Left-sided Heart Failure (Coursework Sample)

Concept Map and Case Study Questions [Student Name] [University] 6457950-109220Clinical symptomsOliguriaDependent peripheral edemaDyspneaTachycardiaBilateral crackles when breathingDecreased tolerance to physical activityPale / Cyanotic skinDizziness, fatigue & weakness1, 200Clinical symptomsOliguriaDependent peripheral edemaDyspneaTachycardiaBilateral crackles when breathingDecreased tolerance to physical activityPale / Cyanotic skinDizziness, fatigue & weakness1, 22400300-99695PathogenesisImpaired left ventricle (L.V.) function → ↓ Cardiac output → ↓ systemic blood volume → ↓ Kidney perfusion → ↓ Urine output (oliguria) → Peripheral edemaImpaired left ventricle function → ↓ blood flow from left atrium into the left ventricle → ↓Cardiac output → ↑ Pulmonary venous blood volume and pressure → fluid forced from pulmonary capillaries into the pulmonary tissues and alveoli → pulmonary interstitial edema → impaired breathing 1, 200PathogenesisImpaired left ventricle (L.V.) function → ↓ Cardiac output → ↓ systemic blood volume → ↓ Kidney perfusion → ↓ Urine output (oliguria) → Peripheral edemaImpaired left ventricle function → ↓ blood flow from left atrium into the left ventricle → ↓Cardiac output → ↑ Pulmonary venous blood volume and pressure → fluid forced from pulmonary capillaries into the pulmonary tissues and alveoli → pulmonary interstitial edema → impaired breathing 1, 2-371475-109855AetiologyHypertensionHypothyroidismCoronary artery diseaseValvular diseaseCardiomyopathy1, 200AetiologyHypertensionHypothyroidismCoronary artery diseaseValvular diseaseCardiomyopathy1, 2 causes55054502241551514475224155results in 485775205740Prolonged exposure0Prolonged exposure48577543815552450034861500 -371475125095Risk factorsHeart infectionsCongenital heart defectsHypertensionEating foods high in saturated fatsOld ageSmoking Stress 1, 2, 300Risk factorsHeart infectionsCongenital heart defectsHypertensionEating foods high in saturated fatsOld ageSmoking Stress 1, 2, 3 6524625234950DiagnosisHistory & clinical signsComplete physical examChest x-rayEchocardiogramElectrocardiogram.Blood testsCT scan & MRIPulse oximetry test1, 300DiagnosisHistory & clinical signsComplete physical examChest x-rayEchocardiogramElectrocardiogram.Blood testsCT scan & MRIPulse oximetry test1, 32447925291465Left-sided Heart FailureLeft-sided Heart Failure5313997187644Diagnosed byDiagnosed by 2095500181610This is a life threatening condition characterized by the inability of the left side of the heart to pump blood to the body leading to pulmonary congestion.00This is a life threatening condition characterized by the inability of the left side of the heart to pump blood to the body leading to pulmonary congestion.869632440195500839089040132000 4448175988060Therapeutic effect0Therapeutic effect17522831726565Patient survival rate0Patient survival rate485775740410PreventsPrevents485775597535436244984518500-3714751092834Primary PreventionEating balanced, healthy foods e.g. fruits and vegetables. 1, 2Exercising regularly. 1, 2, 3Quit / avoid smoking. 2, 3Maintaining healthy weight. 1Stress management. 1, 300Primary PreventionEating balanced, healthy foods e.g. fruits and vegetables. 1, 2Exercising regularly. 1, 2, 3Quit / avoid smoking. 2, 3Maintaining healthy weight. 1Stress management. 1, 326765252778125ComplicationProlonged diuretic therapy may produce both hypokalemia and hypernatremia resulting in weakness, fatigue, malaise and muscle cramps 100ComplicationProlonged diuretic therapy may produce both hypokalemia and hypernatremia resulting in weakness, fatigue, malaise and muscle cramps 12676525463550Course of diseaseWith Treatment – Vital signs (pulse, blood pressure and respiratory rate) drop to normal range, pulmonary edema diminishes and patient shows tolerance for increased activity.Without Treatment – Decreased tissue perfusion impairs cell metabolism leading to cardiogenic shock, coma then death.1 0Course of diseaseWith Treatment – Vital signs (pulse, blood pressure and respiratory rate) drop to normal range, pulmonary edema diminishes and patient shows tolerance for increased activity.Without Treatment – Decreased tissue perfusion impairs cell metabolism leading to cardiogenic shock, coma then death.1 8095615473075Need for Immediate treatment00Need for Immediate treatment8382000153035046291501864360Surgical placement of an implantable cardioverter defibrillator in patients with irregular heartbeats. Cardiac resynchronization therapy by placement of a pacemaker on the left ventricle to improve left ventricular function.Heart transplantation in patients with end-stage left heart failure. 100Surgical placement of an implantable cardioverter defibrillator in patients with irregular heartbeats. Cardiac resynchronization therapy by placement of a pacemaker on the left ventricle to improve left ventricular function.Heart transplantation in patients with end-stage left heart failure. 146291501616711Surgical00Surgical46291501378585Treatment00Treatment65341511616710Medical00Medical65341501863725Diuretics (e.g. furosemide and thiazide) to minimize edema. 2,3Vasodilators to lower blood pressure and increase blood flow. 1, 2Digitalis to strengthen the hearts contractility. 1Nutritional therapy. Consuming low sodium (2-3g/day) diet and avoiding excessive fluid intake. 1, 3 00Diuretics (e.g. furosemide and thiazide) to minimize edema. 2,3Vasodilators to lower blood pressure and increase blood flow. 1, 2Digitalis to strengthen the hearts contractility. 1Nutritional therapy. Consuming low sodium (2-3g/day) diet and avoiding excessive fluid intake. 1, 3 22574258540742257425854075-2762262854325PrognosisThe five-year mortality rate among patients admitted with pulmonary edema due left sided heart failure is about 42%. The prognosis is therefore poor. 400PrognosisThe five-year mortality rate among patients admitted with pulmonary edema due left sided heart failure is about 42%. The prognosis is therefore poor. 4 References 1. Brunner, L.S., & Suddarth, D.S. (2010). Left-sided heart failure. Textbook of medical-surgical nursing (12th ed., pp. 346-354). Philadelphia, PA: Lippincott Williams and Wilkins. 2. Grossman, S.C., & Porth, C.M. (2013). Left ventricular dysfunction. Porth's pathophysiology: Concepts of altered health states (pp. 588-596). Philadelphia, PA: Lippincott Williams and Wilkins. 3. Rosenkranz, S., Gibbs, S., Wachter, R., De Marco, T., Vonk-Noordegraaf, A., & Vachiery, J. (2015, October 27). Left ventricular heart failure and pulmonary hypertension. European heart journal, 37(12), 942-954. doi: http://dx.doi.org/10.1093/eurheartj/ehv512 4. The survival of patients with heart failure with preserved or reduced left ventricular ejection fraction: an individual patient data meta-analysis. (2011, August 6). European heart journal, 33(14), 1750-1757. doi:dx.doi.org/10.1093/eurheartj/ehr254 Question 1 An acute exacerbation of heart failure is a sudden worsening of the clinical signs associated with heart failure. Decreased blood flow from the pulmonary blood vessels into the left atrium results in an increase in both the pulmonary blood volume and pulmonary blood pressure. The increased pressure forces fluid to flow from pulmonary capillaries into the adjacent lung tissue and alveoli (Brunner & Suddarth, 2008). This movement of fluid results in pulmonary interstitial edema which impairs gaseous exchange at the lung. The normal respiratory rate in an adult human ranges from twelve to twenty breaths per minute (Marieb, Hoehn & Hutchinson, 2014). Respiration is controlled by breathing centers located in the medulla which determine the respiratory rate and the depth of breathing. Fluid accumulating in the pulmonary interstitium affects normal lung ventilation resulting in hypoxia. When hypoxia occurs, there is an increased level of carbon dioxide in the blood stream which is detected by chemoreceptors in the brain and the carotid and aortic bodies. Signals are therefore sent to the breathing centers in the medulla to increase the respiratory rate in an attempt to eliminate the accumulating carbon dioxide and eliminate hypoxia. As the pulmonary edema progresses, fluid moves from the pulmonary interstitium and starts filling the alveoli. Auscultation at the base of the lungs reveals crackles which denotes presence of fluid in the alveolar space. The fluid forms a froth in the alveoli resulting in insufficient alveolar ventilation. The patient then starts experiencing a sense of suffocation which is manifested as severe dyspnea. The froth in the alveoli also further impairs O2-CO2 exchange at the lungs. This results in a further decrease in oxygen uptake at the lungs and increased carbon dioxide retention in blood and tissues. A physician performing the pulse oximetry test will therefore detect a diminished blood oxygen level (SpO2). (Brunner & Suddarth, 2008). According to Grossman & Porth (2013), when low blood oxygen levels are registered, compensatory or adaptive responses are initiated by the body to ensure tissue perfusion is maintained to prevent cell death. The response involves stimulation of the sympathetic nervous system or the hormonal system which occurs minutes to hours after acute heart failure. Both try to maintain the heart’s pumping performance at normal levels. The sympathetic nervous system releases catecholamines into blood which speed up the heart rate and also act on the smooth muscles of blood vessels causing vasoconstriction. Alternatively, the hormonal system caus...