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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2818_Библиотеки_им_академика_М_И_Перельмана
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Lead II 25 mm/s. 10 mm = 1 mV
Lead II 25 mm/s. 10 mm = 1 mV
Lead II 25 mm/s. 10 mm = 1 mV
https://t.me/med1917
Fig. 20.24 Analyse the
rhythm strip
Lead II 25 mm/s. 10 mm = 1 mV
Fig. 20.25 Analyse the rhythm strip
20 Junctional andVentricular Arrhythmias
25 mm/s. 10 mm = 1 mV
Lead II
Fig. 20.26 Analyse the rhythm strip
Fig. 20.27 Analyse the rhythm strip
Fig. 20.28 Analyse the rhythm strip
Lead II 25 mm/s. 10 mm = 1 mV
Lead II 25 mm/s. 10 mm = 1 mV
Lead II 25 mm/s. 10 mm = 1 mV
20.2 Ventricular Arrhythmia
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279
7. Identify the rhythm strip (Fig. 20.29). Give two points in favour of your
diagnosis.
8. A 55-year-old patient had anterior wall myocardial infarction. While undergo-
ing reperfusion therapy, the following abnormality appeared in the bedside cardiac monitor. Can you identify the rhythm strip given in Fig.20.30.
9. Identify the rhythm (Fig.20.31). What is your diagnosis?
10. You were on duty in CCU. Suddenly the cardiac monitor sounded the alarm.
The rhythm strip from the monitor is given in Fig.20.32. Identify the abnormal-
ity. What will you do to manage this patient?
25 mm/s. 10 mm = 1 mV
Lead II
Fig. 20.29 Analyse the rhythm strip
Fig. 20.30 Analyse the rhythm strip
Fig. 20.31 Analyse the rhythm strip
Fig. 20.32 Analyse the rhythm strip
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20 Junctional andVentricular Arrhythmias
Answers
1. True 2. True 3. False 4. False 5. False 6. a 7. c 8. d 9. b 10. d
Case Studies
1. The rhythm strip (Fig.20.23) shows ventricular extrasystoles occurring after
every four normal PQRS complexes. The extrasystoles have wide QRS complex and amplitude and morphology is entirely different from normal PQRS
complexes.
The patient has irregular pulse which means the extrasystoles are occurring
at random without maintaining any rhythm even if the rhythm strip shows them
at a regular pattern occurring after every four normal complexes.
Ventricular extrasystoles are commonly seen in daily clinical practice. In
this patient, investigations should be carried out to rule out any underlying heart
disease. If no underlying heart disease is detected, it indicates good prognosis
and nothing more needs to be done. However, she should be advised to reduce
intake of caffeine. If she becomes symptomatic, she may need beta-blockers to
control the symptoms.
2. The diagnosis is VT (Fig.20.24). There is wide QRS complex with duration
more than 0.14s and ventricular rate is about 166bpm.
Treatment of VT depends upon haemodynamic status. In this drowsy patient,
there is hypotension and pulmonary oedema. This is a medical emergency.
Immediate DC cardioversion should be done. After resuscitation, he should be
evaluated for postoperative myocardial ischaemia or infarction.
In patients with structural heart disease and hemodynamically stable ventricular tachycardia, intravenous procainamide, amiodarone, lidocaine and
sotalol (depending on availability) are recommended for the acute treatment of
ventricular tachycardia.
3. The diagnosis is VF (Fig.20.25). There is undulating baseline with no identiable PQRS complex.
This is a life threatening emergency. Immediately guideline-directed management as per Advanced Cardiac Life Support (ACLS) protocol should be
initiated. He should be shocked immediately with 120–200J on a biphasic debrillator or 360J using a monophasic debrillator. Administer epinephrine and
amiodarone as per ACLS protocol in patients sustaining VF rhythm regardless
of receiving three shocks. Amiodarone signicantly improves survival to hospital admission without affecting survival to hospital discharge. Identifying and
addressing the cause of inciting event is equally important.
4. The rhythm strip shows IVR (Fig.20.26). There is no P wave, and the QRS
complexes are wide, more than 0.14s. The ventricular rate is 37bpm. This is
also called slow VT.
Usually, IVR is a benign rhythm which settles down of its own. Sometimes,
a patient may be symptomatic and may not tolerate idioventricular rhythm secondary to atrioventricular dyssynchrony, fast ventricular rate or degenerated
ventricular brillation of idioventricular rhythm. Atropine may be trialled in
such cases to increase sinus rate.
20.2 Ventricular Arrhythmia
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281
5. The rhythm strip in Fig.20.27 shows premature junctional complex. The fourth
PQRS complex is premature in timing and it is followed by compensatory
pause. The P wave is inverted. Rest all the PQRST complexes are normal.
6. The rhythm strip (Fig.20.28) shows Torsades de pointes, polymorphic VT.The
rst PQRS complex is normal. The second PQRS complex has prolonged Q-T
interval. It is 0.68s. It is followed by VT with big amplitude complexes at the
beginning followed by small amplitude complexes. At the end of the strip again
big amplitude complexes are seen. Hence it is Torsades de pointes precipitated
by long Q-T interval.
Intravenous magnesium is the rst-line pharmacologic therapy in Torsades
de Pointes. The patient has a feeble pulse and blood pressure is normal. Hence
magnesium should be given. The recommended initial dose of magnesium is a
slow 2g IV push. An infusion of 1–4g/h. should be started to keep the magnesium levels greater than 2mmol/L.Magnesium has been shown to stabilize the
cardiac membrane. If the patient becomes unstable haemodynamically, synchronized cardioversion should be performed (100J monophasic, 50J biphasic). Pulseless torsades should be debrillated.
7. The rhythm is IVR (Fig.20.29). Two points in favour of diagnosis are wide
QRS complex, absent P waves and ventricular rate of about 40bpm.
8. The diagnosis is AIVR (Fig.20.30). There are no P waves, wide QRS complex
at a rate of 100bpm. This is also called slow VT.
AIVR is usually a benign and well-tolerated arrhythmia. Most of the cases
will require no treatment. It is frequently seen during reperfusion therapy and it
signies complete reperfusion although many disagree with it. Atropine may be
required sometimes to increase the sinus rate to suppress the arrhythmia.
9. The diagnosis is junctional tachycardia (Fig.20.31). The QRS complex is narrow. The ventricular rate is 125bpm. The P waves are all inverted. Inverted P
wave signies that the rhythm is originating from AV junction. Hence, it is
junctional tachycardia also called junctional ectopic tachycardia.
Junctional tachycardia is more common in infants and children as compared
to adults. It is often seen after cardiac surgery for congenital heart disease in
infants. Beta-blockers, diltiazem and verapamil are recommended for treatment. Amiodarone is often effective in non-postoperative junctional tachycardia. Catheter ablation may be reasonable in patients with junctional tachycardia
when medical therapy is not effective.
10. The diagnosis is VT degenerating into VF ultimately progressing to ventricular
asystole (Fig.20.32). Broad QRS tachycardia indicates VT at the beginning.
There are no P waves. After this suddenly it degenerates into ill-formed complexes, which is VF and the following straight line indicates asystole.
Immediate resuscitation should be started according to current ACLS guidelines. High-quality CPR is the mainstay of treatment. Asystole is a nonshockable rhythm. Therefore, if asystole is noted on the cardiac monitor, no
attempt at debrillation should be made. High-quality CPR should be continued with minimal (less than 5s) interruption. CPR should not be stopped to
allow for endotracheal intubation. Epinephrine (1mg via intravenous or intraosseous line) should be delivered every 3–5min. Cardioversion should be done
the moment VT is diagnosed or else it may be too late.
Chapter 21
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Approach toArrhythmias
Learning Objectives
After studying this chapter, the reader will learn about:
• Analysis of arrhythmias by analysing rate and rhythm
• Analysis of arrhythmias by studying P wave
21.1 Approach toArrhythmia
There are various ways of approaching arrhythmia. The choice of course depends
upon the knowledge and the level of understanding of the reader. The easy method
is to analyse by starting with the rate and regularity and then narrow down to the
various possibilities. While analysing by this method, the following questions
should be asked while inspecting the rhythm strip.
(a) Is the rate normal, fast or slow?
(b) Is the rhythm regular?
(c) If the rhythm is irregular, whether there is pattern of regularity to the rhythm
that is regularly irregular or it is absolutely irregular that is irregularly irregular?
(d) If there are only a few beats interrupting the regularity, then it needs to be seen
whether these are ectopic beats or whether these beats are followed by compensatory pause?
Now let us see the interpretation of these questions.
Ltd. 2024
T. K. Koley, Rapid Review of ECG,
https://doi.org/10.1007/978-981-99-9116-7_21
283© The Author(s), under exclusive license to Springer Nature Singapore Pte
284
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21 Approach toAr rhythmias
21.1.1 Consider theFollowing Possibilities When theRhythm
Is Regular
21.1.1.1 Normal Rate
(a) Sinus rhythm (regular P waves present)
(b) Sinus rhythm absent (regular P waves absent)
(i) Ectopic atrial pacemaker (P′ wave present)
(ii) Accelerated AV nodal rhythm
(iii) Implanted pacemaker (ventricular)
21.1.1.2 Tachycardia
(a) Sinus tachycardia (P waves present, narrow QRS complex)
(b) PSVT/PAT (P waves usually not seen, narrow QRS complex)
(c) Ventricular tachycardia (P waves usually not seen, wide QRS complex)
21.1.1.3 Bradycardia
(a) Sinus bradycardia
(b) Idioventricular rhythm with SA block or complete AV block
(c) AV nodal rhythm with SA block or complete AV block
21.1.2 Consider the Following Possibilities When the Rhythm
Is Irregular
21.1.2.1 Regularly Irregular Arrhythmias
(a) Sinus arrhythmia
(b) Mobitz type I block (Wenckebach block)
(c) Bigeminy or trigeminy of atrial, AV nodal or ventricular origin
21.1.2.2 Irregularly Irregular Arrhythmias
(a) Atrial utter with variable AV block
(b) Atrial brillation
(c) Ventricular brillation
21.1 Approach toArrhythmia
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21.1.2.3 Infrequent Irregularity
(a) Atrial, AV nodal or ventricular premature beats
(b) Mobitz type II AV block
285
21.1.3 Consider theFollowing When There Are Pauses
21.1.3.1 Long Pause
(a) Sinus pause
(b) Complete AV block with failure of escape beat
21.1.3.2 Short Pause
(a) Ventricular ectopic (complete pause)
(b) Atrial ectopic (incomplete pause)
Another method of analysing arrhythmias is by the study of the P wave and its relation with the QRS complexes. Here initially it has to be seen whether sinus rhythm
is present or not. If the sinus rhythm is absent, then the number and the morphology
of the P waves are to be studied and then the irregularities of the P waves are to be
correlated with the QRS complexes. It is always better to mark out all the P waves
in the rhythm strip at the beginning. The duration of the QRS complex should also
be measured because a wide QRS complex points towards the ventricular origin of
the arrhythmia. Let us consider the following:
21.1.3.3 Sinus Rhythm
(a) Regular sinus rhythm
(b) Sinus bradycardia
(c) Sinus tachycardia
(d) Sinus arrhythmia
21.1.3.4 Absent Sinus Rhythm
(a) Absent P waves
(i) Infrequent absence
– Ventricular ectopic
– Premature beat of nodal origin
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21 Approach toAr rhythmias
(ii) Constant absence of P wave (or P wave buried in T wave)
– Atrial brillation
– Ventricular tachycardia
– Nodal rhythm
– Accelerated nodal rhythm
– PSVT/PAT
(b) Abnormal shape of P wave (P′ wave)
(i) Atrial ectopic beat
(ii) Wandering atrial pacemaker
(iii) Incorrect placement of arm electrodes
(iv) Nodal rhythm with retrograde conduction of P waves
(c) More than one P wave for each QRS complex
(i) Complete AV block
(ii) 2:1 or higher AV block (Mobitz type I and II)
(iii) Atrial utter or brillation with second degree AV block (very difcult to
identify P wave in these cases)
One can use either of these methods alone or together to analyse arrhythmia, but it
is easier said than done because analysis of arrhythmia is one of the most difcult
aspects of ECG.This comes not by reading book only, but by constant daily practice.
Part VI
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Miscellaneous ECG
Chapter 22
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ECG inElectrolyte Imbalance
Learning Objectives
After studying this chapter, the reader will learn about:
• Hyperkalaemia
• Hypokalaemia
• Hypercalcaemia
• Hypocalcaemia
• Magnesium effect
Resting membrane potential of a cardiac cell is dependent upon the maintenance of
a normal ionic balance across the cell membranes. Potassium, sodium and calcium
inuence the resting membrane potential as well as generation of action potential.
Potassium is the most important contributor to the resting membrane potential. The
normal ECG depends upon the concentration of these ions across the cardiac cell
membranes. Imbalance in the level of potassium and calcium has profound effect on
the ECG.Electrolyte abnormality is frequently encountered in our day-to-day practice in patients suffering from renal failure, patients on IV uids and severely ill
patients in ICU.
22.1 ECG inPotassium Imbalance
Electrophysiology of cardiac cell is profoundly affected by increase or decrease in
level of potassium ions, thereby affecting the electrical stability of heart. Potassium
ions play a key role in repolarization of cardiac cells. Severe hyperkalaemia and
hypokalaemia can be life threatening and require urgent treatment.
Ltd. 2024
T. K. Koley, Rapid Review of ECG,
https://doi.org/10.1007/978-981-99-9116-7_22
289© The Author(s), under exclusive license to Springer Nature Singapore Pte
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