Chapter 046. Sodium and Water (Part 4)

ExtrarenalNonrenal causes of hypovolemia include fluid loss from the gastrointestinal tract, skin, and respiratory system and third-space accumulations (burns, pancreatitis, peritonitis). Approximately 9 L of fluid enters the gastrointestinal tract daily, 2 L by ingestion and 7 L by secretion. Almost 98% of this volume is reabsorbed so that fecal fluid loss is only 100–200 mL/d. Impaired gastrointestinal reabsorption or enhanced secretion leads to volume depletion. Since gastric secretions have a low pH (high H+ concentration) and biliary, pancreatic, and intestinal secretions are alkaline (high HCO3– concentration), vomiting and diarrhea are often accompanied by metabolic alkalosis and acidosis, respectively.Water...
Nội dung trích xuất từ tài liệu:
Chapter 046. Sodium and Water (Part 4) Chapter 046. Sodium and Water (Part 4) Extrarenal Nonrenal causes of hypovolemia include fluid loss from the gastrointestinaltract, skin, and respiratory system and third-space accumulations (burns,pancreatitis, peritonitis). Approximately 9 L of fluid enters the gastrointestinaltract daily, 2 L by ingestion and 7 L by secretion. Almost 98% of this volume isreabsorbed so that fecal fluid loss is only 100–200 mL/d. Impaired gastrointestinalreabsorption or enhanced secretion leads to volume depletion. Since gastricsecretions have a low pH (high H+ concentration) and biliary, pancreatic, andintestinal secretions are alkaline (high HCO3– concentration), vomiting anddiarrhea are often accompanied by metabolic alkalosis and acidosis, respectively. Water evaporation from the skin and respiratory tract contributes tothermoregulation. These insensible losses amount to 500 mL/d. During febrileillnesses, prolonged heat exposure, exercise, or increased salt and water loss fromskin, in the form of sweat, can be significant and lead to volume depletion. TheNa+ concentration of sweat is normally 20–50 mmol/L and decreases with profusesweating due to the action of aldosterone. Since sweat is hypotonic, the loss ofwater exceeds that of Na+. The water deficit is minimized by enhanced thirst.Nevertheless, ongoing Na+ loss is manifest as hypovolemia. Enhanced evaporativewater loss from the respiratory tract may be associated with hyperventilation,especially in mechanically ventilated febrile patients. Certain conditions lead to fluid sequestration in a third space. Thiscompartment is extracellular but is not in equilibrium with either the ECF or theICF. The fluid is effectively lost from the ECF and can result in hypovolemia.Examples include the bowel lumen in gastrointestinal obstruction, subcutaneoustissues in severe burns, retroperitoneal space in acute pancreatitis, and peritonealcavity in peritonitis. Finally, severe hemorrhage from any source can result involume depletion. Pathophysiology ECF volume contraction is manifest as a decreased plasma volume andhypotension. Hypotension is due to decreased venous return (preload) anddiminished cardiac output; it triggers baroreceptors in the carotid sinus and aorticarch and leads to activation of the sympathetic nervous system and the renin-angiotensin system. The net effect is to maintain mean arterial pressure andcerebral and coronary perfusion. In contrast to the cardiovascular response, therenal response is aimed at restoring the ECF volume by decreasing the GFR andfiltered load of Na+ and, most importantly, by promoting tubular reabsorption ofNa+. Increased sympathetic tone increases proximal tubular Na + reabsorption anddecreases GFR by causing preferential afferent arteriolar vasoconstriction. Sodiumis also reabsorbed in the proximal convoluted tubule in response to increasedangiotensin II and altered peritubular capillary hemodynamics (decreasedhydraulic and increased oncotic pressure). Enhanced reabsorption of Na + by thecollecting duct is an important component of the renal adaptation to ECF volumecontraction. This occurs in response to increased aldosterone and AVP secretionand suppressed atrial natriuretic peptide secretion. Clinical Features A careful history is often helpful in determining the etiology of ECFvolume contraction (e.g., vomiting, diarrhea, polyuria, diaphoresis). Mostsymptoms are nonspecific and secondary to electrolyte imbalances and tissuehypoperfusion and include fatigue, weakness, muscle cramps, thirst, and posturaldizziness. More severe degrees of volume contraction can lead to end-organischemia manifest as oliguria, cyanosis, abdominal and chest pain, and confusionor obtundation. Diminished skin turgor and dry oral mucous membranes are poormarkers of decreased interstitial fluid. Signs of intravascular volume contractioninclude decreased jugular venous pressure, postural hypotension, and posturaltachycardia. Larger and more acute fluid losses lead to hypovolemic shock,manifest as hypotension, tachycardia, peripheral vasoconstriction, andhypoperfusion—cyanosis, cold and clammy extremities, oliguria, and alteredmental status. Diagnosis A thorough history and physical examination are generally sufficient todiagnose the etiology of hypovolemia. Laboratory data usually confirm andsupport the clinical diagnosis. The blood urea nitrogen (BUN) and plasmacreatinine concentrations tend to be elevated, reflecting a decreased GFR.Normally, the BUN:creatinine ratio is about 10:1. However, in prerenal azotemia,hypovolemia leads to increased urea reabsorption, a proportionately greaterelevation in BUN than plasma creatinine, and a ...