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Continuous
ECG
ICD
https://t.me/med1917
A simple 12- lead
disorders, particularly the arrhythmias, come and go and so may be missed at the
time of the
there are many ways of recording the electrical activity over a longer period:
Telemetry An inpatient wears
ECG
monitoring
ECG
only gives a snapshot of the heart’s electrical activities. Many
ECG
recording. If you feel you are missing a paroxysmal arrhythmia,
ECG
leads and the signals are shown on screens
being watched by sta. Thus, if a dangerous arrhythmia occurs, help is immediately available. This is very resource intensive so reserved for those at high risk of
dangerous arrhythmias, eg immediately post-
Exercise
Bruce on a treadmill) and the
s The patient exercises according to a standardized protocol (eg
BP
and
STEMI
.
ECG
are monitored, looking for ischaemic
changes, arrhythmias, and features suggestive of arrhythmia risk, such as
delta waves.
Holter monitors The patient wears an
24
h– 7d whilst they go about their normal life, and this is later analysed. These can
also be used to pick up
ST
changes suggestive of ischaemia.
ECG
monitor which records their rhythm for
Loop recorders These record any
detected arrhythmias, but can be
activated by patients to correlate
symptoms with recordings—
useful if the arrhythmia causes
loss of consciousness: the patient
can press the button when they
wake up. Loop recorders may be
implanted just under the skin (eg
®
or the newer, injectable
Reveal
™
LINQ
device), and are especially
useful in patients with infrequent
episodes as they can continually monitor for months or years
awaiting an event (
Pacemakers and
cord details of cardiac electrical
activity and device activity. This
information can be useful for
establishing an arrhythmic origin
for symptoms.
fig
3.30
s These re-
).
Fig 3.
30
This is a recording from a loop recorder, each
line follows on from the one above. This tracing was
recorded at the time of a syncopal episode, it shows
cardiac slowing then a
to cause syncope! But not long enough to arrange a
ECG
standard
Reproduced from Camm et al., ESC Textbook of
Cardiovascular Medicine,
15
, even if the patient were in hospital.
from Oxford University Press.
s pause: quite long enough
2009
, with permission
121
3 Cardiovascular medicine
Sinus node dysfunction
Sinus node dysfunction, formerly known as sick sinus syndrome, is usually caused
by sinus node fibrosis, typically in elderly patients. Other causes include medications
(eg digoxin, donepezil), toxins, or systemic conditions. The sinus node becomes dysfunctional, in some cases slowing to the point of sinus bradycardia or sinus pauses, in
others generating tachyarrhythmias such as
Symptoms Syncope, pre- syncope, light- headedness, palpitations,
Management
• Thro mboem bolis m prop hylaxis if episod es of AF are dete cted.
• Permanent pacemakers for patients with symptomatic bradycardia or sinus
pauses.
Some patients develop a ‘tachy brady syndrome’, suering from alternating
tachycardic and bradycardic rhythms. This can prove dicult to treat medically
as treating one circumstance (eg tachycardia) increases the risk from the other.
Pacing for bradycardic episodes in combination with rate- slowing medications for
tachycardic episodes may be required if the patient is symptomatic or unstable.
AF
an d atr ial t achy card ia.
SOB
.
3 Cardiovascular medicine
Narrow complex tachycardia
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122
Definition
Narrow
ECG
shows rate of >
QRS
complexes occur when the ventricles are depolarized via the normal
100
bpm and
QRS
complex duration of <
conduction pathways. The arrhythmia originates above or within the His bundle (ie
SVT
) (fig
3.32
a supraventricular tachycardia—
Dierential diagnosis Assess rhythm and P waves (if present— atrial rate, P- wave
morphology, relationship between atrial and ventricular rates, position of
cardiac cycle (short vs long
RP
interval)).
Regular narrow complex tachycardias See fig
).
3.33
.
Irregular narrow complex tachycardias
• Normal variant: sinus dysrhythmia (rate changes with inspiration/ expiration—
regularly irregular); sinus rhythm with frequent ectopic beats.
• Atrial fibrillation (AF)— no P waves present: p
• Atrial flutter with variable block: eg P– P– P–
The atrial rhythm is regular but the ventricular rhythm (hence pulse) is irregular.
• Multifocal atrial tachycardia: like focal atrial tachycardia but there are multiple
groups of atrial cells taking it in turns to initiate a cardiac cycle.
P- P
ology and
Principles of management See p
intervals vary. Usually associated with
791
If the patient is compromised, use DC cardioversion (p
• Identify and treat the underlying rhythm: eg treating sinus tachycardia secondary
to volume depletion with
COPD
by correcting hypoxia and hypercapnia; treating focal atrial tachycardia
to
secondary to digoxin toxicity with digoxin- specific antibody fragments; treating
AV
re- entry tachycardia (
amiodarone; for
• If AV nodal re- entry tachycardia (
ently blocking the
IV
fluids; treating multifocal sinus tachycardia secondary
AVRT
AF
and atrial flutter see p
AVN.
) secondary to
This should break the circuit of an atrioventricular re- entry
rhythm, allowing sinus rhythm to re- establish. If the underlying rhythm is actually
atrial in origin (eg flutter or atrial tachycardia),
rhythm but the paused ventricular activity will unmask the atrial rhythm (
aiding diagnosis and management.
1 Vagal manoeuvres: carotid sinus massage, Valsalva manoeuvre (eg blowing into
a syringe followed by supine repositioning with
45
° angle— this modified Valsalva is the most eective vagal manoeuvre).
at a
2 IV adenosine: see p
• In some cases, narrow complex tachyarrhythmias cause symptomatic episodes of
790
.
127
, fig
3.40
QRS– P– P– QRS
.
(3:1 block then 2:1 block).
COPD
.
.
754
WPW
with flecainide, propafenone, or
126
.
AVNRT)
or
AVRT
are suspected, consider transi-
AVN
blockade will not treat the
AVN
blockade can be achieved by:
15
seconds of passive leg raise
).
sucient severity and frequency to warrant more invasive treatment, eg ablation
therapy for accessory pathways.
120
P
wave in
P
- wave morph-
fig
3.31
ms.
),
32
Fig 3.
31
This patient was given adenosine for tachycardia thought to be due to
The adenosine has slowed the ventricular rate, revealing flutter waves (sawtooth appearance),
disproving an
AVRT/ AVNRT
Holiday heart syndrome
Binge drinking in a person without any clinical evidence of heart disease may
result in acute cardiac rhythm and/ or conduction disturbances, which is called
holiday heart syndrome (note that recreational use of cannabis may have
similar eects). The most common rhythm disorders are supraventricular
tachyarrhythmia and
heart disease who present with new- onset
The prognosis is excellent, especially in young patients without structural heart
disease. As holiday heart syndrome resolves rapidly by abstinence from alcohol
use, advise all patients against the excessive use of alcohol in future.
AVRT
or
AVNRT
diagnosis. Image courtesy of Dr Ed Burns, www.lifein thef astl ane.com
AF
(consider this diagnosis in patients without structural
AF
).
.
Normal conduction
AVRT
AVNRT
SVT
eft
anterior
and
posterior
hemi fascicle
AB
https://t.me/med1917
Normal conduction: initiated by the
SAN
sinoatrial node (
tivity spreads around the atria. The
atrioventricular node (
this activity, pauses, then passes it
), electrical ac-
AVN
on, down the bundle of His which
splits into left and right bundle
branches. These cause depolarization of the ventricular myocardium
from bottom (apex) to top (outflow
tracts).
Regular rhythm tachycardia
See fig
3.33
.
A. Sinus tachycardia Conduction oc-
fig
3.32
curs as per
but impulses are
initiated at a high frequency. Causes
include infection, pain, exercise, anxiety, volume depletion, bleed, systemic
vasodi lation (eg in sepsis), drugs (caffeine, nicotine, salbutamol), anaemia,
PE
, hyperthyroidism, pregnancy,
fever,
retention, autonomic neuropathy
CO
2
(eg inappropriate sinus tachycardia).
B. Focal atrial tachycardia A group
of atrial cells act as a pacemaker,
out- pacing the
ology (shape) is dierent to sinus.
Long
RP
interval.
SAN. P
- wave morph-
C. Atrial flutter Electrical activity circles the atria
‘sawtooth’ baseline, see
resulting in ventricular rates that are factors of
D. A trio ventric ular re- entry tachycardia (
Wol – Parkin son– White (
to pass to the resting atrial myocytes, creating a circuit: atria–
accessory pathway– atria. This direction is called ‘orthodromic’ conduction and
results in narrow
bundle of His. Conduction in the other direction is called ‘antidromic’ and results in
QRS
broad
QRS
complexes as ventricular depolarization is triggered via the
com plexes. No or re trograd e P wave a nd sho rt RP interva l.
E. Atrioventricular nodal re- entry tachycardia (
AVN
, causing narrow complex tachycardias with no or retrograde P wave and
the
RP
interval. This is very common.
short
F. Junctional tachycardia Cells in the
QRS
complexes as impulses reach the ventricles through the normal routes; P
waves may be inverted and late.
G.
with aberrancy Any of the above conditions can result in broad complex
tachycardias if there is bundle branch block (
H. Ventricular tachycardia (VT) This can result from circuits, similar to atrial
flutter, or from focuses of rapidly firing cells. The
is in action and its plane rotates, the
regularly increasing and decreasing amplitudes; this is called torsades de pointes.
) receives
fig
3.40
WPW
SAN
MV
His bundle
Left
bundle
branch
Fig 3.
32
Normal conduction.
AVN
TV
Right
bundle
branch
E
D
Fig 3.
33
Regular tachycardias.
300
, p
127
. The
AVN
), p
129
) allows electrical activity from the ventricles
AVN
become the pacemaker, giving narrow
ECG
shows broad complex tachycardia with
times per minute, giving a
passes some of these impulses on,
300 (150, 100, 75
) An accessory pathway (eg in
p92).
QRS
F
G
+
).
AVN
) Circuits form within
is broad. When a circuit
123
L
3 Cardiovascular medicine
C
H
– ventricles–
3 Cardiovascular medicine
Broad complex tachycardia
SVT
ICD
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124
Definition
plexes, it is
ECG
shows rate of >
VF
or asystole (or problems with the
Principles of management If the patient is unstable or you are uncertain of
what to do, get help fast— the patient may be peri- arrest (
• Identify the underlying rhythm and treat accordingly.
• If in doubt, treat as ventricular tachycardia (
• Giving
AVN
• If
blocking agents to treat
can cause dangerous haemodynamic instability. Treating for
is actually in
SVT
WPW
has less potential for deterioration.
is suspected, avoid drugs that slow AV conduction— see p
Dierential diagnosis Assess rhythm (irregular rhythm suggests AF with ab-
QRS
errancy),
ation present (in keeping with
especially
• Ventricular fibrillation— chaotic, no pattern, fig
•
VT,
• Torsades de pointes (polymorphic VT)— VT with varying axis (fig
VF
• Any cause of narrow complex tachycardias (p
bundle branch block or metabolic causes of broad
• Antidromic
axis (extreme axis deviation suggests VT), whether any AV dissoci-
CAD
, or arrhythmias.
fig
3.15
, p98; fig
3.35
. QT interval is a predisposing factor.
AVRT
(eg
Dierentiating VT from
help. Diagnosis is based on the history (
arrhythmia), a
ECG
findings in favour of VT:
• Fusion beats or capture beats (figs
• + ve or −ve
•
QRS
• Marked axis deviation, or ‘northwest axis’ (
• AV dissociation (
•
RSR
12
- lead
QRS
>
concordance in all chest leads (ie all + ve (R) or all −ve (QS)).
160
ms.
P
S independent of
’ pattern where R is taller than R’. (R’ taller than R suggests
Management See p
Implantable cardioverter defibrillator (
diac death in patients with prior sustained
MI
+
LVE F
eg prior
II– III
) +
≤30%, symptomatic HF (New York Heart Association (
LVE F
≤35% (despite 3mths of optimal medical therapy), certain high- risk
inherited arrhythmia syndromes. A combined
(cardiac resynchronization therapy- defibrillator (
duce mortality in patients with a
ICD
compl ications, p
129
itional transvenous
(eg those at high risk of systemic infection).
Ventr icul ar e xtrasys tole s (e ctop ics) These are common and can be
symptomatic— patients describe palpitations, a thumping sensation, or their
heart ‘missing a beat’. The pulse may feel irregular if there are frequent ectopics. On
or occur in patterns:
• Bigeminy: ectopic every other beat, see fig
• Trigeminy: every third beat is an ectopic.
• Couplet: two ectopics together.
• Triplet: three ectopics together.
ECG
, ventricular ectopics are broad
QRS
and so calculate the rate to be half the true value.
second
Occasional ventricular ectopics in otherwise healthy people are extremely common
and rarely significant. Frequent ectopics (>
should prompt testing for underlying cardiac conditions.
100
and
QRS
complexes >
SVT
with aberrancy when the patient is in VT
VT
), any known history of structural heart disease,
120
ECG
VT)
— the commonest cause.
ms. If no clear
machine or stickers).
p
788
).
VT
3.34
.
QRS
when the patient
106
.
.
3.36
), may look like
122
) when in combination with
QRS
WPW
), p
123
.
with aberrancy This may be dicult; seek expert
IHD
ECG
, and the response (or lack thereof) to certain medications.
789
. Helpful tests include
increases the likelihood of a ventricular
3.37, 3.38
).
QRS
QRS
S) or
2:1
QRS
≥
130
. An entirely subcutaneous
ICD
in patients in whom transvenous leads should be avoided
60
.
positive in aVR).
or 3:1 Mobitz II heart block.
RBBB.
U&E
, troponin,
CXR
)
.
) Used to prevent sudden car-
VT/ VF
or in those at high- risk of same,
ICD
and biventricular pacing device
CRT- D
ms with an
)) is recommended to re-
LVE F
ICD
QRS
complexes; they may be single
3.39
.
ECG
≤35% and
is an alternative to the trad-
machines may disregard the
LBBB
/ h), particularly couplets and triplets,
com-
NYHA
. See
)
Fig 3.
https://t.me/med1917
34
VF (p
878
125
).
Fig 3.
35
VT with a rate of
Fig 3.
36
Torsades de pointes tachycardia.
Fig 3.
37
A fusion beat (*)— a ‘normal beat’ fuses with a VT complex creating an unusual complex.
Fig 3.
38
A capture beat (*)— a normal
QRS
breadth were down to bundle branch block or metabolic causes.
235
/ min.
QRS
amongst runs of VT. This would not be expected if the
3 Cardiovascular medicine
Fig 3.
39
Bigeminy— a normal
tory pause, this pattern then repeats. The ectopic beats have the same morphology as each other
so probably all share an origin.
QRS
is followed by a ventricular ectopic beat (*) then a compensa-
3 Cardiovascular medicine
Atrial fibrillation (AF) and flutter
PAF
ECG
https://t.me/med1917
126
AF
33
is a chaotic, irregular atrial rhythm at
sponds intermittently, hence an irregular ventricular rhythm. Cardiac output drops
10– 20
% as the ventricles aren’t primed reliably by the atria. AF is common in the
by
9
elderly (≤
4
commended if >
%). The main risk is embolic stroke. Warfarin reduces this to 1%/ yr from
%. So, do an
ECG
on everyone with an irregular pulse (opportunistic screening re-
65
yr). If AF started more than 48h ago, intracardiac clots may have
formed, necessitating anticoagulation prior to cardioversion.
Causes Hypertension;
failure; pneumonia; hyperthyroidism; caeine; alcohol; post- op; K
Types Paroxysmal AF (
Long- standing persistent AF Lasts >12mths. Permanent AF Decision made not to
pursue rhythm control strategy.
Symptoms May be asymptomatic or cause chest pain, palpitations, dyspnoea, or
Signs Irregularly irregular pulse, the apical pulse rate is greater than the
faintness.
radial rate, and the
Examine the whole patient: AF is often associated with non- cardiac disease.
Tests
1
Shows absent P waves, irregular
cardiac enzymes, thyroid function tests.
tral valve disease, poor
ECG
may help diagnose
Managing acute AF
• If the patient has adverse signs (shock, myocardial ischaemia (chest pain or
changes), syncope, heart failure):
(synchronized shock, start at
delay treatment in order to start anticoagulation.
• If the patient is stable & AF started <48h ago: rate or rhythm control may be
tried. For rhythm control,
IHD
) or amiodarone. Start heparin in case cardioversion is delayed (see
ease,
‘Anticoagulation and
• If the patient is stable & AF started >48h ago or unclear time of onset: rate control
(eg with bisoprolol or diltiazem). If rhythm control is chosen, the patient must be
anticoagulated for >
• Correct electrolyte imbalances (K+ , Mg
monia); and consider anticoagulation (see
Managing chronic AF The m ain go als are rate co ntrol a nd ant icoag ulation. Rate con-
trol is at least as good as rhythm control,
• symptomatic or
if
corrected precipitant (eg
Rate control - blocker or rate- limiting Ca
LVE F
<40%. If this fails, add digoxin (p
if
CCF
monotherapy in chronic
blockers with verapamil. Aim for heart rate <
DC
cardioversion: do echo first to check for intracardiac thrombi. If there is risk of
cardioversion failure (past failure, or past recurrence) give amiodarone for
before the procedure and
flecainide is
amiodarone instead). In refractory cases,
1
st choice (CI if structural heart disease, eg scar tissue from MI: use IV
ablation, or the maze procedure may be considered.
(eg flecainide or propafenone
systolic, no past
LV
dysfunction. Anticoagulate (see
Consider ablation if symptomatic or frequent episodes.
Atrial flutter See p
control and the need for anticoagulation.
IV
amiodarone may be needed if rate control is proving dicult. Recurrence
version.
rates are high so ablat ion is often re commend ed for lo ng- term management.
300– 600
bpm (fig
3.40
); the AV node re-
IHD
(seen in 22% of MI patients); PE; mitral valve disease; heart
+
; Mg
2
+
.
) Intermittent. Persistent AF Fails to self- terminate in 7d.
‘Lone’ AF This means no cause found.
st heart sound is of variable intensity; signs of
QRS
complexes, fig
LVF
(p
3.40
. Blood tests
784
).
Echo To look for left atrial enlargement, mi-
LV
function, and other structural abnormalities. Ambulatory
PAF
or assess AF burden.
ABCDE
120– 150
DC
cardiovert or give flecainide (CI: structural heart dis-
AF
’).
3
wks first.
, get senior input DC cardioversion
J) ± amiodarone if unsuccessful (p
2
+
2
+
, Ca
); associated illnesses (eg MI, pneu-
BOX
‘Anticoagulation and AF’).
34
but rhythm control may be appropriate
791
); do not
• younger • presenting for 1st time with lone AF • AF from a
U&E
). Anticoagulation See
2
+
blocker are 1st choice. Avoid Ca
107
AF
is only acceptable in sedentary patients. Do not give -
12
months after. Elective pharmacological cardioversion
), then consider amiodarone. Digoxin as
AVN
BOX
‘Anticoagulation and AF’.
110
pm at rest. Rhythm control Elective
2
+
blocker
ablation with pacing, pulmonary vein
Paroxysmal AF ‘Pill in the pocket’
PRN
127
) may be tried if: infrequent AF, BP >
, fig
3.40
. Tre at me nt Similar to AF regarding rate/ rhythm
DC- CV
BOX
‘Anticoagulation and AF’).
is preferred to pharmacological cardio-
100
U&E
ECG
BOX
4
wks
mmHg
,
Anticoagulation and
(a)
(b)
(c)
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AF
Acute AF Use heparin until a full risk assessment for emboli (see below) is
AF
made— eg
48
>
4
+
trans oesophageal- guided cardioversion is an option if urgent cardioversion is required. Use a
(past ischaemic stroke,
arterial disease; evidence of valve disease or
unsure).
factors for emboli, and
structural heart disease, no previous recurrences, no sustained
started <48h ago and elective cardioversion is being planned. If
h, ensure ≥3wks of therapeutic anticoagulation before elective cardioversion
wks afterwards (in patients without long- term need for anticoagulation); NB:
DOAC
(eg apixaban) or warfarin (target
TIA
, or emboli; 75yrs with BP, DM; coronary or peripheral
35
Use no anticoagulation if stable sinus rhythm has been restored, no risk
AF
recurrence unlikely (ie no failed cardioversions, no
INR
2– 3) if high risk of emboli
LV
function/
CCF
— only do echo if
AF
for >1yr).
Chronic AF In all cases, the need for anticoagulation should be assessed using the
CHA2DS
-
VAS
c score to assess embolic stroke risk (consider anticoagulation if score
2
0
, >1), and balancing this against the risks of anticoagulation to the patient,
>
assessed with the
DOAC
(see p
346
) or warfarin.
HAS- BLED
score. Long- term anticoagulation should be with a
DOAC
S should be preferentially used except in the case
of mechanical heart valves or moderate– severe mitral stenosis where warfarin is
the anticoagulant of choice. Where anticoagulation is contraindicated due to high
bleeding risk etc., consider a left atrial appendage occlusion device.
CHA2DS2- VA S
65– 74
2
(
stroke risk of
HAS- BLED
predispose to bleeding (eg
hypertension
• liver disease • stroke history.
Pre- excited
In pre- excited AF, accessory pathways capable of conducting at rapid rates (eg
sometimes in
ventricles, unfiltered by the
>
c— Congestive cardiac failure (1 point), Hypertension (1), Age
yrs (1), Age >74yrs (2), Diabetes (1), previous Stroke/
TIA
/ thromboembolism
), Vascular disease (1), Sex Category (1 if female). A score of 2 = an annual
2.2
%. Online calculators can be helpful (eg www.mdc alc.com).
— 1 point for each of: • labile
INR
NSAID
• age >65 • use of medications that can
S, antiplatelets) • alcohol abuse • uncontrolled
• history of, or predisposition to, major bleeding • renal disease
AF
WPW
syndrome) pass erratic electrical activity from the atria to the
AVN. ECG
200
bpm. High risk of VT and VF.
S will show irregular, broad
QRS
complexes at
127
3 Cardiovascular medicine
†
†
***
*
Fig 3.
40
(a) AF: note the irregular spacing of
ventricular response (sometimes referred to as ‘fast
100
bpm. (c) Atrial flutter with 2:1 bl ock (2 P wav es (*) fo r ev ery 1
rate >
have the classic ‘sawtooth’ appearance. Alternate
QRS
com plexe s and l ack o f P wave s. (b) AF with a rapid
AF
’). No pattern to
P
wav es a re m erge d w ith the
QRS
complex spacing, and
QRS
co mpl ex (†) ). The P waves
QRS
co mpl ex.
3 Cardiovascular medicine
Pacemakers
PPM
S
O
CRT
ECG
https://t.me/med1917
128
In normal circumstances the
areas of myocardium will set the pace (see earlier in chapter). If the heart is not
pacing itself fast enough, artificial pacing may be required. Options include ‘percussion pacing’— fist strikes to the precordium, used only in peri- arrest situations;
transcutaneous pacing— electrical stimulation via defibrillator pads (
porary transvenous pacing (
pacemaker. Leadless pacemakers are a less invasive alternative for single ventricle
RV
only) pacing in patients in whom you wish to avoid transvenous pacing.
(
Indications for temporary cardiac pacing include
• Symptomatic bradycardia, unresponsive to atropine.
• After acute anterior MI, prophylactic pacing is required in:
• complete
• symptomatic Mobitz type
• Mobitz type
• non- adjacent bifascicular, or trifascicular block (p
• After inferior MI, pacing may not be needed in complete AV block if reasonably
stable, rate is >
• Suppression of drug- resistant tachyarrhythmias by overdrive pacing, eg
• Special situations: during general anaesthesia; during cardiac surgery; during elec-
trophysiological studies; drug overdose (eg digoxin, - blockers, verapamil).
See p
AV
blo ck
II AV
40– 50
760
for further details and insertion technique.
Indications for a permanent pacemaker (
• Complete AV block (Stokes– Adams attacks, asymptomatic, congenital).
• Mobitz type II AV block (p91).
• Persistent AV block after anterior MI.
• Symptomatic bradycardias (eg sinus node dysfunction, p
• Heart failure (cardiac resynchronization therapy).
• Drug- resistant tachyarrhythmias.
Pre- operative assessment Bloods
nula, consent, antibiotics as per local protocol.
Post- operative management Prior to discharge, check wound for bleeding or
haematoma; check lead positions and for pneumothorax on
function. During
1
st week, inspect for wound haematoma or dehiscence. The battery
needs changing every
Pacemaker letter codes These enable pacemaker identification (minimum is
3
letters):
• 1st letter the chamber paced (A= atria, V= ventricles, D= dual chamber).
• 2nd letter the chamber sensed (A= atria, V= ventricles, D= dual chamber, O= none).
• 3rd letter the pacemaker response (T= triggered, I= inhibited, D= dual).
• 4th letter (R= rate modulation, P= programmable, M= multiprogrammable).
• 5th letter (P means that in tachycardia the pacemaker will pace the patient.
means that in tachycardia the pacemaker shocks the patient. D= dual ability to
pace and shock.
= neither of these).
Cardiac resynchronization therapy (
diac contraction and reduces mortality
who have an ejection fraction <
biventricular pacing (both septal and lateral walls of the
atrial lead. It may be combined with a defibrillator (
of paced rhythms (fig
ECG
‘spike’ on the
. This spike can be very small with modern bipolar pacing systems.
Ventricular pacing usually has a broad
are usually programmed ‘on demand’ so will only pace when necessary. Modern
systems are generally very reliable but pacing spikes with no capture afterwards
suggests a problem. Programming of devices is complicated so seek help early if
concerned. Many pacemakers store intracardiac electrograms which can be accessed to correlate rhythm with any symptoms.
SAN
plays the role of pacemaker. On occasion, other
p
760
); and a subcutaneously implanted permanent
I AV
blo ck
, and
5– 10
blo ck (Wenc kebach )
QRS
complexes are narrow.
(FBC
, clotting screen, renal function), IV can-
years. For driving rules see p
) Improves the synchronization of car-
36
in people with symptomatic heart failure
35
% and a
3.16
, p99; fig
3.41
). Pacemaker input appears as a vertical
QRS
morphology (similar to
92
) include
QRS
duration >
CRT- D
p
754
).
SVT, VT
121
).
CXR
; check pacemaker
150
.
130
ms.37 It involves
LV
) and, if required, also an
).
LBBB
). Systems
); tem-
.
WPW
LQTS
ARVC
Fig 3.
https://t.me/med1917
41
ECG
of a paced rhythm.
Pacemaker/
ICD
complications
Peri- procedural (3– 6%)
• Bleeding.
• Infection— can be life- threatening; complete removal and antibiotics needed.
• Lead dislodgement.
• Pneumothorax.
• Cardiac perforation.
• Death (rarely).
Long- term
• Infection.
• Lead failure (resulting in failure to pace/ shock or inappropriate shocks).
• Tricuspid valve damage.
• Venous thrombosis.
• Pacing/ defibrillation thresholds.
• Device and/ or lead migration or fracture.
Congenital arrhythmogenic cardiac conditions
As well as the many acquired conditions that can predispose to arrhythmias
p
121
), there are a number of congenital conditions. These may be clinically silent
(
until a fatal attack and are likely to be responsible for most cases of sudden arrhythmic death syndrome (
syndrome (Wol– Parkinson– White; fig
sory conduction pathway between atria and ventricles. Resting
PR
interval, wide
changes. Two types:
V
). Tachycardia can be due to an
in
1
Management may include ablation of the accessory pathway.
(Long QT syndromes.) These are channelopathies that result in prolonged
repolarization phases, predisposing the patient to ventricular arrhythmias; classically torsades de pointes.
and Lange- Nielsen syndrome (
(Arrhythmogenic right ventricular cardiomyopathy.)
placed with fibro- fatty material. Symptoms: palpitations and syncope during ex-
ECG
changes include epsilon wave; T inversion and broad
ercise.
SADS
). They include:
3.42
.) Caused by congenital acces-
QRS
complex (due to slurred upstroke or ‘delta wave’) and ST– T
WPW
type A (+ ve δ wave in
AVRT
p
788
. Conditions associated with
p
690
) and Romano– Ward syndrome (p
V
),
1
or pre- excited
ECG
shows short
WPW
type B (−ve δ wave
AF/
atrial flutter (p
LQTS
include Jervell
696
RV
myocardium is re-
QRS
in
V
–
1
Brugada Sodium channelopathy. Diagnosis: classic coved ST elevation in
ECG
suggestive clinical history.
fever, medications (
www.bruga dadr ugs.org), electrolyte imbalances, and ischaemia.
Many of these patients can be treated medically or conservatively but those at
high risk may require an implantable cardiac defibrillator (
members is important for picking up undiagnosed cases.
changes and arrhythmias can be precipitated by
ICD
). Screening family
129
3 Cardiovascular medicine
126
).
).
V
.
3
V
–
V
plus
1
3
Fig 3.
42
This patient has Wol– Parkinson– White syndrome as they have delta waves (slurred
QRS
upstrokes) in beats 1 and 4 of this rhythm strip. The delta wave both broadens the ventricular
complex and shortens the
diltiazem, verapamil, and digoxin— but procainamide, ibutilide, or flecainide may be used.
PR
interval. If a patient with
WPW
has AF, avoid AV node blockers such as
3 Cardiovascular medicine
Diseases of heart muscle
DCM
HCM
https://t.me/med1917
130
Acute myocarditis This is inflammation of myocardium, often associated with
pericardial inflammation (myopericarditis).
ACS
- like symptoms, heart failure symptoms, palpitations, tachycardia, soft
signs
p44). Tes t s
gallop (
AV
block, QT prolongation. Bloods:
and tests for other likely causes. Echo: diastolic dysfunction, regional wall abnormalities. Cardiac
Supportive. Treat the underlying cause, dysrhythmias, and heart failure (
NSAID
S, heavy alcohol, and exercise as these can precipitate dysrhythmias and se-
Prognosis 50% will recover within 4wks. 12– 25% will develop
verity.
heart failure.
ECG: ST
MR
if clinically stable. Endomyocardial biopsy is gold standard.
DCM
can occur y ears after appare nt recovery.
Dilated cardiomyopathy (
both ventricles. Associations: alcohol,
viral infection, autoimmune, pregnancy, thyrotoxicosis, genetic (
Prevalence 0.2%. Presentation Fatigue, dyspnoea, pulmonary oedema,
cases).
AF, VT
emboli,
tricuspid regurgitation (
ascites.
. Signs Pulse, BP,
Tests Blood:
pulmonary oedema.
progression. Echo: Globally dilated hypokinetic heart and low ejection fraction.
MR, TR, LV
Look for
biventricular pacing,
mural thrombus. Diuretics, - blockers,
Hypertrophic cardiomyopathy (
asymmetric septal hypertrophy.
the young.
70
present at any age. Ask about family history of sudden death.
Sudden death may be the first manifestation of
able to implantable defibrillators), angina, dyspnoea, palpitation, syncope,
pulse; a wave in
Prevalence 0.2%. Autosomal dominant inheritance, but 50% are sporadic.
% have mutations in genes encoding - myosin, - tropomyosin, and troponin T. May
JVP
; double- apex beat; systolic thrill at lower left sternal edge; harsh
ejection systolic murmur.
(inferior + lateral lead s);
septal hypertrophy; small
closure of aortic valve; systolic anterior movement of mitral valve.
p
101
. • Cardiac catheterization helps assess: severity of gradient; coronary artery dis-
ease or mitral regurgitation, but may provoke
be needed (eg if
- blockers or verapamil for symptoms (the aim is reducing ventricular contractility).
Amiodarone (
temic emboli. Septal myomectomy (surgical or chemical (with alcohol) to
tract gradient) is reserved for those with severe symptoms. Consider
www.doc 2do.com/ hcm/ web HCM.html
5.9
%/ yr if <14yrs; 2.5%/ yr if >14yrs. Poor prognostic factors: age <14yrs or syncope at
WPW,
p
130
) for arrhythmias (
presentation; family history of
Restrictive cardiomyopathy Causes Idiopathic; amyloidosis; haemochroma-
tosis; sarcoidosis; scleroderma; Löer’s eosinophilic endocarditis; endomyocardial
Presentation Is like constrictive pericarditis (p
fibrosis.
dominate:
Diagnosis
JVP
, with prominent x and y descents; hepatomegaly; oedema; ascites.
BNP
, echo,
Cardiac myxoma (figs
2:1
. Usually sporadic, but may be familial (Carney complex: cardiac and cu-
: ≈
taneous myxomas, skin pigmentation, endocrinopathy, etc.,
infective endocarditis (fever, weight loss, clubbing,
stenosis (left atrial obstruction,
according to posture.
Causes See table
3.2
. Symptoms and
ch ange s an d T- wave inversion, atrial arrhythmias, transient
CRP, ESR
, & troponin may be raised; viral serology
p
136
DCM
and severe
) Dilatation and impaired contraction of one or
BP
, chemotherapeutics, haemochromatosis,
JVP
MR/ TR)
BNP
(p
ECG:
Tachycardia, non- specific T- wave changes, poor R- wave
ICD
S,
, displaced and diuse apex,
, pleural eusion, oedema, jaundice, hepatomegaly,
134
), Na+ indicates a poor prognosis.
LVAD
S, transplantation. Mortality Variable, eg
) LV outflow tract (
HCM
is the leading cause of sudden cardiac death in
50
% of 'idiopathic'
S
gallop, mitral or
3
CXR
: cardiomegaly,
ACE
- i, anticoagulation,
40
LVOT
) obstruction from
Symptoms and signs
HCM
in many patients (VF is amen-
Te st s •
ECG: LVH
AF; WPW
LV
cavity with hypercontractile posterior wall; mid- systolic
p
129). • Exercise test ± Holter monitor (p
; progressive T- wave inversion; deep Q waves
(p
129
); ventricular ectopics;
VT.
• Electrophysiological studies may
AF, VT
). Anticoagulate for paroxysmal AF or sys-
VT.
• Echo: asymmetrical
121
•
MRI
: see fig
) to risk stratify.
LV
ICD
— use http://
to assess risk of sudden cardiac death. Mortality
HCM
/ sudden death.
132
). Features of
MRI
, cardiac catheterization. Treat the cause.
3.43, 3.44
) Rare benign cardiac tumour. Prevalence ≤5/ 10
p
217
). It may mimic
AF
Tests Echo. Resection.
). A ‘tumour plop’ may be heard, and signs may vary
ESR,
systemic emboli), or mitral
S
). Avoid
RVF
% in 2yrs.
CCF
. Jerky
3.19
outflow
RVF
pre-
000
,
S
1
3
,
,
,
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