Circulatory Control Under Special Circumstances

Haemorrhage

An acute loss of about 5% or more, of the blood volume is accompanied by immediate physiological changes, which can cause a patient to become pale and sweaty with a rapid thready pulse. A rapid respiratory rate and mild cyanosis may also be present. The underlying physiological changes include:

• Decreased systolic and diastolic blood pressures

• Reduced pulse pressure

• Increased heart rate and contractility

• Increased vasoconstriction and venoconstriction

• Diversion of blood centrally from cutaneous, muscular and splanchnic circulations

• Adrenal medulla stimulation with increased circulating catecholamine levels

• Tachypnoea

These initial haemodynamic changes may reverse over about 20 min, depending on the extent of the blood loss. If blood loss is excessive, compensatory mechanisms can only produce transient improvement and haemorrhagic shock ensues, with continued haemodynamic deterioration. Compensation for acute blood loss is mediated via a series of mechanisms:

• The baroreceptor reflex gives rise to selective vasoconstriction of arterioles which increases systemic vascular resistance and preserves cerebral and coronary blood flow

• Chemoreceptor reflexes augment the baroreceptor reflex particularly at lower arterial pressures (< 60 mmHg) where the baroreceptor response is limited by its threshold effect

• Cerebral ischaemic response. At mean arterial pressures below 40 mmHg cerebral ischaemia is associated with direct stimulation of the adrenal medulla augmenting the effects produced by baroreceptor and chemoreceptor reflexes

• Re-absorption of interstitial fluid—vasoconstriction reduces capillary hydrostatic pressures which increases net re-absorption of interstitial fluid. About 0.25 ml/kg/min tissue fluid can be gained through increased reabsorption. Ultimately fluid is also shifted from the intracellular compartment to the interstitial space, this balance probably being influenced by raised cortisol levels stimulated during haemorrhage

• Release of catecholamines. Activation of the sympathetic system via the baroreceptor and chemoreceptor reflexes produces stimulation of the adrenal medulla and increased levels of circulating catecholamines

• Renal conservation of water and salt. Decreased renal perfusion produces secretion of renin from the juxtaglomerular apparatus. The renin converts plasma angiotensinogen, to angiotensin I, which in turn becomes angiotensin II, a potent vasoconstrictor. Stimulation of the adrenal cortex also increases aldosterone levels leading to renal retention of sodium. Reduced intravascular volume decreases firing of atrial stretch receptors and produces increased secretion of antidiuretic hormone (ADH) from the posterior pituitary. This results in the retention of water in the renal collecting ducts. ADH is also a potent vasoconstrictor at higher concentrations. The overall effects are retention of water and sodium which help to restore extracellular fluid volume

Over 6 weeks increased erythropoietin secretion from the kidney stimulates bone marrow to produce more red blood cells and replace haemoglobin lost during haemorrhage.

Valsalva Manoeuvre

The Valsalva manoeuvre is forced expiration against a closed glottis, and provides a good demonstration of autonomic reflex control of heart rate and blood pressure. The manoeuvre produces a square wave rise in intrathoracic pressure of about 40 mmHg (Figure CR.30). The cardiovascular response can be considered in the following stages:

• Initially there is an immediate increase in arterial blood pressure as the step in intrathoracic pressure is transmitted to the pressure in the aorta. The increased intrathoracic pressure also compresses pulmonary veins, forcing their contents into the left atrium, and producing a transient rise in cardiac output

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Figure CR.30 Valsalva manoeuvre

• The sustained increase in intrathoracic pressure is also accompanied by higher intra-abdominal pressure due to contraction of the abdominal wall muscles. Raised pressure in the abdomen and thorax compresses the venae cavae reducing the venous return to the right and left sides of the heart. This causes a decrease in arterial and pulse pressures

• The fall in arterial and pulse pressures results in diminished stimulation of baroreceptors, causing a tachycardia and increased systemic vascular resistance. This restores mean arterial and pulse pressures to about resting values recorded before the manoeuvre

• Opening the glottis releases the positive intrathoracic pressure, producing a sudden fall in aortic pressure. The resulting drop in arterial pressure is maintained briefly as blood fills the pulmonary vessels and central veins, rather than providing venous return to the heart. Baroreceptor reflexes again respond to this sudden drop in arterial pressure, and act to restore venous return and cardiac output

• Finally, as venous return to both sides of the heart increases again, cardiac output is restored, but ejects into a peripheral vascular system already constricted by baroreceptor reflexes. Blood pressure, thus, overshoots its original resting value, until increased stimulation of baroreceptors causes reflex bradycardia and vasodilatation to restore blood pressure to normal once again

The events described above occur even after sympathectomy, because reflex activity can still be mediated if the vagus nerves remain intact. However, in the case of autonomic neuropathy, a persisting fall in blood pressure is caused by the high intrathoracic pressure, and there is no reflex tachycardia. Then, on release of the intrathoracic pressure, no overshoot of arterial blood pressure occurs.

A. M. Valsalva (1666-1723) was an Italian anatomist who described the above manoeuvre for clearing the Eustachian tube.

Exercise

Exercise activates reflex mechanisms that enhance cardiovascular performance. These include:

• Cerebrocortical activation of the sympathetic system due to anticipation of physical activity. This is sometimes referred to as 'central command'

• Cardiovascular reflexes due to stimulation of muscle mechanoreceptors during contraction. The afferent limb is via small unmyelinated fibres which relay centrally by unidentified connections, to activate sympathetic fibres to the heart and peripheral vessels

• Local reflexes stimulated by rapid accumulation of metabolites during muscle contraction

• Baroreceptor reflexes

Peripheral chemoreceptors do not play a significant part during exercise as arterial pH, PaCO2 and PaO2 remain about normal. In addition to the cardiovascular reflexes outlined above, pulmonary reflexes increase the depth and rate of breathing.

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