Cardiovascular physiology forts. Flashcards

Question

Sympathetic constrictor nerve: Role in blood pressure homeostasis? ......... Sympathetic dilator nerve: Role in blood pressure homeostasis? .......

Answer 1

Sympathetic constrictor nerve: Role in blood pressure homeostasis? Very important Sympathetic dilator nerve: Role in blood pressure homeostasis? None

Answer 2

Sympathetic constrictor nerve: Duration of effect? Mostly well sustained. Sympathetic dilator nerve: Duration of effect? Transient.

Answer 3

The alerting or defense response, which is the natural stimulus for sympathetic vasodilator activity in carnivores, is induced by fear-flight-fight situations. It is tempting to assume that the increased blood flow improves muscle nutritions in readiness for action (very limited effect).

Answer 4

Metabolic hyperaemia, by contrast, cause capillary recruitment which facilitates the transfer of all solutes. It cannot be emphasized too strongly that local metabolic factors, not sympathetic vasodilator nerves, cause the hyperemia associated with normal, non-emotional exercise.

Answer 5

Perhaps a greater advantage of the rapid cholinergic vasodilation is that it prevents an excessive rise in blood pressure and afterload when the heart rate suddenly increases, as it does in the alerting response.

Answer 6

The non-cholinergic non-adrneergic (NANC) transmitter seems to be a neuropeptide called vasoactive intestinal polypeptide (VIP).

Answer 7

Parasympathetic perganglionic fibres are much longer than their sympathetic counterparts and leave the central nervous system in 2 outflows: The cranial nerve outflow (e.g. vagus) and the sacral spinal outflow.

Answer 8

The distribution of parasymp vasodilator fibres distribution is less universal than that of sympathetic vasoconstrictor fibres. The long preganglionic fibres synapse with postganglionic neurons within the end-organ, and these send short postganglionic fibres to the arterioles. The fibres are not tonically active, firing only when organ function demands a rise in blood flow.

Answer 9

The postganglionic fibres release the classical neurotransmitter acethylcholine, which hyperpolarizes some VSM cells to cause vascular relaxation. Fig 11.13, resulting in an increased blood flow.

Answer 10

It has become clear in recent years that most parasympathetic postganglionic fibres can release not only acetylcholine but also non-cholinergic, non-adrenergic (NANC) transmitters with a vasodilator action. (accordingly, nerve-induced dilatation of some arteries, is only partially prevented by atropine) The predominant NANC vasodilator transmitter is a neuropeptide, vasoactive intestinal polypeptide (VIP), which aslo occurs in sympathetic cholinergic fibres.

Answer 11

Several endocrine secretions have acute effects on the heart and circulation, but these need to be viewed in perspective; in normal healthy animals hormones are of less importance for short-term cardiovascular regulation than is neural control.

Answer 12

If however neural control is impair, as in transplanted hearts or if a pathological event such as hemorrhage arises, then endocrine secretions become very important.

Answer 13

Hormones such as aldosterone are also of major importance in the long-term regulation of plasma volume.

Answer 14

The medulla (core) of the adrenal gland secretes adrenaline (epinephrine) and noradrenaline (norephinephrine)., which are known collectively as the catecholamines.

Answer 15

Adrenaline is a methylated form of noradrenaline.

Answer 16

The medulla develops, embryologically, from postganglionic sympathetic neurons, and it retained an innervation by preganglionic sympathetic fibres which run in the splanchnic nerve and control the gland.

Answer 17

Although both adrenaline and noradrenaline are secreted, adrenaline forms over 3/4 of the secretion in man

Answer 18

exercise, fear-flight -fight situations, hypotension and hypoglycemia.

Answer 19

Adrenaline affects both the heart and vasculature but these effects are quite small at physiological concentrations compared with the effects of the autonomic nerves and local factors (The metabolic effects of adrenaline are at least as important as its cardiovascular effects; namely the stimulation of liver glycogenolysis, and fat lipolysis, which releases glucose into the blood streatm).

Answer 20

Both hormones stimulate the cardiac beta-adrenoceptors, so their direct action is to increase heart rate and contractility. Both hormones at physiological concentrations cause the arterioles and veins to contract in many tissues and at high concentrations both cause vasoconstriction in all tissues. This is due to activation of the VSM alpha adrenoceptors. (many students have an ingrained belief that adrenaline necessarily causes vasodilatation but this is simply not true).

Answer 21

Skeletal muscle, Myocardium, Liver This is due to the abundance of beta-adrenoceptors in these tissues, coupled with the high affinity of adrenaline for beta-receptors.

Answer 22

Because it activates alpha-receptors too.

Answer 23

Because it has a higher affinity for alpha-receptors than beta receptors.

Answer 24

Noradrenaline and noradrenaline thus have opposite effect on skeletal muscle, the single most abundant tissue in the body (approximately 40% body weight), and as a result their overall effects on the systemic circulation differ considerably in an intact animal.

Answer 25

IV Noradrenaline causes a generalized vasoconstriction, which raises the peripheral resistance and blood pressure markedly. (see Fig 11.15). This elicits a baroreceptor reflex which reduces the sympathetic drive to the heart and increases the parasympathetic drive. These reflexes slow the heart and reduce its output, offsetting the direct stimulatory effect of noradrenaline on the myocardium.

Answer 26

IV adrenaline by contrast reduces the total peripheral resistance slightly, because muscle vasodilatation outweighs vasoconstriction in other tissues. Mean blood pressure therefore changes little, and the direct stimulation of the heart by circulating adrenaline proceeds without signifiant opposition by the baroreflex.

Answer 27

Since adrenaline is the predominant catecholamine secreted by the human medulla, the overall effect of adrenal stimulation is to increase cardiac output.

Answer 28

A rare tumor of the adrenal medulla, the phaeochromocytoma, secretes a mixture of catecholamines, causing hypertension. The latter can be treated with alpha-antagonisists like phentolamine.

Answer 29

The remaining important hormones all have roles in the regulation of renal fluid excretion as well as vascular tone.

Answer 30

Vasopressin is a peptide produced by the magnocellular neurons in the supraoptic and paraventricular nuclei of the hypothalamus. From the cell bodies, the vasopressin is transported along the axons, through the pituitary stalk and into the posterior lobe of the pituitary gland. There, the vasopressin is released into the blood stream.

Answer 31

Partly by hypothalamic cells sensitive to tissue fluid osmolarity (osmoreceptors) and partly by cardiovascular pressure receptors.

Answer 32

To promote water retention by the kidney.

Answer 33

The cardiovascular effects of vasopressin are seen at higher concentrations, such as occur during haemorrhagic hypotension in response to reduced pressure receptor traffic.

Answer 34

High concentrations of vasopressin cause a strong vasoconstriction in most tissues which helps to support arterial pressure and contributes to the pallor of the hypovolaemic patient.

Answer 35

The cerebral and coronary vessels, by contrast, respond to vasopressin with an EDRF-mediated dilatation; vasopressin thus produces a redistribution of the cardiac output in favor of the brain and heart, as is appropriate in hypovolaemia.

Answer 36

In dogs with diabetes insipid us and in Brattleboro rats, both of which lack vasopressin, blood pressure is abnormally depressed during dehydration or hemorrhage.

Answer 37

Angiotensin II is a circulating octapeptide with a powerful vasoconstrictor action.

Answer 38

Ang II production is initiated by an enzyme: renin, which is secreted into the bloodstream by the juxtaglomerular cells of the kidney in response to hypotension and renal sympathetic nerve activity. Renin enzymatically cleaves a n alpha-globulin in plasma (angiotensionogen) to produce a peptide, ang I. Ang I is then modified by an enzyme on the surface of endothelial cells (converting enzyme) to form any II. This process taking place mainly in the lungs.

Answer 39

At normal plasma concentrations, the main role of angiotensin II is to stimulate the secretions of aldosterone, an adrenal cortical hormone that causes the kidney to retina salt and water.

Answer 40

Not only does it directly stimulate the VSM cell, but it also enhances noradrenaline release by the sympathetic fibres barrier at the area postrema to simulate sympathetic activity (central action).

Answer 41

Renin and angiotensin levels are particularly high after a hemorrhage and help to support the blood pressure in this situation.

Answer 42

this peptide is secreted by specialized myocytes in the atria in respond to high cardiac filling pressures.

Answer 43

ANP. In contrast to vaspressin and the RAAS, ANP enhances the renal excretion of salt and water and has a modest relaxing effect on resistance vessels. It also reduces plasma volume to a greater extent that can be accounted of by diuresis alone, which may be due to a rise in capillary pressure and an increase in the hydraulic conductance of the capillary wall.

Answer 44

Because these vessels govern the distribution of blood volume between the periphery and thorax, they therefore regulate cardiac filling pressure and thereby influence stroke volume.

Answer 45

The passive thoracic vessels and 3 peripheral systems (splanchnic veins, skeletal muscle veins and cutaneous veins).

Answer 46

The veins of the gastrointestinal tract, liver and spleens contain about 20% of the total blood volume at rest. They are well innervated by sympathetic constrictor nerves and possess alpha-adrenoreceptors.

Answer 47

Splanchnic veins are well innervated b sympathetic constriction nerves and possess alpha-adrenoreceptors. They contract actively during exercise and hypotension due to increased sympathetic activity and circulating catecholamines. See Fig 11.17). This helps to maintain CVP at times of circulatory stress.

Answer 48

The intramuscular veins are very poorly enervated. Their volume is influenced chiefly by body posture (i.e gravity) and by the muscle pump. Although direct sympathetic control of these veins is almost nonexistent, their constriction reduces the downstream pressure, allowing the venous system to recoil elastically and displace blood centrally. (Fig 11.11)

Answer 49

Temperature. High core temperature elicit a reduction in cutaneous sympathetic nerve actiity producing venodilatation. Conversely, raised sympathetic activity causes the skin veins to contract strongly, as happens in hypotensive patients as part of the baroreflex.

Answer 50

A sympathetic mediated constriction of the skin veins is also elicited by emotional stress and by deep inspiration.

Answer 51

Most veins and venues have little basal tone i the absence of sympathetic activity, unlike arterioles, and they show little myogenic response to stretch (except for the portal vein). The responsens to certain hormones, autocoids and drugs also differ. Ang II for ex has little direct effect on veins but a powerful effect of sympathetic nerves on human veins (neuromodulatory action), and this action contributes to the intense venoconstrciton seen in patients with cardiac failure, who commonly hava high angiotension levels.

Answer 52

Histamine causes veins to constrict but arterioles to dilate.

Answer 53

Glyceryl trinitrate has a greater dilator effect on veins than on arterioles, and its efficacy in relieving angina is now recognized as being due partly to the reduction of cardiac filling pressure (and therefore cardiac work) following ventilation.

Answer 54

The lowest level of control is the Bayliss myogenic response, which tends to maintain a constant blood flow and capillary pressur in the face of arterial pressure fluctuations (auto regulation).

Answer 55

The second level of control is that exerted by local metabolites, which reset blood flow and auto regulation to a level appropriate to the tissue's metabolic activity. This process is predominant in the heart and brain, and in exercising skeletal muscle.

Answer 56

The third levels of control is the neuroendocrine system, which manipulates the vasculature of tissues like the skin and the splanchninc region for the benefit of the organism as a whole, or rather, for the benefit of the brain, which has ultimate control over the vasculature

Answer 57

Specialization in individual circulations: The coronary circulation must deliver oxygen at a high rate to keep pace with cardiac demand. Autoregulation is well developed in the coronary circulation and is reset by metabolic vasodilatation to operate at a higher flow.

Answer 58

From the aorta immediately above the cusps of the aortic valve, the left coronary artery supplying mainly the left ventricle and septum and the right artery mainly the right ventricle; though this distribution is somewhat variable in man.

Answer 59

Most of the venous blood drains via the coronary sinus directly into the RA (95%) and the rest drains into the cardiac chambers via the anterior coronary and theBesian veins.

Answer 60

The coronary circulation is the shortest in the body, the mean transit time of the coronary blood being only 6-8 s at rest.

Answer 61

Special tasks of the coronary circulation: The coronary circulation must deliver oxygen at a high rate to keep pace with cardiac demand. Even in a resting subject, the myocardial oxygen consumption is very high, namely approximately 8 ml of oxygen per min per 100 g; this is 20 times greater than in resting skeletal muscle.

Answer 62

In exercise, where cardiac work rate can increase over fivefold, the coronary circulation must increase its delivery of oxygen correspondingly

Answer 63

Myocardial capillary density is very high; there being 3000-5000 capillaries per mm2 cross-section, or roughly one capillary per myocyte. See Fig 12.1. This facilitates the efficient delivery of oxygen and nutrients to the cell, partly be creating a very large endothelial area for exchange and partly by reducing the maximum diffusion distance to only 9 um (the myocyte being approximately 18 um wide)

Answer 64

In a resting subject, the blood flow per unit weight of myocardium is roughly ten times the average value for the whole body. Even so, the myocardium extracts 65-75% of the oxygen from the coronary blood, in contrast to the whole body average of 25% at rest. See Fig 12.2. The high extraction reduces the oxygen content from 195 ml/litre in arterial blood to only 50-70 ml/litre in coronary sinus blood.

Answer 65

The corresponding oxygen pressure (PO2) in coronary venous blood is only 20 mmHg, and in the myocardial fibre itself the PO2 is only about 6 mmHg, falling further during exercise.

Answer 66

In heavy exercise, coronary oxygen extraction can rise to 90% leaving just 20 ml oxygen in each litre of venous blood at a PO2 of only 10 mmHg.

Answer 67

The extraction of fatty acid from coronary blood is also high (40-70%), but glucose extraction is usually low (2-3%), reflecting the substrate preference of myocardium.

Answer 68

The extra oxygen required at high work rates is supplied chiefly by an increase in blood flow rather than extraction; the latter can increase only modestly.

Answer 69

Coronary blood flow increases in almost linear proportion to myocardial oxygen consumption at light to moderate work rates, whilst at high work rates the flow increase lags a little and oxygen extraction rises. Fig 12.3

Answer 70

Myocardial metabolism evidently generates vasodilator messags in a quantitate manner (metabolic hyperemia). The nature of the vasodilator substances, however, remains a well-sought but carefully guarded secret of nature.

Answer 71

The major contenders for the role are interstitial hypoxia and adenosine released by myocytes following ATP degradation. Both candidates dilate coronary arterioles, and the adenosine versus hypoxia controversy remains unresolved.

Answer 72

Autoregulation is well developed in the coronary circulation and is reset by metabolic vasodilatation to operate at a higher flow.

Answer 73

Autoregulation protects myocardium against underperfusion during periods of low blood pressure, though only down to about 50 mmHg.

Answer 74

Myocardial arteries and arterioles are well innervated by sympathetic vasoconstrictor fibres, whose tonic discharge contributes to the arteriolar tone.

Answer 75

This effect is overcome, in a graded fashion, during metabolic vasodilatation. If all the sympathetic fibres to the heart are excited, including those to the pacemaker and myocytes, the ensuing increase in heart rate and contractility raises the cardiac work and the concomitant metabolic vasodilatation outweighs the increased vasoconstrictor nerve activity: blood flow increases. This metabolic "over-riding" of vasoconstriction ensures that any generalize activation of the sympathetic system does not adversely affect the blood flow to this vital organ.

Answer 76

Adrenaline, secreted at times of stress, reinforces the coronary hyperemia by preferentially activating beta-adrenoreceptors on the coronary VSM, causing dilatation. There is some evidence that parasympathetic cholinergic fibres too can dilate coronary arteries but this is not though to be important in exercise.

Answer 77

The branches of the coronary arteries within the myocardium are compressed during each systole. This effects is at its worst in the LV during isovolumetric contraction when pressure with the ventricular wall reaches approximately 240 mmHg and coronary vessels transiently closes them so that coronary blood flow ceases briefly and even reverses in early systole. See Fig 12.4.

Answer 78

A modest coronary flow is restored during the ejection phase as stress in the ventricle wall eases and the arterial pressure rises, but flow is only restored fully during diastole. Roughly 80% of coronary flow occurs in diastole at basal heart rates.

Answer 79

Although cross-connection exist between the branches of the coronary arteries they are few in number and small in diameter in man, and can transmit only a low flow.

Answer 80

Human coronary arteries have been called "functional" end arteries: because if an atheromatous artery is suddenly blocked by thrombosis, the residual blood flow to the tissue downstream is less than 10% of normal, which is insufficient to support normal contraction and metabolism (ischemia).

Answer 81

The ischaemic myocardium becomes acidotic, causing severe cardiac pain and malfunction. The residual flow may be so low that myocutes begin to die after a few hours (necrosis see Fig 1.2). This sequence of events is called myocardial infarction or a heart attack, and is the single commonest cause of death in the West.

Answer 82

Because the wall stress during systole is greatest here and selectively curtails endocardial blood flow at low perfusion pressures.

Answer 83

Angina pectoris can be relieved by nitrodilator drugs, like glyceryl trinitrate which causes peripheral ventilation and vasodilation. This lowers the filling pressure and arterial pressure, which in turn reduced cardiac work and oxygen demand; this lowers the filling pressure and arterial pressure, which in turn reduced cardiac work and oxygen demand.

Answer 84

Beta-adrenergic blockers like propranolol reduce oxygen demand by reducing heart rate and contractility.

Answer 85

Assessment of human coronary circulation: located by arteiography (coronary angiography). PET (positron emission tomography) is another method for imaging myocardial perfusion.Assessment of human coronary circulation: located by arteiography (coronary angiography). Blood flow can be measure more quantitatively by the coronary sinus thermodilution method. PET (positron emission tomography) is another method for imaging myocardial perfusion.

Answer 86

In common :predominance of metabolic control But there are aslo some marked differences, such as the greater role of nervous reflexes in the regulation of resting skeletal muscle flow.

Answer 87

During exercise, the circulation must deliver oxygen and glucose to the muscle fibres at an increased rate and remove waste products and heat at a increased rate.

Answer 88

The regulation of arterial pressure is a less obvious but very important duty of skeletal muscle vascular. Skeletal muscle constitutes about 40% of the adult body mass, and the resistance of this large vascular bed has a substantial effect on blood pressure.

Answer 89

Skeletal muscle arterioles are richly innervated by sympathetic vasoconstrictor fibres whose tonic discharge enhances arteriolar tone in resting muscle; a high arteriolar tone is of course a prerequisite if dilatation (loss of tone) is to be possible.

Answer 90

The vasoconstrictor nerve activity is controlled reflexly by blood pressure receptors in the thorax and neck, and when vasoconstrictor activity is increased by these reflexes (as in orthostasis and hypovolemia) the resistance of the muscle circulation increases. Aided by similar changes in the splanchnic and renal circulations this plays an important part in the regulation of arterial pressure, which depends on peripheral resistance and cardiac output.

Answer 91

After a severe haemorrhage, the vasoconstrictor discharge to skeletal muscle reaches its maximum rate, namely 6-10 per s, and flow is reduced to around 1/5 the normal level ---an exceedingly low perfusion indeed.

Answer 92

During strenuous exercise the mean flow through phasic muscle can increase more then 20-fold; indeed, it is estimated that if all the muscle groups were maximally vasodilator at the same time the output capacity of the heart would be greatly exceeded. During strenuous exercis, the muscle blood flow in fact accounts for up to 80-90% och the cardiac output (cf. 18% at rest)

Answer 93

The muscle hyperemia during exercise is due almost entirely to a fall in vascular resistance occasioned by metabolic vasodilatation, rather than to the relatively modest changes in arterial pressure.

Answer 94

Skeletal muscle: As in myocardium, the flow rises almost linearly with local metabolic rate, and the nature of the vasodilator agents is again controversial.

Answer 95

Skeletal muscle: During the first few minutes of exercise, potassium ions released locally by the contracting muscle raise the interstitial potassium concentration around the vessels, causing dilatation. The local venous concentration of potassium is up to 0.1 mM higher than the arterial value, and this causes a gradual rise in mixed plasma potassium.

Answer 96

A rise in interstitial osmolarity is important in the early stages of exercise too; the venous effluent osmolarity can increase by 20-30 mOsm. The vasodilator effect of both these factors (potassium ion release locally and increased interstitial osmolarity) is potentiated by local hypoxia. 'The osmolarity level soon decreases, and there are conflicting reports on the potassium levels over long periods,so it is far from clear what maintains the vasodilatation during prolonged exercise.

Answer 97

Only about a third of the capillaries in resting skeletal muscle is well perfused at any one instant. (see Fig 11.1). metabolic vasodilatation increases the well perfused fraction by dilating the terminal arterioles. The capillary recruitment shortens the extravascular diffusion distances and thus speeds up the exchange process.

Answer 98

Resting skeletal muscle extracts only 25-30% of the oxygen from blood, whereas in severe exercise the extraction can reach 80-90%.

Answer 99

Intracellular oxygen tension, which in only few mmHg even at rest, falls so low in severe exercise than anaerobic glycolysis begins to predominate and lactic acid production increases. The quantity of lactate formed is an index of the deficit in oxygen supply and this "oxygen dept" can reach several litres.

Answer 100

The local lactic acidosis stimulates nociceptive C fibres, causing pain and the termination of violent exercise. The lactate also stimulates muscle "work receptors" involved in the reflex control of the circulation.

Answer 101

At the end of exercise, a period of post exercise hyperemia re-supplies the muscle with oxygen (which takes only seconds) and more gradually washes out the accumulated lactate and other vasodilator substances. Only a little of the lactate is oxidized locally; most diffuses into the bloodstream and is either taken up by the liver for resynthesis into glycogen or by the heart as a primary substrate.

Answer 102

Although exercise hyperaemis is due chiefly to a fall in vascular resistance, the massaging effect of rhythmic muslce contrition on the deep veins assists limb perfusion. 2 other special adaptions of the skeletal muscle circulation are the sympathetic vasodilator nerves found in predators like cats and dogs, and the vasodilator response of skeletal muscle arterioles to adrenaline.

Answer 103

When skeletal muscle contracts with 30-70% of its maximum voluntary force, it compresses the intramuscular vessels sufficiently to impair the blood flow. In sustained strong contraction, however, the impairment of flow is maintained, and since the store of oxygen in the muscle's myoglobin only suffices for 5-10 s of ischemia, the fibres quickly before hypoxic and lactate accumulates, leading to pain and fatigue. The rapid loss of strength during a strong sustained contraction will be familiar to anyone who has struggled along with a heavy suitcase.

Answer 104

The problem of fluid translocation across capillaries in exercising muscle, leading to a 10-15% fall in plasma volume, was described din section 9.9.

Answer 105

The temperature of the human "core" (the brain, thoracic and abdominal organs) is normally kept within a degree or so of 37 grader in people by balancing the internal heat production and the heat loss from the surface. The surface in question depends on the species; the skin in man, the tongue in dogs and the ears in rabbits.

Answer 106

Heat is lost by 4 processes: radiation, conduction, convection and evaporation. (See fig 12.5)

Answer 107

The cutaneous circulation participates in many cardiovascular reflexes: Hypotension, caused by hypovolemia or acute cardiac failure (shock) reflexly elicits a constriction of the cutaneous veins and arterioles producing the pale, cold skin characteristic of shock. The rise in cutanesous vascular resistance helps to support arterial pressure while the venoconstriction displaces blood centrally and helps to support central venous pressure.

Answer 108

The life-preserving vale of venoconstriction became clear on the battlefields of France during World War I; when it was noticed that wounded men who were rescued quickly and warmed in blankets (producing cutaneous dilatation) survived severe hemorrhages less successfully than the men who could not be reached for some time, and therefore inadvertently retained their natural cutaneous vasoconstriction.

Answer 109

Exercise initially evokes a sympathetically mediated vasoconstriction in skin, but this later gives way to dilatation if core temperature rises.

Answer 110

Exercise initially evokes a sympathetically mediated vasoconstriction in skin, but this later gives way to dilatation if core temperature rises.

Answer 111

Dilatation of cutaneous veins in a hot environment can lower the central venous pressure and thereby predispose the subject to postural fainting, the classic example being the guardsman who faints while standing at attention in hot weather. Cutaneous vasodilatation also increases the local capillary filtration pressure leading to interstitial swelling; this is why a ring often feels tighter on the finger during hot weather.

Answer 112

The brain receives 14% of the resting cardiac output and most of this goes to the grey matter.

Answer 113

Cerebral circulation: 1. Need for a totally secure oxygen supply. Grey matter has a very high rate of oxidative metabolism, and its oxygen consumption accounts for nearly 20% of human oxygen consumption at rest. Grey matter is exquisitely sensitive to hypoxia, and in man consciousness is lost after just a few seconds of cerebral ischaemia, with irreversible cell damage following within minutes. The primary task of the cerebral circulation, and indeed of the entire cardiovascular system, is therefore to secure an uninterrupted delivery of oxygen to the brain.

Answer 114

Cerebral circulation: special tasks: 2. Adjustment of local supply to local demand. Many mental functions are localized in well-defined regions; for example visual interpretation is located in the occipital visual cortex. External monitoring of the uptake of radio labeled glucose and oxygen in the human brain has proved that local neuronal activity increases the local metabolic rate. The cerebral circulation must therefore be capable of regional adjustment to meed the varying metabolic rate of each region.

Answer 115

Cerebral blood flow, like that to other tissues, depends on vascular conductance and arterial pressure. Unlike any other organ, however, the brain is able to safeguard its own blood supply by controlling the cardiac output and the vascular resistance of other organs via its autonomic outflow. Perfusion of peripheral organs (except the heart) is scarified to preserve cerebral perfusion, when necessary.

Answer 116

Cerebral autoregulation: Autoregulation is very well developed in the brain; a fall in blood pressure causes the resistance vessels to dilate and thereby maintain flow (see Fig 12.7). Below approximately 50 mmHg, however, autoregulation fails and cerebral blood flow declines steeply leading to mental confusion and syncope.

Answer 117

Cerebral auto regulation: The upper limit of autoregulation is probably 175 mmHg. Cerebral auto regulation seems to involve both myogenic and metabolic mechanisms.

Answer 118

Cerebral vessels have a well-developed response to arterial carbon dioxide: Hypercapnia causes vasodilatation and hypocapnia vasoconstriction (see Fig 12.7). These effects are mediated by changes in the carbonic acid concentration, and therefore hydrogen ion concentration, in the interstitial fluid around the cerebral vessels.

Answer 119

Cerebral vessels have a well-developed response to arterial carbon dioxide: Other intravascular acids like lactic acid are ineffective because unlike carbon dioxide they cannot penetrate the blood-brain barrier.

Answer 120

If arterial PCO2 is reduced to 15 mmHg by hyperventilation (normal value 40 mmHg), cerebral blood flow shelved and vasoconstriction can be observed directly in the retina. the retina being embryologiallcy an extension of the brain. Owing to this effect, hysterical hyperventilation can lead to disturbed vision, dizziness, and even fainting. The traditional remedy is said to be a paper bag over the subject's head to cause rebreathing of expired carbon dioxide.

Answer 121

Cerebral vessels dilate in response to local hypoxia, but if the arterial blood is hypoxic it stimulates ventilation too, and the ensuing hypocapnia causes vasoconstriction.

Answer 122

A rise in interstitial H+ concentration and adenosine concentration, secondary to increased neuronal metabolism.

Answer 123

The intracerebral arterioles are innervated rather poorly whereas the cerebral arteries outside the substance of the brain are well innervated by sympathetic vasoconstrictor nerves. Paricipation of brain vessels in the baroreceptor refelc is, however, negligible, which is clearly a good thing teleologically.

Answer 124

The cerebral vessels have few alpha-adrenoreceptors, and the vasoconstriction is probably mediated chiefly by neuropeptide Y, which is abundant in cerebral sympathetic fibres.

Answer 125

The role of the vasoconstrictor innervation may be to protect the blood-brain barrier against disruption should arterial pressure rise suddenly.

Answer 126

Perivascular nerve fibres also contain 5-hydroxytryptamine, possibly co-stored with noradrenaline; 5-HT hasa powerful vasoconstrictor effect on cerebral arteries and, along with a high K+ level, is though to contribute to the vasospasm that follows a subarachnoid hemorrhage.

Answer 127

Cerebral arteries are innovated by dilator fibres, probably of parasympathetic origin. They contain acetylcholine and VIP but their role is obscure.

Answer 128

Lipid-soluble molecules like oxygen, carbon dioxide and xenon diffuse freely between the plasma and brain interstitium but ionic solutes like the dye Evans blue fail to penetrate from plasma into most regions of the brain, demonstrating the existence of a barrier to lipid-insoluble solutes.

Answer 129

Because of the blood-brain barrier, the neuronal environment is the most tightly-controlled cellular environment on the body, and the neurons are protected from the fluctuating levels of ions and catecholamines in the bloodstream.

Answer 130

The blood-brain barrier can be disrupted experimentally by hyperosmotic infusions, and is disrupted clinically by acute hypertension or cerebral ischaemia. There are a few regions where the barriers is normally absent; these being regions where plasma solutes have access to receptors (e.g to the osmoreceptores in the circumventricular regions.)

Answer 131

Gravity influence cerebral blood flow indirectly in that central venous pressure and stroke volume are reduced in the upright posture. The ensuing postural hypotension can reduce cerebral flow to the point of dizziness or fainting (postural syncope) in the absence of brisk autonomic reflexes.

Answer 132

Any space occupying lesion ( a cerebral tumour or hemorrhage) raises the intracranial pressure and forces the brainstem down into the foramen magnum. As the brainstem becomes compressed, altered activity in the neurons controlling the sympathetic system causes a rise in sympathetic vasomotor drive, and thus a rise in arterial blood pressure (Cushing's reflex).

Answer 133

Cushing's reflex: The elevated blood pressure also evokes a bradycardia via the baroreceptor reflex, and the combination of bradycardia and acute hypertension is recognized by neurologists as the hallmark of a large, space-occupying lesion

Answer 134

The lung circulation differs very substantially from the various systemic circulations. The entire output of the right ventricle flows through the alveoli, so their perfusion vastly exceeds their nutritional needs and metabolic factors exert no influence on flow.

Answer 135

The metabolic needs of the bronchi are met by an independent systemic, bronchial circulation.

Answer 136

There is only a low basal tone in the pulmonary circulation and no auto regulation. Sympathetic vasomotor nerves exist but have no well-defined physiological role.

Answer 137

Pulmonary vascular resistance is about an eighth that of the systemic circulation so the arterial pressure is low: Typically 20-25 mmHg in systole and 6-12 mmHg in diastole.

Answer 138

Pulmonary arteries and arterioles are shorter and have thinner, less muscular walls than systemic vessels and whereas arterioles dominate vascular resistance in most systemic organs, resistance in the lungs is shared between the arterial vessels (30%), microvasculature: arterioles to venues (50%) and veins (20%).

Answer 139

Resistance in the lungs is shared between the arterial vessels (30%), microvasculature: arterioles to venues (50%) and veins (20%) Consequently, the capillary pressure (8-11 mmHg) is roughly midway between mean arterial pressure (12-15 mmHg) and left atrial pressure (5-8 mmHg).

Answer 140

Elevation of the left atrial pressure to 20-25 mmHg raises capillary pressure sufficiently to create pulmonary edema, but smaller rises are within the safety margin against edema.

Answer 141

Blood flow is distributed unevenly in the lung of an upright subject. The MAP at heart level is around 15 mmHg, but owing to the effect of gravity, the MAP falls to about 3 mmHg at the apex of the lung and rises to 21 mmHg at the base of the lung.

Answer 142

The MAP at heart level is around 15 mmHg, but owing to the effect of gravity, the MAP falls to about 3 mmHg at the apex of the lung and rises to 21 mmHg at the base of the lung. The high basal pressure distends the thin-walled vessels lowering their resistance and thus increasing flow through the base. Conversely, vessels at the apex actually collapse during diastole because diastolic pressure at heart level is only approximately 9 mmHg, which is insufficient to distend the apical vessels in people (apex being typically 16 cm above heart level). Apical perfusion therefore occurs only during systole and the mean apical flow is about a tenth the basal flow at rest.

Answer 143

Apical perfusion therefore occurs only during systole and the mean apical flow is about a tenth the basal flow at rest. This is an important point, because the efficiency of oxygen transfer in the alveoli depends on the ventilation/perfusion ratio, which should ideally be 0.8-1.0

Answer 144

A standing subject has a higher ventilation/perfusion ratio at the apex than the base, and this ventilation/perfusion mismatch slightly impairs the efficiency of blood oxygenation in the upright, resting subject. In addition, the capillary blood flow is pulsate, especially at the apex, so oxygen uptake is pulsatile.

Answer 145

When a subject is spine, the apex to base gradients are abolished and the ventilation/perfusion ratio becomes more even throughout the lung, increasing the effectiveness of blood oxygenation.

Answer 146

The lungs possess a local mechanism to optimize the local ventilation/perfusion ratio. If the ventilation to a local region is reduced or if local blood flow is increased, the alveolar oxygen content falls and its carbon dioxide content increases.

Answer 147

The small pulmonary arteries which pass close to the surface of small airways respond to airway hypoxia by vasoconstriction, while the bronchiolar smooth muscle respond to airway hypercapnia by relaxation; together these changes maintain an optimal ventilation/perfusion ratio.

Answer 148

he vasoconstriction is thought to be mediated by some unidentified vasoconstrictor intermediary rather than by hypoxia itself because pulmonary arterioles isolated from the surrounding lung tissue are unresponsive to hypoxia.

Answer 149

At high altitude, hypoxia-induced pulmonary vasoconstriction causes high-altitude pulmonary hypertension, even in native residents.

Answer 150

Pulmonary vessels are essentially passive conduits and the downstream vessels in particular are very distensible.

Answer 151

When the pressure driving fluid through an isolated perfused lung is raised, with pulmonary venous pressure set below airway pressure, the pressure-flow is concave (See Fig 12.10a), indicating that vascular conducted increases with perfusion pressure. This is probably due t vascular distension and to the opening up (recruitment) of some venous vessels that were initially closed by the airway pressure.

Answer 152

Physical training by endurance athletes (top cyclists) produces a chronic increase in pulmonary vascular conductance.

Answer 153

During upright exercise, a modest rise in pulmonary artery pressure is beneficial for it improves the perfusion of the apices and thereby increases the area of capillaries available for gas exchange.

Answer 154

Exercise can increase the oxygen transfer capacity of the lungs by around 70% partly due to a rise in the perfused capillary area (by up to 40%), and partly due to an increase in capillary blood volume.

Answer 155

Because the pulmonary vessels are thin-walled, their compliance is high.

Answer 156

If intrathoracic airway pressure is raised by a forced expiration against a closed glottis (the Valsalva manoevre) the external pressure on the vessels can expel up to half of the blood content.

Answer 157

Conversely, forced inspiration, which lowers intrathoracic pressure, can increase the human pulmonary blood volume to about 1 litre.

Answer 158

The high capacitance of the pulmonary circulation allows it to act as a variable blood reservoir; for example, the pulmonary capacitance vessels act as a transient source of blood for the left ventricle when output begins to increase at the start of exercise. The capacitance may be influenced by sympathetic vasoconstrictor nerve activity.

Answer 159

The barorecptors are actually mechanoreceptors; they respond to stretch rather than pressure and if stretch is prevented by applying a plaster cast around the artery, the barorecptors fail to respond to pressure.

Answer 160

Carotid baroreceptors are sensitive to the pulse pressure as well as to mean pressure: the greater the oscillation in pressure about a mean, the greater the aggregate activity in the nerve trunk at the pressure and the greater the ensuing reflex.

Answer 161

From a clinical point of view, baroreflex to a fall in pressure is perhaps more important than the response to a rise because acute hypotension is a common medical emergency.

Answer 162

The heart and blood vessels are controlled by sympathetic and parasympathetic nerves whose activity is regulated and coordinated by the brain. The brain itself is guided by sensory information from peripheral receptors located both within the circulation and outside it.

Answer 163

The 3 elements, namely afferent (sensory) fibres, central relays and efferent fibres, form reflex arcs, as illustrated in Figure 13.1

Answer 164

The high-pressure receptors located around the walls of systemic arteries and the low-pressure receptors located in the heart. Together, their afferent fibres transmit information about arterial pressure and cardiac filling pressure to the brainstem, where it is integrated with information from other sensors such as chemoreceptors and muscle reports.

Answer 165

The process of integration and the computation of an appropriate cardiovascular response involves considerable up -and-down traffic between the brianstem, hypothalamus, cerebellum and cortex.

Answer 166

Sympathetic and parasympathetic outflows then initiate appropriate responses in the heart and blood vessels, and these responses are often (but no inevitably) directed at stabilizing blood pressure.

Answer 167

The reflex response to a rise in blood pressure, for example, is bradycardia and peripheral vasodilatation which tends to lower the blood pressure back to its control level.

Answer 168

barorecptors are sprays of non-encapsulated nerve endings found in the advential layer of arteries at 2 main locations: the aortic arch and the carotid sinus (see Figure 13.2)

Answer 169

The carotid sinus is a thin-walled dilatation at the bottom of the internal carotid artery.

Answer 170

The afferent fibres form the fine carotid sinus nerve and then ascend in the glossopharyngeal nerve (IXth cranial nerve) to the petrous ganglion, where the parent cells are located.

Answer 171

Like all afferent neurones, the parent cells are bipolar and their centrally-directed axons continue with the glossopharyngeal nerve to enter the brainstem, where they terminate in the nucleus tractus solitaries (see later).

Answer 172

The aortic barorecptors are located mainly around the transverse arch of the aorta and their fibres form the aortic or "depressor" nerve (in some species) before ascending in the vagus (Xth cranial nerve). The cell bodies lie in the nodose ganglion and the central axons again terminate in the nucleus tracts solitarius.

Answer 173

The baroreceptors are actually mechanoreceptors; they respons to stretch rather than pressure, and if stretch is prevented by applying a plaster cast around the artery the baroreceptor fail to respond to pressure. Normally, however, a rise in arterial pressure causes arterial distension which in turn excites the mechanoreptors.

Answer 174

In the carotid sinus the transduction of the pressure signal into stretch is enhanced by the thinness of the tunica media which makes the wall stretchy and allows a 15% change in diameter for a normal pulse pressure.

Answer 175

When the carotid sinus is distended by a controlled, sustained rise in blood pressure (see Fig 13.3, fibre 1), an individual baroreceptor fibre fires an initial burst of action potentials as the pressure is changing (the dynamic response), and this signals the rate och change of pressure. The activity then falls back somewhat and settles down to a sustained rate (the adapted response) that signals the new pressure level; the adaption is probably due to mechanical "creep" of the receptor within its disco-elastic environment.

Answer 176

Baroreceptors are also dynamically sensitive to a fall in pressure; they transiently fall silent when pressure is reduced; then resume activity at a new slower rate. As a result of this dynamic sensitivity many baroreceptors in vivo fall silent during diastole and their normal activity pattern consists of burst of potentials during systole (see Fig 13.3, fibre 3).

Answer 177

Threshold refers here to the pressure at which the afferent fibre first begins to discharge action potentials.

Answer 178

Threshold: Baroreceptors fall into 2 main classes in this respect. The large-diameter, myelinated fibres (A fibres) have variable but low thresholds (often ca 50-60 mmHg): such fibres are best suited for signaling moderate hypotension. There are also more numerous, thinner non-myelinated fibres (C-fibres) that have higher activation thresholds (mostly >80 mmHg), and are well suited for signalling acute hypertension.

Answer 179

In general, the carotid sinus receptors have lower thresholds and greater sensitivities than the aortic receptors.

Answer 180

Each individual afferent fibre only responds over a limited pressure range, usually 30 mmHg or so. The baroreceptor nerve trunk, however, has a much wider operating range because it contains many A fibres and even more C fibres; when pressure rises, fibres of progressively higher threshold are recruited and thereby extend the range of pressures signalled in the nerve trunk (see Fig 13.4a and 13.6

Answer 181

Sensitivity to pulse pressure: Carotid baroreceptors are sensitive to the pulse pressure as well as to mean pressure; the greater the oscillation in pressure about a mean the greater the aggregate activity in the nerve trunk at that pressure (See Fg 13.4a) and the greater the ensuing reflex. Fig 13.4b. This is partly due to the dynamic sensitivity of the individual receptors and partly to recruitment of high-threshold fibres during each systole.

Answer 182

In the intact animal, any acute rise in arterial pressure increases the baroreceptor discharge rate and this, via a polysynaptic central pathway, enhances the vagal output to the heart and inhibits the sympathetic outflow to the heart and vasculature.

Answer 183

Multifibre recording from sympathetic nerves to human muscle show that the regular burst of activity accompanying each pulse disappears completely if blood pressure is rapidly raised above 150/90 mmHg. The reduced activity in sympathetic vasoconstriction nerves leads to vasodilatation and a fall in peripheral resistance. At the same time, the reduced cardiac sympathetic nerve activity and increased vagal activity cause a bradycardia and reduced contractility. Since blood pressure is the product of cardiac output and peripheral resistance, these changes together tend to return arterial pressure to normal (See Fig 13.1). The baroreflex thus functions as a "buffer", stabilizing the blood pressure against acute change.

Answer 184

The baroreflex thus functions as a buffer, stabilizing the blood pressure against acute change.

Answer 185

From a clinical point of view, the baroreflex to a fall in pressure is perhaps more important than the response to a rise, since acute hypotensions is a common medical emergency.

Answer 186

This manoeuvre reduces the baroreceptor input to the brainstem, as does hypotension in clinical situations, with the following reflex effects:

Answer 187

This manoeuvre reduces the baroreceptor input to the brainstem, as does hypotension in clinical situations, with the following reflex effects: 1. Tachycardia and increased myocardial contractility. Heart rate increases due to reduced vagal inhibition of the pacemaker and increased sympathetic activity. Increased contractility is mediated sympathetically.

Answer 188

2. Splanchnic venoconstriction. Reflex venoconstrction actively displaces blood from the gut and liver into the central veins (See Fig 11.17), which enhances stroke volume via the Frank-Starling mechanism. In skeletal muscle, the volume of blood in the veins (which are poorly innervated) declines secondarily to the fall in venous pressure caused by arteriolar contraction (see Fig 11.11). Both skin and veins can also be constricted by reflexly secreted adrenaline, vasopressin and angiotensin (see later).

Answer 189

3. Arterial constriction: In most laboratory animals, the baroreflex elicits a sympathetically mediated vasoconstriction involving the skeletal muscle, skin, kidney, and the splnachnic vasulature; this raises peripheral resistance.

Answer 190

In man, compression of the common carotid artery causes a strong reflex vasoconstriction in the splanchnic and renal circulations but relatively little change in the forearm and none in the calf. Direct simulation of the human carotid sinus nerve, on the other hand, does inhibit directly-recorded activity in sympathetic nerve, although sympathetic activity to the skin is unchanged. It seems therefore, that carotid sinus baroreceptors do exert some reflex control over human vessels (but not over the skin), but the sympathetic output to human muscle is probably influenced to a greater extend by the cardiopulmonary receptors.

Answer 191

4. Adrenaline is secreted by the adrenal medulla in response to increased splanchnic nerve activity. Adrenaline stimulates the heart and enhances glycogenesis. a) Arteriolar vasoconstriction lowers capillary pressure producing an absorption of interstitial fluid and expansion of the plasma volume b) Increased renal sympathetic nerve activity stimulates the heart and enhances gluocogenesis.

Answer 192

5. Effects on extracellular fluid volume. The baroreflex affects fluid volume and distribution by several mechanisms: a) Arteriolar vasoconstriction lowers capillary pressure producing an absorption of interstitial fluid and expansion of the plasma volume b) Increased renal sympathetic nerve activity stimulates the heart and enhances gluocogenesis. c) In primates, a fall in baroreceptor traffic evokes the release of vasopressin (ADH) from the posterior pituitary gland, producing an antidiuresis and peripheral vasoconstriction.

Answer 193

In summary: 1. Tachycardia and increased myocardial contractility 2. Splanchnic venoconstriction 3. Arteriolar constriction 4. Adrenaline secretion 5. Effects on extracellular fluid volume

Answer 194

The net result of the baroreflex to acute hypotension is thus to stimulate cardiac output, raise TPR, promote fluid retention and enhance plasma volume, thereby countering the hypotension.

Answer 195

In animal experimente, the sensitivity of the baroreflex can be assessed by isolating the carotid sinus and/or aortic arch and measuring the reflex change in heart rate or systemic pressure in response to controlled distension of the baroreceptors.

Answer 196

In human subjects, baroreceptor activity can be altered by injecting the vasoconstriction drug, phyenylephrine, which raises arterial pressure, of by applying suction to a rigid cuff around the neck, which distends the carotid sinus directly (but not the aortic region). From such measurements, stimulus-response curves can be constructed. The responses prove to be sigmoidal functions of the applied pressure change and the maximum slope of the response curve reveals the optimal sensitivity of "gain" of the reflex. In man, the sensitivity declines with age, and in chronic hypertension, due to a fall in artery wall distensibility. The pressure which the reflex strives to maintain is called its setting or set point, and this can be altered either by neural interactions within the central nervous system (central resetting) or by physical changes in the receptor region (peripheral resetting).

Answer 197

Exercise offers an example of central resetting. The moderate rise in arterial pressure during exercis does not reduce the heart rate even though the baroreflex continues to function. (See Fig 13.6), because the reflex is reset centrally to operate around a higher pressure. Thus, the cardiac output is not suppressed, yet, blood pressure is still buffered around the new level.

Answer 198

Central modulation also occurs during the defense response (see later), which involves a sharp rise i blood pressure and suppression of the baroreflex

Answer 199

Sinus arrhythmia is an example of regular central modulation of the baroreflex; the brainstem neurons that drive inspiration alos inhibit the cardiac vagal motor neurons, rendering them temporarily unresponsive to the baroreceptor input. See Fig 13.13. The resulting fall in vagal activity largely explains the tachycardia associated with each inspiration.

Answer 200

If a rise in arterial pressure is imposed on the circulation the baroreceptor threshold rises to a new, higher pressure within 15 min or so. This shifts the whole stimulus response curve to the right, and in this way the receptors regain a position on the steep part of the stimulus-response curve where they can operate most effectively. Although this extends the pressure-range over which the reflex can effectively buffer sudden pressure fluctuations, it also means that the baroreceptores cannot over long periods, provide the brain with reliable information about the absolute blood pressure; the new pressure may produce the same signal as the old press, after resetting has occurred. The long-term ambiguity of the signal is alos exacerbated by sympathetic motor nerves which inntervate the carotid sinus and can enhance the baroreceptor activity. Because the baroreceptors do not transmit unambiguous info about the absolute blood pressure to the brain, they cannot control absolute pressure in the long term.

Answer 201

Buffering acute changes in arterial pressure in the short-term, but not in regulating the absolute pressure in the long term. If the baroreceptor nerves of a dog are cut under anesthesia and the dog allowed to recover, it is hypertensive for a few days, but the average blood pressure then settles down to a normal level, indicating that arterial baroreceptor are not necessary for the long-term setting of blood pressure. But while the pressure averaged over a period of time returns to normal, the pressure is nevertheless very unstable from minute to minute in the denervated animal, fluctuating over a much wider range than normal. See Fig 13.7b

Answer 202

The major role of the baroreflex is thus to buffer short-term fluctuations in arterial pressure: Walking up a 21-degree incline, for example, raises a normal dog's arterial pressure by approximately 10 mmHg, whereas the baroreceptor-deprived dog experiences a 50 mmHg rise in pressure.

Answer 203

The heart and pulmonary artery are richly innervated by afferent fibres: See Fig 13.8. Like the arterial baroreceptors these fibres have, overall, a tonic inhibitory effect on heart rate and peripheral vascular tone; this is known from the effects of total cardiac deafferentation, which causes a tachycardia, peripheral vasoconstriction and rise in blood pressure.

Answer 204

1) mechanoreceptors around the right and left veno-atrial junctions, connected to myelinated vagal fibres. 2) mechanoreceptors that are scattered diffusely throughout the atria, ventricles and pulmonary artery and are served by non-myelinated fibres traveling i the vagus and cardiac sympathetic nerves. 3) chemosensitive fibres traveling in the vagus and cardiac sympathetic nerves. (Both the vagus and cardiac sympathetic nerves are mixed nerves, i.e carry both motor and sensory fibres). Of these, the veno-atrial receptors are normally the most active.

Answer 205

The veno-atrial stretch receptors: These are branched nerved endings around the junctions of the great veins and atria, served by large myelinated vagal afferents. As Figure 13.8 shows, the receptor dispattern). The charge coincides with either atrial systole (type A pattern) or with the V wave of atrial filling (type B pattern), or with both (intermediate). The receptors therefore signal cardiac filling.

Answer 206

``` If they are stimulated by inflating small balloons at the veno-atrial junction in experimental animals, they elicit a reflex tachycardia and a modest increase in urine flow. This reflex (Brainbridge reflex) is probably the basis of the rapid infusion of saline into a dog's venous system. The reflex diuresis and natriuresis (salt excretion) are still something of a puzzle. ```

Answer 207

Reduced renal sympathetic nerve activity plays a role, for it causes renal vasodilatation, but in addition, a hormone must be involved since blood from a dog subjected to atrial distention can induce diuresis in a denervated kidney. Some atrial muscle cells secrete a natriuretic hormone (atrial natriuretic peptide, ANP) as a direct response to stretch, but this is not a reflex, and plasma ANP concentration does not correlate well with the reflex natriuresis. It is possible, therefore, that a further diuretic hormone awaits discovery. Vasopressin (antidiuretic hormone) too may be involved in the reflex diuresis, for in some species its release can be inhibited by an atrial receptor reflex, as well as by the baroreflex. Changes in plasma vasopressin do not, however, seem to explain the reflex diuresis in dogs.

Answer 208

Around 8+% of the cardiac vagal afferents are small-diameter, unmyelinated fibres and many of these subserve mechanoreception; similar fibres also travel in the cardiac sympathetic nerves. Such mechanoreceptors form a meshwork of fine fibres throughout the heart. Those in the atria respond to distension, and fire during the V wave of atrial diastole, though only during inspiration, when atria filling is greatest. The ventricular fibres, by contrast, fire mainly during ventricular systole, monitoring the speed and force o

Answer 209

The net effect of these atrial and ventricular mechanoreceptors is to induce a reflex bradycardia and peripheral vasodilatation, the dilatation being particularly marked in the kidney. The bradycarda contrast with the reflex tachycardia evoked by the myelinated veno-atrial group.

Answer 210

Some unmyelinated vagal afferents are chemosenstive, and discharge in response to capsaicin, bradykinin and prostaglandins, the last of which is known to be released by ischaemic myocardium.

Answer 211

Some unmyelinated sympathetic afferents are chemosensitive too, responding to bradykinin and to other substances released directly by hypoxic myocardium, such as lactic acid and K+ ions.

Answer 212

The sympathetic chemosensitive afferents are though to mediate the pain of angina and myocardial infarctionThe sympathetic chemosensitive afferents are though to mediate the pain of angina and myocardial infarction. The sympathetic afferents ascent the spinal cord in the spinothalamic tract, in which there is considerable convergence with somatic afferent fibres, and this convergence could explain why cardiac pain is usually experienced as emanating from the chest wall and arms (referred pain).

Answer 213

As indicated earlier, the overall effect of cardiopulmonary receptor activity is tonic inhibition of heart rate and vasoconstrictor tone, depressing blood pressure.

Answer 214

the overall effect of cardiopulmonary receptor activity is tonic inhibition of heart rate and vasoconstrictor tone, depressing blood pressure. This depress effect seems to be involved in the long-term regulation of blood pressure, for it dogs are deprived of their cardiopulmonary receptor input as well as their arterial baroreceptor input they experience a sustained hypertension (See Fig 13.7) as well as the excessive fluctuations in pressure that characterize baroreceptor denervation alone. Nevertheless, patiens with transplanted, denervated heart, have no problem in long-term blood pressure regulation.

Answer 215

It is difficult to establish the relative importance of the various intrathoracic receptors in human subjects, but it is clear that the cardiopulmonary group as a whole acts as a sensor of the volume of blood within the low-pressure, central compartment of the cardiovascular system. The cardiopulmonary receptors are, therefore, often referred to as "central volume receptors" or "low-pressure receptor (jämfört med )the high-pressure arterial baroreceptors).

Answer 216

The cardiopulmonary receptors can detect change in blood volume which are too small to affect arterial pressure significantly. This is thought to explain how a rise in intrathoracic blood volume, without significant accompanying change in arterial pressure, causes a reflex vasodilatation in the human forearm. Conversely, a fall in central blood volume (e.g in response to orthostasis or a hemorrhage) leads to a reflex peripheral vasoconstriction, which complements the concomitant baroreceptor reflex.

Answer 217

Human cardiopulmonary receptors are thought to be as important as the baroreflex in controlling the muscle circulation and also the splanchnic veins.

Answer 218

The central volume receptors also stimulates an expansion of body fluid volume. The total diastolic volume of the heart rises after stimulation: stroke volume increases by about 30% via the Frank-Starling mechanism and arterial pressure rises approximately 10 mmHg

Answer 219

A substantial diuresis ensues owing to a reflex renal vasodilation, a fall in plasma vasopressin concentration and a rise in plasms ANP. There is also a slower-acting fall in aldosterone level due to a fall in renin secretion. It is likely that these changes (aside from ANP secretion) are initiated by both the cardiopulmonary receptors and the arterial baroreceptors.

Answer 220

As well as the cardiopulmonary and baroreceptor depressor reflexes, which serve to stabilizes the blood pressure, there are excitatory reflexes which help the cardiovascular system to respond positively to stresses such as exercise and hypoxia.

Answer 221

Arterial chemoreceptors are nerve terminals which respond to hypoxia, hypercapnia and acidosis. They are located mainly in the carotid and aortic bodies, which are small, highly vascularized nodules adjacent to the carotid sinus and aorta (see Fig 13.2).

Answer 222

Their afferent fibres accompany with the baroreceptor afferents in the IXth and Xth cranial nerves.

Answer 223

The chief role of the arterial chemoreceptors concerns the regulation of breathing, and their influence on the circulation is slight at normal gas tensions.

Answer 224

When excitation is increased by hypoxia and hypercapnia, they elicit a sympathetically-mediated constriction of the splanchnic capacitance vessels. If breathing is held constancy by artificial ventilation they also elicit a modest bradycardia but in spontaneously breathing animals the chemoreflex induced an increase in tidal volume, which in turn excites stretch receptors within the lungs. The pulmonary stretch receptors themselves elicit a "lung inflation reflex", consisting of a modest vasodilation and a marked tachycardia, and the latter opposes the direct bradycardial effect of the chemoreflex.

Answer 225

The chemoreflex is important during severe hemorrhage; severe hypotension impairs the perfusion of the chemoreceptor bodies and the resulting "stagnant hypoxia" excites the chemoreceptors very strongly. Further stimulation is produced by the metabolic acidosis that develops during clinical hypotension, and the chemoreceptor-driven rise in sympathetic vasoconstrictor activity helps to support the blood pressure. This is particularly important in severe hypotension where the baroreflex has reached the limit of its range; the baroreceptor fibres fall silent below about 70 mmHg, whereas the chemoreceptors become progressively more excited the lower the perfusion falls.

Answer 226

The chemoreflex also initiates the rapid breathing that is characteristic of hypotensive shock.

Answer 227

Exercise elicits a rise in heart rate, myocardial contractility and, in moderate to severe exercise, arterial blood pressure. The rise in pressure is especially marked during isomeric exercise and is called the pressor response.

Answer 228

The responses to exercise are initiated in part by the higher regions of the brain but they are also in part a reflex response initiated by receptors in the exercising muscle.

Answer 229

their receptors are activated by chemicals released during exercise, notably K+ ions and H+ ions (due to lactic acid formation), and also by local pressure and active muscle tension. The reflex is strongest when the active muscle becomes ischaemic and produces lactic acid, so the reflex is probably best regarded as a system for sensing underperfusion of active muscle.

Answer 230

Cardiovascular responses can also be evoked by receptors not concerned primarily with cardiovascular control. Somatic pain, for example, causes tachycardia and hypertension while severe visceral pain causes bradycardia, hypotension and even fainting.

Answer 231

Ambient cold causes a rise in blood pressure, which increases LV work.

Answer 232

To fall abruptly to around 40 mmHg, due to peripheral vasodilatation. This established that normal sympathetic vasoconstrictor activity depends on a tonic, net excitatory drive from the brain to the spinal sympathetic neurons..

Answer 233

Normal sympathetic vasoconstrictor activity depends on a tonic, net excitatory drive from the brain to the spinal sympathetic neurons. This tonic excitatory drive arises within the medulla oblongata, which is the most caudal (tail-end) part of the brainstem. See Fig 13.11.

Answer 234

The medulla is by no means the only part of the brain involved in cardiovascular regulation; integration of the vast influx of sensory information relevant to the circulation required the participation of the hypothalamus, cerebellum and the cortex. These central pathways are complex and are only partially characterized at present.

Answer 235

Its true role may in fact be to regulate the excitability of spinal neurones in general. The moderne view emphasizes longitudinal traffic up and down the brain between medulla, hypothalamus and cerebellum (see Fig 13.11) as much as transverse traffic within the medulla.

Answer 236

1. To receive the cardiovascular receptor traffic. The dorsomedial medulla contains an elongated nucleus tracts solitaries (see Fig 13.11 and 13.12), which is the site of first synapse for virtually all the cardiovascular afferents--baroreceptors, cardiopulmonary afferents, arterial chemoreceptors, pulmonary stretch receptors and muscle work receptors.

Answer 237

hypertension.

Answer 238

pressor response.

Answer 239

The output of the nucleus tracts solitaries is relayed to various parts of the medulla, hypothalamus and cerebellum (see Fig 13.11). Within the medulla, a polysynaptic path relays a signal to the nucleus ambiguous, which contains the vagal cardiac motor neurons. Signals are also relayed to the caudal ventrolateral medulla, which influences sympathetic output by inhibiting the rostral ventrolateral medulla. The nucleus tractus solitaries also relays information up to the hypothalamic cells that synthesize vasopressin, and to the hypothalamic depressor area.

Answer 240

The cell bodies of the vagal preganglionic fibres controlling the cardiac pacemaker are located chiefly in the nucleus ambiguus (see Fig 13.12 and 13.13) and to a lesser extent in the dorsal motor nucleus. These vagal nuclei used to be called the cardioihibitory centre

Answer 241

When the anesthetic pentobarbitone is applied locally to the surface of the rostral ventrolateral medulla, a severe fall in blood pressure results. This led to the discovery of a rostral ventrolateral group of neurons that exert a tonic excitatory effect upon the sympathetic preganglionic neurons of the spinal intermediolateral columns. In addition there is a more direct descending inhibitory influence on the spinal sympathetic neurones, arising from the raphe nuclei of the brainstem.

Answer 242

Role of the hypothalamus: The hypothalamus contains many regions involved in cardiovascular regulation, including the hypothalamic depressor area, the altering or defense area, the temperature-regulating area and the magnocellular vasopressin-secreting nuclei.

Answer 243

When stimulated electrically, the depressor area mimics the baroreflex; i.e it activates the cardiac vagal fibres and inhibits sympathetic outflow. Although lesions here impair the barorefelx, they do not abolish it, so the region is evidently only one component in the central processing of the baroreflex

Answer 244

Tachycardia Acute hypertension Splanchnic and renal vasoconstriction and dilatation in skeletal muscle mediated by sympathetic cholinergic fibres.

Answer 245

A discrete defense area of the hypothalamus, and electrical stimulation evokes not only the cardiovascular response but also the behavioral manifestations of fear or rage (spitting, snarling and piloerection in cats)

Answer 246

The defense area in the hypothalamus is probably normally activated by the amygadala of the limbic system, a system known to be involved in generating emotional behavior patterns. Stimulation of the defense area indirectly inhibits those neurons in the nucleus tractus solitarius that are excited by baroreceptor traffic.

Answer 247

The hypothalamic defense area can also, by other pathways, influence the cardiac vagal motor neurons and the rostral ventrolateral medulla neurones that govern sympathetic outflow.

Answer 248

Exhibited by the opossum and young creatures like in in the rabbit in the face of danger. it involves a profound bradycardia and hypotension, being in this respect the opposite of the defence response. The response originates in the limic system. Avoidance of a threatening situation by collapse.

Answer 249

Major role: coordinate muscular movement, and during exercise this region helps coordinate the cardiovascular response too.

Answer 250

The areas involved are the fastigial nucleus and the associated vernal cortex, which receive projections from the medulla. Stimulation of the vernal cortex elicits renal vasoconstriction and muscle vasodilatation, i.e, the pattern seen in exercise, while destruction of the fastigial nucleus reduced both the tachycardia and pressor response of dogs to exercise.

Answer 251

The hypothesis proposes that the cerebral cortex, which initiates muscular exercise, also initiates many of the cardiovascular responses by a direct action on the brainstem regions controlling vagal and sympathetic outflow.

Answer 252

Overview of central pathways controlling the circulation: | Figures 13.13 and 13.14 summarize, in an extremely simplified fashion, the central cardiovascular pathways.

Answer 253

1. One route, of short latency, remains within the medulla and passes from the nucleus tracts solitaries to the vagal motor nuclei, not necessarily directly. 2. The other, of longer latency, passes from the nucleus tractus solitarius up to the hypothalamic depressor centre and from there to the vagal motor neurones.

Answer 254

Control of spinal preganglionic neurones: The central pathways linking the nucleus tractors solitaries to the spinal sympathetic neurons are more complex and less well understood. Higher regions are again involved to some degree.. Whatever the intermediate pathways, baroreceptor activation ultimately inhibits the descending excitatory drive from the rostral ventrolateral medulla to the spinal sympathetic pre-ganglion neurones. In addition, there is a direct descending spinal inhibitory pathway from the brainstem raphe nuclei.

Answer 255

A 13-fold increase in the rate of oxygen absorption by the pulmonary circulation during strenuous exercise is not achieved by a 13-fold change in any one parameter but by the integration of, typically, a 1,5-fold rise in stroke volume, a threefold rise in heart rate, and a threefold increase in the arteriovenous difference in oxygen concentration across the lung.

Answer 256

Movement from a supine to a standing position (orthostasis): Effect of gravity on the distribution of venous blood. Rise in transmural pressure in the most dependent vein, increasing the dependent venous volume. The redistribution of blood causes a fall in intrathoracic blood volume over about 15 s in people. Cardiac filling pressure falls several cmH2O, and the energy of myocardial contraction is reduced by the Frank starling mechanism. Stroke volume declines, so pulse pressure falls substantially. Mean pressure falls only transiently owing to reflex corrections, but even so the transient hypotension can be severe enough to impair cerebral perfusion and cause dizziness and visual fading.

Answer 257

Even healthy individuals occasionally expericen postal giddiness, especially when warm conditions cause cutaneous ventilation, which further reduces central filling pressure.,

Answer 258

In healthy subjects, the cardiopulmonary and carotid sinus reflexes quickly restore mean arterial pressure and prevent postural dizziness.

Answer 259

Cardiopulmonary receptor traffic is reduced by the fall in cardiac blood volume. Cardiac baroreceptor traffic is reduced by the fall in pulse pressure and by the fall in sinus pressure due to the direct effect of gravity. The reduced input to the nucleus tractus solitaries informs the brain of the gravity of the situation, eliciting a reflex reduction in vagal outflow to the heart and an increase in sympathetic outflow to the heart and vasculature. HR increases due chiefly to the carotid sinus reflex. combined with a sympathetically.mediated rise in contractility, this limits the fall in cardiac output to ca 20%. Sympathetically-mediated vasoconstriction in the skeletal muscle, splanchnic and renal vascular beds raises the peripheral resistance which not only restores MAP but even increases it above the supine value.

Answer 260

Splanchnic venoconstrction partially compensated for the dependent venous pooling but there is no sustained reflex venoconstriction in muscle or skin during orthostasis.

Answer 261

The effect of orthostasis on capillary filtration, leads to a fall in plasma volume over about 40 min in people. Renal salt and water excretion is cut down by reflexly-induced increases in plasma vasopressin, renin, angtiotensin and aldosterone, acting in combination with the reflex renal vasoconstriction.

Answer 262

A rise in cerebral vascular resistance, which may be due partly to the increased ventilation that accompanies orthostasis and lowers the arterial PCO2, partly due to a sympathetically-induced constriction of cerebral vessels and partly to the collapse of the excranial veins that drain cerebral blood.

Answer 263

It is a forced expiration against a closed or narrowed glottis, and this is a normal accompaniment to defaecation, coughing, lifting heavy weights, singing a top A or playing the trumpet.

Answer 264

Valsalva manoeuvre: The manoeuvre creates a high intrathoracic pressure which evokes a complex circulatory response with 4 phases.

Answer 265

Initially arterial pressure rises because the high intrathoracic pressure presses upon the thoracic aorta. (phase 1)

Answer 266

MAP and pulse pressure then begin to fall because the high intrathoracic pressure impedes venous return, reducing EDV and impairing stroke volume by the Frank'starling mechanism (phase 2)

Answer 267

As pressure falls, cardiovascular receptors elicit a reflex tachycardia and peripheral vasoconstriction which halts the fall in pressure. When the Valsalva manoeuvre is stopped, there is a sudden mechanical drop in blood pressure as periaortic pressure returns to normal (phase 3)

Answer 268

The drop in intrathroacic pressure allows venous blood to surge into the thorax, distending the heart and increasing the stroke volume. As a result, the pulse pressure and mean pressure rebound rapidly (phase 4), causing the baroreceptors to elicit a reflex bradycardia.

Answer 269

The Valsalva response is therefore a useful test of the competence of the barorefex i man. If the reflex is interrupted by a neurological disorder, the Valsalva test shows a continuing pressure fall in phase 2 and no pressure overshoot or bradycardia in phase 4. Individuals showing such a pattern are probe to postural hypotension.

Answer 270

1. Pulmonary blood flow met be increased to enhance gas exchange 2. Blood flow through the working muscle must be raised to enhance gas exchange 3. A reasonably stable blood pressure must be maintained..

Answer 271

1. Pulmonary blood flow met be increased to enhance gas exchange. This first requirement , a rise in pulmonary perfusion, is met by an increase in RV output.

Answer 272

By local metabolic vasodilation which reduces the resistance to blood flow through the working muscle, but in addition, and increase in LV output is necessary to supply the extra flow.

Answer 273

By a variable degree of vasoconstriction in non-active tissues.

Answer 274

The diversion of an increasing fraction or the raised LV output into working muscle, as illustrated in Fig 14.3.

Answer 275

During exercise, the heart shows a remarkable ability to increase its output in direct, almost linear proportion to whole-body oxygen consumption. See Fig 14.4.

Answer 276

Partly to the rise in cardiac output and partly to an increase in oxygen uptake per litre of pulmonary blood; the latter can increase just over threefold, owing to the low oxygen content of venous blood entering the lungs. Applying the Fick principle to such data, we find that the pulmonary oxygen uptake rate can increase by around 13 fold (in people).

Answer 277

Partly to withdrawal of vagal inhibition of the pacemaker and partly to sympathetic stimulation.

Answer 278

The relative contributions of heart rate and stroke volume to the increased cardiac output depend partly on posture; In supine exercise, almost all of the increased output is due to tachycardia, stroke volume increasing at most by a mere 10-20%, whereas in the upright position stroke volume starts from a lower value and can increase by 50-100%.

Answer 279

The enhancement of stroke volume during exercise is achieved partly by a rise in filling pressure which increases the ventricular EDV, and partly by a rise in EF which lowers the ESV. Filling pressure rises by around 1 mmHg due to the skeletal muscle pump and sympathetically-mediated splanchnic venoconstriction. EF and ejection velocity are raised by a sympathetically-mediated improvement in myocardial contractility.

Answer 280

The hyperemia to muscle groups (can increase locally as much as 40 times), is due chiefly to metabolic vasodilatation, aided in upright exercise by the muscle pump's amplification of the pressure gradient. The fall in muscle vascular resistance also has a vital permissive effect on cardiac output; LV output would otherwise be severely curtailed by a high rise in arterial pressure which would oppose ejection.

Answer 281

Metabolic dilatation of terminal arterioles also causes capillary recruitment, shortening the diffusion distance to the contracting fibres.

Answer 282

The increased capillary blood flow, capillary recruitment and decreased tissue concentration together raise the glucose transport rate into active fibres by an order of magnitude. Arteriolar vasodilatation raises capillary pressure, and capillary filtration can reduce volume by as much as 600 ml during prolonged heavy exercise in people.

Answer 283

Coronary blood flow increases in proportion ot cardiac work owing to metabolic vasodilatation.

Answer 284

This calls for a further rise i cardiac output, yet at the same time the cutaneous venodilatation is reducing the cardiac filling pressure. Consequently, the stroke volume tends to decline during prolonged heavy exercise while heart rate increases to compensate.

Answer 285

The fall in , peripheral resistance occasioned by vasodilatation in skeletal muscle, myocardium and skin is so great during hard exercise that blood pressure would fall by 12-40 mmHg, despite the raised cardiac output, were it not for a compensatory vasoconstriction in the splanchnic and renal vascular beds and in non-exercising muscle. The true importance of the vasoconstrictor response lies the most in supporting the arterial pressure.

Answer 286

systemic arterial pressure during exercise depends very much on the severity duration and nature of the exercise. In dynamic exercise (i.e. alternating contraction and relaxation), mean pressure rises by 20 mmHg or less. Systolic pressure and pulse pressure increase more than this, owing to the rise in stroke volume and ejection velocity, but diastolic pressure rises little or even falls.

Answer 287

In static exercise, there is by contrast a large rise in diastolic pressure; simply supporting a 20 kg suitcase for 2-3 min, can raise diastolic pressure by 30 mmHg (the pressor reflex). This increases LV work considerably.

Answer 288

the rise in plasma adrenaline and noradrenaline that occurs during exercise. If cardiac stimulation by the circling catehcolamines is blocked by a beta-adrenoceptor antagonist, the execise tachycardia is prevented.

Answer 289

The skeletal muscle pump, which raises the cardiac filling pressure and hence stroke volume by the Frank' Starling mechanism.

Answer 290

Aside from metabolic vasodilatation, the cardiovascular changes in exercise are caused by altered autonomic nerve activity. It is not entirely clear, however, what causes the brainstem to initiate these changes in autonomic activity. 2 main hypotheses have been put forward; the central command hypothesis and the peripheral reflex hypothesis, and there is evidence that both play a part. It seems likely that both central command and muscle work receptors drive the cardiac response to exercise. Even so, the near-linear relation between CO and whole-body oxygen consumption is a mystery only partially resolved.

Answer 291

The major effect of training on the vasculature of skeletal muscle is to stimulate the growth of new capillaries. This increases the exchange area and prevents an increase in diffusion distance, which muscle hypertrophy would otherwise cause.

Answer 292

Dynamic training also affects cardiac structure and function. Structurally, the ventricular wall grows thicker, myocardial vascularity increases and the ventricular cavities enlarge.

Answer 293

Ventricular EDV increases from approximately 120 ml in the untrained resting adult to as much as 220 ml in the resting athlete, and the stroke volume is 100-125 ml at rest (cf normal 70-80 ml) in people.

Answer 294

The resting cardiac index (output per unit body surface area) is the same in trained and untrained individuals but owing to a higher stroke volume the trained subject achieves his resting output at a lower heart rate (40-50 beats/min). The resting bradycardia is produced by vagal inhibition of the pacemaker.

Answer 295

During exercise, the athlete achieves bigger stroke volumes than the untrained subject. The athlete's maximum HR is about the same as the untrained subject's, but since the athlete starts with a slower heart rate, he can achieve a proportionately greater change (a rise in HR from 40 beats/min to 180 beats/min is a 4,5 fold increase, in contrast to a rise from 70 beats/min to 180 beats/min, which is only a 2,6 fold increase. Along with the enhanced stroke volume this enables the athlete to increase his cardiac output up to 7 fold, outputs of up to 35 litres/min having been recoded in certain individuals.

Answer 296

Hypovolemic shock Septicemic chock Cardiogenic shock.

Answer 297

A 10% body loss elicits little change in mean blood pressure and does not produce the shock syndrome.

Answer 298

Although shock responses pre sever cerebral and myocardial perfusion, the patient is left with a reduced perfusion of most major organs and a reduced body content of water, electrolytes, plasma protein and red cells.

Answer 299

As blood pressure depends on the balance between cardiac output and peripheral resistance, hypertension must be regarded as an imbalance in cardiovascular regulation.

Answer 300

Stiffening of the carotid artery wall reduces the sensitivity of the baroreflex in hypertensive patients, but this is an effect rather than a cause of the hypertension.

Answer 301

Cardiac work can be reduced by rest, by reducing arterial pressure, and by reducing filling pressure.

Answer 302

Acute failure of the cardiovascular system to perfuse the tissues of the body adequately.

Answer 303

the skin is pale, cold and sweaty with constricted veins. The pulse is rapid and weak, due to a tachycardia and low stroke volume. Arterial pressure may be reduced or normal, but pulse pressure is always reduced. Breathing is rapid and shallow, urine output is impaired and the general condition is one of muscular weakness and reduced mental awareness or confusion.

Answer 304

External fluid loss (hemorrhage, diarrhea, and vomiting, dehydration) or to Internal fluid loss (extensive burns, crushing injuries, pancreatitis).

Answer 305

A gram-neg organisms that release a powerful cardiovascular toxin called endotoxin.

Answer 306

An acute organic impairment of cardia function such as myocardial infarction, myocarditis or an arrhythmia.

Answer 307

Although the details of the physiological response vary to some degree with the cause of shock, there is a shared pattern.

Answer 308

Haemorrhagic hypotension: A 10% blood loss (the volume withdrawn during a blood donation) elicits little change in mean blood pressure, and does not produce the shock syndrome. A 20-30% blood loss lowers mean pressure to 60-80 mmHg and produces the shock syndrome, but does not usually threaten life. A 30-40% blood loss lowers pressure to 50-70 mmHg and causes severe, sometimes irreversible shock, with anuria and impaired cerebral and coronary perfusion.

Answer 309

The Frank-Staling mechanism; acute hypovoleamia lowers central blood volume and hence ventricular EDV, which reduced the energy of contraction. Stroke volume therefore declines, reducing the arterial pressure. Arterial hypotension is thus an indirect rather than direct consequence of a bleed, being quite unlike the loss of pressure in a punctured tyre in this respect.

Answer 310

Cardiopulmonary volume-receptor activity and arterial baroreceptor activity decline or cease, while arterial chemoreceptor activity increase, owing to metabolic acidosis (See Fig 15.1) and impaired chemoreceptor perfusion (stagnant hypoxia).

Answer 311

The chemoreceptor input stimulates the rapid ventilation that characterizes shock. The altered inputs to the nucleus tractus solitaries evoke a reflex increase in sympathetic outflow and reflex secretion of adrenaline and vasopressin, and these reflexes play a vital role in the immediate defence against hypovolemia.

Answer 312

1) The responses which are effective within seconds, 2) those that act more slowly (5-60 min) and 3) those that act over longer periods (days - weeks).

Answer 313

Fig 15.1: responses to shock induced by blood withdrawal in the dog.

Answer 314

The resistance vessels in the cutaneous, skeletal muscle, splanchnic and renal vascular beds; raising the total peripheral resistance and supporting arterial pressure.

Answer 315

Muscular weakness, lactic acidosis, oliguria (low urine flow) and pallor.

Answer 316

The adhesion of white cells to the walls of micro vessels.

Answer 317

The peripheral venoconstrictions partially restores thoracic blood volume and cardiac filling pressures. the attending physician often becomes aware of cutaneous venoconstriction when he attempts to cannulate a vein for intravenous fluid replacement.

Answer 318

Adrenaline, Vasopressin Angiotensin II

Answer 319

Vasopressin is secreted by the hypothalamic magnocellular neurones as a reflex response to the fall in cardiac receptor and barorecptor inputs.

Answer 320

Vasopressin enhances the peripheral vasoconstriction.

Answer 321

Ang II contributes the to peripheral vasoconstriction by both local and central actions, and account for about 30% of the initial recovery in blood pressure in venesected dogs.

Answer 322

1) high renal sympathetic nerve activity, 2) reduced renal artery pressure and 3) reduced sodium load at the macula dense.

Answer 323

Because of the compensatory changes in peripheral resistance, venous capacitance and cardiac performance, the arterial pressure may not fall much after a moderate hemorrhage, making arterial pressure an unsafe guide to the severity of shock.

Answer 324

As a result; the osmotic pressure of the plasma proteins predominates across the capillary wall for a while, and causes the absorption of up to 500 ml if interstitial fluid into the vascular compartment i a human adult.

Answer 325

Intermediate term response; the "internal transfusion": As a result of the plasma volume expansion, the haemaotcrit and plasma protein concentration fall soon after a hemorrhage.

Answer 326

The water and salt deficiencies are corrected first by reduced renal excretion and increased fluid intake.

Answer 327

Glomerular filtration rate is cut down by a sympathetically-mediated constriction of the afferent arterioles, while salt and water reabsorption is stimulated by a rise in plasma aldosterone and vasopressin (ADH).

Answer 328

The high plasma conc of Ang II not only stimulates aldosterone secretion but also stimulates the subfornicular organ of the brain, producing the intense thirst that patients experience after a hemorrhage.

Answer 329

The resulting increase in water intake, in combination with the oliguria, quickly replenishes the body water content. Salt retention by the renal tubules, combined with a normal dietary intake of salt (2-10 g/d), replenishes the extracellular salt mass withi a few days.

Answer 330

The synthesis of albumin by the liver gradually restores plasma protein mass over the course of a week.

Answer 331

An erythropoetic factor secreted by the kidney, resting the haematorcrit to normal over a period of some weeks; provided that iron intake is adequate.

Answer 332

If, however, the loss exceeds 30% and has laster over 3-4 h before fluid replacement begins (as in Fig 15.1), shock is often irreversible, even if the whole loss is subsequently made good by transfusion. In such cases, blood pressure may be maintain for a while by the high sympathetic -adrenal outflow, but pressure then begin to fall, leading to myocardial hypoperfusion and possibly death.

Answer 333

some workers attribute i to depression of myocardial contractility while others attribute it to failure of peripheral vasoconstriction caused by peripheral neurotransmitter depletion, accumulation of competing metabolic vasodilator substances and changes in a central opioid pathway within the brain.

Answer 334

Acute tubular necrosis: a form of acute renal failure caused by hypoxic damage to the renal tubules, This is heralded by failure of the urine output to improve after a day or so. For this reason, the urine output of a patient in shock is closely monitored. Antoher serious complication in patients with pre-existing ischaemic heart disease is myocardial infarction, triggered by the fall in perfusion pressure.

Answer 335

A sudden loss of consciousness that occurs when cerebral blood falls to less than half normal owing to an abrupt fall in arterial pressure.

Answer 336

A pathophysiological stress such as hypovolaemia or orthostasis, or it may be a physiological stress such as fear, pain or horror. See Fig 15.2.

Answer 337

Tachycardia, Muscle vasodilatation Cutaneous vasoconstriciton Sweating (people)

Answer 338

Then a sudden increase in vagal outflow causes a profound bradycardia, and at the same time the peripheral resistance vessels dilate, due probably to a fall in sympathetic vasoconstrictor drive. As a result, blood pressure falls precipitously, and reduced cerebral perfusion is followed within seconds by loss of consciousness.

Answer 339

As a result, blood pressure falls precipitously, and reduced cerebral perfusion is followed within seconds by loss of consciousness. This sequence is sometimes called a vaso-vagal attack.

Answer 340

Vaso-vagal attack: the cause of the sudden changes i vagal and vasomotor activity is not certain: int encase of phychogenic fainting, the response could be related to the playing dead response of small animals, which emanates from the cingulate gyrus. In the case of post-haemorrhagic syncope, the response may be initiated by activation of LV mechanoreceptors in the near-empty heart at end-systole.

Answer 341

The supine position resulting from a faint raises the intrathroacic blood volume and filling presseue, and cardiac output and arterial pressure are quickly restored. Consciousness is recovered in about 2 min. It is a mistake, albeit a well-intentioned one, to prop up the patient during a faint, since this deprives him of the benefit of the Frank-Starling mechanism.

Answer 342

Definition and classification: The medical condition "hypertension" can be defined as a chronic, usually progressive, raised arterial pressure.

Answer 343

Since blood pressure depends on the balance between cardiac output and peripheral resistance, hypertension muse be regarded as an imbalance in cardiovascular regulation.

Answer 344

In the early stages of the disorder, when hypertension is both marginal and labile, the cardiac output is raised while the peripheral resistance is only slightly above normal. When the disease is well established, however, the cardiac output is normal or slightly reduced ad the hypertension is therefore due to an increase in peripheral resistance.

Answer 345

Rarefaction is a reduction in the number of vessels present in unit volume of tissue, and the occurrence of rarefaction has recently been confirmed in both the retina and the intestine of hypertensive patients.

Answer 346

Narrowing of the arterioles is due to increased vascular tone in the early stages, and is fully reversible by vasodilator drugs at this stage. As time passes, however, the smooth muscle of the tunica media responds to the chronically raised pressure load by hypertrophying, and this leads to organic narrowing of the lumen. The elevated resistance can then no longer be fully abolished during maximal vasodilatation.

Answer 347

Medial hypertrophy takes only a few weeks to develop in rats subjected to experimental hypertension by clipping one of the renal arteries (which stimulates the RAAS).

Answer 348

What initiates the hypertension? The answer to this question remains uncertain in people. The long-term control of blood pressure involves neural, endocrine and renal mechanisms, and many workers suspect that hypertension develops only if more than one regulatory process is abnormal. Whatever the initial cause, the process is thought to become self-perpetuating once medial hypertrophy develops, since a rise in pressure evokes further hypertrophy.

Answer 349

The treatment of hypertension is based on diuretic drugs to lower extracellular fluid volume, captopril to block the angiotensin-converting enzyme and therefore reduce angiotensin and aldosterone levels, peripheral vasodilators such as calcium-channel blocker (verapamil, nifedipine), and alpha-adrenoreceptor blockers (prazosin) to lower peripheral resistance, and beta-adrenoreceptor blockers like propranolol to reduce cardiac output.

Answer 350

An intrinsic inability of the heart to maintain an adequate perfusion of the tissues at a normal filling pressure. This contrasts with the "disorder" shock, where the low output state is secondary to a low filling pressure.

Answer 351

Starling, working with the isolated heart preparation, noted long ago that when a heart begins to fail, it requires a higher filling pressure and higher end-diastolic volume to maintain its stroke volume, at a normal filling pressure the stroke volume became subnormal. Thus, the immediate cause of cardiac failure is a fall in the energy of contraction at any given EDV, in other words, a reduction in contractility.

Answer 352

Studies of myocardium from failing hearts indicate that although contractility is impaired, energy production is normal, judging by the normal levels of ATP and creatine phosphate. Energy utilization, however, is impaired; both myofibrilar ATPase activity and myofibril content per gram of myocardium are low.

Answer 353

The most serious abnormality may involve intracellular calcium, the key factor in excitation-contraction coupling; calcium transport into the SR is impaired, so the internal calcium store may be low. Possible impairment of the affinity of troponin for calcium is also being investigated.

Answer 354

Owing to the reduction in contractility, the ventricular function curve of the failing ventricle is depressed and its slope is reduced. See Fig 15.3 The pump function curve (stroke volume against arterial pressure) is depressed too.

Answer 355

The rate of tension development is slow in CHF patents, and the ejection fraction falls from the normal 66% to as little as 10-20%. In severe failure, this reduces the stroke volume, but in mild ´failure, the stroke volume may be almost normal owing to a compensatory increase in EDV.

Answer 356

The cardiac output at rest may be either within the normal range (compensated failure) or subnormal (decompensated failure).

Answer 357

The impaired cardiac performance becomes much more obvious during an exercise test, because the failing heart cannot increase its output to a normal extent.

Answer 358

Impairment of the heart rate response.

Answer 359

The decreased sensitivity to filling pressure (i.e, the reduced slope of the ventricular function curve), by the decreased ability to cope with a rise in arterial pressure, and by a decrease in the responsiveness of contractility to catecholamines.

Answer 360

Partly by a depletion of noradrenaline from the cardiac sympathetic nerve terminals due to a fall in tyrosine hydoxylase activity, and partly by down regulation of the myocyte beta 1-adrenoreceptors, that is to say, a decrease in the number and affinity of the receptors.

Answer 361

Pathophysiological response to heart failure: The responses of the circulation and other systems to heart failure include compensatory influences on the heart, the redistribution of cardiac output, renal retention of salt and water, and edema.

Answer 362

An increase in filling pressure and an increased level of circulating catecholamine.

Answer 363

A combination of increased plasma volume and peripheral venoconstriction. The resulting cardiac dilatation can be gross, and is readily detected in chest radiograms.

Answer 364

Moreover, excessive cardiac dilatation can be harmful because contraction becomes mechanically inefficient: the active tension required to generate systolic pressure increases with ventricular diameter (see Laplace effect. Fig 6.), raising the energy cost of systole in a ventricle that can ill afford extra energy costs.

Answer 365

In addition, gross dilatation can widen the AV orifice to such an extent that the atrioventricular valve becomes functionally incompetent, further reducing the ventricular ejection fraction.

Answer 366

A further ill-effect of a high filling pressure is the generation of edema. There are thus several reasons for trying to reduce the filling pressure in severe cardiac failure, even though this does shift the ventricle back along the Starling curve.

Answer 367

Stimulation by circulating catecholamines: The cardiac nerves themselves become depleted of catecholamine level, but there is...........in severe failure which helps to support the inotropic state. The support is somewhat mitigated, however, by a down regulation of myocardial beta 1 adrenoceptors as the disease progresses.

Answer 368

Heart failure patients: Changes in peripheral vascular beds: The limited cardiac output is preferentially distributed to the coronary , cerebral and skeletal muscle circulations at the expense of other peripheral tissues (see Fig 15.5). The perfusion of the renal splanchninc and cuteneous vascular beds is severely reduced, owing to sympathetic vasoconstrictor nerve activity coupled with a rise in plasma Ang II.

Answer 369

The peripheral vasoconstriction maintains the arterial pressure, which would otherwise be threatened by the low cardiac output.

Answer 370

The increases in sympathetic outflow and circulating Ang II also induce cutaneous and splanchnic venoconstriciton, which contribute to the rise in cardiac filling pressure. Although these changes may be beneficial in mild failure, they cause problems in severe failure, due partly to the harmful effects of excessive cardiac dilatation and partly to the curtailment of stroke volume when a failing ventricle has to eject against a normal arterial pressure.

Answer 371

The kidneys retain salt and water in isotonic proportion in cardiac failure, expanding the extracellular fluid compartment by up to 30% and contributing to cardiac dilatation and edema formation.

Answer 372

The mechanisms underlying the salt and water retention are only partially understood but they include altered renal haemodynamics and stimulation of the RAAS. Plasma aldosterone is further elevated by a reduced degradation rate in the congested underperfused liver.

Answer 373

Peripheral and pulmonary oedema in cardiac failure: Oedema of the lungs and/or periphery is a prominent clinical feature in cardiac failure. The edema is caused primarily by a rise in capillary pressure following the rise in venous pressure. Another contributing factor is the fall in plasma colloid osmotic pressure by approximately 7 mmHg due to plasma volume expansion. These changes tip the balance of Starling forces across the venous capillary wall in favor of an excessive filtration rate, leading to edema. The edema may be worse in the periphery or in the lungs depending on whether the right side or left side filling pressure is more severely affected.

Answer 374

Due to the operation of the Frank-Starling mechanism which ensures that left output equals right output, even in failure.

Answer 375

If the left side transiently pumps out less blood than the right, more blood enters the left side, raising left ventricular filling pressure until by the Frank-Starling mechanism, the LV output achieves parity with the right. (see Fig 15.3).

Answer 376

Because pulmonary venous pressure is raised, edema develops in the lungs and such patients display pulmonary vein congestion (see Fig 15.4), reduced lung compliance, pulmonary interstitial edema, and dyspnea (difficulty in breathing). This form of dyspnea is especially marked during the night (paroxysmal nocturnal dyspnea) because the supine position increases pulmonary congestion and pulmonary capillary filtration pressure.

Answer 377

In moderate pulmonary edema, the excess fluid collects mainly in the pulmonary interstitium around the bronchi and larger vessels but in severe pulmonary edema the fluid flood into the alveolar spaces too, impairing oxygen transport with potentially fatal results.

Answer 378

If the RV fails (for example secondary to pulmonary hypertension caused by lung diease), the combined effects of the Frank-Starling mechanism and renal salt-and-water retention is to raise the systemic venous pressure). This gives rise to peripheral edema in the dependent tissues. Such patients show signs of distended jugular veins. Not infrequently both ventricles fail and edema occurs both in the periphery and the lungs.

Answer 379

1) To reduce cardiac work 2) To reduce the excessive plasma volume and cardiac dilatation. 3) To improve myocardial contractility if possible.

Answer 380

By rest By reducing arterial pressure By reducing filling pressure.

Answer 381

To this end, peripheral vasodilator drugs are used, such as alpha-adrenoreceptor blocker prazosin and the calcium-channel blocker nifedipine. By reducing the arterial pressure opposing ejection such drugs improve the cardiac ejection fraction. Peripheral venodilators like nitroglycerine and nitroprusside lower filling pressure and relieve pulmonary congestion. Captopril and enalaprin (angiotensin-convering enzyme inhibitors) are beneficial too.

Answer 382

Cardiac dilatation, plasma volume and edema can be reduced by diuretic drugs like furosemide and the thiazides, or by captopril, which blocks angiotensin-converting enzyme and so reduces aldosterone levels.

Answer 383

The advantage of reducing gross cardiac dilatation is that the heart can the operate at a better mechanical advantage (Laplace's law), which more than makes up for the concomitant movement down the ventricular function curve. It is interesting to note that both vasodilator and diuretic drugs are partially reversing the natural compensatory responses to cardiac failure; one can view the natural compensations as "overdone" in cardiac failure.

Answer 384

The third line of attach is to enhance myocardial contractility by the iontoropic drug digoxin. Its mechanism of action (enhancing the intracellular store of calcium) is explained there. However, digoxin is also rather cardiotoxic and difficult to control therapeutically, and its use has fallen out of favor recently. An exception is made in cases of failure associated with atrial fibrillation (a common association), where digoxin also helps to slow and regularize the heart beat. In other cases, however, good response are often obtained simply by a combination of rest, vasodilator and diuretic therapy.

Cardiovascular physiology forts. Flashcards

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