NMS. Surgery

13

Chapter 1 ♦ Principles of Surgical Physiology

Table 1-4: Acid–Base Disorders

Expected Compensation 1–4 mEq/L HCO 3 − for each 10 mm Hg Pco 2 rise

−

Disorder

Phase

Pco 2

HCO 3

pH

↑

Respiratory acidosis

Acute

Normal

<7.35

↑

↑

Compensated

7.35–7.40

↓

Respiratory alkalosis

Acute

Normal

>7.45

2–5 mEq/L HCO 3 − for each 10 mm Hg Pco 2 drop

↓

↓

Compensated

7.40–7.45

↓

Metabolic acidosis

Acute

Normal

<7.35

Expected Pco 2 = 1.5(HCO 3

− ) + 8

↓

↓

Compensated

7.35–7.40

↑

Metabolic alkalosis

Acute

Normal

>7.45

Expected Pco 2 = 0.7(HCO 3

− ) + 20

↑

↑

Compensated

7.40–7.45

COAGULATION Hemostasis Mechanism Phases I. Primary Hemostasis

A. Platelet adherence: The first step in controlling hemorrhage is platelet adherence via glycoprotein (Gp) receptor Ib in conjunction with von Willebrand factor. B. Platelet activation: Activated platelets produce thromboxane A 2 and other vasoconstrictors, which reduce blood flow. Expression of Gp IIb/IIIa promotes platelet–platelet adhesion (fibrinogen required) and platelet plug formation. II. Clot formation: Tissue factor exposed due to vessel injury or in response to inflammation begins the clotting cascade (traditionally taught as having an intrinsic and extrinsic pathway; however, in vivo, both pathways act in concert). A. Extrinsic pathway: Tissue factor binds factor VII and activates it (VIIa). VIIa subsequently activates factor X. Xa then converts prothrombin to thrombin.