ECG: Pattern recognition Flashcards
What are the ECG features of Brugada syndrome?
Type 1: Coved ST-segment elevation displaying J-point amplitude or ST-segment elevation ≥2 mm, followed by a negative T wave.
Type 2: ≥2 mm J-point elevation, ≥1 mm ST-segment elevation and a saddleback appearance, followed by a positive or biphasic T-wave.
Type 3: It has either a saddleback or coved appearance, but with an ST-segment elevation <1 mm.
It should be stressed that type 1 is the only ECG diagnostic pattern of BS while types 2 and 3 should only be considered suggestive
How is Brugada syndrome diagnosed?
ECG findings PLUS 1 of:
- Documented VF or polymorphic VT
- Inducibility of VT with electrical stimulus
- Family history of sudden cardiac death <45 yo
- ECG findings in family member
- Syncope
- Nocturnal agonal respiration
What is the clinical features of pericarditis (hx and o/e)
History
- Pleuritic chest pain radiating to trapezoids
- Worse on lying down, relieved by sitting forward
- Associated with fever, dyspnoea, cough, nausea, anorexia
Physical examination
- Tachycardia, tachypnoeic
- Pericardial rub (best heard at LLSE)
- Complications –> Effusion: muffled heart sounds, distended neck veins, hypotension (Becks’ triad
What are the investigations to be done for pericarditis + what are the characteristic ecg findings?
ECG
• Widespread concave ST elevation and PR depression throughout most of limb leads (I, II, III, aVL, aVF) and precordial leads (V2-6)
• Reciprocal ST depressions and PR elevation in lead aVR (±V1)
• Sinus tachycardia due to pain and ± pericardial effusion
Most commonly viral; hence ix to prove viral investigation & check for complications
Inflammatory markers (CRP, ESR)
- FBC (WCC)
- If suspecting effusion 🡪 2D Echocardiogram 🡪 especially if electrical alternans
- CXR: signs of pericardial effusion 🡪 globular heart, cardiomegaly
What is the management of pericarditis?
ABCs
High dose Aspirin/NSAIDs (Ibuprofen 600-800mg tds x2-3/52)
Or Aspirin 300mg, 3x a day (high dose)
With Colchicine (for patients not responding to NSAIDs)
Prednisolone (for patients not responding to NSAIDs/colchicine or recurrent) 🡪 however steroid therapy is generally discouraged
Will interfere with ventricular healing
What are the ecg features of pericardial effusion?
In a large effusion, heart may rotate freely within the sac 🡪 axis of the heart changes with each beat = Electrical alternans
Low voltage in all leads (dampening of electrical output from effusion)
what are the clinical features of pericardial effusion?
Beck’s Triad – muffled heart sounds, elevated JVP and Hypotension 🡪 feature of cardiac tamponade
Pulses Paradoxus – SBP drops >10mmHg on inspiration
How is pericardial effusion managed?
ABCs
Transthoracic echocardiogram
Pericardiocentesis
What are the features of long QT syndrome?
- normal sinus rhythm
- normal axis and QRS complexes
- prolonged QT interval: : QT interval > half of R-R interval = Prolonged QT
What are the clinical features of long qt sydrome?
- ‘inherited channelopathy’
- mostly autosomal dominant
- risk of Sudden Cardiac Death
What are the classic triggers of long qt syndrome?
- LQTS 1 -> sports (esp. swim) 🡪 Classically almost drowns when swimming due to paroxysmal TDP
- LQTS2 -> noise
- LQTS 3 -> sleep
What are the ECG features of hypertrophic cardiomyopathy (HCM)?
- left ventricular hypertrophy
- marked T wave inversions in the anterolateral leads I, II, aVL, V4-V6
What are the differentials for T wave inversions?
- Exertional dyspnoea secondary to heart failure (most common)
- Fatigue, angina, (pre)syncope, palpitations
- Sudden cardiac death from sustained ventricular tachyarrhythmia
What are the physical signs of HCM?
Jerky pulse due to sudden deceleration of blood due to the development of mid-systolic obstruction to blood flow and partial closure of the aortic valve
Aortic flow murmur characteristically louder after the pause that follows an extra-systole
4th heart sound
ESM best heard at apex due to systolic anterior motion of the anterior mitral valve leaflet leading to significant LVOT obstruction
- Heard best at apex and LLSE
- Accentuated by valsava, standing and nitroglycerin which enhances obstruction
- Made softer by squatting, sitting or lying down
MR from SAM of mitral valve
What is the management of hypertrophic cardiomyopathy?
Beta-blockers the cornerstone of treatment
ICD if patient at high-risk of sudden cardiac death form ventricular arrhythmia
What is the pathophysiology of digoxin toxicity?
- a competitive Na+/K+ ATPase inhibitor
- Hence HypoK predisposes pt on Digoxin into Digoxin toxicity (less K+ to bind to Na/K ATPase, hence more Digoxin binds to exert effects)
- Digoxin toxicity may push pt into HyperK due to it preventing extracellular K moving into cells
- Digoxin increases automaticity of the heart at the SA node 🡪 may predispose to SVT
- Causes inhibition of the AV node 🡪 can lead to heart blocks
- Hence it can result in a whole range of presentations
What are the ECG features of digoxin toxicity?
- Down sloping ST depression
- Flattened, inverted, or biphasic T waves (most common)
- Shortened QT interval
- ventricular ectopy (PVCs)
- atrial tachyarrhythmias and AV nodal depression causing high degree of AV block
- Paroxysmal atrial tachycardia (PAT) with block
- severe bradycardia
- accelerated junctional rhythm
- bidirectional ventricular tachycardia
- almost any rhythm except SVT with 1:1 conduction
What are the ecg features of raised ICP?
Widespread giant T-wave inversions (“cerebral T waves”)
QT prolongation
Bradycardia (the Cushing reflex – indicates imminent brainstem herniation)
Others:
- ST elevation/depression
- Increased U wave amplitude
- Rhythmic disturbances
What are the ecg stages of AMI?
T wave changes
- Tall T waves
- T wave inversion
ST elevation
- Concave, merges with T wave
- reciprocal ST depression
Q waves
- Infarcted tissue is electrically silent, hence electrical forces will be directed away from this area, and leads over it will record a negative deflection
- Pathological Q wave >0.04s wide and >0.1mV deep in any 2 leads of a contiguous lead group
- Will have reciprocal changes
What are the ecg features in wellen’s syndrome?
- Deeply-inverted (type B) or biphasic (type A) T waves in V2 and V3
- Isoelectric or minimally-elevated ST segment
- No precordial Q waves
- Preserved precordial R wave progression
- Recent history of angina
- Highly specific for a critical stenosis of the left anterior descending artery (LAD)
- Patient is typically pain-free at the time of the ECG but are at extremely high risk for extensive anterior MI within the next few days to weeks
- Normal or slightly elevated serum cardiac markers
What are the ecg changes seen in pulmonary embolism?
- Sinus tachycardia (most common and sometimes the only finding)
- RV hypertrophy with strain pattern
- Right BBB
- P pulmonale (Right atrial enlargement)
- Negative T waves in leads lll and V1
S1Q3T3 (rare)
- Deep S wave in lead I
- Q wave in lead III
- T wave inversion in lead III
What are the ecg features of mild hyperK?
- peaked t waves
- prolonged pr segment
What are the ecg features of moderate hyperK?
- loss p waves
- prolonged qrs complex
- st segment elevation
- ectopic beats and escape rhythms
What are the ecg features of severe hyperK?
- progressive widening of QRS complex
- sine wave
- ventricular fibrillation
- axis deviations
- asystole
- bundle branch blocks
- fasicular blocks
What are the ecg features of hypoK?
- st depression
- flattening of T wave
- U wave
What are the differentials for ST elevations other than STEMI?
Coronary related
• Coronary dissection
• Coronary spasm (printzmetal)
Myocardium / Pericardium / Pulmonary artery
• Myo / pericarditis
• Stress cardiomyopathy (takotsubo cardiomyopathy)
• Blunt force myocardial injury
• LV aneurysm
Channelopathy (at cell membrane level) or conduction abnormality
• Brugada syndrome
• Early repolarization syndrome
• Left bundle branch block
Electrolytes / external factors
• Hyperkalemia
• Hypercalcemia
• Hypothermia
