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AMC MCQ - You Can Do It!!!!!❤️❤️ > ECG diagnoses > Flashcards

ECG diagnoses Flashcards

1
Q

P wave duration, amplitude & Characteristics

A

P duration < 0.12 sec = 3 small squares

P amplitude < 2.5 mm

Notched P waves “P mitrale” = Left atrial enlargement. Normal amplitude but increased duration (> 3 small squares )

If the P is not seen in LII, look for it in V1

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2
Q

FREQUENCY CALCULATION

A

Vertical bar every 15 big squares

30 bigs squares = 6 sec

Number of Rs x 10 in 6 sec = Heart frequency

300, 150, 100, 75, 60, 50, 40

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3
Q

PR interval duration

A

0.12 - 0.20 sec

3 - 5 small squares

1 big square = 0.20 seg = 200 ms

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4
Q

Prolong PR interval cause

A

> 1 big square or > 220 ms

1st degree AV Block

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5
Q

Short PR interval cause

A

< 0.12 sec or < 3 small squares

Presence of an accessory pathway

Asocc with delta wave = WPW

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6
Q

ECG Normal Axis

A

Lead I: QRS (+)

AVF: QRS (+)

(0 to +90)

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7
Q

ECG Left deviated Axis

A

Lead I: QRS (+)

AVF: QRS (-)

(0 to +90)

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8
Q

CAUSES OF LEFT AXIS DEVIATION

A

Left ventricular hypertrophy

Left bundle branch block

Wolff-Parkinson-White Syndrome

Horizontally orientated heart: Short patient, pregnant or ascites

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9
Q

ECG Rigth deviated Axis

A

Lead I: QRS (-)

AVF: QRS (+)

(+90 to +180)

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10
Q

CAUSES OF RIGHT AXIS DEVIATION

A

Right ventricular hypertrophy

Pulmonary embolism

Lateral/posterior wall STEMI

Chronic lung disease: COPD

Sodium-channel blockade: TCA poisoning

Wolff-Parkinson-White syndrome

Dextrocardia

Normal paediatric ECG <2yo

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11
Q

Left Ventricle Hypertrophy (LVH) in the ECG

A

Left deviated Axis
V6: QRS (+) & T (-)
V1: QRS (-) & T (+)

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12
Q

Left Ventricle Hypertrophy (LVH) CAUSES

A
  1. Essential hypertension
  2. Hypertrophic Obstructive Myocardiopathy (HCOM)
  3. Subaortic and Aortic stenosis
  4. Aortic regurgitation
  5. Mitral regurgitation
  6. Coarctation of the aorta
  7. Ventricular septal defect (VSD)
  8. Infiltrative cardiac processes: Amyloidosis, Fabry disease, Danon disease
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13
Q

HYPERTROPHIC OBSTRUCTIVE CARDIOMYOPATHY (HCOM) in the ECG

A

Classic dagger Q waves on the left precordial leads

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14
Q

Right Ventricle Hypertrophy (LVH) in the ECG

A

Right deviated Axis:
V6: QRS (-) & T (+)
V1: QRS (+) & T (-)

Normal QRS duration

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15
Q

Right Ventricle Hypertrophy (LVH) causes

A
  1. Acyanotic Congenital Heart Diseases: ASD & VSD
  2. Pulmonary valve stenosis (Amiodarone)
  3. Tricuspid valve regurgitation
  4. Tetralogy of Fallot
  5. Lung diseases: Pulmonary fibrosis, chronic obstructive pulmonary disease, and sleep apnoea.
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16
Q

Lead II Isoelectric meanings

A
  1. Right Ventricle Hypertrophy (RVH)
  • Mechanical: Right deviated Axis
  • Electrical Conduction impaired: Normal Axis
  1. Left Branch Bundle Block (LBBB)
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17
Q

Left Branch Bundle Block (LBBB) in the ECG

A

Lead II : P wave wide & prolong PR interval

Axis will be normal or Left deviated

V6: QRS (+) usually notched & T (-) with ST depression

V1: QRS (-)

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18
Q

Rigth Branch Bundle Block (RBBB) in the ECG

A

V1: QRS (+) Wide-notched and T (-) with ST depression

V6: Prominent S

  • RsR’ on V1 –V2

Axis will be normal or Right deviated

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19
Q

QRS Duration

A

0.06 - 0.10 sec

1.5 - 2.5 small squares

> 2.5 small squares = Wide QRS

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20
Q

Wide QRS causes

A
  • Hyperkalemia.
  • Hyper- or hypo-magnesemia.
  • Supraventricular tachycardia (SVT) + bundle branch block (BBB)
  • SVT with aberrant conduction.
  • Atrial fibrillation (Afib) + Wolff-Parkinson-White syndrome (WPWS)
  • Mono-morphic ventricular tachycardia (VT)
  • Sodium Channel Blockers: Phenytoin, Lidocaine, Triamterene, Lamotrigine, Oxcarbazepine, and Amiloride
  • Drug overdose and toxicities: TCA’s, digoxin, cocaine, lithium, diphenhydramine
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21
Q

Q wave present indicates

A
  1. Post STEMI
  2. Pulmonary Embolism: S1Q3T3
  3. HCOM: Dagger Q waves in left leads
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22
Q

S waves meaning

A

Final DEPOLARIZATION of the ventricles (Purkinje fibers)

Mirror effect, shows the opposite side

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23
Q

U waves meaning

A

Represent REPOLARIZATION of the ventricles (Purkinje fibers).

Best seen in the right precordial leads. Usually not seen.

Amplitude is usually < 1/3 T wave amplitude in the same lead.

Increment in U wave amplitude = Premature ventricular complexes (PVC)

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24
Q

QT segment Duration

A
  • Normal = 0.4 to 0.44 sec
    (2 big squares)
  • Short QT < 0.35 sec
  • Prolong QT > 0.44 sec Predecessor of Torsade pointes(PVT) then VF
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25
Q

Prolong QT Causes

A
  1. HYPOS:
    - Hypokalaemia
    - Hypomagnesaemia
    - Hypocalcaemia
    - Hypothermia
  2. Raised intracranial pressure
  3. Drugs
  4. Congenital:
    - Romano Ward syndrome (AD)
    - Jervell and Lange Nielsen syndrome (AR) - bilateral sensorineural hearing loss -
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26
Q

Prolong QT Causes: Drugs

A
  • Antipsychotics
  • TCAs
  • SSRIs: Citalopram, Escitalopram
  • SNRIs: Venlafaxine
  • Apitypical Antidep: Bupropion
  • MAOIs: Moclobemide
  • Antihistamines
  • Antiarrhythmics: Quinidine, procainamide, flecainide, sotalol,
    and Amiodarone.
  • Antimalarial: Chloroquine, Hydroxychloroquine, and quinine
  • Macrolides: Erythromycin, and Clarithromycin

Digoxin

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27
Q

TCA Intoxication ECG

A
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28
Q

Prolong QT Symptom

A

Syncope

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29
Q

Prolong QT Management

A
  1. Correct underline causes
  2. B-Blockers
  3. Implantable cardioverter-defibrillator (ICD)

UNSTABLE: Torsade de Pointes Treatment

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30
Q

Raised Intracranial Pressure ECG changes

A

Widespread giant T-wave inversions (“cerebral T waves”)

QT prolongation

Bradycardia

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31
Q

Short QT Causes

A

HYPERS:
Hypercalcemia
Hyperkalemia
Hyperthermia

Digoxin: Salvador Dali Sign

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32
Q

PULMONARY EMBOLISM IN ECG

A

S1 Q3 T3 : Cor Pulmonale

  • Deep S in Lead I
  • Q in Lead III
  • T inverted In Lead III

✓ SINUSAL TACHICARDIA

✓ RBBB can be associated

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33
Q

Causes of ST-Segment Elevation

A
  • Being an MI until proven otherwise
  • Pericarditis
  • Ventricular aneurysm
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34
Q

Causes Of ST-segment Depression

A
  • Myocardium Ischaemia – Non-Stemi
  • Unstable Angina
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35
Q

ACUTE PERICARDITIS ECG CHANGES

A

ST-segment elevation with reciprocal PR-segment depression in all leads except V1 and AVR

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36
Q

Aneurism ECG changes

A

V1 - V3 ST elevation with concave morphology

Deep Q waves

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37
Q

Brugada syndrome ECG changes

A

ST-segment elevation V1-V3 followed by a negative T wave.

Association with clinical criteria:
- Family history of sudden cardiac death at <45 years old .
- Young, Male, Southeast Asian patient
- Syncope

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38
Q

Takotsubo Cardiomyopathy (Broken Heart) ECG changes

A

Same ECG that STEMI: T wave inversion leads II, III, aVF, V3-6

In the context of:

  • Pregnancy with CHF
  • Sepsis with CHF
  • Alcohol Cardiomyopathy
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39
Q

ECG MI: Anterior wall

A

Leads Affected: V2 to V4

Vessel Involved: Left Anterior Descending artery (LAD) – Diagonal branch

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40
Q

ECG MI: Septal wall

A

Leads Affected: V1 and V2

Vessel Involved: Left Anterior Descending artery (LAD) – Septal branch

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41
Q

ECG MI: Lateral wall

A

Leads Affected: I, aVL, V5, V6

Vessel Involved: Left Coronary Artery (LCA) – Circumflex branch

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42
Q

ECG MI: Inferior wall

A

Leads Affected: II, III, aVF

Vessel Involved: Right Coronary Artery (RCA) – Posterior descending branch

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43
Q

ECG MI: Posterior wall

A

Leads Affected:
V1 to V4 Mirror image ST depression
V7-V9

Vessel Involved:
*Left Coronary Artery (LCA) – Circumflex branch
*Right Coronary Artery (RCA) – Posterior descending branch

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44
Q

Hyperkalemia ECG changes

A

5.5 - 6.5 *Peaked T waves

6.5 - 7 *P waves widening,
flattening or absent
*Prolong PR interval

7 - 9 *Bradyarrhythmias
*Prolonged QRS

> 9 *Asystole
*Ventricular fibrillation
*PEA

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45
Q

Hypokalemia ECG changes

A

K < 2.7 mmol/L

  • Increased P wave amplitude (>2,5 mm)
  • Prolongation of PR interval (> 1 big square)
  • Widespread ST depression and T wave flattening/inversion
  • Prominent U waves - PVC (best seen in V2-V3)
  • Apparent long QT interval due to fusion of T and U waves (= long QU interval)
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46
Q

Digitalis toxicity in ECG

A
  1. ST depression and T wave inversion in V5-6 in a reversed tick pattern.
  2. Bradycardia
  3. Prolonged PR
  4. Shortened QT
  5. Arrhythmias, especially heart block or bigeminy
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47
Q

Amiodarone overdose ECG Changes

A

Widening of QRS complex
Prolongation of the PR and QT intervals
Ventricular tachycardia and ventricular fibrillation

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48
Q

Amiodarone overdose ECG Changes

A

Widening of QRS complex
Prolongation of the PR and QT intervals
Ventricular tachycardia and ventricular fibrillation

49
Q

List: Narrow Complex (Supraventricular) Tachycardia: ATRIAL – REGULAR

A
  • Sinus tachycardia (ST)
  • Atrial tachycardia (AT)
  • Atrial flutter
50
Q

List: Narrow Complex (Supraventricular) Tachycardia: ATRIAL – IRREGULAR

A
  • Atrial fibrillation (AF)
  • Atrial flutter with variable block
  • Multifocal atrial tachycardia (MAT)
51
Q

ATRIAL TACHYCARDIA (AT) & PAROXYSMAL AT: Clinical features

A

A rapid atrial rate overrides the SA Node and becomes the dominant pacemaker

Rhythm arround 150 bpm

In a px that has Hx of Heart disease (long standing AHT, valvar deseas, etc) or cocaine use

Paroxysmal: SVT and then stop

52
Q

FA important facts

A

Prevalence:
< 55 yo = 0.1%
> 80 yo = 10%

Risk Factors:
- HTA (Most important 20%)
- Ischaemic heart disease
- Tirotoxicosis
- Reumatic fever (aboriginal and in developing countries)

Complications:
1) Stroke - Risk:
< 65 yo 2.5 - 3%
> 65 yo 10%
2) Femoral artery embolism

53
Q

Paroxysmal AF Clinical Features

A

Spontaneous ends in less than 7 days (usually in 24 h)

After heavy alcohol, drugs

54
Q

Paroxysmal AF Management

A

Rapid = Convert

No rapid = No convert

NEEDS BETTER EXPLANATION

55
Q

Persistent AF Management

A

Fails to revert within 7 days

Usually converts with syncronized cardioversion

Elderly with previous heart conditions, just rate control and anticoagulants.

Definitive treatment: AV node ablation + permanent pacemaker

56
Q

Atrial fibrillation (AF): STABLE < 48H Management

A
  1. Rate control (Aim < 110 bpm):
    A) B-Blockers or CCB (Verapamil. Contraindicated EF<40)
    B) EF<40 = Amiodarone
    C) If the previous didn’t work or contraindications: Add Digoxin

If pharmacological failure WITHOUT left Ventricle systolic dysfunction: Pharmacological cardioversion with Flecainide (EF<40)/Amiodarone or Synchronized CV

  • CHA2DS2VaSc
  • Definitive treatment: AV ablation + permanent pacing (pacemaker)
57
Q

Atrial fibrillation (AF): STABLE > 48H Management

A
  1. Rate control (Aim < 110 bpm):
    A) B-Blockers or CCB (Verapamil. Contraindicated EF<40)
    B) EF<40 = Amiodarone
    C) If the previous didn’t work or contraindications: Add Digoxin
  2. Anticoagulation: LMWH x 5 days. Add Warfarine (INR 2-3) FOR 1 MONTH
  3. Synchronized Cardioversion
58
Q

Atrial fibrillation (AF): UNSTABLE

A

Synchronized Cardioversion

59
Q

CHA2DS2VaSc

A

CHF (EF<40%)
Hypertension
Age > 65 yo /// Age > 75 yo = 2
Diabetes mellitus
Stroke (no hemorrhagic) or TIA = 2
Vascular disease (PVD)
Female

60
Q

CHA2DS2VaSc score

A

0: No anticoagulation or aspirin

1: Antiplatelets

2 or more: Anticoagulation is recommended if not at high risk of bleeding.

61
Q

Atrial flutter: Clinical Features

A

AV Node conducts impulses to the Ventricle at a 2:1, 3:1, 4:1 or more.

  • Degree may be consistent or variable
  • The foci do not have enough electricity to conduct and produce a Ventricular contraction.
  • Ps of the foci and the P of SA node that is conducted.
  • Can be quick rate or normal rate
62
Q

Atrial flutter: ECG Characteristics

A

Rhythm= Regular

P= 4:1 – only P conducted from SA node (Saw-tooth)

PR = short

QRS= width normal

63
Q

Atrial flutter: Management

A

Same as AF STABLE < 48H

Permanent:
- Radiofrequency ablation
- Medical: Sotalol, amiodarone

64
Q

Multifocal atrial tachycardia (MAT): ECG Characteristics

A

Rhythm= Irregular

P= DIFFERENTS but all conducted

PR= normal

QRS= width normal

3 or more P waves, each different in the same ECG

65
Q

Narrow Complex Supraventricular Tachycardia (SVT) : ATRIOVENTRICULAR – REGULAR

A
  • Atrioventricular re-entry tachycardia (AVRT WPW)
  • AV nodal re-entry tachycardia (AVNRT)
66
Q

Wolf Parkinson White (WPW): ECG Characteristics

A
  • Rhythm: Regular
  • P: PR is short
  • W: wide QRS
  • S: slurring of upstroke (delta wave)

(+ FA Irregular rhythm)

67
Q

How to differentiate AVRT of AVNRT

A

Valsava maneuver are effective in the termination of AVRT

NOT to AVNRT

REVIEW!!!!!!

68
Q

WPW Management

A

Refer to cardiologist.

Definitive Therapy: Ablation of the accessory pathway.

AVOID:
- Adenosine
- CCB

69
Q

SVT: ECG Characteristics

A

AVNRT More common (> 60%) than AVRT

Heart rate: Regular 150-160 bpm.

P waves hidden in T waves

QRS: Narrow complex

70
Q

SVT STABLE Management

A

Step 1: Carotid massage/Valsalva manoeuvre

Step 2: Adenosine x 2 (2min)

Step 3: Verapamile x 2 (30 min)

Step 3: Direct current (DC) cardioversion or pharmacological cardioversion (amiodarone or overdrive pacing may be required.

Recurrent: Ablation or amiodarone

71
Q

AF + WPW ECG

A

Irregular and wide complex tachi with delta wavw

72
Q

SVT + WPW ECG

A

Regular and narrow but abnormal QRS

73
Q

Wide Complex Tachycardia: REGULAR

A
  • Ventricular tachycardia (VT)
  • Regular SVT with bundle branch block or aberrant.
74
Q

Wide Complex Tachycardia: IRREGULAR

A
  • Ventricular fibrillation (VF)
  • Polymorphic VT (PVT)
  • Torsade de Pointes
  • AF with Wolff-Parkinson-White syndrome
  • Irregular SVT with bundle branch block.
75
Q

Ventricular arrhythmias (WIDE complex) list

A
  • Premature ventricular contractions(PVCs)
  • Accelerated idioventricular rhythm
  • Monomorphic ventricular tachycardia
  • Polymorphic ventricular tachycardia
  • Ventricular fibrillation
  • Torsades de pointes
  • Arrhythmogenic right ventricular dysplasia
  • Re-entry ventricular arrhythmia
76
Q

Premature ventricular contractions(PVCs): Clinical Features

A
  • PVC or Ventricular extrasystoles (95% benign)
  • Patient feels like he skipped a beat.
  • The PVC does not generate a beat, because the ventricles are half-filed.
77
Q

Premature ventricular contractions(PVCs): ECG Characteristics

A

P= normal P conducted

PR = normal

QRS= normal and a PVC following a T, Then a compensatory pause (always)

78
Q

PVCs in bigeminy

A

Premature ventricular beats occurring after every normal beat are termed(1:1)

1 Normal QRS 1 PVC (repeat)

79
Q

PVCs in trigeminy

A

PVCs that occur at intervals of 2 normal beats to 1 PVC (1:2)

80
Q

PVCs in couplet

A

Normal QRS + PCV + PVC (repeat)

81
Q

PVCs in triplet

A

Normal QRS + PVC + PVC + PVC (Repeat)

82
Q

Non-sustained ventricular tachycardia(NSVT) Definition

A

Groups of three PVCs (Couplets or Paired PVCs) and last less than 30 seconds

(> 30 sec = VT)

83
Q

Non-sustained ventricular tachycardia(NSVT) STABLE: Management

A

◦ First line: metoprolol (BB)

◦ Second line: Verapamil (CCB) or flecainide if BB are Contraindicated. NO OPTION FOR EF <40

◦ If symptoms persist: amiodarone.

◦ Last option: catheter ablation.

84
Q

MONOMORPHIC VT: Characteristics

A

QRS = Same shape and amplitude

T = WIDE COMPLEX

  • Pulseless or perfusing
  • Can deteriorate into VF or unstable VT if sustained and not treated.

Mechanism: Re-entry loop from one ectopic area so all the QRS look the same.

85
Q

Usually cause of MONOMORPHIC VT

A

MI (ischaemia) in 1 area

86
Q

SUSTAINED VT STABLE: Management

A

Sustained VT w/ no structural heart disease:

  • First Line: beta-blockers (never a BB is acute left heart failure) (eg: atenolol, metoprolol tartrate/IV)
  • Second Line or if CI to BB: flecainide or verapamil.

◦ Sustained VT w/ structural heart disease

  • First line: Amiodarone or sotalol.
87
Q

POLYMORPHISM VT: Characteristics

A

QRS = Different shape and amplitude

  • Can be non-perfusing or perfusing
  • Consider electrolyte abnormalities or drugs toxicity as the possible etiology
  • Re-entry loop from multiple ectopic areas, different areas with different morphology on ECG.
88
Q

TORSADE DE POINTES: Characteristics

A
  • QRS reverses polarity and the strips shows a spindle effect.
  • It is a variant of polymorphic VT with normal or long QT intervals
  • Can deteriorate to VT or VF
  • Drugs that causes prolonged QT and electrolyte abnormalities like hypomagnesemia can cause Torsade de points.
89
Q

STABLE TORSADE DE POINTES: Management

A

Magnessium Sulphate 10 mmol in slow IV bolus

NEVER Sodium Bicarbonate!!!

90
Q

UNSTABLE TORSADE DE POINTES: Management

A

UNSYNCRONIZED (DC) CARDIOVERSION

91
Q

TORSADE DE POINTES: Most common cause

A

Drugs toxicity (QT prolonging medications)

92
Q

VENTRICULAR FIBRILLATION (VF): Characteristics

A
  • Chaotic electrical activity with no ventricular depolarization or contraction.
  • There is no pulse or cardiac output.
  • Small amplitude – no pulse is possible or rhythm
93
Q

Unstable Tachys and VF - SHOCKABLE -Management

A

UNSYNCRONIZED CARDIOVERSION

Adrenaline 1 mg after 2nd shock

Amiodarone 300 mg after 3rd shock

Note: CPR X 2 min between shocks

94
Q

PULSELESS ELECTRICAL ACTIVITY (PEA)

A
  • Electrical rhythm, with no pulse detected.
  • PEA can be called electromechanical dissociation
  • CONSIDER AND CORRECT:

“4H and 4T”

95
Q

Non-Shockable Rhythms

A

PEA

Asystole

SINUS BRADY + NO PULSE

96
Q

Non-Shockable Rhythms Management

A

Adenaline 1 mg inmediatly

Then every 2 CPR (X 2 min) Adrenaline again.

97
Q

UnstableList of Bradyarrhythmias with P WAVES PRESENT

A
  1. Sinus bradycardia
  2. Sinus node dysfunction
    a) Sinus Pause.
    b) Sinus Arrest.
    c) SA Nodal Exit Block.
  3. AV Blocks (I, II, III)
98
Q

SINUS Bradyarrhythmia causes

A

Normal in athletes and during sleep.

In acute MI it may be protective and beneficial.

B-blockers can cause sinus bradycardia

99
Q

Bradyarrhythmia: SINUS NODE DYSFUNCTION ECG Characteristics

A

Rhythm= Irregular

P= all same

PR= constant - Normal

QRS= width normal

Mechanism: SA node discharges irregularly

  • The pacing rate of SA node varies with respiration, specially in children and elderly
100
Q

SINUS BRADY + NO PULSE Causes

A

Tension Pneumothorax

Cardiac Tamponade

NO SHOCKABLE!!!!

101
Q

Bradyarrhythmia: SINUS ARREST – DROPPED BEAT ECG Characteristics

A

Rhythm= irregular

P= all same - dropped beat

PR= Normal

QRS= width normal. After the dropped beat, cycles continue on time.

  • Cardiac output may decrease causing syncope or dizziness.
102
Q

Sinus arrest Investigation

A

Holter

103
Q

Bradyarrhythmias Emergency Management

A

People with asymptomatic bradycardia usually need no treatment

A) Correction of the cause (cardiac infections, Ischaemia, hypos, drugs: digoxin, beta-blockers, CCB, amiodarone)

B) Pharmacological:
1. Atropine 0.5 mg bolus IV (Repeat every 3-5 min - MAX 3 mg)
2. Isoprenaline
3. Adrenaline / Epinephrine (Hypotension)
4. Dobutamine (CHF)

C) Transcutaneous Pacemaker (If ineffective pharmacological or MOBITZ 2 / 3rd degree AV Block)

104
Q

Combinations of drugs that block the atrioventricular (AV) node

A

Verapamil + Beta-blocker

105
Q

Bradycardia due to drug toxicity MANAGEMENT: B-Blockers

A

First-line antidote: Glucagon

Second-line: Inotropes (adrenaline, dobutamine, ­isoprenaline)

106
Q

Bradycardia due to drug toxicity MANAGEMENT: Calcium channel blockers

A

First-line antidote: Calcium gluconate

Second-line: Glucagon

107
Q

Bradycardia due to drug toxicity MANAGEMENT: Digoxin

A

Digoxin-specific antibodies (Fab fragments)

Allergenic and expensive.

Only to be used in life-threatening ­arrhythmias attributed to digoxin.

108
Q

Bradyarrhythmias: AV Blocks List

A

The most common cause of bradycardia.

Mechanism: AV node dysfunction

  • First-degree heart block, which manifests as PR prolongation
  • Second-degree heart block
    • Type 1 Second-degree heart block, also known asMobitz IorWenckebach
    • Type 2 Second-degree heart block, also known asMobitz II or Hay
  • Third-degree heart block, also known ascomplete heart block
109
Q

Bradyarrhythmias: 1ST DEGREE AV BLOCK ECG Characteristics

A

Rhythm= Regular

P= Normal - all conducted

PR= PROLONGED

QRS= width normal

  • Benign
  • If associated with MI, it can lead to AV defects.
  • Usually caused by drugs.
110
Q

Drugs that cause 1st degree AV Block

A

Antiarrhythmics:
Quinidine, procainamide, disopyramide, flecainide, encainide, propafenone, beta-blockers, amiodarone, sotalol, calcium channel blockers

Digoxin

Magnesium

111
Q

ECG Characteristics: 2ND DEGREE TYPE 1 / MOBITZ I / WENCKEBACH

A

Rhythm= Irregular

P= normal – a P is blocked

PR = Progressively longer until one P wave is totally blocked and produces no QRS.

QRS= width normal

112
Q

Causes: 2ND DEGREE TYPE 1 / MOBITZ I / WENCKEBACH

A
  1. B-blockers
  2. Digoxin
  3. Calcium channel blockers
  4. Ischaemia involving the right coronary artery.
113
Q

ECG Characteristics: 2ND DEGREE TYPE 2 / MOBITZ II / HAY.

A

Rhythm= Regular

P = Look normal at the same pace, all regular. Some P’s are blocked (Eg 3:1)

PR = Normal in the conducted P

QRS= Width normal

Mechanism: Conduction error in the bubble of His.

114
Q

Clinical features: 2ND DEGREE TYPE 2 / MOBITZ II / HAY

A

ALWAYS SYMPTOMATIC: Dizziness, palpitations, weakness, and syncope.

ALWAYS URGENT REFER AND PACEMAKER

115
Q

ECG Characteristics: 3RD DEGREE AV BLOC

A

Rhythm= Regular 25 - 50 rpm

P= look normal at a regular pace – none conducted

PR = Absent

QRS= abnormal

116
Q

Clinical Features: 3RD DEGREE AV BLOCK

A

Mechanism: Lack of conduction of atrial impulse to ventricle leading to independent contractions.

Signs & Symptoms:

  • Hypotension
  • Large volume pulse
  • Increased JPV (CANNON WAVE)
  • Systolic murmur

Can lead to asystole and cardiac arrest.

ALWAYS PACEMAKER

117
Q

Pacemaker in the ECG

A

Spike + QRS + T

No p wave

118
Q

The Reversible Causes of Cardiac Arrest: 4 Hs, 4 Ts

A

Hypoxia
Hypokalaemia/hyperkalaemia
Hypothermia/hyperthermia
Hypovolaemia

Tension pneumothorax
Tamponade
Thrombosis
Toxins

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