19- Regulation of [H+] in body fluids Flashcards
why is regulating H+ important?
-H+ affects protein function (enzymes, structurally)
- must be regulated within a narrow range and if it isn’t then…
- too little H+ increases excitability of neurons (seizures)
- too much H+ decreases excitability of neurons (comatose)
relationship of H+ and seizures
too little H+ increases excitability of neurons
relationship of H+ and comatose state
excess H+ decreases excitability of neurons
arterial pH
7.4
venous pH
7.35
intracellular fluid pH
6.0 - 7.4
cerebral spinal fluid pH
7.32
urine pH
4.5 - 8.0
acid vs base
acid
-compound which donates H+ or proton
base
-compound which accepts H+ or proton
H+ in respiratory system
CO2 + H2O —> H2CO3 —> [H+] + HCO3-
metabolic H+
H2PO4- —> H+ + HPO4
H+ disorders
- Respiratory acidosis
- Respiratory alkalosis
- meabolic acidosis
- metabolic alkalosis
respiratory acidosis
increased CO2
-hypoventilation
CAUSES
- depression of respiratory centers (anesthetics, sedatives, opioids, brain injury/disease, severe hypercapnia, hypoxia)
- neuromuscular disorders (spinal cord/phrenic nerve injury, polio, tetanus, myasthenia gravis, curare drugs, respiratory muscle disease)
- chest wall restriction (kyphoscoliosis, obesity)
- lung restriction (lung fibrosis, sarcoidosis, pneumothorax)
- pulmonary diseases (pneumonia, edema)
- airway obstruction (COPD, upper airway obstruction)
respiratory alkalosis
decreased CO2
-hyperventilation
CAUSES
- origin in central nervous (anxiety, hyperventilation syndrome, encephalitis, meningitis, tumors)
- drugs or hormones (sacicylates, progesterone)
- bacteremias, fever
- pulmonary diseases (asthma, emboli)
- overventilation with mechanical ventilators
- hypoxemia, high altitude
Metabolic acidosis
HCO3- decreased
CAUSES
- ingestion of toxic substances (methanol, ethanol, salicylates, ammonium chloride)
- loss of HCO3- (diarrhea, renal dysfunction)
- lactic acidosis (hypoxemia, anemia, shock severe exercise, acute respiratory distress syndrome)
- ketoacidosis (diabetes, alcoholism, starvation)
- renal dysfunction
Metabolic alkalosis
HCO3- increased
CAUSES
- loss of H+ (vomiting, gastric fistulas, diuretic therapy)
- treatment with or overproduction of steroids (aldosterone)
- ingestion of excess HCO3- or other bases (antacids_
if you have an arterial blood sample, how do you tell if its acidosis or alkalosis
pH
<7.4 = acidosis
>7.4 = alkalosis
if you have an arterial blood sample with a pH of <7.4, how can you tell whether its metabolic or respiratory?
Metabolic acidosis has a HCO3- < 24mEq/L
Respiratory acidosis has a PCO2 > 40mmHg
if you have an arterial blood sample with a pH of >7.4, how can you tell whether its metabolic or respiratory?
Metabolic alkalosis has a HCO3- >24mEq/L
Respiratory alkalosis has a PCO2 <40mmHg
How to make up for respiratory acidosis and alkalosis
Renal Compensation
acidosis: HCO3- >24mEq/L
alkalosis: HCO3- <24mEq/L
How to make up for metabolic acidosis and alkalosis
Respiratory compensation
acidosis: PCO2 <40mmHg
alkalosis: HCO3- >40mmHg
CO2 hydration reaction
CO2 + H2O —> [H+] + HCO3-
Respiratory acidosis
CO2 is above normal
Metabolic acidosis
CO2 is below normal
physical-chemical buffering is a result of
compounds in a solution minimize the charge in H+ in the solution when a strong acid or base are added to the solution
NaOH –> Na+ + OH —> NaHCO3 + H2O
ion contents of extracellular fluid
HCO3-
HPO4
Proteins
ion contents of intracellular fluid
HPO4
Proteins
isohydric principle
when H+ is altered in a solution all buffer pairs will be affected
determinants of H+ buffering
- concentration or amount of the buffer pair in the solution
- pK of the buffer pair relative to the pH of the solution
pH and pK buffering
pH solution = pK buffer pair
equal amounts of
- H+
- acid
- base
when adding an acid or base, conditions are optimal for buffering around 6ish
Physiologic H+ regulation
processes in the body that can alter the amount of the physical-chemical buffers
- transmembrane exchange
- pulmonary ventilation
transmembrane exchange
- Intracellular fluid
- High concentration of physical- chemical buffers
Example: Respiratory or Metabolic Acidosis
Extracellular Fluid Buffering of H+ is through movement of H+ into cells in exchange for Na or K+.
pulmonary ventilation
-H+ buffering through HCO3- - H2CO3 buffer pair
Example: During metabolic acidosis such as lactacidosis, the following reaction occurs:
lactic acid –> lactate + H+ –> H+ + HCO3- –> H2CO3 –> H2O + CO2 and the CO2 is eliminated by the respiratory system
*each CO2 that comes out takes care of one of the H+ ions made by the anaerobic cycle
renal regulation of H+
- excretion of titratable acid
- reabsorption of bicarbonate
- HCO3- regeneration
-sulfuric acid
-phosphoric acid
-lactic acid
-other
Results in buffering
-H+ by HCO3-
-forming H2CO3-
-dissociates into H2O and CO2
-eliminated by the lungs
how does the brain regulate H+ concentrations
blood-brain barrier
blood-brain barrier
-restricts charged particles movement (such as H+)
- systemic metabolic acidosis and alkalosis
- -cerebrospinal fluid [H+] changes only 10% (of the change in the blood [H+])
- but its ineffective in buffering of respiratory acidosis and alkalosis
- -glial cells in the brain increase production of NH3 and lactic acid during respiratory acidosis and alkalosis respectively
On admission a patient was lethargic, but 7 hours after correcting arterial pH with HCO3 infusion, he became comatose. There was no further treatment, but 22 hours later he was wide awake. explain this
the coma was due to too much H+ in the system after the HCO3 infusion but once everything settled and more CO2 and H2O were produced from the HCO3 the person woke up and was fine
the brain was eventually able to correct itself with time (between 7 and 22 hours)
Between 7 and 24 hours after treatment, CSF pH and HCO3- both increased as a result of HCO3- crossing the blood brain barrier or generation of HCO3- in the brain.
H+ buffering or regulating mechanisms
Respiratory Component
- rapid-acting
- limitedbyHCO3-availability
Transmembrane Exchange
- slightlyslower
- limited by phosphate sites
Renal
- slow to respond
- minimal limitations in a healthy human
- -in patient with renal dysfunction limited capability for excreting the acid
clinical use of anion gap
Anions and Cations
- Must be equal to maintain electrical neutrality
- Clinically Na+ (144mM) is the only cation usually measured
- Only anions measured are Cl- (108 mM/L and HCO-3 (24 mM/L).
- Difference between anions and cations is 12mM/L
- During metabolic acidosis, HCO-3 is decreased, but there is an increase in some anion such as lactate- to maintain electrical neutrality.
- A clinically useful term to assess the degree of acidosis is the anion gap which in metabolic acidosis increases.
