1. Acid-Base Balance Flashcards
Causes of Acid-Base imbalance
- Respiratory Acidosis
% chronic lung disease eg asthma
Blood pH < 7.40
PCO2 > reference point of 40 mmHg = hypoxic
Most common=dec alveolar ventilation=dec breathing rate
Restrictive lung disease ie COPD
Causes
-excess CO2 in inspired air
-decreased alveolar ventilation
»central respiratory depression
»nerve or muscle disorders (e.g., myasthenia gravis)
»lung or chest wall defects (e.g., restrictive lung disease)
»airway disorders (e.g., asthma)
» external factors eg strangling
-Increased production of CO2
»Hypercatabolic disorders (e.g., malignant hyperthermia)
COPD=A group of lung diseases that block airflow and make it difficult to breathe.
-Damage to the lungs from COPD can’t be reversed.
-Symptoms include shortness of breath, wheezing, or a chronic cough.
-Rescue inhalers and inhaled or oral steroids can help control symptoms and minimize further damage.
ie Emphysema=destruction and enlargement of air spaces (move less O2 into blood)
ie bronchitis=increased mucus and inflammation
Causes of Acid-Base imbalance
- Respiratory Alkalosis
% hyperventilation, drug-induced toxicity (analeptics, salicylates)
Arterial pH > 7.40
PCO2 < reference point
Causes
-increased alveolar ventilation
»central causes ─ direct action via respiratory center (various drugs e.g., analeptics, propanidid, salicylate intoxication)
»>High salicylates found in aspirin
»Hypoxemia ─ acts via peripheral chemoreceptors
»pulmonary causes ─ act via intrapulmonary receptors (pulmonary emboli (blood clot))
»Iatrogenic (non-medical causes)─ act directly on ventilation (excessive controlled ventilation)
Causes of Acid-Base imbalance
- Metabolic Acidosis
% increased ketogenesis, diarrhea, kidney failure
(Ketone bodies=acidic-inc in untreated diabetics and inc when fasting
Diarrhea-loss of bicarbonate (base) from gut
Kidney failure-fail to retain bicarbonate or fail to excrete H)
Arterial pH < 7.40
Plasma HCO3- less than expected
Gain of organic acid or loss of base
In other words, high anion gap or normal anion gap metabolic acidosis
Causes
-normal anion-gap acidosis (hyperchloremic)
>(renal, gastrointestinal tract, other)
»Renal eg kidney fail to reabsorb sufficient HCO3- but reabsorb high Cl- (compensation)
»GI eg diarrhea-excessive loss of HCO3
-high anion-gap acidosis (normochloremic)
>(ketoacidosis, lactic acidosis, renal failure, toxins)
»Renal failure eg inability of kidney to secrete acids
–
if low K+ > ignore bc much lower than Na+
glc is 4+ = 4x normal
Normal glc= 70-110 mg/dL
Postprandial (after meals)- glc <140 mg/dL
Causes of Acid-Base imbalance
- Metabolic Alkalosis
% administration of salts of metabolic acids eg antacids, vomiting (lose stomach acids)
–
Arterial pH > 7.40
Plasma HCO3- greater than expected
Loss of strong acid or gain of base
Causes
-loss of H+ via kidneys (diuretics) or gut (vomiting)
-gain of alkali from exogenous source (NaHCO3 infusion) or endogenous source (metabolism of ketoanions)
Most important biological buffer systems
Bicarbonate/CO2 (blood) pKa = 6.1
Phosphate (Intracellular) pKa = 6.8
Hemoglobin (blood) pKa = 7.8
Blood Plasma pH is 7.4
Intracellular pH is 6.9
pKa=pH at which acid:base ratio is 1
Intracellular buffered by phosphate-close pH, pKa
Blood plasma maintained both by bicarbonate/CO2 and hb action
Application of Henderson Hasselbalch equation to CO2/Bicarbonate buffer system
CO2 + H2O H2CO3 H+ + HCO3-
pH=6.1 + log [HCO3-]/[CO2]
You can measure bicarbonate and CO2 concentrations. Clinically, however, CO2 is usually measured as a partial pressure, PCO2 or PaCO2, in units of mm of Hg. This is the pressure of CO2 in the gas in contact with the blood.
[CO2] = 0.03 X PCO2
Usu [ ] in milliequivalents units
The CO2/ Bicarbonate system is unique in that the pH is regulated in part through the release and uptake of a gas
CO2 levels are controlled by lungs (alveoli)
Bicarbonate levels are controlled by kidneys
Role of Kidney in
Acid-Base Balance
Kidneys contribute to acid-base balance in three ways:
- Reabsorption of HCO3- (bicarbonate)
- Production of new HCO3-
- Excretion of H+ as NH4+
Carbonic anhydrase (CA) plays an important role in the reabsorption of filtered bicarbonate as well as in the production of new bicarbonate
Lungs-slow breathing rate-inc CO2 and H+
Diag in words:
In lumen-
CA role from H2CO3 -> H2O + CO2
(H2CO3 from HCO3- joining w H+ that came from cell)
In proximal tubule cell-
CA role from CO2+ H2O -> H2CO3
(H2CO3 then -> HCO3- (goes into blood) + H+ (goes into lumen via Na+/H+ antiport)
In blood-
X CA role in diag, but Na+, HCO3- out into blood from cell, K+ into cell from blood
Basic principles of physiologic acid-base imbalance
- Respiratory: (cause is pulmonary)
- Acidosis: If the respiratory rate decreases, CO2 is retained, PCO2 increases, and pH falls (i.e., respiratory acidosis).
- Alkalosis: If the respiratory rate increases, CO2 loss is increased, PCO2 decreases, and pH rises (i.e., respiratory alkalosis). - Metabolic: (cause is metabolic)
- Acidosis: If excess acid is produced and/or base lost by a non-respiratory process, metabolic acidosis results.
- Alkalosis: If acid is lost and/or excess base is produced, metabolic alkalosis results.
- Doesn’t involve lungs
- Involves kidney function or other metabolic funcs
Compensation
Overall objective: try to keep pH around 7.4. If the causative process does not cease on its own, an opposing process must compensate for it.
CO2 + H2O H+ + HCO3
pH = 6.1 + log [HCO3-] / (0.03 x PCO2)
In eq, if change both terms in numerator and denom, can compensate for any changes
pH>7.4 if high [HCO3-]
- Respiratory acidosis (↑PCO2) is compensated by metabolic alkalosis (increased renal retention and production of HCO3-).
- Repiratory alkalosis (↓PCO2) is compensated by metabolic acidosis (increased excretion of HCO3- by kidneys).
- Metabolic acidosis (↓[HCO3-]) is compensated by respiratory alkalosis (hyperventilation to decrease PCO2).
- Metabolic alkalosis (↑[HCO3-]) is compensated by respiratory acidosis (hypoventilation to increase PCO2).
Respiratory-much faster than metabolic compensation, so can have acute/chronic respiratory acidosis/alkalosis
In a true pathologic state, pH is not fully compensated (to 7.4) until acidifying cause removed. The same is true for alkalosis.
Ie COPD causes high pCO2 (respiratory acidosis, pH 7.1)
Compensate with inc HCO3-
Treatment – dec pCO2
Anion Gap - Usefulness in distinguishing between loss of base and gain of acid
Metabolic acidosis results from a decrease in serum HCO3- due to
-a lack of renal reabsorption or production (thus, loss of base), or
-an excess of “other” anions (i.e. organic acids) that titrate HCO3- (lactate, ketones or acids from exogenous poisons like methanol or ethylene glycol)
»Dec HCO3- avail for buffering
The primary use of AG is to distinguish between these two possibilities
In the first case, AG would be normal (due to ↑Cl-) while in the second case, it would be elevated
Anion Gap - Definition
Serum contains both cations and anions in near balance to yield the normal pH of 7.4
Principal cation is Na+ while minor (unmeasured) cations are K+, Ca2+, Mg2+ and γ-globulin
Principal anions are HCO3- and Cl- while other (unmeasured) anions are lactate, phosphate, sulfate, ketones and albumin (and exogenous anions)
Serum anion gap is a measure of such “other” anions and is defined as [Na+] – ([Cl-] + [HCO3-])
(Slightly more cations than anions)
but try to get anions=cations
In metabolic acidosis, [HCO3-] decreases
This loss of HCO3- may be made up by Cl- (hyperchloremic), leaving the AG unchanged
If instead of Cl-, “other” anions accumulate (normochloremic), then AG would be elevated
