Created by Amelia Claire
about 7 years ago
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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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