W2 D3/4 - ECG Theory Atrial Flashcards
What is re-entry?
Atrial cells begin firing on their own
* the impulse travels to the AV node and into the ventricle BUT also makes it way back to the atrial cells
* the impulse does not go through every time because the AV node is in absolute refractory
* 150-350 impulses a min from atrial cells
the reentry can cause atrial flutter
If a clot forms in the arterties or in the heart, where could it travel?
What are your concerns?
To the organs, brain, major arteries throughout body.
Concerned for stroke or occulsive artery; lack of blood flow to extremty
A DVT clot forms in veins and travels up to the lungs
What is a PAC?
What are the causes?
An early beat w/ upright different shaped P wave.
A clump of cells in the atria fire an impulse on their own, depolarizing the atria causing an abnormal P wave followed by a QRS (conducted) or not (non-conducted)
Causes
General
* sympathomimetics
* ischemic heart disease
* stress
* anxiety
* nicotine
* caffeine
Structural
* CHF
* atrial enlargement
* heart valve disease
Treatment
* 1 PAC randomly is ok
* none, investigate underlying cause
* frequent PACs treat symptoms
Differentiate PAC vs. non-conductive PAC
How is sinus pause different?
PAC
* early impulse received by AV node and sent through resulting in early PQRST
Non-conductive PAC
* AV node is still in absolute refractory period so it cannot take the impulse.
* a P wave shows with no QRS
Sinus pause/block does not have PQRST at all
Differentiate sinus pauses: block vs. arrest
Sinoartrial block
* an exact interval of R-R
* blocked impulse from SA node
Sinus arrest
* NOT an exact interval of R-R
* SA node has no impulse
A pause
* general term
* when the rhythm is not sinus but there is a missing PQRST
Describe the patho and diagnosis of atrial tachycardia
A problem with the circuit reentry or automaticity of atrial tissue.
An ectopic site becomes the pacemaker allowing normal depolarizing through the ventricles (QRS)
* HR 150-250, too fast to see P or T
* regular rhythm, normal QRS
* increased oxygen demand
Impact
* increases workload of the heart, myocardial oxygen demand
* lowered diastolic phase, ventricular filling, SV, CO, coronary blood supply
* causing myocardial ischemia and infarction
Causes
General
* sympathomimetics
* ischemic heart disease
* electrolyte imbalance
* hypoxia
* simulants
* stress, nicotine, caffeine
Structural
* atrial scaring
* atrial enlargement
* CHF
* valve disease
* COPD
* pulmonary hypertension
What is the treatment for atrial tachycardia?
Treatment
Symptomatic/unstable
(hypotension, LOC, shock, chest discomfort, acute HF)
* syncronized cardioversion
Asymptomatic
* vagal maneuvers
* beta blockers: metoprolol
* CCB: diltiazem
* amiodarone
* adenosine (stable only, 6 or 12 mg, 10 sec., fast IV + 20 mL flush, asystole/bradycardia, chest discomfort)
Differentiate atrial tachycardia and sinus tachycardia?
Atrial tach. eats the P wave
* usually 150-250
Sinus tach. has all components of PQRST
* usually 100-150
How does syncronized cardioversion work?
Electrical shock is delivered outside of the second half of the T wave (refractory period)
* could cause fatal arrhythmias if shocked during repolarization / last half of T wave
* syncronized is safest
Explain atrial flutter
Variable vs. non-variable conduction
What is the patho?
A saw tooth atrial pattern with flutter waves between R-R intervals.
The atria is creating its own impulses at more than 250 BPM with a varying ventricular rate as the AV node does not accept every impulse. This is d/t:
* reentry; continuous impulses sent to AV node but not allowed through, sent back to atria
* altered automaticity; atria cells firing on their own without SA node
Variable vs. non to variable conduction
* variable has inconsistent conduction ratio
* non-variable has same conduciton ratio through strip and between all R-Rs
* small waves are atrial contraction
* big waves / QRS is ventricle
Causes
General
* sympathomimetics, ischemic heart disease, electrolyte imbalance, hypoxia, pericarditis, myocarditis
Structural
* valve heart disease, cardiomypathy, CHF, cardiac surgery, hypertension, chronic lung disease
Explain atrial fibrillation
Controlled vs. uncontrolled
An irregular rhythm with fibrillatory waves. The atria is quivering from atrial impulses of 300-600 BPM
* Only QRS is normal
* no P or T waves
* irregular
The AV node tries to stop too many impulses from getting through to the ventricles
* unsuccessful = uncontrolled above 100 BPM
* successful = controlled under 100 BPM
A-flutter may lead to a-fib
Causes
General
* sympathomimetics, ischemic heart disease, electrolyte imbalance, hypoxia, hypertension, pericarditis, myocarditis
Structural
* valve heart disease, cardiomypathy, CHF, cardiac surgery, hypertension, chronic lung disease
What are the treatments for A-fib and flutter?
Treatment goals
RATE control or more than 48 hours
* meds that work on beta 1 to control rate
* … metoprolol and diltiazem
* anticoagulants
RHYTHM control less than 48 hours ONLY
* unstable; electrical conversion
* stable: amiodarone first, then EC
* over 48hours we do not treat rhythm, risk of emboli
Hypomagnesemia common cause
Criteria…
* critical / chronic?
* stable / unstable?
* less than / more than 48 hours?
* afib is the cause of instability / instability causing afib?
* rate control / rhythm control?
Explain the cause of variations in P wave and PR interval
no P wave
* no impulse at all
peaked/pointed upright P wave
* right atrial enlargement or unequal impulse strength from one atria
* ectopic atrial cells
double bump P-wave
* left atrial enlargement
inverted P wave
*
lengthened PR interval
* longer than 0.20 sec
* may indicate 1st degree heart block
shortened PR
* pre-excitation, precense of accessory pathway from atria to ventricles
* AV junctional rhythm
Explain the cause of variations in QRS & QT intervals
Not yet learned in week 2
Wide QRS complex
* more than 0.10/0.12 sec wide
* bundle branch block
* ventricular rhythm
* hyperkalemia
Lengthened QT
* more than 450 msec
* torsades de pointes / ventricular arrhythmias
* hypokalemia
* hypomagnesaemia
* hypocalcemia
* hypothermia
* MI, post ROSC, ^ ICP
* meds!!!
Explain the cause of variations in ST interval & T wave
not yet learned week 2
Elevated ST
* acute STEMI
* pericarditis
* left bundle branch block
Depressed ST
* myocardial ischemia / NSTEMI
* posterior MI
* digoxin
* hypokalemia
* SVT
* right or left bundle branch block
T-wave
Peaked
* hyperkalemia
* early STEMI
Inverted
* myocardial ischemia / infarction
* bundle branch block
* ventricular hypertrophy
* PE
* cardiomyopathy
Flattened T wave
* non-specifc
* ischemia
* hypokalemia
