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ACID-BASE BALANCE AND OXYGENATION M.R.CUENO, RN Blood gases I. Physiological controls A. Chemical buffer systems in ICF and ECF 1. Bicarbonate-carbonic acid a. Ratio of bicarb to carbonic acid is 20:1 b. Responsible for 45% of all H+ buffering 2. Inorganic phosphates 3. Plasma proteins 4. Intracellular buffers - proteins, organic & inorganic phosphates 5. RBC buffers - hemoglobin B. Respiratory - removal of CO2 1. PaCO2 is an acid, serum CO2 is a base 2. Rise in PaCO2 is powerful stimulus for increased respirations - tidal volume & rate 3. Consistent PaCO2 > 50 mm Hg desensitizes the respiratory center 4. Compensation a. metabolic acidosis - increased respirations b. metabolic alkalosis - decreased respirations c. respiratory compensation has limits C. Renal regulation 1. Bicarbonate is reabsorbed from kidney tubules. Kidney manufactures bicarbonate 2. Hydrogen ion - excreted during acidosis and retained during alkalosis 3. Kidneys can compensate for respiratory imbalances over a period of days II. Tests to measure acid-base A. Anion gap Na + - (CL - + HCO2) = 12 -15 mEq/L 1. Determines if metabolic acidosis is from excessive acid or loss of bicarbonate B. pH - reflects H + concentration C. Total serum CO2 - indirect measure of bicarbonate

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Page 1: Acid-Base Balance

ACID-BASE BALANCE AND OXYGENATION

M.R.CUENO, RN

Blood gases

I. Physiological controlsA. Chemical buffer systems in ICF and ECF

1. Bicarbonate-carbonic acida. Ratio of bicarb to carbonic acid is 20:1b. Responsible for 45% of all H+ buffering

2. Inorganic phosphates3. Plasma proteins4. Intracellular buffers - proteins, organic & inorganic phosphates5. RBC buffers - hemoglobin

B. Respiratory - removal of CO2

1. PaCO2 is an acid, serum CO2 is a base2. Rise in PaCO2 is powerful stimulus for increased respirations - tidal

volume & rate3. Consistent PaCO2 > 50 mm Hg desensitizes the respiratory center4. Compensation

a. metabolic acidosis - increased respirationsb. metabolic alkalosis - decreased respirationsc. respiratory compensation has limits

C. Renal regulation1. Bicarbonate is reabsorbed from kidney tubules. Kidney manufactures

bicarbonate2. Hydrogen ion - excreted during acidosis and retained during alkalosis3. Kidneys can compensate for respiratory imbalances over a period of days

II. Tests to measure acid-baseA. Anion gap Na+ - (CL- + HCO2) = 12 -15 mEq/L

1. Determines if metabolic acidosis is from excessive acid or loss of bicarbonate

B. pH - reflects H+ concentrationC. Total serum CO2 - indirect measure of bicarbonate

1. Increased in metabolic acidosis 2. Decreased in metabolic alkalosis3. Total CO2 is 95% HCO3 and 5% CO2 gas and H2CO3

D. Blood gases1. Normal values

a. pH  7.35-7.45  (usually fatal if < 6.8 or > 7.6)b. PaCO2 35-45 mm Hgc. PaO2 80-100 mm Hgd. HCO3 22-26 mEq/L

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e. O2 saturation (SaO2) 95-100%  - Oxyhemoglobin dissociation curve

f. Base excess/deficit  -2 to +2 mEq/Lg. O2 content  -  15-23 vol%  - measurement of total O2 in blood,

including that bound to Hgb and free dissolved in plasma)2. Pediatric procedures

a. Transcutaneous pO2 monitoring - 50-100 mm Hgi. special heated electrode placed on head, chest or thigh

ii. warmth causes O2 to diffuse out of capillariesiii. electrode measures O2 at skin surfaceiv. proportional to capillary O2

b. Fetal scalp vein pH  7.25-7.40i. Helps determine if cesarean section is needed

III. How to analyze ABGsA. Determine if acidosis or alkalosis by looking at pHB. Determine the primary disturbance

1. Look at the HCO3 and CO2 - which one goes in the same direction as the pH? If the CO2 is in the same direction, it is respiratory; if the HCO3 is in the same direction, it is metabolic.

a. CO2 > 40   = acidosisb. CO2 < 40   = alkalosisc. HCO3 > 24 = alkalosisd. HCO3 < 24 = acidosis e. May have a combined cause

C. Compensation1. Look at the value that is not the same as primary cause. If it is going in the

opposite direction (alkalosis or acidosis) as the primary problem, then compensation is occurring. Compensation may be partial or complete. Renal can completely compensate for respiratory.

IV. Metabolic acidosis - base deficitA. Causes

1. Excess acida. Ketoacidosis - diabetes or starvationb. Lactic acidosis - burns, myocardial infarction, shockc. Salicylate poisoningd. Uremiae. Methanol or ethylene glycol toxicity

2. Decreased basea. GI losses - diarrhea, fistula, NG drainageb. Ureteroconduits - gain of chloride from urinec. Acetazolamide (Diamox)

B. Clinical picture1. Headache, confusion, drowsiness2. Deep rapid respirations (Kussmaul)3. Nausea & vomiting4. Peripheral vasodilation

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5. Hyperkalemia often presentC. Compensation

1. Hyperventilation to remove CO2

2. Kidneys excrete more H+ and produce more HCO3

D. Nursing considerations1. Protect confused patients from injury2. Good pulmonary hygiene3. Good oral care4. Monitor potassium

V. Metabolic alkalosisA. Causes

1. GI losses - vomiting, gastric suctioning, pyloric stenosis2. Hypokalemia - potassium-losing diuretics, kidneys excrete H+ and try to

conserve K3. Hyperaldosteronism, Cushing's syndrome4. Excessive antacid intake5. Diuretics6. Placing patient with COPD on mechanical ventilation, relief of chronic

respiratory acidosisB. Clinical picture

1. Depressed respirations2. Hypocalcemia - decreased ionized Ca - dizziness, tingling of fingers &

toes, circumoral paraesthesia, carpopedal spasm, hypertonic muscles3. Hypokalemia often present

C. Compensation1. Hypoventilation - retain CO2

2. Kidneys excrete more HCO3

D. Treatment1. Treat underlying cause2. Give NS for kidney to absorb Na and Cl allowing excretion of HCO3

E. Nursing considerations1. Replace GI losses with isotonic fluids, flush NG tube with NS2. Teach patient not to use baking soda as antacid3. Monitor K levels

VI.   Respiratory acidosis - excess CO2

A. Causes1. Lung diseases - COPD, ARDS2. Neuromuscular diseases affecting respirations - Guillian-Barre, multiple

sclerosis3. Anesthesia4. Pneumonia

B. Clinical picture1. Acute

a. Feeling of fullness in head - cerebral vasodilationb. Confusion, dizziness, lethargy, restlessness, decreased attention

span

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c. Decreased respirationsd. Dysrhythmias

2. Chronica. Weakness, dull headacheb. Barrel chest, use of accessory muscles to breathe

C. Compensation1. Kidneys retain HCO3

D. Treatment1. Administer oxygen - low concentration if chronic2. Keep airway clear, postural drainage & vibration, humidified air3. Force fluids4. Promote lung expansion - incentive spirometer, blowing up balloons.

E. Nursing considerations1. Assess respiratory status frequently- effort, accessory muscle use, lung

sounds, skin color, mental status2. Monitor serial ABGs3. Assist patient into comfortable positions that facilitate lung expansion -

Semi- or high Fowlers4. Be prepared to intubate5. Teach exercises to enhance expiration - pursed lip breathing

VII. Respiratory alkalosis - deficit of CO2

A. Causes 1. Hyperventilation

a. extreme anxietyb. hypoxemiac. high feverd. early salicylate poisoninge. bacteremiaf. CNS lesionsg. pulmonary embolismh. overventilation with mechanical ventilatorsi. pregnancy

B. Clinical picture1. Lightheadedness - cerebral vasoconstriction2. inability to concentrate3. hypocalcemia - numbness & tingling of extremities, circumoral

paresthesiaC. Compensation - kidneys excrete increased HCO3

D. Treatment - treat causeE. Nursing considerations

1. Teach patient to focus on controlled breathing, relaxation techniques2. Monitor rate and depth on mechanical ventilators