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1. A SEMINAR ON
“SHOCK”
by,
Dr.Prasanna Kumar Y.S
Post-Graduate student
Department of Preventive and Community dentistry

2. SHOCK…
Various attempts to define shock are;
“ It is a condition in which circulation fails to meet the nutritional
needs of the cells and at the same time fails to remove the
metabolic waste products”
“ It is a clinical condition characterised by signs and symptoms
arising when the cardiac output is insufficient to fill the arterial
tree with blood under sufficient pressure to provide all the organs
with adequate blood flow”
Shock is classified into various types depending on the
Causes.They are:
 Haematogenic shock
 Traumatic shock
 Neurogenic shock àVasovagal shock
àPsychogenic shock
 Cardiogenic shock
 Septic shock
 Miscellaneous types àAnaphylactic shock
àInsulin shock

3. Haematogenic or Hypovolaemic shock:
Pathophysiology:
Such shock is usually due to sudden loss of blood volume or loss
of fluid from the vascular space.Most common causes include
hemorrhage,vomiting and other states of dehydration.
In case of hemorrhagic shock there is loss of blood resulting in
decreased filling to the right heart.
The decreased filling results in an a drop of arterial pressure and
thus consequential hypotension.
The compensatory mechanisms put forth by the body are:
1.Adrenergic discharge
2. Hyperventilation
3. Release of vasoactive amines
4. Collapse
5. Resorption of fluid from the intracellular and extracellular
space
6. Renal conservation of body water and electrolytes
1. ADRENERGIC DISCHARGE
It starts within 60 seconds of blood loss.The constriction of
venules and small veins displaces blood to the right atrium and
ventricle.This causes an increase in the diastolic blood pressure
and stroke volume thus compensating the systemic hypotension.

4. Adrenergic discharge constricts sphincters in the splanchic
viscera,kidneys and the skin.This selective vasoconstriction
improves filling of the right heart and increases cardiac output.
2.HYPERVENTILATION
This occurs in response to metabolic acidaemia that develops
shortly after haemorrhage.
Spontaneous deep breathing sucks blood from extrathoracic sites
to the heart and lungs.This results in increased filling to the left
ventricle.
“Both adrenergic discharge and hyperventilation occur within one
minute of blood loss”
3.RELEASE OF VASOACTIVE AMINES
A hormone known as RENIN is released from the kidney in
response to low perfusion.Renin releases AngiotensinI from the
liver which is converted to Angiotensin II in the lungs.This
Angiotensin II is a potential vasoconstrictor.
Another hormone of importance is VASOPRESSIN.
It is released in response to the stimulation of baroreceptors
situated in the Carotid bodies of the aortic arch.It acts as a
systemic vasoconstrictor and diverts the blood flow towards the
brain and heart increases cardiac output.

5. EPINEPHRINE is also a vasoactive hormone released from the
aderenal medulla as a consequence of discharge from the
adrenergic nervous system.
“The release of vasoactive amines usually occurs after 1 to 2
minutes of Haemorrhage”
4.COLLAPSE
“Assumption of the recumbent posture due to collapse
automatically displaces blood from the lower part of
the body to the heart and increases cardiac output”
5.RESORPTION OF FLUID FROM THE
INTRACELLULAR AND THE EXTRACELLULAR SPACE
Release of epinephrine from the adrenal medulla,cortisol from the
adrenal cortexand glucagons from the pancrease results in high
extracellular glucose concentration.This causes hyperosmolarity
of
the extracellular tissue which draws water out of the
Cells.Interstitial pressure increases as a result water,sodium and
chloride are forced into the vascular space.
6.RENAL CONSERVATION OF BODY WATER AND
ELECTROLYTES
Adrenocorticotropic hormone is release by any stress or
shock.This along with AngiotensinII stimulate the synthesis and

6. release of hormone Aldosterone which helps in resorption of
sodium and water by the Kidneys.
CLINICAL FEATURES OF HYPOVOLAEMIC SHOCK
Based on the degree of loss of blood volume and the duration(time
elapsed) the clinical features can be described under 3 Phases.
 MILD SHOCK
 MODERATE SHOCK
 SEVERE SHOCK
1.MILD SHOCK
Loss of less than 20% of blood volume is included under this
category.The clinical findings include:
 Paleness of extremities which become cool-due to peripheral
vasoconstriction which in turn is due to theaction of
adrenergic discharge
 There is sweating in the forehead and palms again due to
adrenergic discharge.
 Urinary output and pulse rate and BP remain normal
 Patient feels thirsty and cold
2.MODERATE SHOCK
Loss of blood volume from 20% to 40% is seen.
In consistence with the features of mild shock what is
seen here is OLIGURIA.

7. “Oliguria is due to adrenergic discharge along with the effects of
circulating aldosterone and vasopressin.”
The pulse beats is around 100 beats per min. Initially the BP will
be normal but progressively falls later on.
3.SEVERE SHOCK
Loss of blood volume more than 40% usually causes this form of
shock.
Characterized by:
1.Palor(paleness of skin and extrmities)
2.Low urinary output
3.Rapid pulse
4.Low BP
CLINICAL MONITORING:
 Measurement of BP
 By measuring respiratory rate
 Urine output
 Measuring central venous pressure.
TREATMENT
1.RESUSCICATION
2.IMMEDIATE CONTROL OF BLEEDING
3.EXTRACELLULAR FLUID REPLACEMENT
- Usually Normal saline supplemented with 1 or 2 ampules of
Sodium bicarbonate.

8. 4.DRUGS-In this case usually only in the form of sedatives.
TRAUMATIC SHOCK
Pathophysiology:
The peculiarity of this type of shock is that the traumatised tissues
activate the co-agulation system and release MICROTHROMBI
into circulation. These occlude the pulmonary Microvasculature.
The humoral products of the thrombi increase the capillary
permeability resulting in depletion of vascular volume.
CLINICAL FEATURES
The features are very much similar to that of hypovolaemic shock
except there are two differentiating features.
 Presence of pulmonary and peripheral oedema in this type of
shock
 Infusion of large volumes sufficient for hypovolaemic type is
not sufficient for traumatic shock
TREATMENT
1.Resuscitation
2.Local treatment of trauma and control of bleeding
à usually by surgical debridement of ischaemic and dead tissues
3.Fluid replacement

9. 4.Use of anticoagulant therapy-One intravenous dose of 10,000
units of heparin.
CARDIOGENIC SHOCK
PATHOPHYSIOLOGY:
This type of shock is primarily due to dysfunction of one of the
ventricles.It may be because of myocardial infarction,chronic
congestive heart failure,cardiac arrythmias or pulmonary
embolism.
“In cardiac compressive shock there is compression on the heart
from outside resulting in decreased output. Causes may be tension
pneumothorax and pericardial tamponade”
CLINICAL FEATURES
 In the beginning the skin is pale and the urinary output is
low.
 Gradually the pulse becomes rapid and the arterial pressure
falls.
 In case of right ventricular dysfunction the neck veins
become distended and the liver is also enlarged
 In left ventricular dysfunction the characteristic third heart
sound is heard and presence of Bronchial rales.
TREATMENT
The treatment of cardiogenic shock involves;
1.Airway clearance for adequate oxygenation

10. 2.In case of massive pulmonary embolus-Large doses of Heparin
is given intravenously
3.Pain is dealt with by Morphine
4. Persistent pulmonary oedema should be treated with a Diuretic
NEUROGENIC SHOCK
CAUSES:
1.Trauma to the spinal cord such as in crush injuries
2.Any blockade to the sympathetic nervous system wherein there is
loss of arterial and venous tone resulting in peripheral pooling of
blood.
3.Paraplegia and quadriplegia also have been known to be
involved
Two types of Neurogenic shock are seen:
1.Vasogenic type: It occurs in case of peripheral dilatation of blood
vessel resulting in reduced blood flow to the brainàCerebral
hypoxiaàUnconciousness
2.Psychogenic type: It follows sudden fright or unexpected bad
news
In the psychogenic type there is dilatation of the systemic
vasculature which lowers the systemic arterial pressure.
CLINICAL FEATURES

11. “The peculiar feature is that the skin remains warm,pink and well
perfused.Urine output is also normal but the Heart rate is
rapid and the BP is low”
TREATMENT
1.Assuming the TRENDELENBURG position is an important
aspect so as to displace blood from the systemic venules and thus
increase the cardiac filling.
2.Use of Vasoconstrictors saves the patient from sudden low BP
and low cardiac output thus savin organs such as Brain,kidney
and heart from ischaemic damage.
SEPTIC SHOCK
Such a type of shock is usually due to Gramnegative septicemia.
The common organisms responsible for it are:
1.E.Coli
2.Klebsiella aerobacter
3.Proteus
4.Pseudomonas
PATHOPHYSIOLOGY
In this type of shock there is wide spread dissemination of the
exotoxin elaborated by the organism.Sometimes Gram positive
such as Clostridium tetani infections result in fulminating
infections and sepsis.Here there is massive fluid loss resulting in
progressive hypotension

12. CLINICAL FEATURES
It is often recognised by:
1. Development of chills
2. Elevated temp.above 100 C
There are two types here:
 Early warm shock-Cutaneous vasodilation
 Late cold shock- increased vascular permiability due to
persistence of septic focus.
TREATMENT
Here there are two lines of treatment:
1. Treatment of infection by early surgical debridement or
drainage and use of antibiotics
2.Use of fluid replacement for shock followed by steroid therapy
and administration of vasoconstrictors if necessary
COMMON EVENTS OF SHOCK ENCOUNTERED IN
CLINICAL PRACTICE
The incidence of shock like features or shock itself in clinical
practice should always be anticipated.
These include in order of common occurrence:
1.Nausea
2.Perspiration
3.Apprehension

13. These features may subside or herald the onset of further
complications.
The complications include;
 Syncope
 Hypertension followed by hypotension
 Peripheral loss of color and generalised paleness later on.
 Visual disturbances followed by dizziness
The features as mentioned are basically due to
APPREHENSION precipitated by PAIN AND STRESS
MEASURES TO BE TAKEN:
1.The patient should first be placed in TRENDELENBURG
position so as to increase the blood flow to the heart and to the
brain.
In case of pregnancy the patient should be in LEFT LATERAL
DECUBITUS POSITION.
2.Secondly monitoring of BP,pulse and respiratory rate should be
done.
If the patient still continues to have Bradycardia Then:
ATROPINE-0.5 to 1 mg should be administered and
repeated every 5 minutes to a maximum dose of 3mg.

14. Full recovery in this case should occur after in 20 minutes.If loss
of conciousness takes longer than 20 minutes then Emergency
Medical service should be called upon (Priorly informed!!)
Finally what can be said is that the very word SHOCK creates an
impression of a Life threatening procedure. It is so….but what is
needed is more of a preventive based approach keeping in mind the
factors related to shock that may be encountered in day today
events.A calm and calculated approach from the Clinician as a
result of previous training for such situations goes a long way in
saving lives.