Hemodynemic

Hemodynamic
Disorders,
Thromboembolism
and Shock
Dr. Raghad Hanoon

LEC. 4
Outlines
• Edema
• Hyperemia and congestion
• Hemorrhage
• Hemostasis and thrombosis
• Embolism
• Infarction
• Shock
• References
Infarction
Infarction
● Infarction: are area of ischemic necrosis caused by occlusion of either
arterial supply or venous drainage in particular tissue.
● Causes of vascular obstruction:
1. Vast majority of infarctions results from thrombotic or embolic events &
almost all result from arterial occlusion.
2. Uncommon causes include:
a. Local vasospasm
b. Expansion of an atheroma secondary to intraplaque hemorrhage
c. Extrinsic compression of vessels e.g. by tumor, or edema within a
confined space (e.g., in anterior tibial compartment syndrome). and
entrapment in a hernia sac.
d. Vessel twisting (e.g., in testicular torsion or bowel volvulus),
e. Traumatic vascular rupture.
Morphology of infarction
● Infarcts may be either red (hemorrhagic) or white (pale, anemic) and may
be either septic or sterile..
1. Red Infarct:
occur with:
1- Venous occlusion (e.g. ovarian torsion).
2- Loose tissues (e.g. lung that allow blood to diffuse through and collect in
infarcted zone).
3- Tissues with dual blood supply (e.g. lung & small intestines). It allows
blood flow from an unobstructed parallel blood supply into infarcted zone.
4- Previously congested tissue because of sluggish venous outflow.
5- Re-established blood flow to a site of previous arterial occlusion and
necrosis, e.g. following coronary angioplasty of an obstructed coronary
artery.
2. White Infarct:
Occur with:
1. Arterial occlusions
2. In solid organs
3. With end-arterial circulation without a dual blood supply (e.g. heart,
spleen, and kidney)
4. Tissue with increased density which prevents the diffusion of RBCs
from adjoining capillary beds into the necrotic area.
(A) (B)
 Infarcts tend to be wedge shaped, with the occluded vessel at the apex and the organ
periphery forming the base (A) Hemorrhagic, pulmonary infarct (red infarct). (B) Pale infarct in the
spleen (white infarct).
 Histologically:
● In most tissues, the main histologic finding associated with infarcts is
ischemic coagulative necrosis.
● Inflammatory response begin within few hours along margin & becomes
well defined in 1-2 days caused by necrotic tissues then gradual degradation
of dead tissues with phagocytosis by inflammatory cells.
● Reparative response begin in margin & most infarction replaced by scar
tissues.
● Infarction in the central nervous system (CNS) results in liquefactive
necrosis.
● Septic infarctions occur when infected heart valve vegetations embolize or

when microbes seed an area of necrosis; the infarct converted in to an
abscess.
Remote kidney infarct, now replaced by a large fibrotic scar .
Factors that Influence Development of an Infarct
● The outcomes of vascular occlusion can range from no effect to death of a tissue or
person.
● Major determinants of outcome include:
1. Anatomy of the vascular supply (The presence or absence of an alternative blood
supply): Dual supply (i.e., lung, liver) or anastomosing circulations (i.e., radial and
ulnar arteries, circle of Willis, small intestine) protect against infarction. By contras,
obstruction of end-arterial vessels generally causes infarction (i.e., spleen, kidneys).
2. Rate of occlusion: Slowly developing occlusions less often cause infarction by allow
time for the development of collateral blood supplies. (e.g., collateral coronary
circulation).
3. Tissue vulnerability to hypoxia: Neurons undergo irreversible damage after 3 to 4
minutes of ischemia; myocardial cells die after only 20 to 30 minutes. In contrast,
fibroblasts within ischemic myocardium are viable even after many hours.
4. Oxygen content of blood: Anemia, cyanosis, or CHF (with hypoxia) can cause
infarction in an otherwise insignificant blockage.
Shock
Shock
● Shock: is a state of systemic hypo-perfusion caused by reduction
either in cardiac output or in the effective circulating blood volume,
that lead to; hypotension, impairs tissue perfusion and cellular
hypoxia.
● Initially , the cellular injury is reversible; however, prolonged

shock eventually leads to irreversible tissue injury and is often fatal.
● Shock is categorized in to:

1- Hypovolemic shock:
● Result from low cardiac output due to loss of blood or plasma volume.
Examples include:
 Hemorrhage ( external or internal)
 Fluid loss as in severe vomiting, diarrhea & extensive burns.
2- Cardiogenic shock:
● Results from low cardiac output due to myocardial pump failure. It may be
caused by:
 Myocardial damage (infarction),
 Ventricular arrhythmias,
 Extrinsic compression (cardiac tamponade)
 Outflow obstruction (e.g., pulmonary embolism).
3- Septic shock:
● Results from vasodilation and peripheral blood pooling caused by microbial
infections associated with severe systemic inflammatory response syndrome.
 Causes:
● Overwhelming bacterial infection (Gram-positive bacteria, followed by Gram-
negative bacteria and fungi. (Hence, an older synonym, “endotoxic shock,” is no
longer appropriate).
 Pathogenic mechanism:
● Bacterial toxin or microbial cell wall components cause;
1. Activation of leucocytes and endothelial cells and trigger release of inflammatory
cytokines that cause peripheral vasodilatation & increase vascular permeability .
2. Endothelial cell injury and direct activation of coagulation and complement
cascades lead to increased thrombotic tendencies with DIC (disseminated
intravascular coagulopathy).
● These end with multi-organ failure ; since hypotension, edema, and small vessel
thrombosis all reduce oxygen and nutrient delivery to tissues.
Pathogenesis of Septic Shock
● Less commonly shock:
4- Neurogenic shock:
● Result from a loss of vascular tone associated with anesthesia or secondary to
a spinal cord injury.
5- Anaphylactic shock:
● Results from systemic vasodilation and increased vascular permeability that is
triggered by an immunoglobulin E–mediated hypersensitivity reaction.
Stages of shock
● Shock is a progressive disorder often culminating in death.
● Shock tend to evolve through three phases:
1. Non-progressive phase: during which reflex neurohumoral compensatory
mechanisms are activated (catecholamines, sympathetic stimulation, ADH,
renin-angiotensin axis, etc.) to maintain cardiac output, blood pressure and
perfusion of vital organs.
The compensatory mechanisms include:
a- Arteriolar constriction leading to increase peripheral vascular resistance and
blood pressure.
b- Increase heart rate leading to increase cardiac output.
c- Retention of fluid through increase secretion of ADH & activation of rennin
angiotensin aldosterone axis to retain fluid.
● If the underlying causes are not corrected, shock passes imperceptibly
to the progressive phase.
2. Progressive phase: characterized by tissue hypo-perfusion and worsening circulatory and
metabolic abnormalities, since persistent tissue hypoxia lead to anaerobic glycolysis and
lactic acidosis. The acidosis also reduces the vasomotor response, causing vasodilation.
● In the absence of appropriate intervention, or in severe cases, the process eventually
enters an irreversible stage.
3. Irreversible Phase: In which cellular and tissue injury is so severe that even if the
hemodynamic defects are corrected, survival is not possible.
 Widespread cell injury is reflected in lysosomal enzyme leakage, further aggravating
the shock state.
 Myocardial contractile function worsens, in part because of increased Nitric oxide
synthesis.
 The ischemic bowel may allow intestinal flora to enter the circulation, and thus
bacteremic shock may be superimposed.
 Commonly, further progression to renal failure occurs as a consequence of ischemic
injury of the kidney, and despite the best therapeutic interventions, the downward spiral
frequently culminates in death.
Pathological Changes
● The cellular and tissue changes are those of hypoxic injury due to a combination of
hypoperfusion and microvascular thrombosis.
● Although any organ can be affected, the brain, heart, kidneys, adrenals, and gastrointestinal
tract are most commonly involved.
● Brain: Ischemic encephalopathy.
● Heart: coagulation necrosis
● Adrenal: cortical cell lipid depletion is akin to that seen in all forms of stress and reflects
increased use of stored lipids for steroid synthesis.
● Kidneys: acute tubular necrosis which lead to oliguria or anuria &electrolytes disturbances.
● Lungs: diffuse alveolar damage.
● GIT: focal mucosal hemorrhage &necrosis.
● Except of neuron and myocyte loss, virtually all affected tissues can recover completely if
the patient survives.
● Fibrin thrombi can form in any tissue but typically are most readily visualized in kidney
glomeruli.
Clinical Features
● The clinical manifestations of shock depend on the cause.
● In hypovolemic and cardiogenic shock, patients present with hypotension, a
weak rapid pulse, tachypnea, and cool, clammy, cyanotic skin.
● In septic shock, the skin may be warm and flushed owing to peripheral
vasodilation.
● The initial underlying cause that precipitated the shock may be life-threatening
(e.g. myocardial infarct, severe hemorrhage, or sepsis). Later, the organ
dysfunction involving cardiac, cerebral, and pulmonary function worsen the
situation.
● If patients survive the initial complications may develop renal insufficiency
characterized by a progressive decrease in urine output and severe fluid and
electrolyte imbalances.
Prognosis
● The prognosis depends on the cause and duration of shock.
● Patients with hypovolemic shock may survive with appropriate
management (more than 90% of young, otherwise healthy patients survive
with appropriate management)
● Septic shock, or cardiogenic shock associated with worse outcomes,
even with state-of-the-art care.
References
● Chapter 4: Hemodynamic Disorders, Thromboembolism, and Shock
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Hemodynamic

Dr. Raghad Hanoon

● Septic infarctions occur when infected heart valve vegetations embolize or

● Initially , the cellular injury is reversible; however, prolonged

● Shock is categorized in to:

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