Arrhythmias Flashcards
One type of arrhythmia is an irregular rhythm, usually caused by multiple, active automaticity sites which are often parasystolic. What does it mean to be parasystolic?
Insensitive to overdrive suppression
One type of arrhythmia is an irregular rhythm, usually caused by multiple, active automaticity sites which are often parasystolic. What are the 3 main types of irregular rhythms?
Wandering pacemaker
Multifocal atrial tachycardia (MAT)
Atrial fibrillation
Etiology of wandering pacemaker
Produced by pacemaker activity wandering from SA node to nearby atrial automaticity foci
EKG changes with wandering pacemaker
Produces cycle length variation and variation in P’ shape
Overall rate is in normal range
What type of arrhythmia mimics a wandering pacemaker, but with a rate >100bpm?
Multifocal atrial tachycardia
[see varying P’ shape, atrial rate exceeds 100, irregular ventricular rhythm]
Multifocal atrial tachycardia is found in pts with what conditions?
Primarily COPD or digitalis toxicity
[overall association with lung disease includes COPD, pneumonia, ventilator theophylline; also associated with beta agonists, electrolyte abnormalities like hypokalemia, hypomagnesemia, sepsis]
Arrythmia caused by continuous, rapid firing of multiple atrial automaticity foci in which no single impulse depolarizes the atria completely and only the occasional, random atrial depolarization reaches the AV node to be conducted to the ventricles
Atrial fibrillation
“______” refers to a beat or rhythm response of an automaticity focus to a pause in pacemaking activity
Escape
[i.e., an escape rhythm = automaticity focus escapes overdrive suppression to pace at its inherent rate; escape beat = automaticity focus transiently escapes overdrive suppression to emit one beat]
A ____ escape rhythm becomes the dominant pacemaker after sinus arrest, with an inherent range of _____-_____
Atrial; 60-80
A junctional escape rhythm (aka idiojunctional rhythm) occurs after sinus arrest AND failure of atrial automaticity foci; or if there is a complete conduction block in the proximal AV node. What is the inherent range of this type of escape rhythm, and what other changes are seen on ECG?
Inherent range 40-60
Produces a series of lone QRS complexes, may produce retrograde atrial depolarization —> inverted P’ waves with upright QRS
[note that inverted P’ wave may be before, after, or buried within QRS]
Inherent rate and circumstances in which you might see a ventricular escape rhythm (aka idioventricular rhythm)
Inherent rate = 20-40
Occurs with complete conduction block in ventricular system BELOW the AV node; or total failure of SA node and all automaticity foci above the ventricles
[this is RARE — and referred to as downward displacement of the pacemaker]
Specific ventricular escape rhythm in which pacing is so slow that pt loses consciousness and you must constantly maintain/monitor their airway
Stokes Adams Syndrome
Upon transient sinus block of one pacemaking stimulus from the SA node, if the pause is sufficient enough, you may see an atrial _____ _____
Escape beat
ECG finding associated with atrial escape beat
P’ wave that is different shape/appearance than others; the SA node then quickly resumes pacing and tracing returns to normal
If the SA node misses one pacing cycle, and there is no atrial focal response, the result is a junctional escape beat. What is the resulting change on ECG?
There may bay retrograde atrial depolarization, resulting in inverted P’ before or after QRS
If the SA node and all atrial and junctional foci fail, there may be a resulting ventricular escape beat. What usually causes this?
Burst of parasympathetic activity, which depresses SA node, atrial, and junctional foci, leaving ventricular foci to respond
Premature beats occur when there is an irritable focus that spontaneously fires a single stimulus. What are some potential causes of irritable atrial or junctional foci?
Epinephrine from adrenals Sympathetic stimulation (or decreased parasympathetic stim) Caffiene, amphetamines, cocaine, other stimulants Beta 1 agonists Excess digitalis Toxins Ethanol Hyperthyroid Stretch O2 (to some extent)
ECG findings with premature atrial beats
P’ wave earlier than expected (appears different from sinus-generated P) — will be upright when focus is close to SA node, inverted when further away
The SA node then resets to continue pacing one cycle length from premature stimulus (requires that dominant center is depolarized by premature beat)
Why might you see slightly widened QRS following a premature atrial beat?
Aberrant ventricular conduction because the ventricles were still partially refractory when the premature beat occurred
Why might you see a dropped QRS following a premature atrial beat? What ECG finding does this mimic?
If premature atrial beat is not conducted through AV node, may see dropped QRS; mimics heart block
What is it called when you see a premature atrial beat coupled to the end of each normal cycle?
Atrial bigeminy
[atrial trigeminy is coupled to the end of every 2 cycles]
What causes a premature junctional beat? What is seen on ECG?
AV junction spontaneously fires stimulus that depolarizes ventricles and sometimes retrograde to atria (inverted P’)
Often see widened QRS because ventricles are still partially refractory
AV junctional bigeminy (PJB after each normal cycle); AV junctional trigeminy (PJB after every 2 cycles)
Which automaticity foci are considered the most sensitive to O2?
Ventricular automaticity foci - when they sense low O2 they emit a premature ventricular beat (may occur with airway obstruction, absence of air d/t things like drowning, minimal oxygenation at lungs, reduced cardiac output, poor coronary blood supply, etc.)
Other than low O2, what are some causes of premature ventricular beats?
Hypokalemia Mitral valve prolapse Stretch Myocarditis Sometimes beta 1 agonists
Premature ventricular beats usually occur early in the cycle, and are easily recognized by what characteristics on ECG?
Great width and amplitude of QRS, usually opposite the polarity of the other QRS complexes
Premature ventricular beats do NOT depolarize the SA node, so SA node continues pacing on schedule, but the ventricles are refractory d/t extra beat so a pause is seen
ST-T wave moves in opposite direction of QRS
Can also see bigeminy or trigeminy
Can be unifocal (QRS’s appear uniform) or multifocal (multiple QRS morphologies present)
____+ premature ventricular beats in a minute is considered pathologic
Six
______ ______ = premature ventricular contractions coupled to a long series of normal cycles (dual rhythm with pacing from 2 sources)
Ventricular parasystole
Condition characterized by a run of 3+ PVCs in rapid succession (rate of 120-200), usually regular with wide QRS
Ventricular tachycardia
[sustained V-tach when >30 seconds]
If a PVC falles on a ____ wave, it potentiates ischemia in something called ______ phenomenon, which may result in dangerous arrhythmias
T; R on T
Tachyarrhythmias are rapid rhythms originating in very irritable automaticity foci. What are the 3 types of tachyarrhythmias and their associated rates?
Paroxysmal tachycardia = 150-250 bpm
Flutter = 250-350 bpm
Fibrillation = 350-450 bpm
Paroxysmal atrial tachycardia and paroxysmal junctional tachycardia can not typically be distinguished, and are usually treated the same way anyway, so they can generally be referred to using what blanket term?
Paroxysmal Supraventricular Tachycardia
ECG findings with paroxysmal supraventricular tachycardia
P’ waves that appear different from normal P waves, otherwise normal P’-QRS-T cycles; when paroxysmal junctional tachycardia may see retrograde atrial depolarization with inverted P’ before, after, or buried in QRS
May see widened QRS d/t aberrant ventricular conduction (aka still refractory)
ECG findings with paroxysmal atrial tachycardia with AV block
Rapid rate, spiked P’ waves
2:1 ratio of P’:QRS
What should you suspect as the etiology for paroxysmal atrial tachycardia with AV block?
Digitalis excess or toxicity
Paroxysmal junctional tachycardia may lead to AV nodal re-entry tachycardia (AVNRT). What does that mean?
Continuous re-entry circuit develops (including AV node and lower atria) and rapidly paces the atria and ventricles; No P waves are seen
Mechanism:
- Premature atrial impulse enters slow path but is blocked at the fast path
- Impulse is conducted forward through slow path
- Ventricles activated in synchrony
- Impulse is conducted backward through fast path
- Impulse activates atria retrogradely and re-enters slow path
Characteristic ECG pattern of paroxysmal ventricular tachycardia
Enormous, consecutive PVC-like complexes
SA node is still pacing, but it will be buried in the tracing
Signs of AV dissociation or extreme right axis deviation are also characteristic
Paroxysmal ventricular tachycardia is most likely to occur in what pt populations?
Elderly pts with ischemia of ventricles
Type of polymorphic ventricular tachycardia, characterized by shifting sinusoidal waves on EKG; can lead to ventricular fibrillation
Torsades de pointes
Causes of Torsade de Pointes
Hypokalemia K+ channel blockers Congenital abnormalities (long QT syndrome)
Arrhythmia characterized by “sawtooth” appearance on ECG representing atrial depolarization
Atrial flutter
_____ maneuvers increase ____ node refractoriness allowing fewer flutters to be conducted to ventricles and may help to reduce symptoms associated with atrial flutter
Vagal; AV
______ flutter produces a series of smooth sine waves, rarely self resolves, and almost always precedes a deadly arrhythmia
Ventricular flutter (deadly arrhythmia it leads to is ventricular fibrillation)
What usually triggers Afib?
Usually initiated by parasystolic foci in the pulmonary vein ostia of the LA
ECG appearance of Afib; what leads are best to identify it?
Appears as wavy baseline without identifiable P or P’ waves; QRS response is not regular and may be fast or slow
“Irregularly irregular”
Best Leads = II, III, aVF
Condition characterized by totally erratic EKG without identifiable waves with gradually diminishing amplitude as the heart fails
Ventricular fibrillation
Most common type of ventricular pre-excitation syndrome
Wolff-Parkinson-White syndrome
WPW is characterized by abnormal fast accessory condition pathway from the atria to the ventricle (bundle of ____) which bypasses the rate-slowing AV node; thus the ventricles begin to partially depolarize earlier, leading to characteristic _____ wave with ______ QRS and _____ PR interval
Kent; delta; widened; shortened
WPW may result in re-entry circuit, leading to _____ ____
Supraventricular tachycardia
Condition in which AV node is bypassed by extension of the anterior internodal tract; absence of conduction delay in AV node allows “James” bundle to conduct atrial depolarization directly to the His bundle without delay
Lown-Ganong-Levine syndrome
Lown-ganong-levine syndrome allows atrial conduction be transmitted directly to the His bundle without delay. This may lead to what complication?
Rapid atrial arrhythmias like atrial flutter
Autosomal dominant disorder leading to increased risk of ventricular tachyarrhythmias and SCD, most common in asian males
Brugada syndrome
ECG findings associated with Brugada syndrome
RBBB with ST elevation in V1, V2, V3
[these pts need pacemakers/ICD]
Condition characterized by stenosed anterior descending coronary artery in which angioplasty is necessary to prevent impending MI
Wellens syndrome
Long QT syndrome predisposes to dangerous ventricular arrhythmias. What defines a QT segment as long?
A long QT segment exceeds 1/2 the cardiac cycle
What typically causes long QT syndrome? What is the major complication of concern?
Typically caused by ion channel defects, but can also be drug-induced (class IA and class III antiarrhythmics, abx like macrolides, antipsychotics like haloperidol, antidepressants like TCAs, anti-emetics like odansetron)
Major complication of concern is increased risk of SCD d/t torsade de pointes
COPD is associated with ______ hypertrophy, ____ axis deviation, and ______ (arrhythmia)
RV; Right; MAT
ECG findings with pulmonary embolus
[tachycardia, non-specific ST-T changes]
Large S wave in lead I
ST depression in lead II
Large Q wave in lead III (with T wave inversion in V1-4)
Transient RBBB
ECG findings in moderate to severe hyperkalemia
Moderate —> peaked T wave, wide flat P wave, wide QRS
Severe —> No P waves, QRS more widened
May see increased PR interval
ECG findings in hypokalemia
U waves
Increased QT interval
Flat or inverted T wave
ECG findings in hypercalcemia
Short QT
ECG findings in hypocalcemia
Prolonged QT
Medical conditions/situations associated with bradycardia
Normal people, healthy athletes, physiologic components to sleep, fright, carotid sinus massage, carotid hypersensitivity, ocular pressure (glaucoma), obstructive jaundice (effect of bile salts on SAN), sliding hiatal hernia, valsalva maneuver
diseases of atrium or SAN — CAD, inflammation, invasive neoplasm, cardiomyopathy, muscular dystrophy, amyloidosis
Drugs like digitalis, quinidine, HTN drugs like clonidine, methyldopa, reserpine, beta blockers
Acute inferior MI (d/t increased vagal tone), ischemia, acidosis, SSS, convalescence from digitalis toxicity
What is the most common cause of an unexplained pause on ECG?
Nonconducted premature atrial contraction (PAC)
What med is given in sinus bradycardia if HR is <45-50 with hemodynamic compromise/unstable acute situations?
Atropine
can also give epinephrine, isoproterenol, or pacemaker
[note side effects = urinary retention, abdominal distention]
______ = property of a cardiac cell to depolarize spontaneously during phase 4 of AP/leads to generation of an impulse
Automaticity
Treatment of PACs
Only if symptomatic — look to reverse the cause (stress, alcohol, tobacco, coffee, COPD, CAD)
Can give beta blockers — metoprolol
Tx for MAT
Focus on underlying cause
IV verapamil (calcium channel blockers)
Treatment for AVNRT (SVT)
Adenosine (try valsalva first to slow HR); can also give diltiazem, beta blocker, or shock if needed
Treatment of PVCs
If stable, do nothing
If symptomatic or in setting of ACS — give metoprolol
If unstable (in setting of MI, acidosis, etc.), give antiarrhythmic like amiodarone, lidocaine, procainamide, etc.
Fusion beats in the setting of ventricular tachycardia are characteristic of ______ syndrome
Dressler
A 63 y/o man has been in the ED for 1.5 hours with hx of CP. EKG reveals changes consistent with anterior AMI. The pt suddenly becomes cool, clammy, and confused with systolic BP of 70. EKG at that time reveals ventricular tachycardia. What do you do?
Cardioversion required d/t sudden change in status
Tx for Vfib
CPR, defibrillation
Torsade de pointes tx
MgSO4
Overdrive pacing
Isoproternol
If the clinical vignette ever mentions cancer or malignancy, the first electrolyte that should come to mind is _____
Calcium
[hypercalcemia is associated with malignancy, look for short QT interval and/or short ST segment on ECG]
What change in pH reduces the threshold for VF?
Acidosis
ECG findings in hypothermia
Bradycardia and J wave (Osborne wave)
ECG changes with cor pulmonale
Tall, pointed P waves [p-pulmonale]
ECG changes with cerebral hemorrhage
Impressive ST-T changes
[tall T waves, inverted wide T waves, etc.]
Whenever you see widespread flattening or mild inversion of T waves without associated ST segment displacement, always think of __________
Hypothyroidism
Whenever you see widespread flattening or mild inversion of T waves without associated ST segment displacement, always consider hypothyroidism.
The other most constant ECG finding in myxedema (severe hypothyroid) is low voltage of the ________. Sinus bradycardia is less often seen.
QRS complex
