Basic Dysrhythmia Interpretation

NURS 108Spring 2008

Majuvy L. Sulse RN, MSN,CCRN

Cardiac Cycle

Systole-simultaneous contraction of ventricles, lasts 0.28 sec

Diastole- ventricular relaxation, lasts 0.52 sec One cardiac cycle occurs every 0.8 sec

Cardiac Cycle

Stroke volume-volume of blood (70cc) pumped out of one ventricle of the heart in a single contraction

Heart rate- number of contractions per minute(60-100bpm

Cardiac output-amount of blood pumped by the left ventricle in 1 minute (4-8L/min) CO= SV XHR

Cardiac Cycle

Preload-degree of myocardial fiber stretch at the end of diastole Afterload-resistance against which the heart must pump to eject

blood through the semilunar valves and into peripheral vessels STARLING’S Law-the more the muscle fibers are stretched up to a

certain point, the more forceful the subsequent contraction will be. Systemic vascular resistance (impedance)- amount of opposition to

blood flow offered by the arterioles, pressure the heart must overcome to open the aortic valve

Autonomic Nervous System

Sympathetic-prepares for physical activity-fight or flight response-norepinephrine (Adrenergic nerve endings) Alpha-vasoconstriction Beta

Beta 1-increase HR & contractility Beta 2-bronchial dilation & vasodilation

Parasympathetic-rest & digest function Acetylcholine (cholinergic nerve endings)

Electrophysiologic Properties

Automaticity-ability to generate an electrical impulse spontaneously & repetitively

Excitability-ability to be electrically stimulated or respond to an electrical stimulus

Conductivity-ability to receive an electrical stimulus and transmit to other cardiac cells

Contractility-also rhythmicity is the ability to shorten and cause contraction in response to an electrical stimulus-coordination of contraction to produce a regular heartbeat

Major electrolytes that affect Cardiac Function 3 major cations

K-performs a major function in cardiac depolarization and repolarization

Sodium plays a vital part in myocardial depolarization Calcium is important in myocardial depolarization and

contraction. Magnesium-acts as transporter for Na & K across

cellular membranes. Also plays an important function in muscular contraction

Movement of Ions

Resting cardiac cells (Polarization) –inside the cell is negatively charged. K is greater in the cell; Na greater outside the cell (positively charged)-Resting membrane potential

Depolarization (action Potential)-sodium-potassium exchanged pump resulting in positive polarity inside the cell membrane. Myocardial contraction occurs.

Repolarization-recovery or resting phase; positive charges are again on the outside and negative charges in the inside

Refractory Periods

Ensures that the muscle is totally relaxed before another action potential occurs

Atrial muscle-0.15 sec Ventricular muscle-.25-.30 sec

Refractory Periods

Absolute refractory period-cardiac muscle cannot be depolarized. Corresponds to beginning of QRS to peak of T wave

Relative refractory period-cardiac muscles stimulated to contract prematurely if stimulus is stronger than normal. Corresponds with down slope of T wave

Cardiac Conduction System

Electrical Conduction Pathway

SA node (60-100bpm) Internodal pathways AV node ( 40-60bpm) Bundle of His Bundle Branches Purkenje networks (20-40bpm)

EKG

ECG/EKG-a graphic representation of cardiac activity 12 lead-shows electrical activity from 12 different planes of the

heart-used as a diagnostic tool rather than a monitoring device Electrode-adhesive pad that contains conductive gel and

designed to be attached to skin Leads-wires generally color coded. For the EKG to receive a

clear picture of electrical impulses, there must be a positive, a negative and a ground. The exact portion of the heart being visualized depends on lead placement

EKG Leads

Baseline-isoelectric line-no current flow in the heart; consists of positive, negative deflections or biphasic complex

3 or 5 lead- used for monitoring the current cardiac activity of patients at risk for cardiac abnormalities

Lead ll or MCL1-modified chest leads mostly used because of ability to visualize P waves. MCL provides a R sided view of the heart. MCL6-L sided view of the heart

EKG Leads

Limb leads Bipolar leads-measures activity between 2

points (I, II, III) Unipolar leads-positive electrodes only-

aVR, aVL, aVF Chest leads-6 precordial leads

LIMB LEADS & AUGMENTED LEADS

EKG Graph Paper

Segments and Intervals

Segments and Intervals

P wave-deflection representing atrial depolarization PR segment-isoelectric line from end of P wave to beginning

of QRS-impulse is traveling through the AV node. PR interval-0.12-0.20(time for atrial depolarization-AV node-Purkenje fibers)

QRS complex-ventricular depolarization. QRS duration of 0.04-.10 sec from QRS to J-point

ST segment-early ventricular repolarization from J-point to beginning of T wave. Elevations not more than 1 mm or deflections o.5 mm from isoelectric line

T wave- ventricular repolarization, usually rounded, positive deflection

U wave-smaller polarity as T wave-slow repolarization- not normally seen except in hypokalemia

QT interval-total time for ventricular depolarization and repolarization

HR Determination

6 second method count QRS complexes in a 6 sec strip x 10 (30 large boxes in

6 sec strip) P-P or R-R interval method

count number of small blocks in a P- P or R-R interval and divide into 1500 (no. of small blocks in 1 min)

Count the number of large blocks in an interval and divide into 300 (number of large blocks in 1 minute)

Memory method

ECG Rhythm Analysis

Analyze P waves- P wave is present. shape is consistent, must be before each QRS

Analyze QRS complex- QRS complex is present & consistent

Determine atrial rhythm or regularity- check regularity by assessing P-P or R-R

Determine ventricular rhythm or regularity-check regularity by assessing R-R

Determine heart rate-use one of the methods Measure the PR interval-measurement should be

constant and should be between 0.12-0.20 Measure the QRS duration-measurement should be

constant and should be between 0.04-0.10 sec Interpret the rhythm

General Rules

First & most important, LOOK at your PATIENT!

Read every strip from left to right

Apply the systematic approach Avoid shortcuts and

assumptions. Ask and answer each question

in the ECG analysis approach

Artifacts

Waveforms outside the heart-interference caused by: Patient movement wandering baseline Loose or defective electrodes-lost contact with

patient’s skin Improper grounding-in touch with an outside source of

electricity Faulty EKG apparatus

Normal Sinus Rhythm

SA node generated an impulse that followed a normal pathway, the heart rate falls within the range, atrial & ventricular rhythms are regular, P waves preceded every QRS and QRS is within 0.12sec

Sinus Bradycardia

SA node fires slower than normal heart rate-less than 60bpm

Rhythm is regular

P wave upright and same shape

PR is constant .12-.20sec

QRS-normal <.12sec

Sinus Bradycardia

Causes: Vagal stimulation, MI, hypoxia Digitalis toxicity Medication side effects Normal to athletes

Adverse effects: Dizziness, weakness, syncope, diaphoresis, pallor,

hypotension Treatment

According to symptoms, atropine to speed up heart rate, pacemaker

Sinus Tachycardia

SA node fires at a rate faster than normal but conduction pathway is normal. All criteria for interpretation are the same except that the heart rate is faster.

Sinus Tachycardia

Causes Emotionally upset, pain, fever, thyrotoxicosis, hypoxia,

hypovolemia, inhibition of vagus nerve, Caffeine, norepinephrine, theophylline

Adverse effects Angina, dizziness, hypotension, increased in cardiac workload

Treatment Treat the cause Medications may be given- betablockers

Sinus Arrhythmia

The only irregular rhythm from the sinus node and has a cyclic pattern that usually corresponds with breathing

Rate- varies with respiratory pattern Regularity-irregular in a repetitive pattern P waves-Upright in most leads, same shape and one to each QRS

P-P interval is irregular QRS-<.12 sec Cause-usually caused by breathing pattern but can also heart

disease Treatment- usually non required

Atrial Dysrhythmias

SA node fails to generate an impulse Atrial nodes or internodal pathways may initiate an

impulse and follows the conduction pathway Dysrhythmias of this type are not lethal Accessory pathway-irregular muscle connection between

atria and ventricles that bypasses the AV node

Premature Atrial Contractions

Causes- atria becomes hyper and fire early caused by medications, caffeine, tobacco, hypoxia or heart disease

Adverse effects-if frequent can be a sign of impending heart failure or atrial tachycardia or fibrillation

Treatment-O2, omit caffeine, tobacco or other stimulants. Give digitalis or quinidine, treat heart failure.

Premature Atrial Contractions

Rate normal

Rhythm usually regular except for a PAC

P waves shaped differently from a normal P wave or hidden in preceding T wave

PR interval .12 to .20sec

QRS .12sec similar to underlying rhythm

Supraventricular Tachycardia (SVT) Tachycardia (>150 bpm) originating above the ventricles-SA

node, atria, AV nodes P waves not discernible-hidden in T waves Paroxysmal-starts & ends abruptly Causes-same as PAcs Adverse effects- palpitations, light-headedness, dizziness,

shortness of breath, chest pain, fainting =decreased cardiac output

Treatment-vagal maneuvers (cough, bear down), carotid massage, or medications digitalis, calcium channel blockers, beta blockers, Adenosine

Supraventricular Tachycardia (SVT)

Rate 150-250bpm

Rhythm regular

P waves not discernible

PR not discernible

QRS usually less than .10sec

Atrial Flutter

Results when one irritable atrial foci fires out regular impulses at a rapid rate that P waves are in a sawtooth pattern

Av node (gatekeepers) cannot depolarize fast enough to keep up, many impulses never get through to ventricles. Conduction ratio is variable-2:1block, 3:1 block or 4:1 block. Slow ventricular response-VR of <60pm; rapid VR >100-150bpm)

Causes-acute MI, CHF, digitalis toxicity, pulmonary embolism, SA node disease, septal defects

Adverse effects-decreased cardiac output Treatment-digitalis, cardioversion, calcium channel blockers,

ablation

Atrial Flutter

Rate atrial 250-300bpm, ventricles-variable

Rhythm regular if conduction ratio is constant, irregular if conduction rate varies

P waves replaced by fluttery waves

PRnot measurable

QRS <.12sec

Atrial Fibrillation

Most common atrial dysrhythmia in elderly patients Multiple atrial impulses from different locations all at the same time

(350-600bpm) Ventricular response maybe rapid (100-150bpm) or slow (< 60bpm) Causes-maybe chronic MI CHF, valvular heart disease,

hyperthyroidism Adverse effects-decreased cardiac output, blood clots which

can cause MI, stroke or clot in the lung Treatment- Digitalis, quinidine, cardizem, anticoagulant as

coumadin, cardioversion

Atrial Fibrillation

Junctional Rhythms

Arrhythmia originating in AV node HR= 40-60bpm; accelerated =60-100bpm; junctional= 100-140bpm P wave-absent, inverted before or after a QRS PR interval-<.12if P precedes a QRS QRS <.12sec Cause-vagal stimulation, hypoxia, ischemia of SA node, MI, digitalis

toxicity Treatment-varies according to type of arrhythmia. Atropine to

increase HR, withhold or decrease medication that can slow heart rate

Junctional Rhythms

Ventricular Dysrhythmias

Ventricles serves as pacemaker Heart rate significantly reduced (20-40 beats per

min Normal conduction system bypassed QRS bizarre in appearance & >0.12 sec P waves absent (buried or hidden in QRS) Rhythms considered life threatening

Premature Ventricular Complexes (PVCs) A single ectopic (out of place) complex from an irritable site Indicates increased myocardial irritability Precursors of more serious lethal rhythms Cardiac output compromised Causes

Myocardial ischemia, Emotional stress, increased physical exertion, CHF, electrolyte imbalance, digitalis toxicity or acid base imbalances

Treatment- based on symptoms and causative factors O2 and antidysrhythmics

PVCs

Unifocal-arise from one single site Multifocal- originate from different sites Ventricular bigeminy- every other beat is a PVC Ventricular trigeminy-every third beat is a PVC Ventricular quadrigeminy- every 4th beat is a PVC Interpolated- a PVC between two sinus beats Couplet or repititive PVCs- two PVCs occurring together

without a normal complex in between Salvos-3 or more PVCs in a row (Vtach)

Premature Ventricular Contraction (PVC)

Multifocal PVCs

Unifocal PVCs

Premature Ventricular Contraction (PVC

NSR with Couplets

Bigeminy

Ventricular Tachycardia

3 or more PVCs in a row overriding pacemaker Sustained-lasts more than 30 sec Unsustained- less than 30 sec Can be tolerated for short bursts but can cause profound shock if

unconscious or untreated Causes- as with PVCs Treatment

Pulseless Vtach-treated like Vfib Stable-drug intervention

Lidocaine, procainamide, amiodarone Unstable- defibrillation

Ventricular Tachycardia

Rate 100-25bpm

Regularity usually regular

P waves none PR will vary if present

QRS wide & bizarre >0.12

Ventricular Fibrillation (VFib) Fatal, most common initial rhythm in cardiac arrest Myocardial cells quiver rather than depolarized Usually coarse (amplitude > 3mm) then becomes fine (amplitude

less than 3mm) No cardiac output- cardiovascular collapse Causes- MI, drug toxicity or overdose, hypoxia, CAD Treatment- immediate defibrillation must be done, CPR, epinephrine

(medications make defibrillations more successful and prevent recurrence

Ventricular Fibrillation (VFib)

Rate cannot be counted

Regularity rapid, not detectable

P waves none

QRS none detectable

Asystole

Cardiac standstill Absence of all ventricular activity-no waveforms Check on 2 leads-? Very fine Vfib Clinical death-absence of pulse and respirations Causes- MI, cardiac trauma, ventricular aneurysm,

CHB Treatment-atropine to reverse vagal influences,

epinephrine, CPR, pacemaker, dopamine, O2

Ventricular Asystole

Rate zero

Regularity none

P waves none

QRS none

Atrioventricular Blocks

Impulses in the SA node are blocked or delayed-heart blocks- (PR >.20, some Ps not followed by QRS; some P-P with regular interval

Underlying rhythm is sinus Rate normal or slow-symptomatic or asymptomatic Site of block is either AV node or bundle branches

First dgree Second degree

Type l-Mobitz l Type ll- Mobitz 2

Third degree

First degree AV block

Prolonged PR interval that results from a delay in the AV node’s conduction of sinus impulse to ventricles

All parameters are normal except for prolonged PR interval (hallmark of 1st degree)

Usually asymptomatic Causes-AV node ischemia, digitalis toxicity, use of

betablockers or calcium blockers Treatment- treat cause

First Degree AV Block

Rate based on underlying rhythm

Regularity usually regular

P waves upright, one to each QRS

PR interval > .20 sec

QRS <.0.12 sec looks alike

Second Degree Block (Mobitz l (Wenckebach Progressive prolongation of the impulse Cyclic pattern is produced: PR interval continues to

increase in length until an impulse is not conducted (QRS dropped)

Atrial rhythm is regular but ventricles ar irregular Cause-MI, digitalis toxicity, n\medication effects Treatment-atropine if heart rate is slow &

asymptomatic, pacemaker.

Second Degree Block (Mobitz l (Wenckebach)

Rate-Atrial rate normal: ventricular rate less than atria

Regularity-maybe regular or irregular

P waves-normal P; PR interval progressive prolongation

QRS=<0.12 if at AV node > if block is at bundle branch

Second Degree Block-Mobitz ll Increased risk of progression to 3rd degree Ratio of P waves to QRS complexes (2:1 block, 3:1

block or 4:1 block) PR interval is constant or regular for every conducted

beat Intermittent absence of QRS Causes-same as type l Treatment-02, atropine if patient is symptomatic,

epinephrine, dopamine, pacemaker if block continues and symptoms are present

Second Degree Block-Mobitz ll

Rate =atrial 60-100: ventricular half of atrial rate

Regularity=regular

P waves= Normal

PR interval= constant

QRS= <.12 sec or >.12 sec if BBB present

Third Degree or Complete Heart Block (CHB) SA node sends out impulses as usual but not one is conducted

to the ventricles Atria & ventricles beat independently of each other-AV

dissociation Rate- atria-60-100, Ventricles-20-60 Regularity-Regular P waves- no relationship with QRS PR interval- no pattern, varies QRS-based on site of pacemaker Cause-MI, lesion on conduction system, hypoxia, medication

side effects Treatment-pacemaker insertion

Third Degree or Complete Heart Block (CHB)

PACEMAKERS

PACEMAKERS

Device that substitutes for the normal pacemaker of the heart’s electrical conduction system Generator-controls rate & strength of each electrical impulse Lead wires-electrode at the tip relay the electrical impulse from the

generator to the myocardium Types

Temporary-used to sustain HR in an emergency situation Transcutaneous (TCP)-external cardiac pacing Transvenous-lead wire threaded through the skin into a large vein

Permanent- implanted in patient’s chest

Indications for insertion of Pacemakers

Temporary Suppression of ectopic atrial or ventricular rhythm Acute MI with symptomatic bradycardia, 2nd & 3rd degree AV

block or bundle branch block Maintenance of adequate HR during special procedures or as

prophylaxis after an open heart surgery Termination of AV nodal reentry

Permanent- Chronic atrial fibrillation with slow ventricular response Fibrotic or sclerotic changes in the cardiac conduction system Sick sinus syndrome or Sinus node dysfunction Tachyarrhythmias Symptomatic bradycardia and Third degree AV block not

responding to pharmacologic interventions

Permanent Pacemakers

Atrial- lead wire inserted into the Right atrium-stimulates the atrium then travels down the electrical conduction through the ventricles

Permanent Pacemakers

Ventricular- lead wire inserted into the Right ventricle. The electrical impulse from the pacemaker generator produces ventricular depolarization

Permanent Pacemakers

AV sequential- two electrodes on the lead wire one placed on the R atrium & one on the R ventricle. Artificial impulses stimulate or pace first the atria, then the ventricles

Rules for interpretation of Pacemaker Rhythms Same as for dysrhythmias Remember: Properly functioning

pacemakers will produce rhythms with pacemaker spikes. Spikes indicates only that the pacemaker is firing. They do not reveal information relative to ventricular contraction. Assess your patient for presence of symptoms

Code System 1st letter-chamber being paced

A-atrium V-ventricle D-dual (both)

2nd letter- chamber sensed A-atrium V-ventricle D-dual (both O-off

3rd letter- type of response by pacemaker to sensory I-Inhibited (pacemaker will not function when the

person’s heart beats O-none T-triggered D-dual

Code System

4th letter- ability of generator to be programmed O-none P-Simple programmability M-Multi programmability C-Telemetry ability P-ability of rate to change with activity

5th letter-ability of generator to defibrillate P-Antitachycardia S-Shock D-antitachycardia processing & shock O-none

Common Problems associated with Pacemakers Battery failure

Decreased amplitude of pacemaker spike and a slowing pacemaker rate

Immediate transport to the hospital depending on the patient’s symptoms or underlying rhythm

Runaway Pacemakers Rapid rate of electrical impulse discharge results Immediate transport to a hospital

Failure to Sense

Failure to sense -pacemaker fails to sense the patient's own intrinsic rhythm and generates a pacer spike in the intrinsic rhythm's own QRS, absolute or relative refractory period of the T wave. The ventricular capture following the pacer spike may or may not occur. This can cause lethal arrhythmia. Failure to sense can be caused when the sensitivity setting is too low. 

Failure to Sense

EKG Characteristics: Rate: It may be regular or irregular. Rhythm: It can be any intrinsic rhythm in which the pacemaker spike is in the QRS, absolute, or relative refractory period of the T wave. QRS complex: It is within the normal limits of the intrinsic rhythm.

Nursing Intervention: Obtain the blood pressure, pulse, respiratory rate, O2 saturation and notify the MD. Closely observe for ventricular tachycardia caused by failure to sense.

Failure to Capture

Failure to capture of a pacemaker happens when the output is too low, resulting in a failure to depolarize the ventricle, which causes an absence of a mechanical contraction of the ventricle, or no QRS. It can occasionally happen or be constantly happening which results in ventricular standstill and a pulse-less patient.

EKG Characteristics: Rate: It will be irregular due to the failure to produce QRS. Rhythm: The pacemaker spike or spikes will not have a QRS following them. P Wave: It may be absent or present. QRS Complex: A loss of a QRS behind a pacer spike.

Failure to Capture

Nursing Intervention: Should the loss to capture be occasional, one should get a blood pressure, pulse rate, respiration rate, and O2 saturation. This is to determine if the patient is tolerating the failure to capture. If the failure to capture is continuous, the patient will be pulse-less or have a symptomatic bradycardia. This can range from a situation in which medication may be needed, or a code situation in which one would follow hospital protocol. External pacing may be an option for this patient

Pre-procedure & Post procedure care Consent VS Skin prep Pre-op checklist-NPO, dentures, pins Position post op is important Maintain hemodynamic stability Prevent complications

Patient & family Teaching Guides

Follow the instructions for pacemaker site skin care. Report any fever or redness, swelling, or drainage from incision site.

Keep your pacemaker identification card in your wallet and wear a medical alert bracelet

Take your pulse for 1 full minute at the same time each day and record the rate in your pacemaker diary. Take your pulse anytime you feel symptoms of a possible pacemaker failure and report them to your physician.

Patient & family Teaching Guides Know the rate at which your pacemaker is set and the basic

functioning of your pacemaker, battery failure. Know what changes to report to your physician.

Report any of the following symptoms to your physician: dizziness, difficulty of breathing, fainting, chest pain, weight gain, and prolong hiccupping. If you have any of these symptoms, check your pulse and call your physician.

Take all medications, follow prescribed diet, activity restrictions

Do not apply pressure over the generator. Avoid tight clothing or belts.

Patient & family Teaching Guides

Do not operate electrical appliances over pacemaker as they may cause malfunction.

Be sure electrical appliances or motors are properly grounded.

Avoid all transmitter towers for radio, TV and radar. Radios, TV, & other home appliance and antennas do not pose a hazard.

Inform airport personnel and show ID card before passing through the metal detector.

Automatic Implantable Cardioverter-Defibrillator Lead placed via the subclavian into the endocardium Generator is implanted subcutaneously over the pectoralis muscle Monitors HR/rhythm and identifies ventricular tachycardia &

ventricular fibrillation Delivers a shock (25 joules) to the heart muscle upon sensing a

lethal arrhythmia Some newer ICDs are equipped with antitachycardia and

antibradycardia pacers- initiates ovrdrivepacing to prevent painful shocks

Patient & Family teaching guide for AICD

Maintain close follow up with physician for testing ICD function & inspection of site

Medic alert should be worn & information about the ICD should be available

Watch for signs of infection Avoid lifting operative side arm above shoulder for about

a week Avoid direct blows to ICD site

Patient & Family teaching guide for AICD When traveling, inform airport official about presence of

AICD When ICD fires Routine checks with programmer device needed-2-3

months Family members should learn CPR Avoid electromagnetic forces that may turn off device Participate in ICD support groups