This document discusses hemodynamic disorders and provides details on several topics: 1. It defines edema as excess fluid in the interstitial space and describes different types of edema like pulmonary and brain edema. 2. It explains thrombosis as the pathologic formation of an intravascular blood clot, which most commonly occurs in the deep veins of the leg. The pathogenesis of thrombosis involves endothelial injury, turbulence or stasis of blood flow, and hypercoagulability. 3. Locations of thrombus formation are discussed, noting the most common sites for arterial thrombi like the coronary and cerebral arteries, and venous thrombi which most often affect the lower extremities.

1. HEMODYNAMIC
DISORDERS

2. CHAPTER OUTLINE
 Introduction
 Edema
 Hyperemia & congestion
 Hemostasis
 Hemorrhage
 Thrombosis
 Embolism
 Infarction
 Shock

3. INTRODUCTION
 The health of cells and tissues depends on the circulation of blood,
which delivers oxygen and nutrients and removes wastes generated
by cellular metabolism.
 Under normal conditions fluid exchange occur in capillary beds,
 Proteins in the plasma are retained within the vasculature and
 there is little net movement of water and electrolytes into the
tissues.
 This balance is often disturbed by pathologic conditions that
collectively called hemodynamic disorders.

4. EDEMA
 Definition: Presence of excess fluid in the interstitial space (the space
between cells).
 Depending on the site, fluid accumulation in body cavities can be
variously designated as:
a. Subcutaneous edema – excessive fluid accumulation in the subcutaneous
tissue.
b. Pulmonary edema – excessive fluid accumulation in the lung interstitial
space.
c. Brain edema - excessive fluid accumulation in the brain interstitial space.
d. Generalized edema: excessive interstitial fluid accumulation allover the body
e. Anasarca – is a severe & generalized edema of the body with profound
subcutaneous swelling.
f. Effusion: Excess fluid within the body cavities

5. EDEMA…

6. Effusion
 Definition: excess fluid within the body cavities.
a. Pleural effusion – excess fluid accumulation in pleural cavity.
b. Pericardial effusion – excess fluid accumulated in the pericardial cavity.
c. Ascites – fluid accumulation in peritoneal cavity.
 Classification: Transudative versus Exudative
 Transudative effusion
 Edema fluid with low protein content
 Specific gravity <1.020
 Commonly caused by heart failure, cirrhosis, nephrotic syndrome…
 Exudative effusion
 Edema fluid with high protein content and cells
 Specific gravity> 1.020
 Types of exudative effusions: Purulent (pus), Fibrinous, Eosinophilic, Hemorrhagic
 Commonly associated with bacterial infections and cancer.

7. Effusion…
Ascites Pleural effusion

8. Clinical classification of edema
Generalized edema
 Heart failure
 Nephrotic syndrome
 Renal failure
 Liver cirrhosis
 Malnutrition
Localized edema
 Pulmonary edema
 Brain edema
 Lymphedema
 Deep venous thrombosis
can also cause local
edema.

9. Mechanisms of edema
1. Increased capillary
hydrostatic pressure
2. Decreased colloid
osmotic pressure
(Hypoproteinemia)
3. Increased endothelial
permeability
4. Lymphatic obstruction
(lymphedema)

10. Common causes of edema
 Increased capillary hydrostatic pressure: Congestive heart failure (CHF),
Portal hypertension (e.g. liver cirrhosis), Renal failure, Venous thrombosis
(local edema)
 Decreased colloid osmotic pressure (Hypoproteinemia): Liver disease,
Nephrotic syndrome, Protein deficiency (e.g., Kwashiorkor, Protein loosing
enteropathy)
 Increased endothelial permeability: Inflammation, Type I hypersensitivity
reactions, Drugs (e.g.,bleomycin, heroin, etc.)
 Lymphatic obstruction (lymphedema): Tumor, Surgical removal of lymph
node drainage, Parasitic infestation (filariasis/elephantiasis)

11. Congestive heart failure (CHF)
 Structural and/or functional
impairment of the heart
which result defective
ventricular filling or ejection
of blood which intern result
in edema, fatigue, shortness
of breath…
 One of the most common
causes generalized edema
 Edema in CHF is due to
increased capillary
hydrostatic pressure.

12. Mechanism (Pathogenesis) of edema in HF

13. Nephrotic syndrome
 Nephrotic syndrome is renal (kidney) disorder
characterized by heavy proteinuria (protein excretion
greater than 3.5 g/24 hours), hypoalbuminemia (less
than 3.0 g/dL), and peripheral edema.
 It is one of the most common causes of generalized
edema in children.
 The underlying mechanism of edema in nephrotic
syndrome is decreased plasma oncotic pressure due to
hypoalbuminemia followed by other mechanisms.

14. Mechanism of edema in nephrotic
syndrome

15. Brain edema ( Edema of the brain)
 Definition: excessive fluid accumulation
in the brain interstitial space.
 Can be localized or generalized
 The most feared complication of brain
edema is herniation
 Pathophysiology: Edema → ↑ ICP →
herniation → compression of vital centers
→ death of the patient.
 Morphology: Narrowed sulci & distended
gyri.

16. Pulmonary edema
• Definition: excessive fluid accumulation
in the lung interstitial space.
 Usually occurs in left ventricular failure.
 May also occur in adult respiratory
distress syndrome (ARDS).
 Gross: The lungs often are two to three
times their normal weight, and sectioning
shows frothy, sometimes blood-tinged.
 Microscopy: consisting of a mixture of
edema fluid, and extravasated red cells.

17. Lymphedema (lymphatic edema)
 The lymphatic system returns the
small amount of proteinaceous fluid
from the interstisium to the circulation.
 Obstruction of lymphatic channels due
to various causes leads to the
accumulation of the proteinaceous
fluid in the interstitiuml
(lymphedema/lymphatic edema).
 Common causes of lymphatic
obstruction include parasitic
infection e.g. filariasis, neoplastic
infiltration (e.g. breast cancer), surgical
resection or irradiation.

18. HYPERMIA AND CONGESTION
 Definition: Hypermia and congestion can be
defined as a local increase in volume of blood
in a particular tissue.

19. Hypermia
 Is an active process resulting
from an increased inflow of
blood into a tissue because of
arteriolar vasodilation.
 commonly occurs in exercising
skeletal muscle or acute
inflammation.
 Affected tissue becomes red
as there is engorgement with
oxygenated blood.

20. Congestion
 Is a passive process resulting from impaired outflow of blood
from a tissue.
 occurs systemically as in cardiac failure or locally as in isolated
venous obstruction.
 Affected tissue appears blue-red due to accumulation of
deoxygenated blood.
 In long-standing congestion (also called chronic passive
congestion states), poorly oxygenated blood causes hypoxia →
results in parenchyma cell degeneration or cell death.

21. a) Pulmonary congestion
 Can be acute or chronic
 Cut surface: hemorrhagic & wet.
 1. Acute pulmonary congestion:
 Alveolar capillaries engorged with
blood
 Septal edema
 2. Chronic pulmonary congestion:
 Thickened & fibrotic septa
 hemosiderin-laden macrophages
(heart failure cells)
 Can result in pulmonary
hypertension.

22. b) Hepatic congestion
 Caused by obstruction of hepatic venous
outflow e.g. heart failure.
 1) Acute hepatic congestion:
 Central vein & sinusoids are distended
 There may be even central hepatocyte
degeneration.
 Peripheral hepatocytes better oxygenated
& develop only fatty changes.
 2) Chronic passive congestion of liver:
 Central lobules grossly depressed because
of loss of cells & appear red brown
(nutmeg liver).
 Hemosiderin laden macrophages
 In longstanding hepatic congestion,
commonly associated with cardiac failure,
there is a grossly evident hepatic fibrosis
called cardiac cirrhosis

23. HEMOSTASIS
 Hemostasis is the process of blood clot formation at the site
of vessel injury, which serves to prevent or limit the extent
of bleeding.
 When a blood vessel wall is disrupted, the hemostatic
response must be quick, localized, and carefully regulated.
 Components of hemostasis:
 platelets,
 clotting factors, and
 endothelium

24. Steps of hemostasis
a. Arteriolar vasoconstriction
b. Primary hemostasis (
formation of the platelet
plug)
c. Secondary hemostasis
(deposition of fibrin).
d. Clot stabilization and
resorption.

25. a. Arteriolar vasoconstriction
 Arteriolar vasoconstriction occurs immediately and
markedly reduces blood flow to the injured area.
 It is mediated by reflex neurogenic mechanisms and
augmented by the local secretion of factors such as
endothelin*
 This effect is transient, however, and bleeding would
resume if not for activation of platelets and
coagulation factors.

26. b. Primary hemostasis (Platelet plug formation ).
 Platelet plug formation occur in three steps
1. Platelet adhesion: Platelets adhere to the exposed subendothelial
matrix (directly or indirectly via vWf).
2. Platelet activation: Activation of platelets results in a dramatic shape
change (from small rounded discs to flat plates with spiky protrusions,
as well as the release of secretory granules by which they recruit
additional platelets,
3. Platelet plug formation: Fibrinogen forms bridges between activated
platelets by attaching with a receptor called GP IIb/IIIa complex to form
the platelet plug.

27. c. Secondary hemostasis (formation and
deposition of fibrin)
 Characterized by the sequential activation of a series of inactive
precursor proteins (procoagulants) to active proteins
(coagulants/clotting factors), culminating in conversion of
fibrinogen to fibrin which enmeshes and reinforces the platelet
plug.
 All of the procoagulants are synthesized in the liver except VWF,
which is synthesized in megakaryocytes and endothelial cells.
 Traditionally, the clotting cascade is depicted as consisting of an
intrinsic and extrinsic pathway.

28. c. Secondary hemostasis (formation and
deposition of fibrin)

29. b. Secondary hemostasis (deposition of fibrin)…

33. HAEMORRHAGE (BLEEDING)
 Definition: Hemorrhage (bleeding) is
extravasation of blood outside the blood
vessel.
 Can be internal (concealed) or external
(revealed).

34. Causes of hemorrhage
 Physical trauma – Stabbing, Stick injury,
Gunshot, Motor vehicle accident
 Pregnancy and delivery complications:
Placental abruption, uterine atony, uterine
rupture, cervical and vaginal tears…
 Bleeding disorders…

35. Disorders of hemostasis (Bleed disorders)

36. Clinical features of internal bleeding
 Hematoma: Haemorrhage enclosed within a tissue or a cavity is
known as hematoma.
 Bruise: accumulation of blood in subcutaneous tissue
 Petechiae: Minute 1-2 mm hemorrhages occurring in the skin,
mucosal membrane, or serosal surface.
 Purpura: Slightly > 3mm hemorrhage occurring in the skin.
 Eccymosis (bruises): Larger than 1-2cm subcutaneous
hematoma. It is typical after trauma.

37. THROMBOSIS
 Pathologic formation of an intravascular
blood clot (thrombus)
 Can occur in an artery or vein
 Most common location is the deep veins of
the leg below the knee which is called DVT.

38. Pathogenesis
 There are three factors
that predispose to
thrombus formation.
 These factors are called
Virchow’s triad:
 A: Endothelial injury
 B: Stasis or turbulence of
blood flow
 C: Blood hypercoagulability

39. A: Endothelial injury
 It is the most important factor in thrombus formation and by itself can lead to
thrombosis.
 Endothelial injury is particularly important in thrombus formation in the heart
& arterial circulation.
 Causes of endothelial injury include physical injury, infectious agents, abnormal
blood flow, inflammatory mediators, metabolic abnormalities, such as
hypercholesterolemia or homocystinemia, and toxins absorbed from cigarette smoke.
 Irrespective of the cause, the final event is exposure of the highly
thrombogenic subendothelial extracellular matrix, mainly collagen & tissue
factors up on which platelets undergo adherence & contact activation.

40. B: Turbulence or Stasis blood flow
 Under physiologic conditions normal blood flow is laminar, that is,
the cellular elements flow centrally in the vessel lumen separated
from endothelium by slowing moving clear zone of plasma.
 Stasis & turbulence therefore:
 Both promote endothelial cell activation and enhanced
procoagulant activity, in part through flow-induced changes in
endothelial gene expression.
 Stasis allows platelets and leukocytes to come into contact with
the endothelium when the flow is sluggish.
 Stasis also slows the washout of activated clotting factors and
impedes the inflow of clotting factor inhibitors.

41. B: Turbulence or Stasis blood flow…
 Stasis is a major factor in the development of venous thrombi
 while turbulence contributes to arterial & cardiac thrombosis by causing direct
endothelial injury or by forming countercurrents & local pockets of stasis.
 Causes of vascular stasis and turbulence include
a. Ulcerated atherosclerotic plaques not only expose subendothelial ECM but also cause
turbulence.
b. Abnormal aortic and arterial dilations called aneurysms create local stasis and
consequently are fertile sites for thrombosis.
c. Acute myocardial infarction results in focally noncontractile myocardium.
d. Ventricular remodeling after more remote infarction can lead to aneurysm formation.
e. Mitral valve stenosis (e.g., after rheumatic heart disease) results in left atrial dilation and
atrial fibrilation.

42. C: Hypercoagulablity
 Hypercoagulability is any alteration of the coagulation
pathway that predisposes to thrombosis.
 Hypercoagulability is a less common cause of
thrombosis & it can be divided into:
a. Primary (Genetic): Mutations in factor V[Lieden factor], Anti
thrombin III deficiency, Protein C or S deficiency…
b. Acquired: Prolonged bed rest or immobilization, Myocardial
infarction, Atrial fibrillation, Tissue injury (surgery, fracture,
burn), Cancer

43. Locations of thrombi formation.
 Thrombi may develop any where in the
cardiovascular system.
 According to their location, thrombi can be
divided into venous & arterial thrombi.
 Cardiac thrombi can be considered as arterial
thrombi because of certain similarities
between the two).

44. Locations of thrombi formation…
 The most common site of arterial thrombi in descending order are:
 o Coronary arteries
 o Cerebral arteries
 o Temporal arteries
 Thrombi occurring in heart chambers or in the aortic lumen are designated as mural thrombi.
 Mural thrombi is common on the heart valves & in the auricular appendages (especially, of the
right atrium).
 The veins of the lower extremities are most commonly affected (90% of venous thromboses);
 however, venous thrombi also can occur in the upper extremities, periprostatic plexus, or
ovarian and periuterine veins, and
 under special circumstances they may be found in the dural sinuses, portal vein, or hepatic
vein.

45. Morphology of thrombus
 Firmly attached to the wall of
the vessel
 Thrombi can have grossly (and
microscopically) apparent
laminations called lines of
Zahn.
 these represent pale platelet
and fibrin layers alternating
with darker red cell–rich layers.

46. Fates of a thrombus
1. Propagation: The thrombus enlarges through the accretion of additional
platelets and fibrin, increasing the odds of vascular occlusion or
embolization.
2. Embolization: Part or all of the thrombus is dislodged and transported
elsewhere in the vasculature.
3. Dissolution: If a thrombus is newly formed, activation of fibrinolytic factors
may lead to its rapid shrinkage and complete dissolution.
4. Organization and recanalization: Older thrombi become organized by the
ingrowth of endothelial cells, smooth muscle cells, and fibroblasts. Later
recanalized and reestablish the continuity of the original lumen.

47. Clinical significance of thrombi
 Thrombi are significant clinically because:
 They cause obstruction of arteries and veins &
 They are possible source of thromboemboli.

48. A. Venous Thrombosis (Phlebothrombosis)
 Venous thrombosis affects veins of the lower
extremity in 90% of cases.
 It can be divided into superficial & deep vein
thrombosis:

49. 1. Superficial venous thrombosis
 Usually occurs in saphenous venous
system, particularly when there are
varicosities.
 Rarely embolizes
 Causes local edema, pain, and
tenderness (i.e. it is symptomatic)
 Local edema due to impaired venous
drainage predisposes the involved
overlying skin to infection after slight
trauma leading to a condition known as
varicose ulcer.

50. 2. Deep venous thrombosis (DVT)
 Usually starts in deep veins
within the calf muscles.
 They are entirely
asymptomatic in approximately
50% of patients.
 Has higher incidence in middle
aged & elderly people.
 May embolize to the lung,
hence, is more serious than
superficial venous thrombosis.

51. B. Arterial Thrombosis
 In western society atheroma is by far the commonest predisposing
lesion for arterial thrombosis.
 Atheromatous plaques produce turbulence and may ulcerate & cause
endothelial injury, both of which can lead to thrombosis.
 Common arteries involved are the coronary and cerebral arteries.
 Occlusion of these arteries will lead to myocardial infarction (MI) &
cerebral infarction respectively.
 Arterial thrombi may also embolize to brain, kidney or other organs to
cause obstruction and infarction.

52. C. Cardiac thrombosis (mural thrombosis)
 Cardiac thrombi can be caused by infective endocarditis, atrial
dilatation, atrial fibrillation,& myocardial infarction.
 Cardiac thrombosis is common on the heart valves & in the auricular
appendages (especially, of the right atrium).
 Two thirds of intracardiac mural thrombi are associated with left
ventricular wall infarcts and another quarter with dilated left atria
secondary to rheumatic valvular heart disease.
 The remaining (20%) of systemic emboli arise from aortic aneurysm,
thrombi on ulcerated athrosclerotic plaques, or fragmentation of valvular
vegetation.

53. EMBOLISM
 An embolus is a 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.

54. Causes of embolism
 The vast majority (99%) of emboli derive from a
dislodged thrombus (called thromboembolism).
 Less commonly, emboli are composed of
 fat droplets (fat embolism),
 bubbles of air or nitrogen (air embolism),
 atherosclerotic debris (cholesterol emboli),
 tumor fragments (tumor embolism),
 amniotic fluid (amniotic fluid embolism).

55. Thromboembolism
 a) Pulmonary thromboembolism (PTE)
 b) Systemic thromboembolism
 c) Paradoxical embolism thromboembolism

56. a) Pulmonary thromboembolism (PTE)
 PTE is refers to the impaction of an embolus in the pulmonary arteries
& their branches.
 Such an embolus is derived from a thrombus in the systemic veins or
the right side of the heart.
 95% of PTE arise from the deep leg veins (DVT).
 The thromboembolus will travel along with the venous return & reach
the right side of the heart.
 From there, it will go into the pulmonary trunk & pulmonary arteries.

57. a) Pulmonary thromboembolism (PTE)…
 Depending on the size of the embolus and on the state of pulmonary
circulation, the pulmonary embolism can have the following effects:
 Most pulmonary emboli (60%–80%) are small and clinically silent.
 At the other end of the spectrum, a large embolus that blocks a major pulmonary
artery can cause sudden death.
 Embolic obstruction of medium-sized arteries and subsequent rupture of
downstream capillaries rendered anoxic can cause pulmonary hemorrhage.
 Embolism to small end-arteriolar pulmonary branches usually causes infarction.
 Multiple emboli occurring through time can cause pulmonary hypertension and
right ventricular failure (corpulmonale).

58. b) Systemic thromboembolism
 Systemic thromboembolism refers to emboli
travelling within arterial circulation & impacting in the
systemic arteries.
 Most systemic emboli (80%) arise from intracardiac
mural thrombi.
 Unlike venous emboli, which tend to lodge primarily
in one vascular bed (the lung), arterial emboli can
travel to a wide variety of sites.

59. b) Systemic thromboembolism…
 The major sites for arteriolar embolization are the lower
extremities (75%) & the brain (10%), with the rest lodging in
the intestines, kidney, & spleen.
 The emboli may obstruct the arterial blood flow to the tissue
distal to the site of the obstruction.
 This obstruction may lead to infarction (death of the tissue).
 The infarctions, in turn, will lead to different clinical features
which vary according to the organ involved.

60.  Paradoxic embolism
 Fat Embolism
 Air embolism
 Amniotic fluid embolism

61. INFARCTION
 An infract is an area of ischemic necrosis caused by occlusion
of either the arterial supply or venous drainage in a particular
tissue.
 Infarction primarily affecting the heart and the brain is a common
and extremely important cause of clinical illness.
 Other organs infarction such as pulmonary infarction is a common
clinical complication, bowel infarction often is fatal, and ischemic
necrosis of distal extremities (gangrene) causes substantial
morbidity in the diabetic population.

62. Causes of infarction.
 Arterial thrombosis or arterial embolism underlies the vast majority
of infarctions.
 Less common causes of arterial obstruction include
 vasospasm,
 expansion of an atheroma secondary to intraplaque hemorrhage, and
 extrinsic compression of a vessel by tumor, a dissecting aortic aneurysm, or
edema within a confined space (e.g., in anterior tibial compartment syndrome).
 Other uncommon causes of tissue infarction include vessel twisting
(e.g., in testicular torsion or bowel volvulus), traumatic vascular
rupture, and entrapment in a hernia sac.

63. Factors That Influence Infarct Development
 The effects of vascular occlusion range from
inconsequential to tissue necrosis leading to organ
dysfunction and sometimes death.
 The range of outcomes is influenced by the following
three variables:
 A. The nature of the vascular supply: e.g. lung…
 B. The rate of development of occlusion: Slowly developing
occlusions are less likely to cause infarction…
 C. Susceptibility of the tissue for hypoxia e.g. neurons…

64. Morphology of infarcts
 Based on their colour (reflecting the amount
of haemorrhage).
 1. Hemorrhagic (Red) infarcts
 2. Anemic (White) infarcts
 B) Based on the presence or absence of
microbial infection into:
 1. Septic infarcts
 2. Bland infarcts

65. 1. Red infarcts
 Red infarcts occur :
 a) as a result of venous occlusions (as in ovarian torsion)
 b) in loose tissues s (e.g. lung) which allow blood to collect in infarct zone.
 c) In tissues with dual circulations (e.g. lung and intestine), permitting flow of
blood from unobstructed vessel in to necrotic zone.
 d) In tissues that were previously congested because of sluggish outflow of blood.
 e) When blood flow is reestablished to a site of previous arterial occlusion &
necrosis.

66. 2. White infarcts
 White infarcts occur with arterial occlusions in solid organs with end-arterial
circulations (e.g., heart, spleen, and kidney), and where tissue density limits the
seepage of blood from adjoining patent vascular beds.
 Infarcts tend to be wedgeshaped, with the occluded vessel at the apex and the
organ periphery forming the base;
 when the base is a serosal surface, there is often an overlying fibrinous
exudate.
 Lateral margins may be irregular, reflecting flow from adjacent vessels.
 The margins of acute infarcts typically are indistinct and slightly hemorrhagic;
with time, the edges become better defined by a narrow rim of hyperemia
attributable to inflammation.

67. Red vs White infarcts

68. Clinical examples of infarction
 A. Myocardial infarction
 Usually results from
occlusive thrombosis
supervening on ulcerating
atheroma of a major
coronary artery.
 Is a white infarct.
 Microscopically
characterized by
coagulative necrosis.

69. Clinical examples of infarction…
 B. Cerebral infarcts
 May appear as pale or
hemorrhagic
 A fatal increase in intracranial
pressure may occur due to
swelling of large cerebral
infarction.
 Is one type of cerebrovascular
accidents (CVA) or stroke which
has various clinical
manifestations.

70. SHOCK
 Shock is a pathologic state characterized by a significant
reduction of systemic tissue perfusion, resulting in
decreased oxygen delivery to the tissues.
 This creates an imbalance between oxygen delivery and
oxygen consumption.
 Prolonged oxygen deprivation leads to cellular hypoxia
and derangement of critical biochemical processes at the
cellular level, which can progress to the systemic level.

71. Pathophysiology of shock

72. Types of shock
 Hypovolemic shock: is a consequence of decreased preload
due to intravascular volume loss. The principal cause of
hypovolemic shock is Fluid loss (e.g., hemorrhage, vomiting,
diarrhea, burns, or trauma)
 Cardiogenic shock: is a consequence of cardiac pump failure.
Common causes of cardiogenic shock include Myocardial
infarction, Ventricular rupture, Arrhythmia, Cardiac tamponade,
Pulmonary embolism
 Distributive (vasodilatory) shock: is a consequence of
severely decreased SVR. Causes include sepsis, Toxic shock
syndrome, Anaphylaxis and anaphylactoid reactions…

73. Stages of shock
 Non progressive stage (compensated stage): It is characterized by
rapid compensation for diminished tissue perfusion by various
homeostatic mechanisms.
 Progressive stage (Established shock): During this phase the
compensatory mechanisms become overwhelmed and signs and
symptoms of organ dysfunction appear. These include tachycardia,
dyspnea, restlessness, diaphoresis, metabolic acidosis, oliguria, and
cool clammy skin.
 An irreversible stage: Characterized by Progressive end-organ
dysfunction leads to irreversible organ damage and patient death.
During this stage, urine output may decline further (culminating in
anuria and acute renal failure), acidemia decreases the cardiac output
and alters cellular metabolic processes, and restlessness evolves into
agitation, obtundation, and coma.

74. Morphology of shock
 Changes can manifest in any tissue although they
are particularly evident in brain, heart, lungs,
kidneys, adrenals, and gastrointestinal tract.
 The adrenal changes in shock are those seen in all
forms of stress; essentially there is cortical cell lipid
depletion.
 The kidneys typically exhibit acute tubular necrosis.

75. Morphology of shock…
 When shock is caused by sepsis or trauma, diffuse
alveolar damage may develop, the so-called shock lung.
 In septic shock, the development of disseminated
intravascular coagulation leads to widespread deposition
of fibrin-rich microthrombi, particularly in the brain, heart,
lungs, kidney, adrenal glands, and gastrointestinal tract.
 The consumption of platelets and coagulation factors also
often leads to the appearance of petechial hemorrhages
on serosal surface and the skin.

76. Clinical Consequences of shock
 In hypovolemic and cardiogenic shock the patient
presents with hypotension; a weak, rapid pulse;
tachypnea; and cool, clammy, cyanotic skin.
 In septic shock the skin may initially be warm and
flushed because of peripheral vasodilation.
 The initial threat to life stems from the underlying
catastrophe that precipitated the shock (e.g.,
myocardial infarct, severe hemorrhage, or sepsis).

77. Clinical Consequences of shock…
 Rapidly, however, shock begets cardiac, cerebral, and
pulmonary dysfunction, and eventually electrolyte disturbances
and metabolic acidosis exacerbate the dire state of the patient
further.
 The second phase dominated by renal insufficiency and marked
by a progressive fall in urine output as well as severe fluid and
electrolyte imbalances.
 Coagulopathy frequently complicates shock, particularly when
the cause is sepsis or trauma, and can have serious or even fatal
consequences, particularly in patients with severe disseminated
intravascular coagulation.

78. Clinical Consequences of shock…
 The prognosis varies with the origin of shock and its
duration.
 Greater than 90% of young, otherwise healthy patients with
hypovolemic shock survive with appropriate management;
 Septic shock and cardiogenic shock associated with
extensive myocardial infarction, are associated with
substantially worse mortality rates, even with state-of-the-
art care.

79. THANK YOU