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The physiology of edema.
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Edema: The abnormal accumulation of fluid in a specific organ vs generalized. In capillary: Balance between hydrostatic pressure and oncotic (colloid osmotic) pressure.
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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
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Interstitial hydrostatic pressure:
Varies from one organ to another: Subcutaneous tissue: Subatmospheric (-2 mmHg) Liver, kidney: + Brain: As high as 6 mmHg
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Oncotic pressure: Capillary wall usually impermeable to plasma proteins and other colloids. Only water and small solutes cross capillary wall. Crystalloids vs colloids
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These colloids exert an osmotic pressure of about 25 mmHg.
The colloid osmotic pressure due to the plasma colloids=oncotic pressure.
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Edema: Due to disturbance in hydrostatic and/or oncotic pressure between intra-capillary and interstitial component.
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Organ specific: Brain: Cerebral edema
Lung: Intra-alveolar=pulmonary edema, intra-pleural=pleural effusion Peritoneum=ascites Severe generalized edema=anasarca
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Reduced oncotic pressure:
Reduction in production of colloids--- plasma proteins. Liver failure Malnutrition
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Increase in loss of colloids--- plasma proteins.
Nephrotic syndrome Catabolic states
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Increase capillary hydrostatic pressure:
Venous end: Heart failure, deep venous thrombosis, superior vena cava obstruction etc. Arterial end: Pre-capillary dilatation. Calcium channel blockers.
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Increased interstitial oncotic pressure:
Lymphatic obstruction: Primary vs secondary group.
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Capillary leaks: Result of capillary damage:
Pleura: Infections, tumors Alveoli: Inhalation of noxious substance, eg chlorine gas etc
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Diverse causes of edema:
Anaemia Hypothyroidism
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Hormones involved in edema:
Renin angiotensin aldosterone system: secondary hyperaldosteronism ADH (Vasopressin) ANP
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Clinical physiological approach to edema:
Hypervolemia: Vs Normovolemia:
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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
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Normal JVP: Unilateral Unilateral increase in capillary pressure
Deep venous thrombosis OR: Unilateral increase in interstitial colloid osmotic pressure Lymphatic obstruction (radiation, filariasis, congenital)
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Edema due to capillary hypertension with normal venous pressure:
Pre-capillary dilatation: Calcium channel blockers
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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
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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:
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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:
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Sinus rhythm or not. Pulmonary hypertension 3`rd degree heart block Patency between SVC and RA Tricuspid regurgitation and stenosis
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