Clinical Definitions and Diagnostic Aids Respiratory acidosis = PaCO 2 > 45 mmHg Respiratory...

Clinical Definitions and Diagnostic Aids

• Respiratory acidosis = PaCO2 > 45 mmHg

• Respiratory alkalosis = PaCO2 < 35 mmHg

• Metabolic acidosis = HCO3- < 22 mmHg

or Base Deficit of < -2• Metabolic alkalosis = HCO3

- > 28 mmHg or Base Excess of > +2

Case #4

• 22 year old diabetic found unresponsive

• P = 102, BP = 110/80, f = 20, • T = 36.2 C• ABG PaO2 = 90, PaCO2 = 36,

• pH = 7.12, HCO3- = 8, BD = -20

Metabolic Acidosis• Definition: low HCO3

- <22 mEq/L or BD < -2

• Cause: retained fixed acids (or HCO3- loss)

• Treatment:– Correct cause!– Give NaHCO3 if necessary to correct pH to > 7.20

Anion Gap In Metabolic Acidosis• Anion gap:

[Na+] - ([Cl-] + [HCO3-]) = 8-16 mmol/L

• If > 18, there are unmeasured anions, such as:– lactate– ketones– salicylate– ethanol– ethylene glycol (anti-freeze)

Compensation: Opposing Metabolic And Respiratory Effects Aimed At Returning pH Towards Its Normal

Value• Primary Metabolic Acidosis

– Acute or chronic– Decreased HCO3

-

– Response?

For every 1 mEq decrease in HCO3-

PaCO2 is expected to decrease 1-1.5 mmHg

Secondary respiratory alkalosis

So what does this mean?

• Lactic Acid + HCO3 ↔ lactate- + H2O + CO2

So increasing Lactic acid leads to lactate replacing HCO3

If anion gap is unchanged in metabolic acidosis suggest other reason for acidosis (eg diarrhoea – loss of HCO3 but gain in

Cl-

Acid - Base Diagnosis

PaCO2< 35 or >45?

No VentilatoryComponent

PaCO2< 35?

HCO3-<21 or >28?

No

PaCO2>45?

VentilatoryAlkalosis

VentilatoryAcidosis

Yes

Yes

Yes

No

No MetabolicComponent

HCO3->28?

HCO3-<21?

No

Yes

MetabolicAlkalosis

MetabolicAcidosis

Yes

No

Yes

pH<7.35?

Acidemia Yes

pH>7.45?

No

Alkalemia YesNormal pH

NoDiagram source unknown

Case #2

• 36 year old heroin addict found unresponsive with needle in arm

• P = 102, BP = 110/80, f = 5, T = 35.2 C• ABG: PaO2 = 70, PaCO2 = 80,

• pH = 7.00, HCO3- = 23

Ventilatory Acidosis

• Definition – PaCO2 > 45 mm Hg

• Ventilatory insufficiency or failure• Cause:

– Hypoventilation– Low VA (i.e., low VE and/or high VD)

• Treatment:– Increase VE, lower VD/Vt

– Eliminate CNS depression of ventilation


Value• Primary Respiratory Acidosis

– Increased PaCO2

–Chronic (> 3-5 days)• Response?

For every 1 mm Hg increase in PaCO2

HCO3- is expected to increase 0.4

mEq Secondary metabolic alkalosis

Case #5

• 6 week old infant is lethargic with history of vomiting increasing for 1 week


• pH = 7.62, HCO3- = 36, BE = +12

Metabolic Alkalosis

• Definition: high HCO3- >28 mEq/L or BE > +2

• Cause: fixed acids loss

• Treatment:– Correct cause!– Prevent HCO3

- retention (correct pH to <7.50) (How?)

– Give acetazolamide(CA inhibitor) or H+ in extremes


Value• Primary Metabolic Alkalosis

– Acute or chronic– Increased HCO3

-

– Response?

For every 1 mEq increase in HCO3-

PaCO2 is expected to increase 0.5 - 1 mmHg

Secondary respiratory acidosis

• Recall HH – compensation aims to normalize pH by restoring [HCO3]:PCO2 ratio towards normal.

• The “Primary” disturbance is the one that is consistent with the pH

Comments On Compensation…

Case #3

• 16 year old with closed head injury after a fall from 15 feet

• P = 132, BP = 115/90, f = 32, • T = 37.2 C• ABG: PaO2 = 110, PaCO2 = 26,

• pH = 7.52, HCO3- = 22, BD = 1

Ventilatory Alkalosis

• Definition – PaCO2 < 35 mm Hg

• Hyperventilation• Cause:

– Hyperventilation– High VA (i.e., high VE = f x Vt)

• Treatment: (usually none!)– Decrease VA

– Sedation


Value• Primary Ventilatory Alkalosis

– Decreased PaCO2

– Chronic (> 3-5 days)• Response?

For every 1 mm Hg decrease in PaCO2

HCO3- is expected to decrease 2-5

mEq Secondary metabolic acidosis

http://animalsbeingdicks.com/page/6

Davenport diagram showing the relationships among HCO3-, pH, and PCO2. A shows the normal buffer line BAC

pH 7.2, HCO3- 15 mM and PCO2 40 mm Hg ?

metabolic acidosis

Davenport diagram showing the relationships among HCO3, pH, and PCO2. . B shows the changes/compensation occurring in respiratory and metabolic acidosis and alkalosis

Overview of Potassium Homeostasis

Cells exist in a steady state where potassium uptake via the Na/K-ATPase is balanced bypotassium leak through ion channels. Regulation of exchange between intra- and extracellularfluid is known as internal potassium homeostasis.

Factors which affect internal potassium balance

are important in the regulation of plasma [potassium]. Skeletal muscle cells are the major single pool of potassium in the body and are the most important cells in relation to internal potassium homeostasis.

The typical Western diet contains around 80mEq of potassium per day. Maintenance ofpotassium homeostasis requires that the rate of potassium excretion matches daily intake. This is known as external potassium homeostasis. Fine regulation of renal potassium output is the major control mechanism ensuring external balance. Losses from the GI tract in feces are generally about 10% of dietary intake, though this can become a large source of potassium loss in diarrhea.

1) Internal potassium homeostasis.

2)External potassium homeostasis.

Factors Affecting Internal K+ Exchanges

K+

K+ ingestioninsulin

liver, skeletal

muscle

Exercise

epinephrine skeletal muscle (beta2 receptors)

aldosterone (skeletal muscle)

High plasma [K+]

cell

Insulin/glucose infusions are used clinically tocontrol hyperkalemia.

The final common pathway for increased cellular potassium uptake with insulin,aldosterone and epinephrine is increased Na/K-ATPase activity.

Acidosis:

H+

K+

Alkalosis:

H+

H+

K+o

K+o

Acid/Base Balance

(hyperkalemia)

(hypokalemia)

• As hydrogen ions move into and out of the cells in the body, there is a corresponding movement of potassium in the opposite direction by ion transport proteins that link hydrogen ion movement to potassium ion movement. This movement helps maintain electrical balance inside the cells.

A K+ Load Must Be Quickly Removed To Protect Plasma [K+]

0

50

100

% r

e spo

nse

Hours6 12

K+ moved into cells

Renal K+ excretion

K+ load

FE K+ =10 – 150+%

Reabsorption:

PCT (FE=30%), TALH (FE=10%)

Secretion:

DCT & CCD

(FE = 10 to 150%)

Renal K+ Handling Involves Filtration, Reabsorption And Secretion

The rate of renal potassium excretion varies over a wide range according to changes in dietaryintake.

In states of low dietary potassium intake

dietary potassium excess

K+ Excretion Is Determined By K+ Secretion In The Collecting Duct

Lumen Blood

3Na+

K+

Principal cell

aldosterone+

Case #6

• 63 year old with history of COPD due to tobacco abuse


• pH = 7.34, HCO3- = 31, BE = +9

Acid-base status?Primary disorder?Secondary disorder?Compensation?

Case #7• 39 year old with history of chronic

renal insufficiency due to hypertension

• P = 82, BP = 148/95, f = 20, T = 36.1 C

• ABG PaO2 = 88, PaCO2 = 30, pH = 7.33, HCO3

- = 14, BD = -11


Mixed Acid-Base Disorders• Most common acid-base disorders• Multiple disorders• Usually one acidosis and one alkalosis• pH usually partially or completely

corrected

Case #1 Review

• 26 YO male involve in MVC• Hypotensive and tachycardia at crash

scene• Altered mental status and multiple

severe injuries• pH = 7.38; PaCO2 = 30 mm Hg;

• HCO3- = 18 mEq/L, BD = -8 mEq/L


Key Points

• Acid-base disorders are common and important clinical concerns

• Accurate diagnosis is essential to proper treatment

• Primary disorders are complicated by secondary disorders occurring at a different time course

Clinical Definitions and Diagnostic Aids Respiratory acidosis = PaCO 2 > 45 mmHg Respiratory...

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