Atrial Fibrillation

1
Atrial Fibrillation

• Holly Everts, RN, BSN
• Alverno College, MSN 621
• evertshn_at_alverno.edu

2
Tutorial Directions

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Table of Contents
3
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
Electrical System
Definition of Atrial fib
Normal Heart Function
Mechanical System
Signs and Symptoms
Aging processes and Atrial fib
Procedures
Medications
Nursing Implications
5
The Hearts 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)
Click for video
American Heart Association, 2010
6
The Hearts 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).
Used with permission by EKG concepts, 2009
7
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).
QRS complex
P wave
T wave
Used with permission by EKG concepts, 2009
8
Quick Review
Click where the electrical impulse originates in
a normal sinus rhythm.
Try Again
Correct
Try Again
Click on what is repolarizing during the QRS
complex?
Ventricles
Incorrect
Atria
Correct!!
Used with permission by EKG concepts, 2009
9
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.
• What is atrial fibrillation?

10
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
(Porth, 2005)
American Heart Association, 2010
11
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).

12
EKG in Atrial Fibrillation
Notice there are no defined p waves or t
waves but fibrillatory waves are present
instead. The ventricular rate is irregular
Click for video
American Heart Association, 2010
Irregular QRS
Fibrillation waves
Used with permission from P. Schwartz
13
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 node.
Rapid impulses released by multiple locations in
the atria
Incorrect, try again.
Correct!!
Rapid impulses released by the ventricles.
Rapid impulses released by AV node.
Incorrect, try again.
Incorrect, try again.
14
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).

15
Signs and Symptoms of Atrial Fibrillation
Symptoms vary greatly among individuals and
include Palpitations Shortness of
Breath Irregular heart rate Fatigue/weakness Pu
lmonary edema Dizziness Chest pain Risk for
stroke (Porth, 2005)
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Review Question

• Which of Mrs. Bs symptoms are due to decreased
  cardiac output caused by her atrial fibrillation?

Yes! Cardiac demand is greater than output
causing chest pain
Yes! Due to decreased perfusion to muscles
Chest discomfort
Weakness
This would be caused by excited cells in atria
Yes! Due to decreased perfusion to lungs
Palpitations
Shortness of Breath
Yes! Due to decreased cerebral perfusion
Dizziness
17
Cardiac cells and Ions
Ca
Sodium and Calcium enter the cell during
depolarization. Potassium leaves the cell slowly
during depolarization and quickly during
repolarization.
Na
Cell
K
Cell during depolarization
(Porth, 2005)
18
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.
• (Cleveland Clinic, 2010)

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Review Question

• During depolarization of a cell, which ions enter
  the cell? (Click the answers)

Correct!!
Calcium
Correct
Sodium
Try again, potassium is already in the cell
Potassium
Try again
Chloride
20
Review Question

• How does calcium overload in the cells remodel
  the myocytes (cardiac cells)? (Click the correct
  answer).

Does not allow vitamin D to enter the cell
Builds proteins that change the cells function.
Try again
Try again
Activates proteases that breakdown important
cellular proteins.
Inhibits electricity to flow through the cell.
Try again
Correct!!
21
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.
• (Lai, L., Tsai, C., Su, M., Lin, J., Chen, Y.,
  Tseng, Y., Huang, S., 2003).

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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.
• (Lai, L., Tsai, C., Su, M., Lin, J., Chen, Y.,
  Tseng, Y., Huang, S., 2003).

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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
  son-in-law. She starts feeling frequent
  palpitations and short of breath. How might her
  age and stress contribute to her symptoms?

Incorrect! Stress is a normal response of the
sympathetic nervous system (Porth, 2005).
Age can cause genetic mutations that lead to
atrial dysfunction and make cells more
vulnerable to stress hormones
Stress is a genetic response that leads aging
Correct!
25
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).

27
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. Bs stress of cooking dinner for
  everyone increase her free radical production?
  (Click on the correct answer)

Stress neurohormones increase angiotensin 2 and
superoxide levels.
Stress releases calcium from the cells causing
increased nitric oxide.
Correct!!
Incorrect, remember too much calcium in the cell
releases nitric oxide
30
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).

31
Review Question

• How does norepinephrine effect atrial
  fibrillation? (click on the correct answers)

Correct!!
Incorrect
Stimulates beta receptors
Slows Heart Rate
Correct!!
Incorrect
Increases responsiveness of potassium channels
Causes gene mutation
32
Review Question

• Free radicals, (such as nitric oxide and
  superoxide) contribute to atrial fibrillation by
  breaking down proteins and damaging DNA.

False
True
Incorrect
Correct!!
33
Treatment Options
Several approaches are used to treat and prevent
atrial fibrillation
Ablation
Cardio-version
Medications
MAZE procedure
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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).

35
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).

36
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
• Sodium channel blocker
• Multaq
• Beta Blockers
• Metoprolol
• Potassium Channel blocker
• Sotalol, Amiodarone, Tikosyn
• Calcium Channel blocker
• Cardizem
• Other mechanisms
• Digoxin, Adenosine
• How do they work?

Ca
Na
Cell
K
38
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. (Borczuk, 2009)
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Review Question

• Why would Mrs. Bs potassium channel blocker,
  such as amiodarone, be used for rate and rhythm
  control?

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
41
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
Patient is able to conserve energy and build
endurance to complete activities of daily living.
3011 Activity Tolerance (Moorhead et al, 2004).
Activity Intolerance
Decreased cardiac output
Patient is able to eject enough blood to support
systemic circulation.
0400 Cardiac Pump Effectiveness (Moorhead et al,
2004).
Decreased Cardiac Output
Patient is able perfuse tissues and maintain an
appropriate blood pressure.
0401 Circulation Status (Moorhead et al, 2004).
Ineffective Perfusion
Decreased cardiac output
Click on nursing diagnosis for correlating
nursing outcome. Then click on the nursing
outcome for further explanation.
43
Nursing Diagnoses and Outcomes
Patient is able to utilize actions to reduce
stress, tension and apprehension.
1402 Anxiety Self-Control (Moorhead et al, 2004).
Fear and anxiety
Ineffective Coping
Patient is able ask for help and reduce risk
factors for falls. Patient has adequate cerebral
perfusion to prevent falls.
0406 Tissue Perfusion Cerebral (Moorhead et al,
2004).
Risk for Falls
Decreased cardiac output
Click on nursing diagnosis for correlating
nursing outcome. Then click on the nursing
outcome for further explanation.
44
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)

45
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/i23167
  4.html
• American Heart Association. (2010). Atrial
  fibrillation. Retrieved from http//www.americanhe
  art.org/presenter.jhtml?identifier4451.
• 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.medscap
  e.com/article/757370-overview.
• Centers for Disease Control and Prevention.
  (2010). Atrial fibrillation fact sheet. Retrieved
  from http//www.cdc.gov/dhdsp/library/fs_atrial_fi
  brillation.htm

46
References

• Cleveland Clinic. (2010). Mechanisms of atrial
  electrical remodeling. Retrieved from
  http//my.clevelandclinic.org/heart/atrial_fibrill
  ation/afresearch.aspx.
• 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/artic
  le/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.
  Feb123(2)539-44.

47
References

• 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/h
  ealth/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-of-function
  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.

48
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.texasheartinstit
  ute.org/HIC/Anatomy/anatomy2.cfm