AICD and Pacemaker Update. Kathryn Gray CRNA. Terminology:. 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.
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Kathryn Gray CRNA
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.
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.
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 (8.314472 JXK -1)
T- absolute temperature (273.15 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 (9.6485309 X104 cmol-1)
The Goldman-Hodgkin-Katz equation accounts for the ionic potentials of multiple ions across a cell membrane.
EMF= 61.5 X log([Na]iPNa+[K]iPK+[Cl]oPCl)
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.
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.
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.
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.
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.
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
Hypo or Hypercalcemia
Hypo or hyperkalemia
Hypo or hypercarbia
Drug toxicity and adverse drug reactions
Stress and catecholamine release
Chronic lung disease and subsequent corpulmonale
Sick sinus syndrome
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.
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?
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?
Why do we need a grounding pad?
Why are we afraid of bovie with pacemakers and AICD’s?
Motor evoked potentials
The magnet IS NOT
Don’t be lured in to a false sense of security of “I’ll just put a magnet on it” to fix any problems.
What happens when a magnet is applied over a pacemaker?
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!
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?
— Yes: pacemaker (not ICD)
— Yes: ICD and pacemaker
— No: pacemaker (not ICD)
— No: ICD and pacemaker
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.
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, 929-936.
Burns, E. (2013). Pacemaker malfunction. Retrieved on August 12th, 2013 from www.lifeinthefastlane.com
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(2nd ed.). Philadelphia,Pennsylvania: Lippincot-Williams and Wilkins.
Faust, R.J. et al.(2002). Anesthesiology review (3rd ed.). Philadelphia, Pennsylvania: Reed-Elsevier.
Greenburg, M.L. (2008). Catheter ablation. Retrieved October 16th, 2009 from www.emedicine.medscape.com.
Guyton, A.C.,Hall, A.C.(2006).Textbook of medical physiology (11th ed.). Philadelphia, Pennsylvania: Elsevier-Saunders.
Hines, R.L., Marschall, K.E. (2008). Stoelting’s anesthesia and co-existing diseases (5th ed.). Philadelphia, Pennsylvania: Elsevier-Saunders.
Klabunde, R.E. (2009). Cardiovacular physiology concepts. Ohio University. Retrieved on September 26th, 2009 www.cvphysiology.com.
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. s10840-007-9184-z.
Kumar, P. (2007). AICD defibrillators. Retrieved September 26th, 2009 from www.heartonline.org
McChance, K.L., Huether, S.E. (2006). Pathophysiology: The biologic basis for disease in adults and children (5th ed.). Philadelphia, Pennsylvania: Elsevier-Mosby.
McCrossin, C., (2012). Pacemakers and ICDs. Retrieved on August 12th, 2013 from .docstoc.com
Morgan, G.E., Mikhail, M.S., Murray, M.J. (2006). Clnical anesthesiology (4th ed.). New York, New York: Lange.
Nagelhout, J.J., Zaglaniczny, K.L. (2005). Nurse anesthesia (3rd 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 26th, 2009 from www.vaanes.org.
Seok, C. (2008). Fiber optic sensorized tools for cardiology aplications. Retreived October 16th, 2009 from www.bdml.stanford.edu
Sweesy, M.W. (2009). Fundamental electrical relationships:Ohm’slaw,sStrength duration curve & factors affecting thresholds.Cardio Rhythm 2009, Hong Kong, China. Retrieved October 3rd from www.cardiorhythm.com.
Peters, N.S., (2000). Catheter ablation for cardiac arrhythmias: ablation is the safe and curative treatment of choice. British Medical Journal. RetrievedOctober 16th, 2009 from http://findarticles.com/p/articles/mi_m0999/is_7263_321/ai_66238403/?tag=content;col1
Tempelhof, M.W. (2007). Pacemakers: The basics. Retrieved September 26th, 2009 from www.askdrwiki.com.
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 27th, 2009 from www.tyrx.com.
Wallace, A. (2008). Pacemakers for anesthesiologists made incredibly simple. Retrieved September 27th, 2009 from www.cardiacengineering.com.
Williams, C. (2007). Cardaic electrophysiology for the anesthetist.Powerpoint presentation retrieved on September 26th, 2009 from www.medtronicconnect.com.