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In this chapter, we will discuss how plasma osmolality and water balance are maintained. Like Na+ balance, water balance is determined by the amount of water that is ingested and excreted. Therefore, water intake equals water loss. In a normal individual, the major source of water intake is oral fluids. Water is also derived from other sources such as solid foods and intermediary metabolism. Intravenous fluids form the principal source of water intake in hospitalized patients. Dialysis patients may also gain water during treatments.

Hypokalemia is defined as a serum [K+]

Potassium (K+) is the predominant intracellular cation in the body. The intracellular [K+] is 140–150 mEq/L; in blood it is 3.5–5 mEq/L. Serum contains a slightly higher concentration of K+ than plasma because K+ is released from red blood cells during clot formation. Maintenance of a high cellular concentration of K+ is necessary for several cellular functions, including growth, nucleic acid and protein synthesis, and regulation of cell volume, as well as pH and enzyme activation. In addition, a high intracellular concentration of K+ is essential to the maintenance of the resting membrane potential for cellular excitability and contraction. The high intracellular K+ concentration is maintained by the Na/K-ATPase located in the cell membranes of all animal cells. The activity of this enzyme is influenced by a variety of hormones. The kidney is the primary route for K+ excretion. In general, K+ excretion in the urine, called kaliuresis, parallels dietary intake. The other route for K+ excretion is the colon. Under conditions of decreased renal function, K+ excretion by the colon is enhanced.

Unlike patients with congestive heart failure (CHF) and cirrhosis, patients with nephrotic syndrome have some underlying renal disease. Also, effective circulating volume (ECV) is not decreased in all patients with nephrotic syndrome. This syndrome is characterized by proteinuria in excess of 3.5 g/day, hypoalbuminemia, hyperlipidemia, edema, and lipiduria. The mechanism for salt and water retention is not clear. The traditional (“underfill”) theory implies that loss of protein in the urine causes hypoalbuminemia and decreased plasma oncotic pressure. These factors favor fluid movement into the interstitium, resulting in intravascular hypovolemia and activation of salt-retaining mechanisms (Fig. 9.1). Two lines of evidence, however, argue against this traditional theory. First, not all patients with congenital deficiency of albumin (analbuminemia) develop edema. Second, some patients with nephrotic syndrome have either normal or increased intravascular volume despite hypoalbuminemia. This evidence suggests that mechanisms other than hypoalbuminemia and decreased intravascular volume play a role in renal retention of Na+ in nephrotic syndrome.

As stated in Chap. 6, the maintenance of extracellular fluid (ECF) volume is dependent on the extracellular concentration of Na+ ([Na+]). An increase in total body Na+ causes an expansion in ECF volume, and a decrease in total body Na+ reduces ECF volume. Most of the critically ill patients and patients with less availability of salt and water develop volume contraction, because it is rather difficult to induce volume contraction in humans with normal renal function. The signs and symptoms of volume contraction depend on the rapidity of Na+ loss. Sudden loss of Na+ causes a marked reduction in blood pressure and cardiac output, whereas slow and sustained loss results in a slight decrease in blood pressure. Pure water loss results in hypertonicity with high serum [Na+], whereas loss of both Na+ and water leads to low blood pressure.

The role of contrast-induced nephropathy (CIN) remains controversial. Many experts contend that CIN does not exist or is extremely rare. The diagnosis was previously made too frequently and inappropriately in the presence of coexisting and confounding comorbidities and risk factors making it difficult to singularly isolate the etiologic role of intravenous contrast media in acute kidney injury (AKI). It is probable that many patients were denied important diagnostic information from radiocontrast studies for fear of CIN. Recently, a new terminology for CIN was introduced, and the term CIN was replaced by two interrelated new terms: one is contrast-associated acute kidney injury (CA-AKI), and the second one is contrast-induced acute kidney injury (CI-AKI). CA-AKI occurs in association with risk factors or comorbidities, therefore, it is a correlative diagnosis. On the other hand, CI-AKI is a subtype of CA-AKI that results directly from iodinated contrast media. In this review, we present evidence from various studies that argue against CI-AKI and also those that suggest its existence but with much lower frequency. We will also provide the current status of the pathophysiology and management of CA-AKI/CI-AKI.

A 20-year-old athletic man with no significant past medical history is found to have isolated asymptomatic microscopic hematuria on routine phys exam. He is not on any medications, and does not use illicit drugs. Which one of the following observations suggests hematuria of glomerular origin?

Acid–base disorders are extremely common in critically ill patients. They carry increased morbidity and mortality. Therefore, accurate assessment and appropriate therapeutic intervention are necessary to prevent these associated complications.

The arterial blood gas (ABG) determination is an important laboratory test in the evaluation of oxygenation and acid–base status of the body. This ABG test is most frequently done in the emergency department and critical care units. Also, this test is a valuable tool during operative procedures. When an ABG is ordered, four important values are reported: pH, partial pressure of oxygen (pO2), partial pressure of carbon dioxide (pCO2), and bicarbonate (HCO3−). Base excess (BE) is also reported (see Chap. 3), which is used by some clinicians. The percent saturation of hemoglobin with oxygen in the arterial blood (SaO2) is done by either direct measurement using CO-oximetry or estimated from pO2. Only some blood gas analyzers are equipped with CO-oximeter for measurement of SaO2 directly, and other laboratories report calculated value. Mean SaO2 is 98%.

The role of the liver in acid-base regulation is often neglected because of the importance given to the lungs and kidneys. This negligence is partly related to few studies of acid-base disorders in liver disease. In Chap. 2, the roles of the lungs and kidneys in acid-base regulation were discussed. In this chapter, a brief discussion of the role of the liver in acid-base balance and its disorders in liver disease are presented. The role of the liver in acid-base balance is divided into four categories.

Patients undergoing total parenteral nutrition (TPN) have several underlying systemic illnesses such as infection, surgical operations, cachexia, malnutrition, and malfunctioning gastrointestinal tract. Therefore, these patients are subject to both acidotic and alkalotic conditions. In addition, the composition of TPN solutions such as amino acids and glucose can predispose them to these acid-base disturbances. Let us discuss each one of the four primary acid-base disorders in detail.

In Chapters 5 and 6, lactic acidosis and ketoacidosis were discussed. These acidoses are characterized by high anion gap (AG). Other causes of high AG metabolic acidosis include ingestion of alcohols, glycols, salicylates, acetaminophen (paracetamol), toluene, and paraldehyde. This chapter focuses on the following toxins that cause acid-base disorders

The assessment of an acid–base disorder by three methods was discussed in Chap. 3. In this and other chapters, we follow the physiologic method for evaluation of an acid–base disorder. In Chap. 1, we stated that a change in plasma [HCO3−] results in a metabolic acid–base disturbance, whereas a change in arterial pCO2 results in a respiratory acid–base disorder. Clinically, four primary acid–base disorders can be recognized: (1) metabolic acidosis, (2) metabolic alkalosis, (3) respiratory acidosis, and (4) respiratory alkalosis. Values for an arterial blood gas (ABG) for each primary acid–base disorder are shown in Table 4.1. Table 4.2 shows the terminology that is useful to a clinician in the analysis of an acid–base disorder.

During pregnancy, several anatomic and physiologic changes occur in pulmonary system. Pertinent lung volume changes in pregnancy are summarized in Table 19.1.

In the previous chapter, we discussed both hypo- and hyperkalemic hyperchloremic (non-anion gap) metabolic acidoses due to renal causes. There are several other nonrenal causes for hypokalemic hyperchloremic metabolic acidosis. The most important nonrenal cause is gastrointestinal (GI) disorder and certain medications that are handled by the GI tract. Table 9.1 shows GI causes of acid–base disorders. This chapter deals only with hyperchloremic metabolic acidosis caused by GI disorders. D-lactic acidosis due to short bowel syndrome was discussed in Chap. 5.

Acid-base disorders are rather common in surgical patients. These disorders occur in perioperative (preoperative, intraoperative, and postoperative) periods. Disturbances in all four primary acid-base balances have been reported in surgical patients. However, these disturbances are less severe in healthy patients undergoing elective surgery compared to those who undergo emergent surgery.

Renal tubular acidosis (RTA) comprises a group of different renal tubular disorders that are characterized by the inability to excrete H+ in the urine. As a result, there is a positive H+ balance, causing metabolic acidosis. The net acid excretion (NAE) is decreased, and some of the patients are unable to lower their urine pH

As discussed in Chap. 1, the acid–base physiology deals with the maintenance of normal hydrogen ion concentration ([H+]) and pH in body fluids and is precisely regulated by an interplay between body buffers, lungs, and kidneys. In everyday life, the blood pH is under constant threat by endogenous acid and base loads. If not removed, these loads can cause severe disturbances in blood pH and thus impair cellular function. However, three important regulatory systems prevent changes in pH and thus maintain blood pH in the normal range. These protective systems, as stated, are buffers, lungs, and kidneys.

Acid–base disorders are extremely common in patients admitted to the critical care units because of multiorgan dysfunction. Sepsis, septic shock, toxin ingestion, diabetic ketoacidosis, removal of vomitus by nasogastric suction, massive transfusion with citrated blood, and renal as well as respiratory failure are some of the important causes for acid–base disorders. Hyperchloremic metabolic acidosis is frequently seen due to fluid resuscitation with normal saline or fluids that contain high Cl−. Among acid–base disorders, some reports suggested metabolic acidosis as the predominant disorder in critically ill patients. For example, an observational cohort study reported that 64% had acute metabolic acidosis. Other studies showed metabolic alkalosis to be the most common acid–base disorder in critically ill patients. Therefore, it is difficult to predict which acid–base disorder predominates in critically ill patients. It should be noted that any acid–base disorder is associated with high morbidity and mortality in critically ill patients. Lindner et al. (Intensive Care Med 39:399–405, 2013) described an acid–base disorder called hypernatremic alkalosis in critically ill patients. Their study included 51patients who developed hypernatremia (serum Na+ level > 149 mEq/L) after admission to intensive care units (ICUs). Based on an increase in base excess, hypernatremia was accompanied by an increase in serum HCO3− level and pH. The authors suggest that hypernatremic alkalosis should be part of the differential diagnosis of metabolic acid–base disorders. In this chapter, we will discuss the pathophysiology and management of only four primary acid–base disorders (metabolic acidosis, metabolic alkalosis, respiratory acidosis, and respiratory alkalosis) in critically ill patients.