ETIOLOGYPATHOPHYSIOLOGY

 

-Ineffective contraction of left ventricle (Craft, et al 2011)-Reduced cardiac output (Leonard, 2011) -Accumulation of blood in the left atrium and the lungs -Pulmonary congestion, dyspnea and activity intolerance.

 

-Untreated/ inadequately treated hypertension-Myocardial infarction -Arrhythmias (Barry, 2011) -Valvular disease (aortic and mitral valve stenosis) -Cardiomyopathy -Congenital heart disease -Volume overload in renal disease -Alcoholism

LEADS TO THE CLINICAL FEATURES

Failure to thriveWeight loss Poor feeding

Cough, with blood tinged mucusReduced urine production Fatigue, weakness Irregular and rapid pulse Palpitations ( Barry, 2011) Shortness of breath Nocturnal paroxysmal dyspnea Weight gain due to fluid retention

CLINICAL MANIFESTATIONS

IN INFANTS

LIFE STYLE CHANGESLimited sodium (3g/day) Avoiding alcohol consumption Reduce weight Moderate exercises MEDICENES -Beta blockers ( Barry, 2011) -Digitalis to prevent arrhythmias -Diuretics to get rid of excess fluids -Spironolactone to prevent retention of salts -Angiotensin converting enzyme inhibitors, -Hydralazine to lower blood pressure. -Digoxin to increase myocardial contractility -Nesiritide to decrease afterload -Sidenafil to prevent pulmonary hypertension OTHERS Cardiac catheterization, valve surgery, coronary bypass surgery,Defibrillation. Ventricular assist device implantation

DIAGNOSIS

PHYSICAL EXAMIrregular rapid heartbeat, tachypnea, heart murmurs, reduced breath sounds, crackles, pitting edema. TESTS Chest X-rays Echocardiogram Heart stress test Electrocardiogram (ECG) Coronary angiography

 

 

PROGNOSISHeart may not fully recover, but the treatment makes the patient stable and prolongs the life. LIFE STYLE MODIFICATION Limited sodium (3g/day) Avoiding alcohol consumption Reduce weight Moderate exercises (Craft et al., 2011)

TREATMENT

PROGNOSIS AND

ComplicationsPulmonary hypertension Right heart failure ( Craft et al., 2011) Impaired renal function Cardiac cachexia Arrhythmias Fluid build up

PREVENTION

COURSE AND COMPLICATIONS

Question 1.a) Pathogenesis that leads to fluid volume excess.

Heart failure is associated with low cardiac output, under-filling of the arteries and increased preload. The tissues are under-perfused due to low cardiac output. This causes stimulation of the arterial baroreceptors and the sympathetic nervous system. Nonosmotic vasopressin production and activation of renin-angiotensin-aldosterone is activated (Albert, 2012).

Reduction in the tissue perfusion and low blood volume activates the Renin- Angiotensin Aldosterone system (RAAS). This system is sensitive to low cardiac output (CO) and it aims at increasing the fluid volume in the body. Reduction in the fluid that passes through the macular densa causes the juxtaglomelular cells to release Renin enzyme. It causes activation of angiotensinogen to angiotensin I. Angiotensin converting enzyme is a key player in this system because it activates angiotensin I to angiotensin II. RAAS system causes reabsorption of sodium ion from the kidney nephron. Consequently, the water follows the electrolyte by osmosis thus increasing the fluid volume in the body. It is this system that the angiotensin converting enzyme inhibitors and angiotensin II blocker drugs target in an attempt to reduce hypertension that develops in heart failure. They prevent reabsorption of more fluid from the kidney nephron (Albert, 2012).

Fluid retention by the RAAS system causes an increase in the ventricular preload and the cardiac output until the cardiac output again meets the RAAS activation threshold. When ventricular dysfunction continues, the cardiac output can no longer reach the activation threshold of RAAS system. Thus, unable reach a new higher set point, the RAAS system becomes continuously activated in proportion to the low cardiac output in the futile attempt to raise the CO. The continuous activation of the RAAS system becomes ineffective and causes the edema due to the retained fluids (Albert, 2012)

1. b) Discuss two nursing strategies used to manage pulmonary edema, a consequence of fluid volume excess and provide evidence-based rationales for these strategies

Application of strategies to lower the fluid volume in the body and neurohormonal modulation are critical in the management of pulmonary edema. Nurses should administer the prescribed drugs that lower the fluid volume in the body. Furosemide is the hallmark drug in the reduction of the excess fluid. Others includespironolactones, angiotensin converting enzyme inhibitors and aldosterone inhibitors. When the fluid is reduced, there is reduced accumulation of blood in the left atria thus reduced fluid in the lungs. Monitoring of fluid intake and output, and the electrolyte balance is necessary to determine the efficacy of the drugs given (Williams &Wilkins, 2010).

Drugs used in neurohormonal modulations include the beta blockers like carvedilol. They block theactive sites of beta receptors that are activated by Catecholamines. As a result, the effects of catecholamines thatinclude vasoconstriction and tachycardia are blocked.Consequently, there is reduced peripheral resistance and thus reduced accumulation of blood in the ventricles and the atria. This causes vasodilatation of the blood vessels that makes blood to accumulate in the veins rather than the in the pulmonary circulation.(Champion, 2012).

Another strategy employed in the management of pulmonary edema is contractually enhancement therapy, where the nurse may use digoxin. The rational basis of this method to improve the ability of the heart muscle, enabling it to pump ore effectively. This leads to complete emptying of blood from the heart ventricle leading to a decrease in the volume that backs up in the lungs (Champion, 2012).

Question 2 .c) Explain the mechanism of action of Furosemide.

Furosemide is a loop diuretic that prevents absorption of water from the thick ascendingloop of Henle in the kidney neoprene that is nearly impermeable to water. The filtrate that reacheshere is concentrated. Reabsorption of the salts at this point is dependent on the ion transporter NKCC2. It transports sodium ions across the membrane and the water follows due to the change in osmotic potential. Furosemide and other diureticsinhibitthe Na⁺/ k⁺/2Cl^–co-transporter in the thick ascending loop of Henle. This reduces the reabsorption of NaCl and increases the lumen positive potential of the ascending loop of Henle. It preventsthe generation of a hypertonic medulla thus the water lacks a driving force to move it from the renal tubules to the medulla, thus more of it is excreted in the urine.In addition, when the transporter is inhibited, there is an increase in the positive electrical potential in the tubular lumen due to accumulation of the K+ ions. This prevents reabsorption of divalent ions like magnesium and calcium that are excreted in the urine(Bullock& Manias, 2011).

1. d) Discuss the nursing implications when furosemide is given.

Just as the other drugs, Furosemide has its adverse effect to the body. It may lead to electrolyte imbalance that can lead to dysrrythmias and hypotension, especially due to the loss of potassium and magnesium. It can also cause worsening renal function as a result of impaired function of the ion transporter. It is the role of the nurse to monitor and carefully manage electrolyte levels, hemodynamics and overall fluid status of the individual patient. In some patients with advanced heart failure, diuretics may become resistant and unable to excrete excess body fluid. The nurse should apply strategies to overcome this resistance. The strategiesinclude rotating the loop diuretics andinfusing the loop diuretics incontinuous infusion using the infusion set. The infusion set can deliver a small set amount of the diuretics continuously thus ensuring that the action of the dug is also continuous. It can also involve administering two diuretics at the same time. The known diuretics include Furosemide, Torsemide, Bumetadine and Ethacrynic acid (Albert, 2012). Also, to counter potassium loss, it is advisable that the nurse gives Furosemide accompanied with a potassium supplement. The nurse should also be cautious of the drugs that interact with Furosemide to produce adverse effects, such as digoxin.

References.

Albert, M. N.(2012). Fluid management strategies in heart failure.Critical Care Nurse,32 (2), 20-29.

Barry, A .(2011). Heart failure with preserved ejection fraction.European heart journal,2(32), 670-679.

Bullock, S., & Manias, E. (2011).Fundamentals of pharmacology (6th Ed.). French’s Forest, NSW: Pearson Australia

Champion, H.(2012). Pulmonary hypertension: a common complication of left heart disease.Advances in PH Journal, 10(1), 10-23.

Craft, J., Gordon, C., Tiziani, A., Heuther, S., McCance, K., Brashers, V. & Rote, N. (2011).Understanding pathophysiology.Chatswood, NSW: Elsevier.

Leonard, S.L. (2011).Pathophysiology of heart disease: a collaborative project for medical pathogenesis. Philadelphia, PA: Lippincott Williams & Wilkins.

 

William, L.,& Wilkins, 2010.Professional guide to pathophysiology(3^rd Ed). Philadelphia, PA: Lippincott Williams & Wilkins.