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![Diagnostic measures
• ECG
• Lab Investigations
– Troponin I
– Troponin T
– CPK-MB
– CPK [Total]
– SGOT
– CBC & ESR
• X-Ray Chest
• Echocardiogram
• Radioisotope studies
- Stress Thallium
- Rest Thallium
- Multi-gated acquisition scan [MUGA]
• Coronary Angiogram
• MRI](https://image.slidesharecdn.com/acutemi-140506224950-phpapp02/85/Acute-mi-20-320.jpg)
![Enzyme Normal value Onset Peak Return to
normal
Trop. I &
Trop T
<0.2 4-6hrs 24-36 hrs. 10-12days
CPK[Total] 21-232 hrs. 12-24 hrs. 3-5days
CPK– MB <25 . 12-20 hrs. 42-48hrs.
SGOT <40 6-12hrs. 24-48 hrs. ≥10days
LDH 160 – 410 24hrs. 48-72 hrs. 7-10days](https://image.slidesharecdn.com/acutemi-140506224950-phpapp02/85/Acute-mi-24-320.jpg)
![Interventional Management
[PTCA] Percutaneous Transluminal Coronary Angioplasty](https://image.slidesharecdn.com/acutemi-140506224950-phpapp02/85/Acute-mi-41-320.jpg)
![Coronary Artery Bypass Graft
Surgery [CABG]](https://image.slidesharecdn.com/acutemi-140506224950-phpapp02/85/Acute-mi-42-320.jpg)
Uploaded byChandan N
Acute mi
This document discusses acute myocardial infarction (AMI), also known as a heart attack. It defines AMI as necrosis of cardiac muscle due to acute blockage of a coronary artery, usually from a ruptured atherosclerotic plaque forming a thrombus. It lists major risk factors and describes the pathophysiological changes that occur during AMI. It outlines diagnostic tests, treatment including thrombolysis or percutaneous coronary intervention, nursing management, and cardiac rehabilitation post-AMI.
More Related Content
Acute mi
- 1. Acute Myocardial infarction Priya.M. Vincent & Padma Susan Mathew ICCU
- 2. Definition • Necrosis tocardiac muscle due to acute occlusion of coronary artery as a result of plaque rupture and thrombosis
- 3. Coronary Atherosclerosis withThrombus
- 4. Riskfactors • Non-modifiable – Age –Race – Sex – Heredity • Modifiable – Smoking – Hypertension – Diabetes mellitus – Hyperlipidemia. – Obesity – Response to stress
- 5. Understanding Myocardial Infarction Changein the condition of plaque in the coronary artery Activation of platelets Formation of thrombus Ischemia of tissue in the region supplied by the artery Coronary blood supply < demand Myocardial cell death Contractility Stimulation of the sympathetic nervous system Altered repolarization of myocardium Release of lysosomal enzymes Anaerobic Glycolysis Myocardial irritability Dysrhythmia s ST seg. q wave CPK-MB LDH Lactic Acid production Angina
- 6. Contractility Stimulation of the sympatheticnervous system LV function Preload Cardiac Output CVP PCWP LVEF HR O2 NEED After load Vasoco nstricti on Continuation….
- 7.
- 8.
- 9. Myocardial Infarction –1st week
- 10.
- 11.
- 12. MI 18-24 hoursloss of nucleus, contraction bands, coagulative necrosis
- 13. MI 3-4 days– Hemorrhage, inflammation
- 14. MI 1st – 2nd week–Granulation tissue
- 15. MI 2- 4 weeks- Resorption, fibrosis
- 16. MI > 4–6weeks - Collagen Scar
- 17. Clinical features Symptoms: • Prolongedchest pain • Profuse sweating • Nausea & vomiting • Breathlessness • Anxiety • Collapse / Syncope
- 19. Physical signs • Pallor,sweating, vomiting • Tachycardia / Bradycardia • Hypotension, oliguria, cold periphery • Narrow pulse pressure • Raised JVP in RVMI • Lung crepitation • 3rd and 4th heart sounds • Fever
- 20. Diagnostic measures • ECG •Lab Investigations – Troponin I – Troponin T – CPK-MB – CPK [Total] – SGOT – CBC & ESR • X-Ray Chest • Echocardiogram • Radioisotope studies - Stress Thallium - Rest Thallium - Multi-gated acquisition scan [MUGA] • Coronary Angiogram • MRI
- 21.
- 22. Coronary Arteries •Left Coronary A. •L.A.Descending •LeftCircumflex •Right Coronary A. LCx LAD
- 23. Area of myocardium involved Coronaryartery supply Leads Anterior Left coronary artery left anterior descending branch V2,V3,V4 Posterior Right Coronary Artery V1 – V3 Inferior Right Coronary Artery II, III, avf Anteroseptel Left Coronary Artery left anterior descending branch V2 & V3 High lateral Circumflex artery, marginal branch or LCA I, aVL Apical Usually LCA, left anterior branch may be RCA, posterior descending branch V5 & V6
- 24. Enzyme Normal valueOnset Peak Return to normal Trop. I & Trop T <0.2 4-6hrs 24-36 hrs. 10-12days CPK[Total] 21-232 hrs. 12-24 hrs. 3-5days CPK– MB <25 . 12-20 hrs. 42-48hrs. SGOT <40 6-12hrs. 24-48 hrs. ≥10days LDH 160 – 410 24hrs. 48-72 hrs. 7-10days
- 25. Management • Se ek im m e diate m e dicalatte ntio n
- 26. Medical Management • Majorgoals: – Management of the acute attack – Prevention of complications – Rehabilitation
- 27. 1. Management ofAcute attack • History • ECG • IV access • Routine blood investigations • Continuous cardiac monitoring • Invasive monitoring
- 28. General Measures • Paincontrol • Aspirin • Clopidogrel • Nitrates • Beta-adrenoreceptor blockers • ACE inhibitors • Bed rest upto 48 hours • Soft diet • Stool softeners
- 29. Patients with ischemictype discomfort ECG ST elevation ECG strongly suspicious for ischemia ( ST depression, T wave inversion Non diagnostic ECG Eligible for thrombolytic therapy Thrombolytic therapy contraindicated Admit Initial antiischemic therapy or treat as unstable angina Thrombolytic therapy Primary PTCA Continue evaluation Obtain follow up serum cardiac marker levels ECHO Evidence of ischemic infarction Evidence of ischemic infarctionYes NoInitial reperfusion strategy if ST elevation develops Discharge
- 30. Thrombolysis • Streptokinase • Urokinase •Tissue plasminogen activator (t-PA) • Acylated plasminogen streptokinase activator complex (APSAC)
- 31. Criteria forthrombolysis inacute MI Indications: • Chest pain • ECG changes • Time from onset of symptoms <6 hrs. : most beneficial 6-12 hrs. : lesser but still important benefits >12 hrs. : diminishing benefits but may still be used in selected patients
- 32. Absolute contraindications 1. Activeinternal bleeding (excluding menses) 2. Suspected aortic dissection 3. Recent head trauma or known intracranial neoplasm 4. Hemorrhagic CVA 5. Major surgery or trauma < 2weeks.
- 33. Relative contraindications • BP>180/110mmHgon at least 2 readings • History of hypertension • Active peptic ulcer • History of CVA • Current use of anticoagulants • Prolonged or traumatic CPR • Diabetic hemorrhagic retinopathy • Pregnancy • Prior exposure to STK & APSAC
- 34. Protocol followed inICCU • Aspirin 150-325mg chewed, 75mg daily thereafter • Clopidogrel 300mg stat & 75mg daily • Pain relief – Inj. Morphine 3mg + Inj. Phenergan 12.5mg slow IV – Inj. Pethedine 12.5mg IV in patients with asthma • O2 2-4 lit/min for 2-3 hrs. If saturation <95% continue beyond 3hours. • 2 IV access if the patient is for thrombolysis • Inj.Avil 2cc + Inj. Hydrocortisone 200mg+Inj. Ranitidine 50mg IV • Inj.Streptokinase 1.5million /15 lakhs units in 100ml NS over 1hr. • Inj. Heparin 60 units/kg bolus + 12units/kg/hr.infusion 4 hrs. after STK
- 35. • Inj. NTGinfusion x 24-48hrs. in LVF, large anti. MI persistent pain • β blockers to all patients unless contraindicated Metoprolol 12.5mg – 25mg BD use carvedilol 3.125mg OD for anti. MI, LVF, previous MI • Statins if LDL >100mg/dL & TGL>150mg/dL • Stool softeners • Hypnotic – Lorazepam 1-2mg HS • NPO till pain relief Liquid diet x 12 hours. Semisolid diet thereafter, low fat,low cholesterol 1500 calories diet. • Pulse,BP ½ hourly till stable then hourly. • ECG 90 min,180 min after starting STK &daily thereafter till transfer out. • Consider IV beta-blockers in young patients with tachycardia,hypertension(Metoprolol 5mg 3 doses at 5min interval.
- 36. 2. Prevention ofcomplications a. Dysrhythmias b. Cardiogenic shock c. Heart failure & pulmonary edema d. Pulmonary embolism e. Recurrent MI f. Complications due to necrosis of myocardium g. Pericarditis h. Dressler’s syndrome (late pericarditis)
- 37. 3. Rehabilitation Overall goals •Lead a productive life • Remain within the limits of the heart’s ability to respond to increase in activity and stress Sub goals • A programme of progressive physical activity • Health teaching • Help to accept the limitations • Aid the client in adjusting to changes in occupational goal • Change the psychological factors • Reduce risk factors
- 38. Phase I (inhospital) • Bed rest for 1 day with liquid diet • When vital signs get stabilized, patient can move in bed • Passive exercises • As strength is regained - sit on the side of the bed and dangle the feet. • Once transferred from CCU self-care activities are encouraged • Brief walks with supervision • Instruct regarding warning signs of over exertion • Client education
- 39. Phase II (Intermediate) •If no complications, discharge at the end of one week • Sexual intercourse after 4-8 weeks. • Stop smoking completely • Encourage frequent walks • Avoid strenuous activities • Monitored group programmes • Warm up and stretching exercises • Aspirin daily. • Return to work at the end of 8-9 wks. • Follow up in hospital between 8-9 wks.
- 40. Phase – III(Long term) • Periodic evaluation
- 41. Interventional Management [PTCA] PercutaneousTransluminal Coronary Angioplasty
- 42. Coronary Artery BypassGraft Surgery [CABG]
- 43. Nursing Management • NursingDiagnosis: – Acute chest pain related to myocardial ischemia resulting from coronary artery occlusion with loss/restriction of blood flow to an area of myocardium and necrosis of the myocardium. – Dysrhythmias related to electrical instability or irritability secondary to ischemic or infracted tissue. – Decreased cardiac output related to negative inotropic changes in the heart secondary to myocardial ischemia, injury or infarction. – Impaired gas exchange related to decreased cardiac output – Powerlessness related to hospital environment and anticipated life style changes – Fear & anxiety related to hospital admission and fear of death – Altered health maintenance related to MI and implications for life style changes.
- 44.