Acid Base Flashcards
What must happen to maintain acid-base balance?
What are the 2 ways this occurs?
excrete an amount of acid equal to the production of non-volatile acids
Volatile acid - CO2 is “blown off” by the lungs
Kidneys are responsible for the excretion of non-volatile acids (50-150 mEq/day & requires proton acceptors in the tubule)
What are the sources of H+ in the kidney?
This requires what enzyme?
- dissociation of H2CO3
- requires enzyme carbonic anhydrase
What measurement is an index of H+ secretion?
HCO3- reabsorption
What are buffers?
What is the equilbrium constant?
How is equilbrium shifted?
buffers are a mixture of relatively weak acids & its conjugate base
Ka is the equilibrium constant, pKa = -log Ka
Adding or removing H+ causes this equilbrium to shift either left or right
What is the Henderson-Hasselbalch Equation?
pH is dependent on what two factors?
- The [A-]/[HA] ration (regardless of the concentrations)
- the pKa of the buffer system
What are the pH levels & subsequent [H+] under normal, acidosis, and alkalosis situations?
Acid-base regulation refers to what phenomena?
regulation of the [H+] in the body fluids
What 4 systems are involved in the regulation of pH?
- Chemical buffers
- Respiratory system (controling ventilation)
- Kidney (controling excretion fixed acid & generating bicarbonate)
- Bone (long-term)
How quickly do chemical buffers respond to an acid or base challenge?
What is the isohydric principle?
instantaneously - both intracellular & extracellular - due to a change in the acid/base ration
Isohydric principle: all of the chemical buffer systems participate simulatneously in defending against disturbances in acid-base status
How quickly does the respiratory system compensate for challenges to acid/base status?
How does it do this?
minutes to hours
Regulates PaCO2 by altering alveolar ventilation
Acidosis stimulates ventilation
Alkalosis reduces ventilation
- Alveolar ventilation equation
- VCO2 = rate of CO2 production
- VA = rate of alveolar ventilation
How quickly does it take the kidney to compensate for challenges to acid/base status?
What are these responses?
hours to days
- Acidosis:
- excrete more H+ (as NH4+ and TA) and produce and reabsorb more HCO3-
- Alkalosis
- secrete less H+ and excrete more HCO3-
Where do the buffers in the blood come from?
- Most of the buffer is through bicarbonate (plasma & erythrocyte) –53%
- hemoglobin & oxyhemoglobin are also important – 35%
- organis phosphate – 3%
- inorganic phosphate – 2%
- plasma proteins – 7%
What is the most powerful extracellular buffer?
pKa?
Why is it effective at blood pH?
Describe the components of this system & include relevant equations.
CO2 - bicarbonate buffer system
pKa = 6.1
- Effective at pH 7.4 b/c
- CO2 and HCO3- can be controlled independently
- ventilation takes care of CO2
- kidney takes care of bicarbonate
- HCO3- can be replaced nearly as fast as it is used up in buffering pH changes
- CO2 and HCO3- can be controlled independently
- CO2 - volatile acid
- Produce ~15,000 mEq/day from cellular metabolism
- Lungs (respiratory system) regulates arteiral PaCO2 by controlling alveolar ventilation
- HCO3- - base
- kidney contorl body fluid [HCO3-] by excreting excess HCO3- in the urine (in alkalosis), or by makign “new” HCO3- (in acidosis)
Describe the equation for the mass action relationship
because we can independntly regulate CO2 on one side of the system and independnetly regulate HCO3- on the other side of the system
this makes the CO2 / bicarb system important in regulating pH
What are the normal values of the following variables with relation to the mass action equation
PaCO2
Dissolved CO2
Plasma [HCO3-]
pHa
- PaCO2 = 40 mmHg
- Dissolved CO2 = 0.03 * PaCO2 = 1.2
- Plasma [HCO3-] = 24 mM
- pHa = 7.4 or [H+] = 40 nM (40 x 10-9 M)
Do absolute concentrations of HCO3- and CO2 matter?
no, for pH 7.4 all that matter is that the ratio is 20/1
What is the role of “non-respiratory buffers” ?
the H+ are also in equilibrium with “non-respiratory” buffers
so, when we look at changes in CO2 that drive the reaction left or right, these changes in H+ will result in relative changes to the A- / HA form of the “non-respiratory buffers”, which influences our acid/base status
What ratio of HCO3- to dissolved CO2 denotes acidosis?
What ratio of HCO3- to dissolved CO2 denotes alkalosis?
- acidosis
- <20/1
- alkalosis
- `>20/1
Describe what happens variable under acidosis & then under alkalosis?These measurements indicated respiratory or metabolic conditions?
HCO3- / CO2 ratio
PaCO2
plasma HCO3-
- Primary Acid-Base Disturbances
- Acidosis
- HCO3- / CO2 decreases
- Respiratory: increase PaCO2 (decrease VA) - increasing the denominator by decreasing ventilation
- Metabolic: decrease plasma HCO3-
- HCO3- / CO2 decreases
- Alkalosis
- HCO3- / CO2 increases
- Respiratory: decrease PaCO2 (increase VA) - decrease the amount of acid by increasing ventilation
- Metabolic: increase plasma HCO3-
- HCO3- / CO2 increases
- Acidosis
What is the difference between correction & compensation?
- Correction
- the elimination of the cause of the acid-base disturbance
- all values return to normal
- Compensation
-
minimized the pH disturbance by adjusting the ratio of conjugate base to acid
- returning the HCO3- / CO2 ratio toward 20/1
- so, if CO2 goes up, need to increase HCO3- as well
- compensation is NOT corrective and a small pH disturbance will remain
- returning the HCO3- / CO2 ratio toward 20/1
-
minimized the pH disturbance by adjusting the ratio of conjugate base to acid
What type of compensation occurs for respiratory disorder?
What type of compensation occurs for metabolic disorder?
- Respiratory disorder
- compensation is renal (hours to days)
- Metabolic disorder
- compensation is respiratory (minutes to hours) & renal (hours to days)
What does “primary disturbance” refer to?
In what direction do compensatory changes occur
- Primary disturbance is the initial change
- All chemical buffers are involved in any pH change, and the buffering is instantaneous
- Compensatory changes occur in the “same direction” as the primary disturbance, and bring the base/acid ratio back toward 20/1
- respiratory compensation takes minutes to hours ( & typically accompanies the development of the disorder)
- renal compensation takes hours to days
What type of disturbance occurs when the change pH and plasma [HCO3-] occur in the same direction?
metabolic disturbance
pH is directly proportional to [HCO3-]
What type of disturbance occurs when the change of pH and plasma [HCO3-] occur in opposite directions?
respiratory disturbance
pH is inversely proportional to dissolved CO2
Fill out the provided diagram
How can you determine the degree of compensation?
from the change in the “other” variable
if you have had time to compensate & bring the ratio back to 20/1, you will minimize the magnitude of the change in pH
How can you determine if there is a base excess vs. deficit?
Total base in the system is determine by HCO3- + A-
- Base excess
- increase in total base contents (HCO3- + A-)
- Base deficity
- decrease in total base contents (HCO3- + A-)
- base deficit is somethign referred to as “negative base excess”
What impact does hypoventilation have on acid/base status?
- Hypoventilation –> Respiratory Acidosis
- leading to CO2 retention
- increased PaCO2 (hypercapnia)
What conditions indicate acute respiratory acidosis?
How would you calculate [HCO3-]?
- Change in opposite directions
- increased PaCO2 ( >40mmHg)
- decreased pH (increased [H+])
- Small increase in HCO3- – but no base excess
- new HCO3- can be approximated by:
What conditions indicate chronic respiratory acidosis?
How would you calculate [HCO3-]?
- Renal compensation (hours to days)
- The kidneys secrete more H+ (due to increased PaCO2)
- reabsorb all the filtered HCO3-
- increase formation of TA and NH4+
- increase new HCO3- production (increase HCO3-)
- excrete an acidic urine
- plasma HCO3- increases– a base excess develops
- Expected HCO3- at madimal compensation:
- The kidneys secrete more H+ (due to increased PaCO2)
What conditions can lead to acute ihibition of the medullary respiratory center?
Chronic?
- Acute
- drugs, opiates, anesthetics, seditives
- oxygen in chronic hypercapnia
- cardiac arrest
- central sleep apnea
- Chronic
- extreme obesity (Pickwickian syndrome)
- central nervous system lesion (rare)
What disorders of the respiratory muscles and chest wall can lead to acute respiratory acidosis?
Chronic respiratory acidosis?
- acute
- muscle wakness - myasthenia gravis, periodic paralysis, aminoglycosides, Guillain-Barre syndrome, severe hypokalemia or hypophosphatemia
- chronic
- muscle weakness - poliomyelitis, amyotrophic lateal sclerosis, multiple sclerosis, myxedema
- kyphoscoliosis
- extreme obesity
What type of airway obstruction can lead to acute respiratory acidosis?
- acute
- aspiration of foreign body or vomitus
- obstructive sleep apnea
- langospasm
What disorders affecting gas exchange across the pulmonary capillary can cause acute respiratory acidosis?
Chronic respiratory acidosis?
- acute
- exacerbation of underlying lung disease (including increased CO2 production with high carbohydrate diet)
- adult respiratory distress syndrome
- acute cardiogenic pulmonary edema
- sever asthma or pneumonia
- pneumothorax or hemothorax
- chronic
- chronic obstructive pulmonary disease: bronchitis, emphysema
What impact does hyperventilation have on acid/base status?
- Hypoventilation –> Respiratory Alkalosis
- leading to excess CO2 elimination
- decreased PaCO2 (hypocapnia)
What conditions indicated acute respiratory alkalosis?
How would you calculate [HCO3-]?
- Opposite directions
- decrease PaCO2 ( <40 mmHg)
- incrase pH (decrease [H+])
- Small decrease in HCO3 but no base deficit,
- the new HCO3 concentration can be approximated by:
What conditions indicated chronic respiratory alkalosis?
How would you calculate [HCO3-]?
- Renal compensation (hours to days)
- The kidneys secrete less H+ (due to decreased PaCO2)
- fail to reabsorb all the filtered HCO3- and some HCO3- and some HCO3- stays in teh tubule and is excreted
- relatively alkaline urine
- Plasma HCO3- decreases and a base deficit develops
- Expected HCO3- at maximal compensation
- The kidneys secrete less H+ (due to decreased PaCO2)
What conditions can cause hypoxemia, leading to respiratory alkalosis?
- Alkalosis
- pulmonary disease: pneumonia, interstitial fibrosis, emboli, edema
- congestive heart failure
- hypotension or severe anemia
- high-altitude residence
What conditions directly stimulate the medullary respiratory center leading to respiratory alkalosis?
- Stimuation of Medullary Respiratory Center
- psychogenic or voluntary hyperventilation
- hepatic failure
- gram-negative septicemia
- salicylate intoxicatoin
- postcorrection of metabolic acidosis
- pregnancy and the luteal phase of the menstrual cycle (due to progesterone)
- neurologic disorder: cerebrovascular accidents, pontine tumors
What is the primary disturbance in metabolic acidosis?
derease in plasma HCO3
- increased H+ (diabetic ketoacidosis)
- loss of HCO3- (diarrhea)
- Combination of decrease in pH and a decrease in [HCO3-] in teh same direction
- a base deficit develops & can be used to assess the severity of the disturbance
Describe respiratory compensation in metabolic acidosis.
How would you calculate the expected PaCO2?
- Respiratory compensation (…minutes to hours)
- low pH stimulates peripheral chemoreceptors which increase ventilatio, leading to a decrease in PaCO2
- no real “acute” phase b/c respiratory system begins increasing ventilation with the onset of the acidosis, and PaCO2 begins to fall
- Tendency for the central chemoreceptors to limit the extent of the hyperventilation (low PaCO2 reduces drive to breathe)
- Expected PaCO2 with respiratory compensation:
Describe renal compensation of metabolic acidosis.
What is the maximally acidic urine?
- Renal compensation (hours to days)
- since the primary disturbance is a fall in plasma HCO3-, the filtered load of HCO3 will be reduced
- Total H+ secretion is reduced (decreaed FLHCO3 and decreased PCO2)
- Instead, the kidney forms more TA and NH4+ and therefore excretes more H+
- Produces more new HCO3 to reduce the base deficit
- maximally acidic urine (~pH 4.5)
Why is there an anion gap in metabolic acidosis & how do you calculate it?
What is the normal value?
Anion gap develops due to the accumulationof fixed acids
Anion gap represents “unmeasured anoins” taht balance Na+ in place of the lost HCO3-
normal value is 9-13
What are the most common causes of metabolic acidosis with an anion gap?
MULEPAK
- M: methanol
- U: uremia
- L: lactate
- E: ethylele glycol
- P: paraldehyde
- A: aspirin
- K: ketones
What is the primary disturbance of metabolic alkalosis?
increase in plasma HCO3-
- loss of H+ (excessive vomiting)
- gain of HCO3- (overuse of diuretics)
- the combination of increase in pH and increase in HCO3- confirms metabolic alkalosis – change in the same direction
- A base excess ([HCO3-] and [A-]) develops and can be used to assess the severity of the disturbance
Describe respiratory compensation of metabolic alkalosis
How would you calculate the expected PaCO2?
not very good & doesn’t last very long
- Respiratory compensation (minutes to hours)
- High pH inhibits peripheral chemoreceptors which decreases ventilation, leading ot an increase in PaCO2
- tendency for the chemoreceptors to limit the extend of the hypercapnia (central) and hypoxemia (peripheral) due to hypoventilation
- Expected PaCO2 with respiratory compensation:
Describe renal compensation of metabolic alkalosis
- Renal compensation (hours to days)
- since the primary disturbance is an increase in plasma HCO3-, the filtered load of HCO3- is increased
- the increased PaCO2 increases renal H+ secretion and increases HCO3- reabsorption, compromising the degree of compensation
- excess HCO3- is excreted resultin in a realtively alkaline urine
Renal compensation of metabolic alkalosis is impaired under what two conditions?
Describe why this is the case.
- Volume depletion
- increase aldosterone release increases distal nephron Na+ reabsorption and increases H+ (and K+) secretion
- increase in new HCO3-
- increase aldosterone release increases distal nephron Na+ reabsorption and increases H+ (and K+) secretion
- K+ - depletion
- decreases in Na+- K+ exchange in the distal nephron and increases H+ secretion ( to offset the reduced K+ secretion)
- increase new HCO3-
- decreases in Na+- K+ exchange in the distal nephron and increases H+ secretion ( to offset the reduced K+ secretion)
- BOTH conditions increase new HCO3- production and reabsorption perpetuating the alkalosis
Why might someone fail to achieve the expected degree of compensation?
It is possible to have 2 acid-base disorders at the same time
this may reflect a mixed disorder
What conditions might suggest that a person has mixed acidosis and alkalosis conditions?
pH in the normal range
PaCO2 and HCO3- out of normal ranges
one is probably a chronic condition
