Blood Pressure & Capillary Exchange

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Normal response of the heart rate and blood pressure when one changes from supine position to sitting and standing

The normal heart rate is in is 80-100 beats per minute, and the normal BP is 120/80. From sitting to standing, blood pressure decreases initially, as a result of the pooling of blood in the venous circulation. This results in decreased venous return and, thus, decreased stroke volume. This leads to decreased cardiac output and, hence, lowers blood pressure. The blood pressure should not fall by greater than 20mmHg systolic and greater than 10mmHg diastolic. This is due to the baroreceptor reflex, whereby, stretch receptors in the carotid artery are not stimulated resulting in less stimulation of the cardiovascular center. This results in decreased vagal activity and increased sympathetic stimulation of the heart. Stimulation of beta 2 adrenergic receptors results in an increased rate of contraction of the heart muscles, thereby, increasing heart rate. Stimulation of alpha 1 receptors results in constriction of the arteries, increasing peripheral vascular resistance and, consequently, blood pressure.

List of dysfunctional locations in the cardiovascular system that could affect the baroreceptor reflex

The carotid sinus
The heart such as in cardiomyopathy
The blood vessels
Decreased blood oxygen-carrying capacity such as, in anemia and decreased blood volume.
The cardiovascular center in medulla oblongata.
The aortic arch body
The afferent nerves (glossopharyngeal).
The efferent nerve (vagus).
The receptors such as beta 2, M2 and M3
Neurotransmitter deficiency
A lymphatic system such as, in obstructed vessels
Autonomic nervous system

Preganglionic fibers

Ganglia
Postganglionic fibers
Receptors on effector cells

Role of the muscarinic system in blood pressure regulation

M3 receptors are located in vascular endothelium, smooth muscle and in glands. They are G-coupled receptors. Their stimulation results in activation of the phospholipase C-inositol triphosphate cascade. This results in vasodilatation. This reduces total peripheral resistance (TPR) and lowers the blood pressure because (Blood pressure) BP= Cardiac output (CO) × TPR.

Blockade of the M3 receptors did not result in a change in the heart rate. This is abnormal because stimulation of M3 receptors should cause vasodilatation lowering TPR and, hence, lowering BP. This should be followed by reflex tachycardia if the baroreceptor mechanism is intact. Blockade of the vagus nerve will result in uninhibited sympathetic stimulation of the sinoatrial node. This causes tachycardia due to sympathetic stimulation.

Account for these results

The heart rate did not change, because the sympathetic system is not working properly. The muscarinic blockade should have resulted in tachycardia. This is because the blockade caused vasodilatation and according to the formula mean arterial pressure (MAP) = CO × TPR. The total peripheral resistance is determined by vessel caliber and blood viscosity. In this case, the diameter of the vessel is increased lowering the TPR. This lowers the MAP. Increased heart rate should occur to restore the blood pressure.

Role of the sympathetic nervous system in blood pressure regulation

The sympathetic response is the most important control of blood pressure. It is especially important in rapid minute-to-minute control of BP. It is involved in baroreflex, chemoreflex, and medullary ischemic response. The sympathetic fibers arise from the thoracolumbar (T1-T12 & L1-L3) region of the spinal cord. The nerve endings release and act through catecholamines. They stimulate alpha1 and beta2 receptors found on the target organs.

The sympathetic system stimulates most vessels to constrict but dilates vessels in the cardiac and skeletal muscle. The receptors are found on all vessels except capillaries. In baroreflex, a decrease in BP results in increased sympathetic response leading to increased heart rate and vasoconstriction, therefore, elevating the blood pressure. The chemoreflex refers to the sympathetic response to hypoxemia, hypercapnia and acidosis. The chemoreceptors are located in the carotid and aortic bodies.

Medullary ischaemic response refers to the sympathetic response that results when the medulla is subjected to ischaemia. Stress, anger and arousal can stimulate an increase in blood pressure mediated through the sympathetic nervous system.

This is a normal response. Catecholamines are the neurotransmitters that mediate action in sympathetic activity. They bind to alpha1 receptors on vascular endothelium and on beta2 receptors in the heart. This results in vasoconstriction increased rate and strength of contractility respectively. This results in increased heart rate and blood pressure.

Account for the result

The result is due to sympathetic activity increasing heart rate and total peripheral vascular resistance. According to BP=CO × TPR. Whereby CO= heart rate (HR) × Stroke volume. Increased heart rate increases cardiac output. This, together with the increased TPR results in increased blood pressure.

The system affected

The patient’s problem lies in the sympathetic nervous system. The patient suffers from orthostatic hypotension. The results demonstrate that the cardiovascular effectors (sinoatrial node, ventricular myocardium, vascular smooth muscle) receive their normal tonic inputs over the autonomic pathways. The SA node is responding normally to its parasympathetic and sympathetic inputs (normal resting HR of 70beats/min changes appropriately when the sympathetic input is stimulated). The myocardium and blood vessels respond normally to increased levels of catecholamines.

It is, subsequently, hypothesized that the patient’s problem lies either between the baroreceptors and the central nervous (either the baroreceptors do not respond normally, or the signal does not reach the brainstem) or within the brain itself (if the information from the baroreceptors is not processed correctly). In either case, the patient’s heart rate does not increase upon standing up.

The major clinical problems for patients with orthostatic hypotension are dizziness and fainting in the erect position.

Compensatory mechanisms of the cardiovascular system upon consumption of seawater

Seawater differs from blood in composition and concentration. Blood is constituted mostly by water; the rest is made up of cells. Electrolytes such as sodium and potassium are found in the plasma. Nutrients such as amino acids and glucose are also found in plasma. The cells are made up of white blood cells, red blood cells and platelets. Sea water on the other hand is made up of water salt, iodides and potassium. It can also contain toxins such as lead causing heavy metal poisoning if taken in large quantities.

The major problem caused by consuming large quantities of sea water lies in its increased sodium concentration which is about 3.5%. This is about three times the sodium concentration in blood which is about 0.9%. When the body is subjected to this large concentration, there is osmotic pulling of fluid from the intracellular to the extracellular compartment. This leads to dehydration of cells and eventually cell death if the situation is not corrected.

The increased intravascular volume increases the work load of the heart since, there is increased venous return. The end diastolic volume increases and according to Starling’s law, there is increased stretching of the muscle fibers and increased stroke volume. The net result is increased cardiac output and, therefore, increased mean arterial pressure. This means that there is development of hypertension in a heart that is already deprived of water. There increased rate of contraction means that there is reduced perfusion of the heart as the heart is perfused during diastole. Cardiomegally results in the long run, as the heart muscles hypertrophy in order to meet the demands of pumping more fluid. This compounds the already existing problem of lack of cardiac perfusion, as the number of cells has now increased. In the long run there is decompensation according to the Starling’s law of the heart, and heart failure develops.

Drinking sea water, especially by people out at sea, should be discouraged. This is because it does not serve to hydrate the body; on the contrary, it only increases thirst. The kidneys function to remove the excessive sodium from the body by increasing sodium losses. The loss in sodium leads to increased water loss as the water is osmotically pulled into the lumen of the tubules. This leads to hypovolemia and the RAAS system is activated. Then angiotensin II produced stimulates thirst, causes vasoconstriction and stimulates the synthesis of aldosterone. This hormone stimulates the reabsorption of sodium, and the vicious cycle begins again. The net result is hypertension as the total peripheral vascular resistance increases. The compensatory mechanisms of the cardiovascular system fail in the long run and the end result is, death.

How starvation alters capillary exchange and causes edema

Capillary exchange is determined by the Starling forces. They include capillary hydrostatic pressure, interstitial hydrostatic pressure, plasma colloid osmotic pressure and interstitial colloid osmotic pressure. The plasma colloid osmotic pressure is contributed by the plasma proteins and is usually about 28mmHg. The capillary hydrostatic pressure opposes plasma oncotic pressure and is about 30mmHg at the arterial end and 10mmHg at the venous end. The interstitial colloid osmotic pressure is due to plasma proteins that have leaked into the interstitium. It pulls fluid into the interstitium opposing the capillary hydrostatic pressure and is about 8 mmHg. The interstitial fluid hydrostatic pressure opposes capillary hydrostatic pressure and is about 3mmHg. The net inward force is 7mmhg while net outward force is about 13mmHg. This means that there is a difference of 6mmHg allowing fluid to filter out of the capillaries and supply tissues with nutrients. The fluid is reabsorbed at the venous end back into the blood vessels but some is left behind and drains into the lymphatic system.

Starvation results in a wide variety of biochemical changes in the body which result in breakdown of body stores to provide glucose to meet the metabolic requirements of various tissues. The catabolism of proteins in particular has significant effect on microfiltration at the capillary level. Low protein level lowers the plasma colloid pressure. This increases the net outward force and increases the fluid that leaks out. Increased interstitial fluid leads to pitting edema. The effect of this is to reduce the blood volume. Hypovolemia results in compensatory mechanisms of the cardiovascular system. There is increased heart rate in order to meet the needs of the body. The kidneys increase the reabsortion of sodium under the influence of aldosterone whose release is stimulated by the rennin angiotensin aldosterone system.

Starvation leads to hypoprotenemia that results from breakdown of proteins into amino acids that are utilized for gluconeogenesis. Chief among the vital proteins is albumin, which is an essential contributor to oncotic pressure, not to mention, it is a carrier protein for substances such as heme. Proteins are vital for formation of immunoglobulins, and for contributing to plasma colloid pressure that opposes the hydrostatic pressure. The resulting imbalance of starling forces causes fluid to leak out of capillaries and causes edema. This can be treated using diuretics and a high protein diet.

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