Arrhythmias

Valerie Seabaugh MD

Jerry L Pettis Memorial VA Hospital

Today’s discussion

Normal ECG components Normal wave conduction physiology Bradycardia Tachycardia Pacemakers and Automatic internal

cardiac defibrillators (AICD)

Normal ECG By convention, electrical pulses

conducted toward the ECG lead are positive those conducted away are negative

The P wave

Represents atrial depolarization

Duration is measure of time required for depolarization to spread through the atria to the AV node

Is usually upright in I, II, and aVF

Negative in aVR variable in III, aVL

The PR interval

Represents time required for a supraventricular impulse to depolarize the atria, traverse the AV node, and enter the ventricle

Normal is 0.12 to 0.20 seconds, greater than 0.20 is considered first degree AV block

The QRS complex Represents ventricular

depolarization Q wave – first negative

deflection R wave – first positive

deflection after a P wave S wave – negative

deflection following an R wave

Normal is between 0.06 and 0.10 sec

The ST segment

The isoelectric segment following depolarization and preceding ventricular repolarization

From the end repolarization of the QRS to the beginning of the T wave

In contrast to PR and QRS intervals, the ST segment length can be variable

Elevation or depression of the ST segment by 0.1 mV from the baseline is abnormal

The T wave

Represents ventricular repolarization T wave vector normally “tracks” with

the QRS vector. If QRS is predominantly negative an inverted T wave is not necessarily abnormal

The QT interval

From the beginning of the QRS complex to the end of the T wave

Represents electrical systole Is usually <0.425 seconds duration

when corrected for heart rate (QTc = corrected QT interval)

Membrane potential in the ventricle, atria, and Purkinje system

Phase 0 – Na+ enters the cell

Phase 1 – initial repolarization by K+ moving out of the cell

Phase 2 – plateau of action potential caused by Ca++ moving into cell

Stoelting p 69

Membrane potential in the ventricle, atria, and Purkinje system

Phase 3 – Ca++ conductance decreases but K+ conductance increases with K+ moving out of cell

Phase 4 – K+ moving out returns cell to resting potential

This differs in the SA node where influx of Ca++ starts action potential

Effect of electrolyte disturbance on cardiac rhythm

Effect of electrolyte disturbance on cardiac rhythm

Hypocalcemia – prolonged QT interval, ST segment, V Tach, Torsades

Hypercalcemia – shortened QT interval

Hypomagnesemia – widened QRS, cardiac irritability

Bradycardia – Disturbances of cardiac impulse conduction

First degree AV heart block Second degree

Mobitz I Mobitz II

Unifasicular block R bundle branch block L bundle branch block Third degree (trifascicular ) heart block Defined as HR less than 60

First degree AV block

Think of ischemia if it is a new onset for the pt.

Can also be caused from digitalis, aortic regurgitation, increased vagal tone

Usually asymptomatic

2nd degree AV block

Mobitz I (Wenckeback) progressive prolongtion of PR until a beat is entirely blocked

2nd degree AV block Mobitz II

Sudden interruption of the conduction of an impulse without prior prolongation of the PR

2nd degree AV block Mobitz II

More serious than Mobitz I because it is more likely to progress to complete heart block

More likely to require pacemaker “Missing a beat without warning is

TWICE as scary”

Right bundle branch block

Conduction block over the R bundle branch which is present in 1% of hospital patients

May be seen in pts with pulm dz, ASD, or increased R ventricular pressures

Often clinically insignificant

Right bundle branch block

QRS complex exceeds 0.1 second

Broad rSR complex in V1 an V3

L bundle branch block

Often associated with ischemic heart disease, LVH/chronic HTN, or valve disease

Difficult to diagnose MI in the presence of LBBB

L bundle branch block

QRS complex more than 0.12 seconds with wide notched R waves in all leads

Unifascicular block

3 fascicles of the His-Perkinje system Right fascicle, Left anterior fascicle, Left posterior fascicle

A block of one of the L fascicles can occur One of the L fascicles plus RBBB can lead to complete heart

block

Complete heart block

Complete absence of conduction of impulse from atria to ventricle If block is proximal to AV node HR will be 45-

55 BPM If block is distal to AV node (infranodal) HR

will be 30-40 BPM with a wide QRS (ventricular in origin)

Can be caused by fibrotic degeneration, ischemia, cardiomyopathy, ankylosing spondylitis, iatrogenic (cardiac surgery), drugs, hyperkalemia

TX is pacing

Bradycardia

1001 Differential dxs for bradycardia including: Hypovolemia, hypoxia, acidosis,

hypoglycemia, hypothermia, hyperkalemia, overdose, tension pneumo, increased ICP, pesticide exposure, noxious surgical stimulation (ocular pressure, scrotal/ovarian traction, abd insufflation, laryngoscopy), PE, MI, carotid sinus stimulation, narcotics, succinylcholine, sleep apnea, normal physiology of well-trained athlete, hypothyroidism . . . etc

Tachycardia(Heart rate greater than 100)

Three key questions:IS THE PATIENT STABLE?Is the QRS narrow or wide?Is the rhythm regular or irregular?

Tachycardia

Narrow complex Regular rhythm is

probably a reentrant tachycardia

Irregular rhythm is probably A fib or A flutter

Wide complex Regular rhythm

could be SVT with aberrant waveform or VT

Irregular rhythm could be A fib with aberrant waveform, polymorphic V tach, torsades

Narrow versus wide complex tachycardia

Narrow complex more likely from an atrial originAka SVT (supraventricular

tachycardia) Wide complex more likely from a

ventricular originVT more serious since the concern is

that the rhythm may degrade to V Fib

Narrow complex tachycardiaSinus tachycardia

Most common cause of tachycardia Rhythm originates from AV node in

response to stress Hypovolemia Pain Fever Exercise Substance withdrawl Agitation (in the ICU) . . . etc

Treatment is to identify and treat the stressor (if necessary)

Narrow complex tachycardiaSupraventricular tachycardia

SVT can be loosely defined in 3 types Atrial tachycardia-AV node passively

conducts impulse from atria to ventricles• A fib, A flutter, atrial tachycardia

Atrioventricular nodal reentrant tachycardia-reentrant focus is adjacent to AV node and AV node propogates reentrant impulse

AV reentrant tachycardia-accessory pathway bypasses the AV node

• WPW

Narrow complex tachycardiaSupraventricular tachycardia

Atrial tachycardiaEctopic atrial focus (outside the atrial

node) becomes irritable and can override atrial rhythm

• See P waves of different morphology

Narrow complex tachycardia

Atrial fibrillation with RVRAtrial depolarization rate is 400 –

600/minuteAV node acts as gatekeeper and only

conducts 100-180 of these depolarizations each minute

Atrial Flutter Atrial depolarization rate is

250-450/minute

Narrow complex tachycardiaA fib/A flutter

A Fib

A flutter

Narrow complex tachycardiaA fib/A flutter

TreatmentIf patient is unstable tx is always

cardioversion • 50 J for A flutter, 100-200 for a fib

progressing to 200, 300, 360

For stable patients control rate with B blockers, diltiazem, consider amiodorone for new onset

Narrow complex tachycardiaAVNRT & AVRT

Reentry tachycardia requires two pathways over which impulses are conducted at different velocities

Can originate adjacent to the AV node

Pathway may completely bypass AV node (giving rise to WPW)

Narrow complex tachycardiaAVNRT & AVRT

If the supraventricular tachycardia is due to AV node reentry then it should be terminated by anything that transiently blocks the AV nodeCarotid massageValsalvaAdenosine

Definitive tx is ablation of the accessory pathway

Narrow complex tachycardiaAVNRT & AVRT

Accessory pathway which bypasses AV node poses risk for sudden cardiac death due to tachyarrhythmiasWPW syndrome on ECG has delta

wave or slurred deflection of beginning of QRS, QRS greater than 0.12 sec

Pacemakers and AICDs

Chamber paced

Chamber sensed

Response of generator

Prgrammable functions of the generator

V = ventricle V = ventricle T = triggered P = programmable rate

A = atrium A = atrium I = inhibited M= multiprogrammable

D = dual (atrium and ventricle

D = dual D = dual C= communicating

O = none (asynchrynous)

O = none (asynchrynous)

O = fixed function

ICD (implantable/internal cardiac defibrillator)

For patients with a high risk or personal history of ventricular fibrillationDevice delivers a defibrillating shock if

V tach or V fib is sensed

Things to consider in pacemaker/ICD patients

Central venous line placement can displace recently placed transvenous electrodes

Grounding pad needs to be placed far away from device

If cautery is used near device, current should be as low as possible and delivered in short bursts

Things to consider in pacemaker/ICD patients Should defibrillation be necessary in

pacemaker patient, paddles should not be placed directly over the pulse generator and patient may have lower stimulation threshold

For ICDs it is usually prudent to disable the device since sensing of electrocautery may trigger shock External defibrillator should be readily

available and device should be turned on immediately post op

THINGS TO REMEMBER

Your response to a patients dysrhythmia is dependent on whether the patient is stable or unstable Bradycardia of 45 in an Olympic athlete is

acceptable for a BP of 120/80 but not for 60/40

A heart rate of 130 is NORMAL in an infant but could cause an MI for a 78 year old hypertensive, diabetic, smoker

You are walking down the hall of the surgical floor when a nurse recognizes that you are on the surgical team and stops you regarding Mr. Brown. He is a 28 y/o that had an appendectomy at midnight last night. His heart rate was 120 when the CNA took his vitals 5 minutes ago. What is your next step?

You go to see Mr. Brown. He does not appear to be in pain, but does look pale and anxious. You pick up his wrist and count a thready pulse of 135.

His vitals are RR 28, BP 85/65, Temp 100.9

He states he has no heart problems or history of syncope. He runs 2 miles a day. His father died of an MI at 54.

On further exam you notice Mr. Brown’s abdomen seems more tender than you would expect.

The lab calls with a panic value of Hgb of 5.2 for Mr. Brown

You receive a stat page to the ward because Mr. Jones has been found to be lethargic this morning. He is only mumbling incomprensibly when you ask him questions or shake his shoulder.

Mr. Jones is a 78 year old that had a total knee replacement yesterday.

Vital signs are SpO2 85%, HR 45, RR 6, BP 82/40

Mr. Jones is lying in bed with his mouth hanging open. His eyes are rolled back. He is making course, snoring sounds with his respirations. His dressing looks clean and dry. He has NS for IVF running at 120/hour and a morphine PCA.

After oxygen mask is placed his saturation improves to 95%

0.5 mg of atropine improves his heart rate to 85

His mental status improves somewhat but he is still extremely somnalent

On further exam Mr. Jones is noted to have a PCA basal dose of 4 mg/hour of morphine.

After administering naloxone, Mr. Jones becomes responsive, conversant and begins asking for a breakfast tray