Stoelting Study 17 Fluid And Blood

Front 1

2. What body fluid compartments can total body water be divided into?

Back 1

2. Total boCy water can re divided into 1he extracellular and intracellular fluid compartments. Included in the extracellular fluid compartments are the interstitial fluid and the plasma volume.

Front 2

3. What is the plasma volume? What percent of body weight is made up by the plasma volume?

Back 2

3. The plasma volume is the fluid contained within the vasculature excluding the erythrocytes. About 5% of body weight is made up of the plasma volume.

Front 3

4. What is the interstitial fluid? What percent of body weight is made up by the Interstitia! fluid volume?

Back 3

4. The interstitial fluid i; the fluid that is external to the blood vessels and cells. About 15% of body weight is made up of the interstitial fluid volume. The interstitial fluid volume serves as a reservoir from which water and/or electrolytes can be taken into the plasma volume at times of need.

Front 4

6. How can a patient's intravascular fluid volume status be assessed preoperatively?

Back 4

6. A patient's intravascular fluid volume status can be assessed preoperatively by evaluating the patient's mental status, history of recent intake and output, supine and upright arterial blood pressures and heart rates, skin turgor, mucous membrams, urine output, arterial gas pH and base deficit, hematocrit, electrolytes, and central venous pressure. Certain disease states or medicines may also provide an indication of possible intravascular fluid depletion.

Front 5

7. Why is it important to assess a patient's intravascular fluid volume status before the delivery of anesthesia?

Back 5

7, Assessment of a patient's intravascular fluid volume status may help to predict and avoid potentially adverse effects of anesthesia on a hypovolemic patient. Anesthetics can cause hypotension secondary to systemic vasodilation and/or myocardial depression, and this effect may be more pronounced in the and/or myocardial depression, and this effect may be more pror.ounced in the patients frequently fast, have blood drawn, or have their bowels cleared in preparation for surgery. Patients who appear to have an intravascular fluid volume defuit preoperatively should have their volume augmented with the administration of intravascular fluids before the induction of anesthesia.

Front 6

9. What is orthostatic hypotension?

Back 6

9. Orthostatic hypotension is a physical examination finding that indicates a patient may be hypovolemic. The test for orthostatic hYJDtension involves taking a patient's blood pressure and heart rate first while the patient is supine and then repeating blood pressure and heart rate measurements after the patient stands. Orthostatic hypotension is defined as a decrease in blood pressure by greater than 20 mm Hg. This may correspond to a fluid volume deficit of 6% to 8% of body weight, but there is a great degree of variability among patients. This limits the usefulness of this test, particularly among the young and healthy or the elderly.

Front 7

15. How can hyponatremia be treated?

Back 7

15. The treatment of hyponatremia ranges from fluid restriction to the administra· tion of hypertonic saline with osmotic and loop diuretics, depending on the severity of the symptoms. Of great importance is the time course for correction of the serum sodium levels drring treatment. Correction of the serum sodimn levels too rapidly can result in neurologic damage and central pontine myelinolysis. Cerebral edema typically resolves when the serum sodium level is 130 mEq/L or greater.

Front 8

21. What are some adverse effects of hyperkalemia? ·

Back 8

21. A.dverse effects of hyperkalemia include areflexia, weakness, paralysis, paresthesias, and caniJac conduction abnormalities. The potential effects of hyperkalemia on the heart are of the most concern for the anesthesiologist. Sequentim changes thm may be seen on the electrocardiogram as the serum potassium level rises are narrowing and peaking of the T waves, first-degree atrioventricular block, QRS widening, and ST segment depression progressing to merging of the QRS and T waves to a sine wave. Tachycardia and ventricular fibrillation may also occur. Low serum levels of sodium and calcium will augment the adverse effects of hyperkalemia

Front 9

22. How can hyperkalemia be treated?

Back 9

22. The primuy ~oal of the treatment of acute hyperkalemia is the avoidance of the adverse cardiac effects of hyperkalemia. The treatment of acute hyperkalemia with insulin and glucose causes a shift of potassium from the serum into cells and increases the membrane threshold. Hyperkalemia may also be treated with the intravenous administration of calcium to antagonize the adverse effects of hyperkalemia on the heart. Systemic alkalosis, as is produced by hyperventilation of the lungs or the administration of intravenous sodium bicarbonate, may also be used to treat acute hyperkalemia.

Front 10

23. What serum potassium level is often considered to be the upper limit acceptable for patients who are scheduled to under go elective operative procedures?

Back 10

23, Because of the potential morbidity and mortality that can result from intraoperative hyperkalemia, a serum potassium level of 5.5 mEq/L is often considered to be the upper limit acceptable for patients who are scheduled to undergo elective Dperative procedures. (

Front 11

33. What are some manifestations of hypercalcemia. How can hypercalcemia be treated?

Back 11

33. Manifestations of hypercalcemia induce anorexia, nausea, constipation, and cognitive depression. Manifestations on the electrocardiogram include a prolonged PR interval, a shortened QT interval, and premature ventricular contractions. The treatment of hypercalcemia is by treatment of the underlying cause and volume expansion. Sodium inhibits the renal tubular absorption of calcium, making its administration useful in hypercalcemia. Intraoperative hypercalcemia should be managed with the admnistration of adequate fluids and maintenance of the urine output. (

Front 12

35. What are some manifestations of hypocalcemia? How can hypocalcemia be treated?

Back 12

35. Manifestations ofhypocalceroia include neuromuscular irritability, weakness, vasodilation, myocardial dysfunction, bradycardia, and heart block. Neuromuscular irritability may manifest as tetany, laryngospasm, and hyperactive . deep tendon reflexes. The treatment of hypocalcemia is by calcium replacement. Intraoperatively, hypocalcemia may also be treated with the institution of hyperventilation andrespiJatory alkalosis.

Front 13

38. What day postoperatively do third space fluid losses become mobilized?

Back 13

38. Third space fluid losses become mobilized on about the third day postoperatively. Clinically, this may manifest as an increase in the intravascular fluid volume on this day. Patients with limited cardiac reserve or with renal dysfunction may have hypervolemia or pulmonary edemt if the mobilization of fluids is sufficiently large.

Front 14

39. What are crystalloids?

Back 14

39. Crystalloids are a class of fluids that can be administered intraoperatively to maintain normal body fluid composition and replace losses. Crystalloids contain water and electrolytes. Crystalloids cross plasma membranes easily and may dilute plasma proteins, resulting in a reduction of the plasma oncotic pressure. Although crystalloids lfe effective at increasing the intravascular I fluid volume, the administration of crystalloids may be associated with an increased risk of pulmonary edema than that of colloids if administered in sufficient volumes

Front 15

40. What volume of crystalloid fluid should be administered to patients to correct intraoperative blood loss?

Back 15

40. It is recolllJlV-nded that the volume of crystalloid fluid administered to replace intraoperative blood loss be three times the vo1une of the estimated blood loss. This is because volume replacement is nct just to replenish the volume lost from the intravascular space but also to replenish volume that is transferred from the extravascular spaces to the intravascular spaces to maintain the plasma volume during times of acute blood loss. C

Front 16

41. What are colloids? How should they be administered to correct blood loss?

Back 16

41. Colloids include albumin, Plasmanate, hetastarch, and dextran. These all contain large molecules that do not readily cross plasma membranes. For this reason they can be administered in a l:l ratio to replace blood loss. Colloids may be advantageous in that they may maintain the plasma oncotic pressure and remain in the intravascular space for longer than crystalloids. About 20 mL of water is held in the circulation for every gram of colloid administered. There is no evidence that colloids are superior than crystalloids for replacing the intravascular fluid volume. The main advantage of colloids for transfusionis their lack of risk of the transmission of disease. The risk of transmission of hepatitis is eliminated by the pretreatment with heat to 60°C for 10 hours. Disadvantages of colloids include their lack of oxygen-carrying capacity and coagulation factors and their increased cost. (

Front 17

42. What are some potential adverse effects of using hetastarch and dextran for volume replacement?

Back 17

42. The administration of hetastarch and dextral in large volumes can result in a dilutional coagulopatllY. Hetastarch can cause a decrease in factor vm when administered in a volume gteater than 1000 mL in a 70-kg patient. Dextran appears to decrease platelet adhesiveness and has the potential to cause an anaphylactoid or anaphylactic eaction. Dextran has the added disadvantage of interfering with the ability to subsequently crossmatch a patient's blood secondary to the agglutination of red blood cells. (:

Front 18

43. What is the primary indication for the transfusion of 5% albumin? What is the primary indication for be transfusion of 25% albumin?

Back 18

43, The primary indication for the transfusion of 5% albumin is for rapid intravascular fluid volume expansion, and the primary indication for the transfusion of 25% albumin is hypoalbuminemia. C:

Front 19

47. How well can vasoconstriction compensate for intraoperative blood loss?

Back 19

47. Vasoconstriction of the splanchnic and venous capacitance vessels occurs in response to blo()d loss. A oss in blood volume of approximately 10% or greater can be masked by this compensatory change. This compensatory · mechanism may be interfered with by the administration of anesthetia

Front 20

48. What are the indications for the transfusion of blood?

Back 20

48. The primary indication for the transfusion of blood is to increase the oxygencarrying capacity of tIE blmd. Because there are no direct measures of the oxygen-carrying capacity, other measures must be used. Typically, the : hemoglobin concentration is the basis on which the decision to transfuse is made. Blood transfusion is almost always justified when the hemoglobin value is less than 6 gldL and is rarely justified when the hemoglobin value is greater than 10 gldL

Front 21

49. How should the acute loss of large volumes of blood be managed.

Back 21

49. The acute loss of large volumes of blood should be managed with the administration of blood because the administration of crystalloids to these patients in volumes necessary to replace the intravascular volume will result in an inadequate oxygen-carrying capacity of the blood. Typically, this corresponds to a blood loss of greater than one third of the entire blood volume and/or blood loss leading to hypovolemic shock. Whole blood is preferable to packed red blood cells in these situations because the blood loss is sufficiently large to warrant the expansion of blood volume as well as the administration ()f red blood cells

Front 22

50. How can the adequacy of blood replacement be assessed?

Back 22

50. The adequacy of blood replacement may be assessed through the evaluat~on of the systemic blood pressure, heart rate, central venous pressure, urine output, arterial oxygenation, arterial pH, base deficit, and serial hematocrit levels. (239)

Front 23

57. How long can blood be stored?

Back 23

57. Blood can be stored for 21 to 35 days. The duration of the storage of blood is determined by the requirement that at least 70% of the red blood cells be viable for more than 24 hours after transfusion.

Front 24

58. What is the temperature at which blood is stored'? Why?

Back 24

58. Blood is stored at a temperature of 1 'C to 6°C. This slows down the rate of glycolys:s in red blood ceUs and increases their survival time in storage.

Front 25

59. What is the volume of blood, the volume of citrate-containing preservative, and the hematocrit in a given unit of whole blood?

Back 25

59. In a given unit of whole blood the volume of blood is 450 mL, the volume of citrate-contaning preservative is 65 mL, and the hematocrit is about 40%. The total volume of a unit of whole blood is about 515 mL.

Front 26

60. Name the components that can be derived from whole blood. What is the advantage of using components for blood therapy instead of whole blood?

Back 26

60. Components that ~an be derived from whole blood include packed red blood cells, platelet concentrates, flesh frozen plasma, cryopreapitate, albumin, plasma protein fraction, leukocyte-poor blood, factor VIII, and antibody concentrates. The advantage of using components for blood therapy instead of whole blood is that a patient's specific deficiency can be directly corrected. It also allows for prolonged storage, the retention of unnecessary components for other patients who may need them, and the avoidance of transfusing unnecessary components that could potentially contain antigens or antibodies.

Front 27

67. When is the administration of platelets indicated during surgery?

Back 27

67. The administration of platelets during su:gery is usually indicated for platelet counts less than 50,000 cellslmm3, Both laboratory analysis and the clinical situation must be taken into consideration. For instance, in cases of surgical trauma or in cases of bleeding in the brain, eye, or airway the transfusion of platelets at a higher number may be warranted.

Front 28

68. How ouch will the platelet count increase after the administration of 1 unit of platelets?

Back 28

68. The platelet count will increase by 5,000 to 10,000 cells/mm after the administration of 1 unit of platelets to a 70-kg adult. (240; 1636-1637)

Front 29

69. What are some of the risks associated with the administration of platelets?

Back 29

69. Risks associated with the administration of phte1ets include the transmi~sion of viral diseases and sensitization to the human leukoclte antigens present on the plztelet cell membranes. Platelets may also cause bacterial infection in 1 in 12,000 transfusion. Aliliough the risk is small, platelet-related sepsis shoun be considered in a patient who develops a fever after receiving platelet therapy

Front 30

70. What is fresh frozen plasma? What is contained in fresh frozen plasma?

Back 30

70. Fresh frozen plasma is the plasma portion of 1 unit of donated blood. The plasma is frozen within 6 hours of collection. All plasma proteins are contained in fresh frozen plasma. Included are all the cagulation factors except platelets. This included factors V and VIll, which decrease in concentration during the storage of packed red blood cells.

Front 31

73. What is cryoprecipitate? What is contained in cryoprecipitate?

Back 31

73. Cryoprecipitate is the plasma fraction that precipltates when fresh frozen plasma is thawed. Cryoprecipitate contains high concentrations of factor vrn, von Willebrand factor, factor XIII, fibrimgen, and fibronectin.

Front 32

74. What is cryoprecipitate useful for treating?

Back 32

74. Cryoprecipitate is useful for the treatment of factor VIII deficiency as in hemophilia A, von Willebrand factor deficiency, and fibnnogen deficiency.

Front 33

79. How are febrile transfusion reactions treated?

Back 33

79. Febrile transfusion reactions are treated by decreasing the rate of the infusion of blood and administering antipyretics.

Front 34

82. Why are hemolytic transfusion reactions thought to occur?

Back 34

82. Hemolytic transfusion reactions are thought to occur as a result of the administration of an erroneous unit of blood to a patient. Transfused donor cells are attacked by the recipient's antibody and complement, resulting in intravascular henolyus As little as 10 mL of donor blood can result in a hemolytic transfusion reaction, which can be fatal. The severity of a transfusion reaction is proportional to the volume of transfused blood.

Front 35

86. What is the treatment for a hemolytic transfusion reaction?

Back 35

86. The first step in the treatment of a hemoly:ic transfusion reaction is to stop the transfusion. Subsequent treatment interventions are gearec toward preventing renal failure by maintaining urine output. It IS believed that renal failure occurs as a result Df precipi,ates in the renal tubules. The urine output is recommended to be maintained at about 100 mlJhr through the administration of lactated Ringer's solution and mannitol and/cr furosemide as necessary. The urine may also be alkalinized with bicarbonate. Laboratory analysis should be perfonned, including diagnostic tests of urine and plasma hemoglobin concentrations as well as baseline coagulation studies. Finally, unused blood slOuld be sent to the blood bank along with a sample from the patient for a repeat type and crossmatch analysis.

Front 36

90. How does the transfusion of blood affect the patient's arterial pH? .

Back 36

90. The pH of a unit of blood is about 7.1 after collection and is 6.9 after being stored for 21 days. This is partly due to a high PC02 of the blood being stored, but it is also due to the addition of acidic preservatives. Although it would seem that the recipient's arterial pH might decrease with the administration of blood products, it actually increases. This probably occurs for two reasons. First, the elevated PC02 of blood can be quickly corrected on transfusion through the ventilation of the lungs of the recipient. More significandy, blood products contain the preservative citrate that metabolizes to bicarbonate on transfusion. The increased bicarbonate levels actually increase the arterial pH of the recipient, frequently resulting in a metabolic alkalosis with the transfusion of large volumes of blood. Therefore, any treatments of the recipient's arterial pH should be baled on laboratory analysis and not be done empirically.

Front 37

91. How much does the serum potassium level increase in patients after the transfusion of blood?

Back 37

91. Potassium concentrations in blood stored for 21 days may be as high as 20 to 30 roEqlL. Even after the transfusion of large volumes of blood, serum potassium levels rarely increase with the transfusion of blood. This is in part because the high concentration of potassium exists in a small volume and the total potassium content is small. Nevertheless, hyperkalemia resulting from blood transfusions is occasionally reported. In most cases it was associated with large volumes of blood rapldly infused, typically at rates greater than 20 m/min.

Front 38

92. How do concentrations of 2,3-diphosphoglycerate changes with the prolonged storage of blood? How does this affect Oxygen delivery to the tisses?

Back 38

92. Concentrations of 2,3-diphosphoglycerate in erythrocytes decrease with the prolonged wrage of blood. Decreased concentrations of 2,3-diphosphoglycerate are associated with a shift of the oxyhemoglobin dissociation curve to the left and an increase in the affinity of hemoglobin for oxygen. This could result in a decrease in the delivery of oxygen tc the tissues. This effect of a decrease in 2,3-diphosphoglycerate could be further compounded by the presence of acidosis and hypotheonia. Although of concern for the effect on oxygen delivery to the tissues, there appears to be little clinical consequence of the decreased level of 2,3-diphosphoglycerate

Front 39

93. How does the administration of citrate in blood products affect the recipient's serum calcium concentration?

Back 39

93. The infusion of citrate preservative during the transfusion of blood can result in a metabolic alkalosis and hypocalcemia. The metabolic alkalosis results from the metabolism of citrate in the liver to bicarbonate. Hypocalcemia can result from the binding of citrate to calcium in the intravascular space but is usually attenuated by the mobilization of calcium stores in bone. Hypocalcemia can be augmented by hypothermia, liver disease, or hyperventilation because these will all decrease the rate of metabolism of citrate to bicarbonate. Under these circumstances, the infusion of large volumes of citrate combined with the decreased metabolism of citrate can result in hypocalcemia. Indeed, serum ionized calcium has been found to begin to decrease with a rate of infusion of 1 unit of blood every 10 minutes. Hypocalcemia can result in I hypotensIon, a narrow pulse pressure, and elevated central venous pressures.

Front 40

94. How does the administration of citrate in blood products affect the recipient's arterial pH?

Back 40

94. The infusion of citrate preservative during the transfusion of blood can result in a metabolic aIkalosis. The metabolic alkalosis results from the metabolism of citrate in the liver to bicarbonate. This metabolic alkalosis is offset somewhat by the acidic pH of the transfused unit of blood. Metabolic alkalosis can accompany the transfusion of large volumes of blood, however.

Front 41

97. What are some ways in which massive blood transfusions can result in coagulation disorders?

Back 41

97. Massi\e blood transfusions can result in two different coagulation disorders: a diluticnal thrombocytopenia and a dilution of some of the coagulation factors necessary to clot blood. In either Clse, it may manifest clinically as continued frank: bleeding without clotting in the mrgical sileo It may also manifest as hematuria, gingival bleedirg, and spontaneous oozing fran vari

Front 42

98. What is dilutional thrombocytopenia? What is the treatment of dilutional thrombocyopenia?

Back 42

98. Dilutional thrombocytopenia refers to the dilution of platelets from its baseline concentration to a decreased concentration by virtue of the loss of platelets during bleeding without subsequent replacement, as with the administration of crystalloid, colloid, or non-platelet-containing blood products. This occurs even with the transfusion of blood because platelet activity has decreased to about 5% of nonnal after just 2 days of blood storage. The risk of a dilutional thrombocytopenia is the loss of the ability of blood to clot. When platelet counts decrease to less than 75,OOO/mm3, a bleeding disorder is likely to occur. T

Front 43

105. What are some complications that may accompany the intraoperative salvage of blood for autologous blood transfusions?

Back 43

105. Complications of intraoperative blood salvaging include a dilutional coagulopathy, the re-infusion of blood treated with anticoagulants, hemolysis, air embolism, fat embolism, sepsis, and disseminated intravascular coagulation.