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The intravenous fluid given to this patient was too concentrated with sodium and chloride. Because these ions diffuse freely between the plasma and the interstitial fluid, increases in plasma sodium and chloride concentrations will cause increases in interstitial fluid sodium and chloride concentrations.


Interstitial fluid that is hypertonic to intracellular fluid will cause water to shift by osmosis from the cells to the interstitial fluid. Hence, the cells will osmotically shrink. This can be particularly detrimental to the intracellular architecture, causing deformation of the vital organelles required for cell function.

Introducing hypertonic saline into this patient made the plasma and interstitial fluid sodium concentrations rise. As the plasma sodium level rises, more water than normal is passively, osmotically drawn from the renal tubules into the peritubular capillaries of the kidneys. This raises blood volume and blood pressure, causing a shift of water from the plasma into the interstitial spaces. Thus, the patient develops edema (i.e. swelling) in tissues.

This process is exacerbated by the patient's underlying chronic renal failure and heart attack. His failing kidneys have a difficult time excreting the excess sodium and chloride ions introduced into his body. Furthermore, his recent heart attack places him at increased risk of developing congestive heart failure. His left coronary artery blockage probably caused damage to his left ventricle. The osmotic increase in blood volume places an increased pre-load work requirement on an already impaired left ventricle. If this ventricle cannot pump blood out into the aorta at a rate equal to that of blood entering the left ventricle from the left atrium, hydrostatic pressure will rise in the left ventricle, left atrium, and ultimately the pulmonary circulation "upstream." An increase in pulmonary capillary hydrostatic pressure will force more water to be filtered from the bloodstream into the interstitial spaces of the lung tissue. As fluid builds up in these spaces, it may begin to collect in the alveolar air spaces and terminal bronchioles (a condition called "pulmonary edema"). If this happens, rales (i.e. crackling sounds) may be heard with a stethoscope when the patient inhales. These are the sounds of obstructed airways "popping open."

The function of aldosterone is to increase the tubular reabsorption of Na+ ions from the distal renal tubules into the bloodstream in exchange for the tubular secretion of K+ and/or H+ ions from the bloodstream into the distal renal tubules. It probably does this indirectly by stimulating the production of the requisite transport protein in the distal renal tubular cells. Thus, aldosterone helps the body correct hyponatremia (i.e. a lower-than-normal blood Na+ level) and hyperkalemia (i.e. a higher-than-normal blood K+ level). Furthermore, aldosterone helps increase the blood volume because water in the renal tubular fluid follows the Na+ ions by osmosis into the bloodstream. Hence, aldosterone helps the body maintain an adequate blood pressure.

There are several physiologic factors that stimulate the release of aldosterone from the adrenal cortex, the most important of which are (1) elevated blood-K+ level, (2) decreased blood-Na+ level, (3) decreased blood pressure (via stimulation of the renin-angiotensin-aldosterone axis), and (4) increased secretion of adrenocorticotropic hormone (ACTH) from the anterior pituitary gland. The opposite of each of these conditions decreases the release of aldosterone. In our patient's case, the elevated blood-Na+ level will inhibit release of aldosterone, and thus enhance the excretion of the excess Na+ ions into the urine.

Osmoreceptors in the hypothalamus monitor the osmolarity of the extracellular fluid and make adjustments accordingly. In this patient the hyperosmolarity of the blood will stimulate the hypothalamus thirst center, making him feel thirsty and want to drink water to dilute the blood. The hypothalamus also responds to an increased extracellular fluid osmolarity by releasing anti-diuretic hormone (ADH), also known as vasopressin. This hormone, in turn, increases the permeability of the nephrons' collecting duct walls to water. Thus, when urinary filtrate passes through the collecting duct, water is reabsorbed into the peritubular capillaries, resulting in the production of a smaller-than-normal volume of hypertonic urine. This ADH mechanism is a "double-edged sword" for our patient. On the one hand, it helps correct the patient's hypernatremia, but on the other hand, it increases blood volume and may thus trigger congestive heart failure or exacerbate already existing congestive heart failure.

Osmotic shrinkage of cells during hypernatremia can cause shrinking of the brain and concomitant central nervous system symptoms such as lethargy, confusion, coma, convulsions, and respiratory paralysis. Muscular tremor, rigidity, and hyperreflexia may also occur.


This process is exacerbated by the patient's underlying chronic renal failure and heart attack. His failing kidneys have a difficult time excreting the excess sodium and chloride ions introduced into his body. Furthermore, his recent heart attack places him at increased risk of developing congestive heart failure. His left coronary artery blockage probably caused damage to his left ventricle. The osmotic increase in blood volume places an increased pre-load work requirement on an already impaired left ventricle. If this ventricle cannot pump blood out into the aorta at a rate equal to that of blood entering the left ventricle from the left atrium, hydrostatic pressure will rise in the left ventricle, left atrium, and ultimately the pulmonary circulation "upstream." An increase in pulmonary capillary hydrostatic pressure will force more water to be filtered from the bloodstream into the interstitial spaces of the lung tissue. As fluid builds up in these spaces, it may begin to collect in the alveolar air spaces and terminal bronchioles (a condition called "pulmonary edema"). If this happens, rales (i.e. crackling sounds) may be heard with a stethoscope when the patient inhales. These are the sounds of obstructed airways "popping open."