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Physiology Block 2 > 19- Regulation of [H+] in body fluids > Flashcards

19- Regulation of [H+] in body fluids Flashcards

1
Q

why is regulating H+ important?

A

-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)
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2
Q

relationship of H+ and seizures

A

too little H+ increases excitability of neurons

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3
Q

relationship of H+ and comatose state

A

excess H+ decreases excitability of neurons

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4
Q

arterial pH

A

7.4

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5
Q

venous pH

A

7.35

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6
Q

intracellular fluid pH

A

6.0 - 7.4

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7
Q

cerebral spinal fluid pH

A

7.32

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8
Q

urine pH

A

4.5 - 8.0

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9
Q

acid vs base

A

acid
-compound which donates H+ or proton

base
-compound which accepts H+ or proton

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10
Q

H+ in respiratory system

A

CO2 + H2O —> H2CO3 —> [H+] + HCO3-

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11
Q

metabolic H+

A

H2PO4- —> H+ + HPO4

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12
Q

H+ disorders

A
  1. Respiratory acidosis
  2. Respiratory alkalosis
  3. meabolic acidosis
  4. metabolic alkalosis
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13
Q

respiratory acidosis

A

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)
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14
Q

respiratory alkalosis

A

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
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15
Q

Metabolic acidosis

A

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
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16
Q

Metabolic alkalosis

A

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_
17
Q

if you have an arterial blood sample, how do you tell if its acidosis or alkalosis

A

pH
<7.4 = acidosis
>7.4 = alkalosis

18
Q

if you have an arterial blood sample with a pH of <7.4, how can you tell whether its metabolic or respiratory?

A

Metabolic acidosis has a HCO3- < 24mEq/L

Respiratory acidosis has a PCO2 > 40mmHg

19
Q

if you have an arterial blood sample with a pH of >7.4, how can you tell whether its metabolic or respiratory?

A

Metabolic alkalosis has a HCO3- >24mEq/L

Respiratory alkalosis has a PCO2 <40mmHg

20
Q

How to make up for respiratory acidosis and alkalosis

A

Renal Compensation

acidosis: HCO3- >24mEq/L
alkalosis: HCO3- <24mEq/L

21
Q

How to make up for metabolic acidosis and alkalosis

A

Respiratory compensation

acidosis: PCO2 <40mmHg
alkalosis: HCO3- >40mmHg

22
Q

CO2 hydration reaction

A

CO2 + H2O —> [H+] + HCO3-

23
Q

Respiratory acidosis

A

CO2 is above normal

24
Q

Metabolic acidosis

A

CO2 is below normal

25
Q

physical-chemical buffering is a result of

A

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

26
Q

ion contents of extracellular fluid

A

HCO3-
HPO4
Proteins

27
Q

ion contents of intracellular fluid

A

HPO4

Proteins

28
Q

isohydric principle

A

when H+ is altered in a solution all buffer pairs will be affected

29
Q

determinants of H+ buffering

A
  • concentration or amount of the buffer pair in the solution

- pK of the buffer pair relative to the pH of the solution

30
Q

pH and pK buffering

A

pH solution = pK buffer pair

equal amounts of

  • H+
  • acid
  • base

when adding an acid or base, conditions are optimal for buffering around 6ish

31
Q

Physiologic H+ regulation

A

processes in the body that can alter the amount of the physical-chemical buffers

  1. transmembrane exchange
  2. pulmonary ventilation
32
Q

transmembrane exchange

A
  • 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+.

33
Q

pulmonary ventilation

A

-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

34
Q

renal regulation of H+

A
  1. excretion of titratable acid
  2. reabsorption of bicarbonate
  3. 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
35
Q

how does the brain regulate H+ concentrations

A

blood-brain barrier

36
Q

blood-brain barrier

A

-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
37
Q

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

A

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.

38
Q

H+ buffering or regulating mechanisms

A

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
39
Q

clinical use of anion gap

A

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.

Physiology Block 2 (21 decks)

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