This document discusses various cardiac dysrhythmias including their causes, characteristics, signs and symptoms, and treatment. It begins with an overview of the normal cardiac conduction system and electrocardiogram. It then defines dysrhythmias as abnormal cardiac rhythms and lists common causes. Several specific dysrhythmias are described in detail including sinus bradycardia, sinus tachycardia, premature atrial contractions, paroxysmal supraventricular tachycardia, atrial flutter, atrial fibrillation, and junctional dysrhythmias. For each, the document outlines defining features on ECG, potential signs and symptoms, and recommended treatment approaches.

1. DYSRRHYTHMIAS
ANIE GLADSTIN G.L
MSC NURSE
LECTURER

2. INTRODUCTION
• NORMAL CONDUCTION SYSTEM
• Conduction System Four properties of cardiac cells enable the conduction
system to start an electrical impulse, send it through the cardiac tissue, and
stimulate muscle contraction. The heart’s conduction system consists of
specialized neuromuscular tissue located throughout the heart. A normal
cardiac impulse begins in the sinoatrial (SA) node in the upper right atrium.
It spreads over the atrial myocardium via interatrial and internodal
pathways, causing atrial contraction. The impulse then travels to the
atrioventricular (AV) node, through the bundle of His, and down the left
and right bundle branches. It ends in the Purkinje fibers, which transmit the
impulse to the ventricles.

6. ECG
• An electrocardiogram is a record of the electrical activity of the heart
over a period of time.

8. DYSRHYTHMIA
• Abnormal cardiac rhythms, called dysrhythmia.
• Dysrhythmia is a disorder of the formation or the electrical impulses
within the heart.

9. SITES OF ORGIN OF DYSRHYTHMIA
• Sinoatrial Node
• Atria
• Atrioventricular Node
• Ventricles

10. COMMON CAUSES OF DYSRHYTHMIAS
• Cardiac Conditions
• Accessory pathways
• Cardiomyopathy
• Conduction defects
• Heart failure
• Myocardial ischemia, infarction
• Valve disease

11. • Other Conditions
• Acid-base imbalances
• Alcohol
• Caffeine, tobacco
• Connective tissue disorders
• Drug effects (e.g., antidysrhythmia drugs, stimulants, β-adrenergic blockers)
or toxicity
• Electric shock
• Electrolyte imbalances (e.g., hyperkalemia, hypocalcemia) • Emotional
crisis
• Herbal supplements
• Hypoxia
• Metabolic conditions (e.g., thyroid dysfunction)
• Sepsis, shock
• Toxins

12. Types of Dysrhythmias
SINUS BRADYCARDIA
• Sinus bradycardia is a sinus node dysfunction with a rate that is lower than
normal. In humans, bradycardia is generally defined to be a rate of under
60 beats per minute. .A normal heartbeat in human is usually at a rate of 60
to 100 beats per minute.

13. SIGNS AND SYMPTOMS
• The decreased heart rate can cause a decreased cardiac output resulting
in symptoms such as lightheadedness, dizziness, hypotension, vertigo,
and syncope. Bradycardia is not necessarily problematic. People who
practice sports may have sinus bradycardia, because their trained
hearts can pump enough blood in each contraction to allow a
low resting heart rate.

14. ETIOLOGY
• Sinus bradycardia is commonly seen in normal healthy persons and athletes in
the absence of pathophysiological diseases or conditions.
• Different factors or etiologies could lead to the dysfunction of the sinus node,
causing a malformation or prolongation of the impulse.

15. CONTD…
• In terms of pathophysiological diseases, sinus rhythm may be caused by:
• Diseases/Conditions:
• Acute myocardial infarction, carotid sinus syndrome, eating disorders (such as anorexia
nervosa), hypothermia, hypothyroidism, infections (such as diphtheria, acute rheumatic fever, or
viral myocarditis), intrinsic disease of the SA node
• Physiological causes:
• increased intracranial pressure
• Medications, most commonly: digitalis glycosides, beta-blockers, quinidine, adenosine, calcium channel
blockers, class I antiarrhythmic agents, ivabradine, clonidine, reserpine, cimetidine, lithium, amitriptyline.

16. ECG CHARACTERISTICS
• Rate: Less than 60 beats per minute.
• Rhythm: Regular.
• P waves: Upright, consistent, and normal in morphology and
duration.
• PR interval: Between 0.12 and 0.20 seconds in duration.
• QRS complex: Less than 0.12 seconds in width

18. TREATMENT
• Adminster atropine (anticholinergic drugs)
• If atropine is ineffective, dopamine or epinephrine infusion is considered.
• Permanent pacemaker may be needed.
• If bradycardia is due to drugs, these may need to be held, discontinued or
given in reduced dosages.

19. SINUS TACHYCARDIA
• Sinus tachycardia is an elevated sinus rhythm characterized by an increase
in the rate of electrical impulses arising from the sinoatrial node.
• In adults, sinus tachycardia is defined as a heart rate greater than 100
beats/min.
• The normal resting heart rate is 60–90 bpm in an average adult.
• Sinus tachycardia is a normal response to physical exercise, when the heart
rate increases to meet the body's higher demand for energy and oxygen,
but sinus tachycardia can also indicate a health problem.

20. SIGNS AND SYMPTOMS
• Tachycardia is often asymptomatic. It is often a resulting symptom of
a primary disease state and can be an indication of the severity of a
disease. If the heart rate is too high, cardiac output may fall due to the
markedly reduced ventricular filling time. Rapid rates, though they
may be compensating for ischemia elsewhere, increase myocardial
oxygen demand and reduce coronary blood flow, thus precipitating an
ischemic heart or valvular disease. Sinus tachycardia accompanying
a myocardial infarction may be indicative of cardiogenic shock .

21. Causes
• Sinus tachycardia is usually a response to physiological stress, such as exercise, or
an increased sympathetic tone with increased catecholamine release, such as
stress, fright, flight, and anger. Other causes include:
• Pain
• Fever
• Anxiety
• Dehydration
• Malignant hyperthermia
• Hypovolemia with hypotension and shock
• Anemia
• Hyperthyroidism
• Mercury poisoning
• Kawasaki disease
• Pheochromocytoma
• Sepsis

22. • Pulmonary embolism
• Acute coronary ischemia and myocardial infarction
• Chronic obstructive pulmonary disease
• Hypoxia
• Intake of stimulants such as caffeine, theophylline, nicotine, cocaine
• Electric shock
• Drug withdrawal
• Porphyria
• Acute inflammatory demyelinating polyradiculoneuropathy
• Postural orthostatic tachycardia syndrome
• Mitral Valve Prolapse

23. ECG CHARACTERSITICS
• Rate: Greater than or equal to 100.
• Rhythm: Regular.
• P waves: Upright, in leads I, II and aVL, and negative in lead aVR;
• Each P wave is followed by a QRS and T waves

24. • TREATMENT
 If the patient is experiencing tachycardia from pain, effective pain
management is important to treat tachycardia.
 Administer beta blockers- metoprolol
 Calcium channel blockers- diltiazem
 If clinically unstable patients, synchronized cardioversion is used.

25. PREMATURE ATRIAL CONTRACTION (PAC)
• Premature atrial contractions (PACs), also known as atrial premature
complexes (APC) or atrial premature beats (APB), are a
common cardiac dysrhythmia characterized by premature heartbeats
originating in the atria. While the sinoatrial node typically regulates
the heartbeat during normal sinus rhythm, PACs occur when another
region of the atria depolarizes before the sinoatrial node and thus
triggers a premature heartbeat.

26. RISK FACTORS
• Hypertension
• Increased age
• Abnormal body height
• Family history of heart disease
• History of cardiovascular disease (CV)
• Hypoxia
• COPD
• Elevated cholesterol

27. SIGNS AND SYMPTOMS
• Palpitations (fast, forceful heartbeats in an irregular rhythm)
• A missed or skipped heartbeat
• Chest pain or shortness of breath
• Lightheadedness, dizziness, or feeling faint
• Tiredness with exercise or activity

28. ECG CHARACTERISTICS
• Rhythm is irregular
• P wave has a different shape or it may hidden
• PR interval is shorter or longer than the PR interval coming from the SA
node
• QRS complex is usually normal
• QRS interval is 0.12 second or more.

29. TREATMENT
• Treatment depends on patients symptoms.
• Withdrawl of sources of stimulation such as caffine or
sympathomimetic drugs may be needed.
• Beta adrenergic blockers may be used to decrease PACs.

30. PAROXYMAL SUPRAVENTRICULAR TACHYCARDIA
• Paroxysmal supraventricular tachycardia (PSVT) is a type
of supraventricular tachycardia, Often people have no
symptoms. Otherwise symptoms may include palpitations, feeling
lightheaded, sweating, shortness of breath, and chest pain. PSVT is a
dysrhythmia starting in a ectopic focus anywhere above the bifurcation of
the bundle of His.

31. Causes Not known[3]
Risk factors Alcohol, caffeine, nicotine, psychological stress, Wolff-Parkinson-White
syndrome[

32. SIGNS AND SYMPTOMS
• Symptoms may include palpitations, feeling faint, sweating, shortness
of breath, and chest pain. Episodes start and end suddenly.

33. ECG CHARACTERISTICS
• HR is 150 to 220 beats/ minute.
• Rhythm is regular or slightly irregular
• P wave is hidden, if seen it may have an abnormal shape.
• QRS complex is usually normal.
•

34. TREATMENT
• IV adenosine is the drug of choice to convert PSVT to a normal sinus
rhythm.
• Beta blockers
• Calcium channel blockers
• Potassium channel blockers- amiodarone
• If drug therapy is ineffective , cardioversion is used.

35. ATRIAL FLUTTER
• Atrial flutter (AFL) is a common abnormal heart rhythm that starts in the atrial
chambers of the heart.
• When it first occurs, it is usually associated with a fast heart rate
• Atrial flutter is characterized by a sudden-onset (usually) regular abnormal heart
rhythm on an electrocardiogram (ECG) in which the heart rate is fast.
• Symptoms may include a feeling of the heart beating too fast, too hard, or
skipping beats, chest discomfort, difficulty breathing, or loss of consciousness.

36. CAUSES
• Rapid contractions in the atria (upper chambers of the heart), which may spread
to the ventricles (lower chambers) causes a rapid heartbeat. The exact cause is
unknown but factors which contribute may inlcude:
• Conditions like coronary heart disease, atherosclerosis, or a blood clot which
decreases the blood flow to the heart
• Hypertension
• Abnormalities in heart valves
• Enlarged chamber of the heart
• Open heart surgery
• Hyperthyroidism
• Chronic lung diseases, such as COPD
• Stimulants like cocaine, caffeine or amphetamines
• Risk factors include:
• Uncontrolled diabetes
• Uncontrolled high blood pressure

37. • Obesity
• Alcohol consumption
• Hyperthyroidism
• Advanced age
• Pulmonary embolism - a blood clot in the blood vessel of the lungs

38. SYMPTOMS
Common symptoms include:
• Lightheadedness
• Fatigue
• Palpitations
• Mild shortness of breath
• Blurry vision
• Chest pain
• Fainting

39. ECG CHARACTERISTICS
• Atrial rate is200 to 350 beats/ minute.
• Atrial rhythm is regular.
• Ventricular rhythm is regular.
• PR interval is variable and not measurable.
• QRS complex is usually normal.
• AV node can delay signals from the atria.

40. TREATMENT
• Drugs used to control ventricular rate include calcium channel
blockers and beta adrenergic blockers.
• Electrical cardioversion may be performed to convert the atrial flutter
to sinus rhythm
• Antidysrhythmic drugs are used-Amiodarone, ibutilide, dronedarone.
• Radiofrequency catheter ablation is used

41. ATRIAL FIBRILLATION
• Atrial fibrillation is an irregular and often very rapid heart rhythm
(arrhythmia) that can lead to blood clots in the heart.
• Atrial fibrillation increases the risk of stroke, heart failure and other
heart-related complications.
• It is total diosorganization of electrical activity because of multiple
ectopic foci, resulting in loss of effective atrial contraction.
• It is the most common type.

42. CAUSES
• Problems with the heart's structure are the most common cause of atrial
fibrillation. Possible causes of atrial fibrillation include:
• Coronary artery disease
• Heart attack
• Heart defect that you're born with (congenital heart defect)
• Heart valve problems
• High blood pressure
• Lung diseases

43. • Physical stress due to surgery, pneumonia or other illnesses
• Previous heart surgery
• Problem with the heart's natural pacemaker (sick sinus syndrome)
• Sleep apnea
• Thyroid disease such as an overactive thyroid (hyperthyroidism) and
other metabolic imbalances
• Use of stimulants, including certain medications, caffeine, tobacco
and alcohol
• Viral infections
• Some people who have atrial fibrillation have no known heart
problems or heart damage.

44. Risk factors
• Things that can increase the risk of atrial fibrillation (A-fib) include:
• Age. The older a person is, the greater the risk of developing atrial fibrillation.
• Heart disease. Anyone with heart disease — such as heart valve problems, congenital
heart disease, congestive heart failure, coronary artery disease, or a history of heart
attack or heart surgery — has an increased risk of atrial fibrillation.
• High blood pressure. Having high blood pressure, especially if it's not well controlled
with lifestyle changes or medications, can increase the risk of atrial fibrillation.
• Thyroid disease. In some people, thyroid problems may trigger heart rhythm problems
(arrhythmias), including atrial fibrillation.

45. • Other chronic health conditions. People with certain chronic
conditions such as diabetes, metabolic syndrome, chronic kidney
disease, lung disease or sleep apnea have an increased risk of atrial
fibrillation.
• Drinking alcohol. For some people, drinking alcohol can trigger an
episode of atrial fibrillation. Binge drinking further increases the risk.
• Obesity. People who have obesity are at higher risk of developing
atrial fibrillation.
• Family history. An increased risk of atrial fibrillation occurs in some
families.

46. SYMPTOMS
• Sensations of a fast, fluttering or pounding heartbeat (palpitations)
• Chest pain
• Dizziness
• Fatigue
• Lightheadedness
• Reduced ability to exercise
• Shortness of breath
• Weakness

47. ECG CHARACTERISTICS
• Atrial rate may be high as 350 to 600 beats/ minute.
• P waves are replaced by fibrillaory waves.
• Ventricular rate varies, and rhythm is usually irregular.
• PR interval is not measurable.
• QRS complex is usually normal shape and duration.

48. TREATMENT
• Calcium channel blockers-diltiazem
• Beta adrenergic blockers-metoprolol
• Antidysrhythmic drugs-amiodarone, ibutilide
• Cardioversion
• Blood thinners: These medications thin the clot formation. (cardioversion).But
they can raise the risk of bleeding.The most common are:
• Apixaban (Eliquis)
• Aspirin
• Dabigatran (Pradaxa)
• Enoxaparin (Lovenox)
• Heparin
• Rivaroxaban (Xarelto)
• Warfarin (Coumadin, Jantoven)
• Catheter ablation procedure

49. PREVENTION
• Healthy lifestyle choices can reduce the risk of heart disease and may
prevent atrial fibrillation. Here are some basic heart-healthy tips:
• Eat a nutritious diet
• Get regular exercise and maintain a healthy weight
• Don't smoke
• Avoid or limit alcohol and caffeine
• Manage stress, as intense stress and anger can cause heart rhythm problems

50. JUNCTIONAL DYSRHYTHMIAS
• Junctional dysrhythmias that start in the area of the AV node.
• They result because the SA node fails to fire or the signal is blocked. When this
occurs, the AV node becomes the pacemaker of the heart.
• The impulse from the Av node usually moves in retrograde (backward )fashion.
• This produces an abnormal P wave that occurs just before or after the QRS
complex or that hidden in the QRS complex.

51. CAUSES
• CAD
• HF
• Cardiomyopathy
• Electrolyte disturbances
• Inferior MI
• Rheumatic heart disease
• Certain drugs- digoxin, nicotine

52. SIGNS AND SYMPTOMS
• Fainting spells
• Dizziness
• Heart palpitations
• Fatigue
• Feeling lightheaded
• Shortness of breath

53. ECG CHARACTERISTICS
• HR is 40 to 60 beats / minute.
• Rhythm is regular
• P wave is abnormal in shape and inverted or it may be hidden in the
QRS COMPLEX.
• PR interval is less than 0.12 second.
• QRS complex is usually normal

54. TREATMENT
• Atropine can be used
• Beta adrenergic blockers
• Calcium channel blockers
• Amiodarone
• Cardioversion should not be used.

55. AV BLOCK
FIRST DEGREE AV BLOCK
• It is a type of AV block in which every impulse is conducted to the
ventricles but the time of AV conduction is prolonged. After the
impulse moves through the AV node, the ventricles usually respond
normally.

56. CAUSES
• MI
• CAD
• Rheumatic fever
• Hyperthyroidism
• Electrolyte imbalance- hypokalemia
• Drugs such as digoxin, beta blockers, calcium channel blockers.

57. SIGNS AND SYMPTOMS
• First degree AV block is usually not serious but can be a sign of higher
degree of AV block.
• Patients with first degree AV block is asymptomatic.

58. ECG CHARACTERSITICS
• HR normal
• Rhythm is regular
• P wave is normal
• PR interval is prolonged (greater than 0.20 second)
• QRS complex has a normal shape and duration.

59. TREATMENT
• There is no treatment for first degree AV block.
• Monitor patients for any new changes in heart rhythm ( eg. More
serious AV block)

60. SECOND DEGREE AV BLOCK/ Mobitz I /Wenckebach heart block/
TYPE 1
• It is gradual lengthening of PR interval.
• It occurs because of a prolonged AV conduction time until an arterial
impulse is not conducted and a QRS complex is blocked( missing).
• Type I AV block most commonly occurs in AV node, but it can also occur in
the His purkinje system.

61. CAUSES
• Drugs such as digoxin or beta blockers
• CAD- It can slow the AV conduction
SIGNS AND SYMPTOMS
• 1.Chest pain
• 2. Dizziness
• 3. Fainting
• 4. Fatigue
• 5. Nausea
• 6. Shortness of breath

62. TREATMENT
• If the patient is symptomatic, atropine is used to increase HR.
• Temperory pacemaker may be needed, especicially patient had MI.
• If the patient is asyptomatic, the rhythm is closely observed with a
transcutaneous pacemaker on standby.

63. SECOND DEGREE AV BLOCK, TYPE II, Mobitz II heart block
• P wave is not conducted without progressive PR lengthening.
• This is usually occurs when a block in one of the bundle branches is present.
• PR interval is constant.
• It is a serious type of AV block in which a certain number of impulses from the
SA node are not conducted to the ventricles.
• This occurs in ratios of 2:1,3:1( two P waves to one QRS complex, Three P waves
to 1 QRS complex)
• It may occur with varying ratios.

64. CAUSES
• RHD
• CAD
• Anterior MI
• Drug toxicity
SIGNS AND SYMPTOMS
• 1 Shortness of breath 2 Fatigue 3 Diaphoresis 4 Pallor 5 Chest pain 6
Altered mental status 7 Loss of consciousness 8 Bradycardia 9
Hypotension

65. ECG CHARACTERISTICS
• Atrial rate is normal
• Atrial rhythm is regular
• Ventricular rhythm is irregular
• P wave is normal shape
• PR interval may be normal or prolonged in duration and remains constant
on conducted beats.
• QRS complex is usually greater than 0.12 second because of bundle
branch block.

66. TREATMENT
• Insertion of temperory pacemaker may be necessary before the
insertion of permanent pacemaker if the patient becomes symptomatic
( eg. Hypotenson, angina)

67. THIRD DEGREE AV BLOCK/ COMPLETE AV BLOCK
• There is no impulses from the atria are conducted to the ventricles.
• The atria are stimulated and contract independently of the ventricles.
CAUSES
• CAD
• MI
• Myocarditis
• Cardiomyopathy
• Scleroderma
• Drugs like digoxin, beta blockers and calcium blockers.

68. SIGNS AND SYMTOMS
• With third-degree, may get more serious symptoms, like:
• 1. Extreme fatigue
• 2. Irregular heartbeat
• 3. No heartbeat (cardiac arrest)

69. ECG CHARATERISTICS
• Atrial rate is 60 to 100 beats/ minute.
• Ventricular rate depends on the site of block
• Atrial and ventricular rhythm are regular and unrelated to each other.
• P wave is normal in shape
• PR interval is variable
• There is no relationship between P wave and QRS complex.

70. TREATMENT
• Pacemaker
• Atropine, dopamine and epinephrine is a temporary measure to
increase HR and support blood pressure.

71. PREMATURE VENTRICULAR CONTRACTION
• It is a contraction coming from an ectopic focus in the ventricles.
• It is a premature ( early ) occurrence of QRS complex.

72. CAUSES
• The exact causes are unknown but the condition can be triggered by
certain factors which may include:
• Chemical imbalances in the body
• Medications such as decongestants
• Caffeine, tobacco which causes high levels of adrenaline in the body
• Injury to the heart due to coronary heart disease or high blood
pressure
• Risk factors include:
• Anxiety
• High blood pressure
• Excessive intake of caffeine, tobacco
• Heart diseases

73. SIGNS AND SYMPTOMS
• Symptoms may include sensations in the chest, such as
• Missed beats
• Feel of fluttering
• Increased heartbeat
• Jumping
• Flip-flops

74. ECG CHARACTERISTICS
• Rhythm is irregular because of premature beats.
• P wave is rarely visible.
• PR interval is not measurable.
• QRS complex is wide and distorted in shape.
• T wave is generally large

75. TREATMENT
• Oxygen therapy for hypoxia.
• Electrolyte replacement
• Beta blockers
• Procainaimide
• Amiodarone

76. VENTRICULAR TACHYCARDIA
• Fast heart beat rhythm of the ventricles, the lower chambers of the
heart. This may cause dizziness or chest pain.
• In ventricular tachycardia, the heart beats faster, usually 100 or more
beats a minute.
• Sometimes the rapid heartbeat prevents the heart chambers from
properly filling with blood. As a result, the heart may not be able to
pump enough blood to the body. If this happens, may feel short of
breath or lightheaded, or may lose consciousness.
• Ventricular tachycardia episodes may be brief and last only a couple
of seconds without causing harm. But episodes lasting more than a
few seconds can be life-threatening. Sometimes ventricular
tachycardia can cause the heart to stop (sudden cardiac arrest).

77. Symptoms
• Chest pain (angina)
• Dizziness
• Pounding heartbeat (palpitations)
• Lightheadedness
• Shortness of breath
• Ventricular tachycardia may go away on its own within 30 seconds
(nonsustained V-tach) or last more than 30 seconds (sustained V-
tach or VT). Brief episodes may not cause any symptoms. But
sustained VT can cause serious problems, including:
• Fainting
• Loss of consciousness
• Cardiac arrest (sudden death)

78. Risk factors
• Heart disease
• Medication side effects
• Severe electrolyte imbalances
• Use of stimulant drugs such as cocaine or methamphetamine
• A family history of tachycardia or other heart rhythm disorders makes
a person more likely to develop ventricular tachycardia.

79. Classification
Ventricular tachycardia can be classified based on its morphology .
1.Monomorphic ventricular tachycardia means that the appearance of
all the beats match each other in each lead of a
surface electrocardiogram (ECG).

81. 2.Polymorphic ( torsades de pointes )-
• Torsade de pointes is an uncommon
• Characterized by a gradual change in the amplitude and twisting of
the QRS complexes around the isoelectric line

83. ECG CHARACTERISTICS
• Rate is 150 to 250 beats / minute
• Rhythm may be regular or irregular
• AV dissociation may be present
• P waves is usually buried in the QRS complex
• PR interval is not measurable
• QRS complex is distorted in appearance and wide.
• T waves are in opposite direction of QRS complex.

84. TREATMENT
• Electrolyte imbalance is identified and treated.
• Cardioversion
• If a person still has a pulse, it is usually possible to terminate the
episode using electric cardioversion. This should be synchronized to
the heartbeat if the waveform is monomorphic if possible, in order to
avoid degeneration of the rhythm to ventricular fibrillation. An initial
energy of 100J is recommended. If the waveform is polymorphic, then
higher energies and an unsynchronized shock should be provided
(also known as defibrillation).

85. • Defibrillation
• A person with pulseless VT is treated the same as ventricular
fibrillation with high-energy (360J with a monophasic defibrillator, or
200J with a biphasic defibrillator) unsynchronised cardioversion
(defibrillation). They will be unconscious.
• The shock may be delivered to the outside of the chest using the two
pads of an external defibrillator, or internally to the heart by
an implantable cardioverter-defibrillator (ICD) if one has previously
been inserted.

86. Implanted cardioverter defibrillataor

87. Catheter ablation

88. Medication
• For those who are stable with a monomorphic waveform the
medications procainamide or sotalol may be used.
• As a low magnesium level in the blood is a common cause of VT, magnesium sulfate can
be given for torsades de pointes or if a low blood magnesium level is found/suspected.
• Long-term anti-arrhythmic therapy may be indicated to prevent recurrence of VT.
• Beta-blockers and a number of class III anti-arrhythmics are commonly used, such as the
beta-blockers carvedilol, metoprolol, and bisoprolol, and the Potassium-Channel-Blockers
amiodarone, dronedarone, bretylium, sotalol, ibutilide, and dofetilide.
• Angiotensin-converting-enzyme (ACE) inhibitors and aldosterone antagonists are also
sometimes used in this setting.

89. Complications
Possible complications of ventricular tachycardia include:
• unconsciousness
• Heart failure
• Sudden death caused by cardiac arrest

90. VENTRICULAR FIBRILLATION
• It is a severe derangement of the heart rhythm characterized on ECG
by irregular wave forms of varying shapes and amplitude.

92. Risk factors
• The risk of VF during acute myocardial infarction is related to the
amount of ST elevation, the presence of hypokalemia, the absence of
pre-infarction angina, the size of the infarction, and the presence of a
blocked left coronary artery. Other risk factors could include younger
age, male gender, and history of sudden cardiac death in first degree
relatives
•

93. ECG CHARACTERISTICS
• HR is not measurable
• Rhythm is irregular
• P waves are not visible
• PR interval and the QRS interval is not measurable.

94. TREATMENT
• Immediate initiation of CPR and Advanced cardiac life support with
the use of defibrillation and definitive drug therapy such as
epinephrine and vasopressin.

95. ASYSTOLE
• It is the total absence of ventricular electrical activity.
• Occasionally P waves are seen.
• No ventricular contraction occurs.
• Patients are unresponsive and pulseless.it needs immediate treatment.
• Prognosis is very poor.

96. • CAUSES
• Advanced cardiac diseases.
• Severe cardiac conduction disturbances or end stage heart failure
• TREATMENT
• CPR
• Drugs such as epinephrine,vasopressin
• Intubation

97. PULSELESS ELECTRICAL ACTIVITY
• Pulseless electrical activity (PEA) refers to cardiac arrest in which
the electrocardiogram shows a heart rhythm that should produce
a pulse, but does not. Pulseless electrical activity is found initially in
about 55% of people in cardiac arrest.

98. Causes
• Hypovolemia
• Hypoxia
• Hydrogen ions (Acidosis)
• Hyperkalemia or Hypokalemia
• Hypoglycemia
• Hypothermia
• Tablets or Toxins
• Cardiac Tamponade
• Tension pneumothorax
• Thrombosis (e.g., myocardial infarction, pulmonary embolism)
• Tachycardia
• Trauma (e.g., hypovolemia from blood loss)

99. Signs and symptoms
• Pulseless electrical activity leads to a loss of cardiac output, and the
blood supply to the brain is interrupted. As a result, PEA is usually
noticed when a person loses consciousness and
stops breathing spontaneously. This is confirmed by examining
the airway for obstruction, observing the chest for respiratory
movement, and feeling the pulse (usually at the carotid artery) for a
period of 10 seconds.

100. TREATMENT
• CPR
• Drug therapy-epinephrine
• Intubation

101. PRODYSRHYTHMIA
• Antidysrhythmia drugs can cause life threatening dysrhythmias
similar to those for which they are given.
• The patient who has severe left ventricular dysfunction is the most
susceptible to prodysrhythmia.
• For this reason, many oral antidysrhythmia drug regimens are started
in a monitored hospital settings.

102. ANTIDYSRHYTHMIA DRUGS