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Table of Contents 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 Electrical System Mechanical System Definition of Atrial fib Signs and Symptoms ProceduresMedications Nursing Implications Aging processes and Atrial fib Normal Heart Function
Table of Contents 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. 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) American Heart Association, 2010
Table of Contents 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
Table of Contents 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 wave QRS complex Used with permission by EKG concepts, 2009
Table of Contents Ventricles Incorrect Quick Review Click on what is repolarizing during the QRS complex? Click where the electrical impulse originates in a normal sinus rhythm. Atria Correct!! Used with permission by EKG concepts, 2009
Table of Contents 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?
Table of Contents 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)
Table of Contents 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 ratetachycardic (National Heart, Lung, and Blood Institute, 2009).
Table of Contents 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
Table of Contents 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. Correct!!
Table of Contents 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).
Table of Contents 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)
Table of Contents 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
Table of Contents 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
Table of Contents 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)
Table of Contents 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
Table of Contents 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
Table of Contents 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).
Table of Contents Aging and Atrial Fibrillation A study of 88 patients undergoing open heart surgery showed: –Pediatric and Adolescent patients did not have mutated DNA - mtDNA –Older patients had mtDNA –Patients with atrial fibrillation had a higher level of mtDNA 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).
Table of Contents 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).
Table of Contents 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).
Table of Contents 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).
Table of Contents 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 –(Lai, L., Tsai, C., Su, M., Lin, J., Chen, Y., Tseng, Y., Huang, S., 2003).
Table of Contents 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).
Table of Contents Etiologies: Reactive Oxygen Species (Free Radicals) Atrial fib and neurohormonal activation.neurohormonal –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).
Table of Contents 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
Table of Contents 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).
Table of Contents Review Question How does norepinephrine effect atrial fibrillation? (click on the correct answers) Stimulates beta receptors Correct!! Slows Heart Rate Increases responsiveness of potassium channels Causes gene mutation Correct!!Incorrect
Table of Contents Review Question Free radicals, (such as nitric oxide and superoxide) contribute to atrial fibrillation by breaking down proteins and damaging DNA. True False Correct!! Incorrect
Table of Contents Treatment Options Several approaches are used to treat and prevent atrial fibrillation: Medications MAZE procedure Ablation Cardio- version
Table of Contents 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).
Table of Contents 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).
Table of Contents 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)
Table of Contents 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+
Table of Contents 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)
Table of Contents 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)
Table of Contents 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
Table of Contents 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
Table of Contents Nursing Diagnoses and Outcomes 3011 Activity Tolerance (Moorhead et al, 2004) Cardiac Pump Effectiveness (Moorhead et al, 2004) Circulation Status (Moorhead et al, 2004). Activity Intolerance Decreased Cardiac Output Ineffective Perfusion 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.
Table of Contents Nursing Diagnoses and Outcomes 0406 Tissue Perfusion: Cerebral (Moorhead et al, 2004) 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.
Table of Contents 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)
Table of Contents References 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( ). Borczuk, P. (2009). Atrial fibrillation. Emedicine. Retrieved from Centers for Disease Control and Prevention. (2010). Atrial fibrillation fact sheet. Retrieved from
Table of Contents References Cleveland Clinic. (2010). Mechanisms of atrial electrical remodeling. Retrieved from px. 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):
Table of Contents References Lehne, R. (2004). Pharmacology for nursing care, 5 th 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, 7 th edition. Lippincott.
Table of Contents References Ryan, S. (2002). Atrial fibrillation: resource for patients. Retrieved from Texas Heart Institute. (2010). Health Information Center. Retrieved from