Control Of Blood Pressure And Blood Volume - pediagenosis
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Wednesday, February 8, 2023

Control Of Blood Pressure And Blood Volume

Control Of Blood Pressure And Blood Volume.

Control Of Blood Pressure And Blood Volume

Tissues can independently alter their blood flow by changing their vascular resistance. So that this does not have a knock-on effect elsewhere, the pressure head provided by the mean arterial blood pressure (MAP) must be controlled. MAP is determined by the total peripheral resistance (TPR) and cardiac output (MAP = cardiac output × TPR), which is itself dependent on the central venous pressure (CVP) (Chapter 20). CVP is highly dependent on the blood volume. Alterations of any of these variables may change MAP.
Effect of gravity. When standing, the blood pressure at the ankle is 90 mmHg higher than that at the level of the heart, due to the weight of the column of blood between the two. Similarly, the pressure in the head is 30 mmHg less than that at the level of the heart. Blood pressure is always measured at the level of the heart. Gravity does not affect the driving force between arteries and veins because arterial and venous pressures are affected equally.

Acute regulation of the mean arterial blood pressure: the baroreceptor reflex
Physiological regulation commonly involves negative feedback. This requires a sensor that detects the controlled variable (e.g. MAP), a comparator that compares the sensor output to a set point, and a feedback pathway driving effectors that adjust the variable until the difference between the sensor output and the set point is minimized (Chapter 1). The sensor for MAP is provided by baroreceptors (stretch receptors) located in the carotid sinus and aortic arch (Fig. 22a). A decrease in MAP reduces arterial wall stretch and decreases baroreceptor activity, resulting in decreased firing in afferent nerves travelling via the glossopharyngeal and vagus to the medulla of the brain stem, where the activity of the autonomic nervous system (ANS) (Chapter 7) is coordinated. Sympathetic nervous activity consequently increases, causing an increased heart rate and cardiac contractility (Chapter 20), peripheral vasoconstriction, and an increase in TPR and venoconstriction, which increases CVP (Chapter 21). Parasympathetic activity decreases, contributing to the rise in heart rate (Chapter 19). MAP therefore returns to normal (Fig. 22b). An increase in MAP has the opposite effects.
The baroreceptors are most sensitive between 80 and 150 mmHg, and their sensitivity is increased by a large pulse pressure (Chapter 16). They also show adaptation; if a new pressure is maintained for a few hours, activity slowly returns towards (but not to) normal. The baroreceptor reflex is important for buffering short-term changes in MAP, e.g. when muscle blood flow increases rapidly in exercise. Cutting the baroreceptor nerves has a minor effect on average MAP, but fluctuations in pressure are much greater.
Posture. Changes in posture provide a good example of the acute baroreceptor reflex. When standing from a supine position, blood pools in the veins of the legs, causing a fall in CVP; cardiac output and MAP therefore fall (postural hypotension; Chapter 20). Baroreceptor firing is reduced and the baroreceptor reflex is activated. Venoconstriction reduces blood pooling and helps restore CVP which, coupled with an increase in heart rate and cardiac contractility, returns cardiac output towards normal; peripheral vasoconstriction assists the restoration of MAP. The transient dizziness or blackout (syncope) occasionally experienced when rising rapidly is due to a fall in cerebral perfusion that occurs before cardiac output and MAP can be corrected.

Long-term regulation: control of blood volume (Fig. 22c)
The blood volume is dependent on total body Na+ and water. These are regulated by the kidneys, and it is therefore strongly recommended that this chapter is read together with Chapter 35, where the renal mechanisms involved are discussed in detail.
The activation of the baroreceptor reflex by a reduction in MAP leads to renal arteriolar constriction mediated by efferent sympathetic nerves. This and the fall in MAP itself cause a reduction in renal perfusion pressure, which reduces glomerular filtration and so inhibits excretion of Na+ and water in the urine. Sympathetic stimulation and reduced arteriolar pressure also activate the renin–angiotensin system (Chapter 35) and thus the production of angiotensin II, a potent vasoconstrictor that increases TPR. Angiotensin II also stimulates the production of aldosterone from the adrenal cortex, which promotes renal Na+ reabsorption. The net effect is Na+ and water retention, and an increase in blood volume (Fig. 22d). Conversely, a rise in MAP increases Na+ and water excretion.
Changes in blood volume are sensed directly by cardiopulmonary receptors: veno-atrial receptors are located around the join between the veins and atria, and atrial receptors in the atrial wall. These effectively respond to changes in CVP and blood volume. Stimulation (stretch) suppresses the renin–angiotensin system, sympathetic activity and secretion of antidiuretic hormone (ADH, vasopressin), but increases release of atrial natriuretic peptide (ANP) from the atria. Together, these changes promote renal Na+ and water excretion and reduce blood volume (Chapters 34 and 35). A fall in blood volume will induce the opposite effects. The cardiopulmonary receptors normally cause tonic depression – cutting their efferent nerves increases the heart rate and causes vasoconstriction in the gut, kidney and skeletal muscle, thus raising MAP.

Cardiovascular   shock   and   haemorrhage Cardiovascular shock. This is an acute condition with inadequate blood flow throughout the body, commonly associated with a fall in MAP. It can result from reduced blood volume (hypovolumic shock), profound vasodilatation (low-resistance shock) or acute failure of the heart to pump (cardiogenic shock). The most common cause of hypovolumic shock is haemorrhage; others include severe burns, vomiting and diarrhoea (e.g. cholera). Low-resistance shock is due to the pro- found vasodilatation caused by bacterial infection (septic shock) or powerful allergic reactions (e.g. to bee stings or peanuts; anaphylactic shock).
Haemorrhage. Some 20% of the blood volume can be lost without significant problems, as the baroreceptor reflex mobilizes blood from capacitance vessels and maintains MAP. Volume is restored within 24 h because arteriolar constriction reduces the capillary pressure and fluid moves from tissues into the plasma (Chapter 23), urine production is suppressed (see above) and ADH and angiotensin II stimulate thirst. Greater loss (30–50%) can be survived, but only with transfusion within 1 h (the ‘golden hour’) (Fig. 22d). After this, irreversible  shock  generally  develops,  which  is  irretrievable  even  with transfusion. This is because the reduced MAP and consequent profound peripheral vasoconstriction cause tissue ischaemia and the build-up of toxins and acidity, which damage the microvasculature and heart and lead to multiorgan failure.

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