Atrial fibrillation
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Atrial fibrillation

Atrial Fibrillation

Holly Everts, RN, BSN

Alverno College, MSN 621

Tutorial directions

Tutorial Directions

  • Return to the table of contents by clicking the button in the lower left corner.

  • Navigate forward and backward using the buttons in the upper right corner.

Table of


Learning objectives

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.

Table of contents

Table of Contents

Normal Heart Function

Definition of Atrial fib

Electrical System

Mechanical System

Signs and Symptoms

Aging processes and Atrial fib



Nursing Implications

The heart s mechanical system

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.


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

The heart s electrical system

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

Normal ekg rhythm

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

Quick review

Quick Review

Click where the electrical impulse originates in a normal sinus rhythm.

Try Again


Try Again

Click on what is repolarizing during the QRS complex?





Used with permission by EKG concepts, 2009

Case study

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?

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

(Porth, 2005)

American Heart Association, 2010

Pathology of the electrical system

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).

Ekg in atrial fibrillation

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

Fibrillation waves

Irregular QRS

Used with permission from P. Schwartz

Review question

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.


Rapid impulses released by the ventricles.

Rapid impulses released by AV node.

Incorrect, try again.

Incorrect, try again.

Pathology of the mechanical system

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).

  • Signs and symptoms of atrial fibrillation

    Signs and Symptoms of Atrial Fibrillation

    Symptoms vary greatly among individuals and include:


    Shortness of Breath

    Irregular heart rate


    Pulmonary edema


    Chest pain

    Risk for stroke

    (Porth, 2005)

    Review question1

    Review Question

    • Which of Mrs. B’s 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


    This would be caused by excited cells in atria

    Yes! Due to decreased perfusion to lungs


    Shortness of Breath

    Yes! Due to decreased cerebral perfusion


    Cardiac cells and ions

    Cardiac cells and Ions


    Sodium and Calcium enter the cell during depolarization.

    Potassium leaves the cell slowly during depolarization and quickly during repolarization.




    Cell during depolarization

    (Porth, 2005)

    Cardiac cycle and ions

    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)

    Review question2

    Review Question

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





    Try again, potassium is already in the cell


    Try again


    Review question3

    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.

    • Does not allow vitamin D to enter the cell

    Try again

    Try again

    • Inhibits electricity to flow through the cell.

    • Activates proteases that breakdown important cellular proteins.

    Try again


    Aging and atrial fibrillation

    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).

  • Aging and atrial fibrillation1

    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).

  • Etiologies stress and atrial fibrillation

    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 recoveryperiod (Otway, Fatkin & Vandenberg, 2007).

    • A number of potassium (K+) currents arehighly responsive to adrenergic stimuli.

      • Shortens the refractory period.

      • (Otway, Fatkin & Vandenberg, 2007).

    Review question4

    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).

    Stress is a genetic response that leads aging

    Age can cause genetic mutations that lead to atrial dysfunction and make cells more vulnerable to stress hormones


    Etiologies inflammation and atrial fib

    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).

    Etiologies reactive oxygen species free radicals

    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).

    Etiologies reactive oxygen species free radicals1

    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).

    Etiologies reactive oxygen species free radicals2

    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).

    Review question5

    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.


    Incorrect, remember too much calcium in the cell releases nitric oxide

    Etiologies genetics and atrial fibrillation

    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).

    Review question6

    Review Question

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



    Stimulates beta receptors

    Slows Heart Rate



    Causes gene mutation

    Increases responsiveness of potassium channels

    Review question7

    Review Question

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





    Treatment options

    Treatment Options

    Several approaches are used to treat and prevent atrial fibrillation:



    MAZE procedure


    Procedures ablation

    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).

    Procedures for atrial fibrillation

    Procedures for Atrial Fibrillation


    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).

    Procedures for atrial fibrillation1

    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)

    Medications to treat atrial fibrillation

    Anti-arrhythmic medication classes

    Sodium channel blocker


    Beta Blockers


    Potassium Channel blocker

    Sotalol, Amiodarone, Tikosyn

    Calcium Channel blocker


    Other mechanisms

    Digoxin, Adenosine

    How do they work?

    Medications to treat Atrial Fibrillation





    Medications rate control

    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)

    Rhythm control

    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)

    Review question8

    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.



    Nursing implications

    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

    Nursing diagnoses and outcomes

    Nursing Diagnoses and Outcomes

    Patient is able to conserve energy and build endurance to complete activities of daily living.

    Activity Intolerance

    3011 Activity Tolerance (Moorhead et al, 2004).

    Decreased cardiac output

    Patient is able to eject enough blood to support systemic circulation.

    Decreased Cardiac Output

    0400 Cardiac Pump Effectiveness

    (Moorhead et al, 2004).

    Patient is able perfuse tissues and maintain an appropriate blood pressure.

    Ineffective Perfusion

    0401 Circulation Status

    (Moorhead et al, 2004).

    Decreased cardiac output

    Click on nursing diagnosis for correlating nursing outcome.

    Then click on the nursing outcome for further explanation.

    Nursing diagnoses and outcomes1

    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.

    Risk for Falls

    0406 Tissue Perfusion: Cerebral

    (Moorhead et al, 2004).

    Decreased cardiac output

    Click on nursing diagnosis for correlating nursing outcome.

    Then click on the nursing outcome for further explanation.



    • 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)



    • Aikio O, Pokela ML, Hallman M (2002). Pulmonary nitric oxide in preterm and term infants with respiratory failure Retrieved from,

    • American Heart Association. (2010). Atrial fibrillation. Retrieved from

    • American Heart Association. (2008). Atrial Fibrillation for professionals. Retrieved from

    • 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

    • Centers for Disease Control and Prevention. (2010). Atrial fibrillation fact sheet. Retrieved from



    • Cleveland Clinic. (2010). Mechanisms of atrial electrical remodeling. Retrieved from

    • EKG Concepts. (2009). Rapid cardiac arrhythmia tool. EKG Concepts, LLC.

    • Kang, S. (2010). Cardioversion. American Accreditation HealthCare Commission. Retrieved from

    • 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.



    • 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

    • National Heart, Lung, and Blood Institute. (2009). Understanding the Electrical Problem in Atrial Fibrillation. Retrieved from

    • 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.



    • Ryan, S. (2002). Atrial fibrillation: resource for patients. Retrieved from

    • Texas Heart Institute. (2010). Health Information Center. Retrieved from

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