Acid Base Disorder 2011

Disorders of Acid-Base Balance
Antonio L. Diaz Hernandez, MD

Mechanism of Disease, Renal Pathophysiology, UCC
al_diaz41@hotmail.com
787-240-9909
Disorders of Acid-Base
Balance
The Hydrogen Ion concentration is
commonly expressed as the pH, the
negative logarithm of hydrogen ions
in solution.
In biologic fluids, a pH of less than
7.4 is defined as acidic and a pH
greater than 7.4 is defined as basic.
Body acids are formed as end
products of cellular metabolism.
Balance
Body Fluids
Gastric Juices
Urine
Arterial Blood PH
Venous Blood 1.0 -3.0
Cerebrospinal fluid 5.0 6.0
Pancreatic fluid 7.38 7.42
7.37
7.32
7.8 8.0
Balance
Major organs involved in the
regulation of acid-base balance
Kidney
Bones
Lungs
Balance
The Volatile Acid:
Carbonic Acid
Regulated by the
lung, kidney, RBC Non Volatile acids:
CO2 +H2OHCO3
+H+ Sulfuric acid
Phosphate
others
Balance
Volatile acids
Can be eliminated as CO2

Carbonic acid (H CO )
2 3
Balance
Occurs in response

Most important:
to changes in acid-
Buffer systems ECF:
base status
Can absorb
Carbonic Acid-
excessive H+ or OH- Bicarbonate
without significant
change in pH Hemoglobin
Exist as buffer
ICF:
pairs:
weak acid and its Phosphate
conjugate base
Proteins
Located in the ICF
and ECF
Balance
pK
Provides a rate constant for the
chemical reaction.
A buffer system is most effective when
the pK for the buffer is close to the pH
of the fluid in which the buffer is acting.
Balance
Carbonic Acid-Bicarbonate buffering
Operates as buffer in both kidney and
lung
> pCO , more carbonic acid is formed
2
H2CO3 = 0.03 X PCO2

0.03= dissociation constant
The relationship between bicarbonate
and carbonic acid is expressed as a
ratio 20:1
Balance
Compensation
Lungs
Kidney
Balance
Protein buffers
Intracellular buffers
Hemoglobin buffers
Intracellular and extracellular proteins

have negative charges and can serve as
buffers for H+
Balance
Buffering of hydrogen with hemoglobin and carbon dioxide
transport
Balance
Renal Buffering
Distal tubule Principal cells
Secretes hydrogen into the urine
Reabsorbed bicarbonate
Dibasic phosphates (HPO4)
Ammonia (NH3)
Balance
Renal Excretion of Acid
Balance
Other Buffers:
Cellular Ion Exchange
e.g. Potassium
Balance
Balance
Acidemia is defined as a
decrease in blood pH ( or an
increase in the H+
concentration)
Alkalemia is defined as an
elevation in the blood pH (or
a reduction in the H+
concentration)
Balance
Since PCO2 is regulated by
respiration, primary abnormalities in
the PCO2 are called respiratory
acidosis (high PCO2) and respiratory
alkalosis (low PCO2)
Balance
Primary changes in the plasma
HCO3- concentration are referred to
as metabolic acidosis (low HCO3-)
and metabolic alkalosis (high HCO3-)
Balance
The compensatory response always
changes in the same direction as the
primary disturbance.
High PCO2 in respiratory acidosis

results in enhanced renal H+
excretion an appropriate elevation in
the plasma HCO3- concentration.
Disorders of Acid-
Base Balance
Characteristics of the primary acid-base
disturbance
Balance
Metabolic Acidosis
Results from decrease HCO3-
concentration and is associated with a
low pH (or high H+ concentration).
The respiratory compensation consist of
hyperventilation and an elevation in
PCO2.
Balance
Metabolic Alkalosis
Results from an elevation in in the
plasma HCO3- concentration and is
associated with a high pH (or low H+
concentration).
The respiratory compensation consist of
hypoventilation and an elevation in
PCO2.
Balance
Respiratory Acidosis
Decreased effective alveolar ventilation,
resulting in reduced pulmonary
excretion of CO2 and an increase in the
extra cellular PCO2(hypercapnia)
The renal compensation consists of
enhanced H+ excretion, which raises
the plasma HCO3- concentration.
Balance
Respiratory Alkalosis
The primary disturbance in respiratory
alkalosis is hyperventilation, resulting
in a fall in the extra cellular PCO2
(hypocapnia) and an increase in pH (or
reduction in H+ concentration)
The compensatory response consists of
diminished renal H+ secretion,
producing HCO3- loss in the urine and
an appropriate decrease in the plasma
HCO3- concentration.
Balance
Mixed Acid Base Disorders
One or more of the primary
disorders is present
Balance
Clinical use of Hydrogen concentration
[H+] = 24 x PCO2 /[HCO3-]
If one begins at a pH of 7.40 and a H+ concentration of 40 nanoeq/L,

then for every 0.10 increase in pH, the H+ concentration must be
multiplied by 0.8; for every 0.10 decrease in pH, the H+ concentration
must be multiplied by 1.25.
pH = 7.3 [H+] = 40 x 1.25 = 50 nanoeq/L

pH = 7.20 [H+] = 40 x 1.25 x 1.25 = 63 nanoeq/L
pH = 7.50 [H+] = 40 x 0.8 = 32 nanoeq/L
values at less than 0.10-unit steps can be estimated from

interpolation.
Balance
Renal and respiratory compensation to primary acid-base
disturbances in humans
Metabolic Alkalosis
The pathophysiology of metabolic
alkalosis is most easily understood
by asking two separate questions:
How do patients become alkalotic??
Why do they remain alkalotic, since
renal excretion of the excess of HCO3-
should rapidly restore normal acid-base
balance?
Horacio J. Andorgu & Nicolaos E. Midias
Metabolic Alkalosis
Metabolic Alkalosis
Metabolic Alkalosis
Metabolic Alkalosis
Causes of impaired HCO3- excretion
that allow metabolic alkalosis to
persist
Decreased Glomerular filtration rate
a. Ineffective circulating volume
b. Renal Failure ( usually associated with
metabolic acidosis)
Increased Tubular reabsorption
a. Effective circulating volume depletion
b. Chloride depletion (also decreases
bicarbonate secretion)
c. Hypokalemia
d. Hyperaldosteronism
Metabolic Alkalosis
Manifested:
Related to volume depletion and electrolytic losses
Weakness
Muscle Cramps
Hyperactive Reflexes
Tetany may develop
Confusion
Convulsion
Atrial Tachycardia
Shift of the Oxyhemoglobin curve to the left
Metabolic Acidosis
From the reaction of H+ with the
primary extra cellular buffer, HCO3-,
it can be appreciated that metabolic
acidosis can be produced in two
ways:
Addition of H+ ions
Loss of HCO3- ions
Mechanism for the
Development of Metabolic
Acidosis
Accelerate alkali loss into stools and urine
Decrease renal acid titration capacity
Increase endogenous generation,

ingestion or infusion of acid load beyond
normal excretory capacity or rate of
metabolic conversion to neutral
compounds or CO2 and H2O
Acid-Base and Electrolyte Disorders, DuBose, Ham;
Metabolic Acidosis
The response of the body to an
increase in the arterial H+
concentration involves four
processes:
Extra cellular buffering
Intracellular and bone buffering
Respiratory compensation
Renal excretion of the H+ load

Metabolic
Acidosis
Anion Gap
Anion Gap Determination and its significance
Albumi
AG
AG
n
PO4-3
HCO3-
Na+
Cl- AG = Na+ - (Cl- +HCO3-)
Normal AG = 10-12
Anion Gap
AG
AG AG
AG
HCO3- HCO3-
Na+ + HA Na+
Cl- Cl-
Change in AG with Hypoalbuminemia
Before and After High Anion Gap
Metabolic Acidosis
AG Low
albumin AG
AG A- + Albumin
HCO3 -
HCO3-
+ HA
Na+ Na+
Cl- Cl-
Metabolic Acidosis
Clinical manifestation:
Neurologic
Respiratory
Gastrointestinal
Cardiovascular
Metabolic Acidosis
Symptoms:
Headache and Lethargy
Coma
Deep rapid respiration (Kussmaull
Respiration)
Anorexia
Nausea
Vomiting
Diarrhea
Abdominal Discomfort
Life threatening Dysrythmia

Metabolic Acidosis
Lactic Acidosis
Accumulation of lactate in the
circulation, and consequent lactic
acidosis, is generated whenever the
rate of production of lactate is
higher than the rate of utilization
The pathogenesis of this imbalance
reflects:
Overproduction of lactate
Diminish metabolize
Both
Lactic Acidosis
Type A Lactic Acidosis
Type B Lactic Acidosis
Imparmente in
oxygenation Impairment of cellular metabolism
pyruvate production
Enzymatic defects in
glycogenolysis or
gluconeogenesis
Respiratory alkalosis,
including salicylate
intoxication
Pheochromocytoma
Hypovolemia Cyanide
Cardiac Failure Metformin
Sepsis Zidovudine or stavudine
Diabetic Ketosis
Renal Tubular Acidosis
Group of disorders in which tubular
hydrogen ion secretion is impaired
out proportion to any reduction in
the glomerular filtration rate
Characteristics:
Normal Anion Gap (Hyperchloremic metabolic
Acidosis )
Proximal RTA type 2
Excessive HCO
3
Classic Distal RTA type 1
Deficient H+ secretion
Distal RTA type 4 hyperkalemic
Renal Tubular Acidosis
d-Renal Tubular Acidosis
Secondary
Primary Sjgren's syndrome
Idiopathic, Hypercalciuria
Ehlers-Danlos
sporadic Marfan Synd.
Rheumatoid arthritis
Familial Hyperglobulinemia
Balkan
Nephropathy
Autosomal Ifosfamide
dominant
Fabrys disease
Amphotericin B
Autosomal
Wilson disease
Cirrhosis Systemic
recessive Lupus erythematosus
Sickle cell anemia
Obstructive uropathy
Lithium
Renal transplantation
p-Renal Tubular Acidosis
Primary Secondary
Idiopathic, Vitamin D

sporadic
Multiple myeloma deficiency
Familial disorders Drugs Renal
Cystinosis Ifosfamide transplantation
Tyrosinemia Tenofovir Paroxysmal
Hereditary
fructose Carbonic anhydrasenocturnal
inhibitors
intolerance hemoglobinuria
Galactosemia
Amyloidosis
Glycogen storage Heavy metals
disease (type I)
Wilson's disease
Lead Cadmium
Dent syndrome Mercury
Lowe's syndrome Copper
Carbonic
anhydrase
deficiency
Disorders of Acid-
Base Balance
Is characterized by a reduction in
Arterial pH (or increased H+
concentration)
Elevation in pCO2 (hypercapnia)
Variable increases in plasma HCO3
Endogenous metabolism results in production of

aproximatelly, 15,000 mmol of CO2 / day
CO2 + H2O H2CO3 H+ + HCO3-
The elevation in the H+ concentration is then minimized
because most of the excess H+ ions combines with
intracellular buffers, included Hg in red cells
H2CO3 + Hg- HHb + HCO3-
The HCO3- generated leaves the erythrocyte and enters
the extracellular fluid in exchange for extracellular Cl -
Net effect : metabollically generated CO2 is primarily

carried in the bloodstream as HCO3-, with little change in
the extracellular pH.
In the alveoli, as HHg is oxygenated , H+ is released.
These H+ ions combine with HCO3- to form H2CO3 and the
CO2 which is excreted.
Alveolar ventilation provides the oxygen

necessary for oxidative metabolism and
eliminates the CO2 produced by these metabolic
processes.
The main physiologic stimuli to respiration are a
reduction in the arterial pCO2 (hypoxemia) and an
elevation in the arterial pCO2
CO2 stimulus to respiration

Respiratory center in the medulla
Chemoreceptors in the carotid bodies
Carbon dioxide is the major stimulus

to respiration
Minute ventilations are enhanced by
minor elevations in the arterial Pco2
Hypoxemia does not stimulate
ventilation until the Arterial Po2 is
less than
50 60 mmHg
Hypercapnia
Hypercapnia and respiratory acidosis
are almost always due to a reduction in
effective alveolar ventilation
NOT TO AN INCREASE IN CO2
PRODUCTION
Manifestations:
Restlesness
Apprehension
Lethargy
Muscle Twiching
Tremors
Convulsion
Coma
Disorders of Acid-
Base Balance
A primary decrease in Pco2 occurs
when effective alveolar ventilation is
increased to a level beyond that
needed to eliminate the daily load of
metabolically produced CO2
Acute Respiratory Alkalosis
After the onset of respiratory alkalosis H+
move from the cells into the extracellular fluid
They combine with HCO3- , resulting in an
appropriate fall in the plasma HCO3-
concentration
H+ + HCO3- H2CO3 CO2 + H2O
These H+ are derived from
Protein
Phosphates
Hemoglobin
Alkalemia induced Lactic Acidosis
Acute Respiratory Alkalosis
In general enough H+ enter the
extracellular fluid to lower the plasma
HCO3- concentration
2 mEq/L for each 10 mmHg decrease in
Pco2
Chronic respiratory alkalosis
There is a compensatory decrease in renal H+
secretion that begins within 2 hrs. but is not
complete for 2-3 days.
This response is mediated at least in part by a
paralelle rise in renal tubular cell pH, is
manifested by:
HCO3- loss
Decrease amonium excretin
Decrease in HCO3- - conc. In plasma
H+ retention
The combined effect of the cell
buffers and the renal compensation
results in a new steady state in
which the plasma HCO3-
concentration falls,
4 mEq/L for each 10 mmHg fall in the
Pco2
Respiration is physiologically governed by
two sets of chemoreceptors:
Respiratory center in the brainstem, carotid
and aortic bodies
Bifurcation of the carotid arteries
Aortic Archs
Central chemorectors are stimulated by
Pco2, metabolic acidosis, and both appear to
be sensed by a fall in pH in the cerebrospinal
interstitial fluid
Peripheral Chemoreceptors are stimulated by
hypoxemia, although the also contribute to the
acidemic response
Respiratory
Alkalosis
Primary hyperventilation
resulting in respiratory alkalosis
can be produced by Hypoxemia or
Anemia, a reduction in Cerebral
pH ( rare event since
intracerebral pH is elevated in
respiratory alkalosis ) or other
stimuli for hyperventilation, such
as pain, anxiety, stimulation of the
central respiratory center.
Manifestations:
Dizziness
Confussion
Tingling of extremities
Convulsions
Coma
Deep and Rapid Respirations
Urine Anion Gap
urine AG
anions NH4 + NH4+
A
G
Na+ Acidosis Cl- K+
Cl- K+
Na+

Acid Base Disorder 2011

Diunggah oleh

Informasi Dokumen

Hak Cipta

Format Tersedia

Bagikan dokumen Ini

Bagikan atau Tanam Dokumen

Opsi Berbagi

Apakah menurut Anda dokumen ini bermanfaat?

Apakah konten ini tidak pantas?

Hak Cipta:

Format Tersedia

Acid Base Disorder 2011

Diunggah oleh

Hak Cipta:

Format Tersedia

Disorders of Acid-Base Balance

Antonio L. Diaz Hernandez, MD

Can be eliminated as CO2

H2CO3 = 0.03 X PCO2

Intracellular and extracellular proteins

High PCO2 in respiratory acidosis

[H+] = 24 x PCO2 /[HCO3-]

If one begins at a pH of 7.40 and a H+ concentration of 40 nanoeq/L,

pH = 7.3 [H+] = 40 x 1.25 = 50 nanoeq/L

values at less than 0.10-unit steps can be estimated from

Decrease renal acid titration capacity

Increase endogenous generation,

Renal excretion of the H+ load

Life threatening Dysrythmia

Endogenous metabolism results in production of

Net effect : metabollically generated CO2 is primarily

Alveolar ventilation provides the oxygen

CO2 stimulus to respiration

Carbon dioxide is the major stimulus

Anda mungkin juga menyukai