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Disturbance Of Acid-Base Disturbance Of Acid-Base RegulationRegulation

Dr. MatongjunDr. Matongjun

Emergency Department of Emergency Department of Tianjin General HospitalTianjin General Hospital

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ABGABG

pHpH 7.35 – 7.457.35 – 7.45PPCO2CO2 35 – 45 mmHg35 – 45 mmHg

PPO2O2 75 – 100 mmHg75 – 100 mmHg

HCOHCO33-- 22 – 26 mmol/L22 – 26 mmol/L

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Acid-base homeostasisAcid-base homeostasis

Buffer systemCarbonic acid / Bicarbonate

Organ regulationLungs

Characteristic: Sensitive, quickly, but tired easily so can not continue long term

KidneysCharacteristic: powerful but slower (hours

to days)

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pH=pKa+lgpH=pKa+lg [HCO[HCO33－－ ]]

[H[H22COCO33]]

Henderson-Hasselbalch equationHenderson-Hasselbalch equation

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CategoryCategory

SABDpH: acidosis, alkalosisEtiology: respiratory, metabolic

MABDTwo or three SABD are taking place

simultaneously

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Metabolic AcidosisMetabolic Acidosis

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DefinitionDefinition

HCO3－ ↓ , H+↑

pH HCO3- * compensation process

PCO2 *

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manifestationmanifestation

Kussmaul’s respirationNausea ， vomiting and abdominal painTachycardia, cardiac output decrease and

hypotensionHeadache, weakness, lethargy and confusi

on, the level of consciousness is depressed, the deep tendon reflex decrease.

Alter plasma potassium and Calcium concentration

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CategoryCategory

Increased anion gap and normal anion gap Anion Gap

[Na+] - ( [Cl-] + [HCO3-] )

Normal range 8~16 mmol/Lunmeasured anions, consist of proteins

(primarily albumin), sulfates, phosphates, and organic acids

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Anion GapAnion Gap

All anions and cations in Serum

ANIONS CATIONS

Chloride 104 Sodium 140

Bicarbonate 24 Calcium 5

Proteins 15 Potassium 4.5

Organic acids 5 Magnesium 1.5

Phosphates 2

Sulfates 1

TOTAL 151 TOTAL 151

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CategoryCategory

Increased AGHCO3

- decreases and replaced by other anions

Normal AG (hyperchloremic) HCO3

- decreases and replaced by Cl-

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Elevated AG Metabolic AcidosisElevated AG Metabolic Acidosis

Etiology

K Diabetic ketoacidosis

U Uremia

S Salicylate intoxication

S Starvation ketosis

M Methanol ingestion

A Alcoholic lactic acidosis

U Unmeasured osmoles, Ethylene glycol, Aldehydes, Paraldehydes

L Lactic acidosis

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increased serum chloride concentrationsgenerally due to gastrointestinal or renal bicarbonate wastingIngestion of chloride salts or chloride-containing anion exchange resins

Normal AG Metabolic AcidosisNormal AG Metabolic Acidosis

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TreatmentTreatmentRemove the Causealkali therapy

Benefit: decrease the risk of cardiovascular compromise

Risk: 5%NaHCO3 is hyperosmotic, hypernatremia, hypercapnia, cerebrospinal fluid acidosis, and overshoot alkalosis

Indication: renal failure; arterial blood pH below 7.20 or HCO3

- concentration below 10 mmol/L

Goal: Maintain the blood pH >7.20 and plasma HCO3

- concentration > 10 mmol/L

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Metabolic AlkalosisMetabolic Alkalosis

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definitiondefinition

plasma HCO3－ concentration >27 mmolL

arterial blood pH>7.40Compensation

PaCO2↑

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EtiologyEtiology

loss of acid from GI tract or urine, loss fluid with a chloride HCO3

- concentration ratio that is higher than plasma loss of gastric contents, Vomiting or nasoga

stric suctioning. Diuretics (Cl lost )Hyperaldosteronism (H+ and Cl- lost )

alkaline drugs ingestionAntacid overuse (HCO3

-)Blood transfusions (citrate )

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DiagnosisDiagnosis

History Symptoms

Irritability and Possible tetany, tingling , facial twitching, muscle tremors

volume depletion ： weakness, postural dizziness hypokalemia ： muscle weakness, paresthesias

physical examinationrespiratory rateBP(hypertension+Hypokalemia+metabolic alkalosis

suggest primary mineralocorticoid-induced disease)

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TreatmentTreatment

stopping the intake of soda bicarbonate Saline-responsive

Correct volume deficits potassium supplementation ： 4.5-5.5 mmol/LH2R antagonists ： ranitidine, cimetidine, diminish

H+ secretion; pump inhibiter, Omeprarole Saline-unresponsive

remove the mineralocorticoid source or block with spironolactone

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Respiratory AcidosisRespiratory Acidosis

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DefinitionDefinition

Lungs fail to eliminate CO2 so PaCO2 is elevated

Compensation HCO3

－↑

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EtiologyEtiology

inhibition of the respiratory center: head trauma, Neurological disorders, anesthesia

disorders of respiratory muscle: Chest traumaupper airway obstructiondisorders affecting gas exchange across

pulmonary capillaries: COPD, pneumonia, acute or chronic respiratory failure , cardiac arrest

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Signs and SymptomsSigns and Symptoms

respiratory distress, dyspnea level of consciousness If severe, patients may complain of headaches o

r show signs of increased intracranial pressure due to the vasodilatory properties of C02 , increase

cerebral blood flow

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Pathophysiology Pathophysiology

Acute Compensation l mmol/L increase in HCO3

- for each 10mmHg in PCO2

The HCO3- rarely rises above 30mmol/L

Chronic CompensationOver the next 2-3 dthe kidneys increase H+ secretion leading to an

elevation of serum HCO3- by 3~4mmol/L for each

10mmHg increase in PaCO2

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Treatment Treatment

improving ventilationHCO3

- should not be given

Oxygen should also be used with careDiet: Low carbohydrate, high fat

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Respiratory Respiratory Alkalosis Alkalosis

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Definition Definition

decrease in blood PaCO2

compensatory decrease in HCO3－ .

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Causes of Respiratory AlkalosisCauses of Respiratory Alkalosis

Increased CNS drive for respirationAnxietyCNS infection/infarction/traumaDrugs - salicylates/nicotine/aminophyllineFever/sepsis - especially Gram-negative sepsisPregnancy/progesteroneAnemia, Pulmonary edema/pneumonia , Pulmonary emb

oliCarbon monoxide toxicityReduced inspired 02 tension - high altitude

Increased mechanical ventilation

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Signs and SymptomsSigns and Symptoms

hyperventilation: rapid, deep respirations perioral and extremity paresthesias, muscle cra

mps, seizures cardiac arrhythmias K+, Ca+

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Pathophysiology Pathophysiology

Acute Compensation extra-and intra-cellular buffering ， l~2mmol/L fal

l in HCO3－ for every 10mmHg decrease in PaCO2

The HCO3- rarely goes below 18mmol/L.

Chronic Compensationkidneys decrease the secretion of H+ ， serum HC

O3－ decreases 4~5mmol/L for every 10mmHg decr

ease in PaCO2.

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Treatment Treatment

correcting the underlying disorder In ICU, hypoxemia and improper ventilatory settin

gs are the most common causeRebreathing in a paper bag can help the patient wit

h psychogenic hyperventilation

Treatment of the alkalosis is usually not necessary

Antianxiety medications, diazepam

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DiagnosisDiagnosis

The proper evaluation of patients The proper evaluation of patients with suspected acid-base disorders with suspected acid-base disorders requires consideration ofrequires consideration of

The clinical pictureThe clinical pictureBlood Gas ResultsBlood Gas ResultsSerum electrolytesSerum electrolytes

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Diagnosis Diagnosis metabolic or respiratory

determined by the primary change, in HCO3- or

PCO2

acute or chronicAn acute process is measured in minutes to hoursa chronic process is measured in days to weeks or

longer simple or mixed

The primary change of simple disorder is in only one parameter

The primary change of mixed disorder is in both

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ABGABG

The simplest approach to the evaluation of blood gases is to consider pH. Pco2 and HCO3

- separately and then combine the information

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ABG InterpretationABG Interpretation

Identify whether pH, pCO2, and HCO3 are abnormal

pH 7.30

pCO2 55

HCO3 26 Match like disorders

pH and pCO2 are both

the two matching values tell what the problem is – Acidosis or Alkalosis

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ABG InterpretationABG Interpretation

3. Determine if abnormality is due to the kidneys (metabolic ) or the lungs (respiratory)

pH 7.30

pCO2 55

HCO3 26

Match the like abnormalities

Respiratory (lung problem) and Acidosis

= Respiratory Acidosis

Acid

Acid = LUNGS

Normal = Kidneys

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MABDMABD

The compensation can be expected. If the compensation is outside the expected range, it is a MABD

Two methods to diagnose MABDMethod I A rigorous method which involves calcula

tion of the expected compensationsMethod II   Look on a nomogramIf Pco2 and HCO3

- change in opposite direction   consider a MABD

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Method I Method I

Metabolic Acidosis: Expected pCO2 = 1.5 x [HCO3

-] + 8 ± 2

Alkalosis: Expected pCO2=↑6 mmHg per 10 mEq/L  ↑ in HCO3

-

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Method IMethod I Respiratory

Acidosis Acute Expected  ↑HCO3

- = ↑ 1mEq/L for each 10 mm  ↑PCO2

Chronic: Expected  ↑HCO3- = ↑ 3.5mEq/L for ea

ch 10 mmHg  PCO2

Alkalosis Acute Expected↓HCO3

- = ↓2mEq/L for each 10 mm Hg  ↓PCO2

Chronic Expected  ↓HCO3- = ↓5 mEq/L for each

10 mmHg ↓ PCO2

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ExampleExample 11

pH=7.08, pCO2=14, HCO3-=4, Na=140, Cl=104

The pH is low indicating the primary disorder is acidosis.

The anion gap is 140 - (104 + 4) = 32, thus elevatedThe pCO2 is low, the expected compensation

The predicted pCO2 by the above equation is 1.5×4+8 = 14 ， This is the observed pCO2

simple increased anion gap metabolic acidosis

pH=7.08, pCO2=14, HCO3-=4, Na=140, Cl=124 ？

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Example 2Example 2

pH 7.37, pCO2=18, HCO3-=10, Na=140,

Cl=114 the pH to be normalThe anion gap is 16, thus increasedExpected pCO2 is 1.5×10+8 = 23 (21 at

minimum), there must be an element of respiratory alkalosis

a combination of increased anion gap metabolic acidosis and a respiratory acidosis

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ExampleExample 3 3

In a patient with severe COPD, and who is diuretics, the pH=7.42, pCO2 = 65, HCO3

-=41, Na 143, K 3.1, Cl 88

Start with a metabolic alkalosis, why? pCO2 should be 50.2 mmHg

6 mmHg CO2 for each 10 mEq/L HCO3- ， 41-2

4 = 17; 1.7×6 + 40 = 50.2 mmHg

pCO2 is measured at 65, there is a respiratory acidosis

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Thank youThank you