Hyponatremia Hypotension

In an attempt to conserve sodium, the kidney secretes renin increased plasma renin activity increases the release of aldosterone, which regulates the absorption of potassium and leads to kafluresis and hypokalemia. Hypokalemia is responsible in part for decreased glucose intolerance (82). Hyponatremia, postural hypotension, and pre-renal azotemia are considered of tittle consequence. Hypemricemia and hypercalcemia are not unusual, but are not considered harmful. However, hypokalemia, progressive decreased glucose tolerance, and increased semm cholesterol [57-88-5] levels are considered... 

Normal saline is an isotonic fluid composed of water, sodium, and chloride. It provides primarily ECF replacement and can be used for virtually any cause of TBW depletion. Common uses of normal saline include perioperative fluid administration volume resuscitation of shock, hemorrhage, or burn patients fluid challenges in hypotensive or oliguric patients and hyponatremia. 

Monitor for resolution of hypotension, dizziness, dehydration, hyponatremia, and hyperkalemia. Increase the dose as clinically necessary. 

Patients with hypovolemic hyponatremia present with decreased skin turgor, orthostatic hypotension, tachycardia, and dry mucous membranes. 

High-risk patients Hypertensive patients at risk of excessive hypotension include those with the following concurrent conditions or characteristics Heart failure, hyponatremia, high-dose diuretic therapy, recent intensive diureses or increase in diuretic dose, renal dialysis, or severe volume or salt depletion of any etiology. Single doses of enalaprilat as low as 0.2 mg have produced excessive hypotension in normotensive patients with these diagnoses. Because of the potential for an extreme hypotensive response in these patients, initiate therapy under very close medical supervision. The... 

Frequent serum electrolyte analysis is essential during therapy with the high-ceiling diuretics. Overdose may result in a rapid reduction of blood volume, dizziness, headache, orthostatic hypotension, hyponatremia, and hypokalemia. Nausea, vomiting, diarrhea, and loss of appetite are especially common with ethacrynic acid. 

The most extreme manifestation of untreated hypothyroidism is myxedema coma, which even if detected early and appropriately treated, carries a mortality rate of 30 to 60%. Myxedema coma is a misnomer. Most patients exhibit neither the myxedema nor coma. Patients with myxedema coma usually have longstanding hypothyroidism with the classic symptoms of hypothyroidism. Decompensation into myxedema coma may occur when the homeostatic mechanisms of the severely hypothyroid patient are subject to a stressful precipitating event (e.g., infection, trauma, some medications, stroke, surgery). The principal manifestation of myxedema coma is a deterioration of mental status (apathy, confusion, psychosis, but rarely coma). Other common clinical features include hypothermia, diastolic hypertension (early), hypotension (late), hypoventilation, hypoglycemia, and hyponatremia. If myxedema coma is suspected, the patient is usually admitted to an intensive care unit for pulmonary and cardiovascular support... 

Triamterene use may result in hyponatremia (somnolence, dry mouth, increased thirst, lack of energy) or severe hyperkalemia (irritability, anxiety, heaviness of legs, paresthesia, hypotension, bradycardia, ECG changes (tented T waves, widening QRS complex, ST segment depression]), particularly in those with renal impairment or diabetes, the elderly, or severely ill patients. 

When oxytocin is used judiciously, serious toxicity is rare. The toxicity that does occur is due either to excessive stimulation of uterine contractions or to inadvertent activation of vasopressin receptors. Excessive stimulation of uterine contractions before delivery can cause fetal distress, placental abruption, or uterine rupture. These complications can be detected early by means of standard fetal monitoring equipment. High concentrations of oxytocin with activation of vasopressin receptors can cause excessive fluid retention, or water intoxication, leading to hyponatremia, heart failure, seizures, and death. Bolus injections of oxytocin can cause hypotension. To avoid hypotension, oxytocin is administered intravenously as dilute solutions at a controlled rate. 

In a 5-day, double-blind, randomized, placebo-con-trolled study in 74 patients with euvolemic or hypervolemic hyponatremia, oral conivaptan (40 or 80 mg/day) significantly increased serum sodium concentrations (2). The most common adverse events were headache, hypotension, nausea, constipation, and postural hypotension. 

At presentation, the patient was hemodynami-cally unstable. She had a rapid heart rate and exhibited orthostatic hypotension (a fall in blood pressure on assuming an upright posture) and slow mentation. Her fluid deficit was greater than 4 L. Her lab work revealed hyponatremia (low serum sodium), hyperkalemia (high serum potassium), and a severe anion gap metabolic acidosis with dehydration. Her anion gap was 28, and her corrected serum Na+ was 135 mEq/L. 

Side effects that may occur include hypokalemia, hypomagnesemia, hyponatremia, hyperglycemia, hyperuricemia or gout, anorexia, orthostatic hypotension, anorexia, nausea, and photosensitivity. 

Vigorous diuresis may lead to profound water loss and electrolyte depletion, resulting in hypokalemia, hyponatremia, dehydration. Sudden volume depletion may result in increased risk of thrombosis, circulatory collapse, sudden death. Acute hypotensive episodes may also occur, sometimes several days after beginning therapy. 

Depletional hyponatremia (excess loss of Na ) is almost always accompanied by a loss of ECF water, but to a lesser extent tlian the Na loss. Hypovolemia is apparent in the physical examination (orthostatic hypotension, tachycardia, decreased skin turgor). Loss of isosmotic or hypertonic fluid is the cause and this can occur through renal or extrarenal losses. If urine Na is low (generally <10 mmol/L), the loss is extrarenal (see Figure 46-2) because the kidneys are properly retaining filtered Na in response to increased aldosterone (stimulated by the hypovolemia and hyponatremia). Causes of extrarenal loss of Na" in excess of H2O include losses from the gastrointestinal tract or skin (see Figure 46-2). 

Functional renal insufficiency is manifested as increases in serum creatinine and blood urea nitrogen. As cardiac output and renal blood flow decline, renal perfusion is maintained by the vasoconstrictor effect of angiotensin II on the efferent arteriole. Patients most dependent on this system for maintenance of renal perfusion (and therefore most likely to develop functional renal insufficiency with ACE inhibitors) are those with severe heart failure, hypotension, hyponatremia, volume depletion, and concomitant use of NSAIDs. - Sodium depletion (usually secondary to diuretic therapy) is the most important factor in the development of functional renal insufficiency with ACE inhibitor therapy. Renal insufficiency therefore can be minimized in many cases by reduction in diuretic dosage or liberalization of sodium intake. In some patients, the serum creatinine concentration will return to baseline levels without a reduction in ACE inhibitor dose. Since renal dysfunction with ACE inhibitors is secondary to alterations in renal hemodynamics, it is almost always reversible on discontinuation of the drug. ... 

ECF volume deficit (ECFVd) is dependent on the patient s weight, age, and the degree of volume depletion, and is difficult to precisely estimate. An ECFVd loss that is equal to a 10% to 15% decrease in body weight is associated with the development of postural hypotension. An ECFVd loss as low as 5%, however, can result in hyponatremia caused by nonosmotic ADH release as a result of stimulation of baroreceptors located in the chest and neck. The ECFVd of patients can be estimated as illustrated in this case a 42-year-old male weighs 70 kg on initial examination and presents with postural hypotension and has a serum sodium of 125 mEq/L ... 

Hydroxysteroid dehydrogenase (corticosterone methyloxidase deficiency) Hypotension Restricted to zona glomerulosa sole aldosterone defect hyponatremia, hyperkalemia, increased renin Mineralocorticoid replacement without glucocorticoid replacement... 

In hypercalcemia, excessive volume depletion, hyponatremia, and hypotension are major risks associated with the use of loop diuretics, and the side effects of hypokalemia, hyperuricemia, and hyperglycemia are always present. Loop diuretics should not be used concurrently with ototoxic aminoglycoside antibiotics (i.e., streptomycin, gentamicin, kanamycin, tobramycin). 

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