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Cardio > ECG: Pattern recognition > Flashcards

ECG: Pattern recognition Flashcards

1
Q

What are the ECG features of Brugada syndrome?

A

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

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2
Q

How is Brugada syndrome diagnosed?

A

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
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3
Q

What is the clinical features of pericarditis (hx and o/e)

A

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
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4
Q

What are the investigations to be done for pericarditis + what are the characteristic ecg findings?

A

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

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5
Q

What is the management of pericarditis?

A

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

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6
Q

What are the ecg features of pericardial effusion?

A

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)

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7
Q

what are the clinical features of pericardial effusion?

A

Beck’s Triad – muffled heart sounds, elevated JVP and Hypotension 🡪 feature of cardiac tamponade

Pulses Paradoxus – SBP drops >10mmHg on inspiration

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8
Q

How is pericardial effusion managed?

A

ABCs
Transthoracic echocardiogram
Pericardiocentesis

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9
Q

What are the features of long QT syndrome?

A
  • normal sinus rhythm
  • normal axis and QRS complexes
  • prolonged QT interval: : QT interval > half of R-R interval = Prolonged QT
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10
Q

What are the clinical features of long qt sydrome?

A
  • ‘inherited channelopathy’
  • mostly autosomal dominant
  • risk of Sudden Cardiac Death
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11
Q

What are the classic triggers of long qt syndrome?

A
  • LQTS 1 -> sports (esp. swim) 🡪 Classically almost drowns when swimming due to paroxysmal TDP
  • LQTS2 -> noise
  • LQTS 3 -> sleep
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12
Q

What are the ECG features of hypertrophic cardiomyopathy (HCM)?

A
  • left ventricular hypertrophy

- marked T wave inversions in the anterolateral leads I, II, aVL, V4-V6

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13
Q

What are the differentials for T wave inversions?

A
  • Exertional dyspnoea secondary to heart failure (most common)
  • Fatigue, angina, (pre)syncope, palpitations
  • Sudden cardiac death from sustained ventricular tachyarrhythmia
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14
Q

What are the physical signs of HCM?

A

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

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15
Q

What is the management of hypertrophic cardiomyopathy?

A

Beta-blockers the cornerstone of treatment

ICD if patient at high-risk of sudden cardiac death form ventricular arrhythmia

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16
Q

What is the pathophysiology of digoxin toxicity?

A
  • 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
17
Q

What are the ECG features of digoxin toxicity?

A
  • 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
18
Q

What are the ecg features of raised ICP?

A

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
19
Q

What are the ecg stages of AMI?

A

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
20
Q

What are the ecg features in wellen’s syndrome?

A
  • 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
21
Q

What are the ecg changes seen in pulmonary embolism?

A
  • 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
22
Q

What are the ecg features of mild hyperK?

A
  • peaked t waves

- prolonged pr segment

23
Q

What are the ecg features of moderate hyperK?

A
  • loss p waves
  • prolonged qrs complex
  • st segment elevation
  • ectopic beats and escape rhythms
24
Q

What are the ecg features of severe hyperK?

A
  • progressive widening of QRS complex
  • sine wave
  • ventricular fibrillation
  • axis deviations
  • asystole
  • bundle branch blocks
  • fasicular blocks
25
Q

What are the ecg features of hypoK?

A
  • st depression
  • flattening of T wave
  • U wave
26
Q

What are the differentials for ST elevations other than STEMI?

A

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

Cardio (16 decks)

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