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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