Fluid Management in Shock

Fildza Sasri Peddyandhari

Department of Anesthesiology and Intensive Care

University of Indonesia, Cipto Mangunkusumo Hospital
 Objectives

• Body Fluid Compartment

• Hemodynamic Goal

• Fluid Responsiveness

• Shock: definition, classification, pathophysiology, fluid

therapy
 Body Fluid Compartment

Based on average 70 kg male

Morgan and Mikhail’s Clinical Anesthesia, 2013.

Average Blood Volume

Morgan and Mikhail’s Clinical Anesthesia, 2013.

 Fluid Kinetics

osmolality (with an “ℓ”) is a measure of the osmoles (Osm) of solute per kilogram of solvent (osmol/kg or Osm/kg)
osmolarity (with an “r”) is defined as the number of osmoles of solute per liter (L) of solution (osmol/L or Osm/L)
Fluid Kinetics
 Volume Kinetic during Infusion of Fluid
in Healthy and Diseases

Normal condition Critical Illness/ High Risk Surgery

Fluid Infusion Fluid Infusion

Albumin Normal endothelial Albumin Abnormal endothelial gap
synthesis gap synthesis

leakage leakage

lymph lymph

Catabolism Leakage >> lymph flow

Metabolism Urinary/ ⬆ GIT →tissue edema
Urinary/ ⬆ GIT loss
loss Hemorrhage
 The Third Space :
the theory behind the story
1. Decrease blood volume

Intracellular Space Intra

Interstitium Space
ICF vascular

4 2 blood loss
1
urine output
3 GIT production

Third Space ??

2. Negative Net Water Flux The third space in its traditional

interpretation is a functionally
3. Third Space Development (?) separated part of the extra-cellular
compartment which cannot be localised,
4. Intracellular Hyperosmolarity but primarily consumes fluid

M.Jacob et al. Best Practice & Research Clinical Anaesthesiology 23 (2009): 145-157
 Fluids shifts within the
functional extra-cellular
compartment, from the
intravascular towards
the interstitial space,

Whereas the classical

third space is the
location of the lost fluid
remains unclear and
most of studies do not
support the existence of
a third space

M.Jacob et al. Best Practice & Research Clinical Anaesthesiology 23 (2009): 145-157
Hemodynamic Goal

Preload HR
CO
Contractility
SV
DO2
Afterload
Hgb
PaO2 CaO2
Sat %
 Frank-Starling Law

the ability of the heart to change its force of contraction and

therefore stroke volume in response to changes in venous return
 Warnings that Fluid is
Needed

• Symptoms: vomiting, diarrhea, constipation, thirst

• Signs: low UO (oliguria/anuria), increased CRT,

tachycardia, hypotension, decreased consiousness,
decrease in CVP

• Markers: raised Ht, increased serum lactate, increased

Ur:Cr ratio, metabolic acidosis, increased plasma
osmolarity
METHODS OF ASSESSING
FLUID STATUS
1. Clinical assessment of fluid overload (e.g. body weight, peripheral
edema and gas exchange parameters)
2. Haemodynamic parameters of hypovolemia (e.g. hypotension,
tachycardia, poor capillary refill and altered mental status)
3. Filling pressure (central venous pressure)
4. Volume monitors (e.g. EVLW on PiCCO, SVV/PPV, SV and CO)
5. Radiological techniques (e.g. “wet looking” CXR)
6. Bioelectric impedance tomography, Electrical Cardiometry,
Bioreactance
7. Fluid balance: potential useful new biomarker in critically ill
 Fluid Responsiveness

• An increase of stroke volume of 10-15% after the patient receives

500 ml of crystalloid over 10-15 minutes
• Also known as ‘volume responsiveness’
• The definitive test: Fluid Challange
• Fluid responsive patients have ‘preload reserve’ and will have
an increase in stroke volume (and usually cardiac output) when
fluid is administered
Predicting Fluid Responsiveness
Static Test

• 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
• ‘one off’ lactate or SvO2
 Fluid Challange
• Patient assessment before and after fluid challange

✓In an adult classicaly 500 ml crystalloid over 20-30 minutes

✓In a child 10 ml/kg over 20-30 minutes

• Objectives:

✓Target MAP: 65mmHg

✓Target UO: 0.5 ml/kg/h

✓Resolution of tachycardia, improved LOC, falling lactate, rising ScvO2

(aim>70%)

✓Ultrasound and echocardiography (optimal filling state: arterial pressure,

IVC diameter, ventricular filling, EF)

✓Cardiac Output monitoring: CI, SV, SVV

 Fluid Challange
Limits for Safety
• If the limit is reached before the objective, the FC is
stopped

• upper limit or increment of CVP or PAWP

‣ e.g. if CVP increases by 2-5mmHg or PCWP

increases by 3-7mmHg, stop fluid challenge

‣ however, CVP and “deltaCVP” correlate poorly with

blood volume or fluid responsiveness

• if no invasive monitoring:

◦ measure JVP and look for signs of pulmonary

edema

◦ or use IVC ultrasound and lung ultrasound to assess

for ‘fluid tolerance’
 Predicting Fluid Responsiveness
Dynamic Test
Passive Leg raise

• Acute volume expansion 500-700 ml in an adult patient

• Maximal effect occurs at 30-90 seconds

• Assess for a 10% increase in stroke volume (cardiac

output monitor) or using a surrogate such as pulse
pressure (using an arterial line)
 Passive Leg Raise
Pros and Cons
Advantages
• reversible
• non-invasive
• easy to perform in patients breathing spontaneously and with
arrhythmias (but must use measures other than stroke volume
variation and pulse pressure variation)
• can be repeated many times to reassess preload responsiveness
without any risk of inducing pulmonary edema or cor pulmonale in
potential nonresponders
Disadvantages
• unreliable in severely hypovolemic patients: the blood volume
mobilized by leg-raising (which is dependent on total blood volume)
could be small and can show minimal to no increase in CO and blood
pressure, even in fluid responsive patients
• need to stop any other interventions during the test
• positional changes may be contra-indicated in some patients
• not useful in patients with raised intra-abdominal pressure
Predicting Fluid Responsiveness
Dynamic Test
• 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
‣ 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
• systolic pressure, pulse pressure (PPV) and stroke volume (SVV)
‣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
stroke volume (and usually cardiac output, unless
heart rate falls) will improve if fluids are given
• Use different cutoff values for fluid responsiveness
depending on the clinical context. For example,
patients 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
 Hypovolemia
vs
Hypervolemia

Pearse RM, Ackland GL. Perioperative Fluid

Therapy. BMJ 2012;344:e2865 doi:
10.1136/bmj.e2865
Type of Fluid
 CRYSTALLOID
•MW <20 KD
•Advantages
–Cheap
–Easy to store and warm
–Established safety
–Predictable rise in cardiac output
•Disadvantages
–Large volumes needed
–No oxygen carrying capacity
–May Increase ICP
–T ½ = 20-30 min
 COLLOID

•MW >20 KD
•Natural Colloid
- Blood product: PRC, Whole blood
- Plasma and plasma components: Albumin 5%, Albumin
25%, Fresh Frozen, plasmanate
•Synthetic Colloid: MW 40 KD – 400 KD
- Poligelin (gelafundin, haemacell)
- Dextran ( 40 - 10%, dan 70 - 6%)
- Hetastarch
 COLLOID
Advantages
• Smaller volume
- Less pulmonary edema
• Stays in the intravascular
space
- Quicker return to normal
hemodynamics
• Smaller package
• Antioxidant and
antinflammatory effects
Disadvantages
• Transmission of diseases
• Increased bleeding
(HES)
• Hypersensitivity
reactions (Gelatine)
• Renal failure (HES)
• Accumulation
- Taken up by interstitial
- Dose limit (20-33mL/kg)
• Cost
 Distribution of fluids for
increasing the blood volume
Intravascular
Extravascular Intertitial

20% 40% Colloid is ideal for

volume therapy

5 12 30
75 kg
BW

Capillary Cell membrane

membrane

4 14.4 36
5 L of 0.9
NaCl

3 16 34
9.4 L of
D5W

6 12 30 1 L of 6% HES

6 11.6 30 0.6 L of 10%

HES

Body fluid volume

C.H. Svensen et al. / Best Practice & Research Clinical Anaesthesiology 23 (2009) 213–224
 FLUID SHIFTING

Fluid shift into the interstitial space

can be divided into two types:
Type 1 – physiologic shift :
• Colloid-free fluid and electrolytes (crystalloid)
• Vascular barrier intact

Type 2 – pathologic shift :

• Protein-rich fluids (colloid)
• Functionally altered vascular barrier
 APPROACH TO FLUID MANAGEMENT

• Use crystalloids only when replacing urine production and

insensible perspiration.
Minimize type • Use colloids or blood products for substitution of acute blood loss
1 shifting

• Goal-directed method with available parameters

• Conservatively to avoid acute hypervolemia
Minimize type • Use colloids instead of crystalloids.
2 shifting

Chappel D. Matthias Jacob et al. A rational Approach to perioperative Fluid

Management. Anesthesiology 2008; 109:723-40
IV Sites
 Shock
Definition

“Inadequate delivery or utilisation of oxygen for

cellular metabolic needs”

“A clinical state in which disparity of oxygen supply

and demand at cell level results in tissue hypoxia and
incipient failure of cell function”
 Shock
Classification
Traditionally shock is classified into four groups according to the main
mechanism of decompensation:
• Cardiogenic
• Obstructive
• Hypovolaemic
• Distributive

There may be considerable overlap between shock states classified

in this way. For example sepsis, an example of distributive shock,
frequently co-exists with myocardial depression and relative
hypovolaemia.
 Shock Diagnosis based on Hemodynamic Profile

Shock MAP Preload Cardiac Output Afterload

Hypovolemic Decrease Decrease* Decrease Increase

Cardiogenic Decrease Increase Decrease* Increase

Obstructive Decrease Increase Decrease Increase

Distributive Decrease Decrease Decrease Decrease*

*Major Changes
 Cardiogenic Shock
“A state in which ineffective cardiac output caused by a primary cardiac
disorder results in both clinical and biochemical manifestations of
inadequate tissue perfusion”

• Acute Myocardial Infarction

• Left ventricular Dysfunction
• Blunt cardiac injury
• Myocarditis
• Acute valvular failure
• Arrhythmia
• Right ventricular failure

Acute cardiac hemodynamic instability may result from disorders that impair function of the
myocardium, valves, conduction system, or pericardium
 Pragmatic and Clinical Trial
Definition of Cardiogenic Shock

• Persistent hypotension
unresponsive to volume
replacement
• End organ hypoperfusion

Circulation. 2017;136:00–00. DOI: 10.1161/CIR.0000000000000525

Pathophysiology
of Cardiogenic
Shock

Copyright © 2010, 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.
Pathophysiology of Cardiogenic Shock Circulation. 2017;136:00–00. DOI: 10.1161/CIR.0000000000000525
 Potential Hemodynamic Presentation of Cardiogenic Shock

CI: Cardiac Index

PCWP: Pulmonary Capillary Wedge Pressure

SVRI: Systemic Vascular Resistance Index

Circulation. 2017;136:00–00. DOI: 10.1161/CIR.0000000000000525

 Initial Management of
Cardiogenic Shock
• High flow oxygen
• Fluid resuscitation unless edema present
• Opiate analgesia
• Early recourse to mechanical ventilation
• Treatment of associated arrhythmia and electrolyte
abnormalities is essential
• ECG
• Echocardiography
• CVC, Arterial line, Swan-Ganz cathetrization
• Augment cardiac output: Inotropes; Intra-aortic balloon
counterpulsation; Revascularisation (thrombolisis,
percutaneus intervention, CABG)
Initial Vasoactive Management Considerations in Types of CS

Circulation. 2017;136:00–00. DOI: 10.1161/CIR.0000000000000525

Circulation. 2017;136:00–00. DOI: 10.1161/CIR.0000000000000525
 Obstructive Shock

• Pulmonary embolus
release
• Cardiac tamponade
• Tension pneumothorax obstruction !!!!!
 Cardiac
Tamponade
• Over-accumulation of fluid or blood in
cardiac sac

• Pericardial efusion, constrictive pericarditis

• Diagnosis: low blood pressure, jugular

venous distension, pericardial rub, or quiet
heart sounds

• Decreased venous return — decrease SV —

decrease CO

• Th/: Fluid resuscitation as initial treatment

and Pericardiocentesis
Tension Pneumothorax

• Progressive build-up of air within the pleural space —

increase pressure in pleural space and around the heart

• Decreased venous return — decrease SV — decrease CO

• Th/: Needle thoracostomy — chest drain placement

Pulmonary Embolism
Pulmonary Embolism
 Hypovolemic Shock
Loss of intravascular fluid volume

Fluid depletion
• Vomiting and diarrhoea
• Burns
• Polyuria

Haemorrhagic
• Trauma
• Gastrointestinal
• Retroperitoneal
Pathophysiology
of Hypovolemic
Shock

Copyright © 2010, 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.
Hemorrhagic Shock Classification
Circulation with hemorrhage control (ATLS 2018)

Isotonic Fluid
Initial Assessment
2 Liter 1 Liter
(ATLS 2012) (ATLS 2018)

Blood Transfussion
Unresponsive: SHOCK 1:1:1 as part of Massive
Transfusion Protocol

Massive Transfusion Protocol

Coagulopathy Prevention Pre-emptive Tranexamic Acid:

within 3 hours post trauma then
continous drip for another 8
hours
ATLS 2018
 Massive Transfusion
ATLS 2018

Protocol
• Defined as > 10 units of pRBCs within the first 24 hours
of admission or more than 4 units in 1 hour.
• This approach has been termed “balanced,” “hemostatic,”
or “damage- control” resuscitation
• Simultaneous efforts to rapidly control bleeding and
reduce the detrimental effects of coagulopathy,
hypothermia, and acidosis (Lethal Triad)
Massive Transfusion Protocol (MTP)
• HR >120 bpm
Assessment of
• SBP <90 mmHg
Blood Consumption
• FAST (+)
(ABC) score
• Penetrating trauma at Thoracal
(0=No, 1=Yes)
region

ABC score ≥2

Persistent Hemodynamic
Instability
MTP ACTIVATION
Active Bleeding: need
surgical approach

Blood transfusion in
trauma centee Cotton BA, Au BK, Nunez TC, et al. Predefined massive transfusion
protocols are associated with a reduction in organ failure and
postinjury complications. J Trauma2009;66:41–49.
 Massive Transfusion Protocol

Study Protocol 1 Protocol 2 Protocol 3

10 Unit PRC
6 Unit PRC

Cotton et al 4 Unit FFP

4 Unit FFP
Repeat Protocol 2
2 Unit TC 2 Unit TC
6 Unit PRC
6 Unit PRC

6 Unit PRC

Dente et al 6 Unit FFP

6 Unit FFP

6 Unit FFP
1 Unit TC 10 Unit Cryo
5 Unit PRC
5 Unit PRC

5 Unit PRC

O’Keeffee et al 2 Unit FFP

2 Unit FFP

2 Unit FFP
1 Unit TC 10 Unit Cryo
10 Unit PRC

Nunez et al 6 Unit FFP

Repeat Protocol 1 Repeat Protocol 1
2 Unit TC
6 Unit PRC

Riskin et al 4 Unit FFP

Repeat Protocol 1 Repeat Protocol 1
1 Unit TC
 Distributive Shock

• Sepsis
• Neurogenic
• Anaphylaxis
Distributive Shock: Sepsis

Sepsis-3 Definitions
• Sepsis: Life-threatening organ dysfunction
caused by dysregulated host response to
infection
• Septic Shock: Subset of sepsis with
circulatory and cellular/metabolic
dysfunction associated with higher risk of
mortality
JAMA. 2016;315(8):801-810. doi:10.1001/jama.2016.0287
Distributive Shock: Sepsis
Distributive Shock: Sepsis
Initial Resuscitation
• We recommend that in the resuscitation from
sepsis-induced hypoperfusion, at least 30ml/kg
of intravenous crystalloid fluid be given within
the first 3 hours.
(Strong recommendation; low quality of evidence)

• We recommend that following initial fluid

resuscitation, additional fluids be guided by
frequent reassessment of hemodynamic status.
(Best Practice Statement)
Distributive Shock: Sepsis

Fluid Therapy
• We recommend crystalloids as the fluid of
choice for initial resuscitation and subsequent
intravascular volume replacement in patients
with sepsis and septic shock
(Strong recommendation, moderate quality of
evidence).

• We suggest using albumin in addition to

crystalloids when patients require substantial
amounts of crystalloids
(weak recommendation, low quality of evidence).
Distributive Shock: Sepsis

We recommend an initial target mean arterial

pressure of 65 mmHg in patients with septic shock
requiring vasopressors.
(Strong recommendation; moderate quality of
evidence)
Distributive Shock: Sepsis

Vasoactive agents
• We recommend norepinephrine as the first
choice vasopressor
(strong recommendation, moderate quality of
evidence).

• We suggest adding either vasopressin (up to 0.03

U/min) or epinephrine to norepinephrine with
the intent of raising MAP to target, or adding
vasopressin (up to 0.03 U/min) to decrease
norepinephrine dosage.
(weak recommendation, low quality of evidence)
Distributive Shock: Sepsis

If shock is not resolving quickly…..

• We recommend further hemodynamic
assessment (such as assessing cardiac function)
to determine the type of shock if the clinical
examination does not lead to a clear diagnosis.
(Best Practice Statement)

• We suggest that dynamic over static variables be

used to predict fluid responsiveness, where
available.
(Weak recommendation; low quality of evidence)
Distributive Shock: Sepsis

Lactate can help guide resuscitation

• We suggest guiding resuscitation to normalize
lactate in patients with elevated lactate levels as
a marker of tissue hypoperfusion.
(Weak recommendation; low quality of evidence)
Distributive Shock: Sepsis

Recommendation
• Start resuscitation early with source
control, intravenous fluids and antibiotics.
• Frequent assessment of the patients’
volume status is crucial throughout the
resuscitation period.
• We suggest guiding resuscitation to
normalize lactate in patients with elevated
lactate levels as a marker of tissue
hypoperfusion.
 Distributive Shock:
Neurogenic
• Hemodynamic phenomenon that can occur within 30
minutes of a spinal cord injury at the fifth thoracic (T5)
vertebra or above and can last up to 6 weeks
• Results in massive vasodilation leading to pooling of
blood in vessels
• Clinical manifestations
• Hypotension
• Bradycardia
• Temperature dysregulation (resulting in heat loss)
• Dry skin
• Poikilothermia (taking on the temperature of the environment)
Pathophysiology
of Neurogenic
Shock

Copyright © 2010, 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.
 Neurogenic Shock
Treatment
• Relative hypovolemia: vasopressor and isotonic IV Fluid

• Neurogenic shock in trauma patient — think associate

with hemorrhagic shock — initially treated with crystalloid
or colloid (ATLS 2018) and evaluate the ongoing blood
loss.

• Sometimes refractory to fluid resuscitation

• Atropine: block parasymphatic NS

 Distributive Shock:
Anaphylaxis

• Acute
• life-threatening hypersensitivity reaction
• Massive vasodilation
• Release of mediators, ↑ Capillary permeability
 Anaphylaxis Shock
Treatment

• Removal antigenes

• ABCD

• Aggressive fluid resuscitation : up to 5-7L isotonic fluid

• Steroids unlikely to be helpful (delay onset).

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