fluid and blood therapy

1. Fluid and Blood Therapy Foundations of Anesthesia I Krista Yoder March 23, 2009

2. Total Body Water Total body water (60% total body weight) Intracellular volume (40% total body weight) Extracellular volume (20% total body weight)

3. Body Fluid Compartments Intracellular Volume / Fluid Compartment Extracellular Volume / Fluid Compartment Interstitial fluid volume (80% of ECV) Plasma volume (20% of ECV)

4. Total Body Water

5. Total Body Water TBW is 55% of a man�s weight TBW is 45% of a woman�s weight TBW is 80% of an infant�s weight Obese individuals have less TBW per weight than non-obese individuals

7. Fluid Compartments Fluid Compartments are divided by water-permeable membranes. Intracellular space is separated from the extracellular space by the cell membrane. The capillary membrane separates the components of the extracellular space. Intravascular space � capillary membrane � interstitial space

9. Intracellular Fluid Compartment High concentration of Potassium Phosphate Magnesium Sodium-potassium pump maintains the high concentration of K+ in ICF.

10. Sodium-Potassium Pump

11. Extracellular Fluid Compartment High concentration of Sodium Chloride Intravascular Fluid (plasma) High concentration of osmotically active plasma proteins. Albumin Capillary membrane essentially impermeable to plasma proteins and they stay in the vascular space. Interstitial Fluid

14. Fluid Movement Within Body Compartments Fluid movement is affected by: Properties of membranes separating compartments. Concentration of osmotically active substances within a compartment.

15. Intravascular Fluid Space Chief focus of fluid therapy Accessible fluid compartment intravascular space � capillary membrane � interstitial space

16. Starling Forces Hydrostatic pressure in the capillary (Pc) Hydrostatic pressure in the interstitium (Pi) Oncotic pressure in the capillary (pc ) Oncotic pressure in the interstitium (pi )

19. Fluid Volume Disorders Osmolarity The number of osmoles of a solute in a liter of solution Osmolality The number of osmoles of a solute in a kilogram of solution Tonicity How a solution affects cell volume For example � isotonic, hypertonic, hypotonic

20. Hypovolemia versus Dehydration Hypovolemia Loss of extracellular fluid Absolute loss of fluid from the body Reduced circulating volume Dehydration Concentration disorder Insufficient water present in relation to sodium

21. Hypervolemia Excess of fluid volume in an isotonic concentration Not usually a problem in surgical patients Can be seen if CHF Renal failure Over hydration with isotonic IV fluids

22. Disorders of Sodium Balance Na+ is the most abundant electrolyte in the ECF. Na+ and accompanying anion Cl- are responsible for normal osmotic activity of the ECF. All gain/loss of Na+ is accompanied by gain/loss of water.

23. Hyponatremia Hypovolemic hyponatremia Vomiting Diarrhea Diuretics Adrenal insufficiency Normovolemic hyponatremia Syndrome of inappropriate secretion of antidiuretic hormone Renal failure Water intoxication Hypervolemic hyponatremia CHF Liver failure Nephrotic syndrome

25. Clinical Manifestations of Hyponatremia Neurologic Seizure Coma Agitation Gastrointestinal Anorexia Nausea/vomiting Muscular Cramps weakness Headache Cerebral edema Confusion

26. Treatment of Hyponatremia Fluid restriction Administration of hypertonic saline and an osmotic or loop diuretic !!!Correction of serum sodium levels too rapidly can result in neurologic damage and central pontine myelinolysis!!!

27. Causes of Hypernatremia Most common cause is water deficiency d/t: Excessive loss Inadequate intake Also may be caused by: Exogenous Na+ load Primary hyperaldosteronism Diabetes insipidus Renal dysfunction

29. Clinical Manifestations of Hypernatremia Tremulousness Irritability Ataxia Mental confusion Coma d/t cerebral water loss

30. Treatment of Hypernatremia Renal tubular diuretics Hemodialysis Treat central diabetes insipidus with vasopressin !!!Correction of serum sodium level too rapidly can result in neurologic damage secondary to cerebral edema!!!

32. Hypokalemia Causes Gastrointestinal losses Systemic alkalosis Diabetic ketoacidosis Diuretic therapy Sympathetic nervous system stimulation Administration of beta-adrenergic receptor agonists

33. Clinical Manifestations of Hyponatremia Autonomic neuropathy Skeletal muscle weakness Increased sensitivity to Digoxin Cardiac Decreased myocardial contractility Electrical conduction abnormalities Arrhythmias Tachycardia Ventricular fibrillation

34. Hypokalemia and the EKG Prolonged PR interval Prolonged T interval Widening of QRS Flattened T wave

35. Treatment of Hypokalemia Slow IV potassium supplements Anesthesia related concerns: Increased risk of myocardial irritability K+ <2.6 Avoid hyperventilation of the lungs Avoid glucose containing IV solutions Avoid rapid infusion of IV K+ supplements

36. Hyperkalemia Causes Increased total body potassium Renal failure Potassium-sparing diuretics Excessive IV K+ supplements Excessive use of salt substitutes Altered distribution of potassium Metabolic or respiratory acidosis Digitalis intoxication Insulin deficiency Hemolysis Tissue and muscle damage after burns Administration on succinylcholine

37. Clinical Manifestations of Hyperkalemia Areflexia Weakness Paralysis Paresthesia Cardiac conduction abnormalities

38. Hyperkalemia and the EKG Narrowing and peaking of T waves 1st degree AV block QRS widening ST segment depression Progression to merging of QRS an T waves to a sine wave Tachycardia Ventricular fibrillation

39. Treatment of Hyperkalemia Primary goal Avoid adverse cardiac effects Insulin and glucose to shift K+ into cells IV calcium to antagonize cardiac effects of hyperkalemia Anesthesia related concerns: A serum K+ of 5.5mEq/L is upper limit for elective procedures

40. Hypomagnesemia Serum magnesium less than 1.5mEq/L Causes: Inadequate intake of magnesium TPN Gastrointestinal losses Pancreatitis Parathyroid hormone disorders Hyperaldosteronism Ketoacidosis Chronic alcoholism

41. Clinical Manifestations of Hypomagnesemia CNS irritability Seizures Hyperreflexia Skeletal muscle spasm

42. Treatment of Hypomagnesemia IV administration of magnesium sulfate

43. Hypermagnesemia Serum magnesium level greater than 2.5 mEq/L Causes: Iatrogenic administration Preeclampsia Antacids/laxatives Renal failure

44. Clinical Manifestations of Hypermagnesemia CNS depression stupor coma Skeletal muscle weakness respiratory failure Decreased peripheral vascular tone Decreased myocardial contractility Tocolysis

45. Hypermagnesemia and the EKG Prolonged PQ interval Widened QRS

46. Treatment of Hypermagnesemia Supportive care Fluid loading Diuresis Acute hypermagnesemia �IV calcium to counter the elevated magnesium levels

47. Hypocalcemia Causes: Decreased serum albumin concentration Chelation of calcium by citrate Rhabdomyolysis Hypoparathyroidism Pancreatitis Renal failure

48. Clinical Manifestations of Hypocalcemia Neuromuscular irritability Tetany Laryngospasm Hyperactive deep tendon reflexes Weakness Vasodilation Myocardial dysfunction Bradycardia Heart block

49. Treatment of Hypocalcemia Calcium replacement Intraoperative � hyperventilation and respiratory alkalosis

50. Hypercalcemia Causes: Calcium mobilization from bone due to immobility Tumors Hyperparathyroidism

51. Clinical Manifestations of Hypercalcemia Anorexia Nausea Constipation Cognitive depression EKG changes Prolonged PR interval Shortened QT interval PVC�s

52. Treatment of Hypercalcemia Treatment of underlying cause Volume expansion Intraoperative hypercalcemia should be managed with administration of adequate fluids and maintenance of urine output.

53. Intraoperative Fluid Management

54. Factors influencing intraoperative fluid management: Patient�s perioperative fluid status Co-existing disease Intra-operative fluid shifts Intra-operative blood loss Selection of appropriate fluids for replacement of intra-operative losses

55. Intra-operative Fluid loss Insensible loss Third space loss Blood loss

56. Insensible loss Water loss through Urine Feces Sweat Respiratory tract Correct insensible losses with 2ml/kg/hr Crystalloid solution

57. Third Space loss The transfer of fluids from the extracellular space to the interstitial space or other non-intravascular spaces. The volume of fluid transferred corresponds to the degree of manipulation of tissues Intraoperatively. Replacement of 3rd space losses is surgical procedure dependent.

58. Replacement of third space loss Minimal trauma: 3-4 mL/kg Moderate trauma: 5-6 mL/kg Severe trauma: 7-8 mL/kg

59. Third Space loss 3rd space losses become mobilized on about the third day post-op. Clinically this may manifest as an increase in the intravascular volume on this day. Patients with limited cardiac reserve or renal dysfunction may have hypervolemia or pulmonary edema if fluid mobilization is significant.

60. Crystalloids Used intraoperatively to maintain normal body fluid composition and replace losses. Contain water and electrolytes. Cross plasma membranes easily and may dilute plasma proteins resulting in a reduction of plasma oncotic pressure. Are effective at increasing the intravascular fluid volume. Are associated with an increased risk of pulmonary edema if administered in large volumes.

61. Crystalloid replacement of blood loss The volume of crystalloid used to replace intraoperative blood loss should be three times the estimated blood loss. This is because volume replacement must replenish both the volume lost from the intravascular space and the volume transferred from the extravascular space to the intravascular space to maintain the plasma volume during times of acute hemorrhage.

62. Not typically administered intraoperatively. Surgical stress response normally induces hyperglycemia. The exception would be for prevention of hypoglycemia in diabetic patients who have received insulin. Glucose containing solutions:

65. Colloids Albumin Plasmanate Hetastarch Dextran

66. Colloids Large molecules that do not readily cross plasma membranes. Can be uses 1:1 to replace blood loss. May be advantageous because they remain in the intravascular space longer than crystalloids. There is no evidence that colloids are superior to crystalloids for replacing the intravascular fluid volume.

67. Colloids Advantages Lack of risk of disease transmission Risk of transmitting hepatitis eliminated by heat Pretreated to 60*C for 10 hours Disadvantages Lack of oxygen-carrying capacity Lack of coagulation factors Increased cost

68. Hetastarch Infusion of large volumes can cause dilutional coagulopathy. Can cause a decrease in factor VIII when administered in a volume greater than 1000mL in a 70kg individual.

69. Dextran Infusion of large volumes can cause dilutional coagulopathy. Appears to decrease platelet adhesiveness. Potential for anaphylactic/anaphylactoid reactions. Interferes with ability to subsequently crossmatch a patient�s blood secondary to agglutination of red blood cells.

70. 5% Albumin Used for rapid expansion of intravascular fluid volume. Administration of plasma protein fractions may result in hypotension due to a decrease in SVR.

71. 25% Albumin Primary indication is for hypoalbuminemia. Administration of plasma protein fractions may result in hypotension due to a decrease in SVR.

73. Clinical assessment of intraoperative blood loss Tachycardia Hypotension Decrease CVP

74. Clinical assessment of intraoperative blood loss Oliguria A urine output of 0.5 - 1 mL/kg/hr is typically indicative of an adequate intravascular fluid volume. Administration of diuretics will interfere with the utility of intraoperative urine output as a measure of fluid volume.

75. Clinical assessment of intraoperative blood loss Variation of systolic BP with respiratory cycle in mechanically ventilated patients. Normally a 8-10mm Hg variation d/t decrease venous return that occurs with inspiration. Variations greater than 10mmHg may indicate hypovolemia.

76. Clinical assessment of intraoperative blood loss All clinical signs may vary with anesthesia. Young healthy patients may lose 20% of circulating blood volume without demonstrating clinical signs.

77. Physiologic response to acute blood loss Vasoconstriction of splanchnic and venous capitance vessels occurs in response to blood loss. A blood volume loss of approximately 10% can be masked by this compensatory response. Anesthesia may interfere with this response.

78. Indication for blood transfusion The primary indication for blood transfusion is to increase the oxygen carrying capacity of the blood. Typically hemoglobin concentration is basis on which decision to transfuse is made. Transfusion is almost always justified when Hgb is less than 6g/dL. Transfusion is rarely justified when Hgb is greater than 10g/dL.

79. Modification of transfusion threshold: Patient age Medical status / comorbidities Is current anemia acute or chronic The decision to transfuse must be made on an individual basis. Example: patient�s with CAD who are at risk for myocardial ischemia may benefit from a Hgb no less than 10mg/dL.

80. Management of acute hemorrhage: Acute loss of large volumes of blood should be managed with administration of blood. Administration of crystalloid volumes necessary to replace the intravascular fluid loss will result in an inadequate oxygen-carrying capacity of the blood. Blood loss greater than one-third entire blood volume. Blood loss leading to hypovolemic shock. Whole blood is preferred to PRBCs in these situations to expand the circulating blood volume and the red cell volume.

81. Adequacy of blood volume replacement: Evaluation of systemic blood pressure Heart rate Central venous pressure Urine output Arterial oxygenation Arterial pH Base deficit Serial hematocrit levels