A nursing implication, when caring for a person with acute exacerbation of heart failure, is the need to manage fluid volume excess.
Explain the pathogenesis that lead to fluid volume excess when a person has developed an acute exacerbation of chronic heart failure.
Heart failure patients have either a high cardiac output that triggers systemic arterial vasodilation and under-filling of arterial circulation or decreased cardiac output that causes under-filling of the circulation in the arteries. The total quantity of blood is increased by increase in blood volume of the circulation in the veins and after-load rises. Increased after-load and a systolic dysfunction lead to increased left ventricular end-diastolic pressure; this plus pulmonary venous pressure leads to a buildup of alveolar pressure. The ability of the alveoli to absorb is overcome causing pulmonary congestion. In addition, reflexes stimulated by increased pressure in the arteries are minimized by reflexes stimulated by the high-pressure atrial circulation. For example, an increase in total quantity of blood involved with decompensated heart failure triggers the renin-angiotensin-aldosterone system leading to the production of angiotensin II. Angiotensin II leads to a cascade of physiological effects, including renal and peripheral vasoconstriction and increased synthesis of aldosterone. However, in acute heart failure, these effects are reduced by renal vasoconstriction and diminished delivery of sodium to the distal nephron. Arterial under-filling stimulates production of Arginine vasopressin that leads to an increase in plasma and urine osmolalities. This result is peripheral arterial vasoconstriction and increased re-absorption of water in the distal tubule leading to a reduction of sodium levels in the blood. Stimulation of neuro-hormonal system further enhances retention of water and sodium that causes edema, hyponatremia and pulmonary congestion.
Discuss two nursing strategies used to manage pulmonary edema, a consequence of fluid volume excess and provide evidence-based rationales for these strategies.
The objectives of fluid management strategies for left ventricular dysfunction are to provide relief from signs and symptoms of fluid overload, to achieve stability of hemodynamic status with no further damage to cardiac muscle cells and to minimize recurrent fluid overload.
Amelioration of low concentration of oxygen in the blood using non-invasive ventilatory therapies such as continuous positive airway pressure (Heart Foundation, 2011), is critical in order to improve oxygenation and minimize the need for mechanical ventilation and intubation.
Loop diuretics are fundamental in the management of pulmonary edema as an early part of hospital therapy because oral agents are irregularly absorbed altering the pharmacokinetics and pharmacodynamics. Intravenous administration of loop diuretics relieves signs and symptoms of pulmonary edema by lowering left ventricular filling pressures. The start dose of loop diuretics is high, dosage is titrated based on urine output and assessment of signs and symptoms (Albert, 2012). Also, prompt identification of the underlying cause in order to initiate specific therapy.
Intravenous frusemide (Lasix) is used in the management of an acute exacerbation of chronic heart failure.
Explain the mechanism of action of frusemide
Frusemide inhibits the Na-K-2Cl co-transporter in the ascending limb of the loop of Henle in the nephrons. The Na-K-2Cl co-transporter acts on the distal tubules without hindering aldosterone and carbonic anhydrase. The co-transporter eliminates the osmotic gradient in the kidney medulla and blocks positive and negative free water clearance.
When the co-transporter is inhibited, the loop diuretics reduce the re-absorption of sodium and chloride ions. They also decrease the lumen positive potential that arises from potassium recycling. In a physiological state, the lumen positive potential stimulates re-absorption of calcium and magnesium ions in the loop of Henle. Therefore, reducing the potential leads to a decrease in re-absorption of these divalent cations. Since calcium ions are normally reabsorbed in the distal convoluted tubule, loop diuretics cannot cause hypokalemia.
Through disruption of re-absorption of these ions, the renal medulla remains hypotonic, and the osmotic driving force of water is reduced allowing it to leave the collecting duct system. This results to increased urine production and decreased blood volume. Ultimately, pulmonary edema is improved.
Discuss the nursing implications when frusemide is given to a patient with acute exacerbation of chronic heart failure
A nursing implication when frusemide is administered to a patient with acute exacerbation of chronic heart failure is the need to monitor and manage, hemodynamic parameters, electrolyte levels and the overall fluid volume status[ CITATION Alb12 l 1033 ]. This is because use of diuretics can lead to electrolyte imbalance that causes dysrhythmias and hypotension which aggravate renal dysfunction.
Albert, N. M. (2012, April). Fluid management strategies in heart failure. Critical Care Nurse , 20-30.
American Heart Association. (2012, September 20). Types of heart failure. Retrieved August 21, 20114, from American Heart Association Website: http://www.heart.org/HEARTORG/Conditions/HeartFailure/
Heart Foundation. (2011, October). Guidelines for the prevention, detection and management of chronic heart failure in Australia. Retrieved August 21, 2014, from Heart Foundation website: http://www.heartfoundation.org.au/
Kelly, A. L. (1999). Left ventricular systolic heart failure resulting in acute pulmonary oedema; Pathophysiology and nursing management in th emergency department. Australian Emergency Nursing Journal , 5-8.
Williams, L., & Wilkins. (2005). Pathophysiology. In Pathophysiology: A 2-in-1 Reference for Nurses . United States of America: Judith A. Schilling McCann, RN, MSN. pg 183-190