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1 Mohammed A. Almeziny BPharm.RPh. Msc. PhD Clinical Pharmacist.
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Transcript of 1 Mohammed A. Almeziny BPharm.RPh. Msc. PhD Clinical Pharmacist.
ACID AND BASE BALANCE AND
IMBALANCE
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Mohammed A. Almeziny BPharm.RPh. Msc. PhD
Clinical Pharmacist
The Body and pH
Homeostasis of pH is tightly controlled Extracellular fluid = 7.4 Blood = 7.35 – 7.45 < 6.8 or > 8.0 death occurs Acidosis (acidemia) below 7.35 Alkalosis (alkalemia) above 7.45
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Small changes in pH can produce major disturbances
Most enzymes function only with narrow pH ranges
Acid-base balance can also affect electrolytes (Na+, K+, Cl-)
Can also affect hormones
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Small changes in pH can produce major disturbances cont’d Cardiovascular
(e.g., impaired contractility, arrhythmias), Pulmonary
(e.g., impaired oxygen delivery, respiratory muscle fatigue, dyspnea),
Renal (e.g., hypokalemia)
Neurologic (e.g., decreased cerebral blood flow, seizures,
coma).
The body produces more acids than bases
Acids take in with foods Acids produced by metabolism of lipids
and proteins Cellular metabolism produces CO2.
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Maintenance of BalanceBalance maintained by: Buffering systems
Lungs
Kidneys
H2CO3…..HCO3
1-Buffer systems Prevent major changes in pH Act as sponges… 3 main systems• Bicarbonate-carbonic acid buffer• Phosphate buffer• Protein buffer
H+
H+H+
Control of Acids
Bicarbonate buffer
Sodium Bicarbonate (NaHCO3) and carbonic acid (H2CO3)
Maintain a 20:1 ratio : HCO3- : H2CO3
HCl + NaHCO3 ↔ H2CO3 + NaCl
NaOH + H2CO3 ↔ NaHCO3 + H2O
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Phosphate buffer
Major intracellular buffer H+ + HPO4
2- ↔ H2PO4-
OH- + H2PO4- ↔ H2O + H2PO4
2-
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Protein Buffers
Includes hemoglobin, work in blood and ISF Carboxyl group gives up H+ Amino Group accepts H+
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2. Respiratory mechanisms
Exhalation of carbon dioxide respiratory control center in the medulla to
increase the rate and depth of ventilation. Peripheral chemoreceptors (located in the carotid
arteries and the aorta) activated by arterial acidosis, hypercarbia (elevated
PaCO2), and hypoxemia (decreased PaO2).
Central chemoreceptors (located in the medulla). activated by cerebrospinal fluid (CSF) acidosis and by
elevated carbon dioxide tension in the CSF
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2. Respiratory mechanisms Cont’d
Powerful, but only works with volatile acids
Doesn’t affect fixed acids like lactic acid CO2 + H20 ↔ H2CO3 ↔ H+ + HCO3
-
Body pH can be adjusted by changing rate and depth of breathing
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3. Kidney excretion
Can eliminate large amounts of acid Can also excrete base Can conserve and produce bicarb ions Most effective regulator of pH If kidneys fail, pH balance fails
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Rates of correction
Buffers function almost instantaneously Respiratory mechanisms take several
minutes to hours Renal mechanisms may take several
hours to days
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Acid-Base Imbalances
pH< 7.35 acidosis pH > 7.45 alkalosis The body response to acid-base
imbalance is called compensation May be complete if brought back within
normal limits Partial compensation if range is still
outside norms.
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Compensation
If underlying problem is metabolic, hyperventilation or hypoventilation can help : respiratory compensation.
If problem is respiratory, renal mechanisms can bring about metabolic compensation.
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Acidosis Principal effect of acidosis is depression of
the CNS through ↓ in synaptic transmission. Generalized weakness Deranged CNS function the greatest threat Severe acidosis causes
Disorientationcoma death
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Alkalosis Alkalosis causes over excitability of the
central and peripheral nervous systems. Numbness Lightheadedness It can cause :
Nervousness muscle spasms or tetany Convulsions Loss of consciousness Death
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Four Basic Types of Imbalance
Respiratory Acidosis Respiratory Alkalosis Metabolic Acidosis Metabolic Alkalosis
Respiratory Acidosis
Carbonic acid excess caused by blood levels of CO2 above 45 mm Hg.
Hypercapnia – high levels of CO2 in blood
Chronic conditions: Depression of respiratory center in brain that
controls breathing rate – drugs or head trauma
Paralysis of respiratory or chest muscles Emphysema
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Respiratory Acidosis cont’d
Acute conditons: Adult Respiratory Distress Syndrome Pulmonary edema Pneumothorax
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Compensation for Respiratory Acidosis
Kidneys eliminate hydrogen ion and retain bicarbonate ion
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Signs and Symptoms of Respiratory Acidosis
Breathlessness Restlessness Lethargy and disorientation Tremors, convulsions, coma Respiratory rate rapid, then gradually
depressed Skin warm and flushed due to
vasodilation caused by excess CO2
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Treatment of Respiratory Acidosis
Restore ventilation Treat underlying dysfunction or disease
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Respiratory Alkalosis
Carbonic acid deficit pCO2 less than 35 mm Hg (hypocapnea) Most common acid-base imbalance Primary cause is hyperventilation
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Respiratory Alkalosis cont’d
Conditions that stimulate respiratory center: Oxygen deficiency at high altitudes Pulmonary disease and Congestive heart
failure – caused by hypoxia Acute anxiety Fever, anemia Early salicylate intoxication Cirrhosis Gram-negative sepsis
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Compensation of Respiratory Alkalosis
Kidneys conserve hydrogen ion Excrete bicarbonate ion
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Treatment of Respiratory Alkalosis
Treat underlying cause Breathe into a paper bag IV Chloride containing solution – Cl- ions
replace lost bicarbonate ions
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Metabolic Acidosis
Bicarbonate deficit - blood concentrations of bicarb drop below 22mEq/L
Causes: Loss of bicarbonate through diarrhea or renal
dysfunction Accumulation of acids (lactic acid or ketones) Failure of kidneys to excrete H+
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Common Causes of Metabolic AcidosisNormal AG Hypokalemic
Diarrhea Fistulous disease Ureteral diversions Type 1 RTA Type 2 RTA Carbonic anhydrase
inhibitors Hyperkalemic
Hypoaldosteronism Hydrochloric acid or
precursor Type 4 RTA Potassium-sparing
diuretics Amiloride Spironolactone Triamterene
Elevated AG Renal Failure Lactic Acidosis (see
Table 10-5) Ketoacidosis
Starvation Ethanol Diabetes mellitus
Drug Intoxications Ethylene glycol Methanol
Salicylates
AG, anion gap; RTA, renal tubular acidosis.
Symptoms of Metabolic Acidosis
Headache, lethargy Nausea, vomiting, diarrhea Coma Death
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Compensation for Metabolic Acidosis
Increased ventilation Renal excretion of hydrogen ions if
possible K+ exchanges with excess H+ in ECF ( H+ into cells, K+ out of cells)
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Treatment of Metabolic Acidosis
Treat underlying cause IV Bicarbonate solution
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Metabolic Alkalosis
Bicarbonate excess - concentration in blood is greater than 26 mEq/L
Causes: Excess vomiting = loss of stomach acid Excessive use of alkaline drugs Certain diuretics Endocrine disorders Heavy ingestion of antacids Severe dehydration
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Compensation for Metabolic Alkalosis
Respiratory compensation difficult – hypoventilation limited by hypoxia
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Symptoms of Metabolic Alkalosis
Respiration slow and shallow Hyperactive reflexes ; tetany Often related to depletion of electrolytes Atrial tachycardia Dysrhythmias
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Treatment of Metabolic Alkalosis
Treat underlying disorder Electrolytes to replace those lost IV chloride containing solution
0.1 N HCL Infusion rate 0.2 mmol/kg/hr Central line
Acetazolamide
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Laboratory Values in Simple Acid-Base Disorders
Disorder Arterial pH
Primary Change
Compensatory Change
Metabolic acidosis ↓ ↓HCO3
- ↓PaCO2
Respiratory acidosis ↓ ↑PaCO2
- ↑HCO3-
Metabolic alkalosis ↑ ↑HCO3
- ↑PaCO2
Respiratory alkalosis ↑ ↓PaCO2
- ↓HCO3-
Interpreting Lab data
Arterial Blood Gas (ABG) Arterial carbon dioxide tension (PaCO2). Serum bicarbonate (HCO3
-). Arterial oxygen tension (PaO2)
pH <7.35, the patient is considered academic >7.45, the patient is considered alkalemic
ABGs Normal Range
pH 7.36–7.44
PaO2 90–100 mmHg
PaCO2 35–45 mmHg
HCO3- 22–26 mEq/L
Normal Arterial Blood Gas (ABG) Values
Anion Gap (AG)
The concentration of all the unmeasured anions in the plasma eg lactate, acetoacetate, sulphate.
Anion gap = [Na+] - [Cl-] - [HCO3-] Reference range is 8 to 16 mmol/l.
Adjusted AG = AG + 2.5 × (normal albumin – measured albumin in g/dL
Anion Gap (AG) cont’d
Clinical Use of the Anion Gap To signal the presence of a metabolic
acidosis and confirm other findings Help differentiate between causes of a
metabolic acidosis To assist in assessing the biochemical
severity of the acidosis and follow the response to treatment
Osmolal gap OG
Osmolality mOsm/kg H2O= (1.86[Na])+([glucose (mmol/L)])+([BUN mmol/L])
Osmolal gap= measured Osmolality- Calculated Osmolality
exists when the measured and calculated values differ by >10 mOsm/kg
Evaluation of Acid-Base Disorders
Obtain a detailed patient history and clinical assessment.
Check the arterial blood gas, sodium, chloride, and HCO3
-. Identify all abnormalities in pH, PaCO2, and HCO3
-.
Evaluation of Acid-Base Disorders Cont’d
Determine which abnormalities are primary and which are compensatory based on pH. If the pH is <7.40, then a respiratory or
metabolic acidosis is primary. If the pH is >7.40, then a respiratory or
metabolic alkalosis is primary. If the pH is normal (7.40) and there are
abnormalities in PaCO2 and HCO3-, a mixed
disorder is probably present because metabolic and respiratory compensations rarely return the pH to normal.
Evaluation of Acid-Base Disorders Cont’d
Consider other laboratory tests to further differentiate the cause of the disorder. If the AG is normal, consider calculating the
urine AG. If the AGis high and a toxic ingestion is
expected, calculate an osmolal gap. If the AG is high, measure serum ketones and
lactate.
Evaluation of Acid-Base Disorders Cont’d
Always calculate the AG. If ≥20, a clinically important metabolic acidosis is usually present even if the pH is within a normal range.
If the AG is increased, calculate the excess AG(AG-10). Add this value to the HCO3
- to obtain corrected value. If corrected value >26, a metabolic alkalosis is
also present. If corrected value is <22, a nonanion gap
metabolic acidosis is also present.
Evaluation of Acid-Base Disorders Cont’d
Consider other laboratory tests to further differentiate the cause of the disorder. If the AG is normal, consider calculating the
urine AG. If the AGis high and a toxic ingestion is
expected, calculate an osmolal gap. If the AG is high, measure serum ketones and
lactate.
Evaluation of Acid-Base Disorders Cont’d
Compare the identified disorders to the patient history and begin patient-specific therapy.
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Questions?
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END
ACID - BASE BALANCE