SHOCK
Shock is a systemic state of low tissue perfusion, which is
inadequate for normal cellular respiration. With insufficient
delivery of oxygen and glucose, cells switch from aerobic to
anaerobic metabolism. If perfusion is not restored in a timely
fashion, cell death ensues.
Pathophysiology
Cellular
1-As perfusion to the tissues is reduced, cells are deprived of oxygen and must switch
from aerobic to anaerobic metabolism.
2-The product of anaerobic respiration is not carbon dioxide but lactic acid.
3-When enough tissue is under perfused, the accumulation of lactic acid in the blood
produces systemic metabolic acidosis.
4-As glucose within cells is exhausted, anaerobic respiration ceases and there is failure
of the sodium/potassium pumps in the cell membrane and intracellular organelles.
5-Intracellular lysosomes release autodigestive enzymes and cell lysis ensues.
6-Intracellular contents, including potassium, are released into the bloodstream
causing (hyperkalemia).
Microvascular
1-Hypoxia and acidosis activate complement and prime neutrophils, resulting in the
generation of oxygen free radicals and cytokine release.
2-These mechanisms lead to injury of the capillary endothelial cells. These in turn
further activate the immune and coagulation systems.
3-
Da aged e dotheliu loses its i teg it a d e o es leak . Spa es et ee
endothelial cells allow fluid to leak out and tissue oedema ensues, exacerbating
cellular hypoxia.
Systemic
Cardiovascular :
As preload and afterload decrease, there is a compensatory
baroreceptor response resulting in increased sympathetic activity and release of
catecholamines into the circulation. This results in tachycardia and systemic
vasoconstriction (except in sepsis ).
Respiratory:
The metabolic acidosis and increased sympathetic response result in an
increased respiratory rate and minute ventilation to increase the excretion of
carbon dioxide (and so produce a compensatory respiratory alkalosis).
Renal:
Decreased perfusion pressure in the kidney leads to reduced filtration at the
glomerulus and a decreased urine output. The renin
–angiotensin–aldosterone axis is
stimulated resulting in further vasoconstriction and increased sodium and water
reabsorption by the kidney.
Endocrine:
As well as activation of the adrenal and renin
–angiotensin systems, vasopressin
(antidiuretic hormone) is released from the hypothalamus in response to decreased
preload and results in vasoconstriction and reabsorption of water in the renal collecting
system.
Cortisol is also released from the adrenal cortex, contributing to the sodium and water
reabsorption and sensitizing the cells to catecholamines.
Ischaemia
–reperfusion syndrome
During the period of systemic hypoperfusion, cellular and organ damage progresses
because of the direct effects of tissue hypoxia and local activation of inflammation.
Further injury occurs once normal circulation is restored to these tissues. The acid and
potassium load that has built up can lead to direct myocardial depression, vascular
dilatation and further hypotension.
The cellular and humoral elements activated by the hypoxia (complement, neutrophils,
microvascular thrombi) are flushed back into the circulation where they cause further
endothelial injury to organs such as the lungs and kidneys.
This leads to acute lung injury, acute renal injury, multiple organ failure and death.
Reperfusion injury can currently only be attenuated by reducing the extent and
duration of tissue hypoperfusion.
Classification of shock
• Hypovolaemic
• Cardiogenic
• Obstructive
• Distributive
• Endocrine
Hypovolaemic shock
Hypovolaemic shock is caused by a reduced circulating volume.
Hypovolaemia may be due to haemorrhagic or non-haemorrhagic causes.
Non-haemorrhagic causes include
• poor fluid intake (dehydration) and
• excessive fluid loss because of vomiting, diarrhea, urinary loss (e.g. diabetes),
• e apo atio a d thi d-spa i g , i hi h fluid is lost i to the gast oi testi al t a t
and interstitial spaces, as for example in bowel obstruction or pancreatitis.
Hypovolaemia is probably the most common form of shock and is to some
degree a
component of all other forms of shock. Absolute or relative
hypovolaemia must be excluded or treated in the management of the shocked
state, regardless of cause.
Cardiogenic shock
Cardiogenic shock is due to primary failure of the heart to pump blood
to the tissues.
Causes :
• myocardial infarction, cardiac dysrhythmias, valvular heart disease,
blunt myocardial injury and cardiomyopathy.
• Cardiac insufficiency may also be caused by myocardial depression
resulting from endogenous factors (e.g. bacterial and humoral agents
released in sepsis) or exogenous factors, such as pharmaceutical
agents or drug abuse.
Evidence of venous hypertension with pulmonary or systemic oedema
may coexist with the classic signs of
shock.
Obstructive shock:
there is a reduction in preload because of mechanical
obstruction of cardiac filling. Common causes;- cardiac tamponade,
tension pneumothorax, massive pulmonary embolus and air embolus.
In each case there is reduced filling of the left and/or right sides of the
heart leading to reduced preload and a fall in cardiac output.
Distributive shock:
Distributive shock describes the pattern of cardiovascular
responses characterising a variety of conditions including septic shock,
anaphylaxis and spinal cord injury. Inadequate organ perfusion is
accompanied by vascular dilatation with hypotension, low systemic
vascular resistance, inadequate afterload and a resulting abnormally high
cardiac output.
In anaphylaxis, vasodilatation is caused by histamine release, whereas in
high spinal cord injury there is failure of sympathetic outflow and
adequate vascular tone (neurogenic shock). The cause in sepsis is less
clear but is related to the release of bacterial products (endotoxins) and
the activation of cellular and humoral components of the immune system.
There is maldistribution of blood flow at a microvascular level with
arteriovenous shunting and dysfunction of the cellular utilisation of
oxygen.
In the later phases of septic shock there is hypovolaemia from fluid loss
into the interstitial spaces and there may be concomitant myocardial
depression, which complicates the clinical picture.
Endocrine shock:
it may present as a combination of hypovolaemic, cardiogenic
and distributive shock.
Causes :
include hypo- and hyperthyroidism and adrenal insufficiency.
1-Hypothyroidism causes a shock state similar to that of neurogenic shock as a result
of
disordered vascular and cardiac responsiveness to circulating catecholamines.
Cardiac output falls because of low inotropy and bradycardia.
There may also be
an associated cardiomyopathy.
2- Thyrotoxicosis may cause a high-output cardiac failure.
3-Adrenal insufficiency leads to shock as a result of hypovolaemia and a poor response
to
circulating and exogenous catecholamines. Adrenal insufficiency may result
from pre-
e isti g Addiso s disease o it a e a elati e i suffi ie
aused
a pathological
disease state such as systemic sepsis.
Cardiovascular and metabolic characteristics of shock
Hypovolaemia Cardiogenic Obstructive Distributive
Cardiac output Low Low Low High
Vascular resistance High High High Low
Venous pressure Low High High Low
Mixed venous saturating Low Low Low High
Base deficit High High High High
Severity of shock
Compensated shock
In compensated shock there is adequate compensation to maintain the central blood
volume and preserve flow to the kidneys, lungs and brain.
Apart from a tachycardia and cool peripheries (vasoconstriction, circulating
catecholamines) there may be no other clinical signs of hypovolaemia.
However, this cardiovascular state is only maintained by reducing perfusion to the
skin, muscle and gastrointestinal tract.
There is a systemic metabolic acidosis and activation of humoral and cellular
elements within the underperfused organs.
Patients with occult hypoperfusion (metabolic acidosis despite normal urine output
and cardiorespiratory vital signs) for more than 12 hours have a significantly higher
mortality rate, infection rate and incidence of multiple organ failure .
Decompensation
Fu the loss of i ulati g olu e o e loads the od s o pe sato e ha is s
and there is progressive renal, respiratory and cardiovascular decompensation.
In general, loss of around 15% of the circulating blood volume is within normal
compensatory mechanisms. Blood pressure is usually well maintained and only
falls after 30
–40% of the circulating volume has been lost.
Mild shock
:
initially there is tachycardia, tachypnoea and a mild reduction in urine
output and the patient may exhibit mild anxiety. Blood pressure is maintained
although there is a decrease in pulse pressure. The peripheries are cool and
sweaty with prolonged capillary refill times (except in septic distributive shock).
Moderate shock
:
As shock progresses, renal compensatory mechanisms fail, renal
perfusion falls and urine output dips below 0.5 ml/ kg/h. There is further
tachycardia and now the blood pressure starts to fall. Patients become drowsy and
mildly confused.
Severe shock :
In severe shock there is profound tachycardia and hypotension.
Urine output falls to zero and patients are unconscious with laboured respiration.
Capillary refill :
Most patients in hypovolaemic shock will have cool, pale peripheries
with prolonged capillary refill times; however, the actual capillary refill time varies
so much in adults that it is not a specific marker of whether a patient is shocked,
and patients with short capillary refill times may be in the early stages of shock.
In distributive (septic) shock the peripheries will be warm and capillary refill will
be brisk despite profound shock.
Tachycardia :
Ta h a dia a ot al a s a o pa sho k. Patie ts ho a e o β-
blockers or who have implanted pacemakers are unable to mount a tachycardia. A
pulse rate of 80 in a fit young adult who normally has a pulse rate of 50 is very
abnormal. Furthermore, in some young patients with penetrating trauma, when
there is hemorrhage but little tissue damage, there may be a paradoxical
bradycardia rather than tachycardia accompanying the shocked state.
pressure :
It is important to recognize that hypotension is one of the last signs of
shock. Children and fit young adults are able to maintain blood pressure until the
final stages of shock by dramatic increases in stroke volume and peripheral
vasoconstriction. These patients can be in profound shock with a normal blood
pressure.
Consequences
Unresuscitatable shock
Patients who are in profound shock for a prolonged period of time become
unresuscitatable
. Cell death follo s f o ellula ischaemia, and the ability of the
body to compensate is lost.There is myocardial depression and loss of
responsiveness to fluid or inotropic therapy. Peripherally there is loss of the ability
to maintain systemic vascular resistance and further hypotension ensues.
The peripheries no longer respond appropriately to vasopressor agents.Death is
the inevitable result.This stage of shock is the combined result of the severity of
the insult and delayed, inadequate or inappropriate resuscitation in the earlier
stages of shock. When patients present in this late stage and have minimal
responses to maximal therapy it is important that the futility of treatment is
recognised and that valuable resources are not wasted.
Multiple organ failure
As techniques of resuscitation have improved, more and more patients are
surviving shock. When intervention is timely and the period of shock is limited,
patients may make a rapid, uncomplicated recovery; however, the result of
prolonged systemic ischaemia and reperfusion injury is end-organ damage and
multiple organ failure.
Multiple organ failure is defined as two or more failed organ systems. There is no
specific treatment for multiple organ failure. Management is by supporting organ
systems with ventilation, cardiovascular support and haemofiltration/dialysis until
there is recovery of organ function. Multiple organ failure currently carries a
mortality rate of 60%. Thus, prevention is vital by early aggressive identification
and reversal of shock.
RESUSCITATION
Immediate resuscitation maneuvers (ABC) for patients presenting in shock are to
e su e a pate t ai a a d ade uate o ge atio a d e tilatio . O e ai a
a d eathi g a e assessed a d o t olled, atte tio is di e ted to a dio as ula
resuscitation.
Conduct of resuscitation
1-Resuscitation should not be delayed in order to definitively diagnose the source of
the shocked State; however, the timing and nature of resuscitation will depend on
the type of shock and the timing and severity of the insult.
2- Rapid clinical examination will provide adequate clues to make an appropriate first
determination, even if a source of bleeding or sepsis is not immediately
identifiable.
3-If there is initial doubt about the cause of shock it is safer to assume the cause is
hypovolaemia and begin with fluid resuscitation, followed by an assessment of the
response.
4-In patients who are actively bleeding (major trauma, aortic aneurysm rupture,
gastrointestinal hemorrhage) it is counterproductive to institute high-volume fluid
therapy without controlling the site of hemorrhage. Increasing blood pressure
merely increases bleeding from the site, and fluid therapy cools the patient and
dilutes available coagulation factors. Thus, operative hemorrhage control should
not be delayed and resuscitation should proceed in parallel with surgery.
5-Conversely, a patient with bowel obstruction and hypovolaemic shock must be
adequately Resuscitated before undergoing surgery otherwise the additional
surgical injury and hypovolaemia induced during the procedure will exacerbate
the inflammatory activation and increase the incidence and severity of end-organ
insult.
Fluid therapy
In all cases of shock, regardless of classification, hypovolaemia and inadequate
preload must be addressed before other therapy is instituted.
Administration of inotropic or chronotropic agents to an empty heart will rapidly
and permanently deplete the myocardium of oxygen stores and dramatically
reduce diastolic filling and therefore coronary perfusion.
Patients will enter the unresuscitable stage of shock as the myocardium becomes
progressively more ischemic and unresponsive to resuscitative attempts.
First-line therapy, therefore, is intravenous access and administration of
intravenous fluids. Access should be through short, wide-bore catheters that allow
rapid infusion of fluids as necessary. Long, narrow lines such as central venous
catheters have too high a resistance to allow rapid infusion and are more
appropriate for monitoring than fluid replacement therapy.
Type of fluids
1-
stalloid solutio s o al sali e, Ha t a s solutio , ‘i ge s la tate a d
2-colloids (albumin or commercially available products).
Most importantly, the oxygen-carrying capacity of crystalloids and colloids is zero.
If blood is being lost, the ideal replacement fluid is blood, although crystalloid
therapy may be required while awaiting blood products. Hypotonic solutions (e.g.
dextrose) are poor volume expanders and should not be used in the
treatment of shock unless the deficit is free water loss (e.g. diabetes insipidus) or
patients are sodium overloaded (e.g. cirrhosis).
Dynamic fluid response
The shock status can be determined dynamically by the cardiovascular response
to the rapid administration of a fluid bolus. In total, 250
–500 ml of fluid is rapidly
given (over 5
–10 min) and the cardiovascular responses in terms of heart rate,
blood pressure and central venous pressure (CVP) are observed. Patients can
e di ided i to espo de s , t a sie t espo de s a d nonresponders .
Responders show an improvement in their cardiovascular status, which is
sustained. These patients are not actively losing fluid but require filling to a
normal volume status.
Transient responders show an improvement but then revert to their previous
state over the next 10
–20 min. These patients either have moderate on-going
fluid losses (either overt hemorrhage or further fluid shifts reducing
intravascular volume).
Non-responders are severely volume depleted and are likely to have major on-
going loss of intravascular volume, usually through persistent uncontrolled
hemorrhage.
Vasopressor and inotropic support
Vasopressor or inotropic therapy is not indicated as first-line therapy in
hypovolaemia. As discussed above, administration of these agents in the absence
of an adequate preload rapidly leads to decreased coronary perfusion and
depletion of myocardial oxygen reserves.
Vasopressor agents (phenylephrine, noradrenaline) are indicated in distributive
shock states (sepsis, neurogenic shock), in which there is peripheral vasodilatation
and a low systemic vascular resistance, leading to hypotension despite a high
cardiac output. When the vasodilatation is resistant to catecholamines (e.g.
absolute or relative steroid deficiency), vasopressin may be used as an alternative
vasopressor. In cardiogenic shock or when myocardial depression complicates a
shock state (e.g. severe septic shock with low cardiac output), inotropic therapy
may be required to increase cardiac output and, therefore, oxygen delivery. The
inodilator dobutamine is the agent of choice.
Monitoring for patients in shock
Minimum
■ Electrocardiogram
■ Pulse oximetry
■ Blood pressure
■ Urine output
Additional modalities
■ Central venous pressure
■ Invasive blood pressure
■ Cardiac output
■ Base deficit and serum lactate
Cardiovascular
As minimum, cardiovascular monitoring should include:
• Continuous ECG
• Oxygen saturation.
• Pulse waveform
• Non invasive blood pressure.
Patient whose stats of shock is not rapidly corrected with small amounts of fluid
should have:
• CVP monitoring
• Continuous blood pressure monitoring through arterial line.
Central venous pressure
CVP measurement should be assessed dynamically as the response to fluid
challenge. A fluid bolus (250
– 500 ml) is infused rapidly over 5 – 10 min. the
normal CVP response is raise of 2-3 cm H2O, which gradually drift back to the
original level over 10
– 20 minute. Patients with no changes in their CVP are empty
and require further fluid resuscitation. Patient with large, sustain rise in CVP have
high preload and element of cardiac insufficiency or volume overload.
Cardiac output
Cardiac output monitoring allow an assessment of not only the cardiac output
but also the systemic vascular resistance. Invasive cardiac monitoring using
pulmonary cardiac catheter is become less frequent as new non invasive
monitoring techniques such as Doppler ultrasound, pulse waveform analysis and
indicator dilution method provide similar information without many f the
drawbacks of more invasive technique.
Measurement of cardiac output, systemic vascular resistance and preload can
help to distinguish the type of shock that are present ( hypovolemic, distributive,
cardiogenic ) specially when they coexist.
The information provided guides fluid and vasopressor therapy by providing
real
–time monitoring of the cardiovascular response.
measurement of cardiac output is desirable in patient who do not respond as
expected to first-line therapy or who have evidence of cardiogenic shock or
myocardial dysfunction.
early consideration should be given to instituting cardiac output monitoring in
patients who requires vasopressor or intropic support.
Systemic and organ perfusion
Monitoring of organ perfusion should guide the management of shock. The
best measures of organ perfusion and the best monitor of the adequancy of sock
therapy remain the urine output.
The level of consciousness is important marker of cerebral perfusion, but brain
perfusion remained until the very late stages of shock.
The only clinical indicator of perfusion of the gastrointestinal tract and
muscular bed are the global measurement of lactic acidosis (lactic and base deficit)
and the mixed venous oxygen saturation.
Base deficit and lactate
The degree of lactic acidosis, as measured by serum lactate level and/or base
deficit, is a sensitive tool for both the diagnosis of shock and monitoring to
response to therapy. These parameters are measured from arterial blood gas
analysis. The base deficit and/or lactate should be measured routinely in these
patients until they have returned to normal levels.
Mixed Venous oxygen saturation
Normal mixed venous oxygen saturation levels are 50
– 70 %. Level below 50 %
indicate inadequate oxygen delivery and increased oxygen extraction by the cells.
This consistent with hypovolemic or cardiogenic shock.
high mixed venous blood saturation levels (
< 70 %) are seen in sepsis and
some other forms of distributive shock. Levels lower than this indicate that the
patients is not only in septic shock but also in hypovolemic or cardiogenic shock.
Endpoint of resuscitation
It is much easier to know when to start resuscitation than when to
stop. Traditionally, patients have been resuscitated until they have a
normal pulse, blood pressure and urine output. However; these
parameters are monitoring organ systems whose blood flow is preserved
until the late stages of shock. Therefore, a patient may be resuscitated to
restore central perfusion to the brain, lungs and kidneys yet the gut and
the muscle bed continue to be underperfused. Thus activation of the
inflammatory and coagulation may be on going and, when these organs
are finally perfused, it may lead to reperfusion injury and ultimately
multiple organ failure.
this state of normal vital signs and continued underperfusion is termed
occult hypotension (OH). With current monitoring techniques it is
manifested only by persistent lactic acidosis and low mixed venous oxygen
saturation level. The duration that the patient spend in this hypoperfused
state has a dramatic effect on outcome. Patient with OH for more than 12
hours have a two to three times higher mortality rate than that of patient
with limited duration of shock.
Resuscitation algorithms directed at correcting global perfusion end points
(base deficit, lactate, mixed venous saturation) rather than traditional endpoints
have been shown to improves morbidity and mortality in high risk surgical
patients. Whoever, it is clear that despite aggressive regimens, patients cannot be
resuscitated to normal parameters within 12 hour by fluid resusetation alone.