Flashcards
arrhythmia
Cards in this deck (29)
- 1how 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
- 2what 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 - 3tachycardiafaster than normal heart beat
can be in response to exercise or stress
may prevent the heart from pumping an adequate supply of blood - 4bradycardiaslower than normal heart beat
- 5atrial fibrillationmost 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
- 6ventricular fibrillationcauses ventricles to quiver instead of umping blood out of the heart - this prevents blood circulation and can be fatal
- 7causes of cardiac arrhythmiamyocardial infarction (80-90%)
anaesthesia (20-50%)
digoxin (10-20%) - 8target sites for arrhythmia drugsion channels;
drugs for arrhythmia selectively depress tissues displaying abnormal pacemaker activity or conduction - 9auto arrhythmic cells in the heartSA 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 - 10cardiac cycle1 - 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' - 11symptoms of arrhythmiapalpitations
skipped heart beat
light headedness
dizziness
fainting
angina
shortness of breath
sweating - 12triggers of arrhythmia (non medical)emotional distress
physical exertion
fatigue
stimulants
illicits
some Rx - 13medical conditions triggering arrhythmiacoronary artery disease
abnormal valve function
heart failure
cardiomyopathy
electrolyte disturbances
thyroid disease
pneumonia
cardiac surgery - 14medications that can trigger arrhythmiaappetite 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 - 15goals of treatment in arrhythmia- identify and treat the underlying cause
receive symptoms
prevent sudden death
reduce risk of recurrence and complications (e.g. thrombus) - 16non-pharmalogical management of arrhythmiacessation of tobacco smoking
healthy diet
adequate exercise
avoid stress
avoid alcohol and coffee
avoid medications that precipitate arrhythmia - 17pharmacological interventionsvarious drugs and classes: general MOA is to target the ion channels
- 18Vaughn-Williams Classifications SystemClass 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 - 19example vaughn williams system drug Class I Adysopyramide
- 20example vaughn williams system drug Class I Blignocaine
- 21example vaughn williams system drug class I Cflecainide
- 22example vaughn williams system drug Class IIbeta blockers
- 23example vaughn williams system drug class IIIamiodarone
- 24example vaughn williams system drug class IVverapamil
- 25mechanisms 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) - 26mechanisms of Class II beta blockersdrug binds to beta receptors to stop sympathetic action
- 27mechanisms 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 - 28mechanisms of class IV calcium channel blockersnon-dihydropyradines
verapamil and diltiazem -> affect Ca2+ channels at the SA and AV nodes
dihydropyradines
reduce systemic vascular resistance and adrenal pressure - 29digoxinused 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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- oh boy, my heart can't deal with this exam pressure
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