Disorders of Volume Homeostasis: Edema
net effect: decreased effective circulating fluid volume (ECFV) leads to decreased renal sodium and water excretion
ß ECFV has three effects:
Ý plasma oncotic pressure and ß hydrostatic pressure Þ ß GFR
(2) ß Plasma Volume Þ ß venous and arterial pressure Þ Ý sympathetic nervous system activity and Ý renin-angiotensin activity Þ ß GFR, Ý filtration fraction Þ Ý proximal and distal tubular sodium reabsorption
(3) Ý plasma osmolality Þ Ý ADH secretion (also increases due to ß Plasma Volume) Þ Ý distal nephron water reabsorption
thus, sodium and water excretion is decreased and ECFV is preserved
Perturbation in salts and H2O regulatory mechanisms in each of the following conditions
Ý venous Pressure Þ Ý capillary hydrostatic pressure Þ shift in starling forces Þ Ý ECFV = Edema
Forward Failure: ß CO Þ ß Effective Blood VolumeÞ Systemic Hemodynamic Response Þ Ý Plasma Vol ¹ Ý COÞÝ ECFV = Edema
Liver destruction Þ ß Albumin Synthesis Þ ß Capillary oncotic pressure Þ Ý ECFV, EDEMA, Ascites
Liver destruction Þ impedes splanchnic drainageÞ Ý portal venous pressure Þ arterio venous fistula Þ
Þ ß peripheral resistance Þ Ý CO and ß tissue perfusion Þ ß Effective circulating VolumeÞ Systemic Hemodynamic Response Þ Ý Plasma Vol Þ Ý ECFV = Edema, Ascites
Renal damage Þ massive urinary protein loss Þ ß plasma albumin concentration Þ ß capillary oncotic pressureÞ ß Effective blood vol Þ Systemic Hemodynamic Response Þ Ý Plasma Vol Þ Ý ECFV = Edema
In all three conditions the negative feedback loop of Ý ECFV does not occur, resulting in continued edema
palpable swelling produced by expansion of interstitial fluid volume.
can be localized or generalized (anasarca)
There are two steps in edema formation
Þ expanding ECFV
Note: intracellular and extracellular fluid compartments are in osmotic equilibrium.
changes in Na do not determine movement of fluid from plasma to interstitium. In these compartments Na is an ineffective osmolyte; protein is an effective osmolyte.
- (1) change in capillary hemodynamics that favors fluid movement from vascular to interstitial compartment
- (2) Renal retention of Na and H2O
Role of kidney in Edema Formation
Kidney is essential in edema formation. without a change in renal handling of Na and H2O, edema does not occur.
Edema is not clinically apparent until 2-3 L of fluid moves from the vascular to the interstitial compartments.
Retention of Na by the kidney is an appropriate response in this setting, even though it promotes edema, because loss of 2-3 L from CO would otherwise result in shock.
This illustrates primacy of EVC (effective circulating volume-fullness of arterial circulation) in controlling ECFV
Capillary Hemodynamics and Starling’s Law
Fluid movement between the capillary and interstitium is determined by the hydraulic and oncotic pressures in each compartment:
Starling’s Law Net filtration = Kf(D hydraulic pressure - D oncotic pressure)
p cap -p is)]
Kf is the product of the permeability or porosity of the capillary wall x the filtration surface area .
Oncotic pressures are determined primarily by albumin.
Interstitial fluid accumulation is additionally controlled by the rate of fluid removal by the lymphatics.
Net effect is small gradient (0.3mmHg) favoring filtration.
Starling’s Forces: Hydraulic Pressures
Capillary hydraulic pressure is generated by cardiac contraction, but auto regulation makes hydraulic pressure relatively insensitive to variation in mean arterial pressure
Capillary autoregulation is controlled primarily by the precapillary sphincter, which is under local baroreceptor and hormonal control (ie, endothelial-derived paracrine mediators).
Capillary autoregulation is so efficient that patients with hypertension rarely develop edema.
In contrast, resistance at the venous end is not well-regulated, and an Ý in venous pressure can Ý Pcap and Þ edema
Starling’s Forces: Oncotic Pressures
Oncotic pressure in capillary due mainly to plasma protein, ie, albumin. (Note: Na = ineffective osmolyte, freely crosses cap)
Effective interstitial solutes are filtered proteins (ie, albumin) > mucopolysaccharides.
A fall in plasma albumin will reduce the plasma oncotic pressure and favor fluid movement from the capillary into the interstitium.
Mechanisms and Causes of Edema Formation
Þ fluid flow into interstitium
(2) Renal Na retention and expansion of ECFV
Most common change is increased Pcap, especially due to venous obstruction.
Less frequently, edema results from ß p plasma, Ý capillary permeability, or lymphatic obstruction.
Renal Na Retention and Edema
wihtout renal Na retention edema will not form. 2 mechanisms account for renal retention.
- (1) Large change in Starling forces
Appropriate Na retention by kidney restores and preserves ECV: hormones = renin-Ang II-aldo, norepi, ADH
Primary Na retention occurs in advanced stages of renal disease.
Compensated state: mild disease (MI, CHF), renal response = restored ECV at new Steady state, but with edema.
- (1) Compensatory response to depletion of ECV
- (2) Primary retention of Na
Treatment of Edema
Dietary reduction in Na.
Prescribe diuretics to inhibit (control) Na retention by the kidney.