Disorders of Vascular flow and

shock
Hasan Mukhtar
Assistant Instructor
BSN, RN. M.Phil Public Health*
 Objectives
• Define Edema, describe its types, Pathophysiology of edema and its
clinical effects.
• Define hemorrhage, describe its types, Pathophysiology of edema and its
clinical effects.
• Define hyperemia and congestion, describe its types, Pathophysiology of
edema and its clinical effects.
• Define Thrombosis, Embolism, describe its types, Pathophysiology of
edema and its clinical effects.
• Define Infarction, describe its types, Pathophysiology of edema and its
clinical effects.
• Define shock, describe its types, stages of shock Pathophysiology of
edema and its clinical effects.
 Edema
• Distribution of body water:
body water constitute about 60% of body
weight which is distributed Into two
compartments.
1) Intracellular
2) Extracellular
a)interstitial 15%
b)plasma water 5%
 Edema
• Definition: it refers to : “accumulation of
abnormal amounts of fluid in intracellular
tissues space or body cavity” Edema may be
transudate and exudate.
Lights criteria of Pleural Effusions
Anasarca :
It refers to “severe and generalized
edema”.
Hydrothorax:
It refers to “accumulation of edema fluid
in pleural cavity”
Hydrocardium:
It refers to “ accumulation of edema fluid
in pericardial cavity”
Formation and drainage of interstitial
fluid:
Pressures in capillary:
1. Intravascular hydrostatic pressures at arteriolar
end of capillary bed is 25-35mmHg and at venular
end is 12-15mmHg.
2. Plasma colloid osmotic pressure is 20-25mmHg,
rising slightly at venular end due to escape of
fluid.
Formation of interstitial fluid:
Interstitial fluid formed as a result of leakage of
fluid from arteriolar end of capillary due to
intravascular hydrostatic pressure
• Drainage of interstitial fluid:
Interstitial fluid is drained in two ways
1. Into capillary at venular end of due
intravascular hydrostatic pressure.
2. Into lymphatic's and then into blood
stream through thoracic duct or right
lymphatic duct.
 Causes of Edema:
A. Inc. intravascular hydrostatic pressure:
resulting from
a)impaired venous flow
(a) Thrombosis
(b) External Compression by tumors
b)Congestive heart failure
B. Red. Plasma colloid osmotic pressure
(Hypoalbuminemia)
Resulting from
1) Excessive loss of albumin e.g. nephrotic syndrome
2) Decreased synthesis of albumin, cirrhosis of liver,
malnutrition
C. Lymphatic obstruction.
Resulting from
1) inflammatory or neoplastic obstruction
2) fibrosis of lymph nodes & lympahtics in inguinal region in
filariasis
D. Sodium retention with obligate water
retention:
Resulting from
1) Acute renal failure
2) Post streptococcal glumerulonephritis
E. Increased Vascular permeability:
Resulting from
1)inflammatory chemical mediators
2) allergic or immune reactions
3) trauma or burns
 Types of Edema
A. Generalized Edema
seen in
1)CHF.
2)Nephrotic syndrome.
3)cirrhosis of liver.
4) protein malnutrition.
B. Localized Edema
seen in
1)venous obstruction due to thrombosis or external compression
by tumors
2)lymphatic obstruction.
3) increased vascular permeability due to chemical mediators,
allergic reaction or burns.
Pathogenesis of edema in CHF
 Morphology of Edema
1. Subcutaneous edema
• Lower parts of body occurs in CHF (RVF)
2. Sacral edema
• Patients of CHF confined to bed
3. Dependent edema
• Distribution of edema due to gravity.
4. Periorbital edema (eyelids)
• Occur in renal dysfunction.
5. Pitting edema
• Pitted depression when finger pressed over edematous
subcutaneous tissue
6. Pulmonary edema
• Occur if LVF, Renal failure, RDS, &hypersensitivity reactions.
7. Cerebral edema
• Occurs in brain trauma, meningitis, encephalitis, hypersensitive
crisis.
Pitting Edema Periorbital Edema
 Clinical correlation:
• Edema of subcutaneous tissue in cardiac or
renal; failure indicate underlying diseases and
may impair healing of wounds or infection.
• Pulmonary edema impair ventilatory functions &
creates favorable soil for hypostatic pneumonia.
• Cerebral edema may cause herniation of
cerebral tonsils into foramen magnum or
pressure on blood supply to brainstem that
results in failure of medullary centers and death.
 Hemorrhage:
• Definition:
It refers to “the rupture of blood vessels with
loss of blood”
• Causes of Hemorrhage:
1. Trauma.
2. Hemorrhage diathesis.
3. Hypertension.
4. Atherosclerosis.
5. Neoplastic erosion of vessel wall.
 Types of hemorrhage:
• External hemorrhage.
• Internal hemorrhage.
1. Hematoma:
Accumulation of hemorrhagic blood into body tissues e.g.
retroperitoneal hemorrhage.
2. Hemorrhage into body cavities.
A)Hemothorax b)Hemoperitonium
c)Hemoparicardium d)Hemathorasis
3. Petechiae: it refers to “Minute Hemorrhage into skin”
4. Purpura: It refers to “ hemorrhage slightly larger then
Petechiae”
5. Ecchymosis: It refers to “ diameter 1-2cm large
subcutaneous hematoma.
 Clinical correlation
• Jaundice:
released hemoglobin in internal hemorrhage is converted
into bilirubin & the into hemosidrin that results into
excessive bilirubin formation and gives rise to jaundice.
• Hypovolemic shock:
sudden loss of up to 20% of blood volume or slow loss of
large amount of has no clinical significance.
Acute loss of more then 20 % of blood volume causes
Hypovolemic shock.
• Iron deficiency Anemia:
Repeated external hemorrhage ( from skin, GIT, Female
Genital Tract) loss of iron and iron deficiency anemia.
 Hyperemia or Congestion
• Definition: it refers to “ local increase of Volume of
blood caused by dilation of Small vessels”.
• Types:
1) Active Hyperemia:
It results from augmented arterial flow.
It occurs during
a)Exercise b) Sites of inflammation c) In blushing
2) Passive Hyperemia:
It results from diminished venous out flow
it occurs
a) Cardiac Failure b)Obstructed venous disease.
HYPEREMIA/(CONGESTION)
 Thrombosis
• “Refers to the formation of clotted mass of
blood in non interrupted cardiovascular
system thrombus remaining attach to vessel
wall.”
• Thrombus: “a clotted mass of blood in non
interrupted cardiovascular system , attached
to vessel wall.”
Consequences of thrombosis
• Embolus formation:
part or whole of thrombus may detach and
become free to flow down stream “a freely
flowing mass of clotted blood is referred to as
embolus.”
• Infarctions:
when thrombus or embolus block some vital
arterial supply of an organ , it may lead to
ischemic necrosis of cells & tissues, referred to
an infarction.
 THROMBOSIS
• Virchow’s TRIANGLE
ENDOTHELIAL INJURY

ABNORMAL FLOW HYPER-

(NON-LAMINAR) COAGULATION
 Thrombogenesis
Factors that pre dispose to Thrombogenesis
are
A. Endothelial injury.
B. Stasis & Turbulence.
C. Hypercoagulabuility.
D. Autoimmunity.
 Endothelial injury.
Endothelial injury causes thrombosis by following effects
1. Exposure &adherence of sub endothelial collagen platelets.
2. Activation of intrinsic pathway of coagulation system.
3. Activation of extrinsic pathway of coagulation system.
4. Local loss of prostacyclin and plasminogen activator.
Causes of Endothelial Injury:
a)Bacterial toxins.
b)Ulcerated atherosclerotic plaques.
c)Traumatic or inflammatory injury to vessel.
d)Hemodynamic stresses of hypertension.
e) Homocystinuria.
f) Hypercholesterolemia.
g) Injury of endocardium.
h)Products absorbed from cigarette smoking.
 Endothelium:
NORMALLY

IN INJURY
 Stasis & Turbulence.
Statis and turbulence cause thrombosis by following
effects.
1. Disruption of laminar flow that permits platelets to
come in contact with endothelium.
2. Prevention of dilution of activated clotting factors to
sub clinical conc.
3. Retardation of inflow of clotting factor inhibitors
4. Allowing buildup of platelet aggregation& nascent
fibrin in sluggish stream.
5. Turbulence is a mechanism for endothelial injury.
Sites of stasis and Turbulence.
• Sinuses behind valve cusps in deep veins in
lower legs.
• Aneurismal dilatations.
• Auricular appendages of heart when there is
atrial fibrillation or massive dilation of atria in
mitral stenosis.
 Hypercoagulabuility.
It refers to “ alteration of blood or clotting mechanism
that predisposes to thrombosis.
Causes of Hypercoagulabuility:
• Nephrotic syndrome
• Oral contraceptives
• Following severe trauma or surgery
• Aging, bed rest, immobilization.
• Later pregnancy and postpartum stage.
• Hereditary lack of anticoagulant
• Disseminated cancer
 Autoimmunity.
Autoantibodies directed against anionic
phospholipids causes thrombosis e.g. SLE by
• Induction of platelet aggregation
• Interference in generation of protein C
• Inhibition of prostacyclin production by
endothelial cells.
 Types of thrombi
• Morphological types.
o Pale or white thrombi.(Arterial Thrombi)
• These are dry, friable, tangled gray masses that develop in
arteries or heart at the site of endothelial injury or turbulence.
• composed of platelets and fibrin with few entrapped RBC’s.
o Red thrombi.(Venous Thrombi)
• Venous thrombosis is occulusive.venous thrombi are rich in
RBC’s entrapped in fibrin mesh.
• Typically develop in arterial circulation.
o Common sites:
i) Deep calf Vein. ii) Femoral Vein.
iii)Popliteal vein. Iv) Iliac vein
 Types of arterial thrombi
• Mural thrombi: refers to a thrombus that is attached to wall of blood
vessel or heart and do not occlude the vessel lumen.
Common sites:
I. Chambers of heart.
II. Aorta.
III. Aneurysm.
• Occlusive thrombi: refers to a thrombus that completely occludes the
lumen of smaller arteries.
I. Common sites V. Coronary arteries.
II. Cerebral arteries. VI. Femoral arteries.
III. Iliac arteries. VII. Popliteal arteries.
IV. Mesenteric arteries.
• Vegetations: refers to thrombi deposited in heart valve
Vegetations found in
I. Bacterial endocarditis. II.Non Bacterial endocarditis.
III. Verrucous carditis.
MURAL THROMBI, HEART
 Venous Thrombi.
• Thrombophlebitis
Venous thrombosis occurring secondary to acute
inflammation of the vein is called
Thrombophlebitis. This type of thrombus firmly
attached to vessel wall and does not form
embolus. E.g. infected wounds and ulcerations.
• Phlebothrombosis
Venous thrombosis occurring in the absence of
pre-existing inflammation of the vein is called
Phlebothrombosis. e.g. Deep Venous
Thrombosis.
 Fate of thrombus
• Propagation
It may propagate and eventually cause obstruction of
some critical vessel.
• Embolization
It may embolize. And move to other sites in
vasculature.
• Dissolution
It may be removed by fibrinolytic activity.
• Organization and recanalization:
It may go under organization.
Organized thrombi may become recanalized thus
reestablishing continuity of lumen or original vessel.
 Embolism
• It refers to occlusion of some part of
cardiovascular system by impaction of some
mass transported to the site thru blood
stream.
• Emboli:
“Refers to the mass that occlude blood
vessels”
 Classification of emboli
• According to consistency.
i)Solid emboli:
a)part or whole of dislodged thrombus
b)atherosclerotic debris
c)tumor fragments
d)bits of bone marrow
ii)Liquid emboli:
a)Fat droplets
b)Amniotic fluid
iii)Gas emboli:
a) Air
b) Nitrogen gas
• According to site of origin:
Venous emboli
Saddle embolus/PTE
Paradoxical/crossed embolus
Arterial emboli
Intacardiac mural thrombi
Mural thrombi in aortic aneurysm
fragmentations of vegetations on heart valve
• According to sepsis:
Septic emboli
aseptic emboli
 Fat emboli
Refers to “presence of minute fat globulets in circulation”.
Causes of fat emboli:
1)Fractures of long bones 2)Soft tissue trauma
3)Burns
Clinical manifestations:
1)Pulmonary insufficiency 2)Neurological symptoms
7)Anemia 8)Petechial skin rash.
Pathogenesis :
A)Micro aggregates of neutral fat cause occlusion of pulmonary
or cerebral micro vasculature & free fatty acids released from fat
globulets result in toxic injury to vascular endothelium that
results in pulmonary and neurologic symptoms.
B)Myriad fat globules become coated with platelets—Platelet
depletion—thrombocytopenia—Petechial skin rash.
Amniotic Fluid Embolism:
It refers to “presence of amniotic fluid in mother’s blood(
containing epithelial squamous from fetal skin, lanugo
hairs, fat from vernix caseosa, mucin, from fetal GIT)
Occurs in older multiparous pts, who have a tumultuous
labor.
Pathogenesis:
Amniotic fluid enters mother’s circulation thru
endocervical veins uteroplacental sites, or lacerations of
uterus of cervix—Amniotic fluid
vasoactive substances, eg prostaglandins that cause
pulmonary vasoconstriction.
Thrombogenic factors that induce intravascular
coagulation, leading to DIC and its complications.
Clinical Manifestations:
Sudden onset of dyspnea, cyanosis, collapse, hemorrhage,
convulsions followed by coma.
 Infarction
• Infarction refers to “an area of ischemic
necrosis within a tissue or an organ,
produced by occlusion of either its arterial
supply or venous drainage”.
Types of Infarction:
• HEMORRHAGIC vs. ANEMIC
• RED vs. WHITE
– END ARTERIES vs. NO END ARTERIES
• ACUTEORGANIZATIONFIBROSIS
 INFARCTION FACTORS
• NATURE of VASCULAR SUPPLY
• RATE of DEVELOPMENT
– SLOW (BETTER)
– FAST (WORSE)
• VULNERABILITY to HYPOXIA
– MYOCYTE vs. FIBROBLAST
• CHF vs. NO CHF
HEART
 Shock
• Definition:
• Clinical conditions that result in cellular
hypoperfusion are often referred to as shock
states. Which results in inadequacy to deliver
oxygen and nutrients to support vital organs
and cellular function
 Pathophysiology
• Shock begins with cardiovascular system
failure
• Alterations in at least one of four
components:
– Blood volume
– Myocardial contractility
– Blood flow
– Vascular resistance
 Physiological responses to shock
• Hypoperfusion → hypoxia → anaerobic
cellular respiration → lactic acidosis →
metabolic acidosis → cell death → progressive
organ dysfunction
• Hypercoagulability – increasing viscosity of
blood
• Activation of the inflammatory response –
vasoactive mediators i.e. histamine
 Stages of shock
Three stages of shock.

• Stage I (Compensated or Non-progressive).

• Stage II (Decompensated or Progressive).
• Stage III (Irreversible)
 Stage I (Compensated or Non-
progressive)
The body activates compensatory mechanisms in an effort
to maintain circulatory volume, blood pressure, and
cardiac output.
Vasoconstriction, increased heart rate, and increased
contractility of the heart contribute to maintaining
adequate cardiac output. This results from stimulation of
the sympathetic nervous system and subsequent release of
catecholamines (epinephrine and norepinephrine).
Patients display the often-described “fight or flight”
response The body shunts blood from organs such as the
skin, kidneys, and gastrointestinal tract to the brain, heart,
and lungs to ensure adequate blood supply to these vital
organs.
 Medical Management in
Stage 1
Medical treatment is directed toward
• Identifying the cause of the shock
• Correcting the underlying disorder
• Non specific measures such as fluid
replacement and medication therapy can
initiated to maintain an adequate BP and tissue
perfusion
Stage II (Decompensated or Progressive)
• Compensatory mechanisms begin to fail,
metabolic and circulatory derangements
become more pronounced, and the
inflammatory and immune responses may
become fully activated.
Clinical Manifestations of Stage II
• Respiratory Effects
– Respirations are rapid and shallow.
– Crackles are heard over the lung fields.
– Acute respiratory distress syndrome
• Cardiovascular Effects
– Dysrhythmias and ischemia.
– Heart rate is rapid, sometimes exceeding 150 bpm.
– chest pain
– Week pulse
– Low BP
• Neurologic Effects
– changes in behavior or agitation and confusion.
– Subsequently, lethargy increases, and the patient begins to
lose consciousness
Clinical Manifestations of Stage II
• Renal Effects
– ARF, increased BUN and Creatinine
– Low urine output
– Acid base and electrolyte imbalance
• Gastrointestinal Effects
– Stress ulcers in the stomach, putting the patient at risk for GI bleeding
• Hematologic Effects
– Disseminated intravascular coagulation (DIC)
– Ecchymoses, petechiae
• General
– Anxiety or agitation/restlessness
– Bluish lips and fingernails
– Dizziness, lightheadedness, or faintness
– Pale, cool, clammy skin
– Profuse sweating, moist skin
Medical Management in Stage II
• Depends on the type of shock
• Supporting the respiratory system
• Optimizing intravascular volume
• Supporting the pumping action of the heart
• Enteral nutritional support, aggressive hyperglycemic
control with IV insulin
• Antacids, histamine-2 (H2) blockers, or antipeptic
agents to reduce the risk of GI ulceration and bleeding.
• The patient should not be warmed too quickly, and
warming blankets should not be applied, because they
can cause vasodilation and a subsequent drop in BP.
Medical Management in Stage II
• Preventing Complications
• Promoting Rest and Comfort
• Supporting Family Members
 Stage III (Irreversible)
In the final, irreversible stage, cellular and tissue
injury are so severe that the patient’s life is not
sustainable even if metabolic, circulatory, and
inflammatory derangements are corrected.
At this point, full-blown multisystem organ
dysfunction syndrome (MODS) may become
evident.
• The judgment that the shock is irreversible can be
made only retrospectively on the basis of the
patient’s failure to respond to treatment.
 Stage IV: Refractory
• Prolonged inadequate tissue perfusion
– Unresponsive to therapy
– Dysrhythmias
– Pulmonary edema
– Respiratory Distress Syndrome (RDS)
– Cerebral changes
– Renal decreased GFR
– Contributes to multiple organ dysfunction and
death
Systemic Inflammatory Response
Syndrome (SIRS)
• Widespread systemic inflammatory
response
• Associated with diverse disorders
– Infection
– Trauma
– Shock
– Pancreatitis
– Ischemia
• Most frequently associated with sepsis
 Goal of Shock Treatment
Goal of treatment are to reestablish adequate
organ perfusion and oxygenation and to lessen
the inflammatory response as quickly as
possible.
• opportunity that increases the likelihood of
patient survival occurs when aggressive
therapy begins within 6 hours of identifying a
shock state, especially septic shock
 Types of shocks
• Hypovolemic shock
– Hemorrhagic shock
• Cardiogenic shock
• Distributive shock
i. Neurogenic shock
ii. Anaphylactic shock
iii. Septic shock
-Obstructive Shock
 Hypovolemic shock
Hypovolemic shock is a result of inadequate
circulating blood volume, The extracellular body
fluid is found in one of two compartments:
intravascular (inside blood vessels) or interstitial
(surrounding tissues). Hypovolemic shock
occurs when there is a reduction in intravascular
volume by 15% to 30%, which represents a loss
of 750 to 1500 mL of blood in a 70-kg person
Etiology
 Assessment
• History or active bleeding
• ABG’s
• Lactate Levels
• CBC (Hb, HCT)
• Coagulation profile
• BSL
 Cardiogenic Shock
• Definition:
Cardiogenic shock, which results from loss of
contractility of the heart, is an extreme form of
heart failure.
 Causes of Cardiogenic Shock
• Either coronary or non coronary.
• Left ventricular damage from myocardial
infarction
• Papillary muscle rupture
• Ventricular septal rupture
• Cardiomyopathy
• Cardiac tamponade
• Acute myocarditis
• Valvular disease
• Dysrrhythmias
Cardiogenic Shock
Pathophysiology
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 Distributive shock or
Circulatory shock
• The mechanism underlying all distributive
shock states is vasodilation that causes pools
in peripheral blood vessels.
i. Neurogenic shock:- Vasodilation results
from a loss of sympathetic innervation to the
blood vessels.
ii. Anaphylactic shock and septic shock,
vasodilation results from the presence of
vasodilating substances in the blood.
 Neurogenic Shock
• Neurogenic shock results from loss or
disruption of sympathetic tone, most often
due to severe cervical or upper thoracic
spinal cord injury.
 Clinical manifestations
• hypotension with bradycardia, rather than
the tachycardia
• dry, warm skin rather than the cool, moist
skin seen in hypovolemic shock.
 Anaphylactic shock
• Anaphylaxis is an allergic reaction to a
specific allergen that evokes a life-
threatening hypersensitivity response.
Anaphylaxis may be either
immunoglobulin E (IgE)– or non–IgE
mediated.
 Mechanism of anaphylaxis
• IgE-mediated anaphylaxis:- immune response
to a specific antigen.
• 1st time immune system is exposed to the antigen,
a very specific IgE antibody is formed and
circulates in the blood.
• When 2nd time exposure to this antigen occurs,
the antigen binds to this circulating IgE, which
then activates the immune system, triggering the
release of chemical mediators that initiate
anaphylaxis.
 Mechanism of anaphylaxis
• Non-IgE responses (anaphylactoid
reactions):- occur without the presence of IgE
antibodies.
• 1st time the person is exposed to the antigen.
Direct activation of mediators causes this
response. Anaphylactoid reactions are
commonly associated with NSAIDs, including
aspirin.
 Pathophysio of Anaphylaxis
• The antibody–antigen reaction causes the white
blood cells (WBCs) to secrete chemical
mediators that cause
• Systemic vasodilation
• rapid onset of hypotension
• Increased capillary permeability
• Bronchoconstriction
• Coronary vasoconstriction
• Urticaria (hives).
• cardiac
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5
 Septic Shock
• Septic shock, the most common type of
circulatory shock, is caused by widespread
infection
 Clinical Menefestatins
In the early stage of septic shock
• BP may remain within normal limits (or hypotensive but responsive to fluids).
• Heart and respiratory rates elevated.
• High cardiac output with vasodilation.
• Hyperthermia (febrile) with warm, flushed skin, bounding pulses.
• Urinary output normal or decreased.
• Gastrointestinal status compromised (eg, nausea, vomiting, diarrhea, or decreased
bowel sounds).
• Subtle changes in mental status.
As sepsis progresses
• Low cardiac output with vasoconstriction
• BP drops
• Skin cool and pale
• Temperature normal or below normal
• Heart and respiratory rates rapid
• Anuria and multiple organ dysfunction progressing to failure
 Obstructive Shock
• Physical impairment to adequate
circulatory blood flow
• Causes
• Clinical manifestations
– Chest pain
– Dyspnea
– Jugular venous distension
– Hypoxia
– Cause-dependent findings
Obstructive Shock (Cont.)

Figure 12-9. Obstructive shock

 Multiple Organ Dysfunction
Syndrome (MODS)
• Multiple organ dysfunction syndrome
(MODS) is altered organ function in acutely
ill patients that requires medical intervention to
support continued organ function. It is another
phase in the progression of shock states.
 Multiple Organ Dysfunction
Syndrome (MODS)
• Pulmonary dysfunction.
• Renal dysfunction
• Liver dysfunction
• Cardiovascular dysfunction
• Hematologic dysfunction.
• Neurologic dysfunction
 Multiple Organ Dysfunction
Syndrome (Cont.)
• Clinical manifestations
– Tachypnea/hypoxemia
– Petechiae/bleeding
– Jaundice
– Abdominal distension
– Oliguria  anuria
– Tachycardia
– Hypotension
– Change in level of consciousness
 Shock, Sepsis, and MODS
• Patient outcomes
– Improved tissue perfusion
• Alert, oriented
• Normotensive
• Warm, dry skin
• Adequate urine output
• Normal hemodynamics
• Lab values within normal limits
• Absence of infection
• Intact skin
Questions?????