Cardiac2

Front 1

caridac arrhythmias are disorders of the ___ and ___ of the heart, which can occur as the result of abnormal impulse generation or abnormal impulse conduction

Back 1

rate and rhythm

Front 2

nonpharmacologic tx of arrythmias:

Back 2

pacemakers, implantable cardioverter-defibrillator (ICD), radiofrequency ablation.

Front 3

pharmacologic tx of arrythmias:

Back 3

the drugs used in the tx of arrythmias are aimed at correcting the mechanisms of abnormal impulse generation and conduction.

Front 4

arrythmias can originate in:

Back 4

SA node, AV node, His Bundle, Purkinje finers, atrial muscle or ventricular muscle.

Front 5

all arrythmias result from alterations in :

Back 5

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

Front 6

arrythmias that develop can cause the heart to:

Back 6

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.

Front 7

atrial arrythmias:

Back 7

disorders of the artial rhythm or conduction

Front 8

examples of atrial arrythmias:

Back 8

sinus tachycardia, paroxysmal tachycardia, atrial flutter, atrial fibrulation (AFib)

Front 9

supraventricular tachycardias:

Back 9

disorders of atrial rhythm/conduction OR Av node conduction where impulses from atria to ventricles are disrupted

Front 10

examples of supraventricular tachycardias:

Back 10

AV node reentry, wolf-parkinson white syndrome, and paoxysmaland acute supraventriculr tachycardias

Front 11

ventricular tachycardias:

Back 11

disorders of ventricular rhythm or conduction

Front 12

examples of ventricular tachycardias:

Back 12

monomorphic ventricular tachycardia, polymorphic ventricular tachycardia, ventricular flutter and fibrulation

Front 13

sinus tachycardia:

Back 13

rhythms resulting from abnormalities in impulse rate (SA node starts to pace at a much faster rate than it should)

Front 14

heart rates:

Back 14

distance between 2 consecutive QRS complexes= beat to beat heart rate

Front 15

tachycardia:

Back 15

heart rate of more than 100 beats/min "fast heart"

Front 16

bradycardia:

Back 16

heart rate of fewer than 60 beats/min "slow heart"
(SA node starts to pace at a much slower rate than it should)

Front 17

atrial fibrilation:

Back 17

rhythms resulting from abnormalities in impulse conduction

Front 18

mechanism of atrial fibrilation:

Back 18

contimuous rapid firing of multiple ectopic foci of atrial cells

Front 19

characteristics of atrial fibrilation:

Back 19

atrial contractions chaotic and asynchronized. atrial rate = 400-600 bpm

Front 20

atrial fibrilation EKG:

Back 20

the rhythm is irregularly irregular. the sinus P wave is replaced by erratic fibrilatory waves.

Front 21

atrial fibrilation ventricle rhythm:

Back 21

irregular and ventricle filling is sporadic, resulting in weak contractions

Front 22

atrial fibrilation may occur in patients with :

Back 22

coronary artery disease, mitral valve disease, ischemic heart disease, pericarditis, HT, MI, heart failure, digitalis toxicity, and hyperthyroidism

Front 23

supraventricular tachycardias "AV Node reentry" mechanism:

Back 23

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

Front 24

characteristics of supraventricular tachycardia: Av node reentry

Back 24

palpitations, ventricular rhythm very regular, p waves hidden, narrow QRS wave. rate = 170-250 bpm - atria and AV node at high frequency

Front 25

supraventricular tachycardia: av node reentry :caused by abnormal impulse conduction:

Back 25

abnormal rhythm originates above the ventricles. the artia and ventricles start to beat out of synch. disrupts cardiac output (decreases). can cause dizziness, fainting.

Front 26

Reentry:

Back 26

occurs around scar tissue if you've had an MI or if the person has coronary artery disease

Front 27

Reentry:

Back 27

2 conducting pathways need to be present (slow and fast). Fast = long refractory period and slow= slow refractory period.

Front 28

Reentry:

Back 28

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

Front 29

supraventricular tachycardias : wolf-parkinson white syndrome: mechanism:

Back 29

presence of abnormal accessory pathway connecting artia with ventricle. bypasses AV conduction. it short circuits the usual delay at AV node.

Front 30

characteristics of wolf-parkinson white syndrome:

Back 30

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

Front 31

monomorphic ventricular tachycardia:

Back 31

rhythms resulting from abnormalities in impulse conduction. presence of ectopic focus in either ventricle. cause hot spots of contraction.

Front 32

monomorphic ventricular tachycardia:

Back 32

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

Front 33

ventricular tachycardia is caused by:

Back 33

early or late complication of MI, cardiomyopathy, valvular heart disease, myocarditis, low blood K, Ph (acid-base) changes, insufficient oxigenation, or anti-arrhythmic medications.

Front 34

vtach can deteriorate into:

Back 34

vfib (which can cause sudden death)

Front 35

polymorphic ventricular tachycardias: Torsades de pointes:

Back 35

rhythms resulting from abnormalities in impulse conduction

Front 36

polymorphic ventricular tachycardias:

Back 36

form of ventricular tachycardia with a specific variation in the conduction of the ventricular stimulus

Front 37

polymorphic ventricular tachycardias: mechanism:

Back 37

prolonged AP duration caused by early after-depolarizations (EADs)

Front 38

polymorphic ventricular tachycardias: characteristics:

Back 38

prolonged QT wave. ventricular rate: 150-250 bpm

Front 39

cause of polymorphic ventricular tachycardias:

Back 39

congenital, anti-arrythmic meds, calcium channel blockers, digitalis, haloperidol, electrolyte imbalances, MI, HIV, cocaine

Front 40

After depolarizations:

Back 40

occur in nonpacemaker cells. they are spontaneous depolarizations. they can trigger self-sustaining action potentials.

Front 41

Early after-depolarizations (EADs) occur:

Back 41

during Phase 3 of AP via excess calcium flowing into cardiac cell and too little K flowing out

Front 42

Late EADs occur:

Back 42

at the end of phase 3 or early phase 4 of APs via increased cellular calcium (ischemia, digitalis, excess catecholamines)

Front 43

heart block:

Back 43

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.

Front 44

heart block results ffrom defects in cardiac conducting system. atria beat regularly, but ventricles occassionally fail to be stimulated

Back 44

impulses between atria and ventricles can be blocked to varying degrees: once every secnd or third atrial impulse= 2:1 or 3:1 block

Front 45

complete heart block:

Back 45

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.

Front 46

characteristics of heart block:

Back 46

ECG: p waves normal, and QRS and T waves occur regularly, but at a much slower rate, completely independent of P wave rhythm.

Front 47

causes of heart block:

Back 47

scar tissue, fibrosis, medications (beta blockers, digitalis, calcium channel blockers, anti-arrhythmics [class 1 A]), electrolyte imbalances, cardiac surgery, and inflammatory disease

Front 48

hyperkalemia as a mechanism of arrythmia:

Back 48

changes in ECF levels of K has a profound impact on the heart. changes in ECF K alter concentration gradient between ICF and ECF.

Front 49

hyperkalemia= elevated ECF K:

Back 49

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

Front 50

cells that have automaticity include:

Back 50

SA node, AV node, Bundle of His, and purkinje fibers

Front 51

action potentials in the AV node and the purkinje fibers have :

Back 51

S phases caused by different ion currents

Front 52

in the SA node, phase 4 is the result of ____ions.

Back 52

sodium ions. (slow)

Front 53

in the SA node, phase 0 is the result of ____ ions.

Back 53

calcium ions. (voltage dependent)

Front 54

in the SA node, phase 3 is the result of ____ ions.

Back 54

potassium

Front 55

in the purkinje fibers, phase 1 is the result of ____ ions.

Back 55

potassium

Front 56

in the purkinje fibers, phase 2 is the result of ___ ions.

Back 56

calcium

Front 57

in the purkinje fibers, phase 3 is the result of ___ ions.

Back 57

potassium

Front 58

in the purkinje fibers, phase 4 is the result of ___ ions.

Back 58

sodium

Front 59

all arrythmias result from alterations in:

Back 59

impulse generation, conduction or both

Front 60

characteristics of ventricular tachycardia are:

Back 60

increased rate and QRS bizzare

Front 61

characteristics of atrial fibrillation are:

Back 61

chaotic contractions and no P wave

Front 62

characteristics of AV nod reentry are:

Back 62

palpitations and narrow QRS wave and hidden P wave