Table of Contents

The cardiovascular response to exercise consists of a massive increase in cardiac output combined with a massive decrease in peripheral vascular resistance, predominantly of the skeletal muscle vascular beds. The result is tachycardia, an increased stroke volume, and an increase in blood pressure. Systolic blood pressure increases substantially, but the diastolic drops, and so there is only a slight elevation of MAP. These responses are driven partly by baroreceptor feedback mechanisms, but they can also be activated by the motor cortex in anticipation of exercise.

Cardiac output is defined as the volume of blood ejected by the heart per unit time. It is usually presented as [stroke volume × heart rate], in L/min. Its main determinants are heart rate and stroke volume. Stroke volume, in turn, is determined by preload afterload and contractility, each of which have their own determinants, and each of which influence one another.

First order elimination kinetics is where a constant proportion (eg. a percentage) of drug is eliminated per unit time, whereas zero order elimination kinetics is where a constant amount (eg. so many milligrams) of drug is eliminated per unit time. First order kinetics is a concentration-dependent process (i.e. the higher the concentration, the faster the clearance), whereas zero order elimination rate is independent of concentration. Michaelis-Menten kinetics describes "non-linear" elimination, where where a maximum rate of metabolic clearance is reached when drug concentration achieves 100% enzyme saturation.

The cardiovascular response to isovolaemic anaemia resembles the response to hypovolemia, except that there is vasodilation instead of vasoconstriction. Tachycardia and increased cardiac output are also seen, which are mediated by a vagal reflex for which the sensory afferent is the aortic body chemosensor area. The decrease in peripheral vascular resistance is mediated in part by increased nitric oxide activity, and in part by the decreased blood viscosity.

The arterial pressure wave (which is what you see there) is a pressure wave; it travels much faster than the actual blood which is ejected. It represents the impulse of left ventricular contraction, conducted though the aortic valve and vessels along a fluid column (of blood), then up a catheter, then up another fluid column (of hard tubing) and finally into your Wheatstone bridge transducer. A high fidelity pressure transducer can discern fine detail in the shape of the arterial pulse waveform, which is the subject of this chapter.

The cardiovascular response to haemorrhage consists of a fast baroreflex response, which increases heart rate and peripheral vascular resistance in order to maintain cardiac output and blood pressure. The sympathetic efferent part of the baroreflex also stimulates neurohormonal responses, including renin release, vasopressin release, and the liberation of catecholamines from the adrenal glands. The net effect is the preservation of body fluid volume by decreased water and sodium excretion.

The historical eponymous gas laws as identified below have subsequently been combined into the unifying Ideal Gas Law, which is discussed last. A brief summary of the important features is available elsewhere, for the purposes of revision. This chapter is more of a reflective digression on the history of gas research, lingering delicately on the important roles played in it by lamb bladders and mobs of angry French villagers.

This is the discussion of the loss of 1 litre of whole blood; that is to say, about 300ml of cells and 700ml of plasma fluid, as well as all the dissolved electrolytes and proteins.

Cardiac reflexes are reflex loops between the heart and central nervous system which regulate heart rate and peripheral vascular resistance. Some of these have homeostasis-maintaining roles, for example the baroreceptor reflex which maintains stable cardiac output and blood pressure. Others, such as the oculocardiac reflex and the vasovagal reflex, are not homeostatic in their function, but still have various protective roles. The efferent arms of these reflexes are inevitably the vagus nerve and the sympathetic nervous system.

Respiratory compliance is defined as the change in lung volume per unit change in transmural pressure gradient. It is usually about 100ml/cm H₂O. Static compliance is defined as the change in lung volume per unit change in pressure in the absence of flow. Dynamic compliance is defined as the change in lung volume per unit change in pressure in the presence of flow. Specific compliance is lung compliance which is normalised to a lung volume or capacity, which permits comparison between lungs of different size.

Standing from a supine position decreases venous return and therefore cardiac output. At the same time, hydrostatic pressure in the brain and carotid sinus drops, as they are now elevated above the "hydrostatic indifference point" at the level of the heart. The baroreceptors respond to this by increasing heart rate and peripheral vascular resistance (including venius resistance), which restore blood pressure and cardiac output.

If one were asked to name the most important among the factors that will influence drug absorption and penetration to the site of action,  one would have to name the lipid-water partition coefficient, which is determined by the pKa of the drug and the pH of the body fluids. Put simply, in solution the weak acids and bases will be present in some combination of ionised and non-ionised forms. Of these incompletely ionised substances, the non-ionised forms will be lipid soluble, whereas the ionised forms will not. The proportion of the ionised to non-ionised molecules is determined by the pH of the solution and the pKa of the drug (pKa being the pH at which concentration of ionised and non-ionised forms is equal). 

"Factors which influence blood pressure" seems like a really basic fundamental topic, and so it was surprising to discover a vast conspiracy among academic authors to teach it in a way which makes it totally incomprehensible. In short, blood pressure is determined by flow, resistance, and the total energy of the flowing blood. Each of these factors have their own dependent components, and the contribution of each component varies during the cardiac cycle.

The arterial pressure wave travels at 6-10 metres/sec. The cannula in the artery is connected to the transducer via some non-compliant fluid-filled tubing; the transducer is usually a soft silicone diaphragm attached to a Wheatstone Bridge. It converts the pressure change into a change in electrical resistance of the circuit. This can be viewed as waveform.