Congestive Heart Failure Introduction Of Patient Nursing Essay

Congestive Heart Failure Introduction Of Patient Nursing Essay This cases study was conducted on February 13th, 2012. This patient will be identified by the initials AH throughout this paper. AH is a 91-year-old Caucasian female. Her mood is as expected for her age and culture. This patient agreed to work with me during her hospital stay and continuation of follow up information after discharge. AH was admitted to the hospital on February 09th, 2012 onto the medical floor. This patient was brought into the emergency department by her son, DH, at approximately 9:00 a.m. on February 09, 2012. AH stated she had an increase of shortness of breath, weakness throughout her body, and her ankles were swollen. When asked about the history of these symptoms, AH stated these symptoms have been present since Sunday February 05, 2012. AH went into the doctors office in her hometown and was told to go into the emergency department at the hospital by the physician. On assessment at the emergency department, AH had a temperature of 96.9 degrees Fahrenheit, a pulse of 130 beats per minutes, respirations of 20 breaths per minute, blood pressure of 192 systolic over 105 diastolic, and a pain level of 0 out of 10 on the pain rating scale. Assessment findings were crackles, bilaterally with auscultation, a non-productive cough occasionally, irregular heart rate, 3+ pitting edema bilaterally in lower extremities from the knee down and in feet. This patient had a delayed capillary refill and neck vein distension. AH also had palpable pulses with upper extremity pulses being strong and lower extremity pulses being weak. This patient was admitted with congestive heart failure and atrial flutter with rapid ventricular response. This patient has a history of hypertension, arthritis, hard of hearing, occasional urinary tract inf ections and had a myocardial infarction in 1990. AH had two previous surgical procedures in her life. She has had a left hip replacement in 2006 and a right hip replacement in 2007. AH denies any significant family health history. She also denies any current use or history of alcohol consumption, tobacco use, or drug use. She is not on any supplemental oxygen at home. AH was able to state name, dose, and reason for home medications. These medications are Bumex water pill 1 MG orally taken daily, Clonidine blood pressure pill 0.1 MG orally taken three times a day, Metoprolol blood pressure pill 50MG orally taken daily, and Nitroglycerin for heart 2.5MG orally taken two times a day. I was able to do a total head to toe assessment on February 13, 2012. AH is 182.90 pounds, 60.00 inches tall, and has a body mass index of 35.72. AH is categorized as obese with this body mass index result. This patient is alert and oriented to person, place, and time. This patients pupils are equal, responsive, and reacts to light upon inspection. AH does have slight pitosis of the right upper eyelid. This patient does wear eyeglasses to read. Her total Glasgow Coma Scale is rated at a 15 out of 15. This is a perfect score and shows no impairments. This patient communicates verbally with no problems. AH has full movement in all four extremities and has intact circulation, movement, and sensation. When asked about history of falls, AH stated she had no current or past falls. Her skin is pink, warm, and dry without diaphoresis but has slight purplish discoloration bilaterally on shins from knee to ankle. When assessing AH respiratory status, she stated that she was not experiencing an y distress or shortness of breath currently but does experience this with exertion. AH is not on any supplemental oxygen. Her oxygen saturation was at 94% on room air. Upon auscultation this patients lungs were clear bilaterally in upper lobes and diminished bilaterally in lower lobes. Her respirations were at 16 breaths per minute. Her chest configuration is symmetrical. I did observe a weak non-productive cough occasionally during this assessment. During the cardiovascular assessment, apical pulse was 84 and her radial pulse was 80. This showed a pulse deficit of 4 beats per minute, which could be due to the irregular heartbeat (atrial flutter) with the rapid ventricular response. Patient was on telemetry to monitor for abnormalities during admission. S1 and S2 were heart upon auscultation. AH had a blood pressure of 167 systolic over 82 diastolic on her right upper extremity. AH did have distended neck veins upon inspection, which is a sign of congestive heart failure. AH denied any chest pain. This patient does not have any implanted cardiac defibrillator or pacemaker. This patients abdomen was soft and non-tender with bowel sounds active in all four quadrants. She is on a low sodium diet and states that she does follow the diet restrictions but when asked about exact amount of allowed sodium intake patient did not know. During her hospital stay AH was on a fluid restriction of 1.5 liters per 24 hours. Patient was able to adhere to fluid restriction but states she is on no fluid restriction at home. AH is continent of stool and urine but had Foley catheter in place per physician orders. AH is full weight bearing and has a steady gait but does use a walker for an assistive device while at the hospital. AH states she uses a wheelchair at home. AH has active range of motion and shows no limitations or discomfort within normal limits. AH was under no precautions or isolation. She had five different medications that I administered to her during her admission to the hospital that ranged from antibiotics, hypertension medications, to diuretics. These will be discussed individually in the following systems breakdowns. When asked about cancer screenings, AH denied any annual appointments. AH stated that she was not worried about this currently. AH also does not obtain influenza or pneumococcal vaccines annually and her last tetanus vaccine was unknown. From observation, this patients health promotion is low and patient may need education on importance to her health. When assessing this patients home life, AH stated she has never had any physical or emotional abuse. AH lives at home with her son DH. Her husband passed away several years ago so she arranged for her son to come live with her. DH provides transportation and assistance with activities of daily living for AH. She has a loving relationship with her son and he assists her with medical decisions. She states she is not afraid of her living situation. AH complied with medical regimen and asked questions when she was not sure of the situation. When asked about the history of her congestive heart failure and length of time she has been diagnose d, AH did not understand that she had congestive heart failure and did not know how long she has had this condition. She stated she would speak with her new physician. She will be set up with a new primary physician since she does not currently have one. With this information, this indicates an need for additional information about primary condition due to deficient knowledge stated by patient. Pathophysiology of Congestive Heart Failure The heart, blood vessels, and blood are components that make up the cardiovascular system. The pumping action of the heart consists of contraction and relaxation of the myocardial (muscle) layer of the heart. Each contraction and relaxation that occurs consists of one cardiac cycle. During diastole (relaxation), the ventricles fill with blood. Systole (ventricular contraction) then occurs, which propels the blood out of the ventricles and into the circulation. Cardiac performance can be calculated by measuring the cardiac output. Cardiac output is the amount of blood moving through either systemic or the pulmonary circuit per minute. (Huether McCance, 2008) Cardiac output is calculated by multiplying stroke volume (volume of blood ejected per beat during systole) and heart rate. The amount of blood a ventricle ejects during the cardiac cycle is called ejection fraction. Ejection fraction is calculated by stroke volume divided by end-diastolic volume (blood left in the blood after di astole). The normal ejection fraction is from 50%-70%. A decrease of ejection fraction is a hallmark sign of ventricular fraction, such as left-sided heart failure. The factors that determine cardiac output are preload, afterload, contractility, and heart rate. Preload is the volume and associated pressure generated in the ventricle at the end of diastole (ventricular end-diastolic volume). Preload is determined by the amount of venous return to the ventricle and the blood left in the ventricle after systole (end-systolic volume). Afterload is the resistance the heart has to overcome to eject blood from the left ventricle. Heart failure is a term for the inability of the heart to work effectively as a pump. It results from different acute and chronic cardiovascular problems. The major types of heart failure are left-sided heart failure, right-sided heart failure, and high-output heart failure. The focus of this case study will be on left sided heart failure. Most heart failure starts out with failure of the left ventricle and progresses to both ventricles failing. Typical causes of left-sided heart failure are hypertension, coronary artery, and valvular disease. Decreased tissue perfusion from poor cardiac output and pulmonary congestion indicate left ventricular failure. Left-sided heart failure is also known as congestive heart failure; however not all cases of left ventricular failure involve fluid accumulation. Left-sided heart failure can be further broke down to systolic heart failure and diastolic heart failure. (Ignatavicius Workman, 2010) Systolic heart failure happens when the heart is unable to contract forcefully enough during systole to eject sufficient amounts of blood into the circulation. Preload increases with decreased contractility, and afterload increases as a result of increased peripheral resistance in the vascular spaces (hypertension). The percentage of blood ejected from the heart during systole (ejection fraction) drops from the normal range (50%-70%) down to 40%. As this percentage decreases, tissue perfusion decreases and blood backs up into the pulmonary vessels. This creates symptoms of systemic and pulmonary congestion. Diastolic heart failure occurs when the left ventricle cannot relax enough during the rest period. When the ventricle cannot relax enough, stiffening of the ventricle occurs and prevents the ventricle from filling up with sufficient blood to ensure adequate cardiac output. This ventricle becomes less compliant because more pressure is needed to move the same amount of volume compa red to a healthy heart. (Ignatavicius Workman, 2010) When cardiac output is unable to meet the demands of the body, other areas of the body start to increase their workload to improve cardiac output. Theses mechanisms start off helping cardiac output increase but eventually have a damaging effect on the function of cardiac pumping. The compensatory mechanisms of heart failure are stimulation of the sympathetic nervous system, activation of the renin-angiotension system, release of pro-inflammatory cytokines, release of natriuretic peptides, release of vasopressin, and myocardial hypertrophy. (Ignatavicius Workman, 2010) These compensatory mechanisms will be discussed further in the appropriate body systems throughout this case study. There are many presenting signs and symptoms of heart failure that a patient may have. Signs and symptoms of left-sided heart failure are restlessness, confusion, orthopnea, tachycardia, dyspnea with exertion, fatigue, cyanosis, cough, crackles, wheezes, blood-tinged sputum, and tachypnea. AH has several of these problems. She has tachycardia, dyspnea with exertion, fatigue, orthopnea, occasional cough, tachypnea, and crackles heard with auscultation. These problems make AHs activities of daily living hard to perform at times. She does not use any supplemental oxygen during any of these times. AH is also showing signs and symptoms of right-sided heart failure that could indicate that her condition is progressing. These symptoms are distended jugular veins, and dependent edema. These symptoms of right-sided heart failure can be due to her history of a myocardial infarction, which could have caused the right ventricle to try and compensate for the increase in pulmonary circulation. Thi s leads to the right ventricle to dilate and begin to fail. This is the cause of the distended jugular veins and edema because the systemic venous circulation increases with the compensation of the right ventricle. Treatment of these symptoms is managed with the treatment of left-sided heart failure. (Huether McCance, 2008) There are several risk factors that put a patient at risk for heart failure. Common risk factors that put a patient at risk for heart failure are hypertension, coronary artery disease, cardiomyopathy, substance abuse with alcohol and tobacco use, dysrhythmias, cardiac infections and inflammations, diabetes mellitus, family history, obesity, and conditions such as hyperthyroidism. (Ignatavicius Workman, 2010) AH has several of these risk factors. She has a history of hypertension, obesity, atrial flutter (dysrhythmia), and past myocardial infarction. All of these have a negative affect on the cardiovascular system and lead to the worsening this patients heart failure. Lifestyle modifications can be made to decrease how some of these risk factors affect this patient. Dietary changes such as watching weight, low sodium, and balanced meals could reduce this patients obesity and hypertension. Also, adhering to medication regimen assists with controlling hypertension and removing retained water from the body. Chest x-rays can be helpful in the diagnosis of left ventricular failure. The problem with chest x-rays is that it may lag behind the clinical findings as much as 24 hours. You may see that the heart is enlarged (cardiomegaly) which can be due to hypertrophy and dilation. AH had a chest x-ray done on February 08, 2012. The reason this was done was because of dyspnea. Results obtained from physician were trachea midline, mild prominence of interstitial markings in bilateral lung fields without lobar consolidation, basilar atelectasis, elevated left hemidiaphragm, no evidence of pneumothorax or pleural effusion, mild cardiomegaly, ectatic aorta with vascular calcification and degenerative changes involving shoulder joints. Echocardiograms are considered the best tool in the diagnosis of heart failure. You can see changes in the valves, fluid accumulation in the pericardial space (pericardial effusion), chamber enlargement, and ventricular hypertrophy. This test can also determine eject ion fraction, which shows how bad the ventricular hypertrophy is decreasing the amount of blood ejected from that ventricle. An electrocardiogram may show ventricular hypertrophy, dysrhythmias such as atrial flutter with AH, and any degree of myocardial injury but is not helpful in determining the presence or extent of heart failure. (Ignatavicius Workman, 2010). This test would be helpful for this patient due to the fact of having a dysrhythmia and also have a past myocardial infarction. Laboratory assessments can also be helpful in diagnosis of heart failure. Electrolyte imbalances may occur from heart failure or because of side effects of medications, especially diuretics such as Bumex with AH. Regular assessments of sodium, potassium, magnesium, calcium, and chloride, are obtained. Any impairment of renal function resulting from inadequate perfusion causes the patients blood urea nitrogen and serum creatinine to be elevated and a decrease in creatinine clearance levels. A urinalysis can show if there is an increased amount of protein present in the urine and an elevated specific gravity due to the kidneys not adequately working. Hemoglobin and Hematocrit levels should be obtained to check to see if the heart failure is from anemia, which is a low level of red blood cells. This can be caused from the kidneys not creating enough erythropoietin, which regulates red blood cell production. B-Type natriuretic peptide (BNP) is used for diagnosing heart failure in patient s with dyspnea. An increase in BNP helps determine whether it is dyspnea from heart failure or lung dysfunction. Patients with atrial dysrhythmias and renal disease may also have elevated BNP levels. (Ignatavicius Workman, 2010) AH does have an atrial dysrhythmia (atrial flutter), which could cause an elevated BNP level even without the heart failure. Arterial blood gases could show if the patient is hypoxic due to the low oxygen level from fluid filled alveoli. Respiratory alkalosis could occur because of hyperventilation, respiratory acidosis could occur because of the carbon dioxide retention, and metabolic acidosis could be present from accumulation of lactic acid. (Ignatavicius Workman, 2010). AH did not have arterial blood gas values drawn to look at any abnormalities. TEST RANGE DATE: 02-08-12 DATE: 02-11-12 DATE: 02-13-12 WBC 5,000-10,000 mm3 8.89 mm3 10.00 mm3 RBC 4.2-6.1 X10 / g 4.70 5.11 HGB 11.5-17.5 g/dl 13.8 g/dl 14.8 g/dl HCT 40-52% 43.7% 46.8 % PLATELETS 150,000-400,000 mm3 194,000 mm3 207,000 mm3 NEUTROPHILS 55-70% 78.0% 78.8 % LYMPHOCYTES 20-40% 10.3% 9.5 % MONOCYTES 2-8% 8.7% 9.2 % EOSINOPHILS 1-4% 1.7% 1.5 % BASOPHILS 0.5-1.0% 1.3% 1.0 % SODIUM 135-145 mEq/L 142 mEq/L 138 mEq/L 13 mEq/L CHLORIDE 98-106 mEq/L 105 mEq/L 98 mEq/L 93 mEq/L POTASSIUM 3.5-5.0 mEq/L 5.5 mEq/L 5.0 mEq/L 4.2 mEq/L CO2 24-30 mEq/L 28 mEq/L 28 mEq/L 35 mEq/L MAGNESIUM 1.3-2.1 mEq/L 1.9 mEq/L CALCIUM 9.0-10.5 mg/dl 7.7 mg/dl 7.8 mg/dl 7.3 mg/dl BUN 10-20 mg/dl 45 mg/dl 68 mg/dl 68 mg/dl CREATININE 0.5-1.2 mg/dl 1.29 mg/dl 1.58 mg/dl 1.52 mg/dl GFR 39 37 39 GLUCOSE 70-110 mg/dl 108 mg/dl AST 0-35 U/L 47 U/L ALT 4-36 IU/L 112 IU/L BNP 952 361 TROPONIN I 0.10 0.07 Treatments for heart failure are a combination of pharmacologic and non-pharmacologic therapies. Treatment often focuses on a combination of afterload-reduction with angiotension-converting-enzyme (ACE) inhibitors, reduction of catecholamine surges with beta blockers, and preload reduction with diuretics. ACE inhibitors reduce the production of angiotension II, which is a potent vasoconstrictor, from angiotension I. This will allow the patients blood pressure to lower to a normal range by vasodilation and also prevents ventricular remodeling (alteration in the structure and function of the heart). These medications are recommended for all patients with heart failure with lowered systolic function. With these medications you need to monitor for adverse effects such as dry hacking cough, hypotension, and renal dysfunction. AH was given Lisinopril 10MG tab QD during her hospital admission. Beta blockers protect the heart from the harmful effects of norepinephrine and epinephrine which a re circulating neurohormones released as a compensatory mechanism. This is aimed to reverse ventricular remodeling. Beta blockers help reduce mortality when combined with ACE inhibitors. This combination is referred to as the cornerstone of heart failure treatment. AH was given Lopressor 100MG tab BID to inhibit beta 2 adrenorecpetors of bronchial and vascular smooth muscle. (Jones Bartlett, 2010). This medication helps lower blood pressure and relieve patient of symptoms of heart failure. Diuretics are a key aspect in the relief of dyspnea and signs of sodium and water retention. This helps reduce blood pressure by removing extra fluid in the circulation. Also, putting the patient on sodium restriction decreases the resistance of diuretics. These medications can also be the first line of treatment for older adults with heart failure and fluid overload. AH was administered Bumex 1MG tab BID. This is a loop diuretic, which means it inhibits reabsorption of sodium and chloride in the ascending Loop of Henle and enhances potassium excretion. (Jones Bartlett, 2010) With this medication you must monitor the patients labs to prevent hypokalemia. Another treatment option for heart failure is cardiac glycosides. These drugs increase intracellular calcium, which increases contraction of the heart. Their function results from an increased cardiac output by increasing the force of contraction of the heart. (Jones Bartlett, 2010). Digoxin was the cardiac glycoside administered to AH during her hospital admission. AH received 125MCG tab QD. Potential benefits of this medication are increased contractility, reduced heart rate, slowing of conduction through the atrioventricular node and inhibition of sympathetic activity while enhancing parasympathetic activity. (Ignatavicius Workman, 2010). Monitoring potassium levels is very important for this medication due to lower levels causing patients to be more sensitive to digoxin, which can cause digitalis toxicity. These sign s and symptoms are also vague and nonspecific and include; anorexia, fatigue, changes in mental status and dysrhythmias. Watch for a loss of the P wave on an electrocardiogram. Also, you must monitor apical pulse and heart rhythm on these patients. You must make sure the heart rate is above 60 beats per minute. Any drug that increases the workload of the heart will also increase its oxygen demand. Patients should be monitored for chest pain while taking digoxin. Non-pharmacological interventions for heart failure are ventilation assistance, energy management, and nutrition therapy. Ventilation assistance is an important aspect of treatment for heart failure patients. This allows the patient to have adequate oxygen and carbon dioxide exchange in the lungs. Depending on the patients oxygen saturation and dyspnea, they may need supplemental oxygen prescribed by the physician. Positioning the patient in a high Fowlers position, and keeping the head of the bed elevated over 45 degrees will minimize respiratory efforts. AH did not receive supplemental oxygen, but maintained adequate ventilation by sitting in a bed side chair most of the time during her admission. She was unable to sleep in the hospital bed due to complaints of orthopnea so she also needed to sleep in the chair. (Ignatavicius Workman, 2010) Energy management will help prevent fatigue and perform activities of daily living to the best of their ability. Steps to take to promote ener gy management is monitor patient response to activity, determine patients physical limitations, encourage alternate rest and activity periods, arrange physical activities to reduce competition for oxygen supply to vital body functions, encourage physical activity, monitor patients oxygen response, and teach patient techniques of self-care that will minimize oxygen consumption. (Ignatavicius Workman, 2010) AH was able to ambulate to the bathroom when needed, but was unable to ambulate larger distances. She maintained adequate oxygenation with adequate rest periods when she became short of breath. AH is able to identify when these rest periods need to be taken on her own. Nutrition therapy is also a key aspect in the treatment of heart failure. This treatment targets sodium reduction and water retention. Physicians may prescribe sodium restrictions to decrease fluid retention. Since sodium follows water, a decrease in sodium allows for a decrease in retained water. AH was on a sodium restricted diet but was unable to state the exact amount of allowed daily sodium. All she could state was that she was not allowed to add extra salt to meals. Some patients are also placed on fluid restrictions. This allows for the body to excrete retained fluid in the body without having work harder with additional fluid intake. The restriction depends on the patient and the extent of the heart failure. AH was put on fluid restrictions by her physician. She was allowed 1.5 liters of fluid per 24 hours. AH was able to comply with this restriction. Assistive personnel need to be accurate in measuring intake and output for these patients. Weighing these patients daily is a key factor for heart failure. This allows seeing if the patient is retaining extra fluid which could cause congestion and result in worsened heart failure. 1 kilogram of weight gain or loss equals 1 liter of retained or lost fluid. The same scale should be used everyday at the same time of day (morning) wearing close to the same amount of clothing for the most accurate assessment of weight. (Ignatavicius Workman, 2010) Cardiovascular The heart, blood vessels, and blood all make up the cardiovascular system. The hearts pumps the blood through a network of blood vessels and delivers oxygen, carbon dioxide, and nutrients to the cells and tissues of the body. This circulatory system also removes waste products of cellular metabolism. (Huether McCance, 2008). The blood is carried away from the heart by arteries that branch into capillaries and provide the body with all the nutrients needed to properly function. Veins carry the blood from the capillaries throughout the body back to the heart where the system starts the process over. Since AH has congestive heart failure (as described above), hypertension, atrial flutter, and previous myocardial infarction, her cardiovascular system is greatly affected. One compensatory mechanism that occurs in the cardiovascular system due to congestive heart failure is myocardial hypertrophy. This is enlargement of the myocardium and can be with or without dilation of the chamber. The heart walls thicken to provide more muscle mass. This results in more forceful contractions. This further increases cardiac output. Often a hypertrophied heart is slightly oxygen deprived. All the compensatory mechanisms contribute to an increase in consumption of myocardial oxygen. When the demand for oxygen increases, and the reserve of the myocardium has been exhausted, manifestations of heart failure develop. AH has a history of hypertension. Hypertension is a consistent elevation of systemic arterial blood pressure. It is defined as a sustained systolic blood pressure of 140 mm Hg or greater systolic pressure or a diastolic pressure of 90 mm Hg or greater. (Huether McCance, 2008) There are four different classifications of hypertension. These are normal, prehypertension, stage 1 hypertension, and stage 2 hypertension. AH is categorized in stage 2 hypertension with her systolic blood pressure ranging around 167 mm Hg. This stage of hypertension puts her at risk for damage to target organs such as her brain, kidneys, and heart. Since systolic hypertension is the most significant factor causing target organ damage, this puts AH at an even higher risk. AH also has an elevated diastolic blood pressure ranging around 82 mm Hg. She would be categorized as prehypertension with this value. When a patient has hypertension both by systolic and diastolic measurements, they are diagnosed with primar y hypertension. A specific cause for primary hypertension has not been identified but it is found that a combination of environmental and genetic factors can be the cause of development. Factors associated with primary hypertension are family history, advancing age, gender (more common in women after age 55), black race, high dietary sodium intake, glucose intolerance, cigarette smoking, obesity, heavy alcohol consumption, and low dietary intake of potassium, calcium, and magnesium. (Huether McCance, 2008) AH has several of these factors which are a family history of hypertension, advancing age, female gender, obesity, and poor nutritional status. Many of these factors are also risk factors for other cardiovascular disorders. With AH, the history of myocardial infarction and congestive heart failure all accumulate to poor cardiovascular effects. Pathophysiologic mechanisms mediate these effects that include; the sympathetic nervous system, the renin-angiotension aldosterone system, and natriuretic peptides. The systemic arterial pressure is made up of cardiac output and total peripheral vascular resistance. Total peripheral vascular resistance is the resistance of blood flow in systemic blood vessels. Cardiac output is determined by multiplying stroke volume and heart rate. Stroke volume is the amount of blood ejected by the ventricle with each beat of the heart. Control of peripheral vascular resistance (dilation or constriction) is controlled by the autonomic nervous system (sympathetic and parasympathetic) and circulating hormones (epinephrine and norepinephrine). Any factor that affects peripheral vascular resistance, heart rate, or stroke volume affects systemic arterial pressure, which affects the patients blood pressure. If all increase, blood pressure will increase. If all decrease, blood pressure will decrease. Four control systems play a major role in maintaining blood pressure; the arterial baroreceptor system, regulation of body fluid volume, the renin-angiotension aldosterone system and vascular autoregulation. The arterial baroreceptors monitor the arterial pressure and counteract a rise in arterial pressure by mediated cardiac slowing and vasodilation. (Ignatavicius Workman, 2010) Changes in fluid volume and renin-angiotension aldosterone system will be discussed further in the renal system. Patients with hypertension are often asymptomatic, however patients may have headaches, dizziness, fainting, facial flushing. AH had no complaints of any of these symptoms, but I did observe facial flushing. AH stated that she has had blood pressure issues for quite some time now. AH is on several medications to help assist the body in lowering her blood pressure. She is taking Lopressor 100 MG tab BID (beta blocker), Digoxin 125 MCG tab QD (cardiac glycoside), Lisinopril 10 MG tab QD (angiotension converting enzyme inhibitor) and also Bumex (loop diuretic). All of these medication help lower her blood pressure which will decrease the workload of the heart which assists in compensating in the effects of her congestive heart failure. Atrial flutter is a rapid depolarization occurring at a rate of 250 to 350 times per minute. This rapid depolarization is caused from the electrical current circulating in a small circle within the atria instead of moving from one end to the other. This current travels in a circle because conduction is slowed due to heart damage and the myocardial cells are unable to activate. (Huether McCance, 2008). This is considered a supraventricular tachycardia due to the fact that it is above the ventricle. The atrioventricular node (between the right atrium and right ventricle) in the heart blocks the number of impulses that reach the ventricles as a protective mechanism. (Ignatavicius Workman, 2010). Atrial flutter has many causes but two causes that are related to AH are ischemic heart disease (myocardial infarction), and heart failure. Symptoms are palpitations, weakness, fatigue, shortness of breath, nervousness, anxiety, syncope, angina, and signs of heart failure. AH has several of th ese symptoms but they also could be due to her heart failure. The patient with a normal ventricular rate is usually asymptomatic. Due to her left ventricle conducting at a slower rate, she is at risk for having these symptoms. With these