Your SlideShare is downloading. ×
0
944143 634377681641247500
944143 634377681641247500
944143 634377681641247500
944143 634377681641247500
944143 634377681641247500
944143 634377681641247500
944143 634377681641247500
944143 634377681641247500
944143 634377681641247500
944143 634377681641247500
944143 634377681641247500
Upcoming SlideShare
Loading in...5
×

Thanks for flagging this SlideShare!

Oops! An error has occurred.

×
Saving this for later? Get the SlideShare app to save on your phone or tablet. Read anywhere, anytime – even offline.
Text the download link to your phone
Standard text messaging rates apply

944143 634377681641247500

378

Published on

Published in: Health & Medicine
0 Comments
0 Likes
Statistics
Notes
  • Be the first to comment

  • Be the first to like this

No Downloads
Views
Total Views
378
On Slideshare
0
From Embeds
0
Number of Embeds
0
Actions
Shares
0
Downloads
4
Comments
0
Likes
0
Embeds 0
No embeds

Report content
Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
No notes for slide

Transcript

  • 1. Prepared by:malek ahmad
  • 2. Definition and epidemiologyAetiological factors and Risk factorsPathophysiologySign and symptomsInvestigationDifferential diagnosisTreatment and managementComplicationsPrognosis
  • 3. Definition Irreversible necrosis of cardiac myocyte 20 to prolonged ischemic (extention of ACS ( unstable angina, NSTEMI)) Epidemiology 1.5 million cases of MI each year and CVD cause 12million deaths each year High risk among African American and white population in US Male predominance and premenopausal women are protected (E2) Incidence increases with age
  • 4. Aetiological factors Risk factors Atheromatous plaque >  Non-modifiable  Age, Sex, FH cracked and ruptured >  Modifiable thrombus (occlusive or  Smoking and obestity partially)  DM, HPT,Dyslipidemia  Non atherosclerotic causes Coronary artery embolism  Vasculitis Congenital anomaly  Coronary embolism, trauma, spasm (histamine, serotonin) Coronary artery vasculitis  Drugs- coccaine  Congenital – kawasaki disease in  Factor increase O2 child requirement / decrease O2 supply Dissecting aneurysm w  Others coronary occlusion  Homocysteine  Peripheral vascular D  Stress
  • 5.  Imbalance btwn O2 supply and O2 demand > Cellular ischemia Atherosclerotic causes:  Stable angina- fixed narrowing, thus arterial lumen must reduced by 90% -cellular ischemia at rest, 50%- exercise  Unstable angina- fissuring of AP > platelet accumulation > transient thrombotic occlusion > platelet release VasoC factors (TXA2n serotonin) + endothelial dysfunction> compromise flow Perfusion must be restored w/in 40-60m, or lead to irreversible injury due to severe ATP depletion > increased extracellular ca conc, lactic acidosis and free radical
  • 6. Symptoms Signs Chest pain  Sign of hyperlipedemia  Site- central and substernal  Evidence of DM, TD, Gout,  Onset-sudden/exertion tar stained  Character- tight, compress, squeez, ache, burn, sharp  Bradycardia- CO,  Radiation- left arm n neck*back arrhythmia  Associated w  BP  Timing- over 20 mins  LGF  Exacerbate n relieve- exertion n GTN  Normal JVP, JVP- HF SOB-ischemia> EDP / systolic  4th heart sound, 3rd – HF and diastolic dysF > pulmonary  Pericardial friction rub P  MR/ VSD Sweating, palpitation, fatigue , N, V (sympathetic overdrive)  Bibasal crackles Risk factors assesment
  • 7. Blood Imaging • Troponin T(s:3- • Full thickness MI- ant n inf lead> 12h)(p:24-48h) STE, T wave inversion and +QwaveCardiac (r:5-14d) ECG • Subendocardial MI- ST and T wave change, no Q waveenzyme • CK-MB (s:3-12h) • Post MI- no Q wave, tall R wave in VI (p:24h) (r:2-3d) • RV + inf infarct-STE in V3 n V4 • Urine myoglobin • Heart size, +- CHF +- pulmonary edema FBC • Anemia, leukocytosis CXR • Concomitant disease • Exclude DD • Chemistry profile: • Extent of infarction creatinine ECHO • Assess complication- MR, pericardialothers • Lipid profile effusion, LV rupture • CRP-inflamation marker Cardiac cathetherization
  • 8. Anxiety disordersAortic dissection / Aortic sternosischolecystitisEsophageal spasm, esophangitis, GERDMyocarditis, pericarditisPneumothorax, pulmonary embolism
  • 9. Medical care Surgical care Others• Tx based on: • Percutaneous • Diet control i- Restore balance coronary • Minimize activity ii-Pain relief- intervention- • Consultation opiates and STEMI, cardiogenic • Coronary antiemetics shock, whom rehabilitation iii-Prevent and Tx thrombolysis of Cx failed, high • Health education• Thrombolysis- bleeding tendency • Exercise stress test aspirin, alteplase, • Urgent coronary streptokinase artery graft• Nitrates bypass- whom• B-blockade angioplasty failed, patient with• ACE inhibitors mechanical• Anticoagulant- complication-VSD, heparin LV, PM rupture
  • 10. SupraV Arrhythmias- arrhythmia, Sinus VF +- VTachy heart block brady/tachy, AF, A tachy CHF- systolic / Recurrent Cardiogenic diastolic ischemia shock dysfuntion Acute MR- Pericarditis, Ventricularinferopost MI due ventricular rupture at IVS/ to ischemia, aneurysm, mural LV free wallnecrosis, rupture thrombi, HPT
  • 11. 5-10% survivor die within 1st year after MI AMI- Half of allassociated w patients w MI 30% of rehospitalizedmortality rate within 1 year Variable n depend to extent of infarct, residual LV function, revascularization

×