Transcript The physiology of edema. - Department of Library Services

The physiology of edema.
Edema:
• The abnormal accumulation of fluid in a
specific organ vs generalized.
• In capillary: Balance between
hydrostatic pressure and oncotic
(colloid osmotic) pressure.
Hydrostatic pressure:
• Intra-capillary vs interstitial
• Capillary pressures vary:
• Nail bed capillaries: 32 mmHg at arteriolar
end and 15 mmHg at venous end. Mean
25 mmHg.
• Hydrostatic pressure gradient:
• Intra-capillary hydrostatic pressure –
interstitial fluid hydrostatic pressure
Interstitial hydrostatic pressure:
• Varies from one organ to another:
• Subcutaneous tissue: Subatmospheric (-2
mmHg)
• Liver, kidney: +
• Brain: As high as 6 mmHg
Oncotic pressure:
• Capillary wall usually impermeable to
plasma proteins and other colloids.
• Only water and small solutes cross
capillary wall.
• Crystalloids vs colloids
• These colloids exert an osmotic pressure
of about 25 mmHg.
• The colloid osmotic pressure due to the
plasma colloids=oncotic pressure.
Edema:
• Due to disturbance in hydrostatic and/or
oncotic pressure between intra-capillary
and interstitial component.
Organ specific:
• Brain: Cerebral edema
• Lung: Intra-alveolar=pulmonary edema,
intra-pleural=pleural effusion
• Peritoneum=ascites
• Severe generalized edema=anasarca
Reduced oncotic pressure:
• Reduction in production of colloids--plasma proteins.
• Liver failure
• Malnutrition
• Increase in loss of colloids--- plasma
proteins.
• Nephrotic syndrome
• Catabolic states
Increase capillary hydrostatic
pressure:
• Venous end: Heart failure, deep venous
thrombosis, superior vena cava
obstruction etc.
• Arterial end: Pre-capillary dilatation.
Calcium channel blockers.
Increased interstitial oncotic
pressure:
• Lymphatic obstruction:
• Primary vs secondary group.
Capillary leaks:
• Result of capillary damage:
• Pleura: Infections, tumors
• Alveoli: Inhalation of noxious substance,
eg chlorine gas etc
Diverse causes of edema:
• Anaemia
• Hypothyroidism
Hormones involved in edema:
• Renin angiotensin aldosterone system:
secondary hyperaldosteronism
• ADH (Vasopressin)
• ANP
Clinical physiological approach to
edema:
• Hypervolemia:
• Vs
• Normovolemia:
Jugular venous pressure:
• Elevated and pulsating:
• =hypervolemia
• Then edema:
• Due to increased capillary hydrostatic
pressure:
• Cardiac failure, or isolated RV (pulm HT)
• Hypervolemia caused by transfusion
Normal JVP:
• Unilateral
• Unilateral increase in capillary pressure
• Deep venous thrombosis
• OR:
• Unilateral increase in interstitial colloid
osmotic pressure
• Lymphatic obstruction (radiation, filariasis,
congenital)
• Edema due to capillary hypertension with
normal venous pressure:
• Pre-capillary dilatation:
• Calcium channel blockers
Generalized edema without
hypervolemia:
• Decreased capillary colloid oncotic pressure:
liver, kidney, catabolic states, malnutrition.
• Increased interstitial colloid oncotic pressure:
lymphatic.
• Increase in capillary permeability: Inflammation,
toxins, severe anaemia
Pressure changes in the heart:
• Atria: Study curve in Ganong: jugular
venous pressure curve, also known as
flobogram, indicative of pressure
changes in superior vena cava/ right
atrium.
• 3 waves in the curve:
• a-wave: atrial systole
• c-wave: bulging of tricuspid valve into R
atrium
• v-wave: rise in atrial pressure, just before
tricuspid valve opens during diastole.
• Clinical application of these 3 waves:
• Sinus rhythm or not.
• Pulmonary hypertension
• 3`rd degree heart block
• Patency between SVC and RA
• Tricuspid regurgitation and stenosis