Chapter 7 - Acid-Base Balance

volatile acids

acids that can be converted to a gaseous form and eliminated by the lungs

nonvolatile acids

inorganic acids that are formed during metabolism of carbohydrate, protein, and lipid

can the lungs eliminate nonvolatile acids

no

what is the most important volatile acid

carbonic acid H2CO3 - produced in the largest quantity

most predominant base

bicarbonate HCO3-

how do kidneys provide primary reuglation of HCO3-

control the amount of free hydrogen ions and the amount of bicarbonate that is removed or retained

buffer definition

a substance or group of substances that reacts with either acid or base in order to decrease the effect of acid or baes on the pH of the solution

normal serum pH

7.35-7.45

acidosis

accumulation of acid OR loss of base

acidemia

actual decrease in pH within the body to <7.35

alkalosis

process that leads to accumulation of base or loss of acid pH>7.45

bicarbonate-carbonic acid buffer system

primary ECF buffer against non-carbonic-acid changes

protein buffer system

primary ICF buffer; also buffers ECF

hemoglobin buffer system

primary buffer against carbonic changes

phosphate buffer system

important urinary buffer; also buffers ICF

henderson-hasselbalch equation

pH=pK_a+[H2CO3]

ratio of acids to bases

1 part H2CO3 to 20 parts HCO3-

disodium/monosodium phosphate buffer

excretion of H+ would damage kidney so phosphate accepts the H+ and a weaker acid is formed

how will the kidney respond during alkalosis

reduce the amount of HCO3- reabsorbed

how will the kidney respond during acidosis

increase secretion of H+ and increase amount of HCO3- reabsorbed

which is longer: renal regulation or respiratory regulation

renal

minimum pH of urine

4.5

the kidney uses what two buffers in acidic urine

dibasic phosphate and ammonium

how does ammonium act as a buffer

the base, NH3 is formed in renal tubular cells from the amino acid glutamine. free H+ combines with NH3 to form ammonium. ammonium cannot cross back across the cell membrane so H+ is trapped and excreted

renal responses to acidosis: H+ secretion

increase

renal responses to acidosis: H+ excretion

increase

renal responses to acidosis: HCO3- reabsorption

increase

renal responses to acidosis: HCO3- excretion

normal (all filtered is reabsorbed)

renal responses to acidosis: pH of urine

acidic

renal responses to acidosis: compensatory change in plasma pH

alkalinization toward normal

renal responses to alkalosis: H+ secretion

decrease

renal responses to alkalosis: H+ excretion

decrease

renal responses to alkalosis: HCO3- reabsorbption

decrease

renal responses to alkalosis: HCO3- excretion

increase

renal responses to alkalosis: pH of urine

alkaline

renal responses to alkalosis: compensatory change in plasma pH

acidification toward normal

what is the ion that moves opposite direction to HCO3-

chloride

ABGs

arterial blood gases

anion gap definition

difference between unmeasured anions and cations

normal ABG values for assessment of acid-base balance: O2

>80mmHg

normal ABG values for assessment of acid-base balance: CO2

35-45mmHG

normal ABG values for assessment of acid-base balance: pH

7.35-7.45

normal ABG values for assessment of acid-base balance: HCO3-

24-28mEq/L

normal ABG values for assessment of acid-base balance: base excess

>3 mEq/L

normal ABG values for assessment of acid-base balance: anion gap

10-20 mmol/L

8-16 mEq/L

normal ABG values for assessment of acid-base balance: O2 saturation

>95%

uncompensated respiratory acidosis: pH

decreased

uncompensated respiratory acidosis: CO2

increased

uncompensated respiratory acidosis: HCO3-

normal

uncompensated respiratory acidosis: HCO3-/CO2 ratio

20/2

compensated respiratory acidosis: pH

normal

compensated respiratory acidosis: CO2

increased

compensated respiratory acidosis: HCO3

increased

compensated respiratory acidosis: HCO3-/CO2 ratio

40/2 (20/1)

uncompensated respiratory alkalosis: pH

increased

uncompensated respiratory alkalosis: CO2

decreased

uncompensated respiratory alkalosis: HCO3-

normal

uncompensated respiratory alkalosis: HCO3-/CO2 ratio

20/0.5 (40/1)

compensated respiratory alkalosis: pH

normal

compensated respiratory alkalosis: CO2

decreased

compensated respiratory alkalosis: HCO3-

decreased

compensated respiratory alkalosis: HCO3-/CO2 ratio

10/0.5 (20/1)

uncompensated metabolic acidosis: pH

decreased

uncompensated metabolic acidosis: CO2

normal

uncompensated metabolic acidosis: HCO3-

decreased

uncompensated metabolic acidosis: ratio

10/1

compensated metabolic acidosis: pH

normal

compensated metabolic acidosis: CO2

decreased

compensated metabolic acidosis: HCO3-

decreased

compensated metabolic acidosis: HCO3-/CO2 ratio

15/0.75 (20/1)

uncompensated metabolic alkalosis: pH

increased

uncompensated metabolic alkalosis: CO2

normal

uncompensated metabolic alkalosis: HCO3-

increased

uncompensated metabolic alkalosis: HCO3-/CO2 ratio

40/1

compensated metabolic alkalosis: pH

normal

compensated metabolic alkalosis: CO2

increased

compensated metabolic alkalosis: HCO3-

increased

compensated metabolic alkalosis: HCO3-/CO2 ratio

25/1.25 (20/1)

respiratory acidosis

condition resulting from excess acid in the blood secondary to carbon dioxide

hypercapnia

the term used to describe an excess of CO2

common causes of respiratory acidosis

• hypoventilation

• COPD

• severe pneumonia or asthma

• acute pulmonary edema

• pneumothorax

• drugs; opiate, sedative, anesthetic overdose

• excessive oxygen treating chronic hypercapnia

• sleep apnea

• neuromuscular disease such as amyotrophic lateral sclerosis (ALS), gullain barre syndrome

• morbid obesity

• chest wall injury/skeletal deformity

• aspiration

• bronchospasm

• excessive production of CO2

• overfeeding especially w high carb

major cellular buffering defense for respiratory acidosis

expiration of CO2 by lungs.

body stores of HCO3- are released in order to maintain the appropriate ratio of CO2 to HCO3-

respiratory alkalosis

condition resulting from excess base in blood secondary to increased carbon dioxide expiration

relative amount of base (hco3-) as a result of reduction of CO2

common causes of respiratory alkalosis

hyperventilation

respiratory infection

asthma

change in altitude

drugs that stimulate respirations

anxiety

cerebrovascular accident

fever and sepsis

hyperventilation

result of reduction in serum oxygen levels

what can stimulate hyperventilation

malignancy, stroke, fever ,sepsis, drugs (salicylates), anxiety, physical activity

acute response to respiratory alkalosis

shift of acid from ICF to ECF with movement of HCO3- into cells

chronic respiratory alkalosis response

kidneys reduce secretion of H+ and increase excretion of HCO3-

common first step of respiratory alkalosis treatment

provide oxygen therapy

metabolic acidosis

all types of acidosis that are not casued by excessive CO2

what causes metabolic acidosis

excessive loss of base or excessive gain of fixed acids

common causes of metabolic acidosis

kidney loss of HCO3-

CKD

systemic loss of HCO3-

diarrhea

fistula drainage

excessive production of acid

ketoacidosis

lactic acidosis

most common cause of metabolic acidosis

diarrhea

buffer system in metabolic acidosis

bicarbonate-carbonic acid buffer system

kussmaul breathing

rapid deep and labored breathing.

kussmaul breathing is most common in

metabolic acidosis

treatment of metabolic acidosis

focus on underlying cause

metabolic alkalosis

excess amount of base

common causes of metabolic alkalosis

loss of acid

vomiting

hypokalemia

excessive base

intravenous therapy

blood transfusion

excessive or chronic use of antacids

conditions leading to metabolic alkalosis that involve fluid imbalance

prolonged vomiting, NG suction, diurectics