Congestive Heart Failure - Amazon S3



Case Study: Congestive Heart FailureAmazing PERRLA CustomerA Great Undisclosed InstitutionIntroductionThis paper explores the case study of a patient, Mr. John Doe, who has been admitted to a local hospital with diagnoses of congestive heart failure (also referred to as CHF), cardiomegaly, long-standing hypertension, aortic aneurysm, and stroke. To follow will be the normal anatomy and physiology of the heart and cardiovascular system, as well as the pathophysiology of the patient’s diagnoses, will be discussed. The possible causes, sign’s and symptoms, and possible treatments will also be explored. Next, the patient’s signs, symptoms, and treatments will be looked at and compared to the textbook signs, symptoms, and treatments. And lastly, Mr. Doe’s progression will be followed to show if his current treatments are proving to be effective. PathophysiologyNormally, the heart weighs between 7 and 15 ounces and is a little larger than the size of a fist. The heart is located in the center of the chest between the right and left lungs, and it is behind and slightly to the left of the sternum. The heart and circulatory system make up the cardiovascular system. The job of the cardiovascular system is to work as a pump to push blood and oxygen to the rest of the body through the arteries. Blood returns to the heart through a system of veins. The heart itself is divided into four chambers: the right atrium, right ventricle, left atrium, and left ventricle. In comparison, the left ventricle is the largest and strongest of the four chambers of the heart, followed by the right ventricle. A wall of muscle, called the septum, separates the right and left atria and ventricles ("Heart anatomy," n.d.). There are four heart valves that control the direction and flow of blood through the heart system. The four valves are the tricuspid, pulmonary, mitral, and aortic valves. Normal blood flow comes into the heart from the body system via venous return. Venous return has deoxygenated blood, full of carbon dioxide that will be exchanged for oxygen in the lungs. Venous return flows from the body into the superior and inferior vena cava and then into the right atrium. With every heartbeat, or contraction, blood is pumped into the next chamber due to the fact that the valves are one-way. Blood can go through a valve but cannot return back through it into the previous chamber. From the right atrium the blood goes through the tricuspid valve into the right ventricle. From the right ventricle the blood is then pumped through the pulmonary valve into the pulmonary arteries. The pulmonary arteries carry deoxygenated blood to the lungs where carbon dioxide is exchanged for oxygen. The now oxygen rich blood is carried through the pulmonary veins into the left atrium. Upon contraction, the blood is then pumped through the mitral valve into the left ventricle. The left ventricle is the most powerful pump; this chamber holds the largest amount of blood, and contracts the strongest. This powerful pump sends the oxygen rich blood through the aortic valve, and into the aorta. The aorta is the body’s largest artery and the one responsible for sending blood to the rest of the body ("Heart anatomy," n.d.). There is a certain force that the heart must pump against to push blood into the arteries and to the body. The force is exerted on the arterial walls when the left ventricle contracts during systole and the amount of force falls when the ventricle relaxes during diastole. Each heart contraction causes a constant force and relaxation on the artery walls. The system is called blood pressure. The systolic blood pressure is measured as the highest amount of force exerted on the arterial walls and diastolic blood pressure is the lowest pressure measurement on the arterial walls. Normal blood pressure is <120 systolic and <80 diastolic (less than 120/80), measured in mm of mercury. Arteries are made of elastic tissue, this tissue provides give so that they may stretch and relax during systole and diastole (Taylor, Lillis, LeMone, & Lynn, 2011). In the condition of congestive heart failure, the heart fails to work as an effective pump. CHF most commonly describes left sided heart failure with varying degrees of severity and length of time problem has persisted. Systolic heart failure results when the heart cannot contract forcefully enough to eject an adequate amount of blood into circulation. Preload and after load both subsequently increase as a result of increased peripheral resistance. Ejection fraction decreases from a normal 50% - 70% to below 40%. As it decreases blood accumulates in the pulmonary vessels. Diastolic heart failure happens when the left ventricle cannot relax enough after systole, and results in the ventricle not filling with sufficient blood to ensure enough cardiac output. Ejection fraction is more than 40%, but the ventricle becomes less compliant over time because more pressure is needed to move the same amount of volume as a healthy heart would. A common name for left sided heart failure is “forward failure” because cardiac output is decreased and blood will back up into the pulmonary system (Ignatavicius & Workman, 2010). Two of the major causes of congestive heart failure are chronic hypertension and undetected coronary artery disease (Ignatavicius & Workman, 2010). Mr. Doe had never been to the doctor before he presented to the Emergency Department, he has since been diagnosed with long-standing hypertension. Because of the fact the he has never seen a doctor before this hospital admission, it is unknown how long he has had hypertension. Chronic hypertension can cause heart failure because the heart has to work harder to pump against the increased pressure. This will cause the heart muscle to thicken over time. The heart will hypertrophy, causing enlargement of the heart- cardiomegaly, which is one of Mr. Doe’s diagnose. The heart muscles will become so thick that the heart itself cannot get enough oxygen, and will cause chest pain, also known as angina, which is also one of Mr. Doe’s symptoms. (Dugdale & Chen, n.d.). Mr. Doe was also diagnosed with an ascending aortic aneurysm. Aneurysms are a localized dilation of an artery, and the ascending aorta is the major blood vessel that carries blood from the left ventricle to the body. Aneurysms form when the artery is weakened. Causes of aneurysms include atherosclerosis, hypertension, hyperlipidemia, and cigarette smoking (Ignatavicius & Workman, 2010). Mr. Doe ‘s chronic hypertension was most likely a contributing factor to his aortic aneurysm. His lab results also revealed that he has high levels of LDL cholesterol. A combination of hypertension and high level of LDL could be the cause of his aortic aneurysm.Finally, Mr. Doe was also diagnosed with a stroke. A stroke is an interruption of blood flow to a vessel that supplies the brain. There are two types of stroke; ischemic which is caused by either an embolus or a thrombus that has occluded a cerebral artery, and hemorrhagic stroke which is caused by a bleed in one of the vessels that supplies the brain (Ignatavicius & Workman, 2010). Because Mr. Doe’s only risk factor for stroke is an elevated serum LDL level, I believe that this could be the cause of his stroke. He could have had plaque buildup that blocked blood flow to the brain, or plaque buildup somewhere else in the body broke free, forming a thrombus, and lodged in a vessel supplying the brain and cut off blood supply. Signs and SymptomsThe following table shows a comparison between the classic textbook signs and symptoms and Mr. Doe’s signs and symptoms of congestive heart failure. Mr. Doe has a majority of the textbook signs and symptoms, as his is a classic case of congestive heart failure.Table SEQ Table \* ARABIC 1Comparison of Textbook Signs and Symptoms and Mr. Doe's Signs and symptoms(Ignatavicius & Workman, 2010, p. 768)Textbook Signs and SymptomsMr. Doe’s Signs and SymptomsFatigueDecreased energy for past 6 monthsWeaknessWeakness in right hand gripAnginaCrushing feeling in chest- anginaOliguriaPatient reports normal urine outputWeak Peripheral pulsesPeripheral pulses palpable 2+Tachycardia, palpitationsTachycardia initially, but has now slowed to Bradycardia, most likely due to medicationsTachypneaRespirations 20/min, tachypneaDyspnea/breathlessnessShortness of breath- dyspneaCrackles and wheezes of the lungsNo crackles or wheezes, but diminished lung sounds notedIncreased Heart SizeChest X-ray revealed cardiomegalyElectrolyte imbalancesElectrolytes are in balance, normal levelsArterial Blood Gas imbalancesABGs abnormal indicating Respiratory alkalosis due to hyperventilationB-type natriuretic peptide (BNP) elevationBNP elevated- 293 is high, <100 is normalIrregular heart rhythm resulting from PACs, PVCs, or A-FibEKG revealed Sinus Bradycardia with 4 PVCsAbnormal ECG ECG revealed Left ventricular hypertrophy TreatmentIn this section, the common textbook treatments will be compared to the treatments that Mr. Doe is receiving. The most important goals of treatment for this condition is to improve gas exchange and increase the amount of cardiac output. By prescribing diuretics, accumulated fluids can be pulled from the system, allowing the blood pressure to decrease. This will relieve much of the workload on the heart. Many of Mr. Doe’s treatments correlate with the textbook treatments.Table SEQ Table \* ARABIC 2Comparison of Textbook Treatment’s and Patient’s Treatments ("Mayo Clinic," n.d.)Textbook TreatmentsPatient’s TreatmentsSurgery- Heart valve replacement, coronary bypass, heart transplant, myectomyPatient has not undergone any surgeriesMedical Devices- Ventricular assist device (VAD), cardiac resynchronization therapy (CRT), internal cardiac defribrillator (ICD)Patient does not have any medical devicesAce inhibitors- to decrease blood pressure, improve blood flow and decrease the heart’s workloadPrescribed Benazepril, and Ace-inhibitorBeta Blockers- to decrease blood pressure and slow the heart ratePrescribed metoprolol, a Beta-blockerDigoxin- to increase heart contractilityNot prescribed DigoxinDiuretic therapy- to lessen fluid overload in body and lungs and make breathing easierPrescribed Bumex and AldactoneDiet restriction- low fat, low sodium dietTeaching about diet modificationMeds to reduce lipids/cholesterolPrescribed Pravastatin, a lipid lowering agentExerciseTeaching about the importance of exerciseLimiting alcohol and caffeinePatient does not use alcohol or caffeine Smoking cessationPatient does not smokeReducing stressTeaching about stress reduction, and prescribed Ativan as needed for anxietyProgressDuring Mr. Doe’s admission, his progress has been evident. When presenting to the Emergency Department, Mr. Doe had severe chest pain, shortness of breath, and fatigue. With the prescribed medications, ample rest, and continuous monitoring of his condition, Mr. Doe has been able to recover from his recent symptoms. He no longer has chest pain, shortness of breath, or pain, and has an increase in energy. Mr. Doe’s long-standing hypertension and high cholesterol levels, along with no previous screening or regular checkups with a doctor, have led to very severe disease processes, even though Mr. Doe leads a healthy lifestyle, is not overweight, and does not smoke or drink. After reviewing all the risk factors for CHF, and the patient’s actual risk factors, the only conclusion that can be made is that the patient is genetically predisposed to hypercholesteremia and essential hypertension which overtime have led to congestive heart failure. His new medication therapy, lifestyle modifications, and knowledge about the disease process, will help Mr. Doe in controlling his congestive heart failure in the future. The treatment plan has so far been successful.ReferencesAnatomy of the heart - Texas Heart Institute Heart Information Center. (n.d.). Retrieved from heart failure - diagnosis and treatment at Mayo Clinic. (n.d.). Retrieved from , III, D. C., & Chen, M. A. (n.d.). Hypertensive Heart Disease. Retrieved from , D. D., & Workman, M. L. (2010). Medical-Surgical Nursing: patient-centered collaborative care (6 ed.). St. Louis, MO: Saunders Elsevier.Taylor, C. R., Lillis, C., LeMone, P., & Lynn, P. (2011). Fundamentals of nursing: the art and science of nursing care (7 ed.). Philadelphia, PA: Lippincott Williams & Wilkins. ................
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