Heart Rhythms: High

Degree AV block
Management Lethal
Arrhythmias
NUR 4050
Dr. Oliver-McNeil

Objectives
The

student will be able to calculate a patients heart rate

by the ECG strip.

The

student will be able to identify lethal arrhythmias and

high degree AV blocks by TMS

The

student will be able to recognize an anterior and

inferior wall myocardial infarction on the 12 lead ECG

The

student will understand medications used for

controlling heart rates and rhythms

The

student will understand the pacemaker coding system.

Components of the ECG

Electrodes

Disposable disks consisting an adhesive

ring with a conductive substance in the
center.
The conductive media conducts skin
surface voltage changes through color
coded wires.

Applying Electrodes:

Apply on dry skin.

Remove dead/dry skin before
application with a rough paper or cloth.
Clip hair if necessary.
Place on skin over areas with minimal
muscle activity.
Change as needed or daily.

Components of the for telemetry ECG

5 Lead Wire System

Most common set up in acute &

critical care.
White, black, and red electrodes are
located in identical positions to the
3 lead set.
Green electrode is located opposite
the red electrode.
The brown precordial lead V1 is
located to the right of the sternal
border at the 4th intercostal space.

Telemetry
Cardiac monitor
Lead 2
V1

or MCL1

lead analysis for Telemetry

Electrocardiography

(continued)

ECG Analysis

Rhythm

What is the rhythm of the strip?

Is the rhythm regular or irregular?

Slightly irregular
Basically regular
1.

Premature ectopic beats

2.

Escape ectopic beats

3.

Regularly irregular

4.

Irregularly irregular

ECG Analysis Cont.

Rate

What is the rate of the heart beat?

Calculation of heart beat

1500 method (only if rhythm regular)

R-R method (Quickest, easiest)

Count # of small squares between 2 QRS divide into 1500

Find QRS where peak of R falls on heavy dark line (300-150-100-75-60-50)

6 second method

Count # of QRS in 6 sec multiply by 10

Atrial Conduction

Are P waves present?

Are there P waves for each QRS?

Are the P waves before or after the QRS complex?

What are the shape of the P waves?

Do all P waves look alike?

Are there more P waves than QRS?

Atrial Conduction

If ectopic beats, are there any abnormal shaped P waves in relationship to

these beats?

Are the P waves buried?

AV Conduction

Is PR interval normal?

Are all PR intervals the same?

If PR intervals different, is there a pattern?

Ventricular Conduction

Are QRS complexes normal?

Are all QRS complexes of the same duration?

Do all QRS complexes look the same?

Electrocardiography
Dysrhythmia Interpretation

Heart rate and rhythm

P-wave evaluation
PR-interval evaluation
QRS evaluation
QT evaluation

Before a rhythm can be indentified, these are the steps that must be
completed.

Methods of Counting Heart Rates

Counting Heart rates

from the rhythm strip:
Count the number of QRS
complexes in 6 seconds
Count the number of
boxes between the QRS
complexes (if the rate is
regular).
i.e. 300-150-100-75-60-etc)

Sinus Bradycardia
Has a regular rhythm
Rate < 60 beats minute
Normal P wave preceding each QRS
Normal P-R,QRS complex, T wave, and QT interval

Clinical Considerations of Sinus Bradycardia

Signs of poor perfusion- low BP, decreased LOC, dizziness, syncope,

chest pain, dyspnea.
Possible causes -Cardiac ischemia, HR slowing medications (Digoxin,
beta blockers, Ca channel blockers, antiarrhythmics)
Non-cardiac disorders-electrolyte disturbance, Vagal responses,
hypothermia, hypothyroid.

Treating Symptomatic Bradycardia

Assess the ABCs

Assess VS and IV patency.
Administer O2

Atropine 0.5-1.0 mg every 3-5

minutes up to a total of 0.04
mg/kg.
Transcutaneous external
pacemaker SEDATE
IV Dopamine gtt 210mcg/kg/min
IV epinephrine gtt 2-10
mcg/min (1mg of 1:1000
mixed in 500ml .9NS @15ml/min.

Treatment Sinus Bradycardia

DO NOT JUST TREAT THE NUMBER!!!!

TREAT THE PATIENT

It is not uncommon for athletes to have slow heart rates

Treatment is reserved for symptoms

Sinus bradycardia that occurs with sleeping is not abnormal

Sinus Tachycardia
Regular atrial and ventricular rhythms
Heart rates > 100 beats per minute
P waves are of normal size and shape preceding the QRS. May
be superimposed on the preceding T wave with increasing HR.
PR intervals, QRS complex, and T wave are normal. QT interval
usually shortens.

Clinical Significance of Sinus Tachycardia

Decreases cardiac output by reducing diastole. Also increases
myocardial 02 demand in an unhealthy heart.
Assess ABCs, VS, chest pain, dyspnea, palpitations.
Causes: hypovolemia, pain, anxiety, physiologic stress (i.e.
infection, sepsis, anemia, shock states), fever
Presence of stimulants (caffeine, nicotine, amphetamines OTC
drugs, illicit drugs).
Treatments: Underlying cause if possible.
Consider slowing rate with beta blockers or calcium channel
blockers, but be careful maybe compensatory.
Provide reassurance and reduce fear and anxiety if possible.

Atrial Arrhythmias

Electrocardiography Atrial Rhythms

Conducted/nonconducted PACs

Electrocardiography Atrial Rhythms

(continued)

Supraventricular tachycardia
Paroxysmal supraventricular tachycardia

Electrocardiography Atrial Rhythms

Supraventricular tachycardia (continued)

Management
Medications to limit heart rate
Paroxysmal supraventricular tachycardia
Management
Valsalva maneuver
Carotid sinus massage
IV drugs
Adenocard (Adenosine)
Amiodarone
Diltiazem (Cardizem)

SVT vs Sinus Tachycardia

In

Sinus Tachycardia you will see P waves in

the normal direction for that lead

In

Supraventricular Tachycardia the P wave

will be slurred, inverted from normal
direction or not present

SVT

is a generic term that includes atrial

tachycardia, Atrial flutter and Atrial fibrillation
26

Atrial Flutter

Rates-atrial-200-400 beats/min, will be greater than ventricular

rate
Abnormal p waves referred to as flutter or saw tooth waves
QRS complex will usually be normal
P-R interval : atrial-regular, ventricular-irregular
and QT interval are not discernible

Electrocardiography Atrial Rhythms

Atrial flutter
Management
Dependent on ventricular response rate
Pharmacologic cardioversion
Ibutilide, sotalol, procainamide, amiodarone
Pharmacologic rate control
Calcium channel blockers, beta blockers, digoxin
Nonpharmacologic interventions
Cardioversion
Overdrive atrial pacing
Permanent termination
Radiofrequency ablation

Atrial fibrillation
Atrial rate of 350 - 600 times/min of
disorganized chaotic stimulus.
AV node acts as a buffer zone to the
ventricles.
Coordinated atrial emptying during
diastole is impaired.
Effects include:
Loss of atrial kick.
Pooling and clotting of blood in the
atria.
Thromboembolism.

(70,000 strokes annually).

Diagnostic Characteristics of AF
Rhythm: irregularly irregular
Atrial rate: indiscernible; often> 400/min
Ventricular rate: < 100 to > 150/min
P waves absent ,PR interval indiscernible
QRS complex < 0.12 sec, T wave and QT interval indiscernible

Risk factors for A-fib

Hypertension
Advancing
Dilated
Valve

age

Left Atrium

disease (Aortic or Mitral)

Coronary

artery disease

Elevated

glucose

Thyroid

disease

Atrial Fibrillation

Management
Rhythm control: conversion to sinus rhythm
Antidysrhythmic drugs: amiodarone and ibutilide
Cardioversion
Rate control: control ventricular rate
Calcium channel blockers, beta blockers, digoxin
Anticoagulation
Significant threat of emboli

Medical Tx Atrial Fibrillation

Consider
Rate

duration of Onset (48 hrs is window of opportunity)

Control

IV

Infusion Diltiazem (Cardizem): 20mg IV over 10 mins., followed by drip @ 515mg/hr.

IVP

Diltiazem 15-20mg IVP over 2min (0.25 mg/kg)

May

Rhythm
IV

repeat @ 20-25mg over 2 min (0.35mg/kg)

Control

Amiodarone: Max dose 2.2gm/24 hrs IV.

Rapid

infusion: 150mg IV over the first 10 min (15mg/min), followed by

1mg/min for 6 hrs, then 0.5mg/min for 18 hrs

Convert
May

to PO

cause profound vasodilatation and hypotension, may see pauses as convert

to NSR.

Atrial Fibrillation
Procedures
Cox-Maze

procedure

Radiofrequency
Pulmonary

ablation

Vein Isolation

Atrial Fibrillation

Stroke Preventions in Atrial Fibrillation

CHA2DS2VASc
C

Scoring System

=Congestive Heart Failure 1 point

H=

Hypertension 1 point

A2

=Age75 y 2 points

D=

Diabetes 1 point

S2=
V

Stroke 2 points

=Vascular disease 1 point

A =Age65
Sc=

y 1 point

Sex category, female 1 point

36

Stroke Prevention Atrial Fibrillation

CHADS

Score

CHF=1
Hypertension=1
Age

>75=1

Diabetes=1
Stroke

=2

IF a patient is cardioverted within 24-48 hours of onset, then

continue IV heparin,
If over 48 hours either delay DCCV until INR is >2.0, or Dabigatran
(Pradaxa), Eliquis, or Xarelto for 3-4 weeks or TEE DCCV followed
by anticoagulation.

SCORE RISK RECOMMENDATION FOR LONG TERM

ANTICOAGULATION
1=Intermediate
Anticoagulation

is recommended risk vs benefit discussed with patient

or more

Anticoagulation
High

highly recommended

(CHA2DS2 VASc) or Intermediate (CHADS2 classic)

Warfarin

(INR 2.03.0), unless there are reasons to avoid it. Or use of

alternative anticoagulation medications

ula

rR

hy t
hm

Junctional

dysrhythmias-Possible
terminology
Premature junctional contraction
Junctional escape rhythm
Accelerated junctional rhythm
Junctional tachycardia
Characterized by a regular ventricular

rate
without a P wave or very short PR interval

Junctional Rhythm

Ventricular Junctional Rhythm

Monitor BP

Avoid BB and CCB

Pace if hemodynamically compromised

Electrocardiography
Ventricular Dysrhythmias

Managing PVCs
Assess need for treatment
Assess for symptoms
Treat cause
Assess electrolytes
Assess for drugs that cause ventricular ectopy
Pharmacologic management
Beta blockers to reduce sympathetic
stimulation
Antidysrhythmic drugs

Electrocardiography
Ventricular Dysrhythmias

Premature ventricular contractions (PVCs)

Causes
Types
Timing

Ventricular tachycardia (VT)

Management
Dependent upon patient condition
Pulseless VT: life threatening
Stable VT

Premature Ventricular Contractions (PVCs)

Originate in the ventricles below the Bundle of His from a different

pathway.
P waves are absent due to no atrial depolarization..
T waves and QRS complexes deflect in opposite directions .
QRS complex is wider than normal
Can be normal with no tx or a warning of vent. Irritability
http://www.rnbob.tripod.com/prematureventricularcomplexes.htm

Electrocardiography
Ventricular Dysrhythmias

Unifocal vs Multifocal

Ventricular Tachycardia (VT)

3 or more PVCs in a row
Unable to determine atrial rhythm; Ventricular rate >100/min
Ventricular rhythm may or may not be regular
No p waves and unmeasurable P-R intervals.
QRS complex is wide and bizarre with T wave in the opposite
direction.

Electrocardiography
Ventricular Dysrhythmias

Ventricular tachycardia (VT)

(continued)

Electrocardiography
Ventricular Dysrhythmias

(continued)

Ventricular fibrillation (continued)

Life-threatening dysrhythmia
Management
Defibrillation
Cardiopulmonary resuscitation

Ventricular Fibrillation (VF)

Chaotic rhythm
Rate-indeterminate
No p waves; immeasurable PR
Indiscernible T waves.
Waveform may appear as a wavy baseline.
This is one of the primary lethal arrhythmias

http:www.ecglibrary.com/vf.html

Electrocardiography
Ventricular Dysrhythmias

Ventricular fibrillation Fine vs Coarse

(continued)

Clinical significance of VT/VF

Pts with VT and a pulse may need to be cardioverted if
BP is low, versus meds.
In VF, the ventricles actually are quivering instead of
contracting reducing CO to zero.
ABCs are of vital importance.
Check pt responsiveness.
Defibrillate/AED if pt is pulseless.
CPR until defibrillator arrives.

Heart Blocks

First Degree AV Block (Prolong PR-interval)

PR interval >0.20 ms

Second-degree AV block Type 1

Type I: Characterized by Prolongation of PR Interval before QRS Complex

is dropped. No treatment. Can continue BB and CCB

Second-degree AV block Type II

Characterized by normal PR interval followed by QRS complex with

sudden dropping of QRS Complex. Can lead to complete Heart Block

Second Degree AV Block Type II

56

Second-degree AV block Type II

Management
Transcutaneous

pacing
Patient may need a temporary transvenous
pacemaker
Avoid BB and CCB

Third-degree AV block

Characterized by no P wave before QRS complex or P wave

does not occur before QRS complex

Third Degree AV Block

59

Third-degree AV block
Management
Transvenous or Transcutanous Pacemaker
Will need permeant pacemaker
Do NOT give BB, CCB and antiarrhythmics

Asystole
Cardiac Standstill or total absence of ventricular electrical
activity.
Evidenced clinically by no pulse or cardiac output.
No QRSs seen on the monitor.
Caused by ischemia, hypoxia, drug overdose, electrolyte
disturbances, traumatic arrest.
Think about cause as much as treatment.

Pacemakers in the ICU

Pacemakers.
Are artificial pulse generators which
deliver electrical pulses to stimulate
depolarization in the event of
inadequate intrinsic heart beats to
support CO.
Consist of a pacing lead and a pulse
generator (power source).

Types of Pacemakers Leads

Epicardial lead: Wires placed on the surface of the
heart and brought through the skin and attached to a
pulse generator. (Cardiac Sugery)
Temporary pacing- Lead wire inserted through a
catheter into the right ventricle and attached to a
pulse generator.
Permanent pacing- Lead wires implanted surgically or
transvenously and attached to an implanted
generator with a lithium battery (lasts average 8-12
years).

Types of Pacemakers
External PacingElectrodes placed
on the chest
delivers impulses
through the chest
wall.
Chest wall
impedance often
causes great
discomfort or
inability to
capture.

Pacemaker System

(continued)

Indications for Cardiac Pacing

Unstable bradycardia
SBP < 80,mental status changes, SOB,
chest pain
Override or overdrive unstable tachycardias
(causing same symptoms as above) in ICU
Setting.
Brady-asystolic cardiac arrest.
Heart rate support of temporary conduction
problems (MI, heart blocks, drug overdose)

Three Functions of Pacemakers

Firing or Pacing- The pacer delivers an impulse per the programmed
rate. This is seen on the monitor by an observable spike followed by a
p wave (if atria are stimulated) or QRS (if ventricle is the target
chamber).

Three Functions of Pacemakers

Capture the target chamber
http://www.ecglibrary.com/vvi.html

Successfully depolarizes the target chamber (atria or

ventricle) as evidenced on the monitor by a p wave
or QRS after the spike.
If new pacemaker and there is no capture, turn pt on to
left side

Three Functions of Pacemakers

Sensing
The pacers ability to recognize the presence or absence of
intrinsic electrical activity.
If the pacer is too sensitive, it will recognize inappropriate
internal activity and not fire when necessary.
If the pacer is not sensitive, it wont recognize intrinsic activity
and fire on top of ones own electrical stimulations.

Pacemaker Interpretation Codes

Chamber Paced

Chamber Sensed

Response

V:Ventricle

V: Ventricle

I: Inhibited

A: Atrium

A: Atrium

T: Triggered

D: Dual (both A & V)

D: Dual (A & V)

D: Dual (I & T)

0: None

0: None

0: None

Key Interventions
Assess for chest pain
Evaluate Rhythm
Assess & monitor cardiovascular status.
Complete assessment of peripheral circulation.
Monitor VS frequently.
Evaluate clients response to dysrhythmias.
Monitor appropriate lab tests (i.e. lytes, Mg, cardiac enzymes).
Administer antiarrhythmics
Promote stress reduction

12 Lead ECG for the UG Student

Electrode Placement

V1 4th Intercostal space to the right of the sternum

V2 4th Intercostal space to the left of the sternum

V3 Midway between V2 and V4

V4 5th Intercostal space at the midclavicular line

V5 Anterior axillary line at the same level as V4

V6 Midaxillary line at the same level as V4 and V5

RL Anywhere above the ankle and below the torso

RA Anywhere between the shoulder and the elbow

LL Anywhere above the ankle and below the torso

LA Anywhere between the shoulder and the elbow

12- Lead ECG Electrode Placement

Electrocardiography

ECG Lead Analysis

ECG changes of ischemia and infarction

ST-segment and T-wave changes
ST elevation is seen with myocardial injury
ST depression is seen with myocardial ischemia
(Stress)
Q-wave development
Present with a myocardial infarction (Damage)

Electrocardiography
Infarct Location by 12-Lead

Anterior
Inferior
Ventricular septum
Lateral wall
Posterior wall
Right ventricle
Combinations and infarct age
The changes that occur in the corresponding leads is a clue of the
location of the Acute Coronary Syndrome Event

Color Coding ECGs Anterior

2004 Anna Story

Yellow indicates V1, V2, V3, V4

Anterior infarct with ST

elevation

Left Anterior Descending Artery

(LAD)

V1 and V2 may also indicate

septal involvement which
extends from front to the back
of the heart along the septum

Left bundle branch block

Right bundle branch block

2nd Degree Type2

Complete Heart Block

79

Anterior MI

2004 Anna Story

80

Color Coding ECG- Inferior

Blue indicates leads II, III, AVF

Inferior Infarct with ST elevations

Right Coronary Artery (RCA)

1st degree Heart Block

2nd degree Type 1, 2

3rd degree Block

N/V common, Brady

2004 Anna Story

81

Inferior MI

2004 Anna Story

82