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learning basic concept of acid-base disorder for clinical purposes
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ACID-BASE DISORDERS
By: Leonardo Paskah S, MDCardiology & Vascular Medicine of Universitas Padjadjaran
Bandung-Indonesia
INTRODUCTION
• Blood [H+] is only 0.00004 mEq/L & tightly controlled• [H+] is common represented in pH
pH = -log10 [H+]2
Acid substances
Base substances
solution
BUFFER
Playing a key role in regulation of acid-base in the body
Balancing
H+
H+
H+
ACIDOSIS
ALKALOSIS
Normal pH in body fluidBody fluid pH
ECF:-Arterial blood- venous blood- interstitial
7.407.357.35
ICF 6.0-7.40
Urine 4.5-8.0
Gastric juice 0.8
PHYSIOLOGY
Carbohydrate & lipid metabolism
-protein metabolism- internal pathologic process- external pathologic process
rapid
more gradual
REGULATION MECHANISMS1. CHEMICAL BUFFER SYSTEM rapid action, but less effective in severe or chronic cases converting strong acid/ base to weak acid/base there are 3 kinds:
- bicarbonate systems the strongest & most useful in ECF - phosphate - protein
2. VENTILATION (LUNGS) limited capability; only eliminates volatile acid by changing the depth or/and rate of respiration;
3. RENAL more gradual but can lead to total recovery in metabolic disorders by regulating excretion of H+ and excretion/ reabsorption HCO3-
Regulation of respirationCentral chemoreceptors
Peripheral chemoreceptors: carotid and aorta sensitive to ∆ pO2, pCO2, pH
Acid (ammonium) excretion by renal
Henderson-Hasselbalch equation
[H+] = (7.80-pH)x100 mEq/L[H+] in normal pH 7.40 = 40 mEq/L
Respiration Renal
ACIDOSIS or ALKALOSIS
pH correction
Respiratory system CO2 regulation
Kidney HCO3 regulation
Compensation mechanisms
Acid-base nomogram and compensation response
Lang F. Respiration, acid-base balance. In: Silbernagl S, Lang F, editors. Color Atlas of Pathophysiology. NY: Thieme;2000.
Predicted compensation response
Note: Renal and respiration compensation are in the same direction
Disorders For every.. Predicted response
Metabolic acidosis
1↓ HCO3 1↓ HCO3
Metabolic alkalosis
10↑ HCO3 7↑ p CO2
Acute respiratory acidosis
10↑ pCO2 1↑ HCO3
Chronic respiratory acidosis
10↑ pCO2 4↑ HCO3
Acute respiratory alkalosis
10↓ pCO2 2↓ HCO3
Chronic respiratory alkalosis
10↓ pCO2 5↓ HCO3
Blood Gases Analysis (BGA) test
Interpretation of BGA
pH correlated to [H+] acid-base degree
pCO2 Oxygen partial pressure in blood; normal 80-100 mmHg
SaO2 Arterial oxygen saturation; normal 95-100%
pCO2 CO2 partial pressure in blood; normal 35-45 mmHg
HCO3- Bicarbonate in circulation (calculated); normal 22-26 mEq/L
Base Excess (BE)
Deficit or excess of bicarbonate in blood; normal -2 to +2 mEq/L
Oxygenation status Acid-base status
Parameters in BGA test
Parameters for analysis of acid-base disorders
Methods of interpretation
Nomogram of acid-base disorders
Stewart’s SID• Dependent variables: [H+], [OH-], [HCO3-],
[CO3 2-], [HA], [A-]• Independent variables: pCO2, [A-tot], [SID]
– [SID]= [Na]+[K]+[Ca]+[Mg] – [Cl] – [other strong anions]
normal = 40 mEq/L similar numerical value as BE
– [A-tot]= [Pi-tot] + [Pro-tot] + albumin– [CO2] = pCO2 in blood
• Limitation:– Complexity of the chemistry & mathematics– Lack of clinical correlation– SID neglects Hb as a buffer less accurate than BE
www.acid-base.com/strongion.php
Interpretation of Handerson Hasselbalch approach
STEP 1 Re-check the data [H+]=24 x pCO2 / [HCO3-][H+] mEq/L= (7.80-pH)x100
STEP 2 Acidemia (pH <7.37) or alkalemia (pH >7.42) ?
STEP 3 Determining the primary disorder; metabolic or respiratory ? look any ∆ pCO2 and HCO3-
STEP 4 Determining compensatory mechanisms expected or excessive deviation ?
STEP 5 (for metab acidosis)
Anion Gap= [Na]- ( [Cl] + [HCO3])…...... n<12Hypoalbuminemia AGc= AG + (2.5x ∆ albumin)
STEP 6(for AG > 12)
Delta/delta = ∆AG/∆HCO3 = (AG-12)/(24-HCO3)Delta/delta > 1 = metab acidosis + alkalosisDelta/delta < 1 = metab.acidosis gap + non-gap
1. METABOLIC ACIDOSIS
Type of metabolic acidosis
GAP metab. acidosis
• Exogenous: salicylate intoxication, methanol, alcoholic ketoacidosis
• Endogenous: lactic acidosis, diabetic ketoacidosis, starvation, uremia
NON-GAP metab.acidosis• Renal loss: renal
tubular acidosis, carboanhydrase inhibitor
• GI tract loss: diarrhea, fistule, ureterosigmoidostomy
Hyperchloremic acidosis
Alcoholic intoxication
Therapy of metabolic acidosis
• Correct underlying disease • Correct hydration state and electrolyte
imbalance• Bicarbonate controversial - Indicated for severe acidosis (pH <
7.20), esp. GAP metabolic acidosis- total needed (mEq)= Base deficit x BW(kg)/4 ½ doses is given within first 8 h
• Chronic non-severe acidosis: bicarbonate oral for [HCO3-] <18 mmol/L + clinical symptoms
2. METABOLIC ALKALOSIS
Type and therapy of metabolic alkalosis
Chloride-sensitive Chloride-insensitive * [Cl-] urine < 10 mEq/L * prolonged Cl (and H+) loss via urine/GI tract Na and HCO3 retention by renal * GI tract loss: vomit, NGT suction, diarrhrea * renal loss: diuretic * response to NaCl therapy
• [Cl-] > 10 mEq/L• direct stimulation to renal • causa: hyperaldosteronism, steroid therapy, alkali intake• not response to NaCl therapy; therapy focused on underlying cause (ex. stop consuming steroid)
Therapy with strong acid (HCl, NH4Cl) is only for severe alkalosis and resistant with standard therapy
3. RESPIRATORY ACIDOSIS
4. RESPIRATORY ALKALOSIS
5. MIXED ACID-BASE DISORDERS
CLUE: - compensatory response exceeds expected value - ∆ pH is not suitable to known primary disorder
- pCO2 and HCO3 move not in same direction
- pH normal but with abN pCO2 and HCO3
Metab acidosis + resp acidosis
Cardiac arrest, respiratory failure + renal failure
Metab acidosis + resp alkalosis
Salicylate intox., sepsis, advanced liver disease + lactic acidosis
Metab alkalosis + resp alkalosis
Hepatic cirrhosis + vomit/diuretic overuse, pregnancy + hyperemesis, overventilation in COPD
Metab alkalosis + resp acidosis
COPD with diuretic overuse/ vomit
Metab acidosis + metab alkalosis
Uremia/ ketoacidosis + vomit
Triple disorders Ketoacidosis + muntah + liver disease + sepsis
REFERENCES
1. Guyton AC, Hall JE. Textbook of Medical Physiology. 11th ed. Philadelphia: Elsevier Saunders; 20062. Costanzo LS. Physiology. 4th ed. Philadelphia: Elsevier Saunders; 20093. Ganong WF. Review of Medical Physiology. 22nd ed. US: McGraw-Hill; 2005 4. Hennessey IAM, Japp AG. Arterial Blood Gases Made Easy. Philadelphia: Churchill Livingstone; 20075. Al-Khadra E. Disorders of the Acid-Base Status. In: Kiessling SG, Goebel J, Somers MJG, editors. Pediatric Nephrology in the ICU. Berlin: Springer-Verlag;20096. Gomella LG, Haist SA. Clinician’s Pocket Reference. 10th ed. US: McGraw-Hill; 20047. West JB. Respiratory Physiology: The Essentials. 7th ed. Philadelphia: Lippincott Williams & Wilkins; 20058. Interpretation of the Arterial Blood Gas. Orlando Health, Education & Development. 20109. Fehr T, Wuethrich RP. Water, electrolyte, and acid-base disorders. In: Siegenthaler W, editor. Differential Diagnosis in Internal Medicine. NY: Thieme; 2007.p916-2810. Grogono AW. Acid-Base Tutorial. www.acid-base.com. Tulane University Department of Anesthesiology.11. Seifter JL. Acid-base disorders. In:Goldman L, Ausiello D, editors. Cecil Medicine. 23rd ed. Philadelphia: Saunders Elsevier; 2007.Ch.11912. Kasper, Braunwald, Fauci, et al. Harrison’s Principles of Internal Medicine. 16th ed. Volume 1. NY: McGrawHill; 200513. Sue DY, Vintch JRE. Current Essentials of Critical Care. NY: McGraw-Hill; 2005.p65-7014. Lang F. Respiration, acid-base balance. In: Silbernagl S, Lang F, editors. Color Atlas of Pathophysiology. NY: Thieme;2000.p66-91
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