Hypovolemia

Kidney Inhibition of hypovolemia stimulated renin secretion... 

Ineffective Tissue Perfusion related to hypovolemia, blood loss, impaired distribution of fluid, impaired circulation, impaired transport of oxygen across alveolar and capillary bed, other (specify)... 

Hypovolemia Flat neck veins Intravenous fluids... 

Consider withholding insulin bolus in the setting of shock until resuscitation is underway. Rapid lowering of serum glucose can precipitate worsening hypovolemia... 

Hypovolemia, intraprocedural volume depletion, use of large volumes of contrast, and intra-aortic balloon pump... 

Hypovolemia, pregnant state, tuberculosis D Manage underlying condition... 

FIGURE 10-3. Expected neurohumoral response to hypovolemia. ACTH, adrenocorticotropic hormone ADH, antidiuretic hormone CNS, central nervous system Na, sodium. (Reprinted from Jimenez EJ. Shock. In Civetta JM, Taylor RW, Kirby RR, eds. Critical Care. New York Lippincott-Raven 1997 369, with permission.)... 

Patients will be in acute distress although symptoms and signs will vary depending on the severity of the hypovolemia and whether the etiology is hemorrhagic versus non-hemorrhagic. 

FIGURE 10-4. Treatment algorithm for the management of moderate to severe hypovolemia. BP, blood pressure CVP, central venous pressure ECG, electrocardiogram MAP, mean arterial pressure PA, pulmonary artery PAOP, pulmonary artery occlusion pressure PRBCs, packed red blood cells SBP, systolic blood pressure. 

A primary goal of therapy is ameliorating any identifiable underlying causes of ARF such as hypovolemia, nephrotoxic drug administration, or ureter obstruction. Prerenal and... 

Metabolic alkalosis is characterized by an increased arterial pH, a primary increase in the HCOf concentration, and a compensatory increase in the PaC02. Patients will always hypoventilate to compensate for metabolic alkalosis—even if it results in profound hypoxemia. For a metabolic alkalosis to persist there must concurrently be a process that elevates serum HC03 concentration (gastric or renal loss of acids) and another that impairs renal HC03 excretion (hypovolemia, hypokalemia, or mineralocorticoid excess). The etiologies of metabolic alkalosis are listed in Table 25-5. 

Dehydration, hypovolemia, and hyperkalemia (in primary adrenal insufficiency only)... 

Severe dehydration leading to hypotension and shock (circulatory collapse). Hypovolemia may not be responsive to intravenous hydration and may require the use of vasopressors. 

RBC sequestration in the spleen in young children may lead to a rapid drop in hematocrit, resulting in hypovolemia, shock,... 

In patients with peritonitis, hypovolemia is often accompanied by acidosis, so large volumes of a solution such as lac-tated Ringers may be required initially to restore intravascular volume. Maintenance fluids should be instituted (after intravascular volume is restored) with 0.9% sodium chloride and potassium chloride (20 mEq/L) or 5% dextrose and 0.45% sodium chloride with potassium chloride (20 mEq/L). The administration rate should be based on estimated daily fluid loss through urine and nasogastric suction, including 0.5 to 1.0 L for insensible fluid loss. Potassium would not be included routinely if the patient is hyperkalemic or has renal insufficiency. Aggressive fluid therapy often must be continued in the postoperative period because fluid will continue to sequester in the peritoneal cavity, bowel wall, and lumen. 

Vasopressin is a peptide hormone produced by the hypothalamus and secreted by the posterior pituitary in response to stimulation. Normal stimuli for vasopressin release are hyperosmolarity and hypovolemia, with thresholds for secretion of greater than 280 mOsm/kg and greater than 20% plasma volume depletion. A number of other stimuli, such as pain, nausea, epinephrine, and numerous drugs, induce release of vasopressin. Vasopressin release is inhibited by volume expansion, ethanol, and norepinephrine. The physiological effect of vasopressin is to promote free water clearence by altering the permeability of the renal collecting duct to water. In addition, it has a direct vasoconstrictor effect. Consequently, vasopressin results in water retention and volume restoration. In patients with septic shock, vasopressin is appropriately secreted in response to hypovolemia and to elevated serum osmolarity (R14). 

SuccessM treatment of PEA and asystole depends almost entirely on diagnosis of the underlying cause. Potentially reversible causes include (1) hypovolemia, (2) hypoxia, (3) preexisting acidosis, (4) hyperkalemia, (5) hypothermia, (6) hypoglycemia, (7) drug overdose, (8) cardiac tamponade, (9) tension pneumothorax, (10) coronary thrombosis, (11) pulmonary thrombosis, and (12) trauma. 

Fig. 12-1 contains an algorithm summarizing one approach to an adult patient presenting with hypovolemia. 

Direct measures (e.g., treatment of pain, hypovolemia, fever, infection, or salicylate overdose) can be effective. A rebreathing device (e.g., paper bag) can help control hyperventilation. 

Causes of nonosmotic release of arginine vasopressin, commonly known as antidiuretic hormone, include hypovolemia decreased effective circulating volume as seen in patients with congestive heart failure nephrosis cirrhosis and syndrome of inappropriate antidiuretic hormone (SIADH) release. 

In sinus bradycardia or incomplete heart block, lidocaine administration for the elimination of ventricular ectopy without prior acceleration in heart rate (eg, by atropine, isoproterenol or electric pacing) may promote more frequent and serious ventricular arrhythmias or complete heart block. Use with caution in patients with hypovolemia and shock, and all forms of heart block. 

Dopamine (Intropin) [Vasopressor/Adrenergic] Uses Short-tOTn use in cardiac decompensation secondary to X contractility when no hypovolemia is present T organ p fusion (at low dose) Action Renal dose 2-5 mcg/kg/min Inotropic dose 5-10 mcg/kg/min Pressor dose >10 mcg/kg/min Dose Adults Feds. 5-20 mcg/kg/min by cont inf, start at 5 and t by 5 mcg/kg/min to 20 mcg/kg/min max to effect (mix 400 mg in 250 mL DjW to make 1600 mcg/mL) (see Table 1-3) Caution [C, ] Contra Pheochromocytoma (adrenal gland tumor), VF, sulfite sensitivity Disp Inj 40, 80, 160 mg/mL, premixed 0.8, 1.6, 3.2 mg/mL SE Tach, vasoconstriction, 4- BP, HA, N/V, dyspnea Notes >10 mcg/kg/min X renal p fiision Interactions t Effects W/ a-blockers, diuretics, ergot alkaloids, MAOIs, BBs, anesthetics, phenytoin X effects W/ guanethidine EMS Correct hypovolemia before use use microdrip set or inf pump check soln- discolored... 

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