary artery bypass surgery. A multicenter study. Anesthesiology 86, 576 (1997).
  5. Charlson, M.E. et al. The perioperative and intraoperative predictions of postoperative myocardial infarction or ischemia in patients undergoing noncardiac surgery. Ann Surg 210, 637 (1989).
  6. Owens, P. and O’Brien, E.. Hypotension in patients with coronary disease: Can profound hypotensive events cause myocardial ischemia. Heart 82, 477 (1999).
  7. Shoemaker, W.C. et al. Prospective trial of supranormal values of survivors as therapeutic goals in high-risk surgical patients. Chest 94, 1176 (1988).
  8. Boyd, O. et al. The beneficial effects of supranormalization of oxygen delivery with dopexamine hydrochloride on perioperative mortality. JAMA 270, 2699 (1993).
  9. Tuchschmidt, J. et al. Elevation of cardiac output and oxygen delivery improves outcome in septic shock. Chest 103, 216 (1992).
  10. Yu, M. et al. Effect of maximizing oxygen delivery morbidity and mortality in critically ill patients: A prospective randomized controlled study. Crit Care Med 21, 830 (1993).
  11. Gattinoni, L. et al. A trial of goal-directed hemodynamic therapy in critically ill patients. N Engl J Med 333, 1025 (1995).
  12. Hayes, M.A. et al. Evaluation of systemic oxygen delivery in the treatment of critically ill patients. N Engl J Med 330, 1717 (1994).
  13. Heyland, D.K. et al. Maximizing oxygen delivery in critically ill patients: A methodological appraisal of the evidence. Crit Care Med 24, 517 (1996).
  14. Sinclair, S. et al. Intraoperative volume optimization and length of stay after repair of proximal femur fracture: randomized controlled trial. Br Med J 315, 909 (1997).
  15. Mythen, M.G. and  Webb AR. Perioperative plasma volume expansion reduces the incidence of gut mucosal hypoperfusion during cardiac surgery. Arch Surg 130, 423 (1995).
  16. Polonen, P. et al. A prospective randomized study of goal-oriented hemodynamic therapy in cardiac surgical patients. Anesth Analg 90, 1052 (2000).
  17. Rivers, E. et al. Early goal directed therapy in the treatment of severe sepsis and septic shock. N Eng J Med 345, 1368-1377 (2001).
  18. O’Brien, E.R.M. and Nathan, H.J. Coronary physiology and atherosclerosis. In: Cardiac Anesthesia 4th Ed. Edited by Kaplan JA. Philadelphia, WB Saunders 241 (1999).
  19. Drummond, J.C. The lower limit of autoregulation: Time to reverse our thinking? Anesthesiology 86, 1431 (1997).
  20. Mills, L.C. et al. Effects of various sympathetic drugs on renal hemodynamics in normotensive and hypotensive dogs. Am J Physiol 198, 1279 (1960).
  21. Rowell, L.B. et al. Importance of the splanchnic vascular bed in human blood pressure regulation. J Appl Physiol 32, 213 (1972).
  22. Mohr, R. et al. Inaccuracy of radial artery pressure measurement after cardiac operations. J Thorac Cardiovasc Surg 94, 286 (1987).
  23. Bailey, J.M. et al. Relationship between clinical evaluation of peripheral perfusion and global hemodynamics in adults after cardiac surgery. Crit Care Med 18, 1353 (1990).
  24. Rashkin, M.C. et al. Oxygen delivery in critically ill patients. Relationship to blood lactate and survival. Chest 5, 580 (1985).
  25. Zion, M.M. et al. Use of pulmonary artery catheters in patients with acute myocardial infarction: analysis experience in 5841 patients in the SPRINT registry. Chest 98,1331 (1990).
  26. Connors, A.F. et al. The effectiveness of right heart catheterization in the critical care of critically ill patients. JAMA 276, 889 (1996).
  27. Haryadi, D. et al. Partial CO2 rebreathing indirect Fick technique for non-invasive measurement of cardiac output. J Clin Monit 16, 361 (2000).
  28. Mark, J.B. et al. Continuous noninvasive monitoring of cardiac output with esophageal doppler ultrasound during cardiac surgery. Anesth Analg 65, 1015 (1986).
  29. Tibby, S.M. et al. Clinical validation of cardiac output measurements using femoral artery thermodilution with direct Fick in ventilated children and infants. Intensive Care Med 23, 987 (1997).
  30. Chaney, J.C. and Derdak, S. Minimally invasive hemodynamic monitoring for the intensivist: current and emerging technology. Critical Care Med 30, 2338-2345 (2002).
  31. Benson, M.J.A. et al. The echocardiographic assessment of left ventricular function. In: Ventricular Function. Edited by Waltier DC. Baltimore, Williams and Wilkins 253 (1995).
  32. Hanson, R.M. et al. Poor correlation between pulmonary arterial wedge pressure and left ventricular end-diastolic volume after coronary artery bypass graft surgery. Anesthesiology 64, 764 (1986).
  33. Urbanowicz, J.H. et al. Comparison of transesophageal echocardiographic and scintigraphic estimates of left ventricular end-diastolic volume index and ejection fraction in patients following coronary artery bypass grafting. Anesthesiology 72, 607 (1990).
  34. Harpole, D.H. et al. Right and left ventricular performance during and after abdominal aortic aneurysm repair. Ann Surg 209, 356 (1989).

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  • Circulatory
  • Hemodynamics
  • Cardiac output
  • Invasive pressures
  • Temperature
  • Perioperative care
  • Clinical