How do I Quantify Physiologic Reserve?

There is no single indicator of "reserve", although there are many different clinical and laboratory markers of individual organs’ reserve. 

Although the concept of physiologic reserve is very interesting, can it be quantified? There are some simple indicators, but no magical number that can be conjured up. Take, for example, the cardiovascular  system: the purpose of this system is to deliver oxygen and nutrients to the tissues and remove waste products, the reserve is the maintenance of blood pressure (and cardiac output) without provoking myocardial ischemia. This can be quantified – patients with coronary heart disease develop rate related ischemia, they develop angina on exertion, by speeding up the heart (stress electrocardiography or echocardiography), it is possible to determine the rate at which ischemia arises. The difference between the resting heart rate and the ischemic rate is the functional reserve. In intensive care it is more likely that this rate related reserve will be required to maintain blood pressure in the face of pathological vasodilatation, and it is very important.

The pulmonary system has a quantifiable reserve. In a patient who develops acute pneumonia, and asthmatic attack or even acute lung injury, the increased work of breathing is compensated for by an increase in the respiratory rate and minute ventilation: functional reserve. A progressive rise in the partial pressure of CO₂ (PaCO₂) in the blood is an indication that the reserve is running out, and mechanical assistance is required (failure to ventilate). When we wish to liberate patients from the ventilator, we perform a series of respiratory mechanical tests. These tests assess the ability of the patient to suck in against an obstruction (negative inspiratory force - NIF), the tidal volume and respiratory rate. The purpose of these tests is not to see if we can take the patient off the ventilator, but whether or not he will stay off the ventilator. These tests quantify reserve; without a NIF of greater that -25cmH2O, we know that most patients will not be able to take a big enough breath to expand atelatatic lung segments or cough out secretions.

The renal system has an enormous reserve. Most young people have a glomerular filtration rate of approximately 120ml/minute, but rarely require dialysis until this has fallen well below 20ml/minute. The most efficient way of quantifying this is to measure 24 hour creatinine clearance, a test frequently done on patients who have anticipated evolving loss of renal reserve, such as diabetics. It is important to intermittently measure creatinine clearance in intensive care, as the serum creatinine is a poor measure of renal function, particularly in progressively catabolic patients, and many of the drugs used in our practice are nephrotoxic.

The hematopoetic  system is a useful example of reserve. We have a serum hemoglobin of 12 – 14g/l under normal conditions, but we know that most patients can tolerate hemoglobin levels  of 6-7g/l without adverse symptoms. This allows us to lose a considerable amount of blood without dying. Likewise, the normal platelet count is usually greater than 300,000, but significant capillary bleeding does not occur until it has fallen below 50,000. The hematopoetic reserve is severely compromised in critical illness. Most of our patients are anemic as a result of phlebotomy, so hemoglobin is a poor measure. The platelet count is another story. A persistent drop in the platelet count usually means excessive destruction/consumption, or inadequate production, either way it is a bad prognostic sign. Likewise, the inability to mount a white cell response to an infection is an indication that the body’s reserves have been overwhelmed.

Quantification of reserve is difficult in the other systems. The bowel has yards of reserve space, but the usual problem in critical illness is undernutrition, ileus and infection related malabsorption. The liver has an enormous reserve, and overt liver failure is extremely unusual in critical illness; a rise in the serum bilirubin is a sign of functional impairment, even with large amounts of hepatocellular destruction (raised transaminases); the metabolic functions are maintained. Nutritional assessment is notoriously difficult in critical illness – these patients lose muscle rather than weight. It is possible to look at muscle function by measuring nitrogen balance (anabolic function) and performing electromyography, if critical illness polymyopathy is considered.

Of all of the body’s systems, the one that is probably most important for regulating the stress response to illness is the one most often forgotten: the neuroendocrine system. It is known that in the late stages of critical illness a state of neuroendocrine exhaustion occurs. The hypothalamus and pituitary gland throw in the towel. Unfortunately, it is difficult to quantify the level of reserve in these patients, as the stress response to critical illness if usually in full swing by the time these patients arrive in our units. It is possible to measure serum levels of vasopressin, growth hormone, insulin-like growth factors, thyroid hormones and cortisol, but the interpretation of the results in critical illness is uncertain. We know that a large number of critically ill patients develop  relative adrenal insufficiency (normal serum cortisol, but an inadequate response considering the stress involved), and this can be quantified using ACTH (adrenocorticotrophic hormone) stimulation test. However the replacement of other pituitary (or end organ) hormones is controversial.

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