Physiology for MRCEM Primary

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Cardiovascular physiology

Blood pressure regulation

[box type=”warning”] This was not asked in the curriculum, but spare some time to get the basics right to get a good grip over CVS physiology.[/box]

Tissues can independently alter their blood flow by changing their vascular resistance.
Mean arterial blood pressure (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). CVP is highly dependent on the blood volume.

Effect of gravity.

Standing blood pressure at the ankle is ∼90 mmHg higher than that at the level of the heart due to heart. 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.

Acute regulation : the baroreceptor reflex.

Physiological regulation commonly involves negative feedback.
The baroreceptors (stretch receptors) located in the carotid sinus and aortic arch.
A decrease in MAP reduces arterial wall stretch and decreases baroreceptor activity, resulting in decreased firing in afferent nerves via the glossopharyngeal and vagus to the medulla.
Sympathetic activity consequently increases, causing an increased heart rate and cardiac contractility, peripheral vasoconstriction (rise in TPR), and venoconstriction, which increases CVP.
Parasympathetic activity decreases, contributing to the rise in heart rate.
MAP therefore returns to normal. 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.
They also show adaptation; if a new pressure is maintained for a few hours, activity slowly returns towards (but not to) normal.
Cutting the baroreceptor nerves has a minor effect on average MAP, but fluctuations in pressure are much greater.


On 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).
Baroreceptor reflex is activated.
Venoconstriction reduces blood pooling and restores CVP, heart rate and cardiac contractility increase, returning cardiac output towards normal; peripheral vasoconstriction increases TPR and restores 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 : blood volume

The blood volume is dependent on total body Na+ and water.
A drop in MAP activates the baroreceptor reflex which leads to renal arteriolar constriction (sympathetic) reducing renal perfusion pressure, glomerular filtration and inhibition of Na+ and water excretion.
Sympathetic stimulation and reduced arteriolar pressure also activate the renin–angiotensin system, producing 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.
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.
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

Can result from reduced blood volume (hypovolumic shock -haemorrhage; severe burns, vomiting and diarrhoea), profound vasodilatation (low-resistance shock – septic shock, anaphylactic shock) or acute failure of the heart to pump (cardiogenic shock).
Some 20% of the blood volume can be lost without significant problems.
Greater loss (30–50%) can be survived, but only with transfusion within ∼1 h (the ‘golden hour’).
After this, irreversible shock develops, which is irretrievable even with transfusion.
This is because the reduced MAP leads to tissue ischaemia and the build-up of toxins and acidity, which damage the microvasculature and lead to multiorgan failure.