QRS Morpholo gyggyygy Signs and Symptoms of Hemodynamic...

Systematic AnalysisSystematic AnalysisSystematic AnalysisSystematic Analysis

1. What is the rhythm? (regular, or irregular, regularly irregular) 2. What is the P: QRS ratio (1:1) 3. Is the P wave normal? (smooth, rounded) 4. What is the atrial rate? what is the ventricular rate? 5. Is the PRI within normal limits (0.12 – 0.20 sec) 6. Is the QRS within normal limits? (0.06 – 0.10 sec) 7. Is the ST segment isoelectric? (depression = greater that 0.5 mm, elevation =

greater than 1 mm)

Signs and Symptoms of Hemodynamic Signs and Symptoms of Hemodynamic Signs and Symptoms of Hemodynamic Signs and Symptoms of Hemodynamic CompromiseCompromiseCompromiseCompromise

• changes in mental status (restlessness, confusion, possible loss of consciousness

• low blood pressure

• chest pain

• shortness of breath

• signs of shock

• heart failure

• pulmonary congestion

• decreased urine output

• cold, clammy skin

QRS MorpholoQRS MorpholoQRS MorpholoQRS Morphologygygygy

P Wave MorphologiesP Wave MorphologiesP Wave MorphologiesP Wave Morphologies

ArtifactArtifactArtifactArtifact

Artifact occurs when something causes a distortion of the ECG tracing.

Some common causes are AC interference (causes 60 cycle artifact), muscle tremors, respiratory artifact, wandering baseline, loose electrode, broken lead wire.

Sinus RhythmSinus RhythmSinus RhythmSinus Rhythm and Sinus Arrhythmias and Sinus Arrhythmias and Sinus Arrhythmias and Sinus Arrhythmias

RateRateRateRate 60 -100 bpm

P waveP waveP waveP wave positive, one precedes each QRS complex, same morphology

QRSQRSQRSQRS 0.10 sec or less

PR intervalPR intervalPR intervalPR interval 0.12 – 0.20 sec and constant

RhythmRhythmRhythmRhythm P-P and R-R intervals regular

Sinus BradycardiaSinus BradycardiaSinus BradycardiaSinus Bradycardia

RateRateRateRate less than 60 bpm

P waveP waveP waveP wave positive, one precedes each QRS, same shape and size

QRSQRSQRSQRS normal (≤0.10)

PR intervalPR intervalPR intervalPR interval normal and constant beat to beat (0.12 – 0.20)


EtiologyEtiologyEtiologyEtiology ConductionConductionConductionConduction Clinical FeaturesClinical FeaturesClinical FeaturesClinical Features TreatmentTreatmentTreatmentTreatment

• normal variation in athletes, during sleep, or in response to a vagal maneuver

• abnormal with: o heart disease o acute inferior MI o medication effects (digoxin, beta

blocker, calcium channel blocker) o increased intercranial pressure, o sick sinus syndrome o hypothyroidism

• caused by anything that increases parasympathetic tone

• SA node

• if the bradycardia becomes slower than the SA node pacemaker, a junctional rhythm may occur

Mild 45-59 bpm

• probably asymptomatic

Marked 30-45 bpm

• S&S of hemodynamic compromise

• syncope

• weakness

• dizziness

Sinus bradycardia doesn’t require treatment if asymptomatic

Nursing ManagementNursing ManagementNursing ManagementNursing Management

• assess, VS, LOC, symptoms

• oxygen prn

• ensure IV access

• notify MN/NP if symptomatic Medical ManagementMedical ManagementMedical ManagementMedical Management

• treat the underlying cause (i.e. discontinue contributing medications)

• atropine IV push

• transcutaneous/epicardial pacing if patient is hemodynamically compromised

• permanent pacemaker if chronically symptomatic

Sinus Arrhythmia Sinus Arrhythmia Sinus Arrhythmia Sinus Arrhythmia

RateRateRateRate 60-100 bpm but may be slower or faster


QRSQRSQRSQRS normal

PR intervalPR intervalPR intervalPR interval normal and constant beat to beat

RhythmRhythmRhythmRhythm irregular, phasic with respiration

EtiologyEtiologyEtiologyEtiology ConductionConductionConductionConduction Clinical FeaturesClinical FeaturesClinical FeaturesClinical Features TTTTreatmentreatmentreatmentreatment

• commonly associated with the respiratory rate - usually increases with inspiration and decreases with expiration.

• common among infants, children and young adults

• the non respiratory form often present in diseased hearts, common after acute inferior MI, seen with increased intercranial pressure

• can be the result of medications effects or carotid sinus pressure

• originates in the sinus node, follows normal conduction pathway and discharges impulses irregularly

• usually asymptomatic but if bradycardic may have S&S of hemodynamic compromise

• doesn’t usually require treatment unless accompanied by a rate that causes hemodynamic compromise



• Notify MD/NP if symptomatic Medical ManagementMedical ManagementMedical ManagementMedical Management

• treat causes

• if symptomatic due to bradycardia atropine may be indicated

Sinus Tachycardia Sinus Tachycardia Sinus Tachycardia Sinus Tachycardia

RateRateRateRate 101-160 bpm


QRSQRSQRSQRS ≤0.10




• normal response to increased oxygen demands (exercise, fear, fever, HF, PE, pain, stress, MI, medications)

• begins and ends gradually

• caused by anything that increases sympathetic tone or decreases parasympathetic tone

• originates in the SA node and discharges regularly

• rate related; may be none

• decrease in cardiac output, especially those with CAD

• chest discomfort



• treat cause if able (i.e. pain, fever, anxiety)

• oxygen

• notify MD/NP if persistent or symptomatic Medical ManagementMedical ManagementMedical ManagementMedical Management

• treat the underlying cause

• for AMI, beta blockers given to slow HR

Atrial ArrhythmiasAtrial ArrhythmiasAtrial ArrhythmiasAtrial Arrhythmias

Atrial arrhythmias originate form ectopic sites in the atria. Ectopic P waves differ in shape from the normal sinus P waves. The three basic mechanisms that are responsible for ectopic beats and rhythms are altered automaticity, triggered activity, and reentry. Some atrial arrhythmias may be associated with rapid ventricular rates which decreases the time spent in diastole, lessening coronary artery perfusion and less ventricular filling time. Therefore, an excessively rapid heart rate may lead to ischemia and compromised cardiac output.

Premature Premature Premature Premature Atrial Contractions Atrial Contractions Atrial Contractions Atrial Contractions

RateRateRateRate normal but depends on underlying rhythm

P waveP waveP waveP wave premature; usually have a different morphology than sinus P waves because they originate from an ectopic pacemaker

QRSQRSQRSQRS usually normal

PR intervalPR intervalPR intervalPR interval normal, however the ectopic beats may have a different P-R interval

RhythmRhythmRhythmRhythm regular with premature beats; PAC's occur early in the cycle and they usually do not have a complete compensatory pause


• common in both healthy and diseased hearts

• can also result from HF, ischemia, emotional stress, atrial enlargement, valvular heart disease, stimulants

• may be due to altered automaticity or reentry

• an irritable site in the atria fires prematurely

• P-wave morphology is different from an SA node P-wave; QRS is of normal morphology

• may be asymptomatic or unaware

• may c/o skipped beat or palpitations

• if they occur frequently, they may lead to more serious atrial dysrhythmias

(may set off episodes of atrial fibrillation, atrial flutter or PSVT)

Nursing Management Nursing Management Nursing Management Nursing Management


• reduce stress

• reduce stimulants,

• assess electrolytes

• notify MD/NP if frequency increases or patient symptomatic

Medical ManagementMedical ManagementMedical ManagementMedical Management

• PACs usually do not require treatment if they are infrequent

• treatment includes correcting the underlying cause (i.e. electrolytes)

• frequent PACs may be treated with beta blockers, calcium channel blockers and/or anti anxiety medication

Atrial TachycardiaAtrial TachycardiaAtrial TachycardiaAtrial Tachycardia


P waveP waveP waveP wave P wave for each QRS but differ in shape from sinus P waves

QRSQRSQRSQRS normal

PR intervalPR intervalPR intervalPR interval may be shorter or longer than normal

RhythRhythRhythRhythmmmm regular


• stimulants

• infection

• electrolyte imbalance

• acute illness

• MI

• hyperthyroidism

• mitral valve disease

• atrial tachycardia that starts and stops abruptly is called Paroxysmal Atrial Paroxysmal Atrial Paroxysmal Atrial Paroxysmal Atrial Tachycardia (PAT)Tachycardia (PAT)Tachycardia (PAT)Tachycardia (PAT)

• series of rapid beats from an irritable site in the atria overriding the SA node and becoming the pacemaker

• P-wave has abnormal morphology –commonly pointed

• rate related; may be none

• S&S of decreased cardiac output, palpitations, fluttering sensation in chest, dyspnea, chest discomfort, fatigue, dizziness, syncope, lightheadedness


• assess, VS, symptoms, LOC

• determine if palpitations are regular or irregular (?fib)

• oxygen prn; IV access

• notify MD/NP

• call code if unstable

Medical ManagemenMedical ManagemenMedical ManagemenMedical Managementttt

• treat underlying cause

• meds to slow rate (beta blockers, calcium channel blockers)

• adenosine (cardiovert chemically)

• vagal maneuvers

• synchronized cardioversion for very unstable patients

• ablation

Multiformed Atrial Pacemaker (formerly WanderiMultiformed Atrial Pacemaker (formerly WanderiMultiformed Atrial Pacemaker (formerly WanderiMultiformed Atrial Pacemaker (formerly Wandering Atrial ng Atrial ng Atrial ng Atrial PacemakerPacemakerPacemakerPacemaker))))

RateRateRateRate variable depending on the site of the pacemaker; usually 60-100 bpm MAT 100-250 bpm

P waveP waveP waveP wave variable in morphology; at least 3 different P wave configurations are needed for a diagnosis

QRSQRSQRSQRS normal

PR intervalPR intervalPR intervalPR interval PR interval varies depending on the site of the pacemaker

RhythmRhythmRhythmRhythm may be irregular as pacemaker site shifts


• may occur in normal hearts (athletes, during sleep)

• may also be seen in patients with heart disease (ACS, rheumatic heart disease) and digitalis toxicity

• may also be a precursor to multifocal atrial tachycardia

• often seen in patients with COPD

• if rate is great than 100bpm it is known as Multifocal Atrial Multifocal Atrial Multifocal Atrial Multifocal Atrial Tachycardia (MAT)Tachycardia (MAT)Tachycardia (MAT)Tachycardia (MAT)

• MATMATMATMAT may resemble atrial fibrillation or flutter because both rhythms are irregular; however P waves are clearly present in MAT

• shifting of the pacemaker from the SA node to ectopic atria sites and/or AV junction

• P-R interval varies depending on the site of the pacemaker

• must identify at least 3 different P-wave morphologies in a 6 sec strip to diagnose

• usually none

• if rate is increased as in MAT, S&S of decreased cardiac output may occur



• oxygen prn

• check meds (digoxin)

• if rate increases (becomes MAT) notify MD/NP


• transient rhythm that resolves on its own and there is usually no treatment required

• if caused by digitalis withhold drug

• vagal maneuvers

• calcium channel blockers to control rate (Beta blocker contraindicated if pulmonary disease present)

Sinus Pause/ArrestSinus Pause/ArrestSinus Pause/ArrestSinus Pause/Arrest

RateRateRateRate normal but varies due to the pause

P waveP waveP waveP wave those that are present are normal

QRSQRSQRSQRS normal

PR intervalPR intervalPR intervalPR interval normal

RhythmRhythmRhythmRhythm basic rhythm is regular. The length of the pause is notnotnotnot a multiple of the sinus interval.

EtiologyEtiologyEtiologyEtiology ConductionConductionConductionConduction Clinical FeaturesClinical FeaturesClinical FeaturesClinical Features TreatmenTreatmenTreatmenTreatmentttt

• may also occur with hypoxia, myocardial ischemia or infarction, hyperkalemia, medications (beta blockers, calcium channel blockers), and increased vagal tone

• SA node fails to initiate electrical impulse for one or more beats

• a disorder of automaticity

• SA node stops and restarts and disturbs the timing of the next P-wave so underlying rhythm does not resume on time after the pause

• depends on length of arrest

• may produce no symptoms if short

• may cause S&S of decreased cardiac output (weakness, lightheadedness, dizziness or syncope if long or frequent)t




• notify MD/NP if frequent or prolonged

• if episodes are transient and asymptomatic – monitor

• IV atropine

• 5B – temp pacing prn (if wires in situ)

• call code if acutely decompensating


• if episodes are transient and asymptomatic – monitor

• IV atropine

• episodes frequent or prolonged (>3 sec) - temporary or permanent pacing

Sinoatrial Sinoatrial Sinoatrial Sinoatrial or Sinus Exit or Sinus Exit or Sinus Exit or Sinus Exit Block Block Block Block

RateRateRateRate normal or bradycardia and varies because of pause

P waveP waveP waveP wave those present are normal; precede each QRS complex

QRSQRSQRSQRS ≤ 0.10


RhythmRhythmRhythmRhythm basic rhythm is regular (the pause is the same as, or an exact multiple of, the distance between two other P-P intervals)*.

*In a type I SA block, the P-P interval shortens until one P wave is dropped.

*In a type II SA block, the P-P intervals are an exact multiple of the sinus cycle, and are regular before and after the dropped P wave.


• SA block is uncommon and usually occurs transiently

• may occur in healthy patients with increased vagal tone

• found with CAD, inferior MI, myocarditis, heart failure

• medications (dig, procainamide,salicylites)

• failure of cells in SA node to conduct impulse from pacemaker cells to surrounding atrium

• impulse is blocked as it exits the SA node

• disorder of conductivity

• may produce no symptoms

• may cause S&S of decreased cardiac output (weakness, lightheadedness, dizziness or syncope)



• oxygen prn, IV access

• if asymptomatic – observe

• review medications

• 5B – temp pacing prn (if wires in situ)

• IV atropine

• call code if acutely decompensating Medical ManagementMedical ManagementMedical ManagementMedical Management

• hemodynamic compromise – IV atropine

• if episodes of sinus arrest are frequent or prolonged, temporary or permanent pacing

Supraventricular TachycardSupraventricular TachycardSupraventricular TachycardSupraventricular Tachycardiaiaiaia

RateRateRateRate greater than 160 bpm

P waveP waveP waveP wave may not be visible

QRSQRSQRSQRS normal

PR intervalPR intervalPR intervalPR interval usually not measurable

RhythmRhythmRhythmRhythm regular

SupraventricuSupraventricuSupraventricuSupraventricularlarlarlar arrhythmias arrhythmias arrhythmias arrhythmias ( ( ( (SVTSVTSVTSVT) ) ) ) ---- is an umbrella term that includes:

• three main fast rhythms – atrial tachycardiaatrial tachycardiaatrial tachycardiaatrial tachycardia, AV node reentrant AV node reentrant AV node reentrant AV node reentrant tachycardia (AVNRT)tachycardia (AVNRT)tachycardia (AVNRT)tachycardia (AVNRT) and AV reentrant tachycardia (AVRT)AV reentrant tachycardia (AVRT)AV reentrant tachycardia (AVRT)AV reentrant tachycardia (AVRT), or, or, or, or may be used when you run into a very fast rhythm you can’t identify or you are unable to identify P-waves


• CAD, HF, thyroid disease, COPD

• medications, cocaine, caffeine

• structural abnormalities

• unknown etiology

• begins above the bifurcation of the bundle of His

• includes rhythms that begin in the SA node, atrial tissue or the AV junction

• rate related

• palpitations

• S&S of decreased cardiac output (decreased ventricular filling time, hypotension, chest discomfort/pain, altered LOC, dizziness, SOB, nausea)


• dependent on signs and symptoms

• bed rest prn


• oxygen prn, IV access

• notify MD/NP if patient symptomatic

• call code if decompensating MedicaMedicaMedicaMedical Managementl Managementl Managementl Management

• medications (Amiodarone. beta blocker, calcium channel blocker)

• ablation, cardioversion

• vagal maneuvers

Atrial Flutter Atrial Flutter Atrial Flutter Atrial Flutter

RateRateRateRate atrial 250-450 bpm; ventricular conduction varies and depends on the capability of the AV junction (usually not greater than 180 bpm)

P waveP waveP waveP wave not present; usually "saw toothsaw toothsaw toothsaw tooth" flutter waves are present.

QRSQRSQRSQRS normal

PR intervalPR intervalPR intervalPR interval not measurable

RhythmRhythmRhythmRhythm usually regular, but can be irregular if the AV block varies


• usually a paroxysmal rhythm precipitated by a PAC

• causes include PE, hypoxia, COPD, pneumonia, cardiac surgery, cardiomyopathy, ischemic heart disease

• hyperthyroidism

• pericarditis/myocarditis

• valve disease

• alcohol intoxication

• irritable foci in atrium fires regularly at a rapid rate

• AV node protects ventricles from the fast rate and conducts impulses at a rate <180 bpm

• if it is a 2:1 conduction it may be difficult to differentiate it form sinus tachy or atrial tachy

• to determine the conduction ratio divide the atrial rate by the ventricular rate (i.e. 300/75 gives a 4:1 ratio)

• rate related

• S&S of decreased cardiac output

• palpitations, difficulty breathing, fatigue, chest discomfort




• notify MD/NP if symptomatic or new onset

• bed rest prn

• call code if unstable Medical Medical Medical Medical TreatmentTreatmentTreatmentTreatment

• treatment depends on the level of hemodynamic compromise, the ventricular rate, and duration of rhythm

• synchronized cardioversion is used when prompt rate reduction is needed

• digoxin and other antiarrhythmic drugs

• ablation

• anticoagulation if greater than 48 hrs

Atrial Fibrillation Atrial Fibrillation Atrial Fibrillation Atrial Fibrillation

RateRateRateRate atrial rate usually between 400-600 bpm.

P waP waP waP waveveveve no identifiable P waves present; erratic, wavy baseline

QRSQRSQRSQRS normal

PR interval PR interval PR interval PR interval not measurable

RhythmRhythmRhythmRhythm ventricular rhythm is usually irregularly irregular

Atrial fibrillation may occur paroxysmally, but it may become chronic.

A ventricular rate of more than 100 bpm is described as uncontrolleduncontrolleduncontrolleduncontrolled. The ventricular rate is considered rapidrapidrapidrapid if is 150 bpm or more. A ventricular rate of less than 100 bpm is described as controlledcontrolledcontrolledcontrolled.


• idiopathic, HTN, HF, SSS, PE, COPD, after surgery, electrolyte imbalance, hypoglycemia, stress, hypoxia, mitral valve disease

• stress

• excessive caffeine

• hypokalemia

• hypoglycemia

• electrocution

• medication toxicity

• rapid firing of one or more sites in the atria, or reentry, at a rate of 400-600 times/min

• condition of altered automaticity

• rate related

• S&S of decreased cardiac output

• lightheadedness, palpitations, dyspnea, chest discomfort, low BP

• at risk for clot formation

• slow a fib may indicate medication toxicity


• assess VS, symptoms


• bed rest prn

• notify MD/NP if new onset or symptomatic

• call code if unstable Medical ManagementMedical ManagementMedical ManagementMedical Management

• treatment depends on the level of hemodynamic compromise, the ventricular rate, and duration of rhythm

• synchronized cardioversion is used when prompt rate reduction is needed

• digoxin and other antiarrhythmic drugs for rate control

• ablation

Junctional ArrhythmiasJunctional ArrhythmiasJunctional ArrhythmiasJunctional Arrhythmias

The inherent firing rate of the junctional pacemaker cells is 40 to 60 bpm. This rate is fast enough to sustain life with limited activity if injury or illness keeps the sinus node and atrial tissue from functioning properly. Patients with junctional rhythms often don’t realize that they have a rhythm problem, especially at rates in the 50s, as it often allows people to perform normal daily activities. When the AV junction is functioning as the pacemaker, the electrical impulse produces a wave of depolarization that spreads backward (retrograde) into the atria as well as forward into the ventricles. The location of the P wave relative to the QRS complex depends on the speed of conduction.

• if the electrical impulse from the AV junction depolarizes the ventricles first and then depolarizes the atria, the P wave will be after the QRS complex

• if the electrical impulse from the AV junction depolarizes the atria first and then depolarizes the ventricles, the P wave will be in front of the QRS complex

• if the electrical impulse from the AV junction depolarizes both the atria and ventricles simultaneously, the P wave will be hidden in the QRS complex

Retrograde stimulation of the atria is just opposite the direction of atrial depolarization when normal sinus rhythm is present and produces negative P waves in lead II. The PR interval is short (0.10 sec or less) and the ventricles are deporlarizing normally.

Premature Junctional Contractions Premature Junctional Contractions Premature Junctional Contractions Premature Junctional Contractions

RateRateRateRate normal or accelerated.

P waveP waveP waveP wave occur before, during or after the QRS depending on where the pacemaker is located in the AV junction.; P wave may be inverted

QRSQRSQRSQRS normal

PR intervalPR intervalPR intervalPR interval PR interval less than 0.10 sec if P waves are present

RhythmRhythmRhythmRhythm regular with premature beats

..


• if occasional, insignificant

• if frequent, junctional tachycardia may result

• causes include heart failure, ACS, valve disease, stimulants, digixon toxicity

• irritable site in AV junction fires before next SA node impulse is due

• impulse is conducted normally through ventricles

• compensatory pause often follows a PJC

• usually asymptomatic

• may cause palpitations, skipped beats

• S&S of decreased cardiac output if frequent due to loss of atrial kick

Nursing ManageNursing ManageNursing ManageNursing Managementmentmentment


• oxygen prn


• notify MD/NP if they become frequent or patient becomes symptomatic


• usually none required.

• treat cause(decrease contributing meds)

Junctional Escape Rhythm Junctional Escape Rhythm Junctional Escape Rhythm Junctional Escape Rhythm


P waveP waveP waveP wave occur before, during or after the QRS, depending on where the pacemaker is located in the AV junction; may be inverted

QRSQRSQRSQRS usually ≤0.10 sec

ConductionConductionConductionConduction PR interval less than 0.10 sec if present.



• seen in healthy individuals during sinus bradycardia

• causes include ACS, hypoxia, valvular heart disease, after cardiac surgery, SA node disease, medications

• begins in the AV junction

• frequently occurs during episodes of sinus arrest (kicks in as back up pacemaker)

• a junctional escape beat occurs when the SA node fails to pace the heart; usually appears late

• often asymptomatic or,

• S&S of decreased cardiac output due to loss of atrial kick

• hypotension

• chest discomfort/pain

• altered LOC

• lightheadedness

• SOB




• review possible contributing medications

• Notify MD/NP if symptomatic or new onset

• call code if unstable Medical ManagementMedical ManagementMedical ManagementMedical Management

• treat cause (decrease contributing meds like digoxin, beta blocker)

• atropine

• pacing (for symptomatic slow rate) to increase ventricular rate/output

Accelerated Accelerated Accelerated Accelerated Junctional Junctional Junctional Junctional RhythmRhythmRhythmRhythm



QRSQRSQRSQRS usually 0.10 or less

PR intervalPR intervalPR intervalPR interval PR interval usually less than 0.10 sec if present

RhythmRhythmRhythmRhythm very regular

Junctional TachycardiJunctional TachycardiJunctional TachycardiJunctional Tachycardia a a a

EtiologyEtiologyEtiologyEtiology ConductionConductionConductionConduction Clinical FeaturesClinical FeaturesClinical FeaturesClinical Features TTTTreatmentreatmentreatmentreatment

• caused by enhanced automaticity from heart failure, ACS, valve disease, digoxin toxicity, MI, electrolyte imbalance

• begins in the pacemaker cells of the bundle of His

• usually none as rate is that of regular sinus rate

• S&S of decreased cardiac output due to loss of atrial kick



• oxygen prn

• notify MD/NP if new onset or symptomatic


• check electrolytes


• treat cause (decrease contributing meds)



QRSQRSQRSQRS usually 0.10 or less

PR intervalPR intervalPR intervalPR interval PR interval usually less than 0.12 sec if present

RhythmRhythmRhythmRhythm very regular

AV BlocksAV BlocksAV BlocksAV Blocks


• caused by enhanced automaticity from heart failure, ACS, valve disease, digoxin toxicity

• begins in the pacemaker cells of the bundle of His

• caused by enhanced automaticity

• S&S of decreased cardiac output due to inability of ventricles to fill completely and loss of atrial kick

• “racing heart”

• severe anxiety

• syncope, altered LOC

• nausea

• hypotension




• notify MD/NP if symptomatic or new onset

• review contributing meds (digoxin) Medical ManagementMedical ManagementMedical ManagementMedical Management

• treat cause (decrease contributing meds)

• medications to control rate (beta blocker, calcium channel blocker)

• vagal maneuvers and adenosine (to help distinguish it from other tachy arrhythmias)

The term heart block is used to describe arrhythmias in which there is delayed or failed conduction of impulses through the AV node into the ventricles. The PR interval is primarily a measure of conduction between the initial stimulation of the atria and the initial stimulation of the ventricles (normally 0.12 to 0.20 sec). When the PR interval is too long, the signal is “blocked” in the AV node. It may just be delayed longer than usual, or the AV node may be letting some signals through and holding others back, or all the signals may be blocked completely. AV blocks can occur at the level of the AV node, the bundle of His, or the bundle branches. When located at the AV node of bundle of His, the QRS complexes will be normal duration. When located in the bundle branches, the QRS complex will be wide. The clinical significance of an AV block depends on the degree of block, the ventricular rate, and the patient response.

AV Block Decision TreeAV Block Decision TreeAV Block Decision TreeAV Block Decision Tree

Does PRI change?

No Yes

Are QRS complexes missing? Is R to R interval regular?

No Yes Yes No

1111

stststst degree 2 degree 2 degree 2 degree 2ndndndnd degree 3 degree 3 degree 3 degree 3rdrdrdrd degree 2 degree 2 degree 2 degree 2ndndndnd degree degree degree degree type II type II type II type II type I type I type I type I

First Degree AV Block First Degree AV Block First Degree AV Block First Degree AV Block

RateRateRateRate usually within normal range

P waveP waveP waveP wave normal

QRSQRSQRSQRS normal

PR intervalPR intervalPR intervalPR interval impulse originates in the SA node but has prolonged conduction in the AV junction; PR interval is greater than 0.20 sec but constant


First degree AV block is not a dysrhythmia itself but rather a condition describing the prolonged PR interval. Analysis should include a description of the underlying rhythm.


• occurs in both healthy and diseased hearts

• may be due to inferior MI, medications, hyperkalemia, increased vagal tone, and injury to the AV node or junction.

• SA node fires impulse and the impulse is conducted normally but is delayed at the level of the AV node

• often asymptomatic unless marked first degree block



• monitor for progression

• Notify MD/NP if PRI continues to lengthen

• review contributing meds Medical ManagementMedical ManagementMedical ManagementMedical Management


• assess contributing medications

• observe for progression to a more advanced AV block

• if result of AMI, monitor closely

SSSSecond econd econd econd Degree AV Block (Mobitz TDegree AV Block (Mobitz TDegree AV Block (Mobitz TDegree AV Block (Mobitz Type I, Wenkebach) ype I, Wenkebach) ype I, Wenkebach) ype I, Wenkebach)

RateRateRateRate atrial rate is greater than the ventricular rate

P waveP waveP waveP wave normal; constant P-P interval; some P waves not followed by a QRS complex

QRSQRSQRSQRS normal

PR intervalPR intervalPR intervalPR interval the PR interval is progressively longer until one P wave appears without a QRS complex (QRS is dropped)

RhythmRhythmRhythmRhythm atrial regular, ventricular irregular


• occurs in both healthy and diseased hearts

• may be due to inferior MI, medications hyperkalemia, increased vagal tone, and injury to the AV node or junction.

• often caused by right coronary artery occlusions as it supplies the AV node

• may progress to a higher level block but not likely

• Type I AV block is almost always located in the AV node, which means that the QRS duration is usually narrow, unless there is preexisting bundle branch disease.

• failure of some of the sinus impulses to be conducted to the ventricles

• occurs in the AV node above the bundle of His and is caused by a conduction delay within the AV node

• each successive impulse has difficulty passing through the AV node, until finally an impulse does not pass through

• often asymptomatic as ventricular rate is near normal

• S&S of decreased cardiac output if rate is slow



• oxygen prn: IV access


• notify MD/NP if patient symptomatic or new onset

• atropine IV

• 5B – temp pacing prn in PW in situ



• if rate slow atropine or pacing may be indicated

• if result of AMI, monitor closely

Second Degree AV Block (Mobitz TSecond Degree AV Block (Mobitz TSecond Degree AV Block (Mobitz TSecond Degree AV Block (Mobitz Type II) ype II) ype II) ype II)

RateRateRateRate atrial rate is greater than ventricular rate; ventricular rate is often slow

P waveP waveP waveP wave normal; some P waves not followed by a QRS complex

QRSQRSQRSQRS usually 0.10 sec or greater; periodically absent after P wave

PR intervalPR intervalPR intervalPR interval PR interval may be normal or prolonged, but it is constant until one P wave is not conducted to the ventricles (QRS is dropped)

RhythmRhythmRhythmRhythm atrial regular, ventricular irregular

EtiologyEtiologyEtiologyEtiology ConductionConductionConductionConduction Clinical Clinical Clinical Clinical FeaturesFeaturesFeaturesFeatures TreatmentTreatmentTreatmentTreatment

• causes include acute myocarditis, acute anterior MI (left coronary artery supplies bundle branches), degeneration of electrical conduction system

• type II AV block is almost always located in the bundle branches, which means that the QRS duration is wide indicating complete block of one bundle

• advanced or high grade block is used to describe two or more consecutive P waves that are not conducted

• the number of P waves before the QRS complex determines the conduction ratio (3:1, 2:1)

• failure of some of the sinus impulses to be conducted to the ventricles

• block can occur below the bundle of His or at the level of the bundle branches

• may progress into a third degree block or ventricular standstill

• the more frequently the QRS is dropped the more likely the patient will be symptomatic

• S&S of decreased cardiac output due to decreased ventricular rate

• hypotension

• SOB

• heart failure

• chest pain

• syncope

• This is more serious than the Type I block and frequently progresses to third degree

•

Nursing MNursing MNursing MNursing Managementanagementanagementanagement





• notify MD/NP ASAP

• 5B – temp pacing prn if PW in situ




• pacing for slow rate/symptomatic patient

• permanent pacemaker

• atropine notnotnotnot effective and can worsen conduction disturbance. An increase in the rate of SA node discharge could trigger a situation where even fewer impulses are conducted through to the ventricles.

Third Degree or CThird Degree or CThird Degree or CThird Degree or Complete AV Block omplete AV Block omplete AV Block omplete AV Block

RateRateRateRate atrial rate is usually normal; ventricular rate is determined by origin of the escape rhythm

P waveP waveP waveP wave normal with constant P-P intervals, but not "married" to the QRS complexes

QRSQRSQRSQRS may be normal or widened depending on where the escape pacemaker is located in the conduction system

PR intervalPR intervalPR intervalPR interval none as atrial and ventricular activities are unrelated due to the complete blocking of the atrial impulses to the ventricles

RhythmRhythmRhythmRhythm atrial regular, ventricular regular but no relationship between the rhythms


• associated with anterior and inferior MIs

• digoxin toxicity

• acute infection

• degeneration of the conductive tissue

• Narrow QRS rhythm suggests a junctional escape focus for the ventricles with block above the pacemaker focus, usually in the AV node.

• impulses generated by SA node are blocked before reaching the ventricles

• atria and ventricles beat independently of one another

• secondary pacemaker stimulates the ventricles

• atria are paced by SA node and the ventricles are paced by a pacemaker in the AV junction or the ventricles

• width of QRS complex and rate determines where the block is

• S&S of decreased cardiac output due to decreased ventricular rate

Nursing Nursing Nursing Nursing ManagementManagementManagementManagement



• 5B – temp pacing prn if PW in situ


• notify MD/NP ASAP Medical Medical Medical Medical ManagementManagementManagementManagement



• external pacing

• IV atropine (depending on escape pacemaker)

• permanent pacing for chronic complete heart block.

Ventricular ArrhythmiasVentricular ArrhythmiasVentricular ArrhythmiasVentricular Arrhythmias

Ventricular beats and rhythms Originate below the bundle of His in a pacemaker site in either the right or left ventricle. When impulses arise in the ventricles, the impulse does not enter the normal conduction pathway, but travels from cell to cell through the myocardium, depolarizing the ventricles asynchronously. Therefore, the ventricles are not stimulated simultaneously and the stimulus spreads through the ventricles in an aberrant manner, resulting in a wide QRS complex of 0.12 sec or greater. The delivery system is designed to send nearly simultaneous signals to the left and right ventricles. As a result, the two QRS complexes (one for each ventricle) occur together, overlap each other, and merge into one QRS of the expected duration, less than 0.12 seconds. However, when the depolarization begins in the ventricles, the depolarization occurs sequentially, merging to form a much wider QRS. Normal depolarization Depolarization initiated in ventricles Because the ventricles are the least efficient of the heart’s pacemakers, most of ventricular rhythms are (or have the potential to be) life-threatening and demand prompt recognition and treatment.

Premature Ventricular Contractions Premature Ventricular Contractions Premature Ventricular Contractions Premature Ventricular Contractions

RateRateRateRate usually within normal range

P waveP waveP waveP wave not associated with the PVC; usually obscured by the QRS, PST or T wave of the PVC

QRSQRSQRSQRS greater than 0.12 sec; wide and bizarre with the ST segment and the T wave in opposite direction of QRS; may be unifocal or multifocal (exhibit different morphologies)

PR intervalPR intervalPR intervalPR interval none with PVC as ectopic originates in the ventricle

RhythmRhythmRhythmRhythm essentially regular with premature beats; PVC's may occur in singles, couplets or triplets; or in bigeminy, trigeminy or quadrigeminy


• occur in healthy and diseased hearts

• result of increase in sympathetic tone

• stimulants

• hypoxia

• stress, anxiety

• exercise


• HF, MI, ACS

• medications

• irritable site within either ventricle

• occurs earlier than next expected sinus beat

• often a result of enhanced automaticity, re-entry or triggered activity during ventricular repolarization

• compensatory pause usually follows PVC

• usually asymptomatic if infrequent

• S&S of decreased cardiac output if frequent

• may or may not produce a palpable pulse

• may c/o palpitations, racing heart, skipped beats, chest or neck discomfort



• oxygen prn

• check electrolytes (hypokalemia)

• monitor for increasing frequency

• notify MD/NP if patient symptomatic or frequency increases



• most patients with PVCs do not require treatment but if frequent and symptomatic, antiarrthymics may be indicated

Idioventricular RhythmIdioventricular RhythmIdioventricular RhythmIdioventricular Rhythmssss

RateRateRateRate 20 to 40 bpm (IVR) 41 – 100 bpm (AIVR)

P waveP waveP waveP wave absent or with retrograde conduction, may appear after QRS

QRSQRSQRSQRS greater than 0.12 sec; T wave frequently in opposite direction to QRS

PR intervalPR intervalPR intervalPR interval none

RhythmRhythmRhythmRhythm essentially regular

EtiologyEtiologyEtiologyEtiology ConductionConductionConductionConduction Clinical FeaturesClinical FeaturesClinical FeaturesClinical Features TreTreTreTreatmentatmentatmentatment

• causes may include failure of SA node and AV junction to initiate an impulse,

• myocardial infarction

• digoxin toxicity

• metabolic imbalances

• impulse originates in the ventricles as both the SA node and AV tissue fail to initiate an impulse

• intrinsic firing of the ventricles

• IVRIVRIVRIVR exists when 3 or more ventricular escape beats occur in a row at a rate of 20-40 bpm. A A A A (Accelerated) IVR(Accelerated) IVR(Accelerated) IVR(Accelerated) IVR is between 41-100 bpm

• S&S of decreased cardiac output due to slow rate and lack of atrial kick





• notify MD/NP

• call code if patient decompensates Medical ManagementMedical ManagementMedical ManagementMedical Management


• improve cardiac output (vasopressors)


• establish a normal rhythm

• transcutaneous/epicardial pacing

• if pulseless, CPR and ACLS guidelines are indicated

• Caution: Suppressing the ventricular rhythm is contraindicated because that rhythm protects the heart from complete standstill

Ventricular Tachycardia Ventricular Tachycardia Ventricular Tachycardia Ventricular Tachycardia Monomorphic VTMonomorphic VTMonomorphic VTMonomorphic VT : Ventricular tachycardia is called monomorphic VTmonomorphic VTmonomorphic VTmonomorphic VT when the QRS complexes are the same shape and amplitude


P waveP waveP waveP wave may be present or absent; if present they are unrelated to the QRS complexes

QRSQRSQRSQRS greater than 0.12 sec; wide and bizarre; difficult to differentiate between QRS and T wave


RhythmRhythmRhythmRhythm three or more ventricular beats in a row; essentially regular


• anything that decreases oxygen delivery to the ventricles

• common causes are ACS, cardiomyopathy, tricyclic antidepressant overdose, valvular heart disease, cocaine abuse, electrolyte imbalance

• can quickly deteriorate into ventricular fibrillation

• drugs or congenital disease that lengthens the QT interval

• impulse originates in the ventricles

• less than 30 seconds it is called nonnonnonnon----sustained VTsustained VTsustained VTsustained VT

• greater than 30 seconds it is sustasustasustasustained VTined VTined VTined VT

• S&S of decreased cardiac output due to fast rate causing decrease filling time, and loss of atrial kick

• syncope, hypotension, altered mental status, shock, chest pain, SOB, pulmonary congestion



• If patient has pulsepulsepulsepulse: oxygen, bed rest, IV access, notify MD STAT

• If patient is pulselesspulselesspulselesspulseless/unstable: call code, ABCs, CPR


• treat underlying cause ( IV mag sulfate or potassium to correct imbalances, assess medications)

• stablestablestablestable symptomatic patients: oxygen and IV anti-arrhythmics to suppress the rhythm (Amiodarone)

• unstableunstableunstableunstable patients: oxygen and synchronized cardioversion

• pulselesspulselesspulselesspulseless patient: CPR and defibrillation

• ICD, ablation: refractory to pharmacological approaches

Polymorphic VT: Polymorphic VT: Polymorphic VT: Polymorphic VT: When the QRS complexes vary in shape and amplitude from beat to beat the rhythm is polymorphic VT. Polymorphic VT that occurs in the presence of a long QT interval is called Torsades de Pointes. The hallmark of this rhythm is the upward and downward deflection of the QRS complexes around the baseline. The term Torsades de PointesTorsades de PointesTorsades de PointesTorsades de Pointes means "twisting about the points."


P waveP waveP waveP wave absent

QRSQRSQRSQRS greater than 0.12 sec; gradual alteration in amplitude and direction of the QRS complexes


RhythmRhythmRhythmRhythm may be regular or irregular


• anything that decreases oxygen delivery to the ventricles

• bradyarrhthymias, 3 degree block

• excessive antiarrhythmics, haldol


• congenital LQTS

• liquid protein diets

• CNS disorders

• usually occurs when the QT interval is prolonged

• S&S of decreased cardiac output due to fast rate causing decrease filling time, and loss of atrial kick

• syncope, hypotension, altered mental status, shock, chest pain, SOB, pulmonary congestion


• call code, ABCs, CPR Medical ManagementMedical ManagementMedical ManagementMedical Management

• ACLS guidelines, defibrillate

• treat precipitating causes – meds, electrolytes

• ICD for prophylaxis

• Amiodarone is NOT used as it can prolong the QT further

Ventricular FibrillationVentricular FibrillationVentricular FibrillationVentricular Fibrillation

RateRateRateRate unattainable

P waveP waveP waveP wave not discernible

QRSQRSQRSQRS not discernible

PR intervalPR intervalPR intervalPR interval not discernible

RhythmRhythmRhythmRhythm chaotic electrical activity with no pattern or regularity

EtiologyEtiologyEtiologyEtiology ConductionConductionConductionConduction Clinical FeaturesClinical FeaturesClinical FeaturesClinical Features TrTrTrTreatmenteatmenteatmenteatment

• causes include increased SNS activity

• vagal stimulation


• medications (digoxin toxicity)

• ventricular hypertrophy

• ACS

• HF

• arrhythmias

• MI

• metabolic acidosis

• chaotic rhythm originating in the ventricles

• no organized depolarization so no effective ventricular contraction resulting in no effective myocardial contraction and no pulse

• coarse VF – wave 3 mm or higher

• fine VF – wave less than 3 mm in amplitude

• VT usually deteriorates to VF within 3 minutes

• no cardiac output, no peripheral pulses, no BP, pt unconscious

• death imminent if untreated

• coarse VF indicates a more recent onset and more likely to be reversed by defibrillation


• call code, ABC, CPR; IV access Medical ManagementMedical ManagementMedical ManagementMedical Management

• defibrillation, CPR

• ACLS guidelines (epinephrine, vasopressin, Amiodarone, atropine)

Asystole/Ventricular Standstill Asystole/Ventricular Standstill Asystole/Ventricular Standstill Asystole/Ventricular Standstill

RateRateRateRate no ventricular activity but atrial activity may be seen

P waveP waveP waveP wave may be seen, but there is no ventricular response

QRSQRSQRSQRS none

PR intervalPR intervalPR intervalPR interval not measurable

RhythmRhythmRhythmRhythm ventricular not discernible


• may occur temporarily following the termination of atrial, AV junctional or ventricular tachycardias

• causes: o MMMM – MI o AAAA – acidosis o TTTT – tension pneumo o CCCC – cardiac tamponade o HHHH x 5 –

hyper/hypokalemia, hypotension, hypoxia, Hypovolemia

o EEEE – embolus (pulmonary)

o DDDD – drugs or drug overdose

• absence of ventricular activity

• some atrial activity may be present (P waves) but the ventricles are too sick to respond

• S&S of absent cardiac output

• pulseless, unconscious


• call code, ABC, CPR; IV access

• check two leads to ensure it is asystole and not fine VF or leads off


• CPR and defibrillation if a shockable rhythm (VF, VT) resumes

• ACLS guidelines (epinephrine, vasopressin, atropine)

• medications


PacemakersPacemakersPacemakersPacemakers

Some indications for pacing include:

• sinus bradycardia

• sinus arrest

• sinus exit block

• atrial flutter or fib

• sick sinus syndrome

• chronotropic incompetence (SA node incapable of increasing rate in response to activity)

• 2nd degree AV block type II

• 3rd degree AV block If a pacemaker senses a P wave, the pacemaker is inhibited form firing an electrical stimulus. If the pacemaker does not sense a P wave, the pacemaker sends an electrical stimulus to the atrium. Stimulation of the atrium produces a pacemaker spike, followed by a P wave. The pacemaker is programmed to wait, simulating an electronic PR interval (called the AV interval). The same thing happens for the ventricles if it is a dual chamber pacemaker. Dual chamber pacemakers stimulate the atria and ventricles in sequence mimicking normal heart physiology and thus preserving atrial kick. Because the pacemaker lead doesn’t lie in the sinus node or the AV node, the P waves and QRS complexes will vary from normal. Usually the wire is embedded at the bottom of the ventricle (far from the AV node) so QRS complexes are wide and bizarre.

Paced RhythmsPaced RhythmsPaced RhythmsPaced Rhythms

Fusion beatsFusion beatsFusion beatsFusion beats occur when a pacing stimulus and an intrinsic beat partly depolarize the ventricles.

A pseudopseudopseudopseudo----fusionfusionfusionfusion beatbeatbeatbeat occurs when a pacemaker spike precedes an intrinsic QRS complex but doesn’t change it. The pacemaker spike location gives the false impression that the spike influenced the QRS.

Analyzing Pacemaker FunctionAnalyzing Pacemaker FunctionAnalyzing Pacemaker FunctionAnalyzing Pacemaker Function

Step One: Identify the intrinsic rate and rhythmStep One: Identify the intrinsic rate and rhythmStep One: Identify the intrinsic rate and rhythmStep One: Identify the intrinsic rate and rhythm

• Are P waves present? At what rate?

• Are QRS complexes present? At what rate? Step Two: Step Two: Step Two: Step Two: Measure the paced interval Measure the paced interval Measure the paced interval Measure the paced interval

• Measure the paced interval by measuring the distance between two consecutive paced beats – like you would measure R-R except place calipers on pacing spikes. Ex. spike to spike is 19 small boxes = paced interval of 79

Step three: Analyze the rhythm stripStep three: Analyze the rhythm stripStep three: Analyze the rhythm stripStep three: Analyze the rhythm strip

• Determine rate and regularity of paced activity. Analyze the strip for failure to capture, failure to sense, oversensing or failure to pace

AV Sequential PacemakerAV Sequential PacemakerAV Sequential PacemakerAV Sequential Pacemaker with a with a with a with appropriate sensing and capture: ppropriate sensing and capture: ppropriate sensing and capture: ppropriate sensing and capture: each pacing spike is followed by a P and/ or QRS complex

Pacemaker ComplicationsPacemaker ComplicationsPacemaker ComplicationsPacemaker Complications (applies to temporary and permanent pacemakers (applies to temporary and permanent pacemakers (applies to temporary and permanent pacemakers (applies to temporary and permanent pacemakers))))

Failure to PaceFailure to PaceFailure to PaceFailure to Pace/ Fire/ Fire/ Fire/ Fire: : : : when the pacemaker fails to deliver an electrical stimulus or the correct number of electrical stimuli per minute. Failure to pace is recognized by a lack of pacemaker spikes and a return to the rhythm that indicated the need for a pacemaker.


Caused by:

• battery depletion

• disconnection in the system

• lead fracture

• electromagnetic interference

• pacemaker turned off or programmed incorrectly

• pacemaker does not discharge a stimulus to the myocardium

• lack of a pacing spike where expected

• if the pacemaker doesn’t sense an intrinsic beat after 1000 ms (this will vary depending on the base rate) after the last beat, it should fire.

• hypotension

• bradycardia

• syncope

• chest pain

• return of symptoms associated with rhythm for which pacemaker was implanted



• IV access

• Notify MD/NP

• Temp Epicardial pacing – check battery, ensure unit is turned on, replace pulse generator, remove any electromagnetic interference

• call code if unstable, CPR Medical ManagementMedical ManagementMedical ManagementMedical Management

• adjust pacemaker settings

• surgery to replace lead or device

• IV atropine

• ACLS guidelines if pulseless or decompensated

Failure to CaptureFailure to CaptureFailure to CaptureFailure to Capture: is the inability of the pacemaker stimulus to depolarize the myocardium. The pacemaker fires but does not stimulate the ventricle/atria enough to cause contraction. On the strip you will see a pacing spike with no corresponding P wave or QRS complex.

EtiologyEtiologyEtiologyEtiology ConductionConductionConductionConduction ClinicaClinicaClinicaClinical Featuresl Featuresl Featuresl Features TreatmentTreatmentTreatmentTreatment

Caused by:

• battery failure

• scar tissue or edema at electrode tip

• lead fracture or displacement

• energy output too low

• medications

• electrolyte imbalance (alters ability of heart to respond to stimulus)

• pacemaker discharges a stimulus to the myocardium but the myocardium does not depolarize

• pacing spike not followed by a P wave or QRS complex

• hypotension

• bradycardia

• syncope

• fatigue



• reposition patient

• notify MD/NP

• Temp Epicardial pacing – check battery, ensure unit is turned on, replace pulse generator, check all connections

• call code if unstable, CPR


• adjust pacemaker settings (increase output)


• ACLS guidelines if pulseless or decompensated

Failure to SenseFailure to SenseFailure to SenseFailure to Sense UndersensingUndersensingUndersensingUndersensing: occurs when the pacemaker fails to recognize spontaneous myocardial depolarization. This is recognized by the generation of unnecessary pacing spikes (follow too closely behind the patient’s QRS complexes, occur earlier than the programmed escape interval).


Caused by:

• battery failure

• scar tissue or edema at electrode tip

• lead fracture or displacement

• sensitivity too low

• circuitry dysfunction

• myocardial perforation

• medications


• pacemaker does not recognize myocardial activity and fires earlier than it should

• pacing spike not followed by a P wave or QRS complex, generally earlier than it should

• can occur with or without capture

• c/o skipped beats or palpitations

• risk of pacing spike falling on the T wave causing R-on-T




• Notify MD/NP



• adjust pacemaker settings (increase sensitivity)

• pace in asynchronous (fixed) mode until problem fixed

• x-ray to determine lead placement


OversensingOversensingOversensingOversensing: results when there is inappropriate sensing of extraneous electrical signals (skeletal muscle activity, electrical interference). These electrical signals are interpreted by the pacemaker as intrinsic activity and as a result the pacemaker does not fire. It is recognized by absent pacemaker spikes and ventricular asystole. These inappropriate signals may be large P or T waves, skeletal muscle activity or lead contact problems. Abnormal signals may not be evident on ECG.

EtiologyEtiologyEtiologyEtiology ConductionConductionConductionConduction Clinical FeaClinical FeaClinical FeaClinical Featuresturesturestures TreatmentTreatmentTreatmentTreatment

Caused by:

• battery failure

• device programmed incorrectly

• pacemaker is too sensitive and is sensing the wrong signals causing the pacemaker to reset inappropriately increasing the amount of time before the next discharge

• paced beat occurring later than it should

• can be hard to identify unless the minimum heart rate setting is known

• pace

• fatigue

• bradycardia

• hypotension

• syncope




• notify MD/NP



• adjust pacemaker settings (decrease sensitivity)

• reprogram settings (increase minimum heart rate)

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