Acute myocardial infarction Flashcards
What is ischaemic heart disease
When the heart does not receive enough blood and oxygen which causes cells to die.
What is the aetiology of IHD?
Coronary atherosclerosis and thrombosis.
Death in IHD is due to what?
Ventricular fibrillation, heart failure or stroke.
What are the effects of acute myocardial ischaemia in IHD?
Angina, arrhythmias, MI, heart failure, coronary vasospasm.
What is acute myocardial infarction?
Clinical term to describe the first few hours following a heart attack which is a sudden and symptomatic episode of acute myocardial ischaemia (loss of coronary blood flow) in patients with IHD).
How can AMI cause heart failure?
Ischaemia impaired the ability of the heart muscle to contract due to impaired ATP generation (acute heart failure). Ischaemia lasting longer than 30 mins leads to cell death.
How can AMI cause cardiac arrhythmias?
Ischaemia causes many changes that affect electrophysiology e.g. increase in potassium concentration; ventricular cells develop acute local changes in resting membrane potential and action potential duration, this causes regional slow conduction and triggers ventricular premature beats/lethal VF.
What is the early palliative treatment of AMI?
Morphine i.v. which relieves chest pain, reduces stress-related catecholamine drive.
What attempts can be made to limit the death of heart cells?
Repercussion within three hours, percutaneous coronary intervention (angioplasty by balloon or stent); combination of drugs used with the aim of opening the artery and keeping it open; prophylaxis with anti-thrombotic such as aspirin, prasugrel/clopidogrel; anti-platelet therapy; injectable anti-coagulants such as bivalrudin, heparin, enxoaparin.
What is the mechanism of action of heparin and enoxaparin (anti-coagulants)?
They activate anti-thrombin-III which inhibits thrombin activity which is responsible for the cascade for fibrin formation.
What is the mechanism of bivalrudin?
It directly inhibits thrombin which is responsible for the fibrin cascade.
How do Fibrinolytics i.v. limit heart cell death?
Recombinant tissue plasminogen activators such as tenecteplase and alteplase mimic actions of endogenous TPA. They convert inactive plasminogen into active plasmin which is used in thrombolysis to splits platelets linked by fibrin into products.
What is the treatment of arrhythmias in hospital?
Electrical defibrillation is the only way of terminating VF; cardiogenic shock; i.v. beta-adrenoceptor agonists.
What is the prophylaxis against reoccurrence?
Aspirin reduces mortality long term as it inhibits COX so inhibits the synthesis of thrombotic prostanoids such as thromboxane A2; beta-blockers.
