Disorders of Acid-Base Imbalance Lecture 18 PDF

Disorders of acid-base imbalance Lecture 18 Unit 3 Table of contents 1. Metabolic acidosis 2. Metabolic alkalosis 3. Respiratory acidosis 4. Respiratory alkalosis 5. Treatments 6. Differentiating between the disorders 1. Metabolic acidosis Metabolic acidosis H2CO3 ->...

Disorders of acid-base imbalance Lecture 18 Unit 3 Table of contents 1. Metabolic acidosis 2. Metabolic alkalosis 3. Respiratory acidosis 4. Respiratory alkalosis 5. Treatments 6. Differentiating between the disorders 1. Metabolic acidosis Metabolic acidosis H2CO3 -> HCO3 + H+ - characterized by a decrease in bicarbonate (as it combines with available hydrogen ions), resulting in a decrease in pH. - two main types: 1) anion gap metabolic acidosis and 2) non-anion gap metabolic acidosis. Anion gap: Na -[Cl + HCO3]. = 8-16. >12= red flag - what are the main etiologies of AGMA : 1) diabetic ketoacidosis, 2) uremic acidosis, and 3) lactic acidosis, and 4) decrease in electron transport chain activity. - what are the main etiologies of NAGMA : 1) chronic kidney disease and 2) diarrhea. 3 1. Metabolic acidosis Anion gap metabolic acidosis - recall that the anion gap is the difference between sodium (a cation) and the main anions, bicarbonate and chloride; a normal anion gap is 12 mmol/L. organic acids: ketones, sulferic acid, lactic acid - AGMA is caused by elevated levels of organic acids, but where do they come from? Ketosis: normal Occuring in fasting stage: when body out of glycogen -> using fat storage - in diabetic ketoacidosis (DKA), increased ketosis (due to beta cell deficiency and inability to absorb glucose) increases keto acid production. can’t get rid of organic acids because glomeruls and PCT are damaged - in uremic acidosis , caused by acute renal injury or end-stage renal disease, the kidneys are unable to excrete organic acids. 4 1. Metabolic acidosis Anion gap metabolic acidosis shock: hypoperfusion to organs - lactic acidosis (look for elevated lactate) is commonly caused by hypoperfusion associated with shock , or… high levels of lactate Tuberculosis - certain medications (like metformin, isoniazid, aspirin) or deficiencies (like thiamine) can decrease the activity of the electron transport chain, causing cells to rely on anaerobic metabolism. - incidental toxic alcohol ingestion , including methanol, ethylene glycol, and paint thinner. 5 1. Metabolic acidosis RTA: Renal tubule acidosis Non-anion gap metabolic acidosis - when the anion gap is normal, organic acids are not the root case of the acid-base imbalance. - chronic kidney disease a common cause of this type of acidosis (GFR activate calcium sodium channels firing potential - chronic acidemia has major impacts on musculoskeletal system as calcium is leached from bone as it buffers H+ ions from the blood. 8 2. Metabolic alkalosis diaphragm and internal intercostal muscles Metabolic alkalosis - characterized by an increase in bicarbonate causing an increase in - pH. causes commonly include a loss of hydrogen ions whose etiologies include 1) renal losses and 2) GI losses. - renal losses are caused by diuretic use and hyperaldosteronism ; - while GI losses are caused by vomiting and nasogastric suctioning. affects ventilation rate: breathing rate x tidal volume cardiac output = HR x SV 9 2. Metabolic alkalosis Metabolic alkalosis: renal losses - loop diuretics help treat volume overload as during chronic heart failure, while thiazides help treat hypertension; both cause a decrease in blood volume (hypovolemia) by interrupting sodium reabsorption. water follows sodium - a consequence of inhibiting sodium sodium peed out so water peed out Na/K pump in collecting reabsorption via diuretics is H+ ion duct to trigger - secretion in cases of. hyperaldosteronism, ALD is reabsorption of sodium with diuretics, sodium and water overproduced (causing hypervolemia ), stays in the tubules so cant be reabsorbed which increases triggering Na+ reabsorption and K+ while the Na/H+ blood antiporters in volume and K excretion excretion and H+ excretion. collecting duct try hard to increase Na absoprtion at the expense of H+ ions 10 2. Metabolic alkalosis Metabolic alkalosis: GI losses - GI losses result from vomiting and nasogastric suctioning (due to fluid buildup); in this case, H+ ions and chloride ions are lost as gastric fluids contain hydrochloric acid (HCl). - hypochloremia causes cells to move bicarbonate from the ICF to the ECF, resulting in the alkalosis (caused by chloride shift/ Cl-/HCO3- antiporter). - hypochloremia causes the kidneys to compensate by reabsorb more chloride from the tubular fluid at the expense of 11 2. Metabolic alkalosis Metabolic alkalosis: Gain of base - calcium carbonate-based antacids , like Alka-Seltzer and Tums, are bases that are taken orally. - furthermore, excess calcium (hypercalcemia) causes hypovolemia as it inhibits sodium reabsorption , as calcium blocks sodium channels in kidneys, neurons, and muscles. - hypovolemia also stimulates HCO3- reabsorption, but the underlying mechanism remains unclear. 12 2. Metabolic alkalosis albumin usually binds H+ ions. when theyre absent: calcium is bound hemoglobin: buffers the blood Complications of metabolic alkalosis - the complications manifest from one major issue: decreased hydrogen ions in the bloodstream. - normally, potassium levels are maintained via their exchange with hydrogen ions; in their absence, serum potassium remains low. - hypokalemia causes arrhythmias and muscle weakness. - chemoreceptors trigger hypoventilation to help increase pCO2 and acidify the blood. - some patients may display muscular irritability and tetany, as albumin now binds cations like calcium, causing hypocalcemia (↓ free calcium). 13 3. Respiratory acidosis Respiratory acidosis kidneys need to comoensate: takes more time to activate - characterized by an increase in pCO 2 causing an decrease in pH. - the cause is hypoventilation with three main etiologies: 1) respiratory center dysfunction, 2) neuromuscular diseases, or 3) airway obstruction. - in metabolic acid-base imbalances, compensation occurs quickly , as ventilation can be modified immediately. - in respiratory acid-base imbalances, compensation occurs much less quickly because the kidneys must compensate by modifying H+ secretion and bicarbonate reabsorption. 14 3. Respiratory acidosis Respiratory acidosis: etiologies - when the respiratory centers of the pons and medulla oblongata are damaged , as in stroke, or depressed , as in drug overdoses (opioid and benzodiazepines), signals are not sent to the respiratory muscles. - usually accompanied by other neurological issues. - in neuromuscular disease, like ALS and Guillain-Barre, the nerves or neuromuscular junctions are affected , preventing the centers from communicating with the respiratory muscles. - causes shallow breathing due to low tidal volume. 15 3. Respiratory acidosis Respiratory acidosis: airway obstruction - in these patients, residual volume is higher than normal, whereby air is not adequately exhaled, preventing proper exchange of fresh air. - occurs in patients with lung diseases (i.e. COPD ), exacerbated asthma, chest injuries, and pulmonary edema. - hypoxemia is commonly present before acidosis appears, as oxygen diffuses more slowly than CO2, so pCO2 increases more slowly. faster to see than high levels of CO2 inefficient gas exchange: low levels of O2 16 3. Respiratory acidosis Respiratory acidosis: airway obstruction - shallow breathing with wheezing is commonly identified, and this condition is improved with bronchodilators (to increase overall airflow). - in COPD patients; oxygen administration inhibits chemoreceptor control of breathing, causing hypoventilation, further sustaining or inc. pCO2. watch pH levels: decreased resp rate insensitive to CO2, sensitive to O2: Increased compliance in lung tissue of patients with COPD. 17 3. Respiratory acidosis Respiratory acidosis: major complications - CO2 can easily cross the blood-brain barrier, and at elevated levels, it causes vasodilation in the brain; called cerebral vasodilation. - this will cause a greater volume blood to flow to the brain and can result in increases in intracranial pressure. - can lead to cognitive deficiencies and arousal problems , whereby patients experience lethargy, obtundity, and if severe enough, coma. - particularly dangerous if a patient is already suffering from increases in intracranial pressure (intracranial hypertension and subarachnoid hemorrhage). 18 4. Respiratory alkalosis Respiratory alkalosis - much less serious than previous imbalances and is characterized by decrease pCO 2 and elevated pH caused by hyperventilation. - etiologies of hyperventilation include 1) hyperactive respiratory centers and 2) metabolic toxicity. - pain and anxiety can cause hyperventilation by inc. the activity of the resp. centers, while aspirin toxicity inc. the metabolic rate of the neurons in the resp. centers. - early sepsis, pregnancy, and fever can also cause hyperventilation. 19 4. Respiratory alkalosis Respiratory alkalosis - in respiratory alkalosis, the kidneys will compensate by decreasing H+ secretion and decreasing bicarbonate reabsorption. - the major complications of this imbalance is the reverse of resp. acidosis, whereby we see cerebral vasoconstriction. - reduced cerebral blood flow can decrease intracranial pressure and cause syncope. - for this reason, it is common to program a ventilator to cause hypoventilation in a patient suffering from elevate intracranial pressure. vasodilation: reversing vasoconstriction 20 5. Treatments Metabolic acidosis - for patients with diabetic ketoacidosis , insulin is necessary; if the anion gap remains unchanged, give more insulin. - in lactic acidosis caused by hypovolemia, fluid resuscitation is needed; caused by distributive shock, give patient vasoconstrictors; and caused by cardiogenic shock, give patient inotropes to inc. cardiac output. - for uremic acidosis , give the patient sodium bicarbonate. - for alcohol ingestion , give medication that inhibits alcohol dehydrogenase, like fomepizole. - for NAGMA , give patient sodium bicarbonate. 21 5. Treatments Metabolic alkalosis - for hypovolemic patients , provide normosaline (0.9% NaCl); sodium will cause water retention and chloride will increase HCO3- excretion. - for hypervolemic patients , provide acetazolamide to inhibit sodium and bicarbonate reabsorption in the PCT. Respiratory acidosis Respiratory alkalosis - for drug overdoses , naloxone for - for pain and anxiety , opioids and flumazenil for pain medications and - benzodiazepines. for COPD and asthma , bronchodilators, anti-anxiolytics can be steroids, and BIPAP should be used. administered. 22 6. Differentiating between the disorders Differentiating between the disorders 23 6. Differentiating between the disorders Differentiating between the disorders - what is the main criteria identifying metabolic acidosis? - what criteria differentiates acute from chronic metabolic acidosis? - how do we differentiate between metabolic acidosis caused by inc. in fixed acids or hyperchloremia? 24 6. Differentiating between the disorders Differentiating between the disorders - what is the main criteria identifying respiratory acidosis? - what criteria differentiates acute from chronic respiratory acidosis? 25 5. Review Questions - What are the causes, manifestation and treatments of: - metabolic acidosis? - metabolic alkalosis? - Respiratory acidosis? - Respiratory alkalosis? 26