90. Changes in blood volume (hypovolemia and hypervolemia) - etiology, pathogenesis, clinical manifestations.

Changes in the volume of the blood (hypovolemia and hypervolemia) – etiology, pathogenesis, and clinical manifestations.

I. Hypovolemia

Hypovolemia refers to a decrease in the circulating blood volume, most importantly the effective circulating plasma volume, leading to reduced tissue perfusion.

Etiology

Absolute hypovolemia

• Hemorrhage (trauma, gastrointestinal bleeding, ruptured aneurysm).
• Fluid loss:
• Severe vomiting, diarrhea.
• Burns.
• Excessive sweating.

Relative hypovolemia

• Blood volume moves into third spaces:
• Severe pancreatitis (third spacing into retroperitoneum).
• Peritonitis.
• Massive trauma with soft tissue sequestration.

Pathogenesis

1. Decreased blood volume → reduced venous return (preload).
2. Decreased cardiac output → decreased blood pressure.
3. Compensatory mechanisms:

• Sympathetic activation → tachycardia, vasoconstriction.
• Activation of RAAS → sodium and water retention.
• ADH release → water reabsorption.

1. 4 If uncorrected → tissue hypoxia → metabolic acidosis → multi-organ dysfunction → shock.

Clinical manifestations

• Hypotension (especially orthostatic).
• Tachycardia, weak pulse.
• Cold, clammy skin (peripheral vasoconstriction).
• Oliguria.
• Thirst.
• Mental status changes (agitation, confusion, eventually coma).

II. Hypervolemia

Hypervolemia refers to an increase in total blood volume, particularly the extracellular fluid component.

Etiology

• Heart failure → renal sodium and water retention due to decreased effective perfusion.
• Renal failure → decreased excretion of sodium and water.
• Liver cirrhosis → hypoalbuminemia, portal hypertension → secondary hyperaldosteronism.
• Excessive IV fluid administration (iatrogenic).
• Hyperaldosteronism.

Pathogenesis

1. Sodium and water retention → increased plasma volume.
2. Increased hydrostatic pressure → transudation of fluid into interstitial spaces → edema formation.
3. In heart failure → further worsening of cardiac workload → vicious cycle.

Clinical manifestations

• Hypertension (if systemic vascular resistance intact).
• Edema (peripheral or generalized).
• Jugular venous distension.
• Pulmonary congestion:
• Dyspnea.
• Orthopnea.
• Crackles on lung auscultation.
• Weight gain.
• Possible ascites (especially in liver disease).

Summary table