Acute Ischemic Syndromes and Myocardial Infarction

1. clinical presentation of acute MI

Pain

• resembles anginal pain but usually more severe, lasts longer, and may radiate more widely

• may result from release of mediators like adenosine and lactate onto nerve endings

• often referred to C7-T4 dermatomes (neck, shoulders, arms)

• little response to nitroglycerin

• 25% will be asymptomatic (especially diabetics—neuropathy)

Sympathetic NS Response

• combo of pain and hypotension (if present) trigger catecholamine release

• diaphoresis (sweating), tachycardia, cool and clammy skin (vasoconstriction)

Dyspnea

• decreased LV contractility, increased diastolic LV volume and pressure, conveyed to LA and pulmonary veins

• the resultant pulmonary congestion stimulates J receptors which effect a reflex of rapid, shallow breathing

Other Physical Findings

• S4 sound

• S3 sound

• pericardial friction rubs (if inflammation extends to pericardium)

• systolic murmurs (if papillary muscle involvement causes vavular insufficiency or if infact ruptures IV septum)

• systemic responses to inflammation (IL-1, TNF) like low-grade fever and leukocytosis

2. diagnosis of acute MI

Based on:

characteristic history and presentation

• see above

typical EKG changes

• Q wave MI: ST elevation, T wave inversion, Q waves evolve over infarcted areas

• non Q wave MI: ST depression, T wave inversion

serum markers

other

• echocardiography: demonstrate contraction or mechanical abnormailties

• nuclear scans: technetium-99m (collects in necrotic myocardium)

3. treatment strategies in acute MI

   1. thrombolysis

• most Q wave Mis occur as a result of occlusive thrombus formation w/in a coronary artery

• can use streptokinase, anisoylated plasminogen-streptokinase activator complex (APSAC), or recombinant plasminogen activator (t-PA)

• all function by activating plasmin which lyses fibrin clots

• contraindicated in those susceptible to hemorrhage

• matters less which agent is given, compared to how soon it is administered

• generally followed by IV heparin

2. coronary revascularization – role of PTCA

• alternative to thrombolytic therapy

• some centers unable to provide angioplasty

3. adjuvant medical treatment

• bed rest

• oxygen

• aspirin (decreases platelet adhesiveness, should be started upon presentation of MI and continued indefinitely)

• B-blockers (decrease sympathetic drive to myocardium, reduce work, contribute to electrical stability)

• Nitrates (relieve pain, work by venodilation which lowers oxygen demand by lowering preload)

• Morphine (eliminate pain and anxiety thereby reducing oxygen demand, also venodilate)

• Anticoagulants (heparin)

• ACE inhibitors (limit post-MI ventricular remodeling and heart failure, begun early and continued indefinitely)

Category: Cardiology Notes