Diagnostics and data interpretation Flashcards
ECG:
What regions of the heart correspond to which leads?
- Inferior leads: II, III, aVF
- Lateral leads: I, aVL, V5, V6
- Anteroseptal leads: V1 (septal), V2 (anteroseptal), V3 & V4 (anterior)
- Posterior leads (only used if posterior MI is suspected): V7, V8, V9
ECG:
On standard settings, what does each small square (1mm) represent in time (x-axis) and voltage (y-axis)?
Standard settings: 25mm/s, 1mV = 1cm
- Time: 1mm = 0.04s
- Voltage: 1mm = 0.1mV
Each large square equals:
- Time = 0.2s
- Voltage = 0.5mV
ECG:
What are the 10 steps for systematic interpretation of ECGs?
- Rate
- Rhythm
- Cardiac axis
- P-waves
- PR interval
- QRS complexes
- ST segment
- T waves
- QT interval
- U waves
ECG:
Stages 1 & 2: assessment of rate and rhythm
Rate:
- R-R interval: 300/number of large (5mm) boxes between two R waves
- Rhythm strip method: the rhythm strip (long one at the bottom) shows 10s. Count # of complexes in the rhythm strip and multiply by 6.
Rhythm:
- Sinus rhythm has three components: sinus P waves, a regular PR interval, and a QRS after each P wave.
- Sinus P waves are: positive in I, II and aVF, and negative in aVR
ECG:
Stage 3: assessing cardiac axis (look at the Cabrera circle if unsure)
Look at the polarity of leads I and aVF:
- If both leads are positive, the cardiac axis is between 0° and 90° (i.e. normal)
- If I is positive and aVF is negative, the axis is between 0° and -90°. In this case, look at II, if this is positive, the axis is between 0° and -30°; if II is negative, the axis is between -30° and -90°, meaning there is LAD
- If I is negative and aVF is positive, the axis is between 90° and 180°, meaning there is RAD
- If I and aVF are both negative, there is extreme axis deviation
ECG:
Stage 4: assessing P waves.
Features of a normal P wave?
- Positive in I, II, aVF
- Negative in aVR
- Biphasic (i.e. a positive and negative inflection) in V1, with negative inflection < 1mm
ECG:
Stage 4: assessing P waves.
What is P pulmonale? what is it seen in?
- Right atrial enlargement
- Secondary to COPD, pulmonary fibrosis, pulmonary hypertension, PE etc.
- Increased amplitude (≥ 0.25mV) in II
ECG:
Stage 4: assessing P waves.
What is P mitrale? what is it seen in?
- Left atrial enlargement
- Secondary to constrictive pericarditis, rheumatic heart disease
- Bifid in II (𝗠 shaped → P 𝗠itrale)
- Biphasic in V1 with negative inflection > 1mm
ECG:
Stage 5: assessing the PR interval;
Normal PR interval?
- Start of P wave to start of the QRS complex
- Normally 0.12 - 0.20s
- Should be constant
ECG:
Stage 5: assessing the PR interval;
First-degree AV block diagnosis?
Constant PR interval ≥0.20s
ECG:
Stage 5: assessing the PR interval;
Diagnosis of second-degree AV block (Mobitz I/Wenkebach)?
PR interval progressively lengthens until a QRS is dropped
ECG:
Stage 5: assessing the PR interval;
Diagnosis of second-degree AV block (Mobitz II)?
- Constant PR interval with QRS complexes intermittently dropped
- A constant ratio of P waves to QRS complexes (e.g. 2:1, 3:2 etc.)
ECG:
Stage 5: assessing the PR interval;
Diagnosis of third-degree AV block?
- Complete dissociation of atrial and ventricular contractions
- P waves occurring at regular intervals
- QRS complexes at regular, slower intervals (around 40bpm)
ECG:
Stage 5: assessing the PR interval;
Causes of PR depression?
- Pericarditis
- Pericardial effusion
- Atrial ischaemia
ECG:
Stage 6: assessing the QRS complex;
Normal morphology?
- < 0.1s
- Q wave < 0.2mV (2 small 1mm squares)
- Going from V1-V6 𝗦 waves get 𝗦maller, 𝗥 waves 𝗥ise
ECG:
Stage 6: assessing the QRS complex;
What are abnormal Q waves?
- Too deep (≥ 0.2mV)
- Too wide (≥ 40ms; 1 small square)
- > 25% of the size of the R wave in V1-V3
ECG:
Stage 6: assessing the QRS complex;
Diagnosis of bundle branch blocks?
𝗥ight bundle branch block:
- 𝗠a𝗥𝗥o𝗪
- 𝗠 shaped QRS in V1
- 𝗪 shaped QRS in V6
𝗟eft bundle branch block:
- 𝗪i𝗟𝗟ia𝗠
- 𝗪 shaped QRS in V1
- 𝗠 shaped QRS in V6
- QRS duration > 0.1s
ECG:
Stage 6: assessing the QRS complex;
Causes of dominant R waves?
- R wave prominent from V1-V6
- Right ventricular hypertrophy
- RBBB
- Posterior MI
ECG:
Stage 6: assessing the QRS complex;
Causes of poor R wave progression?
- R wave fails to grow from V1-V6
- S wave may be present in all precordial leads
- Anterior MI
- Right heart strain (e.g. massive PE)
- LBBB
ECG:
Stage 6: assessing the QRS complex;
Diagnosis of left ventricular hypertrophy?
- “Sokolov-Lyon criteria”
- S wave depth in V1 + tallest R wave height in V5-V6 > 35 mm
ECG:
Stage 7: assessing the ST segment;
Diagnosis of ST elevation?
- ≥ 0.1mV in limb leads
- ≥ 0.2mV in precordial leads
- Must be significantly elevated in two contiguous leads
ECG:
Stage 7: assessing the ST segment;
Causes of ST elevation?
- 𝗦𝗧𝗘𝗠𝗜: must be reciprocal change (signs of ischaemia i.e. T wave inversion or ST depression) elsewhere on ECG for diagnosis
- 𝗣𝗲𝗿𝗶𝗰𝗮𝗿𝗱𝗶𝘁𝗶𝘀: global ST elevation (in all territories), may be saddle-shaped. Often no reciprocal change.
- 𝗕𝗿𝘂𝗴𝗮𝗱𝗮 𝘀𝘆𝗻𝗱𝗿𝗼𝗺𝗲: 2nd commonest cause of sudden cardiac death (after HCM). Coved ST elevation in V1-V2.
- Coronary artery vasospasm (Prinzmetal’s angina)
ECG:
Stage 7: assessing the ST segment;
Causes of ST depression?
- Downsloping depression: myocardial ischaemia/NSTEMI
- Upsloping depression: with hyperacute T waves = very early MI
- Upsloping ST depression: digoxin toxicity
- Flat ST depression: V1-V3 → posterior MI, hypokalaemia
ECG:
Stage 7: assessing the ST segment;
Causes of J waves (aka Osborn waves)?
- Hypothermia
- Brugada syndrome
- Benign early repolarisation
- Hypercalcaemia
ECG:
Stage 8: assessing T waves;
Abnormalities of T waves?
- Inversion: myocardial ischaemia (cannot localise pathology), ventricular hypertrophy
- Flattening: myocardial ischaemia, hypokalemia
- Peaked T waves: hyperkalemia, hypermagnesemia
- Hyperacute T waves: very early MI
ECG:
Stage 8: assessing T waves;
Difference between peaked T waves and hyperacute T waves?
- The total area under peaked T waves is the same as normal (i.e. thin and tall; ‘tented’)
- Hyperacute T waves have a larger than normal area underneath them (i.e. tall, normal width)
ECG:
Stage 9: assessing the QT interval;
Normal corrected QT interval?
Men: 390-450ms
Women: 390-460ms
ECG:
Stage 9: assessing the QT interval;
Causes of a short QT interval?
- Hypercalcaemia
- Hyperkalaemia
- Digoxin
ECG:
Stage 9: assessing the QT interval;
Causes of a long QT interval?
- Congenital long QT syndrome e.g. Romano-Ward
- Drug side effects (e.g. antipsychotics, citalopram, some antibiotics)
- Hypocalcaemia, hypokalaemia, hypomagnesemia
- Intracranial pathology e.g. SAH
ECG:
Stage 9: assessing the QT interval;
Complications of long QT interval?
Torsades des Pointes (polymorphic VT)
ECG:
Stage 10: assessing U waves;
What are they and when are they present?
- Small inflection after T wave and before P wave
- Physiological in bradycardia (become visible when HR < 65bpm; get larger the slower the HR)
- Also seen in hypokalemia and hypercalcaemia
ABG:
6 stages of ABG interpretation?
- Look at PaO₂
- Look at pH
- Look at PaCO₂
- Look at HCO₃⁻
- Calculate base excess
- Look at the anion gap (if there’s metabolic acidosis)
- Look at the other values on the gas
ABG:
Step 1: PaO₂
What is the normal range? What is type 1 respiratory failure?
- Normal = 10 - 14kPa
- T1RF is when PaO₂ is low and PaCO₂ is normal
ABG:
Step 2: pH
What is the normal range?
- Normal = 7.35 - 7.45
- pH < 7.35 = acidosis
- pH > 7.45 = alkalosis
ABG:
Step 3: PaCO₂
What is the normal range? What is type 2 respiratory failure?
- Normal = 4.5 – 6kPa
- T2RF is when PaO₂ is low and PaCO₂ is high
- Low PaCO₂ suggests hyperventilation. This can be to compensate for a metabolic acidosis, or it may be psychogenic.
ABG:
Step 4: HCO₃⁻
How is this interpreted?
- High: metabolic alkalosis or compensated respiratory acidosis (a very raised carbonate likely indicates chronic acidosis e.g. in a carbon-retaining COPD patient)
- Normal: uncompensated respiratory disorders
- Low: metabolic acidosis or compensated respiratory alkalosis
ABG:
Step 5: base excess
How is this interpreted?
- Base excess shows how much ‘spare’ HCO₃⁻ is present in the blood.
- Distinguishes between metabolic acidosis/alkalosis.
- Only looks at the metabolic component of the blood.
- Normal range is -2 to 2 mEq/L
- High base excess → large amount of HCO₃⁻ → metabolic alkalosis
- Low base excess → deficiency of HCO₃⁻ → metabolic acidosis (look at anion gap to determine cause)
ABG:
Step 6: anion gap
How is the anion gap measured?
- It is a measure of how many anions that are not routinely tested for are present in the blood
- Therefore measures how many acids (other than carbonic acid) are present (e.g. lactic acid, ketoacids etc.)
- (Sum of anions [+ve ions]) - (sum of cations [-ve ions])
- Calculated as: ([Na⁺] + [K⁺]) - ([Cl⁻] + [HCO₃⁻])
- Normal anion gap metabolic acidosis: primary (renal or GI) 𝗹𝗼𝘀𝘀 𝗼𝗳 𝗛𝗖𝗢₃⁻ with 𝗰𝗼𝗺𝗽𝗲𝗻𝘀𝗮𝘁𝗼𝗿𝘆 𝗶𝗻𝗰𝗿𝗲𝗮𝘀𝗲𝗱 𝗖𝗹⁻ 𝗮𝗯𝘀𝗼𝗿𝗽𝘁𝗶𝗼𝗻.
- Raised anion gap metabolic acidosis: 𝗶𝗻𝗰𝗿𝗲𝗮𝘀𝗲𝗱 𝗰𝗼𝗻𝗰𝗲𝗻𝘁𝗿𝗮𝘁𝗶𝗼𝗻 𝗼𝗳 𝗼𝗿𝗴𝗮𝗻𝗶𝗰 𝗮𝗰𝗶𝗱𝘀 such as lactate, ketoacids with 𝗡𝗢 𝗰𝗼𝗺𝗽𝗲𝗻𝘀𝗮𝘁𝗼𝗿𝘆 𝗶𝗻𝗰𝗿𝗲𝗮𝘀𝗲𝗱 𝗖𝗹⁻ 𝗮𝗯𝘀𝗼𝗿𝗽𝘁𝗶𝗼𝗻.
ABG:
Step 6: anion gap
Common causes of a normal anion gap metabolic acidosis?
GI:
- Diarrhoea
- Fistulas
Renal:
- Renal tubular acidosis
- Addison’s disease
- Spironolactone
Iatrogenic:
- Saline administration (too much Cl⁻)
Chest x-ray:
Systematic method for interpretation?
- Identify the patient and the date of the scan
Assess image quality: 𝗥𝗜𝗣𝗘
- Rotation
- Inspiration (5-6 anterior ribs should be visible)
- Projection (AP/PA film)
- Exposure (vertebrae should be 𝘫𝘶𝘴𝘵 visible behind heart)
𝗦ome𝗕ody 𝗧ook 𝗠y 𝗟ovely 𝗗inosaur:
- 𝗦oft tissue (surgical emphysema, ?obese)
- 𝗕ones (rib fractures, rib notching, other fractures etc.)
- 𝗧rachea (?deviated)
- 𝗠ediastinum (aortic knuckle, ?cardiomegaly*, ?pneumomediastinum?
- 𝗟ungs (?consolidation, ?collapse, ?pneumothorax etc.)
- 𝗗iaphragm (should be same height, ?blunted costophrenic angle)
*cardiomegaly can only be assessed on a PA film. In this case, the heart should not be more than 50% the width of the thorax.
