arrhythmia

Question 1

Cardiac Arrhythmias definition

Answer 1

●Cardiac arrhythmia is an abnormality of the cardiac rhythm.
● Arrhythmias may cause sudden death, syncope, heart failure, dizziness, palpitations or no symptoms at all.

Question 2

two main types of arrhythmia:

Answer 2

Bradycardia:Heart rate is slow (< 60 b.p.m).

Tachycardia: Heart rate is fast (> 100 b.p.m).

Question 3

mechanical and electrical activity.

Answer 3

Mechanical activity of the heart refers to atrial and ventricular contraction, the mechanism by which blood is delivered to tissues.

Mechanical activity of the heart occurs as a result of its electrical activity.
Electrical activity of the heart is controlled mainly by: SA node, AV node and the bundle of His.

Depolarization of the atria results in atrial contraction, and ventricular depolarization causes ventricular contraction.

Question 4

Transmembrane potential of cardiac cells is determined by :

Answer 4

concentrations of the ions: Sodium, Potassium & Calcium

The movement of these ions produces currents that form the basis of the cardiac action potential

Question 5

Mechanisms of Cardiac Arrhythmias

Answer 5

(a) Abnormal impulse initiation (formation): due to abnormal automaticity
If SA node automaticity decreases: this results in a reduced rate of impulse generation and a slow heart rate (sinus bradycardia).
If SA node automaticity increases: this results in an inause the impulse re-enters and creased rate of impulse generation and a rapid heart rate (sinus tachycardia)
(b) Abnormal impulse conduction: called also re-entry (because same impulse re-enters & excites areas of the heart)
**c) both.
**

Question 6

Classification of arrhythmia
Names of arrhythmias are generally composed of 2 words:

Answer 6

The 1st indicates: location of electrophysiological abnormality resulting in the arrhythmia (sinus, AV node, atrial, or ventricular)

The 2nd describes the arrhythmia as abnormally slow (bradycardia) or fast (tachycardia), or the type of arrhythmia (block, fibrillation, or flutter).

example: Sinus bradycardia, Atrial fibrillation

Question 7

Supraventricular Arrhythmias:

Answer 7

All arrhythmias above the bundle of His (i.e. SA node or AV node) and are all characterized by a normal QRS complex.
* Paroxysmal supraventricular tachycardia (PSVT)
* Atrial flutter
* Atrial fibrillation (AF)
* Wolff–parkinson– white (WPW) syndrome
* Premature atrial contractions (PAC).

Question 8

Ventricular Arrhythmias:

Answer 8

All arrhythmias originating below the bundle of His (i.e. Ventricles
* Premature ventricular contractions (PVC)
* Ventricular tachycardia (VT)
* Ventricular fibrillation (VF).

Question 9

Risk Factors
Causes of abnormal automaticity

Answer 9

hypoxia, ischemia, or excess catecholamine activity.

Hormones like adrenaline and norepinephrine can increase heart rate and automacity

Question 10

cause of Bundle Branch Block (BBB):

Answer 10

CAD
systemic hypertension
aortic valve stenosis
and cardiomyopathy.

Question 11

causes of Ventricular arrhythmias:

Answer 11

Ischemia, organic heart disease, exercise, metabolic or electrolyte imbalance.

Question 12

TdP (Torsades de Pointes ) causes and symptoms

Answer 12

• Hypokalemia, hypomagnesemia, hypocalcemia,
• concurrent use of >1 QT-prolonging drug,
• advanced age, female gender
• heart disease, treatment with diuretics (due to electrolyte imbalance),
• impaired hepatic drug metabolism

Torsades de Pointes (TdP) is a
rapid polymorphic VT preceded by QTc interval prolongation that can degenerate into VF, making it potentially life threatening.

Question 13

Patient Assessment
af, pstv, conduction block

Answer 13

S & S are dependent on the type of arrhythmia
AF: Palpitations, lightheadedness, dizziness, and reduced exercise tolerance are the most common symptoms. Stroke is one of the most severe complications.
PSVT: tachycardia (180–200 beats/minute), nervousness, anxiety. May progress to angina, heart failure, or shock, depending on underlying conditions.
Conduction Blocks: 1st-degree AV block is usually asymptomatic. In 3rd-degree block, none of the impulses from the SA node reaches the ventricles.

Question 14

Diagnosis of arrythmias

Answer 14

• not symptoms alone -> similarity in symptoms between arrhythmias

History of present illness, presenting symptoms, and 12-lead ECG are needed to make diagnosis

Assess possible correctable etiologies e.g. myocardial ischemia, potassium concentration & thyroid function tests

If the patient is taking pro-arrhythmogenic drug e.g. digoxin, determine the serum concentration and assess the condition

Question 15

Goal of antiarrhythmic drug therapy

Answer 15

• Restore normal sinus rhythm and conduction
• Prevent more serious and possibly lethal arrhythmias from occurring.
• Maintain normal sinus rhythm and conduction
• Prevent other complications e.g. thromboembolic events

Question 16

Non-pharmacological Treatment

Answer 16

Correction of the underlying condition e.g. Valve replacement, electrolyte imbalance

DCC (Direct Current Cardioversion) might be needed e.g. in VF

Long-term management of some types of arrhythmias e.g. sick sinus syndrome may require implantation of a permanent pacemaker.

Question 17

Anti-arrhythmic drugs 4 classes

Answer 17

Ia > Moderate Na+ channel blocker
Ib > Weak Na+ channel blocker
Ic > Strong Na+ channel blocker
II > β blocker
III > K+ channel blocker
IV > Ca++ channel blocker
V > Other Mechanisms (Direct nodal inhibition)

Question 18

drugs example: Ia
Ib
Ic
II
III
IV
V

Answer 18

• Moderate Na+ channel blocker=Quinidine, Procainamide
• Weak Na+ channel blocker= Lignocaine, Mexilitine
• Strong Na+ channel blocker=Flecainide
• β blocker=Atenolol, Metoprolol
• K+ channel blocker=Amiodarone, Sotalol
• Ca++ channel blocker=Verapamil, Diltiazem
• Other Mechanisms (Direct nodal inhibition)=Digoxin, Adenosine

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Question 19

Ia

Answer 19

Atrial and ventricular arrhythmias
Can cause TdP

Quinidine-> increase digoxin , Procainamide rarly use cuz of toxicity sle and tdp

Question 20

IV procainamide

Answer 20

IV procainamide used for hemodynamically stable ventricular tachycardia and acute conversion of AF

Question 21

Ib

Answer 21

Acute (both) & chronic (mexilitine) treatment of ventricular arrhythmias (e.g. VT, VF

Lignocaine DOC FOR acute ventricle arrythmia only iv
Mexilitine

Question 22

SE of Ib drugs

Answer 22

Paresthesias, tremor, convulsions

Question 23

Ic

Answer 23

Suppressing ventricular arrhythmias
-Flecainide: prophylaxis in paroxysmal AF
Severe pro-arrhythmogenic

only orally, Cannot be used in patients with structural heart disease (e.g. HF or severe left ventricle hypertrophy) or after MI.

Question 24

class II betablocker

Answer 24

management of supraventricular & ventricular arrhythmias particularlly trachycardias e.g. PSVT, atrial flutter and AF
Effects additive with digoxin & CCBs
not proarrythmic

Question 25

catecholamine-induced arrhythmias

Answer 25

bb phaeochromocytoma, hyperthyroidism, amphetamine overdose)·

Question 26

III

Answer 26

Supraventricular and ventricular arrhythmias
Can cause TdP

Question 27

IV
ccb

Answer 27

Supraventricular Tachycardias
Effects additive with digoxin & β-blockers
preventing the occurrence of ventricular arrhythmias
Contraindicated: pre-existing depressed heart function . (HF)

ADR: Bradycardia, and asystole especially when given in combination with β-adrenergic blockers

Question 28

why using non dihrdroprydine cbb not dihydropyridne?

Answer 28

Verapamil & diltiazem are used Because they act on the heart

Dihydropyridine CCBs are not used because they only act on peripheral blood vessels

Question 29

Other Antiarrhythmic Drugs (Class V)

Answer 29

Adenosine is DoC for PSVT, It is used only by slow intravenous bolus because it is extremely short acting (15 seconds only)
* It has a low-profile toxicity (might cause bronchospasm)

Digoxin is used to control the ventricular rate in atrial fibrillation or flutter

Question 30

acute ventrical arrythmia DOC

Answer 30

lignocaine

Question 31

prophylaxis in paroxysmal AF

Answer 31

flecainide

Question 32

DoC for PSVT

Answer 32

Adenosine

Question 33

Adenosine MOA

Answer 33

Adenosine activates A1-purinergic receptors decreasing the SA nodal firing and automaticity, reducing conduction velocity, and depressing AV nodal conductivity

Question 34

class IV CCb adv and contracindication

Answer 34

ADR: Bradycardia, and asystole especially when given in combination with β-adrenergic blockers

Contraindicated in patients with pre-existing depressed heart function (e.g. HF) because of their negative inotropic activity

Question 35

arteial fibrillation vs atrial fluterr

Answer 35

In AF electrical signals come from the atria at a very fast & erratic rate.
Ventricles contract in an irregular manner
The ECG shows normal but irregular QRS complexes, fine oscillations of the baseline (so-called fibrillation or f waves) and no P waves.

Electrical signals come from the atria at a fast but even rate, causing ventricles to contract faster and increase the heart rate.
When the signals from the atria are coming at a faster rate than the ventricles can respond to, the ECG pattern develops a signature “sawtooth” pattern, showing two or more flutter waves between each QRS complex.

Question 36

AF diagnosis

Answer 36

• ECG shows absent p-waves and irregular, narrow QRS complexes
• Thyroid function tests: to rule out thyrotoxicosis
• LFTs (including GGT): If elevated, alcohol may be the cause
  * Chest X-ray: to detect pulmonary oedema
• Transthoracic echocardiogram

Question 37

AF treatment for Hemodynamically unstable patients

Answer 37

Emergency conversion to sinus rhythm is necessary using electrical conversion (DCC-direct current cardioversion)
This can quickly and effectively restores 85% - 90% of patients with AF to normal sinus rhythm.

Question 38

Goal 1: Ventricular Rate Control

Answer 38

Can be achieved by inhibiting the proportion of electrical impulses conducted from the atria to the ventricles through the AV node.

Drugs : β-blockers, CCBs, digoxin, and amiodarone
In patients who present to the emergency with symptomatic persistent AF or paroxysmal AF, ventricular rate control is initially achieved using I.V. β-blockers or CCBs.

In HF: β-blockers or digoxin can be used
Initial monotherapy beta-blocker (not sotalol) or a rate-limiting CCBs
digoxin monotherapy: with significant pulmonary oedema and / or acute heart failure symptoms

Question 39

rythm control

Answer 39

dcc: more effective
drugs: flecainide, amidirone, propafenone

if duration of af more thn 48 hnrs or unknown time when symp appear delay restoriing rytm , cuz risk of thrombus formation
use anticogulant 3 weeks prior to dcc
anticogulant 4 weeks after restoring sinus

Question 40

Maintenance of Sinus Rhythm & Preventing further recurrences

Answer 40

only in patients with episodes of paroxysmal AF who continue to experience symptoms despite maximum tolerated doses of drugs for ventricular RATE CONTROL.

continue using anticogulations
Antiarrhythmic agents primarily used in a rhythm-control strategy are: disopyramide (Class IA), flecainide and propafenone (Class IC), and sotalol, and amiodarone (Class III)

**amidarone most effective in maintaing rythm **

Question 41

Goal 4: Prevention of Stroke and Systemic Thromboembolism

Answer 41

for prevention of thromboembolism unless contraindication exist.
Choices available are: warfarin, dabigatran, rivaroxaban, and apixaban
.
dabigatran better cuz no inr, and drug interaction, rapid onset

warfarin is used in mechanical valve, valvular af, end stage RF

Question 42

combining warfarin and antiplatelet for af?

Answer 42

Consider combining warfarin and antiplatelet in patients who have had an MI, have PCI or have undergone CABG
After 12 months, review the continued need for antiplatelet therapy

Question 43

Pill in the pocket
for AF?

Answer 43

Standard agent is FLECAINIDE
May be suitable for some patients with a history of paroxysmal AF.
The patient does not take regular antiarrhythmic therapy but is given a single dose to use if the AF recurs.

Question 44

Outcome Evaluation in AF therpy

Answer 44

Monitor
HR less than 80 BPM for most patients
HR less than 110 BPM may be accepable as long as patients remain asymptomatic and LV systolic function is preserved.
**Monitor ECG **to assess continued presence of AF and to determine whether conversion to sinus rhythm has occurred.

In patients receiving warfarin, monitor INR approximately monthly to make sure it is therapeutic (target: 2.5; range: 2.0–3.0).
Monitor patients for ADR of specific drug therapy.
Monitor patients receiving oral anticoagulation for S&S of bleeding.