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The physiology of edema.

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Presentation on theme: "The physiology of edema."— Presentation transcript:

1 The physiology of edema.

2 Edema: The abnormal accumulation of fluid in a specific organ vs generalized. In capillary: Balance between hydrostatic pressure and oncotic (colloid osmotic) pressure.

3 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

4 Interstitial hydrostatic pressure:
Varies from one organ to another: Subcutaneous tissue: Subatmospheric (-2 mmHg) Liver, kidney: + Brain: As high as 6 mmHg

5 Oncotic pressure: Capillary wall usually impermeable to plasma proteins and other colloids. Only water and small solutes cross capillary wall. Crystalloids vs colloids

6 These colloids exert an osmotic pressure of about 25 mmHg.
The colloid osmotic pressure due to the plasma colloids=oncotic pressure.

7 Edema: Due to disturbance in hydrostatic and/or oncotic pressure between intra-capillary and interstitial component.

8 Organ specific: Brain: Cerebral edema
Lung: Intra-alveolar=pulmonary edema, intra-pleural=pleural effusion Peritoneum=ascites Severe generalized edema=anasarca

9 Reduced oncotic pressure:
Reduction in production of colloids--- plasma proteins. Liver failure Malnutrition

10 Increase in loss of colloids--- plasma proteins.
Nephrotic syndrome Catabolic states

11 Increase capillary hydrostatic pressure:
Venous end: Heart failure, deep venous thrombosis, superior vena cava obstruction etc. Arterial end: Pre-capillary dilatation. Calcium channel blockers.

12 Increased interstitial oncotic pressure:
Lymphatic obstruction: Primary vs secondary group.

13 Capillary leaks: Result of capillary damage:
Pleura: Infections, tumors Alveoli: Inhalation of noxious substance, eg chlorine gas etc

14 Diverse causes of edema:
Anaemia Hypothyroidism

15 Hormones involved in edema:
Renin angiotensin aldosterone system: secondary hyperaldosteronism ADH (Vasopressin) ANP

16 Clinical physiological approach to edema:
Hypervolemia: Vs Normovolemia:

17 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

18 Normal JVP: Unilateral Unilateral increase in capillary pressure
Deep venous thrombosis OR: Unilateral increase in interstitial colloid osmotic pressure Lymphatic obstruction (radiation, filariasis, congenital)

19 Edema due to capillary hypertension with normal venous pressure:
Pre-capillary dilatation: Calcium channel blockers

20 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

21 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:

22 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:

23 Sinus rhythm or not. Pulmonary hypertension 3`rd degree heart block Patency between SVC and RA Tricuspid regurgitation and stenosis


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