EKG lecture 4 pt 1 Flashcards
through slide 53
Describe the Sxs of arrythmia
1) Asymptomatic, incidental findings
2) Clinically apparent symptoms:
Palpitations
Lightheadedness to syncope – decreased C.O.
Angina – 2nd to supply: demand mismatch
Acute HF
ACS/Sudden death
List the causes of arrythmias
1) Hypoxia: irritable myocardium – pulmonary disease/PE
2) Ischemia & Irritability: stable angina, ACS, myocarditis (viral)
3) Inherited: prolonged QT, HOCM
4) Sympathetic stimulation: exercise, stress, hyperthyroidism, HF
5) Bradycardia: low cardiac output, tachy-brady (sick sinus) syndrome
6) Electrolyte d/o: hypoK/hyperK
7) Drugs: antiarrhythmic drugs, others
8) Stretch: hypertrophy, dilation – HFrEF, cardiomyopathies, valvular dz
HIISBEDS
What are rhythm strips?
View rhythm over longer duration than standard 12 lead
When would you use ambulatory monitors? What are 2 different kinds?
1) Intermittent arrhythmias
2) Holter monitor
Zio patch
Besides ambulatory monitors, what are the other 3 types of monitors? When would you use them?
1) Event monitor – infrequent arrhythmias, patient initiated based on symptoms
2) Implantable event monitor
3) Consumer oriented HR monitors – smart watch/phone
List the 4 different ways to determine HR on an EKG
1) Estimate by 300-150-100-75-60-50-42
2) 300/# of large boxes between R-R interval
3) 1500/# of small boxes between R-R interval
4) For slow/irregular rates, count the # QRS complexes noted on the rhythm strip & multiply by 6 (typical EKG runs for 10 seconds)
Arrhythmias of sinus origin (AKA “supraventricular”): List the different kinds
Sinus bradycardia - slow
Sinus tachycardia - fast
Sinus arrhythmia – normal variant
Sinus arrest/exit block………no sinus activity, flat line
Sinus arrest/exit block with junctional escape…..secondary site origin
List all the differentials for sinus bradycardia
1) Enhanced vagal tone (seen in athletes, valsalva)
2) Medications – negative chronotropes - B-blocker, CCB, et. al.
3) Opioids
4) Myocardial ischemia
5) Hypothyroidism
6) hypothermia
7) hyperkalemia
8) Stroke
9) OSA during apneic episodes
10) Sinus node dysfunction – SSS, sinus arrest
11) Many infectious causes
Explain the physiology of sinus arrythmia
Inspiration speeds up the rate (decreased pre-load)
Expiration slows of the heart rate (increased pre-load)
Explain sinus arrest and sinus exit block
1) Sinus arrest: sinus node does not fire = flat line
2) Sinus exit block: SA node fires but no propagation = flat line
-Neither above have P-wave or any electrical activity unless an escape beat emerges (atrial, junctional, ventricular).
-Escape beats = inherent pacemakers in most myocardial cell
Give an overview of the pacemakers of the heart
1) Normal (sinus pacemaker): SA node 60-100 – “over drives” the other pacers
2) Non-sinus pacemakers (ectopic) result in escape beats – rescue beats if SA node does not fire or propagate a wave of depolarization
a) Atrial pacemakers ~ 60-75/minutes
b) Junctional pacemakers (at or near AV node) ~ 40-60/minute – Most common
c) Ventricular pacemakers ~ 30-45/minute
Explain junctional escape
1) Originates near AV node
2) Usual pattern of atrial depolarization does not occur – normal P wave NOT seen
3) Most often, no P wave seen
4) Occasionally a retrograde P wave may be seen – atrial depolarization moving backward from AV node into the atria and axis reverse
Occasionally a retrograde P wave may be seen with junctional escape; explain what this means
1) A normal P wave is upright in lead II and inverted in aVR
2) Retrograde P wave is inverted in lead II, upright in aVR … but may be hidden in QRS complex of follow
Junctional escape beat: When may it occur? Where does i originate?
1) May follow sinus arrest or sinus exit block
2) Originates at or near AV node, rate of ~ 40-60
Junctional escape beat: Explain what it looks like on an EKG
1) P waves may be absent or occasionally retrograde – after QRS
2) QRS is narrow; depolarization progresses down the ventricular conduction system
“No P wave; electrically silent until escape beat occurs and restores electrical activity” describes what?
Sinus arrest or exit block
Sinus arrest = sinus ___________ clinically
exit block
Explain sinus arrest/ sinus exit block
SA node depolarization is not seen on EKG
neither initiates depolarization of atria
so…can’t tell the difference with EKG … result is the same
Medications, infiltrative processes (amyloid, sarcoid), fibrosis, & inflammatory conditions such as Rheumatic fever
What are the 2 main causes of non-sinus arrythmias?
- Ectopic rhythms: enhanced automaticity or d/o of impulse formation
- Re-entrant rhythms: d/o of impulse transmission
Non-sinus rhythms can be single isolated beats or sustained ____________
arrhythmias
When do ectopic rhythms occur?
“Fastest Pacer Drives the heart” – under abnormal circumstances, non-sinus pacer can be stimulated to fire faster & faster and over “take over” the normal SA node pacer
Ectopic rhythms:
1) Define them
2) Are they always sustained?
3) What causes them?
1) Abnormal rhythms that arise from outside the SA node
2) Single/isolated beats or sustained
2) Enhanced automaticity of a non-sinus node site, either single focus or roving site - essentially disorder of impulse formation
What are some common etiologies of ectopic rhythms?
Digitalis toxicity
B-adrenergic stimulation – SABA/LABA (B1 vs. B2 vs. non-cardio select BB)
Caffeine, alcohol
Stimulant drugs – ADHD Rx, cocaine, methamphetamines
Psychological stress
Re-entry rhythms:
1) What causes them?
2) Why do they vary in size?
1) Abnormal electrical activity resulting in a reentry loop
2) Within AV node, entire chamber, or if an accessory pathway can involve atria and ventricle
- Are NORMAL P-waves present? - Normal shaped P waves and normal P wave axis (0-70 degrees therefore + in lead II, - in lead aVR.)
What are the 3 potential answers to this question? Explain each
1) YES … present and normal axis = then origin of arrhythmia is atrial, likely at or near Sinus node
2) YES … present, abnormal axis or appearance = then origin is atrial other than at or near sinus node, retrograde from junctional or accessory pathway from a ventricular origin
3) NO … no P waves present = then origin is below atria in AV node or ventricles
“What is the relationship between the P waves and the QRS complexes?” What may cause this relationship to be abnormal?
A-V dissociation – atria and ventricles depolarize independently of each other, and no association noted
How do you answer the question “Is the rhythm regular or irregular (look at rhythm strip)?” What may it help determine?
Usually immediately obvious
May be most critical in determining rhythm – think A. fibrillation vs. A. flutter
Supraventricular arrythmias:
1) Define these
2) What are 2 different forms? Which is common?
3) How long are they?
1) Arrhythmias originates above the ventricles:
Atria or vicinity of AV node (junctional)
2) Single or sustained
Single - common and of no clinical significance unless initiate more sustained arrhythmias
3) Seconds or life long
Atrial & junctional Premature beats: Describe them
Common
Neither indicating pathology
Do not require treatment
May initiate more sustained arrhythmias
Both usually conducted normally to the ventricles with a resulting narrow QRS complex (supraventricular origin)
Explain atrial premature beats
Amplitude and duration of 1st P-wave?
Different contour of the P wave – depole originates at different site than SA node
Timing – 3rd beat is early resulting in a premature atrial contraction
Junctional premature beat: What do they look like?
Usually, no visible P wave or occasionally retrograde P wave similar to Junctional escape beats with sinus arrest.
What are the 2 forms of junctional premature beat?
Jct premature beat occurs early (A)
VS.
Jct escape beat occurs late (B)
Give examples of Sustained supraventricular arrhythmias
1) AV nodal reentrant tachycardia (AVNRT) – aka paroxysmal supraventricular tachycardia
2) Atrial flutter
3) Atrial fibrillation
4) Multifocal Atrial Tachyccardia (MAT)
5) Paroxysmal Atrial Tachycardia (PAT) – aka ectopic atrial tachy
6) AV reciprocating tachycardia – see preexcitation lecture
Describe AV nodal reentrant tachycardia (AVNRT). What are the S/Sx and what is the etiology?
Common
Sudden onset - usually initiated by premature supraventricular beat (atrial or jct)
Abrupt termination
May occur in normal hearts
S/S: palpitations, SOB, dizziness, syncope
Etiology: Alcohol, coffee, excitement
Describe what AVNRT looks like on an EKG
1) Regular rhythm
2) Rate 150-250/minute
3) Most often driven by reentrant circuit within AV node (carotid massage may terminate rhythm)
4) May see retrograde P waves in lead II or III and V1 pseudo-R’, most buried in QRS complex
Atrial flutter:
1) Is it normal?
2) What is the rhythm?
3) What is the rate?
4) Explain what is occurring
1) Usually indicates underlying pathology – reentrant rhythm around annulus of tricuspid valve (above AV node)
2) Regular rhythm
3) Rate is faster than AVNRT
4) P waves @ rate 250-300 – flutter waves, best seen in leads II and III
Single constant reentrant circuit with regular P waves
Carotid massage increases AV nodal block (slows ventricular rate)
Atrial flutter: Carotid massage increases AV block from 2:1 to 4:1 but does not ____________ as originate above AV node
terminate
Atrial fibrillation:
1) What is it?
2) Describe the P waves
3) What does the AV node do?
4) What may slow ventricular rate?
1) Chaotic atrial activity
Multiple tiny reentrant circuits
2) No true P waves
3) AV node only allows periodic impulses thru generating Irregularly Irregular Rhythm usually between 120-180/min (rapid ventricular response)
4) Carotid massage may slow (via increased AV nodal block) ventricular rate
