Professional Documents
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SHOCK Management
Fajar Perdhana
Dept. Anestesiologi dan terapi Intensif
FK Universitas Airlangga/RSUD Dr Soetomo
Surabaya
Objectives
•Definition of SHOCK
•Pathophysiologic and features of SHOCK
•Preload and fluid responsiveness in SHOCK
•Monitoring cardiac output in SHOCK
•Markers of the regional and microcirculation
in SHOCK
SHOCK Definition
A life-threatening, generalized form of acute circulatory
failure associated with inadequate oxygen utilization
by the cells. It is a state in which the circulation is
unable to deliver sufficient oxygen to meet the
demands of the tissues, resulting in cellular
dysfunction.
Consensus on circulatory shock
and hemodynamic monitoring. 2014.
European Society of Intensive Care Medicine
• Decreased organ perfusion
leads to tissue hypoxia →
anaerobic metabolism →
activation of an
inflammatory cascade →
vital organ dysfunction
Four specific questions :
(1) What are pathophysiologic and features of shock ?
(2) Should we monitor preload and fluid responsiveness in
shock?
(3) How and when should we monitor stroke volume or
cardiac output in shock?
(4) What markers of the regional and microcirculation can be
monitored, and how can cellular function be assessed in
shock?
Features of SHOCK
• Sign of HYPOPERFUSION
• Hypotension, tachycardia,
altered mental status, delayed
capillary refill, decreased urine
output, and cooled skin and
extremities
• Hypotension (SBP < 90 mmHg,
SBP decrease of 40 mmHg
from baseline, or mean arterial
pressure (MAP) <65 mmHg), →
should not be required to
define shock. Shock requires
evidence of inadequate tissue
perfusion on physical
examination
n engl j med 369;18 nejm.org
Pathophysiology of SHOCK
• Decrease in venous return due to a loss of circulating
volume (i.e. due to internal or external loss of fluids).
• Failure of the pump function of the heart that results
from a loss of contractility (resulting from ischemia,
infarction, myopathy, myocarditis) or a major
arrhythmia (such as ventricular tachycardia or a high
degree A-V block).
• Obstruction due to pulmonary embolism, tension
pneumothorax or cardiac tamponade.
• Loss of vascular tone that results in maldistribution of
blood flow (due to sepsis, anaphylaxis or spinal injury)
SHOCK can be associated with four underlying
patterns, of which three are associated with a low flow
state (hypovolemic, cardiogenic, obstructive) and one is
associated with a hyperkinetic state (distributive).
Should we monitor preload and fluid
responsiveness in SHOCK?
• Optimal fluid management is one of the cornerstones of
hemodynamic management in shock.
• Both hypovolemia and hypervolemia are harmful states
• Attempts have to be made to administer the fluids in the best
possible way
• Fluid responsiveness → To optimize preload (then improve hemodynamic) but
avoid complication
• to determine responders (patients who will benefit from if they are given volume) from non-
responders (patients for whom volume expansion may be deleterious).
• In most studies, > 15 % increase in CO is considered as a positive response to
volume challenge.
Responders vs Non Responders
Flat segment
(preload independence)
Give fluid..
Stroke volume
Be careful
(preload dependence)
to give fluid
in this area
Slope
No more fluid !!
Preload
Making an optimal preload is very challenging
Limitation :
Spontaneous
breathing
Ventilator cause : TV <
8 ml/Kgbb
Low Lung compliance
Elevated pulmonal
artery pressure
Arhytmia
Intraabdominal
Hypertension
• Aortic pulse pressure is known to be directly
proportional to the SV.
• Respiratory changes in pulse pressure (PP) in passive
mechanically ventilated patients reflect changes in
the SV.
Passive Leg Raising
• The PLR maneuver is a simple and reliable
method for evaluating preload
dependency in patients with circulatory
failure, both under conditions of
controlled MV and in spontaneous
breathing even in subjects with alterations
in cardiac rhythm & probably with TV < 8
ml/kg.
• The maneuver is regarded as a test rather
than as a treatment, because it is only
temporary
• a significant increase in CO is observed
over the following minutes-reaching a
peak 60-90 s after elevation
Sabatier C, Monge I, et al, Assessment of cardiovascular preload and response to volume expansion,
Med Intensiva. 2012; 36:45-55.
There are many ways that we have not
discussed in this session.......
↓ ↓SVR
CO
↓CO
↓ DO2
Maldistribution
of flow
SHOCK
MODS
Oxygen Delivery
2014
“..echo must be available 24/7..”
27
What markers of the regional
and microcirculation can be
monitored, and how can
cellular function be assessed
in shock?
Lactate
• Microcirculatory inadequacy to sustain tissue oxygen needs → cellular
dysoxia.
• Inadequate perfusion → lactate and hydrogen ions which spill over into the
blood stream, leading to the biological profile of lactic acidosis
• Plasma level of lactate remains a good surrogate for inadequate tissue
perfusion in shock
• The progressive reduction of plasma lactate and correction of acidosis
probably reflects the restoration of organ blood flow
• The degree and duration of hyperlactacidemia, perfusion-related low pH,
and base deficit → development of organ failure and a poor outcome
SvO2 And ScvO2
SvO2 vs ScvO2
• SvO2 → Indicator global DO2 and VO2 balance
• Merefleksi semua darah vena (SVC, IVC, CS)
• PAC