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ZQMS-ARC-REC-002 ASSIGNMENT COVER REGION

ZQMS-ARC-REC-002

ASSIGNMENT COVER
REGION: MIDLANDS
PROGRAMME: BScHNS INTAKE: 19
FULL NAME OF STUDENT: MOYO JAISON
PIN: P1267006Z
MAILING ADDRESS: [email protected]
CONTACT TELEPHONE/CELL: 0773714531 ID.NO: O8-841543X 26
COURSE NAME: PHYSIOLOGY FOR HEALTH SCIENCES VOLUME 2
COURSE CODE: BSHN 111
ASSIGNMENT NO. e.g. 1 or 2: 1
DUE DATE: 10 March 2018
ASSIGNMENT TITLE:
Discuss how the brain’s blood flow is controlled under normal circumstances.

Describe the relationship between the ECG and the cardiac cycle.

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OVERALL MARK:___________________MARKER’S NAME:__________________
MARKER’S SIGNATURE:___________________________________ DATE: ____________
BSHN 111 PHYSIOLOGY FOR HEALTH SCIENCES
Discuss how the brain’s blood flow is controlled under normal circumstances.

The brain uses 20% 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 in part to the prominent distribution of large arteries to vascular resistance.

In addition, parenchymal arteries have considerable basal tone and also contributes to vascular resistance in the brain. The high metabolic demand of neuronal tissue requires tight coordination between neuronal activite and blood flow within the brain that demand it, upstream vessels must dilate in order to avoid reductions in downstream microvascular pressure. Therefore coordinated flow responses occur in the brain, likely due to conducted or flow mediated vasodilation from distal to proximal arterial segments and to myogenic mechanisms that increase flow in response to decreased pressure.

Cerebral Hemodynamics
Brain blood flow can be modelled from a physical stand point as flow in a tube with the assumption that flow is steady and uniform through thinned wall (the wall is ;10% of the lumen) non distensible tubes. These assumptions do not apply to large arteries that have thick walls or in the micro circulation in which flow is non Newtonian. Ohm’s law states that flow is proportional to the difference in inflow and outflow pressure (?P) divided by the resistance to flow(R), flow =?P/R. In the brain, ?P is cerebral perfusion pressure (CPP), the difference between intra-arterial pressure and the pressure in the veins. Venous pressure is normally low (2-5mmHg) and is influenced directly by intra…. pressure (ICP). Therefore ?P is calculated as the difference in CPP and either venous pressure or ICP whichever is greater.

Blood flow is also estimated by Poisenielle’s law that states that flow is directly related to ?P, blood viscosity and the length of the vessel (assumed to b constant) and inversely related to radius to the fourth power: flow = (8*n?L/r4). Thus radius is the most powerful determinant of blood flow and even small changes in human 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.

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 many vascular beds but particularly well developed in the brain, likely due to the need for a constant blood supply and water homeostasis. In normoretensive adults, cerebral blood flow is maintained at 50ml per 100g of brain tissue per minute, provided CPP is in the range of ~60 to 60mmHg. Above and below this limit, auto regulation is lost and cerebral blood flow becomes dependant on mean arterial pressure in a linear fashion. When CPP falls below the limit of auto regulation, 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, including dizziness, altered mental status and eventually irreversible tissue damage (infarction).

The mechanisms of auto regulation in the brain are not completely understood and likely differ with increase versus decrease in pressure. Although a role for neuronal involvement in auto regulation is appealing, studies have shown that cerebral blood flow auto regulation is preserved in symphathetically and parasymphathetically denervated animals, indicating that a major contribution of extrinsic neurogenic factors to auto regulation of cerebral blood flow is unlikely.

Recently a role for neuronal nutric oxide in modulating cerebral blood flow auto regulation has been shown suggesting that although extrinsic innervations may not be involved, intrinsic innervations may have a role.

Bi products of metabolism have also been proposed to have a role in auto regulation. Reduction in cerebral blood flow stimulates release of vaso active substances from the brain that causes arterial dilation. Candidates for these vaso active substances include H+, O2, adenosine and others. Auto regulation of cerebral blood flow when pressure fluctuates at the high end of the auto regulatory curve is most likely due to the myogenic behaviour of the cerebral smooth muscle that constrict in response to elevated pressure and dilate due to decreased pressure. The important contribution of myogenic activity is demonstrated in vitro in isolated and pressurised cerebral arteries that constrict in response to increased pressure and dilate in response to decreased pressure. Auto regulation of pressures below the myogenic pressure range likely involves hypoxia and release of metabolic factors.

The importance of auto regulation in normal brain function is highlighted by the fact that significant brain injury occurs when auto regulatory mechanisms are lost.

For example during acute hypertension at pressures above the auto regulatory limit, the myogenic constriction of vascular smooth muscle is overcome by the excessive intravascular pressure and forced dilation of cerebral vessels occurs. The loss of myogenic tone during forced dilation decreases cerebrovascular resistance, a result that can produce a large increase in cerebral blood flow (300 – 400%) known as auto regulatory breakthrough. In addition, decreased cerebrovascular resistance increases hydrostatic pressure on the cerebral endothelium, causing oedema formation, the underlying cause of conditions such as hypertensive encephalopathy, posterior reversible encephalopathy syndrome and eclampasia.

Although uncommon since the advent of effective auto hypertensive therapy, hypertensive encephalopathy occurs as a result of a sudden sustained rise in blood pressure sufficient to exceed the upper limit of cerebral blood flow auto regulation (;160mmHg).

Early studies on the reaction of cerebral vessels to high blood pressure produced the concept of hypertensive vasospasm. Acute hypertensive encephalopathy was thought the result of spasm – defined as an uncontrolled vasoconstriction of the cerebral arteries, causing brain tissue ischaemia. This concept originated from the observation of Byrom who produced experimental renal hypertension and found 90% of hypertensive rats with neurologic manifestations showed multiple certical spots of trypan extravarsation whereas rats without cerebral symptoms appeared to have normal cerebrovascular permeability.

Segmented Vascular resistance
In peripheral circulations, small arterioles (;100 micro diameter) are typically the major site of vascular resistance. However, in the brain, both large arteries and small arterioles contribute significantly to vascular resistance. Direct measure of the pressure gradient across different segments of cerebral circulation found that the large extracanial vessels (internal carotid and vertebral) and intracranial pial vessels contribute 50% of cerebral vascular resistance. Large artery resistance in the brain is likely important to provide constant blood flow under conditions that change blood flow locally e.g metabolism.

Large artery resistance also alternates 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 pathologically increasing hydrostatic pressure that can cause vasogenic oedema.

Neural astrocyte regulation
Unlike pial arteries and arterioles, parenchymal arterioles are in close association astrocytes and to a lesser extent, neurones. Both these cell types may have a role in controlling local blood flow. Sub cortical micro vessels are innervated from within the brain parenchyma and are unique in that the majority of vericosities adjoin astrocytic end feet surrounding arterioles and this does not have conventional neurovascular junctions. Neurones whose cell bodies are from within the sub cortical brain regions (e.g nucleus basalis, locus ceruleus, raphi nucleus) project to cortical micro vessels to control local blood flow by release of neurotransmitter eg. ACH, norepinephrine, SHT. Release of neurotransmitter stimulate receptors on smooth muscles, endothelium or astrocytes to cause constriction or dilation thereby regulating local blood flow in concert with neuronal demand. It has been known for some time that astrocytes can release vaso active factors. Evidence for the involvement of astrocytes in local control of blood in vivo has recently emerged. Their close opposition to micro vascular.

Describe the relationship between the ECG and cardiac cycle.

The electrocardiogram is one of the simplest and oldest cardiac investigations available, yet it can provide a wealth of useful information and remains an essential part of the assessment of cardiac patients. With modern machines, surface ECGs are quick and easy to obtain at the bedside and are based on relatively simple electrophysiological concepts.

An ECG is simply a representation of the electrical activity of the heart muscle as it changes with time, usually printed on paper for easier analysis. Like other muscles, cardiac muscle contracts in response to electrical depolarisation of the muscle cells. It is the sum of the electrical activity, when amplified and recorded for just a few seconds that we know as an ECG.

The conducting system of the heart
The normal cardiac cycle begins with spontaneous depolarisation of the sino atrial (sinus) node, an area of specialised tissue situated in the high right atrium (RA).

A wave of electrical depolarisation then spreads through the RA and across the inter-atrial septum into the left atrium (LA).

Basic electrophysiology of the heart
The atria are separated from the ventricles by an electrically inert fibrous ring, so that in the normal heart the only route of transmission of electrical depolarisation from atria to ventricles is through the atrioventricular (AV) node.

The AV node delays the electronic signal for a short time, and then the wave of depolarisation spreads down the interventricular septum (IVS), via the bundle of His and the right and left bundle branches, into the right (RV) and left (LV) ventricules.

Hence with normal conduction, the two ventricles contract simultaneously, which is important in maximising cardiac efficiency.

After complete depolarisation of the heart, the myocardium must then repolarise, before it can be ready to depolarise again for the next cardiac cycle.

The ECG
The ECG is measured by placing a series of electrodes on the patient’s skin – so it is known as the surface ECG. A fundamental principle of the ECG recording is that when the wave of depolarisation travels towards a recording lead it results in a positive or upward deflection. When it travels away from a recording lead, this results in a negative or downward deflection.

It will be clear from above that the first structure to be depolarised during normal sinus rhythm is the right atrium, closely followed by the left atrium.

So the first electronic signal on a normal ECG originates from the atria and is known as the P wave. Although there is usually one P wave in most leads of an ECG, the P wave is in fact the sum of the electric signals from the two atria, which are usually superimposed.

There is then a short, physiological delay as the atrioventricular node slows the electric depolarisation before it proceeds to the ventricules.

This delay is responsible for the PR interval, a short period where no electric activity is seen on the ECG, represented by a straight horizontal or isoelectric line.

Depolarisation of the ventricles results in usually the largest part of the ECG signal (because of the greater muscle mass in the ventricles) and this is known as the QRS complex.

In the case of ventricles, there is also an electronic signal reflecting repolarisation of the myocardium. This is known as the ST segment and the T wave. The ST segment is normally isoelectric, and the T wave in most leads is an upright deflection of variable amplitude and duration.

Cardiac cycle
During the period of contraction (systole), the heart pumps blood out through the arteries and fills with blood during the period of relaxation (diastole). One complete sequence of filling and pumping blood is called a cardiac cycle, or heartbeat.

Diastole phase
During the diastole phase, the atria and the ventricles are relaxed (in diastole). The atrial diastole is shorter, blood flows into the left and right atria. The valves located between the atria and ventricles are open, allowing blood to flow through the ventricles. On the ECG this is recorded as the T wave.

The events that occur during the diastole phase can be summarised as follows:
The atria and ventricles are relaxed
Atrioventricular valves are open
Semi lunar valves close preventing back flow into the atria
T wave on ECG
Atrial systole
The SA node depolarises and triggers the atria to contract (atria systole). The atrial systole occurs when the ventricles are still in diastole.

The right atrium contracts first and empties its contents into the right ventricle. The tricuspid valve prevents the blood from flowing back into the right atrium. The left atrium then contracts next empting its contents into the left ventricle. The mitral valve prevents the oxygenated blood from flowing back into the left atrium.

The sinoatrial node depolarisesThe atria empty blood into the ventricles
Recorded as the P wave on the ECG
Ventricular systole phase
During the systole phase, the ventricles contract pumping blood into the arteries. During the systole phase, the ventricles receive impulses from the Purkinje fibres and contracts. The stage is recorded as the QRS complex. At the beginning of the contraction both atrioventricular and semi lunar valves are closed. As the pressure increases in the ventricles, the semi lunar valves open. The right ventricle sends blood to the lungs via the pulmonary artery. The left ventricle pumps blood to the aorta.

The atrioventricular valves are closed and the semi lunar valves open. The de-oxygenated blood is pumped into the pulmonary artery. The pulmonary valve prevents the blood from flowing back into the right ventricle. Oxygenated blood is pumped into the aorta. The valve prevents the oxygenated blood from flowing back into the left ventricle.

Impulse reaches the ventricle via the Purkinje fibresQRS complex
The ventricles contract
Atrioventricular valves close
Semi lunar valves open
Blood flows to either the pulmonary artery or aorta.

At the end the heart rests (diastole).

One cardiac cycle is completed when the heart fills with blood and is then pumped from the heart. The audible sounds that can be heard from the heart are made by the closing of the heart valves. These sounds are reffered to as the lub-dupp sounds. The lub sound is made by the contraction of the ventricles and the closing of the atrioventricular valves. The dupp sound is made by the semi lunar valves closing.

Summary of events of the cardiac cycle
P Wave Atrial depolarization and contraction
Atrial systole Fills the ventricles Cuspid valves open while valves of the vena cava and pulmonary veins are closed
QRS complex Atrial repolarisation and relaxation and simultaneous ventricular depolarisation and contraction ventricular systole Empties the ventricles Cuspid valves are closed while semi lunar valves are open
T wave Ventricular repolarisation and relaxation
Diastole Heart relaxes Cuspid and semi lunar valves are closed
Pause Myocardium at rest Atria fill after a pause of some length Valves are vena cava and pulmonary veins open so atria can fill
Diagram illustrating the ECG in relation to the cardiac cycle.

REFERENCES
Arthur, S.K et al Impairement of Renal sodium excretion in tropical residents: Phenomenological analysis. Biometereology 1999.

Human Physiology and Mechanisms of Diseases. Arthur C.G Publisher WB Saunders 5th Edition.

Lote, C.J. Principles of Renal Physiology, Kluwer Academic Publishers, London, 4th Edition, 2000.

Mayne, P.D. Clinical Chemistry in Diagnosis and Treatment, Edward Arnold, London, 1994.

Musabayane, C.T. Notes in Renal Physiology, Department of Physiology, University of Zimbabwe 2001.