An Overview of  Critical Care

     
       

Fluid and Electrolyte Abnormalities, Renal Dysfunction

         
       

The serum sodium is the major influence on extracellular fluid volume. There are a number of other important ions in the body: potassium, magnesium and phosphate are mostly intracellular cations, and chloride exists in the extracellular space, at electrochemical equilibrium with sodium. An alteration in this ratio can have significant effects on acid base balance – chloride depletion causes alkalosis, chloride excess causes acidosis. The electrical difference between the two exists in protein (albumin, hemoglobin) and phosphate, and is known as the anion gap. Hypernatremia is indicative of fluid depletion, caused by a process overriding the body’s volume control mechanisms – excessive diuresis or diabetes insipidis (29). Hyponatremia is indicative of fluid overload (high total body water) and is caused by overindulgence/overadministration of hypotonic fluids, inappropriate ADH secretion or the presence of osmotically active molecules in the ECF (alcohol, protein or fat) (30). Potassium is intuitively involved in nerve conduction and muscle contraction, too much potassium makes nerves over-excitable (particularly in the heart), too little makes them weak. Magnesium and calcium are co-factors for muscle contraction. Too little calcium makes nerves excitable (31). Magnesium allows potassium be pumped into cells, so a magnesium deficiency can worsen a potassium deficiency (32). Phosphorous is used for chemical energy in every cellular reaction and is a key part in the production of nucleotides (33). Phosphate depletion causes muscle weakness (34).

Oliguria

Acute Renal Success

Acute Tubular Necrosis

The amount of fluid in the body is tightly controlled by a series of cardiovascular reflexes and the kidney. The kidney, which is an extra-ordinarily metabolically active organ, regulates it’s own blood flow (over a wide range of blood pressures), and excretes a dilute urine when the person is overhydrated, and a concentrated urine when the patient is dehydrated. This process requires oxygen, energy and blood flow (35). If the blood flow to the kidney falls, the latter protects itself by avoiding the production of urine (acute renal success (36)). If a sustained injury is applied to the kidney – hypotension, ischemia, and various nephrotoxins, then the renal tubules are damaged and they can no longer concentrate urine (acute tubular necrosis): these patient may produce a lot of urine which is of poor quality (polyuric), or very little urine (oliguric). The best way to prevent renal failure is to prevent it: in ICU most patients develop acute renal failure (ARF) due to volume depletion and hypotension (37). Maintenance of blood volume and renal perfusion pressure (38) are the most effective methods of saving the kidneys. If the kidneys do fail, they usually recover over a series of weeks. If the patient becomes edematous or volume overloaded, then diuretics are often given, to reduce the total body fluid content, without making the kidneys work (39). Under some circumstances, renal replacement therapy may be necessary: hypokalemia, fluid overload, uremia.

Continuous Renal Replacement Therapy

Continuous Veno-venous Hemodiafiltration

Intermittant Hemodialysis

If the patient is hemodynamically unstable it is best to use a slow continuous hemodiafiltration method, which is very gentle (40). If the patient is hemodynamically stable, then intermittent hemodialysis is used.

Metabolic Acidosis

Respiratory Acidosis

Respiratory Alkalosis

Metabolic Alkalosis

Although acid base abnormalities usually stimulate a great deal of discussion, in of themselves, these disorders probably do little harm (41): the importance of an acid-base abnormality is the underlying cause. Acute metabolic acidosis is caused by the presence of additional measured and unmeasured anions in the circulation: if the anion is measured (i.e. chloride) and the patient is acidotic, then we call this a normal anion gap acidosis (42). If the anion is unmeasured (e.g. lactate, ketoacids or renal acids), the anion gap is widened. The pH is rarely very low in acute metabolic acidosis, due to the enormous buffering capacity of bicarbonate and the ability of the body to hyperventilate, and “blow off” carbon dioxide. The treatment for metabolic acidosis is to treat the cause. The use of sodium bicarbonate as an additional exogenous buffer is probably unnecessary (41). Acute respiratory acidosis is characterized by a high PaCO2, a low pH and normal base excess. The pH is usually considerable lower than with an equivalent metabolic upset due to the lack of rapidly available compensatory mechanisms (CO2 is mainly buffered intracellularly, and although this buffering capacity is very large, it is quite slow to equalize). The treatment for respiratory acidosis is increased alveolar ventilation, which usually means artificial ventilation.

Respiratory alkalosis is caused by hyperventilation, it is treated by reversing the cause (overtriggering of the mechanical ventilator), or, in the case of panic attacks, by rebreathing carbon dioxide. Metabolic alkalosis most commonly occurs to over aggressive diuresis and chloride depletion, and this is treated with sodium chloride administration.

         
                   
       

         
     

       
       

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