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Cardiovascular > ECG's > Flashcards

ECG's Flashcards

1
Q

Wide complex tachycardia differentials

A

Regular
- VTach!
- Hyperkalaemia (RRW)
- TCA/Na+ blocker overdose (RRW)
- Sinus/SVT with aberrancy
- Antidromic WPW/AVRT
- AIVR (<120bpm)
- Massive STE with sinus tach
- Post cardioversion
- Pacemaker tachy/runaway pacemaker

Irregular
- VFib!
- AF/flutter with aberrancy
- WPW with AF
- TDP/Polymorphic VT
- Hyper K/Tox

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2
Q

Pathological ECG findings in syncope

A

High grade AV block
Ischaemia
Brugada syndrome
LVH/HOCM (dagger Q waves, high voltage)
ARVC (epsilon waves, TWI V1-3)
Long QT
WPW syndrome

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3
Q

What are the typical findings in HOCM?

A

Tall QRS complexes consistent with LVH
Narrow dagger Q waves in lateral/inferior leads
Deep precordial TWI in apical HOCM
P mitral

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4
Q

What are the indications for activating the Cath lab (STEMI)

A

STE at J point in 2 or more contiguous leads
- M>40 = 2mm V2/3 or 1mm all else
- M<40 = 2.5mm V2/3 or 1mm all else
- W = 1.5mm V2/3 or 1mm all else
- Posterior STEMI signs
- LBBB/Paced rhythm meeting Sgarbossa criteria
- Widespread STD >1mm with STE >1mm in AVR and/or V1
Symptoms consistent with a myocardial infarction (chest pain present for at least 20mins)

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5
Q

Thrombolysis indications in STEMI?

A

If will be >90-120mins to obtaining PCI
+ Symptoms <12hrs
or symptoms 12-24 + large area affected
or ECG still shows acuteness (persistent R waves + STE, upright T waves)

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6
Q

What is the ECG evidence of reperfusion post PCI/thrombolysis?

A

At least 70% reduction in STE segments

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7
Q

Absolute thrombolysis contraindications?

A

Intracranial neoplasm or AVM
Any prior ICH
Ischaemia stroke <3mths
Active bleeding (except menses) internally or externally
Significant head trauma
<2month spinal/brain surgery
Uncontrollable HTN >180/110
If streptokinase, use in last 6 months or known sensitisation

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8
Q

Relative Thrombolysis contraindications?

A

Hx of chronic severe HTN or HTN >180/110 on presentation
Dementia
Ischaemic stroke >3months ago
intracranial path thats not absolute con
Prolonged CPR >10mins
Major surgery <3wks
Major internal bleeding <4 weeks
Non-compressible vascular puncture
Pregnancy, peptic ulcer, already on oral anticoagulants

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9
Q

What is evidence of failure of reperfusion?

A

STE <50% reduction at 90mins
Ongoing ischaemic CP
Haemodynamica instability
Ventricular tachyarrhythmias

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10
Q

ECG findings suggestive of VT

A
  • Concordance in precordial leads
  • Taller left rabbit ear in V1-2
  • Onset of R to nadir of S >100msec ie Brugada sign
  • More likely with QRS >160msec but <200msec
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11
Q

Brugada criteria

A
  1. Concordance in precordial leads
  2. Brugada sign (R to nadir of S >100msec)
  3. AV dissociation (fusion beats, capture beats etc)
  4. Morphology criteria
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12
Q

What are the Morphology criteria for VT?

A

RBBB type: 1. L) rabbit ear bigger V1
2. qR complex in V1
3. Smooth monophasic R wave
4. No R wave in V6 or R/S ratio <1 (+ has LAD)

LBBB type: 1. V1 R wave >40msec
2. Josephson sign (notching of the S wave V1)
3. RS time >70msec
4. QS or QR waves in V6

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13
Q

Causes of VT

A

Acute ischaemia
Hypokalaemia/Hyperkalaemia
Digoxin OD, TCA/Na+ blocker OD
Cardiomyopathy
Myocarditis

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14
Q

Risk factors for VT

A

Age >35
Structural heart disease
Ischaemic heart disease
Known ion channelopathy or long/short QT
Family history of sudden cardiac death or known conditions (ie brugada, ARVD etc)

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15
Q

How do posterior STEMI’s present on ECG?

A

Dominant R waves in V2
Broad R waves (>30msec)
Upright T waves in anterior leads
Horizontal or reverse tombstone ST depression

Posterior leads only need 0.5mm of continguous STE to be deemed a STEMI!

90-95% are associated with inferior/lateral STEMI, unusual to be isolated posterior STEMI

However any inferolateral STEMI consider possibility of posterior infarction as well

Consider posterior STEMI in anyone with acute ischaemic symptoms and new STD in leads V1-3

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16
Q

How is a posterior STEMI confirmed?

A

Posterior leads V7-9
Also can turn the ECG upside down
- R wave becomes q wave
- STD becomes STE
- upright T waves become TWI

Bedside echo can show posterior RWMA
Troponin will be severely elevated

17
Q

How do right sided STEMIs present on ECG?

A

Often in conjunction with inferior STEMI’s, consider in anyone with a inferior STEMI pattern (30% concurrence)

  • STE in V1 with STD in V2 (most specific)
  • Isolated V2 STD with isoelectric V1/3
  • STE in III&raquo_space;> II
  • Triad of hypotension, clear lungs and jugular venous distension
18
Q

How is an NSTEMI diagnosed?

A

Symptoms consistent with a myocardial infarction (ie >20mins of chest pain)
- STD >1mm in 2 or more contiguous leads that is either downsloping or flat in nature (not upsloping)
- or dynamic TWI in contiguous leads
- In the absence of any criteria being met for a STEMI
- + in most cases an elevated troponin level

19
Q

What two ECG findings need to be present when diagnosing BER in the anterior leads in someone with anterior STE?

A
  • An S wave
    AND/OR
  • Notching at the J point (J wave)

If neither an S wave or notching are present then strongly consider ischaemia if otherwise meeting ischaemic criteria

20
Q

What should also be considered when diagnosing an inferior STEMI?

A
  • Is there a conduction abnormality from the ischaemia
  • Do R) sided leads
  • do posterior leads
21
Q

What drugs are associated with monomorphic VT in overdose?

A
  • Digoxin
  • TCA’s
  • Na+ channel blockers
22
Q

What is the importance of high lateral MI’s?

A

Usually STE in I + AVL, but not as much or none in V5/6

Highest risk for ventricular free wall rupture

23
Q

Narrow complex tachycardia differentials?

A

Regular
- Sinus tach
- Atrial tach
- AVNRT
- Orthodromic AVRT
- Atrial flutter
- Narrow complex VT (fascicular)

Irregular
- Tachycardia with PAC/PVC’s
- AF
- A flutter with variable block
- Atrial tach with variable block
- Multifocal atrial tachycardia
- Digoxin toxicity
- Paroxysmal atrial tachycardia

24
Q

What are the differentials for a small QRS complexes (low voltage)

A
  • Altered ECG amplitude
  • Massive pericardial/pleural effusion
  • Subcut emphysema
  • Pneumothorax
  • Lung hyperexpansion (asthma, COPD, barrel chest)
  • Infiltrates ie myxoedema, scleroderma, amyloidosis, haemochromatosis
  • Restrictive pericarditis
25
Q

What are the non-toxicological causes of prolonged QT interval?

A
  • HypoK/Mg/Ca
  • Congenital long QT
  • Acute ischaemia
  • Hypothermia
26
Q

Whats the difference between atrial flutter and AVNRT?

A
27
Q

How should Torsades De Pointes be treated?

A
  • If unstable or arrested then 200j unsynchronised DC shock
  • Load with 4gm IV magnesium over 30-60mins then 1gm/hr aiming Mg level of 1.5-2.0
  • Replete K+ to 4.0-4.5
  • Replete Ca+ to ionised Ca+ >1.1
  • Correct hypothermia if present
  • Cease all QT prolonging agents
  • Consider IV 1mg/kg Lignocaine, followed by 1mg/min infusion (approx 1mg/kg/hr)
  • Medical chronotropy with Adrenaline or Isoprenaline aiming Hr 100-140
  • Electrical chronotropy if medical not working or causing too many premature complexes

Congenital Long QT
- Actually benefits from slowing down the heart with beta blockers
- Beta adrenergic agonists are contraindicated in congenital long QT

28
Q

How is pericarditis differentiated from AMI?

A

Morphology
- Pericardiditis usually concave (saddle back)
- STEMI may be Convex ie tombstoning (but can also be convex)
- Pericarditis unusual >5mm elevation

Distribution
- Pericarditis is generalised
- STEMI isolated to vascular territories

Reciprocal changes
- No reciprocal changes in pericarditis

TWI/Q waves
- New TWI and Q waves don’t occur in pericarditis

PR changes
- Dont occur in STEMI

29
Q

What are the causes of pericarditis?

A

Infectious
- Viral most common (COVID, HIV etc)
- Fungal, bacterial, TB etc

Radiation
- Iatrogenic or environmental

Post cardiac injury
- Dresslers syndrome
- Cardiac surgery, trauma

Metabolic
- Uraemia, myxedema
- OHSS

Malignancy
- especially lung, breast mesothelioma and Hodgkins

Autoimmune
- SLE, Kawasakis

Idiopathic

Toxicological
- Drug induced lupus (phenytoin, isoniazid, methyldopa etc)
- Anti-cancer drugs (oxorubicin)
- Minoxidil

30
Q

What are the typical ECG changes in pericarditis? What is the typical outpatient treatment?

A

Colchicine 500mcg BD for 3 months
+
Ibuprofen 600mg TDS for 1-2 weeks then taper

31
Q

What is the significance and what are the causes of T wave alternans?

A

Significance
- Strongly associated with impending ventricular dysrythmias and sudden cardiac death

Causes
- Congenital long QT syndrome
- Ischaemia
- Brugada
- HOCM
- Unstable CHF
- Arrhythmogenic drug toxicity (Digoxin etc)

32
Q

What are the features of Congenital Long QT syndrome?

A

ECG
- QTC >480, or QT >470 in girls and 450 in boys
- T wave alternans
- Bradycardic for age (paeds)
- Notched T waves (at least 3 leads)
- TdP

Clinical
- Can be associated wit congenital deafness
- Fhx of sudden death in immediate family
- Exertional (rate related) and non-exertional syncope

Treatment
- Beta blockers
- ICD
- L) cardiac denervation
- Made worse by overdrive pacing

33
Q

How is WPW risk stratified in the ED? What other diseases are associated with or causes of WPW?

A
  • HOCM
  • Transposition of the great vessels
  • Endocardial fibroelastosis
  • Mitral valve prolapse
  • Tricuspid atresia
  • Ebsteins anomaly

Cardiovascular (6 decks)

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