4: Fluids, Volume Regulation, and Volume Disturbances

Published on 06/02/2015 by admin

Filed under Anesthesiology

Last modified 06/02/2015

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 0 (0 votes)

This article have been viewed 1264 times

CHAPTER 4 Fluids, Volume Regulation, and Volume Disturbances

James Duke, MD, MBA

1 Describe the functionally distinct compartments of body water, using a 70-kg patient for illustration

Accurate estimations are difficult because ordinarily ideal body weight (IBW) is used as a basis for calculation. Obesity is rampant in our society, making accurate estimations difficult. Figure 4-1 estimates body water compartments in a patient with an IBW of 70 kg.

image

Figure 4-1 Body water compartments in a patient with an ideal body weight of 70 kg. BV, Blood volume; ECF, extracellular fluid; ICF, intracellular fluid; ISF, interstitial fluid.

2 Describe the dynamics of fluid distribution between the intravascular and interstitial compartments

The intravascular and interstitial fluid spaces compose the extracellular fluid and are in dynamic equilibrium, governed by hydrostatic and oncotic forces. Under normal circumstances the capillary hydrostatic pressure produces an outward movement of fluid, whereas the capillary oncotic pressure results in resorption. The sum of the forces leads to an egress of fluids from arterioles; about 90% of the fluid returns into the venules. The remainder of the fluid is subsequently returned to the circulation via the lymphatic system.

3 How are body water and tonicity regulated?

Antidiuretic hormone (ADH) is a primary mechanism; it circulates unbound in plasma, has a half-life of roughly 20 minutes, and increases production of cyclic adenosine monophosphate in the distal collecting tubules of the kidney. Tubular permeability to water increases, resulting in conservation of water and sodium and production of concentrated urine. Stimuli for the release of ADH include the following:

image Hypothalamic osmoreceptors have an osmotic threshold of about 289 mOsm/kg. Above this level ADH release is stimulated.
image Hypothalamic thirst center neurons regulate conscious desire for water and are activated by an increase in plasma sodium of 2 mEq/L, an increase in plasma osmolality of 4 mOsm/L, and loss of potassium from thirst center neurons and angiotensin II.
image Aortic baroreceptors and left atrial stretch receptors respond to volume depletion and stimulate hypothalamic neurons.

4 Discuss the synthesis of antidiuretic hormone

ADH, or vasopressin, is synthesized in the supraoptic and paraventricular nuclei of the hypothalamus. It is transported attached to carrier proteins down the pituitary stalk in secretory granules into the posterior pituitary gland (neurohypophysis). There it is stored and released into the capillaries of the neurohypophysis in response to stimuli from the hypothalamus. ADH-producing neurons receive efferent innervation from osmoreceptors and baroreceptors.

5 List conditions that stimulate and inhibit release of antidiuretic hormone

See Table 4-1.

TABLE 4-1 Conditions that Stimulate and Inhibit Release of Adrenocorticotropic Hormone

  Stimulates Adrenocorticotropic Hormone Release Inhibits Adrenocorticotropic Hormone Release
Normal physiologic states Hyperosmolality Hypo-osmolality
Hypovolemia Hypervolemia
Upright position Supine position
β-Adrenergic stimulation α-Adrenergic stimulation
Pain and emotional stress
Cholinergic stimulation
Abnormal physiologic states Hemorrhagic shock Excess water intake
Hyperthermia Hypothermia
Increased intracranial pressure
Positive airway pressure
Medications Morphine Ethanol
Nicotine Atropine
Barbiturates Phenytoin
Tricyclic antidepressants Glucocorticoids
Chlorpropamide Chlorpromazine
Results Oliguria, concentrated urine Polyuria, dilute urine

6 What is diabetes insipidus?

Diabetes insipidus (DI) is caused by a deficiency of ADH synthesis, impaired release of ADH from the neurohypophysis (neurogenic DI), or renal resistance to ADH (nephrogenic DI). The result is excretion of large volumes of dilute urine, which, if untreated, leads to dehydration, hypernatremia, and serum hyperosmolality. The usual test for DI is cautious fluid restriction. The inability to decrease and concentrate urine suggests the diagnosis, which may be confirmed by plasma ADH measurements. Administration of aqueous vasopressin tests the response of the renal tubule. If the osmolality of plasma exceeds that of urine after mild fluid restriction, the diagnosis of DI is suggested.

7 List causes of diabetes insipidus

See Table 4-2.

TABLE 4-2 Causes of Diabetes Insipidus

Vasopressin Deficiency (Neurogenic Diabetes Insipidus) Vasopressin Insensitivity (Nephrogenic Diabetes Insipidus)
Familial (autosomal-dominant) Familial (X-linked recessive)
Acquired Acquired
Idiopathic Pyelonephritis
Craniofacial, basilar skull fractures Postrenal obstruction
Craniopharyngioma, lymphoma, metastasis Sickle cell disease and trait
Granuloma (sarcoidosis, histiocytosis) Amyloidosis
Central nervous system infections Hypokalemia, hypercalcemia
Sheehan’s syndrome, cerebral aneurysm, cardiopulmonary bypass Sarcoidosis
Hypoxic brain injury, brain death Lithium

8 Discuss alternative treatments for diabetes insipidus

Available preparations of ADH include pitressin tannate in oil, administered every 24 to 48 hours; aqueous pitressin, 5 to 10 units intravenously or intramuscularly every 4 to 6 hours; desmopressin (DDAVP), 10 to 20 units intranasally every 12 to 24 hours; or aqueous vasopressin, 100 to 200 mU/hr. Incomplete DI may respond to thiazide diuretics or chlorpropamide (which potentiates endogenous ADH).

Buy Membership for Anesthesiology Category to continue reading. Learn more here

Related posts:

58: Congenital Heart Disease 59: Fundamentals of Obstetric Anesthesia 34: Heart Failure 66: Epidural Analgesia and Anesthesia 76: Electroconvulsive Therapy 41: Acute Respiratory Distress Syndrome (ARDS)