Module 2, Part 1 of 3 Flashcards
Acid-Base Balance
-body fluids vary i pH but the range of each fluid is mainly limited by a variety of buffer systems
Major Mechanisms to Control pH in Body
-buffer systems (molecular control of free H+)
-exhalation of CO2
-kidney excretion of H+
Buffer Systems
-prevent rapid, drastic changes in pH
-do not remove or create H+
-old or release H+ to regulate changes in body pH
Carbonic Acid-Bicarbonate Buffer System
CO2 + H2O = H2CO3 = HCO3- + H+
-ph too low (high H+), reaction driven to left
-pH too high (low H+) reaction is driven to right
-CO2 excreted in lungs
-H+ excreted in kidneys/urine
Protein Buffer System
-more effective than phosphate and bicarbonate buffer
-carboxyl group COOh can act like an acid and release H+
-amino grop NH2 can act like base and combine with extra H+
-proteins make up most of solute in intracellular fluids and plasma
Phosphate Buffer System
-phosphates are major anions in intracellular and extracellular fluid
-phosphate buffers produce H+ or OH-
-monohydrogen phosphate acts as a weak acid to buffer strong acids and H+
H+ - HPO4 –> H2PO4
-dihydrogen phosphate acts as weak acid to buffer a strong base
H2PO4 + OH –> HPO4 + H2O
Bicarbonate and CO2 Levels
-cells produce tiny amount of H+ and huge amounts of CO2
-high CO2 means low pH
-bicarbonate buffer converts CO2 to H+ to balance equilibrium
-bicarbonate and H+ can make carbonic acid that turns to CO2 and H2O when CO2 levels are low
Na+/H+ Antiporter in the Proximal C.T (Kidney)
*regulates pH
-can take NA from pee into kidney cells through capillaries
-can send H out through pee
-bicarbonate can be released into bloodstram
Lung Exhalation of CO2 Regulates Blood pH
-blood and tissue pH can be modified by changing rate and depth of breathing
-increase breathing rate/depth is an increase in blood pH
-as CO2 declines with increased breathing, more H+ from the blood and extracellular fluid combines with bicarbonate to balance equilibrium
-ve Feedback for pH Control
- decreased blood pH (high H+ concentration)
- receptors (central chemoreceptors in medulla oblongata and peripheral chemoreceptors in aortic and carotid bodies)
- control centre (respiratory area in medulla oblongata)
- effectos (diaphragm contracts more forcefully and frequently so more CO@ is exhaled)
-less H2CO3 forms and fewer H+ present so blood pH increases
H+ excretion in collecting ducts
-collecting ducts are the last part of the kidney so if something is put there, it is most likely excreted as urine
-bicarbonate can easily be sent out as urine
-proton pump in apical membrane pushes H+ out of cell and into fluid in tubule lumen to become urine
High H+ Concentration in Lumen
-high H+ can be buffered by available NH3 ammoniato become ammonium NH4 which is less acidic
Kidney Excretion of H+
-kidneys reabsorb lost bicarbonate that can buffer H+by proximal convuluted tubules
-kidneys directly excrete H+ in urine as the major way to eliminate excess quickly
-renal failure can cause death rapidly due to its role in pH balance and body will become too acidic
Blood pH Levels
normal pH of blood is 7.35-7.45
-acidosis = less than 7.35
-alkalosis = more than 7.5
-around pH blood 7.00, severe depression of CNS and comma occur
-above 7.45, excitability of nervous tissue; convulsions and death
Respiratory Acidosis
-elevation of blood Co2 (pco2) above 45mmhg
-due to lack of removal of Co2 from blood
-ex. pulm. edema, trauma to respiratory centres, airway obstruction, dysfunction of respiratory muscles
-renal compensation inloves increasing H+ exretion and HCO3 reabsortion to raise pH
Respiratory Alkalosis
-Co2 too low below 35mmhg
-hyperventilation, pulm disease, pregnancy
-renal compensation invloves decreasing exretion of H+ and decreasing reapsorbion of bicarbonate
Metabolic Acidosis
-nonrespiratory acidosis so not CO2 levels
-indicated by blood bucarboante ion concentration being too low (below 22) so H+ accumulates
-causes: kidney failing to remove H+ from prtoein metabolism, or ketosis from diabetes/dieting
-respiratory compensation by hyperventilating
Metabolic Alkalosis
-blood bicarb levels too high (above 26) but not because of CO2
-causes = vomitting, diuretic use, excessive intake of alkaline drugs
-respiratory compensation by hypoventilating
In Binder Chart
on metabolic acidosis from Jan 22
Acid-Base Imbalance Diagnosis
if acidosis is present:
-respiratory so elevated PCO2
-metabolic so decreased bicarbonate
if alkalosis is present:
-respiratory so reduced PCO2
-metabolic so increased bicarbonate
Acid-Base Imbalance in Pregnancy and Birth
- mother respiratory alkalosis during pregnancy
- fetal metabolic or respiratory acidoses in pregnancy
- newborn metabolic acidosis and aspyxia (no oxygen so unconscious or dead) during birth process
Acid-Base Imbalance in Pregnancy and Birth Continued
pregnancy = constant state of respiratory alkalosis due to increased breathing rate
-increased breathing results mainly from progesterone which causes an increased sensitivity to CO2
-pregnancy PCO2 typically around 30 because hyperventilation keeps it low
-renal compensation lowers bicarb
Newborn Acid-Base Imbalance
-foetal oxygenation and pH generally decline during the course of normal labour due to changes of placental function
-severe asphyxia may cause brain damage
APGAR CHART - pull it up
-birth asphyxia and hypoxia are related to baby’s appearance and respiratory function is observed by APGAR
-MUST order lab evidence for foetal metabolic acidosis
-low APGAR scores (0-3) longer than 10 minutes correlate to negative neurological outcomes such as cerebral palsy and more
-metabolic acidosis (pH less than 7.00) must be present to define hypoxia
-neonatal neurological unjust can include: seizure, coma and multiorgan failure
