A CARE STUDY OF A PATIENT WITH MYOCARDIAL INFARCTION DEMOGRAPHIC DATA Name: Patient x Age: 45Years Old Sex: Male Nationality: Bangladesh Date of Admission: 16Th February 2013 Complaints : chest pain, Palpitation, SOB and Nausea Diagnosis : Anterior wall MI PHYSICAL ASSESSMENT • • • • • • • • • • • • • • • • • • • • General appearance Patient is looking anxious, restless and orient Vital signs T-36.4 c HR-102/ Mt R-30 / MT B P-100/80 mm hg SPO2-95 % in room air SKIN Cold, pale and diaphoretic HEAD Scalp is normal, hair is black EYES No redness, sclera white and clear, pupils reactive to light NOSE Nasal discharge present, nasal septum straight MOUTH Dry mouth and lips, no gum bleeding NECK No palpable lymph nodes • • • • • • • • • • • • • • • • • • • • • CHEST Bilateral chest movement present Tachypnea noted No crackles, no wheezing HEART Tachycardia notes No murmur ABDOMEN Soft to palpate Positive bowel sound Slight abdominal distention GENITALIA No palpable mass Urethral meatus located ventrally on the end of the penis EXTRIMITIES Full range of motion present Ten fingers and 10 toes present PATIENT HISTORY Past medical history No past medical history of DM, HTN, IHD etc. Patient is a known chronic smoker for more than 10 years • Present medical history • Patient X brought to ER by SRC ambulance with the complaints of chest pain radiating to left arm, chest discomfort, palpitation, SOB, and nausea. Received in ER resuscitation room by stretcher.PT is conscious, oriented, pale and diaphoretic .Vitals checked and recorded .Attached to monitor, started oxygen via face mask 3 l/MT .Seen and examined by ER doctor on duty and cardiologist. ECG done and seen. Tab. ASPIRIN 300 MG , Tab PLAVIX 300 MG , Tab atorvastatin 80 mg , Inj. MORPHINE 5mg ,IV , Inj. Ranitidine 50 MG IV , Inj. PREMOSAN 10 mg iv , NTG PUFF X 2 times s/ l , Inj. CLEXINE 40 mg s/c given as per order. For lab investigations CBC, PT, APTT, ELECTROLYTES, RBS, BUN, CREATININE, CK, CKMB, TROPONIN I QUANTITATIVE sent to lab. Patient is admitted in ccu for further management. • SURGICAL HISTORY • Patient x has no past and present surgical history. • TOPIC PRESENTATIONS Myocardial infarction or heart attack is the death or damage of part of the heart muscles (myocardium) because the supply of blood to the heart muscle is severely reduced or stopped. This is most commonly due to blockage of a coronary artery following the rupture of a vulnerable atherosclerotic plaque. • ANATOMY AND PHYSIOLOGY OF THE HEART • The heart is a roughly cone – shaped hollow muscular organ. It is about 10 cm long and is about the size of the owners fist .It weighs about 225 g in women and heavier in men about 310 g. POSITION The heart lies in the thoracic cavity the mediastinum between the lungs. It lies obliquely, a little more to the left than the right, and presents a bas above ,and an apex below. The apex extends to the level of the 5th intercostal space and the base extends to the level of the 2 nd rib ORGANS ASSOCIATED WITH THE HEART • Inferiorly: The apex rest on the central tendon of the diaphragm • Superiorly: The great blood vessel, (the aorta, superior vena cava, pulmonary artery, and pulmonary veins) • Posteriorly: The esophagus, trachea, left and right bronchus, descending aorta, inferior vena cava and thoracic vertebrae • Laterally: The lungs the left lung overlaps the left side of the heart • Anteriorly: The sternum, ribs and intercostal muscles • • • • • • • • • • • STRUCTUTE The heart is composed of three layers of tissue 1. Pericardium 2. Myocardium 3. Endocardium 1 .Pericardium The pericardium is made up of two sacs .The outer sac consists of fibrous tissue and the inner of a continuous double layer of serous membrane 2. Myocardium It is composed of specialized cardiac muscle found only in the heart. It is not under voluntary control. It is thickest at the apex and thins out towards the base. This reflects the amount of work each chamber contributes to the pumping of blood. It is thickest in the left ventricle. 3. Endocardium This forms the lining of the myocardium and the heart valves. It is a thin, smooth, glistening membrane which permits smooth flow of blood inside the heart. • INTERIOR OF THE HEART The heart is divided into a right and left side by the septum. Each side is divided by an atrioventricular valve into an upper chamber, the atrium, and a lower chamber, the ventricles .The right atrioventricular valve (tricuspid valve) has three flaps or cusps and the left atrioventricular valve (mitral valve) has two cusps. The valves between the atria and ventricles open and close passively according to changes in pressure in the chambers. They open when the pressure in the atria is greater than that in the ventricles.the valves are prevented from opening upwards into the atria by tendinous cords, called chordae tendineae, which extends from the inferior surface of the cusps to little projections of myocardium covered with endothelium, called papillary muscles. FLOW OF BLOOD THROUGH THE HEART • The two largest veins of the body, the superior and inferior vena cava, empty their contents in to the right atrium .This blood passes via the right atrio ventricular valve into the right ventricle, and from there it is pumped in to the pulmonary artery or trunk (the only artery in the body which carries deoxygenated blood).The opening of the pulmonary artery is guard by the pulmonary valve, formed by three semilunar cusps. This valve prevents the back flow of blood into the right ventricle when the ventricular muscles relax. After leaving the heart the pulmonary artery divides into left and right pulmonary arteries, which carry the venous blood to the lungs where exchange of gases takes place; co2 is excreted and o2 is absorbed. • Two pulmonary veins from each lung carry oxygenated blood back to the left atrium .Blood then passes through the left atrioventricular valve into the left ventricle ,and from there it is pumped into the aorta ,the first entry of the general circulation .The opening of the aorta is guarded by the aortic valve ,formed by three semilunar cusps. BLOOD SUPPLY TO THE HEART • Coronary circulation is the circulation of blood in the blood vessels of the heart muscles(myocardium).The vessels that deliver o2 rich blood to the myocardium are known as coronary arteries (right and left)which branch from the aorta immediately distal to the aortic valve.The vessels that remove the deoxygenated blood from the heart muscles are known as cardiac veins.The coronary artery that run on the surface of the heart are called EPICARDIAL CORONARY ARTERY.These relatively narrow vessels are commonly affected by atherosclerosis and can become blocked causing angina or heart attack.The coronary arteries are classified as “end circulation”since they represent the only source of blood supply to the myocardium. CONDUCTING SYSTEM OF THE HEART • The heart is an intrinsic system where by the cardiac muscles is automatically stimulated to contract without the need for a nerve supply from the brain .However ,the intrinsic system can be stimulated or depressed by nerve impulses initiated in the brain and by circulating chemicals including hormones • There are small groups of specialized neuromuscular cells in the myocardium which initiate and conduct impulses causing coordinated and synchronized contraction of the heart muscles. • • • • • • • • • SINOATRIAL NODE (SA NODE) This small mass of specialized cells is in the wall of the right atrium near the opening of the superior vena cava. The SA node is the pace maker of the heart because it normally initiate impulses more rapidly than other groups of neuromuscular cells. ATRIOVENTRICULAR NODE (AV NODE) This small mass of neuromuscular tissue is situated in the wall of the atrial septum near the atrioventricular valves .Normally the AV node is stimulated by impulses that sweep over the atrial myocardium. However, it too is capable of initiating impulses that cause contraction but at a slower rate than the SA node. ATRIOVENTRICULAR BUNDLE (AV BUNDLE OR BUNDLE OF HIS) This is a mass of specialized fibers that originate from the AV node. The AV bundle crosses the fibrous ring that separates atria and ventricles then, at the upper end of the ventricular septum, it divides into right and left bundle branches .Within the ventricular myocardium the branches break up into fine fibres, called the purkinje fibres. The AV bundle, bundle branches and purkinje fibres convey electrical impulses from the AV node to the apex of the myocardium where the wave of ventricular contraction begins, then sweeps upwards and out wards, pumping blood into the pulmonary artery and the aorta. NERVE SUPPLY TO THE HEART The vagus nerves (parasympathetic) supply mainly the SA and AV nodes and atrial muscles. Parasympathetic stimulation reduces the rate at which impulses are produced, decreasing the rate and force of the heart beat The sympathetic nerve supply the SA and AV nodes and the myocardium of atria and ventricles .sympathetic stimulation increases the rate and force of the heart beat • FACTORS AFFECTING HEART RATE – – – – – – – – • • • • • • • • • • • • • • • Autonomic nervous system Circulating chemicals Position Exercise Emotional stress Gender Age Temperature THE CARDIAC CYCLE The heart acts as a pump and its action consists of a series of events known as the cardiac cycle. The period of contraction is called systole and that of relaxation is called diastole. STAGES OF CARDIAC CYCLE The normal number of cardiac cycle per minute ranges from 60 to 80.Each cycle last about 0.8 of a second and consist of Atrial systole (contraction of the atria)-0.1 sec Ventricular systole (contraction of the ventricles)-0.3 sec Complete cardiac diastole (relaxation of atria and ventricles)-0.4 sec HEART SOUND Two sounds .They are described in words as LUB DUP. The first sound, LUB, is fairly loud and is due to the closure of the atrioventricular valve. The second sound, DUP, is softer and is due to the closure of the aortic and pulmonary valves ELECTRICAL CHANGES IN THE HEART The normal ECG tracing shows 5 waves, named as P, Q, R, S, and T The p wave arises when the impulses from the SA node sweeps over the atria The QRS complex represents the very rapid spread of the impulses from the AV node through the AV bundle and the purkinjI fiber and the electrical activity of the ventricular muscles The T wave represents the relaxation of the ventricular muscles. • • • • • • • • • • • • • • • • CARDIAC OUTPUT The cardiac output is the amount of blood ejected from the heart .The amount expelled by each contraction of the ventricles is the STROKE VOLUME. Cardiac output=stroke volume x heart rate. ETIOLOGY A Myocardial infarction (MI) results from occlusion of one of the coronary arteries. The occlusion can stem from atherosclerosis, thrombosis, platelet aggregation, or coronary artery stenosis or spasm. Predisposing risk factors include: Aging Diabetes Mellitus Elevated serum triglyceride, low-density lipoprotein, and cholesterol levels, and decreased serum high-density lipoprotein levels Excessive intake of saturated fats, carbohydrates, or salt Hypertension Obesity Positive family history of coronary artery disease Sedentary lifestyle Smoking Stress or a type a personality (aggressive, competitive attitude, addiction to work, chronic impatience). In addition, use of such drugs as amphetamines or cocaine can cause a Myocardial infarction (MI). • SIGNS AND SYMPTOMS • 1. Chest pain • A. Severe, diffuse, steady sub sternal pain; may be described as crushing, squeezing, or dull • B .Not relived by rest or sublingual vasodilator therapy, but requires opioids • C. May radiate to the arms (usually the left), shoulders, neck, back, and/or jaw • D. Continues for more than 15 mts • E. May produce anxiety and fear, resulting in an increase in heart rate, BP, and respiratory rate. • F. Some patients exhibit no complaints of pain • 2. Diaphoresis, cool clammy skin, facial pallor. • 3. Hypertension or hypotension • 4. Bradycardia or tachycardia • 5. Premature ventricular and /or atrial beats. • 6. Palpitations, severe anxiety, dyspnea. • 7. Disorientation,confusion,restlessness. • 8. fainting, marked weakness • 9. Nausea,vomiting,hiccups • 10. Atypical symptions; epigastric or abdominal distress, dull aching or tingling sensations, shortness of breath, extreme fatigue PATHOPHYSIOLOGY INADEQUATE CORONARY BLOOD FLOW MYOCARDIAL ISCHEMIA DEPRESS CARDIC FUNCTION IMBALANCE BETWEEN MYOCARDIAL O2 SUPPLY AND DEMAND PERSISTENT ISCHEMIA TISSUE NECROSIS AND SCAR TISSUE FORMATION PERMANENT LOSS OF MYOCARDIAL CONTRACTILITY CARDIOGENIC SHOCK II. Classification • a. Type of myocardial infarction (MI) can be identified on the electrocardiogram (ECG). a.i. ST-segment elevation (also called STEMI). a.ii. Non-ST elevation b. Location of MI can be identified on the ECG. i. Anterior wall of the ventricle. ii. Inferior wall of the ventricle. iii. Posterior wall of the ventricle. iv. Lateral wall of the ventricle. • Acute anterior myocardial infarction ST elevation in the anterior leads V1 - 6, I and aVL reciprocal ST depression in the inferior leads Acute posterior myocardial infarction • hyperacute) the mirror image of acute injury in leads V1 - 3 • (fully evolved) tall R wave, tall upright T wave in leads V1 -3 • usually associated with inferior and/or lateral wall MI Acute inferior myocardial infarction • ST elevation in the inferior leads II, III and aVF • reciprocal ST depression in the anterior leads Lateral Wall M.I. • Lateral M.I.: ST elevation in V1 through V6 and in Leads I and aVL. Nursing Interventions • Monitor and record the patient's ECG readings, blood pressure, temperature, and heart and breathe sounds. • Assess pain and give an analgesic as ordered. • Record the severity of pain, location, type, and duration of pain. • Check the patient's blood pressure before and after giving nitroglycerin, especially the first dose. • Frequently monitor ECG rhythm strips to detect rate changes and arrhythmias. If any new arrhythmias are documented, if chest pain occurs, or at least every shift change or according to facility protocol. • Obtain ECG readings and blood pressure and pulmonary artery catheter measurements, if applicable, to determine changes. During episodes of chest pain • Watch for crackles, cough, tachypnea, and edema, which may indicate impending left-sided heart failure. • Monitor daily weight, intake and output, respiratory rate, serum enzyme levels, ECG readings, and blood pressure. • Organize patient care and activities to maximize periods of uninterrupted rest. • Provide a clear liquid diet dietary until nausea subsides. A lowcholesterol, low-sodium diet, without caffeine-containing beverages, may be ordered. • Provide a stool softener to prevent straining during defecation, which causes vagal stimulation and may slow heart rate. • Allow the patient to use a bedside commode, and provide as much privacy as possible. • Assist with ROM exercises. • If the patient is immobilized by a severe Myocardial Infarction (MI), turn him often. • Give Antiembolism stockings to prevent venostasis and thrombophlebitis. • Provide emotional support, and help reduce stress and anxiety . • If the patient has undergone PTCA, sheath care is necessary. Keep the sheath line open with a heparin drip. Observe the patient for generalized and site bleeding. Keep the leg with the sheath insertion site immobile. Maintain strict bed rest. Check peripheral pulses in the affected leg frequently. Provide an analgesic for back pain if needed. • After thrombolytic therapy, administer continuous heparin as ordered. Monitor the partial thromboplastin time every 6 hours, and monitor the patient for evidence of bleeding. DIAGNOSTIC TESTS – Blood tests-troponin level, ck, ckmb,myoglobulin ,white blood cell count – Chest x ray – heart monitor – ECG – Angiogram INVESTIGATIONS PATIENT VALUE NORMAL VALUE 0.628 <0.120 TROPONIN 12.90 10-17 SEC PT CONTROL 13.6 0.94 2-4 SEC INR 41.6 26.1-36.3 SEC APTT CONTROL 33.6 5.8 mmol/L 4.1-5.9 mmol/L 2.8 mmol/L 3.2 – 7.1 mmol/L 75 umol/L 46-110 umol/L 141 mmol/L 137-145mmol/L 4.1mmol/L 3.5-5.1 mmol/L RBS UREA CREATININE NA K+ CK 118 u/L 55-170u/L 23 u/L 0-16 u/L 17.79 4.23-9.07 HB 16.7 13.7-17.5 HDL 0.83 mmol/L 0.9-1.87 mmol/L 3.02 MMOL/L 3.9-4.7 MMOL/L PLT 273-238 163-337 TG 1.26 MMOL/L 0.34-2.30 MMOL/ CK MB WBC LDL Treatment • The treatment of a heart attack focuses on reducing pain, improving blood flow to the heart muscle, and preventing irreversible damage to the heart muscle. Another important feature of heart attack treatment is close monitoring for cardiac. • Initial treatment for a heart attack in the emergency department includes: • Cardiac monitoring • Oxygen therapy • Intravenous fluids Medications for cardiac chest pain: • Medications that improve blood flow through the coronary arteries in those who have suffered a heart attack include: • Aspirin: • Thins the blood, in to order lower the risk of blood clots in the coronary arteries • Heparin: • Thins the blood, in to order lower the risk of blood clots in the coronary arteries • Nitrates: • Open coronary arteries and let the heart work more efficiently • Platelet inhibitors: • This is a group of medications that block the normal blood clotting activity of platelets. • Examples include: aspirin, abciximab (ReoPro), eptifibatide (Integrilin), • Thrombolytic medications: • Clot busting medications that can restore blood flow in a blocked artery • Examples include: streptokinase, tissue plasminogen activator, andurokinase • Morphine: • Reduces anxiety and increases blood flow through the coronary arteries Additional medications that are used to treat myocardial infarction include: • • • • • • • • • • ACE Inhibitors: Lower blood pressure and reduce the work of the heart Beta-blockers: Lower blood pressure and reduce the work of the heart Calcium-channel blockers: Reduce the work of the heart and reduce abnormal heartbeats Statins: Lower cholesterol and reduce inflammation inside the coronary arteries Clopidogrel (Plavix): Thins the blood, in order lower the risk of blood clots in the coronary arteries • Ranolazine (Ranexa): • Helps improve oxygen levels in heart muscle. This drug is most often used when the above anti-anginal medications are not effective. • • • • • • • • • • • • • • • • Additional treatment for a heart attack in the emergency department includes: Early treatment with aspirin Early treatment with heparin Timely decision whether to provide: Thrombolytic medications Angioplasty Coronary artery stent placement Coronary artery bypass surgery Treatment with beta-blocker medications Treatment with ACE inhibitor medications Continued aspirin therapy after hospital discharge Continued beta-blocker therapy after hospital discharge Smoking cessation counseling Cardiac rehabilitation program The long-term treatment for a heart attack may include: Angioplasty for coronary artery disease Coronary artery bypass surgery for coronary artery disease Complication Complication Type Manifestations Ischemic Angina, reinfarction, infarct extension Mechanical Heart failure, cardiogenic shock, mitral valve dysfunction, aneurysms, cardiac rupture Arrhythmic Atrial or ventricular arrhythmias, sinus or atrioventricular node dysfunction Embolic Central nervous system or peripheral embolization Inflammatory Pericarditis Nursing health teaching • • • Explain procedures and answer questions for both the patient and family. Remember that you may need to repeat explanations after the emergency situation has resolved. To promote compliance with the prescribed medication regimen and other treatment measures, thoroughly explain dosages and therapy. Inform the patient of the drug’s adverse reactions, and advise him to watch for and report signs and symptoms of toxicity (for example, anorexia, nausea, vomiting, mental depression, vertigo, blurred vision, and yellow vision, if the patient is receiving a cardiac glycoside). Explain the need to treat recurrent chest pain or Myocardial Infarction (MI) discomfort with sublingual nitroglycerin every 5 minutes for three doses. If the pain persists for 20 minutes, teach the patient to seek medical attention. If the patient has severe pain or becomes short of breath with chest pain, teach the patient to take nitroglycerin and seek medical attention right away – – – – – – – – – – Review dietary restrictions with the patient. If he must follow a low-sodium, low-fat, or low-cholesterol diet, provide a list of foods to avoid. Ask the dietitian to speak to the patient and family. Explore mechanisms to implement diet control, an exercise program, and smoking cessation if appropriate. Encourage the patient to participate in a cardiac rehabilitation exercise program. The physician and the exercise physiologist should determine the level of exercise and then discuss it with the patient and secure his agreement to a stepped-care program. Counsel the patient to resume sexual activity progressively. He may need to take nitroglycerin before sexual intercourse to prevent chest pain from the increased activity. Advise the patient about appropriate responses to new or recurrent symptoms. Advise the patient to report typical or atypical chest pain. Post Myocardial Infarction (MI) syndrome may develop, producing chest pain that must be differentiated from a recurrent MI, pulmonary infarction, and heart failure. Stress the need to stop smoking. If necessary, refer the patient to a support group. Be sure the patient understands all the medications, including the dosage, route, action, and adverse effects. Instruct the patient to keep the nitroglycerin bottle sealed and away from heat. The medication may lose patients potency. Conclusion • Patient X brought to ER by SRC ambulance with the complaints of chest pain radiating to left arm, chest discomfort, palpitation, SOB, and nausea. Received in ER resuscitation room by stretcher.PT is conscious, oriented, pale and diaphoretic .Vitals checked and recorded .Attached to monitor, started oxygen via face mask 3 l/MT .Seen and examined by ER doctor on duty and cardiologist. ECG done and seen. Tab. ASPIRIN 300 MG , Tab PLAVIX 300 MG , Tab atorvastatin 80 mg , Inj. MORPHINE 5mg ,IV , Inj. Ranitidine 50 MG IV , Inj. PREMOSAN 10 mg iv , NTG PUFF X 2 times s/ l , Inj. CLEXINE 40 mg s/c given as per order. For lab investigations CBC, PT, APTT, ELECTROLYTES, RBS, BUN, CREATININE, CK, CKMB, TROPONIN I QUANTITATIVE sent to lab. Patient is admitted in ccu for further management. The patient improved well and discharged from the hospital. In general, nurses has a big role in assisting these patients in attending their activities of living NURSING CARE PLAN FOR MI ASSESSMENT SUBJECTIVE DATA Patient compliance of severe chest pain radiating to left arm and back OBJECTIVE DATA Restleness Fatigue Cold and clammy skin Palpitation Pain scale of 8/10 Respirations, BP, and heart rate are checked , documented NURSING DIAGNOSIS Acute chest pain related to myocardial ischemia resulting from coronary artery occlusion PLANNING Within 5 MTS of nursing intervention the PT will have improved comfort in chest INTERVENTION -Obtain 12 lead ECG during pain -Administered sublingual nitroglycerine and narcotic analgesics as ordered -Maintained bed rest during pain with position of comfort .maintain relaxing environment to promote calmness -Administered o2 3 L/MT with semi fowlersposition RATIONALE -To monitor changes that can give evidence of further cardiac damage and location of MI -To control the pain. -To reduce o2 consumption and demand ,to reduce competing stimuli and reduce anxiety -To give rest to cardiac muscles EVALUATION Goals fully met Within 5 MTS of nursing intervention the pt. improved comfort in chest ASSESSMENT SUBJECTIVE DATA Patient have doubt regarding his condition OBJECTIVE DATA Anxious and fear of death NURSING DIAGNOSIS PLANNING INTERVENTION RATIONALE EVALUATION Knowledge deficit related to new diagnosis and lack of understanding regarding medical condition Patient will be able to verbalize and understanding of information given regarding condition , medication and treatment -Explained the procedures being done to the patient -To provide basic information Patient verbalized and understood about medical condition and treatment - patient ability and readiness to learn noticed -To provide optimal learning environment -To provide -Explained and discussed the role of PT in control of risk factors(smoking) information regarding complications -Explained the cause and risk factors behind MI -To improve daily activity. -Excessive physical activity or over -Discussed importance exertion can cause of being as active as further weakness of possible without the heart becoming exhausted -To provide basic and of rest between information activities -Advised daily deep breathing and walking exercise -Provided physical comfort for the PT -Allow PT to concentrate on what is being discussed -PT understood fully the importance of quit smoking -goals fully met Bibliography • Ross and Wilson Anatomy and Physiology in health and illness – 9th Edition. • Lippincott Manual of nursing practice - 9th Edition • www. Nurse labs.com • www. Wikitedia.com PREPARED BY : DIVYA PRATHAP KUMAR ER STAFF NURSE THANK YOU