? Buffer systems and its efficiency
? Requirement of maintenance of acid base
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balance? Causes of acid base imbalances
? Regulation of acid base balance
--- Content provided by FirstRanker.com ---
? Renal? Respiratory
2
Case report 1
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? A patient with a history of chronic lung
disease has suffered from emphysema which
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has grown progressively worse over a periodof years. The patient experiences chronic
shortness of breath. Analysis of patient 's
--- Content provided by FirstRanker.com ---
blood reveals the following PCO2=60 mmHg:
[HCO3] =34mM pH=7.38
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? What could be the diagnosis?3
Case report 2
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? A man suffering from untreated diabetes
mel itus is admitted to the hospital. Glucose
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and acetoacetate are present in his urine andhe exhibits shal ow breathing. Analysis of his
blood indicates [HCO3-] =16 mM and
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PCO2=30
? The most likely pH of blood is
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4Relationship of pH to hydrogen ion concentration
5
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Scheme demonstrating the relation betweenpH and the ratio of bicarbonate concentration
to the concentration of dissolved CO2.
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6
? What is pH?
? Negative logarithm of H+ concentration in a solution
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? pH Scale:
? Ranges from 0 to 14
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? What is pKa?? Negative logarithm of dissociation constant
? The pH at which an acid is half dissociated, existing as
--- Content provided by FirstRanker.com ---
equal proportions of acid and conjugate base.
7
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What is buffer? A buffer is a mixture of a weak acid and a salt of
its conjugate base that resists changes in pH
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when a strong acid or base is added
to the solution
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.? Functions of a buffer depends on:
? pH
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? pK
? Salt to acid ratio
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8? Does the dilution change the pH of a buffer?
? pH of a buffer solution is directly proportional
to the salt acid ratio. Dilution does not change
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the ratio
? Buffer efficiency:
? Maximum when the ratio of acid/base is
--- Content provided by FirstRanker.com ---
within the range of 10:1 to 1:10
? Over a pH range is equal to pKa?1
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9Requirement of maintenance of acid
base balance
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? For optimum function of biomolecules :
Enzymes, transport molecules, nucleic acid
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? To avoid disruption of structure and functionof cells
? Several serious health consequences: Acidosis,
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alkalosis
10
Buffer systems
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? 1. Bicarbonate/Carbonic acid buffer systems
? Extra cel ular buffer
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? pK=6.1? cHCO3-/cdCO2= ?
? 2. Phosphate buffer
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? pK= 6.8
? cHPO4-/H2PO4-=
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? Intracel ular buffer? 3. Plasma protein and Hemoglobin: Imidazole
group of histidine: pK=7.3
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11
Regulation of Acid-Base balance
--- Content provided by FirstRanker.com ---
1. Respiratory mechanism2. Renal mechanism
12
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Partial pressure ofoxygen and carbon di oxide
13
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Respiratory Response to Acid-Base
Perturbations
--- Content provided by FirstRanker.com ---
? responds immediately to a change in acid -basestatus
? several hours may be required for the response to
--- Content provided by FirstRanker.com ---
become maximal
? in the early stage plasma pH decreases
? H+ ions equilibrate slowly across the blood -brain
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barrier, the pH in CSF remains nearly normal
? Stimulated peripheral chemoreceptor induces
--- Content provided by FirstRanker.com ---
hyperventilation: Plasma pCO2 decreased?
14
--- Content provided by FirstRanker.com ---
? the PCO2 of the CSF decreases immediatelybecause CO2 equilibrates rapidly across the blood
?brain barrier, leading to a rise in pH of the CSF
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that inhibits the central chemoreceptor
? plasma bicarbonate gradual y fal s because of
--- Content provided by FirstRanker.com ---
acidosis, bicarbonate concentration and pH in theCSF wil also eventual y fall
? stimulation of respiration becomes maximal from
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both central and peripheral chemoreceptors.
15
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Role ofRBC and
Hb
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16
Role of RBC and Hb
17
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Renal mechanisms in the regulation of
Acid-Base Balance
--- Content provided by FirstRanker.com ---
? pH of plasma=? 7.4
? PH of urine=
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? 6.0
18
1. Na+-H+ exchange :
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19
2. Reclamation of HCO3-
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203. Renal production of Ammonia and
excretion of Ammonium ions
--- Content provided by FirstRanker.com ---
214. Excretion of H+ as H2PO4-
22
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Conditions associated with abnormal acid basestatus and abnormal electrolyte composition of
the blood
--- Content provided by FirstRanker.com ---
? Metabolic acidosis
? Metabolic alkalosis
? Respiratory acidosis
? Respiratory alkalosis
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23
Simple depiction of the body as a two-vat system
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of acid and base24
Metabolic acidosis (Primary
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bicarbonate deficit)? Decreased plasma HCO3-
? Ratio of cHCO 3- /cdCO 2 is decreased
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Causes
? 1. Production of organic acids that exceeds the
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elimination: Diabetic ketoacidosis? 2. Reduced excretion of acids: Renal failure,
RTA
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? 3. Excessive loss of bicarbonate:
? Diarrhea (loss of duodenal fluid)
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25? An alcoholic has come to you with a complaint
of severe vomiting. His blood test reveals pH
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7.42 and HCO3- 25 mmol/L,
26
Simple depiction of normal gap, anion gap acidosis,
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and nonanion gap acidosis.
27
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Increase in anion gapMethanol
Uremia
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Diabetic ketoacidosis
Paraldehyde
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Iron, Isoniazid, IbuprofenLactic acidosis
Ethylene glycol, Ethanol
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Salicylates, starvation ketoacidosis
28
? Methanol:
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? Metabolized by the liver to formaldehyde and
formic acid
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29Alcohol
Serum Anion Serum Urine
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osmol Gap
acetone oxalate
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gapEthanol
+
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----
-----
--- Content provided by FirstRanker.com ---
-----Methanol +
+
--- Content provided by FirstRanker.com ---
-----
-----
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Isopropanol +---
+
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----
Ethylene
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++
-----
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+
glycol
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30Osmol gap
? OSMg = OSMm - OSMc
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The diff erence between the actual osmolality (OSMm),measure by freezing-point depression, and the calculated
osmolality (OSMc).
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? OSMc (mOsm/kg) = 2 Na (mmol/L)
+ glucose (mg/dL) /18
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+ urea (mg/dL) /2.8? presence of unmeasured osmotically active substances:
Volatile alcohols: methanol, isopropanol , ethylene glycol
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31
Uremia or renal failure
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? (1) decreased ammonia formation,? (2) decreased Na+-H+ exchange, and
? (3) decreased GFR.
? All result in decreased acid excretion.
? Acidosis usually develops if GFR falls below
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20 mL/min.
32
Diabetic ketoacidosis
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? -hydroxybutyrate and 2-oxoglutarate
accumulate
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? decrease in HCO3- and a high anion gap? Ketoacids also accumulate in states of
starvation and alcoholic malnutrition
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33Paraldehyde toxicity
? after chronic paraldehyde ingestion
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? -hydroxybutyric acid? Patients with paraldehyde toxicity have a
pungent, apple-like odor to their breath
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.34
Isoniazid, Iron, or Ischemia (" Three I's")
--- Content provided by FirstRanker.com ---
? accumulating organic acids with a predominanceof lactic acid
? production of toxic peroxides that act as
--- Content provided by FirstRanker.com ---
mitochondrial poisons and interfere with normal
cel ular respiration
--- Content provided by FirstRanker.com ---
? Ischemia results in anaerobic metabolism withaccumulation of organic (mainly lactic) acids.
35
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Lactic acidosis
? Derived mainly from muscle cells and erythrocytes
? end product of anaerobic metabolism and is normally
--- Content provided by FirstRanker.com ---
metabolized by the liver
? An increase in the concentration of lactate to >3 mmol/L with
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the associated increase in H+ is considered lactic acidosis? caused by severe tissue hypoxia is seen in
(1) severe anemia, (2) shock, (3) cardiac arrest, and (4)
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pulmonary insufficiency
? Treatment: origin of lactate (e.g., seizure, hypoxic
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tissue) is rectified : rapidly metabolized to CO2, which thenis eliminated
36
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Ethylene glycol? metabolized primarily to glycolic and oxalic acid s
? lead s to an acidosis with high anion and osmolal
--- Content provided by FirstRanker.com ---
gaps? Precipitation of calcium oxalate and hippurate
crystals in the urinary tract may lead to acute renal
--- Content provided by FirstRanker.com ---
failure
? Patients develop a variety of neurologic symptoms
--- Content provided by FirstRanker.com ---
that may lead to coma37
Salicylate Intoxication
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? blood salicylate concentrations above 30 mg/L
=acidosis develops
? Salicylate, itself an unmeasured anion
? Alters peripheral metabolism, leading to the
--- Content provided by FirstRanker.com ---
production of various organic acids
? stimulates the respiratory center to increase
--- Content provided by FirstRanker.com ---
the rate and depth of respiration? mixed respiratory alkalosis and metabolic acidosis.
38
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Normal anion gap acidosis? Difference between high and normal anion gap acidosis
? high anion gap acidosis= bicarbonate
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is consumed from buffering excess H+
? normal anion gap acidosis= loss of bicarbonate-rich
--- Content provided by FirstRanker.com ---
fluid from the kidney or the gastrointestinal tract :more Cl- ions are reabsorbed with Na+ or
K+ to maintain electrical neutrality so that
--- Content provided by FirstRanker.com ---
hyperchloremia ensues
39
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? Normal anion gap acidosis is dividedinto (1) hypokalemic, (2) normokalemic, and
(3) hyperkalemic acidosis
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40
? Normal anion gap acidosis with Hypokalemia:
? Gastrointestinal loss
? RTA
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41
Gastrointestinal loss
--- Content provided by FirstRanker.com ---
? Diarrhea may cause acidosis as a result of lossof (1) Na+, (2) K+, and (3)HCO3-
? water, K+, an HCO- 3 in the intestine are not
--- Content provided by FirstRanker.com ---
reabsorbed ,
? The resulting hyperchloremia is due to
--- Content provided by FirstRanker.com ---
replacement of lost bicarbonate with Cl-? a hypokalemic, normal anion gap metabolic
acidosis develops
--- Content provided by FirstRanker.com ---
42
Renal tubular acidosis, Type I and I
? Loss of bicarbonate due to decreased tubular
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secretion of H+ = distal or type I R TA
? Decreased reabsorption of HCO3-= Proximal or
--- Content provided by FirstRanker.com ---
type I RTA? proximal and distal RTAs may be differentiated by
measurement of urine pH after administration of
--- Content provided by FirstRanker.com ---
acid :
? proximal R TA, urine pH becomes <5.5, whereas
--- Content provided by FirstRanker.com ---
in distal RTA, the distal tubules are compromisedand urine pH is >5.5
43
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? Hyperkalemic normal Anion gap Acidosis: RTA type IV
? (1) Failure of the kidneys to synthesize renin,
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(2) Failure of the renal cortex to secrete aldosterone,and
(3) renal tubular resistance to aldosterone.
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? inhibits Na+ reabsorption, and both K+ an H+ are thus
abnormal y retained .
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? decreased renal ammonia formation and thereforedecreased elimination of H+.
44
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Normal Anion GapGI fluid loss
Severe diarrhoea
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Hypokalemia
Pancreatitis
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K+ variableRenal tubular acidosis
Proximal (type I ) R TA
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Urine pH <5.5 , K+ normal or low
Distal (typeI) R TA
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Urine pH >5.5 with hypokalemiaType IV R TA
Urine pH < 5.5 with hyperkalemia
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45
Compensation
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? Primary compensation: respiratory system? Stimulation of RS (Kussmaul respiration )
(1) the elimination of carbonic acid as CO2,
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(2) a decrease in PCO2 (hypocapnia), and
(3) ultimately a decrease in cdCO2.
--- Content provided by FirstRanker.com ---
? Secondary compensation : by Kidney: takes 2-3 days? increased excretion of acid and preservation of base by
an increase (1) rate of Na+-H+ exchange, (2) ammonia
--- Content provided by FirstRanker.com ---
formation, and (3) reabsorption of bicarbonate
46
Decrease in Anion Gap
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Laboratory error
1.Increase in unmeasured cations
--- Content provided by FirstRanker.com ---
2.Lithium intoxication3.Increased immunoglobulin
4.Monoclonal gammopathies
--- Content provided by FirstRanker.com ---
5.Nephrotic syndrome
6.Hyperlipidemia
--- Content provided by FirstRanker.com ---
47Metabolic alkalosis
? (1) excess base is added to the system,
--- Content provided by FirstRanker.com ---
? (2) base elimination is decreased ,
? or (3) acid -rich fluids are lost
--- Content provided by FirstRanker.com ---
? Al lead to a primary bicarbonate excess? alter the cHCO-3 / cdCO2
patient wil hypoventilate to raise PCO2
--- Content provided by FirstRanker.com ---
? achieving a PCO2 =55 mm Hg
? Above pH 7.55, tetany may develop:
--- Content provided by FirstRanker.com ---
? cause of the tetany is a decrease concentration ofionized calcium due to increase binding of calcium ions
by albumin as H+ ions decrease
--- Content provided by FirstRanker.com ---
48
? metabolic alkalosis all into
? (1) Cl- responsive,
? (2) Cl- resistant, and
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? (3) exogenous base categories49
1. Cl- Responsive Metabolic Alkalosis
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? Occur as a result of hypovolemia
? contraction alkalosis
? Hypovolemia wil result in
? (1) increase reabsorption of Na+,
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? (2) increase HCO- 3 absorption and? (3) excretion of K+ and H+.
? Urine Cl- wil be less than 10 mmol/L, as both the
available Cl- an HCO3 - are reabsorbed with Na+
--- Content provided by FirstRanker.com ---
50
? Common causes of contraction alkalosis
include
--- Content provided by FirstRanker.com ---
? prolonged vomiting or
? nasogastric suction and
--- Content provided by FirstRanker.com ---
? the use of certain diuretics? Treatment consists of replacing BW with
? (1) water, (2) NaCl tablets, or
--- Content provided by FirstRanker.com ---
? (3) saline in fusion.
51
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2. Cl- Resistant Metabolic Alkalosis? far less common than Cl- responsive MA
? Associated with:
? (1) primary hyper aldosteronism,
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? (2) Cushing syndrome, or? (3) Bartter syndrome, or with excess addition
of exogenous base.
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? urine Cl- will be greater than 20 mmol/L.52
adrenocortical excess
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? K+ an H+ are "wasted " by the kidneys? increased Na+ reabsorption stimulated by
elevated aldosterone or cortisol
--- Content provided by FirstRanker.com ---
? hypokalemia often further contributes to thealkalosis
? stimulates NH3 production and thus renal H+
--- Content provided by FirstRanker.com ---
excretion as NH 4+
53
--- Content provided by FirstRanker.com ---
3. Exogenous Base? include (1) citrate toxicity following massive
blood transfusion,
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(2) aggressive intravenous therapy with
bicarbonate solutions, and
--- Content provided by FirstRanker.com ---
? (3) ingestion of large quantities of antacids(Milk alkali syndrome)
54
--- Content provided by FirstRanker.com ---
Conditions leading to Metabolic AlkalosisChloride responsive (Urine Cl- < 10 mmol/L)
Contraction alkalosis (Hypovolemia)
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Prolonged vomitingUpper duodenal obstruction
Dehydration
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Chloride resistant (Urine Cl- > 10 mmol/L)
Mineralocorticoid Excess
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Primary hyperaldosteronismBilateral adrenal hyperplasia
Secondary hyperaldosteronism
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Glucocorticoid excess
Primary adrenal adenoma
--- Content provided by FirstRanker.com ---
Pituitary adenoma secreting ACTHExogenous cortisol therapy
Bartter syndrome (defective renal Cl- absorption )
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Exogenous base
Bicarbonate containing iv fluid therapy
--- Content provided by FirstRanker.com ---
Massive blood transfusion ( Sodium citrate overload)Milk Alkali syndrome
55
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Compensatory Mechanisms in
Metabolic Alkalosis
--- Content provided by FirstRanker.com ---
? both respiratory compensation and , ifphysiological y possible, renal compensation
? Respiratory compensation:
--- Content provided by FirstRanker.com ---
? Th e increase in pH depresses the respiratory
center,
--- Content provided by FirstRanker.com ---
? causing retention of carbon dioxide? increase in cH2CO3 and cdCO2
? ratio of cHCO- 3 / cdCO2, which was
--- Content provided by FirstRanker.com ---
original y increased , approaches its normal value
56
Renal compensation
--- Content provided by FirstRanker.com ---
? The kidneys respond to the state of alkalosis
by
--- Content provided by FirstRanker.com ---
? decrease(1) Na+-H+ exchange,
(2) formation of ammonia,
and (3) reclamation of bicarbonate
? This response is blunted in conditions of
--- Content provided by FirstRanker.com ---
hypokalemia and hypovolemia.
57
--- Content provided by FirstRanker.com ---
Respiratory acidosis? occurs only through decreased elimination of CO2
? increase in PCO2 (hypercapnia) an dCO2
--- Content provided by FirstRanker.com ---
? decrease in the cHCO3 - / cdCO2 ratio (e.g., the ratio may be28:1.7 [16:1] or a pH of 7.30 )
? conditions may be divided into those caused by factors that
--- Content provided by FirstRanker.com ---
? directly depress the respiratory center
? mechanical obstruction of the airways
? Chronic obstructive pulmonary disease (COPD) is the most
--- Content provided by FirstRanker.com ---
common cause
58
Conditions leading to Respiratory Acidosis
--- Content provided by FirstRanker.com ---
Factors that directly depress the respiratory centre
Drugs such as narcotics
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CNS trauma, tumorInfections of the CNS
Comatose states
--- Content provided by FirstRanker.com ---
Conditions that affect the Respiratory apparatus
COPD (most common)
--- Content provided by FirstRanker.com ---
Severe pulmonary fibrosisDisease of the upper airway e,g laryngospasm, tumor
Impair lung motion due to pleural effusion
--- Content provided by FirstRanker.com ---
ARDS
Others Abdominal distension as in peritontitis and ascites
--- Content provided by FirstRanker.com ---
Extreme obesitySleep disorder, sleep apnea
59
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Compensatory mechanism
? Immediately via buffers
--- Content provided by FirstRanker.com ---
? Over time via kidneys? Excess carbonic acid present in blood is bufferd
by the hemoglobin and protein
--- Content provided by FirstRanker.com ---
? Buffering of CO2 causes a slight rise in cHCO3-
? immediate post hypercapnic state appear as a
--- Content provided by FirstRanker.com ---
metabolic alkalosis60
Response of Kidney for respiratory
--- Content provided by FirstRanker.com ---
acidosis? similarly to the way that they responds to metabolic acidosis
? Increase in
(1) Na+-H+ exchange,
--- Content provided by FirstRanker.com ---
(2) ammonia formation,and(3) reclamation of bicarbonate
? Partially compensated= the plasma pH is returned about half
--- Content provided by FirstRanker.com ---
way toward normalNot effective before 6 to 12 hours and is not optimal until 2
to 3 days.
--- Content provided by FirstRanker.com ---
COPD= full renal compensation
? COPD with superimposed metabolic alkalosis due to
--- Content provided by FirstRanker.com ---
prolonged diuretics61
Respiratory response for respiratory
--- Content provided by FirstRanker.com ---
acidosis
? stimulates the respiratory center
? Increase pulmonary rate and depth of respiration,
--- Content provided by FirstRanker.com ---
provided that the primary defect is not in the
respiratory center
--- Content provided by FirstRanker.com ---
? Elimination of carbon dioxide through the lungsresults in a decrease in c CO2;
62
--- Content provided by FirstRanker.com ---
Respiratory Alkalosis? decrease in PCO2 (hypocapnia) and the resulting
primary defcit in cdCO2
--- Content provided by FirstRanker.com ---
? increased rate and /or depth of respiration
? excess elimination of acid via the respiratory route
--- Content provided by FirstRanker.com ---
? increase in the cHCO3-/ cdCO2 ratio.? shifts the normal equilibrium of the
bicarbonate/carbonic acid buffer system
--- Content provided by FirstRanker.com ---
? reducing the hydrogen ion concentration and
increasing the pH
--- Content provided by FirstRanker.com ---
? Also results in a decrease in cHCO3-63
? causes of respiratory alkalosis have been
--- Content provided by FirstRanker.com ---
classified as? those with a direct stimulatory effect on the
respiratory center
--- Content provided by FirstRanker.com ---
? and those due to effects on the pulmonary
system.
--- Content provided by FirstRanker.com ---
64Factors causing respiratory Alkalosis
Nonpulmonary stimulation of respiratory center
--- Content provided by FirstRanker.com ---
Anxiety, hysteriaFebrile state
Metabolic encephalopathy
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CNS infection
Cerebrovascular accident
--- Content provided by FirstRanker.com ---
HypoxiaDrugs and agents such salicylates, cathecholamines
Pulmonary disorder
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Pnemonia
pulmonary emboli
--- Content provided by FirstRanker.com ---
Interstitial lung diseaseCHF
Respiratory compensation after correction of metabolic acidosis
--- Content provided by FirstRanker.com ---
Others Ventilation induced hyperventilation
65
--- Content provided by FirstRanker.com ---
Compensatory mechanisms forrespiratory alkalosis
? respond in two stages
--- Content provided by FirstRanker.com ---
? 1st stage: erythrocyte and tissue buffersprovide H+ ions that consume a small amount
of HCO3-
--- Content provided by FirstRanker.com ---
? 2nd stage: in prolonged respiratory alkalosis:
renal compensation as metabolic alkalosis
--- Content provided by FirstRanker.com ---
66ABG parameters in various conditions
of acid-base imbalance
--- Content provided by FirstRanker.com ---
ImbalanceStage
pH
--- Content provided by FirstRanker.com ---
HCO3
pCO2
--- Content provided by FirstRanker.com ---
MetabolicUncompensated
<7.3
--- Content provided by FirstRanker.com ---
Low
Normal
--- Content provided by FirstRanker.com ---
acidosisCompensated
Approx 7.35
--- Content provided by FirstRanker.com ---
Low
Low
--- Content provided by FirstRanker.com ---
Respiratory Uncompensated<7.3
Normal
--- Content provided by FirstRanker.com ---
High
acidosis
--- Content provided by FirstRanker.com ---
CompensatedApprox 7.35
High
--- Content provided by FirstRanker.com ---
High
Metabolic
--- Content provided by FirstRanker.com ---
Uncompensated>7.5
High
--- Content provided by FirstRanker.com ---
Normal
alkalosis
--- Content provided by FirstRanker.com ---
CompensatedApprox 7.45
High
--- Content provided by FirstRanker.com ---
High
Respiratory Uncompensated
--- Content provided by FirstRanker.com ---
>7.5Normal
Low
--- Content provided by FirstRanker.com ---
alkalosis
Compensated
--- Content provided by FirstRanker.com ---
Approx 7.45Low
Low
--- Content provided by FirstRanker.com ---
67
Summary
--- Content provided by FirstRanker.com ---
? According to Broensted and Lowry: An acid is defined as a substance , ionor molecule that yields H+ in sollution and base is an ion , molecule or
substance that can combine with H+ ions.
--- Content provided by FirstRanker.com ---
? Human body produces volatile acids( Carbonic acid) and nonvolatile acid (
Sulfuric acid and lactic acid).
--- Content provided by FirstRanker.com ---
? Buffers are the solution that resist the change in pH on addition of acid orbase.
? The pH of blood is maintained in a narrow range around 7.35-7.45 by
--- Content provided by FirstRanker.com ---
extracellular and intracellular buffering.
? The carbonic-biocarbonate system is the major buffering system.
? The partial pressure of CO2 in blood is 40 mmHg
--- Content provided by FirstRanker.com ---
? The pCO2 is regulated by respiratory system.? The phosphate buffer system (Na2HPO4/NaH2PO4) operates in the cell
and contributes to only about 1% of the plasma buffering capacity.
--- Content provided by FirstRanker.com ---
68Summary contd
? Histidine is the most effective amino acid that helps proteins to
--- Content provided by FirstRanker.com ---
work as buffer. Albumin has 16 and Hemoglobin has 38 histidineresidues.
? Kidneys play a very important role in the regulation of extracel ular
--- Content provided by FirstRanker.com ---
pH through reabsorption of bicarbonate and secretion of H+,
synthesis and excretion of ammonia.
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? The clinical disorder associated with accumulation of acids in thetissue and plasma is known as acidosis whereas the build up of
alkali in the body is known as alkalosis.
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? The respiratory acidosis is seen in cases of pulmonary diseases such
as COPD.
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? Metabolic alkalosis occurs as a result of net gain of HCO3- or loss ofnonvolatile acid
? Assessment of the acid-base imbalance is done by estimation of the
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arterial blood pH , cHCO3- and pCO2 along with electrolytes
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MCQ 1? A 64 years old man who develops acute renal failure
while recovering from myocardial infarction. Blood
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chemistry reveals Na+140 meq/L , K=4 meq/L , Cl- 115
meq/L , Co2 =5 meq/L , pH 7.12 , paCO2=13 mm Hg
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, HCo3-=4 meq/L? A. His anion gap of 14 indicates metabolic acidosis
? B. His anion gap of 20 conclusive of respiratory acidosis
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? C. His anion gap of 22 strongly suggestive of metabolic
alkalosis
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? D. His anion gap of 21 indicative of high anion gapmetabolic acidosis
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MCQ2? A 48 year old man with bronchiectasis presents to the
hospital emergency room with 3 days of increasing
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cough, sputum and dyspnea.About 1 month ago his
blood analysis report showed pH 7,38, paO2 55 mmHg,
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HCO3- 32 meq/L. His current vital signs are BP117/65,pulse 123/min, temp 100oF,. His current ABG in the
emergency room pH 7.28, paCO2 70 mmHg, paO2 50 ,
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HCO3- 23 meq/L. Which of the following best
characterizes the acid base status of this patient?
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? A. Compensated metabolic acidosis? B. Compensated metabolic alkalosis
? C. Uncompensated metabolic acidosis
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? D. Uncompensated respiratory acidosis
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MCQ3? A 50 year old chronic alcoholics brought to the
emergency room in semiconscious state. BP was
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100/50 and Heart rate 120/min, Resp rate 35/min,
temp 104oFBlood chemistry: Na+= 150 meq/L, K+2.5
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meq/L, Cl- 107 meq/L, HCO3- 10 meq/L, pH 7.2,pCO2=25 mmHg, Alcohol 40 mmol/L (0), Osmolality 370
mOsm/L (280-295), glucose 50 mg/dl, BUN 50 mg/dl
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(5-22)What is the acid base status?
? A. Metabolic acidosis
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? B. Metabolic acidosis with resp compensation? C. Metabolic alkalosis
? D. Metabolic alkalosis with resp comp
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MCQ4
? Which of the following is most appropriate for a
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17 year old female suffering from IDDM with the
following blood chemistry report:
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? pH 7.2, pO2 108 mmHg, pCo2 12 mmHg, HCO3- 5meq/L
? A. Metabolic acidosis with resp compensation
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? B . Metabolic alkalosis with respiratory
compensation
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? C. Metabolic acidosis? D. Metabolic alakalosis
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