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

Nervous System Control of the Heart

Parasympathetic

nerve

nervous system Vagus

Decreases rate Slows impulse conduction Decreases force of contraction

Nervous System Control of the Heart

Sympathetic

nervous system

Increases rate Increases force of contraction

Intrinsic Rates of the Conduction System

SA

node
node of His, Purkinje fibers

60-100 40-60 20-40

AV

Bundle

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 Normal duration

0.12-0.20 sec

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 Disturbance in bundle branches or in ventricles

Source of variation

QRS variations
not 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 0.12 sec

Normal duration

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 Electrolyte imbalances Ischemia Infarction

Sources of variation

QT Interval

Beginning of QRS complex to end of T wave Represents time taken for entire ventricular depolarization and repolarization Normal duration

0.34-0.43 sec Drugs Electrolyte imbalances Changes in heart rate inverse relationship

Sources of variation

U Wave

Sometimes seen after T wave ?? May be normal May indicate hypokalemia

Rhythm interpretation
A Systematic Approach

Rules for Systematic Interpretation

If the rhythm doesnt 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 shouldnt be there

Calculating Heart Rate

Regular
Small blocks into 1500 Large 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)

Sinus Bradycardia

ECG characteristics

Rhythm

Rate

Regular, slow <60

P wave

PR interval

Normal, one per QRS 0.12-0.20, consistent Normal, <0.12

QRS complex

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

ECG characteristics

Rhythm

Regular, fast 100-200 Normal, one for every QRS 0.12-0.20, consistent Normal, <0.12

Rate

P wave

PR interval

QRS complex

Sinus Tachycardia
Clinical

Associations

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

Sinus Tachycardia
Clinical

Associations (contd)

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

ECG characteristics

Rhythm

Rate

Irregular, but with a pattern Speeds up with respiration 60-100 normal normal normal

P wave

PR interval QRS complex

Sinus Arrhythmia
Clinical

Associations Clinical significance Treatment

Atrial Fibrillation

ECG characteristics Rhythm 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

ECG characteristics

Rhythm

Rate

May be regular or irregular Atrial 200-350 and regular Ventricular - < & > 100 regular or irregular Flutter waves sawtoothed More than QRS complexes may be in a ratio Not measurable Normal

P wave

PR interval

QRS complex

Atrial Flutter
Clinical

Associations

CAD HTN Mitral valve disorders PEs Chronic lung disease Cor pulmonale Cardiomyopathy Hyperthyroidism Digoxin Quinidine Epinephrine

Atrial Flutter
Clinical

significance

Decrease cardiac output Heart failure Increased risk of stroke Slow ventricular response by increasing AV block Calcium channel blockers Beta blockers Cardioversion Amiodarone Rhythmol Ablation

Treatment

Supraventricular Tachycardia

ECG characteristics

Rhythm

Rate

Regular 150-220

P wave

PR interval

Difficult to determine may be hidden Abnormal Normal or shortened Normal

QRS complex

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 Prolonged arrest, may not be resuscitated CPR with ACLS Epinephrine Atropine Intubation Transcutaneous temporary pacemaker

Clinical significance

Treatment

Premature Beats

Premature Atrial Contractions (PACs)

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 (PACs)

Clinical

Associations

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

Premature Atrial Contractions (PACs)

Clinical

significance

In healthy hearts, not significant Symptoms

Heart

skipped beat Palpitations

May be early indication of more serious dysrhythmias

Reduce stimulants Beta blockers

Treatment

Premature Ventricular Contractions (PVCs)

Beat early in cycle with compensatory pause ECG characteristics

Rhythm

Rate

irregular
Dependent on underlying rhythm No P wave with premature beat none

P wave

PR interval

QRS complex

Wide bizarre, >0.12

Premature Ventricular Contractions (PVCs)

Bigeminy

Every other beat is a PVC Every third beat is a PVC All PVCs from same source Look alike Different sources of beat Beats look different Two in a row Runs will turn into V-tach

Trigeminy

Unifocal

Multifocal

Couplet

Premature Ventricular Contractions (PVCs)

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 (PVCs)

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 (PJCs)

Beat occurs early in cycle and no compensatory pause ECG characteristics

Rhythm

Irregular Dependent on underlying rhythm May or may not be present if present will be inverted Different from underlying rhythm if there at all normal

Rate

P wave

PR interval

QRS complex

Premature Junctional Contractions (PJCs)

Clinical

significance &Treatment

Similar to PACs

Junctional Rhythms

Originate below atria and above ventricles

Junctional Rhythm

ECG characteristics 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

ECG characteristics Rhythm 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
Dependent on tolerance Atropine Beta blockers Calcium channel blockers Amiodarone

Treatment

Ventricular Rhythms

Originate in the ventricles

Idioventricular Rhythm

ECG characteristics

Rhythm

Regular 20-40 none absent Wide, bizarre >0.20

Rate

P wave

PR interval

QRS complex

Ventricular Tachycardia

ECG characteristics

Rhythm

Regular R to R Ventricular rate 150-250 none none Wide, bizarre, > 0.12

Rate

P wave

PR interval

QRS complex

Ventricular Tachycardia
Run

of three or more PVCs 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

ECG characteristics

Rhythm

No rhythm present No rate No P waves none none

Rate

P wave

PR interval

QRS complex

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 Immediate CPR & ACLS Immediate defibrillation

Treatment

Ventricular Standstill

ECG characteristics

Rhythm

Regular p waves Atria 60-80 normal

Rate

P wave

PR interval

none
none

QRS complex

Heart Blocks

First Degree AV Block

ECG characteristics

Rhythm

Regular Normal Normal >0.20 normal

Rate

P wave

PR interval

QRS complex

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

Treatment

Second Degree AV Block Type I

Also called Mobitz I or Wenckebach ECG characteristics

Rhythm

Rate

Irregular
Atrial normal and regular Ventricular slightly higher than atrial rate

P wave

PR interval

More p waves than QRS complexes

Progressing lengths until drops QRS Normal and then one dropped

QRS complex

Second Degree AV Block Type I

Clinical Association

Clinical significance

Digoxin Beta blockers CAD

Treatment

Myocardial ischemia or infarction Generally transient and well tolerate May be warning sign for a more serious AV disturbance Symptomatic
Atropine Temporary pacemaker Closely monitored Transcutaneous pacer on standby

Asymptomatic

Second Degree AV Block Type II

Also called Mobitz II ECG characteristics

Rhythm

Rate

Irregular Regular if consistent conduction ratio Atrial normal and regular Ventricular slower, regular or irregular More p waves than QRS complexes, stated in a ratio Normal or prolonged Preceded by two or more P waves

P wave

PR interval

QRS complex

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
Permanent pacemaker

Treatment

Third Degree AV Block

ECG characteristics

Rhythm

Rate

R-R regular P-P regular Atrial 60-100 Ventricular 20-60, dependent on focus Normal, more P waves than QRS complexes No relationship between P waves and QRS complexes Dependent on focus

P wave

PR interval

QRS complex

Third Degree AV Block

Clinical

CAD MI Myocarditis Cardiomyopathy

Association

Severe heart disease

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 Pacemaker Atropine Epinephrine Dopamine Calcium chloride

Treatment

Bundle Branch Blocks

ECG

characteristics
bizarre

QRS complex
Wide,

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/medic al/instant-ecg--an-electrocardiogramrhythms-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 energies Fewer 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 Multifocal atrial tachycardia Digitalis toxicity

Contraindications

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
V-fib

beats

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

ICDs & Pacemakers

Implantable CardioverterDefibrillators (ICDs)

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

ICDs
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 If

25 seconds after detecting VT or VF, ICD delivers <25 joules. first shock is unsuccessful, ICD recycles and delivers successive shocks

ICDS
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

Pacemakers

A, A dual-chamber rateresponsive 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
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

Transcutaneous Transvenous epicardial

Temporary

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 tachydysrhythmias 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 during cardiac surgery leads are passed through the chest wall and can be attached to an external power source one lead on top of chest and one lead posterior

Epicardial
Placed

Transcutaneous
Placed

ICDs & 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-segmentelevation 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