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Oxford Handbook of Clinical Examination > Clinical data interpretation > Flashcards

Clinical data interpretation Flashcards

1
Q

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

A

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.

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2
Q

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

A

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.

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3
Q

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

A

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.

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4
Q

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

A

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.

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5
Q

Electrocardiography (ECG): the ECG trace, waves

A

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.

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6
Q

Electrocardiography (ECG): the ECG trace, rate

A

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.

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7
Q

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

A

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.

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8
Q

Electrocardiography (ECG): the ECG trace, rhythm

A

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

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9
Q

Electrocardiography (ECG): ECG axis, cardiac axis

A

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.

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10
Q

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

A 
Left ventricular hypertrophy.
LBBB.
Left anterior hemiblock (anterior fascicle of the left bundle).
Inferior MI.
Cardiomyopathies.
Tricuspid atresia.
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11
Q

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

A 
Right ventricular hypertrophy.
RBBB.
Anterolateral MI.
Right ventricular strain (e.g. pulmonary embolism).
Cor pulmonale.
Fallot's tetralogy (pulmonary stenosis).
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12
Q

Electrocardiography (ECG): AV conduction abnormalities, overview

A

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’.

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13
Q

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

A

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

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14
Q

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

A

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

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15
Q

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

A

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.

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16
Q

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

A

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.

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17
Q

Electrocardiography (ECG): ventricular conduction abnormalities, overview

A

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).

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18
Q

Electrocardiography (ECG): ventricular conduction abnormalities, RBBB overview

A

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.

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19
Q

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

A

‘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).

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20
Q

Electrocardiography (ECG): ventricular conduction abnormalities, RBBB causes

A 
Hyperkalaemia.
Congenital heart disease (e.g. Fallot's tetralogy).
Pulmonary embolus.
Cor pulmonale.
Fibrosis of conduction system.
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21
Q

Electrocardiography (ECG): ventricular conduction abnormalities, LBBB overview

A

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.

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22
Q

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

A

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

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23
Q

Electrocardiography (ECG): ventricular conduction abnormalities, LBBB causes

A 
Hypertension.
Ischaemic heart disease.
Acute MI.
Aortic stenosis.
Cardiomyopathies.
Fibrosis of conduction system.
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24
Q

Electrocardiography (ECG): sinus rhythms, overview

A

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.

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25
Q

Electrocardiography (ECG): sinus rhythms, sinus bradycardia

A

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).

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26
Q

Electrocardiography (ECG): sinus rhythms, sinus tachycardia

A

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.

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27
Q

Electrocardiography (ECG): supraventricular tachycardias, overview

A

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.

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28
Q

Electrocardiography (ECG): supraventricular tachycardias, atrial fibrillation overview

A

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.

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29
Q

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

A 
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.
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30
Q

Electrocardiography (ECG): supraventricular tachycardias, atrial fibrillation causes

A 
Idiopathic.
Ischaemic heart disease.
Thyroid disease.
Hypertension.
MI.
Pulmonary embolus.
Rheumatic mitral or tricuspid valve disease.
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31
Q

Electrocardiography (ECG): supraventricular tachycardias, atrial flutter overview

A

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.

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32
Q

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

A

‘Saw-tooth’ appearance of baseline.

Normal appearance of QRS complexes.

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33
Q

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

A

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.

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34
Q

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

A

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

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35
Q

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

A

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.

36
Q

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

A

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.

37
Q

Electrocardiography (ECG): supraventricular tachycardias, reentry tachycardia

A

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.

38
Q

Electrocardiography (ECG): ventricular rhythms, overview

A

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.

39
Q

Electrocardiography (ECG): ventricular rhythms, ventricular tachycardia overview

A

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.

40
Q

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

A

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).

41
Q

Electrocardiography (ECG): ventricular rhythms, ventricular tachycardia causes

A

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

42
Q

Electrocardiography (ECG): ventricular rhythms, ventricular fibrillation overview

A

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

43
Q

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

A

No discernible QRS complexes.

A completely disorganised ECG.

44
Q

Electrocardiography (ECG): ventricular rhythms, ventricular fibrillation causes

A 
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.
45
Q

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

A

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.

46
Q

Electrocardiography (ECG): ventricular rhythms, ventricular escape rhythm

A

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.

47
Q

Electrocardiography (ECG): ventricular rhythms, asystole

A

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.

48
Q

Electrocardiography (ECG): ventricular rhythms, agonal rhythm

A

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).

49
Q

Electrocardiography (ECG): ventricular rhythms, torsades de pointes

A

‘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+.

50
Q

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

A

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.

51
Q

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

A

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.

52
Q

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

A

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.

53
Q

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

A

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

54
Q

Electrocardiography (ECG): ST segment, ST elevation

A

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).

55
Q

Electrocardiography (ECG): ST segment, ST depression

A

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).

56
Q

Electrocardiography (ECG): myocardial infarction

A

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.

57
Q

Electrocardiography (ECG): hypertrophy, overview

A

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.

58
Q

Electrocardiography (ECG): hypertrophy, atrial hypertrophy

A

This can lead to changes to the P wave.

59
Q

Electrocardiography (ECG): hypertrophy, ventricular hypertrophy

A

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

60
Q

Electrocardiography (ECG): hypertrophy, left ventricular hypertrophy

A

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).

61
Q

Electrocardiography (ECG): hypertrophy, right ventricular hypertrophy

A

‘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.

62
Q

Electrocardiography (ECG): paced rhythms

A

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.

63
Q

Peak expiratory flow rate (PEFR): interpretation

A

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.

64
Q

Peak expiratory flow rate (PEFR): reversibility testing

A

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.

65
Q

Arterial blood gas analysis: systematic approach

A

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

66
Q

Arterial blood gas analysis: systematic approach, pH

A

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

67
Q

Arterial blood gas analysis: systematic approach, PaCO2

A

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.

68
Q

Arterial blood gas analysis: systematic approach, respiratory acidosis results

A

Low pH <7.35.

Raised PaCO2 >6.0kPa.

69
Q

Arterial blood gas analysis: systematic approach, respiratory alkalosis results

A

High pH >7.45.

Low PaCO2 <4.7kPa.

70
Q

Arterial blood gas analysis: systematic approach, metabolic acidosis results

A

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

71
Q

Arterial blood gas analysis: systematic approach, metabolic alkalosis results

A

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

72
Q

Arterial blood gas analysis: systematic approach, PaO2

A

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.

73
Q

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

A

PaO2 <8.0kPa.

PaCO2 <6kPa.

74
Q

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

A

PaO2 <8.0kPa.

PaCO2 >6kPa.

75
Q

Arterial blood gas analysis: systematic approach, compensatory mechanisms

A

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.

76
Q

Arterial blood gas analysis: reference ranges

A 
pH 7.35-7.45.
PaCO2 4.7-6.0kPa.
PaO2 10-13kPa.
HCO3- 22-26mmol/L.
Base excess -2 to +2.
77
Q

Arterial blood gas analysis: anion gap

A

(Na+ + K+) - (HCO3- + Cl-).

Normal range = 10-18mmol/L.

78
Q

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

A

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

79
Q

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

A

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.

80
Q

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

A

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

81
Q

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

A 
Diabetic ketoacidosis.
Renal failure (urate).
Lactic acidosis (tissue hypoxia or excessive exercise).
Salicylates, ethylene glycol, biguanides.
82
Q

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

A 
Chronic diarrhoea, ileostomy (loss of HCO3-).
Addison's disease.
Pancreatic fistulae.
Renal tubular acidosis.
Acetazolamide treatment (loss of HCO3-).
83
Q

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

A

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

84
Q

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

A

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

85
Q

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

A

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

86
Q

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

A

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

Oxford Handbook of Clinical Examination (13 decks)

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