<3 dysrhyms - patho E3 Flashcards
what do cardiac muscle cells do
1) automaticity
2) excitability
3) conductivity
4) contractility
atrial depolarization
“the squeeze during systole”
P wave (little bump) caused by the SA node
delay at AV node
PR segment
ventricular depolarization
“the squeeze during diastole”
QRS complex (big peak) caused by AV node
ventricular repolarization
“filling the tank”
T wave
no electrical activity
isoelectric line
what are responsible for the left ventricular contractions
bundle of his & purkinje fibers
PR interval
-beginning of the P wave to the tip of R
-interval: 0.12-0.20 seconds
QRS
-narrow
- less than 0.12 sec
sinus rhythm
-rate: 60-100
-rhythm: regular
-P wave: up & round before every QRS
-PR: 0.12-0.20 sec
-QRS: <0.12 sec
sinus arrhythmia
-a degree of variability in the heart rate
-a normal rhythm
-no changes to CO
-rate: 60 to 100
-PR: 0.12-0.20 sec
-QRS: <0.12 sec
**common in younger pop & associated w/ respiration or autonomic nervous system fluctuations
what causes dysrhythmias: inappropriate automaticity
a cell initiates action potentials when it isn’t supposed to
examples: myocardial ischemia & electrolyte imbalance
what causes dysrhythmias: triggered activity
an extra impulse is generated during or just after depolarization
ex: digoxin toxicity, SNS stim, genetics
what causes dysrhythmias: re entry
cardiac impulse in one part of the heart continues to depolarize after the main impulse has finished
ex: myocardial ischemia & electrolyte imbalance
sinus brady
-originates in the SA node
-regular rhythm
-PR: 0.12-0.20 sec
-QRS: <0.12 sec
-rate: <60
causes of sinus brady
-hyperK
-vagal response
-digoxin toxicity
-late hypoxia
-medications (betas, CCB, & amiodarone)
-MI
clinical manifestations of sinus brady
-lightheaded/dizzy
-easily fatigued
-syncope
-dyspnea
-chest pain/discomfort
-confusion
anytime you see an abnormal rhythm, what do you do first (unless lethal rhythm)
assess patient to see if the are symptomatic or not
ex: fit people can live at a lower HR
treatment of sinus brady
-atropine (anticholingeric)
-pace maker
sinus tach
-originates in SA node
-rhythm: regular
-PR: 0.12-0.20 sec
-QRS: <0.12 sec
-rate: 100-150
causes of sinus tach
-exercise, pain, strong emotions
-fever
-fluid volume deficit
-medications
-substances
-early hypoxia
treatment for sinus tach
hypovol = fluids
fever = antipyretics
pain = analgesics
if a heart thing = beta blockers
paroxysmal supraventricular tachycardia (PSVT)
-originates in the AV node, above the ventricles
-rate:150-250
-usually no P wave or will be abnormal
-QRS: <0.12 sec
-will begin & end suddenly “my heart is racing”
-
PSVT causes
over exertion
emotional stress
stimulants
digitalis toxicity
rheumatic heart disease
CAD
WPW (wolff parkinson white diease)
right sided heart failure
PSVT clinical signs & symptoms
palpitations
chest pain
fatigue
lightheadedness / dizzy
dyspnea
decreased CO
Premature Atrial Contractions (PACs)
-early P waves that usually look a little different, usually no consequence but if frequent indicates that a pt is at high (usually afib) risk for dysrhythmias
-PR: 0.12-0.20 sec
-QRS: <0.12 sec
what to do if you see a patient in PACs
check electrolytes
may need O2
atrial flutter
-originates in the AV, overrides the SA node
-caused by reentry impulse that is repetitive & cyclic so regular artial rhythm w/ an atrial rate of >250 bmps
- ventricular rate is slower & QRS doesn’t follow every P wave (Ps look like a sawtooth)
causes of atrial flutter
CHD, cardiomyopathy, heart valve disease, inflammation, high BP, lung disease, electrolytes
a fibrillation
-multiple irritable sports in the atria
-irregularly irregular (both atrial & ventricular)
-HR: 100-175
-no easily seen P wave or T wave
-r to r are not evenly spaced
a fib clinical manifestations (& flutter)
-palpitations
-heart racing
-fatigue
-dizziness
-chest discomfort
-SOB
~asym
what is our main question with afib
is it rate controlled?
idk losing mass amount of cardiac output so their rate is more important then rthymn
A.fib causes
-electrolyte imbalance
-hypoxia
-CAD
A.fib complications
-decreased CO
-heart failure
-embolus that can lead to stroke
treatment of A.fib & A.flutter
-rate control w/ beta blockers, CCB, digitalis, & amiodarone
-prevent stroke w/ anticoags & anti platelets
premature ventricular contractions (PVCs)
-contraction coming from an ectopic focus in the ventricles no atrial contraction
-it comes earlier than the QRS should come & doesn’t follow a normal rhythm or P wave
-wide and distorted in shape compared to normal QRS
causes of PVCs
stimulants
electrolytes
hypoxia
fever
exercise
emotional stress
CVD
to fix treat cause
V. tach
-consists of 3 or more PVCs together (counts in beats “12 beat run of v. tact”)
-ectopic focus within the ventricles takes controls and fires repeatedly -> no atrial contractions occurring no p wave
-seriously decrease CO
-HR between 150-200
Vtach is what type of rhythm
a deadly rhythm
full hands on deck, things need to happen and fast
V.tach is associated w/
MI, CAD, sign electrolyte abnorms, heart failure, drug toxicity & other bad things
how to treat V.tach
-ACLS -> depends on pulse, patient will be symptomatic very quickly unless it converts back to other rhythm
-may need anti dysrhythmic like beta or CCB
-electrolytes replacement
will you have a pulse w/ V.tach
some will, some wont but eventually everyone will lose a pulse
if no pulse, begin CPR immediately
V.FIb
irregular waveforms of varying shapes and sizes (the ventricles are just quivering)
No cardiac output
what to do if you see your patient in A.fib
check pulse and immediately start cpr
