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MI.ppt
- 1. Dr. M. WajidSadiq Resident Medicine CMH/SKBZ Rawlakot
- 2. A 44year old man presented in ER with the 3 hours history of SOB, restlessness, palpitations, nausea and substernal chest pain radiating to jaws and left arm, increasing in intensity with minimal exertion. His BP 140/90mmHg, PaO2 91%, plasma glucose 110mg/dl, pulse 65/min, R/R 22/min at the time of presentation. His past medical history is insignificant for DM or other systemic illness. His ECG was recorded at the time of presentation is given below
- 5. based on history,physical examination and ECG what is next step of management?
- 7. Contents Definition Types ofInfarcts Etiology Pathiophysiology Clinical manifestations Diagnosis Management
- 8. MI isdefined as a diseased condition which is caused by reduced blood flow in a coronary artery due to atherosclerosis and occlusion of an artery by an embolus or thrombus. MI or heart attack is the irreversible damage of myocardial tissue caused by prolonged ischemia and hypoxia.
- 9. According toanatomic region of left ventricle involved: Anterior, Posterior, Lateral, Septal, circumferential and combinations anterioseptal, anteriolateral, posteriolateral. According to thickness of ventricles Transmural, Laminar(subendocardial)
- 10. Tobacco smoking Hypertension DM and other systemic diseases Drug abuse Obesity Stress Alcohol Age and gender
- 11. Most patientswho sustain an MI have coronary atherosclerosis. The thrombus formation occurs most often at the site of an atherosclerotic lesion, thus obstructing blood flow to the myocardial tissues. Plaque rupture is believed to be the triggering mechanism for the development of the thrombus in most patients with an MI. When the plaques rupture, a thrombus is formed at the site that can occlude blood flow, thus resulting in an MI.
- 12. Irreversible damageto the myocardium can begin as early as 20 to 40 minutes after interruption of blood flow. The dynamic process of infarction may not be completed, however, for several hours. Necrosis of tissue appears to occur in a sequential fashion. Reimer and associates demonstrated that cellular death occurs first in the subendocardial layer and spreads like a “wavefront” throughout the thickness of the wall of the heart. Using dogs, they showed that the shorter the time between coronary occlusion and coronary reperfusion, the greater the amount of myocardial tissue that could be salvaged.
- 13. a substantialamount of myocardial tissue can be salvaged if flow is restored within 6 hours after the onset of coronary occlusion. The cellular changes associated with an MI can be followed by: 1. the development of infarct extension (new myocardial necrosis), 2. infarct expansion (a disproportionate thinning and dilation of the infarct zone), or 3. Ventricular remodeling (a disproportionate thinning and dilation of the ventricle).
- 14. Chest pain/chestdiscomfort Dyspnea Fatigue Others (sweating, weakness, nausea, vomiting, palpitations) Anxiety, hypotension, hypertension, arrhythmias.
- 15. Cardiac enzymes Lactate dehydrogenases Cardiac specific troponins ECG (st elevation, t wave inversion, wide deep Q waves can also appear)
- 16. Laboratory Tests CreatineKinase CK-MB appears in the serum in 6 to 12 hours, peaks between 12 and 28 hours, and returns to normal levels in about 72 to 96 hours. Serial samplings are performed every 4 to 6 hours for the first 24 to 48 hours after the onset of symptoms Creatine Kinase Isoforms: CK-MB1 is the isoform found in the plasma, and CK-MB2 is found in the tissues. In the patient with an MI, the CK-MB2 level rises, resulting in a CK-MB2 to CK-MB1 ratio greater than one
- 17. Troponin. (troponinT and troponin I): Troponin I levels rise in about 3 hours, peak at 14 to 18 hours, and remain elevated for 5 to 7 days. Troponin T levels rise in 3 to 5 hours and remain elevated for 10 to 14 days
- 18. Myoglobin: Myoglobinis an oxygen-binding protein found in skeletal and cardiac muscle. Myoglobin’s release from ischemic muscle occurs earlier than the release of CK. The myoglobin level can elevate within 1 to 2 hours of acute MI and peaks within 3 to 15 hours. Because myoglobin is also present in skeletal muscle, an elevated myoglobin level is not specific for the diagnosis of MI. onsequently, its diagnostic value in detecting an MI is limited
- 20. Non pharmacological:counselling and education of patients, life style modification, smoking cessation, avoid alcohol, diet and nutrition, salt restriction Pharmacological: ◦ Thrombolytics ◦ Anticoagulants ◦ Antiplatelets ◦ Antihypertensive agents ◦ Lipid lowering drugs ◦ Analgesics, antiulcers, and sometimes antidepressants
- 21. Give O2to maintain spo2 92-98% and attach cardiac monitor Obtain iv access and send blood for baseline investigations. Provide small increments of IV opioid analgesia Ensure the patient has had 300mg aspirin and 300 mg clopidogrel PO. Contact cardiologist for PCI If PCI is not available consider thrombolysis and monitor carefully.
- 22. If paincontinues, give GTN @ 0.6mg/hr and can increase if necessary Consider atenolol(5mg iv slowly over 5 min and repeat after 15 mins) or metoprolol unless contraindicated (uncontrolled heart failure, hypotension, bradyarrythmias, COPD, asthma) thrombolysis
- 23. ST elevationof >1mm in 2 limb leads or ST elevation of > or equal to 2mm in 2 or more contiguous chest leads or LBBB in the presence of a typical history of acute MI (LBBB has not to be new. PCI is treatment of choice for STEMI, if PCI cant be performed within 90 mins of diagnosis then thrombolysis is an alternative. Patient presenting > 12 hrs after symptoms onset will not benefit from thrombolysis.
- 24. Head injury,recent stroke, previous neurosurgery or cerebral tumor. Recent GI bleeding, menstruation or coagulopathy/warfarin. Severe hypertension(systolic >200mmHg, diastolic>120mmHg), aortic dissection or pericarditis. Puncture of non-compressible vessels e.g subclavian, traumatic CPR, decrease GCS post arrest.
- 25. Major surgerywith in recent weeks. Pregnancy
- 27. Arrythmias Cardiogenicshock CCF Thromboembolism Rupture Cardiac aneurism Pericarditis
- 28. Vascular Complications Recurrentischemia Recurrent infarction Mechanical Complications Left ventricular free wall rupture Ventricular septal rupture Papillary muscle rupture with acute mitral regurgitation Myocardial Complications Diastolic dysfunction Systolic dysfunction Congestive heart failure Hypotension/cardiogenic shock Right ventricular infarction Ventricular cavity dilation Aneurysm formation (true, false)
- 29. Pericardial Complications Pericarditis Dressler’s syndrome Pericardial effusion Thromboembolic Complications Mural thrombosis Systemic thromboembolism Deep venous thrombosis Pulmonary embolism Electrical Complications Ventricular tachycardia Ventricular fibrillation Supraventricular tachydysrhythmias Bradydysrhythmias Atrioventricular block (first, second, or third degree)