ARRHYTHMIAS

BRADYDYSRHYTHMIAS
BRADYDYSRHYTHMIAS

■ SINUS BRADYCARDIA
– Causes
■ Physiologic – Increased vagal tone (e.g., athletes)
■ Pharmacologic – Due to beta blockers, Ca channel blockers, digoxin
■ Pathologic – Due to acute MI, increased ICP (e.g., Cushing’s reflex), hypothyroidism, sick
sinus syndrome
– Treatment
■ If stable, none required
■ If HR <50bpm AND signs of hypoperfusion:
– Atropine 0.5mg IV bolus, q3-5min for a total of 3mg. (pointless in cardiac transplant
pts, whose new hearts are denervated or in high-grade AV block)
– Epinephrine or dopamine
– If beta blocker or Ca channel blocker toxicity  glucagon 3-10mg IV bolus and drip at
1-5mg/hr
– Transcutaneous or transvenous pacing (rarely indicated)
BRADYDYSRHYTHMIAS

■ JUNCTIONAL RHYTHMS
– Causes
■ Can occur when SA node is beating too slowly (e.g., sinus brady <40bpm) or impulses
fail to reach the AV block (e.g., sinus arrest, SA node exit block).
■ The AV node starts to take over at a rate of 40bpm
■ Can be an occasional or isolated escape beat or a sustained junctional escape rhythm
■ Can be seen in CHF, myocarditis, acute MI, hyperkalemia, digoxin toxicity
– Treatment
■ If isolated, infrequent beats, no need to treat
■ If sustained junctional rhythm, treat underlying cause (.e.g, hyperkalemia or dig
toxicity)
■ If unstable, try atropine to help accelerate SA node rate and enhance AV node
conduction
■ If unstable ad not responding to atropine, use transcutaneous or transvenous pacing
BRADYDYSRHYTHMIAS

■ ACCELERATED IDIOVENTRICULAR RHYTHMS

– Causes
■ Due to an ectopic ventricular focus (hence, wide QRS compared to junctional
rhythm, which arises from AV node and has narrow QRS as a result)
■ Can look like VT but without the “T” (tachycardia)
■ Mostly occurring in acute MI after reperfusion
■ Can occur due to sympathomimetic drugs, electrolyte abnormalities,
cardiomyopathy, myocarditis.
– Treatment
■  Well-tolerated, benign, self-limiting arrhythmia
■ Treat any underlying cause
AV BLOCKS
AV BLOCKS
AV BLOCKS

■ First degree AV block

– PR interval > 200ms
– Rate is still regular
– Can be normal (due to increased vagal tone) or due to beta
blocker, Ca chanel blocker, digoxin, myocarditis, acute MI
– Usually benign! Treat any underlying cause if there is one.
AV BLOCKS

■ Second degree AV block

– Mobitz Type I (Wenckebach)
■ Progressively prolonged conduction through AV node until the impulse
is completely blocked
■ PR interval progressively lengthens before a dropped beat
■ Usually transient and associated with acute inferior MI, digoxin
toxicity, or myocarditis, or after cardiac surgery
■ Stable rhythm, since it occurs at the level of the AV node itself
■ No treatment needed, unless slow ventricular rate  in which case,
give atropine
■ Transcutaneous or transvenous pacing is rarely indicated
AV BLOCKS

■ Second degree AV block

– Mobitz Type II
■ Infranodal block
■ Constant PR interval but with occasional dropped beats (e.g., 2:1,
3:1, 4:1)
■ This can be a dangerous rhythm which can progress to third degree
(complete) heart block!
■ These folks require urgent hospitalization for pacemaker placement!
■ If bradycardic and symptomatic, can try atropine, but it may be
ineffective.
■ If these folks come into the ED, put pacer pads on them, just in case
they deteriorate into complete heart block and require
transcutaneous pacing!
AV BLOCKS

■ Third degree heart block

– There is no AV node conduction
– The ventricles are either paced by a junctional escape pacemaker (if the
block occurs at the AV node) or a ventricular escape rhythm (if the block
occurs below the AV node)
– Can be seen in acute MI or other structural damage to the infranodal
conduction system
– This is a dangerous rhythm! These folks need urgent hospitalization for
pacemaker placement!
– If bradycardic and unstable, perform transcutaneous cardiac pacing until a
transvenous pacemaker can be placed.
– If stable, put the pacer pads on them just in case.
TACHYDYSRHYTHMIAS
NARROW COMPLEX

■ Sinus tachycardia
– Find out what’s causing it. Don’t bother treating it
■ Afib
– Multiple small areas of atrial myocardium that are discharging
– Fibrillatory waves with irregular rhythm.

■ Aflutter
– Originates from a small area in the atria
– “Sawtooth waves” are visible, usually with a 2:1 conduction block
or greater.
NARROW COMPLEX

■ TREATMENT for both afib and aflutter

– RATE CONTROL
■ Diltiazem bolus of about 15mg and a grip at 5-15mg/hour to maintain a rate <110
■ Can also consider other AV nodal blocking meds, such as metoprolol or verapamil.
***One important exception to giving AV nodal blocking meds. If the afib is caused by
someone with Wolff-Parkinson-White (look for the delta waves!), do NOT give AV
nodal blocking agents, due to risk of vfib! Give procainamide instead.
– RHYTHM CONTROL
■ Electrical or chemical cardioversion (with ibutilide)
– If unstable  cardiovert
– If stable, cardioversion in the ED is not necessary, but can consider in pts who
have been in afib < 48 hours or who are already on appropriate anticoagulation.
NARROW COMPLEX

■ Supraventricular Tachycardia
– Regular and rapid rhythm with either absence of P waves or rare retrograde P waves (usually
inverted and just before or after QRS complex)
– Can be AVnRT (reentry circuit within AV node) or AVRT (AV bypass tract  conduction can be
orthodromic or antidromic)
– can occur in normal hearts as well as those with infection (rheumatic heart disease, pericarditis)
or structural heart issues (acute MI, MV prolapse) or preexcitation syndromes (WPW)
– TREATMENT:
■ If stable – try Valsalva maneuver, diving reflex, carotid sinus massage. If that doesn’t work, IV
adenosine (first 6mg, then 12mg). If that doesn’t work, other nodal blocking agents, such as beta
blockers or Ca channel blockers can be used. Amiodarone is another possibility.
■ If unstable – synchronized cardioversion
■ Wide complex SVT – may be due to antidromic AVRT. Sometimes it can be very hard to distinguish
between vtach and SVT with abberancy. Approach it as though it is Vtach and use procainamide. Avoid
AV nodal blocking agents because it can lead to vfib!
WIDE COMPLEX

■ Ventricular tachycardia
– Dangerous rhythm that arises from an ectopic pacemaker in the ventricles
– Wide complex QRS with rate >100 (usually 150-200)
– Most commonly arises from ischemic heart disease or acute MI
– TREATMENT:
■ If pulseless --> defibrillate per ACLS protocol!
■ If pulses and unstable  synchronized cardioversion
■ If pulses and stable  can try 150mg of amiodarone IV (with repeated boluses as needed
q10min to a total of 2g). Start amio drip after successfully cardioverting with bolus.
Procainamide and lidocaine are other options.
**Torsades is a special type of vtach that looks sinusoidal. For these, you can try
overdrive pacing at 90-120 and/or magnesium sulfate 1-2g IV bolus and drip. Can also
try isoproterenol, though it increases myocardial demand.
WIDE COMPLEX

■ Ventricular fibrillation
– The ventricles are sending out completely disorganized impulses
with no effective ventricular pumping activity
– These folks are usually in cardiopulmonary arrest!
– TREATMENT: defibrillation as per ACLS protocol!