AMMAR YASSER https://t.

me/equipment100

Cardiac Physiology:

• Automaticity, Excitability, Conductivity, Contractility:

• Automaticity: Generates electrical impulse independently.
• Excitability: Responds to electrical stimulation.
• Conductivity: Passes electrical impulses from cell to cell.
• Contractility: Shortens in response to electrical stimulation

Conduction System Structures and Functions:

• Sinoatrial (SA) node: Dominant pacemaker, located in upper right atrium. Intrinsic rate 60-100 bpm.
• Internodal pathways: Direct electrical impulses between SA and AV nodes.
• Atrioventricular (AV) node: Slows, delay conduction, intrinsic rate 40-60 bpm.
• Bundle of His: Transmits impulses to bundle branches.
✓ Left bundle branch: Leads to left ventricle.
✓ Right bundle branch: Leads to right ventricle.
• Purkinje system: Spreads impulses rapidly throughout ventricular walls. Located at terminals of bundle
branches, Intrinsic rate 20-40 bpm.

Electrophysiology:

• Depolarization: Alters cell's electrical charge, by a shift of electrolytes on either side of the cell
membrane This change stimulates muscle contraction.

• Repolarization: Chemical pumps re-establish internal negative charge, cells return to resting state.

Note: Mechanical and electrical functions influenced by proper electrolyte balance (sodium, calcium,
potassium, magnesium).

Electrocardiography (ECG):

Definition: Process of producing an electrocardiogram (ECG or EKG).

ECG: Graph of voltage vs. time, records heart's electrical activity through cardiac cycles.

Electrodes: Placed on skin, detect small electrical changes during depolarization and repolarization.

limb Leads:

• Electrodes on right arm (RA), left arm (LA), right leg (RL), left leg (LL). With only four electrodes, six leads

• Standard Leads (Bipolar): I, II, III.

• Augmented Leads (Unipolar): aVR, aVL, aVF.

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Limb Lead:

1. Bipolar Leads (I, II, III):

• Consist of two electrodes of opposite polarity (positive and negative).

• Third (ground) electrode minimizes electrical activity from other sources.

2. Unipolar Leads (aVR, aVL, aVF):

• Consist of a single positive electrode and a reference point with zero electrical potential
in the center of the heart’s electrical field.

Right-Sided 12-Lead ECG:

• Limb leads placed as usual; chest leads mirror the standard 12-lead chest placement.

• ECG machine can't recognize lead reversal, may still print "V₁-V6" next to the tracing.

Clinical Tip: Right-sided ECG useful for assessing possible right ventricular infarction in acute inferior MI.

15-Lead ECG:

• Areas not well visualized by standard chest leads: wall of the right ventricle and posterior wall of
the left ventricle.

• Components:

• Includes standard 12 leads.

• Additional leads: V4R, V8, and V9.

• Purpose:

• Increases the chance of detecting a myocardial infarction (MI) in these areas.

Clinical Tip:

• Use a 15-lead ECG when the standard 12-lead is normal but the clinical history suggests an acute
infarction. And ischemia (Troponin also)
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RL = Right Leg (The third (ground) electrode)

aVR :none view

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Components of an ECG:

1. P Wave:

• Appearance: First wave seen, Small, rounded, upright (positive) wave.

• Significance: Indicates atrial depolarization and contraction.

2. PR Interval:

• Definition: Distance between the beginning of the P wave and the beginning of the QRS
complex.

• Purpose: Measures the time during which a depolarization wave travels from the atria to the
ventricles.

3. QRS Interval:

• Definition: Three deflections following the P wave.

• Indication: Represents ventricular depolarization and contraction.

• Subcomponents:

• Q Wave: First negative deflection.

• R Wave: First positive deflection.

• S Wave: First negative deflection after the R wave.

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4. ST Segment:

• Definition: Distance between the S wave and the beginning of the T wave.

• Purpose: Measures the time between ventricular depolarization and the beginning of
repolarization.

5. T Wave: (inverted T wave instable angina)

• Appearance: Rounded, upright (positive) wave following the QRS complex.

• Representation: Represents ventricular repolarization.

6. QT Interval: (prolong QT Azithromycin)

• Definition: Measured from the beginning of the QRS complex to the end of the T wave.

• Significance: Represents the total ventricular activity.

7. U Wave:

• Appearance: Small, rounded, upright wave following the T wave.

• Observation: Most easily seen with a slow heart rate (HR). (electrolyte disturbance)

• Representation: Represents the repolarization of Purkinje fibers.

Reporting an ECG Recording:

Patient Data:

• Check key information on ECG/request form:

• Patient name

• Date of birth

• Identification number (e.g., hospital number)

• Reason for the request

• Relevant past medical history

• Relevant medication
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Technical Data:

• Date and time of recording

• Paper speed and calibration

• Technical quality

• Any atypical settings

• Additional leads (e.g., posterior leads, right-sided chest leads)

• Physiological maneuvers (e.g., ECG recorded during deep inspiration)

• Diagnostic or therapeutic maneuvers (e.g., ECG recorded during carotid sinus massage)

Standard ECG:

• ECGs printed on a grid with the horizontal axis representing time and the vertical axis
representing voltage.

• Standard values on the grid: 25 mm\sec

• Small box: 1 mm × 1 mm (0.1 mV × 0.04 seconds)

• Large box: 5 mm × 5 mm (0.5 mV × 0.20 seconds)

ECG Fundamentals:

1. Rate

2. Rhythm:

• Supraventricular

• Ventricular

• Conduction problems

3. Axis
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ECG Details: using a step-by-step approach

• Individual features:

• P wave

• PR interval

• Q wave

• QRS complex

• ST segment

• T wave

• QT interval

• U wave

Heart Rate:

• Methods for Calculating Heart Rate (Regular rhythms):

• Method 1 (Count Large Boxes): quickly determined Regular rhythms

• Count large boxes between two R waves.

• Divide the count into 300 to calculate bpm.

• Method 2 (Count Small Boxes): for fast heart rates

• Count small boxes between two R waves for fast heart rates.

• Divide the count into 1500 to calculate bpm.

• Method 3 (Six-Second ECG Rhythm Strip):

• The best method for measuring irregular rates with varying R-R intervals per 60
sec(1min)

• Count R waves in a 6-sec strip. (30 Large box)

• Multiply by 10 to get the average bpm for irregular rates.

AMMAR YASSER https://t.me/equipment100

Heart Rate Assessment and Management:

Heart Rate Evaluation:

1. Normal vs. Abnormal:

• Normal heart rate: 60-100/min.

• Bradycardia: Below 60/min.

• Tachycardia: Above 100/min.

2. Bradycardia Assessment:

• Definition: Heart rate below 60/min.

• Identification: Analyze cardiac rhythm and conduction disturbances.

3. Potential Bradycardia Causes:

• Sinus bradycardia

• Sick sinus syndrome (tachy brady syndrome)

Management of Bradycardic Patient:

1. ABCDE Approach:

• Assess airway, breathing, circulation, disability, and exposure.

2. Monitoring and Initial Actions:

• Monitor SpO2; administer oxygen if hypoxic.

• Monitor ECG and blood pressure; record 12-lead ECG.

• Obtain IV access.

3. Identify and Treat Reversible Causes:

• Address electrolyte abnormalities.

4. Assessment for Adverse Features:

• Check for:

• Shock

• Myocardial ischemia

• Syncope

• Heart failure
AMMAR YASSER https://t.me/equipment100

Algorithm for Management:

1. Adverse Features Present?

• Yes:

• Administer Atropine 500 mcg IV.

• Assess response.

• No response

• If unsatisfactory, consider interim measures (repeat Atropine to

maximum of 3 mg, transcutaneous pacing, or Isoprenaline 5 mcg min¹ IV
/Adrenaline 2-10 mcg min¹ IV).

• Seek expert help for transvenous pacing if needed.

• Yes response:

• Assess the risk of asystole (Mobitz II AV block, recent asystole, complete heart
block with broad QRS, ventricular pause >3 s).

• If no risk of asystole Continue observation

2. Adverse Features Absent?

• Absent Adverse Features:

• Assess the risk of asystole (Mobitz II AV block, recent asystole, complete heart
block with broad QRS, ventricular pause >3 s).

• yes, the risk of asystole

If unsatisfactory, consider interim measures (repeat Atropine to maximum of 3

mg, transcutaneous pacing, or Isoprenaline 5 mcg min¹ IV /Adrenaline 2-10 mcg
min¹ IV).

Seek expert help for transvenous pacing if needed

• If no risk of asystole:

• Continue observation.
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Tachycardia Assessment and Management:

Heart Rate Above 100/min:

Definition of Tachycardia:

• Heart rate above 100/min.

Identification Process:

• Check QRS complexes:

1. Narrow (<3 small squares):

• origin possibilities above the ventricles:

• Sinus tachycardia
• Atrial tachycardia
• Atrial flutter
• Atrial fibrillation
• AV re-entry tachycardia (AVRT)
• AV nodal re-entry tachycardia (AVNRT)
2. Broad (>3 small squares):

• Consider ventricular origin possibilities:

• Ventricular tachycardia
• Accelerated idioventricular rhythm
• Torsade's de pointes
Management:

1. Assess Urgency: first step

• Use the ABCDE approach.

• Evaluate for adverse features in the peri-arrest situation.

2. Gather Clues from Patient History:

• Palpitation onset and stop (sudden or gradual).

• Situations triggering palpitations. (e.g. during exercise, lying quietly in bed)

• Duration of palpitations.

• Associated symptoms (dizziness, syncope, falls, fatigue, breathlessness, chest pain).

• Have the patient describe the palpitations (rate, rhythm).

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3. Ask About Related Disorders:

• Inquire about symptoms of related disorders (e.g., hyperthyroidism).

• Obtain a list of current medications.

4. Check for Drug Influence:

• Identify drugs (e.g., salbutamol) that can increase heart rate. (positively chronotropic)

5. Consider Caffeine Intake:

• Ask about caffeine intake from coffee, tea, and energy drinks.

6. Thorough Examination:

• Look for evidence of hemodynamic disturbance (hypotension, cardiac failure, poor

peripheral perfusion).

• Check for coexistent disorders (e.g., thyroid goiter).

7. Use History, Examination, and Further Investigations:

• Utilize the collected information for a diagnosis.

• Conduct additional investigations (e.g., plasma electrolytes, thyroid function tests).

AMMAR YASSER https://t.me/equipment100

Tachycardia Assessment and Management Algorithm:

Assessment:

1. ABCDE Approach:

• Assess airway, breathing, circulation, disability, and exposure.

• Monitor SpO2 and administer oxygen if hypoxic.

• Monitor ECG and blood pressure; record 12-lead ECG.

• Obtain IV access.

• Identify and treat reversible causes (e.g., electrolyte abnormalities).

2. Adverse Features:

• Check for:

• Shock

• Syncope

• Myocardial ischemia

• Heart failure

Unstable (Adverse Features Present):

• Yes (Unstable):

• Synchronized DC Shock(100 J):

• Up to 3 attempts.

• Seek Expert Help:

• Consult with a specialist.

• Amiodarone (cordarone)Administration:

• 300 mg IV over 10-20 min.

• Repeat shock.

• Administer amiodarone 900 mg over 24 h.

AMMAR YASSER https://t.me/equipment100

Stable (No Adverse Features):

Narrow QRS (<0.12 s):

1. Regular Rhythm:

• (Irregular):

• Probable AF:

• Control rate with beta-blocker or diltiazem.

• Consider digoxin or amiodarone if in heart failure.

• Assess thromboembolic risk and consider anticoagulation.

• (regular):

• Vagal Maneuvers (carotid sinus massage):

• Attempt maneuvers.

• Adenosine Administration (pharmacologic DC shock):

• 6 mg rapid IV bolus; if no effect, give 12 mg; if no effect, give further 12

mg.

• Monitor/record ECG continuously.

• First choice for SVT (supra ventricular tachycardia)

• Sinus Rhythm Achieved:

• Probable re-entry paroxysmal SVT:

• Record 12-lead ECG in sinus rhythm.

• If SVT recurs, treat again and consider anti-arrhythmic

prophylaxis.

• Sinus Rhythm Not Achieved:

• Seek expert help.

• Possible atrial flutter:

• Control rate (e.g., with beta-blocker).

AMMAR YASSER https://t.me/equipment100

Broad QRS:

2. QRS Regular:

• Regular:

• If VT (or uncertain rhythm):

• Amiodarone 300 mg IV over 20-60 min, then 900 mg over 24 h.

• If known to be SVT with bundle branch block:

• Treat as for regular narrow-complex tachycardia.

• Irregular:

• Seek Expert Help:

• Possibilities include AF with bundle branch block.

• Treat as for narrow complex.

• Possibly Pre-excited AF:

• Consider amiodarone.

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Approach to Heart Rhythms:

1. Rhythm Strip Analysis:

• Begin with a rhythm strip, often automatically included at the bottom of a 12-lead ECG.

• Standard lead for rhythm strip: Lead II; alternative leads can be used if necessary.

2. Identifying Cardiac Rhythm:

• Primary Questions:

• Where does the impulse arise from?

• Sinoatrial (SA) node

• Atria

• Atrioventricular (AV) junction

• Ventricles

• How is the impulse conducted?

• Normal conduction

• Impaired conduction

• Accelerated conduction (e.g., Wolff-Parkinson-White [WPW] syndrome)

AMMAR YASSER https://t.me/equipment100

• Seven Questions to Narrow Down Diagnoses:

1. How is the patient?

2. Is ventricular activity present?

3. What is the ventricular rate?

4. Is the ventricular rhythm regular or irregular?

5. Is the QRS complex width normal or broad?

6. Is atrial activity present?

7. How are atrial activity and ventricular activity related?

3. Clinical Assessment (ABCDE Approach):

• Assess airway, breathing, circulation, disability, and exposure.

• Evaluate adverse features indicating hemodynamic instability:

• Shock hypotension (systolic blood pressure <90 mmHg), clamminess, sweating, pallor, confusion
or reduced conscious level

• Syncope cerebral hypoperfusion

• Myocardial ischemic chest pain and/or ischemic ECG changes

• Heart failure Pulmonary oedema, elevated jugular venous pressure, peripheral/sacral oedema

4. Is Ventricular Activity Present?

• Check for electrical activity on the ECG.

• If absent, assess patient, electrodes, and gain setting.

5. What Is the Ventricular Rate?

• Ventricular activity is represented on the ECG by QRS complexes

• Calculate the ventricular rate to classify the rhythm as:

• Bradycardia (<60 beats/min)

• Normal (60-100 beats/min)

• Tachycardia (>100 beats/min)

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6. Is the Ventricular Rhythm Regular or Irregular?

• Assess regularity by observing spacing between QRS complexes.

• One way to do this is to place a piece of paper alongside the rhythm strip

• Classify as:

• Regular (equal spacing)

• Irregular (variable spacing)

• Regular rhythms

■ Sinus rhythm

■ Sinus bradycardia

■ Sinus tachycardia

■ Atrial flutter (if constant AV block, e.g. 2:1)

■ Atrial tachycardia

■ AV re-entry tachycardia (AVRT)

■ AV nodal re-entry tachycardia (AVNRT)

■ Accelerated idioventricular rhythm

■ Monomorphic ventricular tachycardia (VT)

■ Polymorphic ventricular tachycardia (torsades de pointes)

■ Third-degree AV block (if regular escape rhythm)

• Irregular rhythms

■ Sinus arrhythmia (rate varies with respiration)

■ Ectopic boats (atrial, junctional, ventricular)

■ Atrial fibrillation

■ Atrial flutter (if variable AV block)

■ Sinus arrest and SA block

■ Mobitz type I second-degree AV block

■ Mobitz type II second-degree AV block

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7. Is the QRS Complex Width Normal or Broad?

use the width of the QRS complex to try to determine how the ventricles were depolarized

• Classify as:

• Narrow (<3 small squares): Supraventricular rhythm

• Broad (>3 small squares):

• Ventricular rhythm arisen from within the ventricles and thus been unable to
travel via the His-Purkinje system

• Supraventricular rhythm with aberrant conduction

8. Is Atrial Activity Present?

• Presence of P waves indicates atrial depolarization.

• P waves may not originate from the SA node. does not mean that the depolarization necessarily
started at the SA node

9. How Are Atrial Activity and Ventricular Activity Related?

• Evaluate the relationship between P waves and QRS complexes:

• every QRS complex is associated with a P wave, this indicates that the atria and ventricles are
being activated by a common source

• Common source (usually SA node). but not necessarily

• AV junctional rhythms will also depolarize both atria and ventricles)

Every QRS Complex Associated with a P Wave:

• Atria and ventricles activated by a common source.

• Usually, the SA node is the common source.

• Note: AV junctional rhythms can also depolarize both atria and ventricles.

More P Waves than QRS Complexes:

• Conduction between atria and ventricles is either partly blocked.

• Some impulses may get through

• Complete block can occur, leading to ventricles developing their own escape rhythm.
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3. More QRS Complexes than P Waves:

• AV Dissociation:

• Ventricles operate independently of the atria.

• Ventricles may be at a higher rate than the atria.

Broad-complex versus narrow-complex rhythms → https://t.me/equipment100/762

Supraventricular rhythms

1. Sinus Rhythm:

• Normal cardiac rhythm.

• SA node acts as the natural pacemaker.

• Discharges at a rate of 60-100/min.

• Characteristic features:

• Heart rate: 60-100/min.

• Normal P wave morphology. (upright in lead II and inverted in lead aVR)

• Every P wave is followed by a QRS complex.

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2. Sinus Arrhythmia:
• Variation in heart rate during inspiration and expiration.
• Characteristic features:
• Heart rate varies with respiration
• Difference between longest and shortest P-P intervals >0.12 s.
• Increased heart rate during inspiration. response to the increased volume of blood
returning to the heart (which triggers baroreceptors that inhibit vagal tone)
• Decreased heart rate during expiration. response to the decreased volume of blood
returning to the heart (vagal tone is no longer inhibited)
• Normal P wave morphology. (upright in lead II and inverted in lead aVR)
• Every P wave is followed by a QRS complex.

3. Sinus Bradycardia:
• Sinus rhythm with a heart rate of less than 60/min.
• Characteristic features:
• Heart rate less than 60/min.
• Normal P wave morphology. (upright in lead Il and inverted in lead aVR)
• Every P wave is followed by a QRS complex.

• Possible causes:

1. Drugs (e.g., digoxin, beta blockers, beta blocker eye drops, atenolol = tenormin).
2. Ischemic heart disease, myocardial infarction
3. Hypothyroidism.
4. Hypothermia.
5. Electrolyte abnormalities.
6. Obstructive jaundice.
7. Uremia.
8. Raised intracranial pressure.
9. Sick sinus syndrome.
AMMAR YASSER https://t.me/equipment100

4. Sinus Tachycardia:
• Sinus rhythm with a heart rate of greater than 100/min.
• Characteristic features:
• Heart rate greater than 100/min.
• Normal P wave morphology. (upright in lead II and inverted in lead aVR)
• Every P wave is followed by a QRS complex.
• Possible causes:
1. Drugs (e.g., adrenaline, atropine, salbutamol =ventolin ,
caffeine and alcohol).
2. Ischemic heart disease. acute myocardial infarction
3. Heart failure.
4. Pulmonary embolism.
5. Fluid loss.
6. Anemia.
7. Hyperthyroidism.

Note: SVT no P wave but Sinus rhythm normal P wave

5. Atrial Ectopic Beats:

• Also known as atrial extrasystoles, APCs, APBs, or PACs. (tow type atrial or ventricular)
• atrial extrasystole
• atrial premature complex Significant
• atrial premature beats
• premature atrial contraction trigeminy or bigeminy
• Identified by a P wave appearing earlier than expected.
• P wave has a different shape than normal.
• Usually conducted to the ventricles, resulting in a QRS complex.
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Other Supraventricular Rhythms:

E Sick Sinus Syndrome
E Atrial Fibrillation
E Atrial Flutter
E Atrial Tachycardia
E Focal Atrial Tachycardia
E Multifocal Atrial Tachycardia
E AVRT (Atrioventricular Re-entry Tachycardia)
E AVNRT (Atrioventricular Nodal Re-entry Tachycardia)

6. Atrial Fibrillation (AF):

• Basis of AF is rapid, chaotic atrial activity.
• No P waves on ECG; baseline consists of low-amplitude oscillations (fibrillation or f waves).
• 400-600 atrial impulses reach the AV node every minute, but only some are transmitted to the
ventricles. (erratic)
• although the rate can be normal or even slow
• Ventricular rate is typically fast (100-180/min), creating an 'irregularly irregular' QRS complex
rhythm.

• Categories of AF:
1. First-diagnosed AF: Patients presenting in AF for the first time.
2. Paroxysmal AF: Self-terminating episodes, lasting <48 hours (up to 7 days).
3. Persistent AF: Continuous AF lasting >7 days or requiring cardioversion.
4. Long-standing persistent AF (chronic): Present for at least one year, with an aim to
restore sinus rhythm.
5. Permanent AF (chronic): Continuous AF where the arrhythmia is accepted with no plan
to restore sinus rhythm.

Normal Atrial Fibrillation (AF) = Fibrillation wave= HR 80

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• Key Management Issues:

• Reducing Stroke Risk:
• AF increases stroke risk fivefold; one in five strokes is AF-related.
• Anticoagulation is recommended for valvular AF and non-valvular AF unless low
risk or contraindications.
• valvular AF (including rheumatic valve disease and prosthetic valves)
• with non-valvular AF anticoagulation is recommended for all (high risk, age>60),
except in those patients who are at low risk (aged <65 years and lone AF)

• Ventricular Rate Control:

• Common drugs: beta blockers, non-dihydropyridine calcium channel blockers
(verapamil, diltiazem).
• Digoxin is good at rest but less effective during exercise. (effective toxicity)
• Amiodarone effective but carries the risk of chemical cardioversion to sinus
rhythm (lead to thromboembolism unless the patient has been anticoagulated,
where appropriate)
• Rate control is preferred in the elderly and those with minimal symptoms.
• Target: resting ventricular rate <110/min; stricter control if symptomatic.
• aiming for a resting heart rate <80/min (with a heart rate <110/min during
moderate exercise)
• If drug therapy cannot attain satisfactory rate control in AF, and restoration of
sinus rhythm cannot be achieved
• alternative strategy is to undertake ablation of the AV node, permanent pacing
• Digoxin, Amiodarone for old age and minimum symptom

• Rhythm Control:
• Consider for symptomatic patients despite rate control.

• Cardioverting to Sinus Rhythm:

• Urgent electrical cardioversion for recent-onset AF and
hemodynamically unstable patients.
• Stable patients presenting within 48 hours can also have urgent
electrical cardioversion.
• Anticoagulant cover with IV unfractionated heparin initially, followed by
at least 4 weeks' oral anticoagulation (unless age <65 and 'lone' AF).

Cardioversion for
hemodynamically unstable
severe hypotension
deferrable consciousness
shock patient

with anticoagulant: Clexane, unfractionated heparin

AMMAR YASSER https://t.me/equipment100

7. Atrial Flutter:
• Atrial rate: Usually 250-350/min, often close to 300/min.
• regular
• AV node can't keep up; common 2:1 block (alternate atrial impulses to AV node), but 3:1, 4:1, or
variable blocks occur.
• Ventricular rate less than atrial rate, often 150, 100, or 75/min in 2:1 block.
• Characteristic Features:
• Atrial rate around 300/min.
• 'Sawtooth' baseline appearance on ECG due to flutter or 'F' waves.
• Thromboembolism Risk:
• Atrial flutter carries a risk of thromboembolism.
• Assessment for anticoagulant therapy similar to guidelines in AF.
• Treatment of Atrial Flutter:
• Medications:
• Heart rate control: Calcium channel blockers, beta-blockers.
• Rhythm control: Antiarrhythmic drugs.
• Procedures:
• Cardioversion: Electrical shock.
• Catheter Ablation: Destroys tissue creating abnormal signals.
• Temporary pacemaker/implantable cardioverter defibrillator ICD setting
change.
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8. Ventricular Fibrillation (VF):

• ECG shows irregular waves with varying morphology and amplitude.
• Dangerous
• Leads to cardiac arres
• shockable rhythm

• Causes:
• Ischemic Heart Disease (IHD).
• Antiarrhythmic drugs.
• Severe hypoxia.

• Management:
• DC Shock First choice or CPR:
• Immediate non-synchronized at 200 J.
• If ineffective, repeat at (200-360 J).
• IF DC shock fails start basic and advanced life support (CPR)

• Drug Therapy:
• Amiodarone (preferred).
• Others: Lidocaine, procainamide.
• Drug may lead AF

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