Fluid and Electrolyte Management of the Cardiac Patient

Symposium on Fluid and Electrolyte Balance

Fluid and Electrolyte Management of the Cardiac Patient John D. Bonagura, D.V.M., M.S. *

The successful management of fluid and electrolyte disorders in the cardiac patient poses a significant clinical challenge. There are inherent problems associated with the restoration of fluid and electrolyte deficits in the patient with a deranged circulation. Unlike most problems involving fluid therapy, the simple administration of electrolyte solutions must also be supplemented with measures that optimize venous pressures, enhance free water excretion, and inhibit sodium retention by the kidney. In order to direct this type of treatment, the clinician must appreciate the pathophysiology of heart failure and the compensatory changes that attend disruptions in normal fluid homeostasis. The purpose of this article is to offer a theoretical and clinical framework by which the practicing veterinarian can treat clinical disorders of fluid and electrolyte metabolism in the small animal patient with heart failure. Pertinent pathophysiology, general principles of therapy, and specific patient subsets will be described. This information is incomplete, as there are formidable problems and many unanswered questions regarding this area of fluid therapy. The guidelines described herein are a compilation of information obtained from canine studies, human medicine, and personal experience.

PATHOLOGIC PHYSIOLOGY AND HEMATOLOGIC ALTERATIONS PRESENT DURING HEART FAILURE THE NORMAL CIRCULATION

The circulation is powered by a synchronized pump and its attendant great vessels. Blood is diverted from central arteries to

*Assistant Professor, Department of Veterinary Clinical Sciences, Ohio State University College of Veterinary Medicine, Columbus, Ohio; Diplomate, American College of Veterinary Internal Medicine (Cardiology and Internal Medicine) Veterinary Clinics of North America: Small Animal Practice - Vol. 12, No.3, August 1982

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diverse regional circulations through a reflex-regulated arterial system. The elements of blood are then partitioned in the microcirculation where the interplay between Starling forces (hydrostatic and oncotic pressures, capillary membrane permeability) and lymphatic and venous drainage are responsible for keeping the cell interstitium and serous body cavities free of excess solute and water. Despite wide fluctuation in daily water and salt intake, normal cardiovascular and renal mechanisms serve to maintain total body water and sodium within precise limits. Of prime importance is the maintenance of a normal "effective plasma volume" in the central circulation, a factor dependent on cardiac output, peripheral resistance, and renal regulation of sodium and water excretion. In circulatory failure, this relationship is disturbed. In order to maintain an effective plasma volume in the presence of decreased myocardial function, reciprocal changes occur in both arterial resistance and renal reabsorption of sodium and water. Accompanying these changes are sodium retention, increased total body water, elevated venous pressure, and edema.

CONGESTIVE HEART FAILURE

Heart failure is a pathophysiologic state in which the heart fails to pump blood at a rate sufficient to meet tissue needs. When congestive heart failure is present, there is transudation of tissue fluid into the interstitial spaces (edema) or serous body cavities (effusions). Important causes of heart failure in animals can be classified into four types. The congestive cardiomyopathies are characterized by ventricular dilatation and marked reduction in ventricular contractility. Systolic hemodynamic overloads include cardiac lesions that tax the heart and circulation during ventricular contraction. Common examples include atrioventricular valve insufficiency, semilunar valve stenosis, dirofilariasis, and congenital left-to-right shunts. Pericardial disease and hypertrophic cardiomyopathy are examples of diastolic filling disorders that inhibit normal ventricular filling and diminish cardiac output. Arrhythmias may complicate or cause heart failure. Myocardial failure causes a decrease in the effective plasma volume and provokes neurogenic, hormonal, cardiac, and renal compensatory responses. Heart failure is associated with increased sympathetic tone. This serves to increase heart rate, myocardial contractility, and total peripheral resistance, and to redistribute blood to the more vital coronary and cerebral circulations. Cardiac responses include ventricular dilatation and hypertrophy, changes that increase cardiac output. The kidneys behave in heart failure as they do in hypovolemia, by reabsorbing more sodium and water. This increases total body water and sodium, expands the plasma and interstitial fluid volumes, and elevates venous pressure, which in turn increases cardiac output but also predisposes to edema.

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Table 1. Possible Mechanisms Leading to Sodium and Water Retention in Heart Failure HORMONAL FACTORS

Increased aldosterone Increased antidiuretic honnone Decreased natriuretic honnone RENAL FACTORS

Decreased renal plasma flow Increased filtration fraction Redistribution of renal blood flow Decreased glomerular filtration rate Increased sensitivity to aldosterone Increased renal vascular resistance Increased renin-angiotensin Increased renal venous pressure Prostaglandins OTHER FACTORS

Increased sympathoadrenal tone Altered atrial stretch receptors Decreased mean arterial pressure Decreased arterial pulsation Decreased extracellular fluid volume Undefined humoral agents Altered diencephalic responses

Edema Heart failure leads to accumulation of fluid in the lung, the pleural and peritoneal spaces, and less frequently in the subcutis. Edema stems from: (1) elevated venous and capillary hydrostatic pressures, (2) decreased synthesis of albumin or loss of protein, and (3) increased membrane permeability caused by elevated pressures and hypoxia. Venous hypertension is the result of both ventricular failure and renal retention of salt and water (Fig. 1). For example, the dog with mitral valve insufficiency has elevated left atrial and pulmonary venous pressures due to left ventricular dilatation and failure and regurgitant blood flow. The decreased anterograde stroke volume triggers expansion of the extracellular fluid volume by means of renal reabsorption of sodium and water. These factors combine to promote formation of edema. Compensatory mechanisms can maintain cardiac output at normal or higher levels; however, the patient may still accumulate fluid and be incapacitated by edema. From an evolutionary standpoint, these acute renal and circulatory responses appear to be less beneficial for the long-term stresses imposed by cardiac failure. The Renal Response The renal response is critical to the pathogenesis and therapy of congestive heart failure, yet numerous studies in dogs have failed to discern a singular mechanism responsible for persistent sodium

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retention. Instead, multiple explanations have evolved, some of which are illustrated in Figure 1 and Table 1. Emphasis has been directed to the increased levels of angiotensin, aldosterone, and antidiuretic hormone found in congestive heart failure, since these factors promote fluid retention by the kidney. Changes in intrarenal blood flow have been considered important. These include redistribution of flow to the salt-conserving juxtamedullary nephrons, and increases in filtration fraction, a tubular phenomenon that maintains glomerular filtration rate but predisposes to reabsorption of water. Insensitivity of atrial stretch receptors, increased formation of angiotensin, inappropriate thirst, increased adrenergic tone, and deficiency of the elusive natriuretic factor are other mechanisms purported to expand the extracellular fluid volume.

ELECTROLYTE AND ACID-BASE ALTERATIONS Sodium Serum sodium is usually normal in heart failure, although total body sodium is increased and distributed to both plasma and interstitial spaces. Sodium, the major extracellular cation, is accompanied by water. Occasionally serum sodium is decreased but this is rarely due to salt depletion. The apparent cause of hyponatremia in congestive heart failure is dilution from markedly reduced renal free water clearance. Continued release of antidiuretic hormone and free access to water are important factors to be considered in the pathogenesis and therapy of this unusual, and usually preterminal, syndrome. Potassium Serum potassium may be normal, increased, or decreased in heart failure. Hyperkalemia is observed in acute low output heart failure owing to abrupt reductions in glomerular filtration rate and may also accompany overzealous supplementation with potassium chloride in conjunction with the administration of potassium-sparing diuretics. Hypokalemia is particularly injurious as it predisposes to digitalis intoxication and may induce cardiac arrhythmias. Numerous factors predispose to hypokalemia in the cardiac patient. Anorexia from chronic disease or digitalis intoxication is often associated with inadequate potassium intake, while cardiac cachexia and tissue wasting lead to potassium loss. Kaliuresis occurs with diuretic therapy unless the potassium-sparing diuretics spironolactone or triamterene are administered. This loss assumes particular importance in anorectic patients. Excretion of potassium is enhanced by increased levels of aldosterone. When reduction in glomerular filtration rate leads to inadequate delivery of sodium to the distal tubule, potassium must be secreted with organic acids. The potent loop diuretics like furosemide also promote kaliuresis by accelerating the delivery of sodium to the distal nephron, leading to an overall increase in the rate of sodiumpotassium exchange. Finally, metabolic alkalosis occurs secondary to

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emesis or drug-induced chloriuresis. Alkalosis increases the concentration of potassium in the renal tubular cell and promotes its excretion in the urine. Acid-Base The pH of the blood in heart failure is the product of competing factors that alter acid-base balance. Complex acid-base disorders are common owing to disturbances in tissue oxygenation, pulmonary and renal function, and serum electrolyte concentration. The simple determination of total CO 2 combining power without direct measurement of blood pH thus can lead to erroneous conclusions. Metabolic acidosis may be caused by a stagnant circulation with hypoxia and lactic acidemia, or by prerenal azotemia. Respiratory acidosis is a less common, but a more serious, complication and indicates the presence of severe respiratory failure, pulmonary edema, or compression atelectasis. Metabolic alkalosis is common and attributable to diuretic therapy, with resultant decreases in serum chloride and potassium. Vomiting, a common complication of digitalis intoxication, also leads to loss of acid and metabolic alkalosis. Since patients with moderate pulmonary edema tend to hyperventilate, respiratory alkalosis may be detected in some patients. In my experience, respiratory alkalosis and metabolic acidosis are the most commonly encountered acid-base disorders.

SERUM PROTEINS Serum protein concentration is frequently depressed in severe heart failure, particularly in dogs with congestive cardiomyopathy. Whether this is secondary to dilution, intestinal or renal loss, or inadequate hepatic synthesis is uncertain, although each of these mechanisms can be invoked in individual patients. Reduction of the plasma volume with diuretic therapy usually increases the serum albumin concentration; however, the total serum protein frequently remains in the subnormal or low normal range. Edema is more likely to occur at lower venous pressures when there is hypoalbuminemia.

MANAGEMENT GENERAL PRINCIPLES

Important principles of fluid, electrolyte, and acid-base management of the cardiac patient include (1) determining the underlying disease and recording baseline values, (2) directing specific or symptomatic therapy to the cardiac and noncardiac disorders, (3) preventing sodium retention, (4) administering saline-deficient fluids, (5) determining appropriate electrolyte supplements and water intake, (6) improving renal and pulmonary function, and (7) carefully monitoring the effects of therapy.

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The medical and surgical management of heart failure are described elsewhere 2 , 3, 9 but include, to varying degrees, specific surgical therapy when possible, rest, sodium restriction, diuretics, digitalis glycosides, vasodilators, bronchodilators, antiarrhythmic agents, oxygen, sedation, potassium supplementation, and cough suppressants. Since edema is partially a consequence of ineffective cardiac output, the first consideration of fluid therapy should be to support the failing circulation with inotropic drugs. Specific examples are discussed below. Therapy must also be directed to correct complicating noncardiac complications such as anemia, vomiting, diarrhea, anorexia, renal disease, and infection since these problems cause contemporary losses or further derangement of fluid, electrolyte, and acid-base balance. MONITORING

Cardiac patients require careful monitoring of clinical, hematologic, cardiac, and hemodynamic variables. A checklist of important factors is given in Table 2. These should be determined at the time of Table 2. Evaluation of the Cardiac Patient INSPECTION AND EXAMINATION

Body weight Body temperature Pulse rate and quality Respiratory rate Pattern of ventilation Cardiac auscultation Pulmonary auscultation Level of consciousness Muscle strength Mucous membrane color and refill time Evaluation for ascites (measurement of girth) LABORATORY EVALUATION

Serum BUN and creatinine Serum electrolytes Blood gas tensions (PO., Pco.) Blood pH and bicarbonate CHEST RADIOGRAPH ELECTROCARDIOGRAM DETERMINATION OR CALCULATION OF:

Central venous pressure Pulmonary capillary wedge pressure Intravenous fluid requirements Oral water intake Urinary output Total daily sodium intake (intravenously) Total daily sodium intake (dietary) Total daily caloric intake Environmental temperature and humidity

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admission and reevaluated as dictated by the severity of the condition. Frequent determination of such simple variables as water and food intake, daily sodium intake, estimated urine output, and body weight gives the clinician important information concerning fluid dynamics. Central Venous and Pulmonary Capillary Wedge Pressures Of major concern is the effect of fluid administration on venous pressure, since this is an important determinant of both cardiac output (heterometric autoregulation) and formation of edema. In heart failure, an "optimum" venous pressure is needed to maintain cardiac output; however, pulmonary venous pressures in excess of 20 mmHg and central venous pressures of greater than 16 cm H 2 0 may be associated with the formation of edema. Central venous pressure is simple to measure using an indwelling jugular venous catheter, and its determination gives quantitative and qualitative (increasing or decreasing) information concerning right heart filling pressures. A central venous pressure of 8 to 11 cm H 2 0 has been suggested as optimal for right ventricular filling in heart failure. Unfortunately, most animals have either isolated left heart or biventricular failure, and central venous pressure is not an accurate reflection of pulmonary venous pressure in these patients. In order to obtain accurate measurement of pulmonary venous and left heart filling pressure, a catheter must be advanced into a lobar pulmonary artery under fluoroscopic or pressure-monitored control (Fig. 2). Special end-hole, balloon-tipped catheters* can be used to temporarily occlude pulmonary arterial flow, permitting measurement of the damped left atrial pressure waveform which is transmitted through the valveless pulmonary venous and capillary bed. The mean value of such a determination is called the pulmonary capillary wedge pressure and is equivalent to the mean left ventricular filling pressure. The clinician can thus measure the pressure filling the left ventricle (preload) and estimate the tendency to form pulmonary edema by determining iflow (lower than 7 mmHg), optimal (14 to 18 mmHg), or high (greater than 20 mmHg) venous pressures are present in the cardiac patient. The rate of fluid administration is guided by these measurements. SELECTION OF FLUID AND ELECTROLYTE THERAPY

Parenteral Solutions Dogs with cardiac failure do not respond normally to a sodium load. When saline is infused into such patients, marked retention of sodium and water occurs. This marked response, especially prominent with activity, is also present in caged dogs. On the other hand, the dog *5 to 7 French (Swan-Ganz) thermodilution catheters. Edwards Laboratories, Santa Ana, California

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Figure 2. Determination of central venous pressure and pulmonary capillary wedge pressure. Determination of right and left ventricular filling pressures (left lateral view). A balloon-tipped, flow-directed catheter (Swan-Ganz) is inserted into the jugular vein and passed through the cranial vena cava (cran VC), right atrium (RA), right ventricle (RV), and pulmonary artery (P A). Two independent catheter lumina permit pressure determinations in both the right atrium and the pulmonary artery. The proximal lumen in the RA measures the central venous pressure (CVP) while the distal tip measures the P A pressure. When the balloon is inflated, blood flow is temporarily occluded and the pulmonary capillary wedge pressure (PCWP) is measured (inset). Caud VC = caudal vena cava.

can maintain normal serum sodium concentration with a diet containing extremely low concentrations of sodium (less than 5 per cent of National Research Council requirements). Based on these concepts, when parenteral fluid therapy is indicated in the cardiac patient, solutions that contain little or no sodium are given. In our hospital, we administer a solution of 5 per cent dextrose, intravenously. Daily fluid volumes are guided by estimated maintenance (40 to 60 ml per kg per day) needs plus dehydration, twice-a-day body weights, oral fluid intake, urinary output, total serum protein, and central venous pressure or pulmonary capillary wedge pressure determinations. Occasionally a 0.45 per cent solution of sodium chloride in 2.5 per cent dextrose (containing sodium at a concentration of 77 mEq per L) is utilized, but total daily sodium intake is limited to 12 mg per kg body weight (approximately 0.5 mEq per kg). If metabolic acidosis is present, sodium bicarbonate is added to the fluid. It is imperative to calculate the amount of sodium given with the bicarbonate (there are 23 mg

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of sodium per mEq of sodium bicarbonate) when tallying total daily sodium intake. Diuretics Diuretics are important adjuncts to the overall fluid and electrolyte management of the cardiac patient. They are given to the patient receiving intravenous fluids when edema cannot be controlled by rest, sodium restriction, vasodilators, and digitalis glycosides. It is difficult to rationalize the concurrent administration of parenteral fluids and diuretics unless one anticipates benefits above those obtained from simple water loss, such as redistribution of water from the lung to the skin and muscle. The thiazides and furosemide initially increase glomerular filtration rate, but following diuresis and contraction of the plasma volume, glomerular filtration rate falls. Thus they may correct oliguria but will not lower serum BUN or creatinine. Both sodium and water are lost during diuresis, and this serves to reduce venous pressure and mobilize edema, important salutory effects of the loop diuretics. However, diuretics mobilize water from both the extracellular fluid volume and the intracellular fluid volume; therefore, cellular dehydration also may occur. This intracellular dehydration may, in part, be corrected by the administration of a sodium-poor solution, but this potential benefit has not been quantitated in dogs or cats with congestive heart failure. Vasodilators (Minipress, 1 mg TID; Nitrol ointment, 0.25 to 0.75 mg every six hours) and the angiotensin-converting enzyme inhibitor captopril (Capoten, 1 to 2 mg per kg TID) may control edema or ascites without leading to marked volume contraction. Potassium Potassium, as the chloride salt, is routinely administered to normokalemic or hypokalemic cardiac patients receiving fluid therapy. Administration of glucose solutions tends to lower the serum potassium and since most of these patients are not eating, hypokalemia is anticipated. Typical intravenous doses of 0.5 to 2.0 mEq per kg per day are given using accepted guidelines for intravenous administration of potassium. For hypokalemic animals, higher doses of potassium chloride are given up to a rate of 0.5 mEq per kg per hour intravenously. Oliguria, hyperkalemia, and the administration of potassium-sparing diuretics are contraindications for parenteral potassium therapy. SPECIFIC PROBLEMS

The Surgical Patient The surgical patient with marginal or mild heart failure can be successfully managed but requires a complete preoperative cardiovascular and medical work-up. Patients in definite cardiac failure should be digitalized by slow oral methods long before undergoing elective

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surgery. Strict cage rest and a good quality, but sodium-restricted, diet are instituted at this time. Cardiac medications are continued throughout the perioperative period. Surgery poses particular problems related to anesthesia, fluid loss, arrhythmias, and pulmonary function. All anesthetics reduce cardiac function; however, some agents (for example, halothane) are particularly depressant and should be avoided. Fluid replacement is guided by determination of intraoperative blood loss and by monitoring central venous pressure, while recognizing the potential disparity between central venous pressure and pulmonary venous pressure. If possible, urinary output is recorded as oliguria in the postoperative period may provoke pulmonary edema. Overinfusion of sodium must be avoided and this ion is best given when the need for bicarbonate administration arises. Adequate ventilation must be maintained, but inappropriate positive pressure ventilation may lead to decreased venous return and hypotension or acute respiratory alkalosis. Narcotics, pain, fear, and anesthetic agents all can stimulate the release of antidiuretic hormone, provoking acute retention of water. Parenteral administration of furosemide (2 to 4 mg per kg) may be useful in the postoperative period to combat oliguria and resultant pulmonary edema. Respiratory depression should be reversed with narcotic antagonists or- other agents if necessary. Serum potassium should be evaluated daily. Low-Output Congestive Heart Failure Severe life-threatening heart failure can occur in association with the congestive (dilated) cardiomyopathies of the dog and cat and advanced valvular heart disease. These patients usually are weak, hypotensive, hypothermic, oliguric, azotemic, and edematous. Large pleural and peritoneal effusions are common. Management of these animals requires intensive monitoring (see Table 2), immediate measures to improve tissue oxygenation, and prompt support of the central arterial circulation. Initial therapy consists of cage rest, oxygen (greater than 40 per cent), sedation (morphine for dogs, 0.2 mg per kg subcutaneously) parenteral furosemide and aminophylline (6 to 8 mg per kg IV or 1M) and aspiration of pleural effusions. Life-threatening pulmonary edema is managed with topical 2 per cent nitroglycerin ointment (0.25 to 0.75 mg every four to six hours) or infusion of sodium nitroprusside; arterial pressure must be monitored with nitroprusside therapy. Diuretics may be ineffective if the glomerular filtration rate is critically low; therefore, measures to increase cardiac contractility and maintain arterial blood pressure are initiated. The patient is digitalized intravenously (Lanoxin, 0.02 mg per kg IV, 25% every hour) and the catecholamine dobutamine (Dobutrex, 5 to 20 fLg per kg per minute) or the catecholamine precursor dopamine (Intropin, 2 to 5 fLg per kg per minute) is infused to increased cardiac contractility and renal plasma flow. The use of these agents has been described elsewhere.2, 3, 9

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With central venous pressure and preferably pulmonary capillary wedge pressure monitoring, a 5 per cent solution of dextrose is infused in order to optimize ventricular filling pressures and to correct dehydration. Judicious doses of sodium bicarbonate (0.5 mEq per kg) are given to treat metabolic acidosis. Initially, potassium chloride is not given since oliguria may result in hyperkalemia. With establishment of a diuresis, potassium supplementation can be initiated. Renal function and serum electrolytes are monitored on a daily basis. Arrhythmias are controlled with appropriate antiarrhythmic agents. Parenteral fluid therapy is given for two to four days, during which time the patient is placed on conventional oral therapy for heart failure with the addition of an oral vasodilator such as hydralazine (Apresoline, 1 to 2 mg per kg BID to TID), prazosin (Minipress), or captopril (Capoten). Dopamine or dobutamine is continued for 24 to 48 hours in an attempt to reestablish myocardial catecholamine levels. Oral intake of food and water is encouraged after two to three days so that parenteral fluid administration can be terminated.

Heart Failure and Renal Failure Renal failure is a common, complicating factor of both cardiomyopathy and chronic valvular disease. Prerenal azotemia may be secondary to decreased cardiac output, volume contraction from diuresis, anorexia, or vomiting caused by digitalis intoxication. In older dogs, concurrent primary renal disease may be present. It is imperative to distinguish pre renal from primary renal failure since the prognosis and long-term therapy of each may differ. Unfortunately, prior treatment with diuretics precludes the evaluation of renal concentrating ability, even if appropriate stimuli for urine concentration, such as dehydration, are present. Therefore, the clinician must assess previous history, palpation of the kidneys, renal size on radiographs, packed cell volume, urine sediment, creatinine clearance, and response to blood volume expansion when determining the origin of azotemia. Principles of fluid and electrolyte management of the patient with azotemia and heart failure include (1) localizing the origin of the azotemia (prerenal versus primary renal), (2) reducing the dose of digoxin (by 25 to 75 per cent) or using digitoxin, (3) controlling vomiting with antiemetics and low sodium antacids (Amphojel), (4) enforcing strict cage rest, (5) rehydrating the patient with sodiumdeficient fluids, (6) correcting acid-base and electrolyte abnormalities, (7) treating anemia, (8) reducing the use of diuretics, and (9) controlling edema with vasodilator therapy. The choice of a cardiac glycoside is important. Digitalis may be needed to maintain renal plasma flow, yet renal failure prevents the normal excretion of digoxin. For this reason, digitoxin (Crystodigin, 0.05 to 0.1 mg per kg, divided TID) is administered to patients with primary renal disease. In patients with prerenal azotemia that are receiving digoxin, the dose is temporarily suspended or lowered until renal function returns to normal. Serum digoxin levels are important guides to treatment. 2

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The choice of intravenous fluids is similar to that previously described. Since the combination of oligemia and primary renal disease may predispose to hyperkalemia, serum potassium must be monitored. Many azotemic dogs are digitalis-intoxicated, so hypokalemia also must be avoided to prevent cardiac rhythm disturbances. The need for increased free-water clearance, natriuresis, and mobilization of edema are reasons to initiate diuretic therapy; however, diuretics usually decrease glomerular filtration rate and elevate serum creatinine. Whenever possible, the dose of the diuretic is reduced and edema is treated with a balanced vasodilator like prazosin or an arterial vasodilator like hydralazine. The vasodilator and angiotensinconverting enzyme inhibitor captopril may prove to be useful because of its ability to decrease sodium retention, increase renal blood flow, and decrease filtration fraction. ACKNOWLEDGMENT I would like to thank Mr. B. K Kramer for the medical illustration and Miss Marinda L. Brohard for typing the manuscript.

REFERENCES 1. Barger, A. C., Yates, F. E., and Rudolph, A. M.: Renal hemodynamics and sodium excretion in dogs with graded valvular damage, and in congestive failure. Am. J. Physio!., 200:601, 1961. 2. Bonagura, J. D.: Cardiopulmonary disorders in the geriatric dog. VET. CLIN. NORTH AM., 11 :705, 1981. 3. Bonagura, J. D.: Acute heart failure. In Kirk, R. W. (ed.): Current Veterinary Therapy VII. Philadelphia, W. B. Saunders Company, 1980. 4. Cannon, P. J.: The kidney in heart failure. N. Eng!. J. Med., 296:26, 1977. 5. Friedberg, C. K (ed.): Heart, Kidney and Electrolytes. New York, Grune and Stratton, 1962. 6. Gottlieb, M. N., and Braunwald, E.: Renal disorders and heart disease. In Braunwald, E. (ed.): Heart Disease. Philadelphia, W. B. Saunders Company, 1980. 7. Hollenberg, N. K, and Cannon, P. J.: The kidney in congestive heart failure: Sodium-homeostasis, renal hemodynamics, and nephron function. Somerville, New Jersey, Hoechst-Roussel Pharmaceuticals Inc., 1975. 8. Kaloyanides, G. J.: Pathogenesis and treatment of edema with special reference to the use of diuretics. In Maxwell, M. H., and Kleeman, C. R. (eds.): Clinical Disorders of Fluid and Electrolyte Metabolism. New York, McGraw-Hill Book Company, 1980. 9. Mason, D. T. (ed.): Congestive Heart Failure. New York, York Medical Books, 1976. 10. Statland, M.: Heart disease. In Statland, H. (ed.): Fluid and Electrolytes in Practice. Philadelphia, J. B. Lippincott Company, 1963. 11. Swan, H. J. C., Ganz, W., Forrester, J., et a!.: Catheterization of the heart in man with use of a flow-directed balloon tipped catheter. N. Eng!. J. Med., 283:447, 1970. College of Veterinary Medicine Ohio State University 1635 Coffey Road Columbus, Ohio 43210