Clinical data interpretation

Question 1

Electrocardiography (ECG): electrophysiology of the heart, cardiac myocytes

Answer 1

In their resting state, the surface of cardiac myocytes (muscle cells) is polarised with a potential difference of 90mV across the cell membrane (negatively charged intracellularly and positively charged extracellularly).
Depolarisation (reversal of this charge) results in movement of calcium ions across the cell membranes and subsequent cardiac muscle contraction.
It is this change in potential difference that can be detected by the ECG electrodes and represented as deflections on a tracing.

Question 2

Electrocardiography (ECG): electrophysiology of the heart, the basics of the tracing

Answer 2

It is easiest to imagine an electrode ‘looking’ at the heart from where it is attached to the body.
Depolarisation of the myocytes that spreads towards the electrode is seen as an upwards deflection, electrical activity moving away from the electrode is seen as a downwards deflection and activity moving neither towards nor away from the electrode is not seen at all.

Question 3

Electrocardiography (ECG): electrophysiology of the heart, electrical conduction pathway

Answer 3

In the normal heart, pacemaker cells in the sinoatrial (SA) node initiate depolarisation.
The depolarisation first spreads through the atria and this is seen as a small upward deflection (P wave) on the ECG.
The atria and the ventricles are electrically isolates from each other.
The only way in which the impulse can progress from the atria to the ventricles normally is through the atrioventricular (AV) node.
Passage through the AV node slows its progress slightly.
This can be seen on the ECG as the isoelectric interval between the P wave and QRS complex, the PR interval.
Depolarisation then continues down the rapidly conducting Purkinje fibres- bundle of His, then down left and right bundle branches to depolarise both ventricles.
The left bundle has 2 divisions (fascicles).
The narrow QRS complex on ECG shows this rapid ventricular depolarisation.
Repolarisation of the ventricles is seen as the T wave.
Atrial repolarisation causes only a very slight deflection which is hidden in the QRS complex and not seen.

Question 4

Electrocardiography (ECG): the 12 lead ECG, leads and orientation

Answer 4

6 chest leads (V1-V6).
6 limb leads (I, II, III, aVR, aVL, aVF).
The 6 limb leads look at the heart in the coronal plane.
aVR looks at the right atrium (all vectors negative in normal ECG).
aVF, II, and III view the inferior or diaphragmatic surface of the heart.
I and aVL examine the left lateral aspect.
The 6 chest leads examine the heart in the transverse plane.
V1 and V2 look at the right ventricle.
V3 and V4 at the septum and anterior aspect of the lateral ventricle.
V5 and V6 at the anterior and lateral aspects of the left ventricle.

Question 5

Electrocardiography (ECG): the ECG trace, waves

Answer 5

P wave represents atrial depolarisation and is a positive (upwards) deflection- except in aVR.
QRS complex represents ventricular depolarisation.
Q wave = negative first QRS deflection; pathological Q waves seen in MI.
R wave = first positive deflection, may or may not follow Q wave.
S wave = negative deflection following R wave.
T wave = ventricular repolarisation, normally positive, concordant with QRS complex.

Question 6

Electrocardiography (ECG): the ECG trace, rate

Answer 6

The heart rate can be calculated by dividing 300 by the number of large squares between each R wave (with machine trace running at the standard speed of 25mm/sec and deflection of 1cm/10mV).
3 large squares between R waves = rate 100.
5 large squares = rate 60.
Normal rate 60-100bpm.
Rate <60 = bradycardia.
Rate >100 = tachycardia.

Question 7

Electrocardiography (ECG): the ECG trace, intervals and timing

Answer 7

PR interval: from the start of the P wave to the start of the QRS complex, represents the inbuilt delay in electrical conduction at the AV node. Normally <0.20 seconds (5 small squares).
QRS complex: width? normally <0.12 seconds (3 small squares).
R-R interval: from the peak of 1 R wave to the next, used to calculate HR.
QT interval: from the start of QRS complex to the end of T wave, varies with HR, corrected QT interval should be 0.38-0.42 seconds.

Question 8

Electrocardiography (ECG): the ECG trace, rhythm

Answer 8

Regular or irregular?
If irregular but in a clear pattern, ‘regularly irregular’, e.g. types of heart block.
Irregularly irregular e.g. atrial fibrillation.

Question 9

Electrocardiography (ECG): ECG axis, cardiac axis

Answer 9

The cardiac axis, or ‘QRS axis’, is the overall direction of depolarisation through the ventricular myocardium in the coronal plane.
0 degrees is taken as the horizontal line to the left of the heart.
Normal cardiac axis = -30 to +90 degrees.
An axis outside of this range may suggest pathology, either congenital or acquired.
Cardiac axis deviation may be seen in healthy individuals with distinctive body shapes.
Right axis deviation if tall and thin, left axis deviation if short and stocky.

Question 10

Electrocardiography (ECG): ECG axis, causes of left axis deviation (

Answer 10

Left ventricular hypertrophy.
LBBB.
Left anterior hemiblock (anterior fascicle of the left bundle).
Inferior MI.
Cardiomyopathies.
Tricuspid atresia.

Question 11

Electrocardiography (ECG): ECG axis, causes of right axis deviation (>+90 degrees)

Answer 11

Right ventricular hypertrophy.
RBBB.
Anterolateral MI.
Right ventricular strain (e.g. pulmonary embolism).
Cor pulmonale.
Fallot's tetralogy (pulmonary stenosis).

Question 12

Electrocardiography (ECG): AV conduction abnormalities, overview

Answer 12

In the normal ECG each P wave is followed by a QRS complex.
The isoelectric gap between is the PR internal and represents slowing of the impulse at the AV junction.
Disturbance of the normal conduction here leads to ‘heart block’.

Question 13

Electrocardiography (ECG): AV conduction abnormalities, causes of heart block

Answer 13

Ischaemic heart disease.
Idiopathic fibrosis of the conduction system.
Cardiomyopathies.
Inferior and anterior MI.
Drugs: digoxin, beta blockers, verapamil.
Physiological (1st degree) in athletes.

Question 14

Electrocardiography (ECG): AV conduction abnormalities, first degree heart block

Answer 14

PR interval fixed but prolonged at >0.20 seconds (5 small squares at standard rate).

Question 15

Electrocardiography (ECG): AV conduction abnormalities, second degree heart block

Answer 15

Not every P wave is followed by a QRS complex.
Möbitz type I: PR interval becomes progressively longer after each P wave until an impulse fails to e conducted at all; the interval then returns to the normal length and the cycle is repeated; Wenckebach phenomenon.
Möbitz type II: PR interval is fixed but not every P wave is followed by a QRS; the relationship between P waves and QRS complex may be 2:1, 3:1, or random.

Question 16

Electrocardiography (ECG): AV conduction abnormalities, third degree heart block

Answer 16

Complete heart block.
There is no conduction of the impulse through the AV junction.
Atrial and ventricular depolarisation occur independent of one another.
Each has a separate pacemaker triggering electrical activity at different rates.
The QRS complex is an abnormal shape as the electrical impulse doesn’t travel through the ventricles via the normal routes.
P waves may be seen ‘merging’ with QRS complexes if they coincide.

Question 17

Electrocardiography (ECG): ventricular conduction abnormalities, overview

Answer 17

Depolarisation of both ventricles usually occurs rapidly through left and right bundle branches of the His-Purkinje system.
If this depolarisation will occur more slowly through non-specialised ventricular myocardium.
The QRS complex, usually <0.12 seconds, will become prolonged (broad).

Question 18

Electrocardiography (ECG): ventricular conduction abnormalities, RBBB overview

Answer 18

Conduction through the AV node, bundle of His, and left bundle branch will be normal but depolarisation of the right ventricle occurs by the slow spread of electrical current through myocardial cells.
The result is delayed right ventricular depolarisation giving a 2nd R wave, R’.
RBBB suggests pathology in the right side of the heart but can be a normal variant.

Question 19

Electrocardiography (ECG): ventricular conduction abnormalities, RBBB ECG changes

Answer 19

‘RSR’ pattern seen in V1.
Cardiac axis usually remains normal unless left anterior fascicle is also blocked (bifascicular block’) which results in left axis deviation.
T wave flattening or inversion in anterior chest leads (V1-V3).
MaRRoW (V1 = M, V6 = W).

Question 20

Electrocardiography (ECG): ventricular conduction abnormalities, RBBB causes

Answer 20

Hyperkalaemia.
Congenital heart disease (e.g. Fallot's tetralogy).
Pulmonary embolus.
Cor pulmonale.
Fibrosis of conduction system.

Question 21

Electrocardiography (ECG): ventricular conduction abnormalities, LBBB overview

Answer 21

Conduction through the AV node, bundle of His, and right bundle branch will be normal but depolarisation of the left ventricle occurs by the slow spread of electrical current through myocardial cells.
Delayed left ventricular depolarisation.
Always considered pathological.

Question 22

Electrocardiography (ECG): ventricular conduction abnormalities, LBBB ECG changes

Answer 22

‘M’ pattern seen in V6.
T wave flattening or inversion in lateral chest leads (V5-V6).
WiLLiaM (V1 = W, V6 = M)

Question 23

Electrocardiography (ECG): ventricular conduction abnormalities, LBBB causes

Answer 23

Hypertension.
Ischaemic heart disease.
Acute MI.
Aortic stenosis.
Cardiomyopathies.
Fibrosis of conduction system.

Question 24

Electrocardiography (ECG): sinus rhythms, overview

Answer 24

Supraventricular rhythms arise in the atria.
May be physiological or caused by pathology within the SA node, atria, or first parts of the conducting system.
Normal conduction through the bundle of His into the ventricles will usually give narrow QRS complexes.

Question 25

Electrocardiography (ECG): sinus rhythms, sinus bradycardia

Answer 25

Bradycardia (rate <60bpm) at the level of the SA node. Heart beats slowly but conduction of impulse is normal. Causes: drugs (beta blockers, verapamil, amiodarone, digoxin); sick sinus syndrome; hypothyroidism; inferior MI; hypothermia; raised intracranial pressure; physiological (athletes).

Question 26

Electrocardiography (ECG): sinus rhythms, sinus tachycardia

Answer 26

Tachycardia at the level of the SA node- the heart is beating too quickly but conduction of the impulse is normal. Ventricular rate >100bpm, normal P wave before each QRS. Causes: drugs (adrenaline, caffeine, nicotine); pain; exertion; anxiety; anaemia; thyrotoxicosis; pulmonary embolus; hepatic failure; cardiac failure; hypercapnia; pregnancy; constrictive pericarditis.

Question 27

Electrocardiography (ECG): supraventricular tachycardias, overview

Answer 27

Tachycardias (rate >100bpm) arising in the atria or AV node. As conduction through the bundle of His and ventricles will be normal (unless there is other pathology in the heart), the QRS completes appear normal. There are 4 main causes of a supraventricular tachycardia: atrial fibrillation, atrial flutter, junctional tachycardia, re-entry tachycardia.

Question 28

Electrocardiography (ECG): supraventricular tachycardias, atrial fibrillation overview

Answer 28

This is disorganised contraction of the atria in the form of rapid, irregular twitching. No P waves on the ECG. Electrical impulses from the twitches of the atria arrive at the AV node randomly, they are then conducted via the normal pathways to cause ventricular contraction. The result is a characteristic ventricular rhythm that is irregularly irregular with no discernible pattern.

Question 29

Electrocardiography (ECG): supraventricular tachycardias, atrial fibrillation ECG features

Answer 29

``` No P waves. Rhythm = irregularly irregular. Irregular QRS complexes. Normal appearance of QRS. Ventricular rate may be increased ('fast AF')- typically 120-160 per minute. ```

Question 30

Electrocardiography (ECG): supraventricular tachycardias, atrial fibrillation causes

Answer 30

``` Idiopathic. Ischaemic heart disease. Thyroid disease. Hypertension. MI. Pulmonary embolus. Rheumatic mitral or tricuspid valve disease. ```

Question 31

Electrocardiography (ECG): supraventricular tachycardias, atrial flutter overview

Answer 31

This is the abnormally rapid contraction of the atria. The contractions are not disorganised or random, unlike AF, but are fast and inadequate for the normal movement of blood. Instead of P waves, the baseline will have a typical 'saw-tooth' appearance (F waves). The AV node is unable to conduct the impulses faster than 200/min. Atrial contraction faster than that leads to impulses failing to be conducted. e.g. an atrial rate of 300/min will lead to every other impulse being conducted giving a ventricular rate and pulse of 150/min- a 2:1 block. Other ratios of atrial to ventricular contractions may occur. A variable block at the AV node may lead to an irregularly irregular pulse indistinguishable from that of AF on clinical examination.

Question 32

Electrocardiography (ECG): supraventricular tachycardias, atrial flutter ECG changes

Answer 32

'Saw-tooth' appearance of baseline. | Normal appearance of QRS complexes.

Question 33

Electrocardiography (ECG): supraventricular tachycardias, junctional nodal tachycardia overview

Answer 33

The area in or around the AV node depolarises spontaneously, the impulse will be immediately conducted to the ventricles. The QRS complex will be of a normal shape but no P waves will be seen.

Question 34

Electrocardiography (ECG): supraventricular tachycardias, junctional nodal tachycardia ECG changes

Answer 34

No P waves. QRS complexes are regular and normal shape. Rate may be fast or normal.

Question 35

Electrocardiography (ECG): supraventricular tachycardias, junctional nodal tachycardia causes

Answer 35

Sick sinus syndrome (including drug-induced). Digoxin toxicity. Ischaemia of the AV node, esp. with acute inferior MI. Acutely after cardiac surgery. Acute inflammatory processes e.g. acute rheumatic fever, which may involve the conduction system. Diphtheria. Other drugs, e.g. most anti-arrhythmics.

Question 36

Electrocardiography (ECG): supraventricular tachycardias, Wolff-Parkinson-White syndrome

Answer 36

There is an extra conducting pathway between the atria and ventricles (bundle of Kent)- a break in the normal electrical insulation. This accessory pathway is not specialised for conducting electrical impulses so does not delay the impulse as the AV node does. It is not linked to the normal conduction pathways of the bundle of His. Depolarisation of the ventricles will occur partly via the AV node and partly by the bundle of Kent. During normal atrial conduction, electrical activity reaches the AV node and the accessory pathway at roughly the same time. Whilst it is held up temporarily at the AV node, the impulse passes through the accessory pathway and starts to depolarise the ventricles via non-specialised cells (pre-excitation'), distorting the first part of the R wave and giving a short PR interval. Normal conduction via the the bundle of His then supervenes. The result is a slurred upstroke of the QRS complex. 'Fusion beat' in which normal and abnormal ventricular depolarisation combine to give a distortion of the QRS complex.

Question 37

Electrocardiography (ECG): supraventricular tachycardias, reentry tachycardia

Answer 37

The accessory pathway may allow electrical activity to be conducted from the ventricles back up to the atria. Electrical activity may be conducted down the bundle of His, across the ventricles and up the accessory pathway into the atria causing them to contract again, and the cycle is repeated.

Question 38

Electrocardiography (ECG): ventricular rhythms, overview

Answer 38

Most ventricular rhythms originate outside the usual conduction pathways meaning that excitation spreads by an abnormal path through the ventricular muscle to give broad or unusually shaped QRS complex.

Question 39

Electrocardiography (ECG): ventricular rhythms, ventricular tachycardia overview

Answer 39

A focus of ventricular tissue depolarising rapidly within the ventricular myocardium. VT is defined as 3 or more successive ventricular extrasystoles at a rate of >120/min. 'Sustained' VTs last for >30 seconds. VT may be 'stable' showing a repetitive QRS shape (monomorphic) or unstable with varying patterns of the QRS complex (polymorphic). It may be impossible to distinguish VT from an SVT with bundle branch block on a 12-lead ECG.

Question 40

Electrocardiography (ECG): ventricular rhythms, ventricular tachycardia ECG features

Answer 40

Wide QRS complexes which are irregular in rhythm and shape. A-V dissociation- independent atrial and ventricular contraction. May see fusion and capture beats on ECG as signs of atrial activity independent of ventricular activity- pathognomonic. Fusion beats = depolarisation from AV node meets depolarisation from ventricular focus causing hybrid QRS complex. Capture beats = atrial beat conducted to ventricles causing a normal QRS complex in amongst the VT trace. Rate can be up to 130-300bpm. QRS concordance: all the QRS complexes in the chest leads are either mainly positive or mainly negative- suggests ventricular origin of tachycardia. Extreme axis deviation (far -ve or far +ve).

Question 41

Electrocardiography (ECG): ventricular rhythms, ventricular tachycardia causes

Answer 41

Ischaemia (acute including MI or chronic). Electrolyte abnormalities (reduced K+, reduced Mg2+). Aggressive adrenergic stimulation (e.g. cocaine use). Drugs- especially anti-arrhtyhmics.

Question 42

Electrocardiography (ECG): ventricular rhythms, ventricular fibrillation overview

Answer 42

This is disorganised, uncoordinated depolarisation from multiple foci in the ventricular myocardium.

Question 43

Electrocardiography (ECG): ventricular rhythms, ventricular fibrillation ECG features

Answer 43

No discernible QRS complexes. | A completely disorganised ECG.

Question 44

Electrocardiography (ECG): ventricular rhythms, ventricular fibrillation causes

Answer 44

``` Coronary heart disease. Cardiac inflammatory diseases. Abnormal metabolic states. Pro-arrhythmic toxic exposures. Electrocution. Tension pneumothorax, trauma, and drowning. Large pulmonary embolism. Hypoxia or acidosis. ```

Question 45

Electrocardiography (ECG): ventricular rhythms, ventricular extrasystoles (ectopics)

Answer 45

These are ventricular contractions originating from a focus of depolarisation within the ventricle. As conduction is via abnormal pathways, the QRS complex will be unusually shaped. Ventricular extrasystoles are common and harmless if there is no structural heart disease. If they occur at the same time as a T wave, the 'R-on-T' phenomenon, they can lead to VF.

Question 46

Electrocardiography (ECG): ventricular rhythms, ventricular escape rhythm

Answer 46

This occurs as a 'back-up' when conduction between the atria and the ventricles is interrupted (as in complete heart block). The intrinsic pacemaker in ventricular myocardium depolarises at a slow rate (30-40bpm). The ventricular beats will be abnormal and wide with abnormal T waves following them. This rhythm can be stable but may suddenly fall.

Question 47

Electrocardiography (ECG): ventricular rhythms, asystole

Answer 47

This is a complete absence of electrical activity and is not compatible with life. There may be a slight wavering of the baseline which can be easily confused with fine VF in emergencies.

Question 48

Electrocardiography (ECG): ventricular rhythms, agonal rhythm

Answer 48

This is a slow, irregular rhythm with wide ventricular complexes which vary in shape. This is often seen in the alter stages of unsuccessful resuscitation attempts as the heart dies. The complexes become progressively broader before all recognisable activity is lost (asystole).

Question 49

Electrocardiography (ECG): ventricular rhythms, torsades de pointes

Answer 49

'Twisting of points'- a form of polymorphic VT characterised by a gradual change in the amplitude and twisting of the QRS axis. 'Cardiac ballet'. Torsades usually terminates spontaneously but frequently recurs and may degenerate into sustained VT and ventricular fibrillation. Torsades results from a prolonged QT interval. Causes include congenital long-QT syndromes and drugs, e.g. anti-arrhythmics. Patients may also have reduced K+ and Mg2+.

Question 50

Electrocardiography (ECG): P and T wave abnormalities, normal P wave

Answer 50

Represents depolarisation of the small muscle mass of the atria. The P wave is thus much smaller in amplitude than the QRS complex. In sinus rhythm each P wave is closely associated with a QRS complex. P waves are usually upright in most leads except aVR. P waves are <3 small squares wide and <3 small squares high.

Question 51

Electrocardiography (ECG): P and T wave abnormalities, abnormal P wave

Answer 51

Right atrial hypertrophy will cause tall, peaked P waves- causes include pulmonary hypertension and tricuspid valve stenosis. Left atrial hypertrophy will cause the P waves to become wider and twin-peaked or bifid- usually caused by mitral valve disease.

Question 52

Electrocardiography (ECG): P and T wave abnormalities, normal T wave

Answer 52

Represents repolarisation of the ventricles. The T wave is most commonly affected by ischaemic changes. The most common abnormality is 'inversion' which has a number of causes. Commonly inverted in V1 and aVR. May be inverted in V1-V3 as normal variant.

Question 53

Electrocardiography (ECG): P and T wave abnormalities, abnormal T wave

Answer 53

Myocardial ischaemia or MI (e.g. non-Q wave MI) can cause T wave invasion- interpret changes in light of clinical picture. Ventricular hypertrophy causes T invasion in the leads focused on the affected ventricle, e.g. left ventricular hypertrophy will give T changes in leads V5, V6, II, and aVL. Bundle branch block causes abnormal QRS complexes due to abnormal pathways of ventricular depolarisation. The corresponding abnormal repolarisation gives unusually shaped T waves which have no significance in themselves. Digoxin causes characteristic T wave inversion with a downscoping of the ST segment known as the 'reverse tick' sign- this occurs at therapeutic doses and is not a sign of digoxin toxicity. Electrolyte imbalances cause T wave changes: - raised K+ can cause tall tented T waves - low K+ can cause small T waves and U waves (broad, flat waves occurring after the T waves) - low Ca2+ can cause small T waves and prolonged QT interval, raised Ca2+ has the opposite effect - other causes of T wave inversion include subarachnoid haemorrhage and lithium use

Question 54

Electrocardiography (ECG): ST segment, ST elevation

Answer 54

The degree and extent of ST elevation is important- determines whether reperfusion therapy (thrombolysis or primary PCI) is considered in acute MI. Causes: acute MI (convex ST elevation in affected leads, 'tombstone', often with reciprocal ST depression in opposite ends), pericarditis (widespread concave ST elevation, saddle-shaped), left ventricular aneurysm (ST elevation may persist over time).

Question 55

Electrocardiography (ECG): ST segment, ST depression

Answer 55

ST depression can be horizontal, upward sloping, or downward sloping. Causes: myocardial ischaemia (horizontal ST depression and an upright T wave, may be result of coronary artery disease or other causes, e.g. anaemia, aortic stenosis), digoxin toxicity (downward sloping, 'reverse tick'), 'non-specific' changes (ST segment depression which is often upward sloping may be a normal variant and is not thought to be associated with any underlying significant pathology).

Question 56

Electrocardiography (ECG): myocardial infarction

Answer 56

In the 1st hour following a MI, the ECG can remain normal. When changes occur, they usually develop in the following order: ST segment becomes elevated and T waves become peaked; pathological Q waves develop; ST segment returns to baseline and T waves invert. Anterior: V2-V5. Antero-lateral: I, aVL, V5, V6. Inferior: III, aVF. Posterior: dominant R wave in V1. Right ventricular: often no ECG changes.

Question 57

Electrocardiography (ECG): hypertrophy, overview

Answer 57

If the heart is faced with having to overcome pressure overload, e.g. left ventricular hypertrophy in hypertension or aortic stenosis, or higher systemic pressures, e.g. essential hypertension, then it will increase its muscle mass in response. The increased muscle mass can result in changes to the ECG.

Question 58

Electrocardiography (ECG): hypertrophy, atrial hypertrophy

Answer 58

This can lead to changes to the P wave.

Question 59

Electrocardiography (ECG): hypertrophy, ventricular hypertrophy

Answer 59

This can lead to changes to the cardiac axis, QRS complex height/depth, and the T wave.

Question 60

Electrocardiography (ECG): hypertrophy, left ventricular hypertrophy

Answer 60

Tall R wave in V6 and deep S wave in V1. May also see left axis deviation. T wave inversion in V5, V6, I, aVL. Voltage criteria for LVH include: R wave >25mm (5 large squares) in V6; R wave in V6 + S wave in V1 >35mm (7 large squares).

Question 61

Electrocardiography (ECG): hypertrophy, right ventricular hypertrophy

Answer 61

'Dominant' R wave in V1, i.e. R wave bigger than S wave. Deep S wave in V6. May also see right axis deviation. T wave inversion in V1-V3.

Question 62

Electrocardiography (ECG): paced rhythms

Answer 62

Temporary or permanent cardiac pacing may be indicated for a number of conditions such as complete heart block or symptomatic bradycardia. These devices deliver a tiny electrical pulse to an area of the heart, initiating contraction. This can be seen on the ECG as a sharp spike. Many different types of pacemaker exist, categorised according to the chamber paced, the chamber used to detect the heart's electrical activity, and how the pacemaker responds. On the ECG look for the pacing spikes which may appear before P waves if the atria are paced, before the QRS complexes if the ventricles are paced, or both.

Question 63

Peak expiratory flow rate (PEFR): interpretation

Answer 63

PEFR readings less than the patient's predicted, or usual best, demonstrate airflow obstruction in the large airways. PEFR readings are useful in determining the severity, and therefore the most appropriate treatment algorithm, for asthma exacerbations. PEFR <75% best or predicted = moderate asthma attack. PEFR <50% best or predicted = acute severe asthma attack. PEFR <33% best or predicted = life-threatening asthma attack.

Question 64

Peak expiratory flow rate (PEFR): reversibility testing

Answer 64

Improvement in PEFR or FEV1 ≥15% following bronchodilator therapy, e.g. salbutamol, shows reversibility of airflow obstruction and can help to distinguish asthma from poorly reversible conditions such as COPD.

Question 65

Arterial blood gas analysis: systematic approach

Answer 65

Focus on pH, PaCO2, and HCO3- in that order.

Question 66

Arterial blood gas analysis: systematic approach, pH

Answer 66

Is it low (acidosis) or high (alkalosis)?

Question 67

Arterial blood gas analysis: systematic approach, PaCO2

Answer 67

If PaCO2 is raised and there is acidosis (pH <7.35) you can deduce a respiratory acidosis. If PaCO2 is low and there is alkalosis (pH >7.45) then the lack of acid gas has led to respiratory alkalosis. If PaCO2 is low and there is acidosis then the respiratory system will not be to blame and there is metabolic acidosis- confirm this by looking at HCO3-, it should be low. If PaCO2 is high or normal and there is alkalosis, there must be a metabolic alkalosis- confirm this by looking at the HCO3-, it should be raised.

Question 68

Arterial blood gas analysis: systematic approach, respiratory acidosis results

Answer 68

Low pH <7.35. | Raised PaCO2 >6.0kPa.

Question 69

Arterial blood gas analysis: systematic approach, respiratory alkalosis results

Answer 69

High pH >7.45. | Low PaCO2 <4.7kPa.

Question 70

Arterial blood gas analysis: systematic approach, metabolic acidosis results

Answer 70

Low pH <7.35. Low PaCO2 <4.7kPa. Low HCO3- <22mmol/L.

Question 71

Arterial blood gas analysis: systematic approach, metabolic alkalosis results

Answer 71

High pH >7.45. Normal or raised PaCO2 >6.0kPa. Raised HCO3- >26mmol/L.

Question 72

Arterial blood gas analysis: systematic approach, PaO2

Answer 72

Note what FiO2 the patient was breathing when the sample was taken. Hypoxia is PaO2 of <8.0kPa and can result from a ventilation-perfusion mismatch, e.g. pulmonary embolism, or from alveolar hypoventilation, e.g. COPD, pneumonia. Type I respiratory failure: hypoxia and PaCO2 <6kPa. Type II respiratory failure: hypoxia and PaCO2 >6kPa. If the PaO2 is very low consider venous blood contamination.

Question 73

Arterial blood gas analysis: systematic approach, type I respiratory failure results

Answer 73

PaO2 <8.0kPa. | PaCO2 <6kPa.

Question 74

Arterial blood gas analysis: systematic approach, type II respiratory failure results

Answer 74

PaO2 <8.0kPa. | PaCO2 >6kPa.

Question 75

Arterial blood gas analysis: systematic approach, compensatory mechanisms

Answer 75

Mechanisms controlling pH are activated when acid-base imbalances threaten. Renal control of H+ and HCO3- ion excretion can result in compensatory metabolic changes. Similarly, 'blowing off' or retaining CO2 via control of respiratory rate can lead to compensatory respiratory changes. A compensated picture suggests chronic disease.

Question 76

Arterial blood gas analysis: reference ranges

Answer 76

``` pH 7.35-7.45. PaCO2 4.7-6.0kPa. PaO2 10-13kPa. HCO3- 22-26mmol/L. Base excess -2 to +2. ```

Question 77

Arterial blood gas analysis: anion gap

Answer 77

(Na+ + K+) - (HCO3- + Cl-). | Normal range = 10-18mmol/L.

Question 78

Arterial blood gas analysis: What results do you expect in respiratory acidosis?

Answer 78

Low pH. Raised PaCO2. HCO3- may be raised if compensated.

Question 79

Arterial blood gas analysis: What conditions can lead to respiratory acidosis?

Answer 79

COPD, asthma, pneumonia, pneumothorax, pulmonary fibrosis. Obstructive sleep apnoea. Opiate overdose causing respiratory depression. Neuromuscular disorders, e.g. Guillain Barré, motor neuron disease. Skeletal abnormalities, e.g. kyphoscoliosis. Congestive cardiac failure.

Question 80

Arterial blood gas analysis: What results do you expect in metabolic acidosis?

Answer 80

Low pH. Low HCO3-. PaCO2 may be low if compensated.

Question 81

Arterial blood gas analysis: What conditions can lead to metabolic acidosis with raised anion gap?

Answer 81

``` Diabetic ketoacidosis. Renal failure (urate). Lactic acidosis (tissue hypoxia or excessive exercise). Salicylates, ethylene glycol, biguanides. ```

Question 82

Arterial blood gas analysis: What conditions can lead to metabolic acidosis with normal anion gap?

Answer 82

``` Chronic diarrhoea, ileostomy (loss of HCO3-). Addison's disease. Pancreatic fistulae. Renal tubular acidosis. Acetazolamide treatment (loss of HCO3-). ```

Question 83

Arterial blood gas analysis: What results do you expect in respiratory alkalosis?

Answer 83

Raised pH. Low PaCO2. HCO3- may be low if compensated.

Question 84

Arterial blood gas analysis: What conditions can lead to respiratory alkalosis?

Answer 84

Hyperventilation, secondary to panic attack (anxiety) or pain. Meningitis. Stroke, subarachnoid haemorrhage. High altitude.

Question 85

Arterial blood gas analysis: What results do you expect in metabolic alkalosis?

Answer 85

Raised pH. Raised HCO3-. PaCO2 may be raised if compensated.

Question 86

Arterial blood gas analysis: What conditions can lead to metabolic alkalosis?

Answer 86

Diuretic drugs, via loss of K+. Prolonged vomiting, via acid replacement and release of HCO3-. Burns. Base ingestion.