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Estimation of Intravascular Flui

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Estimation of Intravascular Flui Powered By Docstoc
					      Estimation of
Intravascular Fluid Status
   and Organ Perfusion

      Mark Lepore, MD
       November 17 &
      December 3, 2008
              Objectives
• Background: Fluid Distribution in the Body
• Relationship of Intravascular Volume
  (Preload) to Perfusion of Organs
• How to Estimate Intravascular Fluid Volume
• How to Measure Organ Perfusion
• Fluid Options
• Illustrative Cases
               Objectives
• Background: Fluid Distribution in the Body
• Relationship of Intravascular Volume
  (Preload) to Perfusion of Organs
• How to Estimate Intravascular Fluid
  Volume
• How to Measure Organ Perfusion
• Fluid Options
• Illustrative Cases
          Total Body Water
• 60% of weight in young males
• 50% of weight in young females

• As age advances, there is less muscle
  mass, and therefore less total body water

• 50% of weight in elderly males
• 45% of weight in elderly females
     Serum Oncotic Pressure
• Primarily depends on 3 components:
  – Protein (―colloid oncotic pressure‖)
  – Sodium (plus other solutes to smaller
       extent)
  – Red Blood Cells
• Serum Osmolality Equation
  – Only looks at Solute
  – Calculated Serum Osm =
       2 [Na] + [Glucose]/18 + [BUN]/2.8
   Fluid compartments in the Body


Extracellular: 1/3         Interstitial                    In cells
                               3/4

                                                           In
                     Intravascular                         vessels
                           ¼
                                                           Inter-
                                                           stitial



                                      Intracellular: 2/3
  Cell Membrane Permeability
• Cell membranes are permeable to water
• Free Water may be administered either via
  the oral route or via IV as D5 Water
  (―D5W‖)
1 Liter of Water added to a patient


        249 ml
                         In cells

                         In
    87 ml                vessels
                 667ml
                         Inter-
                         stitial
  Cell Membrane Permeability
• Cell Membranes are generally
  IMPERMEABLE to Sodium
• Sodium is the major extracellular cation,
  where Potassium is the major intracellular
  cation
• Concentrations of Sodium/Potassium in
  the Extracellular/Intracellular
  Compartements are felt to be close to
  inverse.
1 Liter of Normal Saline Added to a
               Patient


                          In cells
      750 ml
                          In
                          vessels
                          Inter-
               250 ml     stitial
               Objectives
• Physiology of Fluid Distribution in the Body
• Relationship of Intravascular Volume
  (Preload) to Perfusion of Organs
• How to Estimate Intravascular Fluid
  Volume
• How to Measure Organ Perfusion
• Fluid Options
• Illustrative Cases
  Contractility/
   Inotropy          Stroke             Heart
                     Volume             Rate
     Preload

                              Cardiac           Afterload

                              Output

                      Adequacy of Oxygenation
                       of Blood (Hemoglobin)



                         Perfusion of
                           Organs
                                                            Oxygen
    Health of
                                                          Dissociation
Tissues to Utilize
    Available
                     Ability of Organs to               Curve—Ability to
                                                        Release Oxygen
    Oxygen             Utilize Oxygen                      at Tissues
                 Preload
• Preload = Left Ventricular End Diastolic
  Volume at the end of expiration
• Preload is the ―stretch‖ of the myocardium
  prior to systole
• In the face of NORMAL VALVES and
  NORMAL PULMONARY PRESSURES,
  right sided pressures/volumes may be
  indicative of left sided pressures/volumes
               Afterload
• Resistance against which the heart needs
  to pump to generate cardiac output
• Mediated by resistance in medium-sized
  arterioles
• Has much less to do with cardiac output
  than preload and contractility
  Contractility/
   Inotropy          Stroke             Heart
                     Volume             Rate
     Preload

                              Cardiac           Afterload

                              Output

                      Adequacy of Oxygenation
                       of Blood (Hemoglobin)



                         Perfusion of
                           Organs
                                                            Oxygen
    Health of
                                                          Dissociation
Tissues to Utilize
    Available
                     Ability of Organs to               Curve—Ability to
                                                        Release Oxygen
    Oxygen             Utilize Oxygen                      at Tissues
         Cardiac Output:
     The Frank-Starling Curve
                     160
                     140
Stroke Volume (ml)




                     120
                     100
                      80
                      60
                      40
                      20
                       0
                              0


                                      0


                                              0
                       50

                            15


                                    25


                                            35



                            End Diastolic Volume (ml)
Cardiac Output: Effects of Pressors
      and Negative Inotropes
                      180
                      160
                                                         Normal
 Stroke Volume (ml)




                      140                                Cardiac
                      120                                Function
                                                         Pressors/
                      100                                Positive
                       80                                Inotropy
                       60                                Depressed
                                                         Myocardial
                       40                                Function
                       20
                        0
                            50   150     250     350
                             End Diastolic Volume (ml)
               Objectives
• Physiology of Fluid Distribution in the Body
• Relationship of Intravascular Volume
  (Preload) to Perfusion of Organs
• How to Estimate Intravascular Fluid
  Volume
• How to Measure Organ Perfusion
• Fluid Options
• Illustrative Cases
  Contractility/
   Inotropy          Stroke             Heart
                     Volume             Rate
     Preload

                              Cardiac           Afterload

                              Output

                      Adequacy of Oxygenation
                       of Blood (Hemoglobin)



                         Perfusion of
                           Organs
                                                            Oxygen
    Health of
                                                          Dissociation
Tissues to Utilize
    Available
                     Ability of Organs to               Curve—Ability to
                                                        Release Oxygen
    Oxygen             Utilize Oxygen                      at Tissues
 ―Too Dry, Too Wet, or Just Right?‖
• This question needs to be answered daily
  for all patients in the ICU/hospitalized
• The question often arises in the face of
  decreased urine output, particularly in the
  ICU
• Its estimation is a clinical diagnosis
―Too Dry, Too Wet, or Just Right?‖
• Its estimation should rely on assessment
  of multiple data points at the same time;
  no one parameter/value can answer the
  question
• Data is often conflicting
• Volume status often changes from minute
  to minute and hour to hour
    Keys to Proper Estimation of
           Volume Status
• Correctly interpreting the data you have
• Pursuing more data when the answer is
  not clear
• Continuous re-evaluation of responses to
  the therapy that you give (e.g. fluid
  boluses or diuretics)
• Continuous re-evaluation of volume status,
  as it can change from minute to minute
Why is it so difficult in the ICU?
• Patients aren‘t able to regulate their own
  intake of fluids (non-intubated patients
  being kept NPO, intubated patients with
  variable input entirely controlled by
  medical team)
• Output of fluids is also often regulated
  through artificial means (renal replacement
  therapy (dialysis), diuretics)
 Why is it so difficult in the ICU?
• Many diagnostic tests are not valid in the ICU
  – Vital Signs (hypotension and tachycardia can occur
    with cardiogenic shock as much as they can occur
    with severe volume depletion)
  – Physical Exam (volume resuscitation causes edema
    even with intravascularly depletion; many reasons for
    tachycardia/tachypnea besides volume depletion, etc)
  – JVD (differential diagnosis includes increased
    intrathoracic pressures, SVC clot, pericardial effusion,
    tricuspid regurgitation)
  – Supine Chest X-ray (even upright doesn‘t help too
    much)
 Why is it so difficult in the ICU?
• Many diagnostic tests are not valid in the ICU
  – BNP (is nearly universally elevated in septic/ICU
    patients and turns out to be more of a prognosticator
    of mortality in the ICU than it is a measure of volume
    status (one study, only 16% of ICU patients had
    normal BNP; Median BNP for survivors was 378,
    Median BNP for non-survivors was 943)
  – However, a low BNP still has some value in ruling out
    fluid overload (<350 pg/ml has a >95% negative
    predictive value for cardiogenic shock)
  – CVP/PAWP (CVP is terrible unless extreme level;
    Wedge is better but can still be affected by pulmonary
    hypertension, valvular insufficiency)
Why is it so difficult in the ICU?
• Some data points can be abnormal in both
  severe volume overload and severe volume
  depletion
  – BUN:creatinine ratio >20:1
  – Urine Output < 30ml/hour
  – FeNa <1 or FeUrea<35 (severe overload and severe
    volume depletion can BOTH lead to decreased
    cardiac output and hypoperfusion of the kidneys)
  – BNP Elevation (elevated in all septic patients)
  An Approach to Estimation of
   Intravascular Volume Status:
―Too Wet, Too Dry, or Just Right?‖
INTRAVASCULAR
   DEPLETION
      Intravascular Depletion
• History
  – Infection present
  – Vomiting, diarrhea
  – Blood loss
  – s/p paracentesis or thoracentesis
  – etc.
      Intravascular Depletion
• Physical Exam:
• Interstitium
  – Poor skin turgor
  – Sunken eyes/fontanelle
• Intravascular
  – Hypotension
  – Orthostatic hypotension
  – Tachycardia
      Intravascular Depletion
• Labs
  – FeNa <1 **
  – BUN:creatinine>20:1 **
  – High Urine Specific Gravity **
  – Hemoconcentration
  – Markers of Infection (rising WBC, toxic
    granulations, left shift, elevated CRP)

  – Note: BNP<100 or pro-NT BNP<150
    essentially rule out overload but do not rule in
    volume depletion
      Intravascular Depletion
• Fluid balance negative overall with
  worsening clinical status (over prior hours
  to weeks)
      Intravascular Depletion
• Invasive Hemodynamics (if needed)
  – CVP<3-5 is suggestive but not diagnostic (not
    reliable, especially with high PEEP)
  – Pulmonary Artery Wedge Pressure < 10 is
    also suggestive, depending on the clinical
    scenario
      Intravascular Depletion
• O2 Saturation or Arterial Line Waveforms
  rising and falling with respirations is
  indicative of significant variation in venous
  return with the respiratory cycle, and
  consistent with volume depletion
      Intravascular Depletion
• More measurable parameters of this change
  (―Dynamic parameters‖) are as follows, and
  are more reliable than static numbers :
  – ―Δ down‖= expiratory decrease in systolic
    pressure
  – ―Δ pulse pressure‖ = ―ΔPP‖ = respiratory changes
    in pulse pressure
  – ―Δ Right Atrial Pressure‖ = ―ΔRAP‖ = respiratory
    changes in right atrial pressure
  – ―Δ V peak‖ = respiratory changes in aortic blood
    velocity
    Positive and Negative Predictive
    Values of Dynamic Parameters
                    Best               PPV                 NPV
                    threshold
Δ down              5 mm Hg            95%                 93%

ΔPP                 13%                94%                 96%

ΔRAP                1 mm Hg            77-84%              81-93%

Δ V peak            12%                91%                 100%

PPV= Positive Predictive Value; NPV = Negative Predictive Value
EUVOLEMIA
              Euvolemia
• Normal Pulse and Blood Pressure
  compared with patient‘s baseline
• Urine output > 30ml/hour or
  >0.5ml/kg/hour
• Mentating
• No signs or symptoms of Volume
  Depletion or Volume Overload
INTRAVASCULAR
   OVERLOAD
       Intravascular Overload
• History
  – History of volume overload state
     • CHF
     • Cirrhosis
     • Nephrotic Syndrome
  – Recent transfusion, particularly of Packed
    Red Blood Cells
     • PRBCs have a Hematocrit of 60 to 70 and pull fluid
       into the vascular space better than any other fluid
         Intravascular Overload
• Physical Exam
• Intravascular
   – JVD, Hepatojugular reflex
   – S3 Gallop
   – Rales
• Interstitial
   – Peripheral edema
• ? Where
   – Moist mucus membranes
• Pulse and BP usually normal, but can have
  hypotension/tachycardia in cardiogenic shock
      Intravascular Overload
• Labs
  – BNP>500 or NT-pro-BNP>1000 to 1100 are
    suggestive of overload but are not reliable in
    the ICU patient
  – CXR (often supine)
       Intravascular Overload
• Fluid Balance positive with worsening
  clinical status (over prior hours to weeks)
      Intravascular Overload
• Invasive Hemodynamics
  – CVP >16 to 18 is suggestive but not
    diagnostic
  – Pulmonary artery wedge pressure >18 is the
    gold standard, but not reliable in Mitral
    Regurgitation or Pulmonary Hypertension or
    other clinical circumstances
            Echocardiogram
• Echocardiogram is a key tool to assess
  ventricular systolic and diastolic function
  – Systolic heart failure (Ejection Fraction <30%)
    signifies a dysfunctional pump and
    predisposes to volume overload and
    pulmonary edema
  – Diastolic heart failure (―heart failure with
    preserved ejection fraction‖) signifies impaired
    relaxation of the heart, predisposing to
    pulmonary edema with small changes in
    intravascular volume
       Echocardiogram (continued)
• Echocardiogram can be of significant help
  in determining fluid status at one moment
  in time
• Many of the parameters are measured by
  assessing flow across valves and between
  intracardiac chambers
  – Significant valvular stenosis or regurgitation
    may affect measurements
  – Significant pulmonary hypertension, estimated
    by degree of tricuspid regurgitation, can also
    be measured
      Echocardiogram (continued)
• Hyperdynamic systolic function (e.g. EF
  70% or higher) is consistent with
  intravascular depletion
• Absence of cardiomegaly, with a normal
  diastolic function, speaks against fluid
  overload
• Left Ventricular End Diastolic Area,
  measured over time, is an excellent way to
  assess fluid responsiveness (a technique
  sometimes used by TEE during
  anesthesia in unstable cardiac patients)
      Echocardiogram (continued)
• Focal wall motion abnormalities may be
  indicative of ischemia of those areas
  (within seconds of ischemia, affected
  areas cease to contract normally)
        Echocardiogram (continued)
• ―As [echocardiogram is] very sensitive to
  external factors such as image quality, position
  of the probe, Doppler angle of interrogation,
  patient body habitus, the position of the heart in
  the body, etc., care should be taken in
  interpretation and drawing conclusions.
• Therefore, no measurement should stand alone
  as proof of the filling pressures; instead, an
  integrated approach should be used to come to
  the most likely conclusion.‖
          Inferior Vena Cava (IVC)
                  Ultrasound
• May be used to estimate CVP
• Method:
  –   transducer in subxiphoid region (phased array or cardiac)
  –   select cardiac present from patient menu
  –   transducer indicator (concavity on transducer) to patient's head
  –   Set depth as deep as possible
  –   Sweep transducer into RUQ to find IVC running through liver
  –   Try to look at most proximal portion of IVC-you can often see in the
      same screen the IVC and the RA as it enters
  –   use 2D to locate IVC, freeze and measure largest diameter
  –   use M mode to view the IVC diameter in a single point in space over a
      period of time
  –   hit M mode once to enter the mode
  –   hit M mode again to sample a space over time
  –   freeze after collecting a frame in M mode
  –   measure the difference between max IVC diameter (end expiration) and
      min IVC diameter (end inspiration)
       Inferior Vena Cava (IVC)
               Ultrasound
IVC Size     Respiratory      Estimated CVP
             Change
<1.5 cm      Total Collapse   0-5 mm Hg

1.5-2.5 cm   >50% Collapse 5-10 mm Hg

1.5-2.5 cm   <50% Collapse 11-15 mm Hg

>2.5 cm      <50% Collapse 16-20 mm Hg

>2.5 cm      No change        >20 mm Hg
What if it‘s still not clear?
         Clear volume depletion                       Unclear fluid status                 Clear volume overload




     Begin with a bolus of NS                                                           Begin with 20mg Lasix IV in
     (consider 250ml in elderly,                                                        Lasix-naïve patients, may
     500ml in others)                                                                   start higher depending on
                                                                                        how severe the overload is
                                                                                        and how high the blood
                                                                                        pressure is.
     Re-evaluate fluid status after
     the bolus, which may include
     checking response to Blood
     pressure, urine output,                                                            Re-evaluate fluid status after
     physical exam,                                                                     the Lasix, which may include
     BUN/creatinine response…                                                           checking response to Blood
                                                                                        pressure, urine output,
                                                                                        physical exam,
                                                                                        BUN/creatinine response…


 Not improved/                 Improved
     worse
                                                                                       Improved              Not improved/
                                                                                                                 worse
                            Bolus with NS;
Either a) you               consider
guessed wrong               Albumin only in
and they‘re                 cirrhotics with                                         Diurese until
overloaded, or b)                                                                   clinically              Either a) you
                            albumin level
they need more                                                                      euvolemic,              guessed wrong
                            <2 or in those
fluid.                                                                              then diurese            and they‘re dry
                            with recent
                                                                                    500ml-1000ml            or b) you need
                            paracentesis.
                                                                                    per day                 to give more
                                                                                                            diuretic.
Re-evaluate your
data, get more
labs, call your
attending
                                                                                                            Re-evaluate
                                                Determine the patient‘s most                                your data, get
                                                     pressing problem                                       more labs, call
                                                                                                            your attending.

                    e.g. oxygenation or ventilation                        e.g. elevated creatinine
                    problem; wound healing in the                              with concern for
                     face of interstial edema, etc.                       hepatorenal; low BP, etc.


                                                      If no problem ‗wins out‘
   Diurese, following labs and                        consider more invasive                 Give fluid, following labs
     other parameters very                              monitoring with your                and other parameters very
             closely                                         attending.                               closely
            Option #1:
  Look at what takes precedence
• If hypotensive, give fluid (unless
  overwhelming evidence of cardiogenic
  shock—in that case, give pressors)
• If going into hypoxic or hypercarbic
  respiratory failure, consider diuresis
• If going into respiratory failure AND
  hypotensive, trying to toe the line between
  fluids and diuresis does not work; give
  fluids while getting control of the airway
  (have fluids and dopamine or levophed
  ready while intubating)
          Option #1 (continued):
   Look at what takes precedence
• Other factors that may take precedence:
   – severe tachycardia (>140)—give fluid
   – severe anasarca—diurese
   – renal failure when dialysis isn‘t an option
     (e.g. hepatorenal syndrome)—give fluid
• **Note: the first sign of sepsis is
  hyperventilation and respiratory alkalosis;
  if suspecting sepsis, err on the side of
  giving fluid even in a tachypneic patient
           Option #2:
   Response to Fluid or Diuresis
• When there are questions about fluid
  status, ALWAYS MONITOR RESPONSE
  TO FLUIDS OR DIURESIS
• Make your best guess whether to hydrate
  or diurese, and analyze changes in vital
  signs and/or labs with your Fluid
  Bolus/Lasix
            Fluid Challenge
• Bolus of Normal Saline 500-1000 mL is
  reasonable; consider 250 mL for patients
  with known congestive heart failure or
  diastolic dysfunction; recommended to
  administer over ~30 minutes
• Alternatively, may lift the legs
   – Contraindicated if the patient has a
     DVT, as they are at risk for throwing it
     off and creating a Pulmonary Embolus
   – May cause sympathetic activation,
     making the response less clear
            Diuresis Challenge
• Lasix 20-40mg IV in Lasix naïve patients, higher
  dose in patients who have received diuretics in
  the past
• Lasix lasts for six hours, but the majority of the
  effect will be seen in the first 2 hours
• You should attempt to guesstimate how much
  fluid the patient is overloaded by
   – if rales and significant JVD, aim to get 2 or more liters
     off
   – for stable diuresis in total-body-overloaded patients,
     aim total 500-1000ml per day negative fluid balance
               Option #3:
              Get More Data
• More Data about Preload
  – Arterial Line with Cardiac Index (goal Cardiac
    Index>2 in most, higher the better in sepsis)
  – Swan Ganz Catheter
• Data About Perfusion of Tissues
  – Lactate, serially (~ every hour to 2 hours)
  – ABGs, serially (~ every hour to 2 hours)
  – SvO2 monitor
• Data About Both
  – SvO2 + Cardiac Index Arterial Line = ―Vigileo‖
              Cardiac Index
• (=Cardiac Output/Body Surface Area)
• <2.0 is consistent with cardiogenic shock
• Often quite elevated in Septic Shock (in
  the 3.5 to 6 range)
• Can be measured in a number of ways
  – Swan Ganz catheter: thermodilution
  – Continuous Cardiac Output arterial line (tell
    the nurses before they set up for the arterial
    line that they will need the ―continuous cardiac
    output‖ setup)
        Swan Ganz Catheter
• A diagnostic tool when the volume status
  of the patient remains unclear with less
  invasive techniques
• Studies have not borne out the use of this
  instrument to improve mortality, but the
  idea of studying a DIAGNOSTIC TOOL to
  change mortality is inherently flawed
• Probably beneficial in the correct situation,
  though less use begets less experience
  with its use
    Swan Ganz Catheter (continued)
• Cardiac Index (Cardiac Output/Body Surface
  Area)
• Systemic Vascular Resistance Index
• Right Ventricular End Diastolic Volume Index
• Pulmonary Capillary Wedge Pressure (PCWP)=
  Pulmonary Artery Wedge Pressure (PAWP) =
  ―Wedge‖
• Continuous SvO2 (Mixed Venous Oxygen Sat)
• **Note: Absolute values should be interpreted
  with a grain of salt; continuous interpretation of
  other parameters to maximize hemodynamics is
  key.
   Swan Ganz Catheter (continued)
• ―Normal‖ values
  – Cardiac Index = 2.5-4 Liters/minute*meter2
     (cardiogenic shock is C.I. < 2 L/min*m2)
  – Systemic Vascular Resistance
     (1970-2390 dynes/cm2*m2)
  – Right Ventricular End Diastolic Volume Index
     normal = 60-90 ml/m2
     (often need to drive it up to 130 ml/m2 in
     hypotensive septic patients)
  – ―Wedge‖ (PAWP) = ~ 10 mm Hg
     (values as high as 18 may be seen)
    Swan Ganz Catheter (continued)
• Often most helpful in patients with renal
  failure who are going to surgery, where
  massive fluid shifts are to be expected
• May also be helpful in ARDS with renal
  failure, though studies have not borne this
  out.
     Fluid Status: Helpful tips
• Fluid overload is the only time that the
  BUN and creatinine will actually IMPROVE
  with the administration of loop diuretics
  due to improved Starling Curve dynamics
  and improved Cardiac Output
• Renal failure (particularly oliguric) in the
  face of surgery or in the face of developing
  ARDS are the two clinical situations when
  Swan Ganz catheter MAY be helpful
           Documentation
• Documentation of your thought process is
  vital to appropriate care of ICU patients
               Objectives
• Physiology of Fluid Distribution in the Body
• Relationship of Intravascular Volume
  (Preload) to Perfusion of Organs
• How to Estimate Intravascular Fluid
  Volume
• How to Measure Organ Perfusion
• Fluid Options
• Illustrative Cases
  Contractility/
   Inotropy          Stroke             Heart
                     Volume             Rate
     Preload

                              Cardiac           Afterload

                              Output

                      Adequacy of Oxygenation
                       of Blood (Hemoglobin)



                         Perfusion of
                           Organs
                                                            Oxygen
    Health of
                                                          Dissociation
Tissues to Utilize
    Available
                     Ability of Organs to               Curve—Ability to
                                                        Release Oxygen
    Oxygen             Utilize Oxygen                      at Tissues
        Perfusion of Organs
• Brain/Heart are preferentially perfused vs.
  Kidneys/Liver
• Kidneys/Liver are preferentially perfused
  over Skeletal muscle
• Arteriolar constriction via sympathetic
  activation is mostly responsible for this
  shunting
      Surrogates of Perfusion
• If the patient is mentating, the brain is
  being perfused
   – A SYSTOLIC blood pressure of 60 is
      often the minimum needed to perfuse
      the brain
• If the patient is urinating 30ml/hour, the
  kidneys are being perfused
   – A MEAN arterial pressure of 65 is often
      needed to perfuse the kidneys/all vital
      organs
       Goals of Perfusion:
  The Surviving Sepsis Campaign
• ―Goal-Directed       • Step-wise
  Therapy‖:              therapies to
  – MAP>65               achieve goals:
  – Urine                – 2 Liters NS
    Output>30ml/hour     – Continued fluids
  – CVP 8-10             – Pressors + steroids
  – (Lactic Acid <2)     – PRBC‘s to get
  – (SvO2 70-84)           Hb>10
  – (pH>7.2)             – Dobutamine if
                           SvO2 still not
                           optimized
           Oxygen Delivery
• Cardiac output and Perfusion Pressure are
  important factors for oxygen delivery to the
  tissues
• Oxygen carrying capacity of the plasma
  (largely of blood, but a small amount
  diffused in the plasma) is also important
       Oxygen Consumption
• Depends on the ability of blood to release
  oxygen at the tissue level
  – Properties of Blood – recently transfused
    blood is deficient in 2, 3 DPG and thus can
    carry but not release oxygen for 24 or more
    hours
  – Oxygen-Hemoglobin Dissociation Curve
• Depends on the health of tissues to be
  able to extract oxygen and perform
  aerobic metabolism
Oxygen-hemoglobin Dissociation Curve




                          Tissue 02
                          Delivery
     How can Oxygen Delivery/
    Consumption be measured?
• Goals of Surviving Sepsis Campaign
  – Mentation
  – MAP > 65
  – Urine output > 30ml/hour or >0.5ml/kg/hour
• Mixed Venous Oxygen Saturation
• Lactic Acid
• pH > 7.2, Anion Gap closed
 Mixed Venous Oxygen Saturation
• May be monitored continuously or
  intermittently
• Usually obtain a VBG from the distal port
  to correlate

• Note: The ―SvO2 triple lumen catheters‖
  do not fit through a Cordis; Swan Ganz
  SvO2 monitors do fit through the Cordis
 Mixed Venous Oxygen Saturation
• Affected by both delivery and by
  consumption
  – An abnormally low value (<70) reflects either
    inadequate delivery or too high consumption
    by the body‘s organs (or both)
  – An abnormally high value (>82-85) should
    raise concern for inadequate consumption by
    the body‘s organs in the face of adequate
    delivery or shunting of blood from the arterial
    to the venous side
               Lactic Acid
• Lactic Acid is produced when cells have
  decreased access to oxygen or decreased
  ability to utilize delivered oxygen,
  converting to anaerobic metabolism



• Note: Lactic Acid levels should be
  available within ½ hour of blood draws
  (call the lab and also report to your ICU
  attending if there are significant delays)
      Lactic Acid Interpretation
• All values > 2 are abnormal
• A lactate of >3.5 on admission conveys a 57%
  mortality rate
• A rise in serum lactate, as well as a failure to
  return to normal by 48 hours, is associated with
  a 74% mortality

• Note: Lactate in trauma is NOT indicative of
  mortality (5.4% mortality with Lactate elevation),
  but is helpful in assessing adequacy of
  resuscitation
     Sublingual Capnography
• There is some data that this is a more
  ―real time‖ indication of perfusion (or lack
  thereof)
• The machine to measure this is
  $10,000US and has not yet at this
  institution come into enough favor to justify
  the expense
Modifiable Factors for
  Oxygen Delivery
  Contractility/
   Inotropy          Stroke             Heart
                     Volume             Rate
     Preload

                              Cardiac           Afterload

                              Output

                      Adequacy of Oxygenation
                       of Blood (Hemoglobin)



                         Perfusion of
                           Organs
                                                            Oxygen
    Health of
                                                          Dissociation
Tissues to Utilize
    Available
                     Ability of Organs to               Curve—Ability to
                                                        Release Oxygen
    Oxygen             Utilize Oxygen                      at Tissues
         Modifiable Factors for
           Oxygen Delivery
• Increasing Effective Cardiac Output
  – Fluids to increase preload [Right Ventricular
    End Diastolic Volume]
  – For patients with very low Systemic Vascular
    Resistance (e.g. sepsis, neurogenic shock),
    Pressors (e.g. Norepinephrine [Levophed],
    Vasopressin) to keep MAP > 65
        Modifiable Factors for
        Oxygen Delivery (continued)
• Increasing Effective Cardiac Output
  – For patients with relatively high Systemic
    Vascular Resistance (e.g. cardiogenic shock,
    sepsis with myocardial depressant factor),
    ―Perfusers‖ (e.g. Dobutamine) to increase
    cardiac inotropy/chronotropy while decreasing
    systemic vascular resistance
  – For patients with unclear Systemic Vascular
    Resistance but ―relatively bradycardia‖,
    Positive Inotropes (e.g. Dopamine) to
    increase contractility and heart rate
        Modifiable Factors for
        Oxygen Consumption
• Adding ―Box Cars‖(Transfusion of PRBCs)
  – may increase O2 carrying capacity but may
    not release O2 at the tissue level for >24
    hours due to low 2,3 DPG levels
• Optimizing the Oxyhemoglobin
  Dissociation Curve
• Making Tissues Healthier
  – Restoring Perfusion ( Preload, Dobutamine)
  – Antibiotics
  – Decreasing Inflammation or Toxin Production
  – etc.
               Objectives
• Physiology of Fluid Distribution in the Body
• Relationship of Intravascular Volume
  (Preload) to Perfusion of Organs
• How to Estimate Intravascular Fluid
  Volume
• How to Measure Organ Perfusion
• Fluid Options
• Illustrative Cases
      What Fluid to Choose?
• Crystalloid vs. Colloid
• Crystalloid Options
• Colloid Options
      What Fluid to Choose?
• Crystalloid vs. Colloid
• Crystalloid Options
• Colloid Options
     Colloids vs. Crystalloids
• SAFE Trial [2004]
  – Trial of 7000 consecutive ICU Patients
    randomized to colloid (4% Albumin) or
    crystalloid (Normal Saline)
  – No change in Mortality (20.76% vs. 20.82%),
    Length of ICU Stay (6.5 vs. 6.2 days), Days of
    Mechanical Ventilation (4.5 vs. 4.3 days),
    Total Hospital Stay (15.3 vs. 15.6 days), or
    patients with single or multi-organ failure
     Colloids vs. Crystalloids
• Subgroup Analysis
  – Head trauma patients had higher mortality in
    the Albumin group (24.5% mortality with
    Albumin vs. 15.1% with Saline, p = 0.009)
  – Severe sepsis patients had a higher mortality
    in the Saline group (35.3% mortality with
    Saline vs. 30.7% with Albumin, p = 0.06)
  – ARDS also had a trend toward higher
    mortality with Saline, but it was also not
    statistically significant
         Colloids vs. Crystalloids
• Clinical responses to fluids
  – The Albumin group received less overall fluid
    in the first 2 days of ICU stay
     •   Day 1: 1:1.3 (Albumin:Saline)
     •   Day 2: 1:1.6 (Albumin:Saline)
     •   Day 3: 1:1.3 (Albumin:Saline)
     •   Day 4: 1:1.2 (Albumin:Saline)
     •   Overall (days 1-4): 1:1.4 (Albumin:Saline)
  – The Albumin group received MORE overall
    transfusions (on average, 71ml more per
    patient) than the Saline group
      Colloids vs. Crystalloids
• Clinical responses to fluids (continued)
  – Systolic blood pressure was no different
    between the groups
  – Heart rate was 1.7 beats slower in the
    Albumin group by the end of day 1
      Colloids vs. Crystalloids
• Conclusions:
  – Use crystalloids for all situations, unless there
    are compelling reasons to use colloids
  – Albumin is a significant hemodilutor,
    increasing the risk of needing a transfusion
  – There is a trend in severe sepsis towards
    improvement with Albumin, but it was not
    statistically significant
      What Fluid to Choose?
• Crystalloid vs. Colloid
• Crystalloid Options
• Colloid Options
           Normal Saline
       (0.9% Sodium Chloride)
• 154 mEq of Sodium Chloride
• Used as the Standard Fluid Resuscitative
  Solution
  – pH=5.5, Osm=308mOsm/L
           Lactated Ringers
         (a.k.a. ―Hartmann‘s‖)
• Felt to be more ―physiologic‖
• Preferred by our surgical colleagues
• May be beneficial when there is a
  hyperchloremic metabolic acidosis
  – 130 mEq Sodium
  – 109 mEq Chloride
  – 28 mEq Lactate
  – 4 mEq Potassium
  – 3 mEq Calcium
  – pH=6.6, Osm=273mOsm/L
     Saline vs. Lactated Ringers
• No difference in Mortality head-to-head
• The d-isomer of the lactate in Lactated
  Ringers may be responsible for the lack of
  mortality benefit, as the d-isomer causes
  expression of leukocyte genes known to
  be involved in inflammation, cell migration,
  and cellular apoptosis
               D5W
       (5% Dextrose in Water)
• Used as a treatment for hyponatremia, or
  as a source of dextrose
• TO BE AVOIDED in any situation where
  there is significant chance of brain edema
           Hypertonic Saline
              (3% NaCl)
• Often used to draw water out of an
  edematous brain
• Should ONLY be used in hyponatremic
  patients who are seizing, as there is very
  high risk for over-correction of the sodium
  level
• Contraindicated for Serum Osm‘s of >310
  to 320, or a Serum Sodium > 150 (check q
  6 hours or more frequently)
• High risk for Fluid Overload
   Various hypotonic solutions
• e.g. ½ NS, D51/2 NS, ¼ NS, etc.
• Often used as ―maintenance fluid‖
• More physiologic, but there is high risk for
  third-spacing, and should be avoided in
  patients who cannot afford to third-space
  fluids (e.g. s/p CVA, brain edema,
  significant edema with soft-tissue
  infections (theoretically))
      What Fluid to Choose?
• Crystalloid vs. Colloid
• Crystalloid Options
• Colloid Options
                 Colloids
• All colloids carry infectious risks
• Patients who do not have specific
  indications for colloid products should
  receive crystalloids
      Packed Red Blood Cells
• ~350ml per Unit
• Have all plasma removed
• In most patients, 1 Unit will raise the
  Hematocrit by 3 points (and the
  Hemoglobin by 1 point)
• $258 per Unit
• All of the PRBC Units at VCMC are
  Leukodepleted
     Packed Red Blood Cells
• TRICC Trial
  – Randomized 838 anemic ICU patients to a
    restrictive transfusion strategy (Hb 7-9) vs. a
    liberal transfusion strategy (Hb>10)
  – Restrictive transfusion strategy overall
    Mortality 18.7% vs. Liberal transfusion
    strategy Mortality 23.3% (p = 0.11)
  – In patients with ―significant cardiac disease‖
    (e.g. Acute MI, Unstable Angina), restrictive
    strategy Mortality 20.5% vs. liberal strategy
    22.9% (p = 0.69)
     Packed Red Blood Cells
• PRBCs in CABG (2007)
  – Those who received transfusions had a
    stastically significant higher incidence of both
    thrombosis (MI) and of infection
  – Anemia was associated with worse outcome,
    but the TREATMENT of anemia with PRBCs
    was also associated with a worse outcome
  – Observational retrospective cohort study
  – 40% of the transfused group was >70 years
    old, vs. only 20% of the non-transfused group
    = ? Significant selection bias ?
     Packed Red Blood Cells
• THE most volume-expansive fluid (with a
  Hct~60) with VERY high risk for overload
• Risks for
  – Acute Hemolytic Reactions (1:30,000-50,000)
  – Bronchospasm/hypotension (1:1000-2000)
  – Anaphylaxis (1:20,000-50,000)
  – Fever (1:100-200)
  – Bacterial Sepsis (1:1,400,000)
  – TRALI (1:5000 or more common)
  – Viral transmission (<1:170,000)
 Transfusion Recommendations
             Variable                 Transfusion   Goal
                                        Trigger
Generally Critically Ill (no acute        Hb 7      Hb 7-9
bleeding)                                (g/dL)     (g/dL)
Critically Ill with Septic Shock        Hb 8-10     Hb 10
(<6 hours)                               (g/dL)     (g/dL)
Critically Ill with Septic Shock          Hb 7      Hb 7-9
(>6 hours)                               (g/dL)     (g/dL)
Critically Ill with Chronic Cardiac       Hb 7      Hb 7-9
Disease                                  (g/dL)     (g/dL)
Critically Ill with Acute Cardiac       Hb 8-10     Hb 10
Disease (e.g. ACS, MI)                   (g/dL)     (g/dL)
     Packed Red Blood Cells
• CAUTION: The preceding
  recommendations apply to general
  medical ICU patients who are not felt to be
  bleeding
• Goals in acute bleeding are VERY
  DIFFERENT: Get the Hemoglobin up to
  10 and keep the patient hemodynamically
  stable
       Packed Red Blood Cells:
     To Irradiate or Not to Irradiate
• The main reason to irradiate blood is to prevent T cell
  mediated GVHD which is universally fatal when it occurs
  from transfusion.
• Patients immunosuppressed after transplant,
  lymphoma/leukemia patients on steroids, or other
  patients on significant immunosuppression for whatever
  reason should get blood products radiated.
• 1st degree family members who donate for directed use
  for a relative should have the blood radiated because
  genetic similarities may allow donor T cells to survive.
• The other use for radiation is in patients thought to be
  transplant candidates- The idea is that less WBC give
  you less antigenic exposure but I don't think the data is
  very solid for this. Solid tumor patients on standard
  chemo do not need radiated blood products.
                   FFP
• ~225ml per Unit
• Includes all plasma proteins, including
  clotting factors
• In massive blood loss, the ratio of PRBCs
  to FFP should approximate 1:1, with
  frequent assessments of coagulation
  status
• Hypothermia is a significant risk—use the
  ―Blood warmer‖ or the ―Level One‖ in
  trauma and other patients
• $76 per Unit
                Platelets
• 1 ―Pheresis Unit‖ is the equivalent of 5-6
  ―packs‖ or ―platelet concentrates‖ (may just
  order ―1 Unit‖), and is approximately 300ml
• Transfusion should raise platelet counts
  5,000 to 7,000 per platelet concentrate
  (or 25,000-42,000 per ―Pheresis Unit‖)
• $585 per Pheresis Unit
            Cryoprecipitate
• 1 Unit contains Fibrinogen (150mg),
  Factor VIII (80 Units), and von
  Willebrandt‘s Factor, in 15ml usually
  diluted in 10ml of saline or FFP
• Indicated in severe DIC to keep
  Fibrinogen > 150
• Usually transfused as 5 or 10 Units
• 1 individual unit is $70
• 5 Units pooled is $490
              Hetastarch
• High risk for coagulopathy
• Very little role
                       References
• Tung R, et al. Utility of B-type Natriuretic Peptide for the Evaluation
  of Intensive Care Unit Shock. Crit Care Med 2004; 32: 1643-47.
• Resuscitation end points in severe sepsis: Central venous pressure,
  mean arterial pressure, mixed venous oxygen saturation, and …
  intra-abdominal pressure. Crit Care Med 2008; 36 (3): 1012-13.
• Vincent JL, et al. Fluid Challenge Revisited. Crit Care Med 2006; 34
  (5): 1333-7.
• Michard F, et al. Predicting Fluid Responsiveness in ICU Patients.
  Chest 2002; 121: 2000-8.
• A Comparison of Albumin and Saline for Fluid Resuscitation in the
  Intensive Care Unit. New Engl J Med 2004; 350: 2247-56.
• DeLoughery T. Blood Component Therapy. SCCM 2007 Critical
  Care Review Course.
                       References
• Koustova E, et al. Effects of Lactated Ringers Solutions on Human
  Leukocytes. J Trauma. 2002; 52(5): 872-8.
• Murphy G, et al. Increased Mortality, Post-operative Morbidity, and
  Cost after Red Blood Cell Transfusion in Patients Having Cardiac
  Surgery. Circulation. 2007; 116: 2544-52.
• Janette O‘Neal, VCMC Blood Bank Director, 2008.
• Phua J, et al. Lactate, Procalcitonin, and Amino-Terminal Pro-B-
  Type Natriuretic Peptide Verses Cytokine Measurements and
  Clinical Severity Scores for Prognostication in Septic Shock. Shock.
  2008; 29 (3): 328-333.
• Canadian Critical Care Trials Group. Transfusion Requirements in
  Critical Care. New Engl J Med 1999; 340 (6): 409-17.
• Hebert P, et al. Contraversies in RBC Transfusion in the Critically Ill.
  Chest 2007; 131 (5): 1583-90.

				
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