Lecture 1 Acid-base disturbances PDF

ACID-BASE DISTURBANCES Lecture outline Introduction Definition of Acid-base disorder Acid-base homeostasis Assessment of acid-base status Acute and chronic acid-base disorders Simple and complicated acid-base disorders Compensatory Responses What if compensation is inappropriate? A...

ACID-BASE DISTURBANCES Lecture outline Introduction Definition of Acid-base disorder Acid-base homeostasis Assessment of acid-base status Acute and chronic acid-base disorders Simple and complicated acid-base disorders Compensatory Responses What if compensation is inappropriate? Acid-Base disorders Disturbances of acid–base equilibrium occur in a wide variety of illnesses and are among the most frequently encountered disorders in critical care medicine Acid–base disorders may result in significant morbidity and mortality Medications are a frequent cause of acid–base abnormalities. Clinicians must anticipate drug-related problems to avoid or minimize the clinical consequences Acid-Base disorders o Severe derangements can affect any organ system, but the most serious clinical effects are: cardiovascular (arrhythmias, impaired contractility) neurologic (decreased cerebral blood flow, coma, seizures) pulmonary (dyspnea, impaired oxygen delivery, respiratory fatigue, respiratory failure) and/ or renal (hypokalemia) o Changes in acid–base status also affect multiple aspects of pharmacokinetics (clearance, protein binding) and pharmacodynamics Acid-Base disorders Acid–base disorders are caused by disturbances in hydrogen ion (H+) homeostasis When there is a change in H+ concentration, proteins gain or lose H+, resulting in alterations in charge distribution, molecular configuration, and consequently protein function To protect body proteins, acid–base balance must be tightly controlled in an attempt to maintain a normal extracellular pH of 7.35 to 7.45 Daily Acid Load  Acid-Base homeostasis H+ homeostasis is maintained by three distinct mechanisms working in harmony 1. buffering by extracellular bicarbonate (HCO3-) and intracellular proteins, organic and inorganic phosphates and in the RBC, hemoglobin e.g. H2SO4 (strong acid) + 2NaHCO3 → NA2SO4 + 2H2CO3 (weak acid ) →2CO2 + 2H2O + NA2SO4 2. renal excretion of metabolic acids, excretion or reabsorption of filtered (HCO3-) (an alkali), and synthesis of new (HCO3-) 3. pulmonary regulation of carbon dioxide (CO2) (acid) elimination (through changes in the depth and/or rate of respiration)  Acid-Base homeostasis H+ homeostasis is maintained by three distinct mechanisms working in harmony 1. buffering by extracellular bicarbonate (HCO3-) and intracellular proteins, organic and inorganic phosphates and in the RBC, hemoglobin e.g. H2SO4 (strong acid) + 2NaHCO3 → NA2SO4 + 2H2CO3 (weak acid ) →2CO2 + 2H2O + NA2SO4 2. renal excretion of metabolic acids, excretion or reabsorption of filtered (HCO3-) (an alkali), and synthesis of new (HCO3-) 3. pulmonary regulation of carbon dioxide (CO2) (acid) elimination (through changes in the depth and/or rate of respiration) Acid-Base homeostasis An acid base disorder is a change in the normal value of extracellular pH that may result when renal or respiratory function is abnormal or when an acid or base load overwhelms excretory capacity Acid–base status is traditionally represented in terms of pH pH is the -ve log of H+ concentration [H+] pH and [H+] are inversely related Acid-Base homeostasis Kassirer-Bleich equation: [H+] = 24 × PCO2 / [HCO3-] [H+] and accordingly the pH depend only on the ratio of dissolved CO2 to HCO3− and not the absolute amount of either Where PCO2 (PaCO2) is the partial pressure of arterial CO2 in mmHg and [HCO3-] is the bicarbonate concentration in mEq/L or mmol/L PCO2 Acid-Base homeostasis Because the kidneys excrete less than 1% of the estimated 13,000 mEq (13,000 mmol) of H+ ions generated in an average day, renal failure can be present for prolonged periods before life threatening imbalances occur Conversely, cessation of breathing for minutes results in profound acid–base disturbances Laboratory assessment of acid-base status Blood gas analyzers Normal Arterial Blood Gas (ABG) values  Analysis of ABGs pH These are the 4 primary acid-base disorders Acidemia vs alkalemia  Acute and chronic acid-base disorders Because CO2 is a volatile acid, it can rapidly be changed by the respiratory system. If a respiratory acid–base disturbance is present for minutes to hours, it is considered an acute disorder, while if it is present for days or longer it is considered a chronic disorder The metabolic machinery that regulates HCO3− results in slow changes, and all metabolic disorders are chronic acute chronic Usually acute chronic Usually chronic chronic Simple and complicated acid-base disorders Respiratory and metabolic derangements can occur in isolation or in combination. If a patient has an isolated primary acid–base disorder that is not accompanied by another primary acid–base disorder, a simple (uncomplicated) disorder is present. If two or three primary acid–base disorders are simultaneously present, the patient has a mixed (complicated) disorder. More complex clinical situations lead to mixed acid–base disturbances where pH may be normal or abnormal Compensatory Responses Primary acid-base disorders are associated with defense mechanisms referred to as compensatory responses that function to reduce the effects of the particular disorder on the pH They do not restore the pH back to a normal value, this can only be done with correction of the underlying cause In each of these disorders, compensatory renal or respiratory responses act to minimize the change in H+ concentration by minimizing the alteration in the PCO2 /[HCO3-] ratio  Compensatory Responses Primary Initial Compensa- Compensa- Expected level of disorder chemical tory tory compensation change response Mechanism Metabolic ↓HCO3− ↓PCO2 Hyper- ↓PCO2 = 1.2×∆ [HCO3−] Acidosis ventilation Metabolic ↑HCO3− ↑PCO2 Hypo- ↑PCO2 = 0.7 ×∆ [HCO3−] Alkalosis ventilation  Compensatory Responses 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  Compensatory Responses 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 Summary points of Compensatory Responses 1. Compensatory responses never return the pH to normal 2. The basis of compensatory responses is to maintain the PCO2/[HCO3-] ratio 3. Therefore, the direction of the compensatory response is always the same as that of the initial change 4. Compensatory response to respiratory disorders is two-fold; a fast response due to cell buffering and a significantly slower response due to renal adaptation 5. Compensatory response to metabolic disorders involves only an alteration in alveolar ventilation 6. Metabolic responses cannot be defined as acute or chronic in terms of respiratory compensation because the extent of compensation is the same in each case What if compensation is inappropriate? o If the measured values differ markedly from the calculated values i.e. the measured serum HCO3− is greater than (differs by more than) 2 mEq/L [2 mmol/L] from the calculated value or the measured PaCO2 is greater than (differs by more than) 4 mmHg from the calculated value, Then a second acid–base disorder is present Case Study o Case Study 1 A 59-year-old man is undergoing lung transplant evaluation for advanced emphysema. An ABG drawn during the transplant workup shows: a pH of 7.34, a PaCO2 of 70 mm Hg, and a HCO3– of 35 mEq/L (35 mmol/L) 1. What is the primary acid–base disorder? 2. Is their a secondary acid–base disorder?  Case Study 1 model answer The patient’s ABG values: pH of 7.34, PaCO2 of 70 mm Hg, HCO3– of 35 mEq/L 1. Primary A-B disorder: Respiratory acidosis 2. Assess for compensation, if inappropriate, then a second A-B disorder is present Primary Initial chemical Compens- Compensatory Expected level of disorder change atory Mechanism compensation response Respiratory ↑PCO2 ↑HCO3- Generation of new ↑[HCO3-] = 0.35 x Acidosis HCO3- due to the ∆PCO2 Chronic increased excretion of ammonium Measured [HCO3-] = 35 mEq/L The increase in [HCO3-] = ↑[HCO3-] = 35-24= 11 mEq/L Calculated [HCO3-] = 0.35 x ∆PCO2 = 0.35 (70 - 40) = 10.5 mEq/L Then the measured serum HCO3− does not differ by more than 2 mEq/L from the calculated value, i.e. compensation is appropriate and there is no second A-B disorder is present Case Study o Case Study 2 The next patient is a 60-year-old, was admitted to the hospital 4 days ago with peripheral edema and pulmonary congestion consistent with a congestive heart failure exacerbation. Since admission, she has been treated aggressively with furosemide. Her chest radiograph findings and peripheral edema now show considerable improvement with diuresis; however, she now complains of dizziness when she gets out of bed to go to the bathroom. Physical examination reveals a tachycardic (heart rate [HR], 100 beats/minute), thin elderly woman with poor skin turgor and slight muscle weakness. An ABG was drawn and shows the following: pH of 7.50, a PaCO2 of 47 mm Hg, and a HCO3– of 36 mEq/L (36 mmol/L) What is the primary acid–base disorder? Is their a secondary acid–base disorder?  Analysis of ABGs pH These are the 4 primary acid-base disorders Application of basic pathophysiology ↓PCO2 = ↑PCO2 = 1.2×∆ [HCO3−] 0.7 ×∆ [HCO3−]  THANK YOU You can contact me via email [email protected]