5ab dysrhythmia interpretation review...

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5AB Dysrhythmia 5AB Dysrhythmia 5AB Dysrhythmia 5AB Dysrhythmia InterpreInterpreInterpreInterpretation and Management tation and Management tation and Management tation and Management

Review 2014Review 2014Review 2014Review 2014

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This review begins with a discussion of the physiology of cardiac conduction, and then covers the basics of how to interpret an ECG strip, and the normal components of the ECG waveform. It will then examine basic cardiac dysrhythmias, including atrial and ventricular dysrhythmias, and blocks.

This review will help you to:

• Identify basic normal ECG waveform morphology • Describe the normal physiology of cardiac conduction • Distinguish between basic dysrhythmias • Describe the physiological consequences and treatments of basic dysrhythmias • Demonstrate proper electrode placement and maintenance

OverviewOverviewOverviewOverview

Learning IntentionsLearning IntentionsLearning IntentionsLearning Intentions

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In an adult with a healthy heart, the heart rate is usually between 60-100 beats per minute. The excitatory and electrical conduction system of the heart is responsible for the contraction and relaxation of the heart muscle. The sinoatrial node (SA node) is the

pacemaker where the electrical impulse is generated. This node is located along the posterior wall of the right atrium right beneath the opening of the superior vena cava. It is crescent shaped and about 3 mm wide and 1 cm long. The impulse travels from the SA node through the internodal pathways to the atrioventricular node (AV node). The AV node is responsible for conduction of the impulse from the atria to the ventricles. The impulse is delayed slightly at this point to allow complete emptying of the atria before the ventricles contract. The impulse continues through the AV bundle and down the left and right bundle branches of the Purkinje fibers. The Purkinje fibers conduct the impulse to all parts of the ventricles causing contraction (Guyton, 1982).

Abnormal heart rhythms occur for several reasons:

1. Parasympathetic SParasympathetic SParasympathetic SParasympathetic Stimulationtimulationtimulationtimulation: Vagal stimulation of the parasympathetic nervous system can cause a decrease in the rate

at the SA node and can also decrease the excitability of the AV junction fibers. This causes the heart rate to slow and in severe cases a complete blockage of the impulse through the AV junction.

2. Sympathetic StimulationSympathetic StimulationSympathetic StimulationSympathetic Stimulation: Stimulation of the sympathetic nervous system can also affects cardiac rhythm and conduction. It increases the rate at the SA node and increases the rate of conduction and excitability throughout the heart. It also increases the force of myocardial contraction. Subsequently, the overall workload on the heart is increased.

3. Ectopic fociEctopic fociEctopic fociEctopic foci: A small area of the heart can become more excitable than normal which causes abnormal heart beats called ectopy. Ectopic foci are usually caused by an irritable area in the heart. This irritability may be the result of ischemia, stimulants such as nicotine and caffeine, lack of sleep, or anxiety (Guyton, 1982).

Rates of the Heart’s Electrical SystemRates of the Heart’s Electrical SystemRates of the Heart’s Electrical SystemRates of the Heart’s Electrical System

SA Node 60-100 bpm Atrial tissue 75 bpm AV Junction 40-60 bpm Ventricles 20-40 bpm

Physiology of Cardiac ConductionPhysiology of Cardiac ConductionPhysiology of Cardiac ConductionPhysiology of Cardiac Conduction

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Good Skin Prep: Good Skin Prep: Good Skin Prep: Good Skin Prep:

• Clip hair if present. This allows for better contact and less painful removal of patches (Note: Avoid shaving as this may increase skin irritation under the electrode)

• Wash skin with soap and water

• Rinse then dry briskly to remove dead cells and oils Some Dos and Don’ts for Electrode ASome Dos and Don’ts for Electrode ASome Dos and Don’ts for Electrode ASome Dos and Don’ts for Electrode Applicationpplicationpplicationpplication:

• DO use all the same type of electrodes

• DO check the gel to make sure it is fresh and moist

• DO NOT use alcohol or other skin products on the skin

• DO NOT place electrodes over: bones, areas where there is a lot of muscle or fluid movement (i.e. abdominal ascites), irritated skin, incisions

Electrode MaintenanceElectrode MaintenanceElectrode MaintenanceElectrode Maintenance::::

• Replace electrodes every 24 hours or as needed

• Write the date of the application or change on either of the upper electrodes (black or white)

• Follow the steps for good skin prep and electrode application each time the electrodes are changed

• Change or replace electrodes as needed for: loose electrodes caused by pulling or very moist skin, complaints or evidence of skin irritation, when ECG tracing is of poor quality and is causing false alarms

Lead PlacementLead PlacementLead PlacementLead Placement:::: “Smoke over fire, Clouds over Grass”“Smoke over fire, Clouds over Grass”“Smoke over fire, Clouds over Grass”“Smoke over fire, Clouds over Grass” Translation: Black over Red, White over Green BrownBrownBrownBrown: In the 4thintercostal space (space between the ribs) WhiteWhiteWhiteWhite: Below the right clavicle and near the right shoulder GreenGreenGreenGreen: Below the rib cage on the right side of the abdomen BlackBlackBlackBlack: Below the left clavicle and near the left shoulder RedRedRedRed: Below the rib cage on the left side of the abdomen Important Reminders:Important Reminders:Important Reminders:Important Reminders: • DO make sure the V lead (brown electrode) is in the intercostal space and not over the sternum or rib

ElectrodesElectrodesElectrodesElectrodes

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• DO make sure the red and green electrodes are placed below the rib cage DO NOT place electrodes over pacemakers or implanted defibrillators

ECG paper is a grid where time is measured along the horizontal axis.

• Each small square is 1 mm in length and represents 0.04 seconds • Each larger square is 5 mm in length and represents 0.2 seconds

Calculating heart rate from the ECG strip:Calculating heart rate from the ECG strip:Calculating heart rate from the ECG strip:Calculating heart rate from the ECG strip:

Method 1: Large BoxMethod 1: Large BoxMethod 1: Large BoxMethod 1: Large Box For regular rhythms, the rate can be determined by counting the number of large boxes between two R waves and then dividing that number into 300. Method 2: Small BoxMethod 2: Small BoxMethod 2: Small BoxMethod 2: Small Box To calculate the ventricular rate count the number of small boxes between two consecutive R waves and divide into 1500. To calculate the atrial rate count the number of small boxes between two consecutive P waves and divide into 1500. If the rhythm is irregular, give a range. Method 3: RulerMethod 3: RulerMethod 3: RulerMethod 3: Ruler Using a commercially developed ruler place the “0” mark on a complex and the third QRS (or P for atrial rate) complex from here is the rate.

Components of an ECG StripComponents of an ECG StripComponents of an ECG StripComponents of an ECG Strip

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PQRSTU SummaryPQRSTU SummaryPQRSTU SummaryPQRSTU Summary::::

http://alexandria.healthlibrary.ca P waveP waveP waveP wave

• Indicates atrial depolarization, or contraction of the atrium • Normal duration is not longer than 0.11 seconds (less than 3 small squares) • Amplitude (height) is no more than 2.5 mm • Smooth and rounded, no notching or peaking

QRS complexQRS complexQRS complexQRS complex

• Consists of the q wave, R wave and S wave • Indicates ventricular depolarization or contraction of the ventricles. • Normally between 0.06 to 0.10 seconds in duration • The duration of a QRS caused by an impulse originating in an ectopic pacemaker in the Purkinje network or ventricular

myocardium is usually greater than 0.12 sec and often 0.16 sec or greater • Measured from the beginning of the QRS complex to the end of the S wave • R waves are deflected positively (upward) and the Q and S waves are negative (downward)

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T waveT waveT waveT wave • Indicates ventricular repolarization • Rounded and slightly asymmetrical • Direction of the T wave is normally the same as the QRS complex • Tall, “peaked” T waves are commonly seen in hyperkalemia • Negative T waves suggests myocardial ischemia • 5mm or less in standard leads I, II, and III; 10mm or less in precordial leads V1-V6.

UUUU wave wave wave wave

• Occurs after the T wave (not always seen) • Rounded and symmetric • Usually less than 1.5 mm in height and smaller than the preceding T wave. A U wave greater than 1.5 mm in height is

generally considered abnormal ST segmentST segmentST segmentST segment

• Indicates early ventricular repolarization • Begins with the end of the QRS complex (at the J point) and ends with the onset of the

T wave • Normally found on the isoelectric line; may be elevated slightly in some leads (no more

than 1 mm) • Normally not depressed more than 0.5 mm; ST segment depression of more than ½

mm is suggestive of myocardial ischemia; elevation of more that 1mm in limb leads and 2mm in chest leads suggests myocardial injury

PR intervalPR intervalPR intervalPR interval • Indicates AV conduction time • Measured from the beginning of the P wave to the beginning of the QRS complex • Duration time is 0.12 to 0.20 seconds; normally shortens as heart rate increases and

lengthens as heart rate decreases • Duration of greater than 0.20 sec indicates the impulse is delayed as it passes through

the atria or AV node

QT intervalQT intervalQT intervalQT interval • Represents total ventricular activity (from depolarization to repolarization). A prolonged

QT indicates a lengthened refractory period that puts the ventricle at risk for dysrhythmias, such as torsades de pointes

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• Measured from the beginning of the QRS complex to the end of the T wave • General rule: duration is less than half the preceding R-R interval • Varies according to age, gender and heart rate • Electrolyte disorders, medications, or congential disorders can prolong the QT interval

ArArArArtifacttifacttifacttifact

• Distortion of the ECG tracing by electrical activity that is non cardiac in nature is called artifact • Artifact can be caused by loose electrodes, broken ECG wires, muscle tremor, patient movement, 60 cycle interference

(interference caused by improperly grounded electrical equipment or other electrical interference)

Step Step Step Step OneOneOneOne: Determine the rhythm’s regularity. The rhythm is said to be regular when there is a constant distance between similar

waves (P-P or R-R). Generally a variation of 10% is acceptable. For example, if there are 10 small boxes in an R-R interval, an R wave could be off by 1 small box and still be considered regular.

In an irregular rhythm if the variation between the shortest and longest R-R interval is less than four small boxes (0.16

sec) the rhythm is essentially regular. If the R-R intervals vary by more than 0.16 seconds the rate is irregular. A regularly irregular rhythm is where the R-R intervals are not the same and vary by more than 0.16 sec but have a repeating pattern of irregularity.

Steps of Rhythm AnalysisSteps of Rhythm AnalysisSteps of Rhythm AnalysisSteps of Rhythm Analysis

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Step Step Step Step TwoTwoTwoTwo: Calculate the heart rate using one of the methods described earlier. The SmallSmallSmallSmall Box Method Box Method Box Method Box Method is the most accurate. Count the number of small boxes between R-R or P-P and divide by 1500.

Step ThreeStep ThreeStep ThreeStep Three: Identify and examine P waves. One P wave should precede every QRS complex, look similar in shape, size and position. If P waves are absent it indicates the rhythm originates in the AV junction or the ventricles.

Step FourStep FourStep FourStep Four: Assess intervals. Measure the PR interval. Is it constant, lengthening, of normal duration? Measure the QRS intervals. Are they narrow or wide, occur regularly.

Step FiveStep FiveStep FiveStep Five: Evaluate the overall appearance of the rhythm. Determine whether there is depression or elevation of the ST segment from the isoelectric line. Evaluate the T waves to see if they are upright and of normal height.

Step SixStep SixStep SixStep Six: Interpret the rhythm and evaluate its clinical significance. Specify the site the rhythm originates (sinus), the mechanism (bradycardia), and the ventricular rate. Example: sinus bradycardia. Evaluate the patient’s clinical presentation to determine how they are tolerating the rate and rhythm.

Understanding the mechanisms of a particular rhythm helps to determine the potential effects on patients. Some rhythms have little or no symptoms associated with them while others can impart significant hemodynamic compromise.

Signs and symptoms of hemodynamic compromise include:

� changes in mental status (restlessness, confusion, loss of consciousness) � pulmonary congestion � cold, clammy skin � low blood pressure � signs of shock � shortness of breath � chest pain � congestive heart failure � fall in urine output

Nursing Interventions for Patients with DysrhythmiasNursing Interventions for Patients with DysrhythmiasNursing Interventions for Patients with DysrhythmiasNursing Interventions for Patients with Dysrhythmias

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If a patient has a change in their rhythm:If a patient has a change in their rhythm:If a patient has a change in their rhythm:If a patient has a change in their rhythm:

� Assess the patient for signs and symptoms. This includes physical assessment, vital signs, review of lab values, patient history, etc.

� Assess the patient for the underlying cause and contributing factors. In the case of dysrhythmias, this would entail identifying the dysrhythmia and determining if it was causing a decrease in tissue perfusion

� Correct the underlying cause. This may include reduction of pain and anxiety, fluid restriction, fluid replacement, restricting activities that precipitate dysrhythmias (e.g.valsalva), or administering oxygen. Administer cardiac medications

� Administer cardiac medications as ordered

� Maintain patency of all IVs and other invasive lines

� Provide psychosocial support for patient and family members

� Promote adequate rest

� Maintain appropriate nutritional and fluid balances

� Patient Education: includes acute activities such as reporting chest pain, dyspnea or other symptoms to the RN.

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The various dysrhythmias you are responsible for will be reviewed in this section, but first, a review of normal sinus rhythm...

NoNoNoNormal Sinus Rhythm (RSR)rmal Sinus Rhythm (RSR)rmal Sinus Rhythm (RSR)rmal Sinus Rhythm (RSR)

� the name given to a normal heart rhythm � sinus node is the pacemaker � each beat is conducted normally through to the ventricles

Analyze RhythmAnalyze RhythmAnalyze RhythmAnalyze Rhythm

What is the rhythm?What is the rhythm?What is the rhythm?What is the rhythm? R-R and P-P intervals are constant - rhythm is regular. What is the rWhat is the rWhat is the rWhat is the rate? ate? ate? ate? atrial and ventricular rates are equal; heart rate is between 60-100 bpm. Is there a P Wave before each QRS?Is there a P Wave before each QRS?Is there a P Wave before each QRS?Is there a P Wave before each QRS? Are P waves upright and uniform? uniform; one P wave in front of every QRS complex. What is the length of the PRI?What is the length of the PRI?What is the length of the PRI?What is the length of the PRI? measures between 0.12 and 0 .20 sec; constant from beat to beat Do all QRS complexes look alike?Do all QRS complexes look alike?Do all QRS complexes look alike?Do all QRS complexes look alike? What is the length of the QRS complex? yes; less than 0.11 sec

Rhythm reviewRhythm reviewRhythm reviewRhythm review

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Sinus DysrhythmiasSinus DysrhythmiasSinus DysrhythmiasSinus Dysrhythmias

Sinus dysrhythmias result from problems with impulse discharge or conduction from the sinus node. The SA node remains the primary pacemaker for the heart but either discharges impulses too fast, too slow, irregularly, or the impulses are blocked. Note, sinus bradycardia at rest, sinus tachycardia with exercise, and sinus arrhythmia with breathing are considered normal response.

ECG Review 2014

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Sinus Bradycardia Sinus Bradycardia Sinus Bradycardia Sinus Bradycardia

RhythmRhythmRhythmRhythm P-P and R-R intervals regular

RateRateRateRate less than 60 bpm

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

PR intervalPR intervalPR intervalPR interval normal and constant beat to beat

QRSQRSQRSQRS normal

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

• abnormal with heart disease, MI, medication effects (digoxin, beta blockers, calcium channel blockers, increased intercranial pressure, sick sinus syndrome, hypothyroidism

• SA node

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

• QT may be longer than normal due to slower rate

Mild 45-59 bpm

• probably asymptomatic

Marked 30-45 bpm

• S&S of hemodynamic compromise

• AMI: pulm edema, syncope, ST changes, � bio markers

• assess patient - are they symptomatic? are they stable?

• O2 if indicated

• monitor BP and heart rate

• IV access

• notify MD/NP if symptomatic

• treat the underlying cause

• if asymptomatic no treatment is necessary

• atropine, oxygen, transcutaneous pacing if patient is hemodynamically compromised

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Sinus Arrhythmia Sinus Arrhythmia Sinus Arrhythmia Sinus Arrhythmia

RhythmRhythmRhythmRhythm irregular, phasic with respiration

RateRateRateRate 60-100 bpm but may be slower or faster



QRSQRSQRSQRS normal

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• the rate usually increases with inspiration and decreases with expiration.

• the non respiratory form is present in diseased hearts and sometimes confused with sinus arrest

• medications effects

• SA node and follows normal conduction pathway but fires irregularly

• usually asymptomatic but if bradycardic may have S&S of decreased cardiac output


• monitor

• notify MD/NP if symptomatic

• treat causes


• if symptomatic due to bradycardia atropine may be indicated

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Sinus Tachycardia Sinus Tachycardia Sinus Tachycardia Sinus Tachycardia

RhythmRhythmRhythmRhythm P-P and R-R intervals regular

RateRateRateRate 101-180 bpm



QRSQRSQRSQRS normal


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

• SA node and discharges regularly

• rate related; may be none

• �cardiac output, especially those with CAD

• chest discomfort

• assess patient- are they symptomatic? are they stable?

• O2 if indicated


• IV access

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

• notify MD/NP if persistent or symptomatic

• treat the underlying cause


• for AMI, beta blockers given to slow HR

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Sinus Arrest Sinus Arrest Sinus Arrest Sinus Arrest

RhythmRhythmRhythmRhythm the basic rhythm is regular. The length of the pause is not a multiple of the sinus interval.

RateRateRateRate normal but varies due to the pause

P waveP waveP waveP wave those that are present are normal

PR intervalPR intervalPR intervalPR interval normal

QRSQRSQRSQRS normal


• may also occur with hypoxia, myocardial ischemia or infarction, hyperkalemia, medications, and increased vagal tone

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

• may produce no symptoms

• may cause weakness, lightheadedness, dizziness or syncope


• oxygen if indicated

• IV access

• 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

• if compromised- IV atropine

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

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Sinoatrial Block Sinoatrial Block Sinoatrial Block Sinoatrial Block

RhythmRhythmRhythmRhythm basic rhythm is regular*.

RateRateRateRate normal or bradycardia and varies because of pause

P waveP waveP waveP wave those present are normal


QRSQRSQRSQRS normal

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

• also found with CAD, inferior MI, and due to medications

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

• impulse is blocked as it exits the SA node

• may produce no symptoms

• may cause weakness, lightheadedness, dizziness or syncope


• oxygen if indicated, monitor BP and heart rate

• IV access

• if asymptomatic – observe

• review medications

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

• IV atropine

• call code if acutely decompensating

• asymptomatic - observe

• if hemodynamic compromise is present, atropine may be indicated

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

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Atrial DysrhythmiasAtrial DysrhythmiasAtrial DysrhythmiasAtrial Dysrhythmias

Atrial dysrhythmias originate from an ectopic site (a source other than the SA node) in the atria usually as a result of disorders of impulse formation or impulse conduction. Ectopic P waves will differ in shape from the normal sinus P wave. An increased heart rate decreases the amount of time available for coronary artery perfusion and ventricular filling and can therefore compromise cardiac output.

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Premature Atrial ComplexPremature Atrial ComplexPremature Atrial ComplexPremature Atrial Complex

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

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

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

QRSQRSQRSQRS usually normal

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• 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 before the next SA node impulse is due

• 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)

• assess patient - are they symptomatic?

• are they stable?

• monitor

• reduce stress

• reduce stimulants

• assess electrolytes

• notify MD/NP if frequency increases or patient symptomatic

• PACs usually do not require treatment if they are infrequent

• treatment includes correcting the underlying cause

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

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MultiMultiMultiMulti----formed Atrial Rhythm formed Atrial Rhythm formed Atrial Rhythm formed Atrial Rhythm

RhythmRhythmRhythmRhythm may be irregular as pacemaker site shifts

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

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

PR intervalPR intervalPR intervalPR interval P-R interval varies depending on the site of the pacemaker

QRSQRSQRSQRS usually normal

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

• may also be seen in patients with heart disease and digitalis toxicity

• may also be a precursor to multifocal atrial tachycardia

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

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



• VS, LOC, symptoms

• oxygen prn

• assess contributing meds (digoxin)

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

• transient rhythm that resolves on its own and there is usually no treatment required unless it is caused by digitalis then the drug should be withheld

• vagal maneuvers

• calcium channel blockers to control rate

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Atrial TachycaAtrial TachycaAtrial TachycaAtrial Tachycardiardiardiardia

RhythmRhythmRhythmRhythm regular


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

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

QRSQRSQRSQRS normal


• stimulants

• infection

• electrolyte imbalance

• acute illness

• MI

• series of rapid beats from an irritable site in the atria

• irritable site overrides the SA node and becomes the pacemaker

• often confused with ST


• S&S of decreased cardiac output



• bed rest prn

• oxygen prn, IV access, notify MD/NP if patient symptomatic

• call code if decompensating

• treat underlying cause

• oxygen

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

• adenosine

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Atrial Flutter Atrial Flutter Atrial Flutter Atrial Flutter

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

RateRateRateRate atrial 250-450 bpm; ventricular conduction depends on the capability of the AV junction (usually rate of 150-175 bpm)

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

PR intervalPR intervalPR intervalPR interval not measurable

QRSQRSQRSQRS normal


• usually a paroxysmal rhythm precipitated by a PAC

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

• 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

• rate related


• palpitations, difficulty breathing, fatigue, chest discomfort



• oxygen if indicated

• IV access

• notify MD/NP if symptomatic or new onset

• bed rest prn

• call code if unstable

• 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 can be used

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Atrial Fibrillation Atrial Fibrillation Atrial Fibrillation Atrial Fibrillation

RhythmRhythmRhythmRhythm ventricular rhythm is usually irregularly irregular

RateRateRateRate atrial rate usually between 400-600 bpm.

P waveP waveP waveP wave no identifiable P waves present; erratic, wavy baseline

PR interval PR interval PR interval PR interval not measurable

QRSQRSQRSQRS normal


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

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

• rate related


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


• oxygen prn


• IV access

• bed rest prn

• notify MD/NP if new onset or symptomatic


• 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

• catheter ablation

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SupraventrSupraventrSupraventrSupraventricular Tachycardiaicular Tachycardiaicular Tachycardiaicular Tachycardia


RateRateRateRate greater than 150 bpm

P waveP waveP waveP wave not visible

PR intervalPR intervalPR intervalPR interval usually not measurable

QRSQRSQRSQRS normal


• CAD, HF, thyroid disease, COPD, medications, cocaine, caffeine, structural abnormalities, unknown etiology

• begins above the bifurcation of the bundle of His so include rhythms that begin in the SA node, atrial tissue or the AV junction

• rate related



• bed rest prn


• oxygen prn, IV access

• notify MD/NP if patient symptomatic

• call code if decompensating

• dependent on signs and symptoms

• may include medications (Amiodarone, beta blocker, calcium channel blocker)

• ablation, cardioversion

• vagal maneuvers

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Junctional DysrhythmiasJunctional DysrhythmiasJunctional DysrhythmiasJunctional Dysrhythmias

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 depolarizing normally.

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Premature Junctional ComplexPremature Junctional ComplexPremature Junctional ComplexPremature Junctional Complex

RhythmRhythmRhythmRhythm regular with premature beats

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

PR intervalPR intervalPR intervalPR interval P-R interval less than 0.12 sec if P waves are present

QRSQRSQRSQRS normal

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• 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

• may cause palpitations, skipped beats

• S&S of decreased cardiac output if frequent



• oxygen prn


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

• usually not required.

• treat cause(decrease contributing meds)

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Junctional Escape Beats and Rhythm Junctional Escape Beats and Rhythm Junctional Escape Beats and Rhythm Junctional Escape Beats and Rhythm

RhythmRhythmRhythmRhythm regular with late beats

RateRateRateRate usually within normal range

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

ConductionConductionConductionConduction P-R interval less than 0.12 sec if present.

QRSQRSQRSQRS normal

A junctional escape rhythmjunctional escape rhythmjunctional escape rhythmjunctional escape rhythm is several sequential escape beats.

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• 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)

• often asymptomatic


• hypotension, chest discomfort

• altered LOC, lightheadedness

• SOB


• oxygen prn

• IV access

• review possible contributing medications



• treat cause(decrease contributing meds)

• atropine or pacing (for symptomatic slow rate) to increase ventricular rate

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Accelerated Junctional Accelerated Junctional Accelerated Junctional Accelerated Junctional

RhythmRhythmRhythmRhythm very regular



PR intervalPR intervalPR intervalPR interval P-R interval usually less than 0.12 sec if present

QRSQRSQRSQRS 0.11 sec or less


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

• 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

• IV access


• review meds

• check electrolyes

• treat cause (decrease contributing meds)

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JJJJunctional Tachycardia unctional Tachycardia unctional Tachycardia unctional Tachycardia

RhythmRhythmRhythmRhythm very regular



PR intervalPR intervalPR intervalPR interval P-R interval usually less than 0.12 sec if present

QRSQRSQRSQRS normal


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

• begins in the pacemaker cells of the bundle of His

• caused by enhance automaticity


• “racing heart”

• severe anxiety

• syncope, altered LOC


• oxygen prn

• IV access


• review contributing meds (digoxin)

• treat cause (decrease contributing meds)

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

• vagal maneuver and adenosine (to help distinguish it form other tachycardias)

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Ventricular DysrhythmiasVentricular DysrhythmiasVentricular DysrhythmiasVentricular Dysrhythmias

Ventricular beats and rhythms originate below the bundle of His in a pacemaker site in either 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.

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PPPPremature Ventricular Complexremature Ventricular Complexremature Ventricular Complexremature Ventricular Complex

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


P waveP waveP waveP wave usually obscured by the QRS, PST or T wave of the PVC

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

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


• occur in healthy and diseased hearts

• hypoxia

• stress, anxiety

• exercise


• HF, MI, ACS

• medications

• irritable site in ventricles fire before next expected sinus beat

• often a result of enhanced automaticity

• compensatory pause usually follows PVC

• S&S of decreased cardiac output if frequent

• usually asymptomatic if infrequent

• 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, antiarrhythmics may be indicated

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Ventricular Escape Beat/RhythmVentricular Escape Beat/RhythmVentricular Escape Beat/RhythmVentricular Escape Beat/Rhythm

Ventricular escape beat

Ventricular escape rhythm/idioventricular rhythm

RhythmRhythmRhythmRhythm essentially regular with late beats

RateRateRateRate usually normal but depends on underlying rhythm; 20-40 bpm for idioventricular rhythm

P waveP waveP waveP wave usually absent or with retrograde conduction

PR intervalPR intervalPR intervalPR interval none as originates in the ventricles

QRSQRSQRSQRS 0.12 sec or greater, wide and bizarre; T wave frequently in opposite direction of QRS complex

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• a protective mechanism to protect the heart from more extreme slowing

• may also occur as a result of acute coronary syndrome, digoxin toxicity, or metabolic imbalances

• impulse is generated in the ventricles when the SA node or AV junction fail to initiate an impulse, or becomes slower than the intrinsic rate of the Purkinje fibres

• decrease in cardiac output due to loss of atrial kick

• palpitations, weakness, dizziness, hypotension


• IV access

• O2 if indicated

• IV atropine

• 5B patients - may initiate temp pacing if wires in situ

• call code, CPR if unstable


• improve cardiac output (vasopressors)

• assess contributing medications For idioventricular rhythmFor idioventricular rhythmFor idioventricular rhythmFor idioventricular rhythm:

• establish a normal rhythm

• transcutaneous/epicardial pacing

• medications (epinephrine, dopamine)

• if pulselesspulselesspulselesspulseless, CPR and ACLS guidelines are indicated

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

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Accelerated Idioventricular RhythmAccelerated Idioventricular RhythmAccelerated Idioventricular RhythmAccelerated Idioventricular Rhythm

RhythmRhythmRhythmRhythm essentially regular


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

PR intervalPR intervalPR intervalPR interval none as originates in the ventricles

QRSQRSQRSQRS 0.12 sec or greater; wave frequently in opposite direction of QRS complex

EtioloEtioloEtioloEtiologygygygy ConductionConductionConductionConduction Clinical FeaturesClinical FeaturesClinical FeaturesClinical Features Nursing MgmtNursing MgmtNursing MgmtNursing Mgmt Medical MgmtMedical MgmtMedical MgmtMedical Mgmt

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

• myocardial infarction

• digoxin toxicity

• metabolic imbalances

• cardiomyopathy

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

• intrinsic firing of the ventricles

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

• pale, cool skin

• weakness

• dizziness, hypotension

• altered LOC


• oxygen prn

• IV access


• notify MD/NP

• call code if patient decompensates


• improve cardiac output (vasopressors)

• assess contributing medications

• establish a normal rhythm

• transcutaneous/epicardial pacing

• if pulselesspulselesspulselesspulseless, CPR and ACLS guidelines are indicated

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

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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

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


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

PR intervalPR intervalPR intervalPR interval none

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


• common causes are ACS, cardiomyopathy, 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 sustained VTsustained VTsustained VTsustained VT


• syncope

• assess your patient - are they symptomatic? are they stable?

• if patient has pulsepulsepulsepulse: oxygen, bed rest, IV access, notify MD STAT, monitor closely

• if patient is pulselesspulselesspulselesspulseless or or or or unstableunstableunstableunstable: call code, ABCs, CPR, IV access

• treat underlying cause (IV magnesium or potassium to correct imbalances)

• stablestablestablestable symptomatic patients are treated with oxygen and anti-arrhythmics to suppress the rhythm

• unstableunstableunstableunstable patients are treated with oxygen and synchronized cardioversion

• CPR and defibrillation are used to treat the pulselesspulselesspulselesspulseless patient

ECG Review 2014

36Polymorphic VTPolymorphic VTPolymorphic VTPolymorphic 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 pointes means "twisting about the points."

RhythmRhythmRhythmRhythm may be regular or irregular


P waveP waveP waveP wave absent

PR intervalPR intervalPR intervalPR interval none

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


• anything that decreases oxygen delivery to the ventricles

• bradyarrhthymias, 3 degree block

• excessive antiarrhythmics, haldol

• electrolyte imbalance (hypokalemia, hypomagnesemia)

• congenital LQTS

• liquid protein diets

• CNS disorders

• impulse originates in the ventricles

• less than 30 seconds it is called nonnonnonnon----sustaisustaisustaisustained VTned VTned VTned VT

• greater than 30 seconds it is sustained VTsustained VTsustained VTsustained 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

• call code, ABCs, CPR

• ensure IV access

• notify MRP

• ACLS guidelines, defibrillate

• treat precipitating causes – meds, electrolytes

• ICD for prophylaxis

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

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Ventricular FibrillationVentricular FibrillationVentricular FibrillationVentricular Fibrillation

RhythmRhythmRhythmRhythm chaotic electrical activity with no pattern or regularity

RateRateRateRate unattainable

P waveP waveP waveP wave not discernible

PR intervalPR intervalPR intervalPR interval not discernible

QRSQRSQRSQRS not discernible


• causes include increased SNS activity

• vagal stimulation


• medications

• hypertrophy

• ACS

• HF

• arrhythmias

• MI

• chaotic rhythm originating in the ventricles

• no organized depolarization so no effective ventricular contraction

• 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, loss of consciousness

• death imminent if untreated

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

• assess patient

• call code, ABC, CPR

• IV access

• CPR and defibrillation

• ACLS protocols (ephinephrine, vasopressin, Amiodarone, atropine)

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

RhythmRhythmRhythmRhythm ventricular not discernible

RateRateRateRate no ventricular activity but atrial activity may be seen

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

PR intervalPR intervalPR intervalPR interval not measurable

QRSQRSQRSQRS none


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

• same causes as those of cardiac arrest

• absence of ventricular activity

• some atrial activity may be present

• S&S of absent cardiac output

• pulseless

• assess patient

• 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 resumes

• ACLS protocols

• medications

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Atrioventricular BlocksAtrioventricular BlocksAtrioventricular BlocksAtrioventricular Blocks

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.

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



P waveP waveP waveP wave normal

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

QRSQRSQRSQRS normal

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



• monitor for progression

• notify MD/NP if PRI continues to lengthen

• review contributing meds


• observe for progression to a more advanced AV block

• if result of AMI, monitor closely

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SSSSecond Degree AV Block econd Degree AV Block econd Degree AV Block econd Degree AV Block TTTType Iype Iype Iype I

RhythmRhythmRhythmRhythm atrial regular, ventricular irregular

RRRRateateateate 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

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

QRSQRSQRSQRS normal

EtioloEtioloEtioloEtiologygygygy ConductionConductionConductionConduction Clinical FeaturesClinical FeaturesClinical FeaturesClinical Features Nursing MgmtNursing MgmtNursing MgmtNursing Mgmt Medical MgmtMedical MgmtMedical MgmtMedical Mgmt

• 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

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

• often asymptomatic as ventricular rate is near normal




• 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

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SeconSeconSeconSecond Degree AV Block d Degree AV Block d Degree AV Block d Degree AV Block TTTType IIype IIype IIype II

RhythmRhythmRhythmRhythm atrial regular, ventricular irregular

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

PR intervalPR intervalPR intervalPR interval P-R interval may be normal or prolonged, but it is constant until one P wave is not conducted to the ventricles

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

This is more serious than the Type I block.

Atropine should be avoided as it will not improve the block but will increase the rate of SA node discharge which could trigger a situation where even fewer impulses are conducted through to the ventricles.

EtiologyEtiologyEtiologyEtiology ConductionConductionConductionConduction Clinical FeaturesClinical FeaturesClinical FeaturesClinical Features Nursing MgmtNursing MgmtNursing MgmtNursing Mgmt Medical Medical Medical Medical MgmtMgmtMgmtMgmt

• causes include acute myocarditis, acute anterior MI (left coronary artery supplies bundle branches)

• block usually occurs below the bundle of His or at the level of the bundle branches

• may progress into a third degree block

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



• oxygen prn; IV access



• notify MD/NP ASAP

• 5B – temp pacing prn if PW in situ


• assess contributing medications

• if rate slow pacing may be indicated

• permanent pacemaker

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Third Degree or Complete AV Block Third Degree or Complete AV Block Third Degree or Complete AV Block Third Degree or Complete AV Block

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

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

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

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


• associated with anterior and inferior MIs

• digitalis toxicity

• acute infection

• degeneration of the conductive tissue.

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

• atria and ventricles beat independently of one another

• secondary pacemaker stimulates the ventricles

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



• oxygen prn; IV access

• 5B – temp pacing prn if PW in situ


• notify MD/NP ASAP


• external pacing

• atropine (depending on escape pacemaker)

• permanent pacing for chronic complete heart block.

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Paced RhythmsPaced RhythmsPaced RhythmsPaced Rhythms

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 from 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.

Fusion beats occur when a pacing stimulus and an intrinsic beat partly depolarize the ventricles. A pseudo-fusion beat 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.

Fusion beats

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Analyzing Pacemaker Function Analyzing Pacemaker Function Analyzing Pacemaker Function Analyzing Pacemaker Function

Step OneStep OneStep OneStep One: Identify the intrinsic rate and rhythm: Are P waves present? At what rate? Are QRS complexes present? At what rate?

Step TwoStep TwoStep TwoStep Two: 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:Step Three:Step Three:Step 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 pacemaker or 100% AV paced

100% Atrial paced

100% Ventricular paced

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

Failure to PaceFailure to PaceFailure to PaceFailure to Pace Occurs 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.

EtiologyEtiologyEtiologyEtiology Caused by:

• battery depletion • disconnection in the system • lead fracture • electromagnetic interference • pacemaker turned off or programmed incorrectly

ConductionConductionConductionConduction

• 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. Clinical FeaturesClinical FeaturesClinical FeaturesClinical Features

• hypotension • bradycardia • syncope • chest pain • return of symptoms associated with rhythm for which pacemaker was implanted

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47TreatmentTreatmentTreatmentTreatment Nursing Management

• assess your patient - are they symptomatic? are they stable? • VS, LOC, symptoms • IV access • notify MD/NP • if patient on temp epicardial pacing – check battery, ensure unit is turned on, replace pulse generator, remove any

electromagnetic interference • call code if unstable, CPR

Medical 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. Causes may include battery failure, lead fracture, pacing lead displacement, edema or scar tissue formation at electrode tip, output energy set too low.

Etiology Etiology Etiology Etiology Caused by:

• battery failure

• scar tissue or edema at electrode tip

• lead fracture or displacement

• energy output too low

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• medications

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

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

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

• hypotension

• bradycardia

• syncope

• fatigue TreatmentTreatmentTreatmentTreatment Nursing Management



• reposition patient

• notify MD/NP

• if patient on temp epicardial pacing – check battery, ensure unit is turned on, replace pulse generator, check all connections

• call code if unstable, CPR Medical Management

• adjust pacemaker settings (increase output)

• surgery to replace lead or device

• ACLS guidelines if pulseless or decompensated

Failure to SenseFailure to SenseFailure to SenseFailure to Sense –––– Undersensing Undersensing Undersensing Undersensing 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). Causes include battery failure, lead fracture, pacing lead displacement, edema or scar tissue formation at electrode tip, decreased P wave or QRS voltage, circuitry dysfunction, increased sensing threshold, myocardial perforation.

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• battery failure • scar tissue or edema at electrode tip • lead fracture or displacement • generator sensitivity too low • circuitry dysfunction • myocardial perforation • medications • electrolyte imbalance


• 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

Clinical FeaturesClinical FeaturesClinical FeaturesClinical Features

• c/o skipped beats or palpitations • risk of pacing spike falling on the T wave causing R-on-T

TreatmentTreatmentTreatmentTreatment Nursing Management

• assess your patient - are they symptomatic? are they stable? • VS, LOC, symptoms • reposition patient • notify MD/NP • if patient on temp epicardial pacing – check battery, ensure unit is turned on, replace pulse generator, check all connections

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50Medical Management

• adjust pacemaker settings (increase sensitivity) • pace in asynchronous (fixed) mode until problem fixed • x-ray to determine lead placement • surgery to replace lead or device

Failure to Sense Failure to Sense Failure to Sense Failure to Sense –––– 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.


• 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

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51 Clinical FeaturesClinical FeaturesClinical FeaturesClinical Features

• fatigue • bradycardia • hypotension • syncope

TreatmentTreatmentTreatmentTreatment Nursing Management

• assess your patient - are they symptomatic? are they stable? • VS, LOC, symptoms • reposition patient • notify MD/NP • if patient on temp epicardial pacing – check battery, ensure unit is turned on, replace pulse generator, check all connections

Medical Management

• adjust pacemaker settings (decrease sensitivity) • reprogram settings (increase minimum heart rate)

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ReferencesReferencesReferencesReferences

Aehlert, B. (2013). ECGs Made Easy (5th Ed). St. Louis, Missouri: Mosby Elsevier.

Float Nurse (2013). Retrieved from http://floatnurse-mike.blogspot.ca

Geiter, H. B. (2007). E-Z ECG Rhythm Interpretation. Philidelphia, PA: F.A. Davis Company.

Gertsch, M. (2004). The ECG: a two-step approach to diagnosis. Berlin: Springer-Verlad.

Huff, J. (2012). ECG Workout: Exercises in Arrhythmia Interpretation (6th Ed). Philidelphia, PA: Wolters Kluwer.

Mountain West Digital Library. (n.d.) Retrieved Sept 21, 2011 from http://mwdl.org/index.php/home. RNCeus.com (2009). Home page. Retrieved August 30, 2011 from http://www.rnceus.com/course_frame.asp?exam_id=16&directory=ekg. Yanowitz, F. ( n.d.). Home page: The Alan E. Lindsay ECG learning center in cyberspace. Retrieved August 15, 2011 from http://library.med.utah.edu/kw/ecg/index.html

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