CARDIAC OUTPUT MONITORING: why it is needed?

“It is astonishing that no one has arrived, at the following obvious method, by which the amount of blood ejected by the ventricle of the heart with each systole, may be determined directly……”

 -Adolf Fick, July 9, 1870, On Fick Principle, In proceedings of Würzburg Physikalische Medizinische Gesellschaft.

Primary determinant of organ perfusion is blood pressure (mean arterial pressure- MAP). Blood pressure itself is product of cardiac output (CO) and  systemic vascular resistance (SVR).

                                   MAP= CO × SVR

This physiological equation can have variety of permutation and combination in different pathological states.

Low MAP could be the result of,

•         low CO and high SVR (hypovolemic and cardiogenic shock)
•         high CO and low SVR (vasodialatory shock- septic, anaphylactic, neurogenic)

Normal MAP could be the result of

•        low CO and high SVR ( high dose vasopressors in the setting of hypovolemia or cardiac dysfunction, in the background of sepsis or primary cardiac disease).

      Therefore blood pressure could be normal even if CO is low, because of physiological compensation or artificial correction (vasoactive drug). 

     

      Critically ill patients can have primary cardiac dysfunction (of various etiology including coronary artery disease) or secondary cardiac dysfunction (of sepsis, neurogenic, anaphylactic origin).

These patients are treated with fluids, vasopressors, ionotropes and diuretics. Though these interventions can optimize the clinical parameters, but sometimes, at the cost of further distorting the already deranged physiology. 

For example a patient of septic shock, on high dose vasopressors, and optimized MAP, may be having cardiac dysfunction (decreased CO). His normal blood pressure may be due to vasopressors induced vasoconstriction. This high vasopressor will further compromise CO.

Therefore the present therapy is actually distorting the already deranged physiology, instead of correcting it.

Similarly, a patient with acute left ventricular dysfunction with decreased CO and increased SVR, if treated with diuretic may further deteriorate, because of occult hypovolemia. Here diuretic use would be against the derange physiology.

Therefore estimation of optimal end organ perfusion, by arterial pressure alone, could be erroneous, as it will not address the deranged cardiovascular physiology.

Hence critically ill patients, demand assessment and monitoring of comprehensive cardiac function including CO, SVR and MAP.

A low CO may have various causes, like inadequate intravascular volume, poor myocardial contractility, myocardial diastolic dysfunction, increased PVR (increased afterload), valvular dysfunction or arrhythmia. 

Critically ill patient can have any of these causes, in isolation or combination, and during the course of illness, these deranged physiologies fluctuate. Thus an appropriate therapy at one point in time, can become inappropriate, as the physiology changes.

Therefore the role of cardiac function monitoring encompasses, assessment of the initial cardiac function including CO, judging response to therapy, and ongoing evaluation and correction, of change in haemodynamic state, with disease progression.

Since the introduction of Fick principle some 100 years ago, different techniques have evolved to measure CO.

Fick’s Principle: the total uptake or release of a substance, by an organ, is the product of blood flow to the organ and difference between arterio-venous concentrations of the substance.

Indicator dilution method and thermodilution method of CO monitoring are based on Fick’s principle.

Intermittent Bolus Pulmonary Artery Thermodilution (IB PATD) is the clinical  gold standard method of CO monitoring. It requires insertion of Pulmonary artery catheter, therefore is invasive method of CO monitoring.

Transpulmonary Thermodilution (TPTD) and Arterial Pulse waveform analysis (Pulse Contour analysis, Pulse Power analysis, Arterial Pressure based output) are minimally invasive techniques of CO monitoring as they  arterial catheter and or  central venous catheter insertion.

Esophageal Doppler monitoring (EDM) and Thoracic Electrical Bioimpedance (TEB) are non-invasive techniques of CO monitoring, as they do not need any invasive catheter.

Non-invasive finger Cuff technique of cardiac output monitoring uses finger cuff with infrared photoplethysmography to determine vessel size and volume of blood, and a non-invasive blood pressure device. Algorithm is used to determine stroke volume and other dynamic parameters. Continuous Non-invasive Arterial Pressure (CNAP) technology and Edwards ccNexfin device are based on this technology.

Apart from measuring CO, Devices available with these techniques estimate different dynamic variable like Stroke volume (SV), Stroke volume variation (SVV), Systemic vascular resistance (SVR), Global end diastolic volume (GEDV), Pulmonary blood volume (PBV) and Extravascular lung water (EVLW).

However, it is important to appreciate that every device has its inherent limitations, therefoe no cardiac output monitoring device can change patient outcome, unless its use is coupled with an intervention that by itself has been associated with improved patient outcomes.

References:

A brief history of arterial wave mechanics. Kim H. Parker. Med Biol Eng Comput, 2009:47.

Functional hemodynamic monitoring, Pinsky, 2007.

Monitoring cardiac function in intensive care S M Tibby, Murdoch. Arch Dis Child 2003;88.