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arrythmia 1.pptx
1.
2. ARRHYTHMIA
• CARDIAC ARRHYTHMIA (ALSO DYSRHYTHMIA) IS A TERM FOR ANY OF A LARGE AND HETEROGENEOUS
GROUP OF CONDITIONS IN WHICH THERE IS ABNORMAL ELECTRICAL ACTIVITY IN THE HEART.
• THE HEART BEAT MAY BE TOO FAST OR TOO SLOW, AND MAY BE REGULAR OR IRREGULAR.
• NORMAL SINUS RHYTHM (60-90BPM), SA NODE PACEMAKER
3. NORMAL ELECTRICAL ACTIVITY IN THE HEART
Each heart beat originates as an electrical impulse from a small
area of tissue in the right atrium of the heart called the sinus
node or Sino-atrial node or SA node. The impulse initially causes
both of the atria to contract, then activates the atrioventricular
(or AV) node which is normally the only electrical connection
between the atria and the ventricles , which can be called as
main pumping chambers.
The impulse then spread through both ventricles via the Bundle
of His and the Purkinje fibres causing a synchronised contraction
of the heart muscle, and thus, the pulse
4. Normal electrical activity in the heart
• Impulses originate regularly at a frequency of 60-100 beat/ min
• SAN is considered the pacemaker of the heart .
• SAN is characterized by its own automaticity (ability to generate impulse) So
nerve supply of the heart aims at regulation of heart rate not initiation of
rhythm.
SAN
AVN
7. Mechanisms of Cardiac Arrhythmias
Mechanisms of bradicardias:
Sinus bradycardia is a result of abnormally slow automaticity while bradycardia
due to AV block is caused by abnormal conduction within the AV node or the
distal AV conduction system.
Mechanisms generating tachycardias include:
- Accelerated automaticity.
- Triggered activity
- Re-entry (or circus movements)
8. ACCELERATED AUYOMATICITY
Pacemaker cells are present in the SA node, atria, AV node, and
the His-Purkinje system. In the human heart, the normal rate of
discharge of the SA node is between 60 and 100 beats per min
(bpm). Enhanced automaticity of pacemaker cells can increase
the rate of action potential discharge
When this occurs in the SA node, it can lead to an increase in heart
rate, termed sinus tachycardia. This can be physiological, due to
increased sympathetic tone during exercise, or pathophysiological,
due to hypovolemia, fever, ischemia, or electrolyte disturbances.
9. TRIGGERED ACTIVITY
Triggered activity results from the premature activation of cardiac tissues
Myocardial damage can result in oscillations of the transmembrane potential at the
end of the action potential. These oscillations, which are called 'after
depolarizations', may reach threshold potential and produce an arrhythmia.
The abnormal oscillations can be exaggerated by pacing, catecholamines, electrolyte
disturbances, and some medications.
Examples as atrial tachycardias produced by digoxin toxicity and the initiation of
ventricular arrhythmia in the long QT syndrome.
10. Re-entry (or circus movement)
The mechanism of re-entry occurs when a 'ring' of cardiac tissue
surrounds an inexcitable core (e.g. in a region of scarred myocardium).
Tachycardia is initiated if an ectopic beat finds one limb refractory ,
resulting in unidirectional block and the other limb excitable, circus
movement will be maintained, producing a run of tachycardia.
The majority of paroxysmal tachycardias are produced by this
mechanism.
12. ETIOLOGY:
1. Blocked arteries in the heart (coronary heart disease)
2. Scaring from a previous heart attack (myocardial infarction)
3. Changes to the heart's structure (congenital heart disease)
4. Diabetes
5. High blood pressure
6. Overactive thyroid gland
7. Underactive thyroid gland
8. Certain medications (digitalis, symathomimetics, sympatholytics)
9. Stress or anxiety
10. smoking
13. CLINICALPICTURE:
ARRHYTHMIA SYMPTOMS:
• Asymptomatic
• Rapid heartbeat or irregular heartbeat
• A fluttering feeling in your chest
• Chest pain
• Troubled breathing
• Weakness
• Dizziness or light headedness
• Fainting
• Fatigue
• Sweating
• Embolic Manifestations
• Sudden cardiac death
14. Investigations for arrhythmia
1. Resting ECG
2. Holter ECG
3. Loop Recorder
4. Stress ECG
5.Electrophysiological study (EPS)
6. Investigations for the cause
a. Echo
b. Cardiac MRI (Myocardial Scarring in VT-VF)
c. Serum electrolytes- CBC-Thyroid functions
15. Treatment of arrhythmia
A. Emergency ttt (if hemodynamically unstable PT)
1. Atropine then Temporary Pacemaker in high grade AV-
block
2. DC-Cardioversion in Tacchyarrythmia
N.B (Never to give DC-shock to pt with sinus tachycardia
B. Long term
1. TTT of the Cause (IHD-Thyroid dysfunction- Electrolyte imbalance)
2. AV-blocking agents and anti-arrhythmics for tachyarrhythmia .
3. Anti-coagulation (AF-flutter)
4. Intervention (PPM for HB- Ablation for tacch
16. Sinus tachycardia
• Definition
Atrial and ventricular rates are more than 100 beats per minute
• Management
Identify the cause of the tachycardia
Decrease the heart rate to normal by treating the cause
ß blockers and sedatives may be needed
17.
18. • Definition
It is a paroxysmal condition in which there is abnormal focus in
the ventricle that discharge impulses more than SAN(150– 250/
min)
Since the focus in the ventricle and there is no retrograde
conduction in AVN, sow the ventricles will follow the ectopic
focus and the atria will follow the SAN (AV dissociation).
Can cause cardiac arrest
Ventricular tachycardia
19. • Management
1. STABLE PATEINT WITH SUSTAINED VT:
Administer antiarrhythmics (AMIODARONE, LIDOCAINE)
2. UNSTABLE CLIENT WITH VT
antidysrhythmic therapy
Prepare for synchronized cardioversion
3. PULSELESS CLIENT
Defibrillation and cardiopulmonary resuscitation (CPR)
20. P wave : - normal but hidden by the QRS
QRS: - rapid, regular with wide abnormal bizzare shape
No fixed relation between P wave & QRS due to AV dissociation.
21. SINUS BRADYCARDIA
• DEFINITION
IT IS A CONDITION AT WHICH THE SAN DISCHARGE IMPULSES BY A RATE LESS THAN
60/MIN
• CAUSES
1. PHYSIOLOGICAL : DUE TO STRONG VAGAL TONE OR ATHELETIC TRAINING.
2. EXTRINSIC CAUSES ;HYPOTHERMIA, HYPOTHYROIDISM, CHOLESTATIC JAUNDICE AND DRUG THERAPY
WITH BETA-BLOCKERS, DIGITALIS AND OTHER ANTIARRHYTHMIC DRUGS.
3. INTRINSIC CAUSES; ACUTE ISCHEMIA AND INFARCTION
22. • MANAGEMENT
1. ATTEMPT TO DETERMINE CAUSE AND IF A MEDICATION IS SUSPECTED AS CAUSING
THE BRADYCARDIA, HOLD THE MEDICATION .
2. ADMINISTER ATROPINE SULFATE TO INCREASE THE HEART RATE TO 60 BEATS PER
MINUTE
3. MONITOR FOR HYPOTENSION AND ADMINISTER IV FLUIDS AS NEEDED.
4. DEPENDING ON THE CAUSE OF THE BRADYCARDIA, THE PATIENT MAY NEED A
PERMANENT PACEMAKER
23.
24. Paroxysmal Supraventricular tachycardia
• Definition
A condition in which there is abnormal focus in the atrium other than SAN
which discharge regular impulses in a rate ( 150- 250 / min.)
This abnormal focus may initiated in any area of the atria (paroxysmal atrial
tachycardia) or even in AVN (paroxysmal nodal tachycardia).
• Management
Vagal stimulation
Drugs : A, B, C, D
Adenosine
ß blockers
Ca channel blockers(verapamil)
Digitalis
If there is no response or hemodynamically unstable : DC
cardioversion
25. P wave : - in atrial tachycardia : deformed
- In nodal tachy cardia : absent
QRS: - rapid, regular with normal shape
26. Atrial flutter
• Definition
A condition in which there is abnormal focus in the atrium that discharges
rapid regular impulses in a rate ( 250- 350 / min.), but due to physiological
block of AVN not all atrial impulses are conducted to the ventricles – only
½.1/3, ¼ .. Of the atrial impulses will pass to the ventricles.
• Management
Drugs : to control the ventricular rate (↓ AVN conduction)
ß blockers
Ca channel blockers(verapamil)
Digitalis
If there is no response or hemodynamically unstable : DC
cardioversion
27.
28. Atrial fibrillation
• Definition
A condition in which there is rapid irregular impulses (400-600/min) arise
from the atria by multiple ectopic foci (so the atria don’t contract
effectively) & due to physiological delay at the AVN, not all impulses are
conducted to the ventricles.
• Management
Administer oxygen
Administer anticoagulants as prescribed because of the risk of emboli
Administer cardiac medications as prescribed to control the ventricular
rhythm and assist in the maintenance of cardiac output
Prepare the patient for cardioversion as prescribed
Instruct the patient in the use of medications as prescribed to control the
dysrhythmia
29. P wave : -absent & replaced by fibrillation wave
QRS: - normal in shape but irregular rhythm
30. premature atrial contractions (PAC)
A condition in which an atrial pacemaker site above the ventricles sends out an electrical signal
early. The ventricles are usually able to respond to this signal, but the result is an irregular heart
rhythm.
PACs are common and may occur as the result of stimulants such as coffee, tea, alcohol, cigarettes,
or medications.
Treatment is rarely necessary.
31. Two PACs with a compensatory pause seen on an ECG rhythm strip. A "skipped beat" occurs and
rhythm resumes 2 P-to-P intervals after the last normal sinus beat.
32. Premature ventricular contractions(PVCs)
Definition
A condition in which there is an ectopic impulse arising from the ventricles before
the expected next beat causes what is called premature beat.
Management
• Identify the cause and treat based on the cause
• Evaluate electrolytes, particularly the potassium level, since hypokalemia can
cause PVCs
• Administer lidocaine in emergency cases
• Notify the cardiologist if the patient complains of chest pain, if PVCs increase in
frequency, or occur in runs of ventricular tachycardia
33.
34. Nodal ( junctional )Rhythm
Definition
A condition in which heart is controlled by the AVN.
The impulses reach the atria & ventricles at the same time
Management
• Identify the cause and treat based on the cause
• Atropine if needed.
• Artificial peacemaker may be needed in sever cases.
35. P wave : -inverted & come approximately at the same time with QRS
QRS: - normal in shape but slow & regular
36. Atrio ventricular block
1 st degree heart block
Definition
o It is just prolonged PR interval (PR interval ⍩ 0.2 second (2
small square)
o Has no clinical significance.
o May be associated with acute rheumatic fever, diphtheria,
myocardial infarction or drugs as digoxin
37.
38. 2nd degree heart block
MOBITZ TYPE I (WENCHEBACH PHENOMENON):
GRADUALLY INCREASING P-R INTERVALS LEADING FINALLY TO DROPOUT OF QRS & THEN
THE CYCLE IS REPEATED
IT IS USUALLY PHYSIOLOGICAL AND DUE TO INCREASED VAGAL TONE AND ABOLISHED BY
EXERCISE AND ATROPINE.
MOBITZ TYPE II
THE AVN TRANSMIT ONE IMPULSE FOR EACH 2,3 OR 4 ATRIAL
IMPULSES.
PACING IS USUALLY INDICATED IN MOBITZ II BLOCK, WHEREAS PATIENTS WITH WENCKEBACH
AV BLOCK ARE USUALLY MONITORED.
39.
40. 3rd degree heart block
Complete heart block
Definition
o In this condition all impulses from the atria don’t reach the ventricles , so the
ventricles will be controlled by idioventricular rhythm.
o Common in elderly age groups due to idiopathic bundle branch fibrosis.
o Other causes include coronary heart disease, calcification from aortic valve,
sarcoidosis or congenital.
oTreatment is permanent pacing
41.
42. MCQ
Question 1.
Which arrythmia will occur due to damage to the atrioventricular
node(AVN):
a) Atrial fibrillation(AF).
b) Ventricular tachycardia.
c) Complete heart block
43. answer 1.
Which arrythmia will occur due to damage to the
atrioventricular node(AVN):
c) Complete heart block
44. Question 2.
What risk is commonly associated with atrial fibrillation(AF)
a) Cerebrovascular accident (CVA).
b) hemorrhage.
c) Myocardial infarction.
45. answer 2.
What risk is commonly associated with atrial
fibrillation(AF)
a) Cerebrovascular accident (CVA).
46. Question 3.
What is the most common cause of ventricular tachycardia(VT)
a) Electrolyte imbalance.
b) Myocardial infarction.
c) Renal failure.
47. answer 2.
What is the most common cause of ventricular
tachycardia(VT)
b) Myocardial infarction.