Pathophysiology: Edema and Congestion

Distribution of body water

Hemodynamics: study of blood flow and forces that govern it

Body fluids distributed between intracellular and extracellular compartments

Normal Hemodynamics Review

Hydrostatic Pressure: Force exerted upon the vessel walls by the contained fluid

Colloid Osmotic Pressure: Created by the difference in protein concentration within the tissue and blood

Net Filtration Pressure: Determines movement fluid into the tissue or into the blood

Edema

Palpable swelling produced by an increase in interstitial fluid volume

Generalized: Heart failure, liver failure, and renal disorders

Localized: DVT, lymphatic obstruction, and chronic venous insufficiency

Edema: Cause #1

Overall cause: poor venous circulation and resultant fluid accumulation. Portol vein gets blocked by scar tissue

Two forms:

Localized: Impaired venous outflow: DVT, external pressure, Lower extremity inactivity, and liver disease- ascites

Systemic ¤ Congestive heart failure, constrictive pericarditis (layer around heart, inflammation squeezes heart)

Edema: Cause #2

Decreased Plasma Colloid Osmotic Pressure

Overall cause: protein concentration in blood is lower than in ISF. Plasma proteins attract water. Proteins go into tissue and pressure decreases. Filtration occurs. Fluid is pulled out

Most influential protein = albumin (made in liver)

Two forms: Decreased synthesis and increased excretion/loss (damaged glomerular filtrate, causing proteins to be urinated out), malnutrition (not enough albumin)

Consequences of Reduced Plasma Osmotic Pressure

Fluid leaves the plasma and causes a reduced intravascular volume (into tissue), blood volume drops, affecting mean arterial pressure. MAP = HR x SV x TPR (total peripheral resistance)

HR(heartrate) x SV(stroke volume) = CO (cardio output)

Flow - deltaP/R

How does the body handle reduced intravascular volume? Decreased BV decreases EDV, in turn SV, then MAP. Constriction increases resistance. EDV (end of diastole) - ESV (end of systole) = SV. Renin is released as response, angiotensinogen is cleaved, angiotensin 1 cleaved into angiotensin 2 which causes aldosterone release by adrenal cortex and vasoconstriction. Aldosterone increases sodium absorption and potassium secretion. Water gets pulled out of filtrate and enters blood and increases BV and BP. Aldosterone causes ADP increases water reabsorption. Aldosterone increases thirst.

Edema: Cause #3

Na+ and H2O Retention

Primary or secondary

Excessive salt intake with renal insufficiency. If sodium isn’t able to be urinated then there will be buildup. Increased hydrostatic pressure

Increased tubular reabsorption of Na+ RAAS

Causes: Increased hydrostatic pressure and diminished vascular colloid osmotic pressure (retaining lots of fluid, diluting plasma proteins)

Edema: Cause #4

Lymphatic Obstruction

Lymphatic system provides a route for fluid from interstitial spaces to return to circulation

Impaired lymphatic drainage - lymphedema

Usually localized

Causes: Inflammatory, neoplastic, postsurgical, post-irradiation, and parasitic infections (filariasis)

Edema: Cause #5

Increased Vascular Permeability

Caused by inflammation

Histamine and bradykinin cause proteins to leak into tissue and water follows

Edema Morphology

Generally soft and can be moved around

Pitting edema

Non-pitting edema

Dependent edema

Pitting Edema

Pressure applied to swollen area by depressing skin with thumbindentation remains Displacement of fluid

Tells you how much fluid there is by how much it indents and how long it stays indented

Non-pitting Edema

Pressure that is applied to the skin does NOT result in indentation

Certain disorders of the lymphatic system

Thyroid disorders

Localized infection, trauma can cause it

Caused by excess plasma proteins in area and less water

Dependent Edema

Positional- lower extremity edema is more pronounced when in the standing position

Caused by gravity, increases swelling

Caused by increased hydrostatic pressure

Passive Vascular Congestion

Congestion: Increased blood within vessels in a given region

Passive - impairment in drainage of blood from an area. Leads to increased in hydrostatic pressure

Causes:

Local: isolated venous obstruction

Systemic: cardiac failure

Color of tissue: cyanotic (blue)

Big cause of PVC: CHF

Congestive heart failure (CHF): Heart cannot pump sufficiently to maintain adequate blood flow to meet the needs of the body. Diseases that damage (ie. ischemia- myocardial infarction, coronary arteries are blocked) or overload myocardium (ie. increased blood pressure, hypertension)

Left -sided heart failure (most common): Increased pulmonary venous pressure = pulmonary edema. Impaired venous drainage, increased hydrostatic pressure

Right -sided heart failure: Increased systemic venous pressure = systemic edema

Complications: Development of localized or systemic cyanosis, edema, dilation of veins in affected area, varices, permanent tissue changes, tissue hypoxia, and rupture of varices. Big cause is DVT

RAAS

Renin Angiotensin Aldosterone System, compensatory mechanism in response to hearth failure: Response to heart failure. Makes things worse. Sodium and water reabsorpion increased, hydrostatic pressure further increases and edema worsens. Calloid osmotic pressure decreases, also caused edema.

Active Vascular Congestion

Increase in blood flow to an area

Caused by dilation of arterioles

Ex: acute inflammation, delivery of blood due to increased demand, color of tissue: red

Hemorrhage

Definition: Escape of blood from the cardiovascular system, accumulation in tissues or spaces of body and/or actual escape from the body

Associated with: Chronic congestion, hemorrhagic diathesis, and vascular injury (most common cause)

Categories: Bleeding into environment, bleeding into tissue, bleeding into body cavity:

Hemopericardium (bleeding in membrane around heart), Hemothorax (chest cavity), and Hemoperitoneum (abdominal cavity)

Consequences of bleeding depends on: 3 things: rate/volume of blood loss, site of bleeding (vessel, area), loss of iron

Hemorrhage into tissue

Petechiae: Pinpoint, 1-2 mm hemorrhages into skin, mucous membranes, serosal surfaces, associated with: Increased intravascular pressure, low platelet counts, defective platelet function, DIC, infectious diseases, and medications

Purpura: >3 mm. Causes: Same as petechiae PLUS vasculitis and increased vascular fragility. Senile purpura

Ecchymoses AKA: “bruise” (NOT ACTUALLY A BRUISE): >1-2 cm, platelet abnormalities, and coagulopathies