Intravascular volume

Although blood pressure control follows Ohm s law and seems to be simple, it underlies a complex circuit of interrelated systems. Hence, numerous physiologic systems that have pleiotropic effects and interact in complex fashion have been found to modulate blood pressure. Because of their number and complexity it is beyond the scope of the current account to cover all mechanisms and feedback circuits involved in blood pressure control. Rather, an overview of the clinically most relevant ones is presented. These systems include the heart, the blood vessels, the extracellular volume, the kidneys, the nervous system, a variety of humoral factors, and molecular events at the cellular level. They are intertwined to maintain adequate tissue perfusion and nutrition. Normal blood pressure control can be related to cardiac output and the total peripheral resistance. The stroke volume and the heart rate determine cardiac output. Each cycle of cardiac contraction propels a bolus of about 70 ml blood into the systemic arterial system. As one example of the interaction of these multiple systems, the stroke volume is dependent in part on intravascular volume regulated by the kidneys as well as on myocardial contractility. The latter is, in turn, a complex function involving sympathetic and parasympathetic control of heart rate intrinsic activity of the cardiac conduction system complex membrane transport and cellular events requiring influx of calcium, which lead to myocardial fibre shortening and relaxation and affects the humoral substances (e.g., catecholamines) in stimulation heart rate and myocardial fibre tension. 

Plasma proteins are contraindicated in those with a history of allergic reactions to albumin, severe anemia, or cardiac failure in the presence of normal or increased intravascular volume and in patients on cardiopulmonary bypass. Plasma protein fractions are used cautiously in patients who are in shock or dehydrated and in those with congestive cardiac failure or hepatic or renal failure. These solutions are Pregnancy Category C drugp and are used cautiously during pregnancy and lactation. 

KasseU NF, Peerless SJ, Durward QJ, Beck DW, Drake CG, Adams HP. Treatment of ischemic deficits from vasospasm with intravascular volume expansion and induced arterial hypertension. Neurosurgery 1982 11 337-343. 

Maintain intravascular volume status and urine output with normal saline... 

Restore intravascular volume with normal saline if in hypovolemic shock... 

Diuretic pharmacotherapy (strict avoidance of intravascular volume depletion)... 

The major limitation of nitrate therapy is the development of tolerance with continuous use. The loss of anti-anginal effects may occur within the first 24 hours of continuous nitrate therapy. While the cause of tolerance is unclear, several mechanisms have been proposed. These include depletion of the sulfhydryl groups necessary for the conversion of nitrates to nitric oxide, activation of neurohormonal systems, increased intravascular volume, and generation of free radicals that degrade nitric oxide. The most effective method to avoid tolerance and maintain the anti-anginal efficacy of nitrates is to allow a daily nitrate-free interval of at least 8 to 12 hours. Nitrates do not provide protection from ischemia during the nitrate-free period. Therefore, the nitrate-free... 

List the most common etiologies of decreased intravascular volume in hypovolemic shock patients. 

Hypovolemic shock occurs as a consequence of inadequate intravascular volume to meet the oxygen and metabolic needs of the body. 

Heart rate should begin to decrease reciprocally to increases in the intravascular volume within minutes to hours ... 

As previously discussed, increased portal pressure triggers the release of nitric oxide to directly vasodilate the splanchnic arterial bed and decrease portal pressure. Unfortunately, nitric oxide also dilates the systemic arterial system, causing a decrease in blood pressure and a decrease in renal perfusion by lowering the effective intravascular volume. The kidney reacts by activating the renin-angiotensin-aldosterone system, which increases plasma renin activity, aldosterone production, and sodium retention. This increase in intravascular volume furthers the imbalance of intravascular oncotic pressure, allowing even more fluid to escape to the extravascular spaces. 

The target in treating ascites is to effect a fluid loss of approximately 0.5 L per day.22 Because ascites equilibrates with vascular fluid at a much slower rate than does peripheral edema, aggressive diuresis is associated with intravascular volume depletion and should be avoided unless patients have concomitant peripheral edema. Patients with peripheral edema in addition to ascites may require increasing furosemide doses until euvolemia is achieved intravenous diuretics are often necessary.22 Diuretic therapy in cirrhosis is typically lifelong. 

Prerenal ARF is characterized by reduced blood delivery to the kidney. A common cause is intravascular volume depletion due to conditions such as hemorrhage, dehydration, or... 

When determining the appropriate fluid to be utilized, it is important to first determine the type of fluid problem (TBW versus ECF depletion), and start therapy accordingly. For patients demonstrating signs of impaired tissue perfusion, the immediate therapeutic goal is to increase the intravascular volume and restore tissue perfusion. The standard therapy is normal saline given at 150 to 500 mL/hour until perfusion is optimized. Although LR is a therapeutic alternative, lactic... 

For peritonitis, early and aggressive intravenous fluid resuscitation and electrolyte replacement therapy are essential. A common cause of early death is hypovolemic shock caused by inadequate intravascular volume expansion and tissue perfusion. 

Hypotension and shock may develop if intravascular volume is not restored. 

In the early phase of serious intraabdominal infections, attention should be given to preserving major organ system function. With generalized peritonitis, large volumes of intravenous (IV) fluids are required to maintain intravascular volume, to improve cardiovascular function, and to ensure adequate tissue perfusion and oxygenation. Adequate urine output should be maintained to ensure appropriate fluid resuscitation and to preserve renal function. A common cause of early death is hypovolemic shock caused by inadequate intravascular volume expansion and tissue perfusion. 

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. 

The mainstay of treatment for established SOS is supportive care aimed at sodium restriction, increasing intravascular volume, decreasing extracellular fluid accumulation, and minimizing factors that contribute to or exacerbate hepatotoxicity and encephalopathy. Defibrotide has shown promising results in the treatment of SOS.44... 

The answer is c (HardmanT pp 695-697.) Mannitol increases serum osmolarity and therefore pulls water out of cells, cerebrospinal fluid (C5F), and aqueous humor. This effect can be useful in the treatment of elevated intraocular or intracranial pressure. However, by expanding the intravascular volume, mannitol can exacerbate CHF... 

Shock refers to conditions manifested by hemodynamic alterations (e.g., hypotension, tachycardia, low cardiac output [CO], and oliguria) caused by intravascular volume deficit (hypovolemic shock), myocardial pump failure (cardiogenic shock), or peripheral vasodilation (septic, anaphylactic, or neurogenic shock). The underlying problem in these situations is inadequate tissue perfusion resulting from circulatory failure. 

Crystalloids are administered at a rate of 500 to 2,000 mL/hour, depending on the severity of the deficit, degree of ongoing fluid loss, and tolerance to infusion volume. Usually 2 to 4 L of crystalloid normalizes intravascular volume. 

The primary disadvantage is the large volume necessary to replace or augment intravascular volume. Approximately 4 L of normal saline must be infused to replace 1 L of blood loss. In addition, dilution of colloid oncotic pressure leading to pulmonary edema is more likely to follow crystalloid than colloid resuscitation. 

Intravascular volume overload is characterized by high filling pressures (CVP greater than 12 to 15 mm Hg, PAOP greater than 20 to 24 mm Hg) and decreased CO (less than 3.5 L/min). Ifvolume overload occurs, furosemide, 20 to 40 mg, should be administered by slow IV push to produce rapid diuresis of intravascular volume and unload the heart through venous dilation. 

Patients predicted to follow a severe course require treatment of any cardiovascular, respiratory, renal, and metabolic complications. Aggressive fluid resuscitation is essential to correct intravascular volume depletion and maintain blood pressure. IV colloids may be required because fluid losses are rich in protein. Drotrecogin alfa may benefit patients with pancreatitis and systemic inflammatory response syndrome. IV potassium, calcium, and magnesium are used to correct deficiency states. Insulin is used to treat hyperglycemia. Patients with necrotizing pancreatitis may require antibiotics and surgical intervention. 

Aggressive fluid repletion and management are required for the purposes of achieving or maintaining proper intravascular volume to ensure adequate cardiac output, tissue perfusion, and correction of acidosis. 

In the initial hour of treatment, a large volume of IV solution (lactated Ringer s solution) may need to be administered to restore intravascular volume. This may be followed by up to 1 L/hour until fluid balance is restored in a few hours. 

Iso-oncotic colloid solutions (plasma and plasma protein fractions), such as 5% albumin and 6% hetastarch, offer the advantage of more rapid restoration of intravascular volume with less volume infused, but there is no significant clinical outcome differences compared with crystalloids. 

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