Derangements of Homeostasis
and Hemodynamics part
Heperemia and congestion
Hemorrhage
Shock
Haemodynamic Derangements
I. Disturbances in the volume of the circulating
blood. These include:
o Hyperemia & congestion
o Hemorrhage
o Shock
II. Circulatory disturbances of obstructive nature.
These are:
o Thrombosis
o Embolism
o Infarction
Hyperemia and Congestion
Hyperemia and congestion are the terms
used for localized increase in the volume of
blood within dilated vessels of an organ or
tissue.
The increased volume from arterial & arteriolar
dilatation is called hyperemia or active
hyperemia, whereas the impaired venous
drainage is called venous congestion or passive
hyperaemia.
Hyperemia (active hyperemia)
Increased volume in tissue resulting from arterial
& arteriolar dilatation
Affected tissue becomes red (oxygenated blood).
Seen in the following conditions:
o Acute inflammation
o Blushing (flushing of face skin in response to
emotions)
o High grade fever
o Muscular exercise
Passive Hyperaemia (Venous Congestion)
Increased volume dilated veins due to impaired
venous drainage
The affected tissue or organ is bluish in color due
to accumulation of venous blood (cyanosis).
Congestion may be acute (develops rapidly) or
chronic (develops more prolonged & gradual),
the latter being more common & called chronic
venous congestion (CVC).
Obstruction to the venous outflow may be local
or systemic.
Passive Hyperaemia (Venous Congestion)
Local venous congestion
Results from obstruction to the venous
outflow from an organ or part of the body e.g.
portal venous obstruction in cirrhosis of liver.
Systemic (General) venous congestion
It is engorgement of systemic veins e.g. right-
sided heart failure.
Morphology of liver congestion
In acute liver congestion:
- Central vein & sinusoids are distended with
blood with or without central hepatocyte
degeneration.
- Peripheral hepatocytes better oxygenated &
develop only fatty changes.
Acute hepatic congestion
Central vein and sinusoids
are distended with blood
with or without central
hepatocyte degeneration.
Peripheral hepatocytes develop
fatty changes.
In chronic venous congestion (CVC) Liver:
- Grossly: the liver is enlarged. Cut surface shows
characteristic nutmeg appearance, corresponding
to congested center of lobules & peripheral fatty
changes
- Microscopically:
Centrilobular necrosis with loss of hepatocytes,
Hemorrhage and hemosiderin-laden
macrophages.
Morphology of Chronic passive liver congestion
Centrilobular necrosis with loss of hepatocytes,
hemorrhage and hemosiderin-laden macrophages.
Hemorrhage
Definition: Hemorrhage is extravasation of blood
outside the blood vessel due to vessel rupture.
Causes:
1. Trauma to the vessel.
2. Systemic hypertension (cerebral & retinal
hemorrhage)
3. Neoplastic invasion (following vascular invasion).
4. Inflammatory lesions of the vessel wall (ulcer).
5. Vascular diseases e.g. atherosclerosis.
6. Spontaneous hemorrhage e.g. aneurysm rupture.
Types of Hemorrhage
Hematoma: forms tumor like lesion
Petechiae: 1-2 mm hemorrhages occurring in the
skin, mucosal membrane, or serosal surface.
Purpura: hemorrhage > 3mm (in skin).
Eccymosis: > 1-2cm subcutaneous hematoma
(bruises).
Accumulations of blood in
o Pleural cavity is called Hemothorax
o Pericardial space is called Hemopericardium
o Peritoneum is called Hemoperitoneum
o Joints is called Hemarthrosis
Petechiae
Purpura
Ecchymosis
The effects of Hemorrhage
The effects of blood loss depend on:
o The amount of blood loss;
o The speed of blood loss;
o The site of hemorrhage.
The loss up to 20% of blood volume suddenly or
slowly generally has little clinical effects.
Sudden loss of 33% of blood may → serious
consequences (death)
Chronic blood loss → iron deficiency anemia.
Shock
Definition:
Shock is a life-threatening clinical syndrome of
cardiovascular collapse characterized by:
o Hypotension: an acute reduction of effective
circulating blood volume
o Hypoperfusion: an inadequate perfusion of
cells and tissues.
Shock
The term “true (circulatory or secondary) shock”
is used for a circulatory imbalance between
oxygen supply & oxygen requirements at the
cellular level.
The term “initial (or primary) shock” is used for
transient vasovagal attack resulting from sudden
reduction of venous return to the heart caused
by neurogenic vasodilatation e.g. immediately
following trauma, severe pain or emotional
overreaction (fear, sorrow or surprise).
Classification and Etiology
1. Hypovolemic shock
2. Cardiogenic shock
3. Septic shock
4. Neurogenic shock
5. Hypoadrenal shock
Classification and Etiology
Hypovolaemic shock:
Results from inadequate circulatory blood
volume (may be either from loss of red cell
mass & plasma from hemorrhage, or from the
loss of plasma volume alone.
Cardiogenic shock:
Acute circulatory failure with sudden fall in
cardiac output from acute diseases of the
heart (normovolaemia).
Septic (Toxaemic) shock:
Severe bacterial infections or septicemia.
Neurogenic shock.
results from causes of interruption of
sympathetic vasomotor supply.
Hypoadrenal shock.
occurs from unknown adrenal insufficiency in
which the patient fails to respond normally to
the stress of trauma, surgery or illness.
Pathogenesis
In general, all forms of shock involve following 3
derangements:
1) Reduced effective circulating blood volume
2) Impaired tissue oxygenation
3) Inflammatory mediators & toxins induced
cellular injury.
Pathogenesis
1. Reduced effective circulating blood volume: by
i. Actual loss of blood volume (hypovolaemic shock)
ii. Decreased cardiac output without actual loss of
blood (normovolaemia) (in cardiogenic and septic
shock).
2. Impaired tissue oxygenation:
Any of the above two mechanisms → ↓ venous
return to the heart → ↓ cardiac output → ↓ supply
of oxygen to the organs and tissues → tissue anoxia
→ cellular injury.
Pathogenesis
3. Release of inflammatory mediators:
Bacterial Endotoxins in septic shock stimulate massive
release of pro-inflammatory mediators (cytokines).
Several pro-inflammatory inflammatory mediators are
released from monocytes-macrophages, other
leucocytes (tumor necrosis factor- (TNF)-α and
interleukin-1).
a) Activation of complement pathway → endothelial damage.
b) Activation of mast cells → Histamine → ↑capillary
permeability.
c) Activation of coagulation system → thrombi (DIC).
d) Activation of kinin system → vasodilatation & ↑capillary
permeability.
Pathogenesis of circulatory shock
Stages of Shock
Nonprogressive (Compensated, initial, reversible)
shock: perfusion of vital organs is maintained
Progressive decompensated shock: tissue
hypoperfusion & onset of worsening circulatory &
metabolic imbalances, including acidosis
Irreversible decompensated shock: when the
cellular & tissue injury so severe that even if the
hemodynamic defects are corrected, survival is
not possible.
Mechanisms and effects of three stages of shock
Morphology of shock
Eventually, shock is characterized by multisystem
failure. The morphologic changes in shock are
due to hypoxia resulting in degeneration and
necrosis in various organs:
o Brain: - hypoxic encephalopathy
o heart: - petechial hemorrhages in the epi- &
endocardium; focal myocardial infarction
o Lungs: diffuse alveolar damage & interstitial
edema (Acute respiratory distress syndrome
(ARDS))
Morphology of shock
o kidneys - systemic hypotension → ischemia →acute
tubular necrosis → oliguria, anuria, & electrolyte
disturbances → acute renal failure (ARF) & death.
o Adrenals: acute adrenal hemorrhagic necrosis (In
severe shock).
o Gastrointestinal tract: hemorrhagic
gastroenteropathy
o Liver: congestion and necrosis
o Pancreas: ischemic → acute pancreatitis
o Blood: Disseminated intravascular coagulation (DIC)
Clinical features of shock
The classical features of decompensated shock
are characterized by depression of 4 vital
processes:
o Very low blood pressure (Hypotension)
o Feeble & irregular pulse
o Shallow & sighing respiration
o Cold & clammy skin (warm & flushed in septic
shock).
Complications of shock
Acute respiratory distress syndrome (ARDS)
Disseminated intravascular coagulation (DIC)
Acute renal failure (ARF)
Multiple organ dys-function syndrome (MODS)
Stupor, coma & death
Prognosis
80% to 90% of young, otherwise healthy patients
with hypovolemic shock survive with appropriate
management
Cardiogenic shock associated with extensive
myocardial infarction & gram-negative septic
shock carry mortality rates of up to 75%, even
with the best care currently available.
