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Cardiology - paramedicine

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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  
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hydrostatic pressure   the force exerted by a fluid pressing against the wall (changes in APO)  
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osmotic pressure   force that opposes hydrostatic pressure  
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Cardiac output   SV x HR  
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Blood Pressure   CO x R  
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myocardial cells   conduct impulses muscular contraction intercalcated discs  
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pacemaker cells   generation and conduction of electrical impulses phase 4, 3 and 0  
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depolarisation   0- sodium channels open and sodium moves in 1- sodium channels close, potassium exits 2- calcium moves in and potassium leaves  
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repolarisation   3- potassium finishes leaving, calcium pumped out 4- potassium enters and calcium exits  
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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  
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Cardiovascular risk factors   diet, shift workers, age, depression, physical inactivity ...  
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ACS   A spectrum of diseases including UA, NSTEMI and STEMI that share a common pathology of a disrupted atherosclerotic plaque  
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unstable angina   chest pain that is not resolved through therapeutic means (episodic, new onset, easily provoked); non evidence of myocardial injury or necrosis  
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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  
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STEMI   Occurs when the thrombus that has formed and is completely occlusive. Myocardial necrosis results from interruption to myocardial blood supply  
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Initial lesion   1 macrophage infiltration, isolated foam cells  
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fatty streak   2 intracellular lipid accumulation  
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intermediate lesion   3 intracellular lipid accumulation, small extracellular lipid pools  
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atheroma   4 intracellular lipid accumulation, extracellular lipid core  
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fibroatheroma   5 single or multiple lipid cores, fibrotic cap  
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complicated lesion   6 surface defect, haemorrhage, thrombosis  
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ischaemia   occurs when blood supply to tissue is inadequate to meet physiological may have t wave inversion or ST depression  
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injury   prolonged ischaemia ST elevation  
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infarction   tissue or organ necrosis caused by ischaemia may show Q waves  
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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)  
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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)  
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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  
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dilated   -enlargement of chambers, systolic failures  
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hypertrophic   thickening of the heart muscle, diastolic then systolic failure  
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restrictive   stiffness of ventricular wall, diastolic failure  
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Right coronary artery   Avr, 2, 3 and AVF inferior STEMI  
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left coronary artery   high lateral 1, AVL, v5 and v6  
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left anterior descending artery   septal and anterior v1, v2, v3, v4  
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chronotropic   any drug or condition that influences HR  
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dromotropy   any drug or condition that affects conduction speed  
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inotropy   any drug or condition that alters the force or energy of muscular contractions  
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beta 2 receptors   adrenaline - results in vasoconstriction located in the pulmonary, cerebral and coronary arteries  
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beta 1 receptors   increase force of muscular contractions and rate of discharge adrenaline  
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excitation/contraction coupling   primarily achieved through Moving caclium into the myocyte  
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automaticity   The ability of the cell to self depolarise  
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absolute refractory period   when an action potential cannot be conducted ends halfway through phase 3  
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excitability   The ability of a myocyte to respond to an action potential in an adjacent cell  
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gap junctions   present; create a functional syncytium  
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ATP   aerobic supply only  
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sequence of excitation   SA node, AV node, AV bundle, bundle branches, purkinje fibres  
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bathmotropic   Affects cardiac excitability  
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Cardiac pain   heavy/tight, radiating, SOB  
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Pleuritic pain   sharp, localised, SOB on exertion  
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Traumatic pain   sharp, localised, SOB on exertion  
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Functional residual capacity   expiratory reserve vol + residual vol. Reflects the amount of gas remaining in the lung at the end of a normal expiration  
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threshold potential   the all or nothing phenomenon  
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bradycardia   a heartbeat less than 60BPM, usually due to overstimulated receptors. Stable bradycardia is defined as a heart rate between 50-60BPM  
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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  
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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  
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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  
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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  
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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  
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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  
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sodium channel blockers 1A (procainamide, quinidine, disopyramide)   hypotension through reduced CO, ventricular arrhythmias, vertigo, seizures, prolonged WT, QRS widening  
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sodium channel blockers 1B (lignocaine)   dizziness, respiratory arrest, bradycardia, asystole, hypotension  
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sodium channel blockers 1C (Flecainide, Propafenone)   dizziness, prolonged QRS, heart block, asystole, hypotension  
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Selective Beta Blockers   Metoprolol, Atenolol, Bisoprolol  
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Non-selective Beta Blockers   Carvedilol, Sotalol, Propranolol  
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Potassium Channel Blockers (amiodarone, sotalol)   bradycardia and hypotension, ventricular dysrhythmias, prolonged QT interval, t wave inversion  
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Calcium channel blockers (verapamil, diltazem)   bradycardia and hypotension, first degree HB, syncope  
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digoxin   increased parasympathetic innervation and increased intracellular calcium decrease HR, increased contraction force, slows AV node conduction  
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vitamin k inhibitors   warfarin, Phenindione  
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aortic aneurism   Is a dilation (or enlargement) of the aorta  
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True aneurysm   Involves all three layers of the lumen  
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False aneurysm   Blood leaks through Intima but is contained by Media and Adventitia  
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Dissecting aneurysm   Blood penetrated Intima and creates secondary lumen between layers of vessel wall  
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pericarditis   Inflammation and swelling of pericardial sac causes may be viral, bacterial, fungal, idiopathic, autoimmune, post-surgical  
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STEMI mimics   pericarditis, Prinzmetal’s angina, Takotsubo  
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