CVPR Week 5: Acid and Base prework Flashcards
How much of the human body is water?
~60% of human body weight is composed of water
Where is the water in the human body distributed?
2/3 ICF (28L) and 1/3 ECF (14L)
TBW equation =
0.6 x Wt (Kg) = V (L)
What are the main anions and cations in ICF and ECF?

How does H+ effect the cellular environment?
H+ concentration modifies protein structure and enzyme function therefore it is paramount to regulate H+ concentration within tight limits (35-45 nmol/L)
What is the typical H+ concentration in the body?
35-45 nmol/L
H+ concentrations in the ECF compared to other elements
In the ECF, the concentration of H+ is much less compared to other elements. Such as Na is 35 million times higher than that of H+
Why are buffer systems necessary?
Large amounts of H+ are produced during metabolic processes daily
The concentration of H+ must be maintained at low and tight levels
What is a buffer system?
A buffer is a solution that resists changes in pH when an acid or an alkali is added to it
What are buffer’s composed of?
Typically involve a weak acid or an alkali together with one of their salts
How does a buffer system work?
Addition of a strong acid results in the formation of a weak acid and similarly, the addition of a strong base results in the formation of a weak base. Thus a buffer system prevents large changes in pH
Are buffer systems reusable?
If the constituents of a buffer system are consumed and the buffer system loses efficacy if they are not replaced.
Buffer system of the ECF?
Bicarbonate buffer system (H2CO3/HCO3)
Buffer system of the ICF?
Hemoglobin (H/Hb)
Proteins (H/Proteins)
Phosphate (HPO4/H2PO4)
Isohydrolic principle
since the H+ concentration in the body is finite, all of the buffers in a common solution are in equilibrium with the same H+ concentration. So by knowing the status of one system then we know the functioning status of all the buffer systems in the body and thus can assess the acid/base status
How is acid/base status assessed?
Arterial blood gasses (ABGs), serum osmolarity and chemistries (Na, K, Cl, CO2, albumin), urine chemistries (Na, K, Cl) are a few tools used to assess the functioning of the bicarbonate buffer system
ABGs AKA
Arterial blood gases
What are ABGs?
A series of tests that are performed on arterial blood and provide valuable information to assess the oxygenation and acid/base status
PaO2 =
A value that represents the partial pressure of oxygen dissolved in the arterial blood The PaO2 is the primary indicator of whether a patient is hypoxic and is used to diagnose Acute Respiratory Failure
ARF AKA
Acute respiratory failure
What is partial pressure?
In a mixture of gases, the partial pressure exerted by a gas is equal to the amount of gas present in that mixture provided the temperature remains constant
Changes in PaO2 with altitude
At sea level the atmospheric pressure is 760 mmHg. The concentration in air is 21%, therefore the PO2 at sea level will be (760 x 0.21) 159 mmHg. Albuquerque is at an altitude of 6000 ft and the atmospheric pressure here is approximately 603 mmHg. PO2 in Albuquerque is 126 mmHg. Note that the concentration of O2 remains constant but is only represented by a total pressure of 603 mmHg. 603 mmHg x 21% O2 = 0.21 126 mmHg PO2
What serum level of O2 represents hypoxia?
<65 mmHg
SaO2 =
Represents the % of hemoglobin which is saturated with O2
Normal SaO2 levels
Normal SaO2 = > 92%
What describes the relationship between PaO2 and SaO2?
The O2-Hb dissociation curve
FiO2 =
The fraction O2 in the inspired air. An ABG result should list the FiO2 at which the ABG was collected. Room air has a FiO2 of 21%
Shunt equation relevance
This value is calculated by taking the PaO2 from the ABG results and dividing this by the FiO2 being delivered to the patient.
For example: PaO2 of 75 mmHg divided by room air which has a FiO2 of 0.21 (21% oxygen) would give us a ratio of 357
Shunt equation normal values
A PaO2/FiO2 ratio of > 300 is considered normal
pH definition
A term used to indicate the hydrogen ion concentration in the blood. It is the H ion concentration in the negative log (base 10) scale.
pH =
pH = - log(H+) where H+ is expressed in mol/L
Normal pH range of arterial blood
Normal Arterial blood pH = 7.35 - 7.45
pH relation to [H+]
pH is inversely related to H+ ion concentration
A low pH is associated with a high [H+]
Is a given pH considered acidic or basic?
Any values under 7.40 is considered acidic
Any values over 7.40 is considered alkaline
How to calculate H+ ions from pH
[H+] = 10^-pH
PaCO2 =
A value that represents the partial pressure of CO2 in the arterial blood
CO2 in the blood is considered?
CO2 in the blood is considered a volatile acid
How is CO2 regulated in the body?
CO2 is regulated in the lungs, a change in pH due to a change in PaCO2 is labeled as a respiratory abnormality
Normal PaCO2 levels
PaCO2 > 42 mmHg indicates respiratory acidosis
PaCO2 <38 mmHg indicates respiratory alkalosis
HCO3 =
A value that represents the bicarbonate content of the blood
How is HCO3 regulated?
Kidneys regulate HCO3 concentration by reabsorbing and making new HCO3-. A change in pH due to a change in HCO3- is labeled as a “metabolic” abnormality
Normal HCO3 levels
HCO3 < 22 indicates metabolic acidosis
HCO3 > 26 indicates metabolic alkalosis
Acid =
An acid is a substance that can donate a proton
Base =
A substance that can accept a proton
Acidemia =
Acidic blood has a pH < 7.35 (or a H ion concentration > 42 nmol/L)
Acidosis =
A clinical condition or disease process producing a state where the blood pH is < 7.35
Alkalemia =
Basic blood has a pH > 7.45 (or a H ion concentration < 38 nmol/L)
a pH of > 7.45 is labeled as alkalemia
Alkalosis =
A clinical condition or disease process producing a state where the blood pH is > 7.45
How does the bicarbonate system work?
Cells produce H+ ions which enter the circulation Bicarbonate buffer system which comprises a weak acid (H2CO3) and its salt (NaHCO3), prevents sudden changes in the concentration of H+. H+ binds with the salt (Na)HCO3 and forms Carbonic acid (H2CO3) which is catalyzed by carbonic acid
H2CO3 is unstable and immediately breaks down into H2O and CO2
Thereby preventing an increase in H+ ion concentration by converting a strong acid into a weak acid, however, there was depletion of HCO3 and addition of CO2 in the system

What happens to carbonic acid after it is catalyzed by carbonic anhydrase?
H2CO3 is unstable and immediately breaks down into H2O and CO2
For the bicarbonate buffer system to continue preventing pH changes what needs to happen?
CO2 needs to be released and HCO3 needs to be repleted
How is HCO3 replenished?
Kidneys generate new HCO3
How is CO2 removed?
Lungs remove CO2
What is the significance of the Henderson-Hasselbalch Equation?
It is a mathematical representation of the bicarbonate buffer system and tells us the ratio of HCO3 and PCO2 that govern the pH
Bicarbonate buffer system Henderson-Hasselbalch Equation =

How is pH governed in the blood?
pH is governed by the ratio of HCO3 / PCO2
The Henderson-Hasselbalch Equation tells us that pH can only change if PCO2 and/or [HCO3] change
Changes in PCO2 are labeled as?
Respiratory
Changes in [HCO3] are labeled as?
Metabolic
If PCO2 increases then pH will? And lead to?
pH will decrease and lead to respiratory acidosis
If PCO2 decreases then pH will? And lead to?
pH will increase and lead to respiratory alkalosis
If HCO3 increases then pH will? And lead to?
pH will increase and lead to metabolic alkalosis
If HCO3 decreases then pH will? And lead to?
pH will decrease and lead to metabolic acidosis
pH is inversely related to which part of the HHE?
pH is inversely related to PCO2
PH is directly related to which part of the HHE?
pH is directly related to HCO3
The body tries to limit changes to pH by?
Keeping the HCO3/PCO2 ratio constant which is called Compensation
What is compensation?
The body attempting to limit pH changes by keeping the HCO3/PCO2 ratio constant
The compensatory response accuracy?
The compensatory response may overshoot or undershoot
Compensatory response to metabolic acidosis
A decrease in HCO3 will lead to a decreased pH.
Lungs will counteract this by decreasing PCO2 and thus pH will increase
Compensatory response to metabolic acidosis AKA
Respiratory compensation of metabolic acidosis
Respiratory compensation of metabolic alkalosis
An increase in HCO3 will lead to an increased pH
Lungs will counteract this by increasing PCO2 and thereby increasing pH
Metabolic compensation of respiratory acidosis
An increase in PCO2 will lead to a decreased pH
The kidneys will counteract this by increasing HCO3 and thereby increasing pH
Metabolic compensation of respiratory alkalosis
A decrease in PCO2 will lead to an increased pH
The kidneys will counteract this by decreasing HCO3 and thereby decreasing pH
Normal pH values
7.35 - 7.45
Normal PaCO2 levels
38 - 42 mmHg
Normal HCO3 levels
22-26mEq/L
Normal PaO2
80-100 mmHg
Normal SaO2
>92%
Normal Hypoxemic score/shunt equation
>300
How to identify ventilation/perfusion problems?
Evaluate PaO2/FiO2 whenever hypoxia is present
How to determine the acid/base balance
pH is the indicator
pH <7.35 = Acidosis
pH >7.45 = Alkalosis
Is the cause of acidosis respiratory or metabolic?
If PaCO2 is > 42 mmHg then the cause is respiratory
If the HCO3 is < 22 mEq/L then the cause is metabolic
Is the cause of alkalosis respiratory or metabolic?
If PaCO2 is < 38 mmHg then the cause is respiratory
If the HCO3 is > 26 mEq/L then the cause is metabolic
Has compensation occurred?
Find out the magnitude of the compensatory response and assess whether the compensatory response was appropriate or inappropriate
Respiratory Acidosis is caused by?
Decreased elimination of CO2 usually due to a perfusion/ventilation mismatch
Causes of a perfusion/ventilation mismatch?
Depression of the respiratory center in CNS
Interference with gas exchange across alveolar membrane
Reduction in the amount of blood pumped to the lungs
Lab findings of respiratory acidosis
pH < 7.35
PaCO2 > 42 mmHg
Respiratory acidosis compensation
Kidneys increase HCO3 and thereby attempt to increase pH towards normal but not all the way
Respiratory acidosis compensation timeline
It takes time for the kidneys to produce new channels and enzymes to produce new HCO3, therefore metabolic compensation of respiratory acidosis has 2 phases; an acute phase where the compensation is less robust and a chronic phase where the compensation is more robust
Acute phase respiratory Acidosis compensation magnitude
For each 10 mmHg increase in PCO2, the HCO3 increases by 1 mmHg
Chronic phase Respiratory Acidosis compensation magnitude
For each 10 mmHg increase in PCO2, the HCO3 increases by 4 mmHg
Respiratory alkalosis primary defect
CO2 deficit
Causes of the CO2 deficit in respiratory alkalosis
Overstimulation of the respiratory center in the CNS
Hyperventilation - due to exercise
Lab findings in respiratory alkalosis
pH > 7.45
PaCO2 < 38 mmHg
Metabolic compensation of respiratory alkalosis
Kidneys reabsorbs less HCO3-
Compensation corrects pH towards nromal but not all the way
Metabolic compensation of respiratory alkalosis timeline
Metabolic compensation of respiratory alkalosis takes time so there are 2 phases; an acute phase where the compensation is less robust and a chronic phase where the compensation is more robust
Metabolic compensation of respiratory alkalosis Result
A decrease in pH towards normal
Acute phase respiratory Alkalosis compensation magnitude
For each 10 mmHg decrease in PCO2, the HCO3 decreases by 2 mmHg
Chronic phase Respiratory Alkalosis compensation magnitude
For each 10 mmHg decrease in PCO2, the HCO3 decreases by 5 mmHg
Question

Dissociation constant (Ka)

Dissociation constant equation

Henderson-Hasselbalch equations

Causes of acute respiratory acidosis

Causes of chronic respiratory acidosis

Causes of respiratory alkalosis

Acidosis symptoms
6 listed
- Hyperventilaton (Kussmaul breathing)
- Depression of myocardial contractility
- Cerebral vasodilation
- increased blood flow can cause ICP
- Can also get CNS depression
- Hyperkalemia
- H+ shifts into cells in exchange for K+
- Shift in O2Hb dissociation curve to the right reducing Hb’s affinity to O2 and causing more O2 release into tissues
Alkalosis symptoms
5 listed
- Inhibition of respiratory drive
- depression of myocardial contractility
- cerebral vasoconstriction
- decrease in cerebral blood flow
- hypokalemia
- shifts K+ into cells in the absence of H+
- Shift in HbO2 dissociation to the left dcreasing O2 offloading to the tissues
Alkalosis potassium levels
hypokalemia
because in the absence of H+, K+ is more readily shifted into cells
Acidosis potassium levels
Hyperkalemia because the excess of H+ is shifted into cells in the place of K+
Anion gap
for metabolic acidosis only
Renal compensation for acidosis
3 listed
- Excess H+ filtered/secreted into the nephron
- H2CO3- is reabsorbed
- Urinary buffers are excreted (these serve as buffers and bind H+ preventing severe drops in pH)
- HPO42- excreted as H2PO4- (phosphate)
- NH3 is ecreted as NH4+ (ammonium)
Urinary buffers
2 listed
HPO42- excreted as H2PO4- (phosphate)
NH3 is excreted as NH4+ (ammonium)
Renal compensation for alkalosis
3 listed
- Excess H+ reabsorbed from the nephron
- H2CO3- is secreted and excreted
- Urinary buffers are excreted (these serve as buffers and bind H+ preventing severe drops in pH)
- HPO42- reabsorbed H2PO4- (phosphate)
- NH3 is reabsorbed NH4+ (ammonium)
How to recognize mixed acid-base disorders
- Need to determine the expected compensatory response
- and if the actual response isn’t the expected response then a 2nd disorder is present
- If the body cannot compensate for the pH all the way back to the normal range

Common cause of a mixed acid-base disorder
Nausea and Vomiting
- Nausea causes acidosis
- Vomiting causes alkalosis
Mixed acid-base disorder possible combinations
can only have 1 respiratory ventilation imbalance (either acidosis or alkalosis)
Can have 1 or 2 metabolic disorders (can have an alkalotic and acidotic or 2 of the same)
Compensation formulas
- Winter’s Formula
- Metabolic Alkalosis Formula
- Acute/Chronic Respiratory Equations
- Delta-Delta
Metabolic acidosis compensation and the possibility of a mixed disorder
Always hyperventilation to decrease CO2
Winter’s formula tells you the expected PCO2
If the actual ≠ expected then there is a mixed disorder

Metabolic alkalosis compensation and the possibility of a mixed disorder
hypoventilation to increase PCO2
Rule of thumb is ↑ PCO2 0.7 mmHg per 1.0meq/L ↑[HCO3-]
ΔPCO2 = 0.7 x (Δ[HCO3-])
if the actual PCO2 ≠ expected then a mixed disorder is present
Respiratory acidosis compensation and the possibility of a mixed disorder
Acute compensation
- minutes
- Intracellular budders raise [HCO3-]
- Hemoglobin and other proteins
- results in small ↑pH
Chronic compensation
- Days
- Renal generation of ↑[HCO3-]
- results in a ↑↑pH (but not back to normal!)

Compensating back to a normal pH
The body cannot do this so if this is the case there is a mixed disorder
Respiratory alkalosis compensation and the possibility of a mixed disorder

Compensation timeframe for respiratory compensation
- Rapid (minutes)
- change in respiratory rate
Compensation timeframe for metabolic compensation
- Acute occurs in minutes by mild compensation from cells
- Chronic takes days to get a significant compensation from the kidneys
Alkalosis and acidosis compensation summary

Most commonly tested mixed disorder formula
Winters formula

Shunt equation and normal values
PaO2/FiO2
>300 is normal