Hemodynamic 4 Dr. lameia pgathology
Hemorrhage
Hemorrhage is extravasation of blood from vessels into the extravascular space. Causes are:
1. Chronic congestion (capillary bleeding).
2. Hemorrhagic diatheses.
3. Vascular injury (trauma, atherosclerosis, inflammation, neoplastic erosion of vessel wall ).
Patterns of hemorrhage include:
1. External bleeding.
2. Internal bleeding (enclosed within a tissue) ”hematoma”.
**Petechiae: are small (1-2 mm) hemorrhagic spots.
**Purpuras: slightly larger than petechiae (3-5 mm).
**Ecchymoses(bruises): are larger (1-2cm) subcutaneous hematomas
3. hemothorax, hemoperitoneum, hemopericardium, hemarthrosis refer to large
accumulations of blood in pleural cavity, peritoneal cavity, pericardial cavity, and joint space
respectively.
The clinical significance of hemorrhage depends on:
1. Volume of blood loss.
2. rate of bleeding.
3. Site of hemorrhage.
4. Duration (acute versus chronic or recurrent).
Shock :
Also called cardio-vascular collapse, is defined as systemic hypo-perfusion caused by reduction
either in cardiac output or in the effective circulating blood volume.
The end results are:
1. Hypotension.
2. Impaired tissue perfusion.
3. Cellular hypoxia.
Initially, there will be a reversible cellular injury, persistence of the shock eventually causes
irreversible tissue injury and can lead to the death of the patient.
Shock is categorized into:
1. Cardiogenic.
2. Hypovolemic.
3. Septic.
4. Neurogenic.
5. Anaphylactic.
Cardiogenic shock
Myocardial pump failure: which may be caused by :
1-Intrinsic myocardial damage (MI , ventricular arrhythmias )
2-Extrinsic compression (cardiac tamponade)
3-Out flow obstruction (pulmonary embolism)
Principle mechanism is failure of myocardial pump →sudden fall in C.O.
Hypovolemic shock
result from:
loss of blood or plasma volume as in hemorrhage, fluid loss from sever burns, vomiting
&diarrhea or trauma.
Principle mechanism: inadequate blood or plasma volume→ low Cardiac Output
Septic shock
Is caused by microbial infections.
Most commonly(70%) this occurs in the setting of G- infections (endotoxic shock) but it can
also occur after G+ bacteria septicemia or even fungal sepsis.
The toxins produced by these bacteria causes peripheral vasodilatation & pooling of blood;
endothelial activation /injury, leukocyte induced damage and DIC.
Neurogenic shock:
occurs following an anesthetic accident or spinal cord injury. Loss of vascular tone
and peripheral pooling of blood.
Anaphylactic shock :initiated by type 1 hypersensitivity reaction (Ig E mediated) → systemic
vasodilatation & ↑vascular permeability
Shock is the final common pathway for a number of potentially lethal clinical events.
Stages of shock
Unless the insult is massive and rapidly lethal, shock tends to evolve through 3 stages.
1-Initial non-progressive stage:
During which reflex compensatory mechanisms are activated &perfusion of vital organs is
maintained which include: neurohumoral mechanisms help to maintain the cardiac output &
blood pressure.
These compensatory mechanisms include:
baroreceptors reflexes
release of catecholamines
activation of renin –angiotensin axis
release of antidiuretic hormone (ADH)
generalized sympathetic stimulation
The net effect is tachycardia, peripheral vasoconstriction and renal conservation of fluid .
Cutaneous vasoconstriction is responsible for coolness & pallor of skin in shock .
Coronary & cerebral vessels are less sensitive to the sympathetic response & thus maintain
relatively normal caliber, blood flow →oxygen delivery to the vital organs .
Septic shock initially cause cutaneous vasodilatation and thus the patient presents with
warm & flushed skin.
2-progressive phase:
Characterized by tissue hypoperfusion &worsening of circulatory &metabolic imbalance .
if tissue hypoxia is persistent →intracellular aerobic respiration is replaced by anaerobic
glycolysis, with excessive production of lactic acid →metabolic lactic acidosis →↓tissue pH
and blunts the vasomotor response →arteriolar dilatation and pooling of blood in the
microcirculation →worsen the C.O. ,anoxic injury to the endothelial with subsequent DIC.
With this wide tissue hypoxia, vital organs are affected and begin to fail ; clinically the patient
may become confused & urinary output declines.
3-irreversible stage:
Cellular and tissue injury (due to lysosomal enzyme leakage) is so severe that even if the
hemodynamic defects are corrected, survival is not possible. The patient has complete renal
shutdown due to acute tubular necrosis.
Morphology: The cellular and tissue changes are those of hypoxic injury. Most particularly
involved organs are;
brain, heart, lungs, kidneys, adrenals and gastro-intestinal tract.
Clinical features: they depend on the precipitating insult.
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 initially is warm and flushed due to peripheral vasodilation.
Prognosis :
Varies with the origin of shock and its duration.
The best is in a young patient with hypovolemic shock, and the worst is in an old patient with
cardiogenic shock and that with septic shock.