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Semester 2 Case 6: Too Much Pressure
What is the normal anatomy of the blood vessels?
vessels of the circulatory system have 3 coats, or tunics: Tunica intima: Inner lining consisting of a single layer of extremely flattened epithelial cells, the endothelium, supported by delicate connective tissue. Tunica media: Middle layer consisting primarily of smooth muscle. The most variable coat. Arteries, veins, & lymphatic ducts are distinguished by the thickness of this layer relative to the size of the lumen, its organisation, & in the case of arteries, the presence of variable amounts of elastic fibres. Tunica adventitia: Outer connective tissue layer or sheath.
Arteries Blood vessels that carry blood under relatively high pressure from the heart & distribute it to the body. Different types of arteries are distinguished from each other on the basis of overall size, relative amounts of elastic tissue or muscle in the tunica media, thickness of the wall relative to the lumen, & function. There are 3 types of arteries:
Large elastic arteries - AKA: Conducting arteries. Have many sheets of elastic fibres in their walls, which enable them to expand when they receive the cardiac output from the ventricles, minimising the pressure change. They return to normal size between ventricular contractions, as they continue to push the blood into the medium arteries downstream. This maintains arterial blood pressure between ventricular contractions.
Medium muscular arteries - AKA: Distributing arteries. Have walls that consist mainly of circularly-disposed smooth muscle fibres. Their ability to constrict regulates the flow of blood to different parts of the body as required. Pulsatile contractions of their muscular walls temporarily & rhythmically constrict their lumina in progressive sequence, propelling &
distributing blood to various parts of the body.
Small arteries & arterioles: Have relatively narrow lumina & thick muscular walls. Degree of filling of capillary beds & level of arterial pressure within the vascular system are mainly regulated by degree of tonus (firmness) in the smooth muscle of arteriolar walls. (Tonus above normal ? hypertension). Anastomoses between multiple branches of an artery provide numerous potential detours for blood flow in case the usual pathway is obstructed by compression due to the position of a joint, pathology, or surgical ligation. If a main channel is occluded, smaller alternate channels can usually increase in size over a period of time, providing a collateral circulation that ensures blood supply to the structures distal to the blockage. These are usually insufficient to compensate for sudden occlusion or ligation. However, true terminal arteries do not anastomose with any adjacent arteries (eg. Those in the retina). Functional terminal arteries have ineffectual anastomoses & supply segments of the brain, liver, kidneys, spleen,
& intestines. Veins Venous system has lower blood pressure so the walls (specifically the tunica media) are thinner than those of their companion arteries. Normally, veins do not pulsate & do not squirt or spurt blood when severed. There are 3 sizes of veins:
Venules: Drain capillary beds & join similar vessels to form small veins. Magnification is required to observe venules. Small veins are the tributaries of larger veins that unite to form venous plexuses.
Medium veins: Drain venous plexuses & accompany medium arteries. In locations where the flow of blood is opposed by the pull of gravity (eg. In the limbs), medium veins have venous valves, passive flap valves that permit blood to flow toward the heart but not in the reverse direction.
Large veins: Characterised by wide bundles of longitudinal smooth muscle & a welldeveloped tunica adventitia. Veins are more abundant than arteries. Their walls are thinner, giving them a large capacity for expansion. However, their diameters are usually larger than those of the corresponding artery. Veins tend to be double or multiple. Those that accompany deep arteries surround them in an irregular branching network. This arrangement serves as a countercurrent heat exchanger, the warm arterial blood warming the cooler venous blood. The accompanying veins occupy a relatively unyielding fascial vascular sheath with the artery they accompany. As a result, they are stretched & flattened as the artery expands during contraction of the heart, which aids in driving venous blood toward the heart - an arteriovenous pump. Anastomoses occur more commonly between veins than arteries. Blood Capillaries Simple endothelial tubes connecting the arterial & venous sides of the circulation that allow the exchange of materials with the interstitial or extracellular fluid. Generally arranged in capillary beds, networks that connect the arterioles & venules. As the hydrostatic pressure in the arterioles forces blood into & through the capillary bed, it also forces fluid containing oxygen, nutrients, & other cellular materials out of the blood at the arterial end of the capillary bed into the extracellular spaces, allowing exchange with cells of the surrounding tissue. However, walls are relatively impermeable to plasma proteins. At the venous end of the capillary bed, most of this extracellular fluid - now containing waste products & carbon dioxide - is reabsorbed into the blood as a result of the osmotic pressure from the higher concentrations of proteins within the capillary. (Starling hypothesis) Arteriolovenular anastomoses (AV shunts) exist in some regions (eg. Fingers) between the small arterioles & venules proximal to the capillary beds they supply & drain. These permit blood to pass directly from the arterial to the venous side of the circulation.
A portal venous system is where blood passes through 2 capillary beds before returning to the heart (Eg. Hepatic portal system).
How is cardiac output controlled by venous return?
It is the various factors of the peripheral circulation that affect flow of blood into the heart from the veins - venous return - that are the primary controllers of cardiac output. The heart has a built-in mechanism that normally allows it to pump automatically whatever amount of blood that flows into the right atrium from the veins. This mechanism is called the FRANKSTARLING LAW OF THE HEART. This states that when increased quantities of blood flow into the heart, the increased blood stretches the walls of the heart chambers. This stretch causes the cardiac muscle to contract with increased force, and this empties the extra blood that has entered from the systemic circulation. Stretching the heart also causes the heart to pump faster, as the sinus node in the wall of the right atrium is stretched, and this has a direct effect on the rhythmicity of the node itself to increase heart rate. In addition, the stretched right atrium initiates a nervous reflex called the Bainbridge reflex, passing first to the vasomotor centre of the brain and then back to the heart by way of the sympathetic nerves & vagi, also to increase the heart rate.
How can peripheral oedema be related to blood pressure?
Starling's forces can also be used to explain ankle swelling in hypertension. This relates to capillaries and the forces governing fluid "exchange" there. At the arterial end of a capillary, the hydrostatic pressure pushing fluid out from the capillary into the interstitium is greater than the "plasma oncotic" pressure pushing fluid back in (this is the osmotic pressure exerted by dissolved plasma proteins, which cannot exit the capillary and thus osmotically "suck" fluid back in). At the venous end of the capillary, the hydrostatic pressure is less so the net pressure is now back into the capillary. Thus fluid exits the capillary at the arterial end, and re-enters at the venous end - "fluid exchange". The pressure at the arterial end of the capillary is already pretty low, because the small arterioles upstream of the capillary are a major site of resistance and thus pressure beyond them (in the capillary downstream) is low. When these arterioles are dilated (which calcium channel blockers are especially good at), the blood pressure falls (less resistance), but the capillary downstream of the arteriole now "sees" more of this pressure. Thus, the hydrostatic pressure at the arterial end of the capillary is increased, as is net outward movement of fluid
- hence more tissue fluid which is apparent as oedema. Ankle swelling is the most prominent sign of this, oedema being noticeable in the lower half of the body.
What is blood pressure?
term 'blood pressure' refers to arterial pressure. Systemic arterial pressures range from an average of 100mmHg at the entrance to the aorta to roughly 35mmHg at the start of a capillary network. Capillary hydrostatic pressure is the pressure within capillary beds. Along the length of a typical capillary, pressures decline from 35mmHg to about 18mmHg. Venous pressure is the pressure within the venous system, and is quite low. Pressure gradient from venules to the right atrium is only about 18mmHg. The pressure gradient across the entire systemic circuit, sometimes called the circulatory pressure, averages about 100mmHg. For circulation to occur, circulatory pressure must be sufficient to overcome total peripheral resistance.
 Blood pressure = Cardiac Output x Total Peripheral Resistance Arterial pressure rises during ventricular systole & falls during ventricular diastole. Average blood pressure = 120/80mmHg. A pulse is a rhythmic pressure oscillation that accompanies each heartbeat. Pulse pressure = The difference between the systolic & diastolic pressures.
To report a single blood pressure value, we use the mean arterial pressure (MAP): MAP = Diastolic pressure + (Pulse pressure / 3)
How is blood pressure normally controlled?
Aim: Ensure arterial blood pressure is adequate for organ perfusion. Sensors:
- Baroreceptors - Chemoreceptors
-Volume Receptors Osmoreceptors Effectors: - Heart
- Blood vessels
- KidneysNeural: The autonomic nervous system directly influences the heart & blood vessels, and maintains the blood pressure around a set point.
Nucleu s solitarius in the brain stem modulates the activity of the cardiovascular centres. The cardiovascular centres are found in the medulla oblongata. Cardiac centres & vasomotor centres often act independently of one another, but together make up the cardiovascular centres. The cardiac accelerator centre increases cardiac output through sympathetic innervation, &
the cardiac inhibitory centre reduces cardiac output through parasympathetic innervation, via the dorsal motor nucleus of the vagus & the nucleus ambiguus. The vasomotor centres contain 2 populations of neurons; a very large group responsible for widespread vasoconstriction, and a smaller group responsible for the vasodilation of arterioles in skeletal muscles & the brain. Vasomotor effects are transmitted via sympathetic nerve fibers. Control of vasoconstriction: Neurons innervating peripheral blood vessels in most tissues are adrenergic [they release noradrenaline]. Noradrenaline causes the stimulation of smooth muscles in the walls of arterioles, causing vasoconstriction. Control of vasodilation: Vasodilator neurons innervate blood vessels in skeletal muscles & in the brain. Stimulation of these neurons relaxes smooth muscle cells in the walls of the arterioles. Relaxation of smooth muscle cells is triggered by NO in their surroundings. Vasomotor centres may control NO release directly or indirectly. The most common vasodilator synapses are cholinergic [they release acetylcholine]. Acetylcholine stimulates endothelial cells to release NO, causing local vasodilation. Another type of vasodilator synapse is nitroxidergic [release NO as a neurotransmitter]. Baroreceptors (mechano/stretch receptors) monitor the degree of stretch in the walls of expandable organs. The baroreceptors involved in cardiovascular regulation are located in the walls of:
Carotid sinuses (near the bases of the internal carotid arteries, innervated by glossopharyngeal nerve)
Aortic sinuses (pockets in the walls of the ascending aorta adjacent to the heart, innervated by vagus nerve)
Wall of the right atrium Any changes detected by aortic baroreceptors trigger the aortic reflex, which adjusts blood pressure to maintain adequate blood pressure & blood flow through the systemic circuit. Carotid baroreceptors are extremely sensitive as blood flow to the brain must remain constant.
| blood pressure ? | firing rate to cardiac & vasomotor centres: 1) Stimulates cardioinhibitory centre ? | parasympathetic nervous activity to SA node ?
Release acetylcholine ?| heart rate. 2) Inhibits cardioaccelerator & vasomotor centres ? | sympathetic nervous activity to SA node ? | heart rate & vasodilation.
| blood pressure ? | firing to cardiac & vasomotor centres: 1) Stimulates cardioaccelerator & vasomotor centres ? | sympathetic nervous activity to SA node ? Release noradrenaline ?| heart rate, | force of contraction, &
vasoconstriction. 2) Inhibits cardioinhibitory centre ? | parasympathetic nervous activity to SA node ? |
heart rate. In a crisis, sympathetic activation occurs, & its effects are enhanced by the release of both noradrenaline & adrenaline from the adrenal medullae. Net effect = immediate increase in heart rate & stroke volume, & a corresponding rise in cardiac output. The vasoconstriction increases peripheral resistance. These adjustments work together to elevate blood pressure. Atrial baroreceptors monitor blood pressure at the end of the systemic circuit - at the venae cavae & right atrium. The atrial reflex responds to a stretching of the wall of the right atrium. Normally, the heart pumps blood into the aorta at the same rate at which blood arrives at the right atrium. When blood pressure rises at the right atrium, blood is arriving at the heart faster than it is being pumped out. Atrial baroreceptors correct the situation by stimulating the CV centres & increasing cardiac output until the backlog of venous blood is removed. Atrial pressure then returns to normal.
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