ZQMS-ARC-REC-002 ASSIGNMENT COVER REGION
REGION: MASH East SEMESTER: 2 YEAR: 2018
PROGRAMME: BScHN INTAK E: 26
FULL NAME OF STUDEN T: Justice MulungisiPIN: P1720258R
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COURSE NAME: physiology for health sciences 2 COURSE CODE: NSD105
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ASSIGNMENT TITLE: 1. Discuss how the brain blood flow is controlled under normal circumstances (25)
2. describe the relationship between ECG and cardiac cycle (25).
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1.According to ww.ncbi.nih.gov the brain uses 20 % of available oxygen for normal function, making tight regulation of blood flow critical for survival. Under normal circumstances blood flow to the brain is remarkably constant, partly due to the contribution to large arteries to vascular resistance and also to the basal tone of arterioles. In order for flow to increase to areas within the brain that demand it, upstream vessels must dilate in order to avoid reductions in downstream micro vascular pressure. Therefore the coordinated flow in the brain is due to flow mediated vasodilation from distal to proximal arterial segments, also to myogenic mechanisms that increase flow in response to decreased pressure.
Definition of terms
Auto regulation of cerebral blood flow
Auto regulation of cerebral blood flow is the ability of the brain to maintain relatively constant blood flow despite changes in perfusion pressure. Auto regulation is present in vascular beds, but is well pronounced in brain likely due to the need for a constant blood supply. Usually in adults blood flow is maintained at 50mlper 100g of brain tissue per minute. Any deviation from this limit auto regulation is lost and blood flow become dependent on mean arterial pressure in a linear fashion. The reduction in cerebral blood flow is compensated for by an increase of oxygen extracted from the blood to meet metabolic needs. In auto, regulation reduction in cerebral blood flow stimulate release of vasoactive substance from the brain that cause arterial dilation. The importance contribution of myogenic activity to auto regulation is demonstrated in vitro in isolated and pressurised cerebral arteries that constrict in a response to increased pressure and dilate in response to decreased pressure.
Segmental vascular resistance. In peripheral circulation, small arterioles are typically the major site of vascular resistance. However, in the brain both large and small ateries contribute significantly to vascular resistance. Studies shows that, the large extracranial vessels and intracranial vessels contribute 50% of cerebral vascular resistance. Large artery resistance in the brain is likely importance to provide constant blood flow locally. Large artery resistance also attenuates changes in downstream microvascular pressure during increases in systemic arterial pressure. Thus segmental vascular resistance in the brain is a protective mechanism that helps provide constant blood flow in an organ with high metabolic demand without patholofically increasing hydrostatic pressure that can cause vasogenic edema.
Neural Astrocyte Regulation. According to www.ncbi.nih.gov.com, parenchymal arterioles are in close association with astrocytes and, to a lesser extent, neurons. Both thesecell type may have a role in controlling local blood flow. Neurons whose cell bodies are from within the subcortical brain regions project to cortical microvessels to control local blood flow by release of neurotransmitter. Release of neurotransmitter stimulates the receptors on smooth muscle, endothelium, or astrocytes to cause constriction or dilation, thereby regulating local blood flow in concert with local demand. Its known that astrocytes can release vasoactivefactors. Studies shows that direct electrical; stimulation of the neuronal processes raises calcium in astrcytic end feet and causes dilation of nearby arterioles. Stimulation of astrocytes also raises the calcium in the feet and has a similar vasoactive effect. Thus the role of the myogenic response, which may significantly modify any astrocytic derived signals in vivo is not known.
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 produce marked increase in cerebral blood flow. In fact blood flow does not change in the brain until tissue oxygen pressure falls to below 50mmhg below which cerebral blood flow increases substantially. Chronic hypoxia increases cerebral blood flow through an effect on capillary density. Acute hypoxia causes an increase in cerebral blood flow via direct effects on vascular cells of cerebral arteries and arterioles.
Effect of carbon dioxide, according to www.ncbi.nih.gov.com carbon dioxide has 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. The potent vasodilator effect of carbon dioxide is demonstrated by the finding that in humans 5% carbon dioxide inhalation causes an increase in cerebral blood flow by 50% and 7% carbon dioxide inhalation causes a 100% increase in cerebral blood flow. It is therefore logical to conclude that carbon dioxide has a major role in the control of cerebral blood flow.
To cape it all, it is logical in the light of the points above to conclude that, the control of cerebral blood flow is achieved through the action of different mechanisms and processes including, carbon dioxide effect, oxygen effect, neural Astrocyte Regulation and auto regulation among other things.
2. The cadiac cycle is the period of time that begins with the contraction of the atria and ends with ventricular relaxing. Both the atria and ventricular 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
Definition of terms
Period of time between the onset of arterial contraction and vantricula relaxation.
A structure that sets the rate at which the heart beats.
Is a recording of the heart s electricity activity as a graph over a period of time.
Is the period of time when the heart muscle is relaxed and the chamber fill with blood
End diastolic volume
Is the amount of blood in the ventricle at the end of arterial systole just prior to ventricular contraction.
End systolic volume
Is the amount of blood remaining in each ventricular following systo.
Is an unusual heart sound detected by auscultation typically related to spetal or valve defects.
Is the period of time when the heart muscle is contracting.
According to http//www.courses.lumen learning.com, the cardiac cycle go through phases, at the beginning of the cycle both the atria and ventricles are relaxed, blood is flowing into the right atrium. Blood flows into the left atrium from the four pulmonary veins. The two atrio ventricular valves are open so blood flows into the ventricles.
Atrial systole and diastole
Contraction of the atria flows depolarisation, represented by the p wave of the ECG. As the atrial muscles contracts, pressure rises within the atria and blood is pimped within the ventricles. Atrial systole lasts approximately 100ms and end prior to ventricular systole.
It follows the depolarisation of the ventricles and represented by the QRS complex in the ECG. It may be divided into two phases lasting a total of270ms at the end of atrial systole and just prior to the atrial contraction. In a resting adult the ventricles contains 130ml of blood. Initially there is contraction of the ventricular muscles causing a rise in the pressure of blood within the chamber. In the second phase of the ventricular systole, the contraction of the ventricular muscle has raised the pressure within the ventricular to a point that is greater than the pressure in the pulmonary trunk and the aorta, forcing blood into the aorta. Both ventricles pass the same amount of blood and this quantity is known as stroke volume.
Ventricular relaxation or diastole, follows repolarisation of the ventricules and is represented by the T wave of the ECG. It is devided into two phases lasting 430 ms.
During the early phase of ventricular diastole as the ventricular muscle relaxes, pressure on the remaining blood within the ventricules begins to fall. Blood then flows back toward the heart. So the early phase of this is called the isoventricular relaxation phase.
In the second phase of this there is muscle relaxation. When relaxation occurs pressure falls in the ventricules calling for blood flow into the ventricles. Both chambers are in diastole and the cardiac cycle is complete.
The ECG works by detecting and amplifying tiny electrical changes on the skin that occur during heart muscle deporlarisation. The output for the ECG forms a graph that shows several different waves, each corresponding to a different electrical and mechanical event within the heart. Changes in these waves atre used to identify problems with the different phases of heart activity.
The fisrt P wave indicating the atrial depolarisation oin which the atria contract. The QRS complex refers to the combination of the QRS waves and indicates ventricular depolarisation and contraction. The T wave and ST segment. The T wave indicates ventricular repolarisation, in which the ventricles relaxfollowing depolarisation and contraction. Following the T wave is the U wave, which represent the relaxation of the parkinje fibres. It is not always visible on an ECG because it is a very small wave in comparison to the others.
Arthur,S.K, Musabayana, C.T (2001) physiology for health sciences, Harare, Zimbabwe
http//www.course lumen learning.com.