Acid-Base Disturbances Lecture 2 PDF

ACID-BASE DISTURBANCES Lecture 2 Etiology And Treatment of Acid Base Disorders o All of the following must be reviewed in order to establish the etiology of a given acid–base disturbance: the clinical history the patient’s recent medications physical examination findings ABGs s...

ACID-BASE DISTURBANCES Lecture 2 Etiology And Treatment of Acid Base Disorders o All of the following must be reviewed in order to establish the etiology of a given acid–base disturbance: the clinical history the patient’s recent medications physical examination findings ABGs serum electrolytes o Because frequent assessment of the patient’s response to treatment is critical, an arterial line is often placed to minimize patient discomfort with serial ABG collections ETIOLOGY AND TREATMENT Establishing the specific disease process responsible for the observed acid–base disorder is clinically important because treatment of a given disorder will only be accomplished by correcting the underlying disease process However, supportive treatment of the pH and electrolytes is often needed until the underlying disease state is improved  Metabolic acidosis Metabolic acidosis is characterized by: Primary pH Initial Compensatory Compensatory disorder chemical response Mechanism change Metabolic ↓ ↓HCO3− ↓PCO2 Hyperventilation Acidosis Symptoms: appear due to changes in cardiovascular, musculoskeletal, neurologic, or pulmonary functioning Respiratory compensation requires marked increases in minute ventilation and may lead to dyspnea, respiratory fatigue, and respiratory failure Metabolic acidosis Symptoms: Acidemia predisposes to ventricular arrhythmias and reduces cardiac contractility, each of which can result in pulmonary edema and/or systemic hypotension Neurologic symptoms range from lethargy to coma and are usually proportional to the severity of the pH derangement Metabolic acidosis Symptoms: Chronic metabolic acidosis leads to a variety of musculoskeletal problems, including impaired growth, rickets, osteomalacia, or osteopenia These changes are believed to be caused by the release of calcium and phosphate during bone buffering of excess H+ ions Metabolic acidosis Pathophysiology the buffering (consumption of HCO3-) of an exogenous acid an organic acid accumulating because of a metabolic disturbance (e.g., lactic acid or ketoacids) the progressive accumulation of endogenous acids secondary to impaired renal function (e.g., phosphates and sulfates) the serum HCO3– can also be decreased as the result of a loss of bicarbonate-rich body fluids (e.g., diarrhea, biliary drainage, or pancreatic fistula) secondary to the rapid administration of non-alkali– containing IV fluids (dilutional acidosis) Metabolic acidosis Metabolic acidosis can be divided into: an increase in the anion gap metabolic acidosis a normal anion gap metabolic acidosis Metabolic acidosis The concentrations of total anions and cations in the body are equal because the body must remain electrically neutral When acid is added to the body, the [H+] increases and the [HCO3-] decreases. In addition, the concentration of the anion [A-], which is associated with the acid, increases Na++Unmeasured cations = Cl- + HCO3-+Unmeasured anions Metabolic acidosis Anion gap Metabolic acidosis Anion gap The anion gap represents the concentration of unmeasured anions in excess of the concentration of unmeasured cations in the extracellular fluid Na+ + Unmeasured cations = Cl- + HCO3-+ Unmeasured anions Anion gap (Unmeasured anions - Unmeasured cations ) = [Na] – ([Cl-] + [HCO3-]) The concentration of unmeasured anions normally exceeds the concentration of unmeasured cations by 6 to 12 mEq/L Metabolic acidosis Anion gap If the anion of the acid added to plasma is Cl- , the anion gap will be normal (i.e., the decrease in [HCO3-] is matched by an increase in [Cl-]) For example: HCl + NaHCO3 → NaCl + H2CO3 → CO2 + H2O This disorder is called a hyperchloremic acidosis, because of the associated increase in the Cl- concentration Metabolic acidosis Hyperchloremic acidosis (normal anion gap) Addition of HCl GI or renal loss of HCO3- (as the kidney in its effort to preserve the ECV will retain NaCl leading to a net exchange of lost HCO3- for Cl-)  Metabolic acidosis Increased anion gap If the anion of the acid is not Cl- (lactate, β hydroxybutyrate), the anion gap will increase (i.e. the decrease in [HCO3-] is not matched by an increase in the [Cl-] but rather by an increase in the [unmeasured anion]: HA + NaHCO3→ NaA + H2CO3 → CO2 + H2O, where A- is the unmeasured anion Metabolic acidosis Causes Adjusted anion gap (AG) In critically ill patients with hypoalbuminemia, the calculated AG should be adjusted using the following formula: Adjusted AG = AG + 2.5×(normal albumin – measured albumin in g/dL) normal albumin concentration: 4.4 g/dL If a hypoalbuminemic patient (serum albumin, 2.4 g/dL) with a calculated AG of 11 mEq/L AG (adjusted) = 11 mEq/L + 2.5 × [normal albumin – measured albumin] = 16 mEq/L Case study A 60 year old homeless man presents with nausea, vomiting and poor oral intake 2 days prior to admission. The patient reports a 3 day history of binge drinking prior to symptoms Labs : Serum chemistry: Na 131 (nl:135-145mEq/l), K 5.0 (3.5-5 mEq/l), Cl 104 (104 mEq/l), HCO3- 16 BUN 25, Cr 1.3, Glu 75, ABG: pH 7.30, PCO2 29, HCO3-16, PO2 92, Serum albumin 1.4 Does the patient have an abnormal anion gap? Case study 1 Answer The patient is acidemic with a low bicarb and low PCO2, suggesting metabolic acidosis. The patient is hyponatremic with a history of nausea, vomiting and poor intake. In this scenario, the metabolic acidosis may either be due to normal anion gap acidosis secondary to vomiting and/or due to lactic acidosis, ketoacidosis secondary to extreme volume loss and poor intake. To decide, we need to calculate the anion gap Anion gap = (Na-(Cl +HCO3-) = 131 - (104 +16) = 11mEq/l The anion gap appears to be normal, and thus lactic acidosis appears unlikely. However, note also that the patient is severely hypoalbuminemic with a serum albumin of 1.4 Because the anion gap is primarily determined by negatively charged plasma proteins such as albumin, we must adjust the normal value of the anion gap to more accurately reflect the albumin deficiency Case study 1 Answer, continued Therefore in this scenario, the normal anion gap should be: Decline in albumin = 4.4 – 1.4 = 3 g/dl Reduction in normal anion gap = 3 × 2.5 = 7.5 mEq/l Adjusted anion gap = 11 + 7.5 = 18.5 mEq/l Assessment: This patient has an elevated anion gap metabolic acidosis which may be due to lactic acidosis or ketoacidosis. Metabolic acidosis Treatment 1. Correct the cause 2. Bicarbonate: The precise role of adjunctive therapy with sodium bicarbonate (NaHCO3) is not universally agreed upon. However, most practitioners accept that adjunctive therapy with NaHCO3 is indicated: when renal dysfunction prevents adequate regeneration of HCO3− or when severe acidemia (pH less than 7.15) is present Metabolic acidosis Treatment The metabolic acidosis of renal failure, renal tubular acidosis, or intoxication with ethylene glycol, methanol, or salicylates is much more likely to require NaHCO3 therapy. NaHCO3 may be unnecessary in case of metabolic acidosis seen with lactic acidosis and ketoacidosis these generally resolves with therapy targeted at the underlying cause Metabolic acidosis Treatment with sodium bicarbonate If NaHCO3 is used, the plasma [HCO3−] should not be corrected entirely Why ?... to avoid volume overload, hypernatremia, hyperosmolarity, overshoot alkalemia, hypocalcemia and/or hypokalemia Metabolic acidosis Treatment with sodium bicarbonate Acute severe metabolic acidosis Sodium bicarbonate is recommended to raise arterial pH to 7.2. However, no controlled clinical studies have demonstrated reduced morbidity and mortality compared with general supportive care. Metabolic alkalosis Primary Initial Compensa Compensa- Expected level of disorder chemical -tory tory compensation change response Mechanism − Metabolic ↑HCO3 ↑PCO2 Hypo- ↑PCO2 = 0.7 ×∆ [HCO3−] Alkalosis ventilation ↑pH Patients with metabolic alkalosis rarely have symptoms attributable to alkalemia. Rather, complaints are usually related to volume depletion (muscle cramps, positional dizziness, weakness) or to hypokalemia (muscle weakness, polyuria, polydipsia). Metabolic alkalosis Although the spotlight usually falls on metabolic acidosis, the most common acid-base disturbance in hospitalized patients is metabolic alkalosis Metabolic alkalosis, pathogenesis Metabolic alkalosis is defined as an increase in the bicarbonate (HCO3) concentration in extracellular fluid (>26 mEq/L) that is not an adaptive response to hypercapnia This condition can be the result of any of the following: (a) loss of hydrogen ions (H+) from extracellular fluid, (b) a gain in bicarbonate ions in extracellular fluid, or (c) a decrease in extracellular volume. Metabolic alkalosis loss of H+ via the GIT (eg, nasogastric suctioning, vomiting) or kidneys (eg, diuretics, Cushing syndrome) or from gain of bicarbonate (eg, administration of bicarbonate, acetate, lactate, or citrate) metabolic alkalosis is maintained by abnormal renal function that prevents the kidneys from excreting excess bicarbonate decreased HCO3- excretion (hypovolemia, hypokalemia, or mineralocorticoid excess)  Cushing syndrome Laxatives abuse  Metabolic alkalosis treatment algorithm READ ONLY Excess alkali intake Endogenous Spironolactone If no response, mineralocorticoid Amiloride consider surgery excess Triamterene Metabolic alkalosis treatment algorithm, cont’d READ ONLY  Respiratory Acidosis Primary Initial Compens Compensa- Expected level of disorder chemical -atory tory compensation change response Mechanism Respiratory ↑PCO2 ↑HCO3- Acidosis Acute Intracellular ↑[HCO3-] = 0.1 x ∆PCO2 Buffering (hemoglobin, intracellular proteins) Chronic Generation of ↑[HCO3-] = 0.35 x ∆PCO2 new HCO3- due to the increased excretion of ammonium Respiratory Acidosis Because of the lung’s excellent capacity to excrete excess CO2, increases in PCO2 are always due to hypoventilation and never to increased CO2 production Hypoventilation can occur with any interference in the respiratory process Common Causes of Respiratory Acidosis CNS disease Pulmonary disease Central sleep apnea Lower airway obstruction Infection Chronic obstructive pulmonary Intracranial hypertension disease Trauma Status asthmaticus, Pneumonia Tumor Pneumonitis, Pulmonary edema Drugs Restrictive lung disease Aminoglycosides, Anesthetics Ascites β-Blockers, Hypnotics, Narcotics Obesity Neuromuscular blocking agents Pleural effusion Sedatives Neuromuscular disease Smoke inhalation Muscular dystrophy Others Upper airway obstruction Congestive heart failure Obstructive sleep apnea Inadequate mechanical ventilation Respiratory Acidosis Symptoms: Symptoms are caused by acute respiratory acidosis and not by chronic respiratory acidosis and usually include neurologic abnormalities Severe, acute respiratory acidosis produces a variety of neurologic abnormalities. Initially these include headache, blurred vision, restlessness, and anxiety. These may progress to tremors, asterixis, somnolence, and/or delirium If untreated, terminal manifestations include peripheral vasodilation leading to hypotension and cardiac arrhythmias Respiratory Acidosis Treatment Treat underlying disorder Supply oxygen (Oxygen therapy should be initiated carefully and only if the Pao2 is less than 50 mm Hg because the drive to breathe depends on hypoxemia rather than hypercarbia). Corticosteroids and bronchodilators to reduce airway inflammation and resistance. Mechanical ventilator if ventilation fails.  Respiratory alkalosis Primary Initial Compens Compensa- Expected level of disorder chemical -atory tory compensation change response Mechanism Respiratory ↓PCO2 ↓HCO3- Alkalosis Acute Intracellular ↓[HCO3-] = 0.2 x ∆PCO2 Buffering Chronic Decreased ↓[HCO3-] = 0.4 x ∆PCO2 reabsorption of HCO3-, decreased excretion of ammonium Respiratory alkalosis Respiratory alkalosis represents hyperventilation and is remarkably common. etiologies of respiratory alkalosis range from benign (anxiety) to life threatening (pulmonary embolism) It is very commonly induced by what the body or patient perceives as a stressor. The stressor which is often associated with anxiety, pain, and infection stimulates the CNS leading to hyperventilation. Other common causes are hypoxemia, sepsis, liver failure and pulmonary embolism Respiratory alkalosis Clinical presentation In acute respiratory alkalosis, acute onset of hypocapnia can cause cerebral vasoconstriction. Therefore, an acute decrease in PCO2 reduces cerebral blood flow and can cause neurologic symptoms, including dizziness, mental confusion, syncope, seizures, numbness around the mouth Serum electrolytes can be altered; serum chloride is usually increased; serum potassium, phosphorus, and ionized calcium are usually decreased Respiratory alkalosis Salicylates Methylxanthines Progesterone Catecholamines Respiratory alkalosis Treatment Treat the underlying cause For anxious patient, reassurance, rebreathing into paper bag (raises the inspired PCO2). Teach breath holding techniques during episodes. If intubated, reduce ventilation by adjusting ventilatory settings. Usually self limited since muscles weakness will suppress ventilation  THANK YOU Contact me via email: [email protected]