Cardiac DysrhythmiasNuro 438February 2015

Learning ObjectivesAt the completion of this presentation, the nursing student will be able to successfully Describe cardiac anatomy and physiology

Describe the function of the heart, including circulation and automaticity

Describe and define the major cardiac waves in an EKG

Define normal sinus rhythm

Differentiate between rate, conduction, atrial, and ventricular arrhythmias

Recognize life-threatening dysrhythmias

Identify nursing considerations related to various cardiac dysrhythmias

Differentiate types of medications to treat arrhythmias

Identify risks for cardiac arrhythmias

Identify adverse effects associated with cardiac dysrhythmias

Analyze EKG Rhythm strips

Cardiac Anatomy

Cardiac Anatomy4 Chambers, 2 Atria, 2 Ventricles

4 Valves

Acts as a PUMP

Receives deoxygenated blood from body, pumps to lungs

Receives oxygenated blood from lungs, pumps to body

Cardiac Circulation

Cardiac Function

Heart functions a pump to deliver blood to the body

Automaticity

Impulse GenerationUnder Usual circumstances

Impulse generated from pacemaker cells in SA node

Impulse then travels to AV node

Impulse then travels to Bundle of His

Impulse then travels to Right and Left Bundle Branches

Impulse travels to Perkinje Cells that innervate ventricles

Components of an EKG

EKG Graph

X Axis = time Y Axis = amplitude

Displays electrical activity of heart

Electrical impulse precedes contraction

Depolarization and repolarization are depicted as waves Atrial Depolarization = P wave Atrial repolarization occurs during ventricular depolarization Ventricular depolarization = QRS complex Ventricular repolarization = T wave

EKG BasicsBipolar lead: positive and negative electrode.

Measures electrical potential between the electrodes

AKA ‘Standard Limb Leads’

Leads I,II,III

Used to monitor only for dysrhythmias

Lead II most commonly used

Telemetry PlacementRed = Brake (right), Green =

Gas (left)

Smoke (black) over Fire (red), Snow (white) on the Trees (green)

Stars and Stripes

Lead II

12 Lead EKG3 Standard (bipolar) Limb Leads

3 Augmented (unipolar) Leads (aVR, aVL, aVF) Triaxial reference- measures the difference in

electrical potential between one of three extremity electrodes and the central terminal

6 Precordial (unipolar) Leads (V1, V2, V3, V4, V5, V6)

aVR, aVL, aVF

The V Leads

Cardiac Waves

The P wavePacemaker is SA node,

rate 60 - 100

Correlates with atrial depolarization (begins in SA node moves R-> L and down)

PR interval 0.12-0.2

Determine atrial rate

Compare atrial rate to ventricular rate

The QRS ComplexRepresents normal

depolarization of the ventricles

Normal duration 0.06- 0.12

Measured from Q wave (first deviation from isoelectric line) to S wave (the return to isoelectric line)

Abnormal QRS is abnormal depolarization BBB Ventricular pre-excitation Cardiac pacemaker

The T WaveRepresents Ventricular

repolarization

Occurs during end of ventricular systole

Typically in same direction as QRS complex

Lasts 0.10 – 0.25

U WaveFinal stage of

repolarization, thought to be repolarization of Perkinje Fibers

Not usually seen

May indicate Hypokalemia Cardiomyopathy LVH Dig toxicity

EKG Paper

At the 25 mm speed, Each mark at top is 3 secondsThere are three large boxes between each markEach large box is 1 second or 25 mmEach large box has 5 medium boxes in itEach medium box is 0.2 seconds or 5 mmEach medium box is made up of 5 small boxes (or dots)Each small box (dot) = 0.04 seconds or 1 mm

EKG Paper

Steps to Interpreting Cardiac RhythmsDetermine the Heart Rate

Determine the Regularity

Identify and analyze P waves or flutter

Determine PR interval and AV conduction

Identify and analyze QRS complex

Determine site of origin of dysrhythmia

Identify dysrhythmia

Evaluate significance of dysrhythmia

Determine the Heart RateThe Six-second Method

Most common/least accurate Simplest, quickest

Heart Rate Calculator

The Rule of 300 Must be regular

R-R Interval Method Rhythm must be regular Distance between peaks of 2 R

waves and /60

Describe the Rate & RhythmNormal = 60-100

Tacchycardia >100

Bradycardia <60

Regular

Irregular

Regularly-irregular

Sinus ArrhythmiasST = HR >100

SB = HR ,60

Steps to Interpreting Cardiac RhythmsDetermine the Heart Rate

Determine the Regularity

Identify and analyze P waves or flutter

Determine PR interval and AV conduction

Identify and analyze QRS complex

Determine site of origin of dysrhythmia

Identify dysrhythmia

Evaluate significance of dysrhythmia

Measuring the Waves

PR IntervalRepresents progression of electrical

impulse from the SA node or an ectopic pacemaker (in atria or AV junction) through entire conduction system of the heart to the ventricular myocardium

Normal duration 0.12 – 0.20

PR >0.20 represents delayed conduction of impulse

Irregular P WaveRemember P wave represents

atrial depolarization

Irregular P represents altered, damaged, or abnormal atria Increased Right Atrial Pressure

or hypertrophy as seen in COPD and CHF = tall peaked P wave

Increased left atrial pressure or hypertrophy = wide notched P wave

Ectopic P WaveElectrical impulse for ectopic P wave originated

outside SA node or in AV junction

Occur in PAC’s Atrial tacchycardia SVT

PAC’s Premature Atrial Contraction

P wave followed by normal QRS

Generally followed by noncompensatory pause

P waves vary, PR intervals normal

AV Ratio 1:1 Conduction

Causes of PAC’s Increased sympathetic tone

Infection

Emotional Stress

Stimulants

Medications; epinephrine

Hypoxia

Digitalis toxicity

ACS or CHF

QRS ComplexRepresents normal

depolarization of the ventricles

Onset is point where first wave (Q) deviates from isoelectric line

End is where last wave (S) returns to isoelectric line

Duration 0.06 – 0.12

Irregular QRSRepresents

abnormal depolarization of ventricles

Irregular QRS present in Bundle Branch Block Ventricular

preexcitation Cardiac pacemaker

QT IntervalRepresents time it takes for

ventricles to depolarize and repolarize

Prolonged QT associated with pericarditis, myocarditis, MI, LVH, hypothermia, CVA, increased IC trauma or hemorrhage, medication SE, electrolyte imbalances (K, Ca), or liquid protein diets

ST SegmentRepresents early part of

repolarization of right and left ventricles

Duration < 0.20

Normally ST segment is flat

Elevation can be evidence of myocardial ischemia or infarction, coronary vasospasm, pericarditis, LBBB, LVH, raised ICP

Steps to Interpreting Cardiac RhythmsDetermine the Heart Rate

Determine the Regularity

Identify and analyze P waves or flutter

Determine PR interval and AV conduction

Identify and analyze QRS complex

Determine site of origin of dysrhythmia

Identify dysrhythmia

Evaluate significance of dysrhythmia

Arrhythmias Rate Arrhythmias

Tachycardia Bradycardia

Atrial Arrhythmias Afib/Aflutter WPW SVT

Conduction Arrhythmias Bundle Branch Blocks AV Conduction Block (1st, 2nd, 3rd Degree)

Life Threatening Arrhythmias V Fib Complete Heart Block Asystole

Living Arrhythmiashttps://www.youtube.com/watch?

v=TJR2AfxVHsM

Atrial ArrhythmiasAtrial Tacchycardia

Atrial fibrilation

Atrial flutter

Supra Ventricular Tacchycardia

Wolf-Parkinson-White

8 Steps ID P or F waves Conduction ratio, is every P followed by QRS

Atrial TachycardiaRate is usually 160-240 beats

Type of SVT, where generation for impulse is outside SA node

A Fib and Aflutter are most common forms

P waves are uniform

PR intervals are normal

AV conduction is 1:1

Atrial TachycardiaClinical significance

Dependent on presence and extent of heart disease

Palpitations, nervousness, anxiety Perfusion Syncope Workload of heart

Nursing Assessment

Atrial Tachycardia

A FlutterCauses

Cardiomyopathy Atrial dilation Valve Disease Thyrotoxicities Hypoxia CHF ETOH Abuse

A Flutter Risks; Incomplete emptying of ventricles

Thrombi formation Loss of atrial kick Syncope, hypotension CHF

Treatments Beta Blockers CCB Digoxin Warfarin Cardioversion if uncontrolled Ablation

Atrial Flutter Impulse generated by ectopic pacemaker or reentry

pathway

F waves have a saw-tooth appearance

Rate; Atrial 240-360, Ventricular half the atrial rate

Rate is regular

Normal P waves absent

Unable to measure PR intervals

Expressed as ratio 4: 1 Flutter

Atrial FibrillationAtrial Rate 350-600

Ventricular rate < 100 = controlled, >100 = uncontrolled

Irregularly irregular rate

P waves absent, F waves absent

Atrial FibCauses and treatments similar to A Flutter

SVTRapid rhythm (>100) that generated outside

the ventricles

AKA Paroxysmal Atrial Tach (PAT)

Symptoms Palpitations Lightheadedness Dizziness Maybe symptomless, self limiting

Treatments

Beta Blockers, CCB,antiarrhythmics

SVT

WPWVentricular pre-excitation; early activation of

ventricles by impulse that bypasses the AV node

Impulse can be generated in accessory pathway or bypass tract that abnormally

Most frequent AV bypass tract in WPW is Bundle of Kent

Presence of Delta wave

Wandering Atrial Pacemaker

Dysrhythmia originating in multiple pacemaker sites that shift between SA node and AV junction

Rate 60 – 100

Irregular

P waves vary in size and shape

PR intervals are normal to very short

AV Conduction ratio 1:1

Wandering Atrial Pacemaker

Conduction Arrhythmias

Conduction Block/ AV Block

Bundle Branch Block

AV BlocksFirst Degree AV Block

Second Degree Type I AV Block

Second Degree Type II AV Block

Third Degree AV Block

First Degree AV BlockDelay in conduction of electrical impulse,

usually through the AV node

Most common Heart Block

Prolonged PR (> 0.20)

Rate and Rhythm Regular

AV Conduction 1:1

Causes 1* AV Block Acute Inferior Wall MI Ischemic Heart Disease Digitalis Toxicity Medications (B Blockers, CCB) Hyperkalemia

First Degree AV Block

Second Degree Type I AV BlockAKA Wenckebach

Usually temporary condition, and asymptomatic

Prolonging PR form one QRS to the next until one QRS is not conducted or “dropped” then pattern starts over again

P to P intervals are regular

R to R intervals are irregular

More P waves than QRS complexes

Causes; Acute inerior wall MI, Ischemic heart disease, Dig Toxicity, BB, CCB, Hyperkalemia

Second Degree AVB, Type I

Second Degree Type II AV BlockDysrhythmia with constant P-R interval with

missing QRS complexes

Complete block of conduction in one bundle branch and an intermittent block in the other bundle branch

Can present as pattern, ie 2:1 block or 3: 1 block OR without pattern of QRS/ unstable QRS

Causes; Damage to Bundle Branches p MI,

Very high potential to convert to Third Degree (Complete) Heart Block

Excessively slows HRMay require pacemaker, Atropine not effective

Second Degree AVB

Third Degree COMPLETE HBComplete absence of conduction of electrical

impulse through AV node, Bundle of His, and BB

Atria rhythm independent from Ventricular rhythm; Regular P-P and regular R-R

LIFETHREATENING Rhythm, will lead to asystole

Requires Pacing

Causes; Inferior wall MI, Ischemic Heart Disease, Medications (Dig, BB, CCB), hyperkalemia

Complete Heart Block

Treatment of CHBCardioversion or Defibrillation

Transcutaneous pacing for symptomatic bradycardia

Medications Atropine Vasopressors CCB BB

Nursing Assessment

Bundle Branch Block Irregular conduction or block of electrical

pathway through bundle branches

Ventricles do not contract simultaneously

QRS > 0.12, appears “notched”

Ventricular Arrhythmias

PVC’s

Ventricular Tachycardia

Ventricular Fibrillation

Premature Ventricular Contraction, PVC’SAbnormally wide, bizarre QRS complex, not

associated with P wave

Electrical impulse generated in ventricle, Bundle Branch, or Perkinje Fibers

Does not lead to contraction of ventricles, therefor not “perfused”

Usually followed by compensatory pause

Can be observed with or without a pattern

Causes of PVCs Increased Catecholamine and increased sympathetic

tone

Stimulants

Amphetamine and cocaine

Myocardial ischemia or infarction

CHF

Hypoxemia

Acidosis

Dig Toxicity

Hypokalemia

Hypomagnesemia

Significance of PVCs Isolated PVC without hx heart disease are

usually insignificant, and require no treatment

May indicate presence of ventricular abnormality

Can lead to V tach or V fib

Single PVC

Ventricular Bigeminy

Ventricular Trigeminy

Couplet

Run PVC

Ventricular TachycardiaAKA V Tach

Dysrhythmia originating in an ectopic pacemaker in the bundle branches, perkinje fibers, or ventricular myocardium

Rate 100 – 250 bpm

P wave absent

QRS abnormally wide and bizarre

V Tach

Causes of V TachSignificant Cardiac Disease

CAD ACS Cardiomyopathy LVH

Dig Toxicity

QT interval Prolongation

Electrolyte disturbances

Liquid protein diets

Clinical Significance of V TachDetermine inset and termination

More than 3 PVCs is sustained V Tach

Can be short, nonsustained and asymptomatic

Increased frequency can lead to Ventricular Fibrillation which is LIFETHREATENING

PULSELESS V TACH IS TREATED THE SAME AS V FIB!

Ventricular FibrillationNo coordinated ventricular beats are present

No P wave or QRS complexes noted

Electrical Chaos in Heart

Ventricles ‘contract’ at rate of 300 – 500 bpm

EMERGENCY

Cardiac output CEASES

Nursing Considerations

V FIB

AsystoleTotal Absence of electrical activity in heart

Pt is clinically dead

Absence of P wave and QRS complex

Flat line

Remember, if your patient is speaking to you then they are NOT in a systole

TreatmentsCardioversion and Defibrillation

Medical Management Atropine Vasopressors Calcium Channel Blockers Beta Blockers

Nursing Considerations Oxygen, Pain management

AtropineBlocks parasympathetic nervous system

influence on the heart

Accelerates SA node firing rate

Increases HR

Increases conduction velocity

Administered by IV bolus

Used in Symptomatic Bradycardia Second Degree Type I AVB Second Degree 2:1 AVB Third Degree AVB with narrow QRS complexes

Atropine Ineffective in Second Degree Type II AVB

Advanced AVB with wide QRS complexes Third Degree AVB with wide QRS Complexes

Use with Caution Acute MI Worsening myocardial ischemia Heart Transplant patient

VasopressorsCause vasoconstriction on arterioles and

venous circulation

Improves blood pressure

Increases HR and Strength of Contraction Epinephrine Vasopressin (DOC in asystole) Dopamine Norepinephrine Dobutamine Isopreterenol

AntidysrhythmicsAdenosine; depress AV node and Sinus node

activity SVT, Tachycardia Will not terminate Afib/flutter but will slow rate

Amiodarone; Affects NA, K, and Ca channels SVT VT Vfib

Lidocaine; Widely used, ? Effectiveness in VT SE; altered consciousness, seizures, bradycardia

Procainamide; supresses atrial and ventricular dysrhythmias by slowing conduction VT, control of rate in AF/AF, PVST

Calcium Channel BlockersDiltiazem and Verapamil

Slow conduction and increase conduction time through AV node

Used in Afib and A flutter with rapid ventricular response

Contraindicated in 2nd and 3rd Degree AVB With Beta Blocker Therapy Use with caution on CHF and hypotension

Beta BlockersDecrease HR and BP

Used in SVT To control rate in Afib Aflutter

Time for a GameEKG Jeopardy!

jeopardylabs.com/play/ekg-jeopardy#.VOLPYmdso-w.gmail

Fifteen Question EKG Rhythm Strip Analysis

http://www.12leadecg.com/arrhythmias/index.cfm

Wave Matching1. Ventricular

Depolarization

2. Irregular Ventricular Beat

3. Atrial Depolarization

4. 0.12-0.20

5. Ventricular Repolarization

6. Backup pacemaker Rate 40-60

7. Early atrial beat

8. Pacemaker site

9. 0.06-0.12

10. Sets Normal Heart Rate

A. AV Node

B. T wave

C. PAC

D. SA Node

E. PVC

F. P wave

G. QRS Complex

Take Home PointsEKG is measurement of ELECTRICAL activity

Look at the patient

Irregular activity can progress from asymptomatic to life threatening

Causes are similar (electrolytes, hypoxia, ischemia…)

Treatments also very similar (BB, CCB, antiarrhythmic)

Referenceshttp://lifeinthefastlane.com/ecg-library/

http://ekg.academy/learn-ekg.aspx?seq=11&courseid=315

http://my.clevelandclinic.org/services/heart/patient-education