Transcript Holly Everts, 2010. Atrial Fibrillation

Atrial Fibrillation
Holly Everts, RN, BSN
Alverno College, MSN 621
[email protected]
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Learning Objectives
• Define atrial fibrillation and be able to identify
the rhythm.
• Understand the pathophysiology of atrial
fibrillation.
• Discuss different causes of atrial fibriallation
• Identify signs and symptoms of atrial
fibrillation.
• Describe various treatment modalities.
• Identify nursing implications in caring for
patients with atrial fibrillation.
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Table of Contents
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Normal Heart
Function
Definition of
Atrial fib
Electrical
System
Mechanical
System
Signs and
Symptoms
Aging
processes
and Atrial fib
Procedures
Medications
Nursing
Implications
The Heart’s Mechanical System
Your heart has 4 chambers
~left and right atria
~left and right ventricles
The left and right sides of the heart are separated by a
wall of muscles called the septum.
Contractions
The atria contract first and fill the ventricles.
The ventricles contract shortly after and send blood to
the lungs, heart and body.
(Texas Heart Institute, 2009)
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Click
for
video
American Heart
Association, 2010
The Heart’s Electrical System
~Impulse originates in the sinoatrial
(SA) node.
~Signal travels through specific
pathways causing the atria to
contract.
~Signal then moves to the
atrioventricular (AV) node and the
impulse slows.
~Signal leaves the AV node and
travels along a pathway called the
bundle of His and into the purkinje
fibers.
(National Heart, Lung, and Blood
Institute, 2009).
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Used with permission by
EKG concepts, 2009
Normal EKG rhythm
Atria depolarize on the p wave.
Ventricles depolarize on QRS complex and atria repolarize.
Ventricles repolarize on the t wave.
(National Heart, Lung, and Blood Institute, 2009).
P wave
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QRS
complex
T wave
Used with permission by
EKG concepts, 2009
Quick Review
Click where the electrical
impulse originates in a
normal sinus rhythm.
Click on what is
repolarizing during the QRS
complex?
Correct!!
Atria
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Incorrect
Ventricles
Used with permission by
EKG concepts, 2009
Case Study
• Mrs. B comes to the emergency room
complaining of feeling weak, short of breath,
light headedness, palpitations and mild chest
discomfort.
• She is 87 years old with a history of smoking,
hypertension, coronary artery disease and
anxiety.
• You attach her to the EKG and the physician
gives her the diagnosis of atrial fibrillation.
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• What is atrial fibrillation?
What is Atrial Fibrillation?
“Atrial Fibrillation is an arrhythmia characterized by
chaotic impulses propagating in different directions
and causing disorganized atrial depolarization
without effective atrial contraction” (Porth, 2005, p.
592).
The ventricular rate is irregular and can be fast or
slow.
Click
for
video
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American Heart
Association, 2010
(Porth, 2005)
Pathology of the Electrical System
• In Atrial Fib, the heart's electrical signals do not begin
in the SA node.
– Impulses start in other parts of atria
– Impulses can begin in pulmonary veins
• Signal is disorganized
• AV node is flooded with impulses
• Ventricles react with a tachycardic rate
(National Heart, Lung, and Blood Institute, 2009).
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EKG in Atrial Fibrillation
Notice there are no defined “p” waves or “t” waves but
fibrillatory waves are present instead.
Click
for
video
The ventricular rate is irregular
American Heart
Association, 2010
Fibrillation waves
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Irregular QRS
Used with permission from P. Schwartz
Review Question
• Mrs. B is feeling palpitations due to her rapid
heart rate. How is atrial fib causing her rate
to be so fast (click on answer)?
Rapid impulses
released by SA
Incorrect,
node.
try again.
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Rapid impulses
released by the
ventricles.
Incorrect,
try again.
Rapid impulses
released by multiple
Correct!!locations in the atria
Rapid impulses
released by AV
node.
Incorrect,
try again.
Pathology of the Mechanical
System
• In Atrial Fib, blood pools in the atria and is not
pumped completely into the ventricles.
–
(National Heart, Lung, and Blood Institute, 2009).
• The heart's upper and lower chambers do not work
together as they should.
– (National Heart, Lung, and Blood Institute, 2009).
• Amount of blood pumped out to the body is random.
– (National Heart, Lung, and Blood Institute, 2009).
• Stroke volume different with every beat and cardiac
output is decreased.
– (Porth, 2005).
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Signs and Symptoms of Atrial
Fibrillation
Symptoms vary greatly among individuals and
include:
Palpitations
Shortness of Breath
Irregular heart rate
Fatigue/weakness
Pulmonary edema
Dizziness
Chest pain
Risk for stroke
(Porth, 2005)
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Review Question
• Which of Mrs. B’s symptoms are due to
decreased cardiac output caused by her atrial
fibrillation?
Yes! Cardiac demand
Chest
is greater
than output
discomfort
causing
chest pain
Yes! Due to
decreased
perfusion
Weakness
to muscles
Yes! Due to
Shortness of
decreased
Breath
perfusion to lungs
This would be
Palpitations
caused
by excited
cells in atria
Yes! Due to
Dizziness
decreased
cerebral
perfusion
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Cardiac cells and Ions
Sodium and Calcium
enter the cell during
depolarization.
Ca++
Na+
Cell
K+
Potassium leaves the
cell slowly during
depolarization and
quickly during
repolarization.
Cell during depolarization
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(Porth, 2005)
Cardiac Cycle and Ions
• During atrial fibrillation, calcium ions build up
in cells that cause calcium overload.
– High electrical activity makes it difficult for myocytes to remove
calcium from the cells.
• Calcium overload of the cell leads to electrical
and mechanical remodeling.
– Activates proteases that breakdown important
cellular proteins.
– This remodeling enlarges the atria making them
more likely to sustain fibrillatory activity.
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(Cleveland Clinic, 2010)
Review Question
• During depolarization of a cell, which ions
enter the cell? (Click the answers)
Correct!!
Calcium
Correct
Sodium
Try again,
potassium
Potassium
is already
in the cell
Try
Chloride
again
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Review Question
• How does calcium overload in the cells
remodel the myocytes (cardiac cells)? (Click
the correct answer).
Builds proteins that
change the cells
function.Try again
Inhibits electricity to
flow through the cell.
Try again
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Does not allow
vitamin D to enter the
cell Try again
Activates proteases
that breakdown
important cellular
proteins. Correct!!
Aging and Atrial Fibrillation
• Mitochondria are extremely important for
oxidative energy for cells.
– In atrial fib, rapid depolarization leads to higher
demand for energy and oxygen consumption.
• As cells age, mutations of mitochondrial DNA
(mtDNA 4977) accumulate.
– Result – dysfunctional mitochondria
• Impaired oxidative energy production
• Impaired electron transport in metabolism and
accumulation of free radicals.
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– (Lai, L., Tsai, C., Su, M., Lin, J., Chen, Y., Tseng, Y., Huang, S., 2003).
Aging and Atrial Fibrillation
• A study of 88 patients undergoing open heart
surgery showed:
– Pediatric and Adolescent patients did not have
mutated DNA - mtDNA 4977.
– Older patients had mtDNA 4977.
– Patients with atrial fibrillation had a higher level of
mtDNA 4977.
• Conclusion
– Age related changes and mutations are
associated with atrial fibrillation.
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(Lai, L., Tsai, C., Su, M., Lin, J., Chen, Y., Tseng, Y.,
Huang, S., 2003).
Etiologies: Stress and Atrial
Fibrillation
• Stress causes release of stress hormones
• Norepinephrine – stress hormone
– activates beta receptors and the
renin/angiotensin/aldosterone system (Porth,
2005).
– shortens the atrial action potential and recovery
period (Otway, Fatkin & Vandenberg, 2007).
• A number of potassium (K+) currents are highly
responsive to adrenergic stimuli.
– Shortens the refractory period.
– (Otway, Fatkin & Vandenberg, 2007).
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Review Question
• Mrs. B is cooking dinner tonight for her whole
family and is stressed about seeing her sonin-law. She starts feeling frequent
palpitations and short of breath. How might
her age and stress contribute to her
symptoms?
Incorrect!
is a
Stress isStress
a genetic
normal
response
of the
response
that leads
sympathetic
nervous
aging
system (Porth, 2005).
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Age can cause
genetic mutations that
lead to atrial
dysfunction and make
Correct!
cells more vulnerable
to stress hormones
Etiologies: Inflammation and Atrial
Fib
• C-reactive protein correlates to atrial
fibrillation duration.
– proves association between inflammation and
atrial remodelling.
• C-reactive protein values have been found to
decrease post-cardioversion.
• White blood cell (WBC) count has been found
to lower the seventh day post-cardioversion.
(Korantzopoulos, P., Kolettis, T., Siogas, K., Goudevenos, J.,
2005).
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Etiologies: Reactive Oxygen
Species (Free Radicals)
• Review:
• Dysfunctional mitochondria in aged cells
impair electron transport in metabolism.
– Leads to accumulation of free radicals
– Free radicals damage cellular components
and tissues.
– Oxidative stress increases the amount of
mtDNA 4977.
– (Lai, L., Tsai, C., Su, M., Lin, J., Chen, Y., Tseng, Y., Huang, S., 2003).
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Etiologies: Reactive Oxygen
Species (Free Radicals)
• Calcium and reactive oxygen species
• Calcium overload can cause increase nitric oxide
(NO) levels.
– Nitric oxide has pro-oxidative and antioxidative
effects (Cleveland Clinic, 2010).
– The toxicity of NO depends on what molecule it
reacts with (Aikio, Poleka, & Hallman, 2002).
– Reaction of NO and O2- lead to pro-oxidative
damage and the destruction of cellular proteins
and DNA (Aikio, Poleka, & Hallman, 2002).
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Etiologies: Reactive Oxygen
Species (Free Radicals)
• Atrial fib and neurohormonal activation.
– Leads to increased release of Angiotensin II and superoxide
(O2- ).
(Cleveland Clinic, 2010).
• A study done in the UK measured the amount of
vascular superoxide from tissue samples of 79
patients.
• Patients that were prescribed medication to block
angiotensin II showed a significant decrease in
vascular superoxide levels.
– (Berry, C., Anderson, N., Kirk, A., Dominiczak, A., &
McMurray, J., 2001).
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Review Question
• How would Mrs. B’s stress of cooking dinner
for everyone increase her free radical
production? (Click on the correct answer)
Stress
neurohormones
increase angiotensin
2 and superoxide
levels.
Correct!!
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Stress releases
calcium from the
cells causing
increased nitric
Incorrect,
oxide.
remember too
much calcium in
the cell releases
nitric oxide
Etiologies: Genetics and Atrial
Fibrillation
• The Mayo Clinic identified a mutation in DNA that
was linked to atrial fibrillation.
• Gene KCNA5 produces an important heart protein
Kv1.5.
– Kv1.5 is an important protein involved with ion channels
• A mutation in this gene caused a loss of function in
this protein.
• This loss of function made the atria susceptible to
sustain atrial fibrillation.
– (Olson, T., Alekseev, A., Liu. X., Park, S., Zingman, L.,
Bienengraeber, M., Sattiraju, S, Ballew, J., Jahangir, A., & Terzic,
A. 2006).
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Review Question
• How does norepinephrine effect atrial
fibrillation? (click on the correct answers)
Stimulates beta
receptorsCorrect!!
Causes gene mutation
Incorrect
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Slows HeartIncorrect
Rate
Increases
responsiveness
of
Correct!!
potassium channels
Review Question
• Free radicals, (such as nitric oxide and
superoxide) contribute to atrial fibrillation by
breaking down proteins and damaging DNA.
True
Correct!!
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False
Incorrect
Treatment Options
Several approaches are used to treat and prevent atrial
fibrillation:
Ablation
MAZE
procedure
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Cardioversion
Medications
Procedures: Ablation
• A catheter is inserted into the femoral artery to the
area of heart muscle where there's an accessory
(extra) pathway.
• The catheter is guided using fluoroscopy.
• The physician is able to see the exact area on the
heart that is causing the accessory pathway
• Radiofrequency energy is transmitted to the pathway
and destroys the selected heart muscle cells in a very
small area (about 1/5 of an inch).
(American Heart Association, 2010).
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Procedures for Atrial Fibrillation
Cardioversion
Electrode patches are placed on the front and back
of the chest and connected to the defibrillator.
The defibrillator is then synchronized to deliver a
shock on the QRS complex.
This shock interrupts all electrical activity of the
heart and allows the normal heart rhythm to
return.
– (Kang, 2010).
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Procedures for Atrial fibrillation
• MAZE procedure
• Incisions are made in the atria creating scar tissue
that electrical impulses can not travel through.
• This redirects the hearts electrical pathway and
eliminates accessory pathways.
• “The Maze procedure has been very successful with
a 98% success rate in "lone atrial fibrillation" patients
and a 90% success rate overall. Post – Maze
procedure freedom from stroke has been over 99%.”
» (Cleveland Clinic, 2010)
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Medications to treat Atrial
Fibrillation
• Anti-arrhythmic medication classes
Ca++
– Sodium channel blocker
• Multaq
– Beta Blockers
Na+
• Metoprolol
– Potassium Channel blocker
Cell
• Sotalol, Amiodarone, Tikosyn
– Calcium Channel blocker
• Cardizem
– Other mechanisms
• Digoxin, Adenosine
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How do they work?
K+
Medications: Rate Control
• Calcium-channel blockers: slow the influx of calcium
ions into the heart and slow the depolarization and
repolarization periods (Lehne, 2004).
• Beta-blockers: "block" the action of sympathetic
neurotransmitters on beta receptors.
– This slows down conduction of impulses through the heart
and make the AV Node less sensitive.
• Digoxin: slows down the heart rate by blocking the
electrical conduction between the atria and ventricles.
• (Ryan, 2002)
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Rhythm Control
• Sodium Channel Blockers which decrease the speed
of electrical conduction in the heart muscle and
stabilize cell membranes.
• Potassium Channel Blockers slow nerve impulses in
the heart, keep the cell depolarized longer and
stabilize cell membranes.
– (Ryan, 2002)
Conversion of atrial fibrillation
Agents with proven efficacy: dofetilide, amiodarone, ibutilide,
flecainide, propafenone, and quinidine.
Less effective or incompletely studied agents: procainamide,
sotalol, and digoxin.
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(Borczuk, 2009)
Review Question
• Why would Mrs. B’s potassium channel
blocker, such as amiodarone, be used for
rate and rhythm control?
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Potassium channel
blockers slow the rate
of conduction by
slowing the efflux of
potassium
Potassium channel
blockers deplete the
cells of potassium
therefore inhibiting
depolarization.
Correct!
Incorrect
Nursing Implications
• Monitor hemodynamic stability
– Heart rate, blood pressure, oxygenation &
perfusion
• Symptom control
– Anxiety, shortness of breath, dizziness
• Activity intolerance
• Medication management
• Monitor for complications
– Blood clot formation – PE, stroke, MI, DVT
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Nursing Diagnoses and Outcomes
Activity Intolerance
Decreased
cardiac output
0400
Cardiac
Pump
Patient
is able
to eject
Effectiveness
enough blood to support
(Moorhead
al, 2004).
systemic et
circulation.
Decreased Cardiac
Output
Ineffective Perfusion
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Patient is able to conserve
3011 Activity
Tolerance
energy
and build
endurance
et al, 2004).
to(Moorhead
complete activities
of daily
living.
Decreased
cardiac output
0401
Circulation
Status
Patient
is able perfuse
(Moorhead
al, 2004).
tissues andetmaintain
an
appropriate blood pressure.
Click on nursing diagnosis for correlating nursing outcome.
Then click on the nursing outcome for further explanation.
Nursing Diagnoses and Outcomes
Ineffective Coping
Risk for Falls
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Fear and
anxiety
Patient
is able
to utilize
1402
Anxiety
Self-Control
actions to reduce
stress,
(Moorhead
et al, 2004).
tension and apprehension.
Decreased
cardiac output
Patient is able ask for help
0406
Tissuerisk
Perfusion:
and reduce
factors for
Cerebral
falls.
Patient has adequate
(Moorhead
et al, 2004).
cerebral
perfusion
to prevent
falls.
Click on nursing diagnosis for correlating nursing outcome.
Then click on the nursing outcome for further explanation.
Conclusion
• Atrial fib is the most common arrhythmia with
2 million Americans afflicted.
• Atrial fibrillation is responsible for 15 to 20
percent of ischemic strokes.
• By 2050, the CDC estimates that 12 million
Americans will have atrial fibrillation.
(Centers for Disease Control and Prevention, 2010)
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References
• Aikio O, Pokela ML, Hallman M (2002). Pulmonary nitric oxide in
preterm and term infants with respiratory failure Retrieved from,
http://herkules.oulu.fi/isbn9514268512/html/i231674.html
• American Heart Association. (2010). Atrial fibrillation. Retrieved
from
http://www.americanheart.org/presenter.jhtml?identifier=4451.
• American Heart Association. (2008). Atrial Fibrillation for
professionals. Retrieved from http://www.americanheart.org
• Berry, C., Anderson, N., Kirk, A., Dominiczak, A., & McMurray,
J. (2001). Renin angiotensin system inhibition is associated with
reduced free radical concentrations in arteries of patients with
coronary heart disease. Heart. 86(217-220).
• Borczuk, P. (2009). Atrial fibrillation. Emedicine. Retrieved from
http://emedicine.medscape.com/article/757370-overview.
• Centers for Disease Control and Prevention. (2010). Atrial
fibrillation fact sheet. Retrieved from
Table of
http://www.cdc.gov/dhdsp/library/fs_atrial_fibrillation.htm
Contents
References
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Contents
• Cleveland Clinic. (2010). Mechanisms of atrial electrical
remodeling. Retrieved from
http://my.clevelandclinic.org/heart/atrial_fibrillation/afresearch.as
px.
• EKG Concepts. (2009). Rapid cardiac arrhythmia tool. EKG
Concepts, LLC.
• Kang, S. (2010). Cardioversion. American Accreditation
HealthCare Commission. Retrieved from
http://www.nlm.nih.gov/medlineplus/ency/article/007110.htm
• Korantzopoulos, P., Kolettis, T., Siogas, K., Goudevenos, J.,
(2005). The emerging role of inflammation in atrial fibrillation
and the potential of anti-inflammatory interventions. European
Heart Journal. 26(20).
• Lai, L., Tsai, C., Su, M., Lin, J., Chen, Y., Tseng, Y., & Huang,
S., (2003). Atrial fibrillation is associated with accumulation of
aging-related common type mitochondrial DNA deletion
mutation in human atrial tissue. Chest. Feb;123(2):539-44.
References
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Contents
• Lehne, R. (2004). Pharmacology for nursing care, 5th edition.
Elsevier Saunders: Philadelphia.
• Moorhead, S., Johnson, M., & Maas, M. (2004). Nursing
Outcomes Classification (NOC) (3rd ed.). St. Louis, MO: Mosby.
• National Heart, Lung, and Blood Institute. (2009). Understanding
the Heart's Electrical System. Retrieved from
http://www.nhlbi.nih.gov/health/dci/Diseases/arr/arr_whatis.html.
• National Heart, Lung, and Blood Institute. (2009). Understanding
the Electrical Problem in Atrial Fibrillation. Retrieved from
http://www.nhlbi.nih.gov/health/dci/Diseases/af/af_what.html.
• Olson, T., Alekseev, A., Liu. X., Park, S., Zingman, L.,
Bienengraeber, M., Sattiraju, S, Ballew, J., Jahangir, A., &
Terzic, A. (2006). Kv1.5 channelopathy due to KCNA5 loss-offunction mutation causes human atrial fibrillation. Human
Molecular Genetics. 15(14).
• Otway, R., Fatkin, D., & Vandenberg, J., (2007). Genes and
atrial fibrillation. Circulation. 116(7).
• Porth, C. (2005). Pathophysiology, 7th edition. Lippincott.
References
• Ryan, S. (2002). Atrial fibrillation: resource for patients.
Retrieved from http://www.a-fib.com/Medications.htm.
• Texas Heart Institute. (2010). Health Information Center.
Retrieved from
http://www.texasheartinstitute.org/HIC/Anatomy/anatomy2.cfm
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