Tag Archives: Critical Care

“But doctor, he’s vomiting blood!!!” – The NEJM GI Bleed article by Villanueva: Yup, time to reassess transfusion in GI bleed! @FOAMed, @FOAMcc

thinking critical care

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Last january a highly anticipated paper came out in the NEJM (http://www.nejm.org/doi/pdf/10.1056/NEJMoa1211801), which should be a game changer, given a few provisos.  Villanueva et al reported on their large (almost 1,000 patients) randomized study on liberal (<90 mg/dl) vs restrictive (<70 mg/dl) strategy.  Interestingly but no longer surprisingly, the patients in the restrictive strategy did better.

Hmmm…sound familiar?  By now everyone  accepts the TRICC trial threshold of 70 in ICU patients, but when it first came out, there were a fair bit of disbelievers and concerned health care workers.  At the time, they excluded GI bleeds and acute coronary syndromes, understandably,

So what do the numbers say?  First lets see if there was any difference in the actual treatment. Definitely. In the restrictive group, 51% of patients required transfusion, vs 86% in the liberal group.  Sizeable difference. Now in terms of outcomes:

a. rebleeding decreased: 10% vs 16%

b. 6 week…

View original post 1,030 more words

Fluid Management

Fluid Management

Clinical Problems

    There are several clinical problems associated with the need to understand fluid management related to patient care.

  1. How to identify patients who need fluid therapy or are becoming hemodynamically unstable before they progress too far?
  2. How to determine the most appropriate therapy to reverse the primary cause for impending circulatory shock/problem(s)?
    1. For instance,
      1. Which fluid, when to give fluid, how much fluid to give
      2. Predicting fluid response
  3. How to implement the most appropriate therapy for your individual patients?
  4. How to assess your patients fluid response?
    1. Is Cardiac Output Adequate? (Preload Responsiveness)
    2. Is blood flow adequate to meet metabolic demands?
      1. Does the patient have adequate organ perfusion
    3. Will increasing intravascular volume increase cardiac output?
    4. Will decreasing the driving pressure for venous return decrease cardiac output?
    5. Is cardiac output responsive to intravascular fluid loading?
  5. What end points/results from your therapy demonstrate success or a need for further action?

Causes

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“Classic” Blalock 1937

  1. Hematogenic
  2. Neurogenic
  3. Vasogenic
  4. Cardiogenic

Low Cardiac Output states (Carrico: ACS Early Care of the Injured Patient 4th Ed.)

  1. Hypovolemic shock
    1. volume loss
    2. Internal volume loss
  2. Cardiac shock
    1. Impaired inflow
    2. Primary pump dysfunction
    3. Impaired outflow
  3. Low peripheral resistance states
    1. Neurogenic shock
      1. Loss of sympathetic tone
    2. Vasogenic Shock
      1. Septic
      2. Anaphylactic

Tissue oxygen saturation predicts the development of organ dysfunction during traumatic shock resuscitation

SMACC: Johnston on the Assessment of Shock

Fluid resuscitation of hemorrhagic shock

Epocrates – Evaluation of Shock

 

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Acute coagulopathy of trauma shock (ACoTS)

Acute Coagulopathy of Trauma Shock (ACoTS)

  1. Syn:ETIC (Early Trauma Induced Coagulopathy)
  2. Starts in the prehospital period.
  3. Shock & Hypoperfusion is the cause.
  4. Dilution,Hypothermia,Loss of coagulation factors not significant at this stage.
  5. Thrombomodulin-ProteinC pathway is activated in hypoperfusion.
  6. Hypercoagulable state and risk of thrombosis due to Protein C depletion.

LITFL – Shock… Do We Know It When We See It?

Hypothermia and acidosis worsen coagulopathy in the patient requiring massive transfusion

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The Lethal Six Pack

  1. Tissue Injury
  2. Shock
  3. Dilution
  4. Hypothermia
  5. Acidosis
  6. Inflammation

Hypothermia

  1. Causes of Hypothermia
    1. Environmental factors: extrication and transport time
    2. IV fluids and ongoing blood loss
    3. Alteration of normal heat producing metabolism
  2. Effects of Hypothermia
    1. Decreases platelet aggregation and adhesion
    2. Decrease coagulation factor activity by 10% for each degree decrease in core temperature
    3. Both R (Rx Time) & K (Fibrin) prolonged on TEG
    4. 100% fatal when core temperature reaches < 32°C
  3. Coagulation assays are run at 37 °C!

Hypothermia References and Resources

  1. Emcrit – Targeted Temperature Management for Post-Arrest and Critical Care
  2. Hypothermic Resuscitaiton
  3. Induced Hypothermia After Anoxic Brain Injury
  4. Iced Saline in the Field – Induced Hypothermia for EMS
  5. Induced hypothermia does not impair coagulation system in a swine multiple trauma model
  6. Induced Hypothermia in Post Cardiac Arrest Patients
  7. Steady-state and time-dependent thermodynamic modeling of the effect of intravenous infusion of warm and cold fluids
  8. Therapeutic Hypothermia in Survivors of Cardiac Arrest
  9. Therapeutic Hypothermia – The Pharmacologic Inhibition of Thermoregulation
  10. University of Penn – Med – Center for Resuscitation Science – Hypothermia

Impact of prehospital hypothermia on transfusion requirements and outcomes

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Hypothermia in massive transfusion: have we been paying enough attention to it?

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Acidosis

  1. Causes of Acidosis
    1. Decreased perfusion leads to anaerobic metabolism and lactic acid production
    2. LR pH 6.0, normal saline 4.5, no buffering capacity
    3. Red cell unit at two weeks have pH < 7.0
  2. Effects of Acidosis
    1. Reduced clot formation demonstrated by TEG
    2. Spherical platelets devoid of pseudopods
    3. Reduced fibrinogen levels, platelet counts & FXa
  3. Prevention of Acidosis
      1. Dependent on restoration of perfusion
      2. Exogenous bicarb has mixed results

Acute traumatic coagulopathy: initiated by hypoperfusion: modulated through the protein C pathway?

Chapter 19: Using the Stewart Model at the Bedside

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Coagulopathy

Coagulopathy and blood component transfusion in trauma

The interplay between metabolic acidosis, hypothermia and progressive coagulopathy in trauma “Bloody Vicious Cycle”

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Surgical Treatment: Evidence-Based and Problem-Oriented – Abdominal compartment syndrome

Initial Management of Life-Threatening Trauma. Ch 6 Trauma and Thermal Injury. ACS Surgery: Principles and Practice

Abdominal Compartment Syndrome

Abdominal compartment syndrome has emerged as a virtual epidemic in busy trauma centers that practice damage-control surgery and goal-oriented ICU resuscitation. This syndrome is an early event, and its clinical trajectory can be accurately predicted within 3 to 6 hours after ED admission. At admission to the ICU, high-risk patients have significant intra-abdominal hypertension and are in persistent shock. Contrary to conventional wisdom, they do not respond well to pre-load directed resuscitation. In fact, continued aggressive resuscitation precipitates the full-blown syndrome [figure 13].

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Stress Repair Mechanism

The capillary gate component (red) corresponds to the intrinsic pathway of the coagulation cascade. The tissue repair component (blue) corresponds to the extrinsic pathway of the coagulation cascade. Both the SRM and the coagulation cascade generate thrombin (orange), plus soluble fibrin and insoluble fibrin. Inhibitory pathways appear in green.  View a list of SRM terms and concepts here. (30 Years Lost in Anesthesia Theory)

SRM_Diagram

Hemodynamic Values

From Crashing Patient

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Catheters and Flow Rates

(Marino, The ICU Book, 109-110)

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Intravenous extension sets: when more is less

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Composition

Winters – Fluids in the Critically Ill

 

In 1861, Thomas Graham’s investigations on diffusion led him to classify substances as crystalloids or colloids based on their ability to diffuse through a parchment membrane. Crystalloids passed readily through the membrane, whereas colloids (from the Greek word for glue) did not. Intravenous fluids are similarly classified based on their ability to pass from intravascular to extravascular (interstitial) fluid compartments.

From Wikipedia – Volume Expanders

There are two main types of volume expander; crystalloids and colloids. Crystalloids are aqueous solutions of mineral salts or other water-soluble molecules. Colloids contain larger insoluble molecules, such as gelatin. Blood is a colloid.

  • Colloids preserve a high colloid osmotic pressure in the blood, while, on the other hand, this parameter is decreased by crystalloids due to hemodilution.[1] However, there is still controversy with regard to the actual difference in efficacy between colloids and crystalloids.[1] Crystalloids generally are much cheaper than colloids.[1]
  • The most commonly used crystalloid fluid is normal saline, a solution of sodium chloride at 0.9% concentration, which is close to the concentration in the blood (isotonic). Lactated Ringer’s (also known as Ringer’s lactate) and the closely related Ringer’s acetate, are mildly hypotonic solutions often used for large-volume fluid replacement.

Additional information:

  1. Crystalloid solutions – clear fluids made up of water and electrolyte solutions; Will cross a semi-permeable membrane e.g Normal, hypo and hypertonic saline solutions; Dextrose solutions; Ringer’s lactate and Hartmann’s solution.
  2. Colloid solutions – Gelatinous solutions containing particles suspended in solution. These particles will not form a sediment under the influence of gravity and are largely unable to cross a semi-permeable membrane. e.g. Albumin, Dextrans, Hydroxyethyl starch [HES]; Haemaccel and Gelofusine
    1. The colloid solutions contain particles which do not readily cross semi-permeable membranes such as the capillary membrane
    2. Thus the volume infused stays (initially) almost entirely within the intravascular space
    3. Stay intravascular for a prolonged period compared to crystalloids
    4. However they leak out of the intravascular space when the capillary permeability significantly changes e.g. Severe trauma or sepsis
    5. Until recently they were regarded as the gold standard for intravascular resuscitation
    6. Because of their gelatinous properties they cause platelet dysfunction and interfere with fibrinolysis and coagulation factors (factor VIII) – thus they can cause significant coagulopathy in large volumes.

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Common Examples

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Paucis Verbis: Composition of intravenous fluids (Medscape – An Update on Intravenous Fluids)

Fluid Therapy in Hemorrhagic Shock: The ability of sodium to replace interstitial fluid deficits, not blood volume deficits, is the reason that crystalloid fluids containing sodium chloride (saline fluids) gained early popularity as resuscitation fluids for acute blood loss.

 

A physicochemical model of crystalloid infusion on acid-base status

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(LifeInTheFastLane – Strong Ion Difference = SID & Stewart’s Strong Ion Difference)

Crystalloid infusion changes plasma SID by changing the proportion of strong cations to strong anions and, thus, the net charge balance. After crystalloid infusion, plasma SIDad
(admixture) reflects the admixture of the crystalloid SID and plasma SID. The major strong cations and anions will also be diluted by the increment in plasma volume by the infusate. The plasma SIDad from standard state conditions is calculated as follows: SIDss (standard state) plasma volume + SIDci (crystalloid infusate) infusate volume divided by plasma volume + infusate volume. The plasma SIDad calculation after a 1 L infusion of normal saline from standard state can be found in the appendix.

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Association between a chloride-liberal vs chloride-restrictive intravenous fluid administration strategy and kidney injury in critically ill adults

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Clinical review: Volume of fluid resuscitation and the incidence of acute kidney injury – a systematic reviewimage

Base Deficit or Base Excess

The base deficit is the amount (in millimoles) of base needed to titrate one liter of whole blood to a pH of 7.40 (at temperature of 37°C and PCO2 = 40 mm Hg). Because base deficit is measured when the pCo2 is normal, it was introduced as a more specific marker of non-respiratory acid-base disturbances than serum bicarbonate (16). In the injured or bleeding patient, an elevated base deficit is a marker of global tissue acidosis from impaired oxygenation (17). One advantage of the base deficit is its availability. Most blood gas analyzers determine the base deficit routinely using a pC02/HC03 nomogram, and the results are included in the blood gas report. The base deficit (BD) can also be calculated
using the equation below (18), where BD is base deficit in mmol/L, Hb is the hemoglobin concentration in blood, and HC03 is the serum bicarbonate concentration.

BD = [(1 – 0.014 Hb) X HC03] – 24 + [(9.5 + 1.63 Hb) X (pH – 7.4)]

The normal range for base deficit is +2 to -2 mmol/L. Abnormal elevations in base
deficit are classified as mild (-2 to -5 mmol/L), moderate (-6 to -14 mmol/L),
and severe (<-15 mmol/L).

Clinical studies in trauma patients have shown a direct correlation between the magnitude of increase in base deficit at presentation and the extent of blood loss (19). Correction of the base deficit within hours after volume replacement is associated with a favorable outcome (19), while persistent elevations in base deficit are often a prelude to multiorgan failure.

(Marino, The ICU Book, 218)

(Best utilized in combination with serum lactate early (24-36 hours) in the patients ICU stay.)

P-Video: Rule of 15 for Anion Gap Metabolic Acidosis
     

    1. AcidBase.org
    2. Acid-Base Physiology
      1. Acid-Base Physiology – Quantitative Acid-Base Analysis: The Variables
      2.  Acid-Base Physiology – Quantitative Acid-Base Analysis: The Equations
    3. Acid-base balance in peritoneal dialysis patients: a Stewart-Fencl analysis
    4. Wikipedia – Base Excess
    5. Base Excess & Calculated Bicarbonate
    6. Cornell – Base Excess & Calculated Bicarbonate Calculator
    7. EMCrit
      1. Podcast 44 – Acid Base: Part I
      2. Podcast 45 – Acid Base: Part II
      3. Podcast 46 – Acid Base: Part III
      4. Podcast 50 – Acid Base Part IV – Choose the Solution Based on the Problem
      5. Podcast 96 – Acid Base in the Critically Ill – Part V – Enough with the Bicarb Already
      6. Podcast 97 – Acid-Base VI – Chloride-Free Sodium
    8. Life In The Fast Lane – Base Excess Vs Standard Base Excess
    9. Life In The Fast Lane – Strong Ion Difference
    10. P-Video: Rule of 15 in anion gap metabolic acidosis
    11. Stewarts Strong Ion Difference
    12. Strong ions, weak acids and base excess: a simplified Fencl-Stewart approach to clinical acid-base disorders
    13. YouTube Acid Base Videos
      1. Application of Base Deficit in Resuscitation of Trauma Patients
      2. Eric Strong – Introduction and Course Overview (Understanding ABGs – Lecture 1 of 23)
      3. MEDCRAMvideos – Medical Acid Base Explained Clearly! 1 of 8

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When using the base deficit to guide fluid resuscitation in trauma patients, the base deficit should be monitored serially along with the patient’s clinical response.

Elevated Arterial Base Deficit in Trauma Patients: A Marker of Impaired Oxygen Utilization

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Chapter 19: Using the Stewart Model at the Bedside

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The Stewart approach–one clinician’s perspective

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Physical Exam

 

Physical exam in general is not sensitive or specific

  1. Acute weight loss; however, obtaining an accurate weight over time may be difficult
  2. Decreased skin turgor – if you pinch it it stays put
  3. Dry skin, particularly axilla
  4. Dry mucus membranes
  5. Low arterial blood pressure (or relative to patient’s usual BP)
  6. Orthostatic hypotension can occur with significant hypovolemia; but it is also common euvolemic elderly subjects.
  7. Decreased intensity of both the Korotkoff sounds (when the blood pressure is being measured with a sphygmomanometer) and the radial pulse (“thready”) due to peripheral vasoconstriction.
  8. Decreased Jugular Venous Pressure
  9. The normal venous pressure is 1 to 8 cmH2O, thus, a low value alone may be normal and does not establish the diagnosis of hypovolemia.

The rational clinical examination. Is this patient hypovolemic?

(Marik et al. Annals of Intensive Care 2011, 1:1)

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Volume Depletion with Depleted Extravascular Compartment

  1. Acute blood loss
    1. Trauma
    2. GI bleed
  2. Gastrointestinal tract losses (diarrhea, vomiting, fistula)
  3. Decreased fluid intake due to acute medical conditions
  4. Diabetic ketoacidosis
  5. Heat exhaustion
  6. “Dehydration”

Volume Depletion with Expanded Extravascular Compartment

  1. Sepsis
  2. Pancreatitis
  3. Trauma
  4. Surgery
  5. Burns
  6. Liver failure
  7. Cardiac failure

Also: P.E. Marik, Handbook of Evidence-Based Critical Care, DOI 10.1007/978-1-4419-5923-2_8

Permissive Hypotension

Damage Control Resuscitation: The New Face of Damage Control

Permissive Hypotension

The concept behind permissive hypotension involves keeping the blood pressure low enough to avoid exsanguination while maintaining perfusion of end organs. Although hypotensive resuscitation is evolving into an integral part of the new strategy of DCR, the practice itself is not a new concept. Walter Cannon and John Fraser remarked on it as early as 1918 when serving with the Harvard Medical Unit in France during World War I. They made the following observations on patients undergoing fluid resuscitation: “Injection of a fluid that will increase blood pressure has dangers in itself. Hemorrhage in a case of shock may not have occurred to a marked degree because blood pressure has been too low and the flow to scant to overcome the obstacle offered by the clot. If the pressure is raised before the surgeon is ready to check any bleeding that may take place, blood that is sorely needed may be lost.”13 Dr. Cannon’s endpoint of resuscitation before definitive hemorrhage control was a systolic pressure of 70 mm Hg to 80 mm Hg, using a crystalloid/colloid mixture as his fluid of choice.

In World War II, Beecher promulgated Cannon’s hypotensive resuscitation principles in the care of casualties with truncal injuries. “When the patient must wait for a considerable period, elevation of his systolic blood pressure (SBP) to 85 mm Hg is all that is necessary … and when profuse internal bleeding is occurring, it is wasteful of time and blood to attempt to get a patient’s blood pressure up to normal. One should consider himself lucky if a systolic pressure of 80 mm Hg to 85 mm Hg can be achieved and then surgery undertaken.”14

Although these anecdotal reports from earlier generations of surgeons are interesting, more scientific attempts to examine outcomes for permissive hypotension after serious injury have been mixed. The most well-known study that displayed a benefit for delayed aggressive fluid resuscitation until after operative intervention with surgical hemostasis was published in 1994 by Bickell et al. This randomized controlled trial of patients with penetrating truncal injuries compared mortality rates of patients who received immediate versus delayed administration of intravenous (IV) fluids and discovered improved survival, fewer complications, and shorter hospital stays in the delayed group. They demonstrated that, regardless of the victim’s blood pressure, survival was better in their urban “scoop and run” rapid transport system when no attempt at prehospital resuscitation was made.15 The same group published a follow-up abstract in 1995, which was a subgroup analysis of the previous study dividing patients into groups by their injury type. This study demonstrated a lack of affect on survival, in most groups, for patients treated with delayed fluid resuscitation with a survival advantage only for patients with penetrating injuries to the heart (p 0.046).16 This called into question whether study by Bickell et al. was generalizable to trauma population at large. Four years later, Burris et al.17 also suggested that patients could benefit in the short-term by resuscitating to a lower blood pressure. Other studies attempting to replicate these results were unable to find a difference in survival.18,19 Also of note is whether these results in a penetrating trauma population can be extrapolated to the trauma population at large remains to be seen.

In 2006, Hirshberg et al.20 used computer modeling to demonstrate that the timing of resuscitation has different effects on bleeding, with an early bolus delaying hemostasis and increasing blood loss and a late bolus triggering rebleeding. Animal models exploring the effect of fluid administration on rebleeding have been equally contradictory, with some demonstrating that limiting fluids reduces hemorrhage, 21 whereas others demonstrate that fluids do not increase bleeding.22 Moreover, the limited use of fluids during resuscitation efforts is in direct opposition to guidelines put forth by the American College of Surgeons and the Advanced Trauma Life Support protocol.23

The discussion about the risks and benefits of permissive hypotension beg additional questions: even if one believes that permissive hypotension is beneficial, it seems intuitive that some low threshold of safety should exist. How low of a blood pressure can the injured patients tolerate? For how long? Does this theoretical lower limit change when considering not only the initial hypotensive/hypoxic injury but reperfusion injury as well? At the other end of the spectrum, at what level of blood pressure do we “pop the clot” off of spontaneously clotted vessels? Does this point vary with types of resuscitation fluid, time of onset, rate of resuscitation, and the nature of the wound? How does permissive hypotension come into play in the setting of multiple injuries? Most of the work in this modality has been done in penetrating trauma. What is the role of permissive hypotension in blunt trauma? This is an especially pertinent question in injuries where hypotension has been shown to be detrimental, such as brain injury. This important point of contention that, in severe traumatic brain injury (TBI), denying fluids can attenuate the injury by decreasing the intracerebral perfusion pressure has been entertained before.24,25

Unfortunately, no evidence-based recommendations exist from any of the field’s leading trauma organizations. In their absence, the findings from historical military medical sources, modern urban transport studies, and recent laboratory animal models suggest that trauma patients without definitive hemorrhage control should have a limited increase in blood pressure until definitive surgical control of bleeding can be achieved. The potential for rebleeding against the detrimental effects of systemic ischemia and reperfusion require further study. Until more detailed studies are conducted, hard guidelines cannot be put forth.

  1. Anaesthesia for vascular emergencies
  2. Hypotensive Resuscitation in Patients with Ruptured Abdominal Aortic Aneurysm
  3. Immediate versus delayed fluid resuscitation for hypotensive patients with penetrating torso injuries
  4. Jem’s – Permissive Hypotension in Trauma Resuscitation
  5. LifeInTheFastLane – Permissive Hypotension
  6. Permissive hypotension and desmopressin enhance clot formation
  7. Permissive hypotension does not reduce regional organ perfusion compared to normotensive resuscitation: animal study with fluorescent microspheres
  8. Permissive hypotensive resuscitation–an evolving concept in trauma
  9. Target blood pressure for hypotensive resuscitation
  10. Trauma – Permissive Hypotension
  11. Wikipedia – Permissive Hypotension

Anaesthesia for vascular emergencies

For aortic rupture, permissive hypotension should be a standard of care with the aim of keeping the systolic blood pressure 50–100 mmHg as long as consciousness is maintained [1, 36, 57]. Excessive fluid administration, in an attempt to normalise blood pressure, dilutes coagulation factors, disrupts thrombus and can cause expansion and rupture of a contained retroperitoneal haematoma [11].

Haemorrhagic shock, therapeutic management

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Damage control resuscitation from major haemorrhage in polytrauma

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Traumatic Brain Injury or TBI

Why does TBI require a higher systolic BP than required for permissive hypotension?

  1. CPP = MAP- ICP
  2. MAP = [DBP+1/3 (SBP-DBP)]

Progressive Blood Loss

(Committee on Trauma Advanced Trauma Life Support Manual. Chicago: American College of Surgeons; 1997. pp. 103–112.)

(These are ideal conditions/scenario’s and rarely occur together in real life as described below.)

The American College of Surgeons identifies four categories of acute blood loss based on the percent loss of blood volume.

Class I: Loss of 15% or less of the total blood volume. This degree of blood loss is usually fully compensated by transcapillary refill. Because blood volume is maintained, clinical findings are minimal or absent.

Class II: Loss of 15-30% of the blood volume. The clinical findings at this stage may include orthostatic changes in heart rate and blood pressure. However, these clinical findings are inconsistent. Sympathetic vasoconstriction maintains blood pressure and perfusion of vital organs, but urine output can fall to 20-30 ml/hr, and splanchnic flow may also be compromised. Splanchnic hypoperfusion is a particular concern because it can lead to breakdown of the intestinal barrier and translocation of microbes and inflammatory cytokines, setting the stage for systemic inflammation and multiple organ failure.

Class III: Loss of 30-40% of the total blood volume. This marks the onset of decompensated hypovolemic shock, where the vasoconstrictor response to hemorrhage is no longer able to sustain blood pressure and organ perfusion. The clinical consequences include hypotension and reduced urine output (usually 5-15 ml/hr). Systemic vasoconstriction may be attenuated or lost at this stage, resulting in exaggerated hypotension.

Class IV: Loss of more than 40% of blood volume. Hypotension and oliguria are profound at this stage (urine output may be <5 ml/hr, and these changes may be irreversible.

American College of Surgeon’s Classes of Acute Hemorrhage

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The rational clinical examination. Is this patient hypovolemic?

 Oxygen Consumption vs Delivery

(Marino, The ICU Book, 218)

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Clinical review: Hemorrhagic shock

Diagnostic Accuracy of Vital Signs for Acute Blood Loss

  jrc80003t4

Tachycardia in the supine position is absent in a majority of patients with moderate-to-severe blood loss. In fact, bradycardia may be more prevalent in acute blood loss. Orthostatic vital signs have limited value in the evaluation of hypovolemia. According to ATLS the use of the hematocrit to estimate blood loss is unreliable and inappropriate. In the early hours after acute hemorrhage, the hematocrit is a reflection of the resuscitation effort (the type of infusion fluid and the volume infused), not the severity of blood loss. (Marino, The ICU Book, 214-6)

 

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  Diagnostic Accuracy of Physical Signs for Hypovolemia Not Due to Blood Loss

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The Trendelenburg Position

Elevation of the pelvis above the horizontal plane in the supine position was introduced in the latter part of the 19th century as a method of facilitating surgical exposure of the pelvic organs. The originator was a surgeon name Friedrich Trendelenburg, who specialized in the surgical correction of vesicovaginal fistulas. The body position that now bears his name was later adopted during World War I as an antishock maneuver that presumably promotes venous return by shifting blood volume from the legs toward the heart. This maneuver continues to be popular today, despite evidence that it does not perform as expected. (Marino, The ICU Book, 219-220)

  1. Trendelenburg position and oxygen transport in hypovolemic adults
  2. Failure of the Trendelenburg position to improve circulation during clinical shock
  3. Blood volume distribution in the Trendelenburg position

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Transfusion

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One of the important discoveries, I believe…is the realization that anemia is well tolerated… providing blood volume is maintained. Daniel J. Ullyot, M.D. (1992)

Anemia is almost universal in patients who spend more than a few days in the ICU (1), and about half of ICU patients with anemia are given one or more transfusions of concentrated erythrocytes (packed red blood cells) to correct the problem (2). This practice of transfusing red blood cells to correct anemia is one of the most fickle and arbitrary interventions in critical care medicine…The fear of anemia is pervasive but unfounded, because (as indicated in the introductory quote) anemia does not compromise tissue oxygenation as long as the intravascular volume (and hence cardiac output) is maintained. The relative importance of blood volume over blood cells is demonstrated by the fact that hypovolemia is a recognized cause of circulatory shock (impaired tissue oxygenation), whereas anemia is not. (Marino, The ICU Book, 659)

Adverse Events Associated with RBC Transfusions

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The viability of platelets in whole blood and erythrocyte concentrates (packed cells) is almost completely lost after 24 hours of storage. Therefore, large-volume transfusions can produce dilutional thromocytopenia. This effect becomes prominent when the transfusion volume exceeds 1.5 times the blood volume (25). (Marino, The ICU Book, 687)

Transfusion for Massive Blood Loss

Questions from LifeInTheFastLane:

  1. Managing The Critical Bleeder!!
  2. Trauma! Massive Transfusion

LifeInTheFastLane – Transfusion Reactions

MDCalc: TASH Score (Trauma Associated Severe Hemorrhage) for Massive Transfusion

Predicts the need for massive transfusion based on clinical and laboratory data.

Video: CATH HURN on MASSIVE TRANSFUSION & HAEMOSTATIC RESUS

 

 

 

 

Parameters For Fluid Replacement

Static Fluid Measures*

Static tests (less sensitive, less specific and less useful that dynamic tests)

  • Clinical static endpoints (e.g. heart rate, blood pressure, collapsed veins, capillary refill time, previous urine output)
    — not sensitive
    — poor inter-observer reliability
  • CVP/PCWP (also delta CVP post fluid challenge)
    — poor predictors
  • CXR
    — look for pulmonary edema
    — unreliable
  • PiCCO – “PiCCO” means Pulse Contour Cardiac Output. The “i” is only included to have an easy sounding and pronounceable word
    — EVLW and ITBV 
  • ‘one off’ lactate or SvO2 (not useful)

Dynamic Fluid Measures*

Dynamic tests

  • Passive leg raising
    — see Passive leg raise
    — can use with pulse pressure change, PPV, VTI (echo), NICOM, carotid Doppler flow, or ETCO2 (if ventilation and metabolic status constant)
  • End-expiratory occlusion test
    — Occluding the circuit at end-expiration prevents the cyclic effect of inspiration to reduce left cardiac preload and acts like a fluid challenge.
    — A 15 second expiratory occlusion is performed and an increase in pulse pressure or cardiac index predicts fluid responsiveness with a high degree of accuracy.
    — The patient must be able to tolerate the 15 second interruption to ventilation without initiating a spontaneous breath.

Ultrasound (can be used dynamically)

  • Echocardiography
    — subaortic velocity time index (VTI) allows measurement of stroke volume
    — EDV approximates preload
  • Lung ultrasound
    — can be used to detect pulmonary edema, i.e. lack of fluid tolerance
  • IVC ultrasound (see below)

Respiratory variation tests (can be used dynamically)

  • IVC ultrasound
    — assess size and degree of inspiratory collapse
    — correlates with CVP, but CVP is a poor indicator of fluid responsiveness
  • Plethmysography
  • systolic pressure, pulse pressure (PPV) and stroke volume (SVV)
    — see Systolic Pressure Variation
    — generally limited to mechanically ventilated patients in sinus rhythm
  • aortic blood velocity

SIGNIFICANCE

  • Fluid responsiveness does not mean that a patient should be given fluids
  • However, if a patient has low cardiac output that requires correction, fluid responsiveness means that cardiac output will improve if fluids are given
  • It means patients are on the ascending portion of their Starling curve, in other words, they have ‘preload reserve’
  • We should probably use different cutoff values for fluid responsiveness depending on the clinical context. Patient’s with severe respiratory failure need higher specificity and lower sensitivity tests of fluid responsiveness, whereas the opposite may be appropriate in patients with pre-renal failure.

(Clinical Judgment is the most important consideration in evaluating patients needs using the information below, especially consider the many other static and dynamic ways discussed)

Volume status and Frank-Starling curves:

Schema Frank Starling curves.jpg

For the same baseline pre-load (A, assessed by CVP) and same increase in pre-load (amount of fluid given: A -> B), the hemodynamic response assessed by the variation in stroke volume is not significant in patients on the flat portion of the Frank Starling curve (poor LV systolic function) : a = b. In these patients, pre-load increase won’t have beneficial effects and may worsen the patient’s condition. In patients who are on the steep portion of the curve, the same increase of pre-load (A -> B) will lead to significant increase in stroke volume: b’ > a’.

Ideally, the volume status is a “functional assessment”: to induce a change in cardiac preload and observe the effects on cardiac output and arterial pressure.

Predictive Value of Techniques Used to Determine Fluid Responsiveness

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Fluid Challenge

Fluid Resuscitation

What is a fluid challenge?

The fluid challenge is a test that allows the clinician to give fluids and at the same time to test the preload reserve of the patient. The judicious administration of intravenous
fluid is an essential part of the management of many sick patients. An inadequate cardiac output (CO) and systemic arterial pressure reduces the delivery of oxygen to a level below the necessary requirements, leading to a cascade of cellular changes that ultimately can result in organ dysfunction and failure.

When the decision of increasing the CO is made, optimization of preload is usually the first step taken. It goes without saying, therefore, that the primary target of a fluid challenge is an increase in SV or CO. An increase of at least 10–15% is considered a positive response [10].

Corrected flow time
The corrected flow time (FTc), derived from oesophageal Doppler monitoring, has been described as indicating fluid challenge and predicting response in surgical patients [32]. The FTc should not be considered an accurate marker of left ventricular preload [33], being
inversely proportional to systemic vascular resistance, and therefore describing left ventricular afterload.

What fluid?
Fluid challenges may be performed with crystalloid (isotonic or hypertonic) or colloids. The ability of colloids to maintain or increase CO should reduce fluid extravasation into the lung, but increased capillary permeability may negate this advantage…Colloid will stay in the intravascular compartment for longer, and hyperoncotic fluid will draw fluid out of the interstitial space, increasing plasma volume beyond the administered volume. Whether this has clinical relevance for the fluid challenge is unclear.

Rate of administration
Rate of administration is probably more important than the amount of fluid and the type of fluid. The best evidence in terms of outcome comes from studies where the fluid challenge technique has been used in goal directed therapy [5–7,9,24]. In these studies, small
boluses of fluid (250 ml, or 3 ml/kg of usually colloids) were given in a short period of time (5–10 min). A response in terms of SV with a CO monitor was considered positive if the SV increased by 10–15%. An algorithm mandates the clinician to repeat this process until the SV
fails to increase above the chosen threshold. This process is called SV maximization.

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Key points

  1. A fluid challenge identifies and simultaneously corrects volume depletion in order to optimize tissue perfusion.
  2. Administration of fluid using a fluid challenge protocol avoids unnecessary fluid administration and may improve outcome in critically ill and elective surgical patients.
  3. Dynamic noninvasive predictors of volume responsiveness such as SV, PLR and DScVO2 should be used in preference to the CVP and PAOP for guiding fluid therapy.
  4. Continuous CO monitors are the best option to monitor the response to a fluid challenge.
  5. The physiological properties of the fluid and the clinical picture should be considered when choosing which fluid to use.

Predicting fluid responsiveness in ICU patients: a critical analysis of the evidence

Volume expansion is frequently used in critically ill patients to improve hemodynamics. Because of the positive relationship between ventricular end diastolic volume and stroke volume,[1] the expected hemodynamic response to volume expansion is an increase in right ventricular end-diastolic volume (RVEDV), left ventricular end-diastolic volume, stroke volume, and cardiac output. The increase in end-diastolic volume as a result of fluid therapy
depends on the partitioning of the fluid into the different cardiovascular compliances organized in series. The increase in stroke volume as a result of end-diastolic volume increase depends on ventricular function since a decrease in ventricular contractility
decreases the slope of the relationship between end-diastolic volume and stroke volume.[1] Therefore, only 40 to 72% of critically ill patients have been shown to respond to volume expansion by a significant increase in stroke volume or cardiac output in studies [2–13] designed to examine fluid responsiveness. This finding emphasizes the need for predictive
factors of fluid responsiveness in order to select patients who might benefit from volume expansion and to avoid ineffective or even deleterious volume expansion (worsening in gas exchange, hemodilution) in nonresponder patients, in whom inotropic and/or vasopressor support should preferentially be used.

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Intraoperative fluid restriction improves outcome after major elective gastrointestinal surgery

Monitoring of peri-operative fluid administration by individualized goal-directed therapy

  1. Oesophageal Doppler

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Fluid Challenge is potentially risky

Pcap-PAOP difference is high in ALI/ARDS

  1. Collee et al. Anesthesiology 1987
  2. Radermacher et al. Anesthesiology 1989
  3. Radermacher et al. Anesthesiology 1990
  4. Teboul et al J. Appl Physiol 1992
  5. Benzing et al. Acta Anaesthesiol Scand.1994
  6. Rossetti et al. Am J Respir Crit Care Med 1996
  7. Benzing et al. Br J Anaesth. 1998
  8. Nunes et al. Intensive Care Med. 2003
  9. Her et al. Anesthesiology 2005

Degree of pulmonary edema poorly evaluated by Pcap and  lung capillary permeability is often altered in ICU pts

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CVP

Cardiovascular Physiology Concepts – Central Venous Pressure

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CVP Measurement (Synopsis shown listed below, but see the link for more details)

OVERVIEW

  • Central venous pressure (CVP) is the pressure in the central veins (internal jugular, subclavian or femoral)
  • typically referred to as the blood pressure in the proximal SVC, near the junction with the right atrium
  • normal is 0-6mmHg in a spontaneously breathing non-ventilated patient
  • CVP represents the driving force for filling the right atrium and ventricle
  • measurement reflects vascular compliance and changes in volume status
  • Despite the widespread belief that CVP reflects the adequacy of cardiac preload in critically ill patients, there is a large body of evidence suggesting that the relationship between CVP and cardiac output is tenuous
  • CVP represents the interaction between pump function and venous return and can give meaningful information about volume status if some measurement of cardiac function is known

CVP WAVEFORM

a = atrial contraction
c = closing and bulging of the tricuspid valve
x = atrial relaxation
v = passive filling of atrium
y = opening of the tricuspid valve

USE

Diagnosis of:

  • right ventricular infarction
  • PE
  • ARDS
  • cor pulmonale
  • tamponade

Do not use CVP to assess fluid responsiveness

  • very poor relationship between CVP and blood volume and CVP/DeltaCVP is a poor predictor of the hemodynamic response to a fluid challenge.

Venous Function and Central Venous Pressure

Measuring Central Venous Pressure

CVP and Fluid Responsiveness

  • Central venous pressure (CVP) has been used over the last 50 years to assess volume status and fluid responsiveness in critically ill patients.
  • Despite widespread practice habit, CVP has not been shown to reliably predict fluid responsiveness in the critically ill.
  • In a recent updated meta-analysis, Marik et al reviewed 43 studies, totaling over 1800 patients.
    • 57% of patients were fluid responders
    • The mean CVP was 8.2 mm Hg for fluid responders and 9.5 mm Hg for non-responders
    • For studies performed in ICU patients, the correlation coefficient for CVP and change in cardiac index was just 0.28.
  • Bottom line: Current literature does not support the use of CVP as a reliable marker of fluid responsiveness.

References

Marik PE, Cavallazzi R. Does the central venous pressure predict fluid responsiveness? An updated meta-analysis and a plea for some common sense. Crit Care Med 2013:41:1774-1781.

Emcrit – Pressure Transducer Set-up for CVP and A-Lines

PiCCO

  1. Accurate characterization of extravascular lung water in acute respiratory distress syndrome
  2. Extravascular lung water in sepsis-associated acute respiratory distress syndrome: indexing with predicted body weight improves correlation with severity of illness and survival
  3. Extravascular lung water measurements and hemodynamic monitoring in the critically ill: bedside alternatives to the pulmonary artery catheter
  4. Train the Trainer – Advanced Hemodynamic Monitoring – PiCCO Technology
  5. Case Study – Acute Burn Injury with Unclear Fluid Resuscitation
  6. Pulmonary artery catheter versus pulse contour analysis: a prospective epidemiological study
    1. On direct comparison, the use of PiCCO was associated with a greater positive fluid balance and fewer ventilator-free days. After correction for confounding factors, the choice of monitoring did not influence major outcomes, whereas a positive fluid balance was a significant independent predictor of outcome
    2. More recently, new technology (PiCCO [pulse contour cardiac output] System; PULSION Medical Systems AG, Munich, Germany) that provides an alternative to the PAC has been developed and applied [5]. This new technology uses transpulmonary thermodilution and pulse contour analysis to calculate cardiac output, stroke volume variation, intra-thoracic blood volume, and extra-vascular lung water (EVLW). In patients who already have a central line, PiCCO requires only the insertion of a 4-French femoral catheter. Several small studies have been conducted to compare the PAC to PiCCO in terms of physiological relevance (for example, ability to predict fluid responsiveness). They have suggested that PiCCO obtained data such as stroke volume variation or intra-thoracic blood volume index (ITBI) may better predict fluid responsiveness [5-10]. This may or may not affect clinical outcome.
    3. Pulsion – PiCCO Technology – FAQ
    4. Swan Ganz Catheters – A Learning Guide – PiCCO
PiCCO2 – 1. Configuration & Navigation

Passive Leg Raise

  1. Increase in right ventricular preload (Thomas et al 1965)
  2. Increase in left ventricular preload (Rocha 1987, Takagi 1989, De Hert 1999, Kyriades 1994 )
  3. Changes in BP induced by passive leg raising predict response to fluid loading in critically ill patients
    1. Image not available.
    2. Image not available.
    3. Image not available.
    4. In most of the patients, PPrad (radial artery pulse pressure) slightly increased during PLR (Fig 2). This increase in PPrad was positively correlated to the increase in SV during PLR (r 0.77;p  0.001) [Fig 3]
  4. Passive leg raising does not produce a significant or sustained autotransfusion effect
  5. Monitoring volume and fluid responsiveness: From static to dynamic indicators
    1. The passive leg raising (PLR) test has been proposed as another preload challenge taking its advantage to be independent of heart–lung interactions and thus to be used in all patients, even those who are not intubated[45]. Lifting the legs from the horizontal position induces a gravitational transfer of blood from the lower limbs towards the intrathoracic compartment. This significantly increases the right and left cardiac preload[46], supporting the fact that the volume of blood transferred to the heart during PLR is sufficient for challenging the Frank–Starling curve.
    2. The excellent ability of PLR to serve as a test of preload responsiveness was demonstrated in patients with acute circulatory failure [47]. A 10–12% increase in cardiac output or stroke volume during PLR enables us to predict fluid responsiveness, even in patients with cardiac arrhythmias and/or spontaneous ventilator triggering [28]. It is important to note that: (1) changes in arterial pressure cannot be used to assess the hemodynamic response to PLR as it can result in false-negative cases [28] and (2) the cardiac output response to PLR must be assessed with a real-time monitoring device as the effects of PLR are transient and reach their maximum after only 30–90 s [45]. Indeed, probably because of the development of some compensatory mechanisms, the increase in cardiac output during PLR is not sustained when the leg elevation is prolonged. This is particularly marked in septic patients in whom an important capillary leak may account for an attenuation of the PLR effects after 1 min. Thus, real-time cardiac output monitoring technologies and devices such as PiCCO,  FloTrac/Vigileo, oesophageal Doppler, USCOM and echocardiography are perfectly suitable for this purpose as demonstrated by clinical studies [35]. More recently, the real-time changes in end-tidal carbon dioxide, which reflect the changes in cardiac output, were shown to assess the response to PLR and thus to predict fluid responsiveness in mechanically ventilated patients [49,50].
    3. Beyond its reliability and easiness, the PLR test has some limitations [45]. First, it cannot be used in instances in which mobilizing the patient is not possible or allowed, like in the operating theatre or in the case of head injury [51]. Second, the value of the PLR has been questioned in cases of increased intra-abdominal pressure [52], although this has to be confirmed.
  6. Non-invasive assessment of fluid responsiveness by changes in partial end-tidal CO2 pressure during a passive leg-raising maneuver
  7. End-tidal carbon dioxide is better than arterial pressure for predicting volume responsiveness by the passive leg raising test

End-expiratory occlusion test

The end-expiratory occlusion test

This test is another method that takes advantage of heart-lung interactions to predict fluid responsiveness in ventilated patients. During mechanical ventilation, each insufflation increases the intrathoracic pressure and impedes venous return. Thus, interrupting the respiratory cycle at end-expiration inhibits the cyclic impediment in venous return. The resulting increase in cardiac preload may thus help to test preload responsiveness (Figure 1). Indeed, it was demonstrated that if a 15-second end-expiratory occlusion test increased the arterial pulse pressure or the pulse contour-derived cardiac output by more than 5%, the response of cardiac output to a 500 ml saline infusion could be predicted with good sensitivity and specificity [31]. Noticeably, all patients of the latter study were arrhythmic or had mild spontaneous breathing activity. These initial results were recently confirmed [26].

Beyond its simplicity, the main advantage of the end-expiratory occlusion test is that it exerts its hemodynamic effects over several cardiac cycles and thus remains valuable in case of cardiac arrhythmias [31]. Also, the end-expiratory occlusion test can be used in patients with spontaneous breathing activity, unless marked triggering activity interrupts the test. Another limitation is that the effects of the end-expiratory occlusion test, which must be observed over 15 s, are much easier to observe on a continuous display of cardiac output than on the arterial pulse pressure because the value of the latter is not continuously calculated and displayed by bedside monitors.

Hemodynamic parameters to guide fluid therapy

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End-Expiratory Occlusion Test Predicts Preload Responsiveness Independently of Positive End-Expiratory Pressure During Acute Respiratory Distress Syndrome

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Ultrasound

Echocardiography

Predicting fluid responsiveness with transthoracic echocardiography is not yet evidence based

Echocardiography is a well-established method to assess cardiac anatomy and biventricular function. When Doppler technique is added, stroke volume (SV) may be estimated across the aortic valve.(3) When transthoracic echocardiography (TTE) is performed, the method is non-invasive and may be applicable to most intensive care patients.(4) The clinical interest in utilizing TTE by non-cardiologist in intensive care medicine has resulted in echocardiography protocols such as the Focus Assessed Transthoracic Echocardiography and Critical Care Echocardiography.(5,6) Thus, major intensive care societies now recommend that echocardiography should be part of the curriculum of intensive care physicians.(7) As TTE is becoming an integrated tool for circulatory assessment in the intensive care unit, it is imperative to know TTE’s validity as a test for fluid responsiveness. Therefore, the aim of this systematic review was to assess the predictive value of TTE for fluid responsiveness.

F.A.T.E.

Trans-thoracic Echo Standard Views Intro Part 1 of 2 [UndergroundMed]

 

Trans-thoracic Echo Standard Views Intro part 2 of 2 [UndergroundMed]

 

FATE Exam: Focused Assessed Transthoracic Echo

 

Focus Assessed Transthoracic Echocardiography (FATE)

R.U.S.H. Exam

  1. Mount Sinai Emergency Medicine Ultrasound – RUSH
  2. Emcrit – Rapid Ultrasound for Shock and Hypotension – the RUSH Exam
  3. Bedside Ultrasound in Resuscitation and the Rapid Ultrasound in Shock Protocol
  4. SonoCase: 45 yr old female acute respiratory distress…. RUSH, part deux
  5. SonoCase: 78 yr old, hypotensive, altered…Welcome to “RUSH” week!
Rapid Ultrasound for Shock and Hypotension — the RUSH Exam

 

RUSH: Rapid Ultrasound in Shock
Echocardiographic Evaluation of Hypovolemia and Volume Responsiveness

 

Audio for this is found at: Sharon Kay: Echo for Everyone: 5 Things Never to Miss

Trauma Fast Exam (from my previous post)

Lung ultrasound

  1. Fluid administration limited by lung sonography: the place of lung ultrasound in assessment of acute circulatory failure (the FALLS-protocol)
UltrasoundPodcast.com – Ultrasound for Dyspnea

 

Lung ultrasound: a new tool for the cardiologist

  1. The main application of LUS for the cardiologist is the assessment of B-lines. B-lines are reverberation artifacts, originating from water-thickened pulmonary interlobular septa. Multiple B-lines are present in pulmonary congestion, and may help in the detection, semiquantification and monitoring of extravascular lung water, in the differential diagnosis of dyspnea, and in the prognostic stratification of chronic heart failure and acute coronary syndromes.
  2. LUS limitations are essentially patient dependent. Obese patients are frequently difficult to examine because of the thickness of their ribcage and soft tissues. The presence of subcutaneous emphysema or large thoracic dressings alters or precludes the propagation of ultrasound beams to the lung periphery.
  3. The main limitation of B-lines is the lack of specificity. As already mentioned, they are a sign of interstitial syndrome, therefore they are a very sensitive but not specific sign of cardiogenic pulmonary edema. How to distinguish the different etiologies of B-lines has been discussed. However, it must be always reminded that all instrumental data should be evaluated within the clinical context and integrated with patient’s history. No single test alone allows to establish the diagnosis.

Figure 2

Figure 3

Figure 4

Figure 1

Figure 5

Ultrasound Podcast – Lung Ultrasound with Vicki Noble – Part 1

 

Ultrasound Podcast – Lung Ultrasound with Vicki Noble – Part 2

IVC Ultrasound

Anatomy

  1. The inferior vena cava returns blood from the body to the right atrium
  2. Formed by the convergence of the iliac veins
  3. Retroperitoneal
  4. Right of the aorta
  5. Normal size <2.5 cm
  6. Varies w respiration

Stanford University – IVC

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ICU Sonography – Tutorial 4 – Volume status and preload responsiveness assessment

Figure 1: Longitudinal view of the inferior vena cava (IVC): RA: right atrium. From http://www.pifo.uvsq.fr/hebergement/webrea/index.php?option=com_content&amp;task=view&amp;id=36&amp;Itemid=93

Figure 3: Simultaneous measurements of the central venous pressure (CVP) and IVC diameter at the end of expiration in 108 mechanically ventilated patients.: From: http://www.pifo.uvsq.fr/hebergement/webrea/index.php?option=com_content&amp;task=view&amp;id=36&amp;Itemid=93

IVC Ultrasound for Fluid Responsiveness

SCOTT WEINGART (@EMCRIT) ON IVC ULTRASOUND

THE GREAT IVC DEBATE: STONE V. WEINGART. THE RUMBLE IN THE CASTLE 2012! PART 1 (STONE) #FOAMED

Podcast 86 – IVC Ultrasound for Fluid Tolerance in Spontaneously Breathing Patients – EAT IT STONE

Emcrit – IVC for Fluid Responsiveness

SMACC: The Dark Art Of IVC Ultrasound

IVC diameter (cm) IVCCI Estimated RA pressure (mm Hg)
<1.7 >50% 0-5
>1.7 >50% 6-10
>1.7 <50% 11-15
‘dilated’ none >15

Use M-mode assessment in the subxiphoid ling axis, and ideally a sniff test.

It’s probably better for ventilated patients than spontaneously breathing patients (you can remove much of the breath-to-breath variation that confounds so many of these assessment tools). It’s also probably OK at extremes (flat versus full) and serial measurements are probably a good idea.

  • No-one knows where we should measure the IVC. The IVC collapses non-uniformly. Most studies measure the IVC at or around the confluence with the hepatic veins. An influential study by Wallace et al warned against measuring at the junction with the right atrium, but with no gold standard in their study they had no actual justification for this advice.
  • No-one knows how to measure it. Many experts love M-mode, but this has serious flaws when measuring the IVC.
  • We don’t even know where to place the probe. Most studies use the subxiphoid long axis. Some recommend the subxiphoid short axis. Others (such as ACEP) recommend the midaxillary long axis. But every approach has theoretical and actual flaws. Probably the worst is the midaxillary long axis, but then again… no-one knows.
  • The sniff test is a great party trick but not validated. It seems like a waste of time to me.
  • That table above is probably useless. Everyone’s IVC is different and there are plenty of confounding factors (patient size and position, manner of breathing, measurement site…)

Ultrasound Guided Volume Assessment Using Inferior Vena Cava Diameter

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Audio for the following presentation is located at: https://gmep.org/media/14673

 

Emcrit – Ultrasound of the IVC in the Non-Intubated Patient

The respiratory variation in inferior vena cava diameter as a guide to fluid therapy

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Plethmysography

Examining amplitude variation between inspiration and expiration phases has been extended to the plethysmographic waveform. Although this technique has several
similarities to arterial pulse pressure variation, there are several important differences.
The plethysmographic waveform obtained from a standard pulse oximeter probe is
based on transmission and reflection of infrared wavelengths of light by tissue. The
pulsatility is a function of changing tissue volume between systole and diastole,
producing the familiar wave tracing.

The pulse oximeter as a gauge of volume status first was suggested by Partridge [26] in
1987. Variation in the plethysmographic waveform has been referred to by many names:
change in pulse oximetry plethysmography (dPOP), ventilation-induced plethysmographic
variation (VPV), and DPPLET. For the sake of this article, the authors will refer to VPV (VPV(%) 5 100 ([Max amplitude Min amplitude]/[(Max amplitude Min amplitude)/2])). Cannesson and colleagues [27] reported the strong correlation (r2 5 .82,P<.001) of VPV with PPV in 22 mechanically ventilated patients. It should be noted that the precision of this correlation appears to decrease as variation increases. The Cannesson study did not demonstrate volume responsiveness, but only that VPV of greater than or equal to 15% was predictive of having PPV greater than or equal to 13%, the threshold value for volume responsiveness sited in many studies. Wyffels and colleagues [28] reported that in 32 postoperative cardiac surgery patients, PPV and VPV reliably predicted at least a 15% increase in cardiac index in response to administration of 500 mL 6% hydroxyethylstarch with an AUC (95%CI) of 0.937 (0.792 to 0.991) and 0.892 (0.731 to 0.972), respectively. Feissel and colleagues [29] demonstrated in 23 septic patients that a VPV of 14% allowed discrimination of volume responders and nonresponders with a sensitivity of 84% and specificity of 80%.

Although the obvious and tantalizing advantage to the use of the pulse oximeter to
determine fluid responsiveness is the complete noninvasiveness of the technique, at
this time, evidence does not support reliance on this method.

Adapted from Cannesson M. et. al. Br J Anesth 2008;101(2):200-206

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Masimo – Clinical Evidence – Pleth Variability Index (PVI®)

Systolic pressure, pulse pressure (PPV) and stroke volume (SVV)

  1. Advanced Hemodynamic Monitoring – Can We Use Fluid to Improve Hemodynamics?
    1. In clinicians’ quest to achieve optimal oxygen delivery (DO2) they are often faced with imprecise, non-specific information in which to guide their therapy. Traditional hemodynamic monitoring parameters (HR, MAP, CVP, and PAOP) are often insensitive and sometimes misleading in the assessment of circulating blood volume. However, the appropriateness of their interventions is often crucial to avoid the deleterious effects of over-, under-, or inappropriate resuscitation. Volume is one of the first therapeutic interventions clinicians turn to when optimizing DO2.
    2. Stroke volume variation is a naturally occurring phenomenon in which the arterial pulse pressure falls during inspiration and rises during expiration due to changes in intra-thoracic pressure secondary to negative pressure ventilation (spontaneously breathing). Variations over 10mmHg have been referred to as pulsus paradoxus. The normal range of variation in spontaneously breathing patients has been reported between 5-10mmHg.
      Reverse pulsus paradoxus is the same phenomenon with controlled mechanical ventilation, however, in reverse. Arterial pressure rises during inspiration and falls during expiration due to changes in intra-thoracic pressure secondary to positive pressure ventilation. In addition to reverse pulsus paradoxus, it has also been referred to as paradoxical pulsus, respiratory paradox, systolic pressure variation and pulse pressure variation. Traditionally SVV is calculated by taking the SVmax – SVmin / SV mean over a respiratory cycle or other period of time.
    3. SVV and assessing fluid response
      SVV and its comparable measurement, pulse pressure variation (PPV), are not indicators of actual preload but of relative preload responsiveness. SVV has been shown to have a very high sensitivity and specificity when compared to traditional indicators of volume status (HR, MAP, CVP, PAD, PAOP), and their ability to determine fluid responsiveness. The following table of studies demonstrates SVV sensitivity and specificity in predicting fluid responsiveness against a specified infused volume and defined criteria for a fluid responder.
    4. image

        1. Berkenstadt H, et al. Stroke volume variation as a predictor of fluid responsiveness in patients undergoing brain surgery. Anesth Analg 2001;92:984-989.
        2. Michard F. Changes in arterial pressure during mechanical ventilation. Anesthesiology 2005; 103:419-428.
        3. Reuter DA, et al. Usefulness of left ventricular stroke volume variation to assess fluid responsiveness in patients with reduced cardiac function. Crit. Care Med 2003; 31:1300-404.

  2. Pulse pressure variation: beyond the fluid management of patients with shock
    1. In the previous issue of Critical Care, Keyl and colleagues [1] have investigated the effects of cardiac resynchronization therapy on arterial pulse pressure variation (PPV). Many studies [2] have shown that PPV is much more accurate than cardiac filling pressures and volumetric markers of preload to predict fluid responsiveness (that is, the hemodynamic effects of volume loading). PPV is also more reliable than other dynamic parameters such as systolic pressure variation [3,4] or pulse contour stroke volume variation [4]. In this respect, PPV is used increasingly in the decision-making
      process regarding volume expansion in patients with hemodynamic instability [2]. Limitations to the use of PPV do exist (mainly active breathing, cardiac arrhythmia, and low tidal volume) and have been described in detail elsewhere [2,5].
    2. As an indicator of the position on the Frank–Starling curve, PPV is as useful to predict the deleterious hemodynamic effects of fluid depletion as it is to predict the beneficial
      effects of fluid loading [6].
    3. In such clinical situations, fluid management could be refined by PPV monitoring: a large PPV or an increase in PPV indicates that the patient is operating on the steep portion of the Frank–Starling curve, and hence indicates that further ultrafiltration or further fluid restriction/depletion will induce hemodynamic
      instability
    4. Another potential field of application for PPV is the intraoperative fluid optimization of patients undergoing high-risk surgery. Several studies [11-13] have shown that monitoring and maximizing stroke volume by fluid loading (until the stroke
      volume reaches a plateau, actually the plateau of the Frank–Starling curve) during high-risk surgery is associated with improved postoperative outcome.
    5. image
  3. Pulse pressure variation: where are we today?
    1. The dynamic parameters of fluid responsiveness are related to cardiopulmonary
      interactions in patients under general anesthesia with mechanical ventilation. This is far superior to static indicators (such as central venous pressure) [1]. The advantage of these dynamic measurements is that they can be derived from a single arterial pressure waveform [systolic pressure variations (SPV), and pulse pressure variations (PPV)]. Measurement of these indicators can predict an increase in cardiac output induced by volume expansion before volume expansion is actually performed.
    2. Moreover, it is now possible to obtain PPV non invasively using respiratory variations in the pulse oximeter plethysmographic waveform amplitude (DPOP) [7, 8,17, 24–28].
    3. The goal of perioperative fluid optimization is the same than that of the cardiovascular system under normal conditions: an adequate blood flow in vitals and in traumatized
      tissues, as not to compromise the first and to enable effective wound healing in the latter [64].
    4. image
  4. Geneva Hemodynamic Research Group – How to explain simply: Pulse Pressure Variation (PPV)
  5. Systolic Pressure Variation And Stroke Volume Variation
  6. Advanced Hemodynamic Monitoring – Stroke Volume Variation
  7. The effect of graded hemorrhage and intravascular volume replacement on systolic pressure variation in humans during mechanical and spontaneous ventilation
    1. imageimage
    2. Overall, the change in SPV with each 500-mL volume shift was not as consistent during spontaneous ventilation in comparison to mechanical ventilation (Figure 5).

PPV = (Pmax–Pmin)/([Pmax+ Pmin])/2)

Criteria for calculation
–Sinus rhythm
–Passive breathing (AC mode with good synchrony)
–Tidal volume > 8 cc/kg
–Pmax and Pmin must be calculated over the same respiratory cycle

Ability of Pulse Power, Esophageal Doppler and Arterial Pulse Pressure to Estimate Rapid Changes in Stroke Volume in Humans

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Clinical use of respiratory changes in arterial pulse pressure to monitor the hemodynamic effects of PEEP.

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PPV Predicts the Decrease in Cardiac Index with the addition of 10 cm H2O PEEP

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Relation between respiratory changes in arterial pulse pressure and fluid responsiveness in septic patients with acute circulatory failure

Baseline PPV Predicts Volume Responsiveness

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Receiver Operator Characteristic (ROC) Curve for >15% increase in cardiac output to a 500 ml volume challenge in patients in septic shock

 

imagePPV >13%
SPV > 13%
Pra > 8 mm Hg > 8 mm Hg
Ppao > 12 mm Hg

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PULSE PRESSURE VARIATION IN 5 EASY STEPS

Technical Limitations of PPV and SVV for Assessment of Preload for Assessment of Preload-Responsiveness

  1. Requires fixed HR Requires fixed HR
    1. Atrial fibrillation, frequent PVCs Atrial fibrillation, frequent PVCs
  2. Requires positive Requires positive-pressure ventilation pressure ventilation
  3. Requires no spontaneous ventilatory efforts
    1. Can not use during CPAP, PSV, A/C Can not use during CPAP, PSV, A/C
  4. Cor Pulmonale and ventricular interdependence Cor Pulmonale and ventricular interdependence
  5. Magnitude of PPV or SVV will change if tidal Magnitude of PPV or SVV will change if tidal volume changes
  6. Changes in vasomotor tone will alter the Changes in vasomotor tone will alter the PPV/SVV relation

Aortic blood velocity

  1. Respiratory Changes in Aortic Blood Velocity as an Indicator of Fluid Responsiveness in Ventilated Patients With Septic Shock
    1. image
    2. To summarize, our findings suggest that, in contrast with EDAI, DeltaVpeak is an accurate indicator of fluid responsiveness in sedated septic shock patients who are receiving mechanical ventilation and who have preserved LV systolic function. Therefore, an analysis of the DeltaVpeak could facilitate the hemodynamic management of such patients

Other Basic Fluid Management Methods

  1. Maintenance
  2. Deficits
  3. Insensible loss
  4. Estimated blood loss

Maintenance

  1. 4:2:1 Rule or Calculate Wt + 40 cc  [For any person weighing more than 20kg] (Miller, Basics of Anesthesia: Expert Consult, 552)
    1. MD Calc – Maintenance Fluids Calculations
    2. Steps
      1. 4 ml/kg/hr for first 10 kg (=40ml/hr)
      2. then 2 ml/kg/hr for next 10 kg (=20ml/hr)
      3. then 1 ml/kg/hr for any kgs over that
  2. Calculated weight: (IBW + ABW)/2
  3. IBW male: 110 lbs + 7 lbs * in > 5’
  4. IBW female: 100 lbs + 6 lbs * in > 5’
Maintenance Fluids Overview [UndergroundMed]

 

 

4-2-1 Rule for Maintenance Fluid Rate

 

Maintenance Fluids Calculation Derivations [UndergroundMed]

Deficits

  1. NPO status: Calculated Wt x hrs NPO x 0.7
  2. Bowel prep ~ 1200cc
  3. Diuretics/ Urine output
  4. NGT drainage
  5. CT drainage

Insensible loss

(Volume based on Calculated Weight)

(4:6:8 Rule – The postoperative patient and his fluid and electrolyte requirements;  Mass General Handbook, Barash, 5th edition, Miller, 5th edition, Miller and Stoelting, 5th edition)

  1. Replace with Crystalloid (NS, LR, Plasmalyte)
    1. Minor: 4 mL/kg/hr
    2. Moderate: 6 mL/kg/hr
    3. Major: 8 mL/kg/hr
Case Type Volume
Non-open 2-3 cc/kg/hr
Open

4-6 cc/kg/hr

Major Abdominal 6-10 cc/kg/hr
Trauma > 10 cc/kg/hr

Estimated blood loss

  1. The 3: 1 Rule, replace 3 cc crystalloid : 1 cc blood loss (Initial resuscitation of hemorrhagic shock)
  2. The 1:1 Rule, replace 1 cc colloid : 1 cc blood loss

Further Estimating the Total Resuscitation Volume

 

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(Marino, The ICU Book, 236)

Hemodynamic monitoring over the past 10 years

Importantly, no monitoring device, no matter how accurate or complete, would be expected to improve patient outcome, unless coupled to a treatment that itself improves outcome [6].

End Points of Resuscitation

The goal of resuscitation in hemorrhagic shock is to restore three parameters: blood flow, oxygen transport, and tissue oxygenation. The parameters are defined by the end-points shown below.

  1. Cardiac index = 3 L/min/m2
  2. Systemic oxygen delivery (DO2)  > 500 ml/minm2
  3. Systemic oxygen uptake (VO2) > 100 ml/min/m2
  4. Arterial lactate <2 mmol/L or base deficit >-2 mmol/L

Oxygen Delivery (DO2)

The oxygen that enters the bloodstream in the lungs is carried to the vital organs by the cardiac output. The rate at which this occurs is call the oxygen delivery (DO2) The DO2 describes the volume of oxygen (in milliliters) that reaches the systemic capillaries each minute. It is equivalent to the product of the O2 content in arterial blood (CaO2) in mL/L and the cardiac output (Q) in L/min (2,5-7).

DO2 = Q x CaO2 x 10

(The multiplier of 10 is used to convert the CaO2 from mL/dL to mL/L, so the DO2 can be expressed in mL/min.) If the CaO2 is broken down into its components (1.34 x Hb x SaO2), the equation can be rewritten as,

DO2 = Q x 1.34 x Hb x SaO2 x 10

The normal DO2 in adults at rest is 900-1,100 mL/min, or 500-600 mL/min/m2 when adjusted for body size.

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(Marino, The ICU Book, 27)

Oxygen Uptake (VO2)

When blood reaches the systemic capillaries, oxygen dissociates from hemoglobin and moves into the tissues. The rate at which this occurs is called the oxygen uptake (VO2). The VO2 describes the volume of oxygen (in mL) that leaves the capillary blood and moves into the tissues each minute. Since oxygen is not stored in tissues, the VO2 is also a measure of the oxygen consumption of the tissues.

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(Marino, The ICU Book, 28)

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Trend is more important than absolute value

Unfortunately, it is not always possible to reach these end-points despite aggressive volume replacement, and the ability to reach the desired end points is a principal determinant of survival. This is demonstrated in Figure 12.7. The graph in this figure shows the effects of controlled hemorrhage and resuscitation on oxygen uptake (VO2) in an animal model of hemorrhagic shock. Note that in the survivors, the VO2 increases and returns to the baseline (pre-hemorrhage) level in response to resuscitation. In contrast, the VO2 in the nonsurvivors shows no response to resuscitation and actually deteriorates further. Thus when hemorrhagic shock becomes refractory to volume resuscitation, the prognosis is bleak.

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(Marino, The ICU Book, 203)

Blood Lactate vs. % Survival

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Endpoints of Resuscitation What Should We Be Monitoring?

Major resuscitation goals in the management of shock include restoration of adequate tissue perfusion and oxygen balance and normalization of cellular metabolism…Traditional endpoints, such as heart rate, blood pressure, mental status, and urine output are useful in the initial identification of inadequate perfusion, but are limited in their ability to identify ongoing, compensated shock. Many clinicians continue to use these parameters as indicators that systemic oxygenation imbalances have resolved, even though they have been found to be poor indicators of ongoing tissue hypoxia. Additional resuscitation endpoints that more closely evaluate the adequacy of perfusion and oxygenation at the tissue level should also be used when managing the critically ill. Selected endpoints should include a variety of global and regional indicators to guide and evaluate the effectiveness of treatment.

Currently, many clinicians are using additional global and regional indicators of oxygen
transport as endpoints of resuscitation (Table 1). Evaluation of these additional endpoints will allow for rapid treatment and stabilization of systemic oxygenation during resuscitation.
Early detection and aggressive management of tissue hypoxia will assist in decreasing complications, limiting organ dysfunction, and improving outcomes. [11]

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Measurement of acid-base resuscitation endpoints: lactate, base deficit, bicarbonate or what?

Lactate

  1. Acid-Base Physiology – Lactic Acidosis
  2. ALiEM – Geriatric Blunt Trauma: Respect the Lactate
  3. BroomDocs – The Lactate “Debate” with Dr Seth Trueger
  4. Don’t take vitals, take a lactate
  5. EMCrit Podcast 37 – Lactate in Sepsis
  6. Emcrit Lactate FAQ
  7. EMCrit Wee – Is Lactate Clearance a Flawed Paradigm?
  8. Surviving Sepsis Campaign
  9. Trick of the Trade: Serial lactate measurements in sepsis?

Bellomo R, Ronco C. The pathogenesis of lactic acidosis in sepsis. Current Opinion in Critical Care 1999;5:452-7.

Lactic acidosis is a common finding in critically ill patients during severe sepsis/septic shock, and a powerful predictor of mortality. Because of the knowledge that lactate is the end product of anaerobic glycolysis, the presence of hyperlactatemia in sepsis has been taken to indicate the development of anaerobic glycolysis within tissues. Such anaerobic glycolysis is understood to result from oxygen “debt” at cellular level. The metabolic acidosis frequently associated with hyperlactatemia has thus been ascribed to hydrogen ions released from adenosine triphosphate hydrolysis. This simplistic view of the pathogenesis and meaning of hyperlactatemia, however, is not supported by available data. Systemic oxygen transport is usually increased rather than decreased in septic patients. Whenever studied, tissue oxygenation is either preserved or increased in septic animals and humans. In addition, lactate levels may fluctuate in response to inotropic drugs and do not consistently decrease when tissue oxygen delivery is increased. Furthermore, there is strong evidence that large amounts of lactate can be produced and released under aerobic conditions and that the pathogenesis of hyperlactatemia in septic states is complex. Such pathogenesis may involve accelerated glycolytic fluxes, the inhibition of pyruvate dehydrogenase activity, and changes in intermediary metabolism. It may also involve the need to modulate the rate and efficiency of glycolytic flux by controlling the redox state of cytoplasm and mitochondria through lactate accumulation.

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Bench-to-bedside review: Lactate and the kidney

Lactate clearance as a target of therapy in sepsis: a flawed paradigm

RenalFellow – Differential Diagnosis: Lactic Acidosis

Resus.me – Some causes of a raised lactate

Marik PE, Bellomo R, Demla V. Lactate clearance as a target of therapy in sepsis: A flawed paradigm. OA Critical Care 2013 Mar 01;1(1):3.

Glycolytic pathway. Epinephrine-increased glycolysis is coupled to Na[+]/K[+]-ATPase activity. From James et al.[39].

Etiology and Therapeutic Approach to Elevated Lactate Levels

2013 Mayo Foundation for Medical Education and Research n Mayo Clin Proc. 2013;88(10):1127-1140

Lactate levels in clinical practice are often used as a surrogate for illness severity
and to gauge response to therapeutic interventions. The use of lactate as a clinical
prognostic tool was first suggested in 1964 by Broder and Weil1 when they observed
that a lactate level of more than 4 mmol/L was associated with poor outcomes in patients
with undifferentiated shock. Since then, much has been published on the use of lactate in a
variety of patient populations. Moreover, causes of elevated lactate levels apart from tissue
hypoperfusion have been recognized and should be considered in the appropriate clinical
context.

Elevated lactate levels are not clearly and universally defined, but most studies use cutoff
values of 2.0 to 2.5 mmol/L,7 whereas “high” lactate levels have been defined as greater than
4.0 mmol/L in several studies.8-11 Furthermore, the “normal value” may vary depending on the assay used. The terms lactate and lactic acid are often used interchangeably, but lactate (the component measured in blood) is strictly a weak base, whereas lactic acid is the corresponding acid. Lactic acidosis is often used clinically to describe elevated lactate levels, but it should be reserved for cases in which there is a corresponding acidosis (pH <7.35).12 The exact pathogenesis of elevated lactate levels in various conditions is likely multifactorial, patient specific, and disease specific. In general, lactate level elevation may be caused by increased production, decreased clearance, or a combination of both. The etiology of elevated lactate levels is perhaps best studied in shock states. Contributing factors seem to include hypoperfusion due to macrocirculatory or microcirculatory dysfunction, mitochondrial dysfunction (including a potential lack of key enzymatic cofactors), and the presence of a hypermetabolic state, among others.13-18 Liver dysfunction may contribute to increased production and decreased clearance, which becomes even more important in states of hypoperfusion.

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An Evaluation of the End Points of Resuscitation

An integration of the following parameters will allow the intensivist to determine the adequacy of volume resuscitation and if/when a vasopressor agent should be initiated:

  1. Urine output
  2. Urine sodium and osmolarity
  3. Mean arterial pressure (cerebral and abdominal perfusion pressure)
  4. BUN
  5. PPV (or SVV)
  6. Heart rate
  7. Lactate
  8. Arterial pH, BE, and HCO3
  9. Mixed venous oxygen saturation SmvO2 or ScvO2
  10. Mixed venous pCO2
  11. Tissue pCO2 (sublingual capnometery or equivalent)
  12. Gastric impedance spectroscopy
  13. Skeletal muscle tissue oxygenation StO2 as measured by NIRS
  14. Extravascular lung water
  15. Intra-abdominal pressure
  16. Technology yet to be developed

Currently, the preponderance of supporting literature favors blood lactate as the optimal resuscitative end point. Because its measurement does not require specialized or invasive equipment, and because today’s technology provides rapid assay results, it possesses many advantages in addition to its validated accuracy. Other techniques that indirectly reflect
BL, such as BD, gastric mucosal pH, and venous hypercarbia, may in time prove as useful as BL, because they may correct more rapidly to adequate resuscitation than BL (less lag time). Tissue oxygen monitoring also holds promise as an emerging technique to gauge resuscitation adequacy. Further prospective goal-directed human studies in all these latter
modalities should be encouraged.

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Limitations of Static Measures Central Venous Pressure

This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVP/DeltaCVP to predict the hemodynamic response to a fluid challenge. CVP should not be used to make clinical decisions regarding fluid management.

Image not available.

ROC AUC = 0.56

Does central venous pressure predict fluid responsiveness? A systematic review of the literature and the tale of seven mares

AUC data were available for 33 studies and correlation data for 20 studies. Overall 57% ± 13% of patients were fluid responders, with 52% ± 11% of ICU patients being fluid responders as compared to 63% ± 15% of patients in the operating room. The mean baseline CVP was 8.2 ± 2.3 mm Hg in the fluid responders and 9.5 ± 2.2 mm Hg in the nonresponders. The summary AUC was 0.56 (95% CI, 0.54–0.58), with no heterogenicity between studies (Q statistic p = 0.9, I2 = 0%). The summary AUC was 0.56 (95% CI, 0.52–0.60) for those studies done in the ICU and 0.56 (95% CI, 0.54–0.58) for those done in the operating room. Similarly, the summary AUC was 0.56 (95% CI, 0.51–0.61) for the cardiac surgery patients and 0.56 (95% CI, 0.54–0.58) for the noncardiac surgery patients. The summary correlation coefficient between the baseline CVP and the delta SVI/CI was 0.18 (95% CI, 0.1–0.25), being 0.28 (95% CI, 0.16–0.40) in the ICU patients, and 0.11 (95% CI, 0.02–0.21) in the operating room patients.

Does the central venous pressure predict fluid responsiveness? An updated meta-analysis and a plea for some common sense

Organ Specific

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Acidosis Algorithm

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MUDPILES (methanol, uremia, diabetic ketoacidosis, propylene glycol, isoniazid, lactic acidosis, ethylene glycol, salicylates)

Both lactate and BD levels may be used to identify lactic acidosis and predict mortality at admission. Increased lactate levels predict mortality and a prolonged course regardless of the associated BD level, whereas an increased BD level has no predictive value if the lactate level is normal.

Discordance between lactate and base deficit in the surgical intensive care unit: which one do you trust?

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Figure 1. Mean (±SE) Cardiac Index, Oxygen Delivery, and Oxygen Consumption in the Three Study Groups.

For each variable, the incremental area under the curve differed significantly among the three groups (P<0.001). B denotes base line. Measurements were made twice a day for five days after randomization.

A trial of goal-oriented hemodynamic therapy in critically ill patients. SvO2 Collaborative Group

Don’t Overshoot Your Mark!

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Supranormal trauma resuscitation causes more cases of abdominal compartment syndrome

During resuscitation from traumatic hemorrhagic shock, normalization of standard clinical parameters such as blood pressure, heart rate, and urine output are not adequate to guarantee survival without organ system dysfunction. Numerous parameters including hemodynamic profiles, acid-base status, gastric tonometry, and regional measures of tissue O2 and CO2 levels have been studied. Many can be useful for predicting risk of organ failure and death. Studies comparing use of these parameters as endpoints for resuscitation protocols, however, have failed to show clear benefit in terms of patient outcomes. At present, it seems prudent to use one of these endpoints rather than relying on standard clinical parameters.

East Association for the Surgery of Trauma – Resuscitation Endpoints

Concise Evolution in Treatment Strategies (I know this leaves a lot of great people out)

  1. Auto transfusion (“Cell Saver”)
  2. Hyperdynamic “Supranormal” Resuscitation (Shoemaker)
  3. Less is More – Mattox
  4. Trauma Vaccine – Vedder, et al.
  5. Hypertonic Saline
  6. Glue Grant
    1. standardization, endpoints, genetics

Recommendations

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Dr. Rivers speaking on Sepsis from 2008

Emcrit – Fluid Resus in Severe Sepsis (Chad Meyers)

EPISODE 22 – FLUID RESPONSIVENESS

EPISODE 23 – FLUID RESPONSIVENESS PART 2

EPISODE 37 – HANEY MALLEMAT INTERVIEW

 

Miscellaneous

Videos

Scalea – Principles of Resuscitation

Hemostatic Resuscitation with Richard Dutton

 

Hypovolemia and Fluid Responsiveness

 

Fluid Responsiveness in the Critically Ill Patient

 

MEDCRAMvideos – Shock Explained Clearly!

 

MEDCRAMvideos – Shock Treatment Explained Clearly!

 

Slides

 

Other Coagulation presentations

 

 

 

 

 

 

 

 

 

 

 

 

 

 

SlideShare: Cardiac Output, Blood Flow, and Blood Pressure

Hypotension Flow Diagram

Hypotension and Shock

Water Balance

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Indications for Damage Control Surgery

Damage control surgery: it’s evolution over the last 20 years

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Inflammation

Management of the Bleeding Cardiac Surgical Patient

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Guidelines

  1. 2006 – Practice Guidelines for Perioperative Blood Transfusion and Adjuvant Therapies: An Updated Report by the American Society of Anesthesiologists Task Force on Perioperative Blood Transfusion and Adjuvant Therapies
  2. 2010 – Management of bleeding following major trauma: an updated European guideline
  3. 2012 – Clinical Practice Guide on Red Blood Cell Transfusion
  4. Ann Intern Med – Red blood cell transfusion: a clinical practice guideline from the AABB
  5. Australia – National Blood Authority – Patient Blood Management Guidelines
  6. Blood transfusion: indications, administration and adverse reactions
  7. Guidelines for Prehospital Fluid Resuscitation in the Injured Patient
  8. Translating resuscitation guidelines into practice: health care provider attitudes, preferences and beliefs regarding pediatric fluid resuscitation performance
  9. Preferences of critical care registrars in fluid resuscitation of major trauma patients: concordance with current guidelines
  10. Inflammation and the Host Response to Injury, a Large-Scale Collaborative Project: Patient-Oriented Research Core—Standard Operating Procedures for Clinical Care: III. Guidelines for Shock Resuscitation
  11. Trauma Exsanguination Protocol Improves Survival and Blood Product Use
  12. East Association for the Surgery of Trauma – Resuscitation Endpoints
  13. East Association for the Surgery of Trauma – Prehospital Fluid Resuscitation in the Injured Patient
  14. East Association for the Surgery of Trauma – Red Blood Cell Transfusion in Adult Trauma and Critical Care
  15. East Association for the Surgery of Trauma – Geriatric Trauma: Parameters for Resuscitation
  16. Suviving Sepsis 2012 Guidelines

Interesting Studies and Clinical Trials

  1. ARISE-RCT: Australasian Resuscitation In Sepsis Evaluation Randomised Controlled Trial
  2. Crash 2
  3. Falls Protocol
  4. FEAST (Fluid Expansion as Supportive Therapy) Trial
  5. Harborview Study – 7.5% Saline and 7.5% Saline/6% Dextran for Hypovolemic Shock
  6. Matters Study (JAMA Surgery)
  7. ProCESS – Protocolized Care for Early Septic Shock
  8. The prospective, observational, multicenter, major trauma transfusion (PROMMTT) study: comparative effectiveness of a time-varying treatment with competing risks
  9. Resuscitation Outcomes Consortium
  10. Saline vs. Albumin Fluid Evaluation Study (SAFE)
  11. TRICC trial

Blogs, Podcasts, and other Resources

  1. ALiEM
    1. Choosing the right vasopressor agent in hypotension
    2. Deciphering Acid-Base Disorders
    3. Do you know your resuscitation room?
    4. Geriatric Blunt Trauma: Respect the Lactate
    5. P-Video: Rule of 15 in anion gap metabolic acidosis
    6. Patwari Academy video: Early goal directed therapy
    7. Paucis Verbis: Composition of intravenous fluids
    8. Trick of Trade: Rule of 10′s for burn fluid resuscitation
    9. RUSH protocol: Rapid Ultrasound for Shock and Hypotension
    10. Sneak Peak “Trick of the Trade”: IO line for failed IV access
    11. Trick of the Trade: Serial lactate measurements in sepsis?
  2. BoringEM
    1. Normal Saline: The Coke of Crystalloid Fluids
  3. BroomeDocs
    1. Should Normal saline be the norm?
    2. The Lactate “Debate” with Dr Seth Trueger
    3. Remote Resuscitation
  4. CrashingPatient
    1. Fluid Resuscitation
    2. Hemodynamic Monitoring
    3. Predicting Fluid Responsiveness
  5. CriticalCareReviews
    1. Fluid Responsiveness
  6. CriticalEcho
    1. Tutorial 4 – Volume status and preload responsiveness assessment – Volume status and preload responsiveness assessment
  7. Emcrit
    1. Hemostatic Resuscitation by Richard Dutton, MD
    2. Podcast 12 – Trauma Resus: Part I
      1. Thoughts on the Resuscitation of the Critically Ill Trauma Patient
      2. Damage Control Anesthesia
    3. Podcast 13 – Trauma Resus II: Massive Transfusion
    4. Podcast 30 – Hemorrhagic Shock Resuscitation
    5. EMCrit Podcast 37 – Lactate in Sepsis
    6. EMCrit Wee – Is Lactate Clearance a Flawed Paradigm?
    7. EMCrit Podcast 49 – The Mind of a Resus Doc: Logistics over Strategy
    8. Emcrit Acid Base Series

      1. Podcast 44 – Acid Base: Part I
      2. Podcast 45 – Acid Base: Part II
      3. Podcast 46 – Acid Base: Part III
      4. Podcast 50 – Acid Base Part IV – Choose the Solution Based on the Problem
      5. Podcast 96 – Acid Base in the Critically Ill – Part V – Enough with the Bicarb Already
      6. Podcast 97 – Acid-Base VI – Chloride-Free Sodium
    9. Podcast 50 – Acid Base Part IV – Choose the Solution Based on the Problem
      1. Vimeo – Acid Base Lecture Part II
      2. Vimeo – Acid Base III
    10. Podcast 64 – Fluid Responsiveness with Dr. Paul Marik
    11. Podcast 85 – A Confirmation of Prejudices: Chloride and Pressure Poisoning
    12. Podcast 86 – IVC Ultrasound for Fluid Tolerance in Spontaneously Breathing Patients – EAT IT STONE – Can the Inferior Vena Cava Ultrasound guide our fluid administration in the ED? Of course it can!
    13. Podcast 90 – Mind of the Resuscitationist Series: Cliff Reid’s Own the Resus Room
    14. Podcast 109 – Mind of the Resuscitationist from SMACC 2013
    15. Rapid Ultrasound for Shock and Hypotension – the RUSH Exam
      1. Original RUSH Article
    16. SMACC Back 2 – IVC for Decisions on Fluid Status
    17. What Will it Take to Kill off CVP?
  8. Emergency Medicine Literature of Note
    1. Chloride-Restriction & More JAMA Inadequacy
    2. Put Hydroxyethyl Starch Away
  9. ERCast
    1. Chest Trauma with Kenji Inaba
    2. How to put in a chest tube
  10. Intensive Care Network
    1. Cath Hurn: There will be Blood! (Massive Transfusion & Hemostatic Resuscitation)
    2. Drenzla on the Fluid Debate
    3. Fluid Therapy by Prof John Myburgh
    4. Podcast 32: Holley on Transfusion
    5. SMACC: Harris – Cardiac Output in the Resuscitation Room – Have you considered the right side?
    6. SMACC: Myburgh on Fluid Resuscitation
    7. SMACC: Johnston on the Assessment of Shock
    8. SMACC: Weingart – The Mind of the Resuscitationist
  11. LifeInTheFastLane
    1. Shock… Do We Know It When We See It?
    2. Fluid Responsiveness
      1. CCC — Fluid challenge
      2. CCC — Passive leg raise
      3. CCC — Systolic Pressure Variation
    3. Managing the Critical Bleeder
    4. SMACC: The Dark Art Of IVC Ultrasound
    5. CVP Measurement
  12. Medscape
    1. An Update on Intravenous Fluids
    2. Dehydration Treatment & Management
    3. Early Fluid Resuscitation Reduces Sepsis Mortality
    4. Fluid Replacement in Critical Care: A New Look at an Old Issue
    5. Fluid Resuscitation in Sepsis and Hemorrhagic Shock: What Do the Data Show?
    6. Fluid Resuscitation in Septic Shock
    7. Fluid Resuscitation Ups Mortality Risk in Children
    8. Hemodynamic Tools in the ICU
    9. The Great Fluid Debate Revisited
  13. Resus.me
    1. Collapsible IVC predicts ‘low’ CVP
    2. End expiratory occlusion
    3. European Trauma Bleeding Guidelines updated
    4. Evidence refutes ATLS shock classification
    5. Fluids contribute to acid-base disturbance on ICU
    6. Predicting volume responsiveness
  14. Sancrit
    1. Fluid Challenges and Arterial Blood Pressure
  15. ShortCoatsInEM
    1. What’s Your Trigger?
  16. SonoSpot: Topics in Bedside Ultrasound
      1. SonoCase: 45 yr old female acute respiratory distress…. RUSH, part deux
      2. SonoCase: 78 yr old, hypotensive, altered…Welcome to “RUSH” week!
  17. UltrasoundPodcast
    1. Integrated ultrasound approach to Fluid Responsiveness……Canadian Style. #FOAMED
    2. THE GREAT IVC DEBATE: STONE V. WEINGART. THE RUMBLE IN THE CASTLE 2012! PART 1 (STONE) #FOAMED
    3. INTEGRATED ULTRASOUND APPROACH TO FLUID RESPONSIVENESS……CANADIAN STYLE. #FOAMED
    4. EPISODE 22 – FLUID RESPONSIVENESS
    5. EPISODE 23 – FLUID RESPONSIVENESS PART 2
    6. SCOTT WEINGART (@EMCRIT) ON IVC ULTRASOUND
    7. EPISODE 37 – HANEY MALLEMAT INTERVIEW

References

  1. 7.5% Saline and 7.5% Saline/6% Dextran for Hypovolemic Shock
  2. A Comparison of Albumin and Saline for Fluid Resuscitation in the Intensive Care Unit
  3. A Multicenter, Randomized, Controlled Clinical Trial of Transfusion Requirements in Critical Care
  4. A novel method for the assessment of the accuracy of computing laminar flow stroke volumes using a real-time 3D ultrasound system: In vitro studies
  5. A physicochemical model of crystalloid infusion on acid-base status
  6. A randomized, controlled, double-blind crossover study on the effects of 2-L infusions of 0.9% saline and plasma-lyte® 148 on renal blood flow velocity and renal cortical tissue perfusion in healthy volunteers
  7. A rational approach to perioperative fluid management
  8. A trial of goal-oriented hemodynamic therapy in critically ill patients. SvO2 Collaborative Group
  9. Ability of Pulse Power, Esophageal Doppler and Arterial Pulse Pressure to Estimate Rapid Changes in Stroke Volume in Humans
  10. Accurate characterization of extravascular lung water in acute respiratory distress syndrome
  11. Acid-base balance in peritoneal dialysis patients: a Stewart-Fencl analysis
  12. Aggressive early crystalloid resuscitation adversely affects outcomes in adult blunt trauma patients: an analysis of the Glue Grant database
  13. An Evaluation of the End Points of Resuscitation
  14. Application of Base Deficit in Resuscitation of Trauma Patients
  15. Applying dynamic parameters to predict hemodynamic response to volume expansion in spontaneously breathing patients with septic shock
  16. Assessing the diagnostic accuracy of pulse pressure variations for the prediction of fluid responsiveness: a “gray zone” approach
  17. Assessment of fluid responsiveness during increased intra-abdominal pressure: keep the indices, but change the thresholds
  18. Assessment of intravascular fluid status and fluid responsiveness during  mechanical ventilation in surgical and intensive care patients
  19. Assessment of intravascular volume: a comedy of errors
  20. Assessment of intravascular volume status and volume responsiveness in critically ill patients
  21. Assessment of volume responsiveness during mechanical ventilation – recent advances
  22. Association between a chloride-liberal vs chloride-restrictive intravenous fluid administration strategy and kidney injury in critically ill adults
  23. Base deficit as a guide to volume resuscitation
  24. Bench-to-bedside review: Resuscitation in the emergency department
  25. Bioreactance is not reliable for estimating cardiac output and the effects of passive leg raising in critically ill patients
  26. Brachial artery peak velocity variation to predict fluid responsiveness in mechanically ventilated patients
  27. Can changes in arterial pressure be used to detect changes in cardiac index during fluid challenge in patients with septic shock?
  28. Cardiac filling pressures are not appropriate to predict hemodynamic response to volume challenge
  29. Cardiac output measurements using the bioreactance technique in critically ill patients
  30. Causes of death after fluid bolus resuscitation – New Insights from FEAST
  31. Central venous blood oxygen saturation: an early, accurate measurement of volume during hemorrhage
  32. Changes in BP induced by passive leg raising predict response to fluid loading in critically ill patients
  33. Changes in Arterial Pressure during Mechanical Ventilation
  34. Changes in pulse pressure variability during cardiac resynchronization therapy in mechanically ventilated patients
  35. Clinical controversies in the management of critically ill patients with severe sepsis: Resuscitation fluids and glucose control
  36. Clinical review: Acid–base abnormalities in the intensive care unit – part II
  37. Clinical review: Hemorrhagic shock
  38. Clinical review: Myocardial depression in sepsis and septic shock
  39. Clinical review: The meaning of acid–base abnormalities in the intensive care unit – effects of fluid administration
  40. Clinical review: The role of ultrasound in estimating extra-vascular lung water
  41. Clinical review: Update on hemodynamic monitoring – a consensus of 16
  42. Clinical review: Volume of fluid resuscitation and the incidence of acute kidney injury – a systematic review
  43. Clinical use of respiratory changes in arterial pulse pressure to monitor the hemodynamic effects of PEEP.
  44. Colloids and crystalloids: does it matter to the kidney?
  45. Colloids versus crystalloids for fluid resuscitation in critically ill patients
  46. Comparison of an automated respiratory systolic variation test with dynamic preload indicators to predict fluid responsiveness after major surgery
  47. Comparison of arterial pressure and plethysmographic waveform-based dynamic preload variables in assessing fluid responsiveness and dynamic arterial tone in patients undergoing major hepatic resection
  48. Comparison of monitoring performance of Bioreactance vs. pulse contour during lung recruitment maneuvers
  49. Comparison of stroke volume and fluid responsiveness measurements in commonly used technologies for goal-directed therapy
  50. Comparison of three techniques using the Parkland Formula to aid fluid resuscitation in adult burns
  51. Crystalloids vs. colloids: KO at the twelfth round?
  52. Current practice in hemodynamic monitoring and management in high-risk surgery patients – a national survey of Korean anesthesiologists
  53. Damage control hematology: the impact of a trauma exsanguination protocol on survival and blood product utilization
  54. Damage control resuscitation from major haemorrhage in polytrauma
  55. Damage Control Resuscitation: The New Face of Damage Control
  56. Damage control surgery: it’s evolution over the last 20 years
  57. Decreases in organ blood flows associated with increases in sublingual PCO2 during hemorrhagic shock
  58. Determination of the optimal mean arterial pressure for postbleeding resuscitation after hemorrhagic shock in rats
  59. Differences in acid-base behavior between intensive care unit survivors and nonsurvivors using both a physicochemical and a standard base excess approach: a prospective, observational study
  60. Differentiating disseminated intravascular coagulation (DIC) with the fibrinolytic phenotype from coagulopathy of trauma and acute coagulopathy of trauma-shock (COT/ACOTS)
  61. Discordance between lactate and base deficit in the surgical intensive care unit: which one do you trust?
  62. Disseminated intravascular coagulation or acute coagulopathy of trauma shock early after trauma? An observational study
  63. Do colloids in comparison to crystalloids for fluid resuscitation improve mortality?
  64. Does Central Venous Pressure Predict Fluid Responsiveness
  65. Does central venous pressure predict fluid responsiveness? A systematic review of the literature and the tale of seven mares
  66. Does the central venous pressure predict fluid responsiveness – An updated meta-analysis and a plea for some common sense
  67. Don’t take vitals, take a lactate
  68. Dynamic and volumetric variables of fluid responsiveness fail during immediate postresuscitation period
  69. Dynamic changes in arterial waveform derived variables and fluid responsiveness in mechanically ventilated patients – a systematic review of the literature
  70. Echocardiographic Assessment of Preload Responsiveness in Critically Ill Patients
  71. Effect of baseline serum albumin concentration on outcome of resuscitation with albumin or saline in patients in intensive care units: analysis of data from the saline versus albumin fluid evaluation (SAFE) study
  72. Effect of blood pressure on hemorrhage volume and survival in a near-fatal hemorrhage model incorporating a vascular injury
  73. Effects of Fluid Resuscitation With Colloids vs Crystalloids on Mortality in Critically Ill Patients Presenting With Hypovolemic Shock – The CRISTAL Randomized Trial
  74. Effect of Intravenous Albumin on Renal Impairment and Mortality in Patients with Cirrhosis and Spontaneous Bacterial Peritonitis
  75. Elevated Arterial Base Deficit in Trauma Patients: A Marker of Impaired Oxygen Utilization
  76. Emergency Department Bedside Ultrasonographic Measurement of the Caval Index for Noninvasive Determination of Low Central Venous Pressure
  77. Emerging trends in minimally invasive haemodynamic monitoring and optimization of fluid therapy
  78. End-diastolic volume. A better indicator of preload in the critically ill
  79. Endpoints of Resuscitation What Should We Be Monitoring?
  80. End-Expiratory Occlusion Test Predicts Preload Responsiveness Independently of Positive End-Expiratory Pressure During Acute Respiratory Distress Syndrome
  81. End-tidal carbon dioxide is better than arterial pressure for predicting volume responsiveness by the passive leg raising test
  82. Evaluation of stroke volume variations obtained with the pressure recording analytic method
  83. Excess mortality associated with the use of a rapid infusion system at a level 1 trauma center
  84. Extravascular lung water in sepsis-associated acute respiratory distress syndrome: indexing with predicted body weight improves correlation with severity of illness and survival
  85. Extravascular lung water measurements and hemodynamic monitoring in the critically ill: bedside alternatives to the pulmonary artery catheter
  86. Fluid administration limited by lung sonography: the place of lung ultrasound in assessment of acute circulatory failure (the FALLS-protocol)
  87. Fluid challenge revisited
  88. Fluid resuscitation in patients with traumatic brain injury: what is a SAFE approach?
  89. Fluid resuscitation in septic shock: a positive fluid balance and elevated central venous pressure are associated with increased mortality
  90. Fluid resuscitation in traumatic hemorrhagic shock
  91. Fluid Status and Fluid Responsiveness
  92. Fluid Therapy in Resuscitated Sepsis: Less is More
  93. Functional hemodynamic monitoring and dynamic indices of fluid responsiveness
  94. Graphic aids for calculation of fluid resuscitation requirements in pediatric burns
  95. Goal-Directed Fluid Management Based on the Pulse Oximeter–Derived Pleth Variability Index Reduces Lactate Levels and Improves Fluid Management
  96. Goal-directed intraoperative fluid therapy guided by stroke volume and its variation in high-risk surgical patients – a prospective randomized multicentre study
  97. Goal-directed therapy in intraoperative fluid and hemodynamic management
  98. Goal-directed resuscitation in the prehospital setting: A propensity-adjusted analysis
  99. Greater cardiac response of colloid than saline fluid loading in septic and non-septic critically ill patients with clinical hypovolaemia
  100. Hemodynamic monitoring over the past 10 years
  101. Hemodynamic parameters to guide fluid therapy
  102. Hemodynamic pressure waveform analysis in predicting fluid responsiveness
  103. How to measure and interpret volumetric measures of preload
  104. Hydroxyethyl starch 130/0.42 versus Ringer’s acetate in severe sepsis
  105. Hydroxyethyl starch in severe sepsis: end of starch era?
  106. Hypertonic resuscitation of hemorrhagic shock prevents alveolar macrophage activation by preventing systemic oxidative stress due to gut ischemia/reperfusion
  107. Hypotensive Resuscitation in Patients with Ruptured Abdominal Aortic Aneurysm
  108. Hypothermia and acidosis worsen coagulopathy in the patient requiring massive transfusion
  109. Hypothermia in massive transfusion: have we been paying enough attention to it?
  110. Hypovolemic Shock Evaluated by Sonographic Measurement of the Inferior Vena Cava During Resuscitation in Trauma Patients
  111. Hypovolemic shock resuscitation
  112. The ideal crystalloid – what is ‘balanced’?
  113. Ideal permissive hypotension to resuscitate uncontrolled hemorrhagic shock and the tolerance time in rats
  114. Immediate versus Delayed Fluid Resuscitation for Hypotensive Patients with Penetrating Torso Injuries
  115. Impact of prehospital hypothermia on transfusion requirements and outcomes
  116. Impairment of coagulation by commonly used resuscitation fluids in human volunteers
  117. Improved outcome with hypotensive resuscitation of uncontrolled hemorrhagic shock in a swine model
  118. Induced hypothermia does not impair coagulation system in a swine multiple trauma model
  119. In Search of the Optimal End Points of Resuscitation in Trauma Patients: A Review
  120. Inferior Vena Cava Distensibility as a Predictor of Fluid Responsiveness in Patients with Subarachnoid Hemorrhage
  121. Inferior Vena Cava Percentage Collapse During Respiration Is Affected by the Sampling Location: An Ultrasound Study in Healthy Volunteers
  122. Intensivist Bedside Ultrasound (INBU) for Volume Assessment in the Intensive Care Unit: A Pilot Study
  123. Intensive Insulin Therapy and Pentastarch Resuscitation in Severe Sepsis
  124. Intraoperative fluid restriction improves outcome after major elective gastrointestinal surgery
  125. Intravenous fluid resuscitation: was Poiseuille right?
  126. Initial resuscitation of hemorrhagic shock
  127. Integrating lung ultrasound in the hemodynamic evaluation of acute circulatory failure (the fluid administration limited by lung sonography protocol)
  128. Is albumin use SAFE in patients with traumatic brain injury?
  129. Lactate clearance as a target of therapy in sepsis: a flawed paradigm
  130. Language Guiding Therapy: The Case of Dehydration versus Volume Depletion
  131. Less invasive methods of advanced hemodynamic hemodynamic monitoring principles, devices, and their role in the perioperative hemodynamic optimization
  132. Limits of corrected flow time to monitor hemodynamic status in children
  133. Lung ultrasound: a new tool for the cardiologist
  134. Major complications, mortality, and resource utilization after open abdominal surgery: 0.9% saline compared to Plasma-Lyte
  135. Measurement of acid-base resuscitation endpoints: lactate, base deficit, bicarbonate or what?
  136. Measuring cardiac index with a focused cardiac ultrasound examination in the ED
  137. Minimal invasive cardiac output monitoring: get the dose of fluid right
  138. Monitoring of peri-operative fluid administration by individualized goal-directed therapy
  139. Monitoring fluid responsiveness
  140. Monitoring volume and fluid responsiveness – From static to dynamic indicators
  141. Mortality after Fluid Bolus in African Children with Severe Infection
  142. New approaches to trauma management using severity of illness and outcome prediction based on noninvasive hemodynamic monitoring
  143. New insights into fluid resuscitation
  144. New strategies for massive transfusion in the bleeding trauma patient
  145. Non-invasive assessment of fluid responsiveness by changes in partial end-tidal CO2 pressure during a passive leg-raising maneuver
  146. Noninvasive Cardiac Output Monitors: A State-of the-Art Review
  147. Noninvasive Hemoglobin Monitoring: How Accurate Is Enough?
  148. Noninvasive Monitoring of the Autonomic Nervous System and Hemodynamics of Patients With Blunt and Penetrating Trauma
  149. Non-invasive prediction of fluid responsiveness during major hepatic surgery
  150. Novel rapid infusion device for patients in emergency situations
  151. The Use of Normal Saline for Resuscitation in Trauma
  152. Optimizing perioperative hemodynamics – what is new
  153. Outcome prediction by a mathematical model based on noninvasive hemodynamic monitoring
  154. Out-of-hospital hypertonic resuscitation after traumatic hypovolemic shock: a randomized, placebo controlled trial
  155. Passive leg raising: good for everyone?
  156. Passive leg-raising and end-expiratory occlusion tests perform better than pulse pressure variation in patients with low respiratory system compliance
  157. Passive leg raising-induced changes in mean radial artery pressure can be used to assess preload dependence
  158. Passive leg raising predicts fluid responsiveness in the critically ill
  159. Permissive hypotension and desmopressin enhance clot formation
  160. Permissive hypotension does not reduce regional organ perfusion compared to normotensive resuscitation: animal study with fluorescent microspheres
  161. Pleth variability index is a weak predictor of fluid responsiveness in patients receiving norepinephrine
  162. Plethysmographic variation index predicts fluid responsiveness in ventilated patients in the early phase of septic shock in the emergency department – A pilot study
  163. Post hoc ergo propter hoc: the story of the Resuscitation Outcomes Consortium.
  164. Pred of Responsiveness to an IV Fluid Challenge in Patients After Cardiac Surgery with Cardiopulmonary Bypass – A Comparison Arterial Pulse Pressure Variation and Digital Plethysmographic Var Index
  165. Predicting cardiac output responses to passive leg raising by a PEEP-induced increase in central venous pressure, in cardiac surgery patients
  166. Predicting Fluid Responsiveness in ICU Patients – a critical analysis of the evidence
  167. Predicting fluid responsiveness in patients undergoing cardiac surgery: functional haemodynamic parameters including the Respiratory Systolic Variation Test and static preload indicators
  168. Predicting fluid responsiveness
  169. Predicting fluid responsiveness with transthoracic echocardiography is not yet evidence based
  170. Predicting volume responsiveness by using the end-expiratory occlusion in mechanically ventilated intensive care unit patients
  171. Prediction of fluid responsiveness by a continuous non-invasive assessment of arterial pressure in critically ill patients – comparison with four other dynamic indices
  172. Predicting fluid responsiveness in ICU patients: a critical analysis of the evidence
  173. Prediction of fluid responsiveness in patients during cardiac surgery
  174. Predictors of pulmonary edema formation during fluid loading in the critically ill with presumed hypovolemia
  175. Pre-ejection period variations predict the fluid responsiveness of septic ventilated patients
  176. Principles of Doppler Echocardiography and the Doppler Examination #1
  177. Prospective trial of supranormal values of survivors as therapeutic goals in high-risk surgical patients    (commentary)
  178. Pulmonary artery catheter versus pulse contour analysis: a prospective epidemiological study
  179. Pulmonary lactate release in patients with sepsis and the adult respiratory distress syndrome
  180. Pulmonary lactate release in patients with acute lung injury is not attributable to lung tissue hypoxia
  181. Pulse pressure variation: beyond the fluid management of patients with shock
  182. Pulse pressure variation and stroke volume variation: from flying blind to flying right?
  183. Pulse pressure variation: where are we today?
  184. Relation between Respiratory Changes in Arterial Pulse Pressure and Fluid Responsiveness in Septic Patients with Acute Circulatory Failure
  185. Respiratory changes in aortic blood velocity as an indicator of fluid responsiveness in ventilated patients with septic shock
  186. Respiratory variation in aortic blood flow velocity as a predictor of fluid responsiveness in children after repair of ventricular septal defect
  187. Respiratory variations in aortic blood flow predict fluid responsiveness in ventilated children
  188. Respiratory variations of inferior vena cava diameter to predict fluid responsiveness in spontaneously breathing patients with acute circulatory failure: need for a cautious use
  189. Resuscitation and transfusion management in trauma patients: emerging concepts
  190. Resuscitation Fluids
  191. Resuscitation from severe hemorrhage
  192. Resuscitation of the Critically Ill in the ED – Responses of Blood Pressure, Heart Rate, Shock Index, Central Venous Oxygen Saturation, and Lactic Acid
  193. Role of colloids in traumatic brain injury: Use or not to be used?
  194. Sodium Bicarbonate for the Treatment of Lactic Acidosis
  195. Shock: Ultrasound to Guide Diagnosis and Therapy
  196. Steady-state and time-dependent thermodynamic modeling of the effect of intravenous infusion of warm and cold fluids
  197. Stroke volume variation: from applied physiology to improved outcomes
  198. Stroke volume variations
  199. Strong ions, weak acids and base excess: a simplified Fencl-Stewart approach to clinical acid-base disorders
  200. Sublingual capnometry for diagnosis and quantitation of circulatory shock
  201. Sublingual capnometry for rapid determination of the severity of hemorrhagic shock
  202. Supranormal trauma resuscitation causes more cases of abdominal compartment syndrome
  203. Surviving Sepsis Campaign guidelines for management of severe sepsis and septic shock
  204. Target blood pressure for hypotensive resuscitation
  205. The acute coagulopathy of trauma shock: clinical relevance
  206. The Australasian Resuscitation in Sepsis Evaluation (ARISE) trial statistical analysis plan
  207. The biochemical effects of restricting chloride-rich fluids in intensive care
  208. The effect of graded hemorrhage and intravascular volume replacement on systolic pressure variation in humans during mechanical and spontaneous ventilation
  209. The effects of balanced versus saline-based hetastarch and crystalloid solutions on acid-base and electrolyte status and gastric mucosal perfusion in elderly surgical patients
  210. The effect of breathing manner on inferior vena caval diameter
  211. The effects of propofol and dexmedetomidine infusion on fluid responsiveness in critically ill patients
  212. The effects of saline or albumin resuscitation on acid-base status and serum electrolytes
  213. The Efficacy and Safety of Colloid Resuscitation in the Critically Ill
  214. The history of 0.9% saline
  215. The impact of phenylephrine, ephedrine, and increased preload on third-generation Vigileo-FloTrac and esophageal doppler cardiac output measurements
  216. The influence of the airway driving pressure on pulsed pressure variation as a predictor of fluid responsiveness
  217. The Interrater Reliability of Inferior Vena Cava Ultrasound by Bedside Clinician Sonographers in Emergency Department Patients
  218. The prospective, observational, multicenter, major trauma transfusion (PROMMTT) study: comparative effectiveness of a time-varying treatment with competing risks
  219. The rational clinical examination. Is this patient hypovolemic?
  220. The respiratory variation in inferior vena cava diameter as a guide to fluid therapy
  221. The rule regulating pH changes during crystalloid infusion
  222. The Sonodynamic Study: Comparison of Qualitative Versus Quantitative Assessment and Inter-Rater Reliability In Serial Ultrasonography Evaluations of Inferior Vena Cava Dynamics and Left Ventricular Systolic Function In Fluid Resuscitation of Emergency Department Patients With Symptomatic Hypotension
  223. The status of massive transfusion protocols in United States trauma centers: massive transfusion or massive confusion?
  224. The Stewart approach–one clinician’s perspective
  225. The use of bioreactance and carotid Doppler to determine volume responsiveness and blood flow redistribution following passive leg raising in hemodynamically unstable patients
  226. The use of volume kinetics to optimize fluid therapy
  227. The utility of base deficit and arterial lactate in differentiating major from minor injury in trauma patients with normal vital signs
  228. Therapeutic Strategies for High-Dose Vasopressor-Dependent Shock
  229. Tissue oxygen saturation predicts the development of organ dysfunction during traumatic shock resuscitation
  230. Transthoracic echocardiography does not improve prediction of outcome over APACHE II in medical-surgical intensive care
  231. Treatment of lactic acidosis: appropriate confusion
  232. Ultrasound lung comets: a clinically useful sign of extravascular lung water
  233. Ultrasound for the detection of intraperitoneal fluid: the role of Trendelenburg positioning
  234. Ultrasound Guided Volume Assessment Using Inferior Vena Cava Diameter
  235. Ultrasound of the Inferior Vena Cava Does Not Predict Hemodynamic Response to Early Hemorrhage
  236. Use of the Trendelenburg Position as the Resuscitation Position: To T or Not to T?
  237. Use of Ultrasound to Assess Fluid Responsiveness in the Intensive Care Unit
  238. Volume Management in Critically Ill Patients – New Insights
  239. What is a fluid challenge?
  240. What’s new in critical illness and injury science? the ongoing debate on the optimal resuscitative fluid and monitoring parameters
  241. What’s new in resuscitation strategies for the patient with multiple trauma

Sepsis

INTRODUCTION

First, sepsis is a syndrome and not an individual disease. It is the 11th leading cause of death in the US. According to the Global Sepsis Alliance (GSA), “Sepsis is one of the most pressing healthcare challenges faced by the world today.”  The CDC shows sepsis hospital admissions “have grown from around 200 per 1000 inhabitants in 2000, to 340 in 2008. Also, in 2008 the costs for hospital treatment were US $14.8 billion, but these have increased by an annual rate of 11 percent.” According to Dr. Reinhardt “the main way it can be prevented is if it is recognized early and the patient receives adequate measures of treatment. Treatments, like antimicrobials and intravenous fluids must be initiated when the first signs of organ dysfunction appear. If they are given in the first few hours the survival rate may be up to 80 percent, but studies suggest with each hour of delay the mortality rate increases by five to eight percent.” (GSA – Stop Sepsis, Save Lives)

DEFINITION

Sepsis is a potentially deadly medical condition characterized by a whole-body inflammatory state (called a systemic inflammatory response syndrome or SIRS) that is triggered by an infection. The body may develop this inflammatory response by the immune system to microbes in the blood, urine, lungs, skin, or other tissues. A popular term for sepsis is blood poisoning. Severe sepsis is the systemic inflammatory response, infection and the presence of organ dysfunction. Septic Shock is the combination of sepsis with abnormally decreased blood pressure.

(Also, here is another great video about SIRS from the same source.)

PATHOPHYSIOLOGY

At this point in time, the literature richly illustrates that no single mediator / system / pathway / pathogen drives the pathophysiology of sepsis (Am J Pathol. 2007 May; 170(5): 1435–1444. doi:10.2353/ajpath.2007.060872Pathophysiology of Sepsis)

    • The basic pathophysiology of sepsis, severe sepsis, and septic shock includes:
      • Vasodilation
      • Third spacing due to capillary leak
      • Myocardial dysfunction.
    • Vascular endothelium is both a source and target of injury in SIRS / sepsis. Injury may be due to toxins such as LPS (endotoxin) or from ischemia itself. Tissue factor release leads to amplification of the inflammatory response and to DIC via the thrombin pathway. Thrombin not only catalyzes fibrin formation but also causes leukocyte adhesion which leads to further endothelial damage. As DIC progresses, clotting factors are consumed and bleeding occurs.
    • Clotting factors, pro-fibrinolytic, and anti-thrombin factors are consumed leading to loss of fibrinolysis & normal down-regulation of thrombin pathway. This phenomenon is both pro-inflammatory and pro-thrombotic.
    • Protein C depletion has been associated with increased mortality. This has led to a series of clinical trials utilizing protein C, activated protein C (APC), antithrombin III (AT-III), and tissue factor pathway inhibitor to try and disrupt this cycle. Activated protein C has in fact been shown to reduce mortality in severe sepsis in adults. Bleeding problems seems to outweigh the benefits in children.
    • Usually gram negative and usually originating in the urinary or respiratory systems
    • Frequent microbial causes of sepsis

 

IDENTIFYING SEPSIS

(Balk RA. Crit Care Clin 2000;16:337-52Surviving Sepsis Campaign 2008 SSC Guidelines)

Differentials

TREATMENT

DESPERATE MEASURES

These measures can help improve immunohomeostasis (pro/antiinflamatory mediators), improve coagulation response with decreased organ thrombosis, and provide mechanical support for organ perfusion during an acute episode, and may buy some time, but may or may not reduce mortality.

NOVEL THERAPIES

QUALITY

REVIEWS

CLINICAL TRIALS

DR. RIVERS TALK

Dr. Emmanuel Rivers gave a talk on Severe Sepsis Management via the EMCrit Blog. The talk is broken down into the three links to each of the episodes provided below.

ADDITIONAL RESOURCES

In addition, here are some more great resources related to sepsis.

  1. Advances in Sepsis
  2. Crashing Patient Severe Sepsis
  3. Development and Implementation of a Multidisciplinary Sepsis Protocol
  4. EMCrit – Severe Sepsis Resources*
  5. EM Guidlines – Sepsis
  6. Global Sepsis Alliance
  7. International Sepsis Forum
  8. MedicineNet – Sepsis
  9. Medline Sepsis
  10. Sepsis Alliance
  11. Sepsis know from day 1
  12. Stanford SOM – Septris
  13. Surviving Sepsis
    1. The Surviving Sepsis Campaign (SSC) was developed by the European Society of Critical Care Medicinethe International Sepsis Forum,and the Society of Critical Care Medicine, to help meet the challenges of sepsis and to improve its management, diagnosis, and treatment. The agreement between the three founding organizations and funding for the campaign was concluded December 31, 2008. A generous grant has been received to continue the important work of the campaign. The grant funding extends through 2013. Assistance for US hospitals interested in implementing the bundles can be obtained through the Society of Critical Care Medicine’s Paragon program.
    2. Surviving Sepsis Protocol Checklist

Additional References

  1. 2001 SCCM/ESICM/ACCP/ATS/SIS International Sepsis De?nitions Conference
  2. Cleveland Clinic – Sepsis
  3. Genetic Polymorphisms in Sepsis and Septic Shock:Role in Prognosis and Potential for Therapy
  4. New Approaches to Sepsis: Molecular Diagnostics and Biomarkers
  5. Role of oxygen debt in the development of organ failure sepsis, and death in high-risk surgical patients
  6. Oxidative stress as a novel target in pediatric sepsis management
  7. The Pathogenesis of Sepsis
  8. Rapid Treatment of Severe Sepsis
  9. Sepsis in cirrhosis: report on the 7th meeting of the International Ascites Club
  10. Thermo Scientific biomarker procalcitonin
  11. Time is tissue: Why emerging evidence on sepsis urges physicians to watch the clock
    Early volume resuscitation can help avoid organ dysfunction—if you act quickly after making a diagnosis

CONCLUSION

Sepsis poses a significant burden upon the US healthcare system, resulting in an estimated 750,000 hospital admissions, 570,000 Emergency Department visits, 200,000 deaths and $16.7 billion in medical expenditures annually, according to, the online journal article in PLOS ONE, Chronic Medical Conditions and Risk of Sepsis. Mortality rates remain high in severe sepsis, and despite recent therapeutic breakthroughs much remains to be done to advance our understanding and treatment of sepsis. Currently, anti-sepsis initiatives focus on acute care, with ED staff employing the “sepsis bundles,” a series of steps that includes aggressive administration of antibiotics, IV fluids and blood pressure-boosting medications, and management. Additionally, the  Surviving Sepsis Campaign 2012 guidelines will further suggest that in patients with elevated lactate levels as a marker of hypoperfusion, resuscitation should be targeted at normalizing lactate as rapidly as possible (grade 2C). Having said that, however, a normal lactate doesn’t indicate absence of shock. Other factors, such as the patient’s central venous oxygen saturation level, need to be considered as well. The Surviving Sepsis Campaign guidelines are sponsored by 27 medical organizations. Among them are the Society of Critical Care Medicine, ACEP, the Society of Hospital Medicine, the American College of Chest Physicians, the American Thoracic Society, the Infectious Diseases Society of America, the Surgical Infection Society, the Pediatric Acute Lung Injury and Sepsis Investigators, and a host of international groups. Hopefully, strategies will be developed to continue to improve and maximize our efforts towards ameliorating sepsis throughout the world.