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Heart Blocks &

Bradycardia
Heart Blocks
• Background: rhythms in the heart are generated in the SA node which
depolarize approximately once per second, rhythm starts in the SA node!
atrium ! AV node! His-Purkinje System! Ventricles
• At the AV node there is normal slowing of the rhythm reflected in the PR
interval
• Vagal innervation extends from the SA node to the AV node. Increased
vagal tone (parasympathetic drive) decreases the heart rate

First Degree AV Block

• Location: Defect at AV node
• EKG: PR interval is increased
• Prognosis: Good

Second Degree: Mobitz Type I (Wenckebach)

• Location: Defect at AV node
• EKG: progressively prolonged PR interval until there is a P with no QRS
complex
• Prognosis: Good

Second Degree: Mobitz Type II

• Location: Defect in His-Purkinje System
• EKG: QRS follows P wave at normal speed then develops sudden
unexpected loss of P-wave conduction and the QRS is missing
• Prognosis: Poor, need pacemaker as can develop wide complex
bradycardias and asystole

Third Degree AV Block

• Location: complete heart block between atria and ventricles
• EKG: P waves are not coordinated with the QRS complex; can be narrow
or wide QRS depending on location of pacemaker (narrow if at high
junction and wide if low in ventricles)
• Prognosis: Poor, need pacemaker
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Bradycardia: A Simplified Approach

• Think!
• Stable or Unstable?
• Wide or Narrow?
• Very slow or just slow?

Think! Differential?
• Drugs – e.g. Beta Blocker, Calcium Channel Blocker, Digoxin
• Ischemia
• Electrolytes – e.g. hyperkalemia

Stable or Unstable?
• Unstable! act quickly
• Stable !!slow rate alone is bad, patient is using all physiologic reserve to
maintain blood pressure and mentation, be aware they can code

Wide or Narrow?
• Wide complex occurs when the block is below the AV node, they have a
slower rate and are more likely to result in asystole, not atropine sensitive
• Narrow complex is a more stable bradycardia, faster, atropine sensitive
because the block is at the AV node that contains vagal innervation

Very Slow or Just Slow?

• Remember resting heart rate can be low in athletic patients due to high
vagal tone (as low as 30’s!)
• Very slow heart rate can indicate a higher likelihood of an unstable patient

Treatment
• Transcutaneous pacing (often fails)
• Transvenous pacing
• Atropine: blocks action of vagus nerve; narrow complex bradycardia is
responsive to atropine while wide complex is not (due to location of vagal
innervation); administer slowly (especially in ischemic cases); administer
0.25-0.5 mg IV x 1 and repeat q3-5 min. Max 3 mg total
• Dopamine: positive chronotrope to increase speed of conduction
• Epinephrine Drip: 10 mL of 1:10,000 epi = 1000 micrograms; put into 1000
mL bag of normal saline = 1 microgram per mL; run at 2-10 mL/min
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Simplified Arrhythmia
Therapy
6 Step Rule
1. Simplified Approach
• Plan on a very simplified approach: examine the rhythm strip

2. IV, O2, Monitor

• In addition to IV, O2, monitor, ensure advanced airway equipment,
defibrillator and pacemaker are at the bedside
• Remember that the endpoint of bad arrhythmias is electricity – any
intervention can make the patient worse. Antiarrhythmics are
proarrhythmic

3. Is the patient stable or unstable?

• The patient is unstable if they have altered mental status, pulmonary
edema, hypotension, or chest pain
o Note about 70% of patients will have chest pain
o Definition of hypotension is < 90 mmHg systolic, but compare to the
patient’s baseline blood pressure (may be normal for small patient)
• In general, if the patient is unstable = treat with electricity. Sedate patient
during cardioversion
• If patient is stable = try medications to treat the arrhythmia

4. Are P waves present?

• If P waves are present on EKG = sinus; many patients that present with
tachycardia may have sinus tachycardia, e.g. sepsis or a PE. Do not treat
with antiarrhythmics or electricity, treat the underlying cause
• Look for P waves in leads II and v1, and ensure P waves are in the correct
axis (upright in lead II and negative in aVR)
• P waves should be 1:1, prior to every QRS
• Look for “special P waves”
o Multiple chaotic P waves = atrial fibrillation
o 3 or more P waves of variable morphology and tachycardia =
multifocal atrial tachycardia (MAT)
o Flutter waves
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5. Regular or Irregular?
• Differentiate rhythms from above the AV node versus below
• Irregular = from above the AV node = supraventricular
• Irregular = treatment is to block the AV node
• Irregular = rhythm is not ventricular tachycardia
• Irregular = clearly irregular on EKG, march the rhythm out

6. Wide or Narrow?
• Differentiate rhythms from above the AV node versus below
• Narrow = supraventricular
• Narrow = block the AV node
• Narrow = rhythm is not ventricular tachycardia
• Narrow = < 0.12 sec (3 small squares on EKG), or <0.08 in children

Four Groups of Arrhythmias

Narrow, Regular, no P waves, Tachycardia
Differential
• PSVT = paroxysmal supraventricular tachycardia
• AVNRT = AV Nodal reentrant tachycardia. Most common cause of SVT
• Atrial Flutter. Macro-reentry circuit with circus movement in the atrium
firing impulses down AV node with consistent regular block, e.g. 2:1 block
• Orthodromic WPW. Impulse travels down AV node ! His-Purkinje system
!!ventricles!! reentrant accessory pathway to atrium !!repeat
• RARE: Narrow complex ventricular tachycardia
• Treatment for stable patients:
o Adenosine = ultrashort AV nodal blocker. Dose is 6 mg IV rapid
push; if fails 12 mg IV x1; if fails then 12-18 mg IV x1. Tip: lift the
arm up during IV push, bolus needs to be administered to heart
quickly
o Diltiazem = long acting AV nodal blocker. Dose is 2.5 mg/min up to
total of 50 mg, or bolus 15-20 mg over 2 minutes. Tip: be cautious
with high doses in elderly - start with 10 mg IV
o Verapamil = long acting AV nodal blocker. Dose is 2.5-10 mg IV x1,
max dose 20 mg, may repeat 5-10 mg dose after 15-30 minutes
• Treatment for unstable patients:
o Consider adenosine, but immediate cardioversion is also
appropriate
o Cardioversion. Start at 50 J and double every time you need to
shock the patient. Prepare defibrillator
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Narrow, Irregular, Tachycardia

Differential
• Atrial fibrillation
• Atrial flutter with variable block
• Multifocal atrial tachycardia (MAT) – look for differing P waves, similar to
atrial fibrillation but firing from 10-20 locations in the atrium compared to
hundreds of locations in atrial fibrillation
• Treatment for stable patients:
o Diltiazem = long acting AV nodal blocker (calcium channel
blocker). Bolus 10-20 mg over 2 minutes, administer up to 60 mg in
30 minutes, continue to control rate with a drip of 5-10 mg/hour, or
control with 30 mg PO QID
o Verapamil = long acting AV nodal blocker. Dose is 2.5-10 mg IV x 1,
max dose 20 mg, may repeat 5-10 mg dose after 15-30 minutes
o Adenosine will work for several seconds and may reveal underlying
rhythm
o Metoprolol = Beta blocker. Dose is 2.5-5 mg IVP over 2 min, up to 3
doses; if patient responds, then PO load with 25-50 mg
o Esmolol = Beta blocker. Bolus 0.5 mg/kg over one minute followed
by 50 mcg/kg/min, can re-bolus and titrate infusion up to 200
mcg/kg/min
o Avoid using IV Calcium Channel Blocker with IV beta blocker,
can cause severe bradycardia or heart block
o Digoxin = inotropic cardiac glycoside. Consider if beta blockers or
calcium channel blocker has failed. Dose is 0.25-1 mg IV q2 hours
o Amiodarone = antiarrhythmic. Consider if beta blockers, calcium
channel blockers and digoxin do not work. Dose is 150 mg IV over
10 minutes, followed by 1 mg/min x 6 hours, followed by 0.5
mg/min x 18 hours
• Treatment for unstable patients: very difficult to control, most are atrial
fibrillation
o Diltiazem = long acting AV nodal blocker
o Amiodarone = antiarrhythmic
o Magnesium sulfate 2-4 grams IV over 2-4 minutes
o Cardioversion. Start at 50 J and double every time need to shock
patient. Many patients will not convert back to sinus rhythm

Wide, Regular, Tachycardia

Differential
• Ventricular Tachycardia
o Occurs after an MI in ventricular scar tissue that develops micro-
reentry circuits
o Predictors: old age, known CAD, EKG criteria
o EKG criteria: in addition to wide and regular pattern, which is
ventricular tachycardia until proven otherwise, can occasionally get
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a narrow complex, which indicates atrium is also firing in between

ventricular beats (capture beat); can also get a fusion beat (wide
and narrow complex fuse), which is rare but signifies patient has
AV dissociation
• Supraventricular tachycardia with aberrancy (bundle branch block):
impulse is not being conducted down the His-Purkinje system due to BBB
• Antidromic Wolf Parkinson White syndrome: impulse fired down the
accessory pathway into ventricle !!spread through ventricle!!!His-
Purkinje!!!AV node!!!atrium!!!repeat cycle
• Treatment for stable patients: Cardiovert! Medications below typically end
up dropping the blood pressure and patient typically needs cardioversion
o Adenosine 6 mg IV, then 12 mg IV will work for SVT with BBB.
Consider if very stable
o Magnesium sulfate 2-4 grams IV over 2-4 minutes if ventricular
tachycardia is most likely
o Procainamide = antiarrhythmic. Dose is 17 mg/kg IV over 30 min;
consider if ventricular tachycardia is likely
o Amiodarone = antiarrhythmic. Dose above. Consider if ventricular
tachycardia is likely
• Treatment for unstable patients:
o Cardioversion. 100 Joules synced. Double the joules every time
you need to shock the patient

Wide, Irregular, Tachycardia

Differential
• Atrial Fibrillation with BBB (most likely the case)
• Atrial Flutter with variable AV-block and BBB
• Atrial Fibrillation and WPW. Rare, about 1/100 to 1/1000 of wide, irregular
fast patterns
o Accessory pathway conducts extremely well. Impulses from atrial
fibrillation place patient at risk for developing ventricular fibrillation
and death
o Determine if patient has history of WPW? Young patient? More
likely.
o EKG: in addition to having a wide and irregular pattern, the EKG
looks bizarre / “wacky.” EKG contains some wide and some narrow
complexes; pattern is very fast with R-R intervals over 250
• Polymorphic Ventricular tachycardia or Torsades de Pointes
• Treatment for stable patients:
o Same treatment as for narrow and irregular pattern = block the AV
node with e.g. diltiazem, except in WPW.
o Atrial Fibrillation with WPW: do NOT use an AV nodal blocker.
Blocking AV node will cause the accessory pathway to become
more efficient causing polymorphic ventricular tachycardia or
ventricular fibrillation and lead to death. Cardiovert immediately.
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o Atrial Fibrillation with WPW: consider procainamide which can

slow down conduction through the accessory pathway. Dose above.
o If unsure patient has WPW, play it safe and cardiovert.
o Torsades de Pointes: Magnesium sulfate. Dose above.
• Treatment for unstable patients:
o Cardioversion. 100 Joules synced. Double joules as needed.
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Tachycardia Arrhythmia:
Board Basics
Normal Heart Rhythm
• Sinoatrial (SA) node = pacemaker: depolarizes with automaticity !
impulse spreads through the atrium and causes the atrium to contract !
spreads to the atrioventricular (AV) node which slows down the impulse
through a normal delay reflected by the PR interval !!spreads quickly
down the His-Purkinje system and bundle branches!! into the ventricles
!!ventricular depolarization and contraction is reflected by a narrow QRS
complex
• In healthy myocardial tissue conduction occurs through a slow arm and a
fast arm. Normally an impulse travels slowly down the slow arm and
quickly down the fast arm. The impulse that travels down the fast arm
cannot go back up the slow arm due to the slow arm’s refractory period. In
normal tissue the impulse is driven down the fast arm of the pathway.

Tachycardia Arrhythmia Concepts

Sinus Tachycardia
• SA node fires over 100 beats per minute down the normal conduction
pathway
• There is a P wave before every QRS complex best seen in leads II and V1
• P waves are in correct axis when upright in Lead II and negative in aVR

Supraventricular Tachycardia (SVT)

• Indicates rhythm is generated above the ventricles, above the AV node
• Can block the AV node to treat SVT
• SVT has a better prognosis than ventricular arrhythmias
• There are “formally” many types of SVT:
o Sinus tachycardia
o Sinoatrial node reentrant tachycardia
o Atrial tachycardia
o Multifocal Atrial Tachycardia = MAT
o Atrial flutter
o AV nodal reentrant tachycardia = AVNRT
o AV reentrant tachycardia = AVRT, e.g. WPW
o Junctional ectopic tachycardia = JET
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• When discussing “SVT” people are generally talking about AVNRT or

AVRT

Narrow Complex Rhythms

• Indicates rhythm is generated above the ventricles, above the AV node
• Can block the AV node to treat narrow complex arrhythmias
• Narrow rhythms have a better prognosis than wide ventricular arrhythmias
• The impulse uses the normal His-Purkinje conduction system

Wide Complex Rhythms

• Wide rhythms start in the ventricles
• Ventricular tachycardia is generated in tissue around a scar that is
generally due to prior cardiac injury, e.g. myocardial infarction
• QRS complex is wide because the impulse does not use the His-Purkinje
system. The impulse spreads throughout the slowly conducting ventricles
• Ventricular tachycardia is regular because it is generated by a micro-
reentry circuit
• Ventricular tachycardia is a very unstable rhythm in patients that are
typically very sick and elderly with known CAD

Circus Movement: Re-entry Circuits

• Produce very regular rhythms
• If a patient develops a Premature Ventricular Contraction (PVC) or
Premature Atrial Contraction (PAC) and the myocardial tissue’s slow arm
and fast arm have different refractory periods with the ability to conduct
anterograde and retrograde impulses, the impulse from the slow arm can
spread up the fast arm, and the patient can develop re-entry circuits, e.g.
AVNRT
• AVNRT: micro-reentry circuit in the AV node
o EKG: narrow, fast, regular. No P waves. Can be wide with a bundle
branch block and look like ventricular tachycardia = SVT with
aberrancy
• Atrial Flutter: macro-reentry circuit throughout the entire atrium
o EKG: narrow, fast, regular, flutter waves that are symmetrical or
“sawtooth” shape. Can be wide with a bundle branch block
• AVRT = Wolff-Parkinson-White Syndrome (WPW): macro-reentry circuit
o Inappropriate accessory pathway between the atrium and ventricles
allowing impulses to bypass the AV node
o Accessory pathway can become a reentry circuit itself or a direct
communication between the atrium and ventricles
o EKG pattern #1: Orthodromic WPW results in a regular narrow
complex tachycardia where the normal conduction pathway is used.
Impulse travels down AV node ! His-Purkinje system !!ventricles!
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! reentrant accessory pathway to atrium !!repeat cycle, causes a

regular circus movement tachycardia that looks like SVT
o EKG pattern #2: Antidromic WPW results in a regular wide
complex tachycardia because the impulse travels through the slow
conducting ventricular tissue. Impulse is fired down the accessory
pathway into ventricle !!spreads through the ventricle!!!His-
Purkinje!!!AV node!!!atrium!!!repeat cycle, looks like
ventricular tachycardia
o EKG pattern #3: WPW with Atrial Fibrillation results in a mix of
wide/narrow/fusion complexes that are fast, irregular and bizarre.
Impulses are conducted down both the accessory pathway (wide)
and down the AV node (narrow). Very dangerous and can lead to
ventricular fibrillation and death.
o EKG pattern #4: in normal sinus rhythm may see a delta wave,
which is a slurred upstroke in the QRS complex that is associated
with a short PR interval

Accelerated Automaticity
• Produces irregular rhythms
• Atrial Fibrillation
o Atrium is irritable and firing from hundreds of foci, bombarding the
AV node with multiple impulses generating a ventricular response
of 160-180 BPM in acute arrhythmia
o EKG: multiple chaotic P waves, rhythm is irregularly irregular
• Multifocal Atrial Tachycardia (MAT):
o Similar to atrial fibrillation, but there are only 5-10 different foci that
generate impulses
o EKG: 3 or more P waves of different morphology with variable PR
intervals
o Can convert into atrial fibrillation