ischaemic heart disease Flashcards
(31 cards)
how does the respiration differ in myocytes between healthly patients and patients with Ischaemic heart disease (IHD)
normal= aerobic
IHD = anaerobic
how does Ischaemic heart disease effects the heart
-reduces generation of ATP which inpairs interaction of contractile proteins
-reduction (transient) of ventricular systolic contraction + diastole relaxation
(occurs within 60s, reversible if repurfusion occurs
what changes to cell structure happens during IHD
-glycogen depletion
-mitocondrial swelling
develops withing minutes
when does irreversible cell death occurs
20-40 minutes after onset
build up of local metabolites is caused by - and what do they cause
due to lack of blood supply/removal
-Activates pain receptors in C7-T4 distribution (Angina)
-dangerous arrhythmias
what are the factors of myocardial oxygen supply
-O2 carrying capacity
-coronary blood flow (coronary perfusion pressure + vascular resistance
-external compression
-intrinstic factors (local metabolites, endothelial factors, nueronal innervation)
what are the factors of myocardial oxygen demands
wall stress
heart rate
contractibility
there are multiple drugs to treat myocardial infarctions
-oxygen (mask)
-Morphine/diamorphine with an antiemetic
-Nitrates
-antiplatelets
-beta blockers
-ACE inhibitos
-Anti-coagulants
-Antiarrhythmia
-statins
how does oxygen help MI
relieves hypoxia
how does morphine treat MI
-pain relief
-relief from nausea
-venodilation
which drug class reduced the risk of another MI
anti-platelets = aspirin, clopidogrel
how do beta blockers treat MI
improves perfusions and reduce risk of arrhythmias
lengthens diastole
how does ACE inhibitors treat IM
useful in risk of heart failure, left ventricular dysfunction
how do anti-coagulants treat MI
protection from thrombus in at risk patient
give an example of a short acting and long acting nitrates
-GTN (short acting)
-Isosorbide mononitrate (long activity)
what is the mechanism of action of nitrates
-relaxes vascular smooth muscle, some reduction of afterload
-relaxes veins, decrease central venous pressure and redcues preload
-The therapeutic doses have less effect on small resistance arteries than on veins
what is the cellular effects of nitrate
it is metabolised and the released Nitric oxide (NO)
this activates guanylyl cyclase, this increase cGMP, this causes desphosphorylation of myosin light chain
this decrease cytoplasmic Ca2+ which reduction of smooth muscle contraction
-Vasodilates collateral arteries
what is Nitrates used to treat
Angina
IHD & MI
what are the adverse effects of nitrates
postural hypotension
headache
what is angina caused by
caused by the arteries suppling blood to the heart muscles becoming narrowed by a build-up of fatty substances (atherscleosis)
what are the symptoms of angina
-chest pain = tight, dull or heavy. May spread to your arms, neck, jaw or back. Triggered by physical exertion or stress. Stops within a few minutes of resting
-Feeling sick or breathless
what are the risk of angina
-risk of atherosclerosis
-unhealthy diet, lack of exercise, smoking, increased age and family history
what is the difference between stable and unstable angina
-Stable = attacks have triggers (stress/exercise) and stops during rest
-unstable = attacks are more unpredictable (no trigger) and can continue despite resting
Unstable can develop from stable
what are the tests used to confirm angina
Blood pressure
BMI + waist size
Blood test to check cholesterol
ECG/ exercise ECG
coronary angiography - scan after injection of a dye to highlight heart and blood vessels
