Indian Journal of Medicine 2011;1:4-23

Review article
Shock for the Internist
George John*, J V Peter, Kishore Pichamuthu, Binila Chacko

Medical Intensive Care Unit, Christian Medical College Hospital, Vellore, India

*corresponding author email: yokavi@yahoo.com

Published online on 17th Feb 2011

Copyright © 2011 George John. This is an open-access article . The publisher and author permit unrestricted use, distribution, and
reproduction in any medium, provided the original work is properly cited.

Abstract
The traditional approach to the correction of the pathophysiology of shock was cardio-centric. In view of the
suboptimal clinical outcomes when clinical management was based on the classical model, there was an
impetus to change. This review gives a new paradigm for understanding and managing shock.

Keywords: shock, sepsis, haemodynamics, critical care, organ dysfunction

Indian J Med 2011;1:4-23

Definition:1

Shock is an acute, systemic clinical syndrome due to ineffective tissue perfusion resulting in severe
dysfunction of organs vital for survival. The manifestations of shock are:

1. arterial hypotension
2. altered temperature and colour of skin / mucous membranes; prolonged capillary refill time
3. organ dysfunction

Classical paradigm:2,3

Traditional haemodynamic evaluation is cardiocentric. The classical approach to understanding

cardiovascular physiology was to visualize the cardiovascular system as being similar to an electrical
circuit (Figure 1). The heart (cardiac output) was considered as the as the organ to be controlled
using preload and vascular resistance as the parameters to be manipulated. Starling’s Law of the
heart was used to explain the relationship between preload and cardiac output. Inotropes were
considered if there was no response to a change in preload (volume challenge).

On the basis of the above paradigm, the causes of shock (based on deranged physiology) can be due
to 4 basic causes presenting as 3 haemodynamic patterns (Table 1).

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Figure 1: The Electrical Analogy

Table 1: Basic types of shock

Cause Pathophysiology* Patterns of abnormalities

Filling status Cardiac function Systemic resistance

Hypovolemic Loss of volume low low high

Vasogenic Vasodilation low high low

Cardiogenic Pump failure high low high

Obstructive Obstruction to flow Variable** low high

*primary problem mentioned in BOLD ; **depending on site of obstruction

Cadiogenic (pump failure) and obstructive (massive pulmonary embolism) causes have similar
clinical patterns but differing pathophysiology. Therapy based on the above paradigm consisted of
measuring upstream pressures (preload), optimizing it using fluid and then using inotropes if the
cardiac output was still suboptimal. In the traditional perspective, the central venous pressure (or
the Left Atrial pressure or its surrogate, the pulmonary artery occlusion pressure) was considered as
a measure of preload which in turn regulated cardiac output. However it is obvious that Starlings
Law applied to cardiac myofiber length. The corresponding in vivo surrogate for this was end
diastolic volume which was determined by the transmural pressure and not the intramural pressure
measured by the CVP. Hence, in the next era, measures of end diastolic volume were considered as
appropriate measures to control cardiac output. Subsequently the concept of volume
responsiveness was introduced.

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THE NEW PARADIGM: 3,4,5,6

The new paradigm uses several concepts regarding cardiovascular physiology which were already
known but not utilized because of the prevalent “fashion” to use pressure measurements to
optimize haemodynamics. It was only when several studies showed that traditional sophisticated
pressure measurements and their derived variables did not improve clinical outcome in patients 7
that attention was refocused on a new perspective.

In the new paradigm, dynamic movement is not considered the same as control. In a car, the moving
parts of the engine are impressive but it is the driver who controls the car. The primary goal of the
cardiovascular system is to ensure tissue perfusion in order to deliver adequate oxygen and
nutrients. The core function of the heart is to transfer blood from a low energy system to a high
energy system. Therefore the final control of the system is with the tissues which need perfusion.
The heart responds to the need by altering output as required.

1. STRESSED AND UNSTRESSED VOLUMES:6

The major component (70%) of blood in the cardiovascular system does not stretch the walls of the
vessels but merely fills the space. This is the unstressed volume and does not contribute to vascular
pressure (except for the gravitational component). The remaining 30% of the blood volume stretches
the walls producing a measurable change in pressure – the mean circulatory filling pressure (MCFP).
This is known as the stressed volume. This is analogous to a pneumatic tyre where the initial volume
of air does not increase pressure but does so only after the tube is inflated to a certain volume
(Figure 2).

Figure 2: Volume vs Pressure

2. DISTRIBUTION OF BLOOD VOLUME:

The blood volume is distributed as follows in various vascular compartments (Figure 3).

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Figure 3: Blood volume distribution

3. MEAN CIRCULATORY FILLING PRESSURE (MCFP):3,4,5,8

The MCFP is the mean pressure value for the entire circulation when the heart stops beating. It is
the ‘hydrostatic mean pressure’ of the circulation – the pressure in the circulation with no cardiac
activity. When there is no effective cardiac contraction, the arteries recoil and about 4 ml/kg of
blood moves from the arterial side to the venous side (due to elastic recoil) and an overall pressure
of 7 (+2) mm Hg is achieved. This value is less than the capillary pressure but more than the venous
pressure. The pressure in the small veins (< 1mm diameter) is the “pivot locus” as it does not
change. Conceptually, the MCFP (also known as Pmc) is the resultant of two components – the mean
systemic filling pressure (MSFP, Pms) and the mean pulmonary filling pressure (MPFP, Pmp). The
difference in Pmc and Pms is accounted for by variation in Pmp. The capacitance of the pulmonary
circulation is < 1/8 of the systemic but the blood volume in the pulmonary circulation is only 1/10 of
systemic volume. Hence the Pmc and Pms are numerically almost equal under normal conditions as
the mean pulmonary filling pressure does not significantly contribute to the resultant pressure. It is
now possible to obtain a surrogate (analogue) of the Pms (known as the Pmsa) in real time with
input from the circulatory variables (available from the bedside monitors) using special software. 4

4.THE ROLE OF THE HEART:

First, the circulation is not controlled (as opposed to energised) by the heart, but by the tissue flow
requirements for gas exchange and metabolism. Second, unlike most pumps, the heart fills passively
- it is not a suction pump.

Consider the following analogy4 (Figure 4):

There are 2 water tanks connected by a pipe at the floor level. The tanks have unequal heights of
water. Water drains continuously from the larger to the smaller tank because the height of water in
the larger tank is more than in the smaller tank. This is maintained by a pump which pumps water
continuously from the smaller tank to the larger one.

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Figure 4: The New Paradigm

Pms is the mean systemic filling pressure ;Pra is the Right Atrial Pressure

Rvr is the Resistance to Venous Return ;Flow is the venous return into the right atrium

The large reservoir of pressure head (Pms) has an exit pipe of resistance Rvr at the base of the wall.
The pipe fills a small chamber of pressure head Pra. Within the chamber, a pump (the heart) pumps
water back into the reservoir. The “heart” is careful to keep Pra low and constant. The “pumping
output” thus equals the Venous Return Flow into the chamber.

When the right atrial pressure reaches the MCFP, venous return ceases (Figure 5).

Figure 5: Venous return

Thus the true volume status of the body is reflected in the MCFP.

The cardiac output is determined by the intersection of the two curves (Figure 6) 5

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Figure 6: Cardiac output

The pump (the heart) has an efficiency denoted by EH (efficiency of heart function) 4

EH = (Pms – Pra) / Pms = 1 – (Pms / Pra )

This ratio EH is a clinically useful concept to assessing cardiac performance. Consider two extreme
examples:

If the heart stops pumping, Pra = Pms and Pra/Pms = 1 and EH = 1 - 1 = 0.

If the heart is pumping well, Pra = 0; and (Pra / Pms) = 0 and EH = 1- 0 = 1.

Thus, EH may be used as a parameter for assessing the need for inotropes.

A functional perspective would be as follows (Figure 7):

Figure 7: Functional perspective of haemodynamics

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5. THE MICROCIRCULATION:

a. Systemic:

The average pressures (all in mm Hg) in the microcirculation are summarized in Table 2.

Table 2: Pressures in the systemic microcirculation

SYSTEMIC (P)

Capillary Mean = plus 25 (40 = arterial end and 10 =venous

end)
HYDROSTATIC
Interstitial minus 2 (5 – 8) subcutaneous; plus 6 in brain;
positive in kidney / liver

Capillary plus 25 - 28

ONCOTIC
Interstitial plus 8 (0 – 10)

Arterial end = [40 – (-2)] – [28 – 8]

NET FORCE = 42 – 20 = plus 22

(tending to force fluid from capillary into

interstitium)

Venous end =[10 – (-2)]- [28 – 8]

= 12 – 20 = minus 8

(tending to force fluid back into capillary)

Note that as fluid leaves the capillary, the protein concentration and hence the oncotic pressure rises
tending to pull back fluid (this is not shown in the calculation) into the vessel.

The Interstitial Colloid Oncotic Pressure varies in the different organs. Direct measurement is not
possible as samples will be contaminated. The estimation is based on the presumption that
lymphatics drain the interstitial space and estimation of protein content of lymph from various
organs will approximate the interstitial fluid protein.

The filtration reabsorbtion rates also differ in the various organs. In the muscle, there is outward
movement at the arteriolar end and an inward movement at the venous end as shown above. In the
glomeulus, the capillary hydrostatic pressure (CHP) is 50-60 mm Hg and is always much higher than
the capillary colloid oncotic pressure (COP) - hence the flow is outward through the whole length of
the glomerular capillary. In the intestine, the CHP is much less than the COP, thus there is absorption
through the length of the capillary.

b. Pulmonary:

The functional pulmonary unit can be visualized as in Figure 8.

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CAPILLARY INTERSTITIUM ALVEOLI

Figure 8: The pulmonary microstructure

The permeability of pulmonary capillaries to protein is higher than the permeability of systemic
capillaries. This results in more leakage of protein into the pulmonary interstitium. The lymphatics
drain the interstitial space of about 30ml of fluid per hour.

The pressures in the pulmonary microcirculation are given in Table 3.

Table 3: Pressures in the pulmonary microcirculation

CAPILLARY INTERSTITIUM ALVEOLI

(Exposed to atmosphere)

HYDROSTATIC PLUS 7 MINUS 8 Surface tension

ONCOTIC PLUS 28 PLUS 14 Same as interstitial as there is

no protein barrier

NET EFFECT Fluid moves from capillary to interstitium and from alveoli to interstitium; fluid
drained by lymphatics.

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The net negative interstitial hydrostatic pressure of about 1 mm Hg along with the increase in the
interstitial colloid oncotic pressure along with the high capacity for lymphatic drainage in the lungs
keeps the alveoli dry for optimum gas exchange. This also explains why the low albumin in a
condition such as nephrotic syndrome can cause significant peripheral oedema while there is no
pulmonary oedema. This is because:

-The oncotic pressure gradient does not balance out the hydrostatic gradient as per Starlings law –
they are on the same side of the equation.

-The permeability of pulmonary capillaries to protein equalizes the oncotic pressure gradients to a
large extent. Hence pulmonary oedema occurs in response to unbalanced hydrostatic pressures not
due to an imbalance of oncotic pressure.

MANAGEMENT OF SHOCK:1,9,10,11

The management of shock includes early definitive intervention to stabilize haemodynamics, specific
therapy for the cause of shock (e.g transfusion for haemorrhagic shock) and support of failed organ
systems.

The following are important principles:

1. Intervention in shock must be early and appropriate. Hence devices which take time and expertise
(which may not be readily available) to insert are fine in theory but are not likely to improve
outcome in reality.

2. Interventions must be evidence based – not just on normalizing physiology but on improving
outcome.

The following is the broad strategy:

1.EARLY RECOGNITION: The needle of clinical suspicion for shock must have a very high sensitivity in
the appropriate scenario. This includes elderly patients, patients admitted in ICUs, those with
indwelling devices or foreign bodies and post operative or post trauma patients. Unwarranted
reliance on blood pressure “numbers” to diagnose shock will delay initiation of therapy.

2.TARGET THE CAUSE (if feasible): As examples,

a. haemorrhage – stop haemorrhage, replace blood; do not push up blood pressure rapidly if the

source of bleed is not controlled (permissive hypotension)

b. anaphylaxis – remove / stop offending antigen

c. sepsis – drain any infected collection, short lag time (< 1 hour) from recognition to administer first

antibiotic dose

d. cardiogenic due to coronary occlusion: PTCA / thrombolysis as appropriate

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e. pulmonary embolism: thrombolysis

f. tension pneumothorax / cardiac tamponade: evacuate air / fluid

In some cases, it may not be possible to remedy the problem immediately- e.g. septic shock in a
person with a prosthetic valve. In this case, the best available options (adequate antibiotics, support
of failing organ systems) must be implemented till definitive intervention is possible.

3. SUPPORT DYSFUNCTIONAL ORGAN SYSTEMS:

A.CARDIOVASCULAR:

The core principles to keep in mind for optimizing cardiovascular physiology in shock are:

1.The Starling mechanism cannot by itself determine stroke volume- it is not a control mechanism
but an executive mechanism which matches inflow to outflow. It merely guarantees that it pumps
out whatever is put into it, if myocardial function is normal

2.Cardiac output and venous return are interdependent

3.Cardiac output is the product of stroke volume and heart rate and is the cause of arterial pressure
not its consequence. It makes no sense to write the equation as: Cardiac Output = (Mean Arterial
Pressure – RAP) / Systemic Resistance.

4.In a similar vein, the cardiac output is coupled to venous return – in a steady state, both are equal.
If venous return increases, RAP increases and so does Cardiac Output till the output equals intake.
Increasing Cardiac Output will push more blood into the venous system and increase venous return.
The reverse process also occurs.

5.The primary goal of the arterial system is to distribute blood – a fall in arterial pressure generates
two systemic responses: increase in cardiac output and increase in peripheral resistance in addition
to a local response depending on tissue needs (regional changes in resistance).

6.The primary goal of the venous system is to collect blood – in this context venous capacitance is
more important than venous resistance. Thus, in contrast to arteriolar constriction (which increases
resistance to flow), venoconstriction does not result in an increase in venous resistance with a
resultant decrease in return flow to the heart (with decreased cardiac output). Venous constriction
reduces capacitance, shifts blood into the heart and increases cardiac output.

The core haemodynamic goal in critical care is to keep the heart optimally filled, the lungs “dry” (to
allow oxygenation) and the kidneys “wet”. In the absence of appropriate measurable parameters,
this is a juggling act!

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Newer modes of assessment and intervention attempt to answer the following questions:

a) Is the circulation underfilled / responsive to fluid?

b) Does this patient need a higher cardiac output to improve his clinical condition?

c) Will fluid therapy be of benefit (ventricles are fluid responsive)

or

will it do harm (flood the lungs)?

I)IS THE CIRCULATION UNDERFILLED / RESPONSIVE TO FLUID? 9,11,12,13,14

a. The Traditional Parameters: Pressure Measurements: CVP / PAoP:

The CVP was the first parameter measured used to answer this question. It was considered a
surrogate for the “volume status” of the body and hence the filling pressures of the heart. However,
the CVP is only the filling pressure for the right heart. The CVP by itself shown to be an insensitive
and non specific marker (Figure 9) of the body’s total volume status. 6,9

Figure 9: CVP and body fluid status

CVP measurement was thereafter replaced by the PA catheter measurement which also measured
the filling pressures of the left (pulmonary artery occlusion pressure, PAoP) heart in addition to the
CVP. The classical protocol used was to “normalize” filling pressures followed by the use of inotropes
/ vasoactive agents based on measured and calculated parameters such as cardiac output and
peripheral resistance.

The PA catheter has not been shown to alter outcome in several controlled clinical trials. 7

b. The New Parameters:11,12,13,14

Respiratory variation of parameters:

In the following discussion, variation is mathematically calculated as follows:

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Variation % = [(Maximum minus Minimum) / Average] x 100

Variation % = [(Maximum minus Minimum) / {(Max + Min)/2}] x 100

1. IVC diameter variation:

The respiratory variation in superior and inferior vena caval diameter have been used to predict
volume status (preload responsiveness) in ventilated patients. The diameters are measured using
bedside sonology.

The IVC collapse index (IVC-CI) is used:

IVC-CI = (IVCDmax – IVCDmin) / IVCDmean.

In healthy subjects breathing spontaneously, the IVC has a larger diameter in expiration and a
smaller diameter in inspiration.

For those on positive pressure ventilation, the changes in IVC diameters in relation to the respiratory
cycle are the reverse of the measurements compared to those breathing spontaneously (maximum
during positive pressure and minimum during exhalation). The maximum and minimum
measurements can also be made without reference to the respiratory cycle.

A IVC-CI value > 12% indicates that the vascular volume is underfilled.

2.Stroke Volume Variation:

This is based on the fact that positive pressure ventilation causes cyclic changes in intrathoracic
pressure which result in cyclic changes in LV output (stroke volume). These changes are seen best in
mechanically ventilated patients. A value > 12% indicates that the vascular space is underfilled.

3.Pulse Pressure Variation (Figure 10):

Some invasive blood pressure monitors give the pulse pressure variation on the monitor itself –
making it a useful bedside parameter.

Figure 10: Pulse Pressure Variation

The threshold value for an underfilled vascular system using an arterial pulse pressure variation is
> 12%.

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4. Pulse oximetry plethysmogram:

It has been shown that the respiratory changes in the amplitude of the plethsmographic pulse wave
(pulse oximeter) allows the prediction of fluid responsiveness in mechanically ventilated septic
patients. The threshold value for a patient who will respond to volume for the plethysmographic
pulse pressure variation is > 14%.

5. Passive Leg Raising (PLR):

PLR is based on the principle that raising the lower limbs induces an abrupt increase in venous return
secondary to auto-transfusion of peripheral blood from capacitive veins of the lower part of the
body. This is equivalent to an “internal fluid challenge” equivalent to a 300 - 500ml fluid bolus. The
lower limbs are both lifted in a straight line to an angle of 30 o - 45o for 4 minutes. It has the added
advantage that it is reversible on lowering the legs (if pulmonary oedema occurs).

The maximal haemodynamic effects of PLR occurs within the first minute of leg elevation. The value
to be noted is the change systolic blood pressure or the pulse pressure not the change in mean or
diastolic blood pressure. This is intuitive as the systolic / pulse pressure corresponds to the stroke
volume.

The PLR test can be used both for mechanically ventilated and spontaneously breathing patients.

6. Fluid challenge:

This is done to assess the responsiveness of the cardiovascular system to an increase in intravascular
volume. 200 – 500 ml of fluid is given over 10 minutes. Pulse pressure variation or stroke volume
variation in response to the fluid challenge is then measured.

Assessments of predictive tests for fluid responsiveness are most relevant when focused in patients
with hypoxemic or cardiac failure.

II)Does this patient need a higher cardiac output to improve his clinical condition?

The primary goal of any therapeutic intervention is to maintain tissue oxygenation and perfusion.The
finding that a person’s vascular space is “underfilled” or fluid responsive does not imply that fluid
administration is useful or necessary. Even healthy walking persons are fluid responsive!! In addition,
administration of fluid will not result in better perfusion if the myocardium cannot cope with the
increased load. In this case, inotropes will be needed.

The available technology to monitor regional perfusion is neither easily available nor clinically
validated. It is also possible that regional circulations may show heterogeneity of perfusion in shock.
The current measures used are global indicators for adequacy of oxygenation & perfusion. These
are:

a)arterial lactate (a value >2mmmol/L) implies that the tissues have switched to anaerobic
metabolism due to inadequate oxygen delivery (it can also be because of reduced clearance, hence
an overall perspective is essential)

b)ScvO2 is the oxygen saturation of haemoglobin in blood returning to the heart. If the tissues do
not receive adequate oxygen, they will extract more of the oxygen being delivered and the blood
returning to the heart will show more desaturation (SvO 2 < 70%) as compared to those with better
perfusion. The limitation is that if blood is shunted in the periphery (the tissues are bypassed) the
venous blood may not show desaturation even though the tissues are not getting adequate oxygen.

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A recent study15 shows that a high central venous oxygen may also be a surrogate for impaired
tissue oxygenation as the “unused / unusable” oxygen is being “returned”. In the observational
study published in 2011, in patients undergoing cardiac surgery, it was shown that both low
(< 60.8%) and supranormal (>77.4%) ScvO2 were predictors of a complicated post operative period.
Lactate was comparably increased in the patients who died irrespective of whether they had low or
supranormal ScvO2. Lactate was higher in patients who had a supranormal ScvO 2.15 However, this
finding needs to be confirmed in patients with sepsis.

Hence a low as well as a supranormal ScvO2 may be signs of inadequate tissue oxygenation.

c) Veno- arterial carbon dioxide difference:

The veno- arterial carbon dioxide difference is a surrogate marker for cardiac output. It has been
shown in a study that the cardiac output is inversely correlated with the venous-arterial PCO 2. In
states of decreased flow (cardiac output), there is an increase in the difference. As a rule of thumb, if
the difference is >7 mm Hg, the cardiac index is low (< 2.5 l/min/m 2).

III) Will fluid therapy be of benefit (ventricles are fluid responsive) or will it do harm (flood the
lungs)?16

If a maneuver to increase cardiac output results in arterial hypoxia by flooding the lungs, the whole
purpose of improving tissue oxygenation / perfusion is lost. The core of the problem in managing
fluid balance is to achieve a balancing act between sufficient filling of the cardiovascular system
while avoiding pulmonary oedema. The main concern in giving additional fluid is that the lungs will
get “wet” which in turn will affect oxygenation. This would defeat the primary purpose of the goal to
improve tissue oxygenation.

It is also well documented 16 that the amount of Extravascular Lung Water (EVLW) is an independent
predictor of prognosis. Techniques to estimate EVLW) are available. Those with EVLW > 15ml / kg
had a mortality rate of about 65% while those with an EVLW < 10ml / kg had a survival rate of about
67%.

The PICCO (Pulse Contour Cardiac Output) technique utilizes a standard CVP line and a special
arterial catheter with a thermistor to measure EVLW.

Dynamic studies are also useful to answer this question.

1. PLR & S/F ratio:

If the SpO2 is simultaneously noted during PLR and there is no drop in oxygen saturation, there is
likely to be good tolerance to volume expansion. If the SpO 2 drops significantly, it is likely that fluid
administration may cause more harm (pulmonary oedema as the left ventricle cannot cope with the
added volume) than good and inotropes may be indicated.

However, it should be remembered that the SpO 2 must be < 97% for the test to be useful because
the S/F ratios and P/F ratios are concordant only if SpO 2 is < 97%. This is because the maximum
numerical value for SpO2 is 100 while the PaO2 may be 500. If there is good oxygenation, but the
heart cannot take an additional load, an increase in lung water with a drop in PaO 2 from 500 to 200
will not be reflected in the SpO2 which will remain at 100.

The Passive Leg Raising test can answer the two questions stated above but in different time frames.
The change in pulse pressure/systolic blood pressure takes place within a minute but changes in
oxygenaton (as seen in the SpO2) can take up to 5 minutes.

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2. Fluid bolus administration (Fluid Challenge) & Oxygenation Indices:

If the “oxygen transfer” indices (P/F ratio / PA-a difference) is normal, fluid challenge can be
considered safe. However, a low P/F ratio or PA-a difference does not rule out the need for fluid
administration. The oxygen transfer may improve with increasing cardiac output as pulmonary
perfusion improves.

Repeated evaluation of the P/F ratio with bolus administration of fluid will give an idea as to
whether the lungs are becoming “wet” with fluid therapy. Hence the P/F ratio will need to be
reassessed at regular intervals to check for any deleterious increase in lung water with interference
of oxygenation.

It should be noted that these methods of evaluating “safe to fill” have not been clinically validated.

The bedside ECHO17 (Bedside sonology) can also be used to assess cardiac contractility, cardiac
output, lung water and response to fluid therapy.

Remember:

IF

The peripheral tissues need an increase in perfusion

AND

The circulatory system is not fluid responsive OR It is not safe to fill

THEN

inotropes have to be used.

B) RESPIRATORY:

Is the Respiratory System able to meet the need of the body in order to:

1. oxygenate

2. maintain pH

If this is not possible, Mechanical Ventilatory Support may be needed.

C)RENAL:

Is renal function adequate to maintain fluid, electrolyte and acid base homeostasis.

If not, Renal Replacement Therapy is indicated. Acidosis results in a suboptimal response to

inotropes/vasopressors. The exception is vasopressin which acts even in an acidic environment.

D)LIVER:

Is hepatic function adequate to maintain metabolic homeostasis?

Avoid hepatotoxic drugs if hepatic function is impaired.

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E) TARGET MEDIATORS OF INFLAMMATION (if evidence is adequate):

These include activated Protein C (rhAPC), Immunoglobulins or hemoperfusion through a column of

immobilized polymyxin B (PMX-B). There is controversy regarding the usefulness of these modes of
therapy.

COMPONENTS FOR INTERVENTION:

FLUID :18,19

The choice of fluid for resuscitation has been the subject of intense debate for many years.
Physiologically, colloids expand intravascular volume more than crystalloids. Hence, these were
considered, to be the fluid of choice in shock. Others opined that in shock, vascular permeability was
impaired, thus allowing colloid particles to leak into the interstitium thereby pulling more fluid out of
the vascular system into the interstitium.

Clinical trials showed that crystalloid solutions had less complications (renal dysfunction) when used
in resuscitation. The adverse effects are probably related to hyperoncotic colloids which were used
and hence colloid solutions which have lower oncotic pressure are now being suggested for
resuscitation.

INOTROPES: 20,21,22,23,24

The choice of inotropic/vasoactive drugs should be based not only on the pattern of physiological
abnormalities (profile analysis) but also on the evidence of randomized trials showing improved
outcome (and not just improvement in measured parameters). Good quality clinical trials for
inotropes are now available. Appropriate inotropes tailored to the situation should used. Careful
monitoring of the response is mandatory as significant inter individual variability can exist.

Adrenaline vs Noradrenaline:

It has been shown that there is no difference between adrenaline (epinephrine) and noradrenaline
(norepinephrine) plus dobutamine in terms of efficacy or safety when used in patients with septic
shock.

Dopamine vs Noradrenaline / other inotropes:

There is no renal protection in using low dose dopamine in critically all patients.

Early small observational studies had suggested that treatment with dopamine may be detrimental
for patients with septic shock. In a comparison of dopamine and noradrenaline, the results showed
that there was no significant difference in mortality. However, there were more arrhythmic events
among the patients treated with dopamine than in those treated with noradrenaline.

Vasopressin:

Low-dose vasopressin did not reduce mortality rates as compared with norepinephrine among
patients with septic shock. The advantage is that it maintains its action even if there is acidosis.

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First use protocol - Fluids or Inotropes?

It is important to remember that “a numerically acceptable MAP” at the cost of intense

vasoconstriction does not achieve the goal of optimising tissue perfusion. Keeping this in mind, fluids
should generally be used first if it is safe (patient not in pulmonary oedema). However, if the blood
pressure is “crashing” with an impending cardiac arrest, it would be best to start fluids and inotropes
simultaneously, stabilize the blood pressure and then do the tests for fluid responsiveness prior to
further fluid administration.

PUTTING IT ALL TOGETHER A SYN-OPTIC VIEW:

A syn-optic view of managing a patient in shock, termed by its acronym, SITEMAP, is given.
SITEMAP stands for STRUCTURED INTERVENTION by TARGETED EVALUATION to MAINTAIN
ADEQUATE PERFUSION (Figure 11).

Figure 11: SITEMAP

The conceptual points are not to be seen in serial order but simultaneously. Continuing monitoring
and intervention are necessary to ensure that tissue perfusion continues to be optimized.

The central starting conceptual point is the lack of tissue perfusion. This lack of tissue perfusion
should intuitively include significant hypotension but not be the sole criterion. A Mean Arterial
Pressure (MAP) below 60mm Hg will be an inadequate pressure head for perfusion in most people.
Some (e.g chronic hypertensives) will need a higher mean arterial pressure to maintain tissue
perfusion while others (e.g. those with chronic congestive cardiac failure) can manage with a lower
MAP as they have adapted to the low pressure state with time. The other starting point will be
abnormal markers of suboptimal tissue perfusion (lactate, ScvO 2).

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PATTERNS OF SCVO2 AND LACTATE LEVELS:

This may be seen as one of several possible patterns (Table 4).

Table 4: SCVO2 and lactate patterns:

ScvO2 Lactate level Pathophysiological Diagnosis

Peripheral shunt, increased lactate production,

decreased lactate clearance, mitochondrial poison
High15 High interfering with oxidation pathway
(> 77%)

Decreased oxygen delivery – low haemoglobin, low

oxygen saturation or inadequate cardiac output
Low 10,15 High

(<60-70%)

Low Normal Increased oxygen extraction but oxygen delivery is

adequate for need
(<2mmol/l)

HAEMOGLOBIN:

In a critically ill septic patient, the optimum haemoglobin is 7-8 g%. A higher level of 10 g% may be
needed in a critically ill patient with myocardial or cerebral ischemia .

“ADEQUATE” CARDIAC OUTPUT:

The cardiac output should be optimized to the need for tissue perfusion not to a numerically normal
value.Assessment of Cardiac Output should be done only after the Mean Arterial Pressure is
“normalized” (with vasopressors if needed). In the presence of significant reduction in peripheral
resistance, even if the myocardium is hypofunctioning, the cardiac output may be in the
“numerically normal range ”. If the systemic vascular resistance is increased using vasopressors, the
myocardium will then reveal its “true colours” as it is now pumping against an increased resistance
to maintain an adequate MAP. However, most vasopressors used in critical care (dopamine,
noradrenaline, adrenaline) are in fact “inopressors” and not pure vasopressors. Thus the cardiac
output estimated while giving these inopressors will have a component of inotropic effect (it may
show a higher value).Dobutamine is an inodilator as it has a peripheral vasodilator action in addition
to its inotropic effect.

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Indian Journal of Medicine 2011;1:4-23

Conflict of interest: None declared

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