This document discusses critical care in medicine, focusing on the management of critically ill patients and the various mechanisms of brain injury. It outlines the causes and types of brain injuries, as well as the physiological responses and effects of hypoxia, ischemia, and edema. Key aspects of the diagnosis, prognosis, and management of coma and confusional states are also emphasized.

2. Actuality
• Increasing spectrum of diseases
secondary to critical illness
• 1/3 of intensive care units (ICU)
patients, 55% mortality rate
• Increase length of stay and disability
• Systematic approach to identify
potentially reversible etiologies and
prognostic factors
• Increased survival among medical
and surgical.

3.  Concept of extreme
conditions
 Mechanisms of Injury.
Brain injury
 Level of Consciousness
 Coma
 Spinal injury
 Shock

4. Concept of extreme conditions
► Intensive-care medicine or critical-care medicine is a branch of
medicine concerned with the diagnosis and management of life
threatening conditions requiring sophisticated organ support and
invasive monitoring.
► A critically ill patient is one at imminent risk of death; the severity of
illness must be recognised early and appropriate measures taken
promptly to assess, diagnose and manage the illness.
► The approach required in managing the critically ill patient differs
from that required in less severely ill patients with immediate
resuscitation and stabilisation of the patientis condition taking
precedence.
► Priorities are:
hypoglycaemia and dysrhythmias
analysis of the deranged physiology
establishing the complete
diagnosis in stages as further
history and the results of
investigations become available
careful monitoring of the patientis
condition and response to treatment
adhering to advanced life support guidelines and the
principles of cardiorespiratory management
urgent treatment of life-threatening
emergencies such as hypotension
hypoxaemia
hyperkalaemia
prompt resuscitation

5. Mechanisms of Injury
• Injury to brain tissue can result from a number of conditions,
including trauma, tumors, stroke, and metabolic
derangements.
• Brain damage resulting from these disorders involves
several common pathways, including the effects of hypoxia
and ischemia, cerebral edema, and injury caused by
increased intracranial pressure.
• In many cases, the mechanisms of injury are interrelated.

7. BRAIN INJURY
• The brain is protected from external
forces by the rigid confines of the
skull and the cushioning afforded by
the cerebrospinal fluid (CSF).
• The metabolic stability required by its
electricallyactive cells is maintained by
a number of regulatory mechanisms,
including the blood-brain barrier and
autoregulatory mechanisms that
ensure its blood supply.
• Nonetheless, the brain remains
remarkably vulnerable to injury.

8. • One third of all trauma deaths
• 15-45 years of age
• 49%-road traffic accidents,28%-falls,23%-
gun shot injuries and other causes
• Inpatient case fatality rates
all head injuries - 2.6%to6.5%
severe injuries - 15 to 50%
• Good outcome-Glasgow outcome scale of 1or 2
Introduction

9. Category Description % of pts
Good/modera
te
Severe/vegetati
ve
Dead
No CT data 2.3 5.9 0.0 94.1
Diffuse
injury I
No visible pathology on
CT
7.0 61.6 28.8 9.6
Diffuse
injury II
Cisterns visible, shift 0
– 5 mm, no high or
mixed density lesion >
25 cm3
23.7 34.5 52.0 13.5
Diffuse
injury III
(swelling)
Cisterns compressed
or absent, shift 0 – 5
mm, no high or mixed
density lesion > 25 cm3
20.5 16.4 49.7 34.0
Diffuse
injury IV
(shift)
Shift > 5 mm, no high
or mixed density lesion
> 25 cm3
4.3 6.2 37.6 56.2
Evacuated
mass lesion
Any lesion surgically
evacuated
37.0 22.8 38.4 38.8
Nonevacua-
ted mass
High or mixed density
lesion > 25 cm3 not
surgically evacuated
4.8 11.1 36.1 52.8
Brainstem
injury
(no brainstem reflexes
by physical exam)
0.4 0.0 33.3 66.7

10.  Can be minor or serious
 Even small lacerations
can lead to significant
blood loss.
› This blood loss may be
severe enough to
cause hypovolemic
shock.
 They are often an
indicator of deeper,
more serious injuries.

11.  Significant force applied to the head
may cause a skull fracture.
 May be open or closed, depending on
whether there is an overlying laceration
of the scalp
 Injuries from bullets or other
penetrating weapons often result in
skull fractures.
Signs of skull fracture include:
•Patient’s head appears deformed
•Visible cracks in the skull
•Ecchymosis (bruising) that develops
under the eyes (raccoon eyes)
•Ecchymosis that develops behind
one ear over the mastoid process
(Battle’s sign)

12.  Account for about
80% of all skull
fractures
 Radiographs are
often required to
diagnose a linear
skull fracture
because there are
often no physical
signs.
 Linear skull fractures
 Result from high-
energy direct
trauma to the
head with a blunt
object
 Frontal and
parietal bones are
most susceptible
 Bony fragments
may be driven
into the brain
 Compressed skull fractures
 Associated with
high-energy
trauma
 Usually occur
following diffuse
impact to the head
 Signs include CSF
drainage from the
ears, raccoon
eyes, and Battle’s
sign
 Basilar skull fractures
 Result when
severe forces are
applied to the
head
 Often associated
with trauma to
multiple body
systems
 Brain tissue may
be exposed to the
environment
 Open skull fractures

14. Hypoxia and Ischemia
Hypoxia and hypotension are the 2 major causes
of secondary CNS injury following head trauma.
The brain relies on the ability of the cerebral circulation to deliver
sufficient oxygen for its energy needs.
Although the brain makes up only 2% of the body weight, it receives one
sixth of the resting cardiac output and accounts for 20% of the oxygen
consumption.
By definition, hypoxia denotes a deprivation of oxygen with maintained
blood flow and ischemia, a situation of greatly reduced or interrupted
blood flow.
The cellular effects of hypoxia and ischemia are quite different, and the
brain tends to have different sensitivities to the two conditions.
Hypoxia interferes with the delivery of oxygen, and ischemia interferes
with the delivery of oxygen and glucose as well as the removal of
metabolic wastes.

15. Hypoxia and Ischemia
• Hypoxia usually is seen in conditions such as
exposure to reduced atmospheric pressure, carbon
monoxide poisoning, severe anemia, and failure to
oxygenate the blood.
• Contrary to popular belief, hypoxia is fairly well
tolerated, particularly in situations of chronic hypoxia.
• Neurons are capable of substantial anaerobic
metabolism and are fairly tolerant of pure hypoxia; it
commonly produces euphoria, listlessness,
drowsiness, and impaired problem solving.
• Unconsciousness and convulsions may occur when
hypoxia is sudden and severe.
• However, the effects of severe hypoxia (i.e., anoxia)
on brain function seldom are seen because the
condition rapidly leads to cardiac arrest and
ischemia.

16. Hypoxia and Ischemia
• Unconsciousness occurs within seconds of severe global ischemia, such as that
resulting from complete cessation of blood flow, as in cardiac arrest. If circulation is
restored immediately, consciousness is regained quickly. However, if blood flow is
not promptly restored, severe pathologic changes take place.
• Energy sources (i.e., glucose and glycogen) are exhausted in 2 to 4 minutes, and
cellular ATP stores are depleted in 4 to 5 minutes. Approximately 50% to 75% of the
total energy requirement of neuronal tissue is spent on mechanisms for maintenance
of ionic gradients across the cell membrane (e.g., sodium-potassium pump), resulting
in fluxes of sodium, potassium, and calcium ions.
• Excessive influx of sodium results in neuronal and interstitial edema.
• The influx of calcium initiates a cascade of events, including release of intracellular
and nuclear enzymes that cause cell destruction.
Focal ischemia involves a single
area of the brain, as in stroke.
Collateral circulation may provide
low levels of blood flow during focal
ischemia. The residual perfusion
may provide sufficient substrates to
maintain a low level of metabolic
activity, preserving neuronal
integrity.
Global ischemia occurs when
blood flow is inadequate to meet
the metabolic needs of the entire
brain. In contrast to persons with
focal ischemia, those with global
ischemia have no collateral
circulation during the ischemic
event. The result is a spectrum of
neurologic disorders.

17. Hypoxia
and
Ischemia
• Within the brain, certain regions and cell
populations are more susceptible than others to
hypoxic-ischemic injury.
• For example, neurons are more susceptible to
injury than are the glial cells.
• Among the neurons, the pyramidal cells of the
hippocampus, the Purkinje cells of the
cerebellum, and the neurons of the globus
pallidus of the basal ganglia are particularly
sensitive to generalized ischemic-hypoxic
injury.
• The reason for this selectivity is uncertain but
appears to be related at least to some extent on
local levels and metabolism of certain excitatory
neurotransmitters such as glutamate.

18. Cerebral Edema
 Cerebral edema,
or brain swelling,
is an increase in
tissue volume
secondary to
abnormal fluid
accumulation.
 There are
basically two types
of brain edema:
vasogenic or
cytotoxic.

19. Vasogenic Edema
 Vasogenic edema results from an increase in the extracellular fluid
that surrounds brain cells.
 It occurs with conditions such as:
Vasogenic edema occurs primarily in the white matter of the brain,
possibly because the white matter is more compliant than the gray
matter and offers less resistance to fluid accumulation.
Vasogenic edema can be localized, as in the case of abscesses or
neoplasms, or it may be more generalized.
The functional manifestations of vasogenic edema include:
tumors
prolonged
ischemiahemorrhage
infectious processes (e.g., meningitis) that impair
the function of the blood-brain barrier and allow
water and plasma proteins to leave the capillary and
move into the interstitium.
brain injury
focal
neurologic
deficits
disturbances in
consciousness
severe
intracranial
hypertensio

20. Cytotoxic Edema
 Cytotoxic edema involves the swelling of brain cells. It involves an increase in fluid
in the intracellular space, chiefly the gray matter, although the white matter may be
involved.
 Cytotoxic edema can result from hypoosmotic states, such as water intoxication or
severe ischemia, that impair the function of the sodium-potassium membrane pump.
This causes rapid accumulation of sodium in the cell, followed by movement of water
along the osmotic gradient. Depending on the nature of the insult, cellular edema can
occur in the vascular endothelium or smooth muscle cells, astrocytes, the myelin-
forming processes of oligodendrocytes, or neurons.
 Major changes in cerebral function, such as stupor and coma, occur with cytotoxic
edema.
 The edema associated with ischemia may be severe enough to produce cerebral
infarction with necrosis of brain tissue.

22. Cerebral Edema

23. Definition of Terms
 Confusion :
– impaired attention and concentration,
manifest disorientation in time, place
and person, impersistent thinking,
speech and performance, reduced
comprehension and capacity to reason
– Fluctuate in severity, typically worse at
night ‘sundowning’
– Perceptual disturbances and
misinterpret voices, common objects
and actions of other persons
 Confusion is also found in dementia
(progressive failure of language,
memory, and other intellectual
functions)

24. Level of Consciousness
 Alert: normal awake and
responsive state
 Drowsiness: state of apparent
sleep, briefly arousal with oral
command
 Lethargic: resembles
sleepiness, but not becoming
fully alert, slow verbal response
and inattentive. Unable to
adequately perform simple
concentration task (such as
counting 20 to 1)

25. Level of Consciousness
 Somnolent: easily aroused by voice
or touch; awakens and follows
commands; required stimulation to
maintain arousal
 Obtunded/Stuporous: arousable
only with repeated and painful
stimulation; verbal output is
unintelligible or nil; some purposeful
movement to noxious stimulation
 Comatose: no arousal despite
vigorous stimulation, no purposeful
movement - only posturing, brainstem
reflexes often absent

26. Dementia Confusional state
Memory problem
Clouding of
consciousness
Fluctuate
Acute
Varies little
from time to
time
Longstanding
nature
Dementia Confusional state

27. Causes of confusional state
Medical or
surgical disease
• Metabolic disorders
• Hepatic
• Uremic
• Hypo- and
hypernatremia
• Hypercalcemia
• Hypo- and
hyperglycemia
• Hypoxia
• Hypercapnia
 Infectious illness
•Pneumonia
•Endocarditis
•Urinary tract
infection
•Peritonitis
 Congestive heart
failure
 Postoperative and
posttraumatic states
 Drug intoxication
Opiates
Barbiturates
Other sedatives
Diseases of nervous
system
• Cerebrovascular
disease, tumor, abscess
• Subdural hematoma
• Meningitis
• Encephalitis
• Cerebral vasculitis
• Hypertensive
encephalopathy

28. Definition of Terms
COMA - reduced alertness and responsiveness represents
a continuum that in severest form, a deep sleeplike state from
which the patient cannot be aroused.
STUPOR - lesser degrees of unarousability in which the
Patient can be awakened only by vigorous stimuli,
accompanied by motor behavior that leads to avoidance
of uncomfortable or aggravating stimuli.
Drowsiness - which is familiar to all persons,
simulates light sleep and is characterized by easy arousal
and the persistence of alertness for brief periods.
Drowsiness and stupor are usually attended by
some degree of confusion.

29. By definition, coma (decreased
arousal) is produced by:
Bilateral hemispheric damage
Suppression by hypoxia,
hypoglycemia, drugs or toxins
Brain stem lesion or metabolic
derangement that suppresses
Reticular Activating System
(RAS)

30. Level of consciousness
Pattern of breathing (Cheyne-Stokes)
Pupillary changes
Oculomotor responses (ie. Doll’s
eyes)
Motor responses

31. Posturing
 Decorticate
 Flexion of arms,
wrists, fingers
 Adduction of upper
extremities
 Extension of lower
extremities
 Decerebrate
 Extremities in
extension
 Pronation of forearms
and plantar extension
of feet

32. GLASGOW COMA SCORE

33. Mortality
Morbidity
 Brain death – brain stem death – no potential for
recovery – no control of homeostasis
 Cerebral death – death of cerebral hemispheres
not including the brain stem – vegetative state
 Recovery of consciousness
 Residual cognitive dysfunction
 Psychosocial domain
 Vocational domain

34. Prognosis of coma
► Recovery from coma depends primarily on the
causes, rather than on the depth of coma
► Intoxication and metabolic causes carry the best
prognosis
► Coma from traumatic head injury far better than
those with coma from other structural causes
► Coma from global hypoxic-ischemic carries least
favorable prognosis
► At 3rd day, no papillary light reflex or GCS < 5 is
associated with poor prognosis

35. Conditions mimic
coma
• Brain death
• Locked-in syndrome
• Vegetative state
• Frontal lobe disease
• Non-convulsive status epilepticus
• Psychiatric disorder (catatonia,
depression)

36. Vegetative State
Signifies an awake but
unresponsive state. Most of
these patients were earlier
comatose and after a period of
days or weeks emerge to an
unresponsive state in which
their eyelids are open, giving
the appearance of wakefulness.
Yawning, grunting, swallowing,
limb and head movements
persist, but there are few, if
any, meaningful responses to
the external and internal
environment-in essence, an
"awake coma.“
Respiratory and autonomic
functions are retained.
Cardiac arrest and head injury
are the most common causes.

38. Locked-in state Describes a pseudocoma in which
an awake patient has no means of
producing speech or volitional limb,
face, and pharyngeal movements in
order to indicate that he or she is
awake, but vertical eye movements
and lid elevation remain
unimpaired, thus allowing the
patient to signal.
Vertical eye movement and lid
elevation remain unimpaired.
Etiology: infarction or
hemorrhage of the ventral
pons, which transects all
descending corticospinal and
corticobulbar pathways.
Such patients have written entire
treatises using Morse code.

39. Akinetic
mutism
• Partially or fully awake
patient who is able to
form impressions and
think but remains
immobile and mute,
particularly when
unstimulated.
• Causes: damage in the
regions of the medial
thalamic nuclei, the
frontal lobes (particularly
situated deeply or on
the orbitofrontal
surfaces), or from
hydrocephalus.

40. Abulia
• Aboulia or abulia (from the Greek
"αβουλία", meaning "un-will"), in
neurology, refers to a lack of will
or initiative and can be seen as a
disorder of diminished motivation
(DDM).
• Aboulia falls in the middle of the
spectrum of diminished
motivation, with apathy being less
extreme and akinetic mutism
being more extreme than aboulia.
A patient with aboulia is unable to
act or make decisions
independently. It may range in
severity from subtle to
overwhelming. It is also known as
Blocq's disease (which also
refers to abasia and astasia-
abasia).
• Mental and physical slowness and
lack of impulse to activity that is in
essence a mild form of akinetic
mutism with the same anatomic
origins.

41. Catatonia
 Catatonia is a state of neurogenic motor
immobility, and behavioral abnormality manifested
by stupor. It was first described, in 1874, by Karl
Ludwig Kahlbaum in Die Katatonie oder das
Spannungsirresein (Catatonia or Tension Insanity).
 Hypomobile and mute syndrome associated with a major
psychosis.
 Patients appear awake with eyes open but make no
voluntary or responsive movements, although they blink
spontaneously, swallow, and may not appear distressed.
 Eyes are half-open as if the patient is in a fog or light
sleep.
 NO clinical evidence of brain damage.

42. Brainstem Reflexes
pupillary responses to light,spontaneous and elicited
eye movements, corneal responses
PUPILLARY LIGHT RESPONSES:
Simmetrically reactive round
pupils:
Exclude midbrain damage (2 to 5 mm )
Enlarged pupil (>5 mm),
unreactive or poorly reactive:
Intrinsic midbrain lesion (ipsilateral) by mass
effect (contralateral).
Unilateral pupillary enlargement: Ipsilaterall mass.
Oval and slightly eccentric
pupils:
Early midbrain third nerve compression.
Bilaterally dilated and unreactive Severe midbrain damage by transtentorial
pupils: herniation or anticholinergic drugs toxicity.
Reactive bilaterally small but
not pinpoint (1 to 2.5 mm):
Metabolic encephalopathy, deep bilateral
hemispheral lesions as hydrocephalus or
thalamic hemorrhage
Very small but reactive pupil
(Less than 1 mm):
Narcotic or barbiturate overdose or bilateral
pontin damage.

43. Ocular Movements
Eye movements are the second sign of importance in determining
if the brainstem has been damaged.
EYE MOVEMENTS
Adducted eye at rest:
Lateral rectus paresis due to VI nerve lesion. If is
bilateral is due to intracraneal hypertension.
Abducted eye at rest, plus ipsilateral
pupilary enlargement :
Medial rectus due to III nerve dysfunction.
Vertical separation of the ocular Pontin or cerebellar lesion
Globes. (Skew deviation) :
Coma and spontanous conjugate horizontal
roving movements :
Midbrain and pons intact
“Ocular bobbing”. Brisk downward and
slow upward movement of the globes with
loss of horizontal eye movements :
Bilateral pontine damage
“Ocular dipping”. Slower, arrhytmic
downward followed by a faster upward
movement with normal reflex horizontal
gaze :
Anoxic damage to the cerebral cortex.
Thalamic and upper midbrain lesions: Eyes turned down and inward.

44. Brainstem Reflexes
Respiratory pattern
Shallow, slow, well-timed
regular
Suggest metabolic or drug
depression.
Breathing:
Rapid, deep (Kussmaul)
breathing:
Metabolic acidosis or ponto-
mesencephalic lesions.
Cheyne-Stokes breathing, with
light
Mild bihemispherical damage
or metabolic supression.
Coma:
Agonal gasps: Bilateral lower brainstem
damage.
Terminal respiratory pattern.

45. Anatomy and Physiology-
General Structure and Function
Spinal Column:
• Made up of 26 vertebrae stacked
on top of one another
• Divided into 5 areas; cervical,
thoracic, lumbar, sacral, and coccyx
• “Joint” at the superior end of the spinal
“Long Bone” VERY FLEXIBLE:
• Allows flexion, extension, and rotation of
the head
• The head acts as a weighted lever
during acceleration/ deceleration
• Common site of spinal injuries

46.  Bony spinal injuries may or may not be associated with spinal cord injury
 These bony injuries include:
 Compression fractures of the vertebrae
 Comminuted fractures of the vertebrae
 Subluxation (partial dislocation) of the vertebrae
 Other injuries may include:
 Sprains- over-stretching or tearing of ligaments
 Strains- over-stretching or tearing of the muscles
 Cutting, compression, or stretching of the spinal cord
 Causing loss of distal function, sensation, or motion
 Caused by:
 Unstable or sharp bony fragments pushing on the cord, or
 Pressure from bone fragments or swelling that interrupts the blood
supply to the cord causing ischemia

48. Immediate and irreversible loss of sensation and motion
Cutting, compression, or stretching of the spinal cord
Occurs at the time of impact/injury
 Injury Delayed
 Occurs later due to swelling, ischemia, or movement of
sharp or unstable bone fragments
 May be avoided if spine immobilized during extrication,
packaging, treatment, and transport
Incomplete Spinal Cord Injury
Complete injury to specific spinal tracts with reduced
function distally
Other tracts continue to function normally with distal function
intact

49. Mechanism of Injury
 Physical manner and forces
involved in producing injuries
or potential injuries
 Valuable tool in determining if
the a particular set of
circumstances could have
caused a spinal injury
 Mechanisms likely to produce
spinal injuries occur in MVAs,
falls, violence, and sports
(including diving accidents)

51. Hyperextension -
Excessive/abnormal bending back
of the head beyond its normal
range of motion
Hyperflexion - Excessive/abnormal bending
forward of the chin toward the chest. This is
one mechanism seen when patients are
ejected from moving vehicles

52. Flexion injuries
The most common fracture mechanism in cervical
injuries is hyperflexion.
Anterior subluxation occurs when the posterior
ligaments rupture.
Since the anterior and middle columns remain
intact, this fracture is stable.
Simple wedge fracture is the result of a pure
flexion injury. The posterior ligaments remain intact.
Anterior wedging of 3mm or more suggests
fracture. Increased concavity along with increased
density due to bony impaction. Usually involves the
upper endplate.
Unstable wedge fracture is an unstable flexion
injury due to damage to both the anterior column
(anterior wedge fracture) as the posterior column
(interspinous ligament).
Unilateral interfacet dislocation is due to both
flexion and rotation.
Bilateral interfacet dislocation is the result of
extreme flexion. BID is unstable and is associated
with a high incidence of cord damage.
Flexion teardrop fracture is the result of extreme
flexion with axial loading. It is unstable and is
associated with a high incidence of cord damage.
Anterior atlantoaxial dislocation

53. Hyperotation -
Excessive/abnormal
rotation. This may
produce injuries in any
area of the spine.

54. Axial Loading
- Sudden/excessive compression of the
spine. Examples include falling and landing on
your feet or ejection from a vehicle and
landing on your head
Axial compression injuries
 Jefferson fracture is a burst fracture of the
ring of C1 with lateral displacement of both
articular masses.
 Burst fracture at lower cervical level

55. Axial Distraction -
Sudden/excessive elongation of the
spine caused by stretching or
tearing anywhere along the spinal
column. Example: hanging.
This is a hang man’s fracture suffered
by a woman that was ejected from
her car in a roll-over MVA. She
apparently got hung up on the
shoulder belt and got hung.
Lateral radiograph of type II
Hangman's fracture (pars
interarticularis fracture of C2 –
Levine and Effendi's
classification 20,21); it is an
unstable spine because of the
discontinuity of central axial
spinal pillar

58. Shock is a condition in which the cardiovascular
system fails to perfuse tissues adequately
 An impaired cardiac pump, circulatory system,
and/or volume can lead to compromised blood flow
to tissues
 These three parts can
be called the
“perfusion triangle.”
– When a patient is in
shock, one or more of
the three parts is not
working properly.

60. Shock
• Inadequate systemic oxygen delivery
activates autonomic responses to maintain
systemic oxygen delivery
• Sympathetic nervous system
 NE, epinephrine, dopamine, and cortisol release
• Causes vasoconstriction, increase in HR, and increase of cardiac
contractility (cardiac output)
• Renin-angiotensin axis
 Water and sodium conservation and vasoconstriction
 Increase in blood volume and blood pressure

61. Shock
• Cellular responses to decreased systemic oxygen
delivery
• ATP depletion → ion pump dysfunction
• Cellular edema
• Hydrolysis of cellular membranes and cellular death
• Goal is to maintain cerebral and cardiac perfusion
• Vasoconstriction of splanchnic, musculoskeletal, and
renal blood flow
• Leads to systemic metabolic lactic acidosis that
overcomes the body’s compensatory mechanisms

62. Global Tissue Hypoxia
• Endothelial inflammation and disruption
• Inability of O2 delivery to meet demand
• Result:
• Lactic acidosis
• Cardiovascular insufficiency
• Increased metabolic demands

63. Cell death
Inadequate oxygen delivery
Catecholamines and other responses
Anaerobic metabolism
Cellular dysfunction
Generalized State of Hypoperfusion
What is shock?

64. Shock. Kinds of shock.
Mechanisms of disorders of general
hemodynamics and microcirculation at shock.
 Shock is a state of organ hypoperfusion with resultant cellular
dysfunction and death.
 Mechanisms may involve:
decreased circulating volume,
decreased cardiac output,
vasodilation,
sometimes with shunting of blood to bypass capillary exchange beds.
 Symptoms include altered mental status, tachycardia, hypotension,
and oliguria.
 Diagnosis is clinical, including BP measurement and sometimes
markers of tissue hypoperfusion (eg, blood lactate, base deficit).
 Treatment is with fluid resuscitation, including blood products if
necessary, correction of the underlying disorder, and sometimes
vasopressors.

65. STAGES OF SHOCK
 Non-progressive Stage
Reflex compensatory mechanisms are activated.
Profusion of vital organ is maintained
 Progressive Stage
Tissue hypoperfusion.
Circulatory & metabolic imbalances leading to
Acidosis.
 Irreversible Stage
Cellular & tissue injury.
Even with correction of haemodynamic defects,
survival is not possible.

66. Stages of Shock
❇ Initial stage - tissues are under perfused, decreased
CO, increased anaerobic metabolism, lactic acid is
building
❇ Compensatory stage - Reversible. SNS activated
by low CO, attempting to compensate for the decrease
tissue perfusion.
❇ Progressive stage - Failing compensatory
mechanisms: profound vasoconstriction from
the SNS ISCHEMIA Lactic acid production is high
metabolic acidosis
❇ Irreversible or refractory stage - Cellular necrosis
and Multiple Organ Dysfunction Syndrome may occur
DEATH IS IMMINENT!!!!

67.  NEUROHUMORAL MECHANISMS MAINTAIN
CARDIAC OUTPUT AND BLOOD PRESSURE:
 Baroreceptors reflexes
 Release of catecholamine
 Activation of renin-angiotensin axis
 ADH release
 Generalized sympathetic stimulation
 DIFFERENT CLINICAL OUTCOME OF THESE
COMPENSATORY MECHANISMS:
 Tachycardia
 Peripheral vasoconstriction (cool & pale skin)
 Renal conservation of fluid

68.  WIDESPREAD HYPOXIA:
Anaerobic glycolysis
Production of lactic acidosis
pH lead to blunting of vasomotor
response leading to vasodilatation
Peripheral pooling of blood
cardiac output
 DIFFERENT CLINICAL OUTCOME
OF THESE FAILING MECHANISMS:
Feeble, failing pulse
Mental confusion
Urine output
PROGRESSIVE STAGE

69. WIDESPREAD CELLULAR INJURY:
 Damage to the organelle of cells
 Leakage of lysosomal enzymes
 Production of nitric oxide by cells
 Worsened myocardial contractility
DIFFERENT CLINICAL OUTCOME OF
CELLULAR INJURY:
 Septic shock (entry of intestinal flora into
circulation)
 Complete renal shutdown (acute tubular
necrosis)
 Downward clinical spiral
IRREVERSIBLE STAGE

71. COMPENSATORY MECHANISMS:
Sympathetic Nervous System (SNS)-
Adrenal Response
 SNS - Neurohormonal response
Stimulated by baroreceptors
Increased heart rate
Increased contractility
Vasoconstriction (Afterload)
Increased Preload

72. COMPENSATORY MECHANISMS:
Sympathetic Nervous System (SNS)-
Adrenal Response
 SNS - Hormonal: Renin-angiotension
system
Decrease renal perfusion
Releases renin angiotension I
angiotension II potent vasoconstriction &
releases aldosterone adrenal cortex
sodium & water retention ( intravascular
volume)

73. COMPENSATORY MECHANISMS:
Sympathetic Nervous System
(SNS)-Adrenal Response
 SNS - Hormonal: Antidiuretic Hormone
Osmoreceptors in hypothalamus stimulated
ADH released by Posterior pituitary gland
Vasopressor effect to increase BP
Acts on renal tubules to retain water

74. COMPENSATORY
MECHANISMS: Sympathetic
Nervous System (SNS)-Adrenal
Response
 SNS - Hormonal: Adrenal Cortex
Anterior pituitary releases
adrenocorticotropic hormone (ACTH)
Stimulates adrenal Cortex to release
glucorticoids
Blood sugar increases to meet increased
metabolic needs

75. Types of
Shock
• Hypovolemic or
Haematogenic
• Traumatic Shock.
• Septic
• Cardiogenic
• Anaphylactic
• Neurogenic
• Obstructive

77. Complications of Shock
• Acute Respiratory Distress Syndrome

78. Literature:
1. General and clinical pathophysiology / Edited by Anatoliy V. Kubyshkin –
Vinnytsia: Nova Knuha Publishers – 2011. – P. 642–651.
2. Gozhenko A.I. General and clinical pathophysiology / A.I. Gozhenko,
I.P. Gurcalova // Study guide for medical students and practitioners.
Edited by prof. Zaporozan, OSMU. – Odessa. – 2005. – P. 314–320.
3. Essentials of Pathophysiology: Concepts of Altered Health States
(Lippincott Williams & Wilkins), Trade paperback (2003) / Carol Mattson
Porth, Kathryn J. Gaspard. – P. 328 – 336; 725 – 745.
4. Symeonova N.K. Pathophysiology / N.K. Symeonova // Kyiv, AUS
medicine Publishing. – 2010. – P. 531–536.
5. Robbins and Cotran Pathologic Basis of Disease 8th edition./ Kumar,
Abbas, Fauto. – 2007. – Chapter 20. – P. 758–775.
6. Copstead Lee-Ellen C. Pathophysiology / Lee-Ellen C. Copstead,
Jacquelyn L. Banasik // Elsevier Inc, 4th edition. – 2010. – P. 927–930,
936–937.
7. Pathophysiology, Concepts of Altered Health States, Carol Mattson
Porth, Glenn Matfin. – New York, Milwaukee. – 2009. – P. 1299–1453.