clinical definitions and diagnostic aids respiratory acidosis = paco 2 > 45 mmhg respiratory...
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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
Compensation: Opposing Metabolic And Respiratory Effects Aimed At Returning pH Towards Its Normal
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
• P = 122, BP = 85/60, f = 24, • T = 37.2 C• ABG PaO2 = 90, PaCO2 = 44,
• 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
Compensation: Opposing Metabolic And Respiratory Effects Aimed At Returning pH Towards Its Normal
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
Compensation: Opposing Metabolic And Respiratory Effects Aimed At Returning pH Towards Its Normal
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
• P = 92, BP = 135/90, f = 26, • T = 37.0 C• ABG PaO2 = 65, PaCO2 = 55,
• 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
Acid-base status?Primary disorder?Secondary disorder?Compensation?
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
Acid-base status?Primary disorder?Secondary disorder?Compensation?
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