Hemodynamic Disorders- I

1/25/23 Deborah Dalmeida MD 1

 CV2.4: Apply knowledge of biochemical and cellular physiology
to correlate the pathogenic mechanisms resulting in the cellular
alterations in hemodynamics with the pathological changes
Given a clinical case, scenario, laboratory data, graph, or image, the student
should be able to:
CV2.4.1. Interpret the pathophysiologic categories of edema
CV2.4.2. Decipher with examples, how edema can be produced as a result of
changes in hydrostatic pressure or plasma oncotic pressure.

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Factors influencing fluid movement across capillary walls

§ Hydrostatic and osmotic forces are

nearly balanced so that there is
little net movement of fluid out of
vessels

1/25/23 Deborah Dalmeida MD 3

Factors influencing fluid movement across capillary walls
§ Hydrostatic pressure (PH) pushes fluid
out of capillaries/venules

§ PO keeps fluid in vessels.

§ When PH >PO, so fluid is leaving the

vessel and entering the interstitial
space (net transudation) (see left)

§ When both pressures are equal, there

is no fluid movement into the interstitial Starling forces in a capillary/venule

space. (see middle)

§ When PO > PH, there is net

reabsorption of fluid (see right)
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 Lumio Smart activity

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Edema versus Effusions

qEdema qEffusion

§ Accumulation of fluid within tissues § Accumulation of fluid within the

when the net rate of fluid body cavity when the net rate of
movement exceeds the rate of fluid movement exceeds the rate of
lymphatic drainage lymphatic drainage

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 Clinical grading of edema

Pitting versus non-pitting edema

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Pathophysiologic categories of edema
q Congestive heart failure
q Increased Hydrostatic Pressure
§ Left heart failure:
§ Impaired venous return.

ü Congestive heart failure Increased PH in the pulmonary capillaries

ü Constrictive pericarditis transudate enters the alveoli & interstitium of the lungs
ü Ascites (liver cirrhosis)
pulmonary edema
ü Venous obstruction or compression

• Thrombosis § Right heart failure:

• External pressure (e.g., mass)

↑PH in vena cava
• Lower extremity inactivity with
prolonged dependency transudate enters the interstitial tissue around the ankles

and lower leg

Pitting edema
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C. Pulmonary edema in a patient with left-sided heart failure (LHF). This
histologic section shows lung alveoli filled with pink-stained edema fluid (F),
representing a transudate caused by increased PH in the pulmonary capillaries Dependent pitting edema showing depressions in
from LHF the skin around the ankle after gentle pressure
with the finger is applied and then released
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 qDecreased oncotic pressure
qLiver Cirrhosis § Liver cirrhosis
cirrhosis of the liver
Cirrhosis of the liver

the parenchyma is entirely replaced

by fibrous tissue decreased liver synthesis of

the PH within the portal vein albumin (hypoalbuminemia)

markedly increases

Portal hypertension Decrease in PO

ascites
a transudate enters the peritoneal
cavity
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Pathophysiologic categories of edema
q Decreased oncotic pressure

ümalnutrition with decreased protein

intake

ünephrotic syndrome with increased

loss of protein in urine
(>3.5 g/24 hr)

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Pathophysiologic categories of edema
qLymphatic obstruction
§ Lymphedema after a modified
radical mastectomy and
radiation therapy
§ Breast lymphedema
(inflammatory carcinoma), due
to blockage of subcutaneous
lymphatics by malignant cells
§ Lymphedema in filariasis, due
to Wuchereria bancrofti
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Pathophysiologic categories of edema
qSodium and Water Retention • Renal conditions- acute and

§ causes both increased hydrostatic chronic renal failure,

pressure (due to intravascular fluid glomerulonephritis

volume expansion) and diminished • Congestive heart failure

vascular colloid osmotic pressure
(due to dilution)

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Pathophysiologic categories of edema
q Inflammation

§ Increased permeability of
venules

§ Exudate
§ Bee sting
§ Cellulitis

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Miscellaneous - Myxedema
§ increased synthesis of extracellular
matrix components (e.g.,
glycosaminoglycans).

§ T-cell cytokines stimulate fibroblasts to Pretibial myxedema in

Graves disease. Note the
synthesize excess amounts of thickened area of erythema
hyaluronic acid involving the pretibial area
and dorsum of the foot
§ Examples:
a. pretibial myxedema and
exophthalmos in Graves disease Primary hypothyroidism in
a patient with Hashimoto
b. periorbital puffiness in Hashimoto thyroiditis. The patient has
a puffy face, particularly
thyroiditis around the eyes (localized
myxedema), and coarse
hair.
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Summary of Pathophysiologic categories of edema
A. Increased hydrostatic pressure C. Lymphatic obstruction
Congestive heart failure Neoplastic
Ascites in Liver cirrhosis Post irradiation
Lower extremity activity with prolonged D. Sodium retention
dependency
B. Reduced oncotic pressure Excessive salt intake with renal insufficiency
Nephrotic Syndrome E. Inflammation
Liver cirrhosis Bee sting, Cellulitis
Malnutrition
Protein losing gastroenteropathy

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o A 2-question quiz coming up via MS
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Point separately and select the correct
answer for Q1. Scroll down on the
same slide to attempt Q2.
o Multiple attempts
3 ways to access practice
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correct answers immediately after 3. Click on the link located
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submitting the quiz. topic on BlackBoard
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18
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 Thank You

1/25/23 20
Link to Flashcards: https://www.brainscape.com/p/223Q8-LH-6OSSC
Hemodynamic Disorders- I
1/25/23 Deborah Dalmeida MD 1
Morphology qPulmonary edema
§ lungs are two to three times their
qSubcutaneous edema normal weight

§ distribution is § Sectioning yields frothy, blood-tinged

fluid—a mixture of air, edema, and
influenced by gravity
extravasated red cells
§ Dependent
qBrain edema
§ pitting edema
§ localized or generalized
qRenal dysfunction – § generalized edema - the brain is
generalized edema, grossly swollen with narrowed sulci;
periorbital edema. distended gyri show evidence of
compression against the unyielding
skull
The surface of the brain with cerebral edema
demonstrates widened gyri with a flattened surface. The
sulci are narrowed.
1/25/23 Deborah Dalmeida MD 2
Clinical Consequences
§ Subcutaneous tissue edema: impair • Peritoneal effusions (ascites) : prone
wound healing or the clearance of to seeding by bacteria
infection

§ Pulmonary edema: impede oxygen

diffusion, favorable environment for
bacterial infection

§ Brain edema: compression of the

medullary center death

1/25/23 Deborah Dalmeida MD 3

 CV2.4: Apply knowledge of biochemical and cellular physiology
to correlate the pathogenic mechanisms resulting in the cellular
alterations in hemodynamics with the pathological changes
Objective:Given a clinical case, scenario, laboratory data, graph, or image, the
student should be able to:
CV2.4.3. Analyze the clinical, morphological, and physiological significance of
hyperemia, congestion, and hemorrhage with respect to the disease states that
cause them.

1/25/23 Deborah Dalmeida MD 4

Hyperemia and Congestion
Hyperemia Congestion

§ active process § passive process

§ arteriolar dilation à increased blood § results from reduced outflow of blood

flow from a tissue

§ Affected tissues turn red (erythema) § Affected tissues take on a dusky

because of increased delivery of reddish-blue color (cyanosis) due to
oxygenated blood. red cell stasis and the presence of
deoxygenated hemoglobin

§ May be systemic or localized

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Morphologic changes in congestion
qMay be acute or chronic

qAcute passive congestion

§ a consequence of acute left or
right ventricular failure.
§ Acute LVF: blood backs up into
the lungs àtransudate in alveoli
àpulmonary edema.
§ Microscopic features: engorged Alveoli in this lung are filled with a smooth to slightly floccular
alveolar capillaries, alveolar septal pink material characteristic for pulmonary edema. Note also that

edema, and focal intraalveolar the capillaries in the alveolar walls are congested with many red
blood cells.
hemorrhage

1/25/23 Deborah Dalmeida MD 6

Morphologic changes in congestion
qAcute right ventricular failure

§ Acute liver congestion

§ Microscopic features:
§ central vein and sinusoids are
distended.
§ centrilobular hepatocytes may
undergo ischemic necrosis
§ Periportal hepatocytes – fatty change

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Morphologic changes in congestion
b. Thickened and fibrotic alveolar septae
q Chronic passive congestion
c. The pulmonary interstitium becomes
§ Chronic left ventricular failureà left heart fibrotic. The combination of fibrosis and
cannot pump out the blood flowing in from the iron makes the lungs firm and brown
lungsà creating back pressureà chronic (brown induration).
passive pulmonary congestionà alveolar
capillaries experience increased pressureà
become engorged with blood

§ Consequences:

a. Microhemorrhagesà bleeding into alveolar

spaces àerythrocytes are phagocytosedà
degraded by alveolar macrophagesà Released
iron, in the form of hemosiderin, remains in these
macrophages àcalled “heart failure cells”
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Morphologic changes in congestion
qChronic passive congestion of liver:
§ centrilobular regions are grossly red-
brown and slightly depressed
(because of cell death) and are
accentuated against the surrounding
zones of uncongested tan liver
§ Resembles the cut surface of a
nutmeg – ‘nutmeg liver’
§ M/F: centrilobular hemorrhage,
hemosiderin-laden macrophages, and
variable degrees of hepatocyte
dropout and necrosis
1/25/23 Deborah Dalmeida MD 9
o A 1-question quiz coming up via MS
Forms
o Pause the video, open your Power
Point separately and select the correct
answer for Q1.
o Multiple attempts
o Anonymous
o Responders will see their results and
correct answers immediately after
submitting the quiz.

1/25/23 Deborah Dalmeida MD 10

1/25/23 Deborah Dalmeida MD 11
 Thank You

1/25/23 12
Link to Flashcards: https://www.brainscape.com/p/223Q8-LH-6OSSC