shock

Dr. Ali J. Al-Shammari

University of Al-Qadissiyah
College of medicine
Is a systemic state of low tissue perfusion which is inadequate for normal
cellular respiration
• Pathophysiology : -
• 1- 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 lactic acid. When enough tissue
is under-perfused, the accumulation of lactic acid in the blood
produces a systemic metabolic acidosis. As glucose within cells is
exhausted, anaerobic respiration ceases and there is failure of
sodium/potassium pumps in the cell membrane and intracellular
organelles. Intracellular lysosomes release autodigestive enzymes
and cell lysis ensues. Intracellular contents, including potassium
are released into the blood stream.
Pathophysiology :-
• 2- Microvascular :-
• As tissue ischemia progresses, changes result in activation of the
immune and coagulation systems in which activate complement
and neutrophils, 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, exacerbating
cellular hypoxia.
PATHOPHYSIOLOGY :-
• 3- Systemic :-
• a- 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 ).
• b-Respiratory
• The metabolic acidosis and increased sympathetic response result in an
increased respiratory rate
• to increase the excretion of carbon dioxide (and so produce a compensatory
respiratory alkalosis.
• c- 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.
PATHOPHYSIOLOGY :-
• 3- Systemic :-
• d- 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 resorption of water in the
renal collecting system. Cortisol is also released from the adrenal cortex
contributing to the sodium and water resorption and sensitizing the cells to
catecholamines.
Classification of shock : -
• 1- Hypovolaemic shock :
• due to a reduced circulating volume , is probably the most common form of
shock. Hypovolaemia may be due to
• a- haemorrhagic : bleeding from vessels .
• b-non-haemorrhagic causes : include poor fluid intake (dehydration), excessive
fluid loss due to vomiting, diarrhoea, urinary loss (eg. diabetes), evaporation, or
‘third-spacing’ where
• fluid is lost into the gastrointestinal tract and interstitial spaces, as for example
in bowel obstruction or pancreatitis.
Classification of 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
• - cardiomyopathy.
• - Sepsis
• - drug abuse
• Evidence of venous hypertension with pulmonary or systemic oedema may
coexist with the classical signs of shock.
Classification of shock : -
• 3- Obstructive shock
• In obstructive shock there is a reduction in preload due
to mechanical obstruction of cardiac filling. Common
causes of obstructive shock include
•- cardiac tamponade
•- tension pneumothorax
•- massive pulmonary embolus or air embolus. an air
embolism (50 ml of air), obstructing more than 50% of
pulmonary vasculature leads to severe shock and sudden
death.
• 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.
Classification of shock : -
• 4- Endocrine shock
• may present as a combination of hypovolaemic, cardiogenic or
distributive shock. Causes of endocrine shock include
•- hyperthyroidism may cause a high-output cardiac failure.
•- Hypothyroidism causes a shock state similar to that of
neurogenic shock due to disordered vascular and cardiac
responsiveness to circulating catecholamines. Cardiac output falls
due to low inotropy and bradycardia. There may also be an
associated cardiomyopathy.
• - Adrenal insufficiency leads to shock due to hypovolaemia and
a poor response to circulating and exogenous catecholamines.
Adrenal insufficiency may be due to pre-existing Addison’s disease
or be a relative insufficiency due to a pathological disease state,
such as systemic sepsis.
Classification of shock : -
• 5- Distributive shock
• Distributive shock describes the pattern of cardiovascular
responses characterizing a variety of conditions, including ( septic
shock, anaphylaxis and neurogenic shock ). 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
•- in spinal cord injury(neurogenic shock ) there is failure of
sympathetic outflow and inadequate vascular tone.
•- in sepsis ( septic shock ) . 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 utilization of oxygen.
CLINICAL FEATURES OF SHOCK :-
• - In early stage—tachycardia, sweating,
cold periphery, hypotension, restlessness,
air hunger, tachypnoea, oliguria, collapsed
veins.
• - In late stage—cyanosis, anuria, jaundice,
drowsiness.
Severity (degrees ) of shock :-
• 1- Compensated shock : with restlessness, mild tachycardia, normal blood
pressure, urine output, normal respiration and mild lactic acidosis.
• 2- Mild shock : with mild lactic acidosis, tachycardia, tachypnea and
anxiousness.
• 3- Moderate shock: with significant lactic acidosis, decreased urine, tachycardia,
tachypnoea, drowsiness, and mild hypotension.
• 4- Severe shock : with severe lactic acidosis, anuria, tachypnea with gasping,
severe tachycardia,
• profound hypotension and unconsciousness.
INVESTIGATIONS IN SHOCK :-
• a- Essential investigation :
• 1- Regular monitoring of BP, pulse rate, Respiratory rate , ECG
,Measurement of urine output , pulse oximetry.
• b- Additive investigation :
• 2- CVP line (Central venous pressure).
• 3- PCWP (Pulmonary capillary wedge pressure).
• 4- Pus, urine, blood culture in case of septic shock.
• 5- U/S, CT, X-ray depending on location of pathology or septic
focus.
• 6- Arterial PO2 and PCO2 analysis.
• 7- Electrolyte estimation.
• 8- Blood CBC, pH assessment, Serum lactate estimation is an
important prognostic indicator .
TREATMENT OF SHOCK :-
• 1- Treat the cause, e.g. arrest haemorrhage, drain pus.
• 2- Fluid replacement: Plasma, normal saline, Ringer’s lactate, plasma expander
(haemaccel) (maximum1 litre can be given in 24 hours). Initially crystalloids
then colloids are given. Blood transfusion is done whenever required(e.g. Hb <
9 , ongoing bleeding ) . Hypotonic solutions like dextrose are poor volume
expanders and so should not be used in shock.
• 3- Inotropic agents: Dopamine, dobutamine, adrenaline infusions mainly in
distributive shock like septic shock or in cardiogenic shock .
• 4- Correction of electrolyte and acid-base balance.
• 5- Steroid is often life-saving. 500-1000 mg of hydrocortisone can be given. It
improves the perfusion, reduces the capillary leakage and systemic
inflammatory effects.
• 6- Antibiotics in patients with sepsis .
• 7- Catheterisation to measure urine output (30-50 ml/hour or > 0.5 ml/kg/hour
should be maintained).
TREATMENT OF SHOCK :-
• 8- Improve oxygenation by nasal oxygen to or ventilator support with intensive
care unit monitoring has to be done.
• 9- Control pain-using morphine or paracetol or ketamine .
• 10- Haemodialysis may be necessary when sever renal impairment .
• 11- Stress ulcer protection by Injection ranitidine IV or omeprazole IV .
• 12- Activated C protein even though costly is beneficial as it prevents the
release and action of inflammatory response.
• 13- MAST (military anti-shock trouser): Provides circumferential external
pressure of 40 mmHg. It is wrapped around lower limbs and abdomen, and
inflated with required pressure. It redistributes the existing blood and fluid
towards centre. It should be deflated carefully and gradually.
• 14- Control of blood sugar in diabetic patients.
Septic shock :
• Definition :
• as a type of shock due to dys-regulated host response to infection.
• Causative agents :-
• may be due to gram-positive organisms, gram-negative organisms,
fungi, viruses or protozoal origin, or mixed .
• Endotoxic shock:-
• Is gram-negative septicaemia /gram-negative septic shock which
occurs due to gram-negative bacterial infections, commonly seen in
strangulated intestines, peritonitis, gastrointestinal fistulas, biliary
and urinary infections, pancreatitis, major surgical wounds, diabetic
wounds and crush injuries.
Pathophysiology of septic shock:
• Toxins/endotoxins from organisms like E. Coli, Klebsiella,
Pseudomonas, and Proteus Inflammation, Chemotaxis of cells,
cellular activation of macrophages, neutrophils, monocytes
Release of cytokines, free radicals endothelial injury, altered
coagulation cascade—SIRS , toxin induced release of isoform of
nitric oxide synthetase from the vessel wall which causes sustained
prolonged release of high levels of nitric oxide peripheral
vasodilatation causing sever hypotension at early state a
reversible hyperdynamic warm stage of septic shock with fever,
tachycardia, tachypnea which respond to vasopressors , but if
delayed Severe circulatory failure with MODS (failure of lungs,
kidneys, liver, heart) with DIC Hypodynamic, irreversible cold
stage of septic shock .
Stages of septic shock :
• a. Hyperdynamic (warm) shock:
• This stage is reversible stage. Patient is still having inflammatory
response and so presents with fever, tachycardia, and tachypnoea.
Pyrogenic responseis still intact. Patient should be treated properly
at this stage. thus main lines of treatment should implied in this
stage.
• b. Hypodynamic hypovolaemic septic shock (cold septic shock):
• Here pyrogenic response is lost. Patient is in decompensated shock.
It is an irreversible stage along with MODS (Multi-organ dysfunction
syndrome) with anuria, respiratory failure (cyanosis), jaundice (liver
failure), cardiac depression, pulmonary oedema, hypoxia,
drowsiness, eventually coma and death occurs (Irreversible stage).
Treatment of septic shock :
1. Correction of fluid and electrolyte by crystalloids, blood
transfusion.
2. Appropriate antibiotics—third generation cephalosporins/
aminoglycosidesm / imipenims
3. Treat the cause or focus—drainage of an abscess; laparotomy for
peritonitis; resection of gangrenous bowel; wound excision.
4. Pus/urine/discharge/bile/blood culture and sensitivity for
antibiotics.
5. Critical care, oxygen, ventilator support, dobutamine/
dopamine/noradrenaline to maintain blood pressure and urine
output.
6. Activated C protein prevents the release of inflammatory
mediators and blocks the effects of these mediators on cells.
 Treatment of septic shock :
7. Monitoring the patient by pulse oximetry, cardiac status, urine
output, arterial blood gas analysis.
8. Short-term (one or two doses) high dose steroid therapy to
control and protect cells from effects of endotoxaemia. It
improves cardiac, renal and lung functions.
9. Single dose of methylprednisolone or dexamethasone which often
Pitfalls ormay
absence of classic again
be repeated signs inafter
shock4:-hours is said to be effective in
• 1- Capillary re lling shock.
endotoxic :-
• Most patients in hypovolaemic shock will have cool,
warm and capillary re ll will be brisk, despite profound shock.
pale peripheries, with prolonged capillary re ll times. However, the actual capillary re ll time
varies so much in adults that it is not a speci c marker of whether a patient is shocked, and
patients with short capillary re ll times may be in the early stages of shock.
• In distributive (septic) shock, the peripheries will be
Pitfalls or absence of classic signs in shock :-
• 2- Tachycardia :-

Complication of poor shock management : -

• Tachycardia may not always accompany shock.
Patients who are on beta-blockers or who have implanted pacemakers are
• 1-to
• unable Unresuscitatable
mount a tachycardia.shock :- rate of 80 in
A pulse
a t young adult who
• Patients whonormally has a pulse shock
are in profound rate of for
50 is
a very abnormal.
prolonged Furthermore,
period of timein some
young patients with penetrating trauma, where there is haemorrhage but little tissue
become ‘unresuscitatable’. Cell death follows from cellular
damage, there may be a paradoxical bradycardia rather than tachycardia accompanying the
ischaemia and the ability of the body to compensate is lost.
shocked state.
• Centrally
Pitfalls or absencethere is myocardial
of classic depression
signs in shock :- and loss of responsiveness
• 3- Blood pressure
to fluid or inotropic therapy. Peripherally there is loss of the ability
• It is important
to maintainto recognise
systemic that hypotension
vascular is one ofand
resistance the further hypotension
last signs of shock.
ensues. TheChildren and t young
peripheries adultsrespond
no longer are able to maintain bloodto
appropriately pressure until the
nal stages of shock by
vasopressor. dramatic
Death increases
is the in stroke
inevitable volume
result. andstage
This peripheral vasoconstriction.
of shock is the
These patients can be in profound shock with a normal blood pressure. Elderly patients who
combined result of the severity of the insult and delayed,
are normally hypertensive may present with a ‘normal’ blood pressure for the general
inadequate or inappropriate resuscitation
population but be hypovolaemic and hypotensive relative to their usual blood pressure. Beta-
blockers or other medications may prevent a tachycardic response.
Complication of poor shock management : -
• 2- Ischaemia–reperfusion syndrome
• During the period of systemic hypoperfusion, cellular and organ
damage progresses due to 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
the 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.
Complication of poor shock management : -
• 3- Multiple organ failure :
• Go to surgical infection lecture as discussed there .
Pitfalls or absence of classic signs in shock :-
• 1- Capillary re lling :-
• Most patients in hypovolaemic shock will have cool,
warm and capillary re ll will be brisk, despite profound shock.
pale peripheries, with prolonged capillary re ll times. However, the actual
capillary re ll time varies so much in adults that it is not a speci c marker
of whether a patient is shocked, and patients with short capillary re ll
times may be in the early stages of shock.
• In distributive (septic) shock, the peripheries will be
Pitfalls or absence of classic signs in shock :-
• 2- Tachycardia :-
• Tachycardia may not always accompany shock.
Patients who are on beta-blockers or who have implanted pacemakers are
• unable to mount a tachycardia. A pulse rate of 80 in
a t young adult who normally has a pulse rate of 50 is very abnormal.
Furthermore, in some young patients with penetrating trauma, where there
is haemorrhage but little tissue damage, there may be a paradoxical
bradycardia rather than tachycardia accompanying the shocked state.
Pitfalls or absence of classic signs in shock :-
• 3- Blood pressure
• It is important to recognise that hypotension is one of the
last signs of shock. Children and t young adults are able to maintain blood
pressure until the nal stages of shock by dramatic increases in stroke
volume and peripheral vasoconstriction. These patients can be in profound
shock with a normal blood pressure. Elderly patients who are normally
hypertensive may present with a ‘normal’ blood pressure for the general
population but be hypovolaemic and hypotensive relative to their usual
blood pressure. Beta-blockers or other medications may prevent a
tachycardic response.
Dynamic assessment of shock : -
• 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 minutes) and the cardiovascular responses in terms of heart
rate, blood pressure and central venous pressure are observed.
• Patients can be divided into ‘responders’, ‘transient responders’ and
‘nonresponders.
• Responders have 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 have an improvement which then reverts to the previous
state over the next 10–20 minutes. These patients have moderate ongoing fluid
losses (either overt haemorrhage or further fluid shifts reducing intravascular
volume).
• Non-responders are severely volume depleted and are likely to have major
ongoing loss of intravascular volume, usually through persistent uncontrolled
haemorrhage.
Pitfalls or absence of classic signs in shock :-
•The classic cardiovascular responses
described are not seen in every patient. It
is important to recognise the limitations of
the clinical examination and to recognise
patients who are in shock despite the
absence of classic signs.
Pitfalls or absence of classic signs in shock :-
• 1- Capillary refilling :-
• 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.
Pitfalls or absence of classic signs in shock :-
• 2- Tachycardia :-
• Tachycardia may not always accompany shock.
Patients who are on beta-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, where there is
haemorrhage but little tissue damage, there may be
a paradoxical bradycardia rather than tachycardia
accompanying the shocked state.
Pitfalls or absence of classic signs in shock :-
• 3- Blood pressure
• It is important to recognise 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. Elderly patients who are
normally hypertensive may present with a ‘normal’ blood
pressure for the general population but be hypovolaemic
and hypotensive relative to their usual blood pressure.
Beta-blockers or other medications may prevent a
tachycardic response.