Congestive Heart FailureS. Schneider**** **** College

Congestive Heart FailureDefinitionCongestive heart failure (CHF), formerly referring to just left sided heart failure, is a common, yet complex, clinical disorder that can result from any functional or structural cardiac disorder that impairs the ventricles ability to fill with or eject blood.(Figueroa, M. and Peters, J., 2006, pg. 402). Congestive heart failure may be acute or chronic and ranges from mild to severe in nature. There are two sub-types: systolic and diastolic. Systolic heart failure results when the heart has insufficient strength to contract forcefully enough to eject adequate amounts of blood into the circulation. Diastolic heart failure occurs when the left ventricle cannot relax adequately during diastole (relaxation phase) which prevents the ventricle from filling with sufficient blood to ensure normal cardiac output and tissue perfusion.(Ignatavicius, D., and Workman, L., 2013, pg. 715). Within this paper we will be focusing in systolic heart failure.Risk factorsThere are major unmodifiable and modifiable risk factors to congestive heart failure. The major unmodifiable risk factors include age (over 65), family history, congenital heart defects, valvular heart disease, past myocardial infarction (heart attack), irregular heart rhythms, and coronary artery disease. (Mayo Clinic Staff, 2015). The major modifiable risk factors include sedentary lifestyle, obesity, uncontrolled diabetes mellitus, uncontrolled hypertension, poor diet and nutrition, alcohol use, and tobacco use (smoking, chewing, etc.) (American Heart Association (AHA), 2015).PathophysiologyCongestive heart failure (CHF) is both an acute and chronic disorder that develops when the heart is unable to maintain adequate ejection of blood and perfusion of organs. Cardiac dysfunction causes a drop in cardiac output which leads to the activation of several neurohormonal pathways. (Gorbunova, S., n.d.). As noted by Hobbs, R., & Boyle, A. (2014, March 1), in systolic dysfunction the body activates the sympathetic nervous system (through neurohormonal tracts) that increases heart rate and strength of contractions, which results in vasoconstriction that stimulates secretion of renin from the juxtaglomerular apparatus of the kidney due to loss of perfusion. Stimulation of the renin-angiotensin system as a result of increased sympathetic stimulation and decreased renal perfusion results in further vasoconstriction, sodium and water retention, and release of aldosterone. An increased aldosterone level, in turn, leads to sodium and water retention, and other complications. Preload and afterload increase as sodium and water are retained. Angiotensin II furnishes ventricular changes resulting in advancing myocyte contractile dysfunction. Natriuretic peptides are neurohormones that work to boost vasodilation and diuresis through sodium excretion in the kidney tubules. Brain naturietic peptide (BNP) is produced and excreted by the ventricles when the client has fluid volume excess from CHF. (Ignatavicus, D. & Workman, L., 2013). Another compensatory mechanism is the enlargement of the cardiac muscle, with or without the increase in ventricular size. These walls thicken to increase the force of contractions but may hypertrophy faster than collateral circulation can supply adequate blood supply. (Ignatavicius, D., & Workman, L., 2013).Complications The complications of CHF arise from the decrease in tissue perfusion. This decrease in perfusion leads to serious tissue damage and in turn congestion of the circulatory system. Such complications that can arise are: kidney damage/failure, heart valve problems, and liver damage. The kidney damage and/or failure arises from the decrease in blood flow which may require dialysis for treatment. Heart valve problems arise from the damage sustained from high pressure or from the enlargement of the heart muscle. Liver damage is done via the fluid backup which leads to scarring of the liver making it hard for the liver to function properly. (Mayo Clinic, 2015 August 18).

Table 1Client to Textbook Comparison

TextbookClient

Clinical Manifestations1. Cough2. Breathlessness3. Weakness4. Dizziness5. Acites6. Peripheral Edema7. JVD8. Cardiomegaly9. Decreased Mentation10. Decreased SpO211. Reduced Kidney Function12. Chest Pain13. Weight Gain1. None upon assessment2. Exertional related to pain from RLE infection3. Present, unable to hold self over while turning in bed. Weak to moderated grips and plantar/dorsifelxion.4. None noted upon assessment5. None noted upon assessment Abdominal obesity.6. +2-3 pitting edema on bilateral lower extremities, and +1 on bilateral upper extremities.7. None upon assessment or admission8. None noted upon admission9. Some forgetfulness/disorientation at times. Re-orientated easily. Noted that opioid pain medications have caused this in the past.10. Upon admission O2 Sat was in high 90s but currently in low 90s.11. GFR 66/5712. None upon assessment or admission13. Upon admission had gained 2-4 lbs; diuresing with Lasix. Current weight 80.28 kg.

Diagnostic Labs, Tests, Procedures1. History and Physical2. Urinalysis3. Troponin4. BNP5. Serum Electrolytes6. Arterial Blood Gases7. Hemoglobin and Hematocrit8. BUN and Creatinine & Protein9. Chest X-Ray10. Echocardiogram11. EKG12. MUGA1. Past smoker history for 30 years (quit in 2006), HTN, COPD, cataracts (surgeries in 08 and 13) worked as a sales manager at a department store and homemaker.2. Clear, straw colored, voided 25 mL, Sp. Gravity 1.004 (low), pH 5.0 - 9/14/15.3.