SHOCK

AARUSHI BISHT
ROLL NO. 01
BATCH 2019
 SHOCK is a systemic state of
low tissue perfusion that is
inade­quate for normal cellular
DEFINITION respiration.

If perfusion is not restored in a

timely fashion, cell death
ensues.
PATHOPHYSIOLOGY
A.) CELLULAR
Perfusion to the tissues is reduced

Cells are deprived of oxygen (Hypoxia)

Cells switch from aerobic to anaerobic metabolism

The product of anaerobic respiration is lactic acid

Accumulation of lactic acid in the blood produces a systemic metabolic

acidosis.
 A.) CELLULAR
Glucose within cells is exhausted

anaerobic respiration ceases

failure of sodium/potassium pumps in the cell membrane and intracellular organelles

Sodium and calcium enter the cell Intracellular lysosomes release autodigestive
enzymes

Potassium leaks out of the cell

Cell lysis ensues

Causes hyperkalaemia, hyponatraemia and

B.) MICROVASCULAR
As tissue ischaemia progresses

Activation of the immune and coagulation systems

Hypoxia and acidosis activates complement and primes leukocytes

Generation of oxygen free radicals and cytokine release

Injury of the capillary endothelial cells

B.) MICROVASCULAR
Activates the immune and coagulation systems

Damaged endothelium loses its integrity and becomes ‘leaky’

Spaces between endothelial cells allow fluids to leak out

Tissue oedema ensues, exacer­bating cellular hypoxia.

Ischaemic cell death releases potassium into the circulation

Systemic hyperkalaemia and acidosis,

 Preload and afterload decrease

Compensatory baroreceptor response

C.)
SYSTEMIC Increased sympathetic activity

1. CARDIOVASCULAR Catecholamines released into the

circulation

Tachycardia and systemic

vasoconstriction (except in sepsis)
 Due to metabolic acidosis and
increased sympathetic response

C.) Increased respiratory rate and

minute ventilation
SYSTEMIC
2. RESPIRATORY Increases the excretion of carbon
dioxide and oxygen saturation

Produce a compensatory
respiratory alkalosis
 Decreased perfusion pressure in the
kidney

Reduced glomerular fltration rate

C.)
SYSTEMIC Decreased urine output

3. RENAL Stimulation of renin–angiotensin–

aldosterone axis

Vasoconstriction and increased sodium

and water reabsorption by the kidney.
 Due to decreased preload

Vasopressin (antidiuretic hormone) is

released
C.)
SYSTEMIC Vasoconstriction and resorption of
water in the renal collecting system

4. ENDOCRINE
Cortisol is also released from the
adrenal cortex

Sodium and water resorption and

sensitising cells to catechol­amines.
 Platelets are activated forming
small clots in many places
C.)
SYSTEMIC Disseminated intravascular
coagulation (DIC)
(Consumption coagulopathy)
4. BLOOD

Further bleeding.
 Noradrenaline, renin-

STAGES OF angiotensin and antidiuretic

hormone (ADH) gets activated

SHOCK causing vasoconstriction to

divert the blood to heart, lungs
and brain.
1. Stage of compensatory
Apart from a tachycardia and
shock
cool peripheries, there may be
no other clinical signs of
hypovolaemia.
2. Stage of decompensatory 3. Stage of irreversible (refractory) shock:
(progressive) shock:

● Further loss of circulating volume ● Here cellular ATP metabolism is lost

overloads the body’s compensatory completely, leading into MODS
mechanisms and there is progressive (Multiorgan dysfunction syndrome)
renal, respiratory and cardiovascular and MOF (multiorgan failure).
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 circulating volume has been
lost.
CLASSIFICATION OF SHOCK
Based on the initiating mechanism:
 Haemorrhagic cause:
● Loss of blood.

I.) Non­haemorrhagic causes:

HYPOVOLAEMIC ● Poor fuid intake (dehydration)

● Excessive fuid loss due to
SHOCK vomiting, diarrhoea, urinary
loss (e.g. diabetes)
is due to a reduced ● Loss of plasma (burns)
circulating volume. ● ‘third­spacing’ i.e. fluid is lost
into the gastrointestinal tract
and interstitial spaces, as for
example in bowel obstruction
or pancreatitis.
PATHOPHYSIOLOGY OF HAEMORRHAGIC SHOCK: 4 Stages

Class I:

When blood loss is less than 750 ml (< 15% of blood volume), it can be called mild
haemorrhage.

To compensate for the loss of blood volume

Peripheral venoconstriction takes place

Some blood shifts into the central circulation

 Apart from a mild
Withdrawal of fluid from the interstitial tachycardia and thirst, there
spaces.
may be no other symptom or
sign suggesting hypovolaemia.
Correction of blood volume The blood pressure, urine
output and mentation are all
normal in Class I shock.
PATHOPHYSIOLOGY OF HAEMORRHAGIC SHOCK:
Class II:
Loss of 800-1500 ml (15-30% of blood volume) results in moderate (Class II) shock.

Peripheral venoconstriction may not be sufficient to main­tain the circulation.

Sympathoadrenal system

Adrenaline and noradrenaline (catecholamines) released

Powerful vasoconstriction of both arteries and veins.

Increased secretion of ADH

Retention of water and salt.

● Clinically, the patient shows a heart ● Thirst increases.
rate of 100-120 beats/ minute and an
elevated diastolic pressure.
● Extremities may look pale and
● Urine output is reduced to about 0.5 the patient is confused and
ml/kg/h and the capillary refill is more thirsty.
than the normal 2 seconds.
PATHOPHYSIOLOGY OF HAEMORRHAGIC SHOCK:

Class III:
● Loss of 1500-2000 ml(30-40% of blood volume).
● The patient's systolic and diastolic blood pressures fall.
● Heart rate increases to around 120 beats/minute.
● The pulse is thready.
● The respiratory rate increases > 20/minute.
● Urine output drops to 10 to 20 ml/hour.
● The patient appears pale and is aggressive, drowsy or confused.
PATHOPHYSIOLOGY OF HAEMORRHAGIC SHOCK:

Class IV:
● Blood loss of more than 2000 ml (> 40% of blood volume).
● The peripheries are cold and ashen.
● The pulse is thready and more than 120/minute.
● The blood pressures are very low or unrecordable.
 II.) Causes of cardiogenic

CARDIOGENIC shock: Myocardial

infarction
SHOCK ● Cardiac dysrhythmias
● Valvular heart disease
Cardiogenic shock is due to ● Blunt myocardial injury and
primary failure of the heart to ● cardiomyopathy.
pump blood to the tissues.
PATHOPHYSIOLOGY:
Acute cardiac injury

Decreased coronary
Decrease in contractility of the heart
perfusion.
Vasoconstric
fluid retentio
Decrease in stroke volume
Ischemia

Cardiac output reduces

Hypotension Decreased peripheral

perfusion
● Systemic inflammation triggered by acute cardiac injury induces
pathologic vasodilatation.
● Inflammatory cytokines and endothelial and inducible nitric oxide (NO)
synthase may augment production of NO and its by-product, peroxynitrite,
which has a negative inotropic effect and is cardiotoxic.
● Lactic acidosis and hypoxemia reduce the efficacy of catecholamines.
Clinical Presentation:
● Systolic blood pressure <90 mmHg.
● Cardiac index <2.2 L/minute/sq metre.
● Raised PCWP (pulmonary capillary wedge pressure) >15mmHg.
● It is commonly seen in acute Ml with a mortality >50%.

Diagnosis:
● ECG
● Echocardiography
● Arterial blood gas analysis
● Cardiac enzymes
● PCWP
● Electrolyte estimation (hypokalaemia and hypomagnesaemia are common)
 Common causes of

III.) obstructive shock include:

● Cardiac tamponade
OBSTRUCTIVE ● Tension pneumothorax

SHOCK ● Massive pulmonary

embolus or air embolus.
There is a reduction in preload In each case, there is reduced
owing to mechanical obstruction flling of the left and/or right
of cardiac flling. sides of the heart, leading to
low cardiac output.
 IV.) Distributive shock can occur in
DISTRIBUTIVE the following situations:

SHOCK • Septic shock

• Anaphylactic shock
Here, the afterload is excessively
reduced affecting circulation. • Neurogenic shock
A.) SEPTIC SHOCK
● Septic shock is typically a I) Gram-positive septic shock
vasodilatory shock wherein there is ● Due to exotoxin by gram +ve bacteraemia
peripheral vasodilatation causing like Clostridium tetani/welchii,
hypotension which is resistant to staphylococci, streptococci, pneumococci.
vasopressors. ● Fluid loss, hypotension is common; with
● This is due to toxin-induced release normal cardiac output.
of isoform of nitric oxide synthetase
from the vessel wall which causes
sustained prolonged release of high II) Gram-negative septic shock
levels of nitric oxide. ● Gram-negative bacteria cause
endotoxaemia and its effects.
● Urinary/gastrointestinal/ biliary and
respiratory foci are common.
A.) SEPTIC SHOCK
PATHOPHYSIOLOGY:

Toxins/endotoxins from organisms like E.

coli, Klebsiella, Pseudomonas, and Proteus
Reversible hyperdynamic warm stage of
septic shock with fever, tachycardia,
tachypnoea
Inflammation, cellular activation of
macrophages, neutrophils, monocytes
Severe circulatory failure with MODS
(failure of lungs, kidneys, liver, heart) with
Release of cytokines, free radicals DIC

Chemotaxis of cells, endothelial injury, Hypodynamic, irreversible cold stage of

altered coagulation cascade-SIRS septic shock.
Stages of septic shock
I) Hyperdynamic (warm) shock:
II) Hypodynamic hypovolaemic
● This stage is reversible stage. septic shock (cold septic shock):
● Patient is still having ● Here pyrogenic response is lost.
inflammatory response and so ● Patient is in decompensated
presents with fever, shock.
tachycardia, and tachypnoea. ● It is an irreversible stage along
● Pyrogenic response is still with MODS (multiorgan dysfunction
intact. syndrome) with anuria, respiratory
failure (cyanosis), jaundice (liver
● Patient should be treated
failure), cardiac depression,
properly at this stage.
pulmonary oedema, hypoxia,
● The underlying cause is drowsiness, eventually coma and
treated. death occurs (Irreversible stage).
B.) ANAPHYLACTIC SHOCK:
● Occurs on exposure to an allergen the patient is sensitive to.
● It may be pollen, foodstuffs, preservatives in the food or a medication.
● The anaphylactic shock that occurs in the hospital is usually due to some drug, e.g. the
patient is allergic to penicillin.
● They combine with lgE of mast cells and basophils, releasing histamine and large
amount of SRS-A (Slow releasing substance of anaphylaxis).
● The reaction may be in the form of mild rashes with or without bronchospasm or it may
be a full blown anaphylactic shock wherein the patient presents with rashes,
generalised oedema including laryngeal oedema, bronchospasm and hypotension and
if not treated in time, cardiac arrest.
C.) NEUROGENIC SHOCK

● It is usually due to spinal cord injury, which causes dilatation of splanchnic

vessels.
● This type can safely be treated with vasoconstrictor drugs to bring up
theblood pressure.
● There will be bradycardia, hypotension, arrhythmias, and decreased cardiac
output.
● Blood pressure control, oxygen delivery, maintenance of haemodynamics,
airway, fluid therapy, intravenous methylprednisolone therapy should be
done.
● Dopamine and or phenylephrine (alpha agonist) can be used.
V.) ENDOCRINE Causes:

SHOCK ● Hypo­thyroidism
● Hyperthyroidism
● Adrenal insuf­fciency.
May present as a combination
of hypovolae­mic, cardiogenic
or distributive shock.
Adrenal Insufficiency:

Causes Features

Adrenal crisis occurs if the adrenal gland • Headache, profound weakness, fatigue,
is deteriorating as in: slow and lethargic movement, joint pain.

● Primary adrenal insufficiency Nausea, vomiting, abdominal pain, high

(Addison's disease) fever and chills.
● Secondary adrenal insufficiency
• Low blood pressure, dehydration, rapid
(pituitary gland injury)
heart rate and respiratory rate, confusion
or coma.
 In early stage-tachycardia, sweating,
cold periphery, hypotension,
restlessness, air hunger, tachypnoea,

CLINICAL oliguria, collapsed veins.

In late stage-cyanosis, anuria,

FEATURES jaundice, drowsiness.

Clinically shock may be:

1.)Compensated with mild

tachycardia, normal blood pressure,
urine output, normal respiration and
mild lactic acidosis.
 2.) Mild shock with mild lactic
acidosis, tachycardia, tachypnoea and
anxiousness.

CLINICAL 3.) Moderate shock with significant

lactic acidosis,decreased urine (below

FEATURES 0.5 mL/kg/hour), tachycardia,

tachypnoea, drowsiness, and mild
hypotension.

4.) Severe shock with severe lactic

acidosis, anuria, tachypnoea with
gasping, severe tachycardia, profound
hypotension and unconsciousness.
 Most patients in hypovolaemic
CLINICAL shock will have cool, pale
peripheries, with prolonged
FEATURES capillary refill time.

In distributive (septic) shock,

Capillary refill
the peripheries will be warm
and capillary refill will be brisk,
despite profound shock.
Clinical consequences
of shock
 ● The acid and potassium load that has
built up can lead to direct myocardial
depression, vascular dilatation and
further hypotension.
Systemic ● Intracellular molecules are released
into the circulation which activate
Infammatory leukocytes.
Response Syndrome ● Together, they overwhelm the local
antid-infammatory response and are
(SIRS) fushed back into the systemic
● Cellular and organ damage circulation, where they cause injury to
progresses due to the direct distant organs such as the lungs and
efects of tissue hypoxia the kidneys.
● This leads to acute lung injury, acute
and local activation of
renal injury, cerebral oedema,
infammation.
multiple organ failure and death.
 ● There is no specifc treatment
for multiple organ fail­ure.
● Management is support of
Multiple organ systems, with ventilation,
cardiovascular support and
Organ Failure haemofltration/dialysis until
there is recovery of organ
Defined as two or more failed function.
organ systems. ● Prevention is by early
aggressive identifcation and
reversal of shock.
THANK YOU !