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GOAL-DIRECTED THERAPY
 Goal – improved tissue perfusion and clinical outcome
 Based on measuring key physiologic variables
⚫ Cardiac output or
⚫ Global O2 delivery
 Achieved with
administering fluids, and
possibly inotropes, vasopressors, vasodilators, and
RBCs
 Targets are defined physiologic endpoints and not dependant on
objective assessments of fluid status.
TARGETS FOR GOAL-DIRECTED THERAPY ARE AS
FOLLOWS:
 Arterial blood pressure and waveform analysis (MAP >65 mm Hg)
 CVP (8-10 cm H2O)
 Echocardiography (No regional wall motion abnormalities)
 Lactate (<2.0 mmol/L)
 O2 extraction and venous O2 saturation (SvO2) or central venous
saturation (ScvO2)
Special
Considerations/
Patient Factors
HEART FAILURE
 Goals => Preserve CO, preload, contractility, and afterload.
 Ventricles poorly compliant and require adequate preload and adequate diastolic
filling time.
 Excessive volume infusion and preload => Impaired contractility and worsening CO
 Invasive monitoring with either EDM/ PAC for fluid therapy
 Restrictive Fluid therapy or GDT is preferred.
 Striking a balance between hypovolemia and hypervolemia is particularly
important in patients with heart failure,
KIDNEY DISEASE
 Preop assessment should focus on
⚫ the adequacy of chronic dialysis in attaining euvolemia, and
⚫ estimating the normal volume of native urine output.
 Comorbidities should be assessed and optimized.
 Surgery undertaken in a facility where preop and postop dialysis or
hemofiltration done.
 In elective surgery, preop dialysis timed such that the patient enters
the intraop phase with a normal blood volume
 Hypervolemia => risk for pulmonary and peripheral edema, hypertension, and
poor wound healing.
 Hypovolemia => risk for anesthesia-related hypotension and inadequate tissue
perfusion.
 Dialysis the day prior to allow equilibration of fluid and electrolyte.
 Electrolytes on the morning of surgery ( ideal K+ value after dialysis is low-to-
normal range. )
 In emergency surgery, NO sufficient time for dialysis, electrolyte abnormalities
must be managed conservatively, intraop fluid balance.
UPPER GASTROINTESTINAL LOSS
 Progressive dehydration => Increased aldosterone secretion => Na+ is
retained at the expense of K+ and H+ ions, (hypokalemia, and
metabolic alkalosis with a paradoxically aciduria)
 Correction => Gradual rehydration with isotonic saline and K+
supplementation and changing to dextrose- containing saline
depending on electrolyte analysis.
SEPSIS AND ACUTE LUNG INJURY
 The pragmatic targets for patients with sepsis who have tissue
hypoperfusion (blood lactate conc. at or >4 mmol/L) or hypotension
persisting after Initial IV fluid Challenge:
⚫ CVP 8 to 12 mm Hg (12 to 15 mm Hg in patients on Ventilation)
⚫ MAP 65 mm Hg or greater
⚫ Urine output 0.5 mL/kg/hr or greater
⚫ ScvO2 > 70% (or mixed venous O2 saturation > 65%)
 Current recommendations to attain these goals
⚫ 30 mL/kg of suitable crystalloid
⚫ Albumin along with vasopressors and inotropes
⚫ RBC transfusion.
 Patients with establishedARDS for surgical procedures.
⚫ Focus of fluid therapy is the fine balance between avoiding an
increase in lung edema while maintaining adequate tissue
perfusion.
⚫ Early goal-directed fluid therapy may prevent ALI/ARDS
⚫ In established ALI/ARDS a fluid-conservative approach is the
minimum requirement
BURNS
 IV fluid therapy is generally instituted for burns of greater than 15%
total body surface area in adults and 10% total body surface area in
children
 Parkland Burn Fluid Resuscitation Formula
First 8 hours: 2 mL/kg × % TBSA (lactated Ringer solution)
Next 16 hours: 2 mL/kg × %TBSA (lactated Ringer solution)
Next 24 hours: 0.8 mL/kg × %TBSA (5% dextrose) + 0.015 mL/kg × %TBSA (5%
albumin)
 Down-titration of fluid volumes if UO is adequate (0.5 to 1 mL/kg/hr)
 Excessive fluid administration (“fluid creep”) may cause
⚫ Pulmonary edema
⚫ Fasciotomies in nonburned muscle compartments
⚫ Raised IOP
⚫ Conversion of superficial to deep burns
⚫ Intraabdominal hypertension and compartment syndrome
 Haifa formula (New Practice)
⚫ Plasma (cc) - 1.5 x % TBSA x body weight (kg) + RL (cc) - 1 x % TBSA x body weight
(kg).
⚫ Half fluid in first 8 hr and the other half in the next 16 hr
⚫ In the subsequent 24 hr, we give half the amount estimated for the first day.
⚫ The sufficiency of the fluid is judged mainly on the basis of urine output.
HEPATIC FAILURE
 Progressive liver disease and cirrhosis cause
⚫ peripheral vasodilation and
⚫ relative intravascular depletion (total body Na+ and water are retained with
ascites and edema )
 Aim is reduction of total body salt and water
[dietary fluid and salt restriction, diuretics (spironolactone and loop diuretics),
and intermittent or continuous drainage of ascites]
 Excessive isotonic saline => salt and water overload=> further ascites
and edema formation.
 Approach => Assess volume status and replace losses with
appropriate volumes of isotonic crystalloid, colloid, or blood but avoid
salt and water overload.
 Large-volume (>6 L) ascites drainage => hemodynamic instability =>
Albumin is more effective than saline.
 Lactate and other buffered fluids may be used in hepatic failure,
although their metabolism may be slowed in advanced liver disease.
 In decompensated liver disease with encephalopathy, raised ICP may
be present and osmotherapy, such as hypertonic saline or mannitol
should be used to bring plasma Na+ into the high-normal range.
 In chronic compensated liver disease, a degree of hyponatremia is well
tolerated and does not require acute correction.
GERIATRIC:
 Decrease in TBW, GFR, urinary concentrating ability, aldosterone, thirst mechanism, free-water
clearance.
 Increase in antidiuretic hormone (ADH), atrial natriuretic peptide (ANP)
 Renal capacity to conserve sodium is decreased.
 Tendency to lose sodium in the setting of inadequate salt intake.
 Decreased thirst response => risk for dehydration and sodium depletion.
 Diminished ability to respond to an increased salt load => increased Na+ retention during the
periop period.
 Volume expansion SHOULD BE DONE CAREFULLY
 BLOOD BY BLOOD in periop settings.
PEDIATRICS
 Holliday and Segar in 1957=> 4-2-1 volume calculation for maintenance fluid
requirements for
⚫ insensible losses and
⚫ urinary losses
 Glucose-based solutions intraop to reduce high risk for preop hypoglycemia after
prolonged fasting and
 Postop maintenance fluids based on the 4-2-1 calculation using hypotonic
crystalloids.
 Paeds population considered at risk for preop dehydration by fasting (limited urinary
concentrating ability and ongoing insensible losses because of large body surface
area.)
 Intraop replenishment of these volumes using isotonic salt solution
Re-evaluation
 Longer preop fasting discouraged carbohydrate-containing—fluids up to 2 hours
before surgery.
 Preop hypoglycemia incidence is infrequent (<2.5%) & related to
⚫ inappropriately prolonged fasting
⚫ premature infants,
⚫ neonates who are SGA, or
⚫ those with poor nutritional status.
 Surgery + Glucose-containing solutions => hyperglycemia => Complications
⚫ osmotic diuresis
⚫ electrolyte abnormalities => adverse neurologic outcomes (ischemia or hypoxia)
 Glucose-free balanced crystalloid solutions should be used intraop, except in those at
particularly high risk for hypoglycemia.
 Surgical stress and presence of pain and hypovolemia => SIADH => water retention and
hypoosmolar hyponatremia with hypotonic solutions in significant volumes.
 Proposed strategies to avoid this
⚫ Using half to two thirds of calculated 4-2-1 formula maintenance fluids,
⚫ Avoiding the hypotonic fluids (4% dextrose with 0.18% NaCl)
⚫ Returning to oral fluids as early as possible
⚫ Ensuring euvolemia to minimize the ADH response
⚫ Not confusing maintenance requirements with ongoing losses (e.g., GI or blood),
which should be replaced by isotonic crystalloids, colloids, or blood
⚫ Checking electrolytes at least daily in those still receiving IV fluids.
 Isotonic saline “safer” for postop maintenance, but risk of Na+ overload and
hyperchloremic acidosis.
 Dearth of data on colloid volume expansion and goal-directed fluid therapy.
FLUID THERAPY IN IMPORTANT
MAJOR SURGERIES/
SURGICAL FACTORS
TRAUMA
 Goal=> Hemostasis then restoration of normal circulating volume and tissue perfusion
 Permit hypovolemia to achieve cerebration rather than normotension, maintain SBP of
⚫ 70 to 80 mm Hg in penetrating trauma, or
⚫ 90 mm Hg in blunt trauma.
 Rapid radiologic or surgical damage control intervention.
 Large volumes of IV crystalloids or colloids in early resuscitation will cause hemodilution and dilute
clotting factors, and saline-based fluids may aggravate the acidosis .
 pRBCs, FFP and platelets replaced early. “High” ratios of FFP to pRBC (e.g., 1:1 to 1:2) are
associated with the best outcomes
 Avoidance hyponatremia and hypoosmolality to minimize cerebral edema in isolated head
injuries with a MAP >90 mm Hg.
FREE TISSUE FLAP SURGERY
 Flap blood flow depends on
⚫ systemic blood pressure
⚫ blood viscosity
 Hypervolemic hemodilution has traditionally been used
 Conservative fluid strategy improves flap outcome by avoiding
reduction in O2 carrying capacity and potential for flap edema
 Large volumes of crystalloid — favoring increased capillary filtration —
AVOIDED and colloids used for blood volume expansion.
MAJOR INTRAABDOMINAL SURGERY
 Fluid losses during surgery are caused by
⚫ prolonged peritoneal exposure,
⚫ significant blood loss, and
⚫ acute drainage of tumor-related ascites.
 Difficult to quantify, so cardiac output monitoring, CVP, arterial pressure monitoring
and serial blood gas analysis is valuable.
 Intraoperative drainage of ascites may require large volumes to replace the ongoing
loss.
 Consequence of fluid redistribution is electrolyte abnormalities; e.g. hypokalemia
and hypomagnesemia .
LIVER TRANSPLANT
 Guided by invasive monitoring like pulmonary artery catheterization.
⚫ During phase I (preanhepatic), large-volume blood loss and fluid shift resulting from
drainage of ascites.
⚫ During phase II (anhepatic) a major reduction in venous return and CO if the IVC,
portal vein, and hepatic artery are cross-clamped. Crystalloid and colloid infusion
required with vasopressors to maintain arterial pressure.
⚫ Phase III (reperfusion) acute rise in CVP, hepatic congestion and right heart strain.
Systemic vasodilation and cardiac suppression leads to hypotension requiring
vasopressor or inotrope. Fluids should be restricted
 Ongoing infusion of fluids, red cells, and blood products should be guided by clinical
blood loss, maintaining a hematocrit of 26% to 32% .
LIBERAL VERSUS RESTRICTIVE TRANSFUSION STRATEGY
 Restrictive policy = BT only when the Hb value is 7 to 8 g/dL or less.
 Liberal policy = BT when the Hb value is 9 to 10 g/dL or greater.
 If no clinical advantages with the liberal transfusion policy, perhaps the restrictive
approach should be used.

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word 2.pptx

  • 1. GOAL-DIRECTED THERAPY  Goal – improved tissue perfusion and clinical outcome  Based on measuring key physiologic variables ⚫ Cardiac output or ⚫ Global O2 delivery  Achieved with administering fluids, and possibly inotropes, vasopressors, vasodilators, and RBCs  Targets are defined physiologic endpoints and not dependant on objective assessments of fluid status.
  • 2. TARGETS FOR GOAL-DIRECTED THERAPY ARE AS FOLLOWS:  Arterial blood pressure and waveform analysis (MAP >65 mm Hg)  CVP (8-10 cm H2O)  Echocardiography (No regional wall motion abnormalities)  Lactate (<2.0 mmol/L)  O2 extraction and venous O2 saturation (SvO2) or central venous saturation (ScvO2)
  • 4. HEART FAILURE  Goals => Preserve CO, preload, contractility, and afterload.  Ventricles poorly compliant and require adequate preload and adequate diastolic filling time.  Excessive volume infusion and preload => Impaired contractility and worsening CO  Invasive monitoring with either EDM/ PAC for fluid therapy  Restrictive Fluid therapy or GDT is preferred.  Striking a balance between hypovolemia and hypervolemia is particularly important in patients with heart failure,
  • 5. KIDNEY DISEASE  Preop assessment should focus on ⚫ the adequacy of chronic dialysis in attaining euvolemia, and ⚫ estimating the normal volume of native urine output.  Comorbidities should be assessed and optimized.  Surgery undertaken in a facility where preop and postop dialysis or hemofiltration done.  In elective surgery, preop dialysis timed such that the patient enters the intraop phase with a normal blood volume
  • 6.  Hypervolemia => risk for pulmonary and peripheral edema, hypertension, and poor wound healing.  Hypovolemia => risk for anesthesia-related hypotension and inadequate tissue perfusion.  Dialysis the day prior to allow equilibration of fluid and electrolyte.  Electrolytes on the morning of surgery ( ideal K+ value after dialysis is low-to- normal range. )  In emergency surgery, NO sufficient time for dialysis, electrolyte abnormalities must be managed conservatively, intraop fluid balance.
  • 7. UPPER GASTROINTESTINAL LOSS  Progressive dehydration => Increased aldosterone secretion => Na+ is retained at the expense of K+ and H+ ions, (hypokalemia, and metabolic alkalosis with a paradoxically aciduria)  Correction => Gradual rehydration with isotonic saline and K+ supplementation and changing to dextrose- containing saline depending on electrolyte analysis.
  • 8. SEPSIS AND ACUTE LUNG INJURY  The pragmatic targets for patients with sepsis who have tissue hypoperfusion (blood lactate conc. at or >4 mmol/L) or hypotension persisting after Initial IV fluid Challenge: ⚫ CVP 8 to 12 mm Hg (12 to 15 mm Hg in patients on Ventilation) ⚫ MAP 65 mm Hg or greater ⚫ Urine output 0.5 mL/kg/hr or greater ⚫ ScvO2 > 70% (or mixed venous O2 saturation > 65%)
  • 9.  Current recommendations to attain these goals ⚫ 30 mL/kg of suitable crystalloid ⚫ Albumin along with vasopressors and inotropes ⚫ RBC transfusion.  Patients with establishedARDS for surgical procedures. ⚫ Focus of fluid therapy is the fine balance between avoiding an increase in lung edema while maintaining adequate tissue perfusion. ⚫ Early goal-directed fluid therapy may prevent ALI/ARDS ⚫ In established ALI/ARDS a fluid-conservative approach is the minimum requirement
  • 10. BURNS  IV fluid therapy is generally instituted for burns of greater than 15% total body surface area in adults and 10% total body surface area in children  Parkland Burn Fluid Resuscitation Formula First 8 hours: 2 mL/kg × % TBSA (lactated Ringer solution) Next 16 hours: 2 mL/kg × %TBSA (lactated Ringer solution) Next 24 hours: 0.8 mL/kg × %TBSA (5% dextrose) + 0.015 mL/kg × %TBSA (5% albumin)
  • 11.  Down-titration of fluid volumes if UO is adequate (0.5 to 1 mL/kg/hr)  Excessive fluid administration (“fluid creep”) may cause ⚫ Pulmonary edema ⚫ Fasciotomies in nonburned muscle compartments ⚫ Raised IOP ⚫ Conversion of superficial to deep burns ⚫ Intraabdominal hypertension and compartment syndrome  Haifa formula (New Practice) ⚫ Plasma (cc) - 1.5 x % TBSA x body weight (kg) + RL (cc) - 1 x % TBSA x body weight (kg). ⚫ Half fluid in first 8 hr and the other half in the next 16 hr ⚫ In the subsequent 24 hr, we give half the amount estimated for the first day. ⚫ The sufficiency of the fluid is judged mainly on the basis of urine output.
  • 12. HEPATIC FAILURE  Progressive liver disease and cirrhosis cause ⚫ peripheral vasodilation and ⚫ relative intravascular depletion (total body Na+ and water are retained with ascites and edema )  Aim is reduction of total body salt and water [dietary fluid and salt restriction, diuretics (spironolactone and loop diuretics), and intermittent or continuous drainage of ascites]  Excessive isotonic saline => salt and water overload=> further ascites and edema formation.  Approach => Assess volume status and replace losses with appropriate volumes of isotonic crystalloid, colloid, or blood but avoid salt and water overload.
  • 13.  Large-volume (>6 L) ascites drainage => hemodynamic instability => Albumin is more effective than saline.  Lactate and other buffered fluids may be used in hepatic failure, although their metabolism may be slowed in advanced liver disease.  In decompensated liver disease with encephalopathy, raised ICP may be present and osmotherapy, such as hypertonic saline or mannitol should be used to bring plasma Na+ into the high-normal range.  In chronic compensated liver disease, a degree of hyponatremia is well tolerated and does not require acute correction.
  • 14. GERIATRIC:  Decrease in TBW, GFR, urinary concentrating ability, aldosterone, thirst mechanism, free-water clearance.  Increase in antidiuretic hormone (ADH), atrial natriuretic peptide (ANP)  Renal capacity to conserve sodium is decreased.  Tendency to lose sodium in the setting of inadequate salt intake.  Decreased thirst response => risk for dehydration and sodium depletion.  Diminished ability to respond to an increased salt load => increased Na+ retention during the periop period.  Volume expansion SHOULD BE DONE CAREFULLY  BLOOD BY BLOOD in periop settings.
  • 15. PEDIATRICS  Holliday and Segar in 1957=> 4-2-1 volume calculation for maintenance fluid requirements for ⚫ insensible losses and ⚫ urinary losses  Glucose-based solutions intraop to reduce high risk for preop hypoglycemia after prolonged fasting and  Postop maintenance fluids based on the 4-2-1 calculation using hypotonic crystalloids.  Paeds population considered at risk for preop dehydration by fasting (limited urinary concentrating ability and ongoing insensible losses because of large body surface area.)  Intraop replenishment of these volumes using isotonic salt solution
  • 16. Re-evaluation  Longer preop fasting discouraged carbohydrate-containing—fluids up to 2 hours before surgery.  Preop hypoglycemia incidence is infrequent (<2.5%) & related to ⚫ inappropriately prolonged fasting ⚫ premature infants, ⚫ neonates who are SGA, or ⚫ those with poor nutritional status.  Surgery + Glucose-containing solutions => hyperglycemia => Complications ⚫ osmotic diuresis ⚫ electrolyte abnormalities => adverse neurologic outcomes (ischemia or hypoxia)  Glucose-free balanced crystalloid solutions should be used intraop, except in those at particularly high risk for hypoglycemia.  Surgical stress and presence of pain and hypovolemia => SIADH => water retention and hypoosmolar hyponatremia with hypotonic solutions in significant volumes.
  • 17.  Proposed strategies to avoid this ⚫ Using half to two thirds of calculated 4-2-1 formula maintenance fluids, ⚫ Avoiding the hypotonic fluids (4% dextrose with 0.18% NaCl) ⚫ Returning to oral fluids as early as possible ⚫ Ensuring euvolemia to minimize the ADH response ⚫ Not confusing maintenance requirements with ongoing losses (e.g., GI or blood), which should be replaced by isotonic crystalloids, colloids, or blood ⚫ Checking electrolytes at least daily in those still receiving IV fluids.  Isotonic saline “safer” for postop maintenance, but risk of Na+ overload and hyperchloremic acidosis.  Dearth of data on colloid volume expansion and goal-directed fluid therapy.
  • 18. FLUID THERAPY IN IMPORTANT MAJOR SURGERIES/ SURGICAL FACTORS
  • 19. TRAUMA  Goal=> Hemostasis then restoration of normal circulating volume and tissue perfusion  Permit hypovolemia to achieve cerebration rather than normotension, maintain SBP of ⚫ 70 to 80 mm Hg in penetrating trauma, or ⚫ 90 mm Hg in blunt trauma.  Rapid radiologic or surgical damage control intervention.  Large volumes of IV crystalloids or colloids in early resuscitation will cause hemodilution and dilute clotting factors, and saline-based fluids may aggravate the acidosis .  pRBCs, FFP and platelets replaced early. “High” ratios of FFP to pRBC (e.g., 1:1 to 1:2) are associated with the best outcomes  Avoidance hyponatremia and hypoosmolality to minimize cerebral edema in isolated head injuries with a MAP >90 mm Hg.
  • 20. FREE TISSUE FLAP SURGERY  Flap blood flow depends on ⚫ systemic blood pressure ⚫ blood viscosity  Hypervolemic hemodilution has traditionally been used  Conservative fluid strategy improves flap outcome by avoiding reduction in O2 carrying capacity and potential for flap edema  Large volumes of crystalloid — favoring increased capillary filtration — AVOIDED and colloids used for blood volume expansion.
  • 21. MAJOR INTRAABDOMINAL SURGERY  Fluid losses during surgery are caused by ⚫ prolonged peritoneal exposure, ⚫ significant blood loss, and ⚫ acute drainage of tumor-related ascites.  Difficult to quantify, so cardiac output monitoring, CVP, arterial pressure monitoring and serial blood gas analysis is valuable.  Intraoperative drainage of ascites may require large volumes to replace the ongoing loss.  Consequence of fluid redistribution is electrolyte abnormalities; e.g. hypokalemia and hypomagnesemia .
  • 22. LIVER TRANSPLANT  Guided by invasive monitoring like pulmonary artery catheterization. ⚫ During phase I (preanhepatic), large-volume blood loss and fluid shift resulting from drainage of ascites. ⚫ During phase II (anhepatic) a major reduction in venous return and CO if the IVC, portal vein, and hepatic artery are cross-clamped. Crystalloid and colloid infusion required with vasopressors to maintain arterial pressure. ⚫ Phase III (reperfusion) acute rise in CVP, hepatic congestion and right heart strain. Systemic vasodilation and cardiac suppression leads to hypotension requiring vasopressor or inotrope. Fluids should be restricted  Ongoing infusion of fluids, red cells, and blood products should be guided by clinical blood loss, maintaining a hematocrit of 26% to 32% .
  • 23. LIBERAL VERSUS RESTRICTIVE TRANSFUSION STRATEGY  Restrictive policy = BT only when the Hb value is 7 to 8 g/dL or less.  Liberal policy = BT when the Hb value is 9 to 10 g/dL or greater.  If no clinical advantages with the liberal transfusion policy, perhaps the restrictive approach should be used.