This document discusses shock, including its definition, causes, stages, classifications, signs, symptoms, and treatments. Shock is defined as a clinical state of circulatory collapse caused by a reduction in cardiac output or circulating blood volume, resulting in hypotension and impaired tissue perfusion. The stages of shock include compensated, uncompensated, and irreversible. The main types of shock covered are hypovolemic, cardiogenic, distributive (septic, anaphylactic, neurogenic), and obstructive. Treatment aims to restore adequate tissue perfusion through volume expansion and vasopressor support.

2.  INTRODUCTION
 DEFINITION
 PHYSIOLOGIC CAUSES OF SHOCK
 THE STAGES OF SHOCK
 CLASSIFICATION OF SHOCK
 TREATMENT OF SHOCK
 CONCLUSION
 REFERENCE

3.  Shock is considered as a dreaded medical complication or
an emergency condition because of it’s complex nature , its
severity & the complexity of its management & most of all
its unpredictable nature of outcome.
 We should be in a position to recognise the type of shock &
atleast render initial / emergency treatment until medical
help can arrive.

4. Clinical state of circulatory collapse characterised by a
reduction either in cardiac output or in the effective
circulating blood volume resulting in hypotension
followed by impaired tissue perfusion &cellular
hypoxia

5. Circulatory Shock Caused by Decreased C.O
1. Cardiac abnormalities that the ability of the heart to pump blood.
 M.I
 Severe heart valve dysfunction, heart arrhythmias
2. Factors that venous return & also C.O
 Diminished blood volume
Circulatory Shock That Occurs Without Diminished C.O
1.Excessive metabolism of the body, so that even a normal C.O is
inadequate
2.Abnormal tissue perfusion patterns, so that most of the C.O is passing
through blood vessels besides those that supply the local tissues with
nutrition.

6. The arterial pressure level -principal measure of adequacy of
circulatory function.
But it can often be seriously misleading.
 At times, a person may be in severe shock & still have an almost
normal arterial pressure because of powerful nervous reflexes that
keep the pressure from falling.
 At other times, the arterial pressure can fall to half of normal, but the
person still has normal tissue perfusion & is not in shock.
Mostly the Arterial B.P decreases at the same time as the C.O
decreases

7.  10 % of the total blood volume can be removed with almost no effect
on either arterial pressure or C.O, over a period of about 30
minutes.
 But greater blood loss usually
diminishes the C.O 1ST &
later the Arterial pressure
 Both of which fall to 0
when about 35 -45 %of the
total blood volume
has been removed.

8. Compensated Shock
• AKA: Nonprogressive Shock
Uncompensated Shock
• AKA: Progressive Shock
Irreversible Shock
• AKA :Refractory shock

9.  Circulatory system can recover as long as the degree of hemorrhage is no
greater than a certain critical amount.
 Thus,hemorrhage beyond a certain critical level causes shock to become
progressive.
 Ie, the shock itself causes still more shock, & the condition becomes a
vicious circle deterioration of the circulation & to death

10.  If shock is not severe enough to cause its own progression, the
person eventually recovers.
 Therefore, shock of this lesser degree is called Nonprogressive
shock
 It is also called Compensated shock,
ie;sympathetic reflexes & other factors compensate enough to prevent
further deterioration of the circulation.

11. Rapid compensatory mechanism (neural mechanism)
1.Baroreceptor reflexes
2.Chemoreceptor reflexes
3.Central nervous system ischemic response
Intermediate compensatory mechanism
4.Reverse stress-relaxation of the circulatory system
5.Formation of angiotensin by the kidneys
6.Formation of vasopressin (ADH)
Long term compensatory mechanism
7.Compensatory mechanisms that return the blood volume back toward
normal

12. PHYSIOLOGIC SYSTEMS ACTIVATED
NERVOUS
SYSTEM
RENAL
SYSTEM
ENDOCRINE
SYSTEM
LOCAL
REGULATIO
N

13. NERVOUS SYSTEM
Through
VMC
&
Baroceptotor &
chemoreceptors

14. 2.ARTERIOLES
1
3.ADRENAL MEDULLA

15. ↓ Blood flow
↓ Arterial pressure
↓O2
↑ CO2 + H+
Chemoreceptor stimulation ↓ Baroreceptor firing
stimulation
Vasoconstrictor area of VMC
Vasoconstriction
Via sympathetic vasoconstrictor
fibres by release of nor- epinephrine
Arterial pressure
↑ HR
Reduced vagal
activity
↓ tissue perfusion

16. RENAL
SYSTEM
Through
Renin- Angiotensin mechanism

17. Blood pressure
Angiotensinogen
RENIN
Angiotensin 1
Angiotensin 2
ACE
JG CELLS OF KIDNEY
IN LUNGS
Aldosterone sectretion
Adrenal cortex-
Reabsorption of Na & H2O
from renal tubules
Vasoconstriction
Blood pressure Blood vol

18. ENDOCRINE
SYSTEM

19. Blood loss
Arterial pressure
Renin Catecholamines
Adrenal
medulla
kidney
ADH
Baroreceptor
stimulation
Post.
pituitary
Angiotensin 2
Aldosterone
Adrenal
cortex
Na &
H2O
Reabsor-
ption
from
Renal
tubules

20. LOCAL
REGULATION
Through local substances-
vasoconstrictors

21. Blood vessel injury
Stretching of blood vessel
Endothelin secretion
Phospholipase
activation
Thromboxane A 2
activation
Vasoconstriction
Arterial pressure

22.  The sympathetic reflexes become activated within 30 seconds to a
minute after hemorrhage
 The angiotensin and vasopressin mechanisms, as well as the
reverse stress-relaxation that causes contraction of the blood vessels
and venous reservoirs, all require 10 minutes to 1 hour to respond
completely, but they aid greatly in increasing the arterial pressure
or increasing the circulatory filling pressure and thereby
increasing the return of blood to the heart.

23.  Finally readjustment of blood volume by absorption of fluid from
the interstitial spaces and intestinal tract, as well as oral ingestion
and absorption of additional quantities of water and salt, may require
from 1 to 48 hours, but recovery eventually takes place, provided
the shock does not become severe enough to enter the progressive
stage.
 But when this initial response (peripheral vasoconstriction) is
prolonged & treatment is delayed ,it results in the following
sequence of events.

25. Is Caused by a Vicious Circle of Cardiovascular Deterioration
 Cardiac Depression
 Vasomotor Failure
 Blockage of Very Small Vessels—“Sludged Blood.”
 Increased Capillary Permeability
 Release of Toxins by Ischemic Tissue
 Cardiac Depression Caused by Endotoxin
 Generalized Cellular Deterioration
 Tissue Necrosis in Severe Shock—Patchy Areas of Necrosis
Occur Because of Patchy Blood Flows in Different Organs

26. Prolonged vasoconstriction
Tissue anoxia
Live
r
Kidney muscleIntestine
Accumulation of
metabolic waste
Anerobic
glycolysis
Kidney
injury
Lactic acid
Metabolic
acidosis
Arterioles sensitive to catecholamine
vasodilatation Hydrostatic pressure
Interstitial fluid
Blood volume
# inactivation of
VDM
Hemorrhagic
necrosis
Blood loss

27. Blood volume
ischemia
Capillary injury
Vascular permeability
Blood volume
Cerebral ischemia Myocardial ischemia
VM - depression
Venous return Depression of cardiac function
Cardiac output
DECOMPENSATED SHOCK

28. After shock has progressed to a certain stage,transfusion or any other
type of therapy becomes incapable of saving the person’s life. The person
is then said to be in the irreversible stage of shock.
Ironically,even in this irreversible stage, therapy can, on rare occasions,
return the arterial pressure & even the C.O to normal or near normal
for short periods,but the circulatory system nevertheless continues to
deteriorate, and death ensues in another few minutes to few hours.

29. Figure shows that transfusion during the irreversible stage can sometimes cause
the C.O(as well as the arterial pressure) to return to normal.
However, the C.O soon begins to fall again & subsequent transfusions have less
& less effect.
Multiple deteriorative changes in the muscle cells of the heart that may not
necessarily affect the heart’s immediate ability to pump blood but, over a long
period,depress heart pumping enough to cause death
In severe shock,a stage is eventually reached at which the person will die even
though vigorous therapy might still return the C.O to normal for short periods.

30. In severe degrees of shock -the high-energy phosphate reserves
All the creatine phosphate -degraded, and almost all the ATP has
downgraded to ADP, AMP and, eventually, adenosine.
This adenosine diffuses out of the cells into the circulating blood & is
converted into uric acid(cannot reenter the cells)
New adenosine - synthesized at 2 % of the normal cellular amount an
hour, ie;once stores are depleted, its difficult to replenish.
Cellular depletion of high energy compounds causes most
devastating end results & leads to irreversibe stage

31. 1. Hypovolemic shock
2. Cardiogenic shock
3. Distributive shock
i. Septic shock
ii. Anaphylactic shock
iii.Neurogenic shock
4. Obstructive Shock

32. Most common type of shock in the victim of maxillofacial
trauma.
DEFINITION
Defined as a medical condition in which rapid loss of
intravascular blood or plasma volume results in multiple
organ failure due to inadequate perfusion.

33. HYPOVOLEMIC SHOCK
HEMORRHAGIC
SHOCK
NONHEMORRHAGIC
SHOCK

34. Hemorrhage
Filling pressure of the circulation
venous return
Cardiac output
Blood pressure
Velocity of blood flow
Blood supply to vital organs,esp brain
SHOCK

35. HEMORRHAGIC SHOCK- loss of intravascular blood
External source
 Laceration
 Trauma
 Surgical procedure
Internal source
 Gastrointestinal bleeding
 Femoral fracture
 Crush injury
 Ruptered internal organs
 Post partum hemorrhage
“Physiologic response is
proportional to volume of blood
lost”

36. % Blood loss Clinical signs
< 15 Slightly increased heart rate, local swelling, skin-warm,compensate
by baro-receptors mediated reflex ,
vasoconstriction, activation of renin-angiotensin mechanism
15-30
Tachycardia, increased diastolic blood pressure,
prolonged capillary refill
30-50 Above findings plus: hypotension, acidosis, decreased
urine output ,skin-cool , pallor +, cns-lethargic
> 50 Refractory hypotension, refractory acidosis, death ,cyanotic
skin, thready central pulse, anuria, bradycardia

37. NON HEMORRHAGIC SHOCK
Loss of plasma from intravascular compartment than the
loss of whole blood
Increased hemoconcentration
Sluggish blood flow
Decreased blood flow to brain
Shock

38. Plasma due to shift of massive fluid
from intravascular compartment
to extravascular compartment
 Burns
 Crush injuries
 Peritonitis
 Pancreatitis
 Surgical wounds
 Pleural effusion
Plasma due to dehydration
Vomiting/diarrhea
Urinary output in renal
disease
Adrenocortical insufficiency
Excessive sweating
Excessive diuretic use
Diabetes insipidus

39. Early stage -an attempt is made to maintain adequate cerebral &
coronary blood supply by redistribution of blood so that the vital
organs ( heart & brain ) are adequately perfused &oxygenated .
ie. The heart may receive 25% of the C.O, as opposed to its normal 5%
to 8% .
Similarly the brain may receive as much as 80% of the C.O, instead of
its usual 15% to 20%.
Ie.
Blood flow to heart & brain & blood flow to extremities,
kidneys,skin,muscle& GI tract

40. If shock is adequately treated , recovery by the compensatory
mechanism compensated / reversible shock.
In hypovolemic shock a great outporing of epinephrine occurs leading to
intense vasoconstriction.
But this situation results in ischemic anoxia of the involved peripheral
tissues in an all out effort to keep the heart & brain function for
survival .

41.  History is vital in determining the possible cause .
 Symptoms - weakness, lightheadedness, confusion should be assessed
 In pt with trauma ,determine the mechanism of injury & information
of vital organ injuries
 If conscious-pt may be able to indicate location of pain.
 In patient with GI bleeding enquire about hematemesis, melena ,
excessive NSAID use
 In case of burns , enquire about the type of burn &time of occurrence

42. SIGN & SYMPTOMS
MILD HYPOVOLEMIA (<20% of blood loss)
† Mild tachycardia but relatively few external signs especially in a supine resting
young patient
† Cool extremities
† Diaphoresis
† Anxiety
MODERATE HYPOVOLEMIA (20-40% of blood loss)
† Pt becomes increasingly anxious & tachycardic
† Although normal blood pressure can be maintained in the supine position, there
may be significant postural hypotension & tachycardia
† Mild oliguria
SEVERE HYPOVOLEMIA (>40%)
† Blood pressure declines & unstable even in supine position
† Marked tachycardia
† Marked oliguria
† Mental status deterioration (coma)
CLINICAL MANIFESTATION OF HYPOVOLEMIC
SHOCK

44.  Trauma examination –assess airway , breathing &circulation
 Later the circulatory system – evaluate signs & symptoms of shock
 Systolic BP should not be relied upon as main indicator.
compensatory mechanism prevents the significant decrease in
systolic BP until pt has lost 30% of blood volume.
 Attention should be paid to pulse, resp. rate & skin perfusion
 Pts on beta blockers may not have tachycardia regardless degree of
shock
 Plasma loss hemoconcentration & free water loss hypernatremia .
These findings should suggest the presence of hypovolemia

45.  ACID-BASE STATUS
Metabolic acidosis/decreased serum bicarbonate
 OXYGEN SATURATION
 COMPLETE BLOOD COUNT
TC,DC, ESR, Peripheral smear , Hb%
 ELECTROLYTE LEVELS
Na , K, Cl, HCO3 , blood urea, creatinine, Glucose levels
 ARTERIAL BLOOD GAS
This test helps to determine PO2 of blood , assisting in titration of supplemental
oxygen delivery.

46.  The impaired ability of the heart to
pump blood
 Pump failure of the right or left
ventricle
 Most common cause is LV MI
(Anterior)
 Occurs when > 40% of ventricular
mass damage
 Mortality rate of 80 % or MORE

47.  Mechanical: complications of
MI:
 Papillary Muscle Rupture
 Ventricular aneurysm
 Ventricular septal rupture
 Other causes:
 Cardiomyopathies
 Tamponade
 Tension pneumothorax
 Arrhythmias
 Valve disease

48.  Impaired pumping ability of LV
Decreased stroke volume
Decreased CO
Decreased BP
Compensatory mechanism
Decreased tissue perfusion !!!!

49.  Impaired pumping ability of LV leads to…
Inadequate systolic emptying
 Left ventricular filling pressures (preload)
 Left atrial pressures
 Pulmonary capillary pressure
Pulmonary interstitial & intraalveolar edema !!!!

50.  Pulmonary & Peripheral Edema
 JVP
 Hypotension
 Tachypnea,
 Crackles
 PaO2
 Urinary Output
Mean arterial pressure below 70 mmhg compromises coronary
perfusion
(MAP = DBP + PP/3) PP=SPB-DPB

51.  Formerly known as “blood poisoning”
 Refers to a bacterial infection widely disseminated to many areas of
the body, with the infection being borne through the blood from one
tissue to another & causing extensive damage.
 Septic shock is extremely important to the clinician, because other
than cardiogenic shock, septic shock is the most frequent cause of
shock-related death in the modern hospital.

52. 1. Peritonitis caused by spread of infection from the uterus & fallopian
tubes, with instrumental abortion(unsterile conditions)
2. Peritonitis due rupture of the G.I system(intestinal disease &
wounds)
3. Generalized bodily infection due spread of a skin infection such as
streptococcal or staphylococcal infection.
4. Generalized gangrenous infection resulting specifically from gas
gangrene bacilli, spreading first through peripheral tissues and finally
by way of the blood to the internal organs, especially the liver.
5. Infection spreading into the blood from the kidney or urinary tract,
often caused by colon bacilli.

53. Systemic Inflammatory Response Syndrome(SIRS)
manifested by : two or > of following:
 Temp > 38 O C or < 36 O C
 HR > 90/min
 RR > 20 or PaCO2 < 32mmHg
 WBC > 12,000/cu mm
Sepsis syndrome: SIRS with confirmed infectious process
associated with organ failure or hypotension
Septic shock :Sepsis with organ failure & Hypotension (SBP < 90 or >
40 fall from baseline) despite adequate fluid resuscitation

54. Initiated by gram-negative (most common) or gram positive
bacteria, fungi, or viruses
Endotoxins release inflammatory mediators (SIRS)
Vasodilation & increase capillary permeability
Shock due to alteration in peripheral circulation & massive dilation
Cell walls of
organisms

58.  Two phases:
“Warm” shock - early phase (hyperdynamic response,Vasodilation)
“Cold” shock - late phase(hypodynamic response,Decompensated
state)
Early stages –no signs of circulatory collapse but signs of the bacterial
infection positive
Later the circulatory system usually becomes involved either because of
direct extension of the infection or secondarily as a result of toxins from
the bacteria,with resultant loss of plasma into the infected tissues through
deteriorating blood capillary walls.
Finally deterioration of the circulation becomes progressive as in other
types of shock.

59. 1. High fever.
2. Often marked vasodilation throughout the body, especially in the infected tissues.
3. High C.O caused by arteriolar dilation in the infected tissues & by high metabolic
rate & vasodilation elsewhere in the body, resulting from bacterial toxin stimulation
of cellular metabolism & from high body temperature.
4. Sludging of the blood caused by red cell agglutination in response to degenerating
tissues.
5. Development of micro–blood clots in widespread areas of the body, a condition
called DIC. Also, this causes the blood clotting factors to be used up, so that
hemorrhaging occurs in many tissues, especially in the gut wall of the intestinal
tract.

60. 7-17%
Sepsis
400,000
20-53%Severe Sepsis
300,000
Septic
Shock
53-63%

62. Anaphylaxis – a severe systemic hypersensitivity reaction characterized
by multisystem involvement
• IgE mediated
Anaphylactoid reaction – clinically indistinguishable from
anaphylaxis, do not require a sensitizing exposure
• Not IgE mediated

63.  Vasodilatation
 Increased vascular permeability
 Bronchoconstriction
 Increased mucus production
 Increased inflammatory mediators
recruitment to sites of antigen interaction

64. CLINICALMANIFESTATIONS
OF
ANAPHYLACTIC SHOCK

65. SIGNS & SYMPTOMS
1. Skin reactions
2. GI disturbances
3. Respiratory disturbances
4. Cardiovascular collapse

66. 1.SKIN REACTIONS
Feeling of
impending doom sweating
flushing
conjunctivitis
urticaria
Pruritis
rhinitis

67. 2. GI DISTURBANCES
1.Severe abdominal cramps
2.Nausea & vomiting
3.Diarrhea
4.Fecal & urinary incontinence

68. 3. RESPIRATORY DISTURBANCES
4.Laryngeal edema-
stridor 1.Bronchospasm- wheezing
2.dyspnea
3.Cyanosis of nail beds &
mucosa

69. 4. CARDIOVASCULAR DISTURBANCES
1. Tachycardia
2. Palpitations
3. Hypotension
4. Cardiac arrhythmias
6. Cardiac arrest
5. Loss of
consciousness

70.  A type of distributive shock that results from
the loss or suppression of sympathetic tone
 Causes massive vasodilatation in the venous
vasculature,  venous return to heart, 
C.O.
 Most common etiology:
Spinal cord injury above T6
NEUROGENIC SHOCK IS THE RAREST FORM OF SHOCK!

71. Disruption of sympathetic nervous system
Loss of sympathetic tone
Venous &arterial vasodilation
Decreased venous return
Decreased stroke volume
Decreased cardiac output
Decreased cellular oxygen supply
Impaired tissue perfusion
Impaired cellular metabolism

72. A.K.A Extracardiac Obstructive Shock
Due to impairment of ventricular filling during diastole due to some
external pressure on heart
ventricular filling
C.O
CAUSES
 Pericardial temponade
 Tension pneumothorax
 Constrictive pericarditis
 Pulmonary embolism

74. Prevention of further injury & transportation of patient to hospital as
rapidly as possible
Prehospital intervention includes
 Immobilization of the patient
 Securing adequate airway
 Ensuring ventilation
 Maximizing circulation

75.  Pts airway should be assessed immediately.
 Depth &rate of respiration assessed.
 Any pathology that interferes should be addressed
immediately
 High flow supplemental oxygen administered &ventilatory
support given

76. REPLACEMENT THERAPY
 Blood and Plasma Transfusion.
 Shock caused by hemorrhage-best possible therapy -transfusion of
whole blood.
 Shock caused by plasma loss-the best therapy is administration of
plasma.
 When dehydration is the cause-provide -appropriate electrolyte
solution

77.  When Whole blood is unavailable-(battlefield conditions)
Plasma can usually substitute adequately for whole blood
because it increases the blood volume and restores normal
hemodynamics.
 Plasma cannot restore a normal hematocrit, but the human
body can usually stand a decrease in hematocrit to about half
of normal before serious consequences result, if C.O is
adequate.
 When plasma is unavailable-plasma substitutes - - dextran
solution

78. •Principal requirement of Plasma substitute is that it remain in the
circulatory system—
Ie, it shouldnot filter through the capillary pores into the tissue spaces for
which it must contain substance with large molecular size to exert colloid
osmotic pressure.
Eg: dextran- a large polysaccharide polymer of glucose
•Must be nontoxic and
•Must contain appropriate electrolytes to prevent derangement of the
body’s extracellular fluid electrolytes on administration.

79. A sympathomimetic drug -mimics sympathetic stimulation.
Eg:norepinephrine, epinephrine,
1.In neurogenic shock, in which the sympathetic nervous system is severely
depressed.Administering a sympathomimetic drug takes the place of the
diminished sympathetic actions and can often restore full circulatory function.
2.In anaphylactic shock, in which excess histamine plays a prominent role. The
sympathomimetic drugs have a vasoconstrictor effect that opposes the
vasodilating effect of histamine. Therefore, either norepinephrine or another
sympathomimetic drug is often lifesaving.
3.In Hemorrhagic shock it is Not valuable because the sympathetic nervous
system is almost always maximally activated by the circulatory reflexes ,so
much norepinephrine and epinephrine are already circulating in the blood that
sympathomimetic drugs have essentially no additional beneficial effect.

80. TREATMENT BY THE HEAD-DOWN POSITION. in hemorrhagic
and neurogenic shock when BP is too low,placing the patient in
trendenlenburg position promotes venous return, thereby also increasing
C.O.
First essential step in the treatment of many types of shock.
OXYGEN THERAPY.
Frequently is far less beneficial,because the problem in most types of
shock is not inadequate oxygenation of the blood by the lungs but
inadequate transport of the blood after it is oxygenated

82. Treatment with Glucocorticoids (Adrenal Cortex Hormones That
Control Glucose Metabolism).
(1) glucocorticoids frequently increase the strength of the heart in the
late stages of shock;
(2) glucocorticoids stabilize lysosomes in tissue cells and thereby
prevent release of lysosomal enzymes into the cytoplasm of the cells,
thus preventing deterioration from this source; and
(3) glucocorticoids might aid in the metabolism of glucose by the
severely damaged cells.

83.  Life threatening: Early goal directed therapy and regular
monitoring by trained staff will change outcome.
 Early detection : DON’T RELY ON BP
 High index of suspicion
 Monitor casualties susceptible to shock