Search

This chapter describes acid-base and electrolyte homeostasis and pathophysiology and presents an organized approach to critical acid-base and electrolyte disorders. Acid-base homeostasis is achieved by tight control of alveolar ventilation and multiple renal mechanisms. Symptoms of severe acidemia are nonspecific, including altered level of consciousness and cardiovascular instability, although modest acidemia is typically well tolerated. Severe alkalemia is less well tolerated and may result in electrolyte derangements, arrhythmias, seizures, and cerebral and myocardial ischemia. By systematically analyzing the blood gas, serum chemistries, anion gap, and osmolar gap, a comprehensive differential diagnosis of acid-base disorders can be formed. Patients with brain injury, heart failure, certain toxic ingestions, and pregnancy require near-normal pH, whereas other patients with respiratory failure will tolerate permissive hypercapnia. Sodium bicarbonate has many adverse effects and, outside of certain indications, is best used to treat acidemia with cardiovascular collapse as opposed to simply normalizing the serum pH. Severe sodium abnormalities primarily affect the central nervous system, and in patients with neurologic emergencies and a serum sodium less than 120 mEq, rapid correction with hypertonic saline is necessary; in the absence of severe symptoms, slow correction of sodium disorders is critically important. Severe potassium abnormalities primarily affect cardiac conduction and can result in serious arrhythmias. The treatment of severe hyperkalemia focuses on stabilizing the cardiac membrane, shifting potassium intracellularly, and then removing potassium from the body. Hypokalemia and hypomagnesemia may cause cardiac irritability, typically occur together, and are treated concomitantly. Severe hypokalemia and hypophosphatemia can result in significant muscle weakness and ventilatory failure. Hypocalcemia in the context of massive transfusion may be an unrecognized cause of persistent hypotension in a bleeding patient.

Hypovolemic shock occurs when the volume within the circulatory system becomes depleted to the extent that tissue perfusion becomes inadequate. In asanguineous hypovolemic shock, effective management is based on: establishing adequate intravenous or intraosseous access, administering fluids to replete the losses and improve cardiac output, monitoring fluid responsiveness, and tracking endpoints of resuscitation. Further study is needed to clarify: which crystalloid (normal saline vs balanced solution) is superior in certain instances, whether there is a role for albumin in hypovolemic shock subtypes, and what is the ideal timing and agent of pressors when shock persists despite fluid administration.