Download Cardiac Pacing and Sleep- Disordered Breathing

Publication of the Association of Polysomnographic Technologists • Summer 2006 • www.aptweb.org
Cardiac Pacing and SleepDisordered Breathing
BY REGINA PATRICK, RPSGT
leep workers commonly believe that heart rhythm problems are
triggered by sleep-disordered breathing but recent studies suggest that heart rhythm problems may instead trigger sleep-disordered
breathing. Physicians have observed that when an artificial pacemaker
is implanted to treat an abnormal heart rhythm, symptoms of sleep-disordered breathing improve significantly in some people. This finding
suggests that artificial cardiac pacing could be a new treatment for
sleep apnea.
S
An artificial pacemaker consists of two parts: a pulse generator and
one or more leads. The pulse generator (a small round device about the
size of a silver dollar) is implanted just below the collarbone. The leads
are wires which carry a signal from the pulse generator to the heart to
trigger a contraction. A pacemaker in which a lead is placed in one
chamber (i.e., usually the right atrium or right ventricle) is called a single chamber pacemaker. Single chamber pacemakers are typically used
to treat sinus bradycardia, ventricular bradycardia, and second and third
degree AV blocks.
In some patients, both the atria and ventricles need stimulation and
a pacemaker will have one lead going to the right atrium and another
going to the right ventricle. This type of pacemaker is called a dual chamber pacemaker. Dual chamber pacemakers are typically used in patients
with bundle branch block problems.
Rhythm problems (i.e., arrhythmias) occur when signals are not
transmitted normally through the heart. The signal for a heartbeat nor-
mally originates from the sinoatrial (SA)
node which is located on the upper wall of
the right atrium. It quickly spreads
throughout both atria causing them to
contract. The signal travels to the atrioventricular (AV) node which is situated
near the junction between the left and
right atria just above the right ventricle. Regina Patrick
The AV node relays the signal to the bundle of His. The bundle of His is a network of fibers which carry the signal down the heart’s septum. Part way in the septum, the bundle of His
splits into left and right bundles to spread the signal along the muscular
walls of the left and right ventricles causing them to contract.
In some cases, arrhythmias can be treated with medication. When
medication can not correct an arrhythmia, implantation of an artificial
pacemaker may restore a steady rhythm.
Abnormal rhythms that may be treated by pacemaker implantation
are: bradycardia (sinus, junctional, or ventricular), AV block, and bundle
branch block. Each of these rhythms are described below:
Bradycardia
Bradycardia (slow heart beat) is any heart rhythm of less than 60
beats/min. Bradycardia can be classified by which part of the heart is
the origin for the slow rhythm. Hence, a person can have sinus bradycardia (i.e., the SA node is the origin of the slow rhythm); junctional
bradycardia (the AV junction is the origin of the
slow rhythm); or ventricular bradycardia (the bundle of His is the origin of the rhythm). A slow heart
rate reduces the amount of blood available to the
brain and heart. As a result, a person with bradycardia can have: syncope (fainting) or near-syncope; transient dizziness or light-headedness; confusional states resulting from reduced blood flow
to the brain; blurred vision; shortness of breath;
chest pain; fatigue; low exercise tolerance, or congestive heart failure. Some people, however, have
no symptoms of bradycardia.
Sinus bradycardia occurs when the SA node
generates signals at a rate of less than 60
beats/minute [beats/min.]. (Normally, the SA node
acts as the heart’s pacemaker; its intrinsic rhythm
is 60-100 beats/min.)
Junctional bradycardia occurs when the AV junction (the area consisting of the AV node plus the portion of the bundle of His before it branches) takes
over as the heart’s pacemaker. The AV junction’s
intrinsic rhythm is 40-60 beats/min. Junctional
bradycardia can occur when the SA node rhythm
falls below 40 beats/min.
ß
14
Publication of the Association of Polysomnographic Technologists • Summer 2006 • www.aptweb.org
Ventricular bradycardia occurs when the ventricles take over as the
heart’s pacemaker. The intrinsic ventricular rhythm ranges from 20-60
beats/min. Ventricular bradycardia can occur when signals are not
relayed from the SA node (e.g., AV block or asystole).
starts breathing. Cheyne-Stokes breathing results from chemoreceptor
hypersensitivity to changes in blood gases. A slight drop in oxygen can
trigger hyperventilation which subsequently gives way to apnea once
peripheral and central receptors “perceive” that oxygen resaturation
has occurred.
AV block
An AV block occurs when some problem at the AV node, the bundle of His, or His bundle branches impedes a signal from being relayed
through the ventricles. An AV block can be first degree, second degree,
or third degree. In first degree AV block, there is a slight delay in the
signal’s leaving the AV junction after each atrial contraction. In second
degree AV block, the SA node rhythmically produces signals but each
beat takes increasingly longer to stimulate the AV junction until ultimately a signal is not relayed and the ventricles do not contract. An
alternative second degree block is that SA node signals contract the
atria rhythmically but at times there is no subsequent AV junction stimulation (and therefore no ventricular contraction). In third degree AV
block, there is a dissociation between the SA node signal and AV junction signal so that the atria beat at their own rhythm while the ventricles beat at their own rhythm.
Bundle Branch Block
In a bundle branch block, damage occurs in one branch causing a
signal to travel through the affected branch at a slower rate than the
opposite bundle branch. The result is that the heart will have two ventricular beats since the affected ventricle contracts after the unaffected ventricle.
Arrhythmic heart contractions can cause improper filling and emptying of the heart’s chambers. This in turn can stimulate the vagus nerve
which innervates the SA node and the AV node. Vagal stimulation slows
the heart contractions. Vagal stimulation can potentially decrease heart
contractions to the point of sinus arrest (i.e., no heart beat) or AV block.
The vagus nerve also plays a role in respiration. Vagal nerve fibers
relay signals from the aortic bodies and pulmonary stretch receptors to
the respiratory center in the brain. The aortic bodies (glandular tissue
found on the aortic arch) are sensitive to oxygen and carbon dioxide levels in the blood. In response to low levels of oxygen (i.e., hypoxia) or high
levels of carbon dioxide (i.e., hypercapnia), the aortic bodies trigger
hyperventilation. The vagus nerve mediates this response.
Pulmonary stretch receptors stimulate the vagal nerve fibers during
inhalations. As the vagal fibers are stimulated, the inspiratory neurons
in the brain’s respiratory center begin to decrease their activity. The
inspiratory neurons ultimately cease their activity which allows the expiratory neurons in the respiratory center to increase their activity so that
exhalation can occur.
Other neurological input (e.g., carotid bodies and central chemoreceptors) to the respiratory center also help to maintain the rhythmicity
of respiration. If the neurological interplay between the respiratory center, stretch receptors, and chemoreceptors (e.g., the aortic bodies,
carotid bodies, and central chemoreceptors) is altered, Cheyne-Stokes
breathing, central apnea, or obstructive sleep apnea can result.
In Cheyne-Stokes breathing, a person will take a few increasingly
deep breaths followed by increasingly shallower breaths which give way
to apnea. This pattern resumes moments later when the person again
In central apnea, the respiratory center does not send a signal to
breathe. As a result, there is no thoracic effort to inhale or exhale and
oxygen levels fall. Breathing usually resumes when oxygen desaturation
falls to a certain point.
In obstructive sleep apnea (OSA), a person stops breathing intermittently during sleep. Breathing ceases due to tissue blocking the
upper airway as muscles in the upper airway relax during sleep. The
blood oxygen level decreases which ultimately triggers the brain to
arouse. With the arousal, muscle tone returns and the airway opens
allowing the free flow of air and resaturation of the blood. Decreased
vagal activity can reduce muscle tone in the upper airway thereby allowing for upper airway collapse.
Artificial pacing may counteract sleep disordered-breathing through
its action on the vagus nerve1. By restoring steady contractions, artificial pacing counteracts improper heart chamber filling and emptying.
This in turn reduces stimulation of pulmonary vagal fibers. With less
vagal stimulation, the respiratory center does not misperceive that a
person is hyperoxic, hypoxic, hypocapnic, or hypercapnic (thereby preventing Cheyne-Stokes breathing or central apneas) and the upper airway muscles can maintain their tone (thereby preventing OSA).
In 1989, Japanese researchers Ogata et al.2 reported that artificial
pacing improves symptoms of sleep apnea. In their report, they discussed the case of a 41 year old, overweight, male subject with congestive heart failure. Electrocardiogram (EKG) recording revealed that
the subject had severe sinus bradycardia and periods of asystole (lack of
heartbeat) lasting up to 6.2 seconds associated with apneic episodes
during sleep. The patient modified his sleep position and lost weight in
an attempt to counteract his sleep apnea. His apnea and bradycardia
remained despite these changes. Ogata then implanted a pacemaker to
treat the patient’s severe bradycardia. The patient’s apnea symptoms
improved significantly after implantation.
Stephane Garrigue et al. 3 in their 2002 study found that
sleep apnea was reduced in subjects who had been implanted
with an atrial-synchronous ventricular pacemaker (a type of
dual-chamber pacemaker). Their 15 subjects, who averaged
around 69 years old, had sinus bradycardia and either central
or obstructive sleep apnea. All under went a baseline (N1)
polysomnogram before implantation. By the following night
(N2), the subjects had undergone pacemaker implantation
and under went a second polysomnographic study. On this
night, the hear t rhythm of one group of subjects was allowed
to beat in spontaneous rhythm while a second group was in
pacing mode (i.e., the pacemaker would induce contractions
when the rhythm became bradycardic). On the night following
this (N3), the patients had a third polysomnogram and were
crossed over to undergo either spontaneous rhythm (if N2
had been in pacing mode) or pacing mode (if N2 had been in
spontaneous rhythm). The researchers found that respiratory
events reduced from an average of 28 events/hour in sponcontinued on page 27
15
Publication of the Association of Polysomnographic Technologists • Summer 2006 • www.aptweb.org
gence by the lab to oversee and ensure that such protections are
carried out.
If your sleep lab has signed business associate agreements with
technology vendors, consultants, accountants, lawyers, or any other
entity or individual who needs to have access to your patients’ PHI in
order to provide your lab with the services required, your lab should
revisit these agreements in light of the HIPAA security regulations. If
your lab’s business associate agreement involves access to or transmission of electronic PHI, the agreement should include how risk assessment will be conducted by the business associate to identify system vulnerabilities. The business associate should also have its own security
policies and procedures.
When reviewing your sleep lab’s business associate agreements,
you should avoid the following pitfalls:
• Limitation of Liability. Business associate agreements are often
attached as addendums to underlying agreements that might predate the HIPAA regulations. Make sure that your business associate does not limit their liability under the terms of the main contract or any subsequent addendums. Your sleep lab should specifically look at the terms that relate to limitation of liability, insurance, and indemnification.
• Monitoring the Activities of Business Associates. It is imperative that sleep labs take steps to monitor and oversee all services being provided by their business associates. Include provisions in your business associate agreements which give your lab
the right to request and receive information and documents from
your business associates that will enable the lab to monitor
HIPAA compliance.
• Evidence of Safeguards. Your lab’s business associate agreements should contain terms to ensure that your associates agree
not to use or disclose your patients’ PHI or electronic PHI in any
way other than is permitted by the agreement or as required by
law. Make sure that the agreement requires your business associate to provide your lab with evidence of safeguards and written
notice if any of these safeguards are breached or discontinued.
HIPAA Compliance
In order to avoid potential liability and resulting civil and criminal monetary penalties, make sure that your sleep lab continues to allocate the
appropriate resources to monitor and maintain compliance with the
HIPAA privacy and security regulations. Your lab should continually provide education and training for all of its employees and independent contractors. The sleep lab’s privacy officer should periodically conduct an
assessment of the technical, security, and privacy measures and identify all authorized users of PHI and electronic PHI to determine appropriateness of all authorized user’s access to PHI. Make sure that the lab’s
compliance with its policies and procedures, notice of privacy practices,
and business associate agreements are monitored and reviewed on an
ongoing basis. H
About the Author
Jayme R. Matchinski, a partner with the law firm of Harris Kessler & Goldstein LLC, in
Chicago, concentrates on health care law and has counseled sleep disorder centers, physicians, and health care providers nationally. She serves on the Special Projects Team of the
A2Zzz Magazine Editorial Board. She can be reached at (312) 280-0111 and [email protected].
Cardiac Pacing and SleepDisordered Breathing
continued from page 15
taneous rhythm to an average of 11 events/hour when
the subject was in pacing mode. From these results, they
concluded that ar tificial pacemaker implantation could
significantly reduce the apneic episodes.
However, pacemaker implantation does not always improve
sleep-disordered breathing. Simantirakis et al.4 compared the
effect of continuous positive airway pressure (CPAP) vs. artificial
cardiac pacing in 16 patients with sleep apnea. The patients on
CPAP therapy had a significant decrease in the number of events
while the patients on artificial pacing had little change in the number of events. Pepin et al.5 similarly found that artificial pacing did
not decrease the number of obstructive sleep apnea episodes in
their subjects. Their subjects had an average of 46 respiratory
events/hour with the heart in spontaneous rhythm and an average
of 50 respiratory events/hour with cardiac pacing.
Nevertheless, scientists are still intrigued by the potential use
of cardiac pacing to treat sleep-disordered breathing. They are currently working to determine which patients with sleep-disordered
breathing will most benefit from cardiac pacing. For example, more
studies may reveal whether cardiac pacing would be more beneficial for someone who would normally not meet the criteria for pacemaker implantation but who has a certain type of sleep-disordered
breathing (e.g., central apnea or Cheyne-Stokes breathing versus
OSA). If a person does meet the criteria for pacemaker implantation, future studies may reveal whether implanting a pacemaker for
certain types of cardiac arrhythmias is more likely to reduce sleepdisordered breathing. Once this is fully determined, cardiac pacing
for sleep-disordered breathing may be useful in preventing not only
symptoms of disordered breathing but also associated disorders
(e.g., hypertension, stroke, etc.). H
References
1. Garrigue S, Bordier P, Barold SS, Clementy J, “Sleep apnea: a new indication for
cardiac pacing?”; Pacing and Clinical Electrophysiology; 27(2):204-211, Feb 2004.
2. Ogata N, Takatori H, Kamijima J, Tatsumi K, Kuriyama T, “A case of Pickwickian syndrome treated by implantation of a cardiac permanent pacemaker,” Kokyu to
Junkan. 1989 Jul;37(7):791-795, 1989.
3. Garrigue S, Bordier P, Jais P, et al., “Benefit of Atrial Pacing In Sleep Apnea
Syndrome,” New England Journal of Medicine, 346(6):404-412, Feb 7, 2002.
4. Simantirakis EN, Schiza SE, Chrysostomakis SI, et al., “Atrial overdrive pacing for
the obstructive sleep apnea-hypopnea syndrome,” New England Journal of
Medicine, 353(24):2568-2577, Dec 15, 2005.
5. Pepin JL, Defaye P, Garrigue S, et al., “Overdrive atrial pacing does not improve
obstructive sleep apnea syndrome,” European Respiratory Journal, 25(2):343347, Feb 2005.
About the Author
Regina Patrick, RPSGT, is a noted freelance medical writer and sleep technologist that
works at St. Vincent Mercy Sleep Disorders Center in Toledo, OH. She is a regular contributor and serves on the A2Zzz Magazine Editorial Board as an Associate Editor. She
also contributes to other publications in the sleep field. Patrick is a past recipient of
the APT Dr. Allen DeVilbiss Literary Award for literary excellence for articles published
in A2Zzz Magazine. She may be contacted through the APT National Office at
[email protected].
27