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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  – 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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