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AICD and Pacemaker Update Kathryn Gray CRNA. Excitability: The ability of a cell to respond to a stimulus by depolarizing and propagating an action potential.

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Presentation on theme: "AICD and Pacemaker Update Kathryn Gray CRNA. Excitability: The ability of a cell to respond to a stimulus by depolarizing and propagating an action potential."— Presentation transcript:

1 AICD and Pacemaker Update Kathryn Gray CRNA

2 Excitability: The ability of a cell to respond to a stimulus by depolarizing and propagating an action potential Depolarization: Occurs when there is a decrease in the polarity across a cell membrane. Hyperpolarization: Occurs when there is an increase in the polarity across a cell membrane. Conductivity: The ability of a cell to transmit action potentials to adjacent cells. Rhythmicity: The ability of cells to generate automatic action potentials. Terminology:

3 Cardiac Anatomy and myocardial conduction

4

5 Where it all begins…………

6 Lets get nerdy…  This equation is used to define the electrical gradient across a membrane based on ion concentrations  This can be applied to cardiac myocytes which helps to explain the ion potentials during AP propagation and RMP. Ion[Intracellul ar] [Extracellula r] Equilibrium potential (Em) Sodium10 mM145 mM60 mV Potassium135 mM 4 mM-94 mV Chloride5 mM120 mM-97 mV Calcium mM 2 mM132 mV

7 Nernst Equation Em= (-RT/zF) X log [K] i /[K] o Em is the equilibrium potential of the ion based on transmembrane concentrations. R-universal gas constant ( JXK -1 ) T- absolute temperature ( degrees kelvin) [K]i- potassium concentration on the inside of the cell [K]o-potassium concentration on the outside of the cell. z- the number of electric charges carried by a single potassium ion F- the Faraday constant ( X10 4 cmol -1 ) Paging Dr. Nernst

8 Lets get really nerdy…  The Goldman-Hodgkin-Katz equation accounts for the ionic potentials of multiple ions across a cell membrane.  EMF= 61.5 X log([Na] i P Na +[K] i P K +[Cl] o P Cl ) ([Na] o P Na +[K] o P K +[Cl i P Cl )

9 The SA node is made up of specialized cardiac muscle cells which do not have contractile abilities. The SA node is the primary pacemaker in the cardiac conduction system. It’s intrinsic rate is faster than the other latent pacemakers in the heart and thus overrides them. It’s automaticity and intrinsic rate is dependant upon *calcium leak channels in the sarcoplasmic reticulum. The Sinoatrial Node

10 At the cellular level

11 SA Node conduction

12 This is a portion of the heart with a more rapid rate than the sinus node. Also occurs when transmission from the SA node to A-V node is blocked (A-V block). During sudden onset of A-V block, sinus node impulses do not get through, and next fastest area of discharge becomes pacemaker of heart beat. Delay in pickup of the heart beat is called “Stokes- Adams” syndrome. The new pacemaker is in A-V node or penetrating part of A-V bundle. Ectopic Pacemakers

13 AV node  The AV node contains highly specialized tissue that slows impulse conduction considerably thereby allowing sufficient time for complete atrial depolarization and contraction prior to ventricular depolarization and contraction.

14 Purkinje Fibers  Located in the inner ventricular walls of the heart, just beneath the endocardium.  The Purkinje fibers have the fastest conduction speed of any fibers in the heart.

15 The ventricles Normal ventricular RMP is -80 to -90mV Action potential is accelerated once threshold is reached by the opening of fast Na channels and slow Ca channels.

16 Putting it all together

17 Depolarization during a cardiac cycle

18 Excitation Contraction Coupling

19 The result…….

20 Innervation of the heart  Releases norepinephrine at sympathetic ending  Causes increased sinus node firing rate  Increases rate of conduction impulse  Increases force of contraction in atria and ventricles  Parasympathetic (vagal) nerves,  Release acetylcholine at their endings  innervate S-A node and A-V junctional fibers  Causes hyperpolarization because of increased K + permeability in response to acetylcholine  Muscarinic Acetylcholine Receptors, when stimulated cause decreased heart rate Sympathetic Parasympathetic

21 CNS control of Heart rate

22 Autonomic effects on CO

23 Causes of cardiac dysfunction  Temperature extremes  pH imbalances  Hypo or Hypercalcemia  Malnutrition, cachexia  Hypoxia/Ischemia  Hypo or hyperkalemia  Autonomic imbalances  Hypo or hypercarbia  Magnesium deficiency  Drug toxicity and adverse drug reactions  Stress and catecholamine release  CAD  HTN  Dilated myopathy  Morbid obesity  Advanced age  CHF  Chronic lung disease and subsequent cor pulmonale  Endocrine imbalance  Hypertropic myopathy  Sick sinus syndrome  Increased ICP  Renal disease Physiologic Imbalances Associated Co-motbidities

24 Types of conduction disruptions  - Atrial Fibrillation  - Atrial Flutter  - 1 st degree heart block  - 2 nd degree heart block  - 3 rd degree heart block  - Ventricular fibrillation  - Ventricular tachycardia  - Re-entry arrhythmias

25 The Solution:

26 And the beat goes on….

27

28 Pacemaker coding system Chamber Paced Chamber Sensed Response to Sensing Programmability Antiarrhythmia Function A=Atrium T=TriggeredP=Simple C=Communic ating P=Pacing V=Ventricles I=InhibitedR=Rate modulation S=Shock D=Dual Both atria and ventrical D=Dual Both atria and ventrical D=Dual Both triggered and inhibited M=Multiprogra m D=Dual Both pacing and shock O=None

29 Who gets what? CODEWhat is it?Who gets it? AOOAtrial pace, no sense no inhibitions SSS with intact conduction in the OR with bovie AAIAtrial pace, atrial sense, inhibition by the atrium SSS with intact conduction system VOOVentricular pace, no sense no inhibition Third degree heart block in OR with atrial fibrillation VVIVentricular pace, ventricular sense and ventricular inhibition Third degree heart block with atrial fibrillation DOODual pace, no sense no inhibitions Third degree heart block in OR with bovie DVIDual pace, ventricular sense, ventricular inhibition Third degree heart block with SVT DDDDual pace, dual sense dual inhibit Third degree heart block

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31 The name is Bond, James Bond

32

33 This is a schematic of how each pacemaker will affect the EKG depending on the intrinsic beat and pacemaker mode

34 Rate Responsive Pacemakers  Rate-Responsive Direct metabolic sensors:  1. Mixed Venous O2 saturation  2. Central venous pH  In-Direct metabolic sensors:  1. Ventilation rate  2. Mixed Venous Temperature  Non-Metabolic Physiological sensors  1. QT interval  2. Ventricular Depolarization Gradient  3. Stroke Volume  4. Mean Arterial Blood Pressure  Direct Activity sensors  1. Motion detection

35 Pacemaker effects on CO

36 Anesthesia and in situ pacemakers  Electromagnetic interference is always a problem when taking a person into the OR for a surgical procedure.  Increase in Pacemaker threshold with some drugs in the OR setting.  Physiologic alterations can change pacemaker function.

37 Questions you need to ask before going into the OR  What is the device?  What brand and model?  Does your hospital have a programmer for this make and model?  What is the magnet mode?  Why does the patient have a pacemaker?  What rhythm does the patient have when the pacemaker is shut off?  When was the last time it was interrogated?  How long has it been since the battery has been changed?

38 AICD’s

39 Indications for AICD insertion Common indications for AICD implantation Class I indicationsClass II indications History of prior MI LVEF < 35% & NYHA class II/III LVEF <30% & NYHA class I Hemodynamically unstable History of VF and VT inducible in the EP lab LVEF < 30% or 35% & NYHA class I Recurrent VF and normal LVEF Chronic myocarditis, pericardial disease, hypertrophic or infiltrative cardiomyopathy History of spontaneous, sustained VF/VT associated with primary pathology Non-iscemic dilated cardiomyopathy History of sustained VF/VT and significant LV dysfunction Unexplained syncope & LV dysfunction Reccurrent VF/VT normal LVEF Hyoertrophic cardiomyopathy History of documented VT/VF

40  What do you do when your patient has an existing pacemaker or AICD?

41 Questions to ask the patient : Why do they have an AICD? How long have they had it? Who is the manufacturer? When was the last time it was interrogated? When was the last time they received an AICD shock? How often do they get shocked? Anesthesia for patients with AICD’s

42

43 Danger in the O.R.

44 Electrocautery  Bipolar vs Unipolar  Why do we need a grounding pad?  Why are we afraid of bovie with pacemakers and AICD’s?

45 Electromagnetic interference in the O.R.  Electrocautery  MRI  ESWL  Defibrillation  Motor evoked potentials  Nerve stimulators

46 Oversensing  Cause  Insulation breach  Bipolar impedance

47 Pacemaker oversensing

48 Pacemaker undersensing

49 Failure to capture

50 Innapropriate AICD shock

51 The Magic Magnet  The magnet IS NOT magical!!!  Don’t be lured in to a false sense of security of “I’ll just put a magnet on it” to fix any problems.

52 Magnet Mode  The pacemaker mode temporarily switches to VOO in single chamber devices and DOO in dual chamber devices.  Asynchronous pacing delivers output regardless of intrinsic activity  Pacing rate will be 85 bpm for pacemaker battery levels above ERI (elective replacement indicator) and 65 bpm for battery levels below ERI*  When the magnet is removed, the previously programmed mode returns*  Use when:  Checking pacemaker battery level  EMI is present (surgery, TENS, etc.)  Device troubleshooting (breaking a PMT, assessing capture, etc.) What happens when a magnet is applied over a pacemaker?

53 Magnet Mode  What happens when a magnet is placed over an AICD?  If the patient is not pacemaker dependant….  If the patient is pacemaker dependant…

54 So what are the recommendations?  De-fasciculation prior to succinylcholine is recommended if the patient has a RR pacemaker  Question the use of Nitrous if the pacemaker is new  Inhalation agents and propofol do not affect pacing thresholds.  What other monitors do I need?  YOU DO NOT ALWAYS NEED TO TURN OFF THE AICD OR PACEMAKER!

55 Recommendations  Atropine should be close at hand if the patient should have severe bradycardia.  A patient with an AICD or pacemaker should NEVER be sent home without the device being interrogated by a representative of the device’s company if a magnet has been used.  What about ACLS with AICD’s and pacemakers?

56 Recommendations:  Perioperative management of these patients should be individualized.  The best type of anesthesia for the patient with an AICD or pacemaker depends on the type of surgery and the patient’s co-morbidities  Bipolar is better  If using monopolar cautery, place pad close to incision site and keep bursts to less than 5 seconds.  Cardioversion will reset the device  If below the umbilicus the risk of EMI is very low with a pacemaker.  Surgery below the umbilicus in the patient with an AICD may still create risk of innapropriate shock.

57 Recommendations  All volatile anesthetics depress cardiac contractility by decreasing calcium into cells during depolarization  NEVER TURN OFF A PACEMAKER OR AICD WITHOUT HAVING THE PATIENT HOOKED UP TO EXTERNAL PACING/DEFIBRILLATION PADS!!!!  Important phone numbers  Biotronik  Boston Scientific  Sorin Ela  Medtronic  St. Jude Medical

58 Preoperative Recommendations:  All patients with pacemakers undergoing elective surgery should have had a device check as part of routine care within the past 12 months that identifies the required elements specified below.  All patients with ICDs undergoing elective surgery should have had a device check as part of routine care within the past 6 months.

59 Emergency recommendations  Identify the type of device  Determine if the patient is pacing  Pacemaker dependent — Yes: pacemaker (not ICD) — Yes: ICD and pacemaker — No: pacemaker (not ICD) — No: ICD and pacemaker  What if I need a central line?

60 Procedure specific recommendations  Monopolar electrosurgery CIED evaluated within 1 month from procedure  External cardioversion CIED evaluated prior to discharge or transfer from cardiac telemetry  Radiofrequency ablation CIED evaluated# prior to discharge or transfer from cardiac telemetry  Electroconvulsive therapy CIED evaluated# within 1 month from procedure unless fulfilling Table 9 criteria  Nerve conduction studies (EMG) No additional CIED evaluation beyond routine  Ocular procedures No additional CIED evaluation beyond routine  Therapeutic radiation CIED evaluated prior to discharge or transfer from cardiac telemetry; remote monitoring optimal;  some instances may indicate interrogation after each treatment (see text)  TUNA/TURP No additional CIED evaluation beyond routine  Hysteroscopic ablation No additional CIED evaluation beyond routine  Lithotripsy CIED evaluated# within 1 month from procedure unless fulfilling Table 9 criteria  Endoscopy No additional CIED evaluation beyond routine  Xray/CT scans/mammography No additional CIED evaluation beyond routine  #This evaluation is intended to reveal electrical reset. Therefore, an interrogation alone is needed. This can be accomplished in person or by remote

61 Pacemaker and AICD policy  Each facility should have a pacemaker and AICD policy. You should find and become familiar with yours.  When dealing with patients who have pacemakers or AICD’s, please use these policies to guide you since these are what you will be measured by if there are any problems.

62 References:  Atlee, J.L. (1996). Arrhythmias and pacemakers: Practical management for anesthesia and critical care medicine.Philadelphia,Pennsylvania:W.B. Saunders.  Björn, C.K., Roden, D.M. (2008). Genetic framework for improving arrhythmia therapy. Nature, 451,  Burns, E. (2013). Pacemaker malfunction. Retrieved on August 12 th, 2013 from  Byong, J.,Mashahiro, O., shien-Fong, L.,Peng- Sheng, C. (2009). The Calcium and Voltage Clocks in Sinoatrial Node Automaticit. Korean circulation journal. June; 39(6): 217–222.  Charney, W. (1999). Handbook of modern hospital safety. Philadelphia, Pennsylvania: Elsevier-Mosby.  Crossley, G. et al. (2011). The heart rhythm society, american society of anesthesiologist expert consensus statement on the perioperative management of patients with implantable defibrillators, pacemakers and arrhythmia monitors: Heart Rhythm Society.  Ellenbogen, K.A., Kay, G.N., Wilkoff, B.L. (2000). Clinical cardiac pacing and defibrillaiton.Philadelphia,Pennsylvania: W.B.Saunders.  Estafanous,F.G., Barash, P.G., Reves, J.G. (2001). Cardiac anesthesia principals and clinical practice(2 nd ed.). Philadelphia,Pennsylvania: Lippincot-Williams and Wilkins.  Faust, R.J. et al.(2002). Anesthesiology review (3 rd ed.). Philadelphia, Pennsylvania: Reed-Elsevier.  Greenburg, M.L. (2008). Catheter ablation. Retrieved October 16 th, 2009 from  Guyton, A.C.,Hall, A.C.(2006).Textbook of medical physiology (11 th ed.). Philadelphia, Pennsylvania: Elsevier- Saunders.  Hines, R.L., Marschall, K.E. (2008). Stoelting’s anesthesia and co-existing diseases (5 th ed.). Philadelphia, Pennsylvania: Elsevier-Saunders.  Klabunde, R.E. (2009). Cardiovacular physiology concepts. Ohio University. Retrieved on September 26 th,  Kanagaratnam, P., Koa-Wing, M., Wallace, D.T., Goldenburg, A.S., Peters, N.S., Davies, D.W. (2007). Experience of roboticcatheter ablation in humans using a novel remotely steerable catheter sheath. Journal of interventional cardiac electrophysiology. s z.

63 References:  Kumar, P. (2007). AICD defibrillators. Retrieved September 26 th, 2009 from  McChance, K.L., Huether, S.E. (2006). Pathophysiology: The biologic basis for disease in adults and children (5 th ed.). Philadelphia, Pennsylvania:Elsevier- Mosby.  McCrossin, C., (2012). Pacemakers and ICDs. Retrieved on August 12 th, 2013 from.docstoc.com  Morgan, G.E., Mikhail, M.S., Murray, M.J. (2006). Clnical anesthesiology (4 th ed.). New York, New York: Lange.  Nagelhout, J.J., Zaglaniczny, K.L. (2005). Nurse anesthesia (3 rd ed.). St. Louis, Missouri: Elsevier-Saunders.  Roizen, M.F., Fleisher, L.A. (1997). Essence of anesthesia. Philadelphia,Pennsylvania: W.B.Saunders. Philadelphia,Pennsylvania:Elsevier-Saunders.  Rooke, A.G. Pacemakers. University of Washington. Retrieved September 26 th, 2009 from  Seok, C. (2008). Fiber optic sensorized tools for cardiology aplications. Retreived October 16 th, 2009 from  Sweesy, M.W. (2009). Fundamental electrical relationships:Ohm’s law,sStrength duration curve & factors affecting thresholds.Cardio Rhythm 2009, Hong Kong, China. Retrieved October 3 rd from  Peters, N.S., (2000). Catheter ablation for cardiac arrhythmias: ablation is the safe and curative treatment of choice. British Medical Journal. RetrievedOctober 16 th, 2009 from 99/is_7263_321/ai_ /?tag=conten t;col1  Tempelhof, M.W. (2007). Pacemakers: The basics. Retrieved September 26 th, 2009 from  Trankina, M.F. (2002). Peripoerative pacemaker-ICD management. American Society of Anesthesiologists.Whats new in…., vol.66 pp 1-2.  TyRx (2009). AgisRx: Site specific delivery- global impact. Retrieved on September 27 th, 2009 from  Wallace, A. (2008). Pacemakers for anesthesiologists made incredibly simple. Retrieved September 27 th, 2009 from  Williams, C. (2007). Cardaic electrophysiology for the anesthetist.Powerpoint presentation retrieved on September 26 th, 2009 from

64 Questions? Thank You!!!


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