Dysrhythmias Flashcards
normal electrical conductivity of heart
Rate 60-100 Regular rhythm P waves: upright and round, one before every QRS, regular rhythm PR interval 0.12-0.20 sec QRS: <0.12 sec
sinus arrythmia
normal
variability in HR 60-100bpm
common in young people
HR fluctuates with respiration or Autonomic nervous system
what is a dysrhythmia
abnormality of cardiac rhythm
problems with impulse generation or conduction
what causes dysrhythmia’s?
inappropriate automaticity
triggered activity re-entry
what are the different types of sinus rhythms?
sinus rhythmmia sinus arrhythmia sinus tachycardia sinus bradycardia paroxysmal supraventricular tachycardia
sinus bradycardia
SA node
regular rate less than 60
normal rhythm
normal PR (.12-.20) and QRS interval (< 0.12)
causes of sinus brady
hyperkalemia vagal response digoxin toxicity late hypoxia meds MI
manifestations of sinus brady
lightheadedness/ dizziness with exertion easily tired syncope or near syncope dyspnea chest pain/discomfort confusion
treatment of symptomatic bradycardia
atropine: anticholenergic
if drug not effective: pacemaker
sinus tachycardia
SA node HR: 100-150 regular rhythm p wave similar or partially hidden normal PR (.12-.20)interval and QRS (<0.12)
causes of tachycardia
catecholamines: (exercise, pain, strong emotions) fever fluid volume deficit meds (epi, albuterol, beta agonists) substances (caffeine, nicotine, cocaine) hypoxia
treatment for sinus tachycardia
based on cause
hypovolemia= fluids
fever= anti-pyretic
pain= analgesics
paroxysmal supraventricular tachycardia (PSVT)
caused by re-entry phenomenon begins and ends suddenly "feel like my heart is racing" HR 150-250 AV node usually no P wave if present, abnormal QRS looks normal (<0.12)
causes of PSVT
over exertion emotional stress stimulants digitalis toxicity rheumatic heart disease CAD Wolff- Parkinson-White right sided heart failure ( Cor pulmonale)
clinical signs and symptoms of PSVT
palpitations chest pain fatigue lightheaded/dizziness dyspnea
premature atrial contractions (PACs)
early P waves that look different normal PR interval (12-20) QRS does follow PAC usually not a problem but frequent PAC's cause pt high risk for dysrhythmia's check electrolytes may need O2
two types of atrial dysrhythmias
atrial flutter
atrial fibrillation
atrial flutter
AV node, overrides SA node re-entry impulse that is repetitive and cyclic Atrial pulse Rate >250 bpm, regular atrial rhythm ventricular rate is slower P was "SAWTOOTH" QRS narrow may be 2:1, 3:1, or 4:1 ( ex: 2 p wave per 1 QRS complex)
causes of atrial flutter
CHD cardiomyopathy heart valve disease congenital heart disease inflammation of heart (myocarditis) high BP overactive thyroid, lung disease electrolytes
atrial fibrillation
multiple irritable spots in atria (all sending signals)
irregularly irregular (atrial and ventricular)
HR 100-175
no identifiable P wave
fibrillation waves
clinical manifestations of Atrial Fibrilation
palpitations heart racing fatigue dizziness chest discomfort sob may be asymptomatic
complications and causes of Afib
electrolytes hypoxia cardiovascular disease decreased cardiac output heart failure embolus/ stroke
untreated a-fib doubles your risk of heart-related ____, and causes a 4-5 times greater risk of ____
death, stroke
treatment of Afib
beta blockers, CCB, digitalis, amiodarone
stroke prevention: anticoagulants, antiplatelets
ablation
cardioversion
types of ventricular dysrhytmias
PVC’s
VTACH
VFIB
PVCs
contraction coming from ectopic focus in ventricles
PVC’s come earlier than QRS and doesn’t follow normal rhythm or p-wave
wide and distorted QRS ( >.12)
no atrial contraction, no P wave
causes of PVC’s
stimulants electrolytes hypoxia fever exercise emotional stress CVD
treatment of PVC’s
treat cause
three sub-types of PVC’s
bigeminy
trigeminy
quadrigeminy
VTACH
3 or more PVC’s together
seriously decreases cardiac output
ectopic focus within the ventricles takes control and fires repeatedly, NO atrial contractions
DEADLY RHYTHM
VTACH presentations
Rate: 150-200, usually regular
no p-wave evident, PR measurable
VTACH associated with
MI, CAD, significant electrolyte abnormalities, HF, drug toxicity
treatment of VTACH
ACLS
depends on pulse, pt symptomatic very quickly unless converts back to rhythm
may need anti-dysrhythmic (beta blocker or CCB)
electrolyte replacement
VFIB
irregular wave forms of varying shapes and sizes
ventricles are QUIVERING
NO CARDIAC OUTPUT
cardiac muscle cells have
automacity
excitability
conductivity
contractility
automacity
ability to generate electrical impulse
excitability
ability of cell to interpret impulse
conductivity
ability to receive and conduct signal
contractility
ability to shorten in respond to impulse. “squeezing”
depolarization
light switch turning on, occurs during systole causing squeezing
repolarization
makes cells ramp up
atrial depolarization
P wave
ventricular depolarization
QRS complex
ventricular repolarization
T wave
atrial repolarization
do not typically see
what does potassium-ATP pump cause
causes action potentials
SA node
stimulates atria to contract
P wave
atrial contraction
AV node
makes ventricular go off
After P wave and before QRS
perkinjie fibers
LT ventricular contractions
what causes dysrhythmias?
inappropriate automaticity
triggered activity
re-entry
inappropriate automaticity
a cell initiates action potential when its not supposed to
triggered activity
an extra impulse generated during or just after repolarization
re-entry
cardiac impulse in one part of the heart contributes to depolarization after main impulse has finished
wolfe-parkinson-white
precipitates PSVT, r/t other rhythm abnormalities
