Study Guide
Acid-Base Balance
-
University:
Kentucky State University -
Course:
BIO 303 | Human Physiology Academic year:
2021
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Views:
2
Pages:
60
Author:
garciavelascogr18
1
Acid-Base Homeostasis CH 4 Acid-Base Homeostasis
Blood hydrogen ion concentration maintained
within tight Limits in health.
Normal levels lie between 35-45 nmol/l
(pH 7.35-7.46) in extracellular fluid.
In intracellular fluid is slightly higher but
also tightly controlled
• Normal pH of body fluids
– Arterial blood is 7.4
– Venous blood and interstitial
fluid is 7.35
– Intracellular fluid is 7.0
2
Acid-Base Homeostasis CH 4 • Alkalosis or alkalemia – arterial blood pH rises
above 7.45
• Acidosis or acidemia – arterial pH drops below 7.35
(physiological acidosis)
3
Acid-Base Homeostasis CH 4 Acid-Base Homeostasis CH 4
Sources of Hydrogen Ions
Most hydrogen ions originate from cellular metabolism
• Breakdown of Sulfur-containing proteins releases H into the ECF
• Incomplete oxidation of energy substrates generates acids like:
• Anaerobic respiration of glucose produces lactic acid
• Fat metabolism yields organic acids and ketone bodies, these intermediates will
be further metabolized and consumed (e.g., lactate in gluconeogenesis, oxidation
of ketones).
• Temporary imbalances between the rates of production and consumption may
occur in health (e.g., the accumulation of lactic acid during anaerobic exercise),
Transporting carbon dioxide as bicarbonate releases hydrogen ions
In disease states increased hydrogen ion production is an important cause of acidosis.
The total amount of hydrogen ion produced each day is
100,000 times more acid than normal !
This just does not happen because excess hydrogen ions are efficiently excreted
4
in urine. 5
Acid-Base Homeostasis CH 4 Acid/Base Homeostasis: Overview
6
Acid-Base Homeostasis CH 4 •
Hydrogen Ion Regulation
Concentration of hydrogen ions is regulated sequentially by:
– Chemical buffer systems – act within seconds
– The respiratory center in the brain stem – acts within 1-3 minutes
– Renal mechanisms – require hours to days to effect pH changes
Chemical Buffer Systems
•
Three major chemical buffer systems
– Bicarbonate buffer system
– Phosphate buffer system
– Protein buffer system
•
Any drift in pH is opposed by the entire chemical buffering system
7
Acid-Base Homeostasis CH 4 Buffering of hydrogen ions
Acid-Base Homeostasis CH 4
As hydrogen ions are generated they are buffered, thus limiting the rise in
hydrogen ion concentration which would otherwise occur.
A buffer is: a solution of the salt or a weak acid
which is able to bind hydrogen ions.
If hydrogen ions are added to a buffer,
some will combine with the conjugate base
and convert it to the undissociated acid.
Buffering does not remove hydrogen ions from the body. Buffers temporarily
wash up any excess hydrogen ions which are produced. …. In the same way that a
sponge soaks up water.
Buffering is only a short term solution to the problem of excess hydrogen ion.
Eventually, the body must get rid of the hydrogen ions by renal excretion.
The efficacy of any buffer is limited by …..its concentration
and by the
position of the equilibrium
8 The body contains Three major chemical buffer systems to resist sudden changes in
hydrogen ion production
Phosphate buffer system: Phosphate is a minor buffer in
the ECF but is of fundamental importance in the urine.
Protein buffer system: hemoglobin in the erythrocytes
has a high capacity for binding hydrogen ion
Bicarbonate buffer system: it is the most important in the ECF
Bicarbonate (HCO3-) combines with hydrogen ion to form carbonic acid (H2CO3)
The addition of hydrogen ions increasing the amount of carbonic acid and consuming
bicarbonate ions.
Conversely, if the hydrogen ion concentration falls, carbonic acid dissociates, thereby
generating hydrogen ions.
This buffer system is unique in that
the H2CO3, can dissociate to water and carbon dioxide.
9
Acid-Base Homeostasis CH 4 Bicarbonate Buffer System
• A mixture of carbonic acid (H2CO3) and its salt, sodium bicarbonate
(NaHCO3) (potassium or magnesium bicarbonates work as well)
• If strong acid is added:
– Hydrogen ions released combine with the bicarbonate ions and
form carbonic acid (a weak acid)
– The pH of the solution
decreases only slightly
• If strong base is added:
– It reacts with the carbonic acid to form sodium bicarbonate (a
weak base)
– The pH of the solution rises only slightly
• This system is the most important ECF buffer
10
Acid-Base Homeostasis CH 4 Simple buffers rapidly become ineffective as the association of the hydrogen ion and
the anion of the weak acid reaches equilibrium.
The bicarbonate system keeps working because the carbonic acid is removed as CO2.
CO2 + H2O * H2CO3 H+ + HCO3The limit to the effectiveness of the bicarbonate system is the initial concentration of
bicarbonate.
Only when all the bicarbonate is used up does the system have no further
buffering capacity.
The capacity of the bicarbonate system in the body is
greatly enhanced by the fact that carbonic acid can
readily be formed from carbon dioxide
or disposed of by conversion into carbon dioxide and water.
Buffering by the bicarbonate system effectively removes hydrogen ion from the ECF
at the expense of bicarbonate. The extracellular fluid contains a large amount of
bicarbonate but it falls as H+ is increased
To maintain the capacity of the buffer system, the bicarbonate must be regenerated.
11
Acid-Base Homeostasis CH 4 Bicarbonate reabsorption and hydrogen ion excretion
The glomerular filtrate contains the same concentration of bicarbonate ions as the
plasma If not reabsorbed large amounts would be excreted in the urine depleting
the body’s buffering capacity causing an acidosis
Virtually all the filtered bicarbonate is reabsorbed.
The luminal surface of renal tubular cells is
impermeable to bicarbonate and therefore direct
reabsorption can not occur.
Bicarbonate is reabsorbed indirectly: within the renal tubular cells, ….carbonic acid is
formed from carbon dioxide and water This reaction is catalyzed in the kidney by the
enzyme carbonic anhydrase.
The carbonic acid thus formed dissociates to give hydrogen and bicarbonate ions.
The bicarbonate ions pass across the basal border of the cells into the interstitial fluid.
The hydrogen ions are secreted across the luminal membrane in exchange for sodium
ions, which accompany bicarbonate into the interstitial fluid.
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Acid-Base Homeostasis CH 4 Acid-Base Homeostasis CH 4
Bicarbonate reabsorption
13 Acid-Base Homeostasis CH 4
Bicarbonate reabsorption
14 Hydrogen ion excretion
Although hydrogen ions are secreted into the tubular fluid, there is no net hydrogen
ion excretion, as the formation of hydrogen ions provides the means for the
reabsorption of bicarbonate.
Hydrogen ion excretion depends upon the same reactions occurring in the renal
tubular cells but, in addition, requires the presence of a suitable buffer system in the
urine.
The excreted hydrogen ions must be
buffered in urine OR the [H+] would rise
to very high levels.
Phosphate acts as one such buffer, while
ammonia is another.
15
Acid-Base Homeostasis CH 4 Bicarbonate reabsorption and hydrogen ion
excretion
The principal urinary buffer is phosphate.
This is present in the glomerular filtrate (HPO42-).
This combines with hydrogen ions and is converted
to H2PO4-.
HPO4 2- + H + H2PO4 Ammnia, produced by the deamination of
glutamine by glutaminase enzyme in renal tubular
cells,
Ammonia can readily diffuse across cell
membranes and ammonium ions are formed and
excreted.
NH3 H NH4
16
Acid-Base Homeostasis CH 4 Acid-Base Homeostasis CH 4
Bicarbonate reabsorption and hydrogen ion excretion
17 18
Acid-Base Homeostasis CH 4 Transport of Carbon dioxide
Acid-Base Homeostasis CH 4
Carbon dioxide, produced by aerobic metabolism, diffuses out of cells and dissolves
in the ECF.
A small amount combines with water to form carbonic acid, thereby increasing the
hydrogen ion concentration of the ECF.
In
red blood cells, metabolism is anaerobic and little carbon dioxide is
produced. Carbon dioxide thus diffuses into red cells down a gradient and carbonic
acid is formed, facilitated by carbonate dehydatase (Carbonic unhydrase)
The overall effect of this process is that
carbon dioxide is converted to bicarbonate in red blood cells.
This bicarbonate diffuses out of the red cells with…. exchange with…. chloride ions
(the chloride shift).
19 In the lungs, the reverse process occurs because of the low partial pressure of
carbon dioxide in the alveolar capillaries.
Carbon dioxide is produced from bicarbonate and diffuses into the alveoli to be excreted
in the expired air.
How is CO2 Exported?
Most of the carbon dioxide
in the blood is present in the
form of bicarbonate.
Dissolved carbon dioxide,
carbonic acid and
carbamino compounds
(compounds of carbon
dioxide and protein) account
for less than 2.0 mmol/L in a
total carbon dioxide conc.
Of appro. 26 mmol/L.
The term ‘bicarbonate’ and ‘total carbon dioxide’ are
frequently used synonymously.
Acid-Base Homeostasis CH 4
20 21
Acid-Base Homeostasis CH 4 Assessing Acid-base Status
Acid-Base Homeostasis CH 4
An indication of the acid-base status of the patient can be obtained by measuring the
components of the bicarbonate buffer system.
H + + HCO3 - H
H22CO
CO33 H2O CO2
H + is proportinal to
PCO2
HCO3-
Excess hydrogen ions are buffered by bicarbonate the formed carbonic acid dissociates
carbon dioxide is lost in the expired air limits
the potential rise in hydrogen
ion concentration at the expense of a reduction in bicarbonate
The hydrogen ion concentration in blood varies as
the bicarbonate concentration
and
PCO2
If everything else remains constant:
change.
Adding hydrogen ion, removing bicarbonate or increasing the PCO2……..
will all have the same effect an increase in [H+].
Removing hydrogen ions, adding bicarbonate
will all cause the [H+] to fail.
Blood [H+] is 40 nmol/l
and is controlled by
the functioning of our kidneys.
22
or lowering PCO2 ………….
our normal pattern of respiration
and Acid Base Balance Disorders of hydrogen ion homeostasis
1. “Metabolic” acid-base disorders
are those that directly cause a change in the bicarbonate concentration,
like diabetes mellitus because of the absence of insulin
building up of [H+], of ketone
bodies
or
loss of bicarbonate from the extracellular fluid.
2. “Respiratory” acid-base disorders affect PCO2 Impaired respiratory
function causes a build up of CO2 in blood or in the case of
hyperventilation causes a decreased PCO2
Compensation
The body has physiological mechanisms which try to restore [H+] to normal
these processes are called 'compensation',
The observed [H+] in any acid-base disorder reflects
the balance between the primary disturbance and the amount of compensation.
Renal Compensation: where lung function is compromised (primary respiratory disorder).
The body attempts to increase the excretion of hydrogen ion via the renal route.
Renal compensation is slow to take place.
Respiratory compensation: where there are metabolic disorder
some compensation is possible by lung
Acid-Base Homeostasis
CH 4
24 Remember
25
When you see “respiratory”, think PCO2
When you see “metabolic”, think [HCO3]
Acid-Base Homeostasis CH 4 26
Acid-Base Homeostasis CH 4 Respiratory compensation:
where there are metabolic disorder
Acid-Base Homeostasis CH 4
some compensation is possible by lung
27 Disorders of hydrogen ion homeostasis
‘Acidemia' and 'alkalemia'
refer simply to whether the
[H+] in blood is higher or
lower than normal
28
PCO2
H
HCO3+
Acid-Base Homeostasis CH 4 Disorders of hydrogen ion homeostasis
Acidosis and alkalosis are clinical terms which define the primary acid-base disturbance.
They can be used even when the [H+] is within the normal range. i.e. when the disorders
are fully compensated.
The definitions are:
H+
PCO2
HCO3 -
1. Non-respiratory (Metabolic) acidosis: The primary disorder is
a decrease in bicarbonate concentration.
2.
Non-respiratory (Metabolic) alkalosis: The primary disorder is
an increased bicarbonate.
3. Respiratory acidosis: The primary disorder is an increased PCO2.
4. Respiratory alkalosis: The primary disorder is a decreased PCO2.
5. Primary mixed acid-base disorders, that is, disorders of combined respiratory
and non-respiratory origin,
‘Acidemia' and 'alkalemia' refer simply to whether the [H+] in blood is higher or lower
than normal
29
Acid-Base Homeostasis CH 4 30
Acid-Base Homeostasis CH 4 1. Non-respiratory (metabolic) acidosis
The primary abnormality in non-respiratory acidosis is either:
increased production
or
decreased excretion
of hydrogen ions.
In some cases,
both of these may contribute.
Loss of bicarbonate
and
retention of hydrogen ions may result in acidosis
in patients
losing alkaline secretions from the small intestine.
Causes of non-respiratory acidosis
* Increased H+ formation
ketoacidosis (usually diabetic, also alcoholic)
lactic acidosis
poisoning: e.g., ethanol, methanol, ethylene glycol and salicylate
* Acid ingestion
acid poisoning
* Decreased H+ excretion
renal tubular acidosis
generalised renal failure
carbonate dehydratase inhibitors
* Loss of bicarbonate
diarrhea
pancreatic, intestinal and biliary fistulae or drainage
31
Acid-Base Homeostasis CH 4 The characteristic biochemical changes seen in the blood in nonrespiratory acidosis
can be summarized as follows:
Non-respiratory acidosis (metabolic)
high [H+], Low pH,
low PCO2
and
Low [HCO3-]
Compensation is effected by hyperventilation, which
increases the removal of carbon dioxide
and
lowers the PCO2.
Hyperventilation is a direct result of the increased [H+] stimulating the respiratory centre.
Respiratory compensation cannot completely normalize the [H+] since it is
* the high concentration itself [H+] that stimulates the compensatory hyperventilation.
* Also the increased work of the respiratory muscle produces carbon dioxide,
so……
limiting the extent to which the pCO2 can be lowered.
In a healthy person, hyperventilation would produce a respiratory alkalosis.
If renal function is normal in a patient with non-respiratory acidosis, excess hydrogen ions
can be excreted by the kidneys.
32
Acid-Base Homeostasis CH 4 The complete correction of a non-respiratory acidosis
requires reversal of the underlying cause,
for example, rehydration and insulin for diabetic
ketoacidosis.
Hyperkalaemia
is common in acidotic patients.
H+
K+
K+
K+
K+
K+
33
H+
H+
K+
H+
H+
H+
ACIDOSIS
H+
HYPERKALEMIA
H+
H+
Acid-Base Homeostasis CH 4 Clinical effects of acidosis
The compensatory response to metabolic acidosis is
hyperventilation,
since the increased [H+] acts as
a powerful stimulant of the respiratory centre.
The deep,
rapid
and
gasping (wheezing) respiratory
pattern is known as Kussmaul breathing.
Hyperventilation is the appropriate physiological response to acidosis
and it occurs rapidly.
A raised [H+] leads to increased neuromuscular irritability.
There is a hazard of …..arrhythmias progressing to cardiac arrest,
this will be more likely in the presence of hyperkalaemia which will
accompany the acidosis
Depression of consciousness can progress to
34
Acid-Base Homeostasis CH 4
coma and death. 35
Acid-Base Homeostasis CH 4 2- Metabolic Alkalosis (Non-respiratory alkalosis): is characterized by a
* primary increase in the ECF bicarbonate concentration,
with
* a consequent reduction in [H+] (increase pH).
Normally, an increase in plasma bicarbonate concentration leads to
incomplete renal tubular bicarbonate reabsorption and
excretion of bicarbonate in the urine.
BUT in non-respiratory (metabolic) alkalosis,
high renal
bicarbonate reabsorption occurs.
Factors which may be responsible for this include
a decrease in ECF volume,
mineralocorticoid excess increased Sod
along with carbonate reabsorption
and
potassium depletion.
Massive quantities of bicarbonate must be ingested to produce a
sustained alkalosis.
36
Acid-Base Homeostasis CH 4 Metabolic Alkalosis (Non-respiratory alkalosis):
The causes of a metabolic alkalosis are:
Loss of Hydrogen ion in gastric fluid
during vomiting especially when there is
no parallel loss of bicarbonate.
Ingestion of an absorbable alkali
as sod bicarbonate: very large quantities are required
except there is renal impairment
In sever potassium depletion (consequences of
diuretic therapy) hydrogen ions are retained inside
cells to replace missing potassium ions.
In renal tubules more hydrogen
are exchanged for reabsorption of sod.
So, despite there being an alkalosis, the patient passes
acidic urine. This often referred to as a
‘paradoxical’ acid urine,
because in other causes of metabolic alkalosis
urinary
[H+] usually falls.
37
Acid-Base Homeostasis CH 4 Acid-Base Homeostasis CH 4
38 Clinical effects of metabolic alkalosis
The clinical effects of alkalosis include:
hypoventilation,
confusion
and
eventually coma.
Muscle cramps,
tetany
and paraesthesia
(any abnormality in sensation) may be a consequence of
a decrease in the unbound plasma calcium concentration
which is a consequence of the alkalosis.
39
Acid-Base Homeostasis CH 4 Metabolic Alkalosis (Non-respiratory alkalosis. Increase in HCO3 with less H):
The correction of non-respiratory alkalosis
primary cause
and
requires reversal both of the
for the mechanism for its maintenance.
The expected compensatory would be an increased in PCO2 which would
increase the ratio PCO2/[HCO3] and thus [H+].
A low arterial [H+] inhibits the respiratory centre, causing
hypoventilation,
and thus an
increase in PCO2.
However, since an increase in PCO2 is itself a powerful stimulus to respiration, this
compensation, particularly in acute non-respiratory alkalosis, may be self-limiting.
In more chronic disorders,
significant compensation may occur,
presumably
because the respiratory centre becomes less sensitive to carbon dioxide.
Should hypoventilation lead to
significant hypoxaemia,
provide a powerful stimulus to respiration
40
however, this will
and prevent further compensation.
Acid-Base Homeostasis CH 4 Management:
The management of a non-respiratory alkalosis depends upon:
the severity of the condition
and
upon the cause.
When hypovolaemia are present, they can be simultaneously corrected by
an infusion of isotonic sodium chloride solution (normal saline) which
will also
improve renal perfusion
and
allow excretion of the
bicarbonate load.
It is very rarely necessary to attempt rapid correction of
non-respiratory alkalosis,
for example, by administration of ammonium
chloride.
The mild alkalosis commonly associated with potassium depletion may
require correction
41
Acid-Base Homeostasis CH 4 “Respiratory” acid-base disorders
42
Acid-Base Homeostasis CH 4 3- Respiratory acidosis:
The primary disorder is an
increased PCO2
Respiratory acidosis is characterized
by an increase in PCO2, (CO2
retention)
For every hydrogen ion produced
a bicarbonate ion is generated
BUT the effect of adding one H+ to a
concentration of 40 nmol/l is much
greater than adding one bicarbonate
molecule to a concentration of 26
mmol/l.
The majority of hydrogen ions are
buffered by intracellular buffers,
particularly hemoglobin.
43
Acid-Base Homeostasis CH 4 Respiratory acidosis: The primary disorder is an increased PCO2
Respiratory acidosis: Respiratory acidosis may be acute or chronic.
Acute conditions occur within minutes or hours, they are uncompensated.
Renal compensation has no time to develop as the mechanisms that adjust
bicarbonate reabsorption take 48-72 hours to become fully effective.
The primary problem in acute respiratory acidosis is alveolar hypoventilation If
airflow is completely or partially reduced,
the PCO2 in the blood will rise immediately
and
the [H+] will rise quickly.
A resulting low PO2 and high PCO2 causes coma.
If this is not relieved rapidly, death results.
Examples of acute respiratory acidosis are:
Acute airway obstruction:
* choking (obstruction of the flow of air from the environment into the lungs)
* bronchopneumonia, * acute exacerbation of asthma.
Depression of respiratory centre:
* Anaesthetics, *Sedatives
Acid-Base Homeostasis CH 4
44 Chronic respiratory acidosis:
usually results from chronic obstructive airways disease
(COAD) and is usually a long-standing condition,
accompanied by maximal renal compensation.
In a chronic respiratory acidosis the primary problem is also
usually impaired alveolar ventilation, but renal compensation
contributes markedly to the acid-base picture.
Compensation may be
The kidney
and
partial or complete.
increases hydrogen ion excretion
ECF bicarbonate levels rise.
Blood [H+] tends back towards normal
45
Acid-Base Homeostasis CH 4 Acid-Base Homeostasis CH 4
46 Management of Acidosis
The aim when treating respiratory acidosis is to
improve alveolar ventilation
and
lower the PCO2.
In acute alveolar hypoventilation:
hypoxia causes the
main threat to life If ventilation is stopped abruptly, death from
hypoxia will occur
In chronic respiratory acidosis, it is rarely possible to correct the
underlying cause
and treatment
is directed at
maximizing alveolar ventilation by,
for example,
utilizing physiotherapy,
bronchodilators and antibiotics.
47
Acid-Base Homeostasis CH 4 4- Respiratory alkalosis
Respiratory alkalosis is much less common than acidosis
but can occur when respiration is stimulated
or
is no longer subject to feedback control.
Usually these are acute conditions, and there is no renal
compensation.
Renal compensation in a respiratory alkalosis develops slowly, as
it does in respiratory acidosis.
The treatment is to inhibit or remove the cause of the
hyperventilation, and the acid-base balance should return to
normal.
Causes are:
1. hysterical over-breathing,
2. mechanical over-ventilation in an intensive care patient,
3. raised intracranial pressure, or hypoxia, both of which may
48
stimulate
the respiratory centre.
Acid-Base Homeostasis CH 4 49
Acid-Base Homeostasis CH 4 Acid-Base Homeostasis CH 4
50 5- Mixed acid-base disorders
Patients can have more than one acid-base disorder.
A patient may have both a metabolic and respiratory acidosis, such as
the chronic bronchitic patient who develops renal impairment
the PCO2 will be increased and the bicarbonate concentration will be low,
Hyperventilation causing a respiratory alkalosis, with
prolonged nasogastric suction that causes a metabolic alkalosis
Sometimes the two acid-base conditions are antagonistic in the way they affect the [H+],
a metabolic acidosis and a co-existent respiratory alkalosis, Some examples of mixed acidbase disorders commonly encountered are:
A patient with chronic obstructive airways disease, causing a respiratory acidosis,
with thiazide-induced potassium depletion and consequent metabolic alkalosis
Salicylate poisoning in which respiratory alkalosis occurs due to stimulation of the
respiratory centre, together with metabolic acidosis due to the effects of the drug on
metabolism.
51
Acid-Base Homeostasis CH 4 Interpretation of Acid-Base Data
A comprehensive understanding of the pathophysiology of acid-base homoeostasis is
essential for the correct interpretation of laboratory data, but these data should always be
considered in the clinical background.
The starting point in any evaluation should be the hydrogen ion concentration or pH.
This will indicate whether the predominant disturbance is an acidosis or an alkalosis.
However, a normal value does not exclude an acid-base disorder.
There may be either a fully compensated disturbance or
Two primary disturbances where effects on hydrogen ion concentration cancel
each other out.
If the PCO2 is abnormal, there must be a respiratory component to the disturbance;
if the PCO2 is raised in an acidosis, the acidosis is respiratory and the value of the hydrogen
ion concentration will indicate whether there is an additional metabolic component.
If the PCO2 is low in an acidosis, the acidosis is non-respiratory and there is an
additional respiratory component, which will often reflect compensation.
A similar rationale applies to alkalotic states.
52
Acid-Base Homeostasis CH 4 Interpretation of
Acid-Base Data
53 Acid-Base Homeostasis CH 4 Case 1
A 70-year-old man was admitted to hospital as an emergency. He gave a history of dyspepsia and epigastric pain extending
over many years. He had never sought medical attention for this. One week prior to admission, he had started to vomit, and
had since vomited frequently, being unable to keep any food. He was clinically dehydrated, and had marked epigastric
tenderness, but no signs of abdominal rigidity. Analysis of an arterial blood specimen gave the following results.
Plasma Analysis
Urea
Sodium
Potassium
Creatinine
17.3 mmol/L
117 mmol/L
2.2 mmol/L
250 mol/L
(2.5-6.6)
(132-144)
(3.3-4.7)
(55-120)
Blood Gas Analysis
Hydrogen
PCO2
Bicarbonate
PO2
26 nmol/L
6.2 kPa
44 mmol/L
9.5 kPa
(36-44)
(4.4-6.1)
(21.0-27.5)
(12-15)
How would you describe this patient’s acid-base status? What might have caused the various abnormalities revealed by these
results? Why is the plasma potassium so low?
=======================================================================================
The patient had a metabolic alkalosis. This was caused by his persistent vomiting, the vomit being likely to consist almost
entirely of gastric contents. In this age group, the cause could be carcinoma of the stomach or chronic peptic ulceration with
associated fibrosis, leading to obstruction of gastric outflow.
Gastric juice potassium is about 10 mmol/L. Also, in the presence of an alkalosis, potassium shifts from the ECF into cells.
Furthermore, dehydration causes secondary hyperaldosteronism, in order to maintain ECF volume, and sodium avidly
retained by the kidneys in exchange for hydrogen and potassium. Patients such as this man, despite having an alkalosis and
despite hyperkalemic, often excrete acidic urine containing large amounts of potassium.
54
Acid-Base Homeostasis CH 4 Case 2
A young woman was admitted in a confused and restless condition. History taking
was not easy, but it seemed that she had been becoming progressively unwell over
the preceding week or two. Acid-base analysis was preformed, and results were as
follows:
Blood Gas Analysis
Hydrogen
78 nmol/L
(36-44)
PCO2
3.2 kPa
(4.4-6.1)
Bicarbonate
6 mmol/L
(21-27.5)
PO2
11.8 kPa
(12-15)
What is her acid-base disorder? What are the most likely causes, and what
investigations could narrow this down?
==========================================================
•She has a metabolic acidosis. Despite the long list of possible causes of metabolic
acidosis, the commonest causes are diabetic ketoacidosis, renal failure, salicylate
overdose and lactic acidosis. These can usually be differentiated on the basis of
history; by measuring U & Es, glucose, and salicylates if indicated; and
performing urinanalysis (using dipstick, and looking especially for ketones).
Lactate can also be measured if required, but is not often necessary. This woman
was a newly presenting Type I diabetic.
55
Acid-Base Homeostasis CH 4 Case 2
An elderly man was brought into the ER after collapsing in the street. He was deeply
comatose and cyanosed, with unrecordable blood pressure. The results of acid-base
analysis were as follows:
Blood Gas Analysis
Hydrogen
124 nmol/L
(36-44)
PCO2
10.4 kPa
(4.4-6.1)
Bicarbonate
15.4 mmol/L
(21-27.5)
PO2
4.8 kPa
(12-15)
What is the acid-base status? What are possible causes?
============================================================
•He has a combined metabolic and respiratory acidosis. The combination of the
elevated hydrogen and PCO2 may initially suggest that he has a respiratory acidosis, but
the bicarbonate would not be reduced in a simple respiratory acidosis. This means that
there is an additional component of a metabolic acidosis present. Results of this sort are
seen in patients with markedly impaired circulatory and respiratory function, such as
occurs after a cardiac arrest. This man had a large abdominal aortic aneurysm that had
ruptured.
56
Acid-Base Homeostasis CH 4 57
Acid-Base Homeostasis CH 4 58
Acid-Base Homeostasis CH 4 59
Acid-Base Homeostasis CH 4 60
Acid-Base Homeostasis CH 4
Acid-Base Balance
of 60
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