Cardio 10 Deck 3 Flashcards

(45 cards)

1
Q

Arrhythmias are caused by

A

physiological and/or anatomical consequences to prevent normal cardiac action potentials.

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2
Q

Normal HR depends on

A

the intrinsic electrical impulses initiated at the sinoatrial (SA) node and conducted to the AV node and over the ventricles.

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3
Q

Absolute refractory period

A

Regardless of the strength of a stimulus, the cell cannot be depolarized.

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4
Q

Relative refractory period

A

Stronger-than-normal stimulus can induce depolarization

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5
Q

Refractoriness

A

State of the cardiac cell which determines depolarization.

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6
Q

Damaged heart cells

A

may maintain a constant rate of refractoriness or may not be refractory at all.

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7
Q

Spontaneously depolarizing cells

A

SA nodes, AV nodes, His-Purkinje, special atrial cells

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8
Q

Automaticity

A

Ability of a heart cell to spontaneously depolarize and generate an action potential

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9
Q

Automaticity may be

A

altered, enhanced, decreased by:

Cell damage, biochemical disturbance, pharmacological agents, environmental toxins

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10
Q

Automacity is the target

A

Target for antiarrhythmic drugs

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11
Q

Reentry Phenomena

A

Reentry is the cause of some arrhythmias.

It depends on two anatomically or physiologically distinct electrical pathways.

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12
Q

Normally, impulses from the

A

AV node are conducted down both pathways in the same direction, bifurcating to cover the entire ventricle.

Sometimes this will get interupted and go out of order and this is wher eyou will have atopic irregular beats. Reentry phenomena

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13
Q

Reentry Phenomena

If a block is encountered

A

by the action potential in one of the pathways, then the impulse can only be conducted down the other pathway.

The impulse can return to the initial point of bifurcation and reexcite the myocardium

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14
Q

Short-circuiting conducting tissue can occur

A

and cause premature contraction.

PVC and PAC

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15
Q

If reentry is

A

repetitive, sustained ventricular arrhythmias, such as ventricular tachycardia, can occur.

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16
Q

Class I: sodium channel blockers

MOA

A

A: lengthen the duration of action potential
B: shorten the duration of action potential
C: minimally increase action potential

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17
Q

Class II: beta blockers

MOA

A
Reduce adrenergic activity in the heart
Sotalol: considered a class II and III drug
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18
Q

Class III: potassium channel blockers

MOA and example

A

Prolong effective refractory period and reduce speed of conduction
Amiodarone

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19
Q

Class IV calcium channel blocker MOA

A

Block the influx of calcium, reduce contractility (negative inotropism), decrease SA and AV node conduction
Significantly reduce afterload but little effect on preload

20
Q

Class IV calcium channel blocker example

A

Verapamil, diltiazem, bepridil

21
Q

potassium will

A

prolong the effect of refractory period to reduce the speed of conduction. This can stop the heart.

22
Q

I. Membrane-stabilizing agents (sodium channel blockers)

examples A,B,C

A

Quinidine, procainamide, disopyramide
Lidocaine, phenytoin
Encainide, Iorcainide, flecainide

23
Q

Beta blocker examples

A

Propranolol, metoprolol, sotalolol, and others

24
Q

III. Agents that prolong duration of the action potential (potassium channel blockers)

examples

A

Amiodarone, bretylium

25
. Agents that prolong duration of the action potential (potassium channel blockers) examples
Amiodarone, bretylium
26
IV. Calcium channel blockers examples
Verapamil, diltiazem, bepridil
27
Pharmacological management of arrhythmias requires
an office that is prepared, ready, and able to handle emergencies.
28
Drugs for arrhythmias you will see these patients for
infections, depression, anemia, fatigue, and so on. Be aware of actions and adverse drug interactions.
29
Beta Adrenergic Blockers various types include
include nonspecific beta antagonists, selective beta-antagonists, and those with or without intrinsic sympathomimetic activity (ISA)
30
Beta blockers are commonly seen in
In post-MI patients, cardioselective agents without ISA are preferred.
31
some beta blockers are used as
aniarrhythmics
32
Drugs with ISA may help
avoid a decrease in cardiac output (CO) and HR. May be preferred for patients who experience bradycardia with other BBs.
33
Beta Adrenergic Blockers more effective in
African American and older patients
34
BBs may NOT be
abruptly withdrawn, because it will increase beta receptor sensitivity
35
BB are no longer
first-line HTN drug choice
36
Amiodarone class
III antiarrhythmic
37
Amiodarone onset of action
oral – 2 days to 3 weeks
38
Amiodarone duration of action
7 to 50 days
39
Amiodaraone excreted in
feces, 1% in urine
40
Amiodarone watch out for
for use of grapefruit juice! inhibits the absorption and will cause the pts to get the wrong dose.
41
Dose of Amiodarone
Ventricular arrhythmias: 800 to 1,600 mg twice daily for 1 to 3 weeks, then decreased to 300 to 400 mg twice daily, maintenance 400 mg/day
42
Amiodarone ARR
thyroid, neurological, blue skin discoloration, bradycardia, lung damage not evident until advanced
43
Amiodarone drug interactions
many
44
For All Antiarrhythmics Monitoring
Potassium, blood urea nitrogen (BUN), creatinine, therapeutic drug levels Electrocardiography (ECG)
45
For All Antiarrhythmics Patient education
Take exactly as prescribed; do not double doses. Be aware of food–drug interactions. Monitor HR for regularity of rate and rhythm. Monitor BP at home.