atrial fibrillation holly everts, rn, bsn alverno college, msn 621 [email protected]
TRANSCRIPT
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Tutorial Directions
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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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Electrical System
Mechanical System
Definition of Atrial fib
Signs and Symptoms
Procedures MedicationsNursing
Implications
Aging processes and
Atrial fib
Normal Heart Function
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The Heart’s Mechanical System
Click for
video
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.
ContractionsThe 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)
American Heart Association, 2010
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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).
Used with permission by EKG concepts, 2009
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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 T waveQRS
complex
Used with permission by EKG concepts, 2009
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VentriclesIncorrect
Quick Review
Click on what is repolarizing during the QRS complex?
Click where the electrical impulse originates in a normal sinus rhythm.
AtriaCorrect!! Used with permission by
EKG concepts, 2009
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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?
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What is Atrial Fibrillation?
Click for
video
“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.
American Heart Association, 2010
(Porth, 2005)
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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
Used with permission from P. Schwartz
Click for
video
American Heart Association, 2010
Notice there are no defined “p” waves or “t” waves but fibrillatory waves are present instead.
The ventricular rate is irregular
Irregular QRSFibrillation waves
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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
Rapid impulses released by the
ventricles.
Rapid impulses released by AV
node.
Incorrect, try again.
Incorrect, try again.
Incorrect, try again.
Correct!!
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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:
PalpitationsShortness of BreathIrregular heart rateFatigue/weaknessPulmonary edemaDizzinessChest painRisk for stroke
(Porth, 2005)
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Yes! Cardiac demand is greater
than output causing chest pain
Chest discomfort
Yes! Due to decreased
perfusion to lungs
Yes! Due to decreased cerebral
perfusion
Yes! Due to decreased perfusion
to muscles
This would be caused by excited
cells in atria
Review Question
• Which of Mrs. B’s symptoms are due to decreased cardiac output caused by her atrial fibrillation?
Weakness
Shortness of Breath
Dizziness
Palpitations
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Cardiac cells and Ions
Sodium and Calcium enter the cell during depolarization.
Potassium leaves the cell slowly during depolarization and quickly during repolarization.
Cell
Ca++
K+
Na+
(Porth, 2005)
Cell during depolarization
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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)
Calcium
Sodium
Potassium
Chloride
Correct!!
Try again, potassium is already in the cell
Correct
Try again
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Review Question
• How does calcium overload in the cells remodel the myocytes (cardiac cells)? (Click the correct answer).
Activates proteases that breakdown
important cellular proteins.
Does not allow vitamin D to enter the
cell
Builds proteins that change the cells
function.
Inhibits electricity to flow through the cell.
Correct!!
Try again Try again
Try again
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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?
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!
Incorrect! Stress is a normal response of
the sympathetic nervous system (Porth, 2005).
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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.
Stress releases calcium from the
cells causing increased nitric
oxide.Correct!!
Incorrect, remember too
much calcium in the cell releases
nitric oxide
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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!! Slows Heart Rate
Increases responsiveness of
potassium channelsCauses gene mutation Correct!!Incorrect
Incorrect
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Review Question
• Free radicals, (such as nitric oxide and superoxide) contribute to atrial fibrillation by breaking down proteins and damaging DNA.
True FalseCorrect!! Incorrect
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Treatment Options
Several approaches are used to treat and prevent atrial fibrillation:
MedicationsMAZE
procedure
AblationCardio-version
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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).
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Procedures for Atrial Fibrillation
CardioversionElectrode 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– 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?
Cell
Ca++
K+
Na+
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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 fibrillationAgents 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. B’s 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
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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
3011 Activity Tolerance (Moorhead et al, 2004).
0400 Cardiac Pump Effectiveness(Moorhead et al, 2004).
0401 Circulation Status(Moorhead et al, 2004).
Activity Intolerance
Decreased Cardiac Output
Ineffective Perfusion
Decreased cardiac output
Decreased cardiac output
Click on nursing diagnosis for correlating nursing outcome.Then click on the nursing outcome for further explanation.
Patient is able to conserve energy and build endurance to complete activities of daily
living.
Patient is able to eject enough blood to support
systemic circulation.
Patient is able perfuse tissues and maintain an
appropriate blood pressure.
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Nursing Diagnoses and Outcomes
0406 Tissue Perfusion: Cerebral(Moorhead et al, 2004).
1402 Anxiety Self-Control (Moorhead et al, 2004). Ineffective Coping
Risk for Falls Decreased cardiac output
Fear and anxiety
Click on nursing diagnosis for correlating nursing outcome.Then click on the nursing outcome for further explanation.
Patient is able to utilize actions to reduce stress,
tension and apprehension.
Patient is able ask for help and reduce risk factors for falls. Patient has adequate
cerebral perfusion to prevent falls.
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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 http://www.cdc.gov/dhdsp/library/fs_atrial_fibrillation.htm
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References
• Cleveland Clinic. (2010). Mechanisms of atrial electrical remodeling. Retrieved from http://my.clevelandclinic.org/heart/atrial_fibrillation/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/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.
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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/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-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.
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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