Reflex control of the circulation

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Intrinsic reflexes

Cardiovascular reflexes represent rapidly acting mechanisms to control the circulation using the central and autonomic nervous systems.16 Reflex control of the circulation can be initiated either from within the cardiovascular system (intrinsic reflexes) or from other organs or systems (extrinsic reflexes). Intrinsic reflexes are the most important short term regulators of arterial pressure. These reflexes are produced by changes in arterial pressure or special chemical stimuli. Alterations in blood pressure are sensed by stretch receptors, pressoreceptors, baroreceptors, or mechanoreceptors. Chemoreceptors are sensitive to chemical stimuli, regulate respiration, and, secondarily, also influence the circulation.

Arterial baroreceptor reflexes - Arterial baroreceptors are specialised, pressure sensitive, nerve endings in walls of the aortic arch and internal carotid arteries just above the carotid bifurcation (carotid sinus) (Fig. 6.3). Afferent fibres from the baroreceptors travel in the aortic and carotid sinus nerves, which join the vagus and glossopharyngeal nerves, respectively, and connect with the cardiovascular centres in the medulla, commonly in the nucleus tractus solitarius. Cells from the nucleus tractus solitarius project to the C-l area and inhibit this region by secretion of y-aminobutyric acid (GABA). There is a small tonic discharge from baroreceptor afferents at a normal arterial pressure. When the baroreceptor endings are stretched, action potentials are generated and propagated at a frequency that is approximately proportional to the pressure change in the artery. Hence, increased arterial pressure sensed by the baroreceptors will increase the frequency of impulses travelling to the CNS. Afferent input produces greater activity in the medullary depressor area and inhibits the pressor and cardiac areas, causing decreases in myocardial contractility and heart rate, and reducing vasoconstrictor tone of both arterioles and veins. Therefore, increased blood pressure leads to reflex activity aimed at reducing the pressure back to a normal set point (the depressor reflex). The opposite effect for declines in blood pressure is also true (the pressor reflex). The arterial baroreceptor reflex provides a negative feedback mechanism for homoeostasis of arterial pressure.16

The baroreceptor reflex plays an important role in rapid control of arterial pressure, for example when rising from a recumbent position. The baroreceptor response can be experimentally elicited during sudden decreases or increases in arterial pressure produced by intravenous administration of sodium nitroprusside or phenylephrine, respectively (Smyth's procedure) (Fig. 6.4). The slope of the plot of heart rate (or R-R interval) versus systolic pressure during rapid changes in pressure obtained

Baroreceptor Reflex Arc
Fig 6.3 Diagram of the central connections of the aortic and carotid sinus baroreceptors. (Reprinted with permission from Smith and Kampine.7)
Baroreceptor Reflex

Fig 6.4 Baroreceptor reflex in a human subject. (a) A recording of the baroreceptor response after intravenous infusion of sodium nitroprusside. Note the increase in heart rate and sympathetic nerve activity in response to the decline in blood pressure. (b) The baroreceptor mediated decrease in heart rate and sympathetic nerve activity after an intravenous infusion of phenylephrine. (Reprinted with permission from Ebert.12)

Fig 6.4 Baroreceptor reflex in a human subject. (a) A recording of the baroreceptor response after intravenous infusion of sodium nitroprusside. Note the increase in heart rate and sympathetic nerve activity in response to the decline in blood pressure. (b) The baroreceptor mediated decrease in heart rate and sympathetic nerve activity after an intravenous infusion of phenylephrine. (Reprinted with permission from Ebert.12)

by this technique is a measure of the "sensitivity" of the baroreflex.12 It has been proposed that such sensitivity may be reduced in patients prone to sudden death. Clamping of the common carotid artery or damage to the carotid sinus nerve during carotid endarterectomy surgery may elicit dramatic haemodynamic changes through alterations in the arterial baroreflex.

Arterial baroreceptors respond most effectively to the rate of change of arterial pressure. The response is greatest to changes of arterial pressure in the physiological range (80-150 mm Hg). Several subcategories of baroreceptors exist that respond to different pressure ranges. Arterial baroreceptors respond more actively to declines in arterial pressure than increases. Evidence suggests that the carotid baroreceptors are more sensitive to pressure changes than the aortic baroreceptors and operate at lower ranges of arterial pressure. Experimental investigations have determined that arterial baroreceptors primarily influence reflex control of cardiac rate and contractility. Control of systemic vascular resistance is of secondary importance. The vessels most influenced by arterial baroreceptors are splanchnic arterioles and venules, with the venules being important in increasing venous return to the heart during the pressor reflex. Evidence also suggests that the arterial baroreceptors participate in stimulating the renin-angiotensin system via an increase in sympathetic tone.18 Decreased baroreceptor responsiveness occurs with advancing age, hypertension, and coronary artery disease.

An important property of arterial baroreceptors is the ability to adapt to prolonged changes in arterial pressure. Arterial baroreceptors continue to function in hypertensive individuals or even during acute hypertensive episodes or exercise, but reset at a higher blood pressure range.19 The higher pressure ultimately forms a new baseline range, but can be reversed if the increase in pressure is relieved. This resetting of the baroreceptor range demonstrates that these reflexes probably have no role in long term blood pressure regulation but, instead, respond only to acute changes in arterial pressure. In fact, resetting can be demonstrated within minutes to hours. The efferent portion of the baroreceptor reflex arc is blocked by many drugs used for the treatment of hypertension. As a result, orthostatic hypotension commonly occurs and, if severe, may lead to syncope. This condition may also be present secondary to pathological processes such as diabetes. Such "autonomic insufficiency" can lead to haemodynamic instability especially during anaesthesia.

Atrial and vena caval low pressure baroreceptors - The right and left atria and inferior and superior vena cava near the junction with the right atrium also contain specialised low pressure mechanoreceptors that respond to increases in central venous pressure.7 These baroreceptors respond to pressure change but in a much lower range that arterial baroreceptors. The low pressure baroreceptors send impulses via large myelinated fibres in the vagus nerves to the CNS when the atria or vena cava are distended. The efferent portion of the reflex consists of SNS fibres to the sinoatrial node and subsequently causes tachycardia. This increase in heart rate caused by atrial stretch is known as the Bainbridge reflex and is abolished by vagotomy. Although the Bainbridge reflex has been observed in numerous species, the heart rate response to atrial filling in humans is complicated by numerous other factors, including the dominant arterial baroreflex, so this reflex probably plays only a secondary role.

Other baroreceptors have been isolated that are also stimulated by filling and distension of the atria but send impulses via unmyelinated vagal fibres to the CNS.11 The reflex heart rate response is the opposite of that which occurs in the Bainbridge reflex, and the overall response is analogous to that of the arterial baroreceptors. An increase in venous return increases and positive pressure ventilation reduces discharge from the receptors. Arterial distension results in decreases in SNS activity, causing a decline in vasoconstriction of skeletal muscle, renal, and mesenteric arterioles, an increase in splanchnic venous capacitance, and a reduction in heart rate. The decrease in SNS activity is accompanied by a decline in renin secretion. Reduced circulating angiotension and aldosterone also decrease arteriolar vasoconstriction and lead to a diminution in plasma volume.

As with arterial baroreceptors, atrial baroreceptors adapt to a continuous increase in pressure by resetting.7 This has been demonstrated in experimental animals where congestive heart failure leads to prolonged atrial distension, increased atrial pressure and attenuation of this reflex. This adaptation is reversed if the heart failure is relieved. It is also important to note that these atrial baroreceptors are stimulated not only by stretch but also by atrial muscle contraction. Hence, it is believed that the diuresis observed in certain clinical and experimental pathological conditions, such as paroxysmal atrial tachycardia and atrial fibrillation, may be the result of the unusual contractile activity in the atrial wall. Atrial natriuretic peptide may also play an important role. The low pressure baroreceptors are significant in the control of extracellular fluid volume. When volume is reduced, these receptors cause a reflex release of vasopressin and enhanced sympathetic tone, which activates the renin-angiotensin-aldosterone axis. In addition, SNS reflex constriction of the afferent arterioles occurs to conserve intravascular volume.^These actions increase volume and homoeostasis is maintained.

Ventricular reflexes - The ventricles contain receptors that are also stimulated by stretch or by strong ventricular contraction.7 These receptors provide afferent input to the medulla via unmyelinated vagal fibres. The medulla responds by decreasing sympathetic tone and causing bradycardia and vasodilation. A very similar reflex response (that is, bradycardia and vasodilation accompanied by apnoea) can be elicited by injecting the drug, veratridine, into the heart or coronary circulation (especially the left circumflex perfusion territory in canine experiments). The unusual coronary chemoreceptor response is referred to as the Bezold-Jarisch reflex. Investigation suggests that this reflex may also be triggered by intracoronary injections of other pharmacological agents, including serotonin, capsaicin, nicotine, bradykinin, histamine and digitalis. A similar reflex has been noted after injection of contrast media during coronary angiography and in certain pathological conditions when specific metabolites accumulate in the coronary circulation, for example, in myocardial necrosis. It has been proposed that the coronary chemoreceptor reflex may be elicited during inferior wall myocardial infarction.

Arterial chemoreceptors - There are also arterial chemoreceptors located in the carotid and aortic bodies, small masses of tissue lying in close proximity to the carotid sinus and the aortic arch receptors (see Fig. 6.3), which have prominent effects on respiration and the circulation. The carotid body is the major chemoreceptor. The special nerve endings respond to decreases in the arterial partial pressure of oxygen (PaO2), increases in the arterial partial pressure carbon dioxide (PaCO2), and increases in arterial hydrogen ion concentration. The afferent pathway is located in the same nerves as the adjacent baroreceptors. Arterial chemoreceptors serve primarily to cause an increase in respiratory minute volume, but secondarily these receptors produce sympathetic vasoconstriction during hypotension. This response is additive to that produced by arterial baroreceptors. The ''secondary" circulatory reflex actions improve oxygen delivery to heart and brain through generalised peripheral vasoconstriction and increased arterial pressure. The increased arterial pressure occurs during hypotension secondary to severe depletion of intravascular volume and subsequent reduction in blood flow and ischaemia of the carotid and aortic bodies. The chemoreceptor response also contributes to formation of Mayer waves during recording of arterial pressure. Decreases in perfusion of the chemoreceptors during hypotension causes activation of the reflex and results in increases in arterial pressure. Increases in flow then deactivate the chemoreceptors and declines in arterial pressure occur. The repetitive cyclisation leads to large swings in pressure (Mayer waves) at a frequency of 2-3 cycles/min.

Extrinsic reflexes

Receptors of the afferent limbs of extrinsic reflex arcs are external to the circulatory system. These reflexes are less consistent than intrinsic reflexes and, in normal circumstances, play only a minor role in circulatory control. On the other hand, extrinsic reflexes are important and protective during certain types of environmental stresses and pathophysiological circulatory states. Afferent impulses enter the CNS via somatic nerves but the central processing of these reflexes is still uncertain. Examples of extrinsic reflexes include pain and cold, oculocardiac, CNS ischaemic, and Cushing reflexes.

Pain reflex - Pain, depending on severity, produces variable haemodynamic responses. Mild to moderate pain results in tachycardia and increases in arterial pressure mediated by the somatosympathetic reflex. This is a common finding in the postoperative period if analgesia is inadequate. Severe pain, as experienced by deep bone trauma or stretching of abdominal or perineal viscera, may elicit bradycardia, hypotension, and, at times, circulatory collapse and syncope.

Cold reflex - Cutaneous thermosensitive nerve endings respond to cold temperature and send impulses through somatic afferent fibres to the hypothalamus. This results in cutaneous vasoconstriction and piloerection. An example of this reflex is the cold pressor test in which application of intense local cold, such as immersion of a hand in ice water, leads to stimulation of both pain and cold receptors with a subsequent increase in arterial pressure. In certain patients with coronary artery disease, the cold pressor test can produce angina by either reflex coronary vasoconstriction or abruptly increased left ventricular afterload.

Oculocardiac reflex - Receptors stimulated by pressure or stretch in the extraocular muscles, conjunctiva, and globe send impulses through the ophthalmic division of the trigeminal nerve (cranial nerve V) to the CNS.20 This leads to bradycardia and hypertension and possibly to more severe cardiac arrhythmias including asystole. This reflex does have a tendency to fatigue with repeated stimulation, most probably at the level of the cardioinhibitory centre.

CNS ischaemic reflex - The CNS ischaemic response occurs when severe hypotension (as in circulatory shock) reduces perfusion and causes hypoxia of the medullary vasomotor centre.21 Chemoreceptors in the vasomotor centre sense local increases in PCOj and decreases in pH. As a result, there is an intense increase in SNS activity leading to a profound and generalised vasoconstriction. Simultaneously, an increase in PNS activity reduces heart rate. This reflex does not become active until mean arterial pressure decreases below 50 mm Hg (6 7 kPa) and is maximal at mean pressures of 15-20 mm Hg (2-0-2-7 kPa). The CNS ischaemic response does not participate in regulation of normal arterial pressure but is an emergency control system to restore cerebral blood flow when it is dangerously reduced.

The Cushing reflex - The Cushing reflex is another reflex that has an origin directly in the CNS. When intracranial pressure is acutely elevated, cerebral vessels are compressed. The decrease in cerebral perfusion pressure causes a reduction in arterial blood flow, and the CNS ischaemic response occurs. The decrease in blood flow to the vasomotor area results in an increase in SNS activity. This leads to progressive elevations in arterial pressure in an effort to exceed intracranial pressure and maintain adequate cerebral perfusion. Simultaneously, decreases in heart rate are observed which are mediated by the baroreceptor reflex.

Spinal shock and autonomic hyperreflexia

When the spinal cord is acutely trans-sected, all cord functions, including reflexes mediated through the CNS, are interrupted below the level of injury.20 Vasoconstrictor tone regulated by the ANS is disrupted below the cord lesion and, if the spinal cord injury occurs at a high level (that is, C6-C7), spinal shock may result. Spinal shock is characterised by a fall in blood pressure as a result of lack of arteriolar and venular constriction as well as a loss of skeletal muscle pump action. The efferent limb of cardiovascular reflexes cannot compensate for the reduction in arterial pressure. This condition is analogous to the loss of control of blood pressure during spinal anaesthesia. Spinal shock typically lasts from one to three weeks.

After this period, local reflexes in the spinal cord below the level of disruption gradually return and a chronic stage, characterised by SNS overactivity or autonomic hyperreflexia, begins. Hyperreflexia occurs in response to cutaneous or visceral stimulation below the level of cord lesion in 85% of patients with spinal cord injury at or above the T6 level. The stimulus sends afferent impulses into the spinal cord, causing local activation of preganglionic sympathetic nerves and subsequent vasoconstriction. This reflex is normally modulated by inhibitory impulses from higher centres, but as a result of the trans-section, such impulses are blocked. The vasoconstriction causes hypertension and elicits the baroreceptor depressor reflex. The reflex mediated decline in SNS activity and increase in PNS activity occur only above the level of the cord trans-section, whereas vasoconstriction continues below this level. With high levels of trans-section, circulatory reflexes are insufficient to offset the effects of vasoconstriction, leading to persistent and sometimes severe hypertension.

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