oxford case of histories in cardiology

Oxford Case
Histories
Oxford Case Histories
Series Editors
Sarah Pendlebury and Peter Rothwell
Published:
Neurological Case Histories (Sarah Pendlebury, Philip Anslow, and
Peter Rothwell)
Oxford Case Histories in Cardiology (Rajkumar Rajendram, Javed Ehtisham,
and Colin Forfar)
Oxford Case Histories in Gastroenterology and Hepatology (Alissa Walsh,
Otto Buchel, Jane Collier, and Simon Travis)
Forthcoming:
Oxford Case Histories in Nephrology (Chris Pugh, Chris O’Callaghan,
Aron Chakera, Richard Cornall, and David Mole)
Oxford Case Histories in Respiratory Medicine (John Stradling, Andrew
Stanton, Anabell Nickol, Helen Davies, and Najib Rahman)
Oxford Case Histories in Rheumatology (Joel David, Anne Miller, Anushka
Soni, and Lyn Williamson)
Oxford Case Histories in Stroke and TIA (Sarah Pendlebury, Ursula Schulz,
Aneil Malhotra, and Peter Rothwell)
1
Oxford Case
Histories in
Cardiology
Dr Rajkumar Rajendram
Specialist Registrar
General Medicine and Intensive Care
John Radcliffe Hospital
Oxford, UK

Dr Javed Ehtisham
Cardiology Specialist Registrar
John Radcliffe Hospital
Oxford, UK
Professor Colin Forfar
Consultant Cardiologist and Senior Lecturer in Medicine
John Radcliffe Hospital and Oxford University
Oxford, UK

1
Great Clarendon Street, Oxford OX2 6DP
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Preface
Post-graduate medicine is evolving. The core curriculum developed for all medical
specialties is a competence-based document dictating the knowledge, skills and atti-

tudes which a trainee should obtain before a certificate of completion of training (CCT)
can be awarded. Mandatory knowledge and performance-based assessments are being
conducted in order to ensure these standards are met. Although ‘student-centred
learning’ is encouraged in order to develop mastery of the core curriculum, there are
few books available to direct higher trainees preparing for these examinations.
We firmly believe that the use of clinical material is one of the best methods of
learning and teaching medicine. This is just as true for experienced consultants as for
first year clinical medical students. However, although many collections of cases are
available for medical students and as preparation for the MRCP(UK), there are few
that challenge the experienced clinician or trainee specialist. It is for this reason that
the cases are not only challenging, but also, we hope, entertaining and informative.
The general medical council is now issuing licences to practice and re-validation will
soon be a requirement. We envisage that use of advanced clinical texts such as this
could be included in a portfolio of continuing medical education that could be used to
support a process of specialist re-validation.
The book consists of 50 case presentations each describing the clinical history and
progress of a patient. Each case includes a set of questions to which we have given
detailed evidence-based answers. Where evidence is unclear and clinical judgement is
required we have expressed our opinion.
The selection of cases covers the breadth of cardiology including acute emergencies
requiring rapid diagnosis and treatment and chronic diseases which require thoughtful
management.
The major topics of the cardiology core curriculum are covered but it is not the aim
of this book to give the answers to all cardiological questions. Rather the Socratic
method of questions and answers is intended to guide towards deeper thought about
clinical issues.
The questions and answers format also ensures that this book will be suitable for
those preparing for specialist examinations in acute medicine and cardiology.
However, perhaps more importantly, this book bridges the gap between the acute
physician and the cardiologist through the discussion of cases from their initial acute

presentation to the on-take team through to the management initiated by cardiologists
in a tertiary centre.
We would like to thank the many colleagues who contributed cases and illustrations
and made helpful comments on the manuscript, in particular Dr Jim Newton for
providing several echocardiographic images. We also thank our families for their
support whilst we worked late evenings, early mornings, and weekends!
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Contents
Abbreviations ix
Cases 1–50 1
List of cases by diagnosis
405
List of cases by principal clinical features at diagnosis
406
Index
407
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Abbreviations
2D 2-dimensional
AAA Abdominal aortic aneurysm
A-a pO2 Arterial–alveolar oxygen
ABG Arterial blood gas
ACC/AHA American College of
Cardiology/American Heart
Association
ACE Angiotensin-converting
enzyme
ACS Acute coronary syndrome
ADP Adenosine diphosphate
AF Atrial fibrillation

AIDS Acquired immuno deficiency
syndrome
AL Amyloid light chain
ALCAPA Anomalous left coronary artery
arising from the pulmonary
artery
ALP Alkaline phosphatase
ALT Alkaline transaminase
AP Anterior–posterior
APTT Activated partial
thromboplastin times
ARB Angiotensin receptor blocker
ARDS Acute respiratory distress
syndrome
ARF Acute renal failure
ARVC Arrhythmogenic right
ventricular cardiomyopathy
ARVD Arrhythmogenic right
ventricular dysplasia
AS Aortic stenosis
ASD Atrial septal defect
AST Aspartate transaminase
AT Anaerobic threshold
ATN Acute tubular necrosis
ATP Adenosine triphosphatase
AV Aortic valve
aVF Augmented vector foot
aVR Augmented vector right
AVR Aortic valve replacement
AVID Antiarrhythmas vs implantable

defibrillators trial
aVL Augmented vector left
AVN Atrioventricular node
BMW Balanced middle weight
BP Blood pressure
BPEG British Pacing and
Electrophysiology Group
bpm Beats per minute
BSA Body surface area
CABG Coronary artery
bypass graft
CAD Coronary artery disease
CASH The Cardiac Arrest Study
Hamburg
CCB Calcium channel blockade
CCU Coronary care unit
CEA Carcinoembryonic antigen
CFA Common femoral artery
CHB Complete heart block
CI Confidence interval
CIDS Canadian Implantable
Defibrillator Study
CIN Contrast-induced nephropathy
CK Creatine kinase
CKD Chronic kidney disease
CK-MB Creatine Kinase-muscle and
bone isoform
CLOSURE 1 A prospective, multicenter,
randomized controlled trial to
assess the safety and efficacy of

the STARFlex® septal closure
device against medical therapy
after a stroke and/or transient
ischemic attack due to
presumed paradoxical
emboslism through a patent
foramen ovale.
x
ABBREVIATIONS
CMRI Cardiovascular magnetic
resonance imaging
CMT Circus movement
tachycardia
CMR Cardiac magnetic resonance
CNS Central nervous system
CO Cardiac output
COPD Chronic obstructive pulmonary
disease
COPE COlchicine for acute
PEricarditis
CPAP Continuous positive airways
pressure
CPEX Cardiopulmonary exercise
CPVT Catecholaminergic
polymorphic ventricular
tachycardia
CRP C-reactive protein
CPR Cardiopulmonary resuscitation
CRT Cardiac resynchronization
therapy

CSF Cerebrospinal fluid
CT Computerise tomography
CTEPH Chronic thromboembolic
pulmonary hypertension
cTnI Cardiac troponin I
cTnT Cardiac troponin T
CTPA Computed tomographic
pulmonary angiography
CURE Clopidogrel in Unstable Angina
to precent Recurrent Events
CVA Cerebrovascular accident
CXR Chest X-ray
DBP Diastolic blood pressure
DC Direct current
DCM Dilated cardiomyopathy
DDDR Dual-chamber rate-responsive
DIC Disseminated intravascular
coagulopathy
DIGAMI Diabetes Mellitus, insulin
Glucose infusion in Acute
myocardial infarction
DVLA Driver and Vehicle Licensing
Agency
DVT Deep vein thrombosis
ECG Electrocardiograph
ED Emergency department
EDD Estimated delivery date
EEG Electroencephalography
EF Ejection fraction
eGFR Estimated glomerular filtration

rate
ELISA Enzyme-linked immuno
sorbent assays
ELISPOT Enzyme-linked immunospot
EMD Electromechanical dissociation
ENT Ear, nose, and throat
ESC European Society of
Cardiology
ESD End systolic diameter
ESR Erythrocyte sedimentation rate
ET Endotracheal
ETT Exercise tolerance test
EuroSCORE European System for Cardiac
Operative Risk Evaluation
FBN-1 Fibrillin-1 gene
FFP Fresh frozen plasma
GCS Glasgow coma score
GFR Glomerular filtration rate
GGT Gamma-glutamyl transferase
GI Gastrointestinal
GISSI Gruppo Italiano per l0 studio
della Streptochinasi nell’
infarto miocardico (Itallian
Group for the study of the
survival of myocardial
infraction)
GP General practitioner
GTN Glyceryl trinitrate
GUSTO Global utilization of
streptokinase and tissue

plasminogen activator for
occulded coronary arteries
HACEK Group of slow growing gram
negative organisms
Hb Haemoglobin
HCM Hypertrophic cardiomyopathy
HDL High density lipoproten
H&E Haematoxylin and eosin
HERG Human Ether-à-go-ge Related
Gene
HGV Heavy goods vehicle
xi
ABBREVIATIONS
HIV Human immunodeficiency
virus
HR Heart rate
IABP Intra-aortic balloon pump
IAS Interatrial septum
ICD Implantable cardioverter
defibrillator
IFN Interferon
IgG Immunoglobulin G
IgM Immunoglobulin M
IHD Ischaemic heart disease
INR International normalised ratio
IPAH Idiopathic PAH
IPPV Intermittent positive pressure
ventilation
ITU Intensive care unit
iv Intravenous

IVC Inferior vena cava
IVS Interventricular septum
IVUS Intravascular ultrasound
JVP Jugular venous pressure
KCNH2 Gene encoding potassium
channel
KDOQI Kidney Disease Outcomes &
Quality Initiative
LA Left atrium
LAD Left anterior descending
LAO Left-anterior-oblique
LBBB Left bundle branch block
LDH Lactate dehydrogenase
LDL Low density lipoprotein
LM Left main coronary artery
LMWH Low-molecular-weight heparin
LQTS Long QT syndrome
LR Likelihood ratio
LV Left ventricular
LVAD Left ventricular assist devices
LVEDP Left ventircular end diastotic
pressure
LVEF Left ventricular ejection
fraction
LVF Left ventricular ejection
fraction
LVH Left ventricular hypertrophy
LVOT Left ventricular outflow tract
MAP Mean arterial pressure
MCV Mean cell volume

MDR Multidrug-resistant
MDRD Modification of diet in renal
disease study
MET Metabolic equivalent of task
MFS-2 Marfan’s syndrome type 2
MI Myocardial infarction
MR Mitral regurgitation
MRI Magnetic resonance imaging
MV Mitral valve
MVR Mechanical mitral valve
replacement
NAC N-acetylcysteine
NASPE North American Society of
Pacing and Electrophysiology
NKDA No known drug allergies
NICE National Institute for Health
and Clinical Excellence
NR Normal ranage
NSAIDS Non-steroidal anti-
inflammatory drugs
NSTE-ACS Non-ST elevation acute
coronary syndrome
NSTEMI Non-ST elevation myocardial
infarction
NSVT Non-sustained ventricular
tachycardia
NYHA New York Heart Association
OASIS Organization to assess
strategies in ischemic
syndromes

od Once daily
OGD Oesophagogastroduodensocopy
OM1 First obtuse marginal
OR Odds ratio
PA Posteroanterior
PA Pulmonary artery
PAC Preoperative assessment clinic
PAH Pulmonary artery hypertension
PAP Pulmonary artery pressure
PAR Pulmonary arterial resistance
PCI Percutaneous coronary
intervention
xii
ABBREVIATIONS
PCM Peripartum cardiomyopathy
PCR Polymerase chain reaction
PE Pulmonary embolism
PEEP Positive end expiratory
pressure
PFO Patent foramen ovale
PH Pulmonary hypertension
PLE Protein-losing enteropathy
PLV Posterior left ventricular
po Per os (oral)
POISE Perioperative Ischemic
Evaluation
PRKAR1a Cyclic adenosine
monophosphate-dependent
protein kinase A
PPM Permanent pacemaker

PR Pulmonary regurgitation
PS Pressure support
PVL Paravalvular leak
PVR Pulmonary vascular resistance
PVT Prosthetic valve thrombosis
PW Pulsed wave
qds Four times a day
RA Right atrium
RALES Randomized aldactone
evaluation study
RAO Right-anterior-oblique
RAP Right atrial pressure
RBBB Right bundle branch block
RBC Red blood cell
RCA Right coronary artery
RCRI Revised cardiac risk index
RCT Randomized controlled trials
RESPECT Randomized evaluation of
recurrent stroke comparing
PFO closure to established
current standard of care
RIFLE Risk, injury, failure, loss,
endstage renal disease (ESRD)
RLN Recurrent laryngeal nerve
RR Respiratory rate
RRT Renal replacement therapy
rtPA Recombinant tissue
plasminogen activator
RV Right ventricular
RVH

RVOT Right ventricular outflow tract
RVSP Right ventricular systolic
pressure
SAM Systolic anterior motion
SAP Serum amyloid P-component
SBP Spontaneous bacterial
peritonitis
SCD Sudden cardiac death
SCD-HeFT Sudden cardiac death in heart
failure trial
SEC Spontaneous echo contrast
SHOCK SHould we emergently
revascularize Occluded
Coronaries for cardiogenic
shock
SLE Systemic lupus erythematosus
SPECT Single photon emission
computed tomography
SpO2 Oxygen saturation
STEMI ST elevation myocardial
infarction
SVC Superior vena cava
SVR Systemic vascular resistance
SVT Supraventricular
tachyarrhythmia
TB Tuberculosis
TCPC Total cavopulmonary
connection
TGF Transforming growth factor
THR Total hip replacement

TIA Transient ischaemic attack
TIMI Thrombolysis in myocardial
infarction
TOE Transoesophageal
echocardiography
TOF Tetralogy of Fallot
TR Tricuspid regurgitation
TT Thrombin time
TTE Trans-thoracic
echocardiogram?
UA Unstable angina
UFH Unfractionated heparin
VA Ventriculoatrial
xiii
ABBREVIATIONS
VF Ventricular fibrillation
VLDL Very low density lipoprotein
VP Ventriculo-peritoneal
V/Q Ventilation/perfusion
VSD Venticular septal defect
VT Ventricular tachycardia
VTE Venous thrombo-embolism
VVI Single-chamber ventricular
demand
WBC White blood cell
WCC White cell count
WPW Wolff–Parkinson–White

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CASE 1

1
Case 1
A 79-year-old man with type II diabetes mellitus, New York Heart Association (NYHA)
class II–III heart failure, and a permanent pacemaker (PPM) presented to the
emergency department (ED) with a 3-week history of increasing shortness of breath.
His exercise tolerance had reduced and he also reported orthopnoea and paroxysmal
nocturnal dyspnoea. He denied chest pain, palpitations, or loss of consciousness. The
PPM had been implanted for complete heart block 7 years prior to this presentation.
Examination revealed a regular tachycardia (120 beats per minute (bpm)), blood
pressure (BP) 102/68 mmHg and a jugular venous pressure (JVP) that was visible
at his ear lobes sitting upright. On auscultation, a pansystolic murmur was audible
and coarse crackles consistent with pulmonary oedema were present in the mid and
lower zones bilaterally.
The admission electrocardiograph (ECG) is shown in Fig. 1.1 . The cardiology registrar
was asked to review the patient. Immediately after initiation of the appropriate
treatment the heart rate slowed and the patient’s breathlessness began to improve.
The ECG was then repeated (Fig. 1.2 ). Echocardiography demonstrated moderate to
severe impairment of left ventricular (LV) function and an estimated left ventricular
ejection fraction (LVEF) of 30 % .
CASE HISTORIES IN CARDIOLOGY
2
Fig. 1.2 ECG after treatment.
Fig. 1.1 ECG on admission.
CASE 1
3
Questions
1. Report the admission ECG shown in Fig. 1.1 .
2. Report the repeat ECG shown in Fig. 1.2 .
3. If the patient did not know the type of pacemaker that was implanted or the
manufacturer how could this information be obtained?

4. What was the cardiology registrar asked to do? What intervention was made?
5. What is the effect of placing a magnet over a PPM? Is the response different
with an implantable cardioverter defibrillator (ICD)?
6. How should the patient’s current arrhythmia be treated?
7. What are the chances of improvement in cardiac function?
CASE HISTORIES IN CARDIOLOGY
4
Answers
1 ) Report the admission ECG shown in Fig. 1.1 .
Figure 1.1 shows a broad complex tachycardia at a rate of 120 bpm with left axis
deviation. The pacing potential before each QRS complex suggests that this is a paced
tachycardia. The left bundle branch block (LBBB) pattern demonstrates that the
patient is being paced from the right ventricle. Atrial pacing potentials are not seen.
The fast ventricular response suggests an atrial wire is present with inappropriate
sensing and ventricular response.
There is a narrow complex fusion beat at the 14th paced complex on the rhythm
strip. This is conducted along the normal activation pathway. However, it is
followed by an inverted T wave. T-wave changes can be classified as primary or
secondary. Primary T-wave changes are caused by changes in the shape of the
action potential and may be due to ischaemia or electrolyte abnormalities.
Secondary T-wave changes are caused by alterations of the activation sequence
such as during ventricular pacing, intermittent LBBB, ventricular tachycardia,
ventricular extrasystoles, and ventricular pre-excitation. These secondary changes
can persist after the normal supraventricular activation pattern resumes. The
mechanism underlying this T-wave ‘memory’ is not yet understood.
2) Report the repeat ECG shown in Fig. 1.2 .
The ECG in Fig. 1.2 was recorded after the pacemaker was checked. It dem-
onstrates atrial fibrillation (AF) with a ventricular response rate of 72 bpm.
Ventricular pacing is initiated when the rate slows at end of the rhythm strip. The
period of pacing is followed by a fusion beat with normal conduction. The QRS

axis is normal. There is infero-lateral T-wave inversion. Although this could
represent myocardial ischaemia, persisting T-wave memory is more likely as his
pacemaker has recently been active.
3) If the patient did not know the type of pacemaker that was implanted or the
manufacturer how could this information be obtained?
Most patients will carry a card with information about their pacemaker. However,
if this is not available, the patient’s general practitioner (GP) or cardiologist should
be contacted as soon as possible. Examination of the surface ECG may reveal pac-
ing potentials and bundle branch block [usually LBBB morphology if the pacing
lead is located within the right ventricular (RV)] if the patient is paced. However,
this information may not be available if the patient is not pacemaker dependent.
A chest X-ray can reveal the type of pacemaker (single or dual chamber, biven-
tricular, ICD) and the manufacturer (logo visible by X-ray).
A pacemaker can be interrogated by the programmer provided by the manufac-
turer of that pacemaker. Most departments will have programmers for the most
commonly used makes (Medtronic, St Jude, Boston Scientific, and Biotronik). If
the manufacturer is not known, interrogation can be attempted with the program-
mers from each manufacturer until the correct one is found. The pacemaker
programmer performs several functions. It can assess battery status, modify pacing
CASE 1
5
settings, and access diagnostic information stored in the pacemaker (e.g. heart rate
trends and tachyarrhythmia recordings).
4) What was the cardiology registrar asked to do? What intervention was made?
A pacemaker should not pace at a rate of 120 bpm in a patient at rest. As malfunc-
tion was suspected, a cardiology registrar was asked to review the patient and
interrogate the pacemaker. Interrogation revealed that it was a functioning dual-
chamber device, with leads in the right atrium and ventricle, programmed to
an atrio-ventricular synchronising dual-chamber rate-responsive (DDDR) mode
(see Table 1.1 for the naming conventions of pacing modes). The electrocardio-

grams obtained from these endocardial leads demonstrated that the underlying
rhythm was AF. The AF sensed by the atrial lead was triggering the pacemaker,
which was pacing the ventricle at 120 bpm, the set upper rate limit.
The pacemaker should have automatically switched to a single-chamber ventricu-
lar demand (VVI) mode when the patient developed AF. However, the mode-
switching algorithm was disabled. When this algorithm was enabled the pacemaker
automatically switched to VVIR pacing and ignored the atrial lead inputs. This
slowed the heart rate. The previous pacemaker check had found paced sinus
rhythm only and so the initial programming error was not spotted.
Classification of cardiac pacemakers
The North American Society of Pacing and Electrophysiology (NASPE) and the British
Pacing and Electrophysiology Group (BPEG) have published a joint pacemaker code
(Table 1.1 ). The code was initially published in 1983 and was last revised in 2002. It
describes the five-letter code for operation of implantable pacemakers and defibrillators.
The first two positions of this code indicate the chambers paced and sensed. The
third position indicates the programmed response to a sensed event, which can be
either to inhibit further pacing or to trigger it. Of the most frequently used modes,
VVI is the simplest form, utilizing a single lead (V- -) that is able to sense ventricular
activity (- V -) and inhibit pacing if it is present (- - I) or pace at a set rate.
DDD offers maintenance of atrial and ventricular synchrony with two leads (A - - +
V - - = D - -) by allowing the atrial lead to sense intrinsic activity, inhibiting atrial pac-
ing (I) and triggering ventricular pacing (- - I + - - T = - - D) in the absence of sensed
ventricular activity. Rate responsiveness is achieved by ventricular tracking of atrial
activity. The fourth position, rate modulation, increases the patient’s heart rate in
response to patient exercise and is useful in dual-chamber mode when sinus node
dysfunction is present and with single-chamber ventricular pacing. A number of
parameters (such as QT interval, movement, blood temperature, chest wall impedence,
and pressure) are used to detect patient exercise. As the exercise wanes, the sensor
indicated rate returns to the programmed lower rate. The fifth position describes
multisite pacing functionality — ventricular multisite pacing is a treatment for heart

failure in the presence of dysynchonous LV contraction.
Dual-chamber pacing is desirable to optimize atrio-ventricular synchrony.
However, ventricular tracking of rapid atrial rates can occur during supraventricular
CASE HISTORIES IN CARDIOLOGY
6
tachyarrhythmias (SVT) if standard dual-chamber pacing modes are used. In the
early 1990s, the introduction of mode-switching algorithms allowed automatic switch-
ing from DDD to VVI, preventing inappropriate tracking of the atrial response. This
case emphasizes the importance of enabling automatic mode switching at implanta-
tion to ensure safe functioning, especially in patients with known paroxysmal AF
or SVT.
5) What is the effect of placing a magnet over a pacemaker? Is the response
different with an ICD?
Placing a magnet over the pacemaker pulse generator closes an internal magnet-
sensitive ‘reed switch’ but this was never intended for the management of pace-
maker emergencies. The response to switch closure varies between pacemaker
manufacturers, models, and programmed settings (magnet mode). Sensing is usu-
ally inhibited and the PPM is often set to pace in an asynchronous (non-sensing of
native electrical activity), fixed rate (‘magnet rate’), overdrive mode in either a
single- or dual-chamber configuration (VOO/DOO; see Table 1.1 ).
Importantly, this reprogramming response is not universal and is usually only
temporary (i.e. whilst the magnet is in situ ). Most models have unique asynchro-
nous rates set for the ‘beginning of life’, an ‘elective replacement indicator’, and the
‘end of life’. Hence, magnet placement can determine whether the battery needs
replacement. However, application of a magnet to a pacemaker with depleted
batteries may result in pacing output instability and could even stop pacing
output. Some possible responses to placement of a magnet and the corresponding
magnet modes are listed in Table 1.2 . Manufacturers can provide information on
the magnet modes of each model of pacemaker.
The response of ICDs differs from that of pacemakers. Some ICDs are temporarily

programmed to monitor-only mode (will not deliver a shock even if programmed
criteria are met) whilst the magnet remains in situ . Other ICDs will remain in
monitor-only mode permanently if activation of the reed switch is sustained for
> 25 seconds. This response depends on the magnet mode program of the device.
Table 1.1 NASPE/BPEG Revised in 2002 Pacemaker Code
Position I Position II Position III Position IV Position V
Chamber
paced
Chamber
sensed
Response to
sensed event
Programmability,
rate modulation
Multisite
pacing
O O O O
A A I A
V V T O V
D
(A & V)
D
(A & V)
D
(T & I)
R D
(A & V)
O, none; A, atrium; I, inhibited; V, ventricle; T, triggered; D, dual; R, rate modulation.
CASE 1
7

6) How should the patient’s current arrhythmia be treated?
If AF has persisted for over 48 hours, management must take into consideration
the risk of thromboembolism. If the onset cannot be determined, patients should
be managed as if the AF has been present for over 48 hours. This is discussed
further in Case 44.
7) What are the chances of improvement in cardiac function?
Tachycardia can induce changes in ventricular structure and function if persistent
and prolonged. Fortunately these changes may be reversed with rate or rhythm
control. The mechanisms responsible are unclear. However, once heart failure
develops, adrenergic stimulation could enhance the ventricular response, resulting
in a vicious cycle with further reduction of cardiac output and amplification of
cardiac failure. Improvement in LV function generally begins within days to weeks
after termination of the tachycardia and may continue over months.
In this case there was immediate symptomatic improvement, with further resolu-
tion over the next few months. An echo performed 3 months after presentation
demonstrated only mild impairment in LV function (EF 45 % ).
Further reading
Guidelines for cardiac pacing and cardiac resynchronization therapy ( 2007 ). The Task Force
for Cardiac Pacing and Cardiac Resynchronization Therapy of the European Society of
Cardiology . Eur Heart J ; 28 : 2256 – 2295 .
ACC/AHA/HRS ( 2008 ). Guidelines for Device-Based Therapy of Cardiac Rhythm
Abnormalities: A Report of the American College of Cardiology/American Heart
Association Task Force on Practice Guidelines . Circulation ; 117 : 350 – 408 .
Kaszala K , Huizar JF , Ellenbogen KA ( 2008 ). Contemporary pacemakers: what the primary
care physician needs to know . Mayo Clin Proc ; 83 : 1170 – 1186 .
Trohman RG , Kim MH , Pinski SL ( 2004 ). Cardiac pacing: the state of the art . Lancet ; 364 :
1701 – 1719 .
Rajappan , K ( 2009 ). Education in Heart: Permanent pacemaker implantation technique .
Heart ; Part I 95 : 259–264; Part II 95 : 334 – 342 .
Table 1.2 Pacemaker responses to magnet placement and magnet modes

i. Asynchronous high-rate
pacing (rate varies by
model)
a. Sustained
b. Brief (10–100 beats) burst then return to
standard program
ii.
No apparent rhythm
or rate change
a. No magnet sensor (no reed switch)
b. Magnet mode disabled
c. ECG storage mode enabled
d. Program rate pacing in already paced patient
e. Inappropriate monitor settings (pace filter on)
iii.
Continuous or transient
loss of pacing
Diagnostic threshold test mode
CASE HISTORIES IN CARDIOLOGY
8
Case 2
A 45-year-old male presented with shortness of breath and fast palpitations that
developed suddenly 1 hour prior to presentation. The admission ECG is shown in
Fig. 2.1 . Intravenous adenosine was administered whilst a rhythm strip was recorded
from lead V2 (Fig. 2.2 ).

Questions
1. What is the differential diagnosis of a broad complex tachycardia?
2. Report the findings in ECG Fig. 2.1 .
3. What are the contraindications to administration of adenosine?

4. Which drugs interact with adenosine?
5. How should adenosine be administered for the diagnosis or treatment of
an SVT?
6. What is the effect of adenosine on this arrhythmia? What is the mechanism of
this action?
7. What drugs should be avoided in this condition?
8. How should the patient be managed acutely?
9. What is the long-term management?
CASE 2
9
Fig. 2.1 12 lead ECG on admission.
Fig. 2.2 10-second rhythm strip recorded from lead V2 after administration of
adenosine.
CASE HISTORIES IN CARDIOLOGY
10
Answers
1 ) What is the differential diagnosis of a broad complex tachycardia?
Causes of broad complex QRS tachycardia may be of ventricular or supraven-
tricular origin and may be regular or irregular. See Cases 33–35, Table 2.1 , and
further discussion below for further discussion of broad complex tachycardia.
2) Report the findings in ECG Fig. 2.1
Fig. 2.1 shows a tachyarrhythmia. During the last 4 seconds of the rhythm strip
there is an irregularly irregular narrow complex tachycardia AF at a rate of approx-
imately 150 bpm. During this arrhythmia the QRS axis is probably normal.
The QRS complex of the single narrow complex capture beat in leads I and II is
predominantly positive. This part of the ECG demonstrates AF, which is
conducted via the atrioventricular node (AVN) to the ventricles.
Table 2.1 Causes of regular and irregular broad complex tachycardias
Supraventricular
Regular

SVT, AF, and AV nodal re-entry tachycardia with pre-existing or functional bundle branch
block

1
Orthodromic CMT with pre-existing or functional bundle branch block
Antidromic CMT with anterograde conduction via an accessory pathway and retrograde
conduction via AV node
SVT with conduction though an accessory pathway
Irregular
AF with bundle branch block with aberrant conduction (pre-existing or functional)
AF with pre-excitation
Ventricular
Regular
Monomorphic ventricular tachycardia

2
Fascicular tachycardia
Right ventricular outflow tract tachycardia
Paced ventricular rhythm
Irregular
Polymorphic ventricular tachycardia

1
CMTs are described in more detail below.

2
Fascicular tachycardia is an uncommon arrhythmia that originates around of the fascicles of the left
bundle branch (usually posterior) and propagates partly via Purkinje fibres. It is often misdiagnosed as an
SVT as the QRS complexes are relatively narrow (0.11–0.14 seconds). The QRS complexes have an RBBB
pattern with left axis deviation if it originates from the posterior fascicle but right axis deviation if the

anterior fascicle is the origin. Fascicular tachycardias are rare and generally do not respond to lignocaine
but can be terminated by intravenous verapamil.