Download AICD and Pacemaker Update

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.
•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.
Cardiac Anatomy and
myocardial conduction
Cardiac Anatomy and
myocardial conduction
Where it all begins…………
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 Equilibrium
potential (Em)
r]
Sodium
10 mM
145 mM
60 mV
Potassium
135 mM
4 mM
-94 mV
Chloride
5 mM
120 mM
-97 mV
Calcium
0.00000010 mM
2 mM
132 mV
Paging Dr. Nernst
Nernst Equation
•Em
Em= (-RT/zF) X log [K]i/[K]o
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)
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]iPNa+[K]iPK+[Cl]oPCl)
([Na]oPNa+[K]oPK+[CliPCl)
The Sinoatrial Node
•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.
At the cellular level
SA Node conduction
Ectopic Pacemakers
•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 “StokesAdams” syndrome. The new pacemaker is in A-V
node or penetrating part of A-V bundle.
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.
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.
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.
The ventricles
Putting it all together
Depolarization during a cardiac
cycle
Excitation Contraction Coupling
The result…….
Innervation of the heart
Sympathetic




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

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
CNS control
of Heart rate
Autonomic effects on CO
Causes of cardiac dysfunction
Physiologic Imbalances











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
Associated Co-motbidities












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
Types of conduction disruptions
-
Atrial Fibrillation
 - Atrial Flutter
 - 1st degree heart block
 - 2nd degree heart block
 - 3rd degree heart block
 - Ventricular fibrillation
 - Ventricular tachycardia
 - Re-entry arrhythmias
The Solution:
And the beat goes on….
Pacemaker coding
system
Chamber
Paced
Chamber
Sensed
Response to
Sensing
Programmability
Antiarrhythmia
Function
A=Atrium
A=Atrium
T=Triggered
P=Simple
P=Pacing
V=Ventricles
V=Ventricles
I=Inhibited
R=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
O=None
O=None
O=None
O=None
C=Communic
ating
CODE
What is it?
Who gets it?
AOO
Atrial pace, no sense
no inhibitions
SSS with intact
conduction in the OR
with bovie
AAI
Atrial pace, atrial
sense, inhibition by
the atrium
SSS with intact
conduction system
VOO
Ventricular pace, no
sense no inhibition
Third degree heart
block in OR with atrial
fibrillation
VVI
Ventricular pace,
ventricular sense and
ventricular inhibition
Third degree heart
block with atrial
fibrillation
DOO
Dual pace, no sense
no inhibitions
Third degree heart
block in OR with
bovie
DVI
Dual pace,
ventricular sense,
ventricular inhibition
Third degree heart
block with SVT
DDD
Dual pace, dual
sense dual inhibit
Third degree heart
block
Who gets what?
The name is Bond, James
Bond
This is a
schematic of
how each
pacemaker will
affect the EKG
depending on
the intrinsic
beat and
pacemaker
mode
 Rate-Responsive


1. Mixed Venous O2 saturation
2. Central venous pH
Rate Responsive Pacemakers
 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

Direct metabolic sensors:
Activity sensors
1. Motion detection
Pacemaker effects on CO
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.
Questions you need to ask
 What
is the going
device? into the OR
before
 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?
AICD’s
Indications for AICD insertion
Common indications for
AICD implantation
Class I indications
Class 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
Hyoertrophic
cardiomyopathy
•History of documented
VT/VF
•Unexplained syncope &
LV dysfunction
•Reccurrent VF/VT normal
LVEF
What
do you do when
your patient has an
existing pacemaker or
AICD?
Anesthesia for patients
with AICD’s
•Questions
•Why
to ask the patient:
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?
Danger
in the
O.R.
Electrocautery
Bipolar
vs Unipolar
Why do we need a grounding
pad?
Why are we afraid of bovie
with pacemakers and AICD’s?
Electromagnetic interference in the O.R.
Electrocautery
MRI
ESWL
Defibrillation
Motor
evoked potentials
Nerve stimulators
Oversensing
 Cause
 Insulation breach
 Bipolar impedance
Pacemaker oversensing
Pacemaker undersensing
Failure to capture
Innapropriate AICD shock
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.
Magnet Mode
What happens when a magnet is applied over a pacemaker?

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.)
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…
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!
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?
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.
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 800.547.0394
Boston Scientific 651.582.4000
Sorin Ela 800.352.6466
Medtronic 800.328.2518
St. Jude Medical 800.722.3774
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.
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?
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
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.
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, 929-936.
Burns, E. (2013). Pacemaker malfunction.
Retrieved on August 12th, 2013 from
www.lifeinthefastlane.com
Byong, J.,Mashahiro, O., shien-Fong, L.,PengSheng, 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: ElsevierSaunders.
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.
References:









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:
ElsevierMosby.
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’s law,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_m09
99/is_7263_321/ai_66238403/?tag=conten
t;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 deliveryglobal 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.
Thank Questions?
You!!!