Cardiac arrhythmias are irregular heartbeats resulting from abnormal electrical conduction, manifesting in various forms such as sinus tachycardia, bradycardia, atrial flutter, atrial fibrillation, and ventricular tachycardia. Management strategies vary based on the type of arrhythmia and patient stability, often including medication, cardioversion, or pacemaker insertion. Nursing interventions focus on monitoring symptoms, administering appropriate medications, and educating patients to improve outcomes.

1. CARDIAC
ARRYTHMIAS
BRENDA NABAWANUKA(BSN,MSN,SWS Fellow)

2. DEFINITION
• Also known as cardiac dysrhythmias, are abnormal electrical
conduction or automatic changes in heart rate and rhythm.
• They vary in severity, from those that are mild, asymptomatic, and
require no treatment to catastrophic ventricular fibrillation, which
necessitates immediate resuscitation.
• It can be the result of a primary cardiac disorder, a response to a
systemic condition, the result of electrolyte imbalance, or drug
toxicity.

3. ECG

4. EKG

5. Electrocardiogram

6. The Electric Conduction System Of The Heart

7. SINUS TACHYCARDIA
• Sinus tachycardia is a heart rate greater than 100 beats per
minute originating from the sinus node.
• Rate: 100 to 180 beats per minute
• P waves precede each QRS complex
• PR interval is normal
• QRS complex is normal
• Conduction is normal
• Rhythm is regular

8. CAUSES OF SINUSTACHYCARDIA
• may include
• Exercise,
• Anxiety
• Fever
sinus tachycardia is often asymptomatic.
Management, however is directed at the treatment of the primary cause.
Carotid sinus pressure (carotid massage) or a beta-blocker may be used
to reduce heart rate.
• drugs
• anemia,
• heart failure,
• hypovolemia, and shock.

9. SINUS BRADYCARDIA
• is a heart rate of less than 60 beats per minute and originates from the sinus
node (as the term “sinus” refers to the sinoatrial node. It has the following
characteristics
• Rate is less than 60 beats per minute
• PWaves precede each QRS complex
• PR interval is normal
• QRS complex is normal
• Conduction is normal
• Rhythm is regular

10. ECG With Labels

11. CAUSES OF SINUS BRADYCARDIA
1. Drugs
2. vagal stimulation
3. hypoendocrine states
4. hypothermia, or sinus node involvement in MI.
5. This arrhythmia may be normal in athletes as they
have quality stroke volume.

12. MANIFESTATIONS OF SINUS BRADYCARDIA
• It is often asymptomatic but manifestations may include:
syncope(fainting or passing out)
fatigue
dizziness.
• Management includes treating the underlying cause and administering
anticholinergic drugs like atropine sulfate as prescribed

13. ATRIAL FLUTTER
• is an abnormal rhythm that occurs in the atria of the heart.
Atrial flutter has an atrial rhythm that is regular but has an
atrial rate of 250 to 400 beats/minute. It has sawtooth
appearance. QRS complexes are uniform in shape but
often irregular in rate.
• Normal atrial rhythm
• Abnormal atrial rate: 250 to 400 beats/minute
• Sawtooth P wave configuration
• QRS complexes uniform in shape but irregular in rate

14. Sawtooth Pattern

15. Causes Includes
• heart failure
• tricuspid valve or mitral valve diseases
• pulmonary embolism
• cor pulmonale
• inferior wall MI
• carditis and digoxin toxicity.

16. MANAGEMENT
• Management if the patient is unstable with ventricular rate of greater
than 150 bpm, prepare for immediate cardioversion.
• If patient is stable, drug therapy may include calcium channel blocker,
beta-adrenergic blockers, or antiarhythmics.
• Anticoagulation may be necessary as there would be pooling of
blood in the atria

17. ATRIAL FIBRILLATION
• is disorganized and uncoordinated twitching of atrial musculature caused
by overly rapid production of atrial impulses.
• This arrhythmia has the following characteristics:
• Atrial Rate: 350 to 600 bpm
• Ventricular Rate: 120 to 200 bpm
• P wave is not discernible with an irregular baseline
• PR interval is not measurable
• QRS complex is normal
• Rhythm is irregular and usually rapid unless controlled.

18. Atrial Fibrillation ilustration

19. Clinical Manifestations And Mgt
• Atrial fibrillation may be asymptomatic but clinical
manifestation may include palpitations, dyspnea, and
pulmonary edema.
Nursing goal is towards administration of prescribed
treatment to decrease ventricular response, decrease
atrial irritability and eliminate the cause.

20. CAUSES
• includes
• atherosclerosis,
• heart failure,
• congenital heart disease,
• chronic obstructive pulmonary disease,
• hypothyroidism and thyrotoxicosis

21. Premature Junctional Contraction (PJC)
• occurs when some regions of the heart becomes excitable than normal. It has
the following characteristics.
• PR interval less than 0.12 seconds if P wave precedes QRS complex
• QRS complex configuration and duration is normal
• P wave is inverted
• Atrial and ventricular rhythms irregular
• .

22. Premature Junctional Contraction (PJC)

23. Causes Of PJC
• may include
• myocardial infarction or ischemia
• digoxin toxicity
• excessive caffeine or amphetamine use

24. Management
• correction of underlying cause
• discontinuation of digoxin if appropriate.

25. Atrioventricular Blocks
• AV blocks are conduction defects within the AV junction that
impairs conduction of atrial impulses to ventricular pathways.
• The three types are
first degree
 second degree
 third degree.

26. FIRST DEGREE HEART
BLOCK
Rate is usually 60 to 100 bpm
PR intervals are prolonged for
usually 0.20 seconds
QRS complex is usually normal
Rhythm is regular
.

27. CAUSES
• First degree AV block is asymptomatic and may be caused by
• inferior wall MI or ischemia
• hyperkalemia
• hypokalemia
• digoxin toxicity
• calcium channel blockers,
• amiodarone and use of antidysrhythmics

28. . Management
• Includes correction of underlying cause.
• Administer atropine if PR interval exceeds 0.26 second
or symptomatic bradycardia develops

29. SECOND DEGREE AV BLOCK MOBITZ I (WENCKEBACH)
• Atrial rhythm is regular
• Ventricular rhythm is irregular
• Atrial rate exceeds ventricular rate
• PR interval progressively but only slightly, longer with each
cycle until QRS complex disappears (dropped beat)

30. 2nd
Heart Degree Block
• PR Interval shorter after dropped
beat.
• .Treatment includes correction of
underlying cause, atropine or
temporary pacemaker for
symptomatic bradycardia and
discontinuation of digoxin if
appropriate.

31. Clinical Manifestations
• include vertigo
• weakness,
• irregular pulse.
• This may be caused by
• Inferior wall MI
• cardiac surgery
• acute rheumatic fever
• vagal stimulation

32. Second Degree AV Block Mobitz II
• Atrial rhythm is regular
• Ventricular rhythm maybe regular or irregular depending on the degree
of block
• P-P interval constant
• QRS complex periodically absent or disappears

33. Clinical Manifestations
• Same As Mobitz I.
• Causes Includes:
• Severe Coronary Artery Diseases
• AnteriorWall MI
• Acute Myocarditis
• Digoxin Toxicity.

34. Treatment
• includes:
• Atropine
• epinephrine,
• dopamine for symptomatic bradycardia.
• Discontinuation of digoxin if appropriate.
• Installation of pacemaker

35. Third Degree AV Block (Complete Heart Block)
• Atrial rhythm regular
• Ventricular rhythm regular and rate slower than atrial rate
• No relation between P waves and QRS complexes
• NO constant PR interval
• QRS interval normal or wide and bizarre

36. Manifestations
•include hypotension,
•angina,
•heart failure

37. Causes
• This May Be Caused By
• Congenital Abnormalities,
• Rheumatic Fever,
• Hypoxia, MI, Lev’s Disease,
• Lenegre’s Disease And Digoxin Toxicity

38. Management
• includes atropine, epinephrine, and dopamine for bradycardia.
Installation of pacemaker may also be considered.

39. PREMATUREVENTRICULAR CONTRACTIONS (PVC)
• Early or premature ventricular contractions are caused by increased automaticity of ventricular
muscle cells.
• PVCS usually are not considered harmful but are of concern if more than six occur in 1 minute, if
they occur in pairs or triplets if they are multifocal or if they occur or near a t wave.

40. • Atrial rhythm is regular
• Ventricular rhythm is irregular
• QRS complex premature, usually followed by a complete compensatory pause
• QRS complex is also wide and distorted, usually >0.14 second.
• Premature QRS complexes occurring singly, in pairs, or in threes

41. CLINICAL MANIFESTATIONS
• Includes
• palpitations
• Weakness
• lightheadedness but it is most of the time asymptomatic.

42. MANAGEMENT
• includes assessment of the cause and treat as indicated.
• Treatment is indicated if the client has underlying disease because PVCs may precipitate
ventricular tachycardia or fibrillation.
• Assess for life threatening PVCs.Administer antiarrhythmic medication as prescribed.

43. Ventricular Tachycardia
• Ventricular tachycardia (VT) is three or more consecutive PVCs. it is con
medical emergency because cardiac output (CO) cannot be maintained b
decreased diastolic filling (preload)
• Rate is 100 to 250 beats per minute
• P wave is blurred in the QRS complex but the QRS complex has no asso
P wave.
• PR Interval is not present
• QRS complex is wide and bizarre;T wave is in the opposite direction
• Rhythm is usually regular

44. CLINICAL MANIFESTATIONS
• ofVT includes
• lightheadedness
• weakness
• dyspnea and unconsciousness.

45. Causes
• includes MI
• Aneurysm
• CAD
• rheumatic heart
diseases
• mitral valve prolapse
• Hypokalemia
• Hyperkalemia
• pulmonary embolism.
• Anxiety may also causedVT.

46. PULSELESSVENTRICULAR TACHYCARDIA
• Management for PulselessVT: Initiate cardiopulmonary resuscitation; follow ACLS
protocol for defibrillation, ET intubation and administration of epinephrine or
vasopressin
• Ventricular Tachycardia with Pulse

47. Management With PulseVT
If hemodynamically stable, follow ACLS protocol for
administration of amiodarone, if ineffective, initiate synchronized
cardioversion.

48. Ventricular Fibrillation
• Ventricular fibrillation is rapid, ineffective quivering of ventricles that may be
rapidly fatal.
• Rate is rapid and uncoordinated, with ineffective contractions
• Rhythm is chaotic
• QRS complexes wide and irregular
• P wave is not seen
• PR interval is not seen

49. Causes
• of ventricular fibrillation is most commonly myocardia ischemia
or infarction.
• It ma result from untreated ventricular tachycardia, electrolyte
imbalances, digoxin or quinide toxicity, or hypothermia.

50. clinical manifestations
• may include loss of consciousness, pulselessness, loss of blood
pressure, cessation of respirations, possible seizures and sudden
death.
• Start CPR is pulseless. Follow ACLS protocol for defibrillation,
ET intubation and administration of epinephrine or vasopressin

54. Nursing Management
• Nursing care planning for patients with cardiac arrhythmia due to
digitalis toxicity includes prompt assessment of the patient’s
condition, prompt treatment of symptoms, and investigation of the
cause.

55. Nursing Problem Priorities
• The following are the nursing priorities for patients with cardiac
arrhythmias:
• Treat life-threatening dysrhythmias.
• Assess and identify cause or precipitating factors.
• Providing patient education and health teachings.

56. Nursing Problem Priorities
• The following are the nursing priorities for patients with
cardiac arrhythmias:
• Treat life-threatening dysrhythmias.
• Assess and identify cause or precipitating factors.
• Providing patient education and health teachings.

57. Nursing Assessment
• Assess For The Following Subjective And Objective Data:
• Heart Rate.Assessing The Heart Rate Is Essential To Identify
The Presence And Type Of Dysrhythmia.
• Variations From The Normal Range Can Indicate Tachycardia
(Fast Heart Rate) Or Bradycardia (Slow Heart Rate),Which Are
Common Dysrhythmias.
• .

58. • Rhythm. Determining the regularity or irregularity of the
heart rhythm is crucial in identifying dysrhythmias.
• Blood pressure. Measuring and monitoring blood pressure
provides information about the patient’s hemodynamic
stability and helps detect any abnormalities associated with
dysrhythmias, such as hypertension or hypotension

59. • Dysrhythmias can impair cardiac output and lead to variations in blood
pressure, indicating compromised cardiovascular function.
• Assess for factors related to the cause of cardiac arrhythmias:
• Altered electrical conduction
• Reduced myocardial contractility
• Nursing Diagnosis
• Decreased cardiac output

60. Nursing Goals
• The client will maintain/achieve adequate cardiac output with blood
pressure and pulse within the normal range, appropriate urinary
output, palpable pulses of equal quality, and a normal level of
mentation.
• The client will experience a reduced frequency or absence of
dysrhythmias.
• The client will actively engage in activities that decrease the workload
on the heart.

61. • The client will demonstrate understanding of their prescribed
medication, including interactions with other drugs or
substances, and recognize the importance of adhering to the
prescribed regimen.
• The client will identify signs of digitalis overdose and developing
heart failure, and promptly report them to the physician

62. • The client will exhibit no signs of drug toxicity and maintain
serum drug levels within an acceptable range specific to the
individual.
• The client, if utilizing a pacemaker, will comprehend their
condition, prognosis, and the function of the pacemaker.

63. • The client will recognize signs of pacemaker failure.
• The client will verbalize understanding of their therapeutic regimen.
• The client will list the desired actions and potential adverse side effects of
their medications.
• The client will correctly perform necessary procedures and provide
explanations for their actions.

64. Nursing Interventions And Actions
• Cardiac arrhythmias are disturbances in the normal heart rhythm.
• Nursing interventions for managing these conditions involve monitoring and
managing symptoms, administering medications and treatments, and providing
patient education.
• The aim is to control the arrhythmia, prevent complications, and improve the
patient’s quality of life.
• Effective nursing care also involves working closely with the healthcare team to
develop an individualized care plan and ensure proper communication and
coordination of care.

65. NURSING INTERVENTIONS AND ACTIONS CONT..
• Managing Impaired Cardiac Function
• Monitoring Diagnostic Procedures and Laboratory Studies
• Administering Medications and Providing Pharmacological Interventions
• Preventing Digitalis Toxicity & Poisoning
• Reducing Anxiety
• Providing Perioperative Nursing Care
• Providing Patient Education and Health Teachings

66. PHARMACOLOGICAL INTERVENTIONS
• Administer supplemental oxygen as indicated.
• Increases the amount of oxygen available for myocardial uptake, which decreases
irritability caused by hypoxia.
• 2. Potassium
• Dysrhythmias are generally treated symptomatically. Correction of hypokalemia may be
sufficient to terminate some ventricular dysrhythmias. Potassium imbalance is the number
one cause of atrial fibrillation.
• 3.Antidysrhythmics
• Antidysrhythmic are medications used to regulate heart rhythm and treat various types of
arrhythmias.These include:

67. CLASS I DRUGS
• Class I drugs depress depolarization and alter repolarization, stabilizing the cell.
These drugs are divided into groups a, b, and c, based on their unique effects.
• These drugs increase action potential, duration, and effective refractory period
decrease membrane responsiveness, prolonging both QRS complex and QT
interval.
• Useful for the treatment of atrial and ventricular premature beats, and repetitiv
arrhythmias (atrial tachycardias and atrial flutter or fibrillation). Myocardial
depressant effects may be potentiated when class Ia drugs are used in conjunct
with medications possessing similar properties.

68. CLASS IA DRUGS:
• disopyramide (Norpace),
• procainamide (Pronestyl, Procan SR)
• quinidine (Quinaglute, Cardioquin)
• These drugs shorten the duration of the refractory
period (QT interval), and their action depends on the
tissue affected and the level of extracellular potassium.

69. Class Ib
• Class Ib: lidocaine (Xylocaine), phenytoin (Dilantin), tocainide
(Tonocard), mexiletine (Mexitil); moricizine (Ethmozine)
• Drugs of choice for ventricular dysrhythmias are also effective
for automatic and reentrant arrhythmias and digitalis-induced
dysrhythmias.These drugs may aggravate myocardial depression

70. Class Ic
• Class Ic: flecainide (Tambocor), propafenone (Rythmol), encainide (Enkaid)
• These drugs slow conduction by depressing SA node automaticity and decreasing
conduction velocity through the atria, ventricles, and Purkinje fibers.
• The result is a prolongation of the PR interval and a lengthening of the QRS
complex.
• They suppress and prevent all types of ventricular dysrhythmias. Flecainide
increases the risk of drug-induced dysrhythmias post-MI. Propafenone can worsen
or cause new dysrhythmias, a tendency called the “proarrhythmic effect.”
• Encainide is available only for patients who demonstrated good results before the
drug was removed from the market.

71. CLASS II DRUGS
• atenolol (Tenormin), propranolol (Inderal), nadolol (Corgard), acebutolol (Sectral),
esmolol (Brevibloc), sotalol (Betapace); bisoprolol (Zebeta)
• Beta-adrenergic blockers have antiadrenergic properties and decrease automaticity.
Therefore, they are useful in the treatment of dysrhythmias caused by SA and AV
node dysfunction (SVTs, atrial flutter, or fibrillation).
• These drugs may exacerbate bradycardia and cause myocardial depression, especially
when combined with drugs that have similar properties.

72. CLASS III DRUGS:
• bretylium tosylate (Bretylol), amiodarone (Cordarone), sotalol (Betapace),
ibutilide (Corvert)
• These drugs prolong the refractory period and action potential duration,
consequently prolonging the QT interval.
• They are used to terminate ventricular fibrillation and other life-threatening
ventricular dysrhythmias or sustained ventricular tachyarrhythmias,
especially when lidocaine and procainamide are not effective

73. CLASS III …..
• Sotalol is a nonselective beta-blocker with characteristics of both class II and class III.

74. CLASS IV DRUGS
• verapamil (Calan), nifedipine (Procardia), diltiazem (Cardizem)
• Calcium antagonists (also called calcium channel blockers) slow
conduction time through the AV node (prolonging PR interval) to
decrease ventricular response in SVTs, and atrial flutter/fibrillation.
• Calan and Cardizem may be used for bedside conversion of acute atrial
fibrillation.

75. • 3.5. ClassV drugs: atropine sulfate, isoproterenol (Isuprel)
• Miscellaneous drugs are useful in treating bradycardia by increasing SA and AV
conduction and enhancing automaticity.
• 4. Cardiac glycosides: digoxin (Lanoxin)
• Cardiac glycosides may be used alone or in combination with other antiarrhythmic drugs
to reduce ventricular rate in the presence of uncontrolled or poorly tolerated atrial
tachycardias or flutter and fibrillation. First-line treatment for paroxysmal
supraventricular tachycardia (PVST).

76. • 5.Adenosine (Adenocard)
• Slows conduction and interrupts reentry pathways in the AV node. Note: Contraindicated in patients with second or third-
degree heart block or those with sick sinus syndrome who do not have a functioning pacemaker.
• 4. Preventing Digitalis Toxicity & Poisoning
• Preventing digitalis toxicity and poisoning is essential in patients with cardiac arrhythmias who are taking digoxin to control
their heart rate. Digitalis toxicity can cause serious side effects such as nausea, vomiting, and arrhythmias, which can worsen
the patient’s condition. Regular monitoring of the patient’s digoxin levels and symptoms of toxicity is necessary to prevent
adverse reactions and ensure safe and effective treatment.
• 1. Discuss the necessity of periodic laboratory evaluation:

77. PROVIDING PERIOPERATIVE NURSING CARE
• Assist with insertion and maintenance of pacemaker function.
• 2. Prepare for invasive diagnostic procedures and surgery as
indicated.
• 3. Prepare for implantation of a cardioverter or defibrillator
(ICD) when indicated.
• This device may be surgically implanted in those patients with
recurrent, life-threatening ventricular dysrhythmias
unresponsive to tailored drug therapy.

78. PROVIDING PATIENT EDUCATION AND HEALTH
TEACHINGS
• Assess the patient and significant other‘s (SO) level of knowledge and ability and desire to
learn.
• 2. Be alert to signs of avoidance: changing the subject away from information being
presented or extremes of behavior (withdrawal or euphoria).
• 4. Provide information in written form for the patient/SO to take home.
• 5. Reinforce explanations of risk factors, dietary and activity restrictions, medications, and
symptoms requiring immediate medical attention.

79. • Encourage identification and reduction of individual risk factors: smoking and alcohol consumption, and
obesity.
• Review normal cardiac function and electrical conduction.
• Explain and reinforce specific dysrhythmia problems and therapeutic measures to the patient and SO.
• Identify adverse effects and complications of specific dysrhythmias: fatigue, dependent edema,
progressive changes in mentation, and vertigo.
• .

80. • Encourage the development of a regular exercise routine, avoiding overexertion. Identify
signs and symptoms requiring immediate cessation of activities: dizziness,
lightheadedness, dyspnea, and chest pain.
• Review individual dietary needs and restrictions: potassium, and caffeine.