Principles of Acid-Base Imbalance
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"The body maintains a balance of acids and bases in order to constantly maintain blood pH within a narrow range, despite the continuous generation of metabolic products. In turn, this allows the body to maintain cell enzyme systems in good operation conditions, together with the proper concentration of ionized (active) forms of various electrolytes such as Ca and Mg . This influences the speed of metabolic reactions and trans-membrane transportation systems (pharmacokinetics and pharmacodynamics)." - Luis Núñez Ochoa, Facultad de Medicina Veterinaria y Zootecnia, Unam, Mexico
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Principles of Acid-Base Imbalance
- 2. Acid-Base Balance (ABB) Fundament to homeostasis Maintenance of a constant pH Animal diseases lead to abnormalities in ABB
- 3. Key Terms • Acid: substance that can donate H+ • Base: substance that can accept H+ • pH: the overall conc. H+ in body fluids
- 5. pH = 7.35-7.45 A pH ˃ 7.45 = Alkalosis A pH ˂ 7.35 = Acidosis pH = ˂6.8 or ˃7.8 Copyright The McGraw-Hill Companies
- 6. Sources of [H+] • Carbonic acid formation – major source of H+ is from metabolically produced CO2. • Inorganic acids produced during nutrient breakdown • Organic acids from intermediary metabolism
- 7. Acids Volatile acids (20,000 mEq/kg/day) Produced by oxidative metabolism of CHO, fat, protein. Excreted through the LUNGS as CO2. Fixed acids (1 mEq/kg/day) Remain in body fluids until eliminated in the KIDNEYS. Examples: sulfuric, phosphoric, organic acids
- 8. CO2+ H2O H2CO3 HCO3-+ H+ ACID ACIDBASE
- 9. CO2+ H2O H2CO3 HCO3-+ H+ Body Compensations: Buffering System (H2CO3; HCO3-) Respiratory Compensation (CO2) Renal Compensation (HCO3-)
- 10. When pH is decreased, the lungs tend to increase ventilation so that more CO2 is eliminated and pH increases. When pH is increased, the lungs tend to decrease ventilation so that CO2 is accumulated and pH decreases.
- 11. PCO2 An increased PCO2 level indicates hypoventilation from shallow breathing. A decreased PCO2 level indicates hyperventilation.
- 13. CO2+ H2O H2CO3 HCO3-+ H+ When blood is acidic, the kidneys reabsorb HCO3- and excrete H+ When blood is alkaline, the kidneys excrete HCO3- and retain H+ KIDNEY
- 15. Acid Base Disorder Represents a change in the normal extracellular pH that may result when renal or respiratory function is abnormal. 2 disorders of ABB: acidosis & alkalosis Origin: metabolic or respiratory
- 17. Acid Base Disorder • Respiratory – primary disturbance in pCO2 levels • acidosis • alkalosis • Metabolic – primary disturbance in [HCO3 -] levels • acidosis • alkalosis
- 18. Acid Base Disorder If the respiratory system is responsible, look for the PaCO2 or serum CO2. If the metabolic system, look for serum HCO3 -.
- 19. AB Disorder SIMPLE: A primary disturbance and the expected adaptive (or secondary) response in the opposite system. MIXED: two (rarely 3) separate primary disturbance present in the same individual.
- 21. Metabolic acidosis A primary gain in acid or loss of base. Most common acid-base disorder in vet. medicine.
- 22. Metabolic acidosis Associated pH change Associated H+ change What was the primary disturbance? What is the secondary response? PCO2HCO3-
- 23. Metabolic acidosis Uremia (uremic acids) Ketosis (keto acids) Lactacidemia (lactic acid) Ethylene glycol toxicity Aspirin toxicity (acetylsalicylic acid)
- 24. Metabolic acidosis Clinical signs: Hyperpnea CNS depression
- 25. Metabolic acidosis UCs = calcium, magnesium UAs = PO4, SO4, organic acids (e.g., lactate, citrate, ketones) Anion Gap (AG) difference between the quantitiy of unmeasured cations (UCs) and unmeasured anions (UAs) in the blood. [Na+] + [K+] – [Cl-] + [HCO3 -]
- 26. Anion Gap Example: • Na+ = 135 • K+ = 3.0 • HCO3 - = 22 • Cl- = 106 138 – 128 = 10 Normal AG = 13 – 25 mEq/L
- 27. High AG Increased organic acid in the blood. Organic acids causing high AG: • Lactic acid • Ketoacids • Formic acid • Oxalic acid
- 28. High AG • Lactic acidosis (salicylates, shock) • Diabetic ketoacidosis • Methanol poisoning • Ethylene glycol poisoning • Renal failure (increased PO4 & SO4)
- 29. Normal AG Due to bicarbonate loss. aka MA with no acid gain. Causes: Diarrhea Renal tubular acidosis
- 30. Metabolic acidosis Na+ Cl- AG HCO3 - normal anion gap Na+ Cl- AG HCO3 - physiologic situation Na+ Cl- AG HCO3 - high anion gap Normochloremic Hyperchloremic
- 31. Metabolic acidosis Initial treatment – Prompt diagnosis & specific treatment of underlying disease. – Correct electrolyte imbalance – Maintain efficient kidney function – Support kidney perfusion
- 32. Metabolic acidosis Administration of crystalloid fluids – Lactated Ringer’s solution Administration of alkalinizing agents – Conservative administration of NaHCO3 - if pH decreases below 7.1- 7.2 to avoid cardiovascular complications.
- 33. Metabolic alkalosis Characterized by an excess of HCO3, caused by a deficit of H+ in the ECF. Excessive [H+] loss • Excessive vomiting (GIT obstruction), or via urinary tract in hyperaldosteronism. • Renal losses for compensation of respiratory acidosis.
- 34. Metabolic alkalosis Base gain Administration of NaHCO3 - to treat metabolic acidosis Administration of organic ions which are metabolized to HCO3 - (e.g., citrate in blood transfusions
- 35. Metabolic alkalosis Clinical signs • Depressed breathing (slow & shallow) • Nervous excitement (i.e., tetany, convulsions • Muscular hypertonicity
- 36. Metabolic alkalosis Associated pH change Associated H+ change What was the primary disturbance? What is the secondary response? PCO2HCO3-
- 37. Metabolic alkalosis Treatment Treatment of underlying cause Use of acidifying solutions: NaCl (0.9%), NH4Cl (1.9%), Ringer’s solution
- 38. Respiratory acidosis Involves retention of CO2 as a consequence of alveolar hypoventilation. Causes: Primary pulmonary dss. (i.e., respiratory obstruction) Neuromuscular disorders Drugs (i.e., general anesthetics, sedatives)
- 39. Respiratory acidosis Associated pH change Associated H+ change What was the primary disturbance? What is the secondary response? HCO3-PCO2
- 40. Respiratory acidosis Clinical signs Respiratory distress CNS depression with progressive disorientation Weakness Coma (CO2 narcosis)
- 41. Respiratory acidosis Initial treatment Elimination of the cause Oxygen administration Contraindication: NaHCO3
- 42. Respiratory alkalosis Develops when the lungs eliminate too much CO2. The most common cause is hyperventilation. Compensation for primary metabolic acidosis Any cause of hypoxemia (CHF, hypotension, anemia)
- 43. Respiratory alkalosis Associated pH change Associated H+ change What was the primary disturbance? What is the secondary response? HCO3-PCO2
- 44. Respiratory alkalosis Clinical signs Tachypnea Hyperpnea CNS stimulation with or without convulsions
- 45. Respiratory alkalosis Treatment Identification & correction underlying cause. Correction of the observed hypocapnia. O2 administration Administration of analgesics and sedatives
- 46. Patterns associated w/ AB disorders Disorder Associated pH change Associated H+ change Primary disturbance Secondary response Metabolic acidosis Metabolic alkalosis Respiratory acidosis Respiratory alkalosis HCO3 - HCO3 - HCO3 - HCO3 - PCO2 PCO2 PCO2 PCO2
- 47. Compensatory responses for AB disturbances in dogs Primary disorder Compensatory response Metabolic acidosis 1.0 mmHg in PCO2 per 1.0 mEq/L in HCO3 - Metabolic alkalosis 0.7 mmHg in PCO2 per 1.0 mEq/L in HCO3 -
- 48. Compensatory responses for AB disturbances in dogs Primary disorder Compensatory response Acute respiratory acidosis 0.15 mEq/L in HCO3 - per 1.0 mmHg in PCO2 Chronic respiratory acidosis 0.35 mEq/L in HCO3 - per 1.0 mmHg in PCO2 Acute = ˂ 48 h Chronic = ˃ 48 h
- 49. Compensatory responses for AB disturbances in dogs Primary disorder Compensatory response Acute respiratory alkalosis 0.25 mEq/L in HCO3 - per 1.0 mmHg in PCO2 Chronic respiratory alkalosis 0.55 mEq/L in HCO3 - per 1.0 mmHg in PCO2 Acute = ˂ 48 h Chronic = ˃ 48 h
- 51. Results Interpretation Reference value pH 7.27 7.39 PCO2 27 37 HCO3 - 12 22 Acidemia Metabolic acidosis Respiratory compensation: 22-12 = 10 (HCO3 -) 10 x 1 = 10 37-10 = 27 Physiological respiratory compensation Acute renal failure
- 52. Results Interpretation Reference value pH 7.33 7.39 PCO2 57 37 HCO3 - 29 22 Slight acidemia Physiological metabolic compensation Metabolic compensation: 57-37 = 20 (PCO2) 20 x 0.35 = 10 (HCO3 -) 22+7 = 29 mEq/L Respiratory acidosis Coughing & dyspnea (1 week)
- 53. Results Interpretation Reference value pH 7.05 7.39 PCO2 44 37 HCO3 - 12 22 Acidemia Metabolic acidosis Mixed metabolic & respiratory acidosis Respiratory acidosis Seriously ill dog
- 54. pH PaCO2 HCO3 Diagnosis 7.4 40 24 Normal 7.26 60 27 Metabolic compensation: 60-40 = 20 (PCO2) 20 x 0.35 = 7 (HCO3 -) 24+7 = 31 mEq/L Examples of Blood Gas Abnormalities Uncompensated respiratory acidosis
- 55. pH PaCO2 HCO3 Diagnosis 7.4 40 24 Normal 7.38 60 36 Metabolic compensation: 60-40 = 20 (PCO2) 20 x 0.35 = 7 (HCO3 -) 24+7 = 31 mEq/L Examples of Blood Gas Abnormalities Partially compensated respiratory acidosis
- 56. pH PaCO2 HCO3 Diagnosis 7.4 40 24 Normal 7.2 40 15 Respiratory compensation: 24-15 = 9 (HCO3 - ) 9 x 1 = 9 (PaCO2) 40-9 = 31 Examples of Blood Gas Abnormalities Uncompensated metabolic acidosis
Editor's Notes
- Fundamental to physiologic homeostasis Refers to the way in which the body maintains a relatively constant pH despite continuous production of metabolic end products. Animal disease states lead to abnormalities of body fluid, electrolytes and ABB, the ability to interpret acid-base data enables the practitioner to identify the cause of the imbalance and provide appropriate treatment.
- ACID. Examples include hydrochloric acid (HCl), nitric acid, the ammonium ion, lactic acid, acetic acid, and carbonic acid (H2CO3). BASE. Examples include ammonia, lactate, acetate, and bicarbonate (HCO3-). The pH is used to express H+
- pH: the negative logarithm of H+ The ratio is inverse, the higher the H+ ion concentration, the lower the pH; the lower the H+ conc., the higher the pH.
- Blood is slightly alkaline – for normal enzyme/cell function and metabolism, pH must remain within a narrow range. ACIDOSIS – a process that involves a gain of acids or a loss of bicarbonate. ALKALOSIS – a process that involves a chlorine loss or decreased PCO2. If blood becomes acidic, cardiac contraction force is decreased; if it becomes alkaline, neuromuscular function is impaired. A blood pH below 6.8 or above 7.8 is usually fatal.
- Where are these extra acids in the boy come from? Endogenous or exogenous Inorganic acids produced during nutrient breakdown – dietary proteins contain a large quantity of sulfuric acid and phosphoric acid. Organic acids from intermediary metabolism – lactic acid and fatty acids Exogenous sources: excess acids may be introduced into the body in cases of ethylene glycol toxicity
- In the body, there are mechanisms in order to regulate changes in pH. Here are the three main mechanisms for doing so. Buffering system Main players are bicarb and carbonic acid; when we have increased H+, bicarb starts to attach H+ and give us carbonic acid. When there is reduced H+, carbonic acid will dissociate to give us more H+ and bicarbonate. Respiratory compensations Works by regulating the CO2 in the body. Renal compensation Works by regulating HCO3- in the body.
- PCO2: partial pressure of arterial CO2 reflects the level of CO2 in the blood. The respiratory system responds within minutes, but provides only a temporary compensation.
- Respiratory Regulation of Blood pH. The respiratory system can reduce blood pH by removing CO2 from the blood.
- Figure 3. Conservation of Bicarbonate in the Kidney. Tubular cells are not permeable to bicarbonate; thus, bicarbonate is conserved rather than reabsorbed. Steps 1 and 2 of bicarbonate conservation are indicated.
- ACID BASE DISORDER – may also result when an excess acid or base overwhelms excretory capacity. ACIDOSIS: too much acid/not enough base in the blood. ALKALOSIS: too much base/too little acid in the blood. These disturbances are either metabolic or respiratory in origin.
- The 3 key pieces of data to consider when assessing ABB and/or AB Disorder are pH, PCO2 and HCO3.
- Simple: when compensation is appropriate Mixed: when compensation is inappropriate
- Metabolic disorder Most common acid-base disorder in dogs, cats, and horses.
- Patterns associated with Metabolic Acidosis
- 5 Most common cause of metabolic acidosis in veterinary medicine
- The clinical signs most commonly associated with metabolic acisosis are hyperpnea and CNS depression. Hyperpnea is an increased minute ventilation.
- Anion Gap The amount of ions in the blood that cannot be measured. Measurement of the balance between cations and anions. Na+ - (Cl- + HCO3-) [Na+] + [K+] – [Cl-] + [HCO3-] {measured cations – measured anions} Unmeaured NS = [Na+] + [K+] ;
- 135 + 3 = 138 22 + 106 = 128 The normal AG varies with the species but is approximately 13 – 25 mEq/L in dogs and cats. AG is most often use to identify causes of metabolic acidosis. Categories : High or increased AG and Normal AG
- Organic acids causing high AG: Lactic acid Ketoacids Formic acid (methanol metabolite) Oxalic acid (ethylene glycol metabolite)
- *Causes of high anion gap acidosis Thus, high anion gap occurs due to more organic acids produced or ingested.
- Metabolic acidosis with no acid gain (non-volatile acids within the normal range). Iatrogenic (hospital-acquired) causes: Carbonic anhydrase inhibitors Ammonium chloride Cationic amino acids (arginine, lysine) Dilutional acidosis – infusion of high chloride solution such as normal saline
- In the case of HIGH ANION GAP, because of the increased amount of organic acids such as lactic acid, the HCO3- levels (measured) decreases because HCO3- buffers H+ that are generated from dissociation of organic acids. Metabolic acidosis with acid gain (high non-volatile acid levels). Examples: endogenous acidosis due to lactic acid gain, ketone bodies, phosphates, sulfates, or in exogenous acidosis caused by ingestion of salicylates, oxalic acid or methanol. The Cl- usually remains unchanged so that this is called as normochloremic metabolic acidosis. The increased organic acid corresponds to the increase of the anion gap. NORMAL ANION GAP is also known as METABOLIC ACIDOSIS WITH NO ACID GAIN (high non-volatile acids within normal range). In other words, due to bicarbonate loss (diarrhea). The negative charge is replaced not by those organic acid anions in the mystery box but by chloride The kidneys compensate for bicarbonate loss by increasing chloride reabsorption keeping serum electroneutral. It can therefore also be referred to as hyperchloremic acidosis because the levels of chloride increases. Anion gap remains normal; the serum remains electroneutral with the same amount of negative charge accounted for. Causes of bicarbonate loss: Diarrhea Renal tubular acidosis – there are several types of RTA, the most common of which is decreased bicarbonate reabsorption in the distal convoluted tubule.
- Initial treatment Prompt diagnosis & specific treatment of underlying disease (e.g., insulin & fluids for diabetes). Correct electrolyte imbalance (e.g. hypovolemia & dehydration)
- Initial treatment Prompt diagnosis & specific treatment of underlying disease (e.g., insulin & fluids for diabetes). Correct electrolyte imbalance (e.g. hypovolemia & dehydration) Administration of crystalloid fluids When metabolic disorder is due to loss of bases or where the increase in acids is observed.
- Vomiting – most common cause of acid loss in small animals Excessive [H+] loss Vomiting (stomach contents, e.g. pyloric obstruction) Diuretic therapy (e.g. furosemide) Cushing’s disease (hyperadrenocorticism)
- BASE GAIN – less common than acid loss
- Metabolic alkalosis is much more common in ruminants.
- Patterns associated with Metabolic Alkalosis Compensation for metabolic alkalosis requires the kidneys to excrete HCO3- and retain H+.
- NH4Cl (1.9%) [NH3+ is conjugated to urea in the liver, which frees H+ and Cl-) Ringer’s solution – supplies Na+, K+, Ca++, & Cl- (in metabolic alkalosis, there is lowered [Cl-], variable [Na+] and low serum [K+]
- Respiratory acidosis Caused by hypoventilation or decreased gas exchange in the alveoli, and develops when the lungs fail to adequately eliminate CO2. Causes: Primary pulmonary dss. (i.e., respiratory obstruction) Neuromuscular disorders that impair the mechanics of breathing Drugs (i.e., general anesthetics, sedatives) – respiratory depression Impaired respiration can be caused by pneumonia, pulmonary edema, emphysema, pneumothorax, respiratory muscle paralysis, morphine, barbiturate, or anesthetic poisoning.
- Patterns associated with Respiratory Acidosis Laboratory analysis of blood will show a decreased blood pH, increased serum HCO3- (renal reabsorption of HCO3-) and a decrease in serum Cl- because of renal excretion. Hypoventilation results in CO2 retention, an excess of H2CO3, and thereby an excess of H+. The compensatory mechanism is for the kidneys to conserve HCO3 and excrete H+.
- Treatment of respiratory acidosis Initial treatment Elimination of the cause Administration of drugs that suppress the respiratory system should be discontinued. Oxygen administration Beneficial since it is often accompanied by varying degrees of hypoxemia. Administration of alkalinizing solution NaHCO3 is contraindicated as it leads to an increase in CO2 in the blood.
- The most common cause is overactive positive pressure ventilation during anesthesia (iatrogenic). Respiratory system: asthma, pneumonia, pulmonary edema Respiratory center: brain tumors, traumatic brain injury, heat stroke, liver failure Other causes include fever, stimulation of respiratory centers by encephalitis, salicylate intoxication, hypoxia, heat prostration, hysteria.
- Patterns associated with Respiratory Acidosis Laboratory analysis reveals increase urine and blood pH, decreased serum HCO3- Compensation occurs by renal excretion of HCO3 and retention of H+.
- Clinical signsHyperpnea (with or without panting) Tachypnea is an excessively high rate of breathing, with the implication that the breathing is shallow Hyperpnea is an increased minute ventilation. Hyperpnea (with or without panting) Tachypnea is an excessively high rate of breathing, with the implication that the breathing is shallow Hyperpnea is an increased minute ventilation.
- Hypocapnia – reduction in the partial pressure of CO2 in the blood. Oxygen administration and hypoxaemia O2 is mandatory when hypoxaemia coexists. O2 decreases induced hyperventilation. Administration of analgesics and sedatives For the treatment of fear, pain or stress, analgesic or sedative drug has been proven to be a satisfactory therapeutic measure.
- For simple AB imbalance, a rule exists where PCO2 and HCO3- always follow the same direction.
- In METABOLIC ACIDOSIS, for each mEq/L that the HCO3- decreases, a PCO2 decrease of 1.0 mmHg is expected. In METABOLIC ALKALOSIS, for each mEq/L that the HCO3- increases, a PCO2 increase of 0.7 mmHg is expected.
- The chronic form of RA has a higher compensation (0.35 vs. 0.15 mEq/L) because in chronic process, not only hemoglobin, PO4 act as buffer, but also the kidneys. The increase generation of bicarbonate of the kidneys account for the additional increase in blood bicarbonate concentration.
- In ACUTE RESP. ALKALOSIS, for each mmHg that the PCO2 decreases, a HCO3- decrease of 0.25 will occur. In CHRONIC RESP. ALKALOSIS, for each mmHg that the PCO2 decreases, a HCO3- decrease of 0.55 will occur.
- This is the arterial blood gas results from a dog with acute renal failure. Is an acid base disturbance present? YES. Is the acidosis metabolic or respiratory? The PCO2 is low, so this can’t be respiratory acidosis. The HCO3 is low, hence this must be metabolic acidosis. To assess the possibility of a mixed disturbance, it must be determined whether the secondary response is as expected. The observed HCO3 is 10 mEq/L lower than normal (22-12). A normal dog can lower its PCO2 by 1.0 mmHg for every 1 mEq/L decrease in HCO3. Therefore, the expected PCO2 should be 27 mmHg. The observed PCO2 is 27 mmHg, and the adaptive response is appropriate. The patient has a simple metabolic acidosis with appropriate respiratory compensation.
- This is the arterial blood gas results from a dog sick for a week with coughing and dyspnea. Is an acid base disturbance present? YES. Slight acidemia Is the acidosis metabolic or respiratory? The HCO3- is high, so this can’t be metabolic acidosis. The PCO2 is high, hence this must be respiratory acidosis. To assess the possibility of a mixed disturbance, it must be determined whether the secondary response is as expected. The observed PCO2 is 20 mmHg higher lower than normal (57-37). A normal dog can increase its HCO3- by 0.35 mEq/L for every 1 mmHg increase in PCO2 in a chronic disturbance. Therefore, the expected HCO3- should be 29 mEq/L. The observed HCO3- is 29 mEq/L, and the adaptive response is appropriate. The patient has a simple respiratory acidosis with appropriate metabolic compensation.
- This is the arterial blood gas results from a seriously ill dog. Is an acid base disturbance present? YES. Acidemia Type of AB disturbance. Severe acidosis. Is the acidosis metabolic or respiratory? The PCO2 is high, so this could be respiratory acidosis; But the HCO3 is low as expected for metabolic acidosis. From this data, it can be said that the secondary response is not as expected. If this disorder were a simple metabolic acidosis, the PCO2 would be low in response. If it were a simple respiratory acidosis, the HCO3 would be high in response. This disturbance represents a mixed metabolic and respiratory acidosis.
- For one mmHg increase in PaCO2, there should be a 0.35 mEq/L increase in HCO3.
- Per one mmHg increase in PaCO2, there should be a 0.35 mEq/L increase in HCO3.
- Per one unit decrease in HCO3, there should be a one unit decrease in PCO2.