MI Flashcards
Epidemiology. Risk factors. Pathogenesis
- necrosis or irreversible damage of the myofibril caused by a prolonged ischemia, occlusion of coronary artery due to thrombosis.
Epidemiology :
- more than a million cases in US, Russia.
- Mortality is more than 15% (primary infarction); if secondary (re-occur disease) up to 30%.
- more in men
- 1-5 million cases are reported each year
- 1 of every 25 patients who survives the initial hospitalization dies in the 1st yr after acute attack.
- survival is reduced in elderly patients (over age 75).
RISK FACTORS
- Familial hypercholesterolaemia
- Smoking
- Stress
- Family history of MI
- Hypercoagulability of blood
- Hypodynamia
- High intake of fatty food
- hypertension,
- diabetes,
- obesity,
- alcoholism.
- Surgical manipulations
- previous history of AP
- Age – male (45-55 yrs); female (55 and above ).
- Sex – male (mostly); female (after menopause).
- Hyperlipidemia.
- Estrogen-progesterone containing drugs.
- triggering factors : physical exhaustion and mental stress.
Pathogenesis :
Pathogenesis :
- coronary thrombosis/ stenotic coronary sclerosis spasm/ disruption of atherosclerotic plaque, vasospasm, platelet aggregation leading to coronary artery occlusion.
- no blood supply to the myocardium, necrosis of the myocardium.
- 1st period: Moderate ischemia-activity decreased, slow.
- 2nd period(After 30 minutes): Deep ischemia-no activity. Cells don‘t function.
- 3rd period: Damage of myofibrils-Necrotic mass. Irreversible pathological stage.
Classification
Classification
- Acc investigation of ECG: ST elevation, Non-ST elevation
1. Acc etiology :
- caused by atherosclerosis
- caused by other reasons such as trauma, embolism, atheritis
2. Acc Clinical Pic
- Typical
- Atypical : Asthmatic form, Abdominal form, Cerebral form, Arrythmic form, Painless/Silent form
3. Location: Anterior, Posterior, Lateral, apex, septum
4. Stages: Acutus, Acute, Subacute, Chronic
5. Morphological: Transmural, Subendocardial
6. Acc to square: Transmural, Q MI, Non Q MI
Typical clinical picture
Typical clinical picture
- Pain - heavy, crushing, pressing, squeezing, & exarcebate in time. impossible to overcome pain. Next day, pain disappears because of damage of all tissue.
- Pain is located in the substernal area.
- Pain prolonged more than ½ hour till next day. patient may fall to shock.
- Irradiation to left shoulder, neck, jaw, left arm & sometimes right shoulder.
- Pain more severe from hour to hour.
- Affect of nitroglycerine is absent. sit flat calmly not useful.
- restless.
- Associated symptoms:
Fear of death. Anxiety Cold sweat Short dyspnoea Palpitations
Weakness Bad mood Discomfort in chest. Fever (38)
Sinus tachycardia
Rapid weak pulse
Clinic of atypical variants
Clinic of atypical variants
1. Asthmatic Type :
- Pain is absent; attack of symptom like cardiac asthma.
- tachypnoe, cold sweat, palpitation, fear of death, weakness, orthopnoe, apnoea & rales.
- inspiratory dyspnea, tachycardia, dizziness, peripheral cyanosis, intestitial edema
- 1st Group: Old people 65-70 years, with cardioclerosis
- 2nd Group: Previous MI. Secondary infarction
2. Arrythmic Type :
- without pain. In some case, Accompanied by pain at rest
- Presence of palpitation, dizziness, fast & irregular pulse.
- Often in patient more than 40 years old.
- sudden attack, ventricular arrhythmia, tachycardia, extrabeats, transient arrythmias.
- predispose to fibrillation
3. Central/Brain Dependant Type :
- like stroke; loss of consciousness, weakness, dizziness, vomiting, vertigo, nausea, headache.
- Impaired movement extremities one side; impaired feeling of skin, paresis of muscle.
- When infarction area is big, cause hypoxaemia
4. Silent Infarction :
- No symptoms showing heart disorder
- Might have discomfort in chest, pain in the teeth or tip of finger.
- necrosis isn‘t so large.
- sudden weakness, soft vertigo, diminish activity of heart
- normally for pt with nerve insensitivity eg; DM
5. Abdominal variant:
- Abdominal(epigastric pain). GIT dysfunctions (meteorism, diarrhea, nausea, vomiting).
- Bradycardia. Paralysis of bowel.
- Irritation of phrenic/vagus nerve
- associated with irritation of intestine dyspepsia (belching, distention, flatulence)
- palpation in upper abdomen is painful.
Investigation
Investigation
1. Lab Test :
- creatine phosphokinase (MB fraction). after pain appear at the 1st 6 hours & peak for the next 24hours. Next day, enzyme is absent.
- AST, ALT. It increases gradually in 1st 6 hours & peak next day till 3rd-4th day; then disappears.
- LDH. Max 5th-7th day after onset of infarction & disappear after 2weeks.
- Troponins are elevated at end of 1st & 2nd day.
- Leucocytosis Reactive – Max 1-2days; disappears at end of 1st week. ESR ↑ in 1st week, slowly disappears during 10-14 days. ↑ band leucocytes (in 1st 1-3days).
- C-rective proteins increases till 1 week
- transmural infarction: Aneosinophilia in 1st/2nd after infarction, it reappears again. ↑ myoglobin in blood. transient hyperglycaemia;
- ECG
Transmural Type: ↑ ST
a. Acutus: 6 hours, increase ST with T wave
b. Acute: 6 hours to 5th/7th day
- R disappears.
- ST elevation presence.
- QS complex/syndrome.
- Elevated T-wave.
- c. Subacute: QS, prominent –ve T
d. Chronic: QS wave, ST normalizes (after 8th week), +ve T
Non Transmural Type :
- Subendocardial & intramural.
- It can stay 2 days after onset of infarction.
- Change in ST & T-wave only; Q-wave don‘t exist. (Last more than 30 minutes)
- Comes quick, 2nd/3rd day S may disappear. (-T) till 8th week.
- After 8 weeks, there is no trace of any changes.
- So if it is transmural, after 8th week, we will not see (-T)
non-Q wave MI - no ST elevation and no Q wave. Q wave MI - ST elevation, and evolve Q wave
- Ultrasound :
- discoordination of myofibrils. No contraction
- aneurysm of heart, dyskinesis or akinesis of myofibrils. - Imaging methods :
- many changes in MI. using contrast
- echocardiography: abnormality of wall motion, estimation of Left Ventricle function.
- angiography abt the coronary vessels. - Auscultation: S3, S4, Open-snap phenomenon. S2 Accentuation. Low S1.
Differential diagnosis of unstable angina
Differential diagnosis of unstable angina
AP MI
Pain synd Present Absent
NTG Effective Not effective
ECG Changes disappears after NTG Present changes.
Enzyme No changes Changes present
Main principles of tactic
Main principles of tactic
reduce the chest pain:
- Nitrates
- beta blockers (Metoprolol/Esmolol)
- morphine sulfate
To stop pain:
- Analgesic – Analgine
- Sublingual Nitroglycerin
- Narcotics: Morphine
- Neuropeptic drug: Doperidole + Fentanyl
Thrombolytic treatment / Fibrolytics:
- Streptokinase.
- Urokinase
- Tissue type plasminogen activator
antiplatelet /antiaggregant agents: Aspirin
anticoagulating / antithrombin agents:
- Heparin (unfractioned heparin)
- Enoxaparin (Lovenox).
- Dalteparin (Fragmin)
Treatment of pain syndrome (tachi- & bradiarrhythmias)
Treatment of pain syndrome (tachi- & bradiarrhythmias)
1. Treatment of pain syndrome.
a. morphine
b. nitroglycerin
c. beta blockers -metoprolol
d. Opioid(synthetic alkaloid)+Neuroleptic Neuroleptanalgesia Fentanyl or Droperidol
2. Treatment of arrhythmic syndrome
a. sustained ventricular tachycardia - Lidocaine
b. ventricular fibrillation
- prompt defibrillation (200-360 J)
- -recurrences treated with lidocaine infusion
c. atrial fibrillation -IV digoxin or IV amiodarone, verapamil, cloradole
d. sinus bradycardia - IV atropine,
3. To treat arrhythmia :
- Quinidine
- Amiodarone/Sotalol
- Ca-channel antagonist: Verapamil (for supraventricular arrhythmia)
- Beta-blockers: reduce chance of ventricular arrhythmia, reinfarction. Supraventricular arrhythmia. Propanol, Metaprolol
- AV Block – Atropine, Euphiline or Prednisolone
Anticoagulant & fibrinolytic therapy
Anticoagulant & fibrinolytic therapy
Anticoagulant Therapy: Heparin, Warfarin
- Unfractioned heparin - initial dose is i/v 10000, then 5000 or 2500 unit acc to weight of the pt.
- low molecular weight heparin (LMWH).
Fibrinolytic therapy:
- tPA, streptokinase, tenecteplase, reteplase, alteplase, urokinase, prourokinase.
- -converts plasminogen to plasmin and lysis the thrombi.
- side effects like allergy, hemorrhage, arrhythmias, relapsing of the thrombosis.
- Contraindications:
Active internal bleeding Aortic dissection Previous hemorrhagic shock Intracranial neoplasm
Complications of early period.
Complications of early period. Causes
- Rupture of myocardium. Tamponade. Heart does not relax.
- Intraventricular rupture. right overdilated. right-sided failure
- Rupture papillary muscle in left ventricle
- Dysfunction of mitral valve. Regurgitation to aorta and back to atrium. Edema (irreversible). Death
- Ventricular septal defect
- Aneurysm (Acute, subacute)
- Unstable coronary blood flow, Prolonged infarction
- Exacerbation of thrombosis in 1st/2nd day
Post myocardial infarction syndrome:
- Fever, chest pain
- Due to autoimmune pericarditis, pleuritis, pneumonitis.
Systemic embolization
- acute coronary failure, edema of the lung, cardiogenic shock, rupture of the aneurysm, arrhythmias, thromboembolism of pulmonary, acute LV insuff, acute pericardiatis
Clinical symptoms & diagnosis
Clinical symptoms & diagnosis
- Cardiogenic shock
Symptom :
- pale with cyanosis skin.
- very low Bp.
- pulse is weak and rapid.
- severe bradycardia
- oliguria
- tachypnea, Cheyne-stokes resp, and jugular vein distension.
- S1 very soft, and S3 may be audible.
Diagnosis :
- blood analysis- leucocytosis
increase BUN and creatinine.
- ECG
- echocardiography with color Doppler
- chest Xray
- Pulmonary edema
symptom : dyspnea at rest. Tachypnea, tachycardia, wheezing, HT Diagnosis :
- Xray- diffuse haziness, and Kerley B lines of interstitial edema.
- echocardiography – to diff betw cardiogenic or noncardiogenic cause.
- ballon flotation catheter – measures diff betw high and normal pressure causes of pulmonary edema. - Pulmonary embolism:
Symptom : dyspnea, chest pain, hemoptysis, cough Diagnosis :
- blood test- polymorphonuclear leucocytosis, elevated ESR, increase LDH
- chest X-ray—raised hemidiaphgram, previous infarct seen as opaque linear scars.
- pulmonary angiography – can detect emboli - Acute cardiac failure:
Symptom : dyspnea, orthopnea, edema, tachycardia, memory, emotional disturbances Diagnosis : chest X-ray, ECG, Echo, blood test , ventriculagraphy, cathetarization chamber of the heart, US
Cardiogenic shock. Types.
- Cardiogenic shock crisis of microcirculation due to the spread of infarction - systemic hypoperfusion, depression of the cardiac index, systolic hypotension. 4 types :
- True cardiogenic shock .
- Reflex cardiogenic shock.
- In permanent ventricular/fibrillation
- Areactive shock
Cardiogenic shock. Pathogenesis.
Pathogenesis :
- Decreased ejection due to blocking in MI/spasm of peripheral vessels.
- reduced coronary perfusion, hypoxemia and lactic acidosis develop
- blood decrease in brain, kidney.
- blood move slow, stagnate in peripheral area, decreased preload, liquid blood come out to the interstitial system.
- After 6-12hrs, organ start to die – Reduced liver activity, etc.
- After 12hrs, it changes to irreversible organ type of shock.
