Left Bundle Dranch Blockade and Atrial Fibrillation - Essay Example

Left Bundle Branch Blockade and Atrial Fibrillation: A case study Introduction Older adults are more vulnerable to experience postoperative complications like cardiovascular, pulmonary, and neurologic aberrations due to the effects of aging on the physiological capabilities of their body systems. For instance, they tend to have lower levels of plasma proteins and decreased plasma osmotic pressure, which causes some loss of blood into the interstitial space (Huether and McCance 876). Arrhythmias, sometimes termed as dysrhythmias, frequently occur as a result of significant blood loss from surgery, electrolyte imbalance and failure of the natural body system to regulate the quantity of acids and bases. As a matter of fact, cardiac rhythm irregularities appear even on non cardiac surgeries caused by the overall injury and trauma. Homeostatic balance can be more difficult and challenging to manage in this particular age group. In this paper, a case study of an older patient diagnosed with Left Bundle Branch Block (LBBB) and fast Atrial Fibrillation (AF) after a Total Knee Replacement (TKR) will be discussed, including the assessment, pathophysiology, treatment and management. Atrial fibrillation (AF) may result after a Total Knee Replacement (TKR) especially in older adults as a consequence of hypercoagulability and proinflammatory states associated with anaesthesia and surgical trauma, hyperadrenergic state related to perioperative stress, hypoxia, and hypovolemia leading to increased myocardial oxygen demand. Specifically, tachycardia as the heart’s compensatory mechanism to supply the systemic circulation leads to subsequent arrhythmias. In addition to AF, Left Bundle Branch Block (LBBB) also occurs as an associated condition in older adults above 75 years old due to vascular incompetency and stasis. Usually, people with AF experience palpitations, dyspnea, syncope, fatigue and other cardiovascular and pulmonary manifestations. However, the most important danger posed by LBBB and AF is the hemodynamic stagnation which promotes the thrombus formation and decreased cardiac output. Patient History The patient is an 83-year-old gentleman who had undergone a total knee replacement on August 16, 2011. His past medical history was significant for hypertension and arthritis. He reported to have past medical history of atrial fibrillation. On the other hand, he stated independence on performing most of his activities of daily living including household chores without difficulties. He claimed not having episodes of orthopnea or paroxysmal nocturnal dyspnea. He was able to walk half a mile before becoming short of breath. Impaired with worsening arthritis, the involved knee caused immobility problems and extremely debilitating pain that occurred usually after an exertion. In a short walk, the patient’s knee was traumatically injured that prompted surgical intervention. The patient qualified for the operation after the panel of pre operative assessment was carried out. However, the patient manifested shortness of breath and chest pain two days after the operation. He was then transferred to an orthopaedic centre to manage the acuteness of the symptoms. Also, the patient was connected to a cardiac monitor and an electrocardiographic reading was taken. He was initially given Bisoprolol 2.5 mg but the condition showed no improvement. At that same night, the patient was transferred to Critical Care Unit of Royal Sussex County Hospital where blood studies were run through. His final diagnosis is Left Bundle Branch Block (LBBB) and fast Atrial Fibrillation (AF). Assessment Cardiac complications resulting from surgery are the result of an intricate and dynamic relationship among patient- related risk factors including the patient’s functional capacity, procedure-related risk factors, and the circumstances surrounding the operation. Preoperative patient evaluation begins with obtaining a detailed history and physical examination (Fleisher et al. 165). After the total knee replacement operation, the patient was having Cell Trans drain in situ. This was used at the end of the operation to allow the patient to have blood that he lost returned to him. He was generally anxious, but oriented to time, place and person. He experienced dizziness and light- headedness. Speech, sensory and motor function also remained intact. The patient also experienced shortness of breath and chest pain that prompted urgent management and referral to critical care unit. His heart rate was noted to be 148 beats per minute. Blood results indicated plasma urea of 12.0 mg/dL, plasma creatinine of 134 mmol/L, and plasma troponin of 431. In addition, his hemoglobin was noted to be at 8.9 g/dL, platelet count of 131,000 mm3, red blood cell count of 2.79 million/µliter, and plasma calcium level of 2.11 mmol/L. The surgical dressing was intact. Nevertheless, the patient was connected to a cardiac monitor and electrocardiographic readings were taken. PR interval was indiscernible. QRS rate was variable and the rhythm was irregular. Left bundle branch block was clinically evident on the readings. Pathophysiology The heart pumps blood through a synchronized pattern and automatically regulated conduction of electrical impulses across its innate nerve- conducting tissues. This conduction system consists of the sinoatrial (SA) node, atrioventricular (AV) junction, and bundle branch system. Electrical impulse starts in the SA node, which is richly innervated by the sympathetic and parasympathetic nervous system. It fires at a rate of 60 to 100 beats per minute sufficient to cause atrial depolarisation. This should be reflected as a P wave on the ECG with a resulting atrial muscle contraction (Ignatavicius and Workman 709). From the SA node, the impulse spreads through the atria to the AV node. At the AV node, the impulse is delayed briefly to give the atria time to finish contracting. It then passes rapidly through the AV bundle branches and the Purkinje fibbers, resulting in a “wringing” contraction of the ventricles that begins at the heart apex and moves towards the atria. This contraction effectively ejects blood superiorly into the large arteries leaving the heart (Marieb 355). Significant blood loss, such as in a total knee replacement surgery, reduces the total amount of circulating blood in the body. With this, lesser amount of blood returns to the heart to sustain another cycle of circulation. In an attempt to sustain the systemic demands of oxygen, tachycardia results as an automatic response. Eventually, this increased heart rate evolves into fatal arrhythmias such as atrial fibrillation and bundle branch blockade. In the case of atrial fibrillation, multiple rapid impulses from many atrial foci, at a rate of 350- 600 times per minute, depolarize the atria in a disorganized manner. The result is chaos, with no P waves, no atrial contractions, and an irregular ventricular response. A rapid ventricular response reduces the time for ventricular filling, resulting in a smaller stroke volume. The atria merely quiver in fibrillation. Thus, there is a marked uncoordinated twitching of the atrial musculature. Because this rhythm causes the atria and ventricles to contract at different times, the atrial kick (the last part of diastole and ventricular filling, which accounts for 25% to 30% of the cardiac output) is also lost. This leads to symptoms of irregular palpitations, fatigue, and malaise. There is usually a pulse deficit, a numerical difference between apical and radial pulse rates. The shorter time in diastole reduces the time available for coronary artery perfusion; thereby increasing the risk for myocardial ischemia. Besides that, the significant reduction in the cardiac output caused by AF further compromises the heart’s perfusion ability. Eventually, dilation and blood stagnation in the atria can lead to thrombus formation, and this increases the risk of stroke or other embolic events (Ignatavicius and Workman 727). It may start and stop suddenly. In addition, atrial fibrillation may occur for a very short time (paroxysmal), or it may be chronic. Recurrent episodes of AF eventually lead to sustained AF. Essentially, atrial fibrillation is associated with advanced age, valvular heart disease, coronary artery disease, hypertension, cardiomyopathy, hyperthyroidism, pulmonary disease, acute moderate to heavy ingestion of alcohol, or the aftermath of a traumatic surgery including total knee replacement and total hip replacement surgery. Sometimes it occurs in people without any underlying pathophysiology, known as lone atrial fibrillation. On the other hand, left bundle branch block (LBBB) occurs when the electrical impulse, which normally depolarizes the right and left bundle branches at the same time, depolarizes the right bundle branch but not the left bundle branch. When left bundle branch is blocked, the supraventricular impulse is able to descend only down the right bundle branch and depolarise that ventricle. The left ventricle is depolarized afterward as the wave of depolarisation from the right ventricle proceeds from cell to cell to the left ventricle. This dyssynchronous electrical stimulation of the ventricles causes the right ventricle to contract before the left ventricle, which can lead to further decreased ejection fraction. On account of the left ventricular compromise, there is lesser blood that enters the right ventricle for pulmonary circulation. LBBB is frequently found in patients with systolic dysfunction (Smeltzer and Bare 796). The consequence of the intertwining phenomena of LBBB and AF lead to embolic problems such as in pulmonary embolism and neurologic stroke. In the patient’s case, shortness of breath and chest pains were the clinical signs manifested indicative of pulmonary complications. When an embolus travels in the pulmonary tree, it disrupts the microscopic vasculature and rapidly affects the surrounding tissues. This progression compromises gas exchange function of the respiratory system (Smeltzer and Bare 548). Management The therapeutic management of atrial fibrillation depends on its cause and duration and the patient’s symptoms, age, and comorbidities. In many patients, atrial fibrillation converts to sinus rhythm within 24 hours and without treatment. However, in this case, atrial fibrillation occurred simultaneously with left bundle branch block. Most importantly, the clinical manifestations of the client (SOB and chest pain) indicated pulmonary involvement, possibly embolism. Diagnostic Tools. The 12-lead ECG is still considered as an important tool for initial evaluation of patients undergoing non cardiac surgery. ECG records the heart’s electrical impulse conduction from the atrial depolarisation up to ventricular contraction and relaxation. This graphical presentation is helpful in identifying specific areas of the cardiac cycle that has been compromised. For example, a delay in depolarisation that prolongs the QRS duration to 0.12 seconds or longer indicate bundle branch block. (Ignatavicius and Workman 735). The presence of specific ECG changes, like ST-segment depression or left ventricular hypertrophy, in intermediate- or high-risk patients may indicate increased perioperative and long-term cardiac morbidity. Furthermore, Transesophageal Echocardiography may be performed to assess for the presence of atrial clots. These clots need to be cleared first before attempting for cardioversion. Drug Therapy. Since the initial findings of this client were shortness of breath and chest pain, oxygen therapy is given as a priority management even if the diagnosis of pulmonary embolism is not established yet. Adequate ventilation and rest are particularly prescribed for this patient to ensure hasty recovery from the TKR surgery and reduce systemic oxygen demands. For clients considered to have a high- risk of developing clots, as in this case, may be given anticoagulant therapy such as heparin and warfarin. Aspirin may be substituted for warfarin for those with contraindications to warfarin and those who are at lower risk of stroke (Revell 7). Moreover, antidysrhythmic drugs can be classified into Vaughn- Williams Classification according to their effects on the action potential of cardiac cells (Ignatavicius and Workman 736). Class I antidysrhythmics are membrane- stabilizing agents, such as quinidine sulphate and procainamide hydrochloride, which can be prescribed for acute phase of atrial fibrillation. Beta- adrenergic blockers, such as Bisiprolol prescribed in this client, belong to Class II. This class of antidysrhythmics compete with beta- adrenergic receptor sites to decrease heart rate and conduction velocity (Lewis et al. 305). To prevent recurrence and to maintain sinus rhythm, Class III antidysrhythmics like amiodarone hydrochloride may be prescribed. Finally, the Class IV drugs like verapamil hydrochloride can be used to treat atrial fibrillation by slowing down the ventricular response. This is accomplished by impeding with the inflow of calcium into the cells during depolarisation, thereby depressing the automaticity of the SA and AV nodes, decreasing heart rate, and prolonging the AV nodal refractory period and conduction. Other drugs not classified under Vaughn- Williams Classification, such as digoxin, are particularly useful in increasing vagal tone, and slowing AV nodal conduction. Although digoxin does not convert AF to sinus rhythm, it is useful in controlling the rate of ventricular response in chronic AF. Also, use of digoxin is recommended to control the ventricular rate in those patients with poor cardiac function (ejection fraction less than 40%). Cardioversion. Cardioversion is a synchronized countershock performed usually during emergency when hemodynamic instability pose fatal risk to the patient. The shock intentionally depolarises a critical mass of myocardium simultaneously during intrinsic depolarisation. However, chronic AF greater than 12 months’ duration is not likely to respond to this intervention. Surgical Intervention. Patients with recurring and symptomatic AF, as in this case, resistant to medical therapies may need to undergo radiofrequency catheter ablation to the bundle of His to block all conduction between the atria and ventricles. However, pacemaker implantation or surgery is further indicated for these patients because the procedure itself does not stop the atria from fibrillating. In the use of pacemakers, the leads are placed on the inner wall of the right atrium, right ventricle and on the outer wall of the left ventricle. This pacing device will provide synchronized electrical stimulation to the heart. Another surgical intervention indicated for patients with uncompensated AF is the maze procedure. This is an open chest surgical technique in which the surgeon places the mazes of sutures in strategic places in the atrial myocardium, pulmonary artery, and possibly the superior vena cava to prevent electrical circuits from developing and perpetuating AF. Sinus impulses can then depolarize the atria before reaching the AV node and preserve the atrial kick (Ignatavicius and Workman 728). Conclusion The progressive physiological changes caused by aging renders the person susceptible for post operative complications. In this particular case study, the intertwining of cardiac rhythm irregularity such as left bundle branch block and atrial fibrillation demands specialized and highly sophisticated medical intervention. The cardiac irregularity can be attributed to the effects of anaesthesia and other medications administered, and the overall surgical trauma during the total knee replacement surgery. Other patient-related factors also contributed to the cardiac dysrhythmias. Severe hypertension should be controlled before surgery when possible. The decision to delay surgery because of elevated blood pressure should take into account the urgency of surgery and potential benefit of more intensive medical therapy. Continuation of preoperative antihypertensive treatment through the perioperative period is critical. The presence of an arrhythmia or cardiac conduction disturbance should incite a careful evaluation for underlying cardiopulmonary disease, drug toxicity, or metabolic abnormality. Treatment should be prioritised for symptomatic or haemodynamically significant dysrhythmias, first to reverse an underlying cause and second to treat the specific arrhythmia. Indeed, management of older people undergoing a traumatic surgery can be quite challenging even for the most expert doctors. It is virtually impossible to predict accurately the outcome of any procedure since metabolic imbalances may not be reported even after a comprehensive pre operative assessment. Thus, the management of dysrhythmias should be taken as an individualized case. Patient- related and procedure- related risks should be considered as these may affect the outcome of any surgery. Works Cited Fleisher, LA, Beckman, JA, Brown, KA, Calkins, H, Chaikof, E, Fleischmann, KE, Freeman, WK, Froehlich, JB, Kasper, EK, Kersten, JR, Riegel, B, Robb, JF. “ACC/AHA 2007 guidelines on perioperative cardiovascular evaluation and care for noncardiac surgery: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines on Perioperative Cardiovascular Evaluation for Noncardiac Surgery).” Journal of American College of Cardiology 50 (2007): 159 –241. Print. Huether, Sue E. and Kathryn L. McCance. Understanding Pathophysiology, 3rd ed. St. Louis: Mosby, 2004. Print. Ignatavicius, Donna D. and M. Linda Workman. Medical- Surgical Nursing: Critical Thinking for Collaborative Care. Singapore: Elsevier, 2006. Print. Lewis, SL, Dirkse, SR, Heitkemper, MM, Bucher, L, and I Camera. Medical-Surgical Nursing: Assessment and Management of Clinical Problems, 7th ed. St. Louis: Mosby, 2007. Print. Marieb, Elaine N. Essentials of Human Anatomy and Physiology, 8th ed. Singapore: Pearson Education, 2006. Print. Revell, MR. Listing for Surgery Total Knee Replacement. Birmingham: NHS Foundation Trust, 2008. Print. Smeltzer, Suzanne C. and Brenda G. Bare. Brunner and Suddarth’s Textbook of Medical-Surgical Nursing10th ed. Philadelphia: Lippincott Williams and Wilkins, 2003. Print. Read More