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Applied Cardiovascular Physiology in Theatre: Measuring the Cardiovascular Effects of Propofol Anaesthesia

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Author: M. R. Pinsky

Br J Anaesth. 2016;116(6):736-738.

Cardiovascular homeostasis is a complex and beautiful interplay between the functional differences between various vascular circuits in the body and their tissue’s metabolic demand, the physical nature of the endothelial barrier to fluid flux, the circulating blood volume, and reflex-mediated autonomic tone. When at rest, as occurs during anaesthesia, basal metabolic demand is both constant and low. Thus, impairments in autoregulation or sudden decreases in blood volume, as may happen during surgery, are thankfully less detrimental to tissue wellness than might otherwise be the case under conditions of metabolic stress. However, such physiologic reserve though comforting to the anaesthetist and forgiving to the patient, has clearly defined limits. Anaesthesia by its nature decreases central nervous system activity and by default, impairs autonomic responsiveness and at high enough concentrations impairs vascular tone and cardiac contractility. These concepts form the basis for anaesthetic selection in specific patient groups. But mostly all these considerations have focused on the left ventricle (LV) and arterial tone, ignoring venous return by simply placating it with increased fluid resuscitation, vasopressor infusion and/or decreased concentration of anaesthesia if the patient becomes hypodynamic.

However, the circulation is much more interactive in its components defining cardiac output than those described by left ventricular preload and contractility and arterial pressure and arterial vasomotor tone. Fundamental principles of cardiovascular physiology, as originally described by Guyton and colleagues[1] more than 50 yr ago,[1]identified venous return as the primary determinant of cardiac output and that LV function is remarkably insensitive in defining this level of flow, only the required backpressures needed for that flow. We collectively argued these points relative to cardiopulmonary bypass surgery in a physiologic commentary.[2] Until recently, just knowing that venous return was the primary determinant of cardiac output did little to help the bedside clinician manage complex and changing surgical patients. One understood that mean circulatory filling pressure (Pmcf) was the best surrogate for effective circulating blood volume, but its measure and its own determinants were difficult to ascertain at the bedside and nearly impossible to measure repeatedly over time. The effective circulating blood volume represents a balancing act between total circulating blood volume, blood flow distribution amongst various organs with varying degrees of capacitance and unstressed volume, and the resistance to venous return (RVR), which has more of a conductance determinant to its value that actual physical resistive.[3] Importantly, multiple lines of investigation have led to the development of several methods to quantify Pmcf at the bedside using only arterial pressure, central venous pressure (CVP), and cardiac output. A detailed review of these various techniques is found elsewhere.[4] However, presently three techniques are readily available and can be used for the bedside assessment of venous return.

The first approach uses an analogue estimate of Pmcf by assuming a constant proportion of compliance and resistances within the arterial and venous circuit.[5] We recently validated this breath-by-breath analogue approach in a canine model during normal and endotoxic shock state.[6] Using this analogue approach Cecconi and colleagues[7] examined the effect of fluid boluses on Pmcf, the driving pressure for venous return (Pmcf-CVP), and cardiac output in a large postoperative surgical patient population. They showed that fluid loading universally increased Pmcf, if only transiently, and unaltered RVR. However, for cardiac output to increase the driving pressure for venous return also needed to increase. Thus, if fluid loading did not increase cardiac output, CVP increased, whereas in those whose cardiac output increased CVP remained stable. The observation that volume loading does not alter RVR has been known for more than 30 yr,[8] and is the basis for increases in CVP during fluid loading being a ‘stopping rule’ for fluid infusion therapy.[9]

The second method used is the end-inspiratory pause technique wherein several small end-inspiratory hold manoeuvres are done for 10–15 s each at 5, 7.5, 10 and 15 cm H2O airway pressure and the resultant steady state Pra, cardiac output values are used to construct the venous return curve.[10] This technique was validated in postoperative cardiac surgery patients[11] and remains the standard technique by which to validate other estimates of Pmcf.

The final approach is to measure the stop flow radial arterial pressure from an indwelling arterial catheter 15 to 20 s after total limb occlusion by rapid inflation of a proximal sphygmomanometer cuff.[12] This approach is attractive because it only requires a simple measure of radial arterial pressure. Geerts and colleagues[13] defined the cardiovascular effects of dobutamine in a porcine model using this approach. Importantly, they identified that dobutamine, a known vasodilator, not only decreased Pmcf but also decreased RVR, such that cardiac output did not decrease as much as would have otherwise been the case if only Pmcf had decreased. And in responsive heart failure patients who are not hypovolemic, the associated decrease in CVP resulted in the expected increase in cardiac output. These data underscore the central role that RVR has in defining cardiac output under conditions in which vasomotor tone varies.

Vasopressor agents such as norepinephrine increase global vasomotor tone, increasing arterial tone, arterial pressure, Pmcf and the RVR. The resultant change in cardiac output is a function of LV contractile reserve. In healthy patients with preserved contractility who can tolerate the increase in arterial pressure without dilating, cardiac output increases, whereas in those who cannot, cardiac output reduces.[14] Similarly, in septic pressor-dependent patients undergoing weaning from vasopressor support, the decreasing norepinephrine concentrations are associated with both a decrease in Pmcf and RVR, such that cardiac output usually remains constant.[15] These findings are relevant to anaesthetists because removing vasopressors may be similar to adding anaesthetics, as both should decrease basal vasomotor tone. In sepsis this is most likely because of decreased sympathomimetic activity and in general anaesthesia as a result of decreased central sympathetic output.

All these interactions form the basis for the recent study by de Wit and colleagues[16]who studied the effect of increasing doses of propofol during surgery on global haemodynamics. They studied three doses of propofol approximating low, medium and high infusion rates that correspond to mean BIS scores of 52, 39 and 29, respectively. Not surprisingly, they showed that as propofol dose increased arterial resistance and arterial pressure decreased. However, both cardiac output and CVP were unchanged. Similarly, with the reduction in LV afterload, both pulse pressure variation and stroke volume variation increased. Not surprisingly, Pmcf also decreased with increasing doses of propofol, probably as a result of an increase in unstressed circulatory volume, as the arterial vasodilation caused blood to perfusion increasing more vascular beds. Why then did cardiac output not decrease? Because if all that happened was a decrease in stressed volume decreasing Pmcf, cardiac output should decrease. Or for that matter, why did cardiac output not go up if CVP remained constant and LV afterload decreased? Ignoring the reality that CVP does not reflect volume responsiveness,[17] it would otherwise be surprising to see that propofol had such a minimal effect of cardiac output. The reason is that RVR also decreased as more parallel venous circuits were opened, increasing vascular conductance. In fact, the decrease in RVR paralleled the decrease in arterial tone, that when coupled with no change in LV contractility cause cardiac output to remain constant. These findings underscore the complex and important interactions that anaesthetics have with the circulation and how by not measuring the determinants of cardiovascular function the bedside anaesthetist may both misunderstand and mistreat their patients. It also adds new meaning to the phrase ‘balanced anaesthesia.’

Now that we have the tools necessary to apply the knowledge already known about cardiovascular physiology in theatre, it will be very interesting to see how other general and regional anaesthetics alter cardiovascular function, and do so across patients with varying degrees of cardiovascular reserve.

References

  1. Guyton AC, Lindsey AW, Abernathy B,et al. Venous return at various right atrial pressures and the normal venous return curve. Am J Physiol 1957; 189: 609–15
  2. Pinsky MR, Permutt S, Wang Y-YL,et al. The classical Guyton view that mean systemic pressure, right atrial pressure, and venous resistance govern venous return is correct. J Appl Physiol 2006; 101: 1528–30
  3. Rothe CF. Venous system: physiology of the capacitance vessels.Comprehensive Physiology 1983
  4. Pinsky MR. Mean systemic pressure monitoring. In: Cannesson M, Pearse R, eds.Perioperative Hemodynamic Monitoring and Goal Directed Therapy. Cambridge University Press, 2014; 157–62
  5. Parkin WG, Leaning MS. Therapeutic control of the circulation.J Clin Monit Comput 1993; 22: 391–400
  6. Lee JM, Ogendele O, Pike F, Pinsky MR. Effect of acute endotoxemia on analogue estimates of mean systemic pressure.J Crit Care 2013; 28: 880.e9–15
  7. Cecconi M, Ayes HD, Geison M,et al. Change in mean systemic filling pressure during fluid challenge in postsurgical intensive care patients. Intensive Care Med 2013; 39: 1299–305
  8. Pinsky MR, Matuschak GM. Cardiovascular determinants of the hemodynamic response to acute endotoxemia n the dog.J Crit Care 1986; 1: 18–31
  9. Pinsky MR, Kellum JA, Bellomo R. The CVP is a stop rule, not a target of resuscitation.Crit Care Resuscitation 2014; 16: 246
  10. Versprille A, Jansen JR. Mean systemic filling pressure as a characteristic pressure for venous return.Pflugers Arch 1985; 405: 226–33
  11. Maas JJ, Geerts BF, de Wilde RBC, van den Berg PCM, Pinsky MR, Jansen JRC. Assessment of venous return curve and mean systemic filling pressure in post-operative cardiac surgery patients.Crit Care Med 2009; 37: 912–8
  12. Maas JJ, Pinsky MR, Geerts BF, deWilde RB, Jansen JR. Estimating mean systemic filling pressure in postoperative cardiac surgery patients with three methods.Intensive Care Med 2012; 38: 1452–60
  13. Geerts BF, Maas JJ, Lagrand WK, Aarts LP, Pinsky MR, Jansen JRC. Partitioning the resistances along the vascular tree: effects of dobutamine and hypovolemia in piglets with an intact circulation.J Clin Monit Comp 2010; 24: 377–84
  14. Maas JJ, Pinsky MR, deWilde RB, de Jonge E, Jansen JR. Cardiac output response to norepinephrine in postoperative cardiac surgery patients: interpretation with venous return and cardiac function curves.Crit Care Med 2013; 41: 143–50
  15. Persichini R, Silva S, Teboul JL,et al. Effects of norepinephrine on mean systemic pressure and venous return in human septic shock. Crit Care Med 2012; 40: 3146–53
  16. deWit F, van Vliet AL, deWilde RB,et al. The effect of propofol on haemodynamics: cardiac output, venous return, mean systemic filling pressure, and vascular resistances. Br J Anaesth 2016; 116: 784–9
  17. Marik PE, Cavallazzi R. Does the central venous pressure predict fluid responsiveness? An updated meta-analysis and a plea for some common sense.Crit Care Med 2013; 41: 1774–81

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