Acid-Base Regulation I Flashcards
1
Q
Maintained by the coordinated actions of the renal and respiratory systems
A
Acid-base homeostasis
2
Q
Changes in ventilation result in changes in the partial pressure of
A
CO2 in blood (PCO2)
3
Q
The kidneys conserve and produce the main physiologic buffer, which is
A
Bicarbonate (HCO3-)
4
Q
In the kidneys there is a linear relationship between endogenous acid production and
A
H+ excretion
5
Q
Minor fluctuations in [H+] produce substantial changes in
A
pH
6
Q
Physiologically, H+ originates from
A
Carbonic and non-carbonic acids
7
Q
Mainly weak acids which reversibly consume or release H+, and in doing so minimize changes in pH
A
Buffers
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+
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
10
Q
A deviation in charge equates to a change in conformation, which results in altered function of the
A
Molecule
11
Q
Carbonic acids and noncarbonic acids constitute the so-called
A
Physiologic acids
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
13
Q
The production of H2CO3 from CO2 and H2O is a very slow reaction without the presence of
A
Carbonic Anhydrase (CA)
14
Q
Abundant within both the lung alveoli and the renal peritubular epithelium
A
Carbonic anhydrase (CA)
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-
16
Q
A major source of alkali in the body is from the metabolism of
A
Anionic amino acids
17
Q
Simply shows that pH depends upon the ratio of HCO3- to H+
A
H-H equation
18
Q
Half the acid will ionize and lose H+ if
A
pH = pKa
19
Q
The acid will lose H+ if?
A
pH is greater than pKa
20
Q
What is the pKa for the bicarbonate buffer system?
A
6.1
21
Q
The main extracellular buffer
A
HCO3-
22
Q
The most important contributors to maintaining plasma pH are
A
CO2 and HCO3-
23
Q
Intracellular buffers consist of
A
Proteins and inorganic phosphates
24
Q
The key intracellular buffer within erythrocytes
A
Hemoglobin (Hb)
25
Represents a massive reserve of base which can be released in response to reduced pH
Skeletal System
26
Up to 40% of buffering of an acute acid load occurs via
Bone-mediated mechanisms
27
The bone buffers include
NaHCO3, KHCO3, CaCO3, and CaHPO4
28
Bone buffering is associated with a drop in plasma HCO3- and is less effective during
Respiratory acidosis (increased PCO2)
29
Occurs essentially immediately upon introduction of an acid load
Plasma HCO3- buffering mechanism
30
Approximately 15 minutes after introduction of an acid load, some buffering is provided by
Interstitial HCO3-
31
Under normal circumstances, the relative contribution of HCO3- and non-bicarbonate buffering is relatively
Equal
32
With decreased HCO3-, we see a much larger importance of
Non-bicarbonate buffering (i.e. bone and intracellular)
33
The utilization of non-bicarbonate buffering occurs after approximately
2-4 hours after acid load introduction
34
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:
1. ) Cl- (primarily in erythrocytes)
| 2. ) Swapping of intracellular K+/Na+ for H+
35
Depending on the underlying cause of the acid-base disorder, changes in ventilation begin within
Hours
36
Within several hours to days, the kidneys mediate
H+ excretion (complete within 5-6 days)
37
The normal pH of arterial blood is
7.38-7.43
38
Venous blood is somewhat more acidic due to its increased
CO2 content
39
Gastric secretions can achieve a maximal acidic pH of approximately
0.7
40
Secreted pancreatic fluid has an approximate pH of
-most basic in body
8.1
41
Results when [H+] rises such that pH drops below 7.38
Acidosis
42
Results when [H+] falls such that pH breaches 7.43
Alkalemia
43
Tissue function is comprised when blood pH is
Less than 7.20 or greater than 7.60
44
Conditions which tend to alter arterial [H+]
Acidosis and alkalosis
45
What are the four primary acid-base disturbances?
1. ) Respiratory acidosis
2. ) Respiratory alkalosis
3. ) Metabolic acidosis
4. ) Metabolic alkalosos
46
These conditions can exist singly or as combined pathologies. The only IMPOSSIBLE combination is a
Respiratory alkalosis with respiratory acidosis
47
CO2 generated via metabolism is carried in blood as
HCO3-, carbaminohemoglobin, and protonated hemoglobin
48
CO2 is directly coupled to H+ via
HCO3-
49
Results from the impaired ability to expire CO2
Respiratory Acidosis
50
Since CO2 equates with H=, pH decreases as plasma CO2
Rises
51
Can be caused by resistance of the diffusion barrier at the level of the alveolus and/or an abnormally decreased respiration rate
Respiratory acidosis
52
Resistance of the diffusion barrier at the level of the alveolus and/or an abnormally decreased respiration rate each lead to
Hypercapnia
53
Can be acute or chronic
Respiratory acidosis
54
Can result from inhibition of the medullary respiratory center, pathologies of the respiratory muscles and chest wall, and disorders affecting gas exchange
Respiratory acidosis
55
What are some of the causes of ACUTE respiratory acidosis?
Obstructive sleep apnea, aspiration of a foreign body or vomit, or laryngospasms
56
Upon an increase in PCO2, there is immediate buffering via the
Bicarbonate system
57
Additional H+ is buffered by intracellular mechanisms; this is mediated by the swap of extracellular H+ for
Intracellular K+
58
Following the inward diffusion of CO2, erythrocytes provide
HCO3-
59
This occurs through the exchange of intracellular HCO3- for
Extracellular Cl-
60
Within cells, can be metabolized into CO2 and H2O or enter the gluconeogenic pathway for the production of glucose
Lactic acid produced by the Na-lactate buffering system
61
a 1 meq/L increase in HCO3- per 10 mmHg increase in PCO2 is predicted during an acute phase of
Respiratory acidosis
62
Represents the partial pressure of CO2 in the blood that is not bound to Hb
PCO2
63
This rise in HCO3- occurs by and large because of the
HCO3-CL exchange system
64
Over approximately 4-5 days of respiratory acidosis (i.e. chronic respiratory acidosis) the kidneys respond with increased
H= excretion
65
H+ excretion by the kidneys not only removes H+, but remarkably equates to enhanced renal production and retention of
HCO3-
66
During CHRONIC respiratory acidosis, for every 10 mmHg increase in PCO2, we see a predicted increase in HCO3- or
4 meq/L
67
Thus, a more accuate diagnosis of acute vs. chronic respiratory acidosis can be made by knowing the
Rise of HCO3- (referred to as compensation)
68
When levels of compensation exceed the predicted values, the patient should be evaluated for the presence of a
Mixed acid-base disturbance (i.e. combined respiratory acidosis w/ metabolic alkalosis)
69
Results from a pathologic increase in the respiratory drive, which lowers PCO2
Respiratory alkalosis (pH greater than 7.43)
70
In order to compensate for respiratory alkalosis, we must reduce plasma levels of
HCO3-
71
During alkalosis, thereis a favorable gradient for
H+ to leave cells
72
Results from an increase in intracellular H+ translocation to the extracellular fluid
Acute compensation for respiratory alkalosis
73
For every 10 mmHg decrease in PCO2, ACUTE compensation for respiratory alkalosis results in an HCO3- decline of
2 meq/L
74
During persistant hypocapnia, the kidneys decrease
H+ excretion
75
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
Driving pH downward
76
The full effect of this compensatory mechanism for CHRONIC respiratory alkalosis results in a
5 meq/L decrease in HCO3- for every 10 mmHg decrease in PCO2
77
The etiology of respiratory alkalosis involves factors which would drive ventilation
Above normal
78
What two things will increase ventilation?
1. ) Hypoxemia (low blood O2; main stimulus)
| 2. ) Acidic pH
79
Hypoxemia due to pulmonary disease, congestive heart failure, hypotension, severe anemia, or high altitude resistance are common causes of
Respiratory alkalosis
80
Can also be stimulated by a number of factors including psychogenic causes, salicylate intoxication, elevated progesterone, and post-correction of metabolic acidosis
MEdullary respiratory centers
81
Stem from an inability of the renal system to handle acidic and bicarbonate loads
Metabolic acidosis and alkalosis
82
Responsible for the chronic regulation of blood pH through:
1. ) Reabsorption/reclamation and generation of HCO3-
2. ) The excretion of nonvolatile acids
The Kidneys
83
The kidneys aggressively oversee normal acid-base balance in which three ways?
1. ) HCO3- reclamation/reabsorption
2. ) Generation of new HCO3-
3. ) H+ excretion
84
Results from:
1. ) Inability of kidneys to handle dietary acid load
2. ) Increase in plasma [H+]
3. ) Decrease in plasma [HCO3-]
Metabolic acidosis
85
Arguably the most common acid-base disturbance that is encountered
Metabolic acidosis
86
The first line of defense for metabolic acidosis is via
Intracellular buffers (i.e. proteins, phosphates, and bone buffers)
87
The main factors which drive ventilation are
Hypoxemia and hypercapnia
88
Coupled to the pH-sensitive chemoreceptors located within the carotid bifurcations and aortic bodies
Hypercapnia
89
During metabolic acidosis, these chemoreceptors are signaled by
Low pH (elevated [H+]
90
The drop in pH is then relayed to the medullary respiratory center via
CN IX and X
91
The medullary respiratory center then triggers an increase in ventilation for the purpose of blowing-off CO2, thereby lowering
Plasma [H+]
92
The resultant acute drop in PCO2 actually induces an acute elevation in pH within the
CSF and cerebral intersitium
93
This is because when plasma PCO2 drops with increased ventilation, CO2 rapidly moves down its concentration gradient and crosses the
Blood-brain barrier (from CSF to plasma)
94
Unlike CO2, requires a transporter mediated mechanism which takes time
HCO3-
95
Because of this, central chemoreceptors actually sense an alkalemia, and the central ventilatory drive is
Suppressed
96
Over approximately the first 24 hours, [HCO3-] drops within the CSF, which means
CSF pH drops and central respiratory drive is stimulated
97
What are the 7 causes of metabolic acidosis?
1. ) Renal failure
2. ) RTA
3. ) Lactic acidosis
4. ) Drugs and toxins
5. ) Diabetes, alcoholism, starvation
6. ) GI HCO3- loss
7. ) Ingestions
98
The patterns of breathing associated with metabolic acidosis compensation is known as
Kussmaul breathing
99
Characterized as deep, sighing type breaths, which is the result of an increase in tidal volume more so than an increase in respiratory rate
Kussmaul breathing
100
The effectiveness of respiratory compensation for metabolic acidosis is limited to
Several days at best
