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Acid Base Disorders
Acid Base Disorders
Acid Base Disorders
Normal homeostasis It is aimed at maintaining the systemic arterial pH between 7.35 to 7.45 pH of < 7.35 is referred to as acidosis pH of > 7.45 is referred to as alkalosis
General Functions A buffer: ~ resists sudden changes in pH ~ temporarily helps prevent body fluids getting too acidic or too basic
A buffer contains:
~ a weak acid & its salt or ~ a weak base & its salt
The metabolic and respiratory components that regulate systemic pH are described by the HendersonHasselbalch equation:
Chemical buffers First to respond in acid base disturbance Acts in less than 1 sec. Temporarily tie up excess acids & bases Buffer systems are Bicarbonate carbonic acid Phosphate Protein
Carbonic Acid Bicarbonate Buffer System Respiratory component CO2 + H2O H2CO3 Renal component H+ + HCO3
Respiratory buffer mechanism Normal p CO 2 is 40 mmHg ^ causes acidosis and causes alkalosis Exhalation of carbon dioxide CO2 + H20 H2CO3 H+ + HCO3Body pH can be adjusted by changing rate and depth of breathing 2nd to respond Takes 1-3 minutes Respiratory centre involved Removes CO2 & therefore H2CO3
Renal mechanism Can eliminate large amounts of acids Eg phosphoric, uric & lactic acids; ketone bodies Can also excrete bases Can conserve and produce bicarbonate ions Most effective regulator of pH If kidneys fail, pH balance fails 3rd to respond but most potent Takes hours to days
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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
Metabolic acidosis 1.pH < 7.35 2.Bicarbonate is low Causes 1.Lactic acidosis 2.Renal failure 3.Diabetic ketoacidosis 4.Ethylene glycol toxicity 5.Diarrhoea
Metabolic acidosis has profound effects on the respiratory, cardiac, and nervous systems. The fall in blood pH is accompanied by a characteristic increase in ventilation, Kussmaul respiration. Intrinsic cardiac contractility may be depressed, but inotropic function can be normal because of catecholamine release. Both peripheral arterial vasodilation and central venoconstriction can be present; the decrease in central and pulmonary vascular compliance predisposes to pulmonary edema with even minimal volume overload. Central nervous system function is depressed, with headache, lethargy, stupor, and, in some cases, even coma.
Treatment 1.Treat the cause 2.Hydrate the patient 3.Only if HCO 3 is < 10 meQ/L or patient is comatosed severe acidemia is present, Bicarbonate infusion is warranted Aim at bringing the pH to 7.15 and HCO3 to > 10 meQ/L Never do aim at bringing them to normal
Metabolic alkalosis It is manifested by an elevated arterial pH > 7.45 ^ in serum [HCO3] > 24 meQ/L ^ in PaCO2 due to compensatory alveolar hypoventilation It is often accompanied by hypochloremia and hypokalemia. Metabolic alkalosis frequently occurs in association with other disorders respiratory acidosis or alkalosis or metabolic acidosis. Isolated occurrence rare
Causes 1.Alkali ingestion 2.Vomiting 3.Continuous gastric aspiration 4.Diuretic therapy 5.potassium and magnesium depletion 6.Cushings disease 7.High/ low renin states like renal artery stenosis, adenomas
Treatment
Respiratory acidosis pH < 7.35 pCO2 > 40 mm Hg Compensatory increase in HCO3 ions
control
Neuromuscular 1. Poliomyelitis 2. Kyphoscoliosis 3. Myasthenia 4. Muscular dystrophies Miscellaneous 1. Obesity 2. Hypoventilation 3. Permissive hypercapnia
Clinical features vary according to severity and duration of the respiratory acidosis, the underlying disease accompanying hypoxemia. A rapid increase in PaCO2 cause anxiety, dyspnea, confusion, psychosis, hallucinations coma
sleep disturbances, loss of memory, daytime somnolence, personality changes, impairment of coordination, motor disturbances tremor, myoclonic jerks, asterixis. Headaches papilledema, abnormal reflexes, focal muscle weakness,
The management of respiratory acidosis severity rate of onset. Acute respiratory acidosis is life threatening tracheal intubation and assisted mechanical ventilation. Oxygen administration should be titrated carefully Aggressive and rapid correction of hypercapnia should be avoided, falling PaCO2 may provoke cardiac arrhythmias, reduced cerebral perfusion, and seizures. The PaCO2 should be lowered gradually in chronic respiratory acidosis, aiming to restore the PaCO2 to baseline levels
Respiratory alkalosis pH > 7.45 pCO2 < 40 mmHg wash out compensatory HCO3 reduction Causes
Central nervous system stimulation
1. Pain 2. Anxiety, psychosis 3. Fever 4. Cerebrovascular accident 5. Meningitis, encephalitis 6. Tumor 7. Trauma
Hypoxemia or tissue hypoxia 1. High altitude, PaCO2 2. Pneumonia, pulmonary edema 3. Aspiration 4. Severe anemia
Drugs or hormones 1. Pregnancy, progesterone 2. Salicylates 3. Cardiac failure Stimulation of chest receptors 1. Hemothorax 2. Flail chest 3. Cardiac failure 4. Pulmonary embolism
Miscellaneous 1. Septicemia 2. Hepatic failure 3. Mechanical hyperventilation 4. Heat exposure 5. Recovery from metabolic acidosis
Clinical features
Paresthesia Circumoral numbness, Chest wall tightness or Pain, Dizziness, Inability to take an adequate breath Tetany Arterial blood-gas analysis acute or chronic respiratory alkalosis hypocapnia 1530 mmHg and no hypoxemia
Treatment
Directed toward alleviation of the underlying disorder.
If respiratory alkalosis complicates ventilator management, changes in dead space, tidal volume, and frequency can minimize the hypocapnia.
Patients with the hyperventilation syndrome benefit from reassurance, rebreathing from a paper bag attention to underlying psychological stress. Antidepressants and sedatives are not recommended Adrenergic blockers may ameliorate peripheral manifestations of the hyperadrenergic state.
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Compensatory Response Increase [HCO3-] Decreased [HCO3] Decrease pCO2 Increased pCO2
Alkaline urine
Hyperventilation
Hypoventilation
Anion gap Level of unmeasured anions in the body The total number of POSITIVE ions = total number of NEGATIVE ions
Used to determine if a metabolic acidosis is due to an accumulation of non-volatile acids (e.g. lactic acid) OR a net loss of bicarbonate (e.g. diarrhea)
High anion gap acidosis 1. Ketoacidosis 2. Lactic acid acidosis 3. Toxin-induced metabolic acidosis 4. Renal failure acidosis 5. Ethylene glycol toxicity 6. Salicylate toxicity
Normal anion gap acidosis 1.Renal tubular acidosis 2.Starvation 3. Colonic fistulas 4. Hyperglycemic hyperosmolar state Even in the presence of acidosis, the anion gap will be normal
(2) The addition to the blood of abnormal cations, such as lithium (lithium intoxication) or cationic immunoglobulins (plasma cell dyscrasias) (3) A reduction in the major plasma anion albumin concentration (nephrotic syndrome) (4) A decrease in the effective anionic charge on albumin by acidosis (5) Hyperviscosity and severe hyperlipidemia,
Case no 1 A patient is in intensive care because he suffered a severe myocardial infarction 3 days ago. The lab reports the following values from an arterial blood sample: pH 7.3 HCO3- = 20 mEq / L ( 22 - 26) pCO2 = 40 mm Hg (35 - 45)
.Metabolic acidosis
Case no 2
A 17 year anxious girl present to ER with features of acute breathlessness. Her vitals are stable and there is no chest sign. C/o tingling sensation in the fingers and chovsteks sign was positive.
ABG showed pH 7.60 pCO2 28 mmHg HCO3 24 meQ/L Whats the diagnosis???
Respiratory alkalosis ..
Case no 3 ABG of a patient reveals 1.pH 7.2 2.HCO3 36 meQ/L 3.pCO 2 60 mmHg What is the acid base disorder here??