Atrial Fibrillation Case Study - Essay Example

Pathophysiology Case Study Introduction Atrial fibrillation (AF or A-Fib) is one of the most common types of cardiac arrhythmia or abnormal heart rhythm which involves the atria of the heart (Wyndham, 2000). Since the heart muscles of the atria failed to have coordinated contraction, the patients’ heartbeats normally failed to occur at regular intervals. Cases of A-Fib are dangerous since failure to provide immediate medical intervention could result to stroke or damages in the major organs like heart and brain which could result to other forms of illness like dementia and more serious heart problems (Grubitzsch et al., 2008; Elias et al., 2006; Gillinov, Blackstone, & McCarthy, 2002; Savelieva & Camm, 2000). To prevent A-Fib from progressing to a more serious health problem, there is a strong need for health care professionals like nurses to learn more about the signs and symptoms, assessment information, proper medical management and treatment, diagnosis method, and nursing intervention when taking care of patients with A-Fib. As a nurse who is currently working in a critical care setting, my personal experiences with regards to handling patients with A-Fib will be tackled in this report. As part of going through the case of D.B.S. which I have encountered once in my entire nursing profession, the pathophysiology behind A-Fib, assessment information, medical management and treatment including the best nursing management will be tackled in details. In line with this, analyzing how the patient have responded to the pathological changes that normally occur in A-Fib is useful in terms of having a better understanding on how the said disease would progress over time. Eventually, three (3) nursing diagnosis with its corresponding nursing intervention will be provided at the end of this report. Case of D.B.S. With the complaints of weakness, fatigue, dizziness, fainting smell, palpitation, irregular heartbeat, and difficulty of breathing, D.B.S. is a 49 year-old African American who was admitted at the emergency ward of X hospital last January 2010. Having suspected a sign of heart problem, I immediately prepared the machine and assisted the physician in taking the electrocardiogram (ECG) in order to record the patient’s electrical activity of the heart through the use of skin electrodes. Diagnostic Test for A-Fib As soon as the patient was admitted at the emergency department of X hospital, the patient’s vital signs were taken and recorded. In line with this, the patient’s vital signs includes: BP of 190/110, RR of 25 breaths per minute, temperature of 37.2oC, and pulse rate of 140 beats per minute was recorded. In a normal heart beat, the ECG tracing would normally show a P wave, the QRS complex, a T wave, and the U wave (National Heart Lung and Blood Institute, 2010). Based on the patient’s first ECG test, the ECG result was normal. However, the patient would experience the same difficulty of breathing and shortness of breath. For this reason, I suggested to the physician that the patient should take another ECG test to verify the main cause of heart breathing problem. (See Appendix I – ECG of Normal Heartbeat on page 12) Based on the patient’s second ECG result, there was a clear absence of the P waves and irregular R-R intervals. As explained in the study of Fuster et al. (2006), the main cause of the absence of P waves and irregular R-R intervals is due to the irregular conduction of the ventricles’ impulses. It was eventually verified by the physician that the second ECG result clearly indicates the patient is suffering from an early stage of A-Fib. (See Appendix II – ECG of the Patient with A-Fib on page 13) Right after taking the patient’s ECG test, the physician gave an instruction to subject the patient to a non-invasive transthoracic echocardiogram (TTE) to verify the case of A-Fib before giving the patient the necessary treatment. In general, TTE – is ultrasound-based scan to identify valvular heart disease performed to further diagnose A-Fib. This test is necessary to minimize the risk that the patient would suffer from stroke. Through TTE, the size and function of the patient’s left and right atrium can be monitored. In line with this, significant enlargement of the patient’s left and right atrium suggests that the patient is suffering from A-Fib (Fuster et al., 2006). Since the patient have rapid pulse rate every now and then, the physician ordered that the patient be placed on Holter monitoring system. This particular electronic gadget measures the patient’s heart electrical activity of the central nervous system for a time span of at least 24 hours upon the admission. Eventually, it was confirmed that the patient has fibrillation in the right atrium. Signs and Symptoms of A-Fib A-Fib is normally accompanied by signs and symptoms related to irregular and rapid heart rate. In line with this, the common signs and symptoms that are significantly associated with the presence of A-Fib include: dyspnea (shortness of breath), chest discomfort, dizziness, fatigue, palpitation, and syncope (Fuster et al., 2006; Savelieva & Camm, 2000). Because of the presence of shortness of breath, patients with A-Fib could not tolerate tedious exercises because this type of physical activities could strain the patient’s heart. Since the patient complaints only weakness, fatigue, dizziness, palpitation, irregular heartbeat, fainting smell, and difficulty of breathing suggest that any of combination of the common signs and symptoms of A-Fib may indicate that a person is suffering from A-Fib. In cases of paroxysmal A-Fib, specific symptoms are usually present whereas less specific signs and symptoms are present in a permanent A-Fib (Savelieva & Camm, 2000). Since most of A-Fib cases are secondary to other health problems, other signs and symptoms like angina or chest pain, hyperthyroidism such as excessive loss of weight and diarrhea, high blood pressure, or symptoms of lung-related diseases such as pneumonia, sarcoidosis, or pulmonary embolism may also occur (Fuster et al., 2006). Pathophysiology of A-Fib Genetic factors and inflammation can cause the development of A-Fib. Based on the study of pathophysiology behind A-Fib, it is believed that the progressive fibrosis of the atria caused by atrial dilation is considered as the primary factor that leads to pathologic changes observed in A-Fib (Sanfilippo et al., 1990). The presence of inflammation that could directly affect the heart can lead to the development of A-Fib. This can be explained due to sarcoidosis and/or autoimmune disorders which develop autoantibodies against the myosin chains (Journal of Atrial Fibrillation, 2010). Likewise, the mutation of the lamin AC gene is another pathophysiological explanation behind the development of A-Fib (Journal of Atrial Fibrillation, 2010). As soon as dilation of the atria occurs, the chain of events begins to activate the renin aldosterone agniotensin system (RAAS) which successively increases the development of matrix metaloproteinases and disintegrin (Journal of Atrial Fibrillation, 2010; Yang et al., 2010). Through the loss of mass in the atrial muscle, this process leads to the remodeling of the atrial fibrosis (Grubitzsch et al., 2008). Other than the loss of mass in the atrial muscle, remodeling of the atrial fibrosis can be a result of the sinus node (SA node) and atrioventricular node (AV node) which correlates with the sick sinus syndrome (Journal of Atrial Fibrillation, 2010; Fuster et al., 2006; Manios et al., 2001). With the prolonged episode of A-Fib, the dysfunction of the SA node becomes progressive. In summary, the presence of multiple re-entrant waveforms in the atria significantly affects the atrioventricular (AV) node. This causes the incidence of irregular tachycardia the patient was experiencing. If left untreated, the loss of contraction can result to the blood stagnation in the atrium which eventually leads to the development of thrombus formation (Borczuk, 2010). Assessment of Data There are many factors that can lead to the dilation of the atria. Among the common factors includes the presence of structural abnormality of the heart which can increase the intra-cardiac pressure. Among the common vulvular heart disease that can cause such abnormality in the structure of the heart includes: mitral stenosis, mitral regurgitation, and tricuspid regurgitation, hypertension, and congestive heart failure. In the case of the patient, his vital signs reflect some abnormality in his blood pressure (Yang et al., 2010). Upon admission, it was noted that his BP was 190/110. It only shows that one of the main causes of the patient’s dilation of the atria was due to hypertension. Normally, the heart beats at the rate of 60 to 80 beats per minute. Because of the fact that electrical signals coming from other parts of the heart disrupts the normal rhythm of the heart, the atria tends to beat rapidly up to 600 times per minute (Ryan, 2002). Basically, the right atrium receives blood from the systemic venous through the superior vena cava, inferior vena cava, and coronary sinus. Fibrillation in the patient’s right atrium hinders the blood flow through the patient’s heart’s chamber. This limits the exchange of oxygen and nutrients in the myocardial cells. The fact that the patient has hypertension which leads to right A-Fib explains why the patient was complaining about feeling weak, fatigue, dizzy, palpitation, irregular heartbeat, and problems with breathing during the time he was first admitted at the emergency ward. In general, the sudden onset of a regular tachycardia with the rate more than 140 beats per minute suggests a supraventricular tachycardia. In line with this, the rapid and irregular tachycardia with a pulse deficit suggests that the patient has A-Fib (Seller, 2000, p. 286). How the Patient Responded to the Pathological Changes in A-Fib Because of the abnormal cardiac functioning in relation to the development of A-Fib related to hypertension, the patient was grasping for air at the time he was admitted at the emergency room. Whenever the patient is experiencing occasional palpitation, the patient was having more difficulty trying to breath in more oxygen. Since it was the first time the patient was admitted for this kind of signs and symptoms, the patient had no idea that he was already going through the health consequences of A-Fib. Medical Management and Treatment As soon as the patient was admitted at the emergency room of X hospital, the patient was immediately placed on cardiac monitor and was given O2 supply. At the same time, the patient’s airways, breathing, and circulation were being monitored by regularly taking the patient’s vital signs. To get a record of the patient’s electrical signals from the heart, ECG, transthoracic echocardiogram, and Holter monitoring system was utilized. In most cases, patients who are diagnosed with A-Fib can be discharged from emergency department provided that they receive immediate medical treatment (Tracy, 2003). To counteract the life-threatening effects of A-Fib, the patient had to undergo medical treatment which includes pharmacologic therapy in order to keep the patient’s in sinus rhythm and control the rate of heartbeat, electrical cardioversion, and prevent the development of thromboembolic disease (Braunwald, 1997, pp. 641 - 656). As a treatment, pharmacologic cardioversion is given to patients with symptomatic signs like short duration of atrial fibrillation or failure in electrical cardioversion (Michael et al., 1999). Based on the study of Alboni et al. (2004), patients with atrial fibrillation can be advised to go through self-administration of either 300 mg of flecainidine or 600 mg of propafenone. IV beta-blockers or calcium channel blockers such as amiodarone, digoxin, diltiazem, or metoprolol can be given for rate control purposes among patients with rapid ventricular response and atrial fibrillation whereas procainamide, disopyramide, propafenone, sotalol, flecainide, amiodarone, ibutilide, and dronedarone can be given to patients with A-Fib and arrythmia (Borczuk, 2010). Nursing Management As part of the nursing management, it is crucial for nurses to monitor the patient’s vital signs. Basically, irregularities in the patient’s vital signs will enable the health care professionals to immediately respond to the needs of the patient. Likewise, nurses should monitor other physical signs like fever, infection or dehydration which can promote the development of tachycardia (Borczuk, 2010). Upon instructing the patient to take the right dose, right medication at the right time, nurses should instruct the patient to immediately consult the physician in case of any signs of discomfort and other health complaints like chest pain takes place upon taking the prescribed medication. Three (3) Nursing Diagnosis with Intervention Decreased Cardiac Output Related to Hypertension In relation to decreased cardiac output related to hypertension, the nurse should regularly monitor the variations in hemodynamic parameters like BP and heart rate. Proposed nursing intervention includes monitoring the BP every 15 – 30 minutes since changes in the patient’s blood pressure may indicate that the patient needs immediate medical intervention. The nurse should monitor the patient’s ECG for arrhythmia since decrease in the cardiac output may lead to significant changes in cardiac perfusion which causes dysrhythmias. Since coffee, cola and chocolates could stimulate cardiac functioning, the nurse should teach the patient to decrease the intake of beverages with caffeine. After 6 hours of nursing intervention, the client is expected to have no increase in the blood pressure. After 4 to 5 days of nursing intervention, the patient will maintain a normal cardiac output. Blurred Vision Related to Ineffective Tissue Perfusion Caused by Hypertension Nursing intervention includes monitoring the patient’s vital signs every 15 – 30 minutes to provide immediate action when necessary. As prescribed by the physician, nurses should administer vasoactive drugs and titrate in order to immediately decrease the blood pressure. Since the blurring of the patient’s vision may indicate cyanide toxicity due to increased intracranial pressure, the nurse should regularly observe and monitor patient’s complaints of blurred vision. After 5 hours of nursing intervention, the patient’s blood pressure will be set within the normal range. After 5 days of nursing intervention, the patient will have adequate tissue perfusion. Ineffective Breathing Pattern Related to Depressant Effect of Analgesics Nurse should assess the signs and symptoms of ineffective breathing patterns like shallow or slow breathing. As part of immediate nursing intervention, the nurse should place the patient in orthopneic position, semi- or high Fowler’s position. Doing so will enable the patient to breath better. Assist the patient with the use of incentive spirometer every hour since the use of this gadget will enable the patient improve the functioning of his lungs. It is also necessary to monitor signs and symptoms of impaired gas exchange such as restlessness, irritability, and significant decrease in the oximetry levels. In line with this, restlessness indicates an early sign of hypoxia. Hypoxia requires immediate medical intervention to avoid cognitive changes like memory loss. On the other hand, significant decrease in the patient’s PaO2 or significant increase in the patient’s PaCO2 indicates respiratory failure. The nurse should also check and assess the patient’s skin color since the development of cyanosis suggests that the patient requires the needed levels of oxygen in the body. Among the common causes of hypoxia includes arterial obstruction and venous obstruction among others. The absence of sufficient oxygen in the blood can lead to a permanent brain damage. In case the patient’s skin has blue discoloration, the nurse should immediately administer oxygen to the patient to avoid further health complications related to hypoxia. After 15 – 30 minutes of nursing intervention, the patient will be able to breathe normally. *** End *** Appendix I – ECG of Normal Heartbeat Appendix II – ECG of the Patient with A-Fib Note: Top ECG result with the red arrow indicates the ECG of a patient with atrial fibrillation. References Alboni, P., Botto, G., Baldi, N., et al. (2004). Outpatient treatment of recent-onset atrial fibrillation with the "pill-in-the-pocket" approach. New England Journal of Medicine , 351(23), 2384-2391. Borczuk, P. (2010, April 23). eMedicine. Retrieved June 5, 2010, from Atrial Fibrillation: http://emedicine.medscape.com/article/757370-overview. Braunwald, E. (1997). Heart disease. In: A Textbook of Cardiovascular Medicine. 5th Edition. Philadelphia, Pa: WB Saunders Co. Elias, M., Sullivan, L., Elias, P., Vasan, R., D'Agostino, R., Seshardri, S., et al. (2006). Atrial Fibrillation Is Associated With Lower Cognitive Performance in the Framingham Offspring Men. Journal of Stroke and Cerebrovascular Diseases , 15(5), 214-222. Fuster, V., Ryden, L., Cannom, D., et al. (2006). ACC/AHA/ESC 2006 Guidelines for the Management of Patients w/ Atrial Fibrillation: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines & European Society of Cardiology Committee for Practice Guidelin. Circulation , 114(7), e257-354. Gillinov, A., Blackstone, E., & McCarthy, P. (2002). Atrial Fibrillation: Current surgical options and their assessment. Annals of Thoracic Surgery , 74(6), 2210-2217. Grubitzsch, H., Menes, A., Modersohn, D., & Konertz, W. (2008). The Role of Atrial Remodeling for Ablation of Atrial Fibrillation. Annals of Thoracic Surgery , 85(2), 474-480. Journal of Atrial Fibrillation. (2010). Retrieved June 5, 2010, from Understand the biology: http://jafib.com/pc/index.php?cont=understand_biology. Manios, E., Kanoupakis, E., Mavrakis, H., Kallergis, E., Dermitzaki, D., & Vardas, P. (2001). Sinus pacemaker function after cardioversion of chronic atrial fibrillation: is sinus node remodeling related with recurrence? Journal of Cardiovascular Electrophysiology , 12 (7), 800-806. Michael, J., Stiell, I., Agarwal, S., & Mandavia, D. (1999). Cardioversion of paroxysmal atrial fibrillation in the emergency department. Annals of Emergency Medicine , 33(4), 379-387. National Heart Lung and Blood Institute. (2010). Retrieved June 5, 2010, from Your Heart's Electrical System: http://www.nhlbi.nih.gov/health/dci/Diseases/hhw/hhw_electrical.html. Ryan, S. (2002). Retrieved June 5, 2010, from Atrial Fibrillation Overview: http://www.a-fib.com/Overview.htm. Sanfilippo, A., Abascal, V., Sheehan, M., Oertel, L., Harrigan, P., Hughes, R., et al. (1990). Atrial enlargtement as a consequence of atrial fibrillation A prospective echocardiographic study. Circulation , 82(3), 792-797. Savelieva, I., & Camm, A. (2000). Clinical Relevance of Silent Atrial Fibrillation: Prevalence, Prognosis, Quality of Life, and Management. Journal of Interventional Cardiac Electrophysiology , 4(2), 369-382. Seller, R. (2000). Differential diagnosis of common complaints. Saunders. Tracy, C. (2003). The Modern Management of Minimally Symptomatic Atrial Fibrillation in the Post-AFFIRM. Current Treatment Options in Cardiovascular Medicine , 5(5), 347-354. Wyndham, C. (2000). Atrial Fibrillation: The Most Common Arrhythmia. Texas Heart Institute Journal , 27(3), 257-267. Yang, B., Chen, Y.-D., Li, T.-D., & Feng, Q.-Z. (2010). Endothelin-1 receptor blockade induces upregulation of renin-angiotensin-aldosterone system expression in terms of blood pressure regulation. Journal of Renin-Angiotensin-Aldosterone System , 11(2), 119-123. Read More