Chapter 38
Dysrhythmias
Dysrhythmias
• Abnormal cardiac rhythms are termed
dysrhythmias.
• Prompt assessment of dysrhythmias and the
patient’s response to the rhythm is critical.
38-2
Properties of Cardiac Cells
• Automaticity- ability to initiate an impulse
spontaneously and continuously
• Excitability- ability to be electrically stimulated
• Conductivity- ability to transmit an impulse along
a membrane in an orderly manner
• Contractility- ability to respond mechanically to
an impulse
38-3
Nervous System
Control of the Heart
• Autonomic nervous system controls
 Rate of impulse formation
 Speed of conduction
 Strength of contraction
38-4
Nervous System
Control of the Heart (Cont.)
• Parasympathetic nervous system: Vagus nerve
 Decreases rate
 Slows impulse conduction
 Decreases force of contraction
• Sympathetic nervous system
 Increases rate
 Increases force of contraction
38-5
Electrocardiogram (ECG) Monitoring
• Graphic tracing of electrical impulses produced
by the heart
• Waveforms of ECG represent activity of charged
ions across membranes of myocardial cells.
38-6
Phases of Cardiac Action Potential
• Please review action potential
38-7
Lead Placement (Cont.)
38-8
Lead Placement (Cont.)
38-9
ECG Paper
• Rhythm strip provides documentation of patient’s
rhythm.
• Allows for measurement of complexes and
intervals and assessment of dysrhythmias
38-10
Assessment of Cardiac Rhythm
38-11
Calculating Heart Rate (HR)
A variety of methods can be used to calculate the
HR from an ECG. The following can be used,
count:
 Number of QRS complexes in 1 minute. or
 R-R intervals in 6 seconds, and multiply by 10. or
 Number of small squares between one R-R interval,
and divide this number by 1 500. or
 Number of large squares between one R-R interval,
and divide this number by 300.
38-12
Assessment of Cardiac Rhythm (Cont.)
38-13
Normal Sinus Rhythm
38-14
Normal Electrical Pattern
38-15
Evaluation of Dysrhythmias
• Holter monitoring
• Event recorder monitoring
• Exercise treadmill testing
• Signal-averaged ECG
• Electrophysiological study
38-16
Sinus Bradycardia
• Sinus node fires <60 bpm
• Normal rhythm in aerobically trained athletes
and during sleep
38-17
Sinus Bradycardia (Cont.)
• Clinical associations
 Occurs in response to
• Carotid sinus massage
• Valsalva manoeuvre
• Increased vagal tone
• Administration of certain medications
38-18
Sinus Bradycardia (Cont.)
• Clinical associations (cont.)
 Occurs in disease states
• Hypothyroidism
• Increased intracranial pressure
• Inferior wall myocardial infarction (MI)
38-19
Sinus Bradycardia (Cont.)
• Clinical significance
 Dependent on symptoms
• Hypotension
• Pale, cool skin
• Weakness
• Angina
• Dizziness or syncope
• Confusion or disorientation
• Shortness of breath
38-20
Sinus Bradycardia (Cont.)
• Treatment
 Atropine
 Pacemaker may be required
 Epinephrine or dopamine infusions
38-21
Permanent Pacemakers
38-22
Sinus Tachycardia
• Discharge rate from the sinus node is increased
as a result of vagal inhibition and is >100 bpm.
38-23
Sinus Tachycardia (Cont.)
• Clinical associations
 Associated with physiological and psychological
stressors
• Exercise
• Fever, pain
• Hypotension
• Hypovolemia
• Anemia
• Hypoxia
38-24
Sinus Tachycardia (Cont.)
• Clinical associations (Cont.)
 Associated with physiological and psychological
stressors (Cont.)
• Hypoglycemia
• MI
• Heart failure
• Hyperthyroidism
• Anxiety, fear
38-25
Sinus Tachycardia (Cont.)
• Clinical significance
 Dizziness, dyspnea, and hypotension due to
decreased cardiac output (CO)
 Increased myocardial oxygen consumption may lead
to angina.
38-26
Sinus Tachycardia (Cont.)
• Treatment
 Determined by underlying cause
• -adrenergic blockers, adenosine, or calcium channel
blockers to reduce HR and myocardial oxygen consumption
• Analgesics to treat pain
38-27
Atrial Flutter
• Atrial tachydysrhythmia identified by recurring,
regular, sawtooth-shaped flutter waves
• Originates from a single ectopic focus
38-28
Atrial Flutter (Cont.)
• Clinical associations: Usually occurs with
 CAD
 Hypertension
 Mitral valve disorders
 Pulmonary embolus
 Chronic lung disease
 Cor pulmonale
 Cardiomyopathy
 Hyperthyroidism
 Medications: digoxin, quinidine, epinephrine
38-29
Atrial Flutter (Cont.)
38-30
Atrial Flutter (Cont.)
• Clinical significance
 High ventricular rates (>100) and loss of the atrial
“kick” can decrease CO and precipitate HF
 Risk for stroke due to risk of thrombus formation in
the atria
38-31
Atrial Flutter (Cont.)
• Treatment
 Primary goal is to slow ventricular response by
increasing AV block
• Medications to slow HR: calcium channel blockers, adrenergic blockers
• Electrical cardioversion may be used to convert the atrial
flutter to sinus rhythm emergently and electively.
38-32
Atrial Flutter (Cont.)
• Treatment (Cont.)
 Primary goal is to slow ventricular response by
increasing AV block (Cont.)
• Antidysrhythmic medications (e.g., amiodarone,
propafenone) to convert atrial flutter to sinus rhythm or to
maintain sinus rhythm
• Radiofrequency catheter ablation can be curative therapy for
atrial flutter.
38-33
Atrial Fibrillation
• Total disorganization of atrial electrical activity
due to multiple ectopic foci, resulting in loss of
effective atrial contraction
• Most common dysrhythmia
• Prevalence increases with age
38-34
Atrial Fibrillation (Cont.)
• Clinical associations: Usually occurs with
underlying heart disease
 Rheumatic heart disease
 CAD
 Cardiomyopathy
 Hypertension
 HF
 Pericarditis
38-35
Atrial Fibrillation (Cont.)
• Clinical associations: Often acutely caused by
 Thyrotoxicosis
 Alcohol intoxication
 Caffeine use
 Electrolyte disturbances
 Stress
 Cardiac surgery
38-36
Atrial Fibrillation (Cont.)
38-37
Atrial Fibrillation (Cont.)
• Clinical significance
 Can result in decrease in CO due to ineffective atrial
contractions (loss of atrial kick) and rapid ventricular
response
 Thrombi may form in the atria as a result of blood
stasis.
 An embolus may develop and travel to the brain,
causing a stroke.
38-38
Atrial Fibrillation (Cont.)
• Treatment
 Goals
• Decrease ventricular rate.
• Prevent cerebral embolic events.
 Medications for rate control: calcium channel blockers
(e.g., diltiazem) and β-adrenergic blockers (e.g.,
metoprolol)
 Long-term anticoagulation therapy
38-39
Atrial Fibrillation (Cont.)
• Treatment (Cont.)
 For some patients, conversion to sinus rhythm may
be considered.
• Antidysrhythmic medications used for conversion:
procainamide, ibutilide, amiodarone, vernakalant
• The nurse must determine that the patient has had atrial
fibrillation or atrial flutter for less than 48 hours.
38-40
Atrial Fibrillation (Cont.)
• Treatment (Cont.)
 Radiofrequency catheter ablation
38-41
Premature Ventricular
Contractions (PVCs)
• Contraction originating in ectopic focus of the
ventricles
• Premature occurrence of a wide and distorted
QRS complex
• Multifocal, unifocal, ventricular bigeminy,
ventricular trigeminy, couplet, ventricular
tachycardia, R-on-T phenomena
38-42
Premature Ventricular
Contractions (Cont.)
• Clinical associations
 Stimulants: caffeine, alcohol, nicotine, aminophylline,
epinephrine, isoproterenol, and digoxin
 Electrolyte imbalances
 Hypoxia
 Fever
 Exercise
 Disease states: MI, mitral valve prolapse, HF, CAD
38-43
Premature Ventricular
Contractions (Cont.)
38-44
Premature Ventricular
Contractions (Cont.)
• Clinical significance
 In normal heart, usually benign
 In heart disease, PVCs may decrease CO and
precipitate angina and HF if >10/minute.
• Monitor patient’s response to PVCs.
• PVCs often do not generate a sufficient ventricular
contraction to result in a peripheral pulse.
 Represents ventricular irritability
38-45
Premature Ventricular
Contractions (Cont.)
• Treatment
 Based on cause of PVCs
• Oxygen therapy for hypoxia
• Electrolyte replacement
• Other treatment according to symptoms
38-46
Ventricular Fibrillation (VF)
• Severe derangement of the heart rhythm
characterized on ECG by irregular undulations
of varying contour and amplitude
• No effective contraction or CO occurs.
38-47
Ventricular Fibrillation (Cont.)
• Clinical associations
 Acute MI, CAD,
cardiomyopathy
 May occur during
cardiac pacing or
cardiac catheterization
 May occur with
coronary reperfusion
after fibrinolytic
therapy
 Accidental
electric shock
 Hyperkalemia
 Hypoxia
 Acidosis
 Drug toxicity
38-48
Ventricular Fibrillation (Cont.)
38-49
Ventricular Fibrillation (Cont.)
• Clinical significance
 Unresponsive, pulseless, and apneic state
 If not treated rapidly, death will result.
38-50
Ventricular Fibrillation (Cont.)
• Treatment
 Assessment of circulation, airway, and breathing
(CAB)
 Immediate initiation of cardiopulmonary resuscitaiton
(CPR) and advanced cardiac life support (ACLS)
measures with the use of defibrillation and definitive
medication therapy
38-51
Asystole
• Represents total absence of ventricular electrical
activity
• No ventricular contraction (CO) occurs because
depolarization does not occur.
38-52
Asystole (Cont.)
• Clinical associations
 Advanced cardiac disease
 Severe cardiac conduction system disturbance
 End-stage HF
38-53
Asystole (Cont.)
• Clinical significance
 Unresponsive, pulseless, and apneic state
 Prognosis for asystole is extremely poor.
38-54
Asystole (Cont.)
• Treatment
 CPR with initiation of advanced cardiac life support
(ACLS) measures
38-55
Pacemakers
• Used to pace the heart when the normal
conduction pathway is damaged or diseased.
 Pacing circuit consists of a power source, one or
more conducting (pacing) leads, and the myocardium.
38-56