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By K. Pavel. James Madison University.
In erect posture cheap voveran sr 100mg spasms quadriplegic, much of the blood from the capillaries pools into the expanded veins, instead of returning to the heart. As venous return diminishes, cardiac output falls, and the effective circulating volume is decreased. Gravity increases pressure in the capillaries, causing excessive fluid to filter out of capillary beds in the lower limbs, producing edema of feet and ankles. Resultant fall in arterial blood pressure on standing from supine position, triggers sympathetic-induced venous vasoconstriction, which moves some of the pooled blood forward. The skeletal muscle pump ‘interrupts’ the column of blood by completely emptying veins blood segments intermittently so that a portion is not subject to the entire column of venous blood from the heart to its level. If a person stands still for a long time, blood flow to the brain is reduced because of the decline in effective circulating blood volume, despite reflexes targeted for maintaining arterial blood pressure, Decreased cerebral blood flow leads to fainting, which returns the person to a horizontal position, thereby eliminating the gravitational effects and restoring effective circulating volume toward normal. Effect of Venous Valves on Venous Return Both venoconstriction and skeletal muscle pump drive blood in the direction of the heart and not backwards because the large veins have one-way valves spaced at 2 - 4 cm gaps, permitting blood to move forward toward the heart but prevent it from moving backward toward the tissue. They also counteract gravitational effects in upright posture by helping minimizing the backflow of blood that tends to occur as a person stands up. Role of Respiratory Activity on Venous Return During respiratory excursions, the pressure within the thoracic cavity averages 5mm Hg less than atmospheric pressure. Blood returning from the lower body parts to heart travels through the chest cavity, where it is exposed to subatmospheric pressure. The venous system of the lower extremity and abdomen is exposed to normal atmospheric pressure. This pressure difference of about 5 mmHg subatmospheric, squeezes blood from lower veins to the chest veins, enhancing venous return. So during exercise, respiratory pump, skeletal muscle pump and venous vasoconstriction enhance venous return. Effect of Cardiac Suction on Venous Return The heart has role in its own filling with blood. During ventricular contraction, the trioventricular valves are pulled downward increasing the atrial cavities, as a result there 170 is transient drop in the atrial pressure, thus increasing vein-to-atria pressure gradient, so that venous return is facilitated. During ventricular relaxation, a transient negative pressure is created in the ventricle, so that blood is ‘sucked in’ from the atria and veins; thus the negative ventricular pressure increasing the vein-to-atria-to-ventricles pressure gradient, further enhancing venous return. The volume of blood returning to the left atrium from the lungs is the same volume, which was released by the right ventricle to the lungs; the output of the right and left ventricles is normally the same. It may be 20 –25 L/min in exercise and in very severe strenuous exercise in a trained athlete 35 – 40 L/min. During anytime, the volume of blood flowing through the pulmonary circulation is the same as flowing through the systemic circulation. Cardiac factors: heart rate & stroke volume, sympathetic stimulation and myocardial contractility; 2. The heart is a “demand pump” adjusting its output to the demand of the body organisms. This action potential spreads through the heart, inducing the heart to contract or have a “heart beat”. Atrial contraction is weakened by a reduction in the slow inward current carried by calcium, reducing the plateau phase. Thus, the heart beats slowly, atrial contraction is weaker, the time between atrial and ventricular contraction is stretched out. These actions are beneficial because parasympathetic controls heart activity in quiet relaxed condition of rest when body is not demanding increase in cardiac output. Sympathetic stimulation increases the rate of depolarization reaching threshold more rapidly mediated via norepinephrine by decreasing potassium permeability by inactivation of potassium channels; greater frequency of action potential and corresponding more rapid heart rate. The overall effect of sympathetic stimulation is to increase heart rate, decrease conduction time, and increase force of myocardial contraction. Heart rate is increased by simultaneous stimulation of sympathetic and inhibition of parasympathetic activity. A decrease in heart rate by stimulating parasympathetic and inhibiting sympathetic activity.
The distal branches of the arterial tree in the brain receive no autonomic innervation voveran sr 100mg line muscle relaxant supplements. Ultrastructurally, tight junctions between the endothelial cell membranes seal the lining of brain capillaries – a major facet of the relatively impermeable blood-brain barrier. Circulatory disorders of the venous system account for a small fraction of cerebrovascular disease and time does not permit a review of the superficial and deep draining pathways of intracranial blood. Physiologic Considerations Hemodynamic as well as anatomic factors play an important role in the vulnerability of brain to disorders of the circulation. The brain comprises only two percent body weight, but it receives fifteen percent of the cardiac output. Blood flow is a function of perfusion pressure (the gradient between mean arterial pressure and venous pressure) and the resistance of the vascular bed (determined mainly at the arteriolar level). Increased intracranial pressure (see the section on Intracranial Hypertension in this syllabus) raises venous pressure and, unless compensated for, lowers the perfusion gradient and the flow of blood. Overall cerebral blood flow is relatively constant over a broad range of arterial pressure. Arteriolar tone is not mediated by the autonomic nervous system or endocrine influences. Cerebral blood flow is clearly affected by oxygen tension, pH, and carbon dioxide tension. But many observations suggest that additional factors, possible oligopeptide neurotransmitters among them, are important determinants of blood flow in the brain. Lack of information in this area is one of the impediments to major advances in cerebrovascular disease. The nerve cell is dependent on oxidative metabolism and a continuous supply of glucose and oxygen for survival. Neuronal function ceases seconds after circulatory arrest; irreversible structural damage follows a few minutes later. Recent work proposes that an excess of excitatory amino acid transmitters and an abnormal influx of calcium into the cell play a decisive role in the death of the nerve cell. Glial cells, especially astroglial and microglia, are more resistant to impaired circulation than nerve cells. The amount of damage and the survival of tissue at risk depends on a number of modifying factors, which include the duration of ischemia, availability of collateral circulation, and the magnitude and rapidity of the reduction of blood flow. Global cerebral ischemia occurs when there is a generalized reduction of cerebral perfusion, such as in cardiac arrest and severe hypotension. Focal cerebral ischemia occurs when there is a reduction or stoppage of blood flow to a localized area of the brain. The resultant localized lesion is referred to as an “infarct” and the pathological process as “infarction. These macrophages slowly leave the field – over a period of weeks and months – and vacated spaces (microcysts) gradually grow larger. The wall of the cavity, where nerve cells and oligodendrocytes may have succumbed but astrocytes survived the acute infarction, includes a network of elaborated astroglial cell processes (glial fibers) that make up the brain’s puny version of scar formation. This is the classical picture of total infarction of brain tissue, but encephalomalacia often stops short of cavitating necrosis. If only the most susceptible members of the neuronal population die while the majority of them survive, little more than a partial loss of nerve cells and astrocytosis may be detectable on microscopic examination. Bear in mind that in the nervous system there is always secondary degeneration of neuronal processes at a distance from the site of injury. Destruction of the motor cortex in the frontal lobe, therefore, leads to secondary degeneration of nerve fibers along the entire length of the lateral and ventral funiculi of the spinal cord (“Wallerian” or “secondary tract degeneration”). In addition, in a number of heavily interconnected neuronal systems of the brain, secondary degeneration occurs transynaptically, othogradely in some systems and retrogradely in others. Sometimes atherosclerotic plaque formation in major arteries is generalized and sometimes the cerebral arteries are affected – or spared – well out of proportion to the degree of involvement of the aortic or coronary systems. The internal carotid arteries at the bifurcation of the common carotid in the neck, the vertebral and basilar arteries, the supraclinoid segment of the internal cartoid artery, and the middle and posterior cerebral arteries are all frequently affected in the usual segmental and eccentric fashion. Involvement of the anterior cerebral artery beyond the anterior communicating artery is distinctly unusual. Otherwise, proximal segments of major branches from the circle of Willis are also affected, but once the arteries reach the cerebral convexities 24 they develop thickening of the intimal layer only in the most advanced cases of atherosclerosis.
