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Acid Base Disorders

ACID BASE DISORDERS 1.ACIDOSIS Respiratory Metabolic 2.Alkalosis Respiratory Metabolic

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

The buffering system of the body is handled by 1.Chemical 2.Renal 3.Respiratory

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:

pH = 6.1 + log HCO 3 PaCO2 * 0.0301

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

(H2CO3 is a volatile acid as CO2 exhaled )

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

Chemical buffer systems Their area of dominance

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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

If underlying problem is metabolic, hyperventilation or hypoventilation can help : respiratory compensation.


If problem is respiratory, renal mechanisms can bring about metabolic compensation.

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

Directed at correcting the underlying stimulus for HCO3 generation

Proton pump inhibitors to reduce H+ loss from GIT


K+ deficits should be repaired

NaCl therapy to reverse the alkalosis if ECFV contraction is present


Renal HCO3 loss can be accelerated by administration of acetazolamide, a carbonic anhydrase inhibitor Dilute hydrochloric acid (0.1 N HCl) is also.

Respiratory acidosis pH < 7.35 pCO2 > 40 mm Hg Compensatory increase in HCO3 ions

Respiratory acidosis caused due to

Severe pulmonary disease Respiratory muscle fatigue Abnormalities in ventilatory

control

Causes of respiratory acidosis


Central 1. Drugs (anesthetics, morphine, sedatives) 2. Stroke 3. Infection Airway 1. Obstruction 2. Asthma Parenchyma 1. Emphysema 2. Pneumoconiosis 3. Bronchitis 4. Adult respiratory distress syndrome 5. Barotrauma

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,

vasoconstriction secondary to loss of the vasodilator effects of CO2.

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.

How to diagnose an acid base disorder

Simple steps to follow..

1.

Note whether the pH is low (acidosis) or high (alkalosis)


Decide which value, pCO2 or HCO3- , is outside the normal range and could be the cause of the problem. If the cause is a change in pCO2, the problem is respiratory. If the cause is HCO3- the problem is metabolic Look at the value that doesnt correspond to the observed pH change. If it is inside the normal range, there is no compensation occurring. If it is outside the normal range, the body is partially compensating for the problem.

2.

3.

4.

Acid-Base Disturbance Respiratory acidosis Respiratory alkalosis

Primary Disturbance Increased pCO2 Decreased pCO2

Compensatory Response Increase [HCO3-] Decreased [HCO3] Decrease pCO2 Increased pCO2

Compensatory Mechanism Acidic urine

Alkaline urine

Decreased [HCO3Metabolic acidosis ] Metabolic alkalosis Increased [HCO3-]

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)

Anion gap = Na (Cl + HCO3)

The unmeasured anions include


anionic proteins, phosphate, sulfate, organic anions. When acid anions, such as acetoacetate and lactate, accumulate in extracellular fluid, the anion gap increases, causing a high anion gap acidosis.

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

Decrease in the Anion gap


(1)

Increase in unmeasured cations

(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)

What is the acid base disorder??

.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??

Respiratory acidosis and metabolic alkalosis