신촌세브란스마취통증의학과 R3 강승연

VO2 = MRO2 36 ATP molecules/ mole glucose

VO2 < MRO2 2 ATP + lactate

Maintain aerobic metabolism !!!

Oxygen delivery (DO2) Amount of O2 delivery to the tissue CO x Hb x 1.34 x SaO2 x 10 Augment C/O Correct Hb Correct SaO2 Maintain BP

Major determinent of O2 delievery

Stroke volume x Heart rate Stroke volume Preload Afterload Contractility

Oxygen consumption (VO2) Arterial O2 delivery – venous O2 delivery (SaO2 – SvO2) Normal SaO2 100%, SvO2 75% Normal O2 extraction: 25% DO2 decrease, O2 extraction increases Maximal of O2 extraction: 50% A decrease in SvO2 to 50%: impending

dysoxia

Decrease in O2 delivery Decrease in Hb Decrease in Arterial O2 saturation (SaO2) Decrease in cardiac output (C/O) Increase in O2 consumption Fever Seizure Shivering Increase work of breathing

Maldistribution of blood flow related to sepsis

Wedge PA catheter

Progressive hypovolemia DO2 ↓ VO2↔ : compensated hypovolemia

D/T Increase in O2 extraction from capilarry

When O2 extraction maximal (50%) VO2 begins to decrease

Onset of unaerobic metabolism, hypovolemic shock

Arterial base deficit and arterial lactate Marker of impaired tissue oxygenation

50% of the body Wt in healthy adults. Volume of total body fluid: 60% LBW in male,

50% LBW in female Blood: 11~12% of total body fluid. Compensatory response of blood loss1)Movement of interstitial fluid up to 15% of blood volume, remain ISF volume deficit2)RA system activation: Na conservation throughout ECF3)Bone marrow: RBC production (~ 2 months) When blood volume loss exceed 15%,

volume replace is necessary.

Class I : loss of 15% or less Fully compensated by capillary refill, Clinical finding with in normal range Class II : loss of 15 to 30% Orthostatic change in HR and BP, Sympathetic vasoconstiction, Urine output decreased, splanchnic hypoperfusion Class III : loss of 30 to 40 % Can not maintain BP and organ perfusion, Impending hypovolemic shock, Systemic vasoconstriction attenuated Class IV : loss of more than 40% Hypotension and oliguia is profound, Irriversible changes

CVP , PCWP Poor correlation between ventricular filling

pressure and ventricular volume -> due to ventricle compliance Cardiac filling pr overestimate the

intravascular volume in hypovolemic pt The cardiac filling pr provide qualitative

information about the general state

EDVI> 138 mL/m2 : no volume resuscitation need< 90 mL/m2 : need volume infusion

SVV (sensitivity, specificity 60 ~70%)> 10 % : volume deficiency status

Mortality in hypovolemic shock directly related to magnitude and duration of organ hypoperfusion

Prompt volume replacement is hallmark of success Rate of volume infustion is determined by

dimenstion of vasclular catheter, not size of the vein

Q = ∆P(πr4/8μL) Rapid volume resucitation, cannulation of peripheral

vein with short catheters is preferred to large central vein with long catheters.

Flow capability is determined by viscosity

Viscosity is a function of cell density (Water = 5% Albumin)

First priority in the bleeding pt is to support cardiac output (VO2 = C/O x 13.4 x Hb x [SaO2 – SvO2])

Infusion volume Colloid > Whole blood> P-RBC

Blood is not the fluid of choice for early resuscitation in acute blood loss (decrease c/o)

Tomato kechap vs Tomato juice

Cardiac index = 3 L/min/m2

Systemic O2 delivery (DO2) > 500 mL/min/m2

Systemic O2 uptake (VO2) > 100 mL/min/m2

Arterial lactate < 2 mmol/L

Base deficit > -2 mmol/L

Rapid restoration of tissue perfusion is the most important goal

Estimate current volume status ! always know fluid in and fluid out Estimate current blood loss ! Wt based estimates (LBW) Calculate the volume deficit Volume deficit = normal blood volume x % volume loss Determine the resuscitation volume for each type

of fluid Whole blood: 100%, Colloid: 50 ~ 75%, Crystalloid: 20 ~ 25% Check Albumin ! Check BE-ECF, Lactate, Urine output ! Tapering Vasopressors V/S, LAB data

Same viscosity (both are cell-free fluids) Crystalloid 20% remain in the vascular space and add to interstitial fluid by 80% (d/t Na distribute evenly in the ECF)

Colloid remain 75~80% in the vascular space and add to plasma volume in few hours

(▲ preload – volume , ▼ afterload – dilutional viscosity)

3 to 4 times Crystalloid = colloid Survival benefit is similar

Normal saline contain 58 g NaCl/ L 0.9% NaCl contain 9 g NaCl /L Higher Na (154 vs 140 mEq/L) Higher Cl (154 vs 103 mEq/L) Lower pH (5.7 vs 7.4) Higher osmolality (308 vs 290 mOsm/L) Metabolic acidosis (Hyperchloremic acidosis)

DDx with lactic acidosis is important!

Contain K and Ca For electrical neutrality: Na is reduced to 130 mEq/L Lactate: buffer for metabolic acidosis Chloride is reduced (d/t lactate) Ca can bind to drugs and citrates (P-RBC anticoagulant) Amiocaproic acid (Amicar), Amphotericin, Ampicillin

and Thiopental should not mix with. H/S not exceeding 50% mix with P-RBC no clot formation 25% Crystallod remain in the vascular space -> no impact on serum lactate levels

Provide calories, Protein sparing effect 1 Gram = 3.4 Kcal, 5% DW (50 g/L) = 170 kcal/L

Predominant cellular swelling effect Metabolic acidosis rather than Energy

production when shock ( 85% glucose -> lactate )

Adverse effect of hyperglycemia Immune suppression, infection risk, ischemic brain injury,

increase mortality

Colloid osmotic pressure 25 mmHg in the upright, 20 mmHg in the supine position More effective expanding plasma volume large, poorly diffusible solute molecule (starling forces)

Large proteins (Albumin) create osmotic pressure 70% : plasma, 30%: ISF 3 times more volume expanding effect than crystalloid Higher colloid osmotic pr, Greater increase in

plasma volume ( Voluven vs Pentaspan) 25% Albumin: increase 3~4 times volume infused

Synthesize continuously by the Liver 120 gram in plasma, 160 gram in the ISF. Principal transport protein and responsible 75%

colloid osmotic pressure in plasma. Buffer, Antioxidant activity Maintain blood fluidity ( inhibiting PLT agg ) Heat-treated preparation of human albumin (5%, 25%)

5% Albumin 20 mmHg colloid osmotic pressure, same as plasma 70% remain in the plasma, dissipate thereafter, Effective duration: 12 hours

25% Albumin hypertonic, 3~4 times increase volume Should not be use as volume expander ( merely shift body fluid )

Chemically modified starch polymer 6% solution in isotonic saline 3 types High MW (450000 dalton), medium (200000 dalton), low (70000 dalton)

High MW greatest oncotic pr, Highest risk 6% HES = 5% Albumin as plasma expander (cost vs hemostasis risk) Inhibition Factor VII and VWF, Impair PLT

adhesion Predominant in High MW, less with medium and

absent with low MW

Limit the infusion volume less than 1500 mL in 24 Hrs

Avoid Coagulopathy ,VWF disease patients Starch hydrolysis by amylase, cleared by

kidney take several weeks, oncotic activity lost after 1 day

Macroamylasemia (▼amylase clearance), not Lipase

Chronic administration - Pruritis (d/t extravasation of starch) Contraindication in the traumatic, infection

patients

Maintain adequate oxygen delivery Normal electrolyte concentrations Normoglycemia The total fluid requirement Compensatory intravascular volume expansion +

Deficit + Maintenance + Loss + Third space

Evaporation from exposed viscera mainly water, electrolyte left behind, Need for water Evaporation proportional to temperature ,

exposed surface area and inversely humidity Excessive urine output (Diuretics, Glycosuria, DI)

replaced with solution base on urinary electrolytes (Na 50 ~ 100 mEq/L, K 20 ~60 mEq/L)

High metabolic demands High ratio of body surface area to weight 100 mL of water is required for each 100

calories of expending energy (4:2:1 regimen) MABL = EBV x (starting Hct – target Hct) Starting hematocrit Hct 20% well tolerate except premature,

cardio-pulmonary disease, term new born Below Hct 30% - incidence of apnea is high

Volume of PRBC = Desired Hct 935) – present Hct (20) x EBV

PRBC Hct (65%) FFP rate exceeding 1.0 mL/ kg/ min Severe ionized hypocalcemia and cardia depression

with hypotension ITP, Chemotherapy pt tolerate PLT

15,000/mm3, no need for PLT transfusion PLT 0.1 ~ 0.3 U/ kg

Arterial underfilling Hypotension -> systemic nervous ->RAS, vasopressin -> Na and water retension ->ascites, edema-> Increase abdominal pr -> renal perfusion decreased -> RAS activation Hypoalbuminemia Low systemic vascular resistance (endotoxemia, vasodilator neurotransmitter) High cardiac output Avoid increase interstitial fluid overload (lasix) Maintain normal potassium Maintain intravascular volume (albumin, inotropics,vasopressor)

Optimize cardiac preload Avoid over administration of sodium Diminish edema Correct common electrolytes Maintain intravascular volume without

expansion of ISF Favor colloid

Maintain cerebral perfusion pressure Avoid CVP elevation and Hypertension Prevention acute and large change in plasma

osmolality (Na 142 ~148 mEq/L ) Avoid Hyperglycemia ( 80~175 mg/dL ) Isotonic crystalloid and colloids Avoid hyponatremia

Avoid excessive ECF volume expansion Correct common electrolytes Maintain normal acid-base status Avoid hypotension Recent dialysis compromise electrolytes, volume

status (12 - 24 hrs later) Crystalloid replacement limited to 1~2 mL/Kg/Hr

Blood loss replace with Colloids and P-RBC Isotonic fluid without Potassium, reduced Chloride

and buffer 30% calculated maintain fluid (70% fluid required use in excreting solutes in kidney) pH, Na, K, Bicarbonate and glucose close

monitoring

Anemia shock ??? Blood save lives ? Anemia dose not compromise tissue oxygenation as

long as the intravascular volume (C/O) is maintained !!!

Until Hb 5 g/dL (JAMA 1998) No deterious effect on tissue oxygenation in Human Isovolemic anemia Increase tissue oxygenation ( paradoxic effect ) ▲tissue PO2 and ▲Ischemic skin lesion -> Skin flap

surgery

Definition: decrease O2 carrying capacity Decrease RBC volume Measured by chromium-tagged erythrocytes (not readily available)

Hb - Hct as a alternative indicator of anemia Hct influenced by plasma volume (e.g. position change)

Hemodynamically unstable, fluid status as well

Hypoalbuminemia

IV infusion and diuretic

Hb - Hct is unreliable marker of anemia

Use of Hct to estimate acute blood loss is unreliable and inappropriate (ATLS manual 1989)

Acute blood loss is whole blood not P-RBC -> Decrease plasma and RBC proportionally. Hct will not change significantly in the early period

after acute blood loss Decrease Hct in the early hours is the result of

volume resuscitation rather than blood loss Asanguinous fluid: Hct decrease Whole blood: Hct maintain P-RBC: Hct increase

O2 extraction up to 50% is maximum compensation – indicator marker for transfusion

Lower Hb level 7 g/dL as transfusion trigger, who do not have coronary a dz

Indicated when Hb less than 6 g/ dL, especially anemia is acute

RBC transfusion based on patient’s risk for Cx of inadequate oxygenation

Hb as a single “trigger” without consider physiologic, surgical factor is NOT recommended

Autologous blood, Normovolemic hemodilution may be beneficial

Ix of autologous is more liberal d/t less risk

Blood loss greater than 20% Hb less than 8 g/dL

Hb less than 10 g/dL with major disease (e.g. Emphysema, Ischemic heart dz)

Hb less than 10 g/dL with autologous blood Hb less than 12 g/dL and ventilator dependent

All blood containing erythrocytes are stored at 4℃, viable for 21 days

Anticoagulant preservatives: Citrate, Phosphate, Dextrose (CPD) - Adenine

Whole blood Contain average 510 mL

(blood + CPD solution)

P-RBC By centrifusing whole blood and removing 250 mL of plasma

supernatant Each unit contain 200 mL eythrocytes 50~100 mL of plasma

and CPD solution Hct 60 ~ 80%, Hb 23 ~ 27 g/dL, Hct 70% Albumin deficiency Leukocyte-poor Red cells Removal of the leukocytes History of febrile, nonhemolytic transfusion reaction Up to 30% of leukocyte remain Washed Red cells Washes with isotonic saline to remove leukocytes and

residual plasma Prevent allergic reaction caused by prior sensitization to

plasma proteins

Saline dilution P-RBC infusion rate: 1/3 of whole blood Only isotonic saline should be used as a diluent Blood filter Trap small clots and cellular debirs Should be replace periodically (every 4 packs) Pore size of 170 to 260 microns Blood warmers Reduce the viscosity of refrrigerated blood Increase infusion rates by 30 ~ 50% Prevention hypothermia Recommended temperature: 33℃ to 35℃ 37℃ or higher: hemolysis

Multi-donor PLT stored for 5 days 5 times higher sepsis incidence than 4 day stored PLT

Bacterial contamination: PLT m/c Bacterial growth related to storage

temperature ( 20℃ ~ 24℃ ) PLT stored at 4℃ 24-48 hr use only, not as effective as routine PLT

Should NOT be given to ITP, prophylactic massive bleeding, prophylactic after

cardiopulmonary bypass, TTP, HIT

Indications Prophylactic PLT transfusion is ineffective (e.g. ITP ) PLT below 50 x 109 / L Known PLT dysfx and microvasclular bleeding Severe thrombocytopenia (< 20,000 cell/mm3) and

Clinical sign of bleeding Use filter with pore size of 170 mm Increase 7000 ~ 10,000 PLT/ pack after 1 hr, Lasts 8 days 0.1 unit/kg will raise 20,000 PLT

Contain all the plasma proteins, F5 & F8 Infection risk Sensitization to foreign proteins Indications Urgent reversal of warfarin- 5 to 8 mL/kg Antithrombin III deficiency, Immunodeficiency Correction of coagulation factors TTP Massive transfusion (when F5, F8 less than 25%) Correction of microvascular bleeding, 1.5 times increase PT or PTT Should be given in calculated dose (30% of plasma

factors) – 10 to 15 mL/kg CIx for augment of plasma volume or Albumin

concentration

Factor VIII, Fibrinogen, Factor XIII Von Willebrand factor & Fibronectin VWF disease, Factor I deficiency FVIII: 5-10 unit FFP = 1 unit Cryoprecipitate Administer through filter and as rapidly as

possible (at least 200 mL/ Hr) Infusion should be completed within 6 hrs of

thawing 0.1 unit/kg is recommended initial doses

Who receives multiple unit of blood, few viable PLT exist (storage over 24 hrs)

10 to 15 unit of blood PLT 100,000/mm3

Old, smaller, preoperative smaller blood volume pt decrease more PLT

PLT should NOT be given as a lab data PLT less than 50,000/mm3 bleeding is d/t

dilutional thrombocytopenia & DIC

Most of factors are stable in store blood Exception is Factor V and VIII 5 to 20% of factor V and 30% of factor VIII

needed for hemostasis Massive transfusion rarely decrease below

20% Most important are volume of blood given,

duration of hypotension or hypoperfusion

Hypoxid acidotic tissue with stagnant blood flow release tissue thromboplastin

Release of tissue plasminogen activator Extrinsic route of coagulation activated by

TNF and endotoxin Intrinsic system contribute hypotension Consumption coagulation factor Fibrinolytic system activated Severity is based on patients’ underlying

disorder Initial antithrombin III best predictor of death in septic patients

Citrate + Calcium = Hypocalcemia Hypotension, Narrow PP, ↑IVEDP etc No vital change if volume is well maintained

and infusion rate less than 1 unit/ 5 mins

Hemodynamic unstable pt: ca decrease even more, not corrected by IV CaCl2

Hypothermia, Liver dz, Liver transplantation and Hyperventilation increase citrate toxicity

10% CaCl2 = 3 times 10% Calcium gluconate

Hyperkalemia Temperature Acid-base abnormality Infusion of microaggregates

Complications 2 ~ 4% Infection (HBV, HCV, HIV etc) Acute hemolytic reactions Febrile nonhemolytic reactions (PLT 30%) Allergic reaction Acute lung Injury (TRALI) FFP Immunomodulation (immunosupression)

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