Ecg

Front 1

Which is not a typical finding on ECG for Hypertrophic cardiomyopathy (HOCM).
A. Peaked P waves of Left atrial enlargement
B. Pathological Q waves in the lateral leads.
C. Deep T inversions in the precordial / lateral leads
D. High precordial voltages.

Back 1

A. Left atrial enlargement = broad, bifid P waves .

Peaked P waves = Right atrial enlargement

Front 2

Which of the 3 Sgarbossa Criteria has the most specificity associated with it ?

Back 2

Concordant ST Elevation > 1mm in leads with a positive QRS complex.

Front 3

List the Ischaemic STEMI equivalents that are found on ECG that are not of the classical variety ( 5).

Back 3

1. Posterior MI
2. Left main occlusion ( STE aVR + inferolateral ST depression)
3. Wellens Syndrome
4. deWinter ST/T wave complex
5. LBBB -Sgarbossa criteria

Front 4

List the causes of ST Elevation on the ECG that are non-ischaemic.

Back 4

1. Benign Early Repolarisation (BER)
2. Acute myopericarditis
3. Left ventricular aneurysm
4. Brugada Syndrome (V1-V3)
5. Cardiomyopathy
6. Hyperkalaemia
7. Subarachnoid Haemorrhage
8. Bundle Branch Block
9. Pacemaker
10. Pre-excitation
11. Normal variant

Front 5

What are the ECG criteria for reperfusion in AMI ?

Back 5

1. ST segment elevation > 1mm in 2/more contiguous LIMB LEADS
2. ST segment elevation > 2mm in 2 / more contiguous CHEST LEADS

Front 6

What are the ECG features for Hypokalemia with K+ < 2.7 mmol / L ?

Back 6

1. P wave - peaking
2. PR interval -prolonged **
3. ST depression
4. T wave flattening
5. U waves
6. QT prolongation

plus : Arrhythmias - SVT / Torsades / VT / VF

Front 7

What are the ECG features of Hyperkalaemia with K+ > 5.5 mmol / L ?

Back 7

1. P wave - loss of
2. PR interval - prolonged **
3. QRS widening
4. T waves tall and peaked
5. Sine wave
6. ventricular arrhythmias
7. Asystole.

Front 8

In regards to the QT nomogram, at what uncorrected QT interval of 500 msec does the heart rate have to be to have an increased likelihood of arrhythmia ?

Back 8

less than 60 bpm.

Front 9

What is Bazett's Formula for the corrected QT interval ?

Back 9

QT (milliSeconds) / Square root RR interval (seconds )

Square root of 1 = 1 therefore QT at rate of 60 (R-R = 1) is uncorrected

Male = 450 msec ( 0.45 sec)
Female = 470 msec.

Front 10

What is the length of 1 small square on the ECG ?

Back 10

40 msec ( 0.04 sec)

Front 11

What is the length of 1 large square on the ECG ?

Back 11

200 msec ( 0.2 sec)

Front 12

What is the normal speed of the paper for the 12 lead ECG ?

Back 12

25 mm/sec.

Front 13

List the ECG features of Hypothermia .

Back 13

1. Tremor artefact
2. Prolongation of intervals :
a. PR
b. QRS
c. QT
3. Bradycardias
a. Junctional
b. AF (slow)
4. Osborne Waves - J waves
"positive deflection in the terminal portion of the QRS + elevation of the J point"
5. Premature Ventricular beats (PVB)
6. Ventricular arrhythmias ( VT / VF )
7. Asystole

Front 14

Which is incorrect regarding Osborn J waves in Hypothermia?
A. They can occur in a single lead only, but tend to be seen in the precordial + lateral leads.
B. They tend to occur at temperatures < 30 degrees.
C. As the temperature drops below 30 degrees, Osborn waves increase in amplitude.
D. They are a " positive deflection in the terminal portion of the QRS".

Back 14

B. Temperature < 32 degrees.

Front 15

What are the ECG features that increase the likelihood of a rapid wide complex tachycardia being VT rather than SVT with aberrancy ? ( 9 )

Back 15

1. Wide complex tachycardia
- > 160 msec
- HR 140-200 bpm
2. Extreme axis deviation
( "Northwest axis " ; + QRS in aVR and negative in I and
aVF)
3. AV dissociation (25%)
4. Capture beats
5. Fusion beats "hybrid complex"
6. Concordance ( + or - in precordial leads )
7. Brugada's sign
( > 100msec distance from QRS onset to nadir of S wave )
8. Josephson's Sign
( notching near nadir if S wave in V1V2 )
9. RSR complex has taller left R wave ( Rsr)

Front 16

Which of the 4 ECG stages of pericarditis has the most prominently recognised ECG findings?

Back 16

Stage I :

1. Diffuse ST elevation
2. PR depression
3. Spodick's sign

Front 17

Best place to look at p wave?

What conditions cause prominent P wave changes ?

P waves all look different?

Back 17

Lead II & V1

Hypokalaemia : peaked P wave

Hyperkalaemia : Flat P wave

Multifocal Atrial Tachycardia

Front 18

What of the following conditions does not cause PR interval lengthening ?
A. Hypothermia
B. Hypocalcaemia
C. Hypokalaemia
D. Hyperkalaemia

Back 18

B. Hypocalcaemia

Front 19

Which Environmental / Electrolyte / drug-induced conditions does not cause QRS widening ?
A. Hypothermia
B. Hyperkalaemia
C. Hypomagnesaemia
D. Hypercalcaemia

Back 19

D.

Front 20

Which Conditions / drugs / electrolytes does not cause QT interval shortening ?
A. Hyperkalaemia
B. Hypokalaemia
C. Hypercalcaemia
D. Digoxin effect

Back 20

B.

Front 21

Which conditions / drugs / electrolytes does not cause QT interval prolongation ?
A. Hypocalcaemia
B. Hyperkalaemia
C. Hypokalaemia
D. Hypothermia and Hyperthermia

Back 21

B.

Front 22

What are the differentials for ST elevation in aVR ? (5)

Back 22

1. Left main coronary occlusion
2. Ventricular tachycardia (VT)
3. Hyperkalaemia
4. Na+ channel blockade
5. Lead placement **

Front 23

What are the ECG features of Hypercalcaemia ?

Back 23

ST segment depression
ST segment shortening
T wave widening
QT interval shortening

"The 3 B's" :
Bradyarrhythmias
Bundle Branch Blocks (BBB)
Block (CHB)

Front 24

List the 7 main categories of causation of a Prolonged QT interval.

Back 24

1. Electrolytes
2. Endocrine
3. Environmental
4. Drugs / Toxins
5. Cardiovascular disease
6. Cerebrovascular disease
7. Hereditary

Front 25

List the electrolyte causes of a Prolonged QT interval.

Back 25

1. Hypokalaemia
2. Hypomagnesaemia
3. Hypocalcaemia

Front 26

List the Endocrine and Environmental causes of a Prolonged QT interval .

Back 26

Endocrine
1. Hypothyroidism

Environmental
1. Hypothermia

Front 27

List the 6 drug / toxin categories that cause a prolonged QT interval.

Back 27

1. Antiarrhythmics ( Ia ; Ic ; III )
2. Antidepressants ( venlafaxine ; TCA )
3. Antipsychotics ( Haloperidol ; quetiapine )
4. Antihistamines (loratidine)
5. Antibiotics ( Flouroquinolones ; erythromycin )
6. Antimalarials ( Chloroquine ; quinine )

Front 28

LVH criteria

Back 28

V5 or V6 >25mm

S in V1 + R V5/6 >35mm

R in lead I + S lead 3 >25mm

R avL >11mm

Front 29

RVH criteria

Back 29

RAD

R in V1 >7mm (or R:S >1 i.e. dominant)

R in V1 + S V5/6 >11mm

(QRS < 120mm i.e. changes not due to RBBB)

Front 30

Causes dominant R wave in V1

Back 30

Posterior MI

WPW type A

RVH

R heart strain = Lung disease

RBBB

Front 31

Changes in pericarditis

Back 31

Widespread STE

PR segment depression

Front 32

Pericardial effusion

Back 32

Electrical alternans - axis changes with each beat

i.e. different QRS complexes

Front 33

ANTERIOR ISCHAEMIA:

'Extensive' - anterolateral

Septal

Anterior

Lateral (apical)

Back 33

Extensive - V1-6; I; avL - Proximal LAD

Septum - V1-3 - Septal perforaters of LAD

Anterior - V4-6 (I; avL) Diagonal (supplies ant LV wall)

Lateral - V5,6; I; avL - Distal LAD or circumflex

Front 34

INFERIOR ISCHAMIA:

Inferior (localised)

Inferior (extended):

Infero-lateral

Inferio-posterior

RV

Back 34

Localised - II, III; avF - RCA or circumflex

Extended - as above, plus:

Inf-lat - I; avL; V5-6 - RCA or dominant Cx

Inf-post - V1-2 - PDA or RCA

RV - V1-3R; V4R - Prox RCA

Front 35

V1/2 prominent R wave + ST depression + TWI

Back 35

Consider posterior leads

Front 36

Prolonged QT - values

Back 36

Normal = 435msec

Prolonged = >50% of R-R interval

F = 460; M = 450

QTc = QT / (sq r) of RR

Front 37

Causes long QT - Congenital

Back 37

Romano-ward syndrome - autosomal dominant

Juville Lane syndrome - autosomal recessive (+ sensorineural deafness)

Front 38

Causes Long QT - Acquired

Back 38

Cardiac - ischaemia; myocarditis; CM

SAH

Electrolytes - Dec Ca/Mg

Drugs:

Antiemetics - droperidol; metoclo; ondans

ABs - erythromycin

Antipsycho - halop

Antidepressants - TCA

Anti-arrhyth - amiodarone; procainamide

Prokinetics - cisapride

Front 39

Digoxin changes

Back 39

AF

ST dep & TWI lateral chest leads

Front 40

U wave

Back 40

Extra wave after T wave:

- Bradycardia (most common cause)

Dec K (characteristic of severe)

- Dec Mg

- Dec Ca

- CM

Front 41

Hypercalcemia

Back 41

Shorted QT

Wide T

J/osborn waves

U wave

Front 42

Hyperkalaemia

Back 42

Tented p; Prolonged PR (5.5-6.5)

Loss of p (6.5-7.5)

Long QRS (7.5-8.5)

Sine wave (>8.5)

VT

Front 43

Hypokalaemia

Back 43

Enlarged P

Prolonged PR

TWI

ST dep

U waves

Long QT

Arrhythmia

Front 44

LAD

Back 44

Left anterior hemiblock

L BBB

WPW type B

Inferior MI

Front 45

RAD

Back 45

L posterior hemiblock

RVH / strain

RBBB

WPW type A

Posterior MI

Front 46

VT criteria

Back 46

Broad complex:

>120 = VT

100-120 = accelerated idioventricular rhythm

<100 = idioventricular rhythm

Front 47

Differentiating VT from SVT with aberrant conduction = Brugada criteria

Back 47

Absence of R-S complexes in each chest lead = VT

RS interval > 100ms (2.5 small squares) = VT

Independent atrial actvity (fusion beat, capture beat) = VT

Typical bundle branch pattern = SVT

Front 48

LBBB - how do you tell if there is ischaemia?

Back 48

Appropriate disconcordance = normal

Inappropriate concordance = ischaemia

Front 49

cc

Back 49

LVH

Front 50

cc

Back 50

RVH

Front 51

ccc

Back 51

Pericarditis

Front 52

cc

Back 52

Pericardial effusion

Electrical alternans

Front 53

cc

Back 53

Long QT

Front 54

cc

Back 54

Digoxin changes:

AF + STD + TWI lateral leads

Front 55

Back 55

Sinus bradycardia & U waves

Anorexia nervosa pt

Front 56

ST depression Morphology

Back 56

Myocardial ischamie:

- Horizontal or downsloping ST depression >0.5mm at the J point in 2 or more contiguous leads

- > 1mm - more specific & worse prognosis

- >2mm in >3 leads - high chance of NSTEMI & high mortality (35% at 30 days)

Upsloping - non-specific for ischaemia

Front 57

Left Main occlusion

Back 57

Pattern of widespread ST depression, with STE in avR

Front 58

Right Heart strain

Back 58

ST depression / T wave inversion in the right precordial (V1-4) and inferior (II, III, aVF) leads

Front 59

ECG Changes in PE

Back 59

Sinus tachy most common

SI Q III T II

Complete or incomplete RBBB

RV strain pattern

RAD

P pulmonale - peaked p wave in lead II>2mm

Simultaneous TWI inferior & R praecordial leads (V1-3)

Front 60

What is Wellens Syndrome

Back 60

ECG abnormality strongly associated with significant left anterior descending coronary artery stenosis

Two types - most common being deep TWI in leads V2-3

Front 61

In Left Atrial Enlargement, the P wave:

A. Increases in amplitude

B. Increases in duration

C. Increases in both amplitude & duration

D. Shows terminal P negativity in lead I

E. All of the above

Back 61

B

Front 62

When interpreting an ECG, right ventricular hypertrophy (RVH) can mimic which of the following conditions?

A. LBBB

B. AV Block

C. True posterior MI

D. LAFB

E. LPFB

Back 62

C

The prominent anterior forces seen in RVH are also seen in a number of other conditions including a true posterior MI. Thus, RVH is sometimes referred to as a pseudoinfarct.

RBBB and WPW could also result in prominent anterior forces but they may be distinguished in other ways. (rSR' morphology in V1, delta waves, and short PR.)

Front 63

Sign of Right atrial enlargement?

Back 63

RAE is recognized by the tall (> 2.5mm) P waves in leads II, III, aVF.

Front 64

Signs of Left Atrial Enlargement?

Back 64

The P-wave is notched, wider than 0.12s, and has a prominent negative (posterior) component in V1. These are all criteria for left atrial enlargement (LAE).

Front 65

Pacemaker Code VOO

Back 65

Asynchronous

No sensing circuitry

Discharges continuous regardless of pt's rhythm

Front 66

PM Code VVI

Back 66

Demand Pacing

Paces when it doesn't sense R waves from V electrode

Doesn't interfere with intrinsic rhythm above a certain rate

Front 67

PM Code DDD

Back 67

Sequential/Dual Pacing

Maintains AV contraction sequence

Pace & sense A & V sequentially

Front 68

What is Wellen's Syndrome?

Back 68

ECG abnormality strongly assoc w significant LAD stenosis

2 Types:

- Symmetric deeply inverted T waves in V2 & V3

- Biphasic T waves in V2 & V3 (less common)

Plus Hx of CP, no Q waves, No STE

Front 69

Measuring PR interval

Back 69

From beginning of p to beginning of QRS

Normal <200ms

Front 70

Normal QT interval

Back 70

Measure from beginning of QRS to end of T wave

At HR = 70, upper limit of QT is 400ms

Add or subtract 20msec for every 10 beats above or below 70

Front 71

Pathological Q wave

Back 71

Either wide >0.04ms

Or deep >30% of QRS height

Front 72

MI - LCx - Region & leads

Back 72

LCx

* Posterior MI
* Dominant R & Tall T V1-2
* STE V7-9 (STD V1-2)

Seek & exclude

LCx + LAD = Posterolateral

LCx + RCA = Inferoposterior

Front 73

MI - Lesion LAD - Type of MI & leads

Back 73

LAD - Combination of following:

* Septal (STE V1-2)
* Anterior (STE V3-4)
* Lateral (STE V5-6; I; aVL)

Front 74

RCA 'Type' MIs - Region & Leads

Back 74

RCA - Occlusion distal to RV:

* Inferior MI - 58% of MI (STE II, III, aVF; STD aVL)
* Inferior & RV MI (as above + STE V1, V4R)
* Increased mortality
* LAD & LCx occlusion in L dominant system

Front 75

What does concordance mean?

Back 75

Throughout chest leads - leads V1-6 show entirely positive (R) or entirely negative (QS) complexes, with no RS complexes seen

Increases likelihood of VT > SVT w aberrant conduction

Front 76

VT vs SVT with aberrant conduction - relative frequencies

Back 76

VT:

- 80% of all broad complex tachycardias (BCT)

- 95% in pts w structural heart disease

So if in doubt - Rx as VT

Front 77

Left Main Occlusion Features

Back 77

STE >1mm in aVR - 95% for LMCA occlusion when there is evidence of ischaemia in other leads (typically widespread STD)

STE in aVR >1.5mm - 75% mortality

Need urgent cath lab

Front 78

WPW Diagnostic criteria (WHO)

Back 78

PR interval <0.12s

Delta wave

QRS >0.12s

Normal p-wave axis

Orthodromic - down AV & back up accessory (most common)

Antidromic - down accessory & back up AV node - ominous as can drive at rapid vent rates (p is after QRS)

Front 79

What is a fusion beat?

Back 79

When a VE occurs just after a sinus beat has started to propagate into the His-Purkinje system - combines morphology of normal sinus beat to the extrasystole

Front 80

What is a capture beat?

Back 80

During VT - when a normal sinus beat sneaks through - normal-shaped QRS & T wave

Front 81

Trifascicular Block

Back 81

Trifascicular block - disease in all 3 fascicles i.e. CHB:

* Right bundle
* Left bundle = Left anterior & Left Posterior
* Bifascicular + 1st (most common) or second degree AV block
* RBBB + LAFB or LPFB

Front 82

LBBB Diagnostic Criteria

Back 82

* QRS duration >120ms
* Dominant S wave in V1
* Broad mono phasic R wave in lateral leads
* Absence of q waves in lateral leads (still allowed in aVL)
* Prolonged R wave peak time >60ms in left praecordial leads

Associated:

- Appropriate DISconcordance - ST & TW in opposite direction to main vector of QRS

- Poor R wave progression

Front 83

Risk of Asystole if Bradycardic

Back 83

* Mobitz II AV block
* Recent asystole
* Ventricular pauses > 3sec
* CHB with broad complex QRS

Front 84

Signs of Digoxin Effect

Back 84

Downsloping ST depression - characteristic "sagging" appearance (most evident in lateral leads)

Flattened, inverted, or biphasic T waves (most common)

Shortened QT

Also - Mild PR prolonged (increased PNS tone); U waves

Front 85

Digoxin Toxicity

Back 85

Clinical Features:

* Nausea; Vomiting; Anorexia
* Yellow-green; Blurred vision
* Palpitations, syncope, dyspnoea
* Confusion; delirium; fatigue
* Multitude of dysrhythmias due to increased automaticity & decreased AV conduction (vagal)
* Classic - SVT w slow vent response
* Other - frequent PVCs; slow AF; brady; an AV block

Front 86

Causes of LVH

Back 86

* HTN
* AS
* AR
* MR
* Coarctation of aorta
* HOCM

Front 87

LV & RV Strain

Back 87

Strain = repolarisation abnormality due to hypertrophy or dilation

LV:

* TWI in lateral leads (V5-6, I & aVL)
* TWI & STD in right praecordial leads (V1-3 & inferior leads - i.e. RV is anterior & inferior)

Front 88

Post-Op Visual Loss - Causes

Back 88

1. Central retinal artery occlusion (external orbital compression)
2. Ischaemic optic neuropathy (anterior or posterior)
3. Compression optic nerve or chasm by pituitary tumour (check cortisol & TSH)
4. Cortical visual loss
5. Functional visual loss

Front 89

Examination post-op visual loss

Back 89

* Visual acuity (doesn't help with Dx as variable findings)
* Pupillary testing
* Visual fields
* External examination
* Ocular motility
* Fundoscopy (dilated)

Front 90

Findings Orbital compression (CRAO)

Back 90

* Usually monocular
* Ocular motility abnormalities
* External oedema
* Chemosis
* Fundus findings of CRAO

Front 91

ION Findings

Back 91

* Afferent pupillary defect if unilateral
* If bilateral -> poorly reactive pupils (although meds can confuse findings)
* Optic nerve:
* Acuity - range normal to 'no light perception'

Front 92

Post-op Visual Loss from intracranial compression - O/E findings

Back 92

Can be unilateral or bilateral. Afferent pupillary defect if unilateral, or bilateral & asymmetric. Visual acuity - variable.

Chiasm compression -> Visual fields are the key

Cortical visual loss - 2 patterns:

1. Unilateral -> homonymous hemianopic visual defect w normal acuity
2. Bilateral -> bilat homnomous hemianopic visual field defects w variable loss of visual acuity

In cortical blindness - even is pt completely blind pupils will be normal reactive w normal fundo.

MRI is critical

Front 93

Post-op Visual Loss - Treatment

Back 93

* Controversial w poor evidence
* Transfuse to Hb 10
* Normal BP & supplementary O2 (unproven but likely harmless)
* No evidence for steroids, IOP-lowering agents or anti-plts