Location via proxy:   [ UP ]  
[Report a bug]   [Manage cookies]                

Lac 3

Download as pdf or txt
Download as pdf or txt
You are on page 1of 14

Al-Esraa University College

Pharmacy Department

Therapeutics I
Lec 3
Arrhythmia
Dr.Mohammed Ali Alobaidy
F.I.C.M.S – Clinical Pharmacy

Background
• Arrhythmia is loss of cardiac rhythm.

• Normal Electrophysiology of the Heart


An impulse normally originates in the SA node
and travels down specialized intranodal pathways
to activate atrial muscle and the AV node.

The AV node holds the impulse briefly before


releasing it to the bundle of His. It then travels to
the right and left bundle branches and out to the
ventricular myocardium via the Purkinje fibers.
SA node Intranodal pathways Activate atrial muscle + AV node

The AV node holds the impulse briefly

Releasing it to the bundle of His

The right and left bundle branches

Ventricular myocardium via the Purkinje fibers

• By convention, these electrical deflections have been labeled the P wave, QRS
complex, and T wave.
✓ The P wave represents: depolarization (contraction) of the atria,
✓ whereas the QRS complex reflects: ventricular depolarization.
✓ The T wave reflects: repolarization (Resting) of the ventricles.

T
P Q S
Etiology

Arrhythmias result from abnormal impulse formation or abnormal impulse


conduction, These changes may be caused by several factors:

• An infarction may cause the death of pacemaker cells or conducting tissue.


• A cardiac tissue disorder, e.g. fibrosis or rheumatic fever, disrupts the
conduction network.
• Sympathetic or parasympathetic control changes, e.g. stress, anxiety, exercise or
smoking.
• Drugs, e.g. antiarrhythmics or inotropes or other substances, e.g. caffeine, or
alcohol.
• Hypothyroidism, hyperthyroidism, hyperkalaemia and hypokalemia or other
electrolyte disturbances may predispose the heart to arrhythmias.
Patients who have pre-existing cardiac disorders including heart failure,
hypertension or a recent infarction are at greater risk of arrhythmias.

Classification of Arrhythmias

1- Supraventricular arrhythmias
All arrhythmias originating above the bundle
of His
2- Ventricular arrhythmias
Arrhythmias originating below the bundle of
His

An alternative method of classifying


arrhythmias is based on the rate:
Bradyarrhythmia (<60 beats/minute) or
Tachyarrhythmia (>100 beats/minute) .
Signs and consequences of arrhythmias
1-Arrhythmias are associated with increased morbidity and mortality . Atrial fibrillation (AF)
roughly doubles the risk of a person having a stroke, triples the risk of heart failure and doubles
mortality risk .

2- Bradycardias tend to cause symptoms that reflect low cardiac output: fatigue, lightheadedness and
syncope (syncope: is a sudden loss of consciousness due to reduced cerebral perfusion).

3-Tachycardias cause rapid palpitation, dizziness, chest discomfort or breathlessness. Extreme


tachycardias can cause syncope because the heart is unable to contract or relax properly at extreme
rates.

4-Palpitations are the awareness of one's heart beat; they may range from a minor sensation to a
distressing problem.

5-Since these signs are not unique to arrhythmias, arrhythmias are not always easy to diagnose
and 24-hour recordings of the ECG (Holter monitoring) may be used

Diagnosis of Arrhythmia

1-Electrocardiogram (ECG)

2-Holter monitoring: Ambulatory, portable ECG monitor that can


record the electrical activity of the heart for 1 to 2
days at a time to detect episodes of arrhythmia.
Pathophysiology
SUPRAVENTRICULAR ARRHYTHMIAS
• Common supraventricular tachycardias requiring drug treatment are Atrial
fibrillation (AF), Atrial flutter, and Paroxysmal supraventricular tachycardia
(PSVT).
• Other arrhythmias that usually do not require drug therapy are not discussed
here (eg, premature atrial complexes, sinus arrhythmia, sinus tachycardia).

• Atrial Fibrillation
AF has extremely rapid (400–600 atrial beats/min) and irregular atrial pulse
(irregular irregularity)

• Atrial Flutter
Atrial flutter has rapid (270–330 atrial beats/min) but regular pulse (regular
irregularity).
Sinus tachycardia
Sinus tachycardia occurs if the heart rate increases but the rhythm remains
unchanged. It is usually due to an increase in sympathetic activity.

Sinus tachycardia is common during exercise or excitation but may also occur
during Infection, Hypovolaemia, Anaemia, Thyrotoxicosis, And Shock.
It can also occur as a side effect of many drugs, such as Beta 2 Agonists, Thyroxine
And Aminophylline.

Paroxysmal Supraventricular Tachycardias


(PSVTs)

AV nodal re-entry tachycardias (AVNRT) and


AV re-entry tachycardias (AVRT)

Wolff-Parkinson-White (WPW) syndrome is the best-


known type of AVRT in which there is an accessory
pathway between atria and ventricles .
Ventricular arrhythmias OR Ventricular tachyarrhythmias
A-Ventricular ectopic beats (extrasystoles, premature beats)
• Ventricular ectopic beats in otherwise healthy subjects: Treatment is not necessary unless the patient is
highly symptomatic, in which case ß-blockers can be used.
• Ventricular ectopic beats associated with heart disease (e.g. recent MI or heart failure): Treatment is
usually needed.

B-Ventricular tachycardias (VT)


• VT is defined as three or more consecutive ventricular ectopic beats.
• VT is defined as non-sustained if it lasts less than 30 seconds and terminates spontaneously; sustained VT
lasts greater than 30 seconds and does not terminate spontaneously, but rather requires therapeutic
intervention for termination.

Torsades de pointes (TdP) is a specific form of VT with prolongation


of the QT interval secondary to drug therapy, particularly anti-
arrhythmics
Torsades de pointes can rapidly degenerate into ventricular
fibrillation and must therefore be treated as a medical emergency.
C-Ventricular fibrillation
Ventricular fibrillation (VF) is a rapid and uncoordinated contraction of the
ventricular tissue. It severely compromises cardiac output (resulting in no cardiac
output) to the extent that patients usually lose consciousness within 10-20 seconds
of onset.

It is responsible for most deaths, caused by myocardial infarction and there is high
risk of VF in patients with severe ischemic heart disease.

Vf is a medical emergency, because without prompt treatment irreversible cerebral


and myocardial damage will occur.

What is this ??
Management
1- Nonpharmacologic therapy of
bradyarrhythmias:
• Cardiac pacemakers
• Artificial cardiac pacemakers are devices that
deliver a small electrical
impulse to a localized region of the heart, thus
initiating an action potential
that then spreads to the remainder of the heart.

• Permanent pacemaker systems are implanted in


a skin "pocket" below
The collar bone. Leads are inserted via a vein
into the heart.

2- Nonpharmacologic therapy of
tachyarrhythmias
A- Direct current cardioversion DCC and
defibrillation
• Cardioversion refers to the process of restoring
the heart's normal rhythm.
• This can be done chemically using drugs
(chemical or pharmacological cardioversion) or
by application of an electric shock across the
chest (electrical cardioversion) DC.

B-Radiofrequency Catheter Ablation for WPWS


and
C- Implantable Cardioverter-Defibrillators (ICD)
Pharmacologic therapy
Classification of antiarrhythmic drugs:

Vaughn Williams classification


The most frequently used classification system is the Vaughn Williams
classification, which categorizes these drugs on the basis of their in vitro
electrophysiologic effect on normal Purkinje fibers.

There are four antiarrhythmic drug classes


Class I drugs, Na-channel blockers,
Class II drugs β-adrenergic blockers,
class III drugs K-channel blockers, and
class IV drugs Ca-channel blockers

Bradycardia
• Treatment of sinus bradycardia is only necessary in patients who become
symptomatic.
1- discontinue any medication(s) that may cause sinus bradycardia whenever
possible .
2- In these patients, a permanent pacemaker may be implanted in order to allow the
patient to maintain therapy with β-blockers .

• Acute treatment of the symptomatic patient consists primarily of administration of


the anticholinergic drug atropine, which may be given in doses of 0.5 mg
intravenously (IV) every 3 to 5 minutes. The maximum recommended total dose
of atropine is 3 mg .

• In patients who are hemodynamically unstable ,epinephrine or dopamine infusion


may be administered.
Tachycardias

A-Sinus tachycardia (ST)


1- treating the underlying cause, for example, using antibiotics to treat infections,
fluid replacement to correct hypotension and hypovolaemia and beta-blockers and
antithyroid agents to manage thyrotoxicosis.

2-Management of inappropriate ST relies on the use of rate-controlling agents such


as beta-blockers or calcium channel blockers.

B-Atrial ectopic beats (extrasystoles, premature beats)


1-They are frequently asymptomatic and require no specific therapy other than
treatment of the underlying disease or avoidance of precipitants .

2-Symptomatic cases usually produce palpitations or the sensation of skipped beats


and can usually be controlled with β-blockers.

C- Atrial fibrillation (AF):


hemodynamically unstable (patients with shock or severe hypotension, pulmonary edema, or
ongoing myocardial infarction or ischemia), emergent conversion to sinus rhythm is necessary
using direct current cardioversion (DCC) + anticoagulation (How?).

In hemodynamically unstable patients who need immediate rate control (There is a potential
risk of thromboembolism in patients undergoing cardioversion who have not received
anticoagulation therapy if atrial fibrillation has been present for > 48 hours).

Hemodynamically stable AF patient The treatment strategy is by rate control or rhythm control

Rate Control Versus Rhythm Control


A-Ventricular Rate Control is achieved by drugs that are effective for ventricular rate control
are those that inhibit AV nodal impulse conduction: β-blockers, diltiazem, verapamil, and
digoxin .

B-Rhythm Control (Restoration of sinus rhythm) can be achieved with DCC or with
antiarrhythmic agents (pharmacological cardioversion )
(type Ic like flecainide , and III like amiodarone are effective ) .
D-Paroxysmal supraventricular tachycardia

Hemodynamically unstable PSVT (e.g., syncope, near syncope, anginal chest pain, severe HF)
should be treated with immediate DCC.

Nondrug measures that increase vagal tone to the AV node (e.g., unilateral carotid sinus massage,
gag reflux, ice bath)

Adenosine is the drug of choice for pharmacologic termination of PSVT


Adenosine Administration??
Adenosine contraindications??

Drugs that may be used for termination of hemodynamically stable PSVT are: Adenosine ,
Verapamil, Diltiazem, Digoxin, B- blockers, amiodarone.

Premature ventricular complexes


drug therapy is unnecessary because PVCs without associated heart disease
In patients with risk factors for arrhythmic death (recent MI, LV dysfunction), chronic drug therapy
should be restricted to β-blockers
Ventricular tachycardia (VT)
A-Acute Ventricular Tachycardia
Hemodynamically unstable VT should be terminated immediately using direct
current cardioversion (DCC) .
Amiodarone is considered the first-line agent for management of VT in patients
with normal left ventricular function, Procainamide and lidocaine is also used.
Amiodarone administrations and Side effects?

However, in patients with HF due to LV dysfunction, procainamide should be


avoided, due to negative inotropic activity, and Amiodarone or dofitilide are used .

B-Sustained Ventricular Tachycardia


Patients with chronic recurrent sustained VT are at extremely high risk for death.
The ICD is a highly effective method for preventing sudden death due to recurrent
VT or VF.

Ventricular fibrillation
1- hemodynamically unstable, due to the absence of
pulse and blood pressure.

2-Initial management includes initiation of


cardiopulmonary resuscitation (CPR).

3-Oxygen should be administered as soon as it is


available.

4- The only mean for terminating VF


and restoring sinus rhythm is electrical
defibrillation (DCC).

5-The vasopressor agents epinephrine or


Vasopressin may be also administered.
Q&A

You might also like