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Sven's Flashcards > 206 - Myocardial Infarction > Flashcards

206 - Myocardial Infarction Flashcards

1
Q

what is the definition of myocardial infarction?

A

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)
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2
Q

what can cause an MI?

A
  • 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
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3
Q

what are the signs and symptoms of an MI?

A
  • 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)
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4
Q

what are the differential for an MI?

A
  • resp - PE, pnemothorax, pleurisy
  • MSK - costochondral pain, rib trauma, nerve compression
  • GI - oesophagitis, spasm, rupture
  • Vascular - aortic dissection, aortic thrombus
  • cardiac - angina, pericarditis
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5
Q

what ST segments changes could be seen in an ECG during and MI?

A
  • 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
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6
Q

what are the sup/inf/lat leads?

A
  • sup - I and aVR
  • inf - II, III and aVF
  • lat - I, aVL, V5/6
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7
Q

what ecg changes can be seen in an MI in mins/hrs/days/weeks?

A
  • 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
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8
Q

what cardiac enzymes tests can be carried out in an MI, what causes it and when can it be tested?

A

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

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9
Q

what other tests should be done in suspected MI?

A

*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

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10
Q

what are the ECG changes for supraventricular tachycardia (SVT)?

A

fast rate without preceding P-wave. regular QRS as pacemakers near AV node

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11
Q

what are the ECG changes for ventricular tachycardia (VT)

A

fast rate and abnormal QRS as low down pacemaker. broad complex and inverted T-waves

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12
Q

what are the ECG changes for atrial fibrillation?

A

no p-waves and irregularly irregular QRS

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13
Q

what are the ECG changes for atrial flutter?

A

saw tooth pattern

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14
Q

what are the ECG changes for wolff parkinson white syndrome?

A

delta wave (deflection of upward R-wave?

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15
Q

what are the ECG changes for 1st degree heart block?

A

long PR interval

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16
Q

what are the ECG changes for 2nd degree heart block?

A 
mobitz I (Wenckebach) - PR becomes longer progressively until a QRS dropped
mobitz II - PR prolonged & QRS dropped at regular intervals
17
Q

what are the ECG changes for 3rd degree heart block?

A

complete AV dissociation - no p-wave-QRS relation

18
Q

what is the immediate treatment for acute coronary syndrome?

A
  • o2 to maintain sp02 of more than 94%
  • GTN - pain and symptoms
  • IV opiate analgesia + anti emetic
  • aspirin - anti platelet
19
Q

when is reperfusion treatment indicated and what are the choices?

A

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.
20
Q

what are the further treatment options for all cases of MI and ACS?

A
  • 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
21
Q

what are the 3 layers of the arterial wall?

A
  • 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
22
Q

what does the structure of a plaque contain?

A
  • 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
23
Q

how does a plaque develop?

A
  • 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
24
Q

what causes nitric oxide (NO) to be produced by the endothelial cells and what does it do?

A

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

25
Q

why does thrombosis occur due to plaques in the blood vessels?

A

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

26
Q

what role does cholesterol have in the body, what are the sources/excretion and regulation?

A
  • 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
27
Q

how are fatty acids metabolised?

A

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)

28
Q

what are the 3 lipid transport pathways?

A
  • 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
29
Q

what do lipoproteins consist of and what types are there?

A

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

30
Q

what causes familial hypercholesterolaemia?

A

LDL receptor dysfunction. Signs - tendon xanthoma (nodules on tendons/ligaments/fascia), xanthelasma (plaques on eyelids), corneal arcus (grey fat deposit at edge of iris). Treatment - statins (reduce cholesterol synthesis in liver & incr. LDL uptake) and fibrates (reduce serum triglyceride)

Sven's Flashcards (32 decks)

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