Lec 15- STEMI NSTEMI Flashcards
MI (STEMI)
3 diagnosis factors- all can be ambiguous
Symptoms
-Prologonged severe chest pain (gripping or crushing, may radiate down arm, across back or up through jaw)
-Sensations of suffocating/doom
-Nausea
-Dizziness
-Sweating
Myocardial infarction
3 diagnosis factors- all can be ambiguous
signs: Dysrhythmias are common; ECG changes-12 lead ECG needed to look for global changes; Increased cardiac component in the blood- troponin T
- Silent AMI
- Estimated that 25% of non-fatal MI’s are not recognised
- Often serious MI will show signs of previous silent episodes
ECG abnormalities
LOOK on BB at the abnormalities
- T wave inversion or elevation: denotes ischemia
- ST-segment elevation: denotes myocardial injury; may be seen as depression in leads viewing electrical potential moving away
- Q wave abnormalities: deep often broad wave usually >25% of following R wave. Denotes infraction
- Non-ST segment elevation ACS: Is less serious. There, maybe no other ECG changes and diagnosis by symptoms and cardiac cell markers
ST segment ECG
ST-segment elevation (STEMI) -Increased R wave amplitude -ST elevation which is sloped upward Prominent Q wave -Prominent Q wave deeper and broader -Elevated ST segments -Inverted 'arrowhead' T waves
Q wave
- Many people who have had prior MI will have an ECG that appears normal
- There may, however, be typical features of previous MI, and the most conspicuous of these is abnormal Q waves
- Often accompanied by reducing R wave
Plasma cardiac components
- Only used cardiac marker is Troponin T- isoenzyme more specific for heart
- Mainly used to distinguish NSTEMI once no ECG changes found
2012 data on MI
- 79,000 hospital admission
- 41% STEMI and 59% NSTEMI
- Twice number of males cf.females
- 30 day mortality 2011-12 8% cf 13% in 2003/4
- 2013 >1 million men and 500k women in the UK who have had an MI
MI: the early stages
- 23% sudden death before hospitalisation
- Another 13% die during admission
- Irreversible damage to the cardiac muscle occurs within 6 hours- but still, some benefit up to 12 hours
- SPEED is vital
- Defibrillators are now common with some airlines and in shopping malls
- Aspirin 300mg should be given if not contra-indicated (chewed)- ASAP
- FAST TRACT FOR PCI
- Even with treatment, 5% die in the 1st year and then about 5% per year indefinitely. prognosis linked to the degree of necrosis- measured by troponin, T elevation and ECG
Immediate complications 1
-Acute left ventricular failure and pulmonary oedema
Lung signs- chest x-ray; increased pulmonary wedge pressure; lung base crack
-All patients to have a bedside echocardiogram to determine EF
May be transient. May then respond to O2 therapy (not COPD; alternatively furosemide oral or IV
Severe is difficult to treat (cardiogenic shock). If CO good then vasodilators to reduce TPR. Need haemodynamic control- monitoring right atrial, pulmonary wedge CO
-Cardiac Arrhythmias: common extra ventricular beats, ventricular tachycardia; ventricular fibrillation. May also see atrial fibrillation; sinus tachycardia and heart block. All patients to have continuous ECG monitoring 48 hrs
Treatment- depends on the type of arrhythmia.
Complication 2
- Cardiogenic shock: hypotension, SBP <90, cold, clammy, cyanosed, hyperventilation, high shallow pulse, oliguria
- 90% mortality even with therapy
- Haemodynamic monitoring
- Dobutamine/Dopamine- positive inotropes minimum effect on rate. Dopamine increases renal blood flow (dopamine R)
- Positive ventilation
- Avoid cardiac glycosides- may increase risk of arrhythmia; increase myocardial O2 consumption
Infarction
- Means stuffing because of (later) collagen scars
- Irreversible damage to heart muscle
- Necrosis occurs first, then infarction
- Transmural or subendocardial (most common)
- The initial injury may spread into adjacent areas. An important therapeutic objective is to limit the infarct size
Cellular events following occlusion
- In affected area, aerobic metabolism –> anaerobic
- ATP levels fall, lactic acid accumulates. Fall in pH; fall in compliance
- Inhibition of Na/K pump (depolarization). Intracellular accumulation of Na and Ca; swelling
- Extracellular accumulation of K, causing electrical instability
- Ca accumulation activates lipases and proteases destroying cell and damaging adjacent tissue
- Necrosis causes a weakening and a thinning of heart wall with a risk of aneurysm rupture
- Necrotic area is invaded by macrophages and replaced by collagen at about 7 days; healing completed at about 7 weeks
Therapeutic strategies
-Non-ST elevation MI is treated like unstable angina
Much less myocardial necrosis
-ST elevation MI- marked myocardial necrosis
-Broad similarities for both- with treatment depending on symptoms
MI: immediate management
- If no pulse: external cardiac massage; electro version (defibrillation)
- Pulse present- severe pain: morphine and anti-emetic
- O2 (40%); if evidence of hypoxia or continued myocardial ischemia (More risk with COPD)
- Bed rest (sedation if required); ECG monitoring
- Antiarrhythmics if necessary
- If signs of failure or shock: vasodilators/diuretic; inotropic
- URGENT PCI LISTING
- Stat loading doses of aspirin and another antiplatelet e.g. prasugrel and clopidogrel
Percutaneous Coronary Intervention PCI- Give loading dose of DAPT before
- insert a stent after balloon angioplasty
- If at point of angiogram no blockage is found- it is not an MI, likely broken heart syndrome for review by team
- If at point of angiogram blockages are not settable- ti be reviewed for possible coronary artery bypass grafting
- Negatives: Metal stent could damage area causing immune response; metal can catch fatty deposits causing blockage
