Download Arrhythmias and EKGs

Arrhythmia and Devices in
HF
Dr Amirhossein Azhari
Electrophysiologist
Premature Ventricular
Contractions (PVCs)
Irritable focus causes ventricles to depolarize before
the SA node fires
Premature beat that has a wide QRS
– QRS and T wave of a PVC usually point in opposite
direction from one another
“Bad PVCs” – more than 6/minute, coupled,
multifocal, and on or near the T wave of the previous
sinus beat
Suppressed by lidocaine.
Coupled PVCs
Multifocal PVCs
R-on-T Phenomenon: May
cause a run of PVCs or Vfib
Vtach: 3 or more PVCs in a
row
Wide QRS with a regular pattern and a rate of 150200
Patient will usually lose consciousness
Treated with lidocaine; may help to have patient
cough if they are still conscious
May require DC shock
Vtach
Vtach
Remember, 3 or more PVCs in a row is a run of Vtach
Vfib
Many ectopic foci firing at the same time
There is no regular pattern as in Vtach
No effective cardiac output!
Requires CPR and DC shock, ie,
Defibrillation
Vfib
This is “coarse” vfib
Vfib
This is “fine” vfib
Epidemiology of VA & SCD
Classification of Ventricular Arrhythmia
by Clinical Presentation
•Hemodynamically stable
♥ Asymptomatic
♥ Minimal symptoms, e.g., palpitations
•Hemodynamically unstable
♥ Presyncope
♥ Syncope
♥ Sudden cardiac death
♥ Sudden cardiac arrest
Epidemiology of VA & SCD
Classification of Ventricular Arrhythmia
by Electrocardiography
•Nonsustained ventricular tachycardia (VT)
♥ Monomorphic
♥ Polymorphic
•Sustained VT
♥ Monomorphic
♥ Polymorphic
•Bundle-branch re-entrant tachycardia
•Bidirectional VT
•Torsades de pointes
•Ventricular flutter
•Ventricular fibrillation
Nonsustained Monomorphic VT
Nonsustained LV VT
Sustained Monomorphic VT
72-year-old woman with CHD
Nonsustained Polymorphic VT
Sustained Polymorphic VT
Exercise induced in patient with no structural heart disease
Bundle Branch Reentrant VT
Ventricular Flutter
Spontaneous conversion to NSR (12-lead ECG)
VF with Defibrillation (12-lead ECG)
Wide QRS Irregular Tachycardia:
Atrial Fibrillation with antidromic conduction in patient
with accessory pathway – Not VT
Epidemiology of VA & SCD
Classification of Ventricular Arrhythmia
by Disease Entity
•Chronic coronary heart disease
•Heart failure
•Congenital heart disease
•Neurological disorders
•Structurally normal hearts
•Sudden infant death syndrome
•Cardiomyopathies
♥ Dilated cardiomyopathy
♥ Hypertrophic cardiomyopathy
♥ Arrhythmogenic right ventricular (RV)
cardiomyopathy
Epidemiology of VA & SCD
Incidence of Sudden Cardiac Death
Events
Incidence
General
population
High-risk
subgroups
Any prior
coronary event
EF<30% or
heart failure
MADIT II
Cardiac arrest
survivor
AVID, CIDS, CASH
Arrhythmia risk
markers, post MI
MADIT I, MUSTT
0
10
20
Percent
30
0
150,0000
SCD--HeFT
300,000
Absolute Number
Reused with permission from Myerburg RJ, Kessler KM, Castellanos A. Circulation 1992;85:12-10.
Mechanisms and Substrates
Mechanisms of Sudden Cardiac Death
in 157 Ambulatory Patients
• Ventricular fibrillation - 62.4%
• Bradyarrhythmias (including advanced AV block and
asystole) - 16.5%
• Torsades de pointes - 12.7%
• Primary VT - 8.3%
Bayes de Luna et al. Am Heart J 1989;117:151–9.
Clinical Presentations of Patients
with VA & SCD
•Asymptomatic individuals with or without electrocardiographic
abnormalities
•Persons with symptoms potentially attributable to ventricular
arrhythmias
♥ Palpitations
♥ Dyspnea
♥ Chest pain
♥ Syncope and presyncope
•VT that is hemodynamically stable
•VT that is not hemodynamically stable
•Cardiac arrest
♥ Asystolic (sinus arrest, atrioventricular block)
♥ VT
♥ Ventricular fibrillation (VF)
♥ Pulseless electrical activity
Therapy
Acute
Hemodynamically Stable
Hemodynamically UnStable
Therapies for VA
Antiarrhythmic Drugs
♥ Beta Blockers: Effectively suppress ventricular ectopic beats &
arrhythmias; reduce incidence of SCD
♥ Amiodarone: No definite survival benefit; some studies have shown
reduction in SCD in patients with LV dysfunction especially when
given in conjunction with BB. Has complex drug interactions and
many adverse side effects (pulmonary, hepatic, thyroid, cutaneous)
♥ Sotalol: Suppresses ventricular arrhythmias; is more pro-arrhythmic
than amiodarone, no survival benefit clearly shown
♥ Conclusions: Antiarrhythmic drugs (except for BB) should not be used
as primary therapy of VA and the prevention of SCD
Therapies for VA
Non-antiarrhythmic Drugs
♥ Electrolytes: magnesium and potassium administration can favorably
influence the electrical substrate involved in VA; are especially useful in
setting of hypomagnesemia and hypokalemia
♥ ACE inhibitors, angiotensin receptor blockers and aldosterone
blockers can improve the myocardial substrate through reverse
remodeling and thus reduce incidence of SCD
♥ Antithrombotic and antiplatelet agents: may reduce SCD by reducing
coronary thrombosis
♥ Statins: have been shown to reduce life-threatening VA in high-risk
patients with electrical instability
♥ n-3 Fatty acids: have anti-arrhythmic properties, but
conflicting data exist for the prevention of SCD
Therapies for VA
ICDs: Results from Primary and Secondary Prevention Trials
Hazard ratio
Trial Name, Pub Year
LVEF, other features
N = 196
MADIT-I
1996
0.35 or less, NSVT, EP
positive
0.46
AVID
1997
N = 1016
Aborted cardiac arrest
0.62
N = 900
CABG-Patch
1997
0.35 or less, abnormal
SAECG and scheduled for
CABG
1.07
N = 191
CASH*
2000
Aborted cardiac arrest
0.83
CIDS
2000
N = 659
Aborted cardiac arrest or
syncope
0.82
MADIT-II
2002
0.30 or less, prior MI
N = 1232
0.69
DEFINITE
2004
0.35 or less, NICM and
PVCs or NSVT
N = 458
0.35 or less, MI within 6 to 40
days and impaired cardiac
autonomic function
0.65
N = 674
DINAMIT
2004
1.08
0.35 or less, LVD due to prior
MI and NICM
N = 1676
SCD-HeFT
2005
0.77
0.4
0.6
ICD better
0.8
1.0
1.2
1.4
1.6
1.8
Therapies for VA
Primary Prevention of SCD (1)
Recommendations in previously published guidelines for prophylactic
ICD therapy based on LVEF are inconsistent:
♥ Different LVEFs were chosen for inclusion in trials
♥ Average EF in such trials was substantially lower than the cutoff
value for enrollment
♥ Subgroup analyses in various trials have not been consistent in
their implications
♥ No trials contained randomized patients with intermediate
LVEF
Therapies for VA
Primary Prevention of SCD (2)
♥ Because of these inconsistencies, the recommendations in this
guideline were constructed to apply to patients with an EF ≤ to a
range of values
♥ The next several slides compare the recommendations of
previously published guidelines with those in this one and the
reasoning behind the writing committee’s decision
Therapies for VA
Primary Prevention of SCD (3)
LV dysfunction due to MI, LVEF ≤ 30%, NYHA class II, III
•
•
•
•
•
2005 ACC/AHA HF: Class I; LOE B
2005 ESC HF: Class I; LOE A
2004 ACC/AHA STEMI: Class IIa; LOE B
2002 ACC/AHA/NASPE PM/ICD: Class IIa; LOE B
2006 ACC/AHA/ESC VA/SCD: Class I; LOE A
Note: The VA/SCD Guideline has combined all trials that enrolled patients
with LV dysfunction due to MI into one recommendation
Therapies for VA
Primary Prevention of SCD (4)
LV dysfunction due to MI, LVEF 30-35%, NYHA class II, III
•
•
•
•
•
2005 ACC/AHA HF: Class IIa; LOE B
2005 ESC HF: Class I; LOE A
2004 ACC/AHA STEMI: N/A
2002 ACC/AHA/NASPE PM/ICD: N/A
2006 ACC/AHA/ESC VA/SCD: Class I; LOE A
Note: The VA/SCD Guideline has combined all trials that enrolled patients
with LV dysfunction due to MI into one recommendation
Therapies for VA
Primary Prevention of SCD (5)
LV dysfunction due to MI, LVEF 30-40%, NSVT, positive EP
study
•
•
•
•
•
2005 ACC/AHA HF: N/A
2005 ESC HF: N/A
2004 ACC/AHA STEMI: Class I; LOE B
2002 ACC/AHA/NASPE PM/ICD: Class IIb; LOE B
2006 ACC/AHA/ESC VA/SCD: Class I; LOE A
Note: The VA/SCD Guideline has combined all trials that enrolled patients
with LV dysfunction due to MI into one recommendation
Therapies for VA
Primary Prevention of SCD (6)
LV dysfunction due to MI, LVEF ≤ 30%, NYHA class I
•
•
•
•
•
2005 ACC/AHA HF: Class IIa; LOE B
2005 ESC HF: N/A
2004 ACC/AHA STEMI: N/A
2002 ACC/AHA/NASPE PM/ICD: N/A
2006 ACC/AHA/ESC VA/SCD: Class IIa; LOE B
Note: The VA/SCD Guideline has expanded the range of LVEF ≤ 30-35% for
patients with LVD due to MI and NYHA class I into one recommendation
Therapies for VA
Primary Prevention of SCD (7)
LV dysfunction due to MI, LVEF ≤ 31-35%, NYHA class I
•
•
•
•
•
2005 ACC/AHA HF: N/A
2005 ESC HF: N/A
2004 ACC/AHA STEMI: N/A
2002 ACC/AHA/NASPE PM/ICD: N/A
2006 ACC/AHA/ESC VA/SCD: Class IIa; LOE B
Note: The VA/SCD Guideline has expanded the range of LVEF ≤ 30-35% for
patients with LVD due to MI and NYHA class I into one recommendation
Therapies for VA
Primary Prevention of SCD (8)
Nonischemic cardiomyopathy, LVEF ≤ 30%, NYHA class II, III
•
•
•
•
•
2005 ACC/AHA HF: Class I; LOE B
2005 ESC HF: Class I; LOE A
2004 ACC/AHA STEMI: N/A
2002 ACC/AHA/NASPE PM/ICD:N/A
2006 ACC/AHA/ESC VA/SCD: Class I; LOE B
Note: The VA/SCD Guideline has combined all trials of nonischemic
cardiomyopathy, NYHA class II, III into one recommendation
Therapies for VA
Primary Prevention of SCD (9)
Nonischemic cardiomyopathy, LVEF 30-35%, NYHA class II, III
•
•
•
•
•
2005 ACC/AHA HF: Class IIa; LOE B
2005 ESC HF: Class I; LOE A
2004 ACC/AHA STEMI: N/A
2002 ACC/AHA/NASPE PM/ICD:N/A
2006 ACC/AHA/ESC VA/SCD: Class I; LOE B
Note: The VA/SCD Guideline has combined all trials of nonischemic
cardiomyopathy, NYHA class II, III into one recommendation
Therapies for VA
Primary Prevention of SCD (10)
Nonischemic cardiomyopathy, LVEF ≤ 30%, NYHA class I
•
•
•
•
•
2005 ACC/AHA HF: Class IIb; LOE C
2005 ESC HF: N/A
2004 ACC/AHA STEMI: N/A
2002 ACC/AHA/NASPE PM/ICD:N/A
2006 ACC/AHA/ESC VA/SCD: Class IIb; LOE B
Note: The VA/SCD Guideline has expanded the range of LVEF to ≤ 30-35% for
patients with nonischemic cardiomyopathy and NYHA class I into one
recommendation
Therapies for VA
Primary Prevention of SCD (11)
Nonischemic cardiomyopathy, LVEF ≤ 31-35%, NYHA class I
•
•
•
•
•
2005 ACC/AHA HF: N/A
2005 ESC HF: N/A
2004 ACC/AHA STEMI: N/A
2002 ACC/AHA/NASPE PM/ICD: N/A
2006 ACC/AHA/ESC VA/SCD: Class IIb; LOE B
Note: The VA/SCD Guideline has expanded the range of LVEF to ≤ 30-35%
for patients with nonischemic cardiomyopathy and NYHA class I into one
recommendation
ICD Leads – Single versus Dual
coil
ICD History
The original AID device had two electrodes, one a spring was placed in
the Vena Cava, the other a cup designed to conform to the cardiac apex
1980
Medtronic Implantable Defibrillators (1989-2001)
209 cc
62 cc
113 cc
49 cc
39.5 cc
80 cc
39 cc
80 cc
39.5 cc
72 cc
39 cc
39.5 cc
54 cc
36 cc
Detection
F
F FF
FF
F
Detection
Fib Zone
1
Detect
2 3 4
5
6
Analyse
7 8 9
10 11 12
Initiate Therapy
Charge
Rate Branch Calculation - Example
VT Detection: 8 intervals < 350 ms
VT Detect
310
340
300
290
330
320
300
310
290
300
300
310
310
320
330
340
Median Ventricular Cycle Length
= (310 + 310) / 2
= 310 ms
ICD Therapies - ATP
ATP Definition
ATP = Antitachycardia Pacing
ATP = Therapeutic intervention using
standard bradycardia pacing algorithms
and energy levels in an effort to bring the
heart out of a reentrant tachycardia and
restore its normal rhythm
VT based on reentry
VT
1 sec
Proparly Timed Electrical Stimulation
ATP
ATP
arrhythmia
ATP
Sinus rhythm
1 sec
ICD and CRT guidelines
2013
primary prevention
Electromagnetic
Interference and
Implantable Devices
It is important to know not only what
sources of interference are of potential
concern, but also how external
interference actually affects pacemakers,
implantable cardioverter-defi brillators
(ICDs) and cardiac resynchronization
therapy (CRT) systems.
Electromagnetic fields have both an
electric field, measured in volts per meter
(V/m), and a magnetic field. The magnetic
flux density is measured in milliteslas
(mT).
Pacemaker and ICD Responses to
Electromagnetic Interference
The most frequent responses :
Inappropriate inhibition
triggering of pacemaker stimuli
reversion to asynchronous pacing
ICD tachyarrhythmia detection.
much less frequent:
Reprogramming of operating parameters
Permanent damage to the device circuitry
Electrode-tissue interface
Sources of Electromagnetic
Interference in Daily Life
Cellular Telephones and Other
Wireless
Communication Devices
Although isolated case reports have
suggested the potential for severe
interactions, most research indicates that
deleterious interactions are unlikely to
happen with normal cellphone use.
There was no clinically significant EMI
episodes when the telephone was placed
in the normal position over the ear..
Maintaining an activated cellphone at least 6
inches (15 cm) from the device prevents
interactions.
The FDA has issued simple
recommendations to minimize the risks:
Patients should avoid carrying their activated
cellphone in a breast or shirt pocket overlying
an implanted device.
A wireless telephone in use should be held
to the ear opposite the side where the device
is implanted.
Gates
No spurious detections occurred during a
10- to 15-second walk through the gates.
All of the patients with serious interactions
had an abdominal implant; however, by
multivariate analysis, diminished R-wave
amplitude and a Ventritex ICD were the
only predictors of interactions.
Metal Detectors
Handheld metal detectors typically operate
at a frequency of 10 to 100 kHz.
one report of a spurious ICD shock
triggered by a handheld metal detector in
an airport.
Guidant ICDs reverted to “monitor-only”
mode after being exposed to metal
detectors.
Current FDA recommendations state that it is safe
for patients with implanted cardiac devices to walk
through a metal detector gate, although the alarm
may be triggered by the generator case.
If scanning with a handheld metal detector is
needed, patients should ask the security
personnel not to hold the detector close to the
implanted device longer than is absolutely
necessary.
A manual personal search can also be requested
Direct Current Cardioversion
and Defibrillation
The risk of damage to the implanted
device depends:
on the amount of energy applied
the characteristics of the device and lead,
and the distance between the paddles or
pads and the pulse generator and leads
Operation with electrocutering
surgery
Incidence of complications was low (0.8
cases per 100 years of surgical
practice).
THE END
Thanks for your
attention