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Cardiovascular and Pulmonary > Acid-Base Regulation I > Flashcards

Acid-Base Regulation I Flashcards

1
Q

Maintained by the coordinated actions of the renal and respiratory systems

A

Acid-base homeostasis

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2
Q

Changes in ventilation result in changes in the partial pressure of

A

CO2 in blood (PCO2)

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3
Q

The kidneys conserve and produce the main physiologic buffer, which is

A

Bicarbonate (HCO3-)

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4
Q

In the kidneys there is a linear relationship between endogenous acid production and

A

H+ excretion

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5
Q

Minor fluctuations in [H+] produce substantial changes in

A

pH

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6
Q

Physiologically, H+ originates from

A

Carbonic and non-carbonic acids

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7
Q

Mainly weak acids which reversibly consume or release H+, and in doing so minimize changes in pH

A

Buffers

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8
Q

The hydrated form of H+, which is small, highly reactive, and both attracted and bound to negative moieties within proteins

A

Hydronium Ion (H3O+

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9
Q

Most biologically relevant molecules can accept or donate H+ ions, which is accompanied by the concaminant change in the

A

Charge on the molecule

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10
Q

A deviation in charge equates to a change in conformation, which results in altered function of the

A

Molecule

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11
Q

Carbonic acids and noncarbonic acids constitute the so-called

A

Physiologic acids

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12
Q

Carbonic and non-carbonic acids originate from the metabolism of

-each day results in approximately 1500 mmol CO2 produced

A

Fats and carbohydrates

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13
Q

The production of H2CO3 from CO2 and H2O is a very slow reaction without the presence of

A

Carbonic Anhydrase (CA)

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14
Q

Abundant within both the lung alveoli and the renal peritubular epithelium

A

Carbonic anhydrase (CA)

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15
Q

Another significant contributor to the daily acid load is the metabolism of proteins via the oxidation of sulfur-containing amino acids, and the hydrolysis of dietary phosphate forming

A

H2PO4-

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16
Q

A major source of alkali in the body is from the metabolism of

A

Anionic amino acids

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17
Q

Simply shows that pH depends upon the ratio of HCO3- to H+

A

H-H equation

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18
Q

Half the acid will ionize and lose H+ if

A

pH = pKa

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19
Q

The acid will lose H+ if?

A

pH is greater than pKa

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20
Q

What is the pKa for the bicarbonate buffer system?

A

6.1

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21
Q

The main extracellular buffer

A

HCO3-

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22
Q

The most important contributors to maintaining plasma pH are

A

CO2 and HCO3-

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23
Q

Intracellular buffers consist of

A

Proteins and inorganic phosphates

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24
Q

The key intracellular buffer within erythrocytes

A

Hemoglobin (Hb)

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25
Q

Represents a massive reserve of base which can be released in response to reduced pH

A

Skeletal System

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26
Q

Up to 40% of buffering of an acute acid load occurs via

A

Bone-mediated mechanisms

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27
Q

The bone buffers include

A

NaHCO3, KHCO3, CaCO3, and CaHPO4

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28
Q

Bone buffering is associated with a drop in plasma HCO3- and is less effective during

A

Respiratory acidosis (increased PCO2)

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29
Q

Occurs essentially immediately upon introduction of an acid load

A

Plasma HCO3- buffering mechanism

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30
Q

Approximately 15 minutes after introduction of an acid load, some buffering is provided by

A

Interstitial HCO3-

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31
Q

Under normal circumstances, the relative contribution of HCO3- and non-bicarbonate buffering is relatively

A

Equal

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32
Q

With decreased HCO3-, we see a much larger importance of

A

Non-bicarbonate buffering (i.e. bone and intracellular)

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33
Q

The utilization of non-bicarbonate buffering occurs after approximately

A

2-4 hours after acid load introduction

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34
Q

After 2-4 hours, we see the translocation of H+ from the interstitial fluid into cells. This results in the subsequent movement of any or all of the following in order to maintain electroneutrality:

A
  1. ) Cl- (primarily in erythrocytes)

2. ) Swapping of intracellular K+/Na+ for H+

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35
Q

Depending on the underlying cause of the acid-base disorder, changes in ventilation begin within

A

Hours

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36
Q

Within several hours to days, the kidneys mediate

A

H+ excretion (complete within 5-6 days)

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37
Q

The normal pH of arterial blood is

A

7.38-7.43

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38
Q

Venous blood is somewhat more acidic due to its increased

A

CO2 content

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39
Q

Gastric secretions can achieve a maximal acidic pH of approximately

A

0.7

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40
Q

Secreted pancreatic fluid has an approximate pH of

-most basic in body

A

8.1

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41
Q

Results when [H+] rises such that pH drops below 7.38

A

Acidosis

42
Q

Results when [H+] falls such that pH breaches 7.43

A

Alkalemia

43
Q

Tissue function is comprised when blood pH is

A

Less than 7.20 or greater than 7.60

44
Q

Conditions which tend to alter arterial [H+]

A

Acidosis and alkalosis

45
Q

What are the four primary acid-base disturbances?

A
  1. ) Respiratory acidosis
  2. ) Respiratory alkalosis
  3. ) Metabolic acidosis
  4. ) Metabolic alkalosos
46
Q

These conditions can exist singly or as combined pathologies. The only IMPOSSIBLE combination is a

A

Respiratory alkalosis with respiratory acidosis

47
Q

CO2 generated via metabolism is carried in blood as

A

HCO3-, carbaminohemoglobin, and protonated hemoglobin

48
Q

CO2 is directly coupled to H+ via

A

HCO3-

49
Q

Results from the impaired ability to expire CO2

A

Respiratory Acidosis

50
Q

Since CO2 equates with H=, pH decreases as plasma CO2

A

Rises

51
Q

Can be caused by resistance of the diffusion barrier at the level of the alveolus and/or an abnormally decreased respiration rate

A

Respiratory acidosis

52
Q

Resistance of the diffusion barrier at the level of the alveolus and/or an abnormally decreased respiration rate each lead to

A

Hypercapnia

53
Q

Can be acute or chronic

A

Respiratory acidosis

54
Q

Can result from inhibition of the medullary respiratory center, pathologies of the respiratory muscles and chest wall, and disorders affecting gas exchange

A

Respiratory acidosis

55
Q

What are some of the causes of ACUTE respiratory acidosis?

A

Obstructive sleep apnea, aspiration of a foreign body or vomit, or laryngospasms

56
Q

Upon an increase in PCO2, there is immediate buffering via the

A

Bicarbonate system

57
Q

Additional H+ is buffered by intracellular mechanisms; this is mediated by the swap of extracellular H+ for

A

Intracellular K+

58
Q

Following the inward diffusion of CO2, erythrocytes provide

A

HCO3-

59
Q

This occurs through the exchange of intracellular HCO3- for

A

Extracellular Cl-

60
Q

Within cells, can be metabolized into CO2 and H2O or enter the gluconeogenic pathway for the production of glucose

A

Lactic acid produced by the Na-lactate buffering system

61
Q

a 1 meq/L increase in HCO3- per 10 mmHg increase in PCO2 is predicted during an acute phase of

A

Respiratory acidosis

62
Q

Represents the partial pressure of CO2 in the blood that is not bound to Hb

A

PCO2

63
Q

This rise in HCO3- occurs by and large because of the

A

HCO3-CL exchange system

64
Q

Over approximately 4-5 days of respiratory acidosis (i.e. chronic respiratory acidosis) the kidneys respond with increased

A

H= excretion

65
Q

H+ excretion by the kidneys not only removes H+, but remarkably equates to enhanced renal production and retention of

A

HCO3-

66
Q

During CHRONIC respiratory acidosis, for every 10 mmHg increase in PCO2, we see a predicted increase in HCO3- or

A

4 meq/L

67
Q

Thus, a more accuate diagnosis of acute vs. chronic respiratory acidosis can be made by knowing the

A

Rise of HCO3- (referred to as compensation)

68
Q

When levels of compensation exceed the predicted values, the patient should be evaluated for the presence of a

A

Mixed acid-base disturbance (i.e. combined respiratory acidosis w/ metabolic alkalosis)

69
Q

Results from a pathologic increase in the respiratory drive, which lowers PCO2

A

Respiratory alkalosis (pH greater than 7.43)

70
Q

In order to compensate for respiratory alkalosis, we must reduce plasma levels of

A

HCO3-

71
Q

During alkalosis, thereis a favorable gradient for

A

H+ to leave cells

72
Q

Results from an increase in intracellular H+ translocation to the extracellular fluid

A

Acute compensation for respiratory alkalosis

73
Q

For every 10 mmHg decrease in PCO2, ACUTE compensation for respiratory alkalosis results in an HCO3- decline of

A

2 meq/L

74
Q

During persistant hypocapnia, the kidneys decrease

A

H+ excretion

75
Q

Since H+ secretion equates to the generation of HCO3-, lowering H+ secretion actually provides a dual mechanism which can assist in

-Usually occurs within hours

A

Driving pH downward

76
Q

The full effect of this compensatory mechanism for CHRONIC respiratory alkalosis results in a

A

5 meq/L decrease in HCO3- for every 10 mmHg decrease in PCO2

77
Q

The etiology of respiratory alkalosis involves factors which would drive ventilation

A

Above normal

78
Q

What two things will increase ventilation?

A
  1. ) Hypoxemia (low blood O2; main stimulus)

2. ) Acidic pH

79
Q

Hypoxemia due to pulmonary disease, congestive heart failure, hypotension, severe anemia, or high altitude resistance are common causes of

A

Respiratory alkalosis

80
Q

Can also be stimulated by a number of factors including psychogenic causes, salicylate intoxication, elevated progesterone, and post-correction of metabolic acidosis

A

MEdullary respiratory centers

81
Q

Stem from an inability of the renal system to handle acidic and bicarbonate loads

A

Metabolic acidosis and alkalosis

82
Q

Responsible for the chronic regulation of blood pH through:

  1. ) Reabsorption/reclamation and generation of HCO3-
  2. ) The excretion of nonvolatile acids
A

The Kidneys

83
Q

The kidneys aggressively oversee normal acid-base balance in which three ways?

A
  1. ) HCO3- reclamation/reabsorption
  2. ) Generation of new HCO3-
  3. ) H+ excretion
84
Q

Results from:

  1. ) Inability of kidneys to handle dietary acid load
  2. ) Increase in plasma [H+]
  3. ) Decrease in plasma [HCO3-]
A

Metabolic acidosis

85
Q

Arguably the most common acid-base disturbance that is encountered

A

Metabolic acidosis

86
Q

The first line of defense for metabolic acidosis is via

A

Intracellular buffers (i.e. proteins, phosphates, and bone buffers)

87
Q

The main factors which drive ventilation are

A

Hypoxemia and hypercapnia

88
Q

Coupled to the pH-sensitive chemoreceptors located within the carotid bifurcations and aortic bodies

A

Hypercapnia

89
Q

During metabolic acidosis, these chemoreceptors are signaled by

A

Low pH (elevated [H+]

90
Q

The drop in pH is then relayed to the medullary respiratory center via

A

CN IX and X

91
Q

The medullary respiratory center then triggers an increase in ventilation for the purpose of blowing-off CO2, thereby lowering

A

Plasma [H+]

92
Q

The resultant acute drop in PCO2 actually induces an acute elevation in pH within the

A

CSF and cerebral intersitium

93
Q

This is because when plasma PCO2 drops with increased ventilation, CO2 rapidly moves down its concentration gradient and crosses the

A

Blood-brain barrier (from CSF to plasma)

94
Q

Unlike CO2, requires a transporter mediated mechanism which takes time

A

HCO3-

95
Q

Because of this, central chemoreceptors actually sense an alkalemia, and the central ventilatory drive is

A

Suppressed

96
Q

Over approximately the first 24 hours, [HCO3-] drops within the CSF, which means

A

CSF pH drops and central respiratory drive is stimulated

97
Q

What are the 7 causes of metabolic acidosis?

A
  1. ) Renal failure
  2. ) RTA
  3. ) Lactic acidosis
  4. ) Drugs and toxins
  5. ) Diabetes, alcoholism, starvation
  6. ) GI HCO3- loss
  7. ) Ingestions
98
Q

The patterns of breathing associated with metabolic acidosis compensation is known as

A

Kussmaul breathing

99
Q

Characterized as deep, sighing type breaths, which is the result of an increase in tidal volume more so than an increase in respiratory rate

A

Kussmaul breathing

100
Q

The effectiveness of respiratory compensation for metabolic acidosis is limited to

A

Several days at best

Cardiovascular and Pulmonary (25 decks)

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