arrhythmia

Question	Answer
how is the heart innervated?	autonomic nervous system regulates the internal organ activities usually involuntarily and automatically. The ANS influences heart rate and myocardial contractility by sympathetic and parasympathetic stimulation. Sympathetic impulses increase heart activity and parasympathetic decrease heart activity - both systems must be in balance otherwise arrhythmia will result
what is arrhythmia ?	arrhythmia is the normal rhythm of the heart, disturbed. normal 60-70bpm (increase with uxercise) the upper chambers contract together, then the lower chambers contract together sinus node sends implies that can be mis interested and cause tacky or bradycardia fibrillation of lower chambers can halt blood flow - very dangerous situation
tachycardia	faster than normal heart beat can be in response to exercise or stress may prevent the heart from pumping an adequate supply of blood
bradycardia	slower than normal heart beat
atrial fibrillation	most common type of heart arrhythmia - the heart's upper chambers quiver quickly, preventing blood from pumping out completely - blood may pool inside the atria and clot. if a clot breaks off and reaches the brain, a stroke may occur
ventricular fibrillation	causes ventricles to quiver instead of umping blood out of the heart - this prevents blood circulation and can be fatal
causes of cardiac arrhythmia	myocardial infarction (80-90%) anaesthesia (20-50%) digoxin (10-20%)
target sites for arrhythmia drugs	ion channels; drugs for arrhythmia selectively depress tissues displaying abnormal pacemaker activity or conduction
auto arrhythmic cells in the heart	SA node AV Node AV bundle Purkinje fibres all are able to direct the basal heart rate it is Na+, K+ and Ca2+ ions that create cardiac potential
cardiac cycle	1 - voltage gated Na+ channels open, Na+ comes into cell (DEPOLARISATION) 2- Ca2+ enters cell (INITIATION OF CONTRACTION) 3 - K+ exits the cell (REPOLARISATION) 4 - recovery - Na+/K+ levels return to 'normal'
symptoms of arrhythmia	palpitations skipped heart beat light headedness dizziness fainting angina shortness of breath sweating
triggers of arrhythmia (non medical)	emotional distress physical exertion fatigue stimulants illicits some Rx
medical conditions triggering arrhythmia	coronary artery disease abnormal valve function heart failure cardiomyopathy electrolyte disturbances thyroid disease pneumonia cardiac surgery
medications that can trigger arrhythmia	appetite suppressants cough preparations psychotropic drugs antihistamines (at high doses) cocaine beta blockers pro-arrhythmic drugs** precipitating factors - caffeine, tobacco, alcohol, fear, stress, anxiety, exams - > overactive ANS, too strong plus heart stimulation
goals of treatment in arrhythmia	- identify and treat the underlying cause receive symptoms prevent sudden death reduce risk of recurrence and complications (e.g. thrombus)
non-pharmalogical management of arrhythmia	cessation of tobacco smoking healthy diet adequate exercise avoid stress avoid alcohol and coffee avoid medications that precipitate arrhythmia
pharmacological interventions	various drugs and classes: general MOA is to target the ion channels
Vaughn-Williams Classifications System	Class I (A,B,C) : sodium channels Class II: anti sympathetic nervous system agents Class III: affect potassium efflux Class IV: affect calcium channels and AV node
example vaughn williams system drug Class I A	dysopyramide
example vaughn williams system drug Class I B	lignocaine
example vaughn williams system drug class I C	flecainide
example vaughn williams system drug Class II	beta blockers
example vaughn williams system drug class III	amiodarone
example vaughn williams system drug class IV	verapamil
mechanisms of class one (sodium channel)	drug binds to Na+ channel to inactivate it binding to inactivate it; binding affinities influence their strength 1A) disopyramide - moderate moderate channel block, prolonged repolarisation 1B) lignocaine - mild mild Na+ channel block with shortened repolarisation 1C)
mechanisms of Class II beta blockers	drug binds to beta receptors to stop sympathetic action
mechanisms of Class III	(amiodarone!) most effective anti arrhythmic available most commonly prescribed blocks K+ channels weakly blocks Na+ and Ca2+ channels and beta receptors activity causing peripheral and coronary dilation
mechanisms of class IV calcium channel blockers	non-dihydropyradines verapamil and diltiazem -> affect Ca2+ channels at the SA and AV nodes dihydropyradines reduce systemic vascular resistance and adrenal pressure
digoxin	used in patients who are symptomatic despite maximal doses of ACE inhibitors digoxin inhibits the Na+/K+ ATPase pump of the myocardium, backing the recovery of the heart muscle in phase 4. Increases force of contraction (calcium), reduces rate of contraction.

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	Created by Amelia Claire almost 7 years ago