Flashcards in 206 - Myocardial Infarction Deck (30):
what is the definition of myocardial infarction?
ischaemic necrosis of the myocardium due to the acute occlusion of a coronary artery. Clinically there must be :
*symptoms of myocardial pain (chest, arms, jaw) +
*ECG changes showing myocardial ischaemia/infarct (ST elevation in ant/lat leads and reciprocal in inf) +
*evidence of cardiac myocyte necrosis (cardiac enzymes troponin T and I)
what can cause an MI?
*atheromatous coronary artery disease - plaque rupture, thrombus formation, emboli
*spontaneous coronary artery thrombosis - procoagulant state
*aortic disection - occludes entrance to coronary arteries
*coronary artery spasm - due to drugs
*arteritis due to SLE
*coronary artery aneurysm or dissection
what are the signs and symptoms of an MI?
*heavy crushing chest pain more than 20 mins with radiation to arms and neck(+ both arms or just right arm, - pleuritic, sharp pain, positional, palpitation)
*sweating, pallor change, nausea
*hyper/hypo tension, brady/tachy cardia, impaired LV function (hypotension, crackles in lungs, murmurs)
what are the differential for an MI?
*resp - PE, pnemothorax, pleurisy
*MSK - costochondral pain, rib trauma, nerve compression
*GI - oesophagitis, spasm, rupture
*Vascular - aortic dissection, aortic thrombus
*cardiac - angina, pericarditis
what ST segments changes could be seen in an ECG during and MI?
*sometimes initial ST depression and T-wave peaking - ischaemia & partial artery occlusion
*then ST elevation (AKA J-point elevation) - ischaemia &total artery occlusion
*t-wave inversion - ischaemia
*pathological Q-waves - >1/3 of R-wave - myocardial death
*new left bundle branch block - wide QRS in V5/6 (I &aVL) with reciprocal in V1/2
what are the sup/inf/lat leads?
*sup - I and aVR
*inf - II, III and aVF
*lat - I, aVL, V5/6
what ecg changes can be seen in an MI in mins/hrs/days/weeks?
*mins - elevated ST, tall peaked T-waves in leads facing
*hrs - path. Q-waves, t-waves invert
*days - normal ST
*weeks - path. Q-waves persist, t-waves may be upright
what cardiac enzymes tests can be carried out in an MI, what causes it and when can it be tested?
Troponin T and I which are released by irreversibly injured cardiac myocytes. It can be tested 4-6 hours after infarction and up to 2 weeks after - needed to be elevated for MI diagnosis but can also be caused by PE, septicaemia, renal failure, cardiac cell death due to CO hypoxia, trauma, myocarditis)
other enzymes - MB-creatine Kinase (MBCK), lactate de-hydrogenase-1 (LDH-1
what other tests should be done in suspected MI?
*FBC (anaemia), U&Es (electrolyte imbalance ie arrythmias), eGFR (creatinine) for renal function prior to ACE inhib, CRP (inflammatory markers), ABG, angiography, echocardiography CXR, myocardia perfusion imaging scintigraphy
what are the ECG changes for supraventricular tachycardia (SVT)?
fast rate without preceding P-wave. regular QRS as pacemakers near AV node
what are the ECG changes for ventricular tachycardia (VT)
fast rate and abnormal QRS as low down pacemaker. broad complex and inverted T-waves
what are the ECG changes for atrial fibrillation?
no p-waves and irregularly irregular QRS
what are the ECG changes for atrial flutter?
saw tooth pattern
what are the ECG changes for wolff parkinson white syndrome?
delta wave (deflection of upward R-wave?
what are the ECG changes for 1st degree heart block?
long PR interval
what are the ECG changes for 2nd degree heart block?
mobitz I (Wenckebach) - PR becomes longer progressively until a QRS dropped
mobitz II - PR prolonged & QRS dropped at regular intervals
what are the ECG changes for 3rd degree heart block?
complete AV dissociation - no p-wave-QRS relation
what is the immediate treatment for acute coronary syndrome?
*o2 to maintain sp02 of more than 94%
*GTN - pain and symptoms
*IV opiate analgesia + anti emetic
*aspirin - anti platelet
when is reperfusion treatment indicated and what are the choices?
indicated in STEMI or ST elevation ACS.
*1st line - immediate Percutaneous coronary intervention - lower stroke risk, most effective within 90mins of symptoms. Used with glycoprotein IIb/IIIa inhibitor (antiplatelet) and heparin
*thrombolysis (streptokinase, urokinase, recombinant tissue plasminogen activators)- when PCI not available, can be given by ambulance, stoke risk. Activates plasminogen to form plasmin which breaks down fibrin.
what are the further treatment options for all cases of MI and ACS?
*antiplatelet therapy - aspirin, clopidogrel, glycoprotein IIa/IIIb inhibitors
*antithrombin therapy - fondaparinux or heparin
*anti-ischaemic therapy - beta blockers (slow HR and contractility incr. diastolic time), ACE inhibitors (decr. BP and cardiac work load)
*statins - reduce cholesterol
what are the 3 layers of the arterial wall?
*intima - endothelium (simple squamous with basal lamina) and subendothelial connective tissue (collagen,elastic fibres, smooth muscle, internal elastic lamina)
*media - thickest layer, elastic and collagen fibres, smc, few fibroblasts
*aventitia - thin layer prevents overstretch. connective tissue fibroblasts, vasa vasorum and nervi vascularis
what does the structure of a plaque contain?
*weak vessel wall - muscle degeneration
*lipid core- oxidised LDLs, cholesterol, cell debris & foam cells (macrophages full of ox LDL)
*shoulder region (edge) - macrophages, foam cells & T-cells
*fibrous cap - collagen, elastin, smc,proteoglycans
*loss of endothelium - incr. thrombus formation
how does a plaque develop?
* ox LDLs damage & enter endothelium
*monocytes attracted become macrophages, take up ox LDL, become foam cells & die attracting more macrophages
*cytokines encourage fibrous cap formation attracting smooth muscle migration to intima to secret collagen & incr. stability.
*plaque grows and then may deterioate
what causes nitric oxide (NO) to be produced by the endothelial cells and what does it do?
in response to shear stress and caused vasodilation, inhibits smc proliferatuon, inhibits monocyte adhesion, antiplatelet effect, promote macrophage apotosis, inhibits lipid oxidation. In endothelial dysfunction reduced NO production
why does thrombosis occur due to plaques in the blood vessels?
plaque eroded due to inflammatory cells causing endothelial cell apotosis or proteases cutting cells from the vessel wall. risk factors for unstable plaques are:
large lipid core, thin fibrous cap, high inflammatory cell conc., low smc density, incr. vaso vasorum
what role does cholesterol have in the body, what are the sources/excretion and regulation?
*role - component of cell membranes and precursor to all steroid hormones, bile acids & vit D
*sources - diet and endogenously from acetyl coA in liver
*excretion in bile acids
*regulation - -ve feedback inhibiting HMG-co-A. insulin incr. secretion glucagon inhibits
how are fatty acids metabolised?
transported from intestines:
long chain - as TAGs in chylomicrons
short & med chain - secreted into blood by intestinal mucosal cells as FFAs (high conc - insulin causes liver uptake, low conc - adipocytes release stores)
what are the 3 lipid transport pathways?
*exogenous - chylomicrons formed in intestinal mucosal cells and enter lymphatics then blood at thoracic duct, broken down to FFAsin capillaries by lipase then onto tissues
*endogenous - vldl synthesised in liver has TAGs removed in capillaries to become IDL which become LDLs
*Reverse cholesterol transport - transports free cholesterol to liver via HDL
what do lipoproteins consist of and what types are there?
non polar lipid core (TAGS & cholesterol esters) & polar outer coat (phospholipid, apolipoprotein & free cholesterol. Types:
chylomircrons - take TAGS from intestine to tissue
VLDL - take TAGs from liver to tissue
IDL - remnants of VLDL
LDL - takes cholesterol esters to tissues
HDL - take free cholesterol to liver