The U wave
ECG 43 was performed on her admission
aVR V1 V4
aVL V2 V5
aVF V3 V6
I
II
II III
43
Answer 43
1 ECG 43 shows sinus rhythm in the initial part. There is a normal axis and no other significant abnormalities. The rhythm strip of the ECG shows sinus rhythm in its initial seven complexes. The eighth complex (arrow) is an atrial ectopic beat as evidenced by a different P wave morphology. This atrial ectopic has led to the development of AF in the remaining part of the rhythm strip. These findings suggest the diagnosis of paroxysmal AF. A 24-hour Holter monitoring should be requested to assess the frequency of paroxysms.
2 Thyroid function tests (free T3, free T4, and TSH) should be requested to confirm the diagnosis of hyperthyroidism. In this patient the presence of thyrotoxicosis was confirmed. The coexisting pernicious anaemia suggests an autoimmune aetiology.
aVR V1 V4
aVL V2 V5
aVF V3 V6
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II
II III
43
A 45-year-old male factory worker involved with heavy mechanical work was found to have ECG 44 during a routine checkup.
1 What does ECG 44 show?
2 What is the significance of this condition?
aVR V1
V1
V4
aVL V2 V5
V5
aVF V3 V6
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II III
44
Answer 44
1 ECG 44 shows sinus rhythm with a normal axis. There is a continuous variation in the PP interval (markers), most obvious in the rhythm strips. The P wave morphology does not change. There are no other abnormalities noted. The diagnosis is sinus arrhythmia. The differential diagnosis includes atrial ectopics and SA block. Atrial ectopics can be differentiated by varying P wave morphology. SA block can be differentiated by an abrupt change in the rhythm.
2 Sinus arrhythmia is a benign condition and does not have any clinical significance. It is commonly found in athletes, people who do heavy mechanical work, and in children.
aVR V1
V1
V4
aVL V2 V5
V5
aVF V3 V6
I
II
II III
44
1What are the findings in ECG 45?
2What is the differential diagnosis?
3What is the association of this condition?
A 34-year-old female with a history of recurrent sinusitis and infertility was found to have ECG 45.
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
45
Answer 45
1 ECG 45shows sinus rhythm with an extreme right axis deviation (RAD). The P wave is upright and R wave is tall in lead aVR. There is a deep S and flattened T wave in lead LI. The height of the QRS complexes gradually decreases from leads V1–V6. The chest leads show a right ventricular pattern with a small R and deep S wave in leads V5 and V6. There is also T wave inversion in leads V1–V3.
2The differential diagnosis is either dextrocardia or improper electrode position with transposition of the right and left arm electrodes. The abnormalities in improper electrode placement are limited to the limb leads. Since the changes in the ECG are also noted in the chest leads, the most likely cause for the abnormality is dextrocardia. This was confirmed on CXR.
3 Dextrocardia may be associated with Kartagener’s syndrome. Other features of Kartagener’s syndrome include recurrent sinusitis, bronchiectesis, situs inversus, and male infertility. It is due to defective motility of the cilia lining the respiratory epithelium and of sperm. Kartagener’s syndrome is an autosomal recessive disorder.
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
45
1 What are the findings in ECG 46a?
2 What does ECG 46b show?
A 78-year-old male presented with a crushing retrosternal chest pain. He was hypotensive with a BP of 80/60 mmHg (10.7/8.0 kPa). The neck veins were engorged and the chest was clear.
aVR V1 V4
aVL V2 V5
aVF V3 V6
I
II
II III
V7
V8
V9
46a
46b
Answer 46
1 ECG 46ashows an irregular rhythm due to AF. There is ST segment elevation in leads LII, LIII, and aVF, and ST segment depression with T wave inversion in leads LI and aVL (arrows). The leads V1, V2, and V3 show ST segment depression and a relatively tall R wave (circles). The diagnosis in this ECG is acute inferior wall MI with lateral wall ischaemia and posterior wall extension.
2 ECG 46bshows the posterior leads V7, V8, and V9. All these leads show ST segment elevation (arrows) confirming the presence of posterior wall MI. One can deduce the presence of acute posterior wall MI from a conventional ECG by finding a tall R wave and ST depression in leads V1 and possibly V2. The R wave is the reciprocal of the Q wave in the posterior leads. The ST segment depression is the reciprocal of the ST segment elevation accompanying the acute infarction.
aVR V1 V4
aVL V2 V5
aVF V3 V6
I
II
II III
V7
V8
V9
46a
46b
1 What are the abnormalities shown in both ECGs and what is the likely cause?
2 How should this patient be managed?
A 74-year-old male with a history of renal failure was admitted with progressive drowsiness. He had a history of hypertension and was found to have a BP of 200/110 mmHg (26.7/14.7 kPa). He was taking co-amilofruse and lisinopril. ECG 47a was taken immediately on admission and ECG 47b was taken after treatment.
aVR V1 V4
aVL V2 V5
aVF V3 V6
I
II
II III
aVR V1 V4
aVL V2 V5
aVF V3 V6
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II
II III
47a
47b
Answer 47
1 ECG 47a shows RAD (170°). P waves are difficult to recognize. The RR interval is regular and QRS complexes are broad, with an M-shaped pattern in V6 as in LBBB (arrows). The T waves are tall and peaked (tented T waves; arrows), seen especially in leads V1–V3. In the context of the clinical history the most likely cause for these abnormalities was hyperkalaemia. In fact the serum K+ on admission was 7.9 mmol/l (7.9 mEq/l). ECG 47b was taken after treatment when the serum K+ had dropped to 6.4 mmol/l (6.4 mEq/l). There is sinus rhythm with clearly visible P waves and a prolonged PR interval (264 ms). The axis is normal and the LBBB appearance in ECG 47a has also disappeared. The QRS complexes are less broad and there is a reduction in T wave amplitude which still remains peaked in V2–V3 (arrows). The changes are consistent with resolving yet residual hyperkalaemia. Other changes seen with hyperkalaemia include junctional escape rhythm and severe broadening of QRS complexes eventually resulting in ventricular fibrillation.
2 The emergency treatment of hyperkalaemia depends on the ECG changes. It should be considered as an emergency in the presence of such changes. Immediate calcium gluconate infusion should be given, followed by insulin and dextrose infusion. More definitive treatment later on includes calcium resonium. In this parti-cular case co-amilofruse and lisinopril should be withheld and alternative antihypertensive agents considered.
aVR V1 V4
aVL V2 V5
aVF V3 V6
I
II
II III
aVR V1 V4
aVL V2 V5
aVF V3 V6
I
II
II III
47a
47b
A 37-year-old female who was partially deaf presented with palpitations.
aVR V1 V4
aVL V2 V5
aVF V3 V6
I
II
III
48 1 What abnormality is shown in ECG 48 and what is the
significance?
2 What further advice needs to be given to the patient?
Answer 48
1 ECG 48shows normal sinus rhythm. The most prominent abnormality is a prolonged QTc of 570 ms (marker). A prolonged QT can be hereditary or acquired. It can lead to development of life threatening ventricular arrythmias such as torsades de pointes and ventricular fibrillation. This can result in sudden cardiac death.
Two varieties of the hereditary form have been reported. The Jervell and Lange-Nielsen syndrome is associated with deafness, while the Romano–Ward syndrome is not. Both of these disorders are autosomal recessive. While some patients remain asymptomatic throughout life, others are highly susceptible to arrhythmias, particularly torsades de pointes. Patients at high risk of sudden cardiac death are characterized by deafness, female gender, syncope, and documented arrhythmias. The acquired form of prolonged QT may be due to drugs, electrolyte abnormalities, hypothermia, and central nervous system injury. Acquired prolonged QT intervals also carry a risk of serious arrhythmias unless the causative factor is corrected.
2 These patients may benefit from an implantable cardiac defibrillator (ICD). Advice should be given to avoid possible precipitating factors especially drugs that can be bought over the counter such as antihistamines. Screening of family members for the condition is also required.
aVR V1 V4
aVL V2 V5
aVF V3 V6
I
II
III
48
1 What are the abnormalities in ECG 49?
2 How should this patient be managed?
A 65-year-old male was admitted with acute inferior wall infarction. While in CCU he had a sudden collapse and the arrhythmia in ECG 49 was noted.
II
III 5V
49
Answer 49
1 ECG 49 is a three lead rhythm strip showing complete heart block in the initial part. After the second normal QRS complex a ventricular ectopic is seen, falling at the end of the T wave (R on T phenomenon;
arrows). This has resulted in the development of polymorphic VT (torsades de pointes).
Torsades de pointes refers to VT characterized by QRS complexes of changing amplitude twisting around the isoelectric line, giving a characteristic undulating pattern with a varying QRS axis. It carries a risk of degenerating into ventricular fibrillation and sudden cardiac death. A prolonged QT interval may predispose to such a cardiac dysrhythmia.
2 This patient was being monitored when this event occurred. Immediate unsynchronized electrical cardioversion should be carried out in this situation along with advanced life support. As this patient has complete heart block an urgent temporary pacing is recommended. Temporary pacing can help to avoid recurrence of the arrhythmia by increasing the heart rate and shortening the QT interval. An isoprenaline infusion may act in a similar manner.
II
III 5V
49
1 What does ECG 50a show?
2 The patient was given adenosine intravenously. What does the rhythm strip ECG 50b show?
3 How may adenosine help in the management of cardiac arrhythmias?
An 85-year-old female was brought in collapse into the accident and emergency department.
She was found to have a BP of 100/55 mmHg (13.3/7.3 kPa) and a pulse of 150 bpm. ECG 50a was performed on initial assessment.
aVR V1 V4
aVL V2 V5
aVF V3 V6
I
II
II III
50a
50b
Answer 50
1 ECG 50ashows an atrial flutter with 2:1 block. There are two P waves (arrows) for every QRS complex.
Some of the P waves can be seen as small deflections superimposed on the T wave (lead V1).
2 ECG 50bshows a profound bradycardia with flutter waves prominently visible between QRS complexes, confirming the diagnosis of atrial flutter.
3 Adenosine is a useful drug that can be used to terminate paroxysmal SVT. It has a very short half-life of about 8–10 seconds and, therefore, should be given as a rapid intravenous bolus followed by a saline flush, preferably in a bigger vein in the antecubital fossa. It can cause profound bradycardia and possible bronchospasm and is contraindicated in second and third degree heart block, sick sinus syndrome, and asthma.
Adenosine can also be used to help in the differential diagnosis of broad and narrow complex tachycardias. It has no effect on broad complex tachycardias if they are of ventricular origin. Adenosine slows AV conduction and ventricular rate and this results in enhancing the morphological features of the arrhythmias, thus helping in the differential diagnosis as demonstrated in the rhythm strip in this example.
aVR V1 V4
aVL V2 V5
aVF V3 V6
I
II
II III
50a
50b
Index
Cases may appear under more than one category; references are to case numbers
atrial rhythm abnormalities 16, 18, 33, 39, 43, 50
atrioventricular (AV) node arrhythmias 5, 6, 13, 17, 21, 23, 33, 35, 40
benign and nonpathogenic conditions 9, 15, 18, 42 cardiac failure 42
electrolyte abnormalities 47 inherited and congenital syndromes
14, 16, 34, 37, 45, 48
ischaemic heart disease 2, 6, 12, 19, 25, 32, 46
myocardial disease/infarction 2, 4, 6, 11, 12, 19, 25, 29, 32, 46 pacemakers/pacing 26, 30, 31, 36,
38
pericardial disease 3, 27, 29, 41 pulmonary heart disease 1, 20, 34
sino-atrial (SA) node arrhythmias 7, 9, 27, 28, 44
sudden cardiac death 48, 49 thyroid disorders 43 valvular heart disease 11, 24 ventricular arrhythmias 22, 49
Note: references are to page numbers action potential 8, 9
adenosine 104, 126 amiodarone 54, 104 anaemia, pernicious 112 aneurysm, ventricular 23, 34 aortic stenosis 74
assessment of ECG 13–25 athletes 40, 56, 114
atria, rhythm abnormalities 14 atrial fibrillation (AF) 106, 108
heart block 92, 102 myocardial infarction 64 paroxysmal 112
WPW syndrome 58, 100 atrial flutter 42, 106, 126
atrial pacemaker, wandering 14, 19, 40
atrial tachycardia 82, 106
atrioventricular (AV) block 42, 104, 106
atrioventricular (AV) dissociation 70
atrioventricular (AV) node 8, 14 blocking drugs 104
intranode re-entry tachycardia (AVNRT) 106
ischaemia 68
atrioventricular (AV) re-entry tachycardia (AVRT) 54, 106 atropine 38, 40
beta blockers 52, 104 bradyarrhythmias 38, 110 bradycardia 46, 56, 88, 126 breast carcinoma 108 bundle branch block
left 36, 92, 110, 120
right 28, 60, 70, 72, 92, 96 calcium channel blockers 52 calcium gluconate 120 calcium resonium 120 capture beat 70 cardiac axis 14–17
causes of deviation 17
deviation around vertical axis 18 left deviation 17, 36, 42, 60, 96 right deviation 17, 36, 60, 66, 94, 116, 120
cardiac conducting system 8–9 cardiac defibrillator, implantable 122 cardiac enzymes 76
cardiac failure, congestive 110 cardiac tamponade 80, 84 cardiomegaly 80
cardiomyopathy, hypertrophic 74 cardioversion, electrical 54, 100, 124 carotid bruits 104
carotid sinus hypersensitivity 88 carotid sinus massage 88, 104 carotid sinus syndrome 88 chest electrodes 5
chest (precordial) leads 6–7, 12 co-amilofruse 120
coronary artery disease 50, 68 cor pulmonale 66
cyanosis 94 deafness 122
delta wave 54, 58, 100 dextrocardia 116 diamorphine 64
digoxin 52, 54, 104, 110 diltiazem 52 ventricular 60, 90, 124 Eisenmenger’s syndrome 94 electrical alternans 32, 80 electrode placement
improper 116 standard 5
escape rhythm, junctional 38, 52 exercise tolerance testing 50 flecainide 54, 104
fluid replacement, intravenous 64
‘flutter/fibrillation’ 42 fusion beats 44, 70
‘F’ waves 42 heart block
bifascicular 60 complete 56, 102, 124 first degree 30, 40, 46, 56 Mobitz type I 56, 68, 96 Mobitz type II 56 trifascicular 96
see also atrioventricular block;
bundle branch block heart rate
calculation 14 and QT interval 25 hemiblock 60 heparin 104
His, bundle of 8, 106
Holter monitoring 110, 112 hyperkalaemia 120
hypertrophy left atrial 34, 48 left ventricular 40, 74 right atrial 66
right ventricular 36, 60, 94 hypotension 64
isoprenaline infusion 38, 124 Jervell and Lange–Nielsen syndrome
122
‘J’ (Osbourne) wave 46 junctional escape rhythm 38, 52 junctional tachycardia 106 Kartagener’s syndrome 116 Kent, bundle of 54, 106 limb electrodes 5 limb leads 6–7, 10–12 lisinopril 120
Lown–Ganong–Levine (LGL) syndrome 82
low voltage complexes 108 mitral valve
anterior wall 30, 60 inferior wall 38, 64, 90, 118 non-ST elevation (partial thickness) 76
posterior wall 118 right ventricle 64
ST segment elevation (STEMI) 22–3, 30, 32, 38, 64
myocardial ischaemia 52 neck veins, engorged 64, 118 nitrates, intravenous 64 normal ECG 8 obesity 108
Osbourne wave (‘J’wave) 46
pacemaker, wandering atrial 14, 19, 40 pacemaker, artificial
coding method 86 dual chamber 86, 88, 98 failure 78, 102
permanent 52, 56, 110 single chamber 78, 98, 102 temporary 38, 124 parasystole 44
pericardial effusion 32, 80, 84 pericarditis, acute 32
P mitrale 34, 36, 48 potassium, serum 120 PP interval 114 P pulmonale 66
P-QRS-T complex 8–9, 10 precordial (chest) leads 6–7, 12 PR interval 10, 19, 62
prolonged 46, 68, 96, 120 short 58, 82, 100
propafenone 104
pulmonary embolism 28, 66, 90 pulmonary hypertension 66, 94 pulmonary stenosis 66
P waves 10, 19, 48, 52, 62, 70, 104
‘hidden’ 106
interpretation of abnormalities 48 P mitrale 34, 36, 48
P pulmonale 66
QRS complex 8–9, 10, 20–1 axis 15
dropped 68, 96 duration 36, 60, 72 height 80, 116 M-shaped 36, 120 wide 70, 72, 96 QT interval 10, 25, 122
corrected (QTc) 25, 122 Q waves 20, 30, 34, 60, 72 reference points, ECG 8, 10 refractory period 8
rhythm strip 14, 68
right ventricular infarction 64 Romano-Ward syndrome 122 RR interval 92
R on T phenomenon 90, 124 R wave 60, 66
tall 74, 90, 94, 116, 118 S1 Q3 T3 pattern 28
saw-tooth flutter waves 42, 106 serotonin re-uptake inhibitors,
selective 88 shunt, right to left 94 sick sinus syndrome 86, 110 sinoatrial (SA) node 8, 114 sinus arrhythmias 14, 40, 114 sinusitis, recurrent 116 sinus rhythm 14 sinus tachycardia 28, 80 sotalol 104
Stoke Adam’s attacks 96 strain pattern 66, 74 streptokinase 30 ST segment 8, 10, 22
depression 118
exercise-induced ischaemia 50 myocardial infarction 30, 38, 64, 118
supraventricular tachycardia 106 ventricular aneurysm 34
ST segment elevation 22–3, 118 myocardial contusion 84
myocardial infarction 22–3, 30, 32, 38, 64 sudden death, risk of 122, 124 supraventricular tachycardia (SVT)
broad complex 58, 70, 92, 100 differentiating broad and narrow complex 126
narrow complex 104, 106 sinus 28, 80
supraventricular 70, 104, 106 ventricular 58, 70, 124 thrombolysis 30, 92 thyroid function 108, 112 torsades de pointes 124 trauma, cardiac 84 tricuspid incompetence 66 troponins, cardiac 76 T wave 8, 10, 24
flat 24, 116
inversion 28, 38, 60, 74, 76, 116, 118
tented 120 12-lead ECG 10–11 U wave 8, 24, 40 vagal tone, resting 40 vagus nerve, stimulation 104 ventricles, rhythm abnormalities 14 ventricular aneurysm 22–3, 34 ventricular fibrillation 46, 54 ventricular septal defect (VSD) 94 ventricular tachycardia 58, 70
polymorphic (torsade de pointes) 124
verapamil 52, 104 warfarin 104, 110
Wenckebach phenomenon 40, 56, 68, 96
Wolff-Parkinson-White (WPW) syndrome 54, 58, 90, 100, 106