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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
Q

Premature Atrial Contractions (PACs)

A

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
Q

Atrial Flutter

A

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
Q

Causes of Atrial flutter

A 
Coronary artery disease
cardiomyopathy
heart valve disease
congenital heart disease
inflammation of the heart
↑BP
Lung disease, overactive thyroid 
Electrolytes
28
Q

Atrial Fibrillation

A 
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
Q

Atrial fibrillation clinical manifestations

A 
Palpitations
heart racing
fatigue
dizziness
chest discomfort
shortness of breath
may be asymptomatic
30
Q

Atrial fib causes and complications

A

electrolytes
hypoxia
cv disease

decreases CO → HF
embolus → stroke

31
Q

Atrial fibrillation treatment

A

Rate control: beta blockers, CCB, digitalis, amiodarone

stroke prevention: anticoagulants, antiplatelets

Non-pharm: abalation, cardioversion

32
Q

Premature Ventricular Contractions (PVCs)

A

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
Q

PVC causes

A 
stimulants
ELECTROLYTES
hypoxia
fever
exercise
emotional stress
CVD

Treat the cause!

34
Q

Ventricular Tachycardia

A

Consists of 3 or more PVCs together

ectopic focus in ventricle takes control, firing repeatedly, no atrial contractions occurring

SERIOUS decrease in CO

35
Q

VTACH causes and treatment

A

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
Q

Ventricular fibrillation

A

irregular waveforms of varying shapes and sizes

NO CARDIAC OUTPUT

Check for pulse, begin CPR

37
Q

dofetilide

indication

A

used to convert afib/aflutter to NSR & maintenance

38
Q

dofetilide

moa

A

selectively blocking the rapid cardiac ion channel carrying K+ currents

39
Q

dofetilide

side effects

A

Torsades (Black Box Warning), SVT, HA, dizziness, chest pain

40
Q

Treatment for PSVT and sinus tach

A

adenosine

41
Q

adenosine side effect

A

short burst of asystole until NSR returns

few others

42
Q

adenosine moa

A

slows the conduction time through the AV node

Short half life

Only given IV

43
Q

Treatment for symptomatic sinus brady

A

atropine

44
Q

atropine moa

A

poisons the vagus nerve, inhibits postganglionic acetylcholine receptors and direct vagolytic action

45
Q

AE of atropine

A

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
Q

nursing implication for atropine

A

DO NOT GIVE UNLESS ON CARDIAC MONITORING

47
Q

Treatment for PSVT, ventricular dysrhythmias

A

amiodarone

48
Q

amiodarone MOA

A

prolongs the action potential duration and the effective refractory period in all cardiac tissues; blocks alpha and beta adrenergic receptors in the SNS

49
Q

amiodarone

AE

A

LOTS, 75% of pts have them
thyroid alterations
corneal deposits
Black box: pulmonary toxicity, hepatotoxicity, cardiac arrythmias

50
Q

Treatment of rate and rhythm control

A

Beta blockers

Calcium channel blockers

Pathopharm 326 (16 decks)

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