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Pathopharm 326 > Dysrhythmias > Flashcards

Dysrhythmias Flashcards

1
Q

inotropic agents

A

Hormones, neurotransmitters, or medications that affect contractility

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2
Q

endogenous positive inotropic agents

A

epinephrine and norepinephrine released by the SNS

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3
Q

endogenous negative inotropic agent

A

acetylcholine released from the vagus nerve

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4
Q

P wave

A

atrial depolarization

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5
Q

QRS complex

A

ventricular depolarization

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6
Q

T wave

A

ventricular repolarization

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7
Q

Isoelectric Line

A

no electrical activity

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8
Q

PR interval

A

0.12-0.20 sec

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9
Q

QRS complex

A

less than 0.12 sec

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10
Q

Sinus arrhythmia

A

a degree of variability in the HR

still originates from SA node

Common in young people

HR still 60-100

HR fluctuates with respiration or ANS

PR and QRS both WNL

Intervals P-P are different–the longest P-P interval differs from the shortest by more than 0.12

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11
Q

Inappropriate automaticity

A

a cell initiates an action potential when it isn’t supposed to

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12
Q

Triggered activity

A

An extra impulse is generated during or right after repolarization

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13
Q

Re-entry

A

A cardiac impulse in one part of the heart continues to depolarize after the main impulse has finished

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14
Q

Any rhythm has sinus before it means what?

A

Originated in the SA (sinoatrial) node

SA node considered the pacemaker of the heart

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15
Q

Sinus bradycardia

A

HR < 60 bpm

Normal PR interval and QRS

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16
Q

Causes of sinus brady

A

hyperkalemia (slows depolarization)

vagal response

digoxin toxicity

late hypoxia

meds

myocardial infarction

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17
Q

Clinical manifestations of sinus brady

A

lightheadedness or dizziness (esp with exertion)

easily fatigued

syncope

dyspnea

chest pain or discomfort

confusion

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18
Q

Treatment of symptomatic bradycardia

A

atropine

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19
Q

Sinus Tachycardia

A

HR 100-150 bpm

P waves similar, may be partially hidden

Normal PR interval and QRS

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20
Q

Causes of Sinus Tachy

A

Catecholamines: exercise, pain, strong emotions

Fever

FVD (sinus tach often 1st sign of FVD)

Meds

Substances

Hypoxia

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21
Q

Treatment for Sinus Tachycardia

A

Dependent on cause

Hypovolemia=fluids
Fever=antipyretics
Pain= analgesics

If no known cause, beta blockers to ↓ HR & myocardial O2 consumption

22
Q

Paroxysmal Supraventricular Tachycardia (PSVT)

A 
HR 150-250 bpm
Originates in AV node
Usually no P wave, if present, look abnormal
QRS normal
Usually caused by re-entry phenomenon
Typically begins and ends suddenly
"feels like my heart is racing"
23
Q

PSVT causes

A 
Over exertion
Emotional stress
Stimulants
Digitalis toxicity
Rheumatic heart disease
CAD
WPW (Wolff-Parkinson-White)
Right sided heart failure
24
Q

PSVT clinical manifestations

A 
Palpitations
Chest pain
Fatigue
Lightheadedness or dizziness
Dyspnea
25
Premature Atrial Contractions (PACs)
Early P waves that usually look a little different Normal PR interval QRS does not follow the PAC Usually no consequences, but if frequent, at risk for other dysrhythmia (usually A-fib) Check electrolytes May need O2
26
Atrial Flutter
Originates in AV node--overrides SA node Reentry impulse that is repetitive & cyclic Atrial rhythm regular with atrial rate > 250 Ventricular rate slower--QRS usually narrow P wave classical sawtooth/shark tooth appearance May be 2:1, 3:1 or 4:1
27
Causes of Atrial flutter
``` Coronary artery disease cardiomyopathy heart valve disease congenital heart disease inflammation of the heart ↑BP Lung disease, overactive thyroid Electrolytes ```
28
Atrial Fibrillation
``` multiple irritable spots in the atria irregularly irregular (both atrial and ventricular) atria and ventricles not communicating HR 100-175 no identifiable P waves ```
29
Atrial fibrillation clinical manifestations
``` Palpitations heart racing fatigue dizziness chest discomfort shortness of breath may be asymptomatic ```
30
Atrial fib causes and complications
electrolytes hypoxia cv disease decreases CO → HF embolus → stroke
31
Atrial fibrillation treatment
Rate control: beta blockers, CCB, digitalis, amiodarone stroke prevention: anticoagulants, antiplatelets Non-pharm: abalation, cardioversion
32
Premature Ventricular Contractions (PVCs)
contraction coming from an ectopic focus in the ventricles comes earlier than the QRS should & doesn't follow normal rhythm or p-wave QRS wide and distorted
33
PVC causes
``` stimulants ELECTROLYTES hypoxia fever exercise emotional stress CVD ``` Treat the cause!
34
Ventricular Tachycardia
Consists of 3 or more PVCs together ectopic focus in ventricle takes control, firing repeatedly, no atrial contractions occurring SERIOUS decrease in CO
35
VTACH causes and treatment
Rate usually 150-200 bpm, usually regular Associated with MI, CAD, significant electrolyte abnormalities, HF, drug toxicity No p-wave evident, PR not measurable Pulse or pulseless--deadly rhythm so need to act quickly Beta blocker or CCB; electrolyte replacement
36
Ventricular fibrillation
irregular waveforms of varying shapes and sizes NO CARDIAC OUTPUT Check for pulse, begin CPR
37
dofetilide | indication
used to convert afib/aflutter to NSR & maintenance
38
dofetilide | moa
selectively blocking the rapid cardiac ion channel carrying K+ currents
39
dofetilide | side effects
Torsades (Black Box Warning), SVT, HA, dizziness, chest pain
40
Treatment for PSVT and sinus tach
adenosine
41
adenosine side effect
short burst of asystole until NSR returns | few others
42
adenosine moa
slows the conduction time through the AV node Short half life Only given IV
43
Treatment for symptomatic sinus brady
atropine
44
atropine moa
poisons the vagus nerve, inhibits postganglionic acetylcholine receptors and direct vagolytic action
45
AE of atropine
xerostomia, blurry vision, photophobia, tachycardia, flushing, hot skin ``` This drug is an anticholinergic so for side effects think: blind as a bat mad as a hatter red as beet hot as a hare dry as a bone ```
46
nursing implication for atropine
DO NOT GIVE UNLESS ON CARDIAC MONITORING
47
Treatment for PSVT, ventricular dysrhythmias
amiodarone
48
amiodarone MOA
prolongs the action potential duration and the effective refractory period in all cardiac tissues; blocks alpha and beta adrenergic receptors in the SNS
49
amiodarone | AE
LOTS, 75% of pts have them thyroid alterations corneal deposits Black box: pulmonary toxicity, hepatotoxicity, cardiac arrythmias
50
Treatment of rate and rhythm control
Beta blockers | Calcium channel blockers

Pathopharm 326 (16 decks)

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