ECG's + Cardiology Flashcards
Syncope ECG Interpretation
2023.1 Junior Doctor Teaching Station
Medical Expertise: Assessment and Diagnosis (40%)
* Interpret ECG
* Outline differential diagnoses
* Identify risk of deterioration in the patient - highlight life threatening features
Medical Expertise: Management (40%)
* Outline resuscitation plan
* Correctly choose time critical interventions based on assessment (to start positive
chronotropes if needed).
* Initiate treatments specific to identified severe abnormalities in circulation (escalating approach)
*address reversible causes
* Outline an overall plan for ongoing treatment.
Scholarship and Teaching (20%)
* Check for level of prior knowledge / understanding.
* Make the learner feel safe and supported.
* Demonstrate a structured approach to the topic.
* Invite questions and clarifies any areas of uncertainty.
* Summarise the session with appropriate emphasis of key elements.
Differential Diagnoses
Syncope ECG Interpretation
2022.2 RMO Interaction Station
Medical Expertise: ECG interpretation (40%)
* Interpret ECG
Medical Expertise: Assessment (40%)
* Elicits a focused, relevant history de novo
* Identifies important historical details (red flags) diagnostic of an important condition
* Describes a focused structured and relevant physical examination
* Explains the reasons for selecting specific tests in the investigation plan.
Prioritisation and Decision Making (20%)
* Highlights high-risk features
* Provides a rationale to explain and justify decisions about ongoing treatment
* Highlights which of selected investigations has/have higher priority.
ABCDE Left to Right
AV block (and bifasicular block)
Brugada
QTc prolongation
Delta wave in WPW
Epsilon waves in arrhythmogenic right ventricular cardiomyopathy
Left ventricular hypertrophy (aortic stenosis & HOCM)
Right ventricular strain pattern in massive PE
Syncope ECG
2023.1 RMO interaction
Advise a junior doctor on the interpretation of an ECG, outline differential diagnoses, and provide initial management.
SYNCOPE ECG INTERPRETATION:
“ABCDE Left to Right”
AV block
Brugada
QTc prolongation
Delta wave of WPW
Epsilon wave (arrythmogenic right ventricular cardiomyopathy)
LVH - AS & HOCM
Right ventricular strain pattern in PE
Tamponade - tachycardia, low voltage, electrical alternans
DIFFERENTIAL DIAGNOSIS
CARDIAC:
Arrythmia:
- bradyarrythmia
- tachyarrythmia
- arrythmogenic right ventricula cardiomyopathy
- WPW
- Prolonged QTc
- Brugada
Obstructive:
- PE
- tamponade
LV outflow obstruction:
- HOCM
- critical AS
Neurological:
- TIA/CVA
- SAH
- Subclavian steel
Anaemia
Massive haemorrhage (ectopic pregnancy)
Autonomic dysfuction:
- parkinsons
- diabetes
Orthostatic hypotension:
- dihydropyridine calcium channel blockers
Dehydration - diarrhoea and vomiting, diuretics
Vasovagal syncope
Hypoglycemia
Seizure
HISTORY:
review the ambulance rhythm strip
sudden syncope - no warning, broken glasses, broken teeth
Palpitations at time of syncope
Syncope on exertion
Syncope while lying down
Pace makers
Family history of sudden unexpected death
Medications:
- beta blockers
- calcium channel blockers
- QT prolonging medications
- diuretics
EXAMINATION:
Auscultation - aortic stenosis
HOCM murmur louder on valsalva, quieter on squatting
POCUS:
- pericardial effusion and tamponade
- PE
INVESTIGATIONS:
Hb - anaemia
Bhcg - ectopic pregnancy
Electrolytes - QTc
Echo
BRADYCARDIA
Causes of bradycardia
- MI (inferior & anterior)
- hypothermia
- hyperkalemia
- hypothyroid myxoedema
- overdose (beta blockers, calcium channel blockers, digoxin)
- raised ICP (cushings reflex)
- neurogenic shock
- BRASH syndrome
AV BLOCK
FIRST DEGREE HEART BLOCK
conduction delay but all p waves conduct to ventricles
PR prolongation >200ms
P waves can be buried in the preceding T wave
benign - not clinically significant
causes - increased vagal tone, athletes, drugs (beta blockers, verapamil, digoxin)
no specific treatment required
SECOND DEGREE HEART BLOCK (MOBITZ TYPE 1)
“Intermittent” failure of AV conduction
Dropped QRS complexes
‘dropped beat’
‘non-conducted p-waves’
Conduction ratio p:QRS
MOBITZ TYPE 1 (Wenchebach)
Progressive PR prolognation
- longest PR interval just before the dropped QRS
- Usually benign
- Asymptomatic patients don’t require treatment
- Symptomatic patients respond to atropine
- Permanent pace maker is rarely required
MECHANISM:
- AV nodal suppression
CAUSES:
- increased vagal tone (athletes)
- drugs (beta blockers, calcium channel blockers, amiodarone, digoxin)
- ischemia (inferior MI)
- post cardiac surgery (valvular)
- myocarditis
- electrolyte disturbance (hyperkalemia)
Bradycardia
SECOND DEGREE HEART BLOCK (MOBITZ TYPE 2)
Dropped QRS complexes
No progressive PR prolongation
RR intervals are fixed
MECHANISM:
- failure at the bundle of His/Purkinje level
- due to structural damage (ischemia, fibrosis, necrosis)
CAUSES:
- Anterior MI
- Idiopathic fibrosis of the conduction system (Lenegre-Lev disease)
- Cardiac surgery - septal surgery
- Infiltrative (amyloidosis, sarcoidosis)
- Myocarditis
- Autoimmune (SLE)
- Electrolytes
- Drugs
CLINICAL SIGNIFICANCE:
- can cause severe bradycardia
- Stokes-Adadms attacks (syncope)
- high risk of sudden cardiac death
- Mandates admission for cardiac monitoring and pacemaker placement
THIRD DEGREE HEART BLOCK:
Severe bradycardia
Complete absence of AV conduction
- No supraventricular impulses are being conducted to the ventricles
- AV dissociation
- Perfusing rhythm is maintained by a junctional escape rhythm
At risk of ventricular standstill –> syncope or sudden cardiac death
Needs admission with cardiac monitoring, back up pacing, and insertion of permanent pacemaker
BRADYCARDIA - BRASH syndrome
Bradycardia
Renal failure
AV blockade
Shock
Hyperkalemia
old people
on beta blocker, calcium channel blocker, digoxin
renal failure
leads to hyperkalemia and accumulation of AV blockade –> bradycardia
MANAGEMENT:
calcium gluconate 2.2mmol (10mL) IV - stabilise the myocardium, cardiac monitoring and serial ECG’s
fluid resuscitation
push dose adrenaline 10-20mcg IV (0.1mcg/kg IV) every 2min
(1ml of 1:10,000 mixed with 9ml saline = 10mcg/ml)
Adrenaline infusion
- Draw up 6 mL of adrenaline 1:1000 solution = 6mg
Add to 94 mL of glucose 5%
insulin + glucose (10units actrapid IV + 10% dextrose 250ml IV)
Infuse at 3 to 50 mL/hour to deliver 3 to 50 micrograms/minute
sodium bicarbonate 50mmol (50mL) IV over 5min
haemodialysis
BRADYCARDIA - Hyperkalemia
ECG changes:
- Peaked T waves
- P wave widening/flattening
- PR prolongation
- bradycardia
- wide QRS
- bizarre QRS morphology
- Sine wave
MANAGEMENT:
calcium gluconate 2.2mmol (10ml) IV
actrapid 10units IV + 10% dextrose 250ml IV
sodium bicarbonate 50mmol/50mL IV
Severe Chest Pain
2021.2 RMO interaction
Discuss with a junior medical officer (role player) an approach to the assessment of a patient who has presented with severe chest pain.
Interpret the ECG (there is ST elevation)
- does it meet STEMI criteria?
- how do you differentiate STEMI from mimics
- consider all other life threatening causes for chest pain
- differentiation between STEMI and pericarditis on ECG
- discuss use of POCUS in chest pain
POCUS pneumothorax video
POCUS PE video
POCUS pericardial effusion
POCUS LV dysfunction
Very important when faced with ST elevation on ECG to be able to differentiate between STEMI and pericarditis
- don’t want to miss STEMI and label as pericarditis
- don’t want to treat pericarditis as STEMI with antiplatelets and anticoagulation and cause a haemorrhagic tamponade
STEMI mimics:
- Pericarditis
- PE
- Benign early repolarisation
- Hypothermia
- Hyperkalemia
- Hypercalcemia
- LBBB
- Pacemaker
- LVH
DIFFERENTIAL DIAGNOSES:
- ACS
- PE
- Aortic Dissection
- Pneumothorax
- Myocarditis
- Oesophageal rupture
- Pericarditis (diagnosis of exclusion)
ACS:
History:
- Crushing or heavy chest pain
- Radiation
- Nausea and diaphoresis
ECG:
- hyperacute T waves,
- ST elevation with reciprocal ST depression
- deWinters T waves (upsloping ST depression with hyperacute T wave)
- Wellens syndrome: deep precordial T wave inversions or biphasic T waves in V2-3, indicating critical proximal LAD stenosis (a warning sign of imminent anterior infarction)
STEMI ECG criteria:
“new ST segment elevation at the J point in at least two contiguous leads of ≥ 2 mm (men) or 1.5 mm (women) in precordial leads or ≥ 1 mm in the limb leads
ECHO:
- regional wall motion abnormalities
PULMONARY EMBOLUS:
ECG:
- tachycardia
- T wave inversion
- right axis deviation
- S1, Q3, T3 patterns
- RBBB
Echo:
- dilated RV (RV > LV)
- McConels sign
- Flat interventricular septum
AORTIC DISSECTION:
ECG:
- non-specific
Echo:
- aortic root dilatation
- aortic regurgitation
- pericardial effusion
- dissection flap
PNEUMOTHORAX:
Echo:
- loss of lung sliding
- lung point of transition point
- loss of comet tails (reverberation artefact)
- absense of seashore sign on m-mode (presence of the barcode sign)
PERICARDITIS:
Echo:
In acute STEMI, a localized wall motion abnormality is typically present that corresponds with the region of the coronary occlusion. In pericarditis, the echocardiogram demonstrates normal wall motion and may also show a pericardial effusion.
DIFFERENTIATING BETWEEN STEMI AND PERICARDITIS:
(1) Distribution of ST elevation:
- Widespread/diffuse ST elevation and PR depression (favours pericarditis)
- Reciprocal ST depression in aVR & V1
- In ACS, ST elevation is localised in the territory of the infarct, this depends on which artery is occluded
inferior = RCA
inferolateral = LAD & L circumflex
Anterior, septal, apical = LAD
(2) ST segment morphology:
- ST elevations are more commonly convex or ‘coved’ shaped in STEMI, while concave upsloping in pericarditis
J point is sharp in pericarditis
J point is indistinct in MI
aVL:
- ST segments should be normal or elevated
- T waves should be upright
- ST depression = inferior MI
- T wave inversion = MI
- aVL is usually normal in pericarditis
Leads II & III
- ST elevation III > ST eleveation II is highly suspicious for inferior STEMI
- ST elevation II > ST elevation III favors pericarditis
Spodick’s sign favors pericarditis.
- down-sloping from the T wave to the QRS segments
- best seen in lead II
T waves:
- hyperacute or inverted in MI
- preserved in pericarditis
Pericarditis
PERICARDITIS:
Diagnostic criteria: (2 out of 4)
1) pericarditis chest pain
- Sharp & Stabbing
- Pleuritic - worse with deep breathing and coughing
- Positional - worse lying down, better sitting forward)
2) pericardial friction rub ‘velcro like’ sound over precordium
3) ECG changes - new widespread ST elevation and PR depression
4) Pericardial effusion
Additional supportive findings:
- raised inflammatory markers (CRP, ESR, WCC)
- signs of pericardial inflammation on CT or cardiac MRI
CAUSES:
Infective - viral (coxsackie), bacterial, fungal, mycobacterium (TB)
Malignancy - primary pericardial mesothelioma, secondary metastases
Autoimmune - SLE, Rheumatoid, sarcoidosis
Trauma
Post MI - dresslers syndrome
Endocrine - hypothryroid myxodedma
Metabolic - uraemia, anorexia
Iatrogenic - Post cardiac surgery, post radiotherapy, PCI, ablation
ECG FINDINGS:
QRS morphology
- CONCAVE/upsloping/Smiling ST elevation
Entire pericardium involved so STE is widespread
Atrial involvement = PR depression
- Reciprocal ST depression and PR elevation in lead aVR (± V1)
- Sinus tachycardia is also common in acute pericarditis due to pain and/or pericardial effusion
PERICARDIAL EFFUSION:
ECG:
- sinus tachycardia
- low voltage QRS
- electrical alternans (beat to beat variation in QRS amplitude)
Low voltage QRS has a differential – including adipose/breast tissue, hyperinflated lungs, pleural effusion, pericardial effusion, and cardiomyopathy
ECHO:
measure effusion size in end-diastole.
Trivial: fluid is only seen in systole
* Small: <10 mm
* Moderate: 10-20 mm
* Large: 21-25mm
* Very Large: >25mm
CARDIAC TAMPONADE:
Cardiac tamponade is a clinical diagnosis, not an imaging one.
5 features occur in the majority of patients with tamponade:
- Dyspnea
- Tachycardia
- Pulsus paradoxus (with pericardial effusion) >10mmHg
- Elevated JVP
- Cardiomegaly on chest radiograph
ECHO:
PoCUS findings suggestive of cardiac tamponade –
scrutinize the right side of the heart and IVC
- A pericardial effusion >25mm (but smaller pericardial effusions
can cause tamponade) - Diastolic right ventricular collapse
- Systolic right atrial collapse
- A plethoric inferior vena cava
Get formal echo
Place arterial line to monitor for pulsus paradoxus
Chest pain ECG
2022.2
Teaching
Adolescent with chest pain
Normal paediatric ECG
ECG of a 42-year-old female patient with resolved chest pain.
2021.2
Chest pain ECG
2021.2 RM interaction
Discuss with a junior medical officer (role player) an approach to the assessment of a patient who has presented with severe chest pain.
Chest pain ECG
2021.1
Inferior STEMI
2018 station
Interpret ECG
ECG:
Identify right ventricular MI (occurs in 1/3 of inferior STEMI)
occlusion of the RCA
- STE in V1
- STE in V1 and ST depression in V2
- STE in III>II
Preload dependent
Avoid nitrites
Need immediate reperfusion
