Ecg analysis, july 2011

McGill/CDH Redevelopment Team

Cardiac Electrophysiology

Rhythm Interpretation

Prepared by Kathleen Brownrigg, BSc, RN, MSNNurse Educator, MUHCJuly 2011

Cardiac Electrophysiology – Rhythm Interpretation Page 1


Chapter One: Electrophysiology and the Cardiac Monitor1.0 Cardiac Monitor and significance1.1 Electrical Activity of the Heart1.2 Linking Conduction to the Cardiac Cycle1.3 ECG Paper1.4 Waveform Analysis

1.4.1 The P Wave1.4.2 PR Interval1.4.3 QRS Complex1.4.4 ST Segment1.4.5 T Wave1.4.6 Summary of ECG Interval

1.5 Monitoring Leads1.6 Trouble Shooting

Chapter Two: Basic Rhythm Interpretation2.0 The Ten Step Method of Rhythm Interpretation2.1 Documentation and Thought Provoking Items

Chapter Three: Rhythms3.0 Normal Sinus3.1 Sinus Dysrhythmia3.2 Sinus Bradycardia3.3 Sinus Tachycardia3.4 Premature Atrial Contractions3.5 Supraventricular Tachycardia3.6 Atrial Flutter3.7 Atrial Fibrillation3.8 Junctional Rhythms3.91 Junctional Escape Rhythm3.92 Premature Junctional Contraction3.93 Junctional Tachycardia4.0 Atrioventricular Blocks

4.1.1 First Degree4.1.2 Second Degree4.1.3 Third Degree

5.0 Premature Ventricular Contractions5.1 Ventricular Tachycardia5.2 Ventricular Fibrillation5.3 Idioventricular5.4 Asystole5.5 Pulseless Electrical Activity (PEA)5.6 Electrolyte Imbalances



Reference List Editorial Note

This module was designed to address the learning needs of the nurse who has no prior knowledge of cardiac rhythms and rhythm disturbances. The module does not use the classification outlined in the ACLS standards. In addressing treatment options and management of dysrhythmias, ACLS protocols should be followed.

Learning Objectives

Upon completion of this learning package and participation in classroom instruction the learner will be able to:

Identify each part of the ECG waveform and normal measurement

Employ the 10-step method of ECG interpretation

Identify basic arrhythmias, their etiology and relate clinical significance



Chapter One: Electrophysiology and the Cardiac Monitor

1.0 Cardiac Monitor and Significance

Continuous electronic monitoring is an adjunct to patient care and

assessment

Monitors are not substitutes for appropriate nursing or physician assessment

Monitors and their alarms provide an alert when the patient’s vital signs deviate outside an identified acceptable range

Monitors provide us with the ability to continuously observe the electrical activity occurring within the cardiac muscle

The current generated by the electrical cells radiate from the heart, through the surface of the skin and into the electrodes placed on the chest

The monitor is able to transform the electrical activity into the waveforms that represent the cardiac cycle

It does not replace actual physical assessment, our “hands on” assessment should correlate with the ECG tracing



It is not enough to say the heart tracing is fast, slow or unusual looking but how the patient is tolerating it (pulse, capillary refill, skin color, temp, BP etc)



1.1 The Conduction System of the Heart

The heart’s primary pacemaker is the sino-atrial node located in the right

atrium near the inflow tract of the superior and inferior vena cava. It has an inherent rate of 60-100 beats per minute. The conduction pathways carry the impulse via the internodal tracts through the atrial tissue and down to the atrio-ventricular node. The AV node is located near the intraventricular septum near the tricuspid valve. Impulses are delayed in the AV node for a few milliseconds to allow the ventricles to fill adequately before systole.

Connected to the AV node in the Bundle of His which is made up of thick

conducting nerve fibres. This bundle divides into the right and left bundle branches and carriers current through the ventricles via the Purkinje Fibres. These fibres are embedded in the myocardium causing depolarization and repolarization.

If the SA node fails, the heart has a protective back up system of pacemakers which continue to stimulate the myocardium. The AV node or secondary pacemaker has an intrinsic rate of 40-50 beats per minute.

If the SA node and the AV node both fail then the tertiary pacemaker is found in the Prukinje Fibres. This process is called inherent rhythmicity. The rate is 20-40 breaths per minute and provides minimal perfusion of vital organs. It usually causes serious symptoms.



1.1 Electrical Activity of the Heart

Intracellular and extracellular fluids contain positive and negative ions

These ions enable each cell to initiate and respond to electrical impulses

The ions flow across the cellular wall membrane creating a wave of electrical conduction

The primary ions of importance are Na + , K + and Ca ++

The resting state, known as polarization, there is no electrical activity taking place within the cell K+ is within the cell and Na+

and Ca++ are outside the cell

The discharge state, known as depolarization, the cell is electrically stimulated causing the ions to pass across the cellular membrane The k+ moves out of the cell and the Na+ and Ca++ move in

The recovery state, known as repolarization, the cell is returning to the resting state and is unable to respond to any further electrical stimulation The k+ once again moves back into the cell and the Na+ and Ca++ moves back out (original state)

All three electrical events (polarization, depolarization and repolarization) will lead to visual waveforms on the cardiac monitor and ultimately is responsible for the mechanical contraction of the heart

The cardiac muscle and purkinji cells are very sensitive to K+ and Ca++ influxes,

therefore electrolyte disturbances

can and will grossly affect the ECG

waveforms and the ultimate cardiac function



1.2 Linking conduction to the Cardiac Cycle

1.2 The Principals of Monitoring

The ECG monitor reflects the electrical activity of cardiac cells. On specialized grid/graph paper, electrical activity of the heart is recorded on two planes at either 25 mm/sec, which is the standard, or at 50 mm/sec, an alternative method often used when drug studies are being conducted.

The Horizontal Axis represents the length of each particular electrical event with its duration in time.

One small block represents 0.04 seconds



Five small blocks form the base of a large block, which is shown by heavier lines and represents 0.20 seconds

One may measure the duration of a waveform or segment by counting the number of blocks and comparing with a normal range

Ticks on the top of the paper represent 3-second intervals (15 boxes) this helps when calculating heart rates

The Vertical Axis represents the electrical voltage in millivolts (mV) oramplitude (mm) of each particular event.

The amplitude/height of the wave segment or intervals is calculated by measuring the number of blocks from the isoelectric line to the highest point of the wave segment or interval.

ECG Paper

1.4 Waveform analysis

On the cardiac monitor one normal cardiac cycle includes:



I. The P waveII. The QRS complex (consisting of a Q, R, and S wave)III. The T wave

These units of electrical activity are further broken down into the following intervals or segments:

I. The PR intervalII. The ST segment

The isoelectric line is the baseline of the cycle with no positive or

negative deflections (the polarized state)



1.4.1 The P Wave:

Reflects atrial depolarization First upright deflection Should be a rounded shape without a notch or peak Indicates the SA node initiated an impulse

1.4.2 PR Interval

Represents AV node delay or conduction The time it takes for the atria to contract and expel the remaining (10-

25%) blood into the ventricles, known as the “atrial kick” Normal PR interval in an infant is 0.08 - 0.13 seconds (2-3 small boxes)

and toddler 0.10- 0.14 seconds (2.5 - 4 small boxes) and adult is 0.12- 0.20 seconds (3-5 small boxes)

For simplicity a PR interval is within normal measures if it is between 2-4 small boxes in newborns and small children

1.4.3 QRS Complex

Represents ventricular depolarization Atrial repolarization occurs but its wave is buried in the QRS complex Begins from the first deflection (either +ve or –ve) that follows the P

wave



Normal QRS duration is 0.04- 0.08 sec in infants and small children extending to 0.12 seconds in adults

For simplicity a QRS is within normal measures if less than three small boxes

1.4.4 ST Segment

Connects the QRS complex to the T wave Under normal circumstances should be at the isoelectric line Represents the time it takes for the ventricles to contract and expel

blood into the major arteries

1.4.5 T wave

Represents ventricular repolarization Should be rounded Changes in T wave may indicate electrolyte imbalance or myocardial

infarction

1.4.6 Summary of ECG interval (note adult norms for time)



1.5 Monitoring leads

Cardiac monitoring provides a continuous assessment of a patient’s heart rate and rhythm. Most bedside cardiac monitors provide a three-lead system which allow one view of the heart to be seen. There is also a 5-lead system which allows two simultaneous views of the heart’s activity.

The leads are often red (+ve), white (-ve) and black (ground)

To recall lead placement for the

3 lead system remember “White

on the right” and “smoke above

the fire” (black lead over the red lead on the left)

Lead II is preferred for observing the patients underlying rhythm, as this



lead produces the most upright waveforms and is best for dysrhythmia detection

With the three lead system, either lead II or the Marriott (MCL) lead is used.

Advantages of Lead II:

1 – Allows for clear visualization of the atrial activity– 2 - Allows for upright R waves which is needed for procedures such as cardioversion

Advantages of MCL

1 – Useful to differentiate L vs. R ventricular ectopic2 – Useful in identifying L vs. R bundle branch blocks.

Advantages of 5 Lead System:

Allows viewing of seven possible modified



Leads including lead I, II, III, AVR, AVL, AVF, and V.

The difference between continuous electronic monitoring and 12 Lead ECG is that the former is used for monitoring only, why the latter provides an additional diagnostic tool for the cardiac patient, either for confirmation or ruling out of a cardiac problem, especially myocardial infarction.

A 12-Lead ECG provides 12 different views of the heart instead of one or two.

1.6 Trouble Shooting

Artifact Lines or waveforms produced on the ECG tracing that are not reflective

of the hearts electrical activity

60-cycle interference a thick fuzzy baseline is displayed on the ECG tracing, often caused by

electrical interference

Wandering baseline the tracing intermittently rises and falls

most common causes

Patient movement Hiccups, shivering, seizures and chest movement related to

respirations Improper electrode placement Electrode gel has not dried out Inadequate contact between electrode and skin Skin excoriation under electrode patch Broken monitor lead wires or cracks Room outlets for damaged plugs Electrical interference from other sources (other equipment)

Straight baseline

No ECG tracing is produced!!

your patient for presence of pulse and respirations (your ABCDs)



then, for all the common causes of artifact above

REMEMBER TO TREAT YOUR PATIENT NOT YOUR

MONITOR

Chapter Two: Basic Rhythm Interpretation

Electrocardiography is the process of creating a visual tracing of the electrical activity of the cells in the heart, for the purpose of identifying and analyzing dysrhythmias.



One must use a systematic approach that enables you to assess the rhythm that you are viewing.

Using a consistent method will help to enhance your assessment, confidence and comfort level.

The Chest Disease Hospital will use a 10-Step Method to Rhythm Analysis which is a clear step by step approach.

2.0 The Ten Step Method

1. Assess your A, B, C, and Ds!2. Assess the ventricular heart rate3. Evaluate the regularity of the rhythm4. Assess the P wave 5. Evaluate the PR interval6. Assess the P:QRS 7. Evaluate the QRS complex8. Assess the ST segment 9. Identify the rhythm10. Determine the clinical significance

**Always analyze a 6 second rhythm strip.

1. Assess your patient (C, A, B, Ds)

Circulation, Airway, Breathing, Disability (or Neurological functioning) If your ABC and D’s are not stable, don’t worry about the rhythm

interpretation. Treat your patient first!!!

2. Assess the Heart Rate (HR)



The simplest method for assessing heart rate is the 10 times method Obtain a 6 second rhythm strip (30 boxes) Count the number of QRS in a 6 second strip and multiply by 10 for the

ventricular rate Count the number of P waves in a 6 second strip and multiply by 10 for

the atrial rate This method works for both regular and irregular rhythms Compare the HR with the normal values as well as the patient’s

baseline.

3. Evaluate the Regularity of the Rhythm

Take a second piece of paper and mark the top of consecutive P waves in the strip; one can then compare the distance between each P-P interval on the strip

This same method can be done to compare the highest point of the QRS complex and then compare all the R-R intervals

If these distances are constant and the measured waves are at regular intervals then the rhythm is said to be regular

If the interval varies then the rhythm is considered irregular If irregular, then note how irregular the rhythm is. Does the

irregularity occur in a pattern? Is it only one irregular (premature/delayed) beat.

4. Assess the P wave

Is it present? It should be before the QRS complex Does every P have a QRS following? It should be upright, rounded and look the same throughout (size and

shape)

5. Assess the PR Interval

Locate the PR Interval from the beginning of the P Wave to the beginning of the QRS complex

Count the number of small boxes and multiply this number by 0.04 to obtain actual seconds

The normal PR interval in an adult is 0.12- 0.20 seconds (3-5 small boxes)

6. Assess the P:QRS relationship

This atrial to ventricular association should be 1:1



Is there a P wave preceding every QRS? Is there only one P wave per QRS? Is there only one QRS for every P wave?

7. Evaluate the QRS complex

The most critical assessment parameter (represents ventricular activity)

Are all QRS complexes the same size and shape? What is the duration of the complex? Count the number of boxes from the beginning of the Q wave to the

end of the S wave where it meets the isoelectric line Normal QRS is less than 3 small boxes (0.12 sec.) in an older

child/adult For simplicity a QRS complex should be ‹ 3 small boxes

8. Assess the ST segment/T wave

Please refer to section 4.4.4 and 4.4.5 Observe the S wave as it returns to the isoelectric line Is it elevated or depressed as it rises towards the baseline? Do the T waves look the same throughout (uniform)? T waves should be ¼ to ½ the QRS height Are the T waves positive (upward), inverted, peaked, rounded or flat?

9. Identify the Rhythm

What is the underlying rhythm? Is it fast? Is it slow? Is it regular? Is it irregular, is it sinus? Are there extra beats? Premature ones? Couplets and so on? Are they atrial or ventricular in nature?

10. Determine the Clinical Significance

Correlate your patient assessment with your ECG interpretation How is your patient tolerating the rhythm? Anticipate the interventions that may be necessary

2.1 Documentation and Thought Provoking Items



Documentation is a necessary part of nursing care

One must document their assessment, plan, implementation and evaluation within the charting record

When a patient is on a cardiac monitor, alarm parameters must be verified at shift change with the routine safety check and signed as such on the flow sheet

HR alarm limits should be set at a maximum of 50% above and 35% below the patient’s baseline

The nursing notes should include when the patient was put on a cardiac monitor and why it was indicated

Nursing notes should also include when and why the monitor was discontinued

Six second recording strips should be printed and included in the patient chart once per shift and in the event of a changing rhythm (dated and timed)

Anytime an arrhythmia is noted, document your assessment of any clinical significance to the patient and any action taken

Remember, assess and treat your patient not the monitor……

AND assess your patient well!!

Chapter Six: Rhythms



Abbreviations used for 10 step method: CRT- capillary refill timeWNL- within normal limitsTx- treatmentbpm- beats per minute

3.0 Normal Sinus

10 steps…

1.

2.

3.

4.

5.

6.

7.

8.

9.

10.

3.1 Sinus Dysrhythmia



Also known as a respiratory arrhythmia Inspiration decreases vagal tone and HR↑, expiration increases the

vagal tone and therefore ↓ HR Extreme variances may be due to airway obstruction or increased ICP

10 steps…

1. Warm, pink, CRT≤ 2 seconds, happy, voiding and VS WNL for age2.3. 4.5. 6.7. 8.9. 10.

Tx-

3.2 Sinus Bradycardia

Slower than normal for age May be normal depending on etiology and length of time sustained Negative consequences if sustained for long periods, with a decrease

in cardiac output (CO)

Etiology: During sleep Vagal stimulation (suctioning, vomiting, bearing down etc.) Hypoxia



Anaesthetic agents Electrolyte imbalances Acid-base imbalances Hypoglycaemia Hypothermia Increased ICP Drug toxicity

Sinus Bradycardia10 steps…

1. symptoms range from none to S&S of decreased CO2.3.4.5.6.7.8.9.10.

Tx-

3.3 Sinus Tachycardia

Faster HR than expected

Etiology: Sympathetic stimulation e.g. anxiety, pain, medication



Infection Fever Hypovolemia Anaemia Respiratory distress ↑ activity Hyperthyroidism Myocarditis/ pericarditis Hydrops

Sinus Tachycardia10 steps…

1. Generally well tolerated but may produce S&S associated with ↓CO2.3.4.5.6.7.8.9.10.

Tx –

3.4 Premature Atrial Contraction(PAC)

An early beat that originates in a pacemaker cell of the atria, other than the SA node

Also known as APBs (atrial premature beats)

Etiology:



SNS stimulation (including caffeine) Hypoxia Anxiety/pain Electrolyte imbalances Sepsis Structural heart disease and following open heart (atrial) surgery Hyperthyroidism Digitalis toxicity

PAC10 steps….

1.2.3.4.5.6.7. 8.9.10.

Tx-

3.5 Supraventricular Tachycardia (SVT)

rapid sustained rhythm with a rate 150 – 250 bpm no change in rate despite activity (fixed rate with no variability) if there is only time for one waveform the larger one will be seen; the P

wave is often hidden or stacked within the T wave

Etiology:



70% are idiopathic (cause unknown) Cardiac defects and/or post cardiothoracic surgery Conduction defects such as Wolff-Parkinson-White syndrome Myocarditis Systemic infections

10 steps…1.2.3.4.5.6.7.8.9.10.

Tx

3.6 Atrial Flutter

Increased automaticity of atrial cells or a re-entry mechanism produces a rapid atrial rate > 250 beats per minute

P waves are saw-toothed in shape S&S of ↓ CO may develop due to loss of atrial kick Ventricular rate may be normal, however irregular in rhythm

Etiology



Usually seen post-op cardiothoracic surgery Structural heart disease with dilated atria

10 steps…

1.2.3.4. 5.6.7.8.9.10.

Tx

3.7 Atrial Fibrillation Disorganized state of electrical activity within the atrium Chaotic baseline producing 400-700 depolarizations a minute Ventricular rate WNL, irregular pulse ↓ CO due to loss of atrial kick

Etiology Infection Hypoxia CHD with dilated atria Pericarditis



Digoxin toxicity Electrolyte imbalance Post-op atrial surgery

10 steps…

1.2.3.4.5.6.7.8.9.10.

Tx

3.8 Junctional Rhythms

Rhythms that originate from the AV node. They replace the activity of the SA node when the latter fails,

therefore, the heart’s secondary pacemaker. P waves may be inverted because the atria are depolarized in a

retrograde conduction. P waves can be closer, lost in or follow the QRS complex. PR Intervals are < 0.12 seconds in the P wave precedes the QRS complex.

Junctional arrhythmias can occur in the presence of organic heart disease, atrial ischemia, myocardial infarction, or excessive digitalis.



3.91 Juntional Escape Rhythm Ventricular rate 40-60 bpm QRS duration < 0.12 sec May lead to heart failure and decreased cardiac output

10 Steps

1.2.3.4.5.6.7.8.9.10.

Tx-



3.9.2Premature Junctional Contraction Can be caused by excessive digitalization, Quinidine, or organic heart

disease. PR Interval < 0.12 sec Also called premature nodal contraction

10 Steps

1.2.3.4.5.6.7.8.9.10.

Tx-

3.9.3 Junctional Tachycardia Rate 100-180 bpm Occurs when the AV junction becomes irritable, speeds up and

overrides higher pacemaker sites Rhythm is regular



4.0 Atrioventricular Blocks

Problems associated with the conduction of an impulse through the AV node or bundle branches

Classified upon the severity of conduction disturbance

Types First Degree Heart Block Second Degree Heart block

Type I second degree = Mobitz I= WenckebachType II second degree = Mobitz II

Third Degree Heart Block= Complete Heart Block= AV dissociation

4.1.1 First Degree Heart Block

PR interval is prolonged, due to the atypical delay of conduction as the sinus impulse travels through the AV node

PR interval is prolonged but constant

Etiology Effects of digitalis, propanolol and quinidine Hyperkalemia Hypoxemia CHD Following heart biopsy, cardiac catheterization or surgery Myocarditis, endocarditis or tumors Rheumatic fever, scarlet fever, mumps or rubella ↑vagal tone (e.g. ↑ ICP, ↑ BP or gastric distension)

10 steps…

1.2. 3. 4.5. 6.



7.8.9.10.

Tx

4.1.2 Second Degree Heart Block

Type I second degree = Mobitz I = Wenckebach

More common than Type II Impulses travelling from the atria are delayed progressively,

lengthening the PRI until one is not conducted at all and results in the QRS complex being dropped

Resultant rhythm irregular Usually transient and prognosis is quite good

Etiology Digitalis or propanolol toxicity ↑ Vagal tone Hypoxemia CHD Degenerative cardiomyopathy Myocarditis Post cardiac surgery Acute rheumatic fever During sleep in healthy children

Mobitz I

10 steps…..

1.2.3.4.5.6.7.



8.9.10.

Tx-

Type II second degree= Mobitz II

More advanced and severe than Type I May progress to Third Degree Heart Block AV conduction is “all or none”, there is either normal AV conduction

with a normal PR interval or the conduction is completely blocked The impulses are blocked intermittently or at a fixed ratio (2:1, 3:1

etc) The PR interval is what differentiates Type I from Type II; in Type I

there is a clear warning as the PR interval lengthens, however, in Type II the PR interval remains constant with the QRS being dropped without warning

Etiology Cardiac drugs Hypoxemia ↑ vagal tone Post cardiac surgery Degenerative cardiomyopathy CHD Myocarditis

*more often more serious causes such as ischemia*

Mobitz II

10 steps…1.2.



3.4.5.6.7.8.9.10.

Tx –

4.1.3 Third Degree Heart Block

Known as complete heart block or divorce (most severe block) No communication between the atria and the ventricles May be congenital requiring a pacemaker within first few days of life The ventricles or AV node generate their own impulses to compensate

and improve CO

Etiology Congenital ( 2° to intrauterine infection, maternal Lupus or connective

tissue disorders) Following cardiac surgery (initially due to swelling or later due to

stunted tissue growth related to scar) Poorly controlled diabetes Collagen disorders Cardiomyopathy, Myocarditis Metabolic disorders Tumors, structural diseases Digitalis toxicity

Third Degree Block



10 steps…

1.2.3.4.5.6.7.8.9. 10.

Tx-

5.0 Premature Ventricular Contractions

Ventricle is a little irritable The increased automaticity of the ventricular cell generates an

electrical impulse, sooner than the expected sinus impulse Produces an earlier wide QRS complex This earlier beat has less stroke volume and often feels like a skipped

beat May have one irritable focus (unifocal) or more than one (multifocal)

which is more serious May occur with increased frequency or regularity causing a pattern

Etiology

Healthy children CHD Hypoxia Electrolyte or acid-base imbalance (hypokalemia, hypocalcemia,

hypomagnesemia, acidosis) Post open heart surgery, inflammation of the heart, cardiac trauma Medications (those that stimulate the Sympathetic Nervous System

e.g. caffeine, epinephrine, aminophylline, dopamine etc.) Invasive lines (central lines, PICC lines, UVCs etc.)



Sympathetic response, stress

10 steps….

1.2.3.4.5. 6.7. 8.9.10.

Tx-



5.10 Ventricular Tachycardia

PVCs are often the precursors to VT Increased irritability of the ventricle causing the ventricles to fire at a

rate close to 200 The longer, more sustained and faster the rhythm, the more dangerous

Etiology

electrocution medications, digitalis toxicity CHD, post open heart surgery, myocarditis Hypoxia Acidosis Electrolyte imbalances

10 steps…

1.2.3.4.5.6.7.8.9. 10.

Tx-

5.2 Ventricular Fibrillation Chaotic, irregular depolarization of the ventricles producing no CO



No discernable P waves or regular QRS complexes seen, only wavy baseline

Lethal yet quickly reversed if defibrillator available

Etiology Post cardiac surgery VT may lead to VF if not terminated Electrolyte imbalances Hypoxia Acidosis Drug ingestions Electrocution

10 steps…

1.2.3.4.5.6.7.8.9.10.

Tx-

5.3 Idioventricular

The dying heart



Ventricular escape mechanism (Purkinje Fibres) takes over pacing in the absence of a higher focus (the SA node and AV junction)

Etiology

Rheumatic fever Myocarditis Severe hypoxia Prolonged vagal stimulation Digitalis toxicity Overdose/ ingestion Hypothermia Idiopathic

10 steps…

1.2.3.4.5.6.7.8.9.10.

Tx-

5.4 Asystole

Also known as ventricular standstill All electrical activity ceases, no exchange of ions



Cannot defibrillate asystole Patients rarely go directly from NSR to asystole, there is usually a

gradual slowing before stopping e.g. the idiopathic rhythm Treatment prognosis is poor; the goal is to prevent the conditions that

cause asystole

Etiology Hypoxia Hyperkalemia Hypokalemia Hypothermia Acidosis Drug overdose

10 steps…

1. Assess your ABCDs Confirm asystole in more than one lead (what appears like

asystole in one lead could be fine VF that may have a chance of converting with defibrillation)

Rule out a technical problem

2. Once asystole confirmed….Forget the 10 steps and start CPR with epinephrine!!

5.5 Pulseless Electrical Activity (PEA)

Organized electrical activity is on the ECG with absent pulses Includes electromechanical dissociation (EMD) Treated the same as asystole



Etiology

Severe hypoxemia Severe acidosis Severe hypovolemia Tension pneumothorax Cardiac tamponade Profound hypothermia Drug ingestions

Tx-

5.6 Electrolyte Imbalances

Electrolyte imbalances most frequently associated with ECG changes include abnormal potassium, calcium and magnesium levels.

Hyperkalemia (serum K+↑)

peaked T wave

Most common ECG change is tall and peaked T waves (monitor may double count HR due to large T waves)

Additional findings may include:-elevated ST segments-widened or flattened P waves-widened QRS complexes-more frequent PVCs and other ventricular arrhythmias

elevated ST segments



Hypokalemia (serum K+↓)

T wave is generally flat or inverted Presence of another wave after the T wave, known as a U wave PR interval may be prolonged QRS may be wide

Hypercalcemia (serum Ca+2 ↑)

QT interval shorter than normal Prolonged PR Interval Severe cases, AV blocks may occur

Hypocalcemia (serum Ca+2 ↓)

Prolonged QT interval



T waves may become flatter

Various wave

patterns indicative of electrolyte imbalances, acid/base disturbances, hypoxia, ischemia, drug ingestions etc.



Remember to assess and treat your patient not the monitor …..AND assess your patient well!!!

Reference List



Aehlert, B. (2002). ECGs Made Easy (2nd ed.). Toronto: Mosby.

Bloedel-Smith, J., Ley, S.J., Curley, M.A., Elixon, E.M., & Dodds, K.M. (1996). Tissue Perfusion. In M.A. Curley, J. Bloedel-Smith & P.A. Moloney-Harmon, Critical Care Nursing of Infants and Children (pp. 155-178). Toronto: W.B. Saunders Company.

Chameides, L., & Hazinski, M.F. (Eds.). (1997). Pediatric Advanced Life Support. American Heart Association.

Chernecky, C. (2002). Real World Nursing Survival Guide: ECGs & the Heart. Toronto: W.B. Saunders Company.

Curley, M.A. (1995). Pediatric Dysrhythmias. London: Prentice Hall.

Dibert, C., & Marville-Williams, C. (2002). Basic Rhythm Interpretation and Intervention. Mississauga: Trillium Health Centre.

van Doornik, N., Edmond, L., & Bruce, E. (2002). Basic Pediatric ECG Interpretation- Level 1. Toronto: Hospital for Sick Children.

Hazinski, M.H. (1999). Nursing Care of the Critically Ill Child . St. Louis: Mosby.

Pilcher, J. (1998). Pocket Guide to Neonatal EKG Interpretation. California: NICU Ink Book Publishers. Sansoucie, D.A., & Cavaliers, T.A. (1997), Transition from Fetal to Extrauterine Circulation. Neonatal Network, 16(2), 5-11.

Slota, M.C.(1998). Core Curriculum for Pediatric Critical Care Nursing . Pennsylvania: W.B. Saunders Company.

Tappero, E.P., & Honeyfield, M.E. (1996). Physical Assessment of the Newborn: A Comprehensive Approach to the Art of Physical Assessment: (2nd ed.). California: NICU Ink Book Publishers.


Ecg analysis, july 2011

Health & Medicine

rhythm disturbances

mcgillcdh redevelopment

mcgillcdh redevelopment

cardiac monitor1

sa node

basic rhythm interpretation2

cardiac cycle1

sinoatrial node