Dysrhythmias Flashcards
inotropic agents
Hormones, neurotransmitters, or medications that affect contractility
endogenous positive inotropic agents
epinephrine and norepinephrine released by the SNS
endogenous negative inotropic agent
acetylcholine released from the vagus nerve
P wave
atrial depolarization
QRS complex
ventricular depolarization
T wave
ventricular repolarization
Isoelectric Line
no electrical activity
PR interval
0.12-0.20 sec
QRS complex
less than 0.12 sec
Sinus arrhythmia
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
Inappropriate automaticity
a cell initiates an action potential when it isn’t supposed to
Triggered activity
An extra impulse is generated during or right after repolarization
Re-entry
A cardiac impulse in one part of the heart continues to depolarize after the main impulse has finished
Any rhythm has sinus before it means what?
Originated in the SA (sinoatrial) node
SA node considered the pacemaker of the heart
Sinus bradycardia
HR < 60 bpm
Normal PR interval and QRS
Causes of sinus brady
hyperkalemia (slows depolarization)
vagal response
digoxin toxicity
late hypoxia
meds
myocardial infarction
Clinical manifestations of sinus brady
lightheadedness or dizziness (esp with exertion)
easily fatigued
syncope
dyspnea
chest pain or discomfort
confusion
Treatment of symptomatic bradycardia
atropine
Sinus Tachycardia
HR 100-150 bpm
P waves similar, may be partially hidden
Normal PR interval and QRS
Causes of Sinus Tachy
Catecholamines: exercise, pain, strong emotions
Fever
FVD (sinus tach often 1st sign of FVD)
Meds
Substances
Hypoxia
Treatment for Sinus Tachycardia
Dependent on cause
Hypovolemia=fluids
Fever=antipyretics
Pain= analgesics
If no known cause, beta blockers to ↓ HR & myocardial O2 consumption
Paroxysmal Supraventricular Tachycardia (PSVT)
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"
PSVT causes
Over exertion Emotional stress Stimulants Digitalis toxicity Rheumatic heart disease CAD WPW (Wolff-Parkinson-White) Right sided heart failure
PSVT clinical manifestations
Palpitations Chest pain Fatigue Lightheadedness or dizziness Dyspnea
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
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
Causes of Atrial flutter
Coronary artery disease cardiomyopathy heart valve disease congenital heart disease inflammation of the heart ↑BP Lung disease, overactive thyroid Electrolytes
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
Atrial fibrillation clinical manifestations
Palpitations heart racing fatigue dizziness chest discomfort shortness of breath may be asymptomatic
Atrial fib causes and complications
electrolytes
hypoxia
cv disease
decreases CO → HF
embolus → stroke
Atrial fibrillation treatment
Rate control: beta blockers, CCB, digitalis, amiodarone
stroke prevention: anticoagulants, antiplatelets
Non-pharm: abalation, cardioversion
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
PVC causes
stimulants ELECTROLYTES hypoxia fever exercise emotional stress CVD
Treat the cause!
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
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
Ventricular fibrillation
irregular waveforms of varying shapes and sizes
NO CARDIAC OUTPUT
Check for pulse, begin CPR
dofetilide
indication
used to convert afib/aflutter to NSR & maintenance
dofetilide
moa
selectively blocking the rapid cardiac ion channel carrying K+ currents
dofetilide
side effects
Torsades (Black Box Warning), SVT, HA, dizziness, chest pain
Treatment for PSVT and sinus tach
adenosine
adenosine side effect
short burst of asystole until NSR returns
few others
adenosine moa
slows the conduction time through the AV node
Short half life
Only given IV
Treatment for symptomatic sinus brady
atropine
atropine moa
poisons the vagus nerve, inhibits postganglionic acetylcholine receptors and direct vagolytic action
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
nursing implication for atropine
DO NOT GIVE UNLESS ON CARDIAC MONITORING
Treatment for PSVT, ventricular dysrhythmias
amiodarone
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
amiodarone
AE
LOTS, 75% of pts have them
thyroid alterations
corneal deposits
Black box: pulmonary toxicity, hepatotoxicity, cardiac arrythmias
Treatment of rate and rhythm control
Beta blockers
Calcium channel blockers
