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Electrophysiology

Cardiology - paramedicine

QuestionAnswer
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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