SHOCK
-Dr.santhosh kumar.M
Shock
● Shock is a systemic state of low tissue perfusion that is inadequate for normal
cellular respiration. With insufficient delivery of oxygen and glucose, cells switch
from aerobic to anaerobic metabolism.
Stages of shock
Deterioration of circulation in shock is a progressive & continuous phenomenon &
compensatory mechanisms becomes progressively less effective.
1. NON-PROGRESSIVE (INITIAL, COMPENSATED REVERSIBLE) SHOCK
2. PROGRESSIVE DECOMPENSATED SHOCK
3. DECOMPENSATED(IRREVERSIBLE)SHOCK
Non progressive shock
In early stage an attempt is made to maintain adequate cerebral and coronary blood
supply by redistribution of blood so that vital organs are adequately perfused and
oxygenated
This is achieved by various neurohormonal mechanism causing
1) Widespread Vasoconstriction
2) By fluid conservation by kidney
• So if the condition that causes shock is adequately treated, compensatory mechanism
may bring about recovery to normal condition. This is called compensated or reversible
shock.
WIDESPREAD FLUID
VASOCONSTRICTION CONSERVATION BY
In response to reduced blood flow and KIDNEY
• Release of ALDOSTERONE from hypoxic
tissue anoxia, the neural and hormonal kidney and ADH due to decreased effective
factors (like baroreceptors, circulating blood volume
chemoreceptors, catecholamines, renins)
are activated • Reduce GFR due to arteriolar constriction
• Shifting of tissue fluid into plasma due to
hypotension
PROGRESSIVE DECOMPENSATED SHOCK
This is a stage when the patient suffer from other stress or risk factor (ex: pre existing
cardiac or lung disease)
• The effect of tissue hypoperfusion leads to:
1) Pulmonary hypoperfusion leading to ARDS & Tachypnoea.
2) Tissue anoxia leading to vasodilation.
Clinically this stage the patient develops confusion and worsening of renal function.
DECOMPENSATED (IRREVERSIBLE ) SHOCK
When the shock is so severe that in spite of compensatory mechanism and therapy and
control of etiologic agent which causes the shock no recovery take place it is called
DECOMPENSATED SHOCK.
Clinically the patient at this stage has features of coma, worsened heart function, and
progressive renal failure due to acute tubular necrosis.
Pathophysiology
Cellular
As perfusion to the tissues is reduced, cells are deprived of oxygen and must switch from
aerobic to anaerobic metabolism. The product of anaerobic respiration is not carbon
dioxide but lactic acid. When enough tissue is underperfused the accumulation of lactic
acid in the blood produces a systemic metabolic acidosis.
Microvascular
As tissue ischaemia progresses, changes in the local milieu result in activation of the
immune and coagulation systems. Hypoxia and acidosis activate complement and prime
leukocytes, resulting in the generation of oxygen free radicals and cytokine release.
These mechanisms lead to injury of the capillary endothelial cells. These, in turn, further
activate the immune and coagulation systems. Damaged endothelium loses its integrity
and becomes ‘leaky’. Spaces between endothelial cells allow fluid to leak out and tissue
oedema ensues, increase cellular hypoxia.
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
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 in response to decreased preload and results in
vasoconstriction and resorption of water in the renal collecting system. Cortisol is also
released from the adrenal cortex, contributing to the sodium and water resorption and
sensitising cells to catecholamines.
Classification of shock
● Haemorrhagic/hypovolaemic shock
● Cardiogenic shock
● Obstructive shock
● Distributive shock
Haemorrhagic and hypovolemic shock
● Hypovolemic shock is due to a reduced circulating volume.
● Hypovolaemia may be due to haemorrhagic or nonhaemorrhagic causes
● Non Hemorrhagic causes include poor fluid intake (dehydration), excessive fluid loss
due to vomiting, diarrhoea, urinary loss (e.g. diabetes), evaporation or ‘third
spacing’, where fluid is lost into the gastrointestinal tract and interstitial spaces, as
for example in bowel obstruction or pancreatitis.
● Hypovolaemia is the most common form of shock, and to some degree is a
component of all other forms of shock.
Lethal triad of hypovolemia
Metabolic acidosis
Hypothermia
Coagulopathy
Cardiogenic shock
● Cardiogenic shock is due to primary failure of the heart to pump blood to the tissues.
Causes of cardiogenic shock include myocardial infarction, cardiac dysrhythmias,
valvular heart disease, blunt myocardial injury and cardiomyopathy.
● Cardiac insufficiency may also be due to myocardial depression caused by
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
classical signs of shock.
Obstructive shock
In obstructive shock there is a reduction in preload owing to mechanical obstruction of
cardiac filling . Common causes of obstructive shock include cardiac tamponade, tension
pneumothorax, massive pulmonary embolism or air embolism. In each case, there is
reduced filling of the left and/or right sides of the heart, leading to low 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 due to histamine release,
● while 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
(endotoxin) 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 cellular utilisation of oxygen.
Initial management of shock
Any shock should be assumed to be hypovolaemic until proven otherwise and, similarly,
hypovolaemia should be assumed to be due to haemorrhage until this has been excluded
Immediate resuscitative measures include the assessment of airway and breathing and
control of life threatening issues as necessary. Large Bore intravenous access should be
instituted and blood drawn for crossmatching (see Cross-matching).
Once haemorrhage has been considered, the site of haemorrhage must be rapidly
identified
Damage control resuscitation
Fluid therapy
● In all cases of shock, regardless of classification, hypovolaemia and inadequate
preload must be addressed before other therapy is instituted.
● As a general rule, the ideal replacement fluid is one that approximates the fluid lost by
the underlying cause of shock.
● If blood is being lost, the replacement fluid is whole blood or its equivalent in
components – although crystalloid therapy may be required while awaiting blood
products.
● Other causes of shock will require crystalloid resuscitation with appropriate electrolyte
supplementation.
● In most studies of shock resuscitation there is no overt difference in response or
outcome between crystalloid solutions (normal saline, Hartmann’s solution, Ringer’s
lactate) and colloids (albumin or commercially available 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).
Vasopressor and inotropic support
● Vasopressor or inotrope therapy is not indicated as first line therapy in hypovolaemia
● Administration of these agents in the absence of adequate preload rapidly leads to
decreased coronary perfusion and depletion of myocardial oxygen reserves.
● Vasopressor agents (phenylephrine, noradrenaline [norepinephrine]) are indicated in
distributive shock states (sepsis, neurogenic shock) where there is peripheral
vasodilatation and a low systemic vascular resistance, leading to hypotension
despite a high cardiac output.
● In cardiogenic shock, or where myocardial depression has complicated 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
Central venous pressure
● There is no ‘normal’ CVP for a shocked patient, and reliance cannot be placed on an
individual pressure measurement to assess volume status.
● Some patients may require a CVP of 5 cmH2O, whereas some may require a CVP of
15 cmH2O or higher. Further, ventricular compliance can change from minute to
minute in the shocked state, and CVP is a poor reflection of end diastolic volume
(preload).
● CVP measurements should be assessed dynamically as the response to a fluid
challenge. A fluid bolus (250–500 mL) is infused rapidly over 5–10 minutes.
● The normal CVP response is a rise of 2–5 cmH2O, which gradually drifts back to the
original level over 10–20 minutes.
● Patients with no change in their CVP are empty and require further fluid
resuscitation. Patients with a large, sustained rise in CVP have high preload and an
element of cardiac insufficiency or volume overload.
Systemic and organ perfusion
Base deficit and lactate
● Lactic acid is generated by cells undergoing anaerobic respiration. The degree of
lactic acidosis, as measured by serum lactate level and/or the base deficit, is
sensitive for both diagnosis of shock and monitoring the response to therapy.
● Patients with a base deficit of more than 6 mmol/L have a much higher morbidity and
mortality than those with no metabolic acidosis.
● Furthermore, the length of time in shock with an increased base deficit is important,
even if all other vital signs have returned to normal
Mixed venous oxygen saturation
● The percentage saturation of oxygen returning to the heart from the body is a
measure of the oxygen delivery and extraction by the tissues.
● Accurate measurement is via analysis of blood drawn from a long central line placed
in the right atrium. Estimations can be made from blood drawn from lines in the
superior vena cava, but these values will be slightly higher than those of a mixed
venous sample (as there is relatively more oxygen extraction from the lower half of
the body).
● Normal mixed venous oxygen saturation levels are 50–70%. Levels below 50%
indicate inadequate oxygen delivery and increased oxygen extraction by the cells.
This is consistent with hypovolemic or cardiogenic shock.
● High mixed venous saturations (>70%) are seen in sepsis and some other forms of
distributive shock.
● Patients who are septic should therefore have mixed venous oxygen saturations
above 70%; below this level, they are not only in septic shock but also in
hypovolaemic or cardiogenic shock.
● Hypovolaemia should be corrected with fluid therapy, and low cardiac output due to
myocardial depression or failure should be treated with inotropes (dobutamine) to
achieve a mixed venous saturation greater than 70% (normal for the septic state).
● New methods for monitoring regional tissue perfusion and oxygenation are becoming
available, the most promising of which are muscle tissue oxygen probes, near
infrared spectroscopy and sublingual capnometry.
End of resuscitation
● 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.
● A patient therefore may be resuscitated to restore central perfusion to the brain,
lungs and kidneys and yet continue to underperfused the gut and muscle beds.
● Thus, activation of inflammation and coagulation may be ongoing and lead to
reperfusion injury when these organs are finally perfused, and ultimately multiple
organ failure.
● This state of normal vital signs and continued underperfusion is termed ‘occult
hypoperfusion’
● It is manifested only by a persistent lactic acidosis and low mixed venous oxygen
saturation
● Resuscitation algorithms directed at correcting global perfusion end points (base
deficit, lactate, mixed venous oxygen saturation) rather than traditional end points
have been shown to improve mortality and morbidity in high risk surgical patients.
Thank you
