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Myocardial infarction
Definition
Stable angina
Unstable angina
NSTEMI
Pathophysiology
Electrocardiogram
Cardiac biomarkers
Diagnostic pathways
Medical therapy
Anti-ischemic therapy
Nitrates
Beta blockers
Antithrombotic therapy
Conservative strategy
Pathophysiology
Clinical presentation
precipitating factor
Physical findings
laboratory findings
Electrocardiogram
total occlusion of an epicardial coronary artery STsegment elevation + Q waves on the ECG
Cardiac imaging
Initial management
Prehospital care
LO 2
Etiology
Cardiogenic shock
Other etiologies
RV failure
Refractory sustained
bradyarrhythmias
Toxic metabolic
Beta blocker/CCB
overdose
Severe acidosis &
hypoxemia
Incidence
Pathophysiology
Inflammatory
cytokines, inducible
nitric oxide synthase
shock
Pump failure
Risk factors
acute MI
older age
female sex
prior MI
diabetes
anterior MI location
reinfarction soon after
MI
Timing
1/4 of MI patients
develop CS rapidly
(within 6 hour of MI
onset)
3/4 later on the 1st
day
Subsequent onset of
CS
reinfarction,
marked infarct
expansion,
a mechanical
complication
Clinical findings
90110 beats/min
Laboratory findings
hypoxemia and
metabolic acidosis
creatine
phosphokinase,
troponin I & T >
ECG
acute MI with LV
failure
1,5 of infarct
anterior
severe left main
stenosis global
ischemia
Chest X ray
pulmonary vascular
congestion
pulmonary edema
CS results from a first
MI hearts size is
normal
Echocardiogram
left-to-right shunt in
patients with VSR
Pulmonary embolism
Proximal aortic
dissection with aortic
regurgitation or
tamponade
Prognosis
Pulmonary edema
Etiology
Pathophysiology (cardiogenic)
Clinical findings
Hypertension
Other examinations
Echocardiography
Electrocardiography
Swan-Ganz catheter
Treatment
Oksigen therapy
Positive pressure ventilation
Diuretics
Nitrates
Morphine
2- to 4-mg IV boluses
ACE-I
Physical Methods
Digitalis Glycosides
Intraaortic Counterpulsation
IABP
LO 3
Cardiac arrest
Cardiac arrest
Etiology
Clinical characteristics
Clinical transition
Treatment
AED
ACLS