Hemodynamics

Question 1

What are edema and effusionaps

Answer 1

Disorders that perturb cardiovascular, renal, or
hepatic function are often marked by the
accumulation of fluid in tissues (edema) or
body cavities (effusions).

Question 2

2 types of localized edema

Answer 2

Inflammatory
– Combination of increased blood flow due to
arteriolar vasodilation AND increased leakiness of
capillary endothelium
• Mechanical
– Blockage of lymph vessels
• Filariasis (nematode infection)
• Neoplasia
• Chemoterapy/radiotherapy damage to lymphatics

Question 3

3 types of systemic edema with examples

Answer 3

• Increased hydrostatic pressure
– Gravity
– Congestive Heart Failure
– Venous Obstruction
• DVT, Vena cava obstruction
• Cirrhosis –backs up blood in hepatic portal system
• Constrictive Pericarditis –similar to CHF, heart can’t pump
• Reduced Osmotic Pressure
– Liver failure (not making enough albumin)
– Nephrotic syndrome (losing too much albumin)
• Sodium (and water) retention
– Acute renal failure

Question 4

Describe hyperemia and congestion

Answer 4

Hyperemia and congestion both stem from increased blood
volumes within tissues, but have different underlying mechanisms
and consequences.
• Hyperemia is an active process in which arteriolar dilation (e.g., at
sites of inflammation or in skeletal muscle during exercise) leads
to increased blood flow. Affected tissues turn red (erythema)
because of increased delivery of oxygenated blood.
• Congestion is a passive process resulting from reduced venous
outflow of blood from a tissue. It can be systemic, as in cardiac
failure, or localized, as in isolated venous obstruction.
• Congested tissues have an abnormal blue-red color (cyanosis) that
stems from the accumulation of deoxygenated haemoglobin in the
affected area.

Question 5

What is hemorrhage

Answer 5

Hemorrhage generally indicates extravasation of blood due to
vessel rupture

Question 6

3 types of hemorrhage

Answer 6

Petechiae: Minute 1- to 2-mm hemorrhages into skin, mucous
membranes, or serosal surface
Purpura: Slightly larger (≥3 mm) hemorrhages.
Ecchymoses: Larger (>1 to 2 cm) subcutaneous hematomas
(i.e., bruises).

Question 7

What is hematoma and give the 4 different types

Answer 7

Hematoma = collection of blood in an organ or tissue:
Hemothorax: in the thorax
Hemoperitoneum: in the peritoneum
Hemopericardium: in the pericardium
Hemarthrosis: in joint

Question 8

What is hemostasis

Answer 8

Sequence of events following vascular injury that
results in the formation of a clot (stasis)

Question 9

2 key regulators of hemostasis

Answer 9

endothelial cells and platelets

Question 10

What is thrombosis

Answer 10

It represents hemostasis in the intact vascular
system.
• It is a process by which a thrombus is formed.
• A thrombus is a solid mass of blood
constituents which develops in artery or vein.
• Is intravascular coagulation of blood often
causing significant interruption to blood flo

Question 11

Pathogenesis of thrombosis

Answer 11

Three primary influences predispose to
thrombus formation, the so-called Virchow
triad:
1. endothelial injury
2. stasis or turbulence of blood flow
3. blood hypercoagulability
In other words it results from interaction
platelets, damaged endothelial cells and the
coagulation cascade.

Question 12

Describe endothelial injury

Answer 12

Endothelial injury:
• Direct injury
• Depletion of anticoagulants
(e.g. PGI2 by Cox-2 inhibitors)
• Upregulation of procoagulants
(e.g. inflammation)

Question 13

Describe abnormal blood flow

Answer 13

Aneurismal dilation of
vessels create local stasis
• Hyperviscosity (too many
erythrocytes in blood)
• Sickle cell anemia
• Turbulence at branchpoints

Question 14

Hypercoagubility

Answer 14

Hypercoagulability:
• Hormonal: estrogen increases production of clotting factors and reduces anticoagulant factors
• Prolonged bed rest or immobilization
• Myocardial infarction
• Atrial fibrillation
• Tissue injury (surgery, fracture, burn)
• Cancer
• Prosthetic

Question 15

The fate of a thrombosis in 4 main points

Answer 15

Dissolution: fibrinolytic activity completely clears thrombus
• Organization and recanalization or incorporation:
thrombi in vessels induce inflammation and fibrosis (organization); these
can recanalize (shown below) or they can become incorporated into the
vessel wall
• Propagation: thrombus stimulates further platelet aggregation and
growth that may eventually occlude vessel lumen
• Embolization: thrombi may break off and plug a distant site

Question 16

Describe venousthrombosis vs arterial thrombosis

Answer 16

Venous thrombosis
• Superficial (varicosities): cause local edema, pain, and perhaps
ulceration; rarely embolize
• Deep (i.e. “DVT”): rarely cause local pain due to collaterals, but often
embolize with significant consequences
Arterial thrombosis
• Atherosclerosis: rupture of plaques induces clotting and occlusion of
vessels
• Mural thrombosis: post-infarction or post-infection damage to lining of
heart induces formation of clots that can break off and plug a distant site.

Question 17

Describe embolism and 3 ways it occurs

Answer 17

Embolus = detached mass that is carried to a site distant
from its origin, for example:
Fat: bone marrow or soft tissue trauma releases adipocytes into blood that can plug
distant sites
Air: rapid depressurization causes gas to bubble out of solution; these gas bubbles within the
circulation can obstruct vascular flow (and cause distal ischemic injury) acting as thrombotic masses.
Bubbles may coalesce to form frothy masses sufficiently large to occlude major vessels.
Amniotic fluid: trauma during childbirth may allow amniotic fluid (and its non-fluid
contents such as dead skin cells, mucus, etc.) to enter maternal circulation and cause remote
blockages.

Question 18

Describe Thromembolism

Answer 18

Embolism causing blockage is derived from a
thrombus
The emboli ultimately lodge in vessels too small
to permit further passage, resulting in partial or
complete vascular occlusion leading to ischemic
necrosis of distal tissue, (infarction). Depending
on the site of origin, emboli may lodge in the
pulmonary or systemic circulations.

Question 19

2 types of thromboembolism

Answer 19

Pulmonary thromboembolism: thrombus (usually from a
DVT) breaks off and goes to right ventricle. From there it
is pumped out to the lungs and blocks pulmonary
arteries. The problem at first is not the ischemia per se,
but instead that this blood is not oxygenated and does
not return to the heart (thus eventually causing systemic
ischemia).
Systemic thromboembolism: thrombus originates in left
ventricular wall or wall of aorta breaks off and causes
infarction at a distant site (brain, kidney, spleen).

Question 20

What is infarction

Answer 20

Area of ischemic necrosis caused by occlusion of
arterial supply or venous drainage.

Question 21

The nature and
extent of damage is influenced by:
3 points

Answer 21

Nature of blood supply: tissues with dual or collateral blood
supply (e.g. lungs, liver, and limbs) are less affected compared to end
organs (muscles, brain, kidney, spleen)
Rate of development: slowly progressing occlusion tolerated
because of development of collateral routes
Tissue vulnerability: neurons can withstand only 3-4 minutes
of hypoxia, myocytes ~30 minutes, fibroblasts can survive many hours
in low oxygen.

Question 22

What is shock

Answer 22

Systemic hypoperfusion caused by reduced cardiac output or reduced
blood volume, resulting in 1) hypotension, 2) impaired tissue
perfusion, and 3) cellular hypoxia.

Question 23

Categories of shock

Answer 23

Cardiogenic: reduced cardiac output
Hypovolemic: reduced blood volume
Hemorrhagic: blood loss
Neurogenic: vasodilation following nerve cord injury
Anaphylactic: systemic vasodilation and respiratory insufficiency
Septic: over-reactive inflammatory response caused by systemic
microbial infection. Most commonly due to gram-negative infections (
endotoxic shock), but it can also occur with gram-positive and fungal
infections.

Question 24

Describe septic shock

Answer 24

Cytokine storm of TNF, IL-1, and IL-6 in response to
bacterial antigens (usu. lipopolysaccharides from
gram-negative bacilli) resulting in:
1) Systemic vasodilation
2) Reduced cardiac contractility
3) Widespread endothelial injury and activation
4) Systemic activation of clotting cascade (Disseminated
Intravascular Coagulation or “DIC”)

Question 25

Describe 3 stages of shock

Answer 25

• Nonprogressive stage: reflex compensatory mechanisms (tachycardia,
peripheral vasoconstriction, renal fluid retention) compensate for
hypoperfusion.
– Causes common symptoms associated with shock: weak, rapid pulse; shallow, rapid
breathing; and cool, clammy skin (the exception is septic shock that may present with
flushing due to widespread inflammatory response).
• Progressive stage: metabolic lactic acidosis blunts vasomotor response and
blood starts to pool in peripheral tissues (increasing hypercoagulative risk),
vital organs perfused less and begin to fail.
– Clinical symptoms associated with this phase are reduced urine output, acidosis, and
electrolyte imbalances
• Irreversible stage: widespread tissue necrosis induces systemic
inflammatory response (vasodilation, etc.), reduced cardiac function, and
acute renal failure.