1. Acid-Base Balance Janis Rusin APN, MSN, CPNP-AC
Pediatric Nurse Practitioner
Lurie Children’s Transport Team

2. Objectives
Discuss the mechanisms for maintaining normal acid-base balance
Define respiratory and metabolic acidosis and alkalosis
Identify the common causes of acid base imbalance
Define and differentiate between respiratory distress and failure
Discuss interventions on transport for a patient with acid-base imbalance

3. Acid-Base Balance
The human body must be maintained in a very narrow range of acid-base balance
We use pH as our measure of acidity or alkalinity
pH stands for “power” of hydrogen
Normal pH is Not a whole lot of wiggle room!
Normal cellular metabolism occurs within this range
The 2 major organs responsible for maintaining acid base balance are:
The lungs-Respiratory balance
The kidneys-Metabolic balance

4. Chemistry Flashback!
An acid is a substance that releases hydrogen ions (when it dissociates)
A base is a substance that accepts the hydrogen ions
A buffer is a substance that protects the pH from derangements by binding with hydrogen ions
HA  H+ + A-

5. The Bicarbonate Buffer System
The bicarbonate buffer system is what we monitor clinically to assess acid base balance
This system works in the plasma
Relationship of carbon dioxide (CO2) to bicarbonate (HCO3-)
CO2 is the acid and HCO3- is the base

6. Balancing Act Lungs Kidneys
CO2 is an end product of normal cellular metabolism
The lungs regulate the CO2 level through respiration
Rapid response-quick fix!
The lungs cannot regulate bicarbonate levels
Kidneys
The renal tubules reabsorb bicarbonate
Excess hydrogen ions are excreted in the urine
Slower process
The kidneys cannot regulate CO2 levels

7. Clinical Applications
Acidosis (blood pH < 7.35)
A pathologic condition that causes an increase in the hydrogen ion concentration
Alkalosis (blood pH > 7.45)
A pathologic condition that causes a decrease in the hydrogen ion concentration
A simple acid base disorder has just one disturbance
The respiratory and metabolic systems compensate for each others deficiencies
If there is more than one disturbance, the patient is said to have a mixed acid base disorder

8. Types of Acid Base Disorders
Metabolic Alkalosis
Metabolic Acidosis
Respiratory Alkalosis
Respiratory Acidosis

9. Metabolic Alkalosis
An elevation in the serum pH associated with a decrease in hydrogen ion concentration and increase in bicarbonate ion concentration
Chloride plays a big role
2 main categories
Chloride Responsive
Chloride levels are < 10 mEq/L
Chloride Resistant
Chloride levels are > 20 mEq/L

10. Metabolic Alkalosis Chloride Responsive Diuretics Post hypercapnia
Hydrogen ions are lost
Vomiting
Loss of HCL from stomach contents, as well as Na and K
Excessive NG suctioning
Loss of both Hydrogen and Chloride ions
The kidneys retain Na and K instead of H in order to maintain the Na-K pump function
Diuretics
Pull H2O from the extracellular space which is low in bicarb
Results in an increased concentration of bicarb
More bicarb available to bind with Hydrogen
Post hypercapnia
Compensation by kidneys to retain bicarb in presence of hypercapnia
Metabolic alkalosis occurs transiently once PaCO2 levels corrected

11. Metabolic Alkalosis Chloride Resistant Bicarbonate is retained
Hypokalemia
Low serum K causes K to shift out of the cells and H to shift into the cells
Excessive base intake
Antacids
Hypertension
Aldosterone levels are elevated
Results in Na and H2O retention
Hydrogen and excess K are dumped by kidney
K shifts into cells

12. Metabolic Acidosis
A decrease in pH associated with a low serum bicarbonate concentration
Three primary mechanisms:
Bicarbonate is lost form the body
Kidney function is impaired and acid cannot be excreted properly
Endogenous or exogenous addition of acid to the body
Common Diagnoses leading to MA
Diarrhea
Insulin Dependent Diabetes Mellitus (IDDM)
Lactic Acidosis
Poor perfusion and shock
Renal Failure

13. Metabolic Acidosis Diarrhea Most common cause of MA
Bicarbonate is lost in excessive stool
The kidneys are unable to keep up with the losses
Potassium is also lost in the stool
Volume depletion results in aldosterone release
Sodium is retained leading to further loss of K
Hypokalemia results

14. Metabolic Acidosis Diabetic Ketoacidosis
Insulin deficiency occurs stimulating the release of excess glucagon
Glucagon stimulates the release of fatty acids from triglycerides
Fatty acids are oxidized in the liver to ketone bodies, beta- hydroxybutrate and aceto-acetic acid
These acids result in MA
In addition, the DKA patient become volume depleted due to excessive urination
Shock develops and further exacerbates the acidosis

15. Metabolic Acidosis Lactic acidosis Renal Failure
Hypoxia or poor tissue perfusion
Cells are forced into anaerobic metabolism producing lactic acid
Shock
Excessive exercise
Ethanol toxicity
Ethanol interferes with gluconeogenesis
Anaerobic metabolism
Renal Failure
Distal RTA
Failure of the distal tubule to properly excrete hydrogen ions
Fanconi syndrome
Failure of the proximal renal tubule to reabsorb bicarbonate, phosphate and glucose
Causes include:
Genetics
Medications such as tetracycline and antiretrovirals
Lead poisoning

16. Anion Gap
Calculation that determines the gap between concentrations of positive (cations) and negative (anions) ions
Useful in determining the cause of metabolic acidosis
Calculated by:
(Na+ + K+) – (HCO3- + Cl-) = 10-12mEq/L

17. Anion Gap Normal Anion Gap
The loss of bicarbonate is compensated for by the retention of chloride
Also known as Hyperchloremic Metabolic Acidosis
Diarrhea
Renal Failure, Proximal RTA
Elevated Anion Gap
MA due to increased H+ load
MUDPILES
Methanol
Uremia
DKA
Propylene Glycol
Isoniazid
Lactic Acid
Ethylene Glycol (antifreeze)
Salicylates

18. Respiratory Alkalosis
A condition in which the carbon dioxide content is significantly reduced (hypocapnia)
Caused by:
Hyperventilation
Occurs within minutes of onset of hyperventilation
Pulmonary disease
CHF
Hypermetabolic states
Fever
Anema
Hyperthyroid

19. Respiratory Acidosis
Occurs when ventilation of CO2 is inadequate and CO2 is retained (hypercapnia)
Causes include airway obstruction, respiratory depression, pneumonia, asthma, pulmonary edema, chest trauma
The renal buffer system is not effective for acute RA
Chronic respiratory acidosis can be well compensated for by the kidneys

20. So, how do we make the diagnosis?
Arterial Blood Gas-Normal Values
pH ( )
PCO2 (35-45)
PO2 (80-100)
HCO3 (22-26)
Base Excess/Deficit (-2 to +2)
Venous Blood Gas-Normal Values
pH ( )
PCO2 (40-50)
PO2 (35-40)
HCO3 (22-26)
Base Excess/Deficit (-2 to +2)

21. Blood Gas Analysis Step 1: Look at the pH Step 2: Look at the PCO2
< 7.35 is acidic
> 7.45 is alkalotic
Step 2: Look at the PCO2
<35 is alkalotic
> 45 is acidic
Step 3: Look at the HCO3
< 22 is acidic
> 26 is alkalotic
Step 4:Match the pH to either the PCO2 or HCO3
Whichever one goes in the same direction as pH determines the primary disorder
Respiratory = CO2
Metabolic = HCO3
Step 5:Which one goes in the opposite direction of the pH?
This is the compensatory system
Step 6: Look at the PO2
Determines presence of hypoxia

22. Blood Gas Interpretation
Blood Gas Analysis 26
HCO3 22
Blood Gas Interpretation 45
PaCO2 35
Normal Values
Respiratory
Acidosis
Metabolic
Alkalosis
Metabolic
Acidosis
Respiratory
Alkalosis pH
Acidemia Alkalemia

23. Mixed Acid Base Disorders
When to suspect a mixed acid base disorder:
The expected compensatory response does not occur
Compensatory response occurs, but level of compensation is inadequate or too extreme
Whenever the PCO2 and HCO3 become abnormal in the opposite direction.
In simple acid base disorders, the direction of the compensatory response will always be in the same as the direction of the initial abnormal change.
pH is normal but PCO2 or HCO3- is abnormal
General rule:
If the pCO2 is elevated and HCO3 is reduced, then both respiratory and metabolic acidosis are present
If the pCO2 is reduced and the HCO3 is elevated, then both respiratory and metabolic alkalosis are present

24. Respiratory Distress
A compensated state in which oxygenation and ventilation are maintained
Define oxygenation and ventilation
How will the blood gas look?
Characterized by any increased work of breathing
Flaring, retractions, grunting
What is grunting?

25. Respiratory Failure Compensatory mechanisms are no longer effective
Inadequate oxygenation and/or ventilation resulting in acidosis
Abnormal blood gas with hypercapnia and/or hypoxia
Will begin to see decreasing LOC due to hypercapnia
Medical emergency! Must protect airway!
Strongly consider intubation

26. Respiratory Failure-Causes
Pulmonary Causes
Diffusion impairment
Atelectasis
Pneumonia
Bronchiolitis
Acute lung injury
Pulmonary edema
Shunting and V/Q mismatch
Non-Pulmonary Causes
Respiratory muscle compromise or fatigue
Impairment of the nervous systems control of breathing
Guillain-Barre
Muscular Dystrophy
Central hypoventilation syndrome
Sedatives
Head injury
Upper airway obstructions

27. Indications for intubation
Inability to protect airway
No cough or gag
Decreasing LOC
GCS < 8
Cardiac or respiratory arrest
Acute respiratory acidosis
Refractory hypoxemia despite 100% FiO2

28. Goals of ventilation Correct acidosis Rest the respiratory muscles
Correct hypoxemia
Allows for delivery of high FiO2
PEEP
Improves cardiac function
Decreases preload
Decreases metabolic demand

29. Initial Ventilator settings
Volume Control
Pressure Control
Rate
Normal for age
Tidal Volume
8-10 cc/kg
PEEP
Start at 5cm H2O and increase as clinically indicated
i-Time
1:2
(Must increase E-time in obstructive processes to avoid air trapping)
Set pressure to produce adequate chest rise and TV’s (8-10/kg)

30. Correction of hypoxia and hypercarbia
To increase PaO2
To decrease PaCO2
Increase FiO2
Increase Rate
Increase PEEP
Increase Tidal Volume or
Pressure control
Increase I-Time

31. Match the Gas Which patient does this gas belong to?
pH 7.09 PCO2 98 PO HCO3 30
A) 22 y/o with Muscular Dystrophy. Severe and worsening muscle weakness
B) 9 y/o with new onset Diabetic Ketoacidosis
C) A 30 y/o patient presenting with a panic attack
D) A 25y/o in a skiing accident presenting in respiratory distress

32. Match the Gas pH 7.09 PCO2 98 Po2 218 HCO3 30
A) 22 y/o with Muscular Dystrophy. Severe and worsening muscle weakness
Chronic Respiratory Failure
Uncompensated Respiratory Acidosis

33. Match the Gas Which patient does this gas belong to?
pH PCO2 28 PO2 63 HCO3- 23
A) 22 y/o with Muscular Dystrophy. Severe and worsening muscle weakness
B) 9 y/o with new onset Diabetic Ketoacidosis
C) A 30 y/o patient presenting with a panic attack
D) A 25y/o in a skiing accident presenting in respiratory distress

34. Match the Gas Which patient does this gas belong to?
pH PCO2 28 PO2 63 HCO3- 23
C) A 30 y/o patient presenting with a panic attack
Hyperventilation
Uncompensated Respiratory alkalosis

35. Match the Gas Which patient does this gas belong to?
pH PCO PO HCO BD -27
A) 22 y/o with Muscular Dystrophy. Severe and worsening muscle weakness
B) 9 y/o with new onset Diabetic Ketoacidosis
C) A 30 y/o patient presenting with a panic attack
D) A 25y/o in a skiing accident presenting in respiratory distress

36. Match the Gas pH 6.94 PCO2 26.6 PO2 55.7 HCO3 5.7 BD -27
B) 9 y/o with new onset Diabetic Ketoacidosis
DKA
Uncompensated Metabolic Acidosis

37. Match the Gas Which patient does this gas belong to?
pH 7.27 PCO PO2 70 HCO3 26 BD -1
A) 22 y/o with Muscular Dystrophy. Severe and worsening muscle weakness
B) 9 y/o with new onset Diabetic Ketoacidosis
C) A 30 y/o patient presenting with a panic attack
D) A 25y/o in a skiing accident presenting in respiratory distress

38. Match the Gas pH 7.27 PCO2 54.8 PO2 70 HCO3 26 BD -1
D) A 25y/o in a skiing accident presenting in respiratory distress
Acute Respiratory Distress
Uncompensated Respiratory Acidosis

39. Questions?