The document discusses metabolic acidosis, defining it as a primary decrease in bicarbonate with a compensatory decrease in PCO2. It notes the causes can include GI or renal bicarbonate loss, lactic acidosis, ketoacidosis from diabetes or alcohol, intoxication from ethylene glycol or methanol, and advanced renal failure. Metabolic acidosis is classified as having a normal or high anion gap, with high anion gap causes including ketoacidosis, lactic acidosis, and certain intoxications.
Concepts of acid base balance and its disorders are very important for practice of medicine.It is for the benefit of medical and students of allied fields.
Biochemical mechanismsof acid base balance and acid base disordersrohini sane
A comprehensive presentation on Biochemical Mechanisms of Acid-Base Balance and Acid Base disorders for undergraduate medical, dental, biotechnology and pharmacology students for self –learning. pH maintained in tissues under physiological conditions are mentioned.
Basic concepts of buffers & their types (Acidic buffer & alkaline) are illustrated. Mechanisms of action of Buffer system for acid base balance is explained for perusal of students. Acids produced in a human body during metabolisms are listed.
Front line defense, second line defense (kidney) and dilution factor in regulation of pH in human body for acid-base balance are presented.
Blood buffers involved in acid base balance are classified. Ratio involved, Advantages and Disadvantages of Bicarbonate Buffer / Phosphate buffer system in acid base balance elaborated for their clinical applications.
Comparison of Buffering action of hemoglobin verses plasma proteins is presented under Protein buffer system. Mechanism of Buffering action of plasma proteins in Acidic and alkaline conditions is explained. Working of Hemoglobin buffer system in lung and tissue is illustrated.
Mechanisms involving hypo ventilation and hyperventilation of respiratory system in acid base balance is presented. Importance of Imidazole group of Histidine of hemoglobin in maintaining blood pH is explained
Role Renal Mechanism during acidosis and alkalosis using Bicarbonate mechanism, Phosphate mechanism, Ammonia mechanism, HCO³⁻ reabsorption and NH ₃ production is simplified. pCO₂, Concentration of K⁺ in ICF (intracellular fluid). Plasma Concentration of Cl⁻ ions and Concentration of adrenal-corticoids Hormones as factors affecting bicarbonate re absorption in proximal renal tubular cells are explained in lucid manner.
Phosphate buffer mechanism (Distal tubular cells) for acid base balance is illustrated.
Importance of Anion Gap in detection of metabolic acidosis & alkalosis presented. Anion Gap in Metabolic acidosis (acid accumulation and bicarbonate ion loss) is elucidated. Urinary anion gap as indicator of effective renal acid secretion during acidosis is explained diagrammatically. Clinical Conditions associated with increase and decrease in Anion Gap are listed. Comparison of Anion Gap between Metabolic acidosis And Metabolic alkalosis is explained diagrammatically.
Importance of Glutaminase, Glutaminase, L- amino acid oxidase, and Glycine oxidase in Ammonia mechanism in kidney-Distal tubular cells for acid base balance is presented.
Comparison of Definition, Ratio, Biochemical findings in Uncompensated and Compensatory phase of between different types of acidosis & alkalosis is done for their laboratory diagnosis. Clinical conditions associated in different types of acidosis & alkalosis are listed. Google images are used to convey the concept of the subject to self-learners.
ABGs or VBGs interpretation made simple straight forward easy to remember and easy to apply. The presentation is designed to help the residents and junior ER physicians. The second part will discuss the oxygenation and the third part will review the "Stewart Approach" while fourth and last part is meant for the Experts.
Concepts of acid base balance and its disorders are very important for practice of medicine.It is for the benefit of medical and students of allied fields.
Biochemical mechanismsof acid base balance and acid base disordersrohini sane
A comprehensive presentation on Biochemical Mechanisms of Acid-Base Balance and Acid Base disorders for undergraduate medical, dental, biotechnology and pharmacology students for self –learning. pH maintained in tissues under physiological conditions are mentioned.
Basic concepts of buffers & their types (Acidic buffer & alkaline) are illustrated. Mechanisms of action of Buffer system for acid base balance is explained for perusal of students. Acids produced in a human body during metabolisms are listed.
Front line defense, second line defense (kidney) and dilution factor in regulation of pH in human body for acid-base balance are presented.
Blood buffers involved in acid base balance are classified. Ratio involved, Advantages and Disadvantages of Bicarbonate Buffer / Phosphate buffer system in acid base balance elaborated for their clinical applications.
Comparison of Buffering action of hemoglobin verses plasma proteins is presented under Protein buffer system. Mechanism of Buffering action of plasma proteins in Acidic and alkaline conditions is explained. Working of Hemoglobin buffer system in lung and tissue is illustrated.
Mechanisms involving hypo ventilation and hyperventilation of respiratory system in acid base balance is presented. Importance of Imidazole group of Histidine of hemoglobin in maintaining blood pH is explained
Role Renal Mechanism during acidosis and alkalosis using Bicarbonate mechanism, Phosphate mechanism, Ammonia mechanism, HCO³⁻ reabsorption and NH ₃ production is simplified. pCO₂, Concentration of K⁺ in ICF (intracellular fluid). Plasma Concentration of Cl⁻ ions and Concentration of adrenal-corticoids Hormones as factors affecting bicarbonate re absorption in proximal renal tubular cells are explained in lucid manner.
Phosphate buffer mechanism (Distal tubular cells) for acid base balance is illustrated.
Importance of Anion Gap in detection of metabolic acidosis & alkalosis presented. Anion Gap in Metabolic acidosis (acid accumulation and bicarbonate ion loss) is elucidated. Urinary anion gap as indicator of effective renal acid secretion during acidosis is explained diagrammatically. Clinical Conditions associated with increase and decrease in Anion Gap are listed. Comparison of Anion Gap between Metabolic acidosis And Metabolic alkalosis is explained diagrammatically.
Importance of Glutaminase, Glutaminase, L- amino acid oxidase, and Glycine oxidase in Ammonia mechanism in kidney-Distal tubular cells for acid base balance is presented.
Comparison of Definition, Ratio, Biochemical findings in Uncompensated and Compensatory phase of between different types of acidosis & alkalosis is done for their laboratory diagnosis. Clinical conditions associated in different types of acidosis & alkalosis are listed. Google images are used to convey the concept of the subject to self-learners.
ABGs or VBGs interpretation made simple straight forward easy to remember and easy to apply. The presentation is designed to help the residents and junior ER physicians. The second part will discuss the oxygenation and the third part will review the "Stewart Approach" while fourth and last part is meant for the Experts.
Presentation by Dr. Mishal Saleem on Topic: Step wise approach to abgs interpretation.
Use of delta ratio and delta gap
Use of Anion Gap
Use of Urinary anion gap
Hypernatremia and hyponatremia for medical students, tonicity, volume and water disorders including syndrome of inappropriate ADH secretion and diabetes insipidus.
4. Definitions
Acid: a substance that may donate protons
(hydrogen ions)
Base: a substance that may receive protons
pH: the negative logarithm of protons
concentration
Strong acids vs. weak acids
Volatile (Co2) vs. nonvolatile acids
Buffers
16. APPROACH TO THE DIAGNOSIS
OF ACID-BASE DISORDERS
Suspicious clinical or lab findings
Identify the major Acid-base disorder
Determine if it is simple or mixed
Establish the cause of the disorder
Direct treatment to the underlying cause unless
the pH is in a dangerous range
(7.10 < or > 7.60)
21. FREQUENCY OF SIMPLE ACID-
BASE DISORDERS
Metabolic
Acidosis 10%
Alkalosis 40%
Respiratory
Acidosis 20%
Alkalosis 20%
22. Consequences of acidosis vs. alkalosis
Impaired cardiac
contractility
Arteriolar dilation
Venoconstriction
Centralization of blood
volume
Increased pulmonary Arteriolar constriction
vascular resistance Reduced coronary blood flow
Cardiovascular Decreased cardiac output Reduced anginal threshold
Decreased systemic BP Decreased threshold for
Decreased hepatorenal cardiac arrhythmias
blood flow
Decreased threshold for
cardiac arrhythmias
Attenuation of
responsiveness to
catecholamines
23. Insulin resistance Stimulation of anaerobic
Inhibition of anaerobic glycolysis
glycolysis Formation of organic acids
Reduction in ATP Decreased oxyhemoglobin
Metabolic synthesis dissociation
Hyperkalemia Decreased ionized Ca
Protein degradation Hypokalemia
Bone demineralization Hypomagnesemia
(chronic) Hypophosphatemia
Tetany
Inhibition of metabolism
Seizures
and cell-volume
Neurologic Lethargy
regulation
Delirium
Obtundation and coma
Stupor
Compensatory
Compensatory
hyperventilation with
Respiratory hypoventilation with
possible respiratory
hypercapnia and hypoxemia
muscle fatigue
24. RESPONSE TO SIMPLE
ACID-BASE DISORDERS
Disturbance Equation Interval Level
Met. Ac. 1 = 1.2 12-24 hr 10
Met. Al. 1 = 0.7 24-36 hr 55
Ac. Resp. Ac. 1 = 0.1 5-10 min 43
Ch. Resp. Ac. 1 = 0.3 72-120 hr 45
Ac. Resp. Al. 1 = 0.2 5-10 min 18
Ch. Resp. Al. 1 = 0.4 48-72 hr 13
29. Or
In metabolic disorders add 15 to HCO3:
Example: if HCO3=10 + 15 = 25 then the PCO2
should be 25, and the last two digits of pH 25
pH=7.25
HCO3=10
PCO2=25
30. Normal Anion Gap
AG = Na – (HCO3+Cl) = 8-12
A-10
HCO3- PaCO2 40
25 pH 7.40
Na
140 CL
105
31. METABOLIC ACIDOSIS
AG = 10 AG = 10
AG = 25
HCO3 =15
HCO3 =25
HCO3 =10
- HCO3 - HCO3
CL- =115
+ CL- CL- =105 + A- CL- =105
HYPERCHLOREMIC NORMAL HIGH AG
32.
33. THE SERUM ANION GAP
AG = Na+ - (HCO3- + CL-), NL = 10 ± 2
AG ≥ 27 INDICATE ORGANIC MET. AC.
AG + HCO3 ≥ 42 INDICATE MET. AL.
AG DECREASED WITH PARAPROTEIN
AG DECREASED WITH LOW ALBUMIN
34. Increased anion gap
metabolic acidosis
ketones, lactate, sulfates, or metabolites of methanol,
ethylene glycol, and salicylate
hyperalbuminemia and uremia (increased
anions)
hypocalcemia or hypomagnesemia (decreased
cations)
35. The effect of low albumin can be
accounted for by adjusting the
normal range for the anion gap
2.5 mEq/L for every 1 g/dL fall in
albumin.
37. ACID-BASE DISORDERS
EXAMPLE OF A SIMPLE DISORDER
pH (7.55) = C * [HCO3-] (18 mmol/L)
PCO2 (21 mm Hg)
Step 1: pH , indicates alkalemia (Met. or Resp)
Step 2: HCO3- , indicates Resp. Alkalosis
Step 3: PCO2 , confirms Resp. Alkalosis
38. The delta gap
The difference between the patient's anion gap
and the normal anion gap is termed the delta gap
considered an HCO3 − equivalent, because for
every unit Rise in the anion gap, the
HCO3 − should lower by 1
The delta gap is added to the measured HCO3 − , the
result should be in the normal range for HCO3 −;
elevation indicates the additional presence of a
metabolic alkalosis
39. ACID-BASE DISORDERS
EXAMPLE OF A MIXED DISORDER
pH (7.55) = C * [HCO3-] (30 mmol/L)
PCO2 (35 mm Hg)
Step 1: Alkalemia
Step 2: HCO3- , indicates Met. alkalosis
Step 3: PCO2 , indicates Resp. alkalosis
Step 4: ∆ HCO3- (25%) > ∆ PCO2 (12.5%)
Step 5: The major disorder is metabolic alkalosis
43. MIXED ACID-BASE DISORDERS
EXAMPLE OF TRIPLE DISORDER
Health NG + Sepsis + Endotox.
pH 7.40 7.49 7.14 7.44
PCO2 40 44 24 12
HCO3 24 32 8 8
AG 9 11 33 35
∆ AG 0 2 24 26
44. Masked disorder
A vomiting, ill-appearing diabetic patient has
laboratory results showing:
Na, 137; K, 3.8; Cl, 90; HCO3 −, 22;
pH, 7.40; Pco2, 41; Po2, 85
anion gap = 137 − (90 + 22) = 25 (normal :10)
Respiratory compensation is evaluated by Winter's formula
Predicted Pco2 = 1.5 (22) + 8 ± 2 = 41 ± 2
delta gap = 15 + 22 = 37
45.
46. Normal ABG?
A diabetic patient presented with gastroentritis
found to have:
pH: 7.4
HCO3: 24
PCO2: 40
Na: 144, K: 4, CL: 95, TCO2: 24, RBS: 520,
Positive test for ketons
What is the acid-base status of this patient?
48. METABOLIC ACIDOSIS
P R IM A R Y : D E C R E A S D H C O 3
RESPO NSE: D EC RESED PC O 2
C AU SES
NO RM A L A G H IG H A G
1 0 m E q /L > 1 5 m E q /L
G I HC O 3 LO SS K E T O A C ID O S ID
RENA L HC O 3 LO SS L A C T IC A C ID O S IS
H Y P O A L D O S T E R O N IS M R E N A L F A IL U R E
TPN IN T O X IC A T IO N
53. METABOLIC ACIDOSIS
KETOACIDOSIS
Diabetes 1 (Insulin lack) leads to fatty acids
oxidation and production of acetoacetate (2) and
B-OH-butyrate (5), which is buffered by HCO 3-,
causing high AG
ETOH (altered cell metabolism)
Starvation (use of fatty acids), usually mild
54. METABOLIC ACIDOSIS
LACTIC ACIDOSIS (Dx by exclusion)
Type A: O2 delivery to cells is inadequate
Shock, mesenteric vascular events, and pulmonary
edema)
Type B: Cells cannot use O2
Hepatic failure, sepsis, acute pancreatitis
Anaerobic glycolysis of glucose to pyruvate and
then lactate (buffered by HCO3-)
55. METABOLIC ACIDOSIS
RENAL FAILURE:
Unable to excrete the daily acid load
Bone buffers keep HCO3-> 15 in CRF
In ARF HCO3- falls by 0.5 mmol/L/day
Retention of sulfate, phosphate, and organic
anions causes the increase in AG
56. METABOLIC ACIDOSIS
NORMAL ANION GAP
GI HCO3- LOSS (Diarrhea, fistula)
RENAL HCO3- LOSS
RTA (Proximal, Distal, Hyperkalemic)
Acetazolamide, hypoaldostironism
Miscellaneous
NH4Cl ingestion, Sulfur ingestion
Pronounced dilution
57.
58. METABOLIC ACIDOSIS
GI. BICARBONATE LOSS
NORMAL AG, HYPERCHLOREMIC
CAUSES
DIARRHEA
EXTERNAL FISTULA
URETEROSIGMOIDOSTOMY OR ILEAL LOOP
CONDUIT
59. METABOLIC ACIDOSIS
RENAL BICARBONATE LOSS
TYPE I RTA (DISTAL, CLASSICAL)
PROTON SECRETION DEFECT
TYPE II RTA (PROXIMAL, FANCONOI)
BICARBONATE REABSORPTION DEFECT
TYPE IV RTA (HYPERKALEMIC)
HYPORENINEMIC HYPOALDOSTERONISM
60.
61.
62.
63.
64. METABOLIC ACIDOSIS
URINARY ANION GAP
UAG = (Na+ + K+) - Cl-
UAG is an estimate of urinary ammonium
Elevated in GI HCO3- loss
Low in distal RTA
UAG: NEGATIVE -20 mEq/L IN GI LOSS
UAG: POSITIVE + 23 mEq/L IN RTA
69. METABOLIC ALKALOSIS
P r im a r y : IN C R E A S E D H C O 3
R E S P O N S E : IN C R E A S E D P C O 2
A p p r o p r ia te r e s p o n s e ?
P C O 2 = 0 .7 H C O 3
U R IN A R Y C H L O R ID E
< 2 0 m E q /L > 2 0 m E q /L
N o rm a l E C V D e c re a s e d E C V N o rm a l E C V D e c re a s e d E C V
A lk a li lo a d G I lo s s E xcess B a r tte r 's
D iu r e tic s M in e r a lo c o r tic o id s H y p o k a le m ia
79. RESPIRATORY ACIDOSIS
P r i m a r y : IN C R E A S E D P C O 2
R E S P O N S E : IN C R E A S E D H C O 3
A p p ro p ria te re s p o n s e ?
A c u te : H C O 3 (1 ) = P C O 2 (1 0 )
C h ro n ic : H C O 3 (3 ) = P C O 2 (1 0 )
CAUSES
P u lm o n a ry N e u ro m u s c u la r
P n e u m o th o ra x COPD C N S d e p re s s a n t P rim a ry h y p o v e n tila tio n
P n e u m o n ia P u lm o n a ry fib ro s is B ra in s te m le s io n s P o lio m y e litis
P u lm o n a r y e m b o lu s S p in a l c o rd le s io n s
P u lm o n a r y e d e m a
81. RESPIRATORY ALKALOSIS
P rim a ry : D E C R E A S E D P C O 2
RESPONSE: DECREASED HCO3
A p p ro p ria te re s p o n s e ?
A c u te : H C O 3 (2 ) = P C O 2 (1 0 )
C h ro n ic : H C O 3 (4 ) = P C O 2 (1 0 )
CAUSES
P E R IP H E R A L CENTRAL
ACUTE C H R O N IC ACUTE C H R O N IC
P n e u m o n ia P u lm o n a ry fib ro s is S a lic y la te o v e rd o s e B ra in tu m o r
P u lm o n a ry e m b o lu s CHF P a in P re g n a n c y
S e p s is C irrh o s is A n x ie ty P a in