Applied Anatomy and Physiology Open inguinal Hernia

Order Description

Assessment task (s) Written assignments of 3000 (learning Outcomes 1, 2, 3) 100% weighting
Pass required 40%
Title Case Study where students will follow a patient through an
Investigation/clinical procedure from admission to discharge to the department/unit

Date of submission 05/01/2014
Place of submission Via Turnitin GradeMark deadline 14.00hrs (2pm)
Release of Marks 01/02/2014
Date of DAP 05/02/2014
Resubmission W/C 21/01/2014
All coursework assignments and other forms of assessment must be submitted by the published
deadline which is detailed above. It is your responsibility to know when work is due to be submitted –
ignorance of the deadline date will not be accepted as a reason for late or non-submission.
Any late work (submitted via Turnitin GradeMark, person or by post) will NOT be accepted and a mark of
zero will be awarded for the assessment task in question.
You are requested to keep a copy of your work.
Assignment
In writing this assignment you should consider the following:
This study is an analysis of physiological data collection derived from patient observation/clinical
procedures, explaining the treatment’s impact on the patient’s physiological parameters relating
this to the underlying theory and its relation to practice.
Choose a patient, procedure etc. that interests you. Do not try to undertake the study of highly
complex areas or procedures. The aim of the case study is to demonstrate your understanding,
knowledge and analytical abilities in relation to the area of anatomy and physiology within your
clinical practice. Keep this statement paramount within your memory whilst undertaking your
study and preparation of the assessments.
The case study would involve you initially identifying a patient who you will be involved with whilst
on duty; this may be for the whole or part of your shift. You will need to collect and collate data
which is relevant to your patient but which does not identify your patient in anyway or form. Such
identification would be a serious breach of confidentiality as would the identification of your
working environment or employer.
Collection of relevant bio-psychosocial data should be directly related to the discussions you
present with regards to the anatomical and physiological aspects of your case study. Data
collection will also involve areas of relevant treatment and care/investigation delivery which leads
to physiological changes or aiding a patient adapting, in a physiological sense, to the procedures
they are undergoing. For instance if a patient has a colloid infusion commenced one would
expect that you would provide an analysis as to why such a fluid is given, the reasons for a
change in the patient’s blood pressure and what physiological effect this administration of such a
fluid would have on the patient. This is not a pharmacological study but some demonstration of 7
knowledge and analysis of drugs and how they were utilised would be required along with their
physiological effects.
All your discussions within your study must be referenced appropriately using a wide variety of
literature and sources to demonstrate you have read sufficiently around your subject matter. You
will need to demonstrate analysis of your chosen subject areas as required at level 2. Overuses
of quotes are best avoided since this does not necessarily demonstrate understanding but only
your ability to copy another author’s work. Read, understand and then incorporate into your work
appropriately. Sometimes it is necessary to quote since paraphrasing may lose the essence of
what the author was trying to convey.
Remember this is an Anatomy and Physiology module and as such should be the focus of you
case study.
In presenting your work for assessment you must be sure that you have addressed all of the learning
outcomes of the module. Your submission will be marked against these learning outcomes and the
assessment criteria. The assessment criteria are a measure of how well you have met the learning
outcomes at this level of academic study.
Guidance on maintaining confidentiality in submitted work is available in your Student Handbook, and
you should read this guidance.
You are required to submit your final assignment via Turnitin GradeMark
For this module you are required to submit your summative assessment (for your written assignment) via
GradeMark.
To check your draft (formative) assignment there will be a class section called ‘Check Originality Report’
(COR) set up in your Turnitin account. You will be able to submit to the Check Originality Report
section as many times as you wish and it will be available throughout your studies. This resource
is also a useful tool to share with your module leader or tutor. You can download your originality report
as a PDF file and email it to your tutor, print the originality report and bring it to the tutorial, or log into
Turnitin whilst in the tutorial to show and discuss your work.

Key text
Clancy, J. and McVicar, A. (2009) Physiology &
Anatomy: A Homeostatic Approach. 3
rd ed. London:
Arnold.
This book relates many of the concepts in
anatomy and physiology to homeostasis and is
highly recommended
Books

Martini F. H., Nath, J. L. and Bartholomew,E. F.
(2012) Fundamentals of Anatomy and Physiology 9
th
ed. London: Pearson Education
Marieb, E. N. (2009) Essentials of Human Anatomy
and Physiology International edition 9th ed. London:
Pearson Benjamin Cummings

McCance, K. L. and Heuther, S. E. (2009)
Pathophysiology The biological basis for Disease in
Adults and Children 6
th ed. St Loius: Mosby Elsevier
This provides in-depth exploration of anatomy
and physiology and complements the lectures
well and is available in the library

This is highly recommended as a text and
informs the lectures with many of the slides
from lectures being gained from this book
This text provides excellent background
information with regards to many pathologies
and complements the normal anatomy and
physiology texts effectively

THIS IS AN EXAMPLE ESSAY GIVEN BY THE LECTURER AS TO HOW WE SHOULD TRY AND FOMURLATE OUR OWN ESSAY it will be fine if you can follow along the same principle xxxxxxxxx

In an ever changing environment, the body is constantly adapting to maintain a relatively steady internal balance. This state of constancy is called homeostasis, a process that begins at a cellular level and relies on the regularity of a water-based medium known as the internal environment (Waugh & Grant, 2006). This environment continually alters and changes within very narrow limits to preserve a state of equilibrium in order to meet the functional needs of the body (Marieb, 2008).
In this assignment, the writer will examine the physiological processes in the maintenance of homoeostasis by following a chosen individual through their anaesthetic induction and operative procedure. The writer aims to demonstrate their understanding of patho- physiology, by analysing the patient’s physiological changes, to include, patient observations through the interpretation of clinical data, the role and function of the endocrine system, the physiological stress response, and the contributions made by other body systems to maintain homeostasis within the body. To respect and maintain confidentiality as specified by the Health Professions Council (2008), Standards of Proficiency 1a .3, the identity of the patient selected for this case study will remain anonymous, and for this reason will be referred to as Mr X.
The patient chosen for this assignment is an otherwise healthy sixty eight year old male, undergoing a carotid endarterectomy under general anaesthesia. This procedure is carried out to reduce the risk of strokes, and involves the surgical removal of fatty deposits called plaque (such as cholesterol and calcium), which build up in the carotid artery. The condition is caused by a disease process called atherosclerosis which narrows and constricts the
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artery causing a reduction in blood flow to the brain (Oxford Concise Colour Medical Dictionary, 2007).
(VascularWeb, 2008)
The process of this physiological study began at pre-assessment, during which time Mr X’s routine observations were checked. These were recorded at a time when Mr X was thought to be calm and relaxed (Darlene Reid & Chung, 2004), and are shown against the normal adult values set out in the table below.
Table 1
????Pre-assessment Observations
?????Mr X’s observations
???Normal Adult Parameters (Darlene Reid & Chung 2004)
???Blood Pressure
???????127/80 mmHg
??????<120/<80 mmHg
???Heart Rate
????80 beats per minute
????60-100 beats per minute
???Respiratory Rate
??14 breaths per minute
?12-16 breaths per minute
???Oxygen Saturation (Sp02)%
???????97%
??????95-100%
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The readings indicated that Mr X’s blood pressure was well within normal adult parameters. Blood pressure, according to Clancy and McVicar (2009), is the force of circulating blood exerted against the inner walls of the blood vessels as it is pumped around the body. Two readings determine this pressure, measured in millimetres of mercury (mmHg). These are the systolic and diastolic pressures. The highest refers to the systolic pressure which is produced when blood is pushed into the aorta following the contraction of the left ventricle. The lower pertains to the diastolic pressure which is obtained when the heart is at rest (Better Health Channel, 2009). Blood pressure is influenced by three primary elements; cardiac output, the peripheral resistance and blood volume. These elements are conveyed in the following formula as suggested by Clancy & McVicar (2009).
Total peripheral resistance, as described by Sells, et al. (2006), is concerned with the forces that oppose blood due to the amount of friction it encounters as it travels through the blood vessels. This is largely determined by the length and width of the vessels, and the thickness or viscosity of the blood itself (Clancy & McVicar, 2009). Peripheral resistance is controlled by the sympathetic nervous system which prompts the blood vessels to dilate and constrict accordingly. Any factors which alter total peripheral resistance will cause a reflex variation in blood pressure (Marieb, 2008).
Godfrey (2004) defines cardiac output as the total amount of blood expelled from the left ventricle every minute. It also works in direct relationship with blood pressure, in that a fluctuation in either one will have the same, direct effect on the other. Cardiac output is the product of heart rate (HR), the number of heart beats per minute based on the rate of ventricular contractions, multiplied by stroke volume (SV), the volume of blood ejected by each ventricle per contraction (Silverthorn, 2010). Stroke volume, as explained by Kindlen (2003), can be controlled either extrinsically (via nerves and hormones), or intrinsically, e.g.
?????Blood pressure (BP) = Cardiac output (CO) x Total peripheral resistance (TPR)
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Starling’s law (Sherwood, 2007). The extrinsic control of cardiac function originates within the sympathetic branch of the autonomic nervous system. This mechanism increases myocardial contractility by stimulating the heart to beat stronger, allowing more blood to be expelled per beat (Clancy & McVicar, 2009). The intrinsic mechanism, as described by McGeown (2007), is concerned with the heart’s innate ability to alter stroke volume. It is directly linked to the force produced by the cardiac muscle during each contraction and is related to the length of the myocardial cells and the end diastolic volume. Klabunde (2004) differentiates stroke volume as a correlation between end-diastolic volume (EDV) and end- systolic volume (ESV). EDV, often referred to as preload, is determined by the amount of blood in each ventricle during diastole (relaxation), and is influenced by the amount of blood returning to the right atrium through the ascending and descending vena cava and pulmonary vein (venous return). According to Marieb (2008) stroke volume is governed by a mechanism known as Starling’s law and is considered to be the most important intrinsic control mechanism in cardiac function. As discussed by Hale (2004) Starling’s law is a phenomenon which deals with variations in venous return and is concerned, more importantly, with the pressure at which the blood is returned to the heart via the central veins. It works on the principle that, the more the heart muscles are stretched, the more powerfully it contracts (Silverthorn, 2010). Therefore, anything that influences an increase in venous return prompts a relevant rise in blood flow to the heart. As the ventricles expand (within certain physiological tolerances), the muscle fibres stretch, stimulating the cardiac muscle to contract more forcibly (Solomon, 2009). As a result, the heart pumps a greater volume of blood into the arteries (Silverthorn, 2010).
When Mr X arrived in the anaesthetic room he appeared to be very nervous and looked extremely pale. An oxygen saturation probe, a non-invasive blood pressure (NIBP) cuff, and a set of electrocardiograph leads were applied to Mr X to monitor his vital signs. These were recorded by the monitoring equipment to reveal the following clinical data:
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Table 2
???Blood Pressure
?????140/85 mmHg
???Heart Rate
???????110 beats per minute
????Respiratory Rate
??16 breaths per minute
???Oxygen Saturation %
???????97%
???It was noticed that Mr X’s blood pressure, heart rate and respiratory rate had increased above the normal limits of his original baseline observations noted at pre-assessment. These increases are suggested as being characteristics of the stress response, an instantaneous reaction which primes the body for “fight or flight” when confronted with a real or perceived threat, either physically or emotionally (Waugh & Grant, 2006). Stimulation of the higher centres of the brain, the cerebral cortex and the hypothalamus, respond to the stress stimulus by activating the sympathetic division of the autonomic nervous system (Biology Encyclopedia, 1998). This activation stimulates the adrenal medulla to release two naturally occurring hormones called catecholamines, these being, adrenaline also known as epinephrine, and noradrenaline, also called norepinephrine, into the bloodstream (Biology Encyclopedia, 1998). As they are released into the circulation they potentiate certain physiological changes within the body, acting as short-term homeostatic effectors of BP by effecting changes within cardiac function and peripheral resistance (Clancy & McVicar, 2009). As explained by Sasada & Smith (2003), adrenaline is a positive inotrope and chronotrope which brings about strengthening of the force of the cardiac muscle contractions and a rise in heart rate respectively. When released into the body adrenaline causes a consequent rise in blood pressure, heart rate and blood glucose levels, and expands the tiny passageways of the lungs (Waugh & Grant, 2006). These increases in metabolic activity increase the demand for more oxygen and glucose and cause a faster movement of blood to the organs of the body, particularly to the brain, heart and the muscles as described by Marieb (2008). Bray et al. (1999) discusses that in response to low blood glucose, a
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polypeptide hormone called glucagon is released by the pancreas. This acts on the liver to promote glycogenolysis, the breakdown of glycogen, and gluconeogensis, the production of glucose from fatty acids and amino acids as a means to increase energy level production through cell respiration, mediated by the release adrenaline and cortisol (Clancy & McVicar, 2009). These changes were reflected in Mr X’s observations and explained the consequent rise in his blood pressure and heart rate when he entered the anaesthetic room given the amount of stress he was under, whereas his respiratory volumes increased as a result of bronchodilation, stimulated by the adrenaline which increased his tidal volume and hence his overall minute volume (Sasada & Smith, 2003) which lead to an increase in his gaseous exchange leading to increased oxygen levels within his blood.
As discussed by Kindlen (2003), noradrenaline also underlies the fight-or-flight response and shares many similarities with adrenaline in the actions caused, i.e. raised heart rate. When noradrenaline is released into the bloodstream it has a greater influence on the blood vessels, in that it potentiates vasoconstriction of the arterioles which prompts a reflex rise in heart rate and stroke volume. According to Ganong (2005), the influencing effects of noradrenaline causes vasoconstriction in organs that are deemed unessential during times of stress, such as the gastrointestinal (GI) tract and the skin (Noble, et al., 2005). This would account for Mr X’s pale and pasty complexion on arrival into theatres which suggested that his peripheral blood vessels had constricted in order to prioritize blood flow to the most important organs of the body. This, therefore, caused a subsequent increase in TPR and a relevant rise in BP as illustrated in table 2.
Another physiological response often seen when circulating amounts of catecholamines increase is the contraction of the spleen. This may be induced under nervous control through intervention of the SNS which prompts the spleen to eject its rich blood supply into
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the central circulatory system, therefore increasing venous return (Ganong, 2005). As a result of this increase, stretch receptors located in the walls of the right atrium detect changes in central venous pressure as well as rising venous return. It is these receptors that provide an input to the brain transmitting impulses through vagal afferents which inhibit parasympathetic activity (Noble, et al., 2005). This in turn leads to an increase in heart rate and a decrease in pressure perpetuated by the movement of blood as it is drawn out of the right atrium and into the left heart (Enu & Obergfell, 2008). The ensuing decrease in right arterial pressure prompts a rise in venous return from the superior and inferior vena cava in a continuing cycle recognised as the Bainbridge reflex which continues until venous return to the right atrium has returned to normal levels (Klabunde, 2004).
In the anaesthetic room the anaesthetist administered 50mcg of Fentanyl through Mr X’s cannula. Fentanyl, as described by Simpson & Popat (2002) is a synthetic opioid medication used to provide the analgesic element of general anaesthesia. According to Sasada & Smith (2003), Fentanyl demonstrates very little effect on the cardiovascular system with the exception of bradycardia. However, as they further discuss, it is an exceptionally powerful respiratory depressant, mediating a decrease in respiratory rate as well as tidal volume, the volume of air inspired and expired out of the lungs during quiet breathing (Costanzo, 2007). In view of this, it can be suggested that the evident fall in Mr X’s heart rate was a result of the bradycardic effects of the drug which, in turn, reduced his blood pressure as shown in table 3 overleaf, reinforcing earlier discussions that heart rate and stroke volume influence cardiac output, and that blood pressure is the product of cardiac output and total peripheral resistance.
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Table 3
?????Blood Pressure
??????126/72 mmHg
????Heart Rate
?91 beats per minute
?????Respiratory Rate
??????14 breaths per minute
????Oxygen Saturation
????99%
??Anaesthetic induction was achieved with an intravenous dose of the non-barbiturate induction agent, Propofol (200mg). Sasada & Smith (2003) state that although cardiovascularly stable, Propofol yields a moderate 15-25% drop in BP and systemic vascular resistance (SVR) without negating an increase in heart rate due to its pharmacological action as a negative inotrope (decreasing myocardial contractility). They further highlight that when given as a bolus dose, Propofol also acts as a respiratory depressant, producing variable periods of apnoea (cease in breathing). This was anticipated by the anaesthetist who pre-oxygenated Mr X with 100% oxygen for a minimum of three minutes prior to induction. According to Wilson et al (2007), the purpose of pre-oxygenation is to increase O2 stores in the lungs, as well as arterial and mixed venous blood, by replacing nitrogen with O2 (de-nitrogenation), therefore maximising PaO2 during apnoea while prolonging arterial desaturation. To facilitate Mr X’s intubation and controlled ventilation, 80mcg of Vecuronium was also administered through his cannula. Vecuronium, as described by Sasada & Smith (2003), is a non-depolarising muscle relaxant that poses minimal cardiovascular or respiratory effect other than apnoea, and allows conditions for adequate intubation within 2 minutes of administration. This allowed the anaesthetist to pass a size 8 endotracheal tube through the patient’s vocal chords and into his trachea while his breathing was controlled and maintained by way of intermittent positive pressure ventilation (IPPV).
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For the purpose of this operation, Mr X’s blood pressure was monitored by means of an arterial line inserted into his radial artery. This was used to provide a constant and accurate real time measurement of his systolic, diastolic and mean arterial blood pressures during the procedure (White, 2004). Sherwood (2007) refers to the difference between systolic and diastolic pressure as the pulse pressure which can be felt when an artery passes close the skin. Mean arterial pressure is the average pressure which drives the blood into the tissues during the cardiac cycle and is equal to one third pulse pressure plus diastolic pressure (Sherwood, 2007). This, Sherwood (2007) continues, is due to the fact that when the heart is at rest, around two thirds of the cardiac cycle is spent in diastole, with only one third in systole. Mean pressure therefore provides a better guide of tissue perfusion than systolic and diastolic values, and is less susceptible to variable measurement, waveform distortion and reflection (Winters, 2008).
On transfer into theatre, Mr X’s anaesthesia was maintained using a combination of oxygen and nitrous oxide dispensed with a potent, inhalational, anaesthetic agent called Isoflurane (Sasada & Smith, 2003). As Simpson & Popat (2002) point out, CO is dependent on venous return to the heart, which again relies on negative intrathoracic pressure as well as the pumping action of muscles adjoining blood vessels. They further state that muscular relaxation coupled with IPPV tends to lessen venous return, thus reducing cardiac output, and in addition, produces vasodilatation and a consequent reduction in BP. According to Treacher & Grant (2006), this is because hypotension normally succeeds anaesthesia due to the direct cardiovascular effects of the drugs and the loss of sympathetic drive. When combined with a muscular blockade positive pressure ventilation may intensify this problem by raising intrathoracic pressure, thus, reducing venous return and therefore cardiac output (Treacher & Grant, 2006). It can be considered, therefore, that the subsequent decrease seen in Mr X’s blood pressure was a result of these influencing factors combined with the pharmacological effects of the anaesthetic drugs administered during induction. However,
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as seen in table 4 below, Mr X’s observations taken before surgical intervention were still well within the accepted physiological parameters.
Table 4
???Blood Pressure
???????120/72 mmHg
????Heart Rate
??87 beats per minute
???Respiratory Rate
???????14 breaths per minute
????Oxygen Saturation
????99%
???Throughout the surgical procedure, this being the carotid endarterectomy, Mr X’s observations remained relatively stable. Frequent and precise readings calculated by the arterial line allowed the anaesthetist to monitor Mr X’s arterial waveforms in addition to his systolic, diastolic and mean arterial pressures (MAP) (Blount, 2007). The importance of this is discussed by Hallett et al (2000) who explain that cerebral perfusion is directly related to MAP. Therefore Mr X’s blood pressure should be maintained in a normotensive to slightly hypertensive range, in order to optimise cerebral perfusion when the carotid artery is cross clamped (Hallett et al (2000). According to Smeltzer, et al (2009), arterial blood flow to the brain arises from the common carotid artery, the first subdivision off the main aorta. As they further explain, bifurcation of the common carotid leads to the internal carotid arteries which supply much of the anterior circulation of the brain. It is these divisions along with the anterior and intermediate cerebral arteries, their connections, and the anterior and posterior communicating arteries, that create the ‘circle of Willis’, allowing blood flow to be redirected on demand (Smeltzer, et al, 2009). As discussed by Jiang (2008), cerebral blood flow (CBF) is regulated by cerebral perfusion pressure (CPP) and cerebrovascular resistance (CVR). He suggests that in normal healthy adults MAP remains relatively steady between 50 mmHg to 150 mmHg as a result of CVR changes determined by the variations in diameter of the small intracranial arteries. This occurrence, as discussed by Jiang (2008), is known as ‘cerebral
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autoregulation’, a mechanism that protects the brain against the risk of hypoxia (inadequate oxygen) and ischemia (inadequate blood supply) at a lower perfusion pressure, or oedema (swelling) at a higher perfusion pressure. When taking these factors into consideration, it can be suggested in Mr X’s case that a significant decrease seen in his blood pressure could potentially lead to hypoperfusion and ischemic infarction of the brain. However, if allowed to become too hypertensive, this would increase the incidence of wound haematoma which, postoperatively, could compromise Mr X’s airway due to direct tracheal compression caused by the pressing haematoma and related oedema. This then further highlights the importance of intraoperative monitoring in which accurate, moment by moment data provided the anaesthetist with crucial blood pressure readings so that any deviations could be corrected in order to maintain Mr X’s normatensive state throughout the procedure.
Anaesthetically, Mr X required little intervention by the anaesthetist intraoperatively as his observations remained stable throughout. On successful completion of the carotid endarterectomy Mr X was taken through to the post-operative care unit where he was extubated and carefully monitored. When fully recovered from the affects of his anaesthesia, Mr X was then transferred back to the ward.
Within this assignment the writer has explored the physiological processes in the maintenance of homeostasis, by observing the changes experienced by Mr X throughout his anaesthetic induction and surgical procedure. A detailed analysis of Mr X’s physiological/clinical data has been incorporated into this study, in which the changes observed, have been discussed from an anatomical and physiological perspective. The writer has explored the physiological processes concerned with hormonal feedback by discussing the stress response, the role and function of the endocrine system, and the contributions made by other body systems in response to maintaining homeostasis. This
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case study has also observed the relationship between blood pressure, cardiac output and total peripheral resistance, and how they are influenced by triggers activated by the higher centres of the brain, the sympathetic nervous system and circulating catecholamines released into the bloodstream. Changes noticed during Mr X’s induction of general anaesthesia were also observed, with emphasis on the pharmacological effects of the drugs, which again, produced variations in his haemodynamics, altering HR, BP and respiratory rate accordingly. This case study has also highlighted the importance of monitoring blood pressure and mean arterial pressure with the use of an arterial line which analysed Mr X’s physiological changes to provide the anaesthetist with up-to-date clinical data, allowing him to monitor Mr X’s vital signs very closely to ensure that blood flow to his brain remained within the recommended physiological values to maintain adequate brain perfusion.
As the writer observed, Mr X’s operative procedure concluded without incident or intervention. Therefore it can be suggested that while Mr X was under the influence of anaesthesia his homeostatic balance was being maintained by the care and treatment of the anaesthetist, and once again highlights the importance of careful and accurate monitoring in which any deviations observed could have been managed and controlled accordingly.
Word Count 3000
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References
Better Health Channel., 2009. Blood Pressure. [Online] (Updated June 2009) Available at: http://www.betterhealth.vic.gov.au/bhcv2/bhcarticles.nsf/pages/Blood_pressure_explained? OpenDocument (accessed 15th October 2009).
Biology Encyclopedia., 1998. Stress Response. [Online] Available at: http://www.biologyreference.com/Se-T/Stress-Response.html (accessed 11th October 2009).
Blount, K., 2007. Hemodynamic Monitoring. In Kaplow, R. & Hardin, S.R. Eds., 2007. Critical Care Nursing: Synergy for Optimal Outcomes. Massachusetts: Jones & Bartlett Publishers. Ch.11.
Bray, J.J. Cragg, P.A. MacKnight, A.D.C. & Mills, R.G., 1999. Lecture Notes on Human Physiology. 4th ed. Oxford: Blackwell Science Limited.
Clancy, J. & McVicar, A.J., 2009. Physiology and Anatomy for Nurses and Healthcare Practitioners :A Homeostatic Approach. 3rd ed. London: Hodder Arnold.
Costanzo, L.S., 2007. Physiology. 4th ed. Philadelphia: Lippincott Williams & Wilkins.
Enu, I & Obergfell, R., 2008. Cardiovascular & Physiology. In Modak, R.K. Eds. Anesthesiology Keywords Review. Philadelphia: Lippincott Williams & Wilkins, 2008, pp. 197.
Ganong, W.F., 2005. Review of medical physiology. 22nd ed. London: McGraw Hill.
Hale, T., 2004. Exercise Physiology: A Thematic Approach. West Sussex: John Wiley & Sons Limited.
Hallett, J.W. Brewster, D.C. & Rasmussen, T.E., 2000. Handbook of Patient Care in Vascular Diseases. 4th ed. Philadelphia: Lippincott Williams & Wilkins.
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Health Professions Council., 2008. Standards of Proficiency – Operating Department Practitioners. London.
Jiang, W.J., 2008. Cerebral Perfusion Imaging. In Heuser, R.R. & Henry, M. Eds., 2008. Textbook of Peripheral Vascular Interventions. 2nd ed. London: Informa Healthcare. Ch. 30.
Klabunde, R.E., 2004. Cardiovascular Physiology Concepts. London: Lippincott Williams & Wilkins.
Marieb, E.N., 2008. Essentials of Human Anatomy and Physiology. 9th ed. London: Pearson Benjamin Cummings.
McGeown, J.G., 2007. Physiology: A Clinical Core Text of Human Physiology with Self- Assessment. 3rd ed. Edinburgh: Churchill Livingstone.
Nobel, A. Johnson, R. Thomas, A. & Bass, P., 2005. The Cardiovascular System. London: Churchill Livingstone.
Oxford Concise Colour Medical Dictionary., 2007. 4th ed. Oxford: Oxford University Press.
Reid, W. Darlene & Chung, F., 2004. Clinical Management Notes and Case Histories in Cardiopulmonary Physical Therapy. United States of America: SLACK Incorporated.
Sasada, M. & Smith, S., 2003. Drugs in Anaesthesia & Intensive Care. 3rd ed. Oxford: Oxford University Press.
Sells, P. & Prentice, W. E., 2006. Impaired Endurance: Maintaining Aerobic Capacity and Endurance. In Voight, M. L. Hoogenboom, B. J. & Prentice, W. E. Eds., 2007. Musculoskeletal Interventions: Techniques for Therapeutic Exercise. United States of America: McGraw Hill. Ch. 9.
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Sherwood, L., 2007. Human Physiology: From Cells to Systems. 7th ed. Belmont, California: Thomson Brooks/Cole.
Silverthorn, D. U., 2010. Human Physiology an Integrated Approach. 5th ed. San Francisco: Pearson Benjamin Cummings.
Simpson, P.J & Popat, M., 2002. Understanding Anaesthesia. 4th ed. London: Butterworth- Heinemann.
Smeltzer, S.C. Bare, B.G. Hinkle, J.L. Cheever, K.H., 2009. Brunner & Suddarth’s Textbook of Medical-Surgical Nursing. 12th ed. Philadelphia: Lippincott Williams & Wilkins.
Treacher, D.F. & Grant, I.S., 2006. Critical Care and Emergency Medicine. In Boon, N.A. Colledge, N.R. & Walker, B.R. Eds., 2006. Davidson’s Principles & Practice of Medcine. 20th ed. Philadelphia: Churchill Livingstone. Ch. 8.
VascularWeb., 2008. Carotid Endarterectomy. [Online] (Updated 19 Dec 08) Available at: http://www.vascularweb.org/patients/NorthPoint/Carotid_Endarterectomy.html (accessed 15th October 2009).
Waugh, A. & Grant, A., 2006. Ross and Wilson: Anatomy and Physiology in Health and Illness. 10th ed. London: Churchill Livingstone.
White, G.C., 2003. Basic Clinical Lab Competencies for Respiratory Care: An Integrated Approach. 4th ed. United States of America: Delmar Learning.
Wilson, W.C. Minokadeh, A. Benumof, J.L. Frass, M. & Barbieri, P., 2007. Definitive Airway Management. In Wilson, W.C. Grande, C.M. & Hoyt, D.B. Eds., 2007. Trauma: Emergency Resuscitation, Perioperative Anesthesia, Surgical Management. Vol 1. New York: Informa Healthcare. Ch.9.
Winters, M.E., 2008. Pearls and Pitfalls in Monitoring the Critically Ill Patient in the Emergency Department. [Online] Medscape Today. Available at: http://www.medscape.com/viewarticle/577221 [Accessed 18 February 2010].
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NB xxxxx Whel l tried to do my on essay during tutorials l was told to adresse the following information

The body internal and external enironment this being what and please explain that to Stalin’s law . Bainridge reflex , Blood pressure as it petains the case study and also the body systems that are affected during this surgical procedure on the this case study …………

NB THE PARAMETERS ======YOU CAN COME UP WITH THOSE AND HOPE YOU CAN EXPLAIN THE CHANGES FOR ME … PLEASE PLEASE PLEASE

NBxxxxxxxxxxxxxxxxxxx PLEASE USE PAST TENSE AS THIS HAS ALREADY OCCURED …..XXXXXX

cite in text ……… as for Referencing please its HAVARD MANY THANKS IN ADVANCE…………..GOODLUCK

Applied Anatomy and Physiology Open inguinal Hernia

Order Description

Assessment task (s) Written assignments of 3000 (learning Outcomes 1, 2, 3) 100% weighting
Pass required 40%
Title Case Study where students will follow a patient through an
Investigation/clinical procedure from admission to discharge to the department/unit

Date of submission 05/01/2014
Place of submission Via Turnitin GradeMark deadline 14.00hrs (2pm)
Release of Marks 01/02/2014
Date of DAP 05/02/2014
Resubmission W/C 21/01/2014
All coursework assignments and other forms of assessment must be submitted by the published
deadline which is detailed above. It is your responsibility to know when work is due to be submitted –
ignorance of the deadline date will not be accepted as a reason for late or non-submission.
Any late work (submitted via Turnitin GradeMark, person or by post) will NOT be accepted and a mark of
zero will be awarded for the assessment task in question.
You are requested to keep a copy of your work.
Assignment
In writing this assignment you should consider the following:
This study is an analysis of physiological data collection derived from patient observation/clinical
procedures, explaining the treatment’s impact on the patient’s physiological parameters relating
this to the underlying theory and its relation to practice.
Choose a patient, procedure etc. that interests you. Do not try to undertake the study of highly
complex areas or procedures. The aim of the case study is to demonstrate your understanding,
knowledge and analytical abilities in relation to the area of anatomy and physiology within your
clinical practice. Keep this statement paramount within your memory whilst undertaking your
study and preparation of the assessments.
The case study would involve you initially identifying a patient who you will be involved with whilst
on duty; this may be for the whole or part of your shift. You will need to collect and collate data
which is relevant to your patient but which does not identify your patient in anyway or form. Such
identification would be a serious breach of confidentiality as would the identification of your
working environment or employer.
Collection of relevant bio-psychosocial data should be directly related to the discussions you
present with regards to the anatomical and physiological aspects of your case study. Data
collection will also involve areas of relevant treatment and care/investigation delivery which leads
to physiological changes or aiding a patient adapting, in a physiological sense, to the procedures
they are undergoing. For instance if a patient has a colloid infusion commenced one would
expect that you would provide an analysis as to why such a fluid is given, the reasons for a
change in the patient’s blood pressure and what physiological effect this administration of such a
fluid would have on the patient. This is not a pharmacological study but some demonstration of 7
knowledge and analysis of drugs and how they were utilised would be required along with their
physiological effects.
All your discussions within your study must be referenced appropriately using a wide variety of
literature and sources to demonstrate you have read sufficiently around your subject matter. You
will need to demonstrate analysis of your chosen subject areas as required at level 2. Overuses
of quotes are best avoided since this does not necessarily demonstrate understanding but only
your ability to copy another author’s work. Read, understand and then incorporate into your work
appropriately. Sometimes it is necessary to quote since paraphrasing may lose the essence of
what the author was trying to convey.
Remember this is an Anatomy and Physiology module and as such should be the focus of you
case study.
In presenting your work for assessment you must be sure that you have addressed all of the learning
outcomes of the module. Your submission will be marked against these learning outcomes and the
assessment criteria. The assessment criteria are a measure of how well you have met the learning
outcomes at this level of academic study.
Guidance on maintaining confidentiality in submitted work is available in your Student Handbook, and
you should read this guidance.
You are required to submit your final assignment via Turnitin GradeMark
For this module you are required to submit your summative assessment (for your written assignment) via
GradeMark.
To check your draft (formative) assignment there will be a class section called ‘Check Originality Report’
(COR) set up in your Turnitin account. You will be able to submit to the Check Originality Report
section as many times as you wish and it will be available throughout your studies. This resource
is also a useful tool to share with your module leader or tutor. You can download your originality report
as a PDF file and email it to your tutor, print the originality report and bring it to the tutorial, or log into
Turnitin whilst in the tutorial to show and discuss your work.

Key text
Clancy, J. and McVicar, A. (2009) Physiology &
Anatomy: A Homeostatic Approach. 3
rd ed. London:
Arnold.
This book relates many of the concepts in
anatomy and physiology to homeostasis and is
highly recommended
Books

Martini F. H., Nath, J. L. and Bartholomew,E. F.
(2012) Fundamentals of Anatomy and Physiology 9
th
ed. London: Pearson Education
Marieb, E. N. (2009) Essentials of Human Anatomy
and Physiology International edition 9th ed. London:
Pearson Benjamin Cummings

McCance, K. L. and Heuther, S. E. (2009)
Pathophysiology The biological basis for Disease in
Adults and Children 6
th ed. St Loius: Mosby Elsevier
This provides in-depth exploration of anatomy
and physiology and complements the lectures
well and is available in the library

This is highly recommended as a text and
informs the lectures with many of the slides
from lectures being gained from this book
This text provides excellent background
information with regards to many pathologies
and complements the normal anatomy and
physiology texts effectively

THIS IS AN EXAMPLE ESSAY GIVEN BY THE LECTURER AS TO HOW WE SHOULD TRY AND FOMURLATE OUR OWN ESSAY it will be fine if you can follow along the same principle xxxxxxxxx

In an ever changing environment, the body is constantly adapting to maintain a relatively steady internal balance. This state of constancy is called homeostasis, a process that begins at a cellular level and relies on the regularity of a water-based medium known as the internal environment (Waugh & Grant, 2006). This environment continually alters and changes within very narrow limits to preserve a state of equilibrium in order to meet the functional needs of the body (Marieb, 2008).
In this assignment, the writer will examine the physiological processes in the maintenance of homoeostasis by following a chosen individual through their anaesthetic induction and operative procedure. The writer aims to demonstrate their understanding of patho- physiology, by analysing the patient’s physiological changes, to include, patient observations through the interpretation of clinical data, the role and function of the endocrine system, the physiological stress response, and the contributions made by other body systems to maintain homeostasis within the body. To respect and maintain confidentiality as specified by the Health Professions Council (2008), Standards of Proficiency 1a .3, the identity of the patient selected for this case study will remain anonymous, and for this reason will be referred to as Mr X.
The patient chosen for this assignment is an otherwise healthy sixty eight year old male, undergoing a carotid endarterectomy under general anaesthesia. This procedure is carried out to reduce the risk of strokes, and involves the surgical removal of fatty deposits called plaque (such as cholesterol and calcium), which build up in the carotid artery. The condition is caused by a disease process called atherosclerosis which narrows and constricts the
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artery causing a reduction in blood flow to the brain (Oxford Concise Colour Medical Dictionary, 2007).
(VascularWeb, 2008)
The process of this physiological study began at pre-assessment, during which time Mr X’s routine observations were checked. These were recorded at a time when Mr X was thought to be calm and relaxed (Darlene Reid & Chung, 2004), and are shown against the normal adult values set out in the table below.
Table 1
????Pre-assessment Observations
?????Mr X’s observations
???Normal Adult Parameters (Darlene Reid & Chung 2004)
???Blood Pressure
???????127/80 mmHg
??????<120/<80 mmHg
???Heart Rate
????80 beats per minute
????60-100 beats per minute
???Respiratory Rate
??14 breaths per minute
?12-16 breaths per minute
???Oxygen Saturation (Sp02)%
???????97%
??????95-100%
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The readings indicated that Mr X’s blood pressure was well within normal adult parameters. Blood pressure, according to Clancy and McVicar (2009), is the force of circulating blood exerted against the inner walls of the blood vessels as it is pumped around the body. Two readings determine this pressure, measured in millimetres of mercury (mmHg). These are the systolic and diastolic pressures. The highest refers to the systolic pressure which is produced when blood is pushed into the aorta following the contraction of the left ventricle. The lower pertains to the diastolic pressure which is obtained when the heart is at rest (Better Health Channel, 2009). Blood pressure is influenced by three primary elements; cardiac output, the peripheral resistance and blood volume. These elements are conveyed in the following formula as suggested by Clancy & McVicar (2009).
Total peripheral resistance, as described by Sells, et al. (2006), is concerned with the forces that oppose blood due to the amount of friction it encounters as it travels through the blood vessels. This is largely determined by the length and width of the vessels, and the thickness or viscosity of the blood itself (Clancy & McVicar, 2009). Peripheral resistance is controlled by the sympathetic nervous system which prompts the blood vessels to dilate and constrict accordingly. Any factors which alter total peripheral resistance will cause a reflex variation in blood pressure (Marieb, 2008).
Godfrey (2004) defines cardiac output as the total amount of blood expelled from the left ventricle every minute. It also works in direct relationship with blood pressure, in that a fluctuation in either one will have the same, direct effect on the other. Cardiac output is the product of heart rate (HR), the number of heart beats per minute based on the rate of ventricular contractions, multiplied by stroke volume (SV), the volume of blood ejected by each ventricle per contraction (Silverthorn, 2010). Stroke volume, as explained by Kindlen (2003), can be controlled either extrinsically (via nerves and hormones), or intrinsically, e.g.
?????Blood pressure (BP) = Cardiac output (CO) x Total peripheral resistance (TPR)
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Starling’s law (Sherwood, 2007). The extrinsic control of cardiac function originates within the sympathetic branch of the autonomic nervous system. This mechanism increases myocardial contractility by stimulating the heart to beat stronger, allowing more blood to be expelled per beat (Clancy & McVicar, 2009). The intrinsic mechanism, as described by McGeown (2007), is concerned with the heart’s innate ability to alter stroke volume. It is directly linked to the force produced by the cardiac muscle during each contraction and is related to the length of the myocardial cells and the end diastolic volume. Klabunde (2004) differentiates stroke volume as a correlation between end-diastolic volume (EDV) and end- systolic volume (ESV). EDV, often referred to as preload, is determined by the amount of blood in each ventricle during diastole (relaxation), and is influenced by the amount of blood returning to the right atrium through the ascending and descending vena cava and pulmonary vein (venous return). According to Marieb (2008) stroke volume is governed by a mechanism known as Starling’s law and is considered to be the most important intrinsic control mechanism in cardiac function. As discussed by Hale (2004) Starling’s law is a phenomenon which deals with variations in venous return and is concerned, more importantly, with the pressure at which the blood is returned to the heart via the central veins. It works on the principle that, the more the heart muscles are stretched, the more powerfully it contracts (Silverthorn, 2010). Therefore, anything that influences an increase in venous return prompts a relevant rise in blood flow to the heart. As the ventricles expand (within certain physiological tolerances), the muscle fibres stretch, stimulating the cardiac muscle to contract more forcibly (Solomon, 2009). As a result, the heart pumps a greater volume of blood into the arteries (Silverthorn, 2010).
When Mr X arrived in the anaesthetic room he appeared to be very nervous and looked extremely pale. An oxygen saturation probe, a non-invasive blood pressure (NIBP) cuff, and a set of electrocardiograph leads were applied to Mr X to monitor his vital signs. These were recorded by the monitoring equipment to reveal the following clinical data:
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Table 2
???Blood Pressure
?????140/85 mmHg
???Heart Rate
???????110 beats per minute
????Respiratory Rate
??16 breaths per minute
???Oxygen Saturation %
???????97%
???It was noticed that Mr X’s blood pressure, heart rate and respiratory rate had increased above the normal limits of his original baseline observations noted at pre-assessment. These increases are suggested as being characteristics of the stress response, an instantaneous reaction which primes the body for “fight or flight” when confronted with a real or perceived threat, either physically or emotionally (Waugh & Grant, 2006). Stimulation of the higher centres of the brain, the cerebral cortex and the hypothalamus, respond to the stress stimulus by activating the sympathetic division of the autonomic nervous system (Biology Encyclopedia, 1998). This activation stimulates the adrenal medulla to release two naturally occurring hormones called catecholamines, these being, adrenaline also known as epinephrine, and noradrenaline, also called norepinephrine, into the bloodstream (Biology Encyclopedia, 1998). As they are released into the circulation they potentiate certain physiological changes within the body, acting as short-term homeostatic effectors of BP by effecting changes within cardiac function and peripheral resistance (Clancy & McVicar, 2009). As explained by Sasada & Smith (2003), adrenaline is a positive inotrope and chronotrope which brings about strengthening of the force of the cardiac muscle contractions and a rise in heart rate respectively. When released into the body adrenaline causes a consequent rise in blood pressure, heart rate and blood glucose levels, and expands the tiny passageways of the lungs (Waugh & Grant, 2006). These increases in metabolic activity increase the demand for more oxygen and glucose and cause a faster movement of blood to the organs of the body, particularly to the brain, heart and the muscles as described by Marieb (2008). Bray et al. (1999) discusses that in response to low blood glucose, a
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polypeptide hormone called glucagon is released by the pancreas. This acts on the liver to promote glycogenolysis, the breakdown of glycogen, and gluconeogensis, the production of glucose from fatty acids and amino acids as a means to increase energy level production through cell respiration, mediated by the release adrenaline and cortisol (Clancy & McVicar, 2009). These changes were reflected in Mr X’s observations and explained the consequent rise in his blood pressure and heart rate when he entered the anaesthetic room given the amount of stress he was under, whereas his respiratory volumes increased as a result of bronchodilation, stimulated by the adrenaline which increased his tidal volume and hence his overall minute volume (Sasada & Smith, 2003) which lead to an increase in his gaseous exchange leading to increased oxygen levels within his blood.
As discussed by Kindlen (2003), noradrenaline also underlies the fight-or-flight response and shares many similarities with adrenaline in the actions caused, i.e. raised heart rate. When noradrenaline is released into the bloodstream it has a greater influence on the blood vessels, in that it potentiates vasoconstriction of the arterioles which prompts a reflex rise in heart rate and stroke volume. According to Ganong (2005), the influencing effects of noradrenaline causes vasoconstriction in organs that are deemed unessential during times of stress, such as the gastrointestinal (GI) tract and the skin (Noble, et al., 2005). This would account for Mr X’s pale and pasty complexion on arrival into theatres which suggested that his peripheral blood vessels had constricted in order to prioritize blood flow to the most important organs of the body. This, therefore, caused a subsequent increase in TPR and a relevant rise in BP as illustrated in table 2.
Another physiological response often seen when circulating amounts of catecholamines increase is the contraction of the spleen. This may be induced under nervous control through intervention of the SNS which prompts the spleen to eject its rich blood supply into
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the central circulatory system, therefore increasing venous return (Ganong, 2005). As a result of this increase, stretch receptors located in the walls of the right atrium detect changes in central venous pressure as well as rising venous return. It is these receptors that provide an input to the brain transmitting impulses through vagal afferents which inhibit parasympathetic activity (Noble, et al., 2005). This in turn leads to an increase in heart rate and a decrease in pressure perpetuated by the movement of blood as it is drawn out of the right atrium and into the left heart (Enu & Obergfell, 2008). The ensuing decrease in right arterial pressure prompts a rise in venous return from the superior and inferior vena cava in a continuing cycle recognised as the Bainbridge reflex which continues until venous return to the right atrium has returned to normal levels (Klabunde, 2004).
In the anaesthetic room the anaesthetist administered 50mcg of Fentanyl through Mr X’s cannula. Fentanyl, as described by Simpson & Popat (2002) is a synthetic opioid medication used to provide the analgesic element of general anaesthesia. According to Sasada & Smith (2003), Fentanyl demonstrates very little effect on the cardiovascular system with the exception of bradycardia. However, as they further discuss, it is an exceptionally powerful respiratory depressant, mediating a decrease in respiratory rate as well as tidal volume, the volume of air inspired and expired out of the lungs during quiet breathing (Costanzo, 2007). In view of this, it can be suggested that the evident fall in Mr X’s heart rate was a result of the bradycardic effects of the drug which, in turn, reduced his blood pressure as shown in table 3 overleaf, reinforcing earlier discussions that heart rate and stroke volume influence cardiac output, and that blood pressure is the product of cardiac output and total peripheral resistance.
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Table 3
?????Blood Pressure
??????126/72 mmHg
????Heart Rate
?91 beats per minute
?????Respiratory Rate
??????14 breaths per minute
????Oxygen Saturation
????99%
??Anaesthetic induction was achieved with an intravenous dose of the non-barbiturate induction agent, Propofol (200mg). Sasada & Smith (2003) state that although cardiovascularly stable, Propofol yields a moderate 15-25% drop in BP and systemic vascular resistance (SVR) without negating an increase in heart rate due to its pharmacological action as a negative inotrope (decreasing myocardial contractility). They further highlight that when given as a bolus dose, Propofol also acts as a respiratory depressant, producing variable periods of apnoea (cease in breathing). This was anticipated by the anaesthetist who pre-oxygenated Mr X with 100% oxygen for a minimum of three minutes prior to induction. According to Wilson et al (2007), the purpose of pre-oxygenation is to increase O2 stores in the lungs, as well as arterial and mixed venous blood, by replacing nitrogen with O2 (de-nitrogenation), therefore maximising PaO2 during apnoea while prolonging arterial desaturation. To facilitate Mr X’s intubation and controlled ventilation, 80mcg of Vecuronium was also administered through his cannula. Vecuronium, as described by Sasada & Smith (2003), is a non-depolarising muscle relaxant that poses minimal cardiovascular or respiratory effect other than apnoea, and allows conditions for adequate intubation within 2 minutes of administration. This allowed the anaesthetist to pass a size 8 endotracheal tube through the patient’s vocal chords and into his trachea while his breathing was controlled and maintained by way of intermittent positive pressure ventilation (IPPV).
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For the purpose of this operation, Mr X’s blood pressure was monitored by means of an arterial line inserted into his radial artery. This was used to provide a constant and accurate real time measurement of his systolic, diastolic and mean arterial blood pressures during the procedure (White, 2004). Sherwood (2007) refers to the difference between systolic and diastolic pressure as the pulse pressure which can be felt when an artery passes close the skin. Mean arterial pressure is the average pressure which drives the blood into the tissues during the cardiac cycle and is equal to one third pulse pressure plus diastolic pressure (Sherwood, 2007). This, Sherwood (2007) continues, is due to the fact that when the heart is at rest, around two thirds of the cardiac cycle is spent in diastole, with only one third in systole. Mean pressure therefore provides a better guide of tissue perfusion than systolic and diastolic values, and is less susceptible to variable measurement, waveform distortion and reflection (Winters, 2008).
On transfer into theatre, Mr X’s anaesthesia was maintained using a combination of oxygen and nitrous oxide dispensed with a potent, inhalational, anaesthetic agent called Isoflurane (Sasada & Smith, 2003). As Simpson & Popat (2002) point out, CO is dependent on venous return to the heart, which again relies on negative intrathoracic pressure as well as the pumping action of muscles adjoining blood vessels. They further state that muscular relaxation coupled with IPPV tends to lessen venous return, thus reducing cardiac output, and in addition, produces vasodilatation and a consequent reduction in BP. According to Treacher & Grant (2006), this is because hypotension normally succeeds anaesthesia due to the direct cardiovascular effects of the drugs and the loss of sympathetic drive. When combined with a muscular blockade positive pressure ventilation may intensify this problem by raising intrathoracic pressure, thus, reducing venous return and therefore cardiac output (Treacher & Grant, 2006). It can be considered, therefore, that the subsequent decrease seen in Mr X’s blood pressure was a result of these influencing factors combined with the pharmacological effects of the anaesthetic drugs administered during induction. However,
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as seen in table 4 below, Mr X’s observations taken before surgical intervention were still well within the accepted physiological parameters.
Table 4
???Blood Pressure
???????120/72 mmHg
????Heart Rate
??87 beats per minute
???Respiratory Rate
???????14 breaths per minute
????Oxygen Saturation
????99%
???Throughout the surgical procedure, this being the carotid endarterectomy, Mr X’s observations remained relatively stable. Frequent and precise readings calculated by the arterial line allowed the anaesthetist to monitor Mr X’s arterial waveforms in addition to his systolic, diastolic and mean arterial pressures (MAP) (Blount, 2007). The importance of this is discussed by Hallett et al (2000) who explain that cerebral perfusion is directly related to MAP. Therefore Mr X’s blood pressure should be maintained in a normotensive to slightly hypertensive range, in order to optimise cerebral perfusion when the carotid artery is cross clamped (Hallett et al (2000). According to Smeltzer, et al (2009), arterial blood flow to the brain arises from the common carotid artery, the first subdivision off the main aorta. As they further explain, bifurcation of the common carotid leads to the internal carotid arteries which supply much of the anterior circulation of the brain. It is these divisions along with the anterior and intermediate cerebral arteries, their connections, and the anterior and posterior communicating arteries, that create the ‘circle of Willis’, allowing blood flow to be redirected on demand (Smeltzer, et al, 2009). As discussed by Jiang (2008), cerebral blood flow (CBF) is regulated by cerebral perfusion pressure (CPP) and cerebrovascular resistance (CVR). He suggests that in normal healthy adults MAP remains relatively steady between 50 mmHg to 150 mmHg as a result of CVR changes determined by the variations in diameter of the small intracranial arteries. This occurrence, as discussed by Jiang (2008), is known as ‘cerebral
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autoregulation’, a mechanism that protects the brain against the risk of hypoxia (inadequate oxygen) and ischemia (inadequate blood supply) at a lower perfusion pressure, or oedema (swelling) at a higher perfusion pressure. When taking these factors into consideration, it can be suggested in Mr X’s case that a significant decrease seen in his blood pressure could potentially lead to hypoperfusion and ischemic infarction of the brain. However, if allowed to become too hypertensive, this would increase the incidence of wound haematoma which, postoperatively, could compromise Mr X’s airway due to direct tracheal compression caused by the pressing haematoma and related oedema. This then further highlights the importance of intraoperative monitoring in which accurate, moment by moment data provided the anaesthetist with crucial blood pressure readings so that any deviations could be corrected in order to maintain Mr X’s normatensive state throughout the procedure.
Anaesthetically, Mr X required little intervention by the anaesthetist intraoperatively as his observations remained stable throughout. On successful completion of the carotid endarterectomy Mr X was taken through to the post-operative care unit where he was extubated and carefully monitored. When fully recovered from the affects of his anaesthesia, Mr X was then transferred back to the ward.
Within this assignment the writer has explored the physiological processes in the maintenance of homeostasis, by observing the changes experienced by Mr X throughout his anaesthetic induction and surgical procedure. A detailed analysis of Mr X’s physiological/clinical data has been incorporated into this study, in which the changes observed, have been discussed from an anatomical and physiological perspective. The writer has explored the physiological processes concerned with hormonal feedback by discussing the stress response, the role and function of the endocrine system, and the contributions made by other body systems in response to maintaining homeostasis. This
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case study has also observed the relationship between blood pressure, cardiac output and total peripheral resistance, and how they are influenced by triggers activated by the higher centres of the brain, the sympathetic nervous system and circulating catecholamines released into the bloodstream. Changes noticed during Mr X’s induction of general anaesthesia were also observed, with emphasis on the pharmacological effects of the drugs, which again, produced variations in his haemodynamics, altering HR, BP and respiratory rate accordingly. This case study has also highlighted the importance of monitoring blood pressure and mean arterial pressure with the use of an arterial line which analysed Mr X’s physiological changes to provide the anaesthetist with up-to-date clinical data, allowing him to monitor Mr X’s vital signs very closely to ensure that blood flow to his brain remained within the recommended physiological values to maintain adequate brain perfusion.
As the writer observed, Mr X’s operative procedure concluded without incident or intervention. Therefore it can be suggested that while Mr X was under the influence of anaesthesia his homeostatic balance was being maintained by the care and treatment of the anaesthetist, and once again highlights the importance of careful and accurate monitoring in which any deviations observed could have been managed and controlled accordingly.
Word Count 3000
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References
Better Health Channel., 2009. Blood Pressure. [Online] (Updated June 2009) Available at: http://www.betterhealth.vic.gov.au/bhcv2/bhcarticles.nsf/pages/Blood_pressure_explained? OpenDocument (accessed 15th October 2009).
Biology Encyclopedia., 1998. Stress Response. [Online] Available at: http://www.biologyreference.com/Se-T/Stress-Response.html (accessed 11th October 2009).
Blount, K., 2007. Hemodynamic Monitoring. In Kaplow, R. & Hardin, S.R. Eds., 2007. Critical Care Nursing: Synergy for Optimal Outcomes. Massachusetts: Jones & Bartlett Publishers. Ch.11.
Bray, J.J. Cragg, P.A. MacKnight, A.D.C. & Mills, R.G., 1999. Lecture Notes on Human Physiology. 4th ed. Oxford: Blackwell Science Limited.
Clancy, J. & McVicar, A.J., 2009. Physiology and Anatomy for Nurses and Healthcare Practitioners :A Homeostatic Approach. 3rd ed. London: Hodder Arnold.
Costanzo, L.S., 2007. Physiology. 4th ed. Philadelphia: Lippincott Williams & Wilkins.
Enu, I & Obergfell, R., 2008. Cardiovascular & Physiology. In Modak, R.K. Eds. Anesthesiology Keywords Review. Philadelphia: Lippincott Williams & Wilkins, 2008, pp. 197.
Ganong, W.F., 2005. Review of medical physiology. 22nd ed. London: McGraw Hill.
Hale, T., 2004. Exercise Physiology: A Thematic Approach. West Sussex: John Wiley & Sons Limited.
Hallett, J.W. Brewster, D.C. & Rasmussen, T.E., 2000. Handbook of Patient Care in Vascular Diseases. 4th ed. Philadelphia: Lippincott Williams & Wilkins.
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Health Professions Council., 2008. Standards of Proficiency – Operating Department Practitioners. London.
Jiang, W.J., 2008. Cerebral Perfusion Imaging. In Heuser, R.R. & Henry, M. Eds., 2008. Textbook of Peripheral Vascular Interventions. 2nd ed. London: Informa Healthcare. Ch. 30.
Klabunde, R.E., 2004. Cardiovascular Physiology Concepts. London: Lippincott Williams & Wilkins.
Marieb, E.N., 2008. Essentials of Human Anatomy and Physiology. 9th ed. London: Pearson Benjamin Cummings.
McGeown, J.G., 2007. Physiology: A Clinical Core Text of Human Physiology with Self- Assessment. 3rd ed. Edinburgh: Churchill Livingstone.
Nobel, A. Johnson, R. Thomas, A. & Bass, P., 2005. The Cardiovascular System. London: Churchill Livingstone.
Oxford Concise Colour Medical Dictionary., 2007. 4th ed. Oxford: Oxford University Press.
Reid, W. Darlene & Chung, F., 2004. Clinical Management Notes and Case Histories in Cardiopulmonary Physical Therapy. United States of America: SLACK Incorporated.
Sasada, M. & Smith, S., 2003. Drugs in Anaesthesia & Intensive Care. 3rd ed. Oxford: Oxford University Press.
Sells, P. & Prentice, W. E., 2006. Impaired Endurance: Maintaining Aerobic Capacity and Endurance. In Voight, M. L. Hoogenboom, B. J. & Prentice, W. E. Eds., 2007. Musculoskeletal Interventions: Techniques for Therapeutic Exercise. United States of America: McGraw Hill. Ch. 9.
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Sherwood, L., 2007. Human Physiology: From Cells to Systems. 7th ed. Belmont, California: Thomson Brooks/Cole.
Silverthorn, D. U., 2010. Human Physiology an Integrated Approach. 5th ed. San Francisco: Pearson Benjamin Cummings.
Simpson, P.J & Popat, M., 2002. Understanding Anaesthesia. 4th ed. London: Butterworth- Heinemann.
Smeltzer, S.C. Bare, B.G. Hinkle, J.L. Cheever, K.H., 2009. Brunner & Suddarth’s Textbook of Medical-Surgical Nursing. 12th ed. Philadelphia: Lippincott Williams & Wilkins.
Treacher, D.F. & Grant, I.S., 2006. Critical Care and Emergency Medicine. In Boon, N.A. Colledge, N.R. & Walker, B.R. Eds., 2006. Davidson’s Principles & Practice of Medcine. 20th ed. Philadelphia: Churchill Livingstone. Ch. 8.
VascularWeb., 2008. Carotid Endarterectomy. [Online] (Updated 19 Dec 08) Available at: http://www.vascularweb.org/patients/NorthPoint/Carotid_Endarterectomy.html (accessed 15th October 2009).
Waugh, A. & Grant, A., 2006. Ross and Wilson: Anatomy and Physiology in Health and Illness. 10th ed. London: Churchill Livingstone.
White, G.C., 2003. Basic Clinical Lab Competencies for Respiratory Care: An Integrated Approach. 4th ed. United States of America: Delmar Learning.
Wilson, W.C. Minokadeh, A. Benumof, J.L. Frass, M. & Barbieri, P., 2007. Definitive Airway Management. In Wilson, W.C. Grande, C.M. & Hoyt, D.B. Eds., 2007. Trauma: Emergency Resuscitation, Perioperative Anesthesia, Surgical Management. Vol 1. New York: Informa Healthcare. Ch.9.
Winters, M.E., 2008. Pearls and Pitfalls in Monitoring the Critically Ill Patient in the Emergency Department. [Online] Medscape Today. Available at: http://www.medscape.com/viewarticle/577221 [Accessed 18 February 2010].
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NB xxxxx Whel l tried to do my on essay during tutorials l was told to adresse the following information

The body internal and external enironment this being what and please explain that to Stalin’s law . Bainridge reflex , Blood pressure as it petains the case study and also the body systems that are affected during this surgical procedure on the this case study …………

NB THE PARAMETERS ======YOU CAN COME UP WITH THOSE AND HOPE YOU CAN EXPLAIN THE CHANGES FOR ME … PLEASE PLEASE PLEASE

NBxxxxxxxxxxxxxxxxxxx PLEASE USE PAST TENSE AS THIS HAS ALREADY OCCURED …..XXXXXX

cite in text ……… as for Referencing please its HAVARD MANY THANKS IN ADVANCE…………..GOODLUCK