Download presentation
Presentation is loading. Please wait.
1
Arrhythmia and Devices in HF
Dr Amirhossein Azhari Electrophysiologist
2
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.
3
Coupled PVCs
4
Multifocal PVCs
5
R-on-T Phenomenon: May cause a run of PVCs or Vfib
6
Vtach: 3 or more PVCs in a row
Wide QRS with a regular pattern and a rate of Patient will usually lose consciousness Treated with lidocaine; may help to have patient cough if they are still conscious May require DC shock
7
Vtach
8
Vtach Remember, 3 or more PVCs in a row is a run of Vtach
9
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
10
Vfib This is “coarse” vfib
11
Vfib This is “fine” vfib
12
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
13
Epidemiology of VA & SCD
Classification of Ventricular Arrhythmia by Electrocardiography Nonsustained ventricular tachycardia (VT) ♥ Monomorphic ♥ Polymorphic Sustained VT Bundle-branch re-entrant tachycardia Bidirectional VT Torsades de pointes Ventricular flutter Ventricular fibrillation
14
Nonsustained Monomorphic VT
15
Nonsustained LV VT
16
Sustained Monomorphic VT 72-year-old woman with CHD
17
Nonsustained Polymorphic VT
18
Sustained Polymorphic VT Exercise induced in patient with no structural heart disease
19
Bundle Branch Reentrant VT
20
Spontaneous conversion to NSR (12-lead ECG)
Ventricular Flutter Spontaneous conversion to NSR (12-lead ECG)
21
VF with Defibrillation (12-lead ECG)
22
Wide QRS Irregular Tachycardia: Atrial Fibrillation with antidromic conduction in patient with accessory pathway – Not VT
23
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
24
Epidemiology of VA & SCD
Incidence of Sudden Cardiac Death Reused with permission from Myerburg RJ, Kessler KM, Castellanos A. Circulation 1992;85:12-10.
25
Mechanisms and Substrates
Mechanisms of Sudden Cardiac Death in 157 Ambulatory Patients Ventricular fibrillation % Bradyarrhythmias (including advanced AV block and asystole) % Torsades de pointes % Primary VT - 8.3% Bayes de Luna et al. Am Heart J 1989;117:151–9.
26
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
27
Therapy Acute Hemodynamically Stable Hemodynamically UnStable
28
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
29
Non-antiarrhythmic Drugs
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
30
ICDs: Results from Primary and Secondary Prevention Trials
Therapies for VA ICDs: Results from Primary and Secondary Prevention Trials 0.6 0.8 1.0 1.2 1.4 MADIT-I AVID 1.6 0.4 CABG-Patch MADIT-II 1996 1997 2002 Aborted cardiac arrest N = 196 N = 1016 N = 900 N = 1232 0.46 0.62 1.07 0.69 Hazard ratio ICD better SCD-HeFT N = 1676 2005 0.77 1.8 LVEF, other features 0.35 or less, NSVT, EP positive 0.30 or less, prior MI 0.35 or less, LVD due to prior MI and NICM 0.35 or less, abnormal SAECG and scheduled for CABG CASH* 2000 N = 191 DEFINITE 2004 N = 458 0.65 0.35 or less, NICM and PVCs or NSVT CIDS N = 659 0.82 Aborted cardiac arrest or syncope DINAMIT N = 674 1.08 0.35 or less, MI within 6 to 40 days and impaired cardiac autonomic function Trial Name, Pub Year 0.83
31
Primary Prevention of SCD (1)
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
32
Primary Prevention of SCD (2)
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
33
Primary Prevention of SCD (3)
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
34
Primary Prevention of SCD (4)
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
35
Primary Prevention of SCD (5)
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
36
Primary Prevention of SCD (6)
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
37
Primary Prevention of SCD (7)
Therapies for VA Primary Prevention of SCD (7) LV dysfunction due to MI, LVEF ≤ %, 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
38
Primary Prevention of SCD (8)
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
39
Primary Prevention of SCD (9)
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
40
Primary Prevention of SCD (10)
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
41
Primary Prevention of SCD (11)
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
43
ICD Leads – Single versus Dual coil
44
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
45
Medtronic Implantable Defibrillators (1989-2001)
113 cc 209 cc 80 cc 80 cc 72 cc 54 cc 62 cc 39 cc 39.5 cc 49 cc 39.5 cc 39.5 cc 36 cc 39 cc
46
Detection VF Detection ! VF Therapy !! F F F F F F F F F F
47
Detection Fib Zone Analyse Detect Initiate Therapy Charge 1 2 3 4 5 6
7 8 9 10 11 12 Detect Initiate Therapy Charge
48
Rate Branch Calculation - Example
VT Detection: 8 intervals < 350 ms VT Detect 340 300 290 330 320 310 290 300 300 310 310 320 330 340 Median Ventricular Cycle Length = ( ) / 2 = 310 ms
49
ICD Therapies - ATP
50
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 As in previous devices, ATP is still available for the VT Zone (for 2 Zone configurations) and for VT-1 and VT-2 (for 3 Zone configurations). The change for Unity is that ATP is now available for Therapy 1and Therapy 2 in these Zones. Even though ATP is now available for more therapy options, the device still has hierarchal rules on what therapies will be available after each therapy is delivered. For example, if VT-1 is detected and ATP and CVRT therapies are all delivered for the VT-1 episode, if the rhythm accelerates to a VT-2 episode, the device will skip ATP therapies and deliver a CVRT shock that is greater than or equal to the last delivered shock. Note: All ATP therapies are considered equal in the hierarchy. An ATP delivery with 200 ms between each burst is not considered more aggressive than an ATP delivery with 400 ms between each burst. It is up to the clinician to program the ATP therapy 2 to be more aggressive than ATP therapy 1.
51
VT based on reentry
52
VT 1 sec
53
Proparly Timed Electrical Stimulation
54
ATP
55
ATP arrhythmia ATP Sinus rhythm 1 sec
58
ICD and CRT guidelines 2013 primary prevention
67
Electromagnetic Interference and Implantable Devices
68
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.
70
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).
72
Pacemaker and ICD Responses to Electromagnetic Interference
73
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
74
Sources of Electromagnetic
Interference in Daily Life
75
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..
76
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.
77
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.
78
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.
79
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
80
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
82
Operation with electrocutering surgery
84
Incidence of complications was low (0
Incidence of complications was low (0.8 cases per 100 years of surgical practice).
85
THE END
86
Thanks for your attention
Similar presentations
© 2025 SlidePlayer.com. Inc.
All rights reserved.