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CLIX > ECG > Flashcards

ECG Flashcards

1
Q

What is the normal calibration for an ECG?

A

10mm/mV
25mm/second

*2tall big swaures x 1 horizontal big square

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2
Q

How do you calculate the rate of an ECG?

A

300/R-R interval

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3
Q

What are the causes of an irregular rhythm?

A
  • sinus arrhythmia
  • sick sinus syndrome
  • ectopic beats (atrial, nodal or ventricular)
  • second degree AV block (usually mobitz I)
  • atrial/ventricular fibrillation
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4
Q

What is the bpm for AV and ventricular nodal escape rhythms?

A

AV nodal escape = 40-60/min

Ventricular escape = 15-40/min

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5
Q

In arrythmias with narrow vs wide QRS complexes, where do the rhythms originate?

A

arrythmias with narrow QRS complex –> rhythms originate in the atria or AV nodal tissue

arrythmias with wide QRS complexes –> rhythms originate in the ventricles

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6
Q

What is the normal ECG axis?

A

-29 –> +90 degrees

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7
Q

What are causes of LAD?

A
  1. marked LVH
  2. left anterior hemiblock
  3. inferior MI
  4. pregnancy
  5. normal variant
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8
Q

What are the causes of RAD?

A
  1. RVH
  2. left posterior hemiblock
  3. lateral MI
  4. acute PE
  5. emphysema
  6. dextrocardia
  7. spurious (L + R arms interchanged)
  8. normal variant
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9
Q

What is P pulmonale and P mitrale?

A

P pulmonale

  • peaked, narrow P waves (>/=2.5mm in height)
  • seen in right atrial hypertrophy
  • best seen in lead II

P mitrale

  • > /=3mm in width
  • humped/bifid P wave
  • seen in left atrial hypertrophy
  • best seen in V1
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10
Q

What causes PR segment depression?

A

pericarditis

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11
Q

What 2 injury currents are seen in acute pericarditis?

A
  1. Atrial injury current
    - PR segment depression
  2. Ventricular injury current
    - ST segment elevation
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12
Q

What is the definition of a pathological Q wave?

A

> /= 1mm deep
/=0.03s (3/4mm) in duration

*normal QRS duration = 0.10s

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13
Q

What are the 3 criteria for LVH?

A
  1. Using the V leads
    - S in V1 + R in V5/V6 –> (>60mm if pt age <30; >40mm if pt age 30-40; >35mm if pt age >40)
  2. Using standard lead I
    - R wave >15mm
  3. Using lead aVL
    - R wave >11mm

N.B only 1 of the 3 required to be fulfilled for LVH**

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14
Q

What is the characteristic finding in RVH?

A

in lead V1 –> R>s followed by T wave inversion with RAD present

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15
Q

When are delta waves seen?

A

Wolff-Parkinson-White syndrome

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16
Q

When are J waves seen?

A

hypothermia

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17
Q

What is the J point

A

junction of ST segment and QRS complex

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18
Q

What is corrected QT and what are the normal vales for males and females?

A

QT calculated for a HR of 60bpm
-QTc = QT/squareroot (R-R)

M=0.43s, F=0.45s

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19
Q

What is the U wave?

A
  • small wave (=25% of T wave) which follows the T wave and represents repolarisation of the purkinje fibres
  • often only visible at slow HR
  • most prominent in R-sided chest leads (V2, V3)
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20
Q

What is normal duration of P wave?

A

<0.12s

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21
Q

What are the ischaemic and non-ischaemic causes of Tall T waves?

A

(>10mm in V leads/>5mm in limb leads)

Ischaemic causes:

  • acute transmural MI (“hyperacute T waves”)
  • coronary artery spasm (prinzmetal’s angina/cocaine)

Non-ischaemic causes:

  • hyperkalemia
  • acute pericarditis
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22
Q

What are the causes of inverted T waves?

A
  • Myocardial ischaemia/infarction
  • ventricular hypertrophy
  • BBB
  • PE (V1-V4)
  • cardiomyopathy
  • digoxin
  • CVA
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23
Q

What are the causes of a short PR duration?

A
  • accessory pathways such as WPW syndrome
  • nodal tachycardia (atria depolarised just before the ventricles)
  • ectopic atrial rhythm (focus close to AV node)
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24
Q

What are the causes of long PR duration?

A
  • elderly
  • rheumatic fever (minor criteria)
  • drugs (ABCD –> Adenosine, B-Blockers, CCB, Digoxin)
  • myocarditis
  • IHD esp. involvement of RCA which supplies AV node in 90% individuals - AV block common in inferior MI
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25
Q

What conditions are pathological Q waves present?

A
  • normal variant (aVR, aVL, aVF, Std III, V1)
  • MI (transmural)
  • LVH, RVH
  • LBBB (absent R waves V1-3; QS waves in these leads)
  • hypertrophic cardiomyopathy
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26
Q

What conditions cause widened QRS complex?

A
  • LBBB/RBBB
  • non-specific intraventricular conduction delay
  • ventricular beats
  • hyperkalemia
  • drugs (e.g. tricyclics)
  • WPW syndrome
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27
Q

What conditions cause low voltage QRS complexes?

A
  • spurious (ECG calibration altered to 5mm/mV)
  • COPD
  • obesity
  • pericardial effusion
  • infiltration of myocardium (hypothyroidism/amyloid)
  • extensive MI
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28
Q

In what conditions is R wave > s wave in lead V1?

A
  • posterior MI (transmural)
  • RVH
  • RBBB
  • WPW syndrome
  • displacement of heart to the R chest
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29
Q

In what conditions is R wave in lead V3 < 3mm?

A

“poor R wave progression”

  • anteroseptal MI
  • LVH/RVH
  • LBBB
  • COPD
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30
Q

What conditions cause ST segment elevation?

A
  • transmural MI (STEMI)
  • coronary artery spasm (Prinzmetal’s angina; cocaine)
  • ventricular aneurysm
  • normal variant (V1-V2, =3mm)
  • LVH (V1-V3)
  • LBBB (V1-V3)
  • acute pericarditis
  • acute myocarditis
  • brugada syndrome
  • hypothermia
  • hypercalcaemia
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31
Q

What conditions cause ST segment depression?

A
  • myocardial ischaemia (angina pectoris; sub-endocardial MI)
  • reciprocal change in acute transmural MI
  • normal variant (only in V1-V2, <1mm)
  • LVH (L chest leads V5-6)
  • RVH (R chest leads V1-2)
  • LBBB (V5-V6)
  • RBBB (V1-V2)
  • digoxin
  • hypokalemia
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32
Q

What conditions cause a short QT interval?

A
  • congenital
  • drugs (digoxin)
  • hyperkalemia
  • hypercalcemia
  • hyperthermia
  • acidosis
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33
Q

What conditions cause prolonged QT interval?

A
  • congenital
  • drugs (amiodarone, erythromycin)
  • hypokalemia
  • hypocalcemia
  • hypothermia
  • IHD
  • myocarditis
  • head injury/SAH/vasovagal
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34
Q

What conditions cause prominent U waves and inverted U waves?

A

Prominent:

  • hypokalemia
  • anti-arryhthmic drugs (amiodarone)
  • LVH
  • SAH

Inverted:
-myocardial ischaemia

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35
Q

What are SVTs?

A

Supra-ventricular tachycardias

  • paroxysmal atrial tachycardia
  • AV nodal re-entrant tachcardia
  • accessory pathway –> re-entrant tachcardia (WPW synd.)
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36
Q

What is the most common cause of sinus arrythmia?

A

respiration

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37
Q

What can happen to the HR in respiratory sinus arrythmia?

A
  • HR increases with inspiration
  • HR decreases with expiration

** due to changes in vagal tone that occur at different phases of respiration

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38
Q

What are some conditions causing sinus bradycardia?

A
  • normal variant
  • drugs that increase vagal tone (digoxin); drugs that decrease sympathetic tone (B-blockers); CCBs
  • hypothyroidism
  • hyperkalemia
  • sick sinus syndrome
  • sleep apnoea
  • carotid sinus hypersensitivity
  • vasovagal reactions
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39
Q

What conditions are commonly associated with sinus tachycardia?

A
  • anxiety, excitement, exertion, pain
  • drugs that increase sympathetic tone (epinephrine, dopamine, TCAs, cocaine)
  • drugs that block vagal tone (atropine)
  • fever, infections, septic shock
  • CHF; PE
  • acute MI (sinus tachy = bad prognostic sign - extensive heart damage)
  • hyperthyroidism
  • phaeochromocytoma
  • intravascular vol. loss due to bleeding, V/D, acute pancreatitis, dehydration
  • alcohol intoxication/withdrawal
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40
Q

What are the ectopic arrythmias originating above the ventricles?

A
  • atrial premature beats (APBs)
  • supraventricular tachycardias (SVTs)
  • atrial flutter
  • atrial fibrillation
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41
Q

What are atrial premature beats and their etiology?

A

-ectopic focus in R/L atrium discharges and depolarises the atria BEFORE the sinus node was due to fire again

etiology:

  • normal hearts (APBs = most common arrythmia)
  • emotional stress
  • excess caffeine
  • drugs (epinephrine, aminophylline)
  • hyperthyroidism
  • structural heart disease (valvular lesions)
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42
Q

What is the compensatory pause in APBs?

A

-long R-R interval following the atrial premature beat complex

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43
Q

What are the causes of atrial flutter?

A

diseased heart:

  • mitral valve disease
  • cardiomyopathy
  • IHD
  • HTN
OR
secondary to:
-COPD
-PE
-complication of cardiac surgery
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44
Q

What is the rate of atrial flutter?

A

250-350bpm (avg. 300)

45
Q

What is Tx. for atrial flutter?

A
  • anticoagulation
  • slow conduction through AV node (B-blocker, CCB, digoxin)
  • antiarrythmics (amiodarone)
  • DC cardioversion
  • radiofrequency ablation of tract
  • atrial pacemaker
46
Q

What is the atrial and ventricular rate seen in AF?

A

atrial rate = 350-600bpm

ventricular rate = 110-180bpm

47
Q

What is the most common clinically significant arrythmia? and what are its hallmarks?

A

AF

  • no recognisable P waves
  • very irregular ventricular response
48
Q

What are the causes of AF?

A

PIRATE-SHIV

Pulmonary - PE, COPD
Idiopathic/Isolated
Rheumatic heart disease (i.e. Mitral Regurgitation/MS)
Alcohol dependence/binging
Thyrotoxicosis
Endocarditis / Echocardiographic changes (ie. Cardiomyopathy)
Sick Sinus Syndrome; Sepsis
Hypertension **commonest **
Ischaemic
Valvular disease
49
Q

What is the Tx for AF?

A
  • pharmacological Tx. (B-blocker, flecainide, amiodarone, digoxin, statins, omega3, ace inhib. –> decrease arrythmogenicity)
  • anticoagulation
  • DC cardioversion
  • surgical Tx. (RF ablation of tissue around pulmonary veins, obliteration of atrial appendages, multiple incisions in both atria to interrupt re-entry pathways -cox maze procedure, ablation of AV node with insertion of ventricular pacemaker
  • atrial defibrillator insertion
50
Q

What is the etiology of ventricular premature beats?

A
  • normal hearts (esp. elderly)
  • anxiety
  • caffeine excess
  • drugs: asthma meds (epinephrine, aminophylline); digoxin (toxicity)
  • electrolyte disturbances (hypokalemia/decr. magnesium)
  • lung disease
  • hypoxia
  • mitral valve prolapse; other valvular lesions
  • HTN; IHD (particularly acute MI)
51
Q

What is the definition of VT?

A
  • a run of 3 or more consecutive VPBs

- non-sustained (3beats - 30s) OR sustained (lasting >30s)

52
Q

Why is sustained VT (>30s) a life-threatening arrythmia?

A
  1. most pts. cannot maintain adequate BP at very rapid ventricular rates –> hypotensive
  2. condition may degenerate into VF (cardiac arrest)
53
Q

What are the causes of sustained VT?

A

some basic underlying structural cardiac abnormality such as:

  • prior MI causing myocardial scar (commonest cause)
  • cardiomyopathy
  • valvular disease associated with fibrosis
  • ventricular enlargement
54
Q

What is the Tx for sustained VT?

A

-insertion of an implantable cardiac device/implantable cardioverter defibrillator (ICD) –> delivers internal electric shock directly to heart during a life-threatening tachycardia

55
Q

What is the etiology of ventricular fibrillation?

A
  • heart disease of any type
  • acute MI
  • drugs (digoxin toxicity, epinephrine, cocaine, increased QT interval - quinidine, erythromycin)
  • preceding ventricular arrhythmias (VPBs or VT)
  • short/long QT interval
  • prominent U waves
  • non-penetrating chest blow
  • electric shock/lightning strike
  • AF occuring in pt. with WPW synd.
56
Q

What factors can cause sinus arrest/block (SA block)?

A
  • sick sinus syndrome
  • hypoxia
  • MI/ischaemia
  • hyperkalemia
  • digitalis toxicity
  • toxic responses to drugs such as B-blockers, CCBs
  • vagal hyperactivity (severe vasovagal episode)
57
Q

What are the 3 degrees of AV block?

A
  1. 1st degree - delay in conduction
  2. 2nd degree - intermittent interruption in conduction
  3. 3rd degree - complete interruption in conduction (atrial and ventricular electrical activity occurs independently-NO transmission of impulses from atria to ventricles)
58
Q

What is 1st degree AV block and its causes?

A

-prolongation of PR interval beyond 0.2s

causes:

  • old age
  • IHD
  • myocarditis (acute rheumatic carditis)
  • drugs (digoxin, B-blockers)
59
Q

What are the 2 types of second degree AV blocks?

A
  1. Mobitz type 1 (Wenckebach phenomenon)
    - successive prolongation of PR interval until a block takes place and impulse fails to be conducted down to ventricles (“drop beat”)
  2. Mobitz type 2
    - constant PR intervals
    - some impulses failing to be conducted through bundle of His
    - always pathological –> pacemaker implantation necessary to avoid deterioration to complete heart block
60
Q

What are the causes of Mobitz type 1 AV block?

A
  • inferior MI
  • drugs (digitalis, B-blockers, CCBs)
  • normal individuals with heightened vagal tone
61
Q

What are the causes of Mobitz type 2 AV block?

A
  • anteroseptal or inferior MI

- calcific disorders of fibrous skeleton of the heart

62
Q

What are the causes of 3rd (complete) AV heart block?

A
  • lenegre’s disease (idiopathic degenerative process involving the conducting system exclusively)
  • Lev’s disease - calcific process involving valves and conducting system in elderly
  • IHD
  • cardiac surgery - interruption of fibres/oedema
  • digoxin toxicity
  • infections (e.g. Chaga’s disease, tumours)
  • congenital heart disease (ASD, VSD)
  • congenital CHB
63
Q

What are the causes of LBBB?

A
  • HTN (*commonest)
  • coronary heart disease
  • left sided valvular lesion (calcification of mitral valve, AS, AR)
  • degenerative changes in conduction system in elderly
  • cardiomyopathy
64
Q

What are the causes of RBBB?

A

May occur in normal hearts or in conditions that affect RIGHT side of the heart:

  • pulmonary HTN (COPD)
  • coronary artery disease
  • R-sided valvular lesions (pulmonary stenosis)
  • degenerative changes in conduction system in the elderly
  • ASD
  • PE
  • CABG
  • normal variant
65
Q

Where would you see an rSR’ complex? and what else would you see on this ECG?

A

RBBB lead V1 with secondary T wave inversions

66
Q

What are the 3 fascicles that make up the ventricular conducting system?

A
  • right bundle
  • anterior fascicle of left bundle
  • posterior fascicle of left bundle
67
Q

Which hemiblock is more common and why?

A

Anterior hemiblock is more common than posterior hemiblock, due to the fact that the posterior fascicle has a dual blood supply from both left and right coronary arteries, whereas the left anterior fascicle is supplied solely by the left anterior descending artery

68
Q

What is a hemiblock?

A

half the left bundle is blocked

-can be anterior (Left axis deviation) or posterior (Right axis deviation)

69
Q

What drugs can cause BBB?

A
  • antiarryhthmics (Na channel blockers –> disopyramide, procainamide, quinidine)
  • TCAs
  • antipsychotics –> phenothiazine

N.B. hyperkalemia can also cause BBBs

70
Q

What would you suspect if a qRS complex is seen in V6?

A

RBBB

71
Q

What are some examples of bifascicular blocks?

A
  • RBBB and LPFB
  • RBBB and LAFB
  • complete LBBB
72
Q

What does the LAD artery supply?

A
  • Anterior wall of LV, apex (V4), lower part of lateral LV (V5, V6) (Diagonal branch)
  • Anterior ⅔ ventricular septum (V1 – V4) (Septal perforator)
73
Q

What does the LCx artery supply?

A
  • Left atrium
  • Upper part of the lateral wall of LV (Std I, aVL)
  • Posterior LV (V7 – V9) and inferior LV (Std II, III, aVF) in 15% of individuals
74
Q

What does the RCA supply?

A
  • Right atrium
  • Virtually entire right ventricle (RV) V1, V3R-V6R
  • Posterior ⅓ ventricular septum
  • Postero-inferior LV in 85 % individuals
75
Q

Summarise RCA and LCA blood supply to the conducting system

A

LCA supplies:

  • Most of LV and left atrium
  • Conducting system below AV node
  • Contributes to SA and AV nodes

RCA supplies:

  • Most of RV and right atrium
  • Inferior and posterior LV (85% of population)
  • SA and AV nodes
  • Contributes to conducting system below AV node
76
Q

What is the criteria for acute MI?

A

increased cardiac biomarker AND >/= 1 of the following:

  • Sx. of ischaemia
  • new ECG changes –> ST segment/T wave changes or new LBBB; pathological Q waves
  • imaging evidence of new loss of viable myocardium or new regional wall motion abnormality
  • angiographic or autopsy identification of an intra-coronary thrombus
77
Q

What does ST elevation in aVR indicate?

A

Lead aVR shows reciprocal ST elevation when there is extensive ST depression in many leads e.g. in a sub-endocardial MI due to left main coronary artery/LAD stenosis or triple vessel disease or ST depression from another cause e.g. LVH.

78
Q

What are the acute and evolving phase ECG changes of a STEMI?

A

acute
-marked by appearance of T elevation and sometimes tall (hyperacute) T waves

evolving
-hrs –> days later; characterised by deep T wave inversions in leads that previously showed ST elevations

79
Q

What are V7-V9?

A

non-standard leads

  • used to identify a posterior STEMI
  • placed on posterior chest beneath L scapula looking directly at epicardial surface of infarcting area
80
Q

What is likely if the ST segment remains elevated ‘ad infinitum’ after an acute MI?

A

ventricular aneurysm

81
Q

Is the myocardium typically viewed from its endocardium or epicardium on a 12-lead ECG?

A

epicardium

82
Q

What are the typical ECG changes of a posterior MI?

A

Acute posterior MI presents as ST depression in leads V1 to V4 – the reciprocal changes that occur because the transmural infarct is being viewed from the endocardial aspect rather than the epicardial, thus resulting in a mirror image of the ST/T changes that would be seen if leads V7 – V9 were being viewed. The evolved and chronic phases show increased R wave amplitude which represent the deep Q waves of the infarcted area

83
Q

How are RV infarctions identified?

A

Acute ST segment elevation of at least 1 mm (0.1 mV) in one or more of leads V3R to V6R (right precordial ECG leads) and Q or QS waves effectively identify RV infarction

84
Q

What are the ECG indicators of NSTEMI?

A
  • ST depression rather than elevation
  • symmetrical T wave inversion
  • no Q wave
  • increased troponin
  • if extensive –> may see reciprocal ST elevation in aVR
85
Q

What are the 3 types of troponins?

A

Troponin C (calcium binding) not cardiac specific, also found in skeletal muscle

Troponin T (tropomyosin-binding) also not cardiac muscle specific – rises in MI as well as in renal failure, pneumonia, PE, liver disease, stroke, carcinomas, CCF

Troponin I (inhibitory) is sensitive and specific to myocardium*****

86
Q

When is CK/CK-MB useful?

A

-to assist in Dx of a recurrent infarct in the acute setting –> when troponin levels may still be elevated from inital infarct, CK remains elevated for only 48hrs

87
Q

What is BNP and its usefulness in Dx?

A

Brain Natriuretic Peptide

  • formed predominantly in ventricular muscle
  • predictor of heart failure and increased mortality
88
Q

What are poor prognostic features post-MI?

A

Clinical features

  • increased age
  • low systolic BP
  • tachycardia
  • pulmonary oedema

ECG features

  • anterior location
  • hyperacute (TALL) T waves
  • marked ST elevation

Markers
-markedly inreased BNP/CRP

89
Q

What is the commonest cause of acute pericarditis?

A

idiopathic

-or due to viral infection

90
Q

What are the clinical manifestations of acute pericarditis?

A
  • chest pain –> sudden, severe with retrosternal or left precordial pain and radiation to back/trapezius area (radiations to arms may occur); chest pain is pleuritic in nature (aggravated by supine, relieved with upright posture)
  • fever
91
Q

What is the characteristic shape of ST segments in acute pericarditis?

A

-typically concave in appearance (“saddle-shaped” elevation)

92
Q

What is the most common ECG finding in PE?

A

T wave inversion V1-V4 due to right ventricular strain

93
Q

What are ECG findings in PE?

A
  • Sinus Tachycardia (one of the most common ECG findings in this situation)
  • T wave inversion V1–V4 due to right ventricular strain (commonest ECG abnormality in PE)
  • Ventricular ectopic beats
  • Atrial fibrillation
  • Right bundle branch block
  • S1Q3T3
94
Q

What is S1Q3T3?

A

ECG anomaly in PE

  • deep S wave in standard lead 1 (signifies development of acute RAD due to sudden increase in R-sided pressure + RV dilatation)
  • deep Q wave + inverted T wave in standard lead 3
95
Q

In children and young athletes, the 2 main causes of SCD are?

A
  1. long QT syndrome

2. hypertrophic cardiomyopathy (HOCM)

96
Q

What are the ECG features of HOCM?

A
  • Left atrial abnormality, due to ↓ventricular compliance and coexistent mitral regurgitation.
  • LVH (tall R waves and LV strain pattern in lateral chest leads)
  • Prominent septal Q waves in the lateral leads (Std I, aVL, V5, V6)
  • Tall, broad R waves in V1
  • AV conduction defects may occur
97
Q

What are the ECG changes in hyperkalemia?

A
  • sinus bradycardia
  • P wave flattens/disappears
  • prolonged PR interval
  • tall, peaked T waves and QT shortens
  • progressive QRS widening

**V. SEVERE –> becomes sine wave pattern –> VF/asystole can occur unless K+ level is reduced timeously

98
Q

What is the earliest change on ECG of hyperkalemia?

A

peaking (“tenting”) of the T waves

99
Q

What condition might you expect in a patient with prominent U waves and flattened/inverted T waves?

A

hypokalemia

100
Q

What are the characteristic ECG changes in hypo and hypercalcemia?

A

Hypocalcaemia prolongs the QT interval by stretching out the ST segment.

Hypercalcaemia decreases the QT interval by shortening the ST segment so that the T wave seems to take off directly from the end of the QRS complex

101
Q

What is the MOA of digoxin?

A

Slows HR
-negative chronotropic effect

Slows AV conduction

  • increases vagal activity via action on CNS
  • useful in AF (increased ventricular filling time)

Increased contractility

  • inhibits Na/K pump
  • increased Na conc. inside myocyte
  • slowed extrusion of Ca via Na/Ca exchange transporter
  • increased Ca stored in sarcoplasmic reticulum –> increased Ca released in each action potential (more powerdul contraction - pos. inotropic effect)
102
Q

What is the clinical use of digoxin?

A
  • To slow rate in AF

- Treatment of heart failure in patients who remain symptomatic despite optimal use of diuretics and ACE-inhibitors

103
Q

What are the characteristic ECG findings on a patient on digoxin Tx.?

A
  • inverted tick appearance of ST segment and T wave
  • prolonged PR
  • short QT interval
104
Q

What are the cardiac/ECG findings suggestive of digoxin toxicity? and which is the most common/often first found*?

A
  • Frequent premature ventricular complexes (ventricular bi- and trigeminy)***
  • Bradyarrhythmias
  • AV block
  • Atrial tachycardia with AV block
  • Junctional tachycardia
  • Bi-directional VT
105
Q

What are the non-cardiac effects of digoxin toxicity?

A
  • fever, malaise, weakness
  • anorexia, N/V/D, abdo. pain
  • headache, dizziness, visual disturbance (flashing lights, halos, blurred etc), confusion, hallucinations, delirium
  • electrolyte disturbance (hyperkalemia often in acute poisoning; hypokalemia more common in chronic toxicity)
106
Q

What is the Tx. of digoxin toxicity?

A
  • acute toxicity –> activated charcoal within 1hr digestion
  • treat electrolyte disturbances (give insulin/glucose for hyperkalemia)
  • digoxin-specific Fab fragments (Digibind)
  • bradycardia + heart block –> atropine, temporary pacemaker if symptomatic
  • VT –> lidocaine/phenytoin (decrease ventricular automaticity without slowing AV node conduction
107
Q

What are the characteristic ECG findings of LBBB?

A

Dominant S wave in V1 with broad, notched (‘M’-shaped) R wave in V6

108
Q

What are the characteristic ECG findings of RBBB?

A

Tall R’ wave in V1-3 (“M” pattern) with wide, slurred S wave in V6 (“W” pattern)

CLIX (4 decks)

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