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