Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
50 Cards in this Set
- Front
- Back
|
276 Which of the following statement(s) is/are true concerning the compensatory mechanisms and treatment of metabolic acidosis?a. Maximal renal compensation for metabolic acidosis occurs before full respiratory compensation can occurb. All patients with lactic acidosis should receive prompt treatment with bicarbonatec. Potassium replacement is essential even in the face of normal or high serum potassium when treating diabetic ketoacidosisd. Sodium bicarbonate administration should begin simultaneous with volume resuscitation in patients with hypoxia secondary to shock
|
Answer: cThe kidney is extremely sensitive to changes in serum bicarbonate concentration and responds by increasing net acid excretion primarily by increasing ammonia excretion. Maximal renal compensation requires 2 to 4 days. Delay in achieving maximal renal response to an increased acid load causes blood pH to decline, which stimulates hyperventilation. Although effective in promptly raising blood pH, ventilatory compensation is only partial, and full respiration compensation requires 12 to 24 hours. The major principal of treatment for mild to moderate acute metabolic acidosis is correction of the underlying cause. In surgical and trauma patients, metabolic acidosis is often the result of hypoxia secondary to inadequate tissue perfusion and subsequent lactic acidosis. Volume and/or blood resuscitation alone may be enough to correct the acidosis. Attempts to correct acidosis with exogenous bicarbonate before correction of inadequate tissue perfusion are usually unsuccessful. The use of bicarbonate for the treatment of lactic acidosis is controversial at best. In several studies the use of bicarbonate in patients with lactic acidosis does not improve clinical parameters or outcome. The correction of both acidosis and hypoglycemia of diabetic ketoacidosis is best achieved by the administration of insulin. Volume resuscitation is also required. Potassium replacement is essential, even in the face of normal or high serum potassium, and as hypokalemia develops as acidosis in hyperglycemia are corrected.
|
|
|
275 Which of the following statement(s) is/are true concerning the osmotic activity of body fluids?a. Urea contributes to the osmolality of a solution but not its tonicityb. The osmolality of the body remains fairly constant at approximately 289 mOsm/kg H2Oc. The two primary regulators of water balance are antidiuretic hormone and aldosteroned. Serum sodium is the most valuable laboratory indicator of abnormal total body water content
|
Answer: a, b, dBody fluids are aqueous solutions composed primarily of water and contained in different compartments of the body. The movement of water from these compartments depends on a number of physical properties, the most important of which is osmosis. According to the principles of osmosis, if two solutions are separated by semipermeable membrane, water moves across the membrane to equalize the concentration of the osmotically active particles. The osmotic activity across a semipermeable membrane is determined by the concentration of solutes on each side of the membrane. The body is capable of fine regulation of solute and water concentrations, so that osmolality remains fairly constant at an average of 289 mOsm/kg H2O. In response to small changes in cell volume, osmoreceptors in the paraventricular and supraoptic nuclei of the hypothalamus send signals to the neuronal centers that control the two primary regulators of water balance, thirst and antidiuretic hormone secretion. Changes in TBW are reflected by changes in extracellular solute concentration. Because sodium is the primary extracellular cation and potassium is the predominant intracellular cation, the serum sodium approximates the sum of the exchangeable total body sodium and exchangeable total body potassium divided by the TBW. Because total body solute content remains relatively stable over time, changes in TBW content result in inversely proportional changes in serum sodium. Thus, abnormalities in serum sodium are the indication of abnormal TBW content. In contrast to impermeable solutes that are excluded from the intracellular space, such as sodium, permeable solutes such as urea can freely cross the cell membranes. Although urea contributes to the osmolality of a solution, it has no effect on tonicity because it distributes equally across membranes, and as such does not contribute to the osmols that affects cell volume.
|
|
|
274 Which of the following statement(s) is/are true concerning the derangement of metabolic acidosis?a. A major source of acid production of the body is sulfuric acidb. Excessive loss of bicarbonate can occur with intestinal or pancreatic fistulasc. Ketoacidosis can occur in conditions of either hyper-or hypoglycemiad. Lactic acidosis is present when serum lactate concentration is > 2 mEq/Le. Lactic acidosis can be associated with ethanol toxicity
|
Answer: a, b, c, eMost clinically significant metabolic acidosis is related to the net loss of bicarbonate, which occurs when consumption due to either loss or titration is greater than bicarbonate generation. Under normal circumstances of ingestion of the average amount of protein in an American diet, about 70 mEq acid is generated daily. The major source of acid production is sulfuric acid from the metabolism of sulphur-containing amino acids. Increased protein intake and tissue catabolism resulting in greater metabolism of sulphur containing amino acids may lead to a generation of increased amounts of sulfuric acid. This excess acid utilizes excess bicarbonate for neutralization. Diarrhea, intestinal or pancreatic fistulas, and burns can cause metabolic acidosis secondary to loss of bicarbonate. The two most common types of organic acidosis are ketoacidosis and lactic acidosis. The abnormality primarily responsible for ketoacidosis is deficiency of insulin whether primary, as in diabetic ketoacidosis, or secondary to hypoglycemia. Under normal conditions a small amount of ketoacids is produced. During prolonged starvation, production of ketoacids increase to modest levels, providing an important source of energy to nonhepatic tissues, particularly the brain. In ketoacidosis, the ketoacid production is excessive because of insulin deficiency. In diabetic acidosis, insulin deficiency also contributes to hyperglycemia by decreasing the metabolism of glucose by extrahepatic tissue and increasing hepatic production of glucose.Lactic acidosis can be divided into type A, caused by tissue hypoxia, and type B, caused by other mechanisms. Hypoxia, the most common cause of lactic acidosis, impairs the mitochondrial oxidation of NADH to NAD that is necessary for glycolysis. Normal serum lactate concentration is below 2 mEq/L. Lactate acidosis is secondary to hypoxemia, usually due to an increased production of lactate as well as decreased use, and serum lactate concentrations greater than 6 mEq/L. The most common cause of type B lactate acidosis is ethanol intoxication.
|
|
|
273 Which of the following statement(s) is/are true concerning abnormalities in serum potassium?a. Hyperkalemia can occur in the otherwise normal surgical patient due to excessive intravenous potassium administrationb. The primary EKG change associated with severe hyperkalemia is peaked T-wavesc. Temporary treatment of hyperkalemia includes administration of calcium, sodium bicarbonate, or glucose and insulind. Alterations in membrane potentials reflected in cardiac and skeletal muscle are common results of both hypo-and hyperkalemiae. A reduction in serum potassium of 1mEq/liter requires replacement of 40mEq of potassium
|
Answer: c, dPotassium is the major intracellular cation and is a major determinant of intracellular osmolality. Because of the large differences between intracellular and extracellular potassium concentrations, a transmembrane potential is generated. Alterations in potassium concentration gradient (both hyper- and hypokalemia) have profound effects on transmembrane potential and consequently on cellular function. This is especially true for cardiac, skeletal, and smooth muscle. Extracellular potassium concentration is primarily determined by renal excretion. About 90% of ingested potassium is secreted by the urine. Hyperkalemia therefore rarely develops from excessive potassium intake in the absence of renal insufficiency, since the capacity for renal potassium excretion is large. In the surgical patient, diminished renal function is perhaps the most common problem leading to hyperkalemia. Both chronic and acute renal failure result in the deficit in potassium excretion. Hyperkalemia can also be associated with cellular disruption, such as with crush injuries or lysed erythrocytes in large hematomas or after massive blood transfusion. The clinical manifestations of hyperkalemia are primarily related to membrane depolarization. The most life-threatening manifestations are related to the cardiac effects of membrane depolarization. Mild hyperkalemia results in peaked T-waves on the EKG and may cause parethesia and weakness. More severe forms of hyperkalemia cause flattened P-waves, prolongation of the QRS complex, and deep S-waves on EKG. Ventricular fibrillation and cardiac arrest may follow. Severe hyperkalemia with EKG abnormalities requires urgent treatment. Rapid infusion of 10% to 20% calcium gluconate may reduce the effects of hyperkalemia on membrane potentials. Administration of sodium bicarbonate is another temporary measure. The increase in serum sodium antagonizes the effects of hyperkalemia on the membrane potential, whereas the increase in extracellular pH shifts potassium into the cells. Movement of potassium into the intracellular compartment can also be achieved by giving insulin and glucose.Hypokalemia is usually caused by total body potassium depletion secondary to the decreased potassium intake, increased extra-renal potassium losses, or increased renal potassium losses. Decreased serum potassium levels may also be secondary to redistribution of potassium into the intracellular space. Symptoms of hypokalemia, like those of hyperkalemia, are manifested by disturbances in membrane potentials. As potassium levels fall below 2.5mEq/L, muscle weakness is common. The primary treatment of hypokalemia is potassium replacement. The route and rate of potassium replacement depends on the presence and severity of symptoms. A reduction in serum potassium of 1mEq/L represents a total body potassium deficiency of 100 to 200 mEq.
|
|
|
272 Which of the following statement(s) is/are true concerning abnormalities in serum sodium?a. The most common cause of hyponatremia is a deficit in total body sodiumb. Hyponatremia can occur in situations of excessive solutec. Most surgical patients with hyponatremia are best treated by free water restrictiond. Central nervous system effects are the predominant symptom of hypernatremiae. Hypernatremia should be rapidly corrected with free water administration
|
Answer: b, c, dThe most common cause of hyponatremia is an excess of free water rather than a deficit of total body sodium. Hyponatremia is frequently seen in the postoperative or post-trauma patients because increased ADH secretion acts on the collecting tubules of the kidney to increase free water reabsorption. Although hyponatremia most often results from excess free water, it can occur in the presence of excess solute. In this situation, TBW content is either normal or diminished but the plasma osmolality is increased. An example of this hyperosmolar-hyponatremic state is untreated hyperglycemia. Excess solute may also be due to exogenous administration or ingestion of mannitol, ethanol, methanol, or ethylene glycol. Most surgical patients with hyponatremia are euvolemic or hypervolemic. Such patients, if asymptomatic, are best treated by free water restriction, since free water overload is the cause of the condition. Hypernatremia is a less common problem in surgical patients than hyponatremia and is usually the result of excess free water loss associated with hypovolemia. Hypernatremia may also be secondary to increased total body content of sodium, which is usually related to exogenous administration of sodium. The symptoms of hypernatremia are related to the hyperosmolar state. CNS effects predominate because of cellular dehydration as water passes into the extracellular space. Once hypernatremia becomes symptomatic, it is associated with significant morbidity and mortality. Prompt treatment of hypernatremia is essential. Rapid correction, however, of hypernatremia is associated with significant risk of cerebral edema and herniation. Because chronic hypernatremia is relatively well tolerated, there are few advantages to rapidly correcting the free water deficit. Moderate degrees of hypernatremia are tolerated well, and symptoms rarely develop unless serum sodium levels exceed 160 mEq/liter. The development of symptoms also depends on the rapidity at which hypernatremia develops.
|
|
|
271 Which of the following statement(s) is/are true concerning the clinical presentation and treatment of severe metabolic alkalosis?a. In most cases clinical signs are obviousb. Correction of potassium and volume depletion corrects most cases of metabolic alkalosisc. Acetazolamide can enhance renal excretion of bicarbonated. Acid replacement should be provided at a molar equivalent basis for excess serum bicarbonate
|
Answer: b, cClinical signs of metabolic alkalosis may not be prominent, since the condition usually develops relatively slowly. Correction of the underlying cause is the mainstay of treatment in this disorder. In general, correction of potassium and volume depletion corrects the metabolic alkalosis. In patients without intravascular volume deficits, renal excretion of bicarbonate can be enhanced by administration of the carbonic acid anhydrase inhibitor acetazolamide. If renal excretion of bicarbonate cannot be increased because of underlying renal insufficiency or if the metabolic alkalosis is severe, acid may be administered to directly titrate the excess extracellular bicarbonate. Acids that can be used include ammonium chloride, arginine hydrochloride, or dilute hydrochloric acid. Partial correction of alkalosis is the initial goal. A general guide is that 2.2 mEq/kg decreases serum bicarbonate by about 5 mEq/L.
|
|
|
270 Which of the following statement(s) is/are true concerning total body water?a. Total body water in men represents a higher percent body weight than in womenb. In infants, water comprises up to 80% of body weightc. Total body water content decreases with increasing aged. Total body water is equally distributed within the intra-and extracellular compartments
|
Answer: a, b, cThe total volume of water within the body is termed total body water. The relationship between total body water (TBW) and body weight is relatively consistent for any given individual and depends on the amount of fat within the body. Because fat contains little water, TBW as a percentage of body weight decreases with increasing body fat. The estimated TBW in men is 60% of body weight, whereas in women, who typically have more adipose tissue, the average TBW is 50% of body weight. The percentage of body weight accounted for by water also varies with age. In infants, water comprises about 80% of body weight. Throughout adult life, a gradual decrease occurs in TBW content because of the amount of fat within the body usually increases with age. In obese patients, estimates of TBW should be decreased by 10% to 20% whereas in lean patients, estimates should be increased by about 10%.TBW is distributed within the intra and extracellular compartments. Intracellular fluid makes up about 2/3 of the TBW, or 40% of body weight.
|
|
|
269 Which of the following statement(s) is/are true concerning abnormalities in calcium concentration?a. Parathyroid hormone affects calcium homeostasis only at the exchange of calcium between bone and extracellular fluidb. About 45% of total plasma calcium is in the ionized state and is responsible for most physiologic actionsc. Changes in plasma protein levels or pH can alter the proportion of calcium in the ionized stated. Intravenous normal saline administration is the first step in treatment of hypercalcemiae. Classic signs of hypocalcemia include hyperactive deep tendon refluxes, Cvostek’s sign and Trousseau’s sign
|
Answer: b, c, d, eCalcium is a divalent cation found in abundance in the human body. About 99% of total body calcium is located in bone in the form of hydroxyapatite crystals. Calcium homeostasis depends on the exchange of calcium between bone and extracellular fluid, renal excretion, and intestinal absorption. These three processes are controlled to a great extent by parathyroid hormone. In extracellular fluid, calcium exists in three forms: ionized calcium, non-ionized calcium, and protein-bound calcium. Ionized calcium, which comprises about 45% of total calcium is responsible for most physiologic actions of calcium in the body, and its level is tightly controlled by a regulatory mechanisms. Some nonionized calcium is complexed with non-protein anions, including phosphate and citrate, and does not easily disassociate. These molecular forms make up only about 15% of total calcium present in plasma. About 40% of extracellular nonionized calcium is bound to proteins, with most being bound to albumin. Changes in either plasma protein levels or pH can alter the proportion of calcium in the ionized state. The most common cause of hypercalcemia is primary hyperparathyroidism. Hypercalcemia can also occur secondary to malignant disease, caused either by a metastasis to bone or by autonomous tumor secretion of hormone-like substances that alter calcium homeostasis. Neuromuscular effects may be the earliest manifestations and include muscle fatigue, weakness, personality disorders, psychosis, confusion, and coma. Elevation of total serum calcium concentrations to greater than 14mg/dL requires prompt treatment to prevent any serious and potentially lethal complications. Immediate measures are directed toward maximizing renal excretion of calcium. Vigorous hydration with 0.9% saline solution to prompt diuresis should be the initial step in treatment. The addition of potassium to the resuscitation fluid as well as the use of furosemide can also be used for treatment.Serum calcium levels below 8 mg/dL may be associated with symptoms and signs that are primary manifestations of neuromuscular abnormalities. These include muscle cramps, perioral tingling, parastesias, laryngeal stridor, tetany, seizures and psychotic behavior. Classic signs of hypocalcemia include hyperactive, deep tendon reflexes, Cvostek’s sign, and Trousseau’s sign. Symptomatic hypocalcemia is best treated with intravenous infusion of calcium in the form of calcium gluconate or calcium chloride.
|
|
|
268 Which of the following statement(s) is/are true concerning maintenance intravenous fluid therapy?a. The total daily water requirement for a 70-kg man is about 2500 mL/dayb. Normal maintenance IV therapy requires administration of sodium, potassium, calcium, phosphate, and magnesiumc. Fluid volume calculations for elderly patients generally are decreased compared to their younger counterpartsd. A child requires a lesser amount of maintenance fluid per kilogram than a larger individual
|
Answer: a, cMaintenance fluid replacement is aimed at replacing fluids normally lost during the course of a day. Calculation of maintenance fluid replacement does not include replacement of preexisting deficits or ongoing additional losses. Formulas exist for calculating maintenance fluid requirements which adjust for differences in body weight and for changes in TBW content. A smaller (or younger) individual who has a high percentage of TBW in relation to body weight requires a greater amount of maintenance fluid per kilogram than a larger individual. The total daily water requirement for a 70-kg man is about 2500 mL/day. Because hypervolemia is poorly tolerated in older individuals and in patients with cardiac disease, the volume calculated is generally diminished in this age group. Normal maintenance therapy requires administration of sodium and potassium. Replacement of calcium, phosphate or magnesium are generally not necessary in patients requiring short-term therapy. In critically ill patients, however, critical deficits in these electrolytes may occur and must be replaced.
|
|
|
267 Which of the following(s) is/are true concerning the control of the volume of body water?a. Osmoreceptors and baroreceptors work equally to control fluid balance during normal conditionsb. The cardiac atrium regulates volume only by means of its sympathetic and parasympathetic connectionsc. The kidney is the primary effector organ in controlling water balanced. The conversion of angiotensin I to angiotensin II is dependent on the amount of the enzyme, renin, availablee. Nitric oxide plays a number of important roles in regulation of renal hemodynamics
|
Answer: c, d, eChanges in volume are detected both by osmoreceptors, which detect changes in plasma osmolality and baroreceptors, which are sensitive to changes in pressure. The osmoreceptors are responsible for day-to-day fine-tuning of volume whereas the baroreceptors contribute relatively little to the control of fluid balance under normal conditions. Changes in effective circulating volume are sensed by the volume receptors of the intrathoracic capacitance vessels and atria, the pressure receptors of the aortic arch and carotid arteries, the intrarenal baroreceptors, and, to a lesser extent, by the hepatic and cerebrospinal volume receptors. These baroreceptors control volume by means of sympathetic and parasympathetic connections. The atria also appear to serve as endocrine organs capable of directing responses to volume changes with the elaboration of the hormone, atrial natriuretic peptide. The major hormonal mediator of baroreceptor modulation of volume control is the renin-angiotensin system. The end result of this complex system of receptors or messengers is a change in sodium and water balance mediated by the kidneys. It is through changes in sodium and water reabsorption that volume and pressure ultimately normalize. Renin is a proteolytic enzyme that is released in response to changes in arterial pressure, changes in delivery of sodium to the macula densa of the distal convoluted renal tubule, increases in beta adrenergic activity and increases in cellular cAMP. Renin cleaves angiotensin I from circulating angiotensinogen. Angiotensinogen is abundant, so this reaction is enzyme dependent rather than substrate dependent. Angiotensin I is further cleaved to angiotensin II which acts with locally and systemically to increase vascular tone. Angiotensin II affects sodium reabsorption by decreasing renal plasma flow and the glomerular filtration coefficient. Finally, angiotensin II increases sodium reabsorption by direct tubular action as well as by stimulation of aldosterone release from the adrenal cortex.The importance of nitric oxide and its many biologic functions has recently been recognized. Nitric oxide participates in the regulation of renal hemodynamics and renal handling of water and electrolytes.
|
|
|
266 Which of the following statement(s) is/are true concerning respiratory acidosis?a. Respiratory acidosis is associated with chronic pulmonary disease far more commonly than is hypoxemiab. The initial buffering effect occurs at the cellular levelc. Renal compensation occurs within 24 hoursd. Correction of hypoxemia in patients with chronic lung disease may worsen respiratory acidosis
|
Answer: b, dRespiratory acidosis, the decrease in extracellular pH from a primary increase in PCO2, is due to inadequate ventilation. Although pulmonary disease commonly causes hypoxemia, respiratory acidosis is far less common, since defusion of O2 is more readily impaired than diffusion of CO2. Increased PCO2 results in increased H2CO3 which disassociates into H+ and HCO3–. Cellular exchange of Na+ and K+ for H+ allows the reaction to continue in this direction with increased extracellular bicarbonate. This tissue buffering is accomplished within minutes. Persistently elevated PCO2 also stimulates increased renal acid excretion. Full renal compensation occurs over 3 to 5 days. The treatment of chronic compensated respiratory acidosis may be complicated by accompanying hypoxemia. In chronic hypercapnia, the chemical chemoreceptors may be insensitive and the accompanying hypoxemia may supply the main respiratory drive through the stimulation of peripheral chemoreceptors. In such patients, complete correction of hypoxemia may further depress respiration and worsen the respiratory acidosis.
|
|
|
265 Which of the following statements(s) is/are true concerning metabolic alkalosis?a. Either increased extracellular bicarbonate concentration or inhibited renal excretion of bicarbonate can cause metabolic alkalosisb. In metabolic alkalosis secondary to prolonged gastric outlet obstruction, the urine pH is usually acidicc. Hypokalemia can lead to metabolic alkalosisd. The respiration compensatory mechanisms for metabolic alkalosis are quite ineffective
|
Answer: b, c, dSustained metabolic alkalosis occurs only if extracellular bicarbonate concentration is increased and renal excretion of excess bicarbonate is inhibited. Alone, neither is sufficient to result in metabolic alkalosis. Extracellular bicarbonate concentration is increased by numerous mechanisms. Loss of HCl is the leading cause of metabolic alkalosis in surgical patients. External loss of gastric acid results in net gain in bicarbonate, which causes metabolic alkalosis. Although the kidney can excrete excess bicarbonate, this must be accompanied by excretion of sodium. Renal excretion of sodium is limited in the face of volume depletion, which also occurs with external losses of gastric secretion. As volume depletion progresses, sodium is conserved in exchange for hydrogen. Thus, in metabolic alkalosis secondary to prolonged gastric outlet obstruction, the urine, although initially alkalotic, becomes paradoxically acidotic in prolonged or uncorrected cases. Hypokalemia and cellular exchange of potassium for hydrogen can also lead to metabolic alkalosis. Hypokalemia results in enhanced proximal tubular bicarbonate reabsorption and distal tubular acid secretion. The major compensatory mechanism in metabolic alkalosis is respiratory, since the presence of metabolic alkalosis implies renal dysfunction in either generating or failing to excrete increased amounts of bicarbonate. Hypoventilation is limited by the development of hypoxemia, which stimulates ventilation. Among the four major types of acid-base disorders, this compensatory mechanism is the least effective.
|
|
|
264 Which of the following statement(s) is/are correct concerning the body fluid compartments?a. Both the extracellular and intracellular components of total body water can be directly measuredb. The intravascular space accounts for the majority of extracellular fluidc. All water in the interstitial space is freely exchangeabled. Transcellular fluid, separated from other compartments by both endothelial and epithelial barriers, constitute about 4% of total body water
|
Answer: dTotal body water (TBW) is distributed within the intracellular and extracellular compartments. Intracellular fluid cannot be measured directly but is calculated as the difference between TBW and the measured extracellular water. Extracellular fluid can be measured directly. The extracellular fluid compartment can be further simplified into the intravascular and interstitial spaces. Intravascular space, which accounts for 20% of the extracellular fluid, contains the plasma volume which is approximately 8% of TBW or 5% of body weight. The interstitial space extends from the blood vessels to the cells themselves and includes the complex ground substance making up the acellular matrix of tissue. Although the water within the space is thought to be freely exchangeable, this water exists in two phases. The free phase contains water that is generally freely exchangeable and in a constant state of flux. The bound or gel phase is composed of water that is closely associated with glycosaminoglycans, mucopolysaccharides, and other matrix components. This water is much less freely exchangeable. An additional extracellular fluid compartment, the transcellular compartment, consists of water that is poorly exchangeable under normal circumstances. This fluid is separated from other compartments by both endothelial and epithelial barriers and includes cerebrospinal fluid, synovial fluid, water within cartilage and bone, fluids of the eye, and the lubricating fluids of the serous membranes. Together, these fluids constitute about 4% of TBW.
|
|
|
263 Which of the following statement(s) is/are true concerning the response to a decrease in functional residual capacity percent (FRC)?a. Supplying supplemental oxygen will always improve the situationb. Respiratory alkalosis may occurc. Decreasing compliance is a common occurrenced. Respiratory rate and depth of breathing generally decrease
|
Answer: b, cPulmonary arterial spasm in response to local hypoxia autoregulates pulmonary blood flow and maintains adequate gas exchange during alveolar collapse—up to a point. However, when the loss in ventilation exceeds the decrease in perfusion, a ventilation-perfusion mismatch occurs, which results in incomplete oxygenation of blood perfusing that area of the lung. The resultant hypoxemia stimulates an increased rate and depth of breathing which may serve to reexpand the person’s inflated area of lung. If it does not, hypoxemia will continue but increased ventilation in other areas of the lung will result in excess CO2 excretion, hypocapnea and respiratory alkalosis. The blood gas picture, hypoxemia with respiratory alklalosis, is the most common abnormality of gas exchange in surgical patients and it is a hallmark of ventilation-perfusion imbalance. Oxygenation of blood in the poorly ventilated area of lung can be improved by increasing concentration of oxygen in the inspired gas. The use of supplemental oxygen, however, treats the symptom rather than the basic cause and may actually make the problem worse by adding to absorption atelectasis, depriving the poorly ventilated area of nitrogen to hold alveoli open. This may result in total alveolar collapse. In this circumstance, blood perfusing the nonventilated area will mix with blood from other areas of the lung, resulting in hypoxemia that does not improve significantly in response of administration of oxygen. Aside from the effects on gas exchange, loss of alveolar space results in changes in the volume-pressure relationships in the lung. A decrease in functional residual capacity always results in a shift in the volume-pressure relationship toward a condition of decreasing compliance.
|
|
|
262 Which of the following statement(s) is/are true concerning the estimation and measurement of energy requirements in the critically ill patient?a. One can only estimate energy expenditure with actual measurement not technically possibleb. The amount of oxygen absorbed through the lungs is equal to the amount of oxygen consumed by metabolic processesc. Metabolic rate, normalized to body surface area, may underestimate metabolism in a fat persond. To convert cc’s of oxygen per minute to calories per day, a conversion factor of 10 kcal of energy per liter of oxygen should be used
|
Answer: b, cThe actual metabolic rate of any patient can be estimated from the predicted basal rate according to the clinical situation. The amount of energy is most conveniently expressed in calories/day. The metabolic rate is normalized to body surface area; however, the actively metabolizing tissue is the lean body cell mass. Consequently, reporting “per square meter” underestimates metabolism in a fat person and overestimates in a very lean person. Although most of studies on nutrition in critical illness have been based on estimated energy expenditure, actual measurement is much more accurate and has become an important aspect of critical care management. The most commonly used method of measurement is indirect calorimetry. In this method, the amount of oxygen absorbed across the lungs into the pulmonary blood is measured over a given period of time. Assuming the patient is at a metabolic steady state during this time, the amount of oxygen absorbed across the lungs is equal to the amount of oxygen consumed in the metabolic process. The metabolic rate, measured in cubic centimeters of oxygen/minute, can be converted to calories/hour or /day if the oxygenated substrates are known. For practical purposes, a conversion factor of 5 kcal of energy/liter of oxygen consumed is a reasonable approximation.
|
|
|
261 Which of the following statement(s) is/are true concerning the use of a ventilator in the treatment of respiratory failure?a. The assist-control mode is appropriate in the paralyzed patientb. Peak inspiratory pressure should be optimized at a level in excess of 40 cm H2Oc. A patient receiving excessive carbohydrate as a nutritional support may have an elevated minute ventilation and may tire with spontaneous breathingd. In general, weaning requires an adequate inspiratory force, vital capacity, and a minute ventilation less than 10 L/min
|
Answer: c, dMost intensivists favor setting the ventilator on the assist-control mode at a low sensitivity. In this fashion, the patient breathes at a rate that regulates the PaCO2 to normal, but each breath is mechanically assisted, providing maximal inflation. The volume of each breath is set by limiting the maximal pressure or maximal volume of each breath. Whichever method is used, the peak inspiratory pressure should not generally exceed 40 cm H2O. If the patient is comatose or paralyzed, the assist mode cannot be used and the rate is set in addition to the volume.Adequate weaning indices are: inspiratory force greater than 20 cm H2O, vital capacity twice the tidal volume, adequate gas exchange at assisted ventilation at FiO2 of 0.3 and 5 cm H2O of PEEP, and minute ventilation less than 10 L/min. If the patient is hypermetabolic or is receiving excessive carbohydrate as nutritional support, the minute ventilation will be elevated, even during assisted mechanical ventilation. If this is the case, the patient will tire rapidly on spontaneous breathing.
|
|
|
260 Which of the following statement(s) is/are true concerning pulmonary mechanics?a. The standard compliance or volume pressure curve is measured during lung inflationb. The decreased compliance in acute respiratory failure occurs because the lung is smaller not stifferc. In acute respiratory failure, higher pressures are required to achieve the same level of inflationd. Areas of normal lungs are more vulnerable to overdistention which may lead to progressive lung dysfunction
|
Answer: b, c, dThe standard compliance or volume pressure curve is drawn by measuring volume and pressure at stages of lung deflation after total inflation. The decreased compliance in acute respiratory distress syndrome occurs because the lung is smaller, not stiffer. In acute respiratory failure, the cause of decreased compliance is almost always associated with a decrease in functional residual capacity (FRC). The decreased FRC represents lost alveoli which are either collapsed or filled with fluid but still perfused with blood. Because the lung is smaller, the compliance curve has shifted to the right and much higher pressures are required to achieve the same level of inflation. Lung damage can be caused by high airway pressure, so that overdistension is not merely inefficient but actually detrimental. Since the most normal areas of lung have the best compliance, they are most vulnerable to overdistension, contributing to the steady progression of lung dysfunction in patients ventilated at high peak pressure.
|
|
|
259 Which of the following statement(s) is/are true concerning the treatment of multisystem organ failure?a. Forced diuresis with negative fluid balance may improve survival and acute respiratory failureb. The titration of ionotropic drugs based on desired blood pressure optimizes the results.c. Nutritional support should be withheld for several days until the patient’s condition stabilizesd. Continuous arteriovenous hemofiltration is preferred to intermittent hemodialysis for most critically ill patientse. Hepatic failure should be treated specifically with pharmacologic manipulation
|
Answer: a, dThe important principles in the management of multiple organ failure are to avoid further episodes of local or systemic ischemia and to keep the brain viable by pharmacologic or mechanical support of the failing organs until organ recovery occurs. Respiratory failure is treated by mechanical assistance for lung inflation and ventilation and by decreasing lung edema as much as possible. Airway intubation is usually required. There is now good evidence that forced diuresis and negative fluid balance is associated with improved survival and acute respiratory failure. Cardiac failure is treated with inotropic drugs. Although ionotropic drugs are usually titrated to achieve a desired arterial blood pressure, it is more sensible to titrate ionotropes to achieve a normal oxygen delivery/oxygen consumption ratio. Pulmonary artery pressure and mixed venous saturation monitoring are essential for intelligent management of the patient with severe respiratory or cardiac failure. Adequate nutrition is also important for recovery from organ failure. Renal failure is treated by mechanical substitution of renal function. Although hemodialysis and peritoneal dialysis can serve this purpose, each has a significant drawback in the critically ill, multiple organ failure patient. Continuous arteriovenous hemofiltration (CAVH) and continuous arteriovenous hemodialysis (CAVHD) are the methods of choice for renal replacement therapy. Hepatic failure often occurs as part of the multiple organ failure syndrome but unfortunately there is no specific treatment.
|
|
|
258 Which of the following statement(s) is/are true concerning various energy sources?a. Carbohydrate is the most efficient source of energyb. Endogenous fat is the major source of energy during starvationc. The respiratory quotient of carbohydrate is greater than either fat or proteind. Ketones can be used as a source of energy during starvation
|
Answer: b, c, dThe major sources of energy are carbohydrates and fats. Carbohydrates are a major source of energy during normal, non-starving existence. The brain, the red cells, and some other organs are obligate glucose users. The brain and red cells can develop the capacity to use ketones as an energy source, a process known as starvation adaptation. Fat is the most efficient source of energy. Fat produces 9 calories of energy per gram of substrate metabolized while carbohydrate produces only 4 calories. The respiratory quotient represents the number of molecules of carbon dioxide for each molecule of oxygen consumed. For carbohydrates it is 1.0, whereas for fat, this respiratory quotient is 0.7. Endogenous fat is the major source of energy during starvation. The glycogen storage is basically depleted after a day of fasting and fat becomes a major energy source with protein breakdown supplying glucose through the process of gluconeogenesis.
|
|
|
257 A 64-year-old diabetic patient develops acute renal failure following an aortic aneurysm repair. Which of the following statement(s) is/are true concerning his diagnosis and management?a. Resting energy expenditure will likely be less than would be expected for a patient with normal renal functionb. Maintenance of positive energy balance reduces protein catabolism and makes the management of renal failure easierc. Expected metabolic abnormalities include hyperkalemia, hypercalcemia, and metabolic alkalosisd. A nonoliguric renal failure is usually associated with a better outcome
|
Answer: b, dIn patients with nonoliguric renal failure, treatment may differ little from that required for identical patients with normal renal function. Management of fluids, solutes, and nutrition is usually unaffected by nonoliguric renal failure, although BUN may be elevated. The extent of renal dysfunction is limited and almost always reversible. The use of renal replacement therapies is rarely necessary. Acute renal failure can result in severe derangements in electrolyte and acid-based physiology. Of all electrolyte abnormalities that might occur, hyperkalemia is the most serious. Other electrolyte abnormalities such as hyponatremia, hyperphosphatemia, hypocalcemia, and metabolic acidosis are common and must be monitored carefully.The metabolic requirements of a patient with acute renal failure are those of a critically ill hospitalized patient. The actual measurements of resting energy expenditure has shown that caloric requirements for multiorgan failure patients with renal failure are often 50% above normal, healthy individuals. Although acute renal failure may require fluid restriction, providing adequate nutrition is an important aspect of their treatment. Positive energy balance may make management of uremia and hyperkalemia less difficult. By providing adequate calories, endogenous protein catabolism with resultant generation of urea and release of potassium can be avoided. Maintenance of positive energy balance with glucose and lipids should reduce protein catabolism, urea generation, and hyperkalemia.
|
|
|
256 Which of the following statement(s) is/are true concerning continuous arteriovenous hemofiltration (CAVH)?a. The technique runs continuouslyb. It is not associated with the hemodynamic instabilityc. Systemic heparin anticoagulation is necessaryd. Fluid balance and correcting electrolyte abnormalities takes several days
|
Answer: a, bContinuous arteriovenous hemofiltration (CAVH) is an extracorporial filtration technique that removes extracellular fluid across a synthetic membrane via hydrostatic pressure gradient created between the indwelling arterial and venous catheters. Arteriovenous access is accomplished by percutaneous cannulation of femoral artery and vein with a low incidence of complications. Although full systemic anticoagulation is not necessary for CAVH, heparinization of the extracorporial circuit is required. CAVH is run continuously for as many days as renal replacement is required. Experience with CAVH has demonstrated very little or no hemodynamic instability with treatment of critically ill renal failure patients. The stable nature of this therapy is attributed to a slow and continuous fluid and solute removal and to the fact that the membrane does not induce compliment activation when in contact with blood. Fluid balance and serum electrolyte concentrations can be titrated to any level in a matter of hours by manipulating the composition and rate of replacement solution. Solute clearance with CAVH is limited by the ultrafiltration and replacement fluid exchange rate. In patients with high urea generation rates, solute removal with CAVH may be inadequate and variations of the technique may be used to enhance clearance.
|
|
|
255 The patient requires renal replacement therapy. Which of the following statement(s) is/are true concerning the differences between hemodialysis and continuous arteriovenous hemodialysis (CAVHD)?a. Anticoagulation is not required for CAVHDb. Hemodynamic instability will be a particular problem with both techniquesc. Both techniques will decrease serum urea ni+62trogen levelsd. CAVHD will likely result in better removal of excessive volumeAnswer: c, d256 Which of the following statement(s) is/are true concerning continuous arteriovenous hemofiltration (CAVH)?a. The technique runs continuouslyb. It is not associated with the hemodynamic instabilityc. Systemic heparin anticoagulation is necessaryd. Fluid balance and correcting electrolyte abnormalities takes several days
|
Answer: a, bContinuous arteriovenous hemofiltration (CAVH) is an extracorporial filtration technique that removes extracellular fluid across a synthetic membrane via hydrostatic pressure gradient created between the indwelling arterial and venous catheters. Arteriovenous access is accomplished by percutaneous cannulation of femoral artery and vein with a low incidence of complications. Although full systemic anticoagulation is not necessary for CAVH, heparinization of the extracorporial circuit is required. CAVH is run continuously for as many days as renal replacement is required. Experience with CAVH has demonstrated very little or no hemodynamic instability with treatment of critically ill renal failure patients. The stable nature of this therapy is attributed to a slow and continuous fluid and solute removal and to the fact that the membrane does not induce compliment activation when in contact with blood. Fluid balance and serum electrolyte concentrations can be titrated to any level in a matter of hours by manipulating the composition and rate of replacement solution. Solute clearance with CAVH is limited by the ultrafiltration and replacement fluid exchange rate. In patients with high urea generation rates, solute removal with CAVH may be inadequate and variations of the technique may be used to enhance clearance.
|
|
|
254 Which of the following statement(s) is/are true concerning various causes of acute renal failure?a. Acute tubular necrosis is the most common pathologic finding of acute renal failureb. Drug-induced renal failure is compounded in situations of hypovolemiac. Myoglobin-induced renal failure can be prevented using diuretics and alkalization of urined. The incidence of radiographic contrast dye-induced renal failure occurs independent of preexisting conditionsMyoglobin is a direct nephrotoxin
|
Answer: a, b, cAcute tubular necrosis results from ischemia to the renal parenchyma and is the most common pathologic finding of acute renal failure. In conditions of diminishing renal blood flow, perfusion to the kidneys is first maintained by vasomotor responses which dilate the afferent arteriole and constrict the efferent arteriole. As continued hypotension occurs, the renin-angiotensin system is activated and vasoconstriction of the afferent arteriole occurs which exacerbates corticohypoperfusion. Pigment nephropathy is a common cause of acute renal failure occurring after trauma, burns, operations, or hemodynamic catastrophe. With ischemia or blunt injury to large muscles, myoglobin is released into the circulation. In the kidney, it is filtered from blood and reabsorbed by the tubule. Although myoglobin is not a direct nephrotoxin, in the presence of aciduria, myoglobin is converted to ferrihemate, which is toxic to renal cells. Prevention of myoglobin-induced renal failure may include the use of diuretics and alkalinization of urine. Drug-induced acute renal failure is responsible for approximately 5% of all cases of acute renal failure. Through normal reabsorption and secretion, the kidney is exposed to high concentrations of drugs and solutes, which may be toxic. This problem is compounded by hypovolemia, which causes increased reabsorption of water and solutes and exposes the lumen to even higher concentrations of toxins. The incidence of radiographic contrast dye induced nephropathy is approximately 1 to 10% and may be predicted according to a number of risk factors which include contrast load, age, preexisting renal insufficiency, and diabetes. The incidence in patients with normal renal function is significantly lower at 1% to 2%.
|
|
|
253 Which of the following statement(s) is/are true concerning pulmonary edema?a. Pulmonary edema effectively narrows bronchi and increases pulmonary vascular resistanceb. Ventilation and perfusion are decreased equallyc. Positive pressure ventilation improves gas exchange by decreasing lung edemad. The condition is frequently caused by decreased plasma protein levels
|
Answer: aThe causes of pulmonary edema are: 1) increased hydrostatic pressure; 2) increased capillary permeability and 3) decreased plasma oncotic pressure. The latter, however, is rarely a problem unless the concentration of plasma protein is very low. When fluid begins to collect in the lung interstitium, it migrates to the loose areolar portion of the lung microanatomy that surround the small bronchioles and pulmonary arteries. The edema in these areas has the effect of narrowing bronchi and increasing resistance in the pulmonary vasculature. This will decrease both ventilation and perfusion in the edematous area, but ventilation is often affected more than blood flow, resulting in a decreased / ratio, with all of its attendant effects on gas exchange. Ventilator treatment of pulmonary edema which increases airway pressure tends to hold the alveoli open, spreading out the space available for water accumulation and overcomes the effect of small bronchial occlusion. Positive pressure ventilation does not, therefore, affect the amount of edema in the lung, only its manifestations.
|
|
|
252 Which of the following statement(s) meet the criteria for organ failure?a. Bilirubin greater than 5 mg/dlb. Creatinine greater than 3 mg/dlc. Alveoloarterial O2 gradient greater than 300 mm Hgd. Glasgow Coma score less than 10
|
Answer: a, b, c, dMultiple organ failure is defined by dysfunction of two or more of the six vital organ systems: cardiovascular, respiratory, nervous system, renal, liver, and host defenses.
|
|
|
251 Which of the following result in a decrease in functional residual capacity?a. Shallow breathingb. Partial airway occlusionc. Absorption atelectasisd. Hemothorax
|
Answer: a, b, c, dA decrease in functional residual capacity is caused by incomplete alveolar inflation related to 1) shallow breathing; 2) partial or complete airway occlusion, which may be generalized (as in bronchospasm) or localized (as in gastric aspiration); 3) absorption atelectasis, which occurs when oxygen is substituted for nitrogen in the inspired gas; or 4) conditions in which air or fluid is occupying a potential alveolar space in the chest such as pneumothorax, hemothorax, or pulmonary edema.
|
|
|
250 Which of the following statement(s) is/are true concerning carbon dioxide kinetics?a. The amount of carbon dioxide produced is equivalent to the amount of oxygen consumedb. Carbon dioxide levels in blood, present mostly as a bicarbonate ion, can quickly changec. Normally the amount of carbon dioxide excreted through the lung is exactly equal to the amount of carbon dioxide produced in peripheral tissuesd. The amount of carbon dioxide excreted is a function of ventilation of perfused alveoli
|
Answer: a, c, dThe total amount of carbon dioxide produced by systemic metabolism is roughly equivalent to the amount of oxygen consumed (100–120 cc/m2/min, 200 cc/min in a typical adult). CO2 production is increased or decreased by each of the factors that causes an increase or decrease in oxygen consumption. Most of the carbon dioxide in blood is present as bicarbonate ion which cannot be changed quickly. However, the metabolically produced CO2 is mostly present as dissolved carbon dioxide, added to the blood in the peripheral tissues and excreted in the lung. In a steady state, the amount of carbon dioxide excreted through the lung is exactly equal to the amount of carbon dioxide produced in peripheral tissues. The amount of carbon dioxide excreted is a function of ventilation of perfused alveoli (i.e. the alveolar ventilation/min). |
|
|
249 Which of the following statement(s) is/are true concerning oxygen delivery?a. The amount of oxygen delivered to peripheral tissues is dependent upon the oxygen content in arterial blood and cardiac outputb. Oxygen content is commonly measured in arterial bloodc. The normal arterial-venous difference is 4 cc O2/dLd. Normal systemic oxygen delivery for a typical adult is approximately 1000 cc/min
|
Answer: a, c, dThe amount of oxygen that is delivered to peripheral tissues is the product of the oxygen content in arterial blood times the cardiac output. Normally, oxygen content of arterial blood is approximately 20 cc/dL, and the normal cardiac index is 5 L/min. Therefore, the normal systemic oxygen delivery is approximately 1000 cc/min. Although oxygen content is the most important measure of oxygen in the blood, PO2 and oxyhemoglobin saturation is more commonly measured in the Intensive Care Unit, hence it is necessary to convert between these measurements. The normal oxygen content of venous blood is 16 cc/dL. Hence, the normal arterial-venous difference is 4 cc O2/dL.
|
|
|
248 Which of the following statement(s) is/are true concerning the outcome in patients with acute renal failure?a. Mortality for ischemic acute tubular necrosis without other organ failure is approximately 6%b. Multiple organ failure complicated with acute renal failure is associated with mortality ranging from 50% to 90%c. Recovery of renal function after six weeks is unlikelyd. There is no difference in survival between oliguric and nonoliguric renal failure
|
Answer: a, b, cSurvival of patients with acute renal failure is a function of the successful treatment of the primary disease from which the renal failure was derived. The mortality for ischemic acute tubular necrosis without organ failure has been reported at approximately 6%. By contrast, mortality of multiorgan failure complicated by acute renal failure ranges from 50% to 90%. In patients who survive the acute phase of illness, recovery of renal function after acute renal failure is dependent on the type and extent of injuries to the renal parenchyma. If renal function is not returned after six weeks, recovery is unlikely. Nonoliguric renal failure is usually limited in its extent and is almost always reversible.
|
|
|
247 Which of the following statement(s) is/are true concerning oxygen consumption (O2)?a. O2 is normally 100–120 cc2/m2/minb. Resting O2 is controlled by the level of thyroid and catecholamine hormonesc. Under steady state conditions the amount of oxygen consumed exceeds the amount of oxygen taken up by the pulmonary capillariesd. O2 is dependent on the status of pulmonary function
|
Answer: a, bOxygen consumed in the process of metabolism is expressed as the volume of oxygen per minute (O2). O2 is normally 100–120 cc2/m2/min, or 200 cc/min for a typical adult. Resting O2 is a function of metabolizing body cell mass, with fine tuning control provided by the level of thyroid and catecholamine hormones. O2 decreases under conditions of hypothermia, paralysis, and hypothyroidism. O2 increases during exercise or muscular activity, hyperthermia, profound hypothalamic injury, hyperthyroidism, catecholamines, and inflammatory mediators, particularly the interleukin cytokines. Under steady state conditions, the amount of oxygen consumed in systemic metabolism is exactly equal to the amount of oxygen taken up by the pulmonary capillaries via the airway. This is true regardless of the status of pulmonary function or dysfunction, so we measure O2 across the lung and assume that it is exactly the amount consumed in the systemic metabolism.
|
|
|
246 Phases of multiorgan failure will include:a. Generalized increased capillary permeabilityb. A hypermetabolic statec. Organ malfunctiond. All of the above
|
Answer: dClinically the multiple-organ failure patient progresses through well-defined phases. These phases include: Phase 1—a generalized increased capillary permeability resulting in edema, weight gain, and intravenous volume replacement, increased protein concentration in urine and lymph. Although the pulmonary microvasculature has been most thoroughly studied, it is apparent that the lung is simply the most obvious end organ in a generalized permeability defect. Phase 2—A hypermetabolic state, with increased oxygen consumption and a compensatory increase in oxygen delivery characterized by tachycardia and high cardiac output. This condition following systemic ischemic and reperfusion is similar to hypermetabolism following endotoxemia, localized sterile inflammation, and infusion of stress hormones, suggesting a common mechanism. Phase 3—Organ malfunction due to localized edema and cellular injury, particularly in the kidney, liver, brain, and host defense system. Hemorrhagic shock predisposes to bacterial translocation and endotoxin absorption from the intestine. Phase 4—In the absence of systemic sepsis, organs may recover to normalcy or may be irreversibly damaged, leading to a need for chronic support. If the organ failure phases lead to systemic infection or irreversible tissue damage in the lung or brain, the death of the entire organ is likely.
|
|
|
245 Useful steps to optimize systemic oxygen delivery include:a. Maintaining mean arterial blood pressure between 50 and 90 mm Hgb. Optimizing PEEP levels by monitoring mixed venous saturationc. Turning the patient proned. Sedation or paralysis
|
Answer: a, b, c, dOptimizing systemic oxygen delivery in relationship to oxygen requirement is the primary goal of management. Improving oxygenation of the blood itself by improving alveolar inflation is only one of the steps in optimizing oxygen delivery. Equally or more important are treating anemia and optimizing cardiac output. Cardiac output should be optimized to maintain delivery of four to five times consumption. In general, this means avoiding those factors which decrease cardiac output, rather than actively trying to increase cardiac output. Blood pressure should be maintained high enough to provide coronary perfusion (over 50 mm Hg mean pressure) but not so high as to limit left ventricular function (over 90 mm Hg mean arterial pressure). Alveolar collapse is treated by cleaning the airways, avoiding 100% oxygen, and moving fluid from the lung or chest, and finally by the use of positive end exploratory pressure to hold open those alveoli which have been opened by other measures. The optimal level of PEEP is that level that maintains arterial oxygenation but does not decrease venous return or cardiac output. This optimal level is best determined by monitoring mixed venous saturation. Another step in optimizing lung function is to take advantage of the gravitational effects on pulmonary blood flow by turning the patient prone or to a full lateral position to direct blood flow to areas of optimal alveolar function. This step will often result in an opening in the closed posterior alveoli which have been compressed by the weight of the fluid in the lungs. At the same time that oxygen delivery is optimized, oxygen consumption should be decreased to normal or even below normal if necessary. Treating infection, providing adequate sedation, and establishing muscular paralysis decrease oxygen consumption, and decrease the need for oxygen delivery.
|
|
|
244 Which of the following statement(s) is/are true concerning the assessment of protein reserve?a. Conventional serum proteins such as albumin and globulin are early indicators of malnutritionb. The total lymphocyte count reflects immune status and not nutritionc. Antigen skin testing reflects patient immunity and not nutritiond. Measurement of urea excretion in urine can be used as a measurement of protein breakdown
|
Answer: dSince protein is the functional and structural chemical of the body, most nutritional assessment techniques are estimates of protein reserves. The actual nitrogen balance can be measured by measuring the amount of nitrogen excreted. This is most conveniently done by measuring the amount of urea excreted in the urine, assuming that urea constitutes 85% of the total nitrogen excretion. Knowing nitrogen excretion, the amount of protein catabolized can be estimated and compared with the amount of protein ingested by the patient. Indirect assessments of protein reserves are based on single measurements of body substances that are dependent on rapid protein synthesis for maintenance of normal levels. Conventional serum proteins such as albumin and globulin are not affected by malnutrition until it is very severe. Proteins such as prealbumen and transferrin, which turn over more rapidly, are better indicators of protein status. Lymphocytes are rapidly destroyed and protein is required for the formation of new cells. Consequently, the absolute lymphocyte count is a useful measure of the status of protein reserves. The lymphocyte count is considered by some the best single “static” measurement characterizing nutritional status. Protein is also required for synthesizing the cells and mediators involved in skin test reactivity. Although skin test reactivity is a manifestation of lymphocyte-mediated immunity, its usefulness in patient assessment is probably that of assessment of the inflammatory response than lymphocyte activity per se. Some chronically and acutely malnourished patients convert from reactive to anergic, and reactivity can be restored by nutritional repletion.
|
|
|
243 Which of the following statement(s) is/are true concerning CO2 transfer in the lung?a. Carbon dioxide excretion is a direct function of alveolar ventilationb. Normally end tidal CO2 should be identical to PaCO2c. The gradient between end tidal and arterial CO2 can be an indirect measure of nonperfused alveolid. Positive pressure ventilation under normal airway pressures creates a significant end tidal PaCO2 gradient
|
Answer: a, b, cThe amount of carbon dioxide excretion is directly related to alveolar ventilation. While oxygenation is a function of matching blood flow to alveoli, carbon dioxide excretion is a direct function of ventilation or hyperventilation of alveoli with some blood flow. Normally the end tidal CO2 represents mixed alveolar gas which is at equilibrium with pulmonary capillary blood, hence with arterial blood. Therefore, the end tidal CO2 and the PaCO2 should be identical. End tidal CO2 measurement is a very useful continuous measurement of PaCO2 which can be used as a monitor when the lung is normal, as in ventilator weaning. Furthermore, the gradient between end tidal and arterial CO2, when it is large, acts as an indirect measure of nonperfused alveoli and/or compression volume. In patients who are ventilated with positive pressure ventilation, a significant end tidal PaCO2 gradient occurs only when peak airway pressures are very high (over 30 cm H2O) and the compression volume is a significant component of each exhaled breath.
|
|
|
242 Which of the following statement(s) is/are true concerning the pathophysiology of gas exchange?a. Hypoventilation in relation to perfusion can result in an oxygen saturation of less than 100%b. Diffusion block and / mismatch can almost completely be overcome by breathing 100% oxygenc. Transpulmonary shunting does not occur under normal circumstancesd. The normal arterial oxygen saturation should be 100%
|
Answer: a, bUnder normal conditions, red blood cells in the pulmonary capillaries become fully saturated and oxygen dissolves in plasma resulting in blood PO2 of 100 and O2 saturation of 100%. This equilibration may be disturbed by hypoventilation in relationship to the perfusion (/ mismatch), diffusion block caused by interstitial fibrosis, or perfusion of nonventilated alveoli. Diffusion block and / mismatch can almost be completely overcome by breathing 100% oxygen, hence hypoxemia during exposure to high alveolar PO2 is caused by total / mismatch, so-called transpulmonary shunting or venous ad mixture. Under normal circumstances, about 5% of the blood entering the left atrium has been shunted away from the pulmonary capillaries, either as the result of bronchial nutritive blood flow or through thebesian veins opening directly into the left side of the heart. This phenomenon, combined with a normal minor / mismatch associated with breathing at rest and positional changes in pulmonary blood flow, result in the fact that normal arterial PO2 is 90–100 mm Hg and the normal O2 saturation is 98%.
|
|
|
241 Which of the following statement(s) is/are true concerning the treatment of pulmonary interstitial edema?a. Diuresis and blood transfusion is a valuable stepb. Salt-poor albumin leaks through the capillaries and worsens the conditionc. Mannitol is contraindicated as a diuretic in this clinical situationd. Isoproterenol is a poor choice as an ionotropic agent
|
Answer: aTreatment of pulmonary edema has two important goals, the first is to improve oxygenation if it is impaired, and the second is to minimize fibrosis and bacterial infection, which often accompany pulmonary edema caused by capillary injury. The treatment of interstitial edema is to maintain the hydrostatic pressure as low as compatible with adequate cardiac output and to raise the oncotic pressure selectively in the vascular space. These measures, combined with fluid restriction and diuresis, will decrease the amount of pulmonary edema. Since it is desirable to maintain filling pressures of the left ventricle as low as possible while maintaining a good cardiac output, inotropic drugs to improve left ventricular contractility are helpful. Isoproterenol or dopamine should be used, with serial cardiac output and filling pressure measurements. The first step in decreasing pulmonary edema is to decrease the pulmonary capillary hydrostatic pressure as low as is compatible with an adequate cardiac output. This is done by diuresis and fluid restriction. As the patient falls behind in blood volume, signs of hypovolemia may appear. Blood volume is then replenished with a fluid that stays in the vascular space. Packed red cells are ideal for this application. When the hematocrit is normal, concentrated salt-poor albumin should be used. This hyperoncotic fluid replenishes the blood volume by attracting interstitial fluid from throughout the body into the vascular space and supplements diuresis. This technique is useful even in the septic patient who may have increased capillary permeability and may loose albumin from the vascular space at a rapid rate. Even if albumin “leaks out”, the short term effects of expanding blood volume and decrease in edema will appear.
|
|
|
240 Which of the following statement(s) is/are true concerning oxygen kinetics in a critically ill, febrile patient?a. Oxygen consumption will likely exceed three times normalb. The high cardiac output and pulse rate are designed to increase oxygen deliveryc. The hyperdynamic response may actually increase oxygen delivery to exceed the increase in oxygen consumptiond. The patient can maintain adequate compensation as long as the oxygen delivery/oxygen consumption rate is greater than 2:1
|
Answer: b, dIn critically ill patients oxygen consumption may be elevated or depressed, but slight to moderate elevations in oxygen consumption is the most common abnormality in critically ill patients. Oxygen consumption will be elevated in proportion to the amount of inflammation. A febrile patient with significant signs of septic toxicity will typically have an oxygen delivery at 1.5 to 2 times normal. It is very unusual for a critically ill patient to experience oxygen consumption greater than twice normal. This occurs only in situations of severe muscular exercise such as seizures or tetanus. During hypermetabolism, a change in oxygen consumption is followed promptly by a proportionate change in oxygen delivery. Hence, it is “normal” for a hypermetabolic patient to have a high cardiac output and pulse rate. Rarely the hyperdynamic response exceeds the increase in oxygen consumption, reflected in a ratio higher than 5:1 and venous saturation greater than 80%. Some patients cannot mount an increased oxygen delivery in response to increased oxygen consumption because of the combination of hypoxemia, anemia, and myocardial failure. If this occurs, then the oxygen delivery/oxygen consumption ratio will be less than 5:1. The patient will compensate for this by increased oxygen extraction, however, and the patient will remain stable as long as the ratio is greater than 2:1.
|
|
|
239 Which of the following statement(s) is/are true concerning O2 venous saturation monitoring?a. The normal saturation of mixed venous blood is 50%b. Mixed venous blood obtained for saturation monitoring can be obtained from any peripheral veinc. If arterial blood is fully saturated, the saturation of mixed venous blood is 80%d. In less than fully saturated blood, the difference between arterial and venous saturation corresponds to oxygen extraction
|
Answer: c, dThe relationship between oxygen delivery and oxygen consumption is reflected in the amount of oxygen in venous blood. Under normal circumstances, oxygen delivery is 1000 cc/min and oxygen consumption is 200 cc/min. The amount of oxygen extracted is 20% of that delivered, and 80% of oxygen is still present in venous blood returning to the heart. Usually arterial blood is fully saturated, and under normal circumstances, the saturation of mixed venous blood (SVO2) will be 80%. This measurement must be made in mixed venous blood since the relative extraction of organs served by the superior and inferior vena cava and coronary sinus are quite different. As long as arterial blood is fully saturated, this observation holds true regardless of the absolute level of oxygen consumption or oxygen delivery. If the arterial blood is less than fully saturated, the difference between arterial and venous saturation corresponds to the oxygen extraction, hence the oxygen delivery/oxygen consumption ratio.
|
|
|
238 Which of the following statement(s) is/are true concerning the autoregulation necessary to maintain oxygen consumption and oxygen delivery?a. A change in oxygen consumption is followed by a proportionate change in oxygen deliveryb. A change in oxygen delivery is followed by a change in oxygen consumptionc. Increases in oxygen delivery are due solely to an increase in cardiac outputd. The normal ratio of oxygen delivery to consumption is 2:1
|
Answer: aThe relationships between oxygen consumption and oxygen delivery represent one of the most interesting regulation systems in homeostasis. First of all, if one of the three components of oxygen delivery is abnormal, endogenous mechanisms regulate the other two until normal oxygen delivery has been restored. The various combinations of compensatory mechanisms supply adequate oxygen for systemic metabolism through a wide range of variations in oxygen delivery. When there is a change in oxygen consumption, there is a proportionate change in oxygen delivery, which occurs almost immediately, mediated completely by a change in cardiac output. Conversely, a primary change in oxygen delivery is not followed by any change in oxygen consumption. The normal ratio of oxygen delivery to consumption is approximately 5:1.
|
|
|
237 Which of the following statement(s) is/are true concerning methods of nutritional support?a. Optimal results for enteral feedings are achieved with approximately half of calories supplied as carbohydrate and half as fatb. Diarrhea is the most common complication of enteral feeds and is due to the high osmolarity of the carbohydrate componentsc. The hyperosmolar nature of parenteral fat solutions requires central venous administrationd. Approximately 25–50% of calories should be provided as fat emulsion in patients receiving total parenteral nutrition
|
Answer: a, b, dMost formulas for enteral feeding range from 1.0 to 2 cal/ml and include 3 to 7% protein. Most of the calories are supplied as glucose or sucrose, so that the solutions have a very high osmolarity. Cramps or diarrhea can result when these high osmolar solutions are placed into the stomach or intestine. Diarrhea is the major complication with most tube feeding formulas. Diarrhea can be minimized by the use of starch or fat as an energy source in tube feedings. This can be supplied as part of the commercial preparation or added in the form of medium chain triglycerides or other oils. The best results are usually achieved by supplying approximately half the calories as carbohydrate and half as fat. In patients receiving total parenteral nutrition, energy source is provided as carbohydrate, fat, and amino acid solutions. Parenteral feeding with carbohydrate is limited by the sclerotic effect of hyperosmolar solutions on veins. Fat is a more efficient energy source and can be given through peripheral veins in concentrations of either 10 or 20%. Most intensivists favor supplementing standard total parenteral nutrition solution with intravenous fat to provide at least 100 grams of fat emulsion each week to preclude fatty acid deficiency. Giving up to 25 to 50% of calories each day as fat emulsion may optimize the delivery of this caloric delivery.
|
|
|
236 Which of the following statement(s) is/are true concerning the relationship between cardiac function and effective blood volume?a. A pulmonary capillary wedge pressure of 5–10 rules out fluid overload as a cause of pulmonary edemab. A shift to the right in the Frank-Starling curve is associated with compromised cardiac functionc. Dilutional anemia may contribute to tachycardia even though blood volume and filling pressures are normald. The sole purpose of a pulmonary artery catheter is to measure pulmonary artery pressure and cardiac output
|
Answer: b, cAlthough physical findings are often adequate to establish a diagnosis and institute management of cardiac failure, direct measurement of filling pressures of the right heart (central venous pressure) or the left heart (pulmonary artery pressure) may be required. Placement of a pulmonary artery catheter allows us to measure cardiac output by thermodilution and, more importantly, to sample mixed venous blood for saturation measurements which tell us the ratio between systemic oxygen delivery and oxygen consumption. From all of these measurements we can determine if cardiac output is normal for the level of filling pressure of the left ventricle, or if contractility is decreased. In the latter case, cardiac output will be lower than predicted for a given level of filling pressure. In the Frank-Starling curve, if the patient is to the right of the normal range, then cardiac function is compromised either because of valvular disease, extrinsic pressure such as pericardial tamponade, or more commonly, a decrease in contractility. If cardiac function and anatomy are normal, then blood volume, filling pressure and cardiac function are related to the Starling curve. The intake and output of fluid and salt is autoregulated to maintain the filling pressure of the left ventricle around 10 mm Hg. Extracellular fluid expansion is usually associated with normal blood volume. Gross expansion of extracelluar space results in deleterious effects if tissue edema can and often do exist with perfectly normal blood volume. In other words, a pulmonary capillary wedge pressure of 5–10 does not rule out fluid overload as a cause of pulmonary or GI dysfunction. In critically ill patients, the fear of hypotension and effect of perfusion usually results in infusion of intravenous salt and water in quantities which exceed losses. Consequently, most patients in the Intensive Care Unit have anemia, dilutional hypoproteinemia, and a compensatory increase in cardiac output. In response to anemia, these patients are tachycardic, even though blood volume is normal, filling pressures are normal, and total body extracellular fluid is excessive.
|
|
|
235 Invasive hemodynamic monitoring using a Swan-Gantz catheter is essential in the optimal management of patients in shock or those suffering post-shock sequelae. Which of the following physiologic characteristics are associated with the various forms of shock?a. Hypovolemic shock: Decreased pulmonary capillary wedge pressure (PCWP), decreased cardiac output, increased systemic vascular resistance (SVR)b. Cardiogenic shock: Increased PCWP, decreased cardiac output, decreased SVRc. Septic shock (hypodynamic): Decreased cardiac output, increased SVRd. Neurogenic shock: Decreased PCWP, increased cardiac output, decreased SVR
|
Answer: a, c
|
|
|
234 Which of the following statement(s) is/are true concerning the multiorgan failure syndrome (MOFS)?a. Changes in the splanchnic and pulmonary microcirculation are critical to the development of MOFSb. Tissue fixed microphages, including the liver Kupffer cell, have little role in the development of MOFSc. MOFS represents systemic consequences of loss of homeostatic control of local inflammation and microcirculatory hypoperfusiond. The nature of MOFS is highly dependent upon the etiology of the underlying problem
|
Answer: a, cThe nature of multiorgan failure syndrome (MOFS) is that of a diffuse cellular injury, developing systemically as a consequence of losing homeostatic control of local inflammation and microcirculatory hypoperfusion. Endothelial injury, platelet aggregation and activation of macrophages and neutrophils occur, and the clotting, fibrinolytic, kinin, and complement cascades are activated, along with the release of potent inflammatory cytokines. The effects of shock, resuscitation, and reperfusion, and the subsequent development of MOFS appear to be critically dependent on changes in the splanchnic and pulmonary microcirculations. These vascular beds appear to be major sites of activation of subsequent inflammatory mediator production that underlies the diffuse systemic inflammatory response. Extensive activation of the liver Kupffer cell and release of inflammatory mediators coupled with the ongoing release of activated neutrophils and by-products of activated gut macrophages is responsible for the injury to the pulmonary microcirculation and secondary induction of alveolar macrophage and additional inflammatory mediator systems. Excessive and persistent macrophage activation plays an essential role in MOFS and is hypothesized to represent the penultimate step in a series of continuous immuno-inflammatory stimulatory events, including local hypoxia, exposure to bacteria and toxins, and mediator release from localized areas of inflammation. When infection is the underlying or major contributing process, the diffuse inflammatory response develops independently of the specific type of microorganism. In noninfectious cases, the response also appears independent of the specific underlying cause.
|
|
|
233 Which of the following statement(s) is/are true concerning the treatment of MOFS?a. Prevention and therapy of MOFS requires control of the infectious or inflammatory sourceb. Restoration of normal clinical parameters such as blood pressure, pulse rate, and urine output ensures optimal resuscitation in most patientsc. Branch chain amino acids play and important role in the nutritional support of the patientd. Because of the nature of gut injury, total parenteral nutrition is preferred for most patients with MOFS |
Answer: a, cThe therapy of MOFS is directed towards interrupting the involving pathophysiologic process and providing an optimal physiologic environment for healing and recovery. Fundamental concerns are control of the source of infection, inflammation or instability; restoration of microcirculatory blood flow and oxygen transfer, and the institution of optimal supportive care. Both the prevention and therapy of MOFS, therefore, requires source control and restoration of adequate profusion. Resuscitation efforts are directed toward restoration of adequate microcirculatory blood flow in all organ systems. Restoration of normal clinical parameters such as blood pressure, pulse rate, urine output, and acid-base balance does not ensure optimal resuscitation. The physiologic endpoint that most closely corresponds with adequate microcirculatory flow is the level of cardiac output and the oxygen delivery at which oxygen consumption and lactate production remain independent of flow.The importance of metabolic support in the patient with MOFS cannot be overemphasized. The malnutrition of MOFS is markedly different than that of starvation and the nutritional requirements also differ. If optimal quantities of appropriately formulated amino acid solutions are given, protein synthetic rates can approach catabolic rates and the goal of nitrogen balance can be achieved. Formulas rich in branch chain amino acids appear to be more efficient in promoting nitrogen retention and minimizing urea production. Whenever feasible, enteral feeding is preferred over TPN because evidence suggests that bacterial translocation from the gut can be limited through the use of enteral feeds. Enteral absorption and processing of nutrients appears superior to TPN and lessens overall complications.
|
|
|
232 Which of the following statement(s) is/are true concerning pharmacologic agents used in the treatment of shock?a. The primary difference between dopamine and dobutamine is the absence of significant a adrenergic activityb. The renal and mesenteric vasoconstrictive effects of norepinephrine complicate and sometimes restrict its usec. The apparent paradoxical use of vasodilators, such as nitroprusside, in shock is indicated as a means to augment cardiac functiond. Isoproterenol with its potent b-adrenergic effect, is a particularly useful agent in the treatment of all forms of shock
|
Answer: a, b, cTherapeutic adjustments of intravascular volume (preload) and systemic vascular resistance (afterload) form the basis of the treatment strategies for all forms of shock. Optimal volume resuscitation should precede measures to augment to contractile function of the heart. Inotropic agents are used in shock when there is inadequate cardiac output despite adequate circulating blood volume. Dopamine and dobutamine are often times first line agents in the pharmacologic treatment of shock. Dopamine, at low doses, stimulates dopaminergic receptors producing renal arteriolar vasodilatation with associated increases in renal blood flow, urine output, and sodium excretion. At moderate doses, stimulation of cardiac b-receptors produces increases in contractility and cardiac output with little effect on heart rate or blood pressure. At higher doses, peripheral vasoconstriction from increasing a activity becomes more pronounced, prompting significant increases in vascular resistance and blood pressure. Dobutamine’s predominant effect is an increasing cardiac contractility with lesser increases in heart rate. Some reduction of peripheral vascular resistance may also occur. When compared to dopamine, dobutamine produces less peripheral vasoconstriction and less chronotropic response. Norepinephrine exerts both a and b-adrenergic effects, with a effects being evident at lower infusion rates and a effects more prominent at high doses. The major use of norepinephrine in current practice is in the patient with hypotension that persists despite appropriate volume resuscitation and the use of inotropic agents. Renal and mesenteric vasoconstrictive effects of norephinepherine complicate its use, especially when support is needed for significant periods of time. Isoproterenol is a potent b-adrenergic agent. With isoproterenol, myocardial oxygen demand is increased and diastolic coronary feeling is limited by tachycardia or diminished diastolic pressure. Indications for the use of isoproterenol are fairly limited, because agents with fewer adverse effects have become available.Vasodilators are used to augment cardiac function through optimization of ventricular filling pressures (preload) and systemic vascular resistance (afterload) both of which reduce demands on the myocardium. Decreases in afterload prompt increases in cardiac output and venodilatation contributes to decreases in pulmonary venous pressure and central venous pressure. Hypotension, however, may develop therefore patients must have careful constant monitoring of arterial pressure and repeated hemodynamic measurements with a pulmonary artery catheter.
|
|
|
231 Which of the following statement(s) is/are correct concerning the cardiovascular response to shock?a. Changes in cardiac contractile function shift the Frank Starling curve up and downb. Venoconstriction from skeletal muscle is a significant contributor to the restoration of blood volume with shockc. Arterial vasoconstriction affects all vascular beds equallyd. The total circulating blood volume is equally split between the arterial and venous system
|
Answer: aCentral in the general cardiovascular response to shock is the action of the heart itself. The principle determinants of cardiac function in the normal heart are the volume of blood available for the heart to pump (preload), the systolic contractile capability, and the diastolic filling of the ventricles. In hypovolemia, the two dynamic variables of cardiac function, ventricular filling and myocardial contractility remain paramount and determine the stroke volume. The product of stroke volume and heart rate in turn determines the cardiac output. Increases in ventricular end-diastolic volume, reflecting venous return, cause ventricular distention. Ventricular distention in turn produces increased volume output with each stroke, the Frank Starling mechanism. Contractile function may vary independent of volume status. Changes in the contractile function shift the Starling curve up and down, producing increases or decreases in stroke volume for any given end-diastolic volume. A fundamental requirement for cardiovascular function is adequate cardiac filling, and cardiac output cannot exceed venous return. The venous system contains nearly two-thirds of the total circulating blood volume, including 20% to 30% within the splanchnic venous system. Most of this volume resides in small veins, which comprise the bulk of venous capacitance. The venous system, especially that of the splanchnic circulation, becomes important in the physiologic compensation to hypoperfusion because it serves as a dynamic reservoir for the autoinfusion of blood volume involving both active and passive mechanisms. The splanchnic circulation makes major contributions to the maintenance of venous return, therefore, it is likely that sympathetic venoconstriction is responsible for a portion of the blood mobilized from the splanchnic venous circulation. Sympathetic mediated venoconstriction in skin and skeletal muscle is probably not as significant as a source of blood volume. Selective vasoconstriction occurs in response to alpha adrenergic receptor stimulation with increased sympathetic activity in shock. Sympathetic stimulation does not cause significant vasoconstriction of either cerebral or coronary vessels, with normal blood flow maintained in these circulations. Blood flow to the skin is sacrificed early, followed by that to the kidneys and splanchnic viscera.
|
|
|
230 Which of the following statement(s) is/are true concerning hypoadrenal shock?a. In the United States, idiopathic adrenal atrophy (Addison’s disease) is the most common causeb. Laboratory abnormalities include hyponatremia, hypochloremia, and hyperkalemiac. Fever may be seen with hypoadrenal shockd. ACTH stimulation test is the diagnostic test of choice to confirm hypoadrenal shock
|
Answer: b, c, dShock of a dramatic nature, poorly responsive to resuscitation, may develop as a consequence of adrenal insufficiency. In this country, adrenal insufficiency most commonly arises as a consequence of the chronic therapeutic administration of high doses exogenous corticosteroids causing adrenal suppression. Other causes include idiopathic adrenal atrophy (Addison’s disease), tuberculosis, metastatic disease, bilateral hemorrhage, and amyloidosis. The stress of illness, operation, or trauma typically requires that the adrenal glands secrete cortisol in excess of that required in the nonstressed state (approximately 3–4 fold). Insufficiency not otherwise apparent may manifest itself only after major physical stress. Findings associated with adrenal insufficiency include weakness, fatigue, anorexia, abdominal pain, nausea, vomiting, and weight loss. Surgical patients with significant adrenal insufficiency need not present with the above findings. More typical is the development of refractory shock, frequently with hyperthermia, in the course of injury or illness. Hypotension may be dramatic despite massive volume resuscitation and pressor support. Laboratory findings suggesting hypoadrenalism include hyponatremia, hypochloremia and hyperkalemia. The diagnosis of adrenal insufficiency may be confirmed or excluded by means of an ACTH stimulation test. A significant major cortisol response should be elicited by ACTH administration.
|
|
|
229 Which of the following statement(s) is/are true concerning the effects of MOFS?a. Pulmonary dysfunction tends to arise early and may resolve within 7 to 10 daysb. Unless the precipitating insult has prompted oliguric acute tubular necrosis, renal function tends to be maintained early in the course of MOFSc. Although hepatic dysfunction is common with MOFS, the GI tract plays little role in this processd. Intercurrent nosocomial infection, most commonly pulmonary, is a common complication providing a “second hit” to the patient
|
Answer: a, b, dPulmonary dysfunction typically arises early in the development of systemic inflammation and may represent mild relatively localized acute lung injury or it may be a prelude to fulminant ARDS. The lung injury, and associated dysfunction, may resolve over the initial 7 to 10 days or persist, depending on the ongoing pathologic process. Many times a “second hit” such as a nosocomial infection, which is most commonly pulmonary, is a complication which can frequently worsen the pulmonary condition. Renal function tends to be maintained early in the course unless the precipitating insult has been prompted by a sudden oliguric acute tubular necrosis. With persistent activation and inflammatory mediators, glomerular filtration falls and the development of oliguric or polyuric renal failure marks the gradual transition into MOFS. Gastrointestinal abnormalities include ileus, stress ulceration, diarrhea, and mucosal atrophy. Breakdown of the mucosal barrier allows translocation of bacteria and endotoxin. Hepatic dysfunction is marked by progressive rise in serum bilirubin levels after a latent period of several days.
|
|
|
228 Which of the following statement(s) is/are true concerning the physiology of the microvascular system?a. Filtration of capillary fluid into the interstitial and the subsequent reabsorption is influenced by Starling’s law of ultrafiltrationb. The most important variable controlling blood to a capillary bed is the length of the vesselc. Most of the resistance to systemic blood flow occurs at the arteriolar leveld. Adrenergic vasoconstriction can arrest blood flow to an entire capillary bed
|
Answer: a, c, dExchange of material between the vascular space and the cell of various tissues via the interstitial space is essential for organ viability and occurs at the capillary level. The filtration of capillary fluid into the interstitium and its subsequent reabsorption into the post capillary venule is governed by microvascular permeability in conjunction with the balance between hydrostatic and oncotic pressures. The relation of these forces to one another (and their net effects) are illustrated by what is termed Starling’s law of ultrafiltration. In normal circumstances, a net filtration from capillary to interstitium is effected by a relatively higher capillary hydrostatic pressure, whereas net reabsorption from the interstitium back into the post capillary venule occurs as hydrostatic pressure falls and oncotic forces predominate. Although the mechanisms controlling blood flow to the capillary bed are complicated and vary among the different tissues, certain concepts are useful. Poiseuille’s law describes the relation between flow of fluid through a tube and the tube length and radius, the fluid viscosity, and the pressure gradient between ends of the tube. The radius of the tube (or vessel) is the single most important variable, because flow is proportional to the radius to the fourth power. Vasoconstrictive and vasodilatory influences directly impact local blood flow, as well as flow to other tissues through secondary effects on the systemic pressure. This secondary effect of peripheral vasoconstriction maintains the pressure gradient for central perfusion of the heart and brain. Systemic blood flow meets most of its resistance at the arteriolar level. While the individual capillary radius is significantly smaller, the vast number of capillaries offers less total resistance. The vascular smooth muscle in arterioles has both a-and b- adrenergic receptors. Alpha stimulation affects vasoconstriction where beta stimulation affects vasodilatation. The efferent sympathetic fibers innervating the precapillary resistance vessels and the venous capacitance vessels release norepinephrine on stimulation, which induces smooth muscle contraction and narrowing of the caliber of the vessels. These contractions are potent enough that blood flow to entire capillary beds can be arrested by adrenergic vasoconstriction.
|
|
|
227 Which of the following statement(s) is/are true concerning ischemia reperfusion injury?a. During ischemia, ATP degradation results in increased plasma and intracellular levels of hypoxanthine and xantheneb. Oxygen free radicals such as the superoxide radical are involved in the expression of the proinflammatory phenotype of endothelial cells, macrophages and neutrophilsc. The intracellular adhesion molecule-1 (ICAN-1) contributes to injury and disruption of the endothelial lining, with extensive capillary leak and resultant interstitial edemad. Animal models have demonstrated that passive immunization with antibodies to neutrophil adhesive complex lessen the ischemic/reperfusion microvascular injury
|
Answer: a, b, c, dDuring the ischemia and hypoperfusion phase, degradation of ATP stores essential to maintain cell integrity and significant loss of diffusible intracellular adenine neuclotides occurs. As ATP further degrades there is an elevation in plasma and intracellular levels of hypoxanthine and xanthene which upon restoration of perfusion and reoxygenation are catalyzed by xanthine oxidase resulting in the formation of superoxide radicals. These radicals plus others such as hydrogen peroxide and hydroxyl radical are generated and lead to endothelial and parenchymal cell injury through membrane lipid peroxidation and activation of critical enzymes. These radicals have also been shown to be involved in the expression of proinflammatory phenotype endothelial cells and on macraphages and neutrophils. The proinflammatory phenotype of the endothelium includes procoagulant activity and the expression of adhesion molecules on the membrane surface, including the intercellular adhesion molecule-1 (ICAN-1) and the selectins. The subsequent adhesion of activated neutrophils to the endothelial leads to an explosive oxidative burst producing additional radicals and extensive release of proteolytic enzymes leading to injury and disruption of the endothelial lining, extensive capillary leak, and massive interstitial edema. Passive immunization of animals with monoclonal antibodies to either the neutrophil adhesive complex or the endothelial selectins dramatically lessens ischemia/reperfusion microvascular injury.
|
