SHOCK

DEFINATION- Shock is a state of poor tissue perfusion with impared cellular metabolism
leading to serious pathophysiological abnormality. This life threatning situation is called Shock.
Maintainence of proper blood circulation depends on three factors—
A. Cardiac Function.
B. Capacity of Vascular bed
C. Circulating blood Volume
Defect of any of these leads to shock.
There is a generalized misunderstanding that shock means haemorrhage and haemorrhage means
shock. But there are other causes of shock.
TYPE OF SHOCK
1) Hpyovolemic Shock
2) Cardiogenic Shock
3) Anaphylactic Shock
4) Neurogenic Shock – Vasovagal or Psychogenic Shock
5) Septic Shock – Hyper dynamic or Warm Shock
6) Traumatic Shock
7) Burn Shock

Hpyovolemic Shock
It is the most common form of shock seen in clinical practice. It is caused by depletion of
circulation blood volume can be caused by loss of either whole blood or ultra filtered plasma
due to increased vascular permeability as seen in peritonitis and burns.

Pathophysiology of Hypovolemic Shock

Loss of varing amount of blood or any of its constituents result in decreased blood volume,
which in turn leads to decreased venous return to heart. The decreased cardiac filling causes fall
in stroke volume which in turn leads to fall in cardiac output and fall in arterial blood pressure.
The fall in the blood pressure is sensed by the stretch receptors present in the carotids
and the aortic arch which increases Sympatheto- adrenal stimulation. In an effort to rise the
blood pressure. This causes increase in heart rate to restore the cardiac output.
This causes increase sympathetic stimulation which causes increase in the heart rate and
contractibility of myocardium. The fall in blood pressure causes hypoxia and change in pH of
blood.
The hypoxia is predominantly sensed by the peripheral chemoreceptor present in carotid and
aortic arch, while the change in pH is predominantly sensed by the central chemoreceptors
present in medulla of brain. All these causes increased sympathetic activity. Heart rate is also
increased by inhibition of the vagal fibres.
Increased sympathetic activity causes peripheral vaso constriction.The peripheral vaso
contriction is more effective in the blood vessels of the skeletal muscles, than the blood vessels
of heart and brain.The vaso contriction reduces the size of the vascular space.
 There is also reduction of capillary hydrostatic pressure. The reduced capillary
hydrostatic pressure encourages the fluid to move from the extra vascular space to the intra
vascular space, thus trying to reduce the hypovolemia and increased the blood pressure.
Other mechanism that helps to maintain the normal circulation after hypovolemia.
I. Reduction of renal blood flow increases the production of enzyme rennin.
II. The rennin leads to formation of Angeotensin II which is a potent
vasoconstrictor.
III. Release of aldosteron from the adrenal cortex which increase sodium
reabsorption and fluid retention by the kidneys.
IV. Release of ADH by the posterior pituitary leads to retention of fluid by the
kidneys.
When the blood loss is 25% or less the compensatory mechanism restores the blood pressure.
The vaso constriction of arterioles is more than the venules, so that hydrostatic pressure in
capillary is low which increase the movement of fluid from extra celluler space to intra vascular
compartment.

CARDIOGENIC SHOCK – Pump failure

Myocardial infarction causing more than 50% of wall of left ventricle. It is also seen in
pulmonary embolism when there is a right sided heart failure.

AMPHYLACTIC SHOCK
There is antigen antibody reaction. The antigen combines with the antibody present over surface
of mast cell and basophils causing release of chemical substances e.g. histamine, SRSA-slow
reacting substance of anaphylaxis leading to laryngeal edema, bronchospasm, respiratory distress
and hypoxia. Beside this the histamine and SRSA causes massive peripheral vasodilation and
hypovolemia shock.

NEUROGENIC SHOCK
Also known as Vasovagal or Psychogenic Shock. There is fainting attack caused by intense
pain or sudden fright. There is sudden paralysis of vasomotor influence, causing peripheral
vasodilation and fall of peripheral vascular resistance and pooling of blood decreases venous
return to heart. Decreased cardiac output and fall of B.P. which causes reflux vagal stimulation
and bradycardia. Cerebral hypoxia causes unconsciousness.
Milder form is treated by removal of offending stimuli that is releaf of pain which causes
rapid gain of vascular tone.
Severe form is treated by IV fluids and vasopressure drugs which causes peripheral
vasocontrition and increase of cardiac output.

SEPTIC SHOCK-- HYPER DYNAMIC OR WARM SHOCK

Septic shock is caused by Gram Positive or Gram Negative bacterial infection. Septic shock is
most commonly caused by Gram Negative bacteria. Gram positive bacterial infection can easily
be controlled so a septic shock caused by gram positive bacterial infection is less dangerous.
Septic shock is mostly caused by the gram negative bacterial infection arising from—
genitourinary, pulmonary, hepatobiliary and gastrointestinal tract.
Septic shock causes derangement of
F Cardiac function
F Capillary permeability
F Vascular resistance
F Cellular metabolism
Gram Negative bacterial infections causing Septic shock are—
E.coli, klebsiella, proteus, pseudomonas and bacteroids.
Enodotoxins are the constituents of bacterial call wall, which are released when the bacteria dies.
Enodoxin causes—
1. Release of kinens and histamine which are vaso active peptides.
2. Endothelial damage causing increased microvascular permeability resulting in fluid
loss from intravascular spaceto extra vascular space. Loss of blood volume resulting in
decreased venous filling, fall in CVP. Cardiac output falls resulting in hypotension.
Hypotension is further aggrevated by kinens, histamines and other vasoactive peptides
which causes peripheral vaso dilation.
The endotoxin released by the bacteria causes activation of coagulation DIC. There is fall in
coagulation factor and platelets.Leading to haemorrhage from various sites. There is upper GI,
lower GI bleeding, hematuria.etc.
The Septic Shock effects nearly all the organs systems of the body but the pulmonary,
cardiovascular, renal and hepatic system are the target organs.
At first there is hyper dynamic state. There is increased cardiac output and trachecardia, warm
and dry skin. The endothelium becomes damaged and endotoxins leaks into the circulation
leading to a generalised inflammatory state.

TRAUMATIC SHOCK
It is due to hypovolemia due to excessive external or internal bleeding. Trauma to the heart itself
may cause pump failure.
When the blood loss is 25% or less then compensatory mechanism restore the blood pressure to
normal. When there is severe internal haemorrhage, Blood collecting into Pleural, peritoneal
space, retro peritoneal and soft tissue blood collection, requires immediate surgical intervention,
rather then to continue with fluid replacement.

BURN SHOCK
When the burn is more than 25% of the body surface area leading to capillary leakage and
hypovolemia. Later the septic shock adds up and worsens the condition.
MANAGEMENT OF SHOCK

¨ HYPOVOLEMIC SHOCK—
Clinical Signs of Shock
(1) Cold and sweating skin.
(2) Pallor
(3) Rapid pulse rate
(4) Fall in blood pressure
(5) Respiration is shallow and rapid
(6) Level of consciousness in reduced
Sign of hypovolemic shock depends on the degree of hypovolemia
Ø Mild hypovolemia -- <20% of blood loss. There is sign of
sympathetic discharge
– Cold and sweating skin particularly of lower limbs and feet.
– Increasing pulse rate
– Blood pressure falls.
Ø Moderate hypovolemia—20 to 40% of blood loss. The Compensatory mechanism to
restore the blood pressure to normal starts. So reduce the sign of sympathetic discharge.
— Urine output is low indicating the ADH release
– Pulse rate is moderately elevated
– Blood pressure may be normal at lying down position
Ø Severe Hypovolemia-- >40% of blood loss
— Signs of sympathetic discharge
— Increase pulse rate
— Blood pressure is low
— Decreased urinary output
— Cerebral ischemia leading to irritability and confusion

PARAMETERS INDICATING CIRCULATORY COMPENSATION

1. Level of cerebral activity
2. SpO2 measurement
3. Hourly urine output it should be 30 to 50 ml per hour.
4. CVP measurement – normally it is 3—5 cms above the maniburosternal angle.
5. Swan Ganz Catheter tracing – pulmonary artery and pulmonary capillary wedge
pressure measurement.
Balloon tipped, flow directed Swan Ganz Catheter is useful in long term care of shocked patient.
The device is not indicated in early management of shock because CVP measurement gives
quick and easy information. The Swan Ganz catheter is introduced through the internal juglar
vein into the right atrium and right ventricle and placed in the pulmonary artery. The pulmonary
artery and pulmonary capillary wedge presuure are measured. Swan Ganz catheter is ideal for
monitoring volume replacement in injured patient with myocardial disease.
TREATEMENT OF HYPOVOLEMIC SHOCK
(1) IV fluid – A large bore IV line should be inserted or a venisection is done.
Initial resuscitation is done by crystalloids (Ringer lactate or sodium chloride) followed
by colloids. Colloids are suitable to replace small blood loss. Among colloids Dextran is used –
(a) Low molecular weight dextran – has an immediate effect in replacing blood volume
but their effect is short lasting as they are rapidly excreated by the kidneys.
(b) High molecular weight dextran—has a delayed effect in restoring blood volume, but
their effect is long lasting.
(c) Gelatine in degraded form—Haemaccoel is mostly used as plasma expander.
(2) Volume infusion is alone not enough to restore the arterial blood pressure and tissue
perfusion, because of low peripheral vascular resistance. Then the use of cardiotonic and
vasoactive drugs are used.
Dopamine – It improves the cardiac function and at the same time causes vaso dilatation
of splanchnic and renal blood vessel and improves blood flow. A Dose of 1—5 mmg/kg/min
is mild inotropic. Successful resuscitation is indicated by warm and dry skin indicating good
tissue perfusion. Rise in urinary output to 30 to 50 ml/hr.
Dobutamine—improves the cardiac function but causes increase in the heart rate and
decrease the peripheral vascular resistance.
(3)Use of steroids are controversial but it has been shown that steroids.
– Improve the cardiac function
– Produce mild peripheral vasodilatation
– Protects the endothelial cells from endotoxins.
So a high dose and a short term use of steroids have no side effects and may be safely
recommended in the management of shock.
(4)Positioning—supine position with limbs elevated
(5)Medical anti shock trousers(MAST)
(6)Sedation-Given IV to reduce pain and fright.

Treatment of Septic Shock

It must be made clear that an established case of septic shock is mostly fatal. So a prompt
recognition and Treatment of infection before septure shock develops is the only way to reduce
mortality.
(1) Patient should be treated in ICU.
(2) Direct arterial blood pressure monitoring.
(3) CVP monitoring, pulmonary capillary wedge pressure monitoring, by Swan Ganz
Catheter.
(4) Arterial and venous blood gas monitoring
(5) Urine output measurement
 (6) Search for source of infection and its treatment. If abscess is present then its drainage.
If abdomen is the source of infection then Exploratory Laparotomy.
(7) Use of antibiotics—culture specimen is to be taken before starting antibiotics. One
antibiotic may not be enough to cover all the organisms. Two antibiotics are used together
once the culture report comes after 48 hr then a specific antibiotic is started.
(8) Maintenance of proper air way and O2 supplementation. If ARDS develops then the use
of positive end expiratory pressure (PEEP) Ventilators are used.

Initial Signs of Gram Negative Sepsis

(1) Chills
(2) Raised body temperature-101o F.
(3) Hyperventilation-- Respiration is shallow and rapid. Mild degree of hypoxia causes
hyperventilation and alkalosis.
(4) Oliguria
(5) Altered Sensorium
(6) White blood cells are raised except in patients very ill patient and those receiving
immuno suppressant.
(7) Fall of platelet count may be early and sensitive indicator of gram negative sepsis.
Clinical signs of septic shock depend on the previous volume status of the patient.
So a septic shock can present as
– Hyper dynamic septic shock
– Hypo dynamic septic shock

HYPER DYNAMIC SEPTIC SHOCK—

In hyper dynamic septic shock the previous volume status of patient (i.e.before sepsis starts) is
normal e.g. septic abortion.
There is –
(a) Hyper ventilation (respiration is shallow and rapid)
(b) High CVP
(c) High Cardiac output
(d) Alkalosis
(e) Oliguria
(f) Low peripheral resistance
(g) Low blood pressure
(h) Warm and dry skin
Aim of treatment is to
i. Further increase of cardiac output
ii. Antibiotic therapy
iii. Early surgical intervension
If the control of infection is delayed patient passes into acidotic phase fall in cardiac output and
further cellular damage. This may not respond to treatment.
HYPODYNAMIC SEPTIC SHOCK –
Is seen in patient who are already hypovolemic or the volume status of the patient is low
before the septic process starts. E.g. Gangrenous intestinal, obstruction, mesenteric artery
thrombosis, peritonitis. There is third space fluid loss.
They present with –
1. Low CVP
2. Low cardiac output
3. Low blood pressure
4. Oliguria
5. Increased peripheral resistance
6. Cold and synoptic limbs