HISTORY OF PATIENT

A) Demographical data of patient Ward: Intensive Cardiac Care Unit (ICCU) Bed no: 3 I.P No: 25626/068 Name of patient: Madan Gopal Udas Age : 70 years Sex: Male Address: Dharan-3,Sunsari, Koshi, Nepal. Marital status: Married Occupation: Retired accountant. Religion: Hindu Date of admission: 068/8/18 Medical diagnosis: Acute Coronary syndrome (ACS) with unstable angina with hypertension with diabetes mellitus type II. Economic status: Upper middle class. Weight: 57kg Height: 170cm Temperature: 98oF Pulse: 60/min Respiration: 14/min Blood Pressure: 120/70mm of hg B) Chief complaints Chest pain, dry cough and shortness of breath since 3days.

C) History of Present Illness(HOPI) Known case of diabetes mellitus type II since 24 years and hypertension since 12 years. He is under antihypertensive and anti diabetic drug regularly. Now presented with chest pain retrosternal, sudden, over course of 3days- constant, non-radiating, not related to exertion, no known relieving factor, no nausea and vomiting, no syncope/ dizziness, no loss of consciousness and no weakness of limbs. There is history of dry cough and shortness of breath since 3 days. D) Personal history Could not remember about immunization Past history of smoking but left many years ago, history of alcoholism 120/day. He is non vegetarian takes major meal 3 times a day snacks two times with fruits. Regular sleeping habit Regular bowel habit.

E) Past history No history of infectious and non infectious diseases in past. Past hospitalization two times before because of chest pain. History of diabetes since 24 years and hypertension since 12 years. No history of surgery and any kind of accidents. No history of environmental, foods, drugs and any other kind of allergies. No history of taking self medications. F) Family History Family Tree

Family history of diseases History of diabetes and hypertension to mother of patient. His son was expired, he was also suffering from diabetes. No family history of cancer other cardiovascular problems, arthritis, blood disorders, tuberculosis and other diseases.

PHYSICAL EXAMINATION OF PATIENT

1. General appearance and behaviour An ectomorphic built, well groomed conscious, oriented, co-operative patient, maintained his eye contact during examination, posture was maintained, gait was balanced, no deformities while looking and personal hygiene was also maintained. 2. Head, neck and face Hair was clean, no extra growth and abnormalities detected. No lymphadenopathy, no stiffness present, no swelling, no injury and scar found. 3. Eye No any abnormalities detected in eyelids, conjunctiva and sclera. Color of sclera was white,B/L pupil size was about 5mm and reacted to light, no discharge from eyes. He had vision problem so, he is using eye glasses. 4. Ear No any abnormalities found in external ear. No discharge from ear, no lesions and polyps found. He has problem in hearing but not using hearing aids. 5. Nose No injury, no blockage of nose, no nasal bleeding, no infection, no polyp, smell is normal, no abnormalities detected in sinuses also. Nasal septum was slightly deviated. 6. Integumentary system Patient's skin color was Asian color(wheat white). No paleness, no icterus, no rashes, no inflammation, no lesions, no oedema, no scar, no pigmentation, no tumours found in skin. Skin elasticity was loose. Shape of nails were normal. 7. Gastrointestinal system No sore lips, no gum bleeding, no toothache, no difficulty in swallowing found but some missing teeth and tooth decay found. No nausea, no vomiting, no diarrhoea and constipation, no abnormal stool found.
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Per abdomen soft, non tender, no hepatospeelnomegaly found. No abdominal mass and no any abnormalities found in gastrointestinal system. Bowel sound was normal. 8. Cardiovascular system History of chest pain but no chest pain present at the time of physical examination. While inspection, patient did not look cyanosis, no signs of pain observed, no clubbing of fingers, . subjectively; no complain of numbness, no complain of palpitation. In auscultation S1 and S2 were normal, no murmur found. No bleeding tendencies, no visible external jugular vein, carotid pulse was 70bpm. No abnormalities in apex beat. Blood pressure was 120/70 bilateral. 9. Respiratory system In inspection of chest, shape was normal, bilateral symmetrical, dry cough was present, no dyspnoea . In auscultation, bilateral air entry was equal, no wheezing was present. No, abnormality in percussion. 10. Urinary system Urine color was straw color, no loin pain, no dysuria, no frequency, urgency and hesitancy. 11. Reproductive system Not complaining any abnormalities. 12. Lymphatic system No enlarge lymph nodes found. 13. Musculoskeletal system Bilateral symmetrical arms and legs, no oedema, no lesions, no rigidity, no flaccidity, normal strength, power and tone. 14. Neurologic system Vertebral column is straight, centrally located. No history of loss of consciousness, sometimes he felt dizziness and irritability. Reflexes are normal. 15. Mental status Oriented to time place and person, memory was intact, well groomed and cooperative. Summary of findings On physical examination, I found dental carries and missing teeth, vision problem so using spectacles, hearing loss, slightly deviated nasal septum and dry cough. Except these things I could not found any major abnormalities.
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LAB INVESTIGATIONS
Investigations Createnine Kinase MB Normal value (CK) Male:50-325U/L Patient`s value First:61U/L After 6hrs: 13U/L After 12 hrs: 14U/L After 18hrs: 14U/L First negative Second negative Albumin : nil Sugar: Trace WBC:0-1HPF RBC: Nil Epithelia cells: 0-1HPF 110mg/dl 29mg/dl 1.1mg/dl 145mmol/l 4.5mmol/l TLC:7400cell/cumm 60% 40% 10.5gm/dl 100,000/cumm 1.7% Shows neutrophilia Normocytic Normochromic Adequate N81 L18 M01 Remarks Normal

Troponine I Urine RE/ ME

0-0.1ng/ml Albumin: nil Sugar: nil WBC:less than 5 HPF RBC: less than 5 HPF 60-140mg/dl 8-25mg/dl 0.2-0.8mg/dl 135-145mmol/l 3.5-5.5mmol/l TLC: 4500-11000/cu mm 45-73% 20-40% 13-18gm/dl in male 150,000-450,000/cumm 0.5-1.5%

Normal Normal

Glucose (random) Urea Cretenine Sodium Potassium CBC DLC: neutrophil lymphocytes Hb% Platelets Reticulocytes count PS for cytology PBS RBC Platelates DLC

Normal Elevated Elevated Normal Normal Normal

Decreased Decreased Elevated Normal

Normocytic normochromic Adequate WBC4500-11000/cu mm N 45-73,L20-40,M2-8 4.4-6.4% ALT 10-40U/L in male AST 10-40U/L in male Cholesterol 150-200mg/dl HDLcholesterol 35-70mg/dl
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Glycohemoglobin Liver function test Lipid profile

8% ALT(SGPT) 40U/L AST (SGOT) 46U/L Cholesterol 114mg/dl HDLcholesterol 45mg/dl

Elevated Normal Elevated Normal Normal

HS-CRP 27mg/L Elevated Angiography Angiography is a way to produce X-ray pictures of the inside of blood vessels. When blood vessels are blocked, damaged or abnormal in any way, chest pain, heart attack, stroke or other problems may occur. Angiography helps your physician determine the source of the problem and the extent of damage to the blood vessel segments that are being examined. Before test Do NOT take any aspirin or any products containing aspirin. Do NOT take dipyridamole (Persantine) or warfarin (Coumadin) within 72 hours before the test, and 24 hours after the test. These medications are often referred to as blood thinning pills. DO take your other medications on schedule as usual, especially any medications for high blood pressure Do NOT take Glucophage (metformin hydrochloride) for 48 hours before the test or 48 hours after the test to reduce the risk of kidney complications On the day of the test Ask the patient not to bring valuables such as jewelry or credit cards. Npo 6hrs. During the test The test itself will take approximately 2 to 3 hours. Mild sedation may be given. During angiography, a long slender tube called a catheter is inserted into a large artery (generally, in the groin area). The catheter is slowly and carefully threaded through the artery until its tip reaches the segment of vessel to be examined by angiography. A small amount of contrast material is injected into the blood vessel segment through the catheter, and X-rays are taken. The contrast agent enables the blood vessels to appear on the X-ray pictures. A physician specially trained in angiography studies the X-ray pictures to determine the source of the problem and the extent of damage to the blood vessel segments that are examined. After the test Do NOT take Glucophage (metformin hydrochloride) for 48 hours after the test to reduce the risk of kidney complications. Do not move the affected foot for 4 hours.

Triglyceride 100-200mg/dl Less than 5mg/L

Triglyceride 116mg/dl

Normal

DISEASE PROCESS
Anatomy of heart

1. 2. 3. 4. 5. 6. 7. 8.

Right Coronary Left Anterior Descending Left Circumflex Superior Vena Cava Inferior Vena Cava Aorta Pulmonary Artery Pulmonary Vein

9. Right Atrium 10. Right Ventricle 11. Left Atrium 12. Left Ventricle 13. Papillary Muscles 14. Chordae Tendineae 15. Tricuspid Valve 16. Mitral Valve 17. Pulmonary Valve

Coronary Arteries Because the heart is composed primarily of cardiac muscle tissue that continuously contracts and relaxes, it must have a constant supply of oxygen and nutrients. The coronary arteries are the network of blood vessels that carry oxygen- and nutrient-rich blood to the cardiac muscle tissue. The blood leaving the left ventricle exits through the aorta, the bodys main artery. Two coronary arteries, referred to as the "left" and "right" coronary arteries, emerge from the beginning of the aorta, near the top of the heart. The initial segment of the left coronary artery is called the left main coronary. This blood vessel is approximately the width of a soda straw and is less than an inch long. It branches into two slightly smaller arteries: the left anterior descending coronary artery and the left circumflex coronary artery. The left anterior descending coronary artery is embedded in the surface of the

front side of the heart. The left circumflex coronary artery circles around the left side of the heart and is embedded in the surface of the back of the heart. Just like branches on a tree, the coronary arteries branch into progressively smaller vessels. The larger vessels travel along the surface of the heart; however, the smaller branches penetrate the heart muscle. The smallest branches, called capillaries, are so narrow that the red blood cells must travel in single file. In the capillaries, the red blood cells provide oxygen and nutrients to the cardiac muscle tissue and bond with carbon dioxide and other metabolic waste products, taking them away from the heart for disposal through the lungs, kidneys and liver. When cholesterol plaque accumulates to the point of blocking the flow of blood through a coronary artery, the cardiac muscle tissue fed by the coronary artery beyond the point of the blockage is deprived of oxygen and nutrients. This area of cardiac muscle tissue ceases to function properly. The condition when a coronary artery becomes blocked causing damage to the cardiac muscle tissue it serves is called a myocardial infarction or heart attack. Superior Vena Cava The superior vena cava is one of the two main veins bringing de-oxygenated blood from the body to the heart. Veins from the head and upper body feed into the superior vena cava, which empties into the right atrium of the heart. Inferior Vena Cava The inferior vena cava is one of the two main veins bringing de-oxygenated blood from the body to the heart. Veins from the legs and lower torso feed into the inferior vena cava, which empties into the right atrium of the heart. Aorta The aorta is the largest single blood vessel in the body. It is approximately the diameter of thumb. This vessel carries oxygen-rich blood from the left ventricle to the various parts of the body. Pulmonary Artery The pulmonary artery is the vessel transporting de-oxygenated blood from the right ventricle to the lungs. A common misconception is that all arteries carry oxygen-rich blood. It is more appropriate to classify arteries as vessels carrying blood away from the heart. Pulmonary Vein The pulmonary vein is the vessel transporting oxygen-rich blood from the lungs to the left atrium. A common misconception is that all veins carry de-oxygenated blood. It is more appropriate to classify veins as vessels carrying blood to the heart. Right Atrium The right atrium receives de-oxygenated blood from the body through the superior vena cava (head and upper body) and inferior vena cava (legs and lower torso). The sinoatrial node sends an impulse that causes the cardiac muscle tissue of the atrium to contract in a coordinated, wavelike manner. The tricuspid valve, which separates the right atrium from the right ventricle, opens to allow the de-oxygenated blood collected in the right atrium to flow into the right ventricle. Right Ventricle
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The right ventricle receives de-oxygenated blood as the right atrium contracts. The pulmonary valve leading into the pulmonary artery is closed, allowing the ventricle to fill with blood. Once the ventricles are full, they contract. As the right ventricle contracts, the tricuspid valve closes and the pulmonary valve opens. The closure of the tricuspid valve prevents blood from backing into the right atrium and the opening of the pulmonary valve allows the blood to flow into the pulmonary artery toward the lungs. Left Atrium The left atrium receives oxygenated blood from the lungs through the pulmonary vein. As the contraction triggered by the sinoatrial node progresses through the atria, the blood passes through the mitral valve into the left ventricle. Left Ventricle The left ventricle receives oxygenated blood as the left atrium contracts. The blood passes through the mitral valve into the left ventricle. The aortic valve leading into the aorta is closed, allowing the ventricle to fill with blood. Once the ventricles are full, they contract. As the left ventricle contracts, the mitral valve closes and the aortic valve opens. The closure of the mitral valve prevents blood from backing into the left atrium and the opening of the aortic valve allows the blood to flow into the aorta and flow throughout the body. Papillary Muscles The papillary muscles attach to the lower portion of the interior wall of the ventricles. They connect to the chordae tendineae, which attach to the tricuspid valve in the right ventricle and the mitral valve in the left ventricle. The contraction of the papillary muscles closes these valves. When the papillary muscles relax, the valves open. Chordae Tendineae The chordae tendineae are tendons linking the papillary muscles to the tricuspid valve in the right ventricle and the mitral valve in the left ventricle. As the papillary muscles contract and relax, the chordae tendineae transmit the resulting increase and decrease in tension to the respective valves, causing them to open and close. The chordae tendineae are string-like in appearance and are sometimes referred to as "heart strings." Tricuspid Valve The tricuspid valve separates the right atrium from the right ventricle. It opens to allow the deoxygenated blood collected in the right atrium to flow into the right ventricle. It closes as the right ventricle contracts, preventing blood from returning to the right atrium; thereby, forcing it to exit through the pulmonary valve into the pulmonary artery. Mitral Value The mitral valve separates the left atrium from the left ventricle. It opens to allow the oxygenated blood collected in the left atrium to flow into the left ventricle. It closes as the left ventricle contracts, preventing blood from returning to the left atrium; thereby, forcing it to exit through the aortic valve into the aorta. Pulmonary Valve

The pulmonary valve separates the right ventricle from the pulmonary artery. As the ventricles contract, it opens to allow the de-oxygenated blood collected in the right ventricle to flow to the lungs. It closes as the ventricles relax, preventing blood from returning to the heart. Aortic Valve The aortic valve separates the left ventricle from the aorta. As the ventricles contract, it opens to allow the oxygenated blood collected in the left ventricle to flow throughout the body. It closes as the ventricles relax, preventing blood from returning to the heart. Physiology of Heart Introduction The cardiovascular system consists of the heart and two vascular systems, the systemic and pulmonary circulations. The heart pumps blood through two vascular systems - the low pressure pulmonary circulation in which gas exchange occurs, and then the systemic circulation, which delivers blood to individual organs, matching supply to metabolic demand. Blood pressure and flow is largely controlled by the autonomic nervous and is also influenced by surgery and anaesthetic drugs. A good working knowledge of cardiovascular physiology is necessary to practice safe anaesthesia. The heart The heart comprises four chambers, and is divided into a right and left side, each with an atrium and a ventricle. The atria act as reservoirs for venous blood, with a small pumping action to assist ventricular filling. In contrast, the ventricles are the major pumping chambers for delivering blood to the pulmonary (right ventricle) and systemic (left ventricle) circulations. The left ventricle is conical in shape and has to generate greater pressures than the right ventricle, and so has a much thicker and more muscular wall. Four valves ensure that blood flows only one way, from atria to ventricle (tricuspid and mitral valves), and then to the arterial circulations (pulmonary and aortic valves). The myocardium consists of muscle cells which can contract spontaneously, also pacemaker and conducting cells, which have a specialised function. Electrophysiology of the heart

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Myocardial contraction results from a change in voltage across the cell membrane (depolarisation), which leads to an action potential. Although contraction may happen spontaneously, it is normally in response to an electrical impulse. This impulse starts in the sinoatrial (SA) node, a collection of pacemaker cells located at the junction of the right atrium and superior vena cava. These specialised cells depolarise spontaneously, and cause a wave of contraction to pass across the atria. Following atrial contraction, the impulse is delayed at the atrioventricular (AV) node, located in the septal wall of the right atrium. From here His-Purkinje fibres allow rapid conduction of the electrical impulse via right and left branches, causing almost simultaneous depolarisation of both ventricles, approximately 0.2 seconds after the initial impulse has arisen in the sinoatrial node. Depolarisation of the myocardial cell membrane causes a large increase in the concentration of calcium within the cell, which in turn causes contraction by a temporary binding between two proteins, actin and myosin. The cardiac action potential is much longer than that of skeletal muscle, and during this time the myocardial cell is unresponsive to further excitation. The cardiac cycle

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There is a similar cycle on both sides of the heart, but the pressures in the right ventricle and pulmonary arteries are less than those in the left ventricle and aorta. Systole refers to contraction, while diastole refers to relaxation. Both contraction and relaxation can be isometric, when changes in intraventricular pressure occur without a change in length of the muscle fibres. The cycle starts with depolarisation at the sinoatrial node leading to atrial contraction. Until this time blood flow into the ventricles has been passive, but the atrial contraction increases filling by 20-30%. Ventricular systole causes closure of the atrioventricular valves (1st heart sound), and contraction is isometric until intraventricular pressures are sufficient to open the pulmonary and aortic valves, when the ejection phase begins. The volume of blood ejected is known as the stroke volume. At the end of this phase ventricular relaxation occurs, and the pulmonary and aortic valves close (2nd heart sound). After isometric relaxation ventricular pressures fall to less than atrial pressures. This leads to opening of the atrioventricular valves and the start of ventricular diastolic filling. The whole cycle then repeats following another impulse from the sinoatrial node. The Heart Sounds The closure of the heart valves and the contraction of the heart muscle produce sounds that can be heard through the thoracic wall by the unaided ear, although they can be heard better when amplified by a stethoscope. The sounds of the heart may be represented as lubb-dubb-pauselubb-dubb-pause. The lubb sound indicates the closing of the valves between the atria and ventricles and the contracting ventricles; the dubb sound indicates the closing of the semilunar valves. In addition, there may also be cardiac murmurs, especially when the valves are abnormal.

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Some heart murmurs, however, may also occur in healthy persons, mainly during rapid or pronounced cardiac action. The coronary circulation Myocardial blood supply is from the right and left coronary arteries, which run over the surface of the heart giving branches to the endocardium (the inner layer of the myocardium). Venous drainage is mostly via the coronary sinus into the right atrium, but a small proportion of blood flows directly into the ventricles through the Thebesian veins, delivering unoxygenated blood to the systemic circulation. Oxygen extraction by the tissues is dependent on consumption and delivery. Myocardial oxygen consumption is higher than in skeletal muscle (65% of arterial oxygen is extracted as compared to 25%). Therefore any increased myocardial metabolic demand must be matched by increased coronary blood flow. This is a local response, mediated by changes in coronary arterial tone, with only a small input from the autonomic nervous system Cardiac Output Cardiac output (CO) is the product of heart rate (HR) and stroke volume (SV): CO = HR x SV For a 70kg man normal values are HR=70/min and SV=70ml, giving a cardiac output of about 5litre/min. The cardiac index is the cardiac output per square metre of body surface area - normal values range from 2.5-4.0 litre/min/m2. Heart rate is determined by the rate of spontaneous depolarisation at the sinoatrial node , but can be modified by the autonomic nervous system. The vagus nerve acts on muscarinic receptors to slow the heart, whereas the cardiac sympathetic fibres stimulate beta-adrenergic receptors and increase heart rate. Stroke volume is determined by three main factors: preload, afterload and contractility. The systemic circulation The systemic blood vessels are divided into arteries, arterioles, capillaries and veins. Arteries supply blood to the organs at high pressure, whereas arterioles are smaller vessels with muscular walls which allow direct control of flow through each capillary bed. Capillaries consist of a single layer of endothelial cells, and the thin walls allow exchange of nutrients between blood and tissue. Veins return blood from the capillary beds to the heart, and contain 70% of the circulating blood volume, in contrast to the 15% in the arterial system. Veins act a reservoir, and venous tone is important in maintaining the return of blood to the heart, for example in severe haemorrhage, when sympathetic stimulation causes vasoconstriction.

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Control of the systemic circulation Arteriolar tone determines blood flow to the capillary beds. A number of factors influence arteriolar tone, including autonomic control, circulating hormones, endothelium derived factors and the local concentration of metabolites. Autonomic control is largely by the sympathetic nervous system, which supplies all vessels except capillaries. Sympathetic fibres arise from the thoracic and lumbar segments of the spinal cord. These are under the control of the vasomotor centre in the medulla, which has distinct vasoconstrictor and vasodilator areas. The Pulmonary Circulation From the right atrium the blood passes to the right ventricle through the tricuspid valve, which consists of three flaps (or cusps) of tissue. The tricuspid valve remains open during diastole, or ventricular filling. When the ventricle contracts, the valve closes, sealing the opening and preventing backflow into the right atrium. Five cords attached to small muscles, called papillary muscles, on the ventricles' inner surface prevent the valves' flaps from being forced backward. From the right ventricle blood is pumped through the pulmonary or semilunar valve, which has three half-moon-shaped flaps, into the pulmonary artery. This valve prevents backflow from the artery into the right ventricle. From the pulmonary artery blood is pumped to the lungs where it releases carbon dioxide and picks up oxygen

Anatomy and physiology of endocrine system

Introduction to the endocrine system The role of the endocrine system is to maintain the body in balance through the release of hormones (chemical signals) directly into the bloodstream. Hormones transfer information and instructions from one set of cells to another. Many different hormones move through the bloodstream, but each type of hormone is designed to affect only certain cells. A gland is a group of cells that produces and secretes chemicals. A gland selects and removes materials from the blood, processes them, and secretes the finished chemical product for use somewhere in the body. The endocrine gland cells release a hormone into the blood stream for distribution throughout the entire body. These hormones act as chemical messengers and can alter the activity of many organs at once. The parts of the endocrine system are grouped together because they release hormones into the blood without going through a duct (which is basically a tube) first. This is different to an exocrine gland, which releases what it creates through a tube to somewhere other than the blood. Hormones can act on some specific cells because they themselves do not actually cause an effect. It is only through binding with a receptor (part of the cell specifically designed to recognize the hormone) like a key into a lock - that causes a chain reaction to occur, changing the activity of the cells. If a cell does not have a receptor for a hormone then there will be no effect. Also, there can be different receptors for the same hormone, and so the same hormone can have different effects on different cells.
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The pancreas

The pancreas is a pinkish-grey organ that lies behind to the stomach. The organ is approximately 15cm in length with a long, slender body connecting the head and tail segments. The endocrine pancreas is separate from the exocrine pancreas which is discussed under the gastrointestinal section. The endocrine pancreas is made up of small clumps of cells within the pancreas, called pancreatic islets, or the islets of Langerhans. These account for only 1% of the pancreatic mass. It is composed of three distinct cell types each producing a different hormone. The two important hormones are: Glucagon Secretion of glucagon is controlled by the level of blood sugar, being released when levels are too low. This greatly increases the output of sugar from the liver and returns blood sugar levels to normal. Insulin Insulin is designed to lower blood sugar levels when they become too high and is released in periods when there is a lot of sugar available, like after a meal. A lack of insulin means the body has to use fat for metabolism rather than sugar and can lead to a condition known as ketoacidosis.

ACUTE CORONARY SYNDROMES

Introduction Acute coronary syndrome (ACS) refers to a spectrum of clinical presentations ranging from those for ST-segment elevation myocardial infarction (STEMI) to presentations found in non ST-segment elevation myocardial infarction (NSTEMI) or in unstable angina. In terms of pathology, ACS is almost always associated with rupture of an atherosclerotic plaque and partial or complete thrombosis of the infarct-related artery. In some instances, however, stable coronary artery disease (CAD) may result in ACS in the absence of plaque rupture and thrombosis, when physiologic stress (eg, trauma, blood loss, anaemia, infection, tachyarrhythmia) increases demands on the heart. The diagnosis of acute
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myocardial infarction in this setting requires a finding of the typical rise and fall of biochemical markers of myocardial necrosis in addition to at least 1 of the following: Ischemic symptoms Development of pathologic Q waves Ischemic ST-segment changes on electrocardiogram (ECG) or in the setting of a coronary intervention Acute coronary syndromes are a group of conditions that are caused by a lack of oxygen to the heart muscle. These conditions include unstable angina, nonQ wave myocardial infarction, and ST segment elevation myocardial infarction. Patients with acute coronary syndromes are at high risk for myocardial infarction and death. Epidemiology Epidemiology of acute coronary syndromes in a Mediterranean country; by Christos Pitsavos in 2005 published in BMC public health. Research was conducted in First Cardiology Clinic, School of Medicine, University of Athens, Greece. Results are The overall incidence rate of ACS observed in our survey was 22.6 events per 10000 of population. annual incidence for men was 34 per 10,000 of people, while the incidence for women was significantly lower, i.e. 11 per 10,000 of people. ACS is the diagnosis in 10-20% of acute chest pain patients in developed world studies. In developing countries, overall prevalence of coronary disease is likely lower and the prevalence of other causes of acute chest pain (e.g. tuberculosis) likely greater compared to developed countries.ACS accounts for almost 1.6 million hospitalization each year. MI was significantly higher in diabetic patients (36.4% vs. 19.2%, P < 0.001). Diabetic patients compare to non diabetic patients were more hypertensive (96% vs. 88.7%, p < 0.005) and had higher serum triglyceride (TG over 200 mg/dl, 35.1% vs. 26.4, p <0.05). 19 out of 20 patients with acute coronary event have at least one of conventional cardiac risk factors. Diabetes and hypertension are leading risk factors, which may directly or indirectly interfere and predict more serious complications of coronary heart disease. Smoking, diabetes, and hypertension are leading risk factors, which may directly or indirectly interfere and predict most serious complications of ACS. In B.P. Koirala Institute of Health Sciences, Dharan Nepal, from January 2011 to December 2011, we found 112 male and 94 female suffering from acute coronary syndrome. Causes Acute coronary syndrome may develop slowly over time by the building up of plaques in the arteries in heart. These plaques, made up of fatty deposits, cause the arteries to narrow and make it more difficult for blood to flow through them. This buildup of plaques is known as atherosclerosis. Eventually, this buildup means that heart can't pump enough oxygen-rich blood to the rest of body, causing chest pain (angina) or a heart attack.

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Another medical term closely related to acute coronary syndrome is coronary artery disease. Coronary artery disease refers to the damage to heart arteries from atherosclerosis. If one of the plaques in coronary arteries ruptures, it can cause a heart attack. In fact, many instances of coronary artery syndrome develop after a plaque ruptures. A blood clot will form on the site of the rupture, blocking the flow of blood through that artery Risk factors The risk factors for acute coronary syndrome are similar to those for other types of heart disease. Acute coronary syndrome risk factors include: Older age (older than 45 for men and older than 55 for women) High blood pressure High blood cholesterol Cigarette smoking Lack of physical activity Type 2 diabetes Family history of chest pain, heart disease or stroke Sign and symptoms according to book Chest pain (angina) that feels like burning, pressure or tightness and lasts several minutes or longer Pain elsewhere in the body, such as the left upper arm or jaw (referred pain) Nausea Vomiting Shortness of breath (dyspnoea) Sudden, heavy sweating (diaphoresis In underlying medical condition, such as diabetes. Some unusual heart attack symptoms include: Abdominal pain Pain similar to heartburn Clammy skin Lightheadedness, dizziness or fainting Unusual or unexplained fatigue Feeling restless or apprehensive. Sign and symptoms observed in patient My patient had diabetes and hypertension also. The sign and symptoms are: Chest pain (angina) that feels like burning, pressure or tightness. Shortness of breath Feeling restless or apprehensive. Diagnostic evaluation according to book Cardiac enzymes in 6-8 hours interval.
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o CK-MB o Troponin-I ECG Myoglobin values first 4-8 hours of onset. Complete blood count (CBC) Blood Glucose Serum Electrolytes Urea Cretenine Levels of brain natriuretic peptide (BNP) C-reactive protein (CRP, an estimate of the extent of systemic inflammation) Chest Radiography Echocardiography Myocardial perfusion imaging Cardiac angiography CT coronary artery Diagnostic evaluation done in patient Cardiac enzymes in 6-8 hours interval. o CK-MB o Troponin-I ECG Blood Glucose Serum Electrolytes Urea Cretenine Cardiac angiography Haemoglobin Lipid profile Liver Function Test CRP Urine RE/ME Treatment and management according to book Initial therapy for acute coronary syndrome should focus on stabilizing the patient's condition, relieving ischemic pain, and providing antithrombotic therapy to reduce myocardial damage and prevent further ischemia. Medicines to use are: Morphine (or fentanyl) for pain control Oxygen Sublingual and/or IV nitroglycerin
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 Soluble aspirin 162-325 mg Clopidogrel with a 300- to 600-mg loading dose Lowmolecular weight heparin (LMWH) Intravenous platelet glycoprotein IIb/IIIa complex blockers (eg, tirofiban, eptifibatide) a beta blocker. Surgical management Angioplasty Angioplasty was not required in my patient because report of angiography was normal. Treatment done in patient Tab. Ecospirin 300mg po OD Tab. Clopilet 300mg stat and 75mg po OD Tab. Metop 12.5mg po BD Tab. Telma 80mg po HS Tab.Esorol 40mg po OD AC Tab. Loree 1mg po HS Tab isodril 5mg sl SOS Inj. Clexon 60mg SC OD Nursing management according to book Assess for location, duration, intensity, and radiation; use a scale of 0 to 10. Assess blood pressure, pulse, and respiration. Obtain ECG as ordered. Administer oxygen as need. Instruct patient to report pain at first onset. Instruct patient to rest during pain. Remain with patient during chest pain until it is relieved. Explain and assist with alternative pain relief measures: Positioning Diversional activities Relaxation techniques Medicate as ordered. Nursing management done in patient Assessed for location, duration, intensity, and radiation Assessed blood pressure, pulse, and respiration. Obtained ECG as ordered. Administered oxygen Sent investigations as ordered
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Kept in propped up position. Provided calm environment and promoted rest. Provided newspaper after relieving pain for diversion. Medication done as ordered.

UNSTABLE ANGINA Unstable angina occurs in patients with worsening CAD and is noted by its changing pattern. Rest does not decrease the chest pain of unstable angina. This pain may even occur when the patient is at rest. The episodes of chest pain with unstable angina increase in frequency and severity, placing the patient at risk for myocardial damage or sudden death. Unstable Angina (UA) is defined as angina pectoris or equivalent ischemic discomfort with at least one of three features: (1) it occurs at rest (or with minimal exertion), usually lasting >10 min; (2) it is severe and of new onset (i.e., within the prior 46 weeks); and/or (3) it occurs with a crescendo pattern (i.e., distinctly more severe, prolonged, or frequent than previously). The diagnosis of NSTEMI is established if a patient with the clinical features of UA develops evidence of myocardial necrosis, as reflected in elevated cardiac biomarkers. Pathophysiology UA/NSTEMI is most commonly caused by a reduction in oxygen supply and/or by an increase in myocardial oxygen demand superimposed on an atherosclerotic coronary plaque, with varying degrees of obstruction. Four pathophysiologic processes that may contribute to the development of UA/NSTEMI have been identified: (1) plaque rupture or erosion with superimposed nonocclusive thrombus, believed to be the most common causeNSTEMI may occur with downstream embolization of platelet aggregates and/or atherosclerotic debris; (2) dynamic obstruction [e.g., coronary spasm, as in Prinzmetal's variant angina ]; (3) progressive mechanical obstruction [e.g., rapidly advancing coronary atherosclerosis or restenosis following percutaneous coronary intervention (PCI)]; and (4) secondary UA related to increased myocardial oxygen demand and/or decreased supply (e.g., tachycardia, anaemia). More than one of these processes may be involved. Among patients with UA/NSTEMI studied at angiography, approximately 5% have left main stenosis, 15% have three-vessel CAD, 30% have two-vessel disease, 40% have single-vessel disease, and 10% have no critical coronary stenosis; some of the latter have Prinzmetal's variant angina (see below). The "culprit lesion" on angiography may show an eccentric stenosis with scalloped or overhanging edges and a narrow neck. Angioscopy may reveal "white" (plateletrich) thrombi, as opposed to "red" thrombi, more often seen in patients with acute STEMI. Patients with UA/NSTEMI often have multiple plaques vulnerable to disruption. Among patients with ACS, apporximately 60%have unstable angina and 40% have MI. Etiology of unstable angina Supply-demand mismatch

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The myocardial ischemia of unstable angina, like all tissue ischemia, results from excessive demand or inadequate supply of oxygen, glucose, and free fatty acids. Increased myocardial oxygen demand may be caused by the following: Fever Tachyarrhythmias (eg, atrial fibrillation or flutter) Malignant hypertension Thyrotoxicosis Pheochromocytoma Cocaine use Amphetamine use Aortic stenosis Supravalvular aortic stenosis Obstructive cardiomyopathy Aortovenous shunts High output states Congestive failure Decreased oxygen supply may be caused by the following: Anemia Hypoxemia Polycythemia Hypotension The above causes must be investigated because a number of them are reversible. For instance, anaemia from chronic GI bleeding is not uncommon in elderly patients. This can coexist with coronary artery disease. However, patients may not benefit or may be harmed by treatments such as anticoagulants and antiplatelet drugs. Avoidance or treatment of the underlying condition is paramount. Excess demand from increased myocardial workload (heart ratesystolic pressure product) or wall stress is responsible for nearly all cases of stable angina and perhaps one third of all episodes of unstable angina. Plaque disruption Accumulation of lipid-laden macrophages and smooth muscle cells, so-called foam cells, occurs within atherosclerotic plaques. The oxidized low-density lipoprotein cholesterol (LDL-C) in foam cells is cytotoxic, procoagulant, and chemotactic. As the atherosclerotic plaque grows, production of macrophage proteases and neutrophil elastases within the plaque can cause thinning of the fibromuscular cap that covers the lipid core. Increasing plaque instability coupled with blood-flow shear and circumferential wall stress lead to plaque fissuring or rupture, especially at the junction of the cap and the vessel wall. Pathogenesis of acute coronary syndromes. The degree and consequence of plaque disruption covers a wide spectrum. Minor fissuring is typically nonocclusive and hence clinically silent, and repeat occult episodes of plaque ulceration
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and healing with a gradual growth of plaque volume have been histologically documented. Moderate to large plaque disruptions commonly result in unstable angina or acute infarction. As many as one half of myocardial infarctions are due to lesions that are angiographically insignificant. Moreover, recurrent major adverse cardiovascular events (MACE) are not caused by the original culprit coronary site in as many as one half of cases (ie, a different lesion is the cause). Hence, angiographically mild lesions can still be dangerous because they have an unstable thin-cap fibroatheroma (TCFA) or because they actually overlie a large amount of vessel wall plaque burden that can occlude or rupture. This means that focal treatments such as percutaneous coronary intervention (PCI) is incomplete and that medical therapy to protect the entire vascular tree is complementary and crucial, particularly in patients with a history of ACS. Vasoconstriction and thrombosis Most patients with acute coronary syndrome have recurrent transient reduction in coronary blood supply because of vasoconstriction and thrombus formation at the site of atherosclerotic plaque rupture. These events occur because of episodic platelet aggregation and complex interactions among the vascular wall, leukocytes, platelets, and atherogenic lipoproteins. Exposure of subendothelial components provokes platelet adhesion and activation. Platelets then aggregate in response to exposed vessel wall collagen or local aggregates (eg, thromboxane, adenosine diphosphate). Platelets also release substances that promote vasoconstriction and production of thrombin. In a reciprocating fashion, thrombin is a potent agonist for further platelet activation, and it stabilizes thrombi by converting fibrinogen to fibrin. The nonocclusive thrombus of unstable angina can become transiently or persistently occlusive. Depending on the duration of occlusion, the presence of collateral vessels, and the area of myocardium perfused, recurrent unstable angina, NQMI, or Q-wave infarction can result. Vasospasm and cyclic flow variation Vasospasm, provoked by either ergonovine or acetylcholine, is a common finding in patients with acute coronary syndrome, particularly in Taiwanese and Japanese patients. Although correlated with chest pain, whether this coronary hyperreactivity causes acute coronary syndrome or is simply an associated finding is not known. Acute coronary syndromes may involve a clot in flux (ie, forming and enlarging, chipping-off and embolizing). This dynamic clot formation and/or lysis, over time, in conjunction with coronary vasoreactivity and resistance in the microvascular bed, causes intermittent and alternating (or cyclical) occlusion and flow. Clinical features Discomfort is usually more intense and easily provoked. ST-segment depression or elevation on ECG may occur. Increased autonomic activity may manifest as diaphoresis or tachycardia, and bradycardia may result from vagal stimulation from inferior wall myocardial ischemia. Others same as acute coronary syndrome. Braunwald Classification of Unstable Angina
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Characteristic Severity

Class/Category I II

Details Symptoms with exertion Subacute symptoms at rest (230 d prior) Acute symptoms (within prior 48 h) Secondary Primary Postinfarction No treatment Usual angina therapy Maximal therapy at rest

III

Clinical factor

precipitating

A B C

Therapy symptoms

during

1 2 3

Canadian Cardiovascular Society Grading System The Canadian Cardiovascular Society Grading System for effort-related angina is widely used since it is a simple and practical classification that is often used to describe symptom severity. The grading system is as follows: Grade I - Angina with strenuous, rapid, or prolonged exertion (Ordinary physical activity such as climbing stairs does not provoke angina.) Grade II - Slight limitation of ordinary activity (Angina occurs with postprandial, uphill, or rapid walking; when walking more than 2 blocks of level ground or climbing more than 1 flight of stairs; during emotional stress; or in the early hours after awakening.) Grade III - Marked limitation of ordinary activity (Angina occurs with walking 1-2 blocks or climbing a flight of stairs at a normal pace.) Grade IV - Inability to carry on any physical activity without discomfort (Rest pain occurs.) Clinical features in patient Mentioned in acute coronary syndrome
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Diagnostic test according to book Serial cardiac biomarkers Haemoglobin Serum chemistry Lipid profile (CK-MB) Troponin levels Brain natriuretic peptide C-reactive protein (CRP, an estimate of extent of systemic inflammation) CBC Urea Cretenine Serum electrolytes ECG Echocardiography MR angiography Exercise testing Diagnostic evaluation done in patient Mentioned above Treatment and management according to book Aspirin Beta-adrenergic blocking agents Lipid-lowering agents (statins) Angiotensin-converting enzyme (ACE) inhibitors Clopidogrel Glycoprotein IIb/IIIa antagonists Nitrates Heparin Patients with unstable angina and the following clinical characteristics should be referred for immediate cardiac catheterization:

Cardiogenic shock Severe left ventricular dysfunction Angina refractory to medical therapy Acute mitral regurgitation New ventricular septal defect Unstable tachyarrhythmias

Treatment in patient
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Mentioned above Nursing management according to book Obtaining a thorough history on a patient admitted with a diagnosis of angina pectoris is important in developing a plan of care and should include the following: How long the patient has had angina Risk factors Triggering activities How pain is relieved If the patient reports chest pain, areas of assessment and documentation should include the following: Type, location, and pain radiation to other areas of the body Vital signs and skin color and temperature Presence of dyspnoea, laboured respirations, diaphoresis, or nausea Oxygen and sublingual NTG are given to the patient with chest pain as ordered. Blood pressure and heart rate are assessed before and after NTG is given. The nurse must promote rest and decrease anxiety for the patient with chest pain. A patient who is experiencing chest pain should never be left alone. Emotional support is important because patients and their families are often afraid that the patient may die. Nursing management done in patient Took history about duration of chest pain, risk factors of angina, alleviating and aggravating factors. Asked about location, radiation of pain. Assessed vital signs Provided oxygen Provided emotional support to patient and family. Medications as per cardex.

HYPERTENSION Introduction Defining abnormally high blood pressure is extremely difficult and arbitrary. Furthermore, the relationship between systemic arterial pressure and morbidity appears to be quantitative rather than qualitative. A level for high BP must be agreed upon in clinical practice for screening patients with hypertension and for instituting diagnostic evaluation and initiating therapy. Because the risk to an individual patient may correlate with the severity of hypertension, a classification system is essential for making decisions about aggressiveness of treatment or therapeutic interventions.

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Based on recommendations of the Seventh Report of the Joint National Committee of Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC VII), the classification of BP (expressed in mm Hg) for adults aged 18 years or older is as follows: Normal - Systolic lower than 120, diastolic lower than 80 Prehypertension - Systolic 120-139, diastolic 80-90 Stage 1 - Systolic 140-159, diastolic 90-99 Stage 2 - Systolic equal to or more than 160, diastolic equal to or more than 100 The classification above is based on the average of 2 or more readings taken at each of 2 or more visits after initial screening. Normal BP with respect to cardiovascular risk is less than 120/80 mm Hg. However, unusually low readings should be evaluated for clinical significance. Epidemiology The public health burden of HTN is enormous, affecting an estimated 60.5 million american adults. And its prevalence is high world wide. Cardiovascular diseases (CVD), most of which are due to atherosclerosis (mainly heart attack and stroke) and often related to arterial hypertension, are responsible for nearly 20% of all deaths world-wide (nearly 10 million). They are the principal cause of death in all developed countries accounting for 50% of all deaths and are also emerging as a prominent public health problem in developing countries, ranking third with nearly 16% of all deaths. They have already become the first cause of death in such countries as Argentina, Chile, Cuba, Mauritius, Singapore, Sri Lanka, Trinidad and Tobago and Uruguay. Many developing countries are now in a phase of epidemiological transition and face the double burden of communicable and non-communicable diseases, with the severe repercussions this has on their very weak economies. In B.P. Koirala Institute of Health Sciences, we found 45male and 48 female of hypertension from January 2011 to December 2011. Pathophysiology The pathogenesis of essential hypertension is multifactorial and highly complex. Multiple factors modulate the blood pressure (BP) for adequate tissue perfusion and include humoral mediators, vascular reactivity, circulating blood volume, vascular caliber, blood viscosity, cardiac output, blood vessel elasticity, and neural stimulation. A possible pathogenesis of essential hypertension has been proposed in which multiple factors, including genetic predisposition, excess dietary salt intake, and adrenergic tone, may interact to produce hypertension. Although genetics appears to contribute to essential hypertension, the exact mechanism has not been established. The natural history of essential hypertension evolves from occasional to established hypertension. After a long invariable asymptomatic period, persistent hypertension develops into complicated hypertension, in which target organ damage to the aorta and small arteries, heart, kidneys, retina, and central nervous system is evident. The progression begins with prehypertension in persons aged 10-30 years (by increased cardiac output) to early hypertension in persons aged 20-40 years (in which increased peripheral resistance is prominent) to

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established hypertension in persons aged 30-50 years, and, finally, to complicated hypertension in persons aged 40-60 years. One mechanism of hypertension has been described as high-output hypertension. High-output hypertension results from decreased peripheral vascular resistance and concomitant cardiac stimulation by adrenergic hyperactivity and altered calcium homeostasis. A second mechanism manifests with normal or reduced cardiac output and elevated systemic vascular resistance due to increased vasoreactivity. Another (and overlapping) mechanism is increased salt and water reabsorption (salt sensitivity) by the kidney, which increases circulating blood volume. Etiology 1. Genetic Considerations Although specific genetic variants have been identified in rare Mendelian forms of hypertension,(like Glucocorticoid-remediable hyperaldosteronism, Polycystic kidney disease etc) these variants are not applicable to the vast majority (>98%) of patients with essential hypertension. 2. Endogenous hormonal causes include the following: Primary hyperaldosteronism Cushing syndrome Pheochromocytoma Congenital adrenal hyperplasia 3. Neurogenic causes include the following: Brain tumor Bulbar poliomyelitis Intracranial hypertension 4. Drugs and toxins that cause hypertension include the following: Alcohol Cocaine Cyclosporine, tacrolimus NSAIDs Erythropoietin Adrenergic medications Decongestants containing ephedrine Herbal remedies containing licorice or ephedrine 5. Other causes include the following: Hyperthyroidism and hypothyroidism Hypercalcemia Hyperparathyroidism Acromegaly Obstructive sleep apnea
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Pregnancy-induced hypertension

Epidemiology Hypertension is a worldwide epidemic; accordingly, its epidemiology has been well studied. An inadequate control rate of hypertension 61%, will almost certainly contribute to the incidence of ACS and its complications. When inadequate BP control is combined with diabetes, then we are treading on dangerous territory. A 2005 survey in the United States found that in the population aged 20 years or older, an estimated 41.9 million men and 27.8 million women have prehypertension, 12.8 million men and 12.2 million women have stage 1 hypertension, and 4.1 million men and 6.9 million women have stage 2 hypertension. In many countries, 50% of the population older than 60 years has hypertension. Overall, approximately 20% of the worlds adults are estimated to have hypertension. The 20% prevalence is for hypertension defined as BP in excess of 140/90 mm Hg. The prevalence dramatically increases in patients older than 60 years. In BPKIHS, Dharan, from January 2011 to December 2011; cases of hypertension were 45 male and 48 female. Diagnostic evaluation in book History taking Physical examination Complete blood count (CBC) serum electrolytes serum creatinine serum glucose uric acid urinalysis Lipid profile (total cholesterol, low-density lipoprotein [LDL], high-density lipoprotein [HDL], and triglycerides)

Investigations done in patient Mentioned above Clinical presentation High blood pressure usually causes no symptoms and high blood pressure often is labelled "the silent killer." People who have high blood pressure typically don't know it until their blood pressure is measured. Sometimes people with markedly elevated blood pressure may develop: Headache Dizziness,
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 Blurred vision Nausea and vomiting Chest pain and shortness of breath. People often do not seek medical care until they have symptoms arising from the organ damage caused by chronic (ongoing, long-term) high blood pressure. The following types of organ damage are commonly seen in chronic high blood pressure: Heart attack Heart failure Stroke or transient ischemic attack (TIA) Kidney failure Eye damage with progressive vision loss Peripheral arterial disease causing leg pain with walking (claudication) Outpunching of the aorta, called aneurysms About 1% of people with high blood pressure do not seek medical care until the high blood pressure is very severe, a condition known as malignant hypertension. In malignant hypertension, the diastolic blood pressure (the lower number) often exceeds 140 mm Hg. Malignant hypertension may be associated with headache, lightheadedness, nausea, vomiting, and stroke like symptoms Malignant hypertension requires emergency intervention and lowering of blood pressure to prevent brain haemorrhage or stroke Clinical presentation in patient Patient is in antihypertensive and blood pressure is maintained in antihypertensive. So, symptoms of hypertension are not seen but still chest pain was present because he is patient of ACS. Treatment and management Angiotensin-converting enzyme (ACE) inhibitors Angiotensin II receptor blockers (ARBs) Diuretics Beta-blockers Calcium channel blockers Alpha-blockers Alpha-agonists Renin inhibitors Combination medications Diuretics are often recommended as the first line of therapy for most people who have high blood pressure. Treatment in patient Mentioned above
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Nursing management following lifestyle changes: Losing weight if you are overweight or obese. Quitting smoking. Eating a healthy diet, including the DASH (Dietary Approaches to Stop Hypertension) diet (eating more fruits, vegetables, and low fat dairy products, less saturated and total fat). Reducing the amount of sodium in your diet to less than 1,500 milligrams a day. Getting regular aerobic exercise (such as brisk walking at least 30 minutes a day, several days a week). Limiting alcohol to two drinks a day for men, one drink a day for women. In addition to lowering blood pressure, these measures enhance the effectiveness of high blood pressure drugs Explain the meaning of high blood pressure, risk factors, and Explain the influences of high blood pressure on the cardiovascular, cerebral, and renal systems. Stresses that Hypertension can never be total cure, only control, of essential hypertension; emphasize the consequences of uncontrolled hypertension. Stress the fact that there may be no correlation between high blood pressure and symptoms; the patient cannot tell by the way he feels whether blood pressure is normal or elevated. Have the patient recognize that hypertension is chronic and requires persistent therapy and periodic evaluation. Present a coordinated and complementary plan of guidance. o Inform the patient of the meaning of the various diagnostic and therapeutic activities to minimize anxiety and to obtain cooperation. o Solicit the assistance of the patients spouse, family, and friends provide information regarding the total treatment plan. o Be aware of the dietary plan developed for this particular patient. Explain the pharmacologic control of hypertension. o Explain that the drugs used for effective control of elevated blood pressure will likely produce adverse effects. o Warn the patient of the possibility that orthostatic hypotension may occur initially with some drug therapy: Instruct the patient to get up slowly to offset the feeling of dizziness, Encourage the patient to sit or lie down immediately if he feels faint o Alert the patient to expect initial effects, such as anorexia, light-headedness, and fatigue, with many medications.

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Inform the patient that the goal of treatment is to control blood pressure, reduce the possibility of complications, and use the minimum number of drugs with the lowest dosage necessary to accomplish this. Educate the patient to be aware of serious adverse effects and report them immediately so that adjustments can be made in individual pharmacotherapy. Note that dosages are individualized; therefore, they may need to be adjusted because it is often impossible to predict reactions. Warn the patient on vasodilating drugs to use caution in certain circumstances that produce vasodilatation a hot bath, hot weather, febrile illness, consumption of alcohol which may exacerbate blood pressure reduction. Warn patients that blood pressure is often decreased when circulating blood volume is reduced as in dehydration, diarrhoea, and haemorrhage so blood pressure should be monitored closely and treatment adjusted

Nursing management for hypertension in patient Explained the patient eating a healthy diet, including the DASH diet. Advised for reducing the amount of sodium in your diet . Advised for getting regular aerobic exercise (such as brisk walking at least 30 minutes a day, several days a week). Advised for limiting alcohol. Explained the meaning of high blood pressure, risk factors, and Explained the influences of high blood pressure on the cardiovascular, cerebral, and renal systems. Stressed that Hypertension can never be total cure, only control, of essential hypertension; emphasize the consequences of uncontrolled hypertension. Instructed the patient to get up slowly to offset the feeling of dizziness, Encourage the patient to sit or lie down immediately if he feels faint. Informed the patient of the meaning of the various diagnostic and therapeutic activities. DIABETES MELLITUS TYPE II Introduction It is the most common form of diabetes. Millions of Americans have been diagnosed with type 2 diabetes, and many more are unaware they are at high risk. Some groups have a higher risk for developing type 2 diabetes than others. Type 2 diabetes is more common in the aged population. In type 2 diabetes, either the body does not produce enough insulin or the cells ignore the insulin. Insulin is necessary for the body to be able to use glucose for energy. When you eat food, the body breaks down all of the sugars and starches into glucose, which is the basic fuel for the cells in the body. Insulin takes the sugar from the blood into the cells. When glucose builds up in the blood instead of going into cells, it can lead to diabetes complications

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In type 2 diabetes mellitus (formerly called adult-onset diabetes mellitus, noninsulin-dependent diabetes mellitus, or NIDDM), some insulin is still made by the pancreas, but in inadequate amounts. Sometimes the amount of insulin is normal or even high, but the tissues are resistant to it and hyperglycaemia results.

Epidemiology Diabetes has grown worldwide at an alarming rate and according to various studies and the World Health Organization (WHO), the number of people with diabetes in the world is at least 240 million, with India, China, and the United States leading the way. The number of people with diabetes is expected to grow by 380 million by year 2025. Based on current trends, >360 million individuals will have diabetes by the year 2030. In B.P. Koirala Institute of Health Sciences, Dharan, from January 2011 to December 2011, cases of diabetes type 2 are 109 male and 89 female. Etiology The etiology of type II diabetes mellitus (non-insulin- dependent diabetes mellitus, NIDDM) is even less clearly understood. Two factors have been identified: a) Impaired insulin release-basal secretion of insulin is often normal, but the rapid release of insulin follows a meal is greatly impaired, resulting in failure of normal handling of a carbohydrate load. In most patients, some level of insulin secretion is maintained, so that the abnormality of glucose metabolism is limited and ketoacidosis is uncommon. In these patients, insulin secretion can be stimulated by drugs such as sulfonylureas. Exogenous insulin is therefore not essential in treatment. It also have been suggested that inheritance of a defective pattern of insulin secretion is responsible for the familial tendency of diabetes. The genetic factor is very strong in type II diabetes, with a history of diabetes present in about 50% of first degree relatives. b) Insulin resistance-a defect in the tissue response to insulin is believed to play a major role. This phenomenon is called insulin resistance and is caused by defective insulin receptors on the target cells. Insulin resistance occurs in association with obesity and pregnancy. In normal individuals who become obese or pregnant, the B cells secrete increased amounts of insulin to compensate. Patients who have genetic susceptibility to diabetes cannot compensate because of their inherent defect in insulin secretion. Thus, type II diabetes is frequently precipitated by obesity and pregnancy. In a few patients with extreme insulin resistance, antibodies against the receptors have been demonstrated in plasma. These antibodies are mostly of the IgG class and act against the insulin receptors, causing the decreased numbers of insulin receptors and defective binding of insulin to receptors.
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Risk factors Family history of diabetes (i.e., parent or sibling with type 2 diabetes) Obesity (BMI 25 kg/m2) Habitual physical inactivity Race/ethnicity (e.g., African American, Latino, Native American, Asian American, Pacific Islander) Previously identified IFG or IGT History of GDM or delivery of baby >4 kg (>9 lb) Hypertension (blood pressure 140/90 mmHg) HDL cholesterol level <35 mg/dL (0.90 mmol/L) and/or a triglyceride level >250 mg/dL (2.82 mmol/L) Polycystic ovary syndrome or acanthosis nigricans History of vascular disease Pathophysiology Type 2 DM is characterized by impaired insulin secretion, insulin resistance, excessive hepatic glucose production, and abnormal fat metabolism. Obesity, particularly visceral or central (as evidenced by the hip-waist ratio), is very common in type 2 DM. In the early stages of the disorder, glucose tolerance remains near-normal, despite insulin resistance, because the pancreatic beta cells compensate by increasing insulin output. As insulin resistance and compensatory hyperinsulinemia progress, the pancreatic islets in certain individuals are unable to sustain the hyperinsulinemic state. IGT, characterized by elevations in postprandial glucose, then develops. A further decline in insulin secretion and an increase in hepatic glucose production lead to overt diabetes with fasting hyperglycemia. Ultimately, beta cell failure may ensue. Clinical features in book Classic symptoms of diabetes mellitus include polydipsia(excessive thirst) polyuria (excessive urination) polyphagia (excessive hunger). Because glucose is unable to enter the cells, the cells starve, causing hunger. The large amount of glucose in the blood causes an increase in serum concentration, or osmolality. The renal tubules are unable to reabsorb all the excess glucose that is filtered by the glomeruli, and glycosuria results. Large amounts of body water are required to excrete this glucose, causing polyuria, nocturia, and dehydration. The increased osmolality and dehydration cause polydipsia. High blood glucose may also cause fatigue, blurred vision, abdominal pain, and headaches. Clinical features in patient Sometimes the following features appears according to patient:
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Polydipsia Polyuria Polyphagia Glycosuria also presents in urine routine examination.

Diagnostic test according to book fasting blood glucose Diagnosis of diabetes mellitus is based on blood glucose levels measured by a laboratory. A normal blood glucose level ranges from 60 to 110 mg/dL, although different laboratories may have slightly different normal values. When the fasting blood glucose (drawn after at least 4 hours without eating) is above 126 mg/dL on two separate occasions, diabetes is diagnosed. oral glucose tolerance test Another test to diagnose diabetes is the oral glucose tolerance test (OGTT). An OGTT measures blood glucose at intervals after the patient drinks a concentrated carbohydrate drink. Diabetes is diagnosed when the blood glucose level is 200 mg/dL or higher after 2 hours. glycohemoglobin The glycohemoglobin test (also called glycosylated haemoglobin, or HbA1c) is used to gather baseline data and to monitor progress of diabetes control. Glucose in the blood attaches to haemoglobin in the red blood cells. Red blood cells live about 3 months in the body. When the glucose that is attached to the haemoglobin is measured, it reflects the average blood glucose level for the previous 3 months. Results should be approximately 4 to 7 percent, depending on the laboratory. This is a helpful measurement when blood glucose levels fluctuate and a single measurement would be misleading. It also assists in determining the degree of effectiveness of a patients treatment plan. Newer methods allow this test to be done in a physicians office while the patient waits. Glycohemoglobin testing might be inaccurate in some people, such as those with anaemia. These individuals may have a glycated serum protein test, which is a similar test that indicates glucose levels over a period of 1 to 2 weeks instead of 3 months. Because diabetes affects so many body systems, additional tests recommended to gather baseline data include a lipid profile, serum creatinine and urine microalbumin levels to monitor kidney function, urinalysis, and electrocardiogram. Investigations done in patient Random blood sugar Glycohemoglobin Urine RE/ME Others mentioned above

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Treatment and management in book The treatment of diabetes is highly individualized, depending on the type of diabetes, whether the patient has other active medical problems, whether the patient has complications of diabetes, and age and general health of the patient at time of diagnosis. A health care professional will set goals for lifestyle changes, blood sugar control, and treatment. Together, the patient and the health care professional will formulate a plan to help meet those goals. Education about diabetes. When the patient is first diagnosed with diabetes, the diabetes care team will spend a lot of time with the patient, teaching them about their condition, treatment, and everything they need to know to care for themselves on a daily basis. The diabetes care team includes the health care professional and his or her staff. It may include specialists in foot care, neurology, kidney diseases, and eye diseases. A professional dietitian and a diabetes educator also may be part of the team. The health care team will see the patient at appropriate intervals to monitor their progress and evaluate goals. Sulfonylureas: These drugs stimulate the pancreas to make more insulin. Biguanides: These agents decrease the amount of glucose produced by the liver. Alpha-glucosidase inhibitors: These agents slow absorption of the starches a person eats. This slows down glucose production. Thiazolidinediones: These agents increase sensitivity to insulin. Meglitinides: These agents stimulate the pancreas to make more insulin. D-phenylalanine derivatives: These agents stimulate the pancreas to produce more insulin more quickly. Amylin synthetic derivatives: Amylin is a naturally occurring hormone secreted by the pancreas along with insulin. An amylin derivative, such as pramlintide (Symlin), is indicated when blood sugar control is not achieved despite optimal insulin therapy. Pramlintide is administered as a subcutaneous injection along with insulin and helps achieve lower blood sugar levels after meals, helps reduce fluctuation of blood sugar levels throughout the day, and improves haemoglobin A1C levels. Incretin mimetics: Incretin mimetics promote insulin secretion by the pancreas and mimics other blood sugar level lowering actions that naturally occur in the body. Exenatide (Byetta) was the first incretin mimetic agent approved in the United States. It is indicated for diabetes mellitus type 2 in addition to metformin or a sulfonylurea when these agents have not attained blood sugar level control alone. Insulins Transplantation of pancreas. Treatment in patient Tab. Glimepride 2mg po OD.
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Diabetic diet

Nursing management according to book Assess knowledge of diabetes selfcare. Assist patient to collaborate with health care provider to determine appropriate blood glucose levels and action to be taken if glucose levels are too high or too low. Teach patient to assess glucose levels before meals and at bedtime or as ordered by health care provider. Ensure that patient knows how to obtain glucose monitor and instruction for home use. Teach patient to administer insulin or oral hypoglycemic agent 30 minutes before meals (15 minutes if patient is using Lispro). Ensure that meal is begun within 30 minutes of medication. Replace any uneaten foods to prevent hypoglycemia. Consult with dietitian for nutrition therapy instruction. Consult with social worker as needed. Provide patient with information regarding comprehensive diabetes education. Remind patient that only survival skills have been taught during initial instruction. Assist patient to obtain medical alert card or tag that identifies diabetes. Nursing management done in patient Monitored blood sugar level every 6hrly and took action accordingly. Provided diabetic diet and taught about diabetic diet. Provided oral hypoglycemic agent according to prescription. Taught about administration of oral hypoglycemic agent. Taught about prevention of complication and care regarding diabetes. Taught about periodic blood sugar monitoring.

DRUG STUDY
1. Ecospirin Generic name: aspirin Pharmacological category: salicylate Antipyretic, Analgesic (non-narcotic), Anti-inflammatory, Antirheumatic, Antiplatelet, NSAID Pregnancy category: D Therapeutic action Analgesic and antirheumatic effects are attributable to aspirin's ability to inhibit the synthesis of prostaglandins, important mediators of inflammation. Antipyretic effects are not fully understood, but aspirin probably acts in the thermoregulatory center of the hypothalamus to block effects of endogenous pyrogen by inhibiting synthesis of the prostaglandin intermediary. Inhibition of platelet aggregation is attributable to the inhibition of platelet synthesis of
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thromboxane A2, a potent vasoconstrictor and inducer of platelet aggregation. This effect occurs at low doses and lasts for the life of the platelet. Higher doses inhibit the synthesis of prostacyclin, a potent vasodilator and inhibitor of platelet aggregation. Dosage Available Forms: Tablets--325, 500, 650, 975 mg; SR tablets--650, 800 mg; suppositories: 120, 200, 300, 600 mg Available in oral and suppository forms. Also available as chewable tablets, gum; enteric coated, sustained release, and buffered preparations (sustained-release aspirin is not recommended for antipyresis, short-term analgesia, or children < 12 y).

Adult Minor aches and pains: 325---650 mg q4h. Arthritis and rheumatic conditions: 3.2---6.0 g/d in divided doses. Acute rheumatic fever: 5---8 g/d; modify to maintain serum salicylate level of 15---30 mg/dL. TIAs in men: 1,300 mg/d in divided doses (650 mg bid or 325 mg qid). MI: 300---325 mg/d. Pediatric Analgesic and antipyretic: 65 mg/kg per 24 h in four to six divided doses, not to exceed 3.6 g/d. Juvenile rheumatoid arthritis: 60---110 mg/kg per 24 h in divided doses at4- to 6-h intervals. Maintain a serum level of 200--300 g/mL. Acute rheumatic fever: 100 mg/kg/d initially, then decrease to 75 mg/kg/d for 4---6 wk. Therapeutic serum salicylate level is 15---30 mg/dL. Kawasaki disease: 80---180 mg/kg per day; very high doses may be needed during acute febrile period; after fever resolves, dosage may be adjusted to 10 mg/kg per day. Uses or Indications Treatment of mild to mederate pain, inflammation and fever; as prophylaxis of myocardial infraction; prophylaxis of stroke; prophylaxis of transient ischemic episode; management of

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rheumatoid arthritis and rheumatoid fever; osteoarthritis and gout; adjunctive therapy in revascularization procedures e.g. PTCA,CABG etc;stent implantation. Low dose have been used to prevent pre-eclampsia, prevention from complications associated with autoimmune disorders. Contraindications Hypersensitive to salicylates, other NSAIDs. Inherited or acquired bleeding disorders. Children under 16 years of age with viral infections. Reye`s syndrome Pregnancy Severe renal and hepatic failure Precautions Dehydration Peptic ulcer diseases 1-2 weeks prior to surgery. Breastfeeding Adverse reactions GI: Nausea, dyspepsia, heartburn, epigastric discomfort, anorexia, hepatotoxicity Hematologic: Occult blood loss, haemostatic defects Hypersensitivity: Anaphylactic reactions to fatal anaphylactic shock Aspirin intolerance: Exacerbation of bronchospasm, rhinitis (with nasal polyps, asthma, rhinitis) Salicylism: Dizziness, tinnitus, difficulty hearing, nausea, vomiting, diarrhoea, mental confusion, lassitude (dose related) Acute aspirin toxicity: Respiratory alkalosis, hyperpnoea, tachypnea, haemorrhage, excitement, confusion, asterixis, pulmonary oedema, convulsions, tetany, metabolic acidosis, fever, coma, cardiovascular collapse,renal and respiratory failure (dose related 20---25 g in adults, 4 g in children Drug interactions Increased risk of bleeding with oral anticoagulants, heparin Increased risk of GI ulceration with steroids, phenylbutazone, alcohol, NSAIDs Increased serum salicylate levels due to decreased salicylate excretion with urine acidifiers (ammonium chloride, ascorbic acid, methionine) Increased risk of salicylate toxicity with carbonic anhydrase inhibitors, furosemide Decreased serum salicylate levels with corticosteroids Decreased serum salicylate levels due to increased renal excretion of salicylates with acetazolamide, methazolamide, certain antacids, alkalinizers Decreased absorption of aspirin with nonabsorbable antacids Increased methotrexate levels and toxicity with aspirin
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Increased effects of valproic acid secondary to displacement from plasma protein sites Greater glucose lowering effect of sulfonylureas, insulin with large doses (>2 g/d) of aspirin Decreased antihypertensive effect of captopril, -adrenergic blockers with salicylates; consider discontinuation of aspirin Decreased uricosuric effect of probenecid, sulfinpyrazone Possible decreased diuretic effects of spironolactone, furosemide (in patients with compromised renal function) Unexpected hypotension may occur with nitroglycerin. Nursing considerations Assessment History: Allergy to salicylates or NSAIDs; allergy to tartrazine; hemophilia, bleeding ulcers, hemmorhagic states, blood coagulation defects, hypoprothrombinemia, vitamin K deficiency; impaired hepatic function; impaired renal function; chickenpox, influenza; children with fever accompanied by dehydration; surgery scheduled within 1 wk; pregnancy; lactation Physical: Skin color, lesions; temperature; eighth cranial nerve function, orientation, reflexes, affect; P, BP, perfusion; R, adventitious sounds; liver evaluation, bowel sounds; CBC, clotting times, urinalysis, stool guaiac, renal and liver function tests Implementation Give drug with food or after meals if GI upset occurs. Give drug with full glass of water to reduce risk of tablet or capsule lodging in the esophagus. Do not crush, and ensure that patient does not chew sustained-release preparations. Do not use aspirin that has a strong vinegar-like odor. Institute emergency procedures if overdose occurs: gastric lavage, induction of emesis, activated charcoal, supportive therapy. 2. Clopilet Generic name:clopidogrel Pharmacologic category: antiplatelet agent Pregnancy category: B Mechanism of action Clopidogrel inhibits platelet aggregation by irreversibly inhibiting the adenosine diphosphate (ADP) pathway for platelet activation, thus suppressing the activation of the glycoprotein IIb/IIIa receptor. Unlike aspirin (ASA), clopidogrel does not affect the cyclo-oxygenase pathway and thromboxane-A2. Indications Clopidogrel is indicated for:
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 Prevention of vascular ischemic events in patients with symptomatic athelosclerosis Acute coronary syndrome without ST-segment elevation, ST elevation MI (STEMI) It is also used, along with aspirin, for the prevention of thrombosis after placement of intracoronary stent or as an alternative antiplatelet drug for patients who are intolerant to aspirin. Contraindications Hypersensitivity Active pathological bleeding Coagulation disorder Precautions to be taken Patient with risk of bleeding Patients with peptic ulcer disease, trauma or surgery. Concurrent treatment with other antiplatelate drugs. Adverse reactions GI: abdominal pain, vomiting, dyspepsia, gastritis and constipation. CV: chest pain, oedema, hypertension. CNS: headache, dizzininess, depression, fatigue. Dermatologic: rash, pruritus. Drug interactions Toxicity A high concentrations, clopidogrel may interfere with the metabolism of amiodarone, cisapride, cyclosporine, phenytoin, quinidine, verapamil, diltiagem, oral hypoglycemic and some NSAIDs. Clopidogrel and naproxen resulted in an increase of GI occult blood loss. Decreased effect Atrovastatin may attenuate the effects of clopidogrel. Some antibiotics may also attenuate the effect of this drug.(clarithromycin, erythromycin etc.) Dosage Oral adults Recent MI, recent stroke or established arterial disease: 75mg once daily Acute coronary syndrome: 300mg loading dose, followed by 75mg OD (in combination with aspirin 75-325mg po OD) Prevention of coronary artery bypass graft closure (saphenous vein) aspirin allergic patients (unlabeled use): loading dose 300mg 6hours following procedure; maintanance 50100mg po per day. Nursing management Assessment Assessment of bleeding, periodic platelets count, neutrophil counts if there are signs of infection.
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Implementation Administer routinely to maximize therapeutic effects. Give the drug with food to minimize GI irritation. Teach patient and family importance of informing to health care professionals about its use specially before dental and surgical procedure. Instruct the patient to prevent injury. Injection Clexane Generic name: Enoxaparin Pregnancy category:B Drug classes: Low-molecular-weight heparin Antithrombotic agent Therapeutic action Low molecular weight heparin that inhibits thrombus and clot formation by blocking factor Xa, factor IIa, preventing the formation of clots. Indications Prevention of deep vein thrombosis, which may lead to pulmonary embolism following hip replacement, knee replacement surgery, abdominal surgery. Prevention of ischemic complications of unstable angina and non---Q-wave MI Treatment of deep vein thrombosis (DVT), pulmonary embolus with warfarin. Prevention of deep vein thrombosis in medical patients who are at risk for thromboembolic complications due to severely restricted mobility during acute illnesses. Contraindications/cautions Contraindications: hypersensitivity to enoxaparin, heparin, pork products; severe thrombocytopenia; uncontrolled bleeding.

Use cautiously with pregnancy or lactation, history of GI bleeding.

Dosage Available Forms: Injection--30 mg/0.3 mL; 40 mg/0.4 mL; 60 mg/0.6 mL; 80 mg/0.8 mL; 100 mg/1 mL Adult: DVT prophylaxis: 30 mg SC bid initial dose soon as possible after surgery, not more than 24 h. Continue throughout the postoperative period for 7---10 d; then 40 mg qd SC for up to 3 wk may be used. Patients undergoing abdominal surgery: 40 mg/d SC begun within 2 h preop for 7---10 d. Outpatient DVT treatment: 1 mg/kg SC q12h. Unstable angina/ non---Q-wave MI: 1 mg/kg SC q12h for 2---8 d.

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Pediatric: Safety and efficacy not established. Adverse effects Hematologic: Haemorrhage; bruising; thrombocytopenia; elevated AST, ALT levels; hyperkalemia Hypersensitivity: Chills, fever, urticaria, asthma Other: Fever; pain; local irritation, hematoma, erythema at site of injection Drug interactions Increased bleeding tendencies with oral anticoagulants, salicylates, penicillins, cephalosporins Increased AST, ALT levels Drug-alternative therapy o Increased risk of bleeding if combined with chamomile, garlic, ginger, gingko, and ginseng therapy Nursing management Assessment History: Recent surgery or injury; sensitivity to heparin, pork products, enoxaparin; lactation; history of GI bleed; pregnancy Physical: Peripheral perfusion, R, stool guaiac test, PTT or other tests of blood coagulation, platelet count, kidney function tests Implementation Give drug as soon as possible after hip surgery, within 12 h of knee surgery, and within 2 h preop for abdominal surgery. Give deep SC injections; do not give enoxaparin by IM injection. Administer by deep SC injection; patient should be lying down. Alternate between the left and right anterolateral and posterolateral abdominal wall. Introduce the whole length of the needle into a skin fold held between the thumb and forefinger; hold the skin fold throughout the injection. Apply pressure to all injection sites after needle is withdrawn; inspect injection sites for signs of hematoma; do not massage injection sites. Do not mix with other injections or infusions. Store at room temperature; fluid should be clear, colorless to pale yellow. Provide for safety measures (electric razor, soft toothbrush) to prevent injury to patient who is at risk for bleeding. Check patient for signs of bleeding; monitor blood tests. Alert all health care providers that patient is on enoxaparin. Discontinue and initiate appropriate therapy if thromboembolic episode occurs despite enoxaparin therapy. Have protamine sulfate (enoxaparin antidote) on standby in case of overdose.
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Treat overdose as follows: Protamine sulfate (1% solution). Each mg of protamine neutralizes 1 mg enoxaparin. Give very slowly IV over 10 min.

Metop Generic name: metroprolol tartrate Pregnancy category: B Drug classes: 1-selective adrenergic blocker, antihypertensive. Therapeutic action Competitively blocks -adrenergic receptors in the heart and juxtaglomerular apparatus, decreasing the influence of the sympathetic nervous system on these tissues and the excitability of the heart, decreasing cardiac output and the release of renin, and lowering BP; acts in the CNS to reduce sympathetic outflow and vasoconstrictor tone. Indications Hypertension, alone or with other drugs, especially diuretics Prevention of reinfarction in MI patients who are hemodynamically stable or within 3---10 d of the acute MI (immediate-release tablets and injection) Treatment of angina pectoris Contraindications/cautions Contraindications: sinus bradycardia (HR < 45 beats/min), second or third-degree heart block (PR interval > 0.24 sec), cardiogenic shock, CHF, systolic BP < 100 mm Hg; lactation. Use cautiously with diabetes or thyrotoxicosis; asthma or COPD; pregnancy. Dosage Available Forms: Tablets--50, 100 mg; ER tablets--50, 100, 200 mg; injection--1 mg/mL Adult Hypertension: Initially 100 mg/d PO in single or divided doses; gradually increase dosage at weekly intervals. Usual maintenance dose is 100---450 mg/d. Angina pectoris: Initially 100 mg/d PO in 2 divided doses; may be increased gradually, effective range 100---400 mg/d. MI, early treatment: Three IV bolus doses of 5 mg each at 2-min intervals with careful monitoring. If these are tolerated, give 50 mg PO 15 min after the last IV dose and q6h for 48 h. Thereafter, give a maintenance dosage of 100 mg PO bid. Reduce initial PO doses to 25 mg, or discontinue in patients who do not tolerate the IV doses. MI, late treatment: 100 mg PO bid as soon as possible after infarct, continuing for at least 3 mo and possibly for 1--3 y. Extended-release tablets
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Hypertension: 50---100 mg/d PO as one dose. Angina: 100 mg/d PO as one dose. Pediatric: Safety and efficacy not established. IV Preparation: No additional preparation is required. Infusion: Inject directly into vein or into tubing of running IV over 1 min. Inject as a bolus; monitor carefully; wait 2 min between doses; do not give if bradycardia of <45 beats/min, heart block, systolic pressure <100 mm Hg. Incompatibilities: Do not mix with amino acids, aztreonam, dopamine.

Adverse effects CNS: Dizziness, vertigo, tinnitus, fatigue, emotional depression, paresthesias, sleep disturbances, hallucinations, disorientation, memory loss, slurred speech GI: Gastric pain, flatulence, constipation, diarrhoea, nausea, vomiting, anorexia, ischemic colitis, renal and mesenteric arterial thrombosis, retroperitoneal fibrosis, hepatomegaly, acute pancreatitis CV: CHF, cardiac arrhythmias, peripheral vascular insufficiency, claudication, CVA, pulmonary oedema, hypotension Respiratory: Bronchospasm, dyspnoea, cough, bronchial obstruction, nasal stuffiness, rhinitis, pharyngitis GU: Impotence, decreased libido, Peyronie's disease, dysuria, nocturia, frequent urination Musculoskeletal: Joint pain, arthralgia, muscle cramp EENT: Eye irritation, dry eyes, conjunctivitis, blurred vision Dermatologic: Rash, pruritus, sweating, dry skin Allergic: Pharyngitis, erythematous rash, fever, sore throat, laryngospasm Other: Decreased exercise tolerance, development of antinuclear antibodies (ANA), hyperglycaemia or hypoglycemia, elevated serum transaminase, alkaline phosphatase Interactions o Increased effects of metoprolol with verapamil, cimetidine, methimazole, propylthiouracil o Increased effects of both drugs if metoprolol is taken with hydralazine o Increased serum levels and toxicity of IV lidocaine, if given concurrently o Increased risk of postural hypotension with prazosin o Decreased antihypertensive effects if taken with NSAIDs, clonidine, rifampin. o Decreased therapeutic effects with barbiturates o Hypertension followed by severe bradycardia if given concurrently with epinephrine o Possible false results with glucose or insulin tolerance tests (oral) Nursing Considerations
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Assessment History: Sinus bradycardia (HR < 45 beats/min), second or third-degree heart block (PR interval > 0.24 sec), cardiogenic shock, CHF, systolic BP < 100 mm Hg; diabetes or thyrotoxicosis; asthma or COPD; lactation Physical: Weight, skin condition, neurologic status, P, BP, ECG, respiratory status, kidney and thyroid function, blood and urine glucose Implementation Do not discontinue drug abruptly after chronic therapy (hypersensitivity to catecholamines may have developed, causing exacerbation of angina, MI, and ventricular arrhythmias). Taper drug gradually over 2 wk with monitoring. Ensure that patient swallows the ER tablets whole; do not cut, crush, or chew. Consult physician about withdrawing drug if patient is to undergo surgery (controversial). Give oral drug with food to facilitate absorption. Provide continual cardiac monitoring for patients receiving IV metoprolol.

Telma Generic name: Telmisartan Drug class: angiotensin II receptor blocker. Prgnancy category:C Therapeutic action Angiotensin II acts as a vasoconstrictor. In addition to causing direct vasoconstriction, angiotensin II also stimulates the release of aldosterone. Once aldosterone is released, sodium as well as water are reabsorbed. The end result is elevation of blood pressure. Telmisartan is a nonpeptide AT1 angiotensin II receptor antagonist. This binding prevents angiotensin II from binding to the receptor thereby blocking the vasoconstriction and the aldosterone secreting effects of angiotensin II. Indications Treatment of hypertension Prevention of MI. Contraindications Hypersensitivity to telmisartan or any component of formulation. Bilateral renal artery stenosis. Pregnancy 2nd and 3rd trimester. Dosage Adults: oral initial 40mg OD, usual maintenance dose 20-80mg/day. Nursing management of patient taking telmisartan. Assessment

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Take medical history, especially of: kidney disease, liver disease, high blood levels of potassium, severe dehydration (and loss of electrolytes such as sodium). Implementation Observe for hypersensitive reaction. Observe signs of an allergic reaction: hives; difficulty breathing; swelling of your face, lips, tongue, or throat. Inform to doctor immediately if muscle pain, tenderness, or weakness especially if you also have fever, nausea or vomiting, and dark colored urine. Ask the patient to limit alcoholic beverages. Tell the patient that;this drug may make you dizzy. Do not drive, use machinery, or do any activity that requires alertness until you are sure you can perform such activities safely.

Esorol Generic name: Esomeprazole Drug category: proton pump inhibitor. Pregnancy category: B Therapeutic action Suppresses gastric acid secretion by inhibition of the H+/K+ ATPase in the gastric parietal cell. Indications Oral/IV Short term treatment of erosive esophagitis. Treatment of symptomatic gastro esophageal reflux diseases(GERD). Multidrug regimen for helicobacter pylori. Prevention of gastric ulcer associated with long term use of NSAIDs. Zollinger- Ellision syndrome. Contraindications Hypersensitivity. Precautions Presence of gastric malignancy. Dosage GERD without Erosive Esophagitis 20 mg PO qDay x4 weeks 20-40 mg qDay IV up to 10 days, switch to PO once patient able to swallow. GERD with Erosive Esophagitis Treatment: 20-40 mg PO qDay x4-8 weeks Maintenance: 20 mg PO qDay up to 6 months 20-40 mg qDay IV up to 10 days, switch to PO once patient able to swallow H. pylori Eradication
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Indicated for combination therapy (with amoxicillin and clarithromycin) to eradicate H. pylori in patients with duodenal ulcer 40 mg PO qDay x 10 d, WITH amoxicillin 1000 mg PO BID, PLUS clarithromycin 500 mg PO BID x 10 days Risk Reduction of NSAID-Associated Gastric Ulcer 20-40 mg PO qDay x up to 6 month Zollinger-Ellison Syndrome 60 mg PO qDay (initial) up to 100 mg PO qDay, OR 60 mg PO BID Pediatric dosage Oral <1 year old: Safety and efficacy not established. 1-11 years old: 10-20 mg PO qDay x up to 8 weeks 12-17 years old: 20-40 mg PO qDay x up to 8 weeks IV Indicated for short-term treatment of GERD with erosive esophagitis when oral therapy is not possible or appropriate. <1 month: Safety and efficacy not established. 1 month-1 year: 0.5 mg/kg IV qDay 1 year or older (<55 kg): 10 mg IV qDay 1 year or older (55 kg or more): 20 mg IV qDay Infuse IV over 10-30 minutes. Administration If patient unable to swallow capsule whole, capsule can be opened, emptied on applesauce, mixed & swallowed immediately Infuse IV over 10-30 min OR not less than 3 min IV injection. Nursing management of patients receiving esomeprazole Administer in empty stomach.

Loree Generic name: lorazepam. Drug classes: Benzodiazepine, Antianxiety agent, Sedative/hypnotic.

Pregnancy category: D
Therapeutic actions Exact mechanisms are not understood; acts mainly at subcortical levels of the CNS, leaving the cortex relatively unaffected. Main sites of action may be the limbic system and reticular

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formation; benzodiazepines potentiate the effects of GABA, an inhibitory neurotransmitter; anxiolytic effects occur at doses well below those necessary to cause sedation and ataxia. Indications Management of anxiety disorders or for short-term relief of symptoms of anxiety or anxiety associated with depression (oral). Preanesthetic medication in adults to produce sedation, relieve anxiety, and decrease recall of events related to surgery (parenteral). Unlabeled parenteral use--management of status epilepticus, chemotherapy-induced nausea and vomiting, acute alcohol withdrawal Contraindications/cautions Contraindications: hypersensitivity to benzodiazepines, propylene glycol, polyethylene glycol or benzyl alcohol (parenteral lorazepam); psychoses; acute narrow-angle glaucoma; shock; coma; acute alcoholic intoxication with depression of vital signs; pregnancy (crosses placenta; risk of congenital malformations and neonatal withdrawal syndrome); labor and delivery ("floppy infant" syndrome); and lactation. Use cautiously with impaired liver or kidney function or debilitation. Dosage Available Forms: Injection--2, 4 mg/mL; oral solution--2 mg/mL; tablets--0.5, 1, 2 mg Adult Oral: Usual dose is 2---6 mg/d; range 1---10 mg/d given in divided doses with largest dose hs. Insomnia due to transient stress: 2---4 mg given hs. IM: 0.05 mg/kg up to a maximum of 4 mg administered at least 2 h before operative procedure. IV: Initial dose is 2 mg total or 0.044 mg/kg, whichever is smaller. Do not exceed this dose in patients older than 50 y. Doses as high as 0.05 mg/kg up to a total of 4 mg may be given 15 to 20 min before the procedure to those benefitted by a greater lack of recall. Pediatric: Drug should not be used in children < 12 y. Geriatric Patients or Those With Debilitating Disease: Initially, 1 to 2 mg/d in divided doses. Adjust as needed and tolerated. IV Preparation: Dilute lorazepam immediately prior to IV use. For direct IV injection or injection into IV line, dilute with an equal volume of compatible solution (Sterile Water for Injection, Sodium Chloride Injection, or 5% Dextrose Injection); do not use if solution is discoloured or contains a precipitate. Protect from light; refrigerate. Infusion: Direct inject slowly, or infuse at maximum rate of 2 mg/min. Y-site Incompatibilities: Do not mix with foscarnet, ondansetron. Adverse effects

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CNS: Transient, mild drowsiness initially; sedation, depression, lethargy, apathy, fatigue, lightheadedness, disorientation, anger, hostility, episodes of mania and hypomania, restlessness, confusion, crying, delirium, headache, slurred speech, dysarthria, stupor, rigidity, tremor, dystonia, vertigo, euphoria, nervousness, difficulty concentrating, vivid dreams, psychomotor retardation, extrapyramidal symptoms; mild paradoxical excitatory reactions during first 2 wk of treatment GI: Constipation, diarrhoea, dry mouth, salivation, nausea, anorexia, vomiting, difficulty in swallowing, gastric disorders, hepatic dysfunction CV: Bradycardia, tachycardia, CV collapse, hypertension and hypotension, palpitations, oedema Hematologic: Elevations of blood enzymes: LDH, alkaline phosphatase, AST, ALT; blood dyscrasias: agranulocytosis, leukopenia GU: Incontinence, urinary retention, changes in libido, menstrual irregularities EENT: Visual and auditory disturbances, diplopia, nystagmus, depressed hearing, nasal congestion Dermatologic: Urticaria, pruritus, skin rash, dermatitis Other: Hiccups, fever, diaphoresis, paresthesias, muscular disturbances, gynecomastia. Drug dependence with withdrawal syndrome when drug is discontinued; more common with abrupt discontinuation of higher dosage used for longer than 4 mo. Drug interactions Increased CNS depression with alcohol Decreased effectiveness with theophyllines Nursing Considerations Assessment History: Hypersensitivity to benzodiazepines, propylene glycol, polyethylene glycol or benzyl alcohol; psychoses; acute narrow-angle glaucoma; shock; coma; acute alcoholic intoxication with depression of vital signs; pregnancy; lactation; impaired liver or kidney function, debilitation Physical: Skin color, lesions; T; orientation, reflexes, affect, ophthalmologic exam; P, BP; R, adventitious sounds; liver evaluation, abdominal exam, bowel sounds, normal output; CBC, liver and renal function tests Implementation Do not administer intra-arterially; arteriospasm, gangrene may result. Give IM injections of undiluted drug deep into muscle mass, monitor injection sites. Do not use solutions that are discoloured or contain a precipitate. Protect drug from light, and refrigerate solution. Keep equipment to maintain a patent airway on standby when drug is given IV. Reduce dose of narcotic analgesics by at least half in patients who have received parenteral lorazepam.

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Keep patients who have received parenteral doses under close observation, preferably in bed, up to 3 h. Do not permit ambulatory patients to drive following an injection. Taper dosage gradually after long-term therapy, especially in epileptic patients.

Glimepride Drug classes: Antidiabetic agent, Sulfonylurea (second generation).

Pregnancy category: B

Therapeutic actions Stimulates insulin release from functioning cells in the pancreas; may improve binding between insulin and insulin receptors or increase the number of insulin receptors; thought to be more potent in effect than first-generation sulfonylureas. Indications As an adjunct to diet to lower blood glucose in patients with type 2 diabetes mellitus whose hypoglycemia cannot be controlled by diet alone. In combination with insulin to better control glucose in insulin-dependent diabetics. Contraindications/cautions Contraindications: allergy to sulfonylureas; diabetes complicated by fever, severe infections, severe trauma, major surgery, ketosis, acidosis, coma (insulin is indicated in these conditions); Type 1 or juvenile diabetes, serious hepatic or renal impairment, uremia, thyroid or endocrine impairment, glycosuria, hyperglycaemia associated with primary renal disease; labor and delivery--if glimepiride is used during pregnancy, discontinue drug at least 1 mo before delivery; lactation, safety not established. Dosage Available Forms: Tablets--1, 2, 4 mg Adult: Usual starting dose is 1---2 mg PO once daily with breakfast or first meal of the day; usual maintenance dose is 1---4 mg PO once daily, depending on patient response and glucose levels. Do not exceed 8 mg/d. Combination with insulin therapy: 8 mg PO qd with first meal of the day with low-dose insulin. Transfer from other hypoglycemic agents: No transition period is necessary. Pediatric: Safety and efficacy not established. Renal Impaired: Usual starting dose is 1 mg PO once daily; titrate dose carefully, lower maintenance doses may be sufficient to control blood sugar.
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Adverse effects CV: Increased risk of cardiovascular mortality (possible) GI: Anorexia, nausea, vomiting, epigastric discomfort, heartburn, diarrhoea Hematologic: Leukopenia, thrombocytopenia, anaemia Endocrine: Hypoglycemia Hypersensitivity: Allergic skin reactions, eczema, pruritus, erythema, urticaria, photosensitivity, fever, eosinophilia, jaundice Drug interaction Increased risk of hypoglycemia with sulfonamides, chloramphenicol, oxyphenbutazone, phenylbutazone, salicylates, clofibrate. Decreased effectiveness of both glimepiride and diazoxide if taken concurrently. Increased risk of hyperglycaemia with rifampin, thiazides. Risk of hypoglycemia and hyperglycaemia with ethanol; "disulfiram reaction" has also been reported. Drug-alternative therapy. Increased risk of hypoglycemia if taken with juniper berries, ginseng, garlic, fenugreek, coriander, dandelion root, celery Nursing Considerations Assessment History: Allergy to sulfonylureas; diabetes complicated by fever, severe infections, severe trauma, major surgery, ketosis, acidosis, coma (insulin is indicated in these conditions); type 1 or juvenile diabetes, serious hepatic or renal impairment, uremia, thyroid or endocrine impairment, glycosuria, hyperglycaemia associated with primary renal disease; pregnancy Physical: Skin color, lesions; T; orientation, reflexes, peripheral sensation; R, adventitious sounds; liver evaluation, bowel sounds; urinalysis, BUN, serum creatinine, liver function tests, blood glucose, CBC. Implementation Monitor urine or serum glucose levels frequently to determine effectiveness of drug and dosage being used. Transfer to insulin therapy during periods of high stress (infections, surgery, trauma, etc.). Use IV glucose if severe hypoglycemia occurs as a result of overdose. Arrange for consultation with dietitian to establish weight-loss program and dietary control. Arrange for thorough diabetic teaching program, including disease, dietary control, exercise, signs and symptoms of hypoglycemia and hyperglycaemia, avoidance of infection, hygiene. Isodril
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Generic name:Isosorbide Dinitrate Pregnancy category: C Drug class: Antianginal agent, Nitrate. Therapeutic actions Relaxes vascular smooth muscle with a resultant decrease in venous return and decrease in arterial BP, which reduces left ventricular workload and decreases myocardial oxygen consumption. Indications Treatment and prevention of angina pectoris

Contraindications/cautions Allergy to nitrates, severe anaemia, head trauma, cerebral haemorrhage, hypertrophic cardiomyopathy, pregnancy, lactation. Dosage Available Forms: Tablets --10, 20, 30, 40 mg; ER tablets--40, 60 mg; ER capsules--40 mg; SL tablets--2.5, 5, 10 mg; chewable tablets--5, 10 mg Adult Angina pectoris: Starting dose: 2.5---5 mg sublingual, 5-mg chewable tablets, 5- to 20-mg oral tablets or capsules. Maintenance: 10---40 mg q6h oral tablets or capsules; sustained release, initially 40 mg, then 40--80 mg PO q8---12h. Acute prophylaxis: Initial dosage: 5---10 mg sublingual or chewable tablets q2---3h. Pediatric: Safety and efficacy not established. Adverse effects CNS: Headache, apprehension, restlessness, weakness, vertigo, dizziness, faintness GI: Nausea, vomiting, incontinence of urine and feces, abdominal pain CV: Tachycardia, retrosternal discomfort, palpitations, hypotension, syncope, collapse, postural hypotension, angina Dermatologic: Rash, exfoliative dermatitis, cutaneous vasodilatation with flushing Other: Muscle twitching, pallor, perspiration, cold sweat Drug interaction Increased systolic BP and decreased antianginal effect if taken concurrently with ergot alkaloids Drug-lab test:False report of decreased serum cholesterol if done by the Zlatkis-Zak color reaction Nursing Considerations
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CLINICAL ALERT! Name confusion has occurred between Isordil (isosorbide) and Plendil (felodipine); use caution. Assessment History: Allergy to nitrates, severe anaemia, GI hypermobility, head trauma, cerebral haemorrhage, hypertrophic cardiomyopathy, pregnancy, lactation Physical: Skin color, temperature, lesions; orientation, reflexes, affect; P, BP, orthostatic BP, baseline ECG, peripheral perfusion; R, adventitious sounds; liver evaluation, normal output; CBC, Hgb.

Implementation Give sublingual preparations under the tongue or in the buccal pouch; encourage the patient not to swallow. Give chewable tablets slowly, only 5 mg initially because severe hypotension can occur; ensure that patient does not chew or crush sustained-release preparations. Give oral preparations on an empty stomach, 1 h before or 2 h after meals; take with meals if severe, uncontrolled headache occurs. Maintain life support equipment on standby if overdose occurs or cardiac condition worsens. Gradually reduce dose if anginal treatment is being terminated; rapid discontinuation can lead to problems of withdrawal.

APPLICATION OF NURSING THEORY

Henderson's definition of nursing Introduction Virginia Henderson graduated from the army school of nursing in 1921. In 1926, she was awarded BS and MA degrees in nursing education from teacher's college, Columbia university, New York City. Her interest in nursing evolved from helping sick and wounded military personnel during world war I. Henderson has received much recognition, including honorary doctoral degrees during her career in nursing practice and education. Definition of Nursing 1. General information Henderson views her work as a philosophical statement rather than a theory because the term theory was not used at the time she formulated her ideas. In her definition, Henderson emphasizes the care of both sick and well individuals; she was one of the first theorists to include spiritual aspects of nursing care.
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According to Henderson, the nurse assists the patient with essential activities to maintain health, recover from illness, or achieve a peaceful death. The patient's independence is an important criterion for health. She identifies 14 basic needs that form the components of nursing care; the nurse helps the patient to meet these needs. Henderson's 14 components are closely parallel to those of Maslow; 1 to 7 relates to physiology, 8and 9 relates to safety, 10 relates to self-esteem, 10 and 11 relate to love and belonging, and 11 to 14 relate to self actualization. Considered together, the 14 basic needs provide a holistic approach to nursing. 2. Henderson's basic needs Breathe normally Eat and drink adequately Eliminate body wastes Move and maintain desirable position Sleep and rest Select suitable clothing Maintain body temperature Maintain body cleanliness and grooming Avoid dangers in the environment. Communicate with others to express emotions, needs fears or opinions. Worship according to one's faith. Work in a way that provides sense of accomplishment. Play or participates in various forms of recreation. Learn, discover or satisfy the courtesy that leads to normal development and health. Henderson's definition and the four concepts of the nursing metaparadism. A. Person Is viewed by Henderson as an individual requiring assistance to achieve health and independence or a peaceful death; the person and family are viewed as a unit. Is affected by both body and mind. Consists of biological, psychological, sociological and spiritual components. Is either sick or well and strives toward a state of independence. Has certain basic needs for survival. Need strength, will, or knowledge to perform activities necessary for healthy living. B. Environment Is not specifically defined by Henderson. Involves the relationship one shares with one`s family. Also involves the community and its responsibility for providing health care; Henderson believes the society wants and expects nurse to provide a service to

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individuals incapable of functioning independently, but in return , she expects society to contribute to nursing education. Can be controlled by healthy individuals; illness may interferes with this ability. Can affect health; personal personal and physical factors play a role in person`s wellbeing. C. Health Refers to an individual`s ability to function independently in relationship to the 14 basic needs. Is a quality of life that is basic to human functioning. Requires strength, will or knowledge. D. Nursing Is defined by Henderson as primarily assisting a sick or well individual to perform activities that contribute to health or peaceful death; the person with sufficient strength, will or knowledge would perform these activities unaided. Helps a person be independent of assistance as soon as possible or achieve a peaceful death. Requires working independently with other members of health care team; the nurse functions independently of the physician but uses the physician`s plan of care to provide holistic care to the patient. Requires basic knowledge of social sciences and humanities; this pioneering belief, which lead to baccalaureate education as the basic training for nurses. Requires knowledge of social costumes and religious practices to assess areas of possible conflict or unmet human needs. Helps the patient to meet the 14 basic needs through the formation of nurse patient relationship ; Henderson identified three levels of nursing function- substitute, helper or partner. Is a logical approach of problem solving that results in individualized care. Involves the use of a written nursing care plan. Assessment Assessment is based on 14 basic needs a. Patient has difficulty in breathing because of chest pain. b. Eating and drinking adequately c. Needs help in elimination because of strict bed rest. d. Moving and maintaining comfortable position in bed. e. Sleep alteration because of hospitalization. f. Wearing suitable clothing. g. Maintaining body temperature. h. Needs assistance in cleanliness and grooming because of bed rest. i. No dangers in environment j. Communicating normally.
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k. Putting tika at forehead which was brought from home after worship. l. No sense of accomplishment of work because of bed rest. m. Not participating in various forms of recreation because he was in intensive cardiac care unit. n. Satisfied from our wishes like Namaste. Nursing diagnosis Difficulty in breathing related to chest pain. Difficulty initiating sleep related to hospitalization. Difficulty in maintaining personal hygiene related to strict bed rest. Nursing care plan is explained below. Intervention and evaluation is done in nursing care plan.

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NURSING CARE PLAN

SN ASSESSMENT 1. Subjective data: patient complains pain. Objective data: increased BP, Pulse, facial expression of patient. NURSING DIAGNOSIS Acute pain related to decreased coronary blood flow. GOAL Patient`s pain will relieve within half hour. INTERVENTION 1. Assess for location, duration, intensity, and radiation. 2. Assess blood pressure, pulse, and respiration. 3. Obtain ECG as ordered. 4. Administer oxygen as ordered. 5. Instruct patient to report pain at first onset. 6. Instruct patient to rest during pain. 7. Remain with patient during chest pain until it is relieved. 8. Explain and assist with alternative pain relief measures: Positioning Diversional activities Relaxation techniques Medicate as ordered. RATIONAL 1. Identifies type and severity of pain. 2. Vital signs may elevate episodes of pain. 3. Identifies location of infarction or ischemia. 4. Helps prevent hypoxia. 5. Helps control pain quickly to prevent further ischemia. 6. Activity increases oxygen demand and can increase chest pain. 7. Provides comfort and reassurance to decrease anxiety and fear. 8. These measures help decrease painful stimuli, allowing the patient to focus on other things. Helps eliminate pain. EVALUA TION Goal was fully met. Patient`s pain was relieved after 20 minutes.

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SN ASSESSMENT 2 Subjective data: patient did not express knowledge regarding care of diabetes and patient is using alcohol regularly. Objective data: patient`s blood sugar is 231mgper dl one reading and glycosurea.

NURSING DIAGNOSIS Risk for ineffective health maintenance related to knowledge deficit

GOAL Patient`s knowledge will be increased after one hour regarding care of diabetes.

INTERVENTION 1. Assess knowledge of diabetes selfcare. 2. Assist patient to collaborate with health care provider to determine appropriate blood glucose levels and action to be taken if glucose levels are too high or too low. 3. Teach patient to assess glucose levels before meals and at bedtime or as ordered by health care provider. Ensure that patient knows how to obtain glucose monitor and instruction for home use. 4. Teach patient to administer insulin or oral hypoglycemic agent 30 minutes before meals (_15 minutes if patient is using Lispro). Ensure that meal is begun within 30 minutes of medication. 5. Consult with dietitian for nutrition therapy instruction.

RATIONAL 1. Teaching should be initiated only if a knowledge deficit exists. 2. Appropriate blood glucose levels are different for each patient and should be determined on an individualized basis. The patient should know what blood glucose levels require notification of the health care provider. 3. Good blood glucose control depends on knowledge of glucose levels and trends. 4. The onset of most diabetes medication is about 30 minutes . If more than 30 minutes passes before a meal, the patient might experience hypoglycemia. 5. The dietitian is trained to provide in-depth meal plan instruction.

EVALUATI ON Goal was fulfilled that patient verbalized knowledge regarding diabetes and asking about timing to consult dietitian.

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SN ASSESSMENT 3 Subjective data: patient`s complain about sleeplessness. Objective data: patient looks fatigue.

NURSING DIAGNOSIS Disturbed sleep pattern related to hospitalization

GOAL Patient will sleep easily and look fresh till next day.

INTERVENTION 1. Identify barriers to sleep.

RATIONAL 1. Anxiety, nocturia, diuretics, orthopnea, or paroxysmal nocturnal dyspnoea can make sleep difficult. 2. Comfortable position promotes sleep.

2. Assist patient in identifying positions of comfort for sleeping. 3. Encourage patient to recline for 30 to 60 minutes before bedtime.

EVALUATI ON Goal was partially met that patient slept more hours than previous day but not slept full night.

4. Give anxiolytic as doctor`s order. 5. Maintain quiet environment

3. Reclining before bedtime redistributes fluid and increases voiding that can occur before going to sleep instead of after going to sleep. 4. To facilitate in initiating sleep. 5. To facilitate sleep.

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Progress Report On admission Sunday 2011.12.04 Patient received from emergency. On admission Patient's general condition was fair. Chest pain and shortness of breath was present. Patient was hemodynamically stable without inotropic support. Spo2 was maintained with oxygen 5l/min via facemask.CK-MB was 61U/l before 6hrs of CCU admission and 13U/l at the time of admission. In the evening at 7pm, random blood sugar was found 231mg/dl by glucometer. So, regular insulin 10 unit was given. Patient was planned for angiography. On Monday 2011.12.05 Patient's general condition was fair. Chest pain was relieved oxygen removed and kept in room air. Patient was hemodynamically stable without inotrops and spo2 was maintained in room air. Patient was strict bed rest. Total intake of last day was 650ml since hospitalization and output was 2950ml. Random blood sugar : 110mg/dl Pulse:70/min Blood pressure:130/70 mm/hg. Spo2:96% in room air. CK-MB:14U/l Patient was prepared for angiography, and angiography was done. Report was normal Post angiography ECG Ventricular rate 55bpm PR interval 186ms QRS duration 90ms QT/QTc interval 402/391. Blood pressure 130/80mm/hg Pulse 60bpm Respiration 14/min On Tuesday Patient was hemodynamically stable without inotropic support. Spo2 was maintained in room air, no need of oxygen. Random blood sugar was maintained. Patient was mobilized. ECG Ventricular rate: 54bpm PR interval: 152ms QRS 355 ms QT/QTc 410/397. Random blood sugar 122mg/dl
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Vital signs Temperature 980F Pulse 60/min Respiration 12/min Blood pressure 120/70mm/Hg Total intake last 24 hours 500ml Total output last 24 hours 950ml. Planned for discharge.

DISCHARGE TEACHING
1. Diet Taught about diet that needed for healthy heart. Like unsaturated fat, fish instead of meat, avoid fatty meat, use of sunflower oil. Encourage eat of whole grains, green leafy vegetables, Drinking a moderate amount of alcohol (up to 1 serving per day for women, up to 2 servings per day for men) with food does not affect blood sugar levels significantly. So, advice to limit alcohol. Use low salt diet 2. Exercise regularly Regular exercise helps improve heart muscle function and keeps blood flowing through arteries. It can also reduce the risk of acute coronary syndrome by helping to achieve and maintain a healthy weight, and control diabetes, elevated cholesterol and high blood pressure. Exercise doesn't have to be vigorous. For example, walking 30 minutes a day five days a week can improve health. 3. Manage stress To reduce your risk of a heart attack, reduce stress in your day-to-day activities. 4. Consult with doctor regularly. 5. Prevention of complications. Complications of diabetes and hypertension and prevention from them. Discharge teaching was focused by keeping literature in mind. Wednesday Patient was discharged and sent to home.

LEARNING FROM STUDY

Revised about anatomy and physiology of cardiovascular system and pancreas. Learned about disease condition. Learned about process to do case study and write report case study. Revised techniques of history taking and physical examination of patient. Revised some drugs. Got opportunity of observing angiography procedure in cath- Lab. Opportunity to care cardiac patient.
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Opportunity to search and look literatures regarding disease conditions.

CONCLUSION
Madan Gopal Udas, 70 years Male from Dharan-3,Sunsari, Koshi, Nepal, admitted in CCU with diagnosis of Acute Coronary syndrome (ACS) with unstable angina with hypertension with diabetes mellitus type II. He came to hospital with complaint of Chest pain, dry cough and shortness of breath since 3days. Known case of diabetes mellitus type II since 24 years and hypertension since 12 years. He is under antihypertensive and anti diabetic drug regularly. Different investigations including angiography was done, HS-CRP, glycohemoglobin and serum urea cretenine were elevated rest investigations normal. Provide drugs as per prescription, monitored vital signs and provided other nursing care also by applying theory. Patient was improved and discharged from hospital after 3 days of admission. I learned many things from this study which are mentioned above.

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REFERENCES
Books 1. Williams LS, Hopper PD understanding Medical Surgical Nursing 2nd edition,2003 F.A. Davis company. 2. Fauci, Braunwald, Kasper, lango H., Jameson, Loscalzo. Harrison's Principles of Internel Medicine,17th edition;2008The McGraw-Hill Companies. 3. Smeltzer SC, Bare BG Brunner and Suddarths Textbook of Medical Surgical Nursing. 10th edition,Philadephia.Lippincot William and wilkins;2004. 4. Karch AM. Nursing Drug Guide. Lippincott Philadephia New York;2002. 5. Lacy CF, Armstrong LL, Goldman MP, Lance LL Drug Information Handbook. 14th edition, LEXI-COMP APhA;2006. 6. Foster C, Mistry N, Pedi PF, Sharma S. The Washington Manual of Medical Therapies. 33rd edition,Lippincott William Wikins;2010. Web sites 7. http://www.nda.ox.ac.uk/wfsa/html/u10/u1002_01.htm. retrieved on 9th December 2011. 8. http://www.nda.ox.ac.uk/wfsa/html/u10/u1002_02.htm, retrieved on 9th December 2011. 9. http://www.virtualmedicalcentre.com/anatomy/endocrine-system/17. retrieved on 9th December 2011. 10. http://www.mayoclinic.com/health/acute-coronarysyndrome/DS01061/DSECTION=riskfactors. retrieved on 9th December 2011. 11. http://emedicine.medscape.com/article/159383-treatment#aw2aab6b6b5. retrieved on 9th December 2011. 12. http://www.gfmer.ch/TMCAM/Hypertension/Epidemiologic_aspects_hypertension_worl d.htm. retrieved on 15th December 2011. Journals 13. Davie AP, Caesar D, Caruana L, Clegg G, Spiller J, Capewell S, Starkey IR, Shaw TR, McMurray JJ: Outcome from a rapid-assessment chest pain clinic. QJM 1998, 91(5):339-343 14. Lamki LA. Acute Coronary Syndrome, Diabetes and Hypertension. Sultan Qaboos Univ Med J. 2011 August; 11(3): 318321. 15. Esteghamat A, Abbasi M et al. Prevalence of diabetes and other cardiovascular risk factors in an Iranian population with acute coronary syndrome. Cardiovascular Diabetology 2006, 5:15.doi:10.1186/1475-2840-5-15 Available at http://www.cardiab.com/content/5/1/15. 16. http://www.gmc.edu.np/journals/vol1-issu1-jan 08/A_study_of_acute_coronary_syndrome_in_western_region_of_Nepal.pdf

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