This is a presentation on the topic of hemodynamic disorders, thromboembolic diseases and shock, prepared by Dr Ashish Jawarkar, he is MD in pathology and a teacher at Parul institute of Medical sciences and research Vadodara.

1. CH 4
Hemodynamic Disorders,
Thromboembolic Disease,
and Shock
Dr Ashish Jawarkar, MD

2. Overview
• Distribution of body water
• Edema and effusions
• Hyperaemia and congestion
• Haemostasis, haemorrhagic
disorders, thrombosis, DIC
• Embolism
• Infarction
• Shock

3. Distribution of
body water

5. Edema and
effusion
• Definitions
• Mechanism
• Types
• Causes
• Clinical features
• Morphology

6. Edema and Effusion
DEFINITION

7. DEFINITION
• Edema
– Accumulation of fluid in tissues
• Effusion
– Accumulation of fluid in body cavities

8. Edema and Effusion
MECHANISMS

9. Mechanisms
of edema and
effusion

10. MECHANISMS OF EDEMA AND EFFUSION
• Increased hydrostatic pressure
– Increases in hydrostatic pressure are mainly caused by disorders that impair
venous return.
• If the impairment is localized (e.g., a deep venous thrombosis [DVT] in a lower
extremity), then the resulting edema is confined to the affected part.
• Conditions leading to systemic increases in venous pressure (e.g., congestive heart
failure) are associated with more widespread edema
• Reduced plasma colloid oncotic pressure
– Under normal circumstances albumin accounts for almost half of the total
plasma protein; conditions leading to inadequate synthesis or increased loss
of albumin from the circulation are common causes of reduced plasma
oncotic pressure
• Reduced albumin synthesis occurs mainly in severe liver diseases (e.g., end-stage
cirrhosis) and protein malnutrition
• An important cause of albumin loss is the nephrotic syndrome

12. Edema and Effusion
TYPES

13. Types –
Inflammatory
(Exudate)
& Non
inflammatory
(Transudate)
• These protein-rich exudates accumulate due to
increases in vascular permeability caused by
inflammatory mediators.
• Usually, inflammation-associated edema is
localized to one or a few tissues, but in systemic
inflammatory states, such as sepsis, that produce
widespread endothelial injury and dysfunction,
generalized edema may appear
Inflammation-related edema
• protein-poor fluids called transudates
• are common in many diseases, including heart
failure, liver failure, renal disease, and severe
nutritional disorders
Noninflammatory edema and effusions

14. Edema and Effusion
CAUSES

15. Causes

16. Edema and Effusion
CLINICAL FEATURES

17. Clinical
features
Subcutaneous edema –
is important primarily because it signals potential underlying
cardiac or renal disease
Pulmonary edema –
fluid collects in the alveolar septa around capillaries and impede
oxygen diffusion, but edema fluid in the alveolar spaces also
creates a favourable environment for bacterial infection
Pulmonary effusions
often accompany edema in the lungs
Peritoneal effusions (ascites)
resulting most commonly from portal hypertension are prone to
seeding by bacteria, leading to serious and sometimes fatal
infections

18. Edema and Effusion
MORPHOLOGY

19. Morphology
• Gross
1. EDEMA
• Subcutaneous edema - can be diffuse or more
conspicuous in regions with high hydrostatic pressures.
• Dependent edema - Its distribution is often
influenced by gravity (e.g., it appears in the legs
when standing and the sacrum when recumbent)
• Pitting edema - Finger pressure over markedly
oedematous subcutaneous tissue displaces the
interstitial fluid and leaves a depression

20. Morphology
• Edema resulting from renal dysfunction
• periorbital edema - often appears initially
in parts of the body containing loose
connective tissue, such as the eyelids
• Pulmonary edema
• the lungs are often two to three times their
normal weight, and sectioning yields frothy,
blood-tinged fluid—a mixture of air, edema,
and extravasated red cells
• Brain edema
• Narrowed sulci and distended gyri, which
are compressed by the unyielding skull

21. Morphology
2. Effusions
• Transudative effusions are typically protein poor,
translucent and straw coloured
• Chylous effusion -peritoneal effusions caused by
lymphatic blockage which may be milky due to
the presence of lipids absorbed from the gut
• Exudative effusions - are protein-rich and often
cloudy due to the presence of white cells.

22. Morphology
• Microscopy
• Clearing and separation of the
extracellular matrix and subtle cell
swelling

23. Hyperaemia &
Congestion
• Hyperaemia
• Congestion
• Pulmonary congestion –
acute/chronic
• Hepatic congestion –
acute/chronic

24. Hyperemia

25. Hyperaemia
• An active process
• Arteriolar dilation leads to increased blood
flow
• E.g. at sites of inflammation or in skeletal
muscle during exercise
• Affected tissues turn red (erythema) because
of increased delivery of oxygenated blood.

26. Congestion

27. Congestion
• Passive process
• Resulting from reduced outflow of blood
from a tissue
• It can be systemic, as in cardiac failure, or
localized, as in isolated venous obstruction
• Congested tissues take on a dusky reddish-
blue color (cyanosis) due to red cell stasis
and the presence of deoxygenated
haemoglobin

28. Pulmonary
congestion
• Acute pulmonary congestion exhibits
engorged alveolar capillaries, alveolar septal
edema, and focal intra-alveolar
haemorrhage. In
• Chronic pulmonary congestion - the septa
are thickened and fibrotic, and the alveoli
often contain numerous hemosiderin-laden
macrophages called heart failure cells

29. Venous congestion-
LIVER
• Acute hepatic congestion –
• the central vein and sinusoids are distended
• centrilobular hepatocytes may undergo
ischemic necrosis while the periportal
hepatocytes—better oxygenated because of
proximity to hepatic arterioles—may only
develop fatty change.
• Chronic passive hepatic congestion –
• the centrilobular regions are grossly red-
brown and slightly depressed (because of cell
death) and are accentuated against the
surrounding zones of uncongested tan liver
(nutmeg liver)
• Microscopically, there is centrilobular
haemorrhage, hemosiderin-laden
macrophages, and variable degrees of
hepatocyte dropout and necrosis

30. Haemostasis,
Haemorrhagic
disorders and
Thrombosis
• Haemostasis
• Haemorrhagic disorders
• Thrombosis

31. Haemostasis
Definition
• Vasoconstriction
• Primary haemostasis
• Secondary haemostasis
• Clot stabilization and resorption
Events
• Platelets
• Clotting cascade
• Fibrinolysis
• Endothelium
Role of

32. Hemostasis
DEFINITION

33. Definition
Haemostasis is a precisely orchestrated process
that occurs at the site of vascular injury
That culminates in the formation of a blood clot
Involving platelets, clotting factors, and
endothelium
Which serves to prevent or limit the extent of
bleeding

34. Hemostasis
EVENTS

35. Events
1. Arterial
Vasoconstriction
• Occurs immediately,
markedly reduces blood
flow to the injured area
• Mediated by reflex
neurogenic mechanisms
• Augmented by the local
secretion of factors such
as endothelin

36. Events
2. Primary Haemostasis –
formation of platelet
plug (adherence,
activation,
aggregation)
• Disruption of the
endothelium exposes
subendothelial von
Willebrand factor (vWF) and
collagen, which promote
platelet adherence and
activation
• Activation of platelets results
release of secretory granules
• Within minutes the secreted
products recruit additional
platelets, which undergo
aggregation to form a
primary haemostatic plug

37. Events
3. Secondary
Haemostasis –
deposition of fibrin
• Tissue factor is exposed at the
site of injury
• Tissue factor binds and activates
factor VII, setting in motion a
cascade of reactions that
culminates in thrombin
generation
• Thrombin cleaves circulating
fibrinogen into insoluble fibrin,
creating a fibrin meshwork
• This sequence, referred to as
secondary haemostasis,
consolidates the initial platelet
plug

38. Events
4. Clot stabilization and
resorption
• Polymerized fibrin and
platelet aggregates
undergo contraction to
form a solid permanent
plug that prevents further
haemorrhage
• At this stage,
counterregulatory
mechanisms (e.g., tissue
plasminogen activator, t-
PA) are set into motion that
limit clotting to the site of
injury and eventually lead
to clot resorption and
tissue repair.

39. Hemostasis
ROLE OF ……

40. Role of -
Platelets
• Platelets main role is in primary haemostasis
• Their function depends on several glycoprotein
receptors, a contractile cytoskeleton, and two
types of cytoplasmic granules.
1. α-Granules
1. have the adhesion molecule P-selectin on
their membranes
2. contain proteins involved in coagulation, such
as fibrinogen, coagulation factor V, and vWF
3. protein factors that may be involved in
wound healing, such as fibronectin, platelet
factor 4 (a heparin-binding chemokine),
platelet-derived growth factor (PDGF), and
transforming growth factor-β.
2. Dense (or δ) granules
1. contain adenosine diphosphate (ADP) and
adenosine triphosphate, ionized calcium,
serotonin, and epinephrine.

41. Role of –
Platelets
Disorders of
platelet
aggregation

42. Role of – Clotting cascade
• The coagulation cascade is series of amplifying enzymatic reactions
that leads to the deposition of an insoluble fibrin clot

43. Role of –
Coagulation
cascade
PT and aPTT
• PT (Prothrombin time) and aPTT (Activated partial
thromboplastin time) assays are of great utility in
evaluating coagulation factor function in patients
• PT
• Tissue factor, phospholipids, and calcium are added to
plasma and the time for a fibrin clot to form is
recorded
• Assesses the function of the proteins in the extrinsic
pathway (factors VII, X, V, II, and fibrinogen)
• aPTT
• In this assay, clotting of plasma is initiated by addition
of negative charged particles (e.g., ground glass) that
activate factor XII (Hageman factor) together with
phospholipids and calcium, and the time to fibrin clot
formation is recorded.
• Screens the function of the proteins in the intrinsic
pathway (factors XII, XI, IX, VIII, X, V, II, and fibrinogen)

44. Role of –
Coagulation
cascade
Thrombin

45. Role of – Coagulation cascade
Limiting coagulation and fibrinolysis
• Once initiated, coagulation must be restricted to
the site of vascular injury to prevent deleterious
consequences
• Limiting factors
1. Dilution; blood flowing past the site of
injury washes out activated coagulation
factors, which are rapidly removed by the
liver.
2. Negatively charged phospholipids which
are mainly provided by platelets that have
been activated are required for
coagulation, are in short supply
3. fibrinolytic cascade that limits the size of
the clot and contributes to its later
dissolution

46. Role of – Coagulation cascade
Fibrinolytic system
• Fibrinolysis is largely accomplished
through the enzymatic activity of
plasmin which breaks down fibrin
• Plasmin is generated by enzymatic
catabolism of precursor
plasminogen, by t-PA (tissue
plasminogen activator)
• This characteristic makes t-PA a
useful therapeutic agent
• Once activated, plasmin is in turn
tightly controlled by
counterregulatory factors such as α2-
plasmin inhibitor
• An elevated level of breakdown
products of fibrinogen (often called
fibrin split products), most notably
fibrin-derived D-dimers, are a useful
clinical markers of several thrombotic
states

47. Role of Endothelium
• The balance between the anticoagulant
and procoagulant activities of
endothelium often determines whether
clot formation, propagation, or
dissolution occurs
• if injured or exposed to proinflammatory
factors, endothelial cells lose many of
their antithrombotic properties
• Antithrombotic factors include –
• Platelet inhibition
• Anticoagulant effects
• Fibrinolysis effects

48. Haemorrhagic
Disorders
•Defects in primary
haemostasis
•Defects in secondary
haemostasis
•Defects involving small
vessel walls

49. Haemorrhagic
Disorders
Defects in primary haemostasis

50. Defects in primary haemostasis
(platelets defects and von Willebrand disease)
• Present with small bleeds in skin or
mucosal membranes
• These bleeds typically take the form
of
• petechiae, minute 1- to 2-mm
haemorrhages or
• purpura, which are slightly larger (≥3
mm)

51. Haemorrhagic
Disorders
Defects in secondary haemostasis

52. Defects in secondary hemostasis
(coagulation factor defects)
• Present with bleeds into soft tissues (e.g.,
muscle) or joints (hemarthrosis) following
minor trauma
• Particularly characteristic of haemophilia

53. Haemorrhagic
Disorders
Defects involving small vessel walls

54. Defects involving small vessels
• Present with “palpable purpura” and
ecchymoses
• Ecchymoses (sometimes simply called bruises)
are hemorrhages of 1 to 2 cm in size
• Characteristic of systemic disorders that disrupt
small blood vessels (e.g., vasculitis) or that lead
to blood vessel fragility (e.g., amyloidosis,
scurvy)

55. Thrombosis
Virchow
Triad
Morphology
of thrombus
Fate of a
thrombus
Clinical
features

56. Thrombosis
Virchow Triad

57. Virchow’s
Triad

58. 1. Endothelial
injury

59. 2. Alterations
in normal
blood flow
• Normal blood flow is laminar
• Stasis and turbulence therefore
• Promote endothelial activation
• Disrupt laminar flow and bring
platelets into contact with the
endothelium
• Prevent washout and dilution of
activated clotting factors by fresh
flowing blood

60. 3. Hypercoagubility
• Any disorder of the blood that
predisposes to thrombosis

61. Heparin induced
thrombocytopenia
Syndrome (HIT)
• HIT occurs following the administration of
unfractionated heparin, which may induce the
appearance of antibodies against heparin and
platelets
• Binding of these antibodies to platelets results
in their activation, aggregation, and
consumption (hence the thrombocytopenia)
• This effect on platelets and endothelial damage
induced by antibody binding combine to
produce a prothrombotic state, even in the face
of heparin administration
• Low-molecular-weight heparin preparations
induce HIT less frequently

62. Anti
phospholipid
antibody
syndrome
• Most important pathologic effects of antibodies are
mediated through binding of to epitopes on protein
antigens that are somehow induced or “unveiled” by
phospholipids
• In APLA, suspected antibody targets include β2-
glycoprotein I, a plasma protein that associates with the
surfaces of endothelial cells
• In vivo, it is suspected that these antibodies induce a
hypercoagulable state through uncertain mechanisms.
• This syndrome (previously called the lupus anticoagulant
syndrome) has protean clinical manifestations, including
• recurrent thromboses,
• repeated miscarriages,
• cardiac valve vegetations, and
• thrombocytopenia.
• The antibodies also frequently give a false-positive
serologic test for syphilis because the antigen in the
standard assay is embedded in cardiolipin.

64. Thrombosis
Morphology of a thrombus

65. Morphology
of thrombus
• Arterial or cardiac thrombi
• usually begin at sites of turbulence or
endothelial injury, whereas
• Venous thrombi
• characteristically occur at sites of
stasis.

66. Morphology of thrombus
Arterial thrombi Venous thrombi
Begin at the site of turbulence Occurs at site of stasis
Grow retrograde (towards heart) Extend in direction of blood flow (towards
heart)
Arterial thrombi are occlusive Venous thrombi are also occlusive
consist of a friable meshwork of platelets, fibrin,
red cells, and degenerating
Leukocytes, superimposed on a ruptured
atherosclerotic plaque
tend to contain more enmeshed red cells (and
relatively few platelets) and are therefore
known as red, or stasis,
thrombi.
Most common sites in decreasing order of
frequency are the coronary, cerebral, and
femoral arteries
veins of the lower extremities are most
commonly involved (90% of cases); however,
upper extremities, periprostatic plexus, or the
ovarian and periuterine veins

68. Morphology
of thrombus
• Antemortem thrombi
• Have grossly and microscopically apparent
laminations called lines of Zahn, which are
pale platelet and fibrin deposits alternating
with darker red cell–rich layers
• focally attached to the underlying vascular
surface
• Postmortem thrombi
• gelatinous and have a dark red dependent
portion where red cells have settled by
gravity and a yellow “chicken fat” upper
portion,
• usually not attached to the underlying
vessel wall.

69. Morphology of thrombus
Mural thrombi
• Occurring in heart chambers or in the
aortic lumen
• Due to
• Abnormal myocardial contraction
(arrhythmias, dilated cardiomyopathy, or
myocardial infarction)
• Endomyocardial injury (myocarditis or
catheter trauma)
• Ulcerated atherosclerotic plaque and
aneurysmal dilation

71. Morphology
of thrombus

72. Thrombosis
Fate of a thrombus

73. Fate of
thrombus

74. Thrombosis
Clinical features

75. Clinical
features
Arterial and
cardiac thrombi
Deep vein
thrombosis

76. Arterial and
cardiac
thrombi
Arterial thrombi
• The chief clinical problem is more related
to occlusion of a critical vessel (e.g., a
coronary or cerebral artery)
• They can also embolize and cause
downstream infarctions
Venous thrombi
• Venous thrombi can cause painful
congestion and edema distal to an
obstruction
• mainly of concern due to their tendency
to embolize to the lungs

77. Disseminated
Intravascular
Coagulation

78. Disseminated intravascular
coagulation (DIC)
• Disorders ranging from obstetric complications to advanced
malignancy to sepsis can cause DIC
• DIC leads to widespread formation of thrombi in the
microcirculation.
• These microvascular thrombi can cause diffuse circulatory
insufficiency and organ dysfunction, particularly of the brain,
lungs, heart, and kidneys.
• To complicate matters, thrombosis “uses up” platelets and
coagulation factors (hence the synonym consumptive
coagulopathy) and often activates fibrinolytic mechanisms.
• Thus, symptoms initially related to thrombosis can evolve into a
bleeding catastrophe, such as haemorrhagic stroke or
hypovolemic shock.

80. Embolism
• Definition
• Types
• Pulmonary
• Systemic
• Fat and marrow
• Air
• Decompression sickness
• Amniotic fluid

81. Embolism
Definition

82. Embolism
• Detached intravascular solid, liquid, or gaseous mass
• That is carried by the blood from its point of origin to a
distant site
• Where it often causes tissue dysfunction or infarction

83. Embolism
Types

84. Pulmonary embolism
• Pulmonary emboli originate from deep venous
thromboses
• Are carried through progressively larger veins and the
right side of the heart before slamming into the
pulmonary arterial vasculature.
• Depending on the size of the embolus, it can occlude
• Main pulmonary artery,
• Straddle the pulmonary artery bifurcation (saddle embolus),
• Pass out into the smaller, branching arteries
• Most pulmonary emboli (60% to 80%) are clinically
silent
• Sudden death, right heart failure (cor pulmonale), or
cardiovascular collapse occurs when emboli obstruct
60% or more of the pulmonary circulation

85. Systemic thromboembolism
• Most systemic emboli (80%) arise from intracardiac mural thrombi
• Arterial emboli can travel to a wide variety of sites; the point of arrest
depends on the source and the relative amount of blood flow that
downstream tissues receive
• Most come to rest in the lower extremities (75%) or the brain (10%)

86. Fat and marrow embolism
• After fractures of long bones /soft tissue trauma/burns
• Microscopic fat globules can be found in the pulmonary
vasculature
• Most cases are asymptomatic
• Fat embolism syndrome is the term applied when it is
symptomatic
• It is characterized by pulmonary insufficiency, neurologic symptoms, anemia
(rbc in fat emboli), and thrombocytopenia (platelets in fat emboli), and is fatal
in about 5% to 15% of cases.

87. Air embolism
• Air can be inadvertently introduced in circulation
• during obstetric or laparoscopic procedures
• consequence of chest wall injury
• Gas bubbles within the circulation can coalesce to form
frothy masses that obstruct vascular flow and cause distal
ischemic injury
• A larger volume of air, generally more than 100 cc, is
necessary to produce a clinical effect

88. Decompression
sickness

89. Amniotic fluid embolism
• Ominous complication of labour and the immediate
postpartum period.
• The underlying cause is the infusion of amniotic fluid or
fetal tissue into the maternal circulation via a tear in the
placental membranes or rupture of uterine veins

90. Infarction
• Definition
• Causes
• Types
• Morphology
• Factors influencing infarct
development

91. Infarction
Definition

92. Infarction
• An area of ischemic necrosis caused by
occlusion of either the arterial supply or the
venous drainage
• Examples
• Myocardial infarction following
atherosclerosis of coronary arteries
• Cerebral infarction (stroke) following DVT
• Pulmonary infarction following DVT
• Bowel following DVT
• Ischemic necrosis of the extremities
(gangrene) in diabetics

93. Infarction
Causes

94. Causes
• Arterial
• Thrombosis or embolism
• Atherosclerosis
• Local vasospasm like Raynaud’s phenomenon
• Haemorrhage into an atheromatous plaque
• Extrinsic vessel compression (e.g., by tumour)
• Torsion of a vessel (e.g., in testicular torsion or bowel volvulus)
• Traumatic vascular rupture
• Vascular compromise by edema (e.g., anterior compartment
syndrome)
• Entrapment in a hernia sac
• Venous
• Although venous thrombosis can cause infarction, the more common
outcome is just congestion
• Infarcts caused by venous thrombosis are more likely in organs with a
single efferent vein (e.g., testis and ovary).

95. Infarction
Types

96. Types
Red infarcts White infarcts
Seen in tissues with
(1) with venous occlusions(e.g.,
testicular torsion),
(2) in loose, spongy tissues (e.g.,
lung) where blood can collect in
the infarcted zone,
(3) in tissues with dual circulations
(e.g., lung and small intestine)
that allow blood to flow from an
unobstructed parallel supply into
a necrotic zone,
(4) in tissues previously congested by
sluggish venous outflow
(5) when flow is re-established to a
site of previous arterial occlusion
and necrosis (e.g., following
angioplasty of an arterial
obstruction)
occur with arterial occlusions in solid
organs with end-arterial circulation
(e.g., heart, spleen, and kidney), and
where tissue density limits the
seepage of
blood from adjoining capillary beds
into the necrotic area.

97. Infarction
Morphology

98. Morphology
• Gross
• Wedge-shaped
• with the
occluded vessel
at the apex and
the periphery of
the organ
forming the base
• When the base is a
serosal surface
there may be an
overlying fibrinous
exudate.

99. Morphology
• Microscopy
• Ischemic coagulative
necrosis
• Acute inflammation is
present along the margins of
infarcts
• Most infarcts are ultimately
replaced by scar

100. Infarction
Factors influencing infarct development

101. Factors influencing infarct development
Anatomy of the vascular supply
• The availability of an alternative blood supply
• Lungs and liver have a blood supply that protects against infarction.
• In contrast, renal and splenic circulations are end-arterial, and vascular obstruction generally causes tissue death.
Rate of occlusion
• Slowly developing occlusions are less likely to cause infarction, because they provide time for development of collateral
pathways
Tissue vulnerability to hypoxia
• Neurons undergo irreversible damage when deprived of their blood supply for only 3 to 4 minutes.
• Myocardial cells die after 20 to 30 minutes of ischemia
• In contrast, fibroblasts within myocardium remain viable even after many hours of ischemia
Hypoxemia
• Understandably, abnormally low blood O2 content (regardless of cause) increases both the likelihood and extent of
infarction

102. Shock
• Definition
• Types
• Pathogenesis
• Stages
• Morphology
• Clinical features

103. Shock
Definition

104. Shock
• Shock is a state in which diminished
cardiac output or reduced effective
circulating blood volume impairs
tissue perfusion and leads to cellular
hypoxia

105. Shock
Types

106. • Neurogenic shock - in the setting of an anaesthetic accident or a spinal cord injury
• Anaphylactic shock - IgE–mediated hypersensitivity reaction
• In both of these forms of shock, acute vasodilation leads to hypotension and tissue
hypoperfusion.
Shock - Types

107. Shock
Pathogenesis

108. Pathogenesis (septic shock)
• With a mortality rate exceeding 20%, septic shock ranks first among the
causes of death in intensive care units
• Its incidence is rising, ironically due to
• improvements in life support for critically ill patients
• growing ranks of immunocompromised hosts (due to chemotherapy,
immunosuppression, advanced age or HIV infection)
• the increasing prevalence of multidrug resistant organisms in the hospital
setting
• Septic shock is most frequently triggered by gram-positive bacterial infections,
followed by gram-negative bacteria and fungi

110. Shock
Clinical features

111. Stages of shock
1. An initial non-progressive phase during
which reflex compensatory
mechanisms are activated and
perfusion of vital organs is maintained
2. A progressive stage characterized by
tissue hypoperfusion and onset of
worsening circulatory and metabolic
imbalances, including lactic acidosis
3. An irreversible stage that sets in after
the body has incurred cellular and
tissue injury so severe that even if the
hemodynamic defects are corrected,
survival is not possible

112. Morphology
• The cellular and tissue changes induced by shock are essentially those of hypoxic
injury
• Adrenal gland - cortical cell lipid depletion
• Kidneys - acute tubular necrosis
• Lungs - diffuse alveolar damage
• Brain, heart, lungs, kidney, adrenal glands, and gastrointestinal tract - Fibrin-
rich microthrombi, particularly in the– due to disseminated intravascular
coagulation
• Petechial haemorrhages on serosal surface and the skin – due to consumption
of platelets and coagulation factors

113. Shock
Stages

114. Clinical features
• Patient presents with hypotension; a
weak, rapid pulse; tachypnoea; and
cool, clammy, cyanotic skin
• Rapidly, however, shock begets
cardiac, cerebral, and pulmonary
dysfunction, and eventually
electrolyte disturbances and
metabolic acidosis