cardiac arrhythmias are abnormal heart rhythms that occur when the electrical signals controlling the heart beat are not working properly.
these can include tachycardia ,Bradycardia,atrial fibrillation and more.
2. These are drugs used to prevent or treat
irregularities of cardiac rhythm.
Nearly 3 out of 4 patients of acute MI & about
half of those given a GA exhibit at least some
irregularities in cardiac rhythm.
Arrhythmias are most common cause of
sudden cardiac death.
Abnormal automaticity or impaired
conduction or both = card arrhythmias.
3. Cardiac action potential –when a stimulus
reaches the cardiac cell, specific ions move
into & out of the cell eliciting an action
potential. (divided into 4 phases )
Phase 0 –is the rapid depolariation of the cell
mem in which – fast entry of Na into the cell
through Na channels.( followed by
repolarisation )
4. Phase-1 is a short, initial rapid repolarisation
due to efflux of K ions.
Phase- 2 is a prolonged plateau phase due to
slow entry of Ca ions in to the cell through the
Ca channels.(cardiac cell differs from other
cells in having this phase of action potential.
Phase- 3 is a second period of rapid
repolarisation with K ions moving out of the
cell.
5. Phase-4 is the resting phase during which K
ions return into the cell while Na & Caions
move out of it & the resting membrane
potential is restored.
During Phase 1 &2, the cell does not
depolarise in response to another impulse,
i.e. it is in absolute refractory period. But in
Phase 3 & 4, the cell is in relative refractory
period &may depolarise in response to
impulse.
9. Arrhythmia Assessment
ECG
24h Holter monitor
Echocardiogram
Stress test
Coronary angiography
Electrophysiology study
10. Mechanism of Arrhthmogensis
1. Disorder of impulse formation.
a) Automaticity.
b) Triggered Activity.
1) Early after depolarization.
2) Delayed after depolarization.
2. Disorder of impulse conduction.
a) Block – Reentry.
b) Reflection.
3. Combined disorder.
13. SINUS TACHYCARDIA
Rate: 101-160/min
P wave: sinus
QRS: normal
Conduction: normal
Rhythm: regular or slightly irregular
The clinical significance of this dysrhythmia depends on the
underlying cause. It may be normal.
Underlying causes include:
increased circulating catecholamines
CHF
hypoxia
PE
increased temperature
stress
response to pain
Treatment includes identification of the underlying cause and
correction.
14.
15. SINUS BRADYCARDIA
Rate: 40-59 bpm
P wave: sinus
QRS: Normal (.06-.12)
Conduction: P-R normal or slightly prolonged at slower rates
Rhythm: regular or slightly irregular
This rhythm is often seen as a normal variation in athletes, during
sleep, or in response to a vagal maneuver. If the bradycardia
becomes slower than the SA node pacemaker, a junctional rhythm
may occur.
Treatment includes:
treat the underlying cause,
atropine,
isuprel, or
artificial pacing if patient is hemodynamically compromised.
16.
17. SINUS ARRHYTHIMIA
Rate: 45-100/bpm
P wave: sinus
QRS: normal
Conduction: normal
Rhythm: regularly irregular
The rate usually increases with inspiration and decreases with
expiration.
This rhythm is most commonly seen with respiration due to
fluctuations in vagal tone.
The non respiratory form is present in diseased hearts and
sometimes confused with sinus arrset (also known as "sinus pause").
Treatment is not usually required unless symptomatic bradycardia is
present.
18.
19. PAROXYSMAL ATRIAL
TACHYCARDIA
Rate: atrial 160-250/min: may conduct to ventricles 1:1, or 2:1, 3:1,
4:1 into the presence of a block.
P wave: morphology usually varies from sinus
QRS: normal (unless associated with aberrant ventricular
conduction).
Conduction: P-R interval depends on the status of AV conduction
tissue and atrial rate: may be normal, abnormal, or not measurable.
PAT may occur in the normal as well as diseased heart.
It is a common complication ofWolfe-Parkinson-White syndrome.
This rhythm is often transient and doesn't require treatment.
However, it can be terminated with vagal maneuvers.
Digoxin, antiarrhythmics, and cardioversion may be used.
20.
21. ATRIAL FIBRILLATION
Rate: atrial rate usually between 400-650/bpm.
P wave: not present; wavy baseline is seen instead.
QRS: normal
Conduction: variableAV conduction; if untreated the ventricular
response is usually rapid.
Rhythm: irregularly irregular. (This is the hallmark of this
dysrhythmia).
Atrial fibrillation may occur paroxysmally, but it often becomes
chronic. It is usually associated with COPD, CHF or other heart
disease.
Treatment includes:
Digoxin to slow the AV conduction rate.
Cardioversion may also be necessary to terminate this rhythm.
22.
23. VENTRICULAR TACHYCARDIA
Rate: usually between 100 to 220/bpm, but can be as rapid as 250/bpm
P wave: obscured if present and are unrelated to the QRS complexes.
QRS: wide and bizarre morphology
Conduction: as with PVCs
Rhythm: three or more ventricular beats in a row; may be regular or
irregular.
Ventricular tachycardia almost always occurs in diseased hearts.
Some common causes are:
CAD
acute MI
digitalis toxicity
CHF
ventricular aneurysms.
Patients are often symptomatic with this dysrhythmia.
Ventricular tachycardia can quickly deteriorate into ventricular fibrillation.
Electrical countershock is the intervention of choice if the patient is
symptomatic and rapidly deteriorating.
Some pharmacological interventions include lidocaine, pronestyl, and
bretylium.
26. CLASSIFICATION
Rate: usually between 150 to 220/bpm,
P wave: obscured if present
QRS: wide and bizarre morphology
Conduction: as with PVCs
Rhythm: Irregular
Paroxysmal –starting and stopping suddenly
Hallmark of this rhythm is the upward and downward deflection of theQRS
complexes around the baseline.The term Torsade de Pointes means "twisting
about the points."
Consider itV-tach if it doesn’t respond to antiarrythmic therapy or treatments
Caused by:
drugs which lengthen the QT interval such as quinidine
electrolyte imbalances, particularly hypokalemia
myocardial ischemia
Treatment:
Synchronized cardioversion is indicated when the patient is unstable.
IV magnesium
IV Potassium to correct an electrolyte imbalance
Overdrive pacing
Class Action Examples Side Effects
1A Fast sodium channel blocker
varies depolarization and
action potential duration
Quinidine,
procainamide,
disopyramide
Class: nausea,
vomiting
Quinidine: hemolytic
anemia,
thrombocytopenia,
tinnitus
Procainamide: lupus
1B lignocaine,
Mexiletine
Lidocaine: dizziness,
confusion, seizures,
coma
Mexiletine: tremor,
ataxia, rash
1C Flecainide,
Propafenone
Flecainide: pro-
arrhythmia, nausea,
dizzyness
2 beta-blockers SA node & AV
node conduction
Propranolol,
metoprolol
Class: CHF,
bronchospasm,
bradycardia,
hypotension
3 Prolong action potential by
blocking K+ channels
Amiodarone,
sotalol
Amiodarone:
hepatitis, pulmonary
fibrosis, thyroid
disorders, peripheral
27. Class 1A agents: Procainamide, quinidine
Uses
Wide spectrum, but side effects limit usage
Quinidine : maintain sinus rhythms in atrial fibrillation and
flutter and to prevent recurrent tachycardia and
fibrillation
Procainamide: acute treatment of supraventricular and
ventricular arrhythmias (no longer in production)
Side effects
Hypotension, reduced cardiac output
Proarrhythmia (generation of a new arrhythmia) eg.
28. Class 1B agents: Lignocaine, phenytoin
Uses
acute : Ventricular tachycardia and fibrillation (esp.
during ischemia)
Not used in atrial arrhythmias or AV junctional
arrhythmias
Side effects
Less proarrhythmic than Class 1A (less QT effect)
CNS effects: dizziness, drowsiness
29. Class 1C agents: Flecainide, propafenone
Uses
Wide spectrum
Used for supraventricular arrhythmias (fibrillation
and flutter)
Premature ventricular contractions (caused
problems)
Wolff-Parkenson-White syndrome
Side effects
Proarrhythmia and sudden death especially with
chronic use (CAST study)
Increase ventricular response to supraventricular
arrhythmias
30. Class II agents: Propranolol, esmolol
Uses
treating sinus and catecholamine dependent tachy
arrhythmias
converting reentrant arrhythmias in AV
protecting the ventricles from high atrial rates (slow AV
conduction)
Side effects
bronchospasm
hypotension
31. Class III agents: Amiodarone, sotalol, ibutilide
Sotalol
Uses
Wide spectrum: supraventricular and ventricular
tachycardia
Side effects
Proarrhythmia, fatigue, insomnia
AMIODARONE- highly lipophilic long acting antiarrythmic drug
with multiple actions.
Prolong APD & QT interval with blocking K+ channels.
Preferentially blocks inactivated Na+ channels.
Partially inhibits myocardial ca+ channels , has noncompititive
beta adrenergic blocking property.
32. Class III agents: Amiodarone, sotalol, ibutilide
Amiodarone
Uses
Very wide spectrum: effective for most arrhythmias
Side effects: many serious that increase with time
Pulmonary fibrosis
Hepatic injury
Increase LDL cholesterol
Thyroid disease
Photosensitivity
May need to reduce the dose of digoxin and class 1
antiarrhythmics
33. Class IV agents: Verapamil and diltiazem
Uses
control ventricular rate during supraventricular
tachycardia
convert supraventricular tachycardia (re-entry around
AV)
Side effects
Caution when partial AV block is present. Can get
asystole if β blocker is on board
Caution when hypotension, decreased CO or sick sinus
Some gastrointestinal problems
34. Additional agents
Adenosine
Administration
rapid i.v. bolus, very short T1/2 (seconds)
Cardiac effects
Slows AV conduction
Uses
convert re-entrant supraventricular arrhythmias
hypotension during surgery, diagnosis of CAD
Magnesium
treatment for tachycardia resulting from long QT
35. Additional agents
Digoxin (cardiac glycosides)
Mechanism
enhances vagal activity, inhibits Na/K ATPase
refractory period, slows AV conduction
Uses
treatment of atrial fibrillation and flutter
Atropine
Mechanism
selective muscarinic antagonist
Cardiac effects
blocks vagal activity to speed AV conduction and
increase HR