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62 Cards in this Set

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caridac arrhythmias are disorders of the ___ and ___ of the heart, which can occur as the result of abnormal impulse generation or abnormal impulse conduction
rate and rhythm
nonpharmacologic tx of arrythmias:
pacemakers, implantable cardioverter-defibrillator (ICD), radiofrequency ablation.
pharmacologic tx of arrythmias:
the drugs used in the tx of arrythmias are aimed at correcting the mechanisms of abnormal impulse generation and conduction.
arrythmias can originate in:
SA node, AV node, His Bundle, Purkinje finers, atrial muscle or ventricular muscle.
all arrythmias result from alterations in :
impulse formation (prob with pacemaker cells), impulse conduction (prob with nerve signals that initiate in pacemaker cells;they fail to reach nonpacemaker cells), or both
arrythmias that develop can cause the heart to:
beat too slowly, beat too rapidly, respond to APs that travel down the conduction pathways outside the conduction system, and/or respond to impulses originating from non SA nodes.
atrial arrythmias:
disorders of the artial rhythm or conduction
examples of atrial arrythmias:
sinus tachycardia, paroxysmal tachycardia, atrial flutter, atrial fibrulation (AFib)
supraventricular tachycardias:
disorders of atrial rhythm/conduction OR Av node conduction where impulses from atria to ventricles are disrupted
examples of supraventricular tachycardias:
AV node reentry, wolf-parkinson white syndrome, and paoxysmaland acute supraventriculr tachycardias
ventricular tachycardias:
disorders of ventricular rhythm or conduction
examples of ventricular tachycardias:
monomorphic ventricular tachycardia, polymorphic ventricular tachycardia, ventricular flutter and fibrulation
sinus tachycardia:
rhythms resulting from abnormalities in impulse rate (SA node starts to pace at a much faster rate than it should)
heart rates:
distance between 2 consecutive QRS complexes= beat to beat heart rate
heart rate of more than 100 beats/min "fast heart"
heart rate of fewer than 60 beats/min "slow heart"
(SA node starts to pace at a much slower rate than it should)
atrial fibrilation:
rhythms resulting from abnormalities in impulse conduction
mechanism of atrial fibrilation:
contimuous rapid firing of multiple ectopic foci of atrial cells
characteristics of atrial fibrilation:
atrial contractions chaotic and asynchronized. atrial rate = 400-600 bpm
atrial fibrilation EKG:
the rhythm is irregularly irregular. the sinus P wave is replaced by erratic fibrilatory waves.
atrial fibrilation ventricle rhythm:
irregular and ventricle filling is sporadic, resulting in weak contractions
atrial fibrilation may occur in patients with :
coronary artery disease, mitral valve disease, ischemic heart disease, pericarditis, HT, MI, heart failure, digitalis toxicity, and hyperthyroidism
supraventricular tachycardias "AV Node reentry" mechanism:
continuous reentry of impulse thru AV junction region (reentry circuit) (should only go in 1 direction)with depolarizing stimulus to atria and ventricle each time it passes thru
characteristics of supraventricular tachycardia: Av node reentry
palpitations, ventricular rhythm very regular, p waves hidden, narrow QRS wave. rate = 170-250 bpm - atria and AV node at high frequency
supraventricular tachycardia: av node reentry :caused by abnormal impulse conduction:
abnormal rhythm originates above the ventricles. the artia and ventricles start to beat out of synch. disrupts cardiac output (decreases). can cause dizziness, fainting.
occurs around scar tissue if you've had an MI or if the person has coronary artery disease
2 conducting pathways need to be present (slow and fast). Fast = long refractory period and slow= slow refractory period.
premature atrial depolarization arrives at at AV node. one pathway is still refractory (conduction slowed) but the other can conduct impulse normally. reentry into atrium occurs when SLOWED impulse undergoes retrograde (backward) conduction into atrium
supraventricular tachycardias : wolf-parkinson white syndrome: mechanism:
presence of abnormal accessory pathway connecting artia with ventricle. bypasses AV conduction. it short circuits the usual delay at AV node.
characteristics of wolf-parkinson white syndrome:
normal rate unless Afib present.
normal rhythm unless Afib present.
short PR interval, delta wave, wide QRS complex
it is a congenital rhythm disorder, young children, adults ages 20-35.
PVST and atrial fibrilation are the 2 most common tachydysrhythmias seen in this syndrome
monomorphic ventricular tachycardia:
rhythms resulting from abnormalities in impulse conduction. presence of ectopic focus in either ventricle. cause hot spots of contraction.
monomorphic ventricular tachycardia:
rate= 100-250 bpm, lethal beat, interferes with pumping action of heart (rest time for ventricular filling). the rhythm is regular. bizzare QRS complex via fusion beat
ventricular tachycardia is caused by:
early or late complication of MI, cardiomyopathy, valvular heart disease, myocarditis, low blood K, Ph (acid-base) changes, insufficient oxigenation, or anti-arrhythmic medications.
vtach can deteriorate into:
vfib (which can cause sudden death)
polymorphic ventricular tachycardias: Torsades de pointes:
rhythms resulting from abnormalities in impulse conduction
polymorphic ventricular tachycardias:
form of ventricular tachycardia with a specific variation in the conduction of the ventricular stimulus
polymorphic ventricular tachycardias: mechanism:
prolonged AP duration caused by early after-depolarizations (EADs)
polymorphic ventricular tachycardias: characteristics:
prolonged QT wave. ventricular rate: 150-250 bpm
cause of polymorphic ventricular tachycardias:
congenital, anti-arrythmic meds, calcium channel blockers, digitalis, haloperidol, electrolyte imbalances, MI, HIV, cocaine
After depolarizations:
occur in nonpacemaker cells. they are spontaneous depolarizations. they can trigger self-sustaining action potentials.
Early after-depolarizations (EADs) occur:
during Phase 3 of AP via excess calcium flowing into cardiac cell and too little K flowing out
Late EADs occur:
at the end of phase 3 or early phase 4 of APs via increased cellular calcium (ischemia, digitalis, excess catecholamines)
heart block:
rhythms resulting from abnormalities in impulse conduction. it is the failure of impulse to get to ventricle from atria. may be partial to full blocking. primary is not very seriuos but tertiary heart block is very serious.
heart block results ffrom defects in cardiac conducting system. atria beat regularly, but ventricles occassionally fail to be stimulated
impulses between atria and ventricles can be blocked to varying degrees: once every secnd or third atrial impulse= 2:1 or 3:1 block
complete heart block:
total dissociation between atrial and ventricular activity. impulses from atria to ventricle are not conducted at all. atrial impulses from SA node normal, but ventricles generate their own much slower impulses.
characteristics of heart block:
ECG: p waves normal, and QRS and T waves occur regularly, but at a much slower rate, completely independent of P wave rhythm.
causes of heart block:
scar tissue, fibrosis, medications (beta blockers, digitalis, calcium channel blockers, anti-arrhythmics [class 1 A]), electrolyte imbalances, cardiac surgery, and inflammatory disease
hyperkalemia as a mechanism of arrythmia:
changes in ECF levels of K has a profound impact on the heart. changes in ECF K alter concentration gradient between ICF and ECF.
hyperkalemia= elevated ECF K:
reduces gradient (K moves out of cell).

reduces resting membrane potential (membrane less negative inside than normal, makes it more excitable & easier to depolarize). the difference in magnitude from normal resting membrane potential to AP is reduced. this prolongs AP duration, slowing ventricular contraction. (broadening QRS complex-->abnormal sequence cardiac conduction -->aberrant cardiac rhythms). the result is: the heart stops beating. the heart muscle is contracting and not relaxing
cells that have automaticity include:
SA node, AV node, Bundle of His, and purkinje fibers
action potentials in the AV node and the purkinje fibers have :
S phases caused by different ion currents
in the SA node, phase 4 is the result of ____ions.
sodium ions. (slow)
in the SA node, phase 0 is the result of ____ ions.
calcium ions. (voltage dependent)
in the SA node, phase 3 is the result of ____ ions.
in the purkinje fibers, phase 1 is the result of ____ ions.
in the purkinje fibers, phase 2 is the result of ___ ions.
in the purkinje fibers, phase 3 is the result of ___ ions.
in the purkinje fibers, phase 4 is the result of ___ ions.
all arrythmias result from alterations in:
impulse generation, conduction or both
characteristics of ventricular tachycardia are:
increased rate and QRS bizzare
characteristics of atrial fibrillation are:
chaotic contractions and no P wave
characteristics of AV nod reentry are:
palpitations and narrow QRS wave and hidden P wave