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Electrophysiology
Cardiology - paramedicine
| Question | Answer |
|---|---|
| perfusion | the passage of fluid though the vessels of a specific organ. It is the ability to provide adequate blood supply to meet nutritional demands and remove waste |
| hydrostatic pressure | the force exerted by a fluid pressing against the wall (changes in APO) |
| osmotic pressure | force that opposes hydrostatic pressure |
| Cardiac output | SV x HR |
| Blood Pressure | CO x R |
| myocardial cells | conduct impulses muscular contraction intercalcated discs |
| pacemaker cells | generation and conduction of electrical impulses phase 4, 3 and 0 |
| depolarisation | 0- sodium channels open and sodium moves in 1- sodium channels close, potassium exits 2- calcium moves in and potassium leaves |
| repolarisation | 3- potassium finishes leaving, calcium pumped out 4- potassium enters and calcium exits |
| sliding filament theory | myosin cross bridge attaches to the actin filament pulls actin filament toward m line ATP attaches to myosin head and cross bridge detaches |
| Cardiovascular risk factors | diet, shift workers, age, depression, physical inactivity ... |
| ACS | A spectrum of diseases including UA, NSTEMI and STEMI that share a common pathology of a disrupted atherosclerotic plaque |
| unstable angina | chest pain that is not resolved through therapeutic means (episodic, new onset, easily provoked); non evidence of myocardial injury or necrosis |
| nSTEMI | reduction in myocardial perfusion – caused by non-occlusive thrombus. The non-occlusive thrombus may become transiently or persistently occlusive (difficult to differentiate between UA and nSTEMI |
| STEMI | Occurs when the thrombus that has formed and is completely occlusive. Myocardial necrosis results from interruption to myocardial blood supply |
| Initial lesion | 1 macrophage infiltration, isolated foam cells |
| fatty streak | 2 intracellular lipid accumulation |
| intermediate lesion | 3 intracellular lipid accumulation, small extracellular lipid pools |
| atheroma | 4 intracellular lipid accumulation, extracellular lipid core |
| fibroatheroma | 5 single or multiple lipid cores, fibrotic cap |
| complicated lesion | 6 surface defect, haemorrhage, thrombosis |
| ischaemia | occurs when blood supply to tissue is inadequate to meet physiological may have t wave inversion or ST depression |
| injury | prolonged ischaemia ST elevation |
| infarction | tissue or organ necrosis caused by ischaemia may show Q waves |
| Heart failure | When the heart is unable to pump an adequate amount of blood to meet the metabolic demands of body tissues (congestive heart failure, congestive cardiac failure) |
| ejection fraction | A measure of the percentage of blood in a ventricle ejected with each contraction; a measure of heart failure (usually left ventricle failure) |
| Starling's law | length tension relationship in muscle fibres relationship is lost in diastolic dysfunction due to inability of the heart to stretch SV drops off because of left ventricular issues |
| dilated | -enlargement of chambers, systolic failures |
| hypertrophic | thickening of the heart muscle, diastolic then systolic failure |
| restrictive | stiffness of ventricular wall, diastolic failure |
| Right coronary artery | Avr, 2, 3 and AVF inferior STEMI |
| left coronary artery | high lateral 1, AVL, v5 and v6 |
| left anterior descending artery | septal and anterior v1, v2, v3, v4 |
| chronotropic | any drug or condition that influences HR |
| dromotropy | any drug or condition that affects conduction speed |
| inotropy | any drug or condition that alters the force or energy of muscular contractions |
| beta 2 receptors | adrenaline - results in vasoconstriction located in the pulmonary, cerebral and coronary arteries |
| beta 1 receptors | increase force of muscular contractions and rate of discharge adrenaline |
| excitation/contraction coupling | primarily achieved through Moving caclium into the myocyte |
| automaticity | The ability of the cell to self depolarise |
| absolute refractory period | when an action potential cannot be conducted ends halfway through phase 3 |
| excitability | The ability of a myocyte to respond to an action potential in an adjacent cell |
| gap junctions | present; create a functional syncytium |
| ATP | aerobic supply only |
| sequence of excitation | SA node, AV node, AV bundle, bundle branches, purkinje fibres |
| bathmotropic | Affects cardiac excitability |
| Cardiac pain | heavy/tight, radiating, SOB |
| Pleuritic pain | sharp, localised, SOB on exertion |
| Traumatic pain | sharp, localised, SOB on exertion |
| Functional residual capacity | expiratory reserve vol + residual vol. Reflects the amount of gas remaining in the lung at the end of a normal expiration |
| threshold potential | the all or nothing phenomenon |
| bradycardia | a heartbeat less than 60BPM, usually due to overstimulated receptors. Stable bradycardia is defined as a heart rate between 50-60BPM |
| RBBB causes | right ventricular hypertrophy pulmonary embolus ischaemic/rheumatic heart disease degenerative disease of conduction system cardiac tumours/surgery congenital heart disease cardiomyopathy acute pericarditis |
| LBBB causes | Chronic - hypertension, ischaemic/rheumatic heart disease, AMI, cardiomyopathy, aortic stenosis, cardiac tumours , hyperkalaemia, digoxin toxicity Acute -anteroseptal MI, congestive heart failure, pericarditis and myocarditis, cardiac trauma |
| left anterior fascicular blocks (LAFB) | Normal conduction interrupted anterior/lateral walls of L ventricle, posterior fascicle and RBB depolarised as normal then transmission via cell conduction to Lateral/anterior walls of L ventricle, QRS generally not widened, Acute Anteroseptal MI |
| Left posterior fascicular block (LPFB) | LPFB is rare RBB/Anterior/lateral wall depolarised as normal, then depolarisation of posterior wall of L ventricle Caused with anteroseptal MI in combination with RV or Inferior MI |
| Bifascicualr block | combination of RBBB with LAFB or LPFB Conduction to the ventricles is via the single remaining fascicle The ECG will show typical features of RBBB plus either left or right axis deviation RBBB + LAFB is the most common of the two patterns |
| Trifascicular block | incomplete (“impending“) trifascicular block can be inferred from: Fixed block of two fascicles with delayed conduction in the remaining fascicle (1st/2nd degree AV block), Fixed block of one fascicle with intermittent failure of the other two fascicles |
| sodium channel blockers 1A (procainamide, quinidine, disopyramide) | hypotension through reduced CO, ventricular arrhythmias, vertigo, seizures, prolonged WT, QRS widening |
| sodium channel blockers 1B (lignocaine) | dizziness, respiratory arrest, bradycardia, asystole, hypotension |
| sodium channel blockers 1C (Flecainide, Propafenone) | dizziness, prolonged QRS, heart block, asystole, hypotension |
| Selective Beta Blockers | Metoprolol, Atenolol, Bisoprolol |
| Non-selective Beta Blockers | Carvedilol, Sotalol, Propranolol |
| Potassium Channel Blockers (amiodarone, sotalol) | bradycardia and hypotension, ventricular dysrhythmias, prolonged QT interval, t wave inversion |
| Calcium channel blockers (verapamil, diltazem) | bradycardia and hypotension, first degree HB, syncope |
| digoxin | increased parasympathetic innervation and increased intracellular calcium decrease HR, increased contraction force, slows AV node conduction |
| vitamin k inhibitors | warfarin, Phenindione |
| aortic aneurism | Is a dilation (or enlargement) of the aorta |
| True aneurysm | Involves all three layers of the lumen |
| False aneurysm | Blood leaks through Intima but is contained by Media and Adventitia |
| Dissecting aneurysm | Blood penetrated Intima and creates secondary lumen between layers of vessel wall |
| pericarditis | Inflammation and swelling of pericardial sac causes may be viral, bacterial, fungal, idiopathic, autoimmune, post-surgical |
| STEMI mimics | pericarditis, Prinzmetal’s angina, Takotsubo |
Created by:
ZoDunk
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