acid base disorders

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

THANK YOU