DYSRHYTMIAS & Hemodynamic Monitoring. Cardiac Rhythm Monitoring 12 lead ECG Telemetry Halter...

DYSRHYTMIAS& Hemodynamic Monitoring

Cardiac Rhythm Monitoring 12 lead ECG Telemetry Halter monitor Bedside monitor

Lead placement 12 lead

12 lead ECG

Diagnostic Structural

changes Ischemia Infarction Enlarged cardiac

chambers Electrolyte

imbalances Drug toxicity

Assessment of dysrhythmias

Lead placement 5 lead

5 lead monitoring

Telemetry monitoring ICU Holter monitors Provides more views

in different leads

Lead placement 3 lead Three Lead

Less lead views Simple monitoring Quick

Patch Considerations

Properly prepare skin Clip excessive hair on

the chest wall with scissors

Gently rub the skin with dry gauze

If skin is oily, wipe with alcohol first

Heart Anatomy& Conduction System

Conduction System

Properties of Cardiac Cells Automaticity

Ability to initiate an impulse spontaneously and continuously

Excitability

Ability to be electrically stimulated

Conductivity

Ability to transmit an impulse along membrane in an orderly

manner

Contractility

Ability to respond mechanically to an impulse

Nervous System Control of the Heart

Autonomic nervous system

controls: Rate of impulse formation Speed of conduction Strength of contraction


Parasympathetic nervous system Vagus nerve Decreases rate Slows impulse conduction Decreases force of contraction


Sympathetic nervous system Increases rate Increases force of contraction

Intrinsic Rates of the Conduction System

SA node 60-100

AV node 40-60

Bundle of His, Purkinje fibers 20-40

Ventricles <20

P Wave Atrial depolarization Firing of SA node Should be upright

Normal duration 0.06-0.12 sec

Source of variation Disturbance in atria

PR Interval

Impulse through atria to AV node, bundle of His

Measured from beginning of P wave to beginning of QRS complex


Source of variation Short – impulse from AV

junction Longer – AV block

QRS Interval Ventricular Depolarization Atrial repolarization

Hidden in wave Measured from the

beginning to end of QRS complex

Normal is not always a traditional wave form

Normal duration < 0.12 sec

Source of variation Disturbance in bundle

branches or in ventricles

QRS variationsnot everyone has “normal” QRS

ST Segment

Time between ventricular depolarization and repolarization

Should be flat (isoelectric) Look for elevation or

depression ST elevation – myocardial

injury ST depression – reciprocal

changes and ischemia Normal duration

0.12 sec Source of variation

Ischemia Injury infarction

T Wave

Ventricular repolarization Should be upright Follows QRS complex Larger than a P wave Inversion indicates ischemia

to myocardium Normal duration

0.16 sec Sources of variation

Electrolyte imbalances Ischemia Infarction

QT Interval Beginning of QRS complex to

end of T wave Represents time taken for

entire ventricular depolarization and repolarization


Sources of variation Drugs Electrolyte imbalances Changes in heart rate – inverse

relationship

U Wave

Sometimes seen after T wave

?? May be normal May indicate hypokalemia

Rhythm interpretationA Systematic Approach

Rules for Systematic Interpretation

If the rhythm doesn’t look right check your patient! Treat the patient not the monitor

Is the rhythm regular or irregular – R to R, then P to P

What is the heart rate Can you identify P waves Can you identify QRS complexes & T waves What is the ratio of P waves to QRS complexes What is the PR interval Anything else you notice that shouldn’t be there

Calculating Heart RateRegular

Small blocks into 1500Large blocks into 300

Irregular = 6-second strip

Divide by 300 between waves

Atrial Rhythms Rhythms that originate in the

atria

Normal Sinus Rhythm

Follows normal conduction pattern Rate

60-100 P wave

Normal , one per QRS PR interval

Normal, consistent (0.12-0.20) QRS complex

Normal (<0.12)

http://www.learnekgs.com/NSR-Generated-LARGE.jpg

Sinus Bradycardia

ECG characteristics Rhythm

Regular, slow Rate

<60 P wave

Normal, one per QRS PR interval

0.12-0.20, consistent QRS complex

Normal, <0.12

Sinus Bradycardia Clinical Associations

Normal in fit, athletic individuals Normal in sleep Increased vagal tone –e.g. vomiting Drugs

Beta blockers Calcium channel blockers

Hypothyroidism MI Increased intracranial pressure Hypoglycemia

Sinus Bradycardia Clinical significance

Dependent on patient tolerance Symptomatic

Pale Cool skin Hypotension Weakness Angina Dizziness Syncope Confusion or disorientation SOB

Sinus Bradycardia Treatment

Atropine Pacemaker Treat underlying cause

Sinus Tachycardia


Regular, fast Rate

100-200 P wave

Normal, one for every QRS PR interval

0.12-0.20, consistent QRS complex

Normal, <0.12

Sinus Tachycardia Clinical Associations

Exercise Anxiety, pain, fear Hypotension Hyperthyroidism Hypovolemia Anemia Hypoxia Hypoglycemia MI Heart failure

Sinus Tachycardia

Clinical Associations (cont’d) Drugs

Epinephrine Norepinephrine Atropine Caffeine Theophylline Nifedipine Hydralazine Sudafed

Sinus Tachycardia Clinical significance

Dependent on tolerance Symptoms

Dizziness Dyspnea Hypotension Angina

Treatment Treat underlying cause Vagal maneuvers Beta blockers

Sinus Arrhythmia


Irregular, but with a pattern Speeds up with respiration

Rate 60-100

P wave normal

PR interval normal

QRS complex normal

Sinus Arrhythmia Clinical Associations Clinical significance Treatment

Atrial Fibrillation


irregular Rate

Atrial 350-600, irregular Ventricular - < & > 100 – irregular

P wave Irregular, chaotic

PR interval Not measurable

QRS complex normal

Atrial Fibrillation Clinical Associations

CAD Rheumatic heart disease cardiomyopathy Hypertensive heart disease Heart failure Pericarditis Thyrotoxicosis Alcohol intoxication Caffeine Electrolyte disturbances Stress Cardiac surgery

Atrial Fibrillation Clinical significance

Most common, clinically significant dysrhythmia Decreased cardiac output Thrombus formation Stroke

Accounts for as many as 20% of all strokes Treatment

Calcium channel blockers Beta blockers Digoxin Amiodarone Cardioversion Anticoagulation therapy

Atrial Flutter


May be regular or irregular Rate

Atrial – 200-350 and regular Ventricular - < & > 100 – regular or irregular

P wave Flutter waves – sawtoothed More than QRS complexes – may be in a ratio

PR interval Not measurable

QRS complex Normal

Atrial Flutter Clinical Associations

CAD HTN Mitral valve disorders PE’s Chronic lung disease Cor pulmonale Cardiomyopathy Hyperthyroidism Digoxin Quinidine Epinephrine

Atrial Flutter Clinical significance

Decrease cardiac output Heart failure Increased risk of stroke

Treatment Slow ventricular response by increasing AV

block Calcium channel blockers Beta blockers Cardioversion Amiodarone Rhythmol Ablation

Supraventricular Tachycardia


Regular Rate

150-220 P wave

Difficult to determine – may be hidden Abnormal

PR interval Normal or shortened

QRS complex Normal

Supraventricular Tachycardia Clinical Associations

Overexertion Emotional stress Deep inspiration Caffeine Tobacco Rheumatic heart disease Digitalis toxicity CAD Cor pulmonale

Supraventricular Tachycardia Clinical significance

Prolonged episodes may precipitate decreased cardiac output

Symptoms Hypotension Dyspnea Angina

Treatment Vagal stimulation

Valsalva maneuver Drugs

Adenosine Beta blockers Calcium channel blockers

Cardioversion

Asystole

There is no electrical activity in the heart during asystole, therefore there will only be a flat line on the rhythm strip

Asystole Clinical Associations

Advanced cardiac disease Severe cardiac conduction system disturbance End stage heart failure

Clinical significance Prolonged arrest, may not be resuscitated

Treatment CPR with ACLS Epinephrine Atropine Intubation Transcutaneous temporary pacemaker

Premature Beats

Premature Atrial Contractions (PAC’s)

Beats occur early in the cycle and there is no compensatory pause ECG characteristics

Rhythm irregular

Rate Dependent on underlying rhythm

P wave Abnormal shape

PR interval Normal Will be different than underlying rhythm

QRS complex Normal

Premature Atrial Contractions (PAC’s) Clinical Associations

Can occur normally Emotional stress Physical fatigue Alcohol Caffeine Tobacco CHF Ischemia COPD Hypoxia Hyperthyroidism CAD

Premature Atrial Contractions (PAC’s)

Clinical significance In healthy hearts, not significant Symptoms

Heart “skipped” beat Palpitations

May be early indication of more serious dysrhythmias

Treatment Reduce stimulants Beta blockers

Premature Ventricular Contractions (PVC’s)

Beat early in cycle with compensatory pause ECG characteristics

Rhythm irregular


P wave No P wave with premature beat

PR interval none

QRS complex Wide bizarre, >0.12

Premature Ventricular Contractions (PVC’s) Bigeminy

Every other beat is a PVC Trigeminy

Every third beat is a PVC Unifocal

All PVC’s from same source Look alike

Multifocal Different sources of beat Beats look different

Couplet Two in a row Runs will turn into V-tach

Premature Ventricular Contractions (PVC’s)

Clinical Associations Caffeine Alcohol Nicotine Aminophylline Epinephrine Digoxin Electrolyte imbalances Hypoxia Fever Exercise Emotional stress MI Mitral valve prolapse Heart failure CAD

Premature Ventricular Contractions (PVC’s) Clinical significance

Usually benign May precipitate

Decreased cardiac output Angina Heart failure

Assess apical-radial pulse rate Treatment

Treat underlying cause Beta blockers Procainamide Amiodarone Lidocaine

Premature Junctional Contractions (PJC’s)

Beat occurs early in cycle and no compensatory pause ECG characteristics

Rhythm Irregular


P wave May or may not be present – if present will be inverted

PR interval Different from underlying rhythm if there at all

QRS complex normal

Premature Junctional Contractions (PJC’s) Clinical significance &Treatment

Similar to PAC’s

Junctional Rhythms Originate below atria and above

ventricles

Junctional Rhythm


regular Rate

40-60 P wave

Inverted, may be hidden in QRS complex PR interval

Shortened or missing QRS complex

normal

Accelerated Junctional Rhythm & Junctional Tachycardia


regular Rate

60-180 P wave

Inverted, may be hidden in QRS complex PR interval

Shortened or missing QRS complex

normal

Junctional Dysrhythmias Clinical Associations

CAD Heart failure Cardiomyopathy Electrolyte imbalances Inferior MI Rheumatic heart disease Digoxin Amphetamines Caffeine Nicotine

Junctional Dysrhythmias Clinical significance

Occur when the SA node has not been effective

If increases to junctional tachycardia patient may become hemodynamically unstable

Treatment Dependent on tolerance Atropine Beta blockers Calcium channel blockers Amiodarone

Ventricular Rhythms Originate in the ventricles

Idioventricular Rhythm


Regular Rate

20-40 P wave

none PR interval

absent QRS complex

Wide, bizarre >0.20

Ventricular Tachycardia


Regular R to R Rate

Ventricular rate 150-250 P wave

none PR interval

none QRS complex

Wide, bizarre, > 0.12

Ventricular Tachycardia Run of three or more PVC’s Clinical Associations

MI CAD Significant electrolyte imbalances Cardiomyopathy Mitral valve prolapse Long QT syndrome Drug toxicity CNS disorders

Ventricular Tachycardia Clinical significance

Stable – patient has a pulse Unstable – no pulse Decreased cardiac output Hypotension Pulmonary edema Decreased cerebral blood flow Cardio-pulmonary arrest

Ventricular Tachycardia Treatment

Treat quickly Identify and treat underlying causes Procainamide Sotalol Amiodarone Lidocaine Beta blockers Magnesium Dilantin Cardioversion CPR & ACLS

Ventricular Fibrillation


No rhythm present Rate

No rate P wave

No P waves PR interval

none QRS complex

none

Ventricular Fibrillation Clinical associations

Acute MI Myocardial ischemia Heart failure Cardiomyopathy Cardiac catheterization Cardiac pacing Accidental electric shock Hyperkalemia Hypoxemia Acidosis Drug toxicity

Ventricular Fibrillation Clinical significance

Symptoms Unresponsive Pulseless Apneic state

If not treated rapidly, patient will die Treatment

Immediate CPR & ACLS Immediate defibrillation

Ventricular Standstill


Regular p waves Rate

Atria 60-80 P wave

normal PR interval

none QRS complex

none

Heart Blocks

First Degree AV Block


Regular Rate

Normal P wave

Normal PR interval

>0.20 QRS complex

normal

First Degree AV Block Clinical Association

MI CAD Rheumatic fever Hyperthyroidism Vagal stimulation Digoxin Beta blockers Calcium channel blockers

First Degree AV Block Clinical significance

Usually not serious Can be a precursor for higher degrees of AV

block Patients are asymptomatic

Treatment No treatment unless caused by medications Monitor patient for increase in block

Second Degree AV Block – Type I

Also called Mobitz I or Wenckebach ECG characteristics

Rhythm Irregular

Rate Atrial – normal and regular Ventricular – slightly higher than atrial rate

P wave More p waves than QRS complexes

PR interval Progressing lengths until drops QRS

QRS complex Normal and then one dropped

Second Degree AV Block – Type I Clinical Association

Digoxin Beta blockers CAD

Clinical significance Myocardial ischemia or infarction Generally transient and well tolerate May be warning sign for a more serious AV

disturbance Treatment

Symptomatic Atropine Temporary pacemaker

Asymptomatic Closely monitored Transcutaneous pacer on standby

Second Degree AV Block – Type II

Also called Mobitz II ECG characteristics

Rhythm Irregular Regular if consistent conduction ratio

Rate Atrial – normal and regular Ventricular – slower, regular or irregular

P wave More p waves than QRS complexes, stated in a ratio

PR interval Normal or prolonged

QRS complex Preceded by two or more P waves

Second Degree AV Block – Type II Clinical Association

Rheumatic heart disease CAD Anterior MI Drug toxicity

Clinical significance Often progresses to third degree AV block Poor prognosis Decreased cardiac output Hypotension Myocardial ischemia

Treatment Permanent pacemaker

Third Degree AV Block


R-R regular P-P regular

Rate Atrial 60-100 Ventricular 20-60, dependent on focus

P wave Normal, more P waves than QRS complexes

PR interval No relationship between P waves and QRS complexes

QRS complex Dependent on focus

Third Degree AV Block Clinical Association

Severe heart disease CAD MI Myocarditis Cardiomyopathy

Amyloidosis Scleroderma Digoxin Beta blockers Calcium channel blockers

Third Degree AV Block Clinical significance

Reduced cardiac output Ischemia Heart failure Shock Syncope possible periods of asystole

Treatment Pacemaker Atropine Epinephrine Dopamine Calcium chloride

Bundle Branch Blocks

ECG characteristics QRS complex

Wide, bizarre

Bundle Branch Blocks Clinical significance Treatment

• http://www.skillstat.com/Flash/ECG_Sim_2004.html

• http://www.nobelprize.org/educational/medicine/ecg/index.html

• http://www.iphoneappsplus.com/medical/instant-ecg--an-electrocardiogram-rhythms-interpretation-guide/index.htm

http://www.skillstat.com/Flash/ECG_Sim_2004.html

http://www.skillstat.com/Flash/ECG_Sim_2004.html

http://www.nobelprize.org/educational/medicine/ecg/index.html



http://www.iphoneappsplus.com/medical/instant-ecg--an-electrocardiogram-rhythms-interpretation-guide/index.htm




Defibrillation & Cardioversion

Including pacemakers and implanted cardioverter defibrillator

Lifepak

Can be used as defibrillator, monitor, or transcutaneous pacer

Defibrillation The use of a carefully controlled electric shock,

administered either through a device on the exterior of the chest wall or directly to the exposed heart muscle, to restart or normalize heart rhythms.

Most effective method of terminating V-Fib and pulseless V-Tach

Deliver energy using a monophasic or biphasic waveform Monophasic defibrillators deliver energy in one

direction. Biphasic defibrillators deliver energy in two

directions. Deliver successful shocks at lower energiesFewer post shock ECG abnormalities

Defibrillation Output is measured in joules or watts

per second. Recommended energy for initial shocks

in defibrillation Biphasic defibrillators: First and

successive shocks: 150 to 200 joules Monophasic defibrillators: Initial shock at

360 joules

Defibrillation

Indications Pulseless v-tach V-fib Always done as emergent

Contraindications Multifocal atrial tachycardia Digitalis toxicity

Cardioversion Restoration of normal heart rhythm: the

use of an electric shock to convert a dangerously rapid, fluttering, and ineffective heartbeat to its normal rhythm Synchronized circuit delivers a counter

shock on the R wave of the QRS Synchronizer switch must be turned

ON

Cardioversion Indications

A-fib If unstable or new witnessed onset – may do

without anticoagulation but preferred method is with anticoagulation three weeks prior

TEE to rule out blood clots A-flutter (if unstable)

Anticoagulation therapy Stable V-tach (with pulse)

If patient does not respond to medications Contraindications

Digitalis toxicity associated tachycardia

Defibrillation & Cardioversion Nursing Considerations

IV access Airway management equipment Sedative drugs Monitor Be aware of possible implanted devices Firm pressure when discharging

Decrease chance for arcing and burns Clear of patient and bed

Defibrillation & Cardioversion Complications

Hypoxia or hypoventilation from sedation Burns

Mostly superficial some deep tissue Dysrhythmias

Premature beats V-fib

Hypotension Pulmonary edema Thromboembolization Myocardial necrosis r/t high energy discharge

ICD’s & Pacemakers

Implantable Cardioverter- Defibrillators (ICD’s)

A, The implantable cardioverter-defibrillator (ICD) pulse generator from Medtronic, Inc.B, The ICD is placed in a subcutaneous pocket over the pectoralis muscle. A single-lead system is placed transvenously from the pulse generator to the endocardium. The single lead detects dysrhythmias and delivers an electric shock to the heart muscle.

Indications for ICD

Spontaneous sustained v-tach Syncope with inducible v-tach/v-fib

during EP study At high risk for future life-threatening

dysrhythmias (cardiomyopathy) Have survived cardiac arrest

ICD’s Consists of a lead system placed via

subclavian vein to the endocardium Battery-powered pulse generator is

implanted subcutaneously ICD sensing system monitors the HR and

rhythm and identifies VT or VF.

Approximately 25 seconds after detecting VT or VF, ICD delivers <25 joules.

If first shock is unsuccessful, ICD recycles and delivers successive shocks

ICD’S ICDs are equipped with anti-tachycardia

and anti-bradycardia pacemakers. Initiate overdrive pacing of

supraventricular and ventricular tachycardias

Provide backup pacing for brady dysrhythmias that may occur after defibrillation discharges

Education is extremely important Participation in an ICD support group

should be encouraged

A, A dual-chamber rate-responsive pacemaker from Medtronic, Inc., is designed to treat patients with chronic heart problems in which the heart beats too slowly to adequately support the body's circulation needs.B, Pacing leads in both the atrium and ventricle enable a dual-chamber pacemaker to sense and pace in both heart chambers.

Pacemakers

Pacemakers Used to pace the heart when the normal

conduction pathway is damaged or diseased Pacing circuit consists of a power source,

one or more conducting (pacing) leads, and the myocardium

Pacemaker types Permanent

Single chamber Dual chamber

Temporary Transcutaneous Transvenous epicardial

Indications for permanent pacemakers

Indications for a temporary pacemaker

Pacemakers Anti-bradycardia pacing Anti-tachycardia pacing: Delivery of a

stimulus to the ventricle to terminate tachy-dysrhythmias

Overdrive pacing: Pacing the atrium at rates of 200 to 500 impulses per minute to terminate atrial tachycardias

Permanent pacemaker: Implanted totally within the body

Cardiac resynchronization therapy (CRT): Pacing technique that resynchronizes the cardiac cycle by pacing both ventricles

Temporary pacemakers Temporary pacemaker: Power source

outside the body Transvenous

Leads threaded through veins to right atrium or ventricle

Epicardial Placed during cardiac surgery – leads are

passed through the chest wall and can be attached to an external power source

Transcutaneous Placed one lead on top of chest and one lead

posterior

ICD’s & Pacemakers Complications

Infection Hematoma formation at sites of insertion Pneumothorax Failure to sense or capture Perforation of atrial or ventricular septum

by the pacing lead Corrosion of leads Battery depletion

ECG Changes Associated with ACS

ECG changes in ACS Ischemia

ST segment depression and/or T wave inversion

ST segment depression is significant if it is at least 1 mm (one small box) below the isoelectric line.

ECG changes in ACS

Changes occur in response to the electrical disturbance in myocardial cells due to inadequate supply of oxygen.

Once treated (adequate blood flow is restored), ECG changes resolve and ECG returns to baseline

ECG changes in ACS Injury

ST segment elevation is significant if >1 mm above the isoelectric line. If treatment is prompt and effective, may avoid

infarction If serum cardiac markers are present, an ST-segment-

elevation myocardial infarction (STEMI) has occurred.

ECG changes in ACS Infarction

Physiologic Q wave is the first negative deflection following the P wave. Small and narrow (<0.04 second in

duration) Pathologic Q wave is deep and >0.03

second in duration

ECG changes in ACS Infarction

Pathologic Q wave indicates that at least half the thickness of the heart wall is involved. Referred to as a Q wave MI Pathologic Q wave may be present

indefinitely. T wave inversion related to infarction

occurs within hours and may persist for months

DYSRHYTMIAS & Hemodynamic Monitoring. Cardiac Rhythm Monitoring 12 lead ECG Telemetry Halter...

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