Cardiac Arrhythmias A Guide For Medical Students William Beaumont Hospital Department of Emergency Medicine A Guide For Medical Students William Beaumont.

Cardiac ArrhythmiasCardiac ArrhythmiasA Guide For Medical Students

William Beaumont HospitalDepartment of Emergency

Medicine

A Guide For Medical Students

William Beaumont HospitalDepartment of Emergency

Medicine

In evaluating arrhythmias -

In evaluating arrhythmias -

Rate - Is it fast or is it slow If slow – is there group to group

beating Rhythm - Is it regular, irregular or

irregularly irregular? P waves - Are they present? QRS - Is it narrow or wide?

Rate - Is it fast or is it slow If slow – is there group to group

beating Rhythm - Is it regular, irregular or

irregularly irregular? P waves - Are they present? QRS - Is it narrow or wide?

Sinus BradycardiaSinus Bradycardia

What is it? What causes it? When do you treat it? How do you treat it?

What is it? What causes it? When do you treat it? How do you treat it?

Sinus BradycardiaSinus Bradycardia A sinus rhythm with normal intervals

and a rate less than 60 bpm Normal variant, beta blocker overdose,

dig, hypothermia, hypothyroidism, brady-tachy syndrome, and SA node ischemia

Requires treatment only if there is evidence of hypoperfusion

Two treatment options Pacing: transvenous or transcutaneous Atropine 0.5 mg IVP

A sinus rhythm with normal intervals and a rate less than 60 bpm

Normal variant, beta blocker overdose, dig, hypothermia, hypothyroidism, brady-tachy syndrome, and SA node ischemia

Requires treatment only if there is evidence of hypoperfusion

Two treatment options Pacing: transvenous or transcutaneous Atropine 0.5 mg IVP

Sinus TachycardiaSinus Tachycardia A sinus rhythm faster than 100 bpm Etiology - usually a physiologic

response to a stressor

Volume depletion / low stroke volume Hypoxia Systemic pathology: fever, anemia,

hyperthyroidism Drugs

Treatment - treat the underlying cause

A sinus rhythm faster than 100 bpm Etiology - usually a physiologic

response to a stressor

Volume depletion / low stroke volume Hypoxia Systemic pathology: fever, anemia,

hyperthyroidism Drugs

Treatment - treat the underlying cause

Atrial ArrhythmiasAtrial Arrhythmias

PACsMATAtrial Fibrillation, atrial flutterSVT

PACsMATAtrial Fibrillation, atrial flutterSVT

Multifocal Atrial Tachycardia

Multifocal Atrial Tachycardia

Diagnosis requires the presence of three distinct p waves in a narrow complex tachycardia

Almost always associated with pulmonary disease

Less often due to hypokalemia or hypomagnesemia

Treat the underlying disorder – usually hypoxia

Unlike the other atrial tachyarrhythmias, cardioversion is of no value in MAT

Diagnosis requires the presence of three distinct p waves in a narrow complex tachycardia

Almost always associated with pulmonary disease

Less often due to hypokalemia or hypomagnesemia

Treat the underlying disorder – usually hypoxia

Unlike the other atrial tachyarrhythmias, cardioversion is of no value in MAT

MAT Rule of ThreesMAT Rule of Threes3 different p waves, 3 different pr

intervals and 3 different r to r intervals3 different p waves, 3 different pr

intervals and 3 different r to r intervals

Causes of A-fibCauses of A-fib

Cardiovascular - CAD, HTN, CHF, myopathy, myo-, endo- and pericarditis, infiltrative disease, valvular, congenital

Metabolic - thyroid, electrolytes Pulmonary - pulmonary HTN, PE Toxic - cocaine, ETOH (holiday heart), beta agonists Sepsis Idiopathic

Cardiovascular - CAD, HTN, CHF, myopathy, myo-, endo- and pericarditis, infiltrative disease, valvular, congenital

Metabolic - thyroid, electrolytes Pulmonary - pulmonary HTN, PE Toxic - cocaine, ETOH (holiday heart), beta agonists Sepsis Idiopathic

ECG Rules for A-fibECG Rules for A-fib Regularity - irregularly irregular Rate - atrial rate usually > 350

Controlled - ventricular rate < 100 RVR - ventricular rate > 100

P wave - none discernable, may be f waves QRS - less that 0.12 seconds (easy dx). If > 0.12

sec must rule out VT (which is usually more regular)

Regularity - irregularly irregular Rate - atrial rate usually > 350

Controlled - ventricular rate < 100 RVR - ventricular rate > 100

P wave - none discernable, may be f waves QRS - less that 0.12 seconds (easy dx). If > 0.12

sec must rule out VT (which is usually more regular)

A-fib with RVRA-fib with RVR A fib with ventricular rate > than 100-120 bpm Patients usually symptomatic requiring rapid tx

Unstable – cardioversion Stable - control rate with calcium channel blockers, beta

blockers or digitalis

A fib with ventricular rate > than 100-120 bpm Patients usually symptomatic requiring rapid tx

Unstable – cardioversion Stable - control rate with calcium channel blockers, beta

blockers or digitalis

A-fib treatmentA-fib treatment Recognize the underlying cause A rate under 120 in an

asymptomatic patient generally requires no emergent treatment

Unstable patients with acute rapid a-fib should receive synchronized cardioversion with 50-100 J

Treatment otherwise depends on the duration

Recognize the underlying cause A rate under 120 in an

asymptomatic patient generally requires no emergent treatment

Unstable patients with acute rapid a-fib should receive synchronized cardioversion with 50-100 J

Treatment otherwise depends on the duration

Treatment of A-fibTreatment of A-fib

Less than 48 hours duration Cardioversion is indicated in any

unstable patient, synchronized if possible, with 50-100 J

May also be used electively in symptomatic but stable patients

Pharmacologic cardioversion may be attempted with procainamide, amiodarone or ibutilide

Less than 48 hours duration Cardioversion is indicated in any

unstable patient, synchronized if possible, with 50-100 J

May also be used electively in symptomatic but stable patients

Pharmacologic cardioversion may be attempted with procainamide, amiodarone or ibutilide

Treatment of A-fib > 48 hours

Treatment of A-fib > 48 hours

Longer duration predisposes the patient to atrial clot formation and failure of conversion

Rate control with diltiazem, beta blockers or digitalis

Do not attempt cardioversion unless emergently indicated

Anticoagulation and arrangement for echo

Longer duration predisposes the patient to atrial clot formation and failure of conversion

Rate control with diltiazem, beta blockers or digitalis

Do not attempt cardioversion unless emergently indicated

Anticoagulation and arrangement for echo

Atrial FlutterAtrial Flutter Patients usually with cardiac or

pulmonary dz Conduction through the AV node may

be at a 2:1, 3:1, 4:1 or 5:1 rate Whenever you see a ventricular rate

close to 150 you should consider a flutter

Frequently is a transient rhythm which may degenerate into a-fib or convert to sinus

Patients usually with cardiac or pulmonary dz

Conduction through the AV node may be at a 2:1, 3:1, 4:1 or 5:1 rate

Whenever you see a ventricular rate close to 150 you should consider a flutter

Frequently is a transient rhythm which may degenerate into a-fib or convert to sinus

Treatment of A-flutterTreatment of A-flutter Hemodynamically unstable -

immediate synchronized cardioversion

Hemodynamically stable Vagal manuevers – if no carotid bruits Adenosine - will not terminate the atrial

tachycardia, but may allow flutter waves to become more apparent

Dig, beta blockers or calcium channel blockers for AV nodal blockade to slow the ventricular rate

Hemodynamically unstable - immediate synchronized cardioversion

Hemodynamically stable Vagal manuevers – if no carotid bruits Adenosine - will not terminate the atrial

tachycardia, but may allow flutter waves to become more apparent

Dig, beta blockers or calcium channel blockers for AV nodal blockade to slow the ventricular rate

SVTSVT

AV nodal reentrant tachycardia Usually you see a regular, narrow

complex tachycardia without p waves

Treatment – adenosine, beta blockers, calcium channel blockers, digoxin

AV nodal reentrant tachycardia Usually you see a regular, narrow

complex tachycardia without p waves

Treatment – adenosine, beta blockers, calcium channel blockers, digoxin

SVT – HR around 150sSVT – HR around 150sIs it SVT, afib, aflutter, sinus tach?Is it SVT, afib, aflutter, sinus tach?

Preexcitation syndromePreexcitation syndrome

Wolf-Parkinson-White syndrome AV re-entrant tachycardia (accessory

pathway) Short PR interval, delta waves Treat like PSVT if the QRS is narrow If the QRS is wide or if afib is present,

use amiodarone or procainamide (slow the atrial rate and increase conduction through the AV node)

Avoid ABCD – adenosine, beta blockers, calcium channel blockers, dig – if WIDE QRS

Wolf-Parkinson-White syndrome AV re-entrant tachycardia (accessory

pathway) Short PR interval, delta waves Treat like PSVT if the QRS is narrow If the QRS is wide or if afib is present,

use amiodarone or procainamide (slow the atrial rate and increase conduction through the AV node)

Avoid ABCD – adenosine, beta blockers, calcium channel blockers, dig – if WIDE QRS

Narrow complex WPWNarrow complex WPW

Wide complex WPWWide complex WPW

Atrioventricular BlocksAtrioventricular BlocksFirst Degree

Second Degree - Type ISecond Degree - Type II

Third Degree

First DegreeSecond Degree - Type ISecond Degree - Type II

Third Degree

Second Degree AV BlocksSecond Degree AV Blocks

Group to group beating Second degree blocks are partial

blocks Two types

Type I, Mobitz I or Wenckebach - transient

Type II, Mobitz II or Classic - often degenerates into 3rd degree heart block

Group to group beating Second degree blocks are partial

blocks Two types

Type I, Mobitz I or Wenckebach - transient

Type II, Mobitz II or Classic - often degenerates into 3rd degree heart block

Second Degree Type ISecond Degree Type I Decremental Conduction: Grouped beats

with progressively longer PR intervals until an impulse is not conducted (a p without a QRS)

Usually narrow QRS Generally requires no treatment – atropine,

temporary pacing if symptomatic May be associated with inferior MI

Decremental Conduction: Grouped beats with progressively longer PR intervals until an impulse is not conducted (a p without a QRS)

Usually narrow QRS Generally requires no treatment – atropine,

temporary pacing if symptomatic May be associated with inferior MI

Second Degree Type IISecond Degree Type II Conduction fails suddenly, without

a change in the PR interval This is not a benign rhythm, is

chronic and often progresses to a complete heart block

Is associated with anteroseptal MI May have wide QRS

Conduction fails suddenly, without a change in the PR interval

This is not a benign rhythm, is chronic and often progresses to a complete heart block

Is associated with anteroseptal MI May have wide QRS

Second Degree Type IISecond Degree Type II No pharmacologic treatment – atropine has no

effect on the His-Purkinje system so not helpful and may worsen the conduction ratio

Emergency treatment - transcutaneous or transvenous pacing

No pharmacologic treatment – atropine has no effect on the His-Purkinje system so not helpful and may worsen the conduction ratio

Emergency treatment - transcutaneous or transvenous pacing

Third Degree BlockThird Degree Block Complete block - there is total AV

Dissociation None of the atrial impulses are conducted

through to the ventricles (P and QRS are independent, P-P and R-R intervals constant

An escape rhythm from a focus below the block will drive the ventricles If the escape rhythm originates in the AV

junction, the ventricular rate will be in the range of 40-60 and the QRS less than 0.12

If the escape is generated from the ventricles, the rate will be in the range of 20-40 with a wide QRS

Complete block - there is total AV Dissociation

None of the atrial impulses are conducted through to the ventricles (P and QRS are independent, P-P and R-R intervals constant

An escape rhythm from a focus below the block will drive the ventricles If the escape rhythm originates in the AV

junction, the ventricular rate will be in the range of 40-60 and the QRS less than 0.12

If the escape is generated from the ventricles, the rate will be in the range of 20-40 with a wide QRS

Third Degree BlockThird Degree Block Although patients may be asymptomatic,

transcutaneous or transvenous pacing is warranted

Autonomic drugs such as atropine will have no effect on ventricular rate

Type I antiarrhythmics should be avoided (they may suppress the escape rhythm)

Although patients may be asymptomatic, transcutaneous or transvenous pacing is warranted

Autonomic drugs such as atropine will have no effect on ventricular rate

Type I antiarrhythmics should be avoided (they may suppress the escape rhythm)

Ventricular ArrhythmiasVentricular Arrhythmias

PVCsV tachV fib

PVCsV tachV fib

Premature Ventricular Contractions

Premature Ventricular Contractions

Generally benign, but may be a consequence of a pathology, esp if multifocal

More concerning causes include hypoxia, ischemia, MI, toxins/drugs, acidosis or alkalosis, hypokalemia

Generally benign, but may be a consequence of a pathology, esp if multifocal

More concerning causes include hypoxia, ischemia, MI, toxins/drugs, acidosis or alkalosis, hypokalemia

Ventricular TachycardiaVentricular Tachycardia

Results from a dysrhythmia originating at or below the bundle of His

Has a wide QRS complex (>0.12 second)

May be monomorphic or polymorphic

Results from a dysrhythmia originating at or below the bundle of His

Has a wide QRS complex (>0.12 second)

May be monomorphic or polymorphic

Monomorphic V-tachMonomorphic V-tach

Morphologically consistent QRS complexes

Most common form of v-tach Seen primarily with cardiac ischemia Also seen in cardiomyopathy, valvular

disease, electrolyte imbalance, myocarditis

Morphologically consistent QRS complexes

Most common form of v-tach Seen primarily with cardiac ischemia Also seen in cardiomyopathy, valvular

disease, electrolyte imbalance, myocarditis

Polymorphic V-tachPolymorphic V-tach

QRS complexes vary in structure and amplitude

Predominantly caused by CAD Associated with more severe

disease

QRS complexes vary in structure and amplitude

Predominantly caused by CAD Associated with more severe

disease

Torsades de pointesTorsades de pointes

A specific form of polymorphic v-tach

Associated with prolonged QT May be due to drugs (tricyclics),

electrolyte imbalance (hypo K, Mg or Ca), or subarachnoid hemorrhage

A specific form of polymorphic v-tach

Associated with prolonged QT May be due to drugs (tricyclics),

electrolyte imbalance (hypo K, Mg or Ca), or subarachnoid hemorrhage

Treatment of Ventricular Tachycardias

Treatment of Ventricular Tachycardias

Unstable - immediate cardioversion 100 – 200 – 300 – 360

Stable - amiodorone 150 mg IVP or lidocaine 1 mg/kg and prepare for elective cardioversion

If torsades de pointes – magnesium 1-2g IV

Unstable - immediate cardioversion 100 – 200 – 300 – 360

Stable - amiodorone 150 mg IVP or lidocaine 1 mg/kg and prepare for elective cardioversion

If torsades de pointes – magnesium 1-2g IV

Ventricular FibrillationVentricular Fibrillation

An irregularly irregular rhythm with no p waves or definite QRS complexes

An irregularly irregular rhythm with no p waves or definite QRS complexes

Treatment of V FibTreatment of V Fib

Defibrillate Adult 360/360/360 joulesChildren 2 joules/kg

Epinephrine 1 mg IVP q 3-5 min (0.01 mg/kg)

Amiodarone, Lidocaine, Magnesium

Defibrillate Adult 360/360/360 joulesChildren 2 joules/kg

Epinephrine 1 mg IVP q 3-5 min (0.01 mg/kg)

Amiodarone, Lidocaine, Magnesium

Osborne WavesOsborne Waves

Not a true arrhythmia, but an EKG abnormality suggestive of underlying pathology Seen primarily in hypothermia, <

35.6 degrees May also be seen in other conditions,

such as hypercalcemia or brain injury Also called J-waves, Camel backs,

hathooks

Not a true arrhythmia, but an EKG abnormality suggestive of underlying pathology Seen primarily in hypothermia, <

35.6 degrees May also be seen in other conditions,

such as hypercalcemia or brain injury Also called J-waves, Camel backs,

hathooks

Osborne Waves - Hypothermia

Osborne Waves - Hypothermia

Osborne Waves - Hypercalcemia

Osborne Waves - Hypercalcemia

Brugada SyndromeBrugada Syndrome

Genetic disease - autosomal dominant Mutation in the gene that controls the Na channel Characteristic ECG – ST segment elevation V1-V3 no signs of ischemia short QT interval Most common cause of sudden death in young males with no underlying cardiac disease Prevalence for Asians Cause of death – polymorphic V tach or V fib Treatment – no medicine will prevent AICD to abort lethal arhythmias

Genetic disease - autosomal dominant Mutation in the gene that controls the Na channel Characteristic ECG – ST segment elevation V1-V3 no signs of ischemia short QT interval Most common cause of sudden death in young males with no underlying cardiac disease Prevalence for Asians Cause of death – polymorphic V tach or V fib Treatment – no medicine will prevent AICD to abort lethal arhythmias

Diagnostic CriteriaDiagnostic Criteria Type I is the only ECG criterion that is diagnostic of

Brugada syndrome. (see figure). Definitive diagnosis - type 1 ST-segment is observed

in >1 right precordial lead (V1 to V3) and one of the following:

documented ventricular fibrillation (VF) polymorphic ventricular tachycardia (VT) a family history of sudden cardiac death at <45 years

old coved-type ECGs in family members inducibility of VT with programmed electrical stimulation syncope nocturnal agonal respiration.

Type I is the only ECG criterion that is diagnostic of Brugada syndrome. (see figure).

Definitive diagnosis - type 1 ST-segment is observed in >1 right precordial lead (V1 to V3) and one of the following:

documented ventricular fibrillation (VF) polymorphic ventricular tachycardia (VT) a family history of sudden cardiac death at <45 years

old coved-type ECGs in family members inducibility of VT with programmed electrical stimulation syncope nocturnal agonal respiration.

Brugada Syndrome Brugada Syndrome

Now for some cases…Now for some cases…

82 yo male with hx HTN c/o weakness dizziness SOB BP 100/50 HR 155

What does the EKG show?What is the treatment?

82 yo male with hx HTN c/o weakness dizziness SOB BP 100/50 HR 155

What does the EKG show?What is the treatment?

35 yo female c/o palpitations, near syncope, occasional episodes of rapid HR

What does the EKG showWhat medicines should be avoided in this

patient?

35 yo female c/o palpitations, near syncope, occasional episodes of rapid HR

What does the EKG showWhat medicines should be avoided in this

patient?

65 yo male with COPD c/o SOB, wheezing and pedal edema

What does the EKG show?What is the treatment?

65 yo male with COPD c/o SOB, wheezing and pedal edema

What does the EKG show?What is the treatment?

91 yo female c/o weakness and syncope.What does the EKG show?

What is the treatment?

91 yo female c/o weakness and syncope.What does the EKG show?

What is the treatment?

26 yo medical student presents with N,V altered mental

status. She has not been eating well. She is on Erythromycin for a URI. Her K=2.1 Mg=1.0

(nl=1.8-3.0) She collapses in the ER and is placed on a monitor.

26 yo medical student presents with N,V altered mental

status. She has not been eating well. She is on Erythromycin for a URI. Her K=2.1 Mg=1.0

(nl=1.8-3.0) She collapses in the ER and is placed on a monitor. What does the monitor show? What is the treatment?

What does the monitor show? What is the treatment?

48 y/o F presents lightheaded after walking. She just started

metoprolol.What does the ecg show?What is the treatment?

48 y/o F presents lightheaded after walking. She just started

metoprolol.What does the ecg show?What is the treatment?

42 y/o F presents with palpitations and DIB?

What does the ecg show?How could you differentiate the rhythm?

42 y/o F presents with palpitations and DIB?

What does the ecg show?How could you differentiate the rhythm?

You are working in the EC. The nurses come get you for this rhythm. It appeared 45 min after giving thrombolytics for AMI. Previously it was

NSR.What is this?

What should you do?

You are working in the EC. The nurses come get you for this rhythm. It appeared 45 min after giving thrombolytics for AMI. Previously it was

NSR.What is this?

What should you do?

86 y/o M c/o weakness and DIB.

86 y/o M c/o weakness and DIB.

What rhythm is this on the monitor?What should you worry about?Are you going to treat this?

What rhythm is this on the monitor?What should you worry about?Are you going to treat this?

61 y/o M with CP, palpitations, and dizziness.

What is the ecg show?What do you want to do?

61 y/o M with CP, palpitations, and dizziness.

What is the ecg show?What do you want to do?

So you cardioverted the previous rhythm and now this is on the

monitor…

So you cardioverted the previous rhythm and now this is on the

monitor…

What is this?What should you check?What should you do (besides soil

yourself)?

What is this?What should you check?What should you do (besides soil

yourself)?

24 y/o pregnant F presents with 3 days of vomiting…

24 y/o pregnant F presents with 3 days of vomiting…

What does the ecg show?What is the treatment of choice?

What does the ecg show?What is the treatment of choice?

52 y/o M who is homeless and found sleeping in an alley.What does the ecg show?What is the treatment?

52 y/o M who is homeless and found sleeping in an alley.What does the ecg show?What is the treatment?

45 y/o M with CKD on HD presents with palpitations and

DIB after missing dialysis.

45 y/o M with CKD on HD presents with palpitations and

DIB after missing dialysis. What does this ecg show?What should you do to treat this?

What does this ecg show?What should you do to treat this?

Had enough yet?Had enough yet?

The EndThe End