Cardiovascular System

Low Molecular Weight Heparin Paper Low molecular weight heparin is typically used for patients who need to be treated for deep vein thrombosis. Deep vein thrombosis (DVT) is a blood clot (thrombus) in a deep vein usually in the legs. These clots are dangerous because they can break loose, travel through the bloodstream to the lungs, and block blood flow in the lungs (pulmonary embolism). There are many reasons why clots form in a patient.

Mainly when a patient is inactive or bedridden for long periods of time, surgery can damage a blood vessel so a clot can form, or even cancer can cause DVT to form. Treatments for DVT are drugs called anticoagulants that can prevent the blood from clotting thus preventing the adverse effects from a clot. Low molecular weight heparin works by binding to a substance called antithrombin III (which is the major inhibitor of thrombin in the blood). The overall effect of heparin is that it turns off the coagulation pathway and prevents clots from forming.

It can be used as a subcutaneous injection which can be given in an outpatient setting with no increased risk of recurrent thromboembolism or bleeding complications. Since most patients with DVT require one or more diagnostic tests, treatment with intravenous heparin and a three to seven day hospital stay thus making low molecular weight heparin a better alternative. (aafp. org1999) However, with low molecular weight heparin, being a subcutaneous injection makes the process easier for the patient since they do not have to spend all that extra time in the hospital.

The ultimate consequence of a blood clot can be stroke or heart attack so prevention of these events is the consequence of this drug. Unfortunately, just like many other drugs there are some serious side effects to taking LMWHs. They are contraindicated with patients with an indwelling epidural catheter; they can be given two hours after the epidural is removed. If it is given before the epidural is taken out then they have found it to be associated with epidural hematoma. Bleeding is the main concern when taking anticoagulation therapy.

Some of the other common adverse effects to heparin are hematoma, nausea, anemia, thrombocytopenia, fever, and edema. There is a low chance for side effects with monitoring and patient awareness. When evaluating a patient on anticoagulants the nurse needs to ensure patients know the side effects to be aware of and arrange follow up care. Cranberry juice should be avoided since it can affect the INR results. Patients should seek emergency medical care for injuries, particularly a head injury, due to the hemorrhage risk.

As a nurse you need to monitor your patient while on these drugs because of the bleeding factor. (nursingtimes. net2012) References Gee, Emma. (2011) How to look after a patient on anticoagulant therapy. January 22, 2011 Retreived from www. nursingnet. net on July 2012 Lilley, Rainforth Collins, Harrington, Snyder. (2011) Pharmacology and the Nursing Process Copyright 2011 Mosby Inc. Rydberg, J Eric MD. (1999) Low Molecular Weight Heparin in Prevention and Treating DVT Retrieved from www. aafp. org

Introduction:

The technological sweetening refering to measurement and information transmittal has led to more inclusive public presentation and Secure characteristic of the patient monitoring merchandises.

In the earlier period, the taking merchandises manufactured by medical device makers are chiefly those for individual parametric quantity measuring. Nowadays nevertheless multi-parameter patient proctors are more extensively and normally used in our infirmary system.

Multi parametric quantity Patient proctor is usage for critical physiological marks of the patient to convey the critical information. Therefore patient proctor has ever been busying a really important place in the filed of medical devices.

The uninterrupted betterment of engineerings non merely helps us set out the critical physiological marks to the medical forces but besides simplifies the measuring and as a consequence addition the monitoring effectivity and now a yearss patient proctor is really flexible and it can supervise multiple physiological Signals.

CLINICAL USED IN HOSPITAL:

The patient proctors are normally used in some clinical countries such as ICU, CCU, operation room and exigency room because the proctor can supply many physiological parametric quantities of the patient to medical forces

Physical PARAMETERS OF PATIENT MONITORS

Some of physiological mark I mention in below are as follows.

1. Electro Cardio Graph ( ECG )
2. Respiration Rate
3. Heart Rate ( HR ) .
4. Non-Invasive Blood Pressure ( NIBP )
5. Oxygen Saturation in Blood ( SpO2 )
6. Invasive Blood Pressure ( IBP )
7. Temperature TEMP

ELECTRO CARDIO GRAPH:

The ECG proctors classify little electromotive forces of about 1 millivolts that appear on the tegument as a consequence of cardiac gesture. Three/five electrodes prearranged in standard constellations called leads are positioned on the tegument to feel these electromotive forces.

At lease two electrodes are required for an ECG lead ; a 3rd electrode is used as a mention to cut down electrical intervention. Each lead presents a bosom, Producing ECG wave form P waves, QRS composite, and T moving ridges vary in amplitude and mutual opposition.

The signals from the different leads provide the heart specialist with a complete presentation of the electrical activity of the bosom, including the Heart rate, which is interpreted as the R~R Interval.

The timing and wave form of ECG Provide Information on whether the patient ‘s bosom rate is characterized by arrhythmia or other altered maps necessitating intervention.

Parameter FOR RESPIRATION Rate:

The method for usage for Respiratory rate by the technique of electric resistance pneumography. Pass a low current with high-frequency bearer signal between two ECG electrodes side of the chest wall the electric resistance of the lungs alterations as the lungs expand and contract and as the volume of air in the lungs alterations.

The alteration in electric resistance creates a alteration in electromotive force across the bearer signal, which is interpret as breathe and from this phenomenal manner we get respiration rate of a forces.

NON-INVASIVE AND INVASIVE BLOOD PRESSURE:

Non Invasive Blood Pressure ( NIBP ) :

Blood force per unit area proctors by and large measure arterial Pressure, This is produced by the contractions of the bosom and continually alterations over cardiac rhythm.

Three blood force per unit area values, articulated in millimetres of quicksilver above so atmospheric pressure.Systolic force per unit area is the maximal rhythm force per unit area occurs during ventricular contraction.

Diastolic force per unit area is the minimal rhythm force per unit area, happening during the ventricle ‘s make fulling stage between contractions of bosom chamber.

Arterial force per unit area is the average value of the blood force per unit area over the cardiac rhythm.

Invasive Blood Pressure ( IBP ) :

Invasive blood force per unit area is measured by agencies of a catheter insert straight into the circulatory system.

Pressure transducer connected to the catheter converts the mechanical force exerted by the blood into an electrical signal by this mean of technique we can acquire the IBP value.

Parameter FOR OXYGEN SATURATION OF THE BLOOD ( SPO2 ) :

Oxygen impregnation technique is based on the soaking up of Pulse blood O to ruddy and infrared visible radiation by agencies of utilizing finger detector and SpO2 mensurating unit.

Electronic transducer in finger detector converts the pulsation ruddy and infrared visible radiation modulates pulse blood O into electrical signal.

By this agencies of technique we calculated value of SpO2.

Parameter FOR TEMPERATURE Detection:

Temperature of the organic structure is measured by agencies of a thermal resistor investigation.

This investigation is made by semiconducting material whose opposition alterations with temperature. By the agencies of temperature alteration get the accurate temperature Value.

STANDARD MODULE of PATIENT MONITOR:

In footings of its functionality, the proctor is made up of following Faculties:

1. Application Faculty
2. Main Processing Module
3. Man-machine interface Module
4. LAN, WLAN, Bluetooth, RJ45 Connector, USB Port Etc
5. Power supply Module

Parameter Measuring Part:

Patient Monitor mensurating the physiological signals of ECG, RespirationNon-invasive blood force per unit area ( NIBP ) , Oxygen impregnation of the blood ( SpO2 ) , Temperature ( TEMP ) , Invasive blood force per unit area ( IBP ) , cardiac end product ( CO ) , CO and Anesthetic gas ( GAS ) .

In this Measuring portion it can transform physiological signals to electrical signals, and procedure and reassign the values, wave forms and dismay information to Main Board, and so expose them by Interface Board.

Main Control Part:

Main board consists of Interface board and Core board. It has CPU/memory, show circuit web circuit and I/O interface. Main board of the integrated board is used to drive man-machine interface, manage parametric quantity measuring and supply other specific maps to the user such as constellation storage, wave form and informations callback, etc.

Interface Part:

The man-machine interfaces are board consists of Screen show, Recorder, Speaker, Indicator, Keys and knobs.

The high-resolution show Screen is the most primary end product interface, exposing real-time current informations and recorded informations of different patients, Speaker gives bosom round tone and audio dismay Indicator provides extra information about power supply

Power Supply Part:

Power supply is an of import portion of the system, dwelling of power board, power patchboard Battery and fan

Different Auxiliary Partss:

RJ45 online upgrade port is available on the proctor, which allows the service applied scientist to upgrade the system package without needfully opening the enclosure of the proctor. This larboard connexion is for usage as Internet map

The cardiovascular system is the first organ system to become fully functional in the vertebrate embryo and its development occurs in a similar way in all vertebrates. It is derived from angioblastic tissue, which arises from mesenchyme, an aggregation of mesenchymal cells derived from the mesodermal tissue of embryos. The main processes involved in the development of the embryonic cardiovascular system are Vasculogenesis, Angiogenesis, Hematopoiesis, Erythropoiesis and Heart Formation. All processes occur under the influence of stimuli from genes and paracrine factors, oligosaccharides, multifunctional cytokines and enzymes.

Vasculogenesis and Angiogenesis

Two distinctive mechanisms, vasculogenesis and angiogenesis implement the formation of the vascular network in the embryo. Embryonic vasculogenesis gives rise to the heart and the primordial vascular plexus within the embryo and its surrounding membranes as the yolk sac circulation. In mammals, it occurs in parallel to hematopoiesis, the formation of blood cells. Vasculogenesis refers to the in situ differentiation and growth of new blood vessels from mesenchymal cells known as angioblasts which aggregate to form isolated angiogenic cell clusters known as blood islands (angiocysts) within the extra-embryonic and intra-embryonic mesoderm. Small cavities appear within these blood islands by the confluence of intercellular clefts.

The peripheral cells within these blood islands flatten to form endothelial cells, triggered by the binding of the Vascular Endothelial Growth Factor (VEGF) to the first of its two receptors, the VEGF-R2 (Flk1) protein, which is responsible for the differentiation of mesodermal cells into endothelial cells and the subsequent proliferation of the endothelial cells. The core cells give rise to blood cells (haematoblasts). The newly formed endothelial cells arrange themselves around the cavities in the blood islands, forming the primitive endothelium. Cellular vacuoles within the developing endothelial cells coalesce and fuse together without cytoplasmic mixing to forma the blood vessel lumen of the initial endothelial tube.

Extracellular matrix deposition by fibroblasts promotes capillary-like tube formation under the influence of the binding of VEGF to its second receptor, VEGF-R1 (Flt1). This is followed by the interaction of the endothelial blood vessel with the supporting mesodermal cells. The Angiopoietin-1 growth factor binds to the Tie2 receptor tyrosine kinase on the cell membrane of the endothelial cells, allowing the blood vessel to recruit the peri-endothelial cells that will surround it as pericytes and the smooth muscle tissue of the blood vessel, thus maintaining the stability of the blood vessels.

The growth and multiplication of this primordial vascular plexus occurs through the process of angiogenesis in which new blood vessels arise from pre-existing vascularity. This process requires the combination of two signals, Angiopoietin 2 and VEGF, in order to promote the loosening of the support cells and the ability of newly exposed endothelial cells to multiply by budding and sprouting into new vessels. Replacement of Ang1 by Ang2 on the Tie2 receptor tyrosine kinase destabilizes the vessel integrity thus facilitating vessel sprouting in response to the VEGF signal. The new endothelial tubule then interacts with the surrounding mesenchymal cells in part as a response to Ang1 which acts on the endothelial cell Tie2 in order to trigger the association of the new tubule with the periendothelial cells.

Hematopoiesis and Erythropoiesis

Blood develops from endothelial cells (haematoblasts) by a process known as hematopoiesis initially in various parts of the embryonic primitive mesenchyme (yolk sac and allantois), and then in the liver and later on in the spleen, bone marrow and lymph nodes. In embryonic development it is known as primitive hematopoiesis. All blood cells develop from pluripotential stem cells committed to three, two or one hemopoietic differentiation pathways but morphologically undistinguishable. These pluripotent stem cells divide infrequently to generate either more pluripotent stem cells (self-renewal) or committed progenitor cells (colony-–forming cells, CFCs) which are irreversibly determined to produce only one or a few types of blood cells.

These colony-forming cells are known as Lymphocyte Forming Colony (LCFC), Megakaryocyte Forming Colony (MCFC), Erythrocyte Forming Colony (ECFC) and Monocyte Granulocyte Forming Colony (MGFC). The progenitor cells are stimulated to proliferate by specific growth factors (colony-stimulating factors, CSFs) but progressively lose their capacity for division and develop into terminally differentiated blood cells which usually live for only a few days or weeks. Erythrocytes (red blood cells) develop by the process of erythropoiesis. In embryos, erythrocytes are nucleated and express embryonic globin chains.

Heart Formation

In vertebrate embryos the heart tube, the earliest formed heart structure, arises in the heart field, an embryonic clustering of cells which arises soon after gastrulation. These early stages of development are almost identical among all vertebrates unlike the subsequent septation of the chambers and of the outflow tract which varies between species.

The heart field is that region of the precardiac mesoderm that contains the cardiac progenitor cells (endocardial and myocardial precursor cells) and is competent in responding to inductive signals.

Precardiac cells from the epiblast lateral to the primitive streak invaginate through the streak and migrate cranio-laterally to form part of the lateral plate. This pattern is maintained in the eventual anteroposterior placement of structures in the heart, with the most cranial cells contributing to the bulbus cordis at the extreme anterior end of the heart and the most caudal cells contributing to the sinoatrial region and the extreme posterior end.

As mentioned above, the cell progeny of this region contributes to all layers of the heart tube (myocardium, endocardium and parietal pericardium), as well as to the endothelial cells in the vicinity of the heart. In the lateral plate the cells maintain their anteroposterior position.

The lateral plate splits to form two epithelial layers, the somatic mesoderm (which also includes migratory precursors for limb musculature) and the splachnic mesoderm which remains an epithelial sheet and includes the cardiac precursors.

The embryo then folds ventrally carrying the splachnic mesoderm with it and bringing it ventral to the foregut which is generated as the lateral folds meet in the ventral midline. The precursors of the endocardium are included in the splachnic mesoderm and begin to form clusters on the foregut side of the epithelial sheet.

The heart fields fuse at the midline to form a primary heart tube, the process beginning cranially and proceeding caudally. This tubular heart consists of an outer myocardial mantle and an endocardial inner lining. Between these two concentric epithelial layers an acellular matrix, the cardiac jelly, is found. As the ventricular region of the heart begins to bend to the right (“cardiac looping”), the cardiac jelly disappears from the future major chambers of the heart (atria and ventricles) and begins to accumulate in the junction between the atria and ventricles (atrioventricular junction, AVJ) and in the developing outflow tract (OFT).

This results in the formation of the endocardial cushion tissues in the AVJ which later contribute to the formation of AV (atrioventricular) septal structures and valves, septation of the OFT and formation of the semilunar valves of the aorta and pulmonary artery.

The vertebrate heart tube is aligned along the antero-posterior axis. Arterial flow is directed from the ventricle at the anterior end of the heart, through the ventral aortic vessel and branchial arches and subsequently travels posteriorly to the dorsal vessel. Blood flow returns to the heart through the venous system to the atrium lying at the posterior end of the heart chamber.

Formation of the Mammalian Embryonic Cardiovascular System

1)  Formation of the primitive cardiovascular system

a)  Extra-embryonic blood vessels

The wall of the yolk sac mesenchyme proliferates and forms isolated cell clusters known as blood islands. Peripheral cells within these islands flatten and differentiate into endothelial cells in order to form endothelial tubes. Centrally- located cells develop into primitive blood cells (hematoblasts). Endothelial tubes approach and fuse with each other forming a primitive vascular network. This primitive endothelial network appears in the chorionic membrane and body stalk and connects to the vitelline circulation.

b)  Intra-embryonic blood vessels

The endothelial tube network appears in the intraembryonic mesenchyme to form an intraembryonic endothelial  tube network. The intraembryonic and extra embryonic tube networks connect to each other forming a diffuse endothelial  tube network which either fuses or disappears to form a primitive cardiovascular system.

2) Development of the Heart

The primitive cardiovascular system consists of the primary heart tube, formed from the fusion of the two bilateral heart fields of the precardiac mesoderm. The primary heart tube gives rise to the endocardium. Blood flows through this primitive heart tube in a cranial position. The mesenchyme surrounding the tube condenses to form the myoepicardial mantle (the future myocardium). Gelatinous connective tissue, the cardiac jelly, separates the myoepicardial mantle from the endothelial heart tube (the future endocardium).

A series of constrictions (sulci) divides the heart into sections: the sinus venosus, in which the common cardinal veins, the umbilical veins and the vitelline veins drain; the primitive common atrium; the primitive common ventricle; and the bulbus cordis through which blood flows to the paired dorsal aortae. The paired dorsal aortae arise when the branchial or pharyngeal arches are penetrated by six pairs of arteries called aortic arches. These arteries arise from the aortic sac and terminate in a dorsal aorta. Initially, the paired dorsal aortae run along the whole length of the embryo but soon fuse to form a single dorsal aorta just caudal to the branchial or pharyngeal arches.

The arterial and venous ends of the heart tube are fixed by the branchial or pharyngeal arches and the septum transversum, respectively. At this stage the heart is beating and the contractions are of myocardial origin and likened to peristalsis.

The primitive atrium loops up behind and above the primitive ventricle and behind and to the left of the bulbus cordis forming the bulboventricular loop.. This looping process brings the primitive areas of the heart into the proper spatial relationship for the further development of the heart.

Embryonic venous circulation consists of three pairs of veins: the vitelline veins which drain blood from the yolk sac, the umbilical veins which bring oxygenated blood from the chorion (early placenta), and the common cardinal veins which return blood to the heart from the body of the embryo. Arterial circulation consists of three paired arteries: the intersegmental arteries, which form 30-35 branches of the dorsal aortae and carry blood to the embryo, the vitelline arteries which pass to the yolk sac and later to the primitive gut, and the umbilical arteries which carry oxygen-depleted blood to the placenta.

3)      Formation of the Heart Chambers

As mentioned above, during cardiac looping the cardiac jelly disappears from

the future major chambers of the heart and begins to accumulate in the    atrioventricular junction (AVJ) and developing outflow tract (OFT). This results in the formation of the endocardial cushion tissues in the dorsal and ventral walls of the AVJ. These cushions are invaded by mesenchymal cells, approach each other and fuse, dividing the atrioventricular canal into the right and left atrioventricular canals.

The primitive atrium is divided into right and left atria by the formation, modification and fusion of the septum primum and the septum secundum. The septum primum grows towards the fusing endocardial cushions from the roof of the primitive atrium creating a curtainlike septum, the foramen primum between the free edge of the septum and the endocardial cushions.

This foramen becomes progressively smaller and eventually disappears when the septum primum fuses with the fused endocardial cushions (atrioventricular septum). The septum secundum grows from the ventrocranial wall of the atrium to gradually overlap the foramen secundum in the septum primum, forming an incomplete separation between the atria in the form of an oval opening, the foramen ovale.

The sinus venosus initially opens into the center of the dorsal wall of the primitive atrium and its left and right horns are of about the same size. The right horn progressively begins to enlarge in respect to the left horn until it receives all the blood from the head and neck via the superior vena cava and the placenta and caudal regions of the body via the inferior vena cava. The left horn forms the coronary sinus.

The wall of the left atrium is formed by the incorporation of the primitive pulmonary vein which develops as an outgrowth of the dorsal atrial wall. As the atrium expands, the primitive pulmonary vein and its branches are gradually incorporated into the wall of the left atrium forming four pulmonary veins with separate openings.

The division of the primitive ventricle into the right and left ventricles is initially indicated by a muscular ridge with a concave free edge in the middle of the ventricular floor near its apex. Initially, most of its increase in height results from the dilation of the ventricles on its each side. Later, however there is active proliferation of myoblasts, forming the thick muscular part of the interventricular septum.

At the beginning a crescentic interventricular foramen exists between the free edge of the interventricular septum and the fused endocardial cushions allowing communication between the right and left ventricles. This foramen closes as the result of the fusion of tissue from three sources: 1) the right bulbar ridge, 2) the left bulbar ridge and 3) the endocardial ridges. The membranous part of the interventricular spetum is derived from tissue extension from the right side of the endocardial cushions. It merges with the aorticopulmonary septum and the thick muscular part of the interventricular septum. When the interventricular foramen closes, the pulmonary trunk is in communication with the right ventricle and the aorta communicates with the left ventricle.

Active proliferation of mesenchymal cells in the walls of the bulbus cordis gives rise to the formation of the bulbar ridges. Similar ridges form in the truncus arteriosus and are continuous with the bulbar ridges. Both the bulbar and the truncal ridges have a spiral orientation and result in the formation of a spiral aorticopulmonary septum when the bulbar and truncal ridges fuse. This septum divides the bulbus cordis and the truncus arteriosus into the aorta and pulmonary trunk.

Due to the spiral orientation of the aorticopulmonary septum, the pulmonary trunk twists around the aorta. The bulbus cordis is incorporated into the walls of the ventricles. In the left ventricle it forms the walls of the aortic vestibule just inferior to the aortic valve. In the right ventricle it forms the infundibulum or conus arteriosus.

Ventricular trabeculation begins in the apical region of the ventricles soon after cardiac looping. The trabeculation serves primarily as a way of increasing the oxygenation of the myocardium in the absence of  a coronary circulation. The compactation of the trabeculae adds to the proportion and thickness of the compact myocardium.

The American physiologist Walter Cannon used the term Homeostasis to describe the body’s ability to maintain a constant stable internal environment despite the changes to the external surrounding1,2. The body has a range of receptors these are used to constantly monitor the body’s internal conditions to keep them in physiological limits.

To achieve this, every organ works together and thus the body works together as a whole.This requires body to communicate with the organs, this is established through two very highly specialized systems; nervous system and endocrine system, they use electrical impulses and hormones to communicate respectively1. It is vital for our body to maintain homeostasis for our survival, this ability of the body allows us to adapt to our environment which is why we can live in a variety of different settings3.The mechanism of every homeostatic control has three interdependent components; the receptor, which is a sensor that responds to a change (stimuli) in the environment, by sending information through the afferent pathway to the control center1. The second component, which is the control center, is where the information received is assessed and it is determined whether the conditions are in limits1. The final component is the effector; it uses the information provided by the control center to respond to the change1.The information travels along the efferent pathway from control center to the effector this result in a response to the stimuli1.

There are two different homeostatic mechanisms; a negative feedback and a positive feedback. Which mechanism is in action depends on the stimuli. During negative feedback the mechanism reacts by producing a response to the variable in opposite directions, this is achieved through reducing the intensity or cutting off the output completely2. For example, you have your central heating on but you open your window this would result in losing heat hence, reducing the temperature of the room.This change would be detected by the thermostat thus signals will be sent to the boiler to increase the activity. This increase in activity would lead to restoring of the temperature. Now if you close the window and the temperature is established the thermostat would detect this and so will again send signals to the boiler to reduce the activity.

For the positive feedback mechanism the body tends to produce a response that increases the activity of the variable so it supports the change1,2. This moves the stimulus further away from its physiological range.This type of control is not as common as the negative control; it has no limits and is more focused on continuous change1. It occurs during the events where frequent adjustment is not required. A very good example for this control is blood clotting. If a blood vessel is damaged, the platelets tend to stick to the site and release chemicals which attract more platelets1. This leads to a rapid accumulation of platelets which eventually forms a clot.

The cardiovascular system consists of the heart and the blood vessels. Its job is to pump the blood to all parts of the body.The system contributes to maintain homeostasis in the body at all times whether it’s to do with providing brain cells with oxygen and glucose so that the control center in the brain carry’s on working to its best potential or working with kidneys to control the blood volume. The system itself is very complex and specialized. The blood flow in the body must be kept constant and steady. This requires the body to work as a whole with the heart being the center of the homeostatic control. The components that control blood pressure in the heart play a significant role in homeostasis.

Cardiac output (CO), Stroke volume, peripheral resistance, blood volume and heart rate all of these contribute towards regulating blood pressure in the body4. The cardiac output “is the volume of blood pumped put by each ventricle in 1 minute”5 . It can be measured by CO= Heart rate x Stroke volume, as the equation shows the CO depends on the heart rate and stroke volume (“ the volume of blood pumped out by one ventricle with each beat”), therefore any changes in one of these would bring a change to the amount of blood pumped out of the ventricles1,6.The heart rate in controlled by the cardioinhibitory center located in medulla which sends signals through the parasympathetic nerves to the heart7. When the heart is at its resting state the stroke volume is controlled by the end diastolic volume1. When the body is under stress the activity on the sympathetic nervous system is increased by the cardioacceleratory center1. This results in increase in the heart rate and stroke volume by increasing the cardiac muscle activity.

The peripheral resistance is adjusted or altered every now and then in order to maintain the fluctuation in blood pressure.The cardiovascular system and nervous system work together to maintain the mean arterial pressure (MAP) by changing the size of the blood vessels diameter, therefore if the blood pressure is low; blood vessels constrict apart from those supplying blood to the heart and the brain1,7. This result in an increase in peripheral resistance hence maintains the blood pressure to its normal range. These type of controls are operated through baroreceptors and vasomotor center located in the medulla.The increase in arterial pressure leads to stretching of baroreceptors; these are located in the aortic arch, carotid arteries and other large arteries8. The stretching of these baroreceptors sends signals to the vasomotor center8. This is responsible for altering the size of blood vessels.

If the blood pressure is higher than this would be detected by the baroreceptors which in return would cause vasodilation of not only arteries but also veins, this dilation of the vessels reduces peripheral resistance1.The dilation of veins declines in the volume of blood returned to the heart therefore the cardiac output is also decreased, baroreceptors sends out impulses that stimulate activity of parasympathetic activity and reduce activity of the cardioacceleratory center therefore reducing the heart rate1,4,8. Similarly, if the blood pressure was low the vessels would constrict causing vasoconstriction; this increases peripheral resistance hence increase in the blood pressure. In addition to this, the body’s temperature has to be maintained for all the metabolic reactions taking place.These reactions are vital for survival and growth therefore the cardiovascular system and skin together maintain the optimum temperature. For example, if the surrounding temperature is low the blood vessels near the skin go under vasoconstriction by the sympathetic vasoconstrictor9. This results in blood not reaching to the skin and restricted to the areas away from the skin.

Therefore heat loss is reduced significantly maintaining the body temperature to physiological range. Whereas if the temperature of the surrounding is high, the body must lose heat in order to keep its optimum temperature.It achieves this by dilating the blood vessels this allows blood to travel even more closely to the skin thus radiating the heat out9. On the other hand, if there is a homeostatic imbalance of the cardiovascular system (CVS) this can be life threatening. An imbalance could be caused by anything it can be a genetic disorder, unhealthy diet or a disease. An example of such a condition of CVS that can cause homeostatic imbalance is atherosclerosis. This condition blocks the artery and therefore leads to hypertension (homeostatic imbalance)10.

The blockage of the artery is caused by damage to the tunica intima, this allows lumps of fatty substances such as lipids, cholesterol and LDLs to accumulate at the ruptured site1. Overtime reactions take place; these oxidize the LDLs which then act as chemotactic agents that attract macrophages8. These take up oxidized LDLs and ingest them, but they become so engorged that they turn into foam cells1,8. The foam cells build up overtime to form atheroma (plaque). Macrophages release chemicals, these make the smooth muscle cells move to the surface of the plaque and forming a covering8.Due to this obstruction the blood pressure and supply is affected, as a result the heart increases the contraction strength to meet the needs of the body causing hypertension. Consequently, the person is at a high risk of other diseases such as congestive heart failure, coronary heart disease, stroke, damage to kidneys and many others10.

It is still not sure what causes atherosclerosis however there are certain risk factors that increase an individual’s chance of having this condition. Some of these factors are diet rich in cholesterol, smoking, hypertension and family history 10,11.Overall, it is very clear how difficult it is to maintain homeostasis; the cardiovascular system plays a very important role and is involved in homeostasis directly and indirectly. However, every organ must carry out its job to maintain a constant internal environment; one small condition can lead to a complete collapse of the system.

CHAPTER ONE

1.0 INTRODUCTION

Cardiothoracic ratio is the maximum transverse diameter of the heart divided by the greatest internal diameter of the thoracic cage (from inside of rib to inside to rib). (Herring, 2003).

In normal people, the cardiothoracic ratio is usually less than 50% but, in black people up to 55% may still be normal (Sutton 1988). Therefore the cardiothoracic ratio is a handy way of separating most normal heart from most abnormal heart. (Herring, 2003).

A heart can be greater than 50% of the cardiothoracic ratio and still be a normal heart (Herring, 2003). This can occur if there is an ultra cardiac cause of cardiac enlargement which include;

1. Pectus excavatum deformity

2. Straight back syndrome

3. Inability to take deep breath because of obesity, pregnancy etc. (Herring 2003).

The ratio may also increase in elderly. This may be to an in folding of ribs, reducing the thoracic component of the ratio (Sutton 1985).

The transverse diameter of the heart can be measured directly on a radiograph at 1.83m (6ft) upper limit of 16cm for men and 15cm for women are usual (Sutton 1985).

The advantage of a single measurement of that it can be held to be compared in serial films. At difference of 2cm is held to be a significant change. This applies only when the heart is originally normal (Sutton 1985).

Normally, the third of the cardiac shadow lies to the left of the midline and one-third to the right (Berry 2003). In normal individual, the transverse diameter of the heart on PA film is usually in the range of 11.5cm to 15.5cm. it lies less than 11.5cm in about 5% of people and only rarely exceeds 15cm (Benny 2003).

The maximum transverse diameters of the cardiac shadow at the chest radiograph film consist mainly of the diameters of the left ventricle and right atrium as shown by radiograph (Hada, 1995). The ratio is influenced by many factors, not only left ventricular dilatation or hypertrophy but also dilatation of the other cardiac chambers and aorta, rotation and shift of the heart, respiratory phase, body posture and measurement errors (Hada, 1995).

Anatomy of the Heart

Development of the Heart

The development of the heart begins in the middle of the third week from the cardiac progenitor cells in the epiblast, immediately lateral to the primitive streak. Cells destined to form cranial segment of the heart, the outflow tract migrate first and cells forming more caudal portion, right ventricle, left ventricle and sinus venosus respectively migrate in sequential order.

Series of developmental processes later leads to formation of a horse-shoe shaped endothelial lined tube surrounded by myoblasts in the cardiogenic field. In addition to cardiogenic region, other clusters of angiogenic cells appear bilaterally, parallel and close to the midline of the embryonic shield. Theseclusters acquire a lumen and form a pair of longitudinal vessel called dorsal aorta. These vessels later gained connections via the aortic arches with the horseshoe shaped region that form the heart tube.

As the embryo folds cephalocaudally, it also folds laterally and as a result, the caudal regions of the paired cardiac primordial merge their caudal most ends.

Simultaneously, the crescent part of the horse- shoe shaped area expands to form the future outflow tract and ventricular regions.

Thus, the heart becomes a continuous expanded tube consisting of an inner endothelial lining an outer myocardial layer. The heart at this stage consist of three layers (a) Endocardium – forming the inner endothelial lining of the heart.

(b) Myocardium- forming the muscular wall

(c) Epicardium or Visceral pericardium- covering the outside of the tube.

Various parts of the heart later develop from the fused heart tube. (Sadler T. W 2000).

Gross Anatomy of the heart

The normal heart lies within the pericardial sac in the middle of the thorax slightly to the left of the middle (Sokolow 1979). The low pressure right atrium and right ventricle occupy the anterior portion of the heart and the higher pressure left ventricle and atrium his posteriorly (Sokolow 1977). The long axis of the heart from the apex of the left ventricle to the root of the aorta runs upwards and backward at an angle of about 300 from the horizontal plane and 450 from the sagital plane of the body (Sokolow 1977). The resisting and position of the heart vary with the build of the patient and with respiration. It assumes a more vertical position during inspiration in tall thin persons and more horizontal position during respiration in persons with heavier body build. (Sokolow1977).

1.2 THE CHAMBERS OF THE HEART

The heart consists of four (4) chambers; that is the right and left atria and the right and left ventricle.

1.2.1 The Right Atrium

The right atrium consists of two (2) embryological portions. (Malcolm 1977). The most posterior thin walled portion into which the vena cava and coronary sinus empty in from form the sinus venosus and is compose of similar tissues to that of the great vein. (Malcolm 1977). The more anterior muscular portion includes the right arterial appendage and the tricuspid valve ring (Malcolm 1977)

The fossa ovalies lies in the site of the foramen ovale (Malcolm 1977). This inter-atrial communication within which is present during fetal life permits the flow of oxygenated blood from the inferior vena cava into the heart (Malcolm 1977).

The patent foramen Ovale remain open or potentially open in about 15% of normal subjects (Malcolm 1977) but since it is a flap value which only allows flow right or left, it is normally functionally closed (Malcolm 1977).

1.2.2 THE RIGHT VENTRICLE

The right ventricle is triangular in shape and forms a cresentric, shallow structure wrapped over the ventricular septum (Malcolm 1977), it can divided into a lower inflow portion containing the tricuspid valve and upper outflow tract from which pulmonary trunk arises. (Malcolm 1977).

The line of demarcation between the two portions consists of bands of muscles formed by the cristasupra ventricularis (Malcolm 1977). The outflow tract of the right ventricles is derived from the embryologically distinct bulbus cordis in contrast to the inflow portion which arises from ventricular tissues (Malcolm 1977).

1.2.3 THE LEFT ATRIUM

The left atrium like the right is composed of a vein like portion which the pulmonary vein drains and make muscular anterior portion which includes the left atrial appendage (Malcolm 1977).

Its wall is slightly thicker than that of the right atrium and the inner area corresponding to the fossa ovale can be seen on its right upper surface (Malcolm 1977).

1.2.4 THE LEFT VENTRICLE

The left ventricular cavity is shaped like an egg. The base or the egg is formed by the mitral valve ring. The wall of the left ventricle accounts for about 75% of the mass of the heart.

The aorta and mitral ring lies close to one another with the layer anterior mole cusp of mitral valve adjacent to the left and posterior cusp of the aortic valve (Malcolm 1977).

The posterior immobile cusp of the mitral valve is shorter and together with the anterior cusp is lethered to the anterior and posterior papillary muscles in a parachute like shared by the two (2) cusps (Malcolm 1977).

The interventricular septum which forms the outright anterior aspect of the left ventricle bulges into the right ventricle making the cross section of the mid portion of the left ventricle circular shape (Malcolm 1977).

1.3 EXTERNAL APPEARANCE OF THE HEART

1.3.1 ANTERIOR ASPECT

As viewing anteriorly, the longest area of the surface of the heart is formed by the triangular shaped right ventricle with the pulmonary trunk arising from the apex of the triangle above and to the right of the right ventricle, one can see right atrium appendages as an ear shape structure overlying the root of the aorta (Sokolow 1997). The grove between the right atrium and ventricle (Coronary sulcus) is often filled with fat and is occupied by the right coronary artery.

Above the right atrium, the superior vena cava is seen entering the right atrium from the back . The anterior aspect of the heart reveals only a small part of the left ventricle lying to the left of the right ventricle and forming the apex of the heart (Sokolow 1977).

The anterior interventricular sulcus often contains fat and is occupied by the anterior descending branch of the left coronary artery (Sokolow 1977).

The only portion of the left atrium visible from the front is the left atrial appendages, which lies side of the origin of the pulmonary trunk. The lungs normally covers most of the anterior surface of the heart especially during inspiration having only a small area opposed to the back of the sternum and left ribs (Sokolow 1977).

1.3.2 LEFT SIDED ASPECT

When viewed from the left side, the ventricle and the left atrium occupy most of the surface of the heart (Sokolow 1977). The posterior interventricular groove separates the left ventricle above from the right ventricle below. The posterior descending branch of the right coronary artery lies in the groove. The anterior ventricular groove runs almost vertically in the view separating the left ventricle from the left atrium (Sokolow 1977). The coronary sinus and circumflex branch of the left coronary artery lies in the groove and complete the ring of blood vessels forming the bases of the corona (crown) after which the blood vessels supplying the heart are named (Sokolow 1977).

1.3.3 POSTERIOR ASPECT

The back of the heart mainly on the diaphragm is largely occupied by the left atrium and ventricle plus portions of the right atrium and ventricle (Sokolow 1977).

The point at which all four (4) chambers meet posteriorly as called the crux at the heart; because of the cross – shape pattern of the blood vessels lying at the function of the posterior interventricular groove and the anterior ventricular groove (Sokolow 1977). The vessels forming the crux are; the coronary sinus and the posterior descending coronary artery. This latter vessel may be a branch of either the right or the circumflex branch of the left coronary artery depending on whether the right or left coronary artery is largely (dominant) (Sokolow 1977).

The pulmonary vein enter the back of the left atrium and the pattern may vary but the two right and the left pulmonary veins are normally present (Sokolow 1977).

1.3.4 Right Side Aspect

When viewed from the right side, the right atrium and ventricle occupies most of the surface (Maurice 1977). The posterior and the anterior vena cava enter the atrium at the back and the aorta runs upward from the middle of the heart (Maurice 1977). The outflow tract of the right ventricle and the pulmonary trunk form the upper border of the heart in this view (Maurice 1977).

1.4 THE HEART WALL

The heart wall is composed of the three layers of tissue, namely the; epicardium, myocardium and endocardium (Stephen 1988). The epicardium and the visceral pericardium are two names for the same structure. The sinus pericardium is called epicardium when considered a part of the heart and the visceral pericardium when considered a part of the pericardium (Stephen 1988).

1.4.2 THE MYOCARDIUM

This is the thick middle layer of the heart, which composed of cardiac muscle cells and is responsible for the ability of the heart to contract, (Stephen 1988).

1.4.3 THE ENDOCARDIUM

This is the smooth inner surface of the heart chamber, which consist of the simple squamous epithelium over a layer or connective tissue (Stephen 1988).

The smooth inner surface allows blood to move easily through the heart. The heart valves are formed by a fold as the endocardium, making a double layer of endocardium with connective tissue in between (Stephen 1988).

1.5 OBJECTIVE OF THE STUDY

The objectives of the study are

To measure the heart diameter, thoracic diameter and cardiothoracic ratio of normal individual in University of Maiduguri Teaching Hospital, Nigeria.
To give the comparison between the heart diameter, thoracic diameter and cardiothoracic ratio between males and females.
CHAPTER TWO

2.0 LITERATURE REVIEW

In 1919, Danzer undertook one of the earliest studies of the cardiothoracic ratio. After investigation nearly 500 patients without the aid of hemodynamic parameters, He determined that any measurement over 0.5 or 50% was suspicious and over 0.52or 52% was definitely pathological.

A latter report by comeau and white in 1942 found that 15 to 25% of normal patient had a cardiothoracic ratio greater than 0.5 or 50% and advised that using CT ratio prediction labels based upon six, image technique and phase of respiration.

A significant relationship was found between the radial measurement and age, which differ within ethnic group groups. The median value of cardiothoracic ratio was 43% in Caucasians, 44% in Asian and 46% in Africans. (Ashcroft Maills’ and Mekol). Mekol concluded that a single upper limit (e.g. 50%) for cardiothoracic ratio is unsatisfactory. It all subject with values of cardiothoracic ratio greater than 50% in the present sample had been recalled for more dedicated cardio logical investigation; this would have affected 2.2% of Caucasians, 4.1% of Asians and 9.3% of Africans limit of 5.3% in Caucasians, 52% in Asian and 53% in Africans would include 2.2%, 2.4% and 2.6% of each subject of these racial groups. (Mekol1982).

Murphy M.L. in 1985 took routine posterior and lateral chest radiograph in 268 patients and analyzed to determine heart size. The coronary artery of this determination was compared with a specific ventricular mass derived from a postmortem cardiac partition technique. The data indicated that in the majority of cases (greater than 70%) a normal sized heart or cardiomegaly can be correctly determined from the chest x – ray either by subjective arterial or chamber enlargement or management of the transverse diameter (Murphy M.L. 1985).

A recent meta-analysis of 29 studies determined that cardiomegaly on the cardiothoracic ratio was the best reason for predicting a reduced ejection fraction, with a sensitivity and specificity of 51% and 79% respectively (Badgett 1996).

Comeau in 1942 said that it is important to recognize compounding factors of cardiomegaly such as an epical fat, a transversely positional heart. An expiratory film or decrease in thoracic width.

In 1987, Kabala used a computed Tomography model in eight patients to show how the heart diameter and cardiothoracic ratio might change between anterior-posterior chest radiograph taken on 103 patients without cardiac failure and 106 with cardiac failure. An upper limit of cardio thoracic ratio of 55% and of heart chamber or 165mm in males and 150mm in females was shown to practice useful discrimination between normal and abnormal heart size (Kabala 1987).

The cardiothoracic ration thoracic ratio increased with age in both sex but females have longer cardiothoracic ratio than men.

Portable films taken in the anterior-posterior and supine position enlarge the appearance of cardiac silhouette (Milne 1988).

CHAPTER THREE

3.0 MATERIALS AND METHODS

3.1 SUBJECTS

A retrospective study was carried out in the university of Maiduguri Teaching Hospital, Department of Radiology, and using normal chest radiograph of two hundred and ninety-one (291) patients.

3.2 SAMPLE SELECTION

The sample includes the normal chest radiographs taken from 2007-2009. All chest radiographs with abnormal result were excluded from the study. The age, sex from the chest radiographs was obtained. Hypertensive subjects were excluded.

3.3 MEASUREMENT

A straight line drawn near the rule meddled of the heart shadow. Another line as in “a” from the right heart border to order to the first line was drown. A third line was drown from the left heart co-order furthest from the in the middle of the heart shown as the “b”. The two were then added together, the cardiothoracic rube as the own of the line “a” and “b” divided by the largest transverse internal diameter of the thoracic cage as shown on the figure 3.1 below.

Figure 3.1 measurement of the cardio thoracic ratio.

Cardiac diameter=>A=B are the maximum extensions of the heart to the left and right of the midline respectively.

CHAPTER FIVE

5.0 DISCUSSION

The cardiothoracic ratio of males and females in the various age groups will be determined in future study.

The ratio increased with age in both sexes but was more marked in females than males.

Oberman in 1967 reported that women have higher cardiothoracic ratio than males. Men had larger cardiac diameter than women. The higher cardiothoracic ratio in women was due to their smaller thoracic diameter. This report supports the present study.

Edge in 1984 also reported that the increase in cardiothoracic ratio with age found particularly in women was mainly due to contraction of the thoracic diameter rather than an increase in the cardiac diameter.

Decrease in the chest diameter with advancing age indicates that cardiothoracic ratio over estimates the heart size in the elderly.

Nikol and Wade in 1982 attributed that Africans have larger cardiothoracic ratio because they have smaller thoracic diameter and larger cardiac diameter.

It was also noted that environmental factors such as poor nutrition and infection may cause cardiac enlargement with resultant increase in cardiac diameter and cardiothoracic ratio.

5.2 CONCLUSION

The higher cardiothoracic ratio in females may suggest the reason of their susceptibility to infections arising from the heart and this could be correlated to clinical data.

5.3 RECOMMENDATION

I recommend that any research on cardiothoracic ratio is best with chest radiographs. Females should always keep good hygiene because of their susceptibility to infections because of their large cardiothoracic ratio.

REFERENCES

Ashcroft MT, Miall WE (1969) cardiothoracic ratio in two Jamaican Communities. AM. J Epidemoil 89: 161-167.

Badgett, R.C. Mulrow, P. Otto and G. Ramirez (1996). How well can the chest radiograph diagnose left ventricular dysfunction. Journal of Internal Medicine 11:625-634(medline)

Comeau W J, White PD(1942).A critical analysis of standard methods of estimating heart size from Roentgen measurements. A M. J Roentgenol 47:665-667

Covoan N R (1964) The heart lung coefficient and the transverse diameter of the heart. Br Heart Journal 26:116-120

Danzer, C. S (1919) The Cardio thoracic ratio A M. J medical sciences 15:512-513

David Sutton (1993) A text of radiography and imaging, normal chest Fifth edition, Great Britain by William Clowes Limited London. P 530

Edge J R, Milliard F C, Reid L, Simon G (1964) The radiographic appearance of the chest in persons of advanced age. Br Heart Journal 26:769-773

Hada Y (1995) Cardio thoracic ratio 26 (1) :51-54

Kabala J T, White P. (1987) The Measurement of the size in the antero-posterior chest radiograph Br journal of Radiology 60 (718) :981-986

Krish namoorthy D M. (2001)100% cardio thoracic ratio Tex heart inst. J.28 (4):334-335

Kono F Suwa M, Hanada H, Hirota Y, Kawanaura K. (1992) Clinical significance of normal cardiac silhouette in dilated cardiomyopathy , Evaluation based upon echocardiography and magnetic resonance imaging . Japanese Journal 56:359-365

Manninen H, Reines J, Partenen K, Tynkkyen P, Mykkannen L, Laakso M, Soimakalio S, Pyorata K. (1991) Evaluation of heart size and pulmonary vasculature conventional chest image intensifier photofluorography

Manorana Berry, sudha Suri, Veena chowdheny , Sina Mukhopadhyay (2003) normal thoracic anatomy on various imaging modalities, Diagnostic radiology chest and cardiovascular imaging second edition , Jaypee brothers medical publishers (P) Ltd. India P(1) 16

Maurice Sokolow (1997) Physiology of the circulatory system clinical cardiology first edition large medical publication carlifornia PP1-9

Milne E N C, K. Burnett, D. Autrichtig, J. Manillian, and T J Imray (1988) Assessment of cardiac size on portable chest films Journal of Thoracic Imaging 3:64-72 (medline)

Murphy M.L, Blue L.R, Thennabadu P N, Philps JR, Fenis EJ. (1998). The reliability of the routine chest roentgenograph for determination of heart size based specific ventricular chamber evaluation at post mortem investigation radiology 20(1) :21-25

Nikol K, Wade AJ. (1982). Radiiographic heart size and cardio thoracic ratio in three ethnic groups basis for a simple screening test for cardiac enlargement in men . Br Journal of Radiology 55(654): 399-403

Oberman A, Mayer A.R, Karuna T.M, Epstein FH, 1967. Heart size of adults in a natural population Feamesh-Michigan circulation 34: 724-733

Philip Thorek. (1985). Anatomy in surgery, thorax. Third edition springer Newyork (PP327)

Rod R Seetey, Trent D. Stephens, Philip Tate (1998) cardiovascular system, Anatomy and Physiology, Fourth Edition. McGraw Hill Newyork pp602-614

Seninge R.P and Lester R.G. History of cardiac radiology. Unpublished report 1970.

Sadler T. W 2000. Langman’s medical embryology 8th edition.

Overview

Deep Vein Thrombosis, also known as DVT is a preventable circulatory disorder which occurs when a blood clot is formed in a deep vein, they usually develop in the lower leg, thigh, or pelvis, but can also occur in the arms. DVT can cause pain and swelling and can lead to complications such as a pulmonary embolism, however DVT is preventable and if diagnosed early treatable. How DVT forms (leg vein)

Veins pass through the deep tissues of the legs; there are superficial veins located just below the surface of the skin and deep veins which run between muscles. These veins transport blood from the legs and feet back up to the heart. When a thrombosis (blood clot) forms in a superficial vein the condition is known as superficial thrombophlebitis, this is different to DVT and is not as serious. DVT occurs when a thrombus builds up in these deep veins which partly or completely block the flow of blood through the vein.

Many blood clots are so small that our bodies can gradually break them down returning the flow back to normal. However when a large blood clot occurs It can completely block the flow of blood causing swelling and tenderness (although symptoms ar e not always visible). Blood clots can become extremely dangerous If a part of it breaks off and travels up to the lungs, this is called a pulmonary embolism, it is extremely dangerous and in worst cases can cause death.

People at risk

Almost anyone can contract DVT but there are factors which can significantly increase someone’s chances of developing the condition, especially if someone has one or more of these risk factors at the same time. Below are some of the factors which could increase the risk of contracting DVT:

• An injury to one of the deep veins caused by a fracture, severe muscle injury or major surgery.
• Slow blood flow caused by paralysis, sitting for a long time (especially with legs crossed, limited movement e. g a leg cast or confinement to a bed. Increased oestrogen for example during pregnancy, when using birth control pills or hormone replacement therapy.
• Certain chronic medical illnesses such as Cancer and it’s treatment, heart disease and lung disease.
• Previous DVT or family history of the disorder.
• Age, obesity, smoking or blood pressure. Symptoms of DVT Small blood clots which the body can gradually break down show no symptoms however large clots which partly or completely block the bloody flow cause symptoms such as swelling to the affected area, pain or tenderness, a change in colour of the skin or skin which feels warm or hot to touch. Diagnosing DVT A GP will ask about the symptoms you have and examine the area. If they think DVT is suspected a referral to a specialist is taken into action, at hospital the following tests will be conducted.
• D-Dimer- A test that measures the substance which develops when a blood clot breaks down, if the test has a negative result it is unlikely that DVT is the problem.
• Doppler Ultrasound- A test using sound waves to look at your blood as it flows through your blood vessels, this is the best test to detect blood clots above the knee. Venogram- This is involves injecting a special dye into the suspected vein which shows up on an X-ray. Treatment When DVT is diagnosed Anticoagulant medicines are the standard treatment, these thin the blood by changing the chemicals wi thin it, they stop new clots from forming and old ones from getting bigger. Anticoagulants can’t dissolve clots you already have as your body will do that over time. Thrombolytic medicines are also sometimes used which dissolve the blood clots, although they can cause bleeding so are not usually the most common of treatments.

Compression socks are also advised to be worn (sometimes for up to two years), these ease the pain, reduce swelling and help to prevent post-thrombotic syndrome

Preventable measures at hospital

After being assessed for the risk of DVT a healthcare team will recommend various things to prevent blood clotting. If going into hospital and the patient is taking the combined contraceptive pill, using HRT or aspirin than they would be asked to stop taking these, usually 4 weeks for contraceptive pills or HRT and one week for aspirin.

During hospital

Whilst at hospital a healthcare team can do a number of things to reduce the risk of DVT such as providing anticoagulant medicines or advising the patient to wear compression stockings helping to keep the blood in your legs circulating or having the patient wear a compression device which is worn the same way as stockings but inflates at regular intervals to squeeze your legs and encourage blood flow. When leaving hospital: If continuing treatment is necessary the patient will be asked to continue wearing compression stockings or taking anticoagulant medicines. Lifestyle:

We can do several things by adapting our lifestyle which will considerably reduce our chances such as getting regular exercise, not smoking, keeping at a healthy weight and eating healthy Travelling: When travelling for long distances it is important to perform leg exercises and keep moving if possible, by drinking plenty of water and avoiding alcohol this will decrease the chances, wearing compression stockings can also help.

References

1. Bupa. (2009) ‘Deep vein thrombosis (DVT)’http://hcd2. bupa. co. uk/fact_sheets/html/deep_vein_thrombosis. html#2 Accessed on 20/10/10 CDC. 2010)
2. ‘Facts about deep vein thrombosis’ http://www. cdc. gov/ncbddd/dvt/508-DVTFactSheet. pdf Accessed on 20/10/10 NHS. (2010)
3. ‘Deep vein thrombosis’ http://www. nhs. uk/conditions/deep-vein-thrombosis/Pages/Introduction. aspx Accessed on 17/10/10 NHS. (2010)
4. ‘Deep vein thrombosis – Prevention’ http://www. nhs. uk/Conditions/Deep-vein-thrombosis/Pages/Prevention. aspx Accessed on 18/10/10 Electronic Journal: Cayley,W. (2007)
5. ‘Preventing deep vein thrombosis in hospital inpatients’ British Medical Journal http://www. bmj. com/content/335/7611/147. full? sid=69a2603d-597a-45dd-b164-699d873e01f5 Accessed on 22/10/10
6. Mackean, D. (2002) Gcse Biology 3rd ed. London, UK: Hodder Education Boyle, M. (2008)
7. Collins Advanced Science – Human Biology 3rd ed. London, UK: Collins Educational Reference Evaluation

All recourses used as a reference have been carefully selected and are reliable based upon many factors including Authors credentials, recent published dates, up to date editions and scholarly publishers. After an initial appraisal I then examined the body of the source, for example the National Health Service is politically accountable to the relevant devolved government and will always hold the most up to date and accurate information.