MARKER’S NAME: M. MUKOSERA DATE: 10 April 2018
OVERALL MARK: 29/50=58%
Source of information not acknowledged
No evidence of wide reading- 2 references cited
Assignment cover missing
Question 1 17/25
Control of cerebral blood flow
The brain uses 20 percent of available oxygen for normal function making tight regulation of blood flow and oxygen delivery critical for survival. In a normal physiological state total blood flow to the brain is remarkably constant due to the prominent contribution of large arteries to vascular resistance. Parenchymal arterioles have considerable basal tone and also contribute significantly to vascular resistance in the brain. The high metabolic demand of neuronal tissue requires tight coordination between neuronal activity and blood flow within the brain parenchyma known as functional hyperemia. In order to flow to increase to areas within the brain that demand it, upstream vessels must direct in order to avoid reduction in downstream microvascular pressure. Therefore coordinated flow responses ok in the brain likely due to conducted or flow mediated vasodilation from distal to proximal arterial segments and to myogenic mechanism that increase flow in responds to decreased pressure. ?
Brain blood flow can be modeled from physical stand point as flow in a tube with the assumptions that flow is steady laminar and uniform through thinned walled, non-distensible tubes. These assumptions do not apply to large arteries that have thick walls or in microcirculation in which flow is non-newtonian. However, Ohm’s law states that flow is proportional to the difference between intra-arterial pressure and the pressure in veins. Venous pressure is normally low and is influenced directly by intracranial pressure. Therefore outflow pressure is calculated as the difference in cerebral perfusion pressure and either venous pressure or intracranial pressure whichever is greater. Blood flow is also estimated by Poiseuielle’s law that states that flow is directly related to outflow pressure, blood viscosity and length of the vessels and inversely related to the radius to the fourth power, thus radius is the most powerful determinant of blood flow and even small changes in lumen diameter have significant effects on cerebral blood flow and it is by this mechanism that vascular resistance can change rapidly to alter regional and global cerebral blood flow. ? did not acknowledge source of information
Autoregulation of cerebral blood flow
This is the ability of the brain to maintain relatively constant blood flow despite changes in perfusion pressure. Autoregulation is present in many vascular beds but is particularly well developed in the brain likely due to the need for a constant blood supply and water homeostasis. When cerebral perfusion pressure falls below the lower limit of autoregulation cerebral ischaemia ensues. The reduction in cerebral blood flow is compensated for by an increase in oxygen extraction from the blood. Clinical signs and symptoms of ischaemia are not seen until the decrease in perfusion exceeds the ability of increased oxygen extraction to meet metabolic needs. At this point clinical signs of hypoperfusion occur, these includes dizziness, altered mental status and eventually irreversible tissue damage. Although a role for neural involvement in autoregulation is appealing studies have shown that cerebral blood flow autoregulation is preserved in sympathetically and parasympatheticallydenervated animals indicating that a major contribution of extrinsic neurogenic factors to autoregulation of cerebral blood flow is unlikely. Biproducts of metabolism have also been proposed to have a role in autoregulation. Reductions in cerebral blood flow stimulate release of vasoactive substances from the brain that cause arterial dilatation. . ?
The importance of autoregulation in normal brain function is highlighted by the fact that significant brain injury occurs when autoregulatory mechanism are lost. For example during acute hypertension at pressures above the autoregulatory limit, the myogenic constriction of vascular smooth muscle is overcome by the excessive intravascular pressure and forced dilatation of cerebral vessels occurs. The loss of myogenic tone during forced dilatation decreases cerebro vascular resistance, a result that can produce a large increase in cerebral blood flow. Decreased cerebrovascular resistance increases hydrostatic pressure on the cerebral endothelium causing oedema formation, the underlying cause of condition such as hypertensive encephalopathy, eclampsia and posterior reversible encephalopathy syndrome. . ?
Segmental Vascular Resistance
In peripheral circulations small arterioles are typically the major site of vascular resistance. However, the brain both large arteries and small arterioles contribute significantly to vascular resistance. Large artery resistance in the brain is likely important to provide constant blood flow under conditions that change blood flow locally for instance metabolism.
Neural astrocyte regulation
Unlike pail arteries and arterioles, parenchymal arterioles are in closer association with astrocyte and a lesser extent neurons. Both these cells type may have a role in controlling local blood flow. Stimulation of astrocyte also raises calcium in end feet and has similar vasoactive effect on parenchymal arterioles however, whether dilation or constriction occurs seems to depend on the level of calcium and not surprisingly resting tone. ? how neurons regulate not fully explained
Effect of oxygen
The brain has a very high metabolic demand for oxygen, compared to other organs and thus it is not surprising that acute hypoxia is a potent dilator in the cerebral circulation that produces marked increase in cerebral blood flow. Generally blood flow does not change in the brain until tissue oxygen partial pressure falls below plus or minus 50mmHg. ?
Effect of carbon dioxide
Carbon dioxide is a profound and reversible effect on cerebral blood flow such that hypercapnia causes marked dilation of cerebral arteries and arterioles and increased blood flow whereas hypocapnia causes constriction and decreased blood flow. ?
Question 2 ?× 12/25
The period of time that begins with the contraction of the atria and ends with ventricular relaxation is known as the cardiac cycle. The period of contraction that the heart undergoes while it pumps blood into circulation is called systole. The period of relaxation that occurs as the chambers fill with blood is called diastole. Both the atria and ventricles undergo systole and diastole and it is essential that these components be carefully regulated and coordinated to ensure blood is pumped efficiently to the body. ?
The cardiac cycle begins with atrial systole and progresses to ventricular systole, atrial diastole and ventricular diastole when the cycle begins again. When the heart chambers are relaxed blood will flow in to the atria from the veins, which are higher in pressure. As blood flows into the atria the pressure will rise so the blood will move passively from the atria into the ventricles. When the action potential triggers the muscles in the atria to contract the pressure within the atria rises further pumping blood into the pulmonary trunk from the right ventricle and into the aorta from the left ventricle. At the beginning of the cardiac cycle both the atria and ventricles are relaxed. Blood is flowing into the right atrium from the superior and inferior venae cavae and coronary sinus. Blood flows into the left atrium from the four pulmonary veins. The atrioventricular valves, tricuspid and mitral valve are both open so blood flows unimpeded from the atria into the ventricles. The two semilunar valves, the pulmonary and aortic valves are closed preventing backflow of blood into the right and left ventricles. Link to ECG
Contraction of the atria follows depolarization represented by the P wave of the ECG. As the atria muscles contract atrial kick pressure rises within the atria and blood is pumped into the ventricles through the open atrioventricular valves. Atrial systole ends prior to ventricular systole as the atrial muscle returns to diastole. Ventricular systole follows the depolarization of the ventricles and is represented by the QRS complex in the ECG. Initially as the muscles in the ventricle contract the pressure of the blood within the chamber rises but not higher enough to open semilunar valves. However blood pressure quickly rises above that of the atria that are now relaxed and in diastole and this causes blood to flow back towards the atria closing the tricuspid and mitral valves. Volume of blood in the chamber remains constant since blood is not being ejected from the ventricles. This initial phase of ventricular systole is known as isovolumic contraction.
In the second phase, the ventricular ejection phase blood is pumped from the heart, pushing open the pulmonary and aortic semilunar valves. Pressure generated by the left ventricle will be greater than the pressure generated by the right ventricle. Nevertheless both ventricles pump the same amount of blood. The quantity is referred to as stroke volume. Ventricular relaxation or diastole follows repolarization of the ventricles and is represented by the T wave of the ECG. During the early phase of ventricular diastole, as the ventricular muscle relax, pressure on the remaining blood within the ventricle begins to fall. When pressure within the ventricles drop below the pressure in both the pulmonary trunk and aorta blood flows back into the heart producing the dicrotic notch seen in blood pressure tracings. In the second phase of ventricular diastole the ventricular muscle relaxes, pressure on the blood within the ventricles drops even further. Eventually it drops below the pressure in the atria, this causes blood to flow from atria into the ventricles pushing open the tricuspid and mitral valves. As the pressure drops within the ventricles blood flows from the major veins into the relaxed atria and into the ventricles. Both chambers are in diastole, the atrioventricular valves are open and the semilunarvalves remain closed. Below is the illustration of the relationship between the cardiac cycle and the ECG. ? relationship not clearly described
In a normal healthy heart there are only two audible heart sounds S1 and S2. S1 is created by the closing of the atrioventricular valves during ventricular contraction and is described as (lub) or fast heart sound. The S2is the sound of the closingof the semilunar valves described as dub. There is also a third heart sound S3, but it is rarely heard in healthy people. It may be heard in youth, athletes and pregnant women. And if heard later in life may indicate congestive cardiac failure. S3may be a sound of blood flowing into the atria or blood slashing back and forth in the ventricle or even tensing of the chordae tendineae. Sound 3 is described as Kentucky gallop. The forth heart sound S4 results from the contraction of the atria pushing blood into a stiff or hypertrophic ventricle indicating failure of the left ventricle. S4 occurs prior to S1 and the collective sounds S4,S1 and S2 are referred to as the Tennessee gallop. The term murmur is used to describe an unusual sound coming from the heart that is caused by the turbulent flow of blood. Murmurs are graded on a scale. It is detected by auscultation typically related to septal or valve defects. × not required
Musabayane, C.T and Arthur, S.K (2004) Physiology for Health Sciences 11: ZOU Statprint Harare
Katheleen, J, Willson, W and Waugh, A (1996) Anatomy and Physiology 11: Churchill Livingstone
https://www.ncbi.nlm.nih.gov/…/ quote author