(21) fluid theraphy - dr. pangku

Fluid Therapy

Dr. Pangkuwidjaja P

Exsanguination

Predictors of death

• Estimated blood loss > 5,000 mls• Red cell transfusion > 4,000 mls• Total blood transfusion > 5,000 mls

OR fluid transfusion > 12,000 mls• Transfusion rates > 12 mls/min

– pH < 7.2– Temp < 34ºC– HCO3 < 15 mmol/l

Trauma and surgery Alters volumes and composition of IC and EC

spaces

Therapeutic infusion further alters compartmental volumes

and composition

Emergency Resuscitation

• How much?

• What Fluid?

• Which Endpoints?

Goals of Fluid Administration

• Maintain good tissue perfusion• Maintain adequate oxygen delivery• Normal electrolyte concentration• Normoglycemia & pH

Goal of Fluid Resuscitation

↑ Cardiac Output↓Hb

DaO2

CO x CaO2

(Hb x SaO2 x 1,34) + (PaO2 x 0,003)

BP = CO x SVR

FLUID THERAPY

MaintenanceResuscitation

Electrolytes NutritionColloidCrystalloid

1. Replace acute loss (hemorrhage, GI loss, 3rd space, etc)

1. Replace normal loss (IWL + urine + faecal)

2. Nutrition support

Compartmental Distribution of Total Body Water

66% ICF

33% ECF

Intracellular Fluid28 L

Plasma 3L

Interstitial Fluid11 L

Total body water

70 kg male TBW 42 L

Water HomeostasisIngested fluids 1300Solid food 800Metabolic water 400

Skin 500Lungs 400

Urine 1500Faeces 100

ICF ECF

Solute Composition of Body Fluid Compartments

280 – 310 mOsm/l

Solutes Solutes

Na+ 10 HPO4- Na+ 140 Cl- 114K+ 150 SO4-- K+ 4 SO4--30Mg++ 4 HCO3-

Prot

Water Water

ICF ECF

Practical Fluid BalanceRule 1

Water without Na expands the TBW (enter both ICF & ECF in proportion to their initial volume)

H2O H2O H2O

ICF ECF


All infused Na+ can not gain access to the ICF because of the Sodium Pump

Na+

Na+

Na+

Na+

Na+

Na+

ICF ECFIsotonic = NO Water Exchange


Change in tonicity of Na solutions (relative to Plasma) causes water exchange

a. Hypotonic saline (¼NS)

Hypotonic = Water Exchange

H2O

Practical Fluid Balanceb. Hypertonic solution

Hypertonic = Water Exchange

Increase Plasma Volume (x times) the originally infused amount

from IFV & ICF

H2O

Dynamics of IV Fluids

• Water solution IntracellularlyAll hypotonic solutions e.g. 5% dextrose called as maintenance type of fluids

• Electrolyte solutionsInterstitial compartmentIsotonicCalled replacement of fluids

Electrolyte Contents

Solution

Electrolyte contents (mEq/l) + g/L

R/PlasmaOsmolarity(mOsmol.L-

1)Na

+Cl- K+ Ca2

+Glucose+ Lactate

Dextrose 5% (D5W)

50 Hypotonic 253

½ NS 77 77 Hypotonic 154

Lactated Ringer 130 109 4 3 28 !! Isotonic 273

N Saline 154 154 Isotonic 308

D5 ¼ NS 38.5

38.5 50 !! Hypotonic 335

D5 ½ NS 77 77 50 !! Hypotonic 432

3% S 513 513 Hypertonic 1026

Regulation of Extracellular Fluid Volume

Renal adaptation to hypovolemia

• Renal autoregulation↓/↑ renal afferent arteriolar resistance

• Reduction in RBF↑ renal afferent arteriolar resistance

redistributed from the kidney• Reduction in GFR• Increased tubular reabsorption


Vasoconstrictive factors• Renal sympathetic nerves• Angitensin II• Catecholamines

Vasodilatory factors• Intrinsic renal

autoregulation• Renal vasodilatory effect

of prostaglandins

Renal perfusion during hypovolemia


PV preservation:

↑ reabsorption of filtered water and NaADHAldosterone

hypoperfusion renin secretion↓ ANP

vasodilatory effect ↑ renal excretion of Na and water

Clinical Implications of Choices Between Crystalloid and Colloid

If membrane permeability intact

Colloids preferentially expand PV rather than IFPV expansion unaccompanied by IF expansion

lower fluid requirementsless peripheral and pulmonary edema accumulationreduce concern about later fluid mobilization

Crystalloids and colloidsCrystalloid Colloid

Intravascular persistance Poor Good

Haemodynamic stabilisation Transient Prolonged

Required infusion volume Large Moderate

Risk of tissue oedema Obvious Insignificant

Enhancement of capillary perfusion Poor Good

Risk of anaphylaxis Nil Low to moderate

Plasma colloid osmotic pressure Reduced Maintained

Cost Inexpensive Expensive

Persistence of Fluids in Circulation

• IMG_2009

Crystalloids (Hypertonic Saline)• Hypertonic Saline 3% and 7.5%

• Increase Plasma Volume from IFV & ICF

• Small Volume Resuscitation

H2O

estimate750 ml

250 ml

Clinical Implication of Hypertonic Fluid Administration

Hypertonic solutions may improveHemodynamics

Cerebral hemodynamicimpermeability of BBB to sodium in uninjured brain

cause brain to shrink in response to acute increase of NaMicrovascular perfusion

through PV expansion

To prolong the therapeutic effectcontinued infusionsubsequent infusion of blood or conventional fluids or addition of colloid

Evaluation of Intravascular Volume

• Physical Examination• Laboratory

Class I Class II Class III Class IV

Blood loss (ml) ≤ 750 750 - 1500 1500 – 2000 ≥ 2000

Blood loss (% of blood volume)

≤ 15 15 - 30 30 - 40 ≥ 40

Fluid replacement (3 : 1 rule)

crystalloid crystalloid crystalloid and blood

crystalloid and blood

Pulse rate < 100 > 100 > 120 ≤ 14

BP normal normal decreased decreased

Pulse pressure Normal or increased

decreased decreased decreased

Capillary refill test normal positive positive positive

Respiratory rate (bpm) 14 – 20 20 – 30 30 – 40 > 35

Urine output (ml/h) ≥ 30 20 - 30 5 - 15 negligible

Mental status sl. anxiety Mild anxiety anxious or confused

confused or lethargic

Hemodynamic ParametersParameter findings Comment

HR Increase

BP Decrease

CVP Decrease < 5 mmHg

Fluid Challenge (250 ml) Increase > 1 – 2 mmHg> 5 mmHg> 12 mmHg (rule out RV dysfunction)

PAOP Decrease < 8 mmHg> 12 mmHg (rule out LV dysfunction)

Laboratory Signs of DehydrationTest Findings

HCT Increase M 0.4 – 0.55 F 0.36 – 0.47

pH < 7.36

Urine Specific Gravity > 1010

UO < 0.5 ml/kg/h

Urinary Sodium < 10 mEq/L

Urinary Osmolality > 450 mOsm/kg

Blood Na+ > 145 mEq/L 133 – 148 mEq/L

BUN/creatinine > 10:11

Delay, not reliable

Surgical Fluid RequirementsSurgical patients require:

replacement of PV and ECFmust compensate for the acute reduction of

functional IF3rd space loss

Degree of Tissue Trauma Fluid Requirement

Minimal (e.g. hemiorraphy) 0-2 ml/kg/hr

Moderate (e.g. cholecystectomy)

2-4 ml/kg/hr

Severe (e.g. bowel resection)

4-8 ml/kg/hr

Blood Replacement Therapy

Replacing Blood Losses

Maintain normovolemia

till the danger of anemia outweighsthe risk of transfusion

ie. 7-8 Gm/dl (HCT of 21-24%)

Crystalloid or

Colloids

Replacing Blood Loses (Vol)

Patients with normal HCT should only be transfused after 10-20% loss of blood volume

One unit of blood pack cellsIncreases Hb by 1 gm/dlOr HCT by 2-3%

10 ml pack cells/kgIncreases Hb by 3 gm/dlOr HCT by 10%

Estimated Blood Volumes

Age Blood volume

Neonates Premature 95 mL/kg

Full term 85 mL/kg

Infants 80 mL/kg

Adults Men 75 mL/kg

Women 65 mL/kg

Replacing Blood Loses (HCT)An 85 kg woman has a preoperative HCT 35%.How much blood loss to decrease her HCT to 30%?

Estimate blood volume 65 ml X kg 85 = 5525 ml

Estimate RBCV at preoperative HCT RBCV preop 5525 X 35% = 1934 ml

Estimate RBCV at HCT 30% RBCV 30% 5525 X 30% = 1658 ml

Calculate RCV lost when HCT 30%RBCV lost = RBCV preop – RBCV 30%

1934 – 1658 = 267 ml

Allowable blood loss = RBCV lost X 3 267 X 3 = 801 ml

Evolution of Transfusion Practices

• 10 ε 30 rule• AIDS

A patient specific approach to the decision to transfuse blood components

RBC transfusion threshold

The rationale??? What Hgb/Hct level poses greater risk to the patient than

the threat of contacting a transfusion-transmitted disease

• greater degrees of anemia could be well toleratedchronically anemic renal failure

• Jehovah’s witness

morbidity and mortality rates did not increaseuntil Hgb level fell below 7 g/dl


The rationale

Adverse physiologic effects of anemiaNo evidence that mild to moderate anemia impairs:

• Wound healingHct < 15

• Increases bleeding• Increases the length of hospital stay• Increases the frequency or severity of postoperative infection


The rationale

• The cause of anemia is thought to be more important in influencing the perioperative course than the severity of anemia

• Maintaining of blood volume was more critical than correcting anemia

RBC transfusion thresholdThe rationale• Goal:

to anticipate, on a patient-by-patient basis, the minimum Hgb level that will avoid organ damage due to O2 deprivation

Do2

Vo2

physiologic capacity for compensatory mechanism

• Decision:should be based upon the clinical judgment that oxygen-

carrying capacity of the blood must be increased to prevent Vo2 from outstripping Do2

Calculation of oxygen delivery (Do2)

Cao2 = Sao2 x Hg x 1.34 + Pao2 x 0.0031

Do2 = Cao2 x CO x 10

Calculation of oxygen consumption (Vo2)

Vo2 = CO x (Cao2 – Cvo2)

normal arteriovenous oxygen content difference is 5 vol%~ Svo2 = 75%

↑Vo2 :

sepsis

hyperthermia

↑ metabolic activity

hyperthyroidism

Oxygen extraction ratio

Fraction of total oxygen delivered is consumed or extracted by the tissues

ER = Vo2 / Do2

= [CO x (Cao2 – Cvo2)] / Cao2 x CO= (Cao2 – Cvo2) / Cao2

Oxygen extraction ratio

Global ≠ Regionalnormal global oxygen delivery may occur in spite of critical levels of regional ischemia

Svo2:vo2 of many vascular beds (global)

heart, under basal condition : 55 – 70%kidney and skin : 7 – 10%

organ with the greatest ER will have the least O2 reserve

Compensatory mechanisms during anemia

• Increased cardiac output• Redistribution of cardiac output• Increased oxygen extraction• Changes in Oxygen-Hemoglobin affinity


Increased cardiac outputWith isovolemic hemodilution

↑ SV↓ SVR

vascular toneviscosity

ageacute or develops slowly

self correcting ↓ oxygen carrying capacity ↑ oxygen transport


Redistribution of cardiac output to organ with greater O2 requirement (brain and heart)

The hearthas a high extraction ratio must rely upon redistribution blood flow to ↑ O2 supply

greatest risk !!!


Increased oxygen extraction

Play an important adaptive rolewhen the normovolemic Hct drops below 25%

↓ mixed venous oxygen saturation

Organs with high ER under basal condition limited capacity to increase Do2 by this mechanism


Changes in Oxygen-Hemoglobin affinity

The sigmoid-shaped oxygen-Hemoglobin dissociation curve:P50 for normal adult Hgb at 37ºC and a pH of 7.4 : 27 mmHg

Left-shiftinghypothermia, alkalosis

Hgb molecule is more ‘stingy’ and requires lower Po2 to release O2 to tissues

Hgb molecules does not release 50% of its O2 until ambient Po2 less than 27 mmHg


Changes in Oxygen-Hemoglobin affinity

When anemia develops slowlythe affinity of Hgb for O2 may be decreased (right-shifted)

accumulation of 2,3 - DPG

Hypovolemic anemia vs Acute blood loss

Acute blood lossstimulation of adrenergic nervous system vasoconstriction and tachycardia! Increased CO does not contribute

Chronic anemiaCO may not change until Hgb decreases to 7 – 8 g/dlsynthesis of supranormal level of 2,3 – DPG begin at Hgb 9 g/dl right shifted

Establishing the RBC transfusion threshold

Transfusion ‘trigger’the Hgb or Hct threshold that justifies RBC transfusion for individual patient

it is presumed that the benefits of RBC transfusion outweigh the risks

• No single criterion could replace clinical judgment as the basis of decision-making

• No evidence that mild-moderate anemia contribute to perioperative morbidity

NIH – Consensus conference on Perioperative Red Cell Transfusion 1988

Establishing the RBC transfusion threshold

Guide therapyclinical assessmentHgb valueLaboratory data (when indicated)

arterial oxygenationmixed venous oxygen tensioncardiac outputoxygen extraction ratioblood volume

estimation of the patient’s myocardial/coronary reserve !!!

Condition that may decrease tolerance for anemia and influence the RBC transfusion threshold

Increased oxygen demandHyperthermiaHyperthyroidismPregnancy

Limited ability to increase COCoronary artery diseaseMyocardial dysfunction (infarction, cardiomyopathy)β-adrenergic blockade

Inability to redistribute COLow SVR state (sepsis, post-CPB)Occlusive vascular disease (cerebral, coronary)

Left shift of O2-Hgb curveAlkalosisHypothermia

Abnormal HemoglobinsPresence of stored Hgb (decreased 2,3-DPG)Hgb S

Acute anemia (limited 2,3-DPG compensation)Impaired oxygenation

Pulmonary diseaseHigh altitude

Target Hemoglobin concentration (g/dl)

4 6 8 10 12

High Risk•Atherosclerotic vasc. Dse•Perioperative ischemia•Pulmonary dse•Rapid blood loss•Anticipated post-op blood loss

Low Risk•Younger patient•Slower blood loss•Chronic anemia•Temporary intra-op hypothermia or hemodilution

PatientConsent

Acute Blood loss and hypovolemia

What donor blood group type may be compatible for transfusion to a particular recipient ?

Focus on which antibodies will be present in the recipient serum !!!reaction of these antibodies with donor RBC antigens

can activate complement hemolysis of RBC

Type O-negative blood universal donorsType AB-positive blood universal recipients

Compatibility testingThe cross-match

Donor RBCs mixed with recipient serumstimulating the actual anticipated transfusion

3 phases1. Immediate phase2. Incubation phase3. Antiglobulin phase

Is cross-match necessary?ABO-Rh status alone 99.8% compatibleWith antibody screen 99.94% compatibleWith complete cross-match 99.95% compatible

Those who have not previously exposed or pregnant

incompatibility : 1 in 1000Those who have previously exposed or pregnant

incompatibility : 1 in 100

Type and Screen orders• When blood is ordered preoperatively for surgical cases in which

transfusion is unlikely• If the need arises the blood can be cross-matched prior to

transfusion

Advantages:• If the blood is not needed

the additional expenses for cross-match is eliminated• If cross-match is performed and compatible unit identified

those unit are held in reserve temporarily out of blood supply if the blood is not used

wastage by outdating

Risk of blood product administration

1. Problems related to blood storage2. Problems related to immune-mediated

transfusion reaction3. Infectious risks


Problems related to blood storage

• Citrate intoxicationCitrate prevent coagulation of stored blood

by chelating ionized Calciumlarge volume (>1 blood volume)administered rapidly (> 1 ml/kg/minor 1 unit/5 mins)impaired liver function temporary reduction of ionized Ca levels

Signs:hypotensionnarrow pulse pressure↑ VEDP↑ CVPECG

prolonged QT intervalwidened QRS complexesflattened T waves



• Acid-base ChangesCPD ↓ pH to 7.0 – 7.1during storage

ongoing metabolism of glucose to lactate production of CO2

Citrate metabolized to bicarbonate

• Decreases in 2,3-DPGleft shift of O2-Hgb dissociation curve

less efficient O2



• Hyperkalemiato maintain electrochemical neutrality

H+ generated during storageRBCs lysis

with normal infusion rate K+ is distributedrates > 90 – 120 ml/min hyperkalemia

aggravated byhypovolemiahypothermiaacidosis



• Hypothermiafrom rapid transfusion of large volumes of cold blood

stored at temp 1 – 6ºC

↓ COtissue perfusion impaired

vasoconstrictionleft-shifting of O2-Hgb dissociation curve

metabolic acidosisshivering

↑ O2 consumption by 300-400%hemostatic dysfunctioncitrate toxicityventricular irritability



• Dilutional coagulopathyplateletsclotting factors

V and VIII

Immediate Hemolytic Transfusion Reactions

hemolysis release hemoglobin to the blood

renal damage↓ renal blood flowmechanical obstruction in the renal tubule

free Hgb, RBC stromadeposition of antigen-antibody complexes (G)deposition of fibrin (DIC)

Signs and symptomsfever, chill, nausea and vomitinghypotension and tachycardiaflushed and dyspneicchest and back painrestlesshemoglobinuriadiffuse bleedingrenal failure

Massive Blood Transfusion

≥ one blood volume< 24 h

• Coagulopathy• Hypothermia• Citrate toxicity• Hyperkalemia• ↓ 2,3 DPG

Emergency Transfusion

Choices:• Type-specific partially cross-matched blood• Type-specific uncross-matched blood• O-negative (universal donor) PRBCs

O-negative (universal donor) whole blood

contains high titers of antibodies

(21) fluid theraphy - dr. pangku

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