Ch.

7 Dysrhythmias

Introduction
 Dysrhythmia interpretation is a fundamental skill
of critical care nurses
 Crucial for early nursing and medical
interventions
 Automaticity
o Cardiac muscle can generate its own
electrical activity
o Special group of cells generate the
automatic impulse
 Cardiac cycle is composed of two activities:
o Electrical (caused by automaticity)
observed on the monitor
o Mechanical (muscular) known as a
contraction

Cardiac Conduction Pathway

Cardiac Cycle
  Two phases of electrical activity
 Depolarization = active
 Repolarization = resting
 ECG is evidence of electrical activity, not contraction
 Electrical activity precedes & causes mechanical activity
 Two mechanical responses
 Systole = active
 Diastole = resting (this is when the
coronary arteries are filling via the
coronary sinus)
 Depolarization = systole = contraction
 Repolarization = diastole = resting or filling phase
 Electrical + mechanical = cardiac contraction

Cardiac Action Potential

 Depolarization
o Na outside cell; K inside the cell
o Change cell permeability
o Na enters cells; K leaves cells
o Ca++ slowly enters
o ATP needed to move electrolytes back to
resting state
 Repolarization begins

Normal Electrical Conduction

 SA node (sinus node)
 AV node
 Conduction
 Bundle of His
 Right and left bundle branches
 Purkinje fibers
 Depolarization = stimulation = systole
 Repolarization = relaxation = diastole

Cardiac Conduction Pathway

 SA node = inherent rate 60 to 100 beats/min
o Depolarization begins
o Atrial contraction or atrial kick (20% cardiac output)
 Intra-atrial and inter-nodal pathways to AV node
 AV node = 40 to 60 beats/min
o Delays impulse to ventricles; allows for filling
o Back-up pacemaker
 Bundle of His = 15 to 40 beats/min
 Left and right bundle branches
 Purkinje fibers

Cardiac Monitoring
 Record and interpret 6-second strip every 4
hours
 Monitor for ST segment changes
 Monitor for dysrhythmias
 Daily 12-lead ECG for cardiac patients
 Graph paper
o Used to standardize tracings
o Vertical boxes measure
voltage/amplitude
o Horizontal boxes measure changes
over time

Measuring Rates and Intervals

 Calculate both atrial and ventricular rates
 Atrial rate = P-P intervals
 Ventricular rate = R-R intervals
 Check P, Q, R, S, and T waveforms
 Each waveform has unique shape
 Comparison of waveform on 6-second strip
 Check for correct sequence of each waveform
 Measure PR interval
 Measure QRS interval
 Measure QT interval

ECG
 P wave
 QRS complex
 T wave
 U wave
 PR interval
 ST segment
 QT interval
 TP interval
 PP interval
 Electrode placement
o Electrode adhesion
 Types of ECG
 ECG interpretation

ECK Graph and Measurement

Duration of Each Segment

Determining Heart Rate and Rhythm

Normal Sinus Rhythms

Relationship Between Electrical Stimulation & Contraction

Rhythm Interpretation
  Dysrhythmia is abnormal cardiac rhythm; preferred term
o Arrhythmia means no rhythm
 Grouped by anatomic areas
o SA node
o Atria
o AV node
o Ventricles
o AV blocks

12 Lead ECG
 The standard three limb leads are I, II, and
III. Limb leads are placed on the arms and
legs.
 These leads are bipolar, meaning that a
positive lead is placed on one limb and a
negative lead on another.
 The bipolar limb leads form Einthoven’s
triangle. This is an equilateral upside-down
triangle with the heart in the center.
 aVR = from heart to right arm
 aVL = from heart to left arm
 aVF = from heart to left foot
 Hexaxial reference system

 Lead I
o Records the magnitude and
direction of current flow between
the negative lead on the right arm to
the positive lead on the left arm.
 Lead II
o Records activity between the
negative lead on the right arm and
the positive lead on the left leg.
o
 Lead III
o Records activity from the negative
lead on the left arm to the positive
lead on the left leg.

Precordial Chest Leads

  The six precordial leads (also called chest leads) are positioned on the chest wall directly over the heart.
These leads provide a view of cardiac electrical activity from a horizontal plane rather than the frontal
plane view of the limb leads.
 Precise placement of these leads is crucial for providing an accurate representation and for comparing
with previous and future ECGs. A misplaced V lead can result in erroneous or missed diagnoses of acute
coronary syndrome and lethal dysrhythmias.
 The precordial leads are unipolar, with a positive electrode and the AV node as a center reference.
Landmarks for placement of these leads are the intercostal spaces, the sternum, and the clavicular and
axillary lines. Positions for these six leads are as follows:
 V1: Fourth intercostal space, right sternal border
 V2: Fourth intercostal space, left sternal border
 V3: Halfway
between V2 and V4
 V4: Fifth intercostal
space, left
midclavicular line
 V5: Fifth intercostal
space, left anterior
axillary line
 V6: Fifth intercostal
space, left
midaxillary line

 Posterior and right

ventricular
electrodes are not
commonly part of
the standard 12-lead
ECG; however, if
indicated, newer ECG machines can record tracings from these areas.

 The 15-lead ECG is an essential

additional assessment that is made
if the patient is suspected of
having an inferior myocardial
infarction, because right
ventricular and posterior
infarctions are common with this
type of infarct.

Heart Rate Variability: Sinus rhythm

  Rate varies with respirations; Inspire = increase the R-R interval; Expire = decrease the R-R interval;
Considered to be the most healthy rhythm due to a greater parasympathetic tone

Sinus Tachycardia
 Sinus rhythm with a rate of 100 to 150 beats/min
 Causes: stimulants, exercise, fever, and alterations in fluid status
 Assess for symptoms of low cardiac output
 Why might prolonged tachycardia result in heart failure?  Heart gets tired

Examples of Unstable Atrial Tachycardias

 Atrial tachycardias: do not originate in SA node
o Atrial fibrillation (thready pulse present)
o Atrial flutter (pulse present)
o Paroxysmal atrial tachycardia (pulse present)
o Re-entry supraventricular tachycardia (SVT) (pulse present)
o Wide-complex tachycardia of an uncertain type (pulse may or may not be present)
Symptomatic Unstable Tachycardia
 Non-sinus in origin
 Heart beating so rapidly that CO is reduced, leading to pulmonary edema, coronary ischemia, and
impaired systemic blood flow to vital organs
 Heart beating so ineffectively that lack of coordination between atria & ventricles reduce CO
 No atrial kick: 20% of stroke volume
 Signs & Symptoms: hypotension, altered mental status, signs of shock, ischemic chest discomfort, AHF

Accelerated Junctional Rhythm and Junctional Tachycardia

 Rhythm initiated from the AV junction
 Rate is 60 to 100 beats/min for accelerated junctional tachycardia
 Rate is greater than 100 beats/min for junctional tachycardia
 The normal intrinsic rate for the AV node and junctional tissue is 40 to 60 beats per minute, but rates
can accelerate.
 An accelerated junctional rhythm has a rate between 60 and 100 beats per minute, and the rate for
junctional tachycardia is greater than 100 beats per minute.
 Patient response: Patient may have a decrease in cardiac output and hemodynamic instability,
depending on the rate.
 Causes: SA node disease, ischemic heart disease, electrolyte imbalances, digitalis toxicity, and
hypoxemia can be causes.
 Care and treatment: Assess and treat the tachycardia if the patient is hemodynamically unstable. Alert
the provider of the change in rhythm.

Premature Junctional Contractions

  Early beats initiated by AV junction
 P-wave changes
 PR interval is shorter than normal
 Usually a noncompensatory pause
 Irritable areas in the AV node and junctional tissue can generate premature beats that are earlier than
the next expected beat.
 These premature beats are similar to PACs but with characteristics of a junctional beat. The
regularity of the underlying rhythm is interrupted by the premature junctional beat.

Premature Atrial Contractions (PACs)

 Early beats initiated in atrium
 Premature P wave
 P waves and PR interval may vary
 P wave may be buried in T wave
 Causes: stress, caffeine; no treatment

Atrial Flutter
 Ectopic foci (other SA node) in atria, heart disease
 Classic “sawtooth” pattern
 Atrial rate fast and regular (250 to 350 beats/min) with AV block
 Degree of conduction varies; may be 1:3, 1:4, etc.
o i.e. 1:3: 1 ventricular contraction for every 3 atrial contractions

Atrial Fibrillation
 Erratic impulse formation in atria
 No discernible P wave (atria are “fibrillating” or quivering)
 Irregular ventricular rate (called “ventricular response”)
 Aberrant (abnormal) ventricular conduction can occur
 Results in loss of atrial kick
 High risk for pulmonary or systemic emboli
 Treatment with blood thinner (warfarin, Coumadin)

Paroxysmal Supraventricular Tachycardia (PSVT)

 Without warning, Heart rate 150 to 250 beats/min
 Regular rhythm, P waves (if present) may merge in T waves
 AV block, QRS complex width is normal
 Hemodynamic effects vary
 If it comes & goes, called “paroxysmal”

Atrial Dysrhythmias
 Increased automaticity in the atria outside the SA node
 P-wave changes
 Causes:
o Stress o Cocaine
o Electrolyte imbalances o Hypothermia
o Hypoxia o Hyperthyroidism
o Atrial injury o Alcoholism
o Digitalis toxicity o Pericarditis
 Paroxysmal Atrial Tachycardia:
When PSVT is sustained….
 Then the rhythm is called Supraventricular Tachycardia (SVT)

Unstable Tachycardia
 KEY TO MANAGEMENT:
o Determine whether pulses are present.
o Rapid recognition of whether patient is symptomatic or unstable.
o Identify whether the patient’s tachycardia is producing hemodynamic instability/signs&
symptoms OR whether the signs/symptoms (pain & distress during AMI) are causing the
tachycardia.
o In absence of poor LV function, a HR > 150 is an inappropriate response to other common
causes of tachycardia, i.e. fever, dehydration, hypotension, anemia, postoperative pain
Symptomatic Tachycardia with Pulse
Secure patent airway, oxygen, cardiac
monitor, vitals, O2 saturation

IV access, 12-LEAD EKG

IF SYMPTOMATIC: SYNCHRONIZED 50-100 J; synchronized electricity delivered

CARDIOVERSION: to R wave

class IV ANTIARRHYTHMIC CAUSING TRANSIENT HEART BLOCK IN THE AV

NODE

IF QRS COMPLEX NARROW, CONSIDER VERY SHORT HALF LIFE, 6 MG RAPID IV PUSH WITH NS FLUSH; SECOND
ADENOSINE: DOSE: 12 MG; CAUSES BRIEF VENTRICULAR ASYSTOLE

USED OFTEN TO TREAT SYMPTOMATIC SVT, AFIB, AFLUTTER

Synchronized Cardioversion
 Abnormally fast heart rate (tachycardia) or cardiac arrhythmia is converted to a normal rhythm using
electricity or drugs.
 Uses a therapeutic dose of electric current to the heart at a specific moment in the cardiac cycle. Click on
‘SYNC’ button.

Tachydysrhythmia Treatment
 Heart rate > 100/min
 Assess whether tachycardia is stable or non-stable
 STABLE SINUS TACHYCARDIA:
o Generated by the SA node
o Usually does not exceed 120-130/min
o Gradual onset & termination
o Lose atrial kick during diastole
o Treat cause: fever, blood loss, hypotension, dehydration, pain, anemia, anxiety
o If AMI present, this is a compensatory tachycardia. CO will fall and further deteriorate cardiac
function. Beta-blockers contraindicated!

Stable Sinus Tachycardia

 IF RHYTHM IS SINUS TACHYCARDIA, CONSIDER CAUSE AND TREAT, WHICH SHOULD
RESOLVE THE RHYTHM:
o This rhythm is due to a physiologic response to extrinsic factors
o ST is generated through a high degree of sympathetic physiologic tone
 o Resolve with treatment of cause: need for IV fluids, blood transfusions, analgesia, anti-anxiety
medication, acetaminophen

Sinus Bradycardia
 Sinus rhythm with rate less than 60 bpm
 Causes: vaso-vagal maneuver, drugs, ischemia, ↑ ICP; normal in physically fit & athletes
 Produce various hemodynamic responses

 What signs and symptoms would you see?

 What drugs cause bradycardia?

Bradydysrhythmia Treatment
 Secure patent airway, oxygen, cardiac monitor, vitals, O2 saturation
 IV access, 12-LEAD EKG
 EKG RHYTHM: SINUS OR 3RD DEGREE HEART BLOCK?
 IF SIGNS & SYMPTOMS PRESENT: hypotension, altered mental status, signs of shock, ischemic
chest discomfort, heart failure -> ATROPINE 0.5 MG BOLUS, REPEAT Q 3-5 MIN; MAX DOSE 3
MG
 IF INEFFECTIVE, consider transcutaneous pacing
 EXPERT CONSULT
 CONSIDER TRANSVENOUS PACING via subclavian vein
 BRADYCARDIA: HR < 60/MIN
 MULITPLE CAUSES: DETERMINE CONTEXT
 DECIDE IF SYMPTOMS ARE DUE TO SLOW HR
 SYMPTOMATIC BRADYCARDIA:
o Symptoms: chest discomfort/pain, sob, decreased loc, weakness, fatigue, light-headedness,
dizziness, syncope
o Signs: hypotension, orthostatic hypotension, diaphoresis, pulmonary congestion, frank hf or
pulmonary edema, frequent pvc’s or vtach

Atrioventricular Blocks
  Block of conduction from atria to ventricles
 Coronary artery disease
 Myocardial infarction (e.g., inferior wall)
 Infections
 Enhanced vagal tone
 Drug effects (e.g., digoxin toxicity)
 AV block, which is also known as heart block, refers to an inability of the AV node to conduct sinus
impulses to the ventricles in a normal manner.
 AV blocks can cause a delay in conduction from the SA node through the AV node, or completely block
conduction intermittently or continuously.
 AV blocks may arise from normal aging of the conduction system or be caused by damage to the
conduction system from ischemic heart disease.
 Always assess for decreased cardiac output and treat cause
 Four types:
o First-degree block
o Second-degree block, Mobitz type I Wenckebach
o Second-degree block, Mobitz type II
o Third-degree block (complete)

First Degree Block

 Delayed conduction from SA node to AV node
 Prolonged PR interval
 Greater than 0.20 seconds
 Same PR interval for each beat
 First-degree AV block describes consistent delayed conduction through the AV node or the atrial
conductive tissue.
 It is represented on the ECG as a prolonged PR interval.

Second-Degree Block: Mobitz Type I

 Steadily lengthening PR interval
 Nonconducted P waves
 PP interval regular
 RR interval irregular
 QRS normal
  Self-limiting; rarely progresses
 May decrease cardiac output
 Also called Mobitz I or Wenckebach phenomenon, second-degree AV block type I is represented on the
ECG as a progressive lengthening of the PR interval until there is a P wave without a QRS complex.
 The AV node progressively delays conduction to the ventricles, resulting in a longer PR interval until
finally a QRS complex is dropped.
 The PR interval following the dropped QRS complex is shorter than the PR interval preceding the
dropped beat. By not conducting this one beat, the AV node recovers and is able to conduct the next
atrial impulse.
 If dropped beats occur frequently, it is useful to describe the conduction ratio, such as 2:1, 3:1, or 4:1.

Second-Degree Block: Mobitz Type II

 More severe AV block
 Often associated with bundle branch block
 PR interval is fixed
 PP interval is regular
 Occasional P wave not followed by QRS
 What is the danger of this block?
 Second-degree AV block type II (Mobitz II) is a more critical type of heart block that requires early
recognition and intervention.
 The conduction abnormality occurs below the AV node, either in the bundle of His or the bundle
branches. A P wave is generated but is not conducted to the ventricles for one or more beats.
 There is no progressive lengthening of the PR interval, which remains the same throughout with the
exception of the dropped beat(s).
 Second-degree block type II is often associated with a bundle branch block and a corresponding
widened QRS complex; however, narrow QRS complexes may be observed.
 Second-degree block type II can progress to the more clinically significant third-degree block and may
cause the patient to be symptomatic.
Third-Degree Block (Complete)
 Atria and ventricles beat
independently of each other
 P waves not associated with QRS
complex
 PP intervals regular
 RR intervals regular
 Junctional or ventricular escape
rhythms
 May need pacemaker
 Hemodynamic status based on
ventricular rate
 Third-degree block is often called
complete heart block because no
atrial impulses are conducted
through the AV node to the
ventricles.
 The block in conduction can occur
at the level of the AV node, the bundle of His, or the bundle branches.
 In complete heart block, the atria and ventricles beat independently of each other because the AV node
is completely blocked to the sinus impulse and it is not conducted to the ventricles.
 Only an escape rhythm arises from the junctional tissue or the ventricles.
 The atria beat at one rate, and the ventricles beat at a different rate. The atrial rate is dictated by the SA
node. The ventricular rate is slow, and usually only a ventricular or junctional escape rhythm is present.
No communication exists between the atria and ventricles. Third-degree block is a type of AV
dissociation.
Ventricular Dysrhythmias
  Impulses initiated from ventricles outside of the normal conduction pathway
 Depolarization does occur, but from ectopic foci, leading to abnormally wide QRS complex
 Common causes:
o Myocardial ischemia, injury, and infarction
o Low potassium or magnesium
o Hypoxia
o Acid-base imbalances

Premature Ventricular Contractions (PVCs)

 Wide and bizarre beats
 Compensatory pause
 Patterns:
o Bigeminy
o Trigeminy
o Couplets
o Triplets
 Wide, bizarre QRS complex greater than 0.10 second
 Irregular rhythm
 Compensatory pause
 Absent P waves because the atria are not contracting

Unifocal Premature Ventricular Contractions

 Unifocal: PVCs have same morphology
 Assess and treat cause of ventricular irritability:
o Hypoxia
o Ischemia
o Electrolyte imbalance
 May need antiarrhythmic agents

Multifocal Premature Ventricular Contractions

 Multifocal = 2 or more different foci
 More unstable
Premature Ventricular Contractions
 Bigeminy: PVC every other beat; In this case, unifocal origin in ventricles

 Couplet: 2 consecutive PVCs, from same foci

 3 PVCs in a row from same foci; more likely to deteriorate- this is often criteria for ventricular
tachycardia
  R on T phenomenon: PVC emerges during repolarization (vulnerable period); could trigger ventricular
tachycardia or ventricular fibrillation

 ...or R on T phenomenon leading to ventricular fibrillation

Ventricular Tachycardia
 Rapid, life-threatening dysrhythmia
 Three or more PVCs in a row
 Fast rate (>100 beats/min)
 Initiated by ventricles
 Wide QRS complex; greater than 0.10 second
 Usually regular
 May or may not have pulse
o Treat pulseless same as ventricular fibrillation
 Hypotension: significant loss of cardiac output
 Frequent PVCs
 Unifocal shape
 3 or more in a row
 Could lead to R on T
 PVC falls into the vulnerable refractory period of the T wave during repolarization
 Ventricular tachycardia or fibrillation can result
Ventricular Fibrillation
 Chaotic pattern, called a lethal dysrhythmia
 No discernible P, Q, R, S, or T waves
 Coarse versus fine ventricular fibrillation
 No cardiac output; life threatening
 Emergent defibrillation for either coarse or fine fibrillation
 Coarse & Fine Ventricular Fibrillation

Course

Fine
Critical Thinking Challenge
 The nurse is talking with the patient. Suddenly, the nurse looks up at the monitor and sees a ventricular
fibrillation pattern.
 Next steps?
o Rhythm below looks like coarse ventricular fibrillation.

Idioventricular Rhythm
 Escape ventricular rhythm from Purkinje fibers
 Rate 15 to 40 beats/min
 Regular rhythm, Wide QRS interval, No P waves
 Do not give lidocaine!

Torsades de pointes
 Torsades de pointes (“twisting about the point”) is a type of VT that is caused by a prolonged QT
interval. Unlike VT, where the QRS complex waveforms have similar shapes, torsades de pointes is
characterized by the presence of both positive and negative complexes that move above and below the
isoelectric line. This lethal dysrhythmia is treated as pulseless VT. Magnesium deficiency is often a
cause of this dysrhythmia. The dysrhythmia can often be prevented by routine measurement of the
 QT/QTc intervals, especially if the patient is receiving drugs that prolong the QT interval. Increases in
QT/QTc interval are reported to the provider, potential drug-related causes are explored, and magnesium
levels are monitored and corrected.

Ventricular Standstill
 Asystole; may have started out as ventricular fibrillation
 No P, Q, R, S, or T waveforms
 Assess in two leads: Why?
 No cardiac output, leads to death if untreated
 Tx: epinephrine; always increase IV fluids after bolus

Pulseless Electrical Activity (PEA)

 Pt has a rhythm but no pulse
o Hypoxia o Tablets (overdose)
o Hypovolemia o Tamponade (cardiac)
o Hypothermia o Tension pneumothorax
o H+ ions (acidosis) o Thrombosis (coronary)
o Hypokalemia or hyperkalemia o Thrombosis (pulmonary)
Emergency Transcutaneous Pacemaker

Bradydysrhythmia Treatment
 Transcutaneous pacing: external delivery of electrical current to stimulate depolarization
o Symptomatic bradycardia
o Heart block
o Myocardial stunning post-AMI

Implantable Pacemakers
 Internal device that delivers electrical impulses to regulate the heart rhythm or to reproduce that rhythm.
 Electrodes placed into the heart, the electronic circuitry and the power supply are implanted (internally)
within the body.
 Pacemakers may function continuously and stimulate the heart at a fixed rate or at an increased rate
during exercise.
 A pacemaker can also be programmed to detect too long a pause between heartbeats and then stimulate
the heart. (on demand)
 Requires minor surgery. Need to stay in the hospital for a day or two. Back to normal activities within a
few days.
 Complications
o Local infection
o Bleeding, hematoma
o Hemothorax
o Ventricular ectopy
o Perforation of ventricular muscle
o Cardiac tamponade
o “Twiddlers” syndrome: malfunction of a
pacemaker due to manipulation of the
device and the subsequent dislodging of the
leads from their intended location.
 Nursing Management: Implanted
o Limit mobility of arm on side of implant for first 24 hours
o Encourage mobility – early ambulation
o Deep breathing
o Pain management
o Prevent infection
Epicardial Pacemakers
 Temporary pacemaker leads are placed on the epicardium—the outer layer of heart muscle—during
cardiac surgery.
o Provide quick access to a temporary pacemaker's pulse generator in case of dysrhythmia in early
postop period.
 Typically 4 wires are placed, attaching one positive and one negative
electrode to both the right atrium and the right ventricle before the
chest is closed.
o The physician loosely sutures the leads onto the epicardium and
threads the wires through to the outside of the chest via small,
stab-like incisions.
o Careful handling of epicardial pacing wires is paramount to
patient's safety.
 Life Pak to Pacer mode

Atrial Pacing

Ventricular Paced Rhythm

Pacemaker Modes