• The body has powerful mechanisms that keep blood volume nearly constant.
• The body has powerful mechanisms that keep extracellular fluid volume nearly constant.
• Some abnormal conditions can cause large increases in blood volume.
• Some abnormal conditions can also cause large increases in extracellular fluid volume.
• Almost all of these conditions are caused by circulatory abnormalities.

Increased Blood Volume and Extracellular Fluid Volume Caused By Heart Diseases

• In congestive heart failure, blood volume may increase by 15% to 20%.
• In congestive heart failure, extracellular fluid volume may increase by 200% or more.
• The reason for these increases is explained in Fig. 30.14.
• Heart failure first reduces cardiac output.
• Reduced cardiac output decreases arterial pressure.
• Low arterial pressure activates several sodium-retaining systems.
• The RAAS is activated.
• The sympathetic nervous system is activated.
• Low blood pressure also causes the kidneys to retain salt.
• Low blood pressure also causes the kidneys to retain water.
• The kidneys retain fluid to restore arterial pressure toward normal.
• The kidneys retain fluid to restore cardiac output toward normal.
• If heart failure is not severe, increased blood volume can restore cardiac output to normal.
• Increased blood volume can also restore arterial pressure to normal.
• Sodium excretion eventually returns to normal.
• Blood volume remains increased.
• Extracellular fluid volume also remains increased.
• The extra fluid helps the weakened heart pump adequately.
• If the heart is severely weakened, arterial pressure cannot increase enough.
• Normal urine output cannot be restored.
• The kidneys continue to retain fluid.
• Severe circulatory congestion develops.
• Pulmonary edema may occur.
• The patient may die unless fluid retention is relieved.
• Improvement of cardiac function can also prevent this outcome.
• In myocardial failure, increased blood volume acts as an important circulatory compensation.
• In heart valvular disease, increased blood volume acts as an important circulatory compensation.
• In congenital heart disease, increased blood volume acts as an important circulatory compensation.
• This compensation helps restore cardiac output toward normal.
• This compensation helps restore blood pressure toward normal.
• This compensation allows the weakened heart to maintain a life-sustaining cardiac output.

Increased Blood Volume Caused By Increased Vascular Capacity

• Any condition that increases vascular capacity also increases blood volume.
• Extra blood volume fills the enlarged vascular capacity.
• Increased vascular capacity first reduces mean circulatory filling pressure.
• This relationship is shown in Fig. 30.14.
• Reduced mean circulatory filling pressure decreases cardiac output.
• Reduced cardiac output decreases arterial pressure.
• The fall in arterial pressure causes the kidneys to retain salt.
• The fall in arterial pressure causes the kidneys to retain water.
• Blood volume increases until the enlarged vascular capacity is filled.
• During pregnancy, vascular capacity increases.
• The uterus contributes to this increase.
• The placenta contributes to this increase.
• Other enlarged organs also contribute.
• Blood volume usually increases by 15% to 25% during pregnancy.
• Large varicose veins also increase vascular capacity.
• In rare cases, varicose veins may hold up to 1 extra liter of blood.
• Blood volume increases to fill the extra vascular capacity.
• The kidneys retain salt.
• The kidneys retain water.
• Blood volume continues to increase until the entire vascular bed is adequately filled.
• Blood pressure rises to the level needed to balance renal fluid output with daily fluid intake.

KEY CONCEPT

• Circulatory abnormalities are the main cause of large increases in blood volume and extracellular fluid volume.
• Heart failure → ↓ Cardiac output → ↓ Arterial pressure → ↑ RAAS + ↑ Sympathetic activity → ↑ Salt & water retention → ↑ Blood volume & ECF volume.
• Mild heart failure allows increased blood volume to restore cardiac output and blood pressure.
• Severe heart failure causes continued fluid retention, circulatory congestion, and pulmonary edema.
• Increased vascular capacity (pregnancy, varicose veins) causes renal salt and water retention until blood volume fills the enlarged vascular bed.
• Figure Mentioned: Fig. 30.14

CONDITIONS THAT CAUSE LARGE INCREASES IN EXTRACELLULAR FLUID VOLUME WITH NORMAL OR REDUCED BLOOD VOLUME

• In some conditions, extracellular fluid (ECF) volume increases greatly.
• In these conditions, blood volume remains normal.
• Blood volume may even become slightly reduced.
• These conditions usually begin with leakage of fluid into the interstitial space.
• Proteins also leak into the interstitial space.
• This leakage tends to reduce blood volume.
• The kidneys respond in the same way as after hemorrhage.
• The kidneys retain salt.
• The kidneys retain water.
• The kidneys attempt to restore blood volume toward normal.
• Much of the retained fluid leaks into the interstitial space.
• This leakage causes more edema.

Nephrotic Syndrome—Loss of Plasma Proteins in Urine and Sodium Retention By the Kidneys

• The general mechanisms of extracellular edema are discussed in Chapter 25.
• Nephrotic syndrome is an important clinical cause of edema.
• In nephrotic syndrome, the glomerular capillaries become more permeable.
• Large amounts of plasma proteins leak into the filtrate.
• Large amounts of plasma proteins are lost in the urine.
• About 30 to 50 grams of plasma protein may be lost in the urine each day.
• Plasma protein concentration may fall to less than one-third of normal.
• Plasma colloid osmotic pressure decreases to very low levels.
• Low plasma colloid osmotic pressure causes capillaries throughout the body to filter more fluid into the tissues.
• More fluid enters the interstitial space.
• Edema develops.
• Plasma volume decreases.
• In nephrotic syndrome, the kidneys retain sodium through multiple mechanisms.
• Leakage of protein and fluid into the interstitial fluid activates these mechanisms.
• The RAAS is stimulated.
• The sympathetic nervous system is stimulated.
• The kidneys continue to retain sodium.
• The kidneys continue to retain water.
• Plasma volume is restored almost to normal.
• Excess sodium and water retention further dilutes the plasma proteins.
• Lower plasma protein concentration causes more fluid to leak into the tissues.
• The kidneys continue retaining fluid.
• Massive extracellular edema develops.
• Treatment is needed to restore plasma proteins.

Liver Cirrhosis—Decreased Synthesis of Plasma Proteins By the Liver and Sodium Retention by the Kidneys

• In liver cirrhosis, plasma protein concentration decreases.
• Liver cell destruction reduces plasma protein production.
• The liver cannot synthesize enough plasma proteins.
• Cirrhosis is also associated with large amounts of fibrous tissue in the liver.
• Fibrous tissue obstructs portal blood flow through the liver.
• Portal capillary pressure increases.
• Increased portal capillary pressure promotes leakage of fluid.
• Increased portal capillary pressure promotes leakage of proteins.
• Fluid and proteins accumulate in the peritoneal cavity.
• This condition is called ascites.
• Loss of fluid and protein from the circulation decreases plasma volume.
• The kidneys respond in the same way as in other conditions with reduced plasma volume.
• The kidneys retain salt.
• The kidneys retain water.
• Plasma volume returns toward normal.
• Arterial pressure returns toward normal.
• In some patients, plasma volume may increase above normal.
• Increased vascular capacity contributes to this increase.
• High portal venous pressure greatly distends the veins.
• Distended veins increase vascular capacity.

KEY CONCEPT

• Increased ECF volume can occur even when blood volume is normal or reduced.
• Fluid and protein leakage into the interstitial space decreases blood volume.
• The kidneys respond by retaining salt and water.
• Nephrotic syndrome: Protein loss in urine (30–50 g/day) → ↓ Plasma proteins → ↓ Colloid osmotic pressure → Edema → Renal sodium retention.
• Liver cirrhosis: ↓ Plasma protein synthesis + ↑ Portal pressure → Ascites → Renal salt and water retention.
• Continued renal fluid retention worsens extracellular edema.