Acid / Base Disorders

Respiratory Alkalosis

Characteristics of Respiratory Alkalosis

·         pCO₂ is determined by metabolic production of CO₂ (VCO₂) and the extent to which CO­₂ can be removed by the lungs (minute ventilation)

o        minute ventilation = tidal volume ´ breaths/min

o        hypoventilation = ­ pCO₂ =  respiratory acidosis

o        hyperventilation = ¯ pCO₂ = defining feature of respiratory alkalosis

·         All of the following conditions can be a likely source of respiratory alkalosis, each of which are associated with hyperventilation:

o        Cardiopulmonary: CHF, lung disease, chest wall abnormality

o        CNS disturbance/head trauma: stimulates respiratory centers in brain

o        Hepatic encephalopathy: e.g., with liver failure, jaundice

o        Sepsis: patients may be febrile, but may also present with hyperventilation

o        Drugs

§         Aspirin: causes respiratory alkalosis and mixed disturbance

·         Peds: although respiratory alkalosis is present, metabolic acidosis predominates

·         Adults: mixed disturbance, but respiratory alkalosis predominates

·         Dr. Baskin indicated that if a patient presents with a severe Aspirin overdose, you can manipulate the blood/urine pH to enhance excretion of Aspirin (this is the “textbook” answer that will appear on the boards).  However, in practice, such manipulation can be dangerous; these patients should be dialyzed instead

§         Theophylline: bronchodilator in the treatment of asthma (phosphodiesterase inhibitor); causes respiratory alkalosis

·         Note Adverse Effects: tachycardia, arrhythmia, hypotension, mental confusion

o        Hysteric: person who is emotionally distraught hyperventilates, and becomes acutely alkalotic

o        Normal pregnancy: at 6-7 months of every normal pregnancy, there is a physiologic respiratory alkalosis

§         ­ Cl^-, ¯ HCO₃^- in a non-pregnant person suggests metabolic acidosis with a normal Anion Gap, but you must do Arterial Blood Gas to determine acid-base status; could also be respiratory alkalosis with compensation

§         ­ Cl^-, ¯ HCO₃^- in a pregnant woman = normal
 

·         To determine whether metabolic compensation is present in respiratory alkalosis, use the following estimates for “expected” HCO₃^- values:

o        Acute respiratory alkalosis: expect 1-2 mEq/L decrease in HCO₃^- for each 10 mmHg decrease in pCO₂

o        Chronic respiratory alkalosis: expect 5-6 mEq/L decrease in HCO₃^- for each 10 mmHg decrease in pCO₂

Clinical Presentation of Respiratory Alkalosis

·         Hysterical patient

o        This is acute respiratory alkalosis without metabolic compensation

§         There is no time for significant renal compensation in acute respiratory alkalosis

§         In chronic respiratory alkalosis, renal compensation takes 3-5 days

o        In practice, you rarely see patients present with acute respiratory alkalosis because the hysteria (and subsequent hyperventilation) is generally transient, and Arterial Blood Gass are not generally performed on these patients

o        Why could a patient who is acutely hyperventilating develop a positive Chvostek sign (i.e., tapping on CN VII causes facial muscle twitches) and carpal-pedal spasms?

§         Ionized Ca²⁺ (physiologically active form) is in pH-dependent equilibrium with albumin-bound Ca²⁺ (physiologically inactive form)

·         Acidosis favors ionized (active) form of Ca²⁺

·         Alkalosis favors bound (inactive) form of Ca²⁺

§         In this case, alkalosis leads to a decrease in ionized form of Ca²⁺ and subsequent tetany

o        Treatment: breathe in/out of a brown bag to elevate pCO₂

·         Acute alcohol intoxication & hallucinations; hyperventilation for 4 days

o        This is chronic respiratory alkalosis with partial compensation

§         If compensated, a 14 mmHg decrease in pCO₂ would be expected to yield an approximate 9 mEq/L decrease in HCO₃

§         In this case, there is a 6 mEq/L decrease in HCO₃, so it is partially compensated

Respiratory Acidosis

Characteristics of Respiratory Acidosis

·         Always due to hypoventilation, which leads to ­ pCO₂

·         Occurs when the minute ventilation is inadequate to handle the metabolic production of CO₂

·         Hypoventilation can arise due to CNS reasons (opiate intoxication), chest wall trauma, etc.

·         To determine whether metabolic compensation is present in respiratory acidosis, use the following estimates for “expected” HCO₃^- values:

o        Acute respiratory acidosis: expect 1-2 mEq/L increase in HCO₃^- for each 10 mmHg increase in pCO₂

o        Chronic respiratory acidosis: expect 3-4 mEq/L increase in HCO₃^- for each 10 mmHg increase in pCO₂

Clinical Presentation of Respiratory Acidosis

·         An asthmatic patient comes into the ER hyperventilating, and is either sedated inadvertently or develops fatigue from this intense respiratory effort, resulting in hypoventilation and a rise in pCO₂

o        This is acute respiratory acidosis without compensation

§         Renal mechanism for compensation takes 3-5 days

o        This asthmatic patient is managed poorly in the ER, and is allowed to become hypoxic.  This results in a decreased pO₂ and the following Arterial Blood Gas values:

§         Decreased pH, decreased HCO₃, and increased Anion Gap imply metabolic acidosis.  So, coupled with the earlier respiratory acidosis, this patient now has a mixed disturbance

§         Hypoxia leads to an increased lactic acid level, which accounts for the decreased pH and increased Anion Gap

o        Acute respiratory acidosis can result in papilledema and retinal hemorrhages

o        Treatment: ventilation

·         A 60 y/o chronic smoker and coal miner presents for his regular monthly checkup at the pulmonary clinic with the following Arterial Blood Gas values:

o        This is chronic respiratory acidosis with appropriate compensation

·         Patient comes to the ER with history of cough and fever x1 week.  CXR shows pneumonia.

o        In the initial Arterial Blood Gas, the patient exhibits chronic respiratory acidosis with appropriate compensation

o        However, the subsequent Arterial Blood Gas reveals an acidotic spike (­ pCO₂, ¯ pH).  This is acute respiratory acidosis without appropriate compensation

o        This patient, therefore, has both acute & chronic respiratory acidosis

o        Treatment: low flow O₂

§         Do NOT give high flow O₂ because in patients with COPD, the respiratory drive is stimulated by hypoxia.  High flow O₂ will cause the patient to stop breathing.

§         This is in contrast to normal patients where the respiratory drive is stimulated by hypercapnea

o        Patient begins to hypoventilate, so the patient is intubated and mechanically-ventilated to blow off enough CO₂ to reach a pCO₂ of 40.

§         Patient is now left with a “burden” of excess HCO₃^- after ventilation, so this presentation is post-hypercapneic metabolic alkalosis, and it will take 3-5 days for renal elimination of the excess HCO₃^-

§         Patient recovers from this episode, and is put on a diuretic.  Patient returns to clinic:

·         Remember, the patient has an underlying chronic respiratory acidosis.  Given a 20 mmHg increase in pCO₂, the patient would be expected to have a HCO₃^- of 32 mEq/L.  However, in this case, the patient has a much greater HCO₃^-

·         In addition to the chronic respiratory alkalosis, the patient now has a primary metabolic alkalosis, which is secondary to the hypokalemic state induced by the diuretic.  Therefore, the patient has a mixed disturbance 

Metabolic Alkalosis

Characteristics of Metabolic Alkalosis

·         Definition: ­ HCO₃^-, ­ pH

·         Four causes of metabolic alkalosis (in bold)

o        Cl^- sensitive (urinary Cl^- <20 mEq/L; treat with normal saline)

§         Vomiting: loss of gastric acid

§         Diuretics (thiazides, loops): lead to metabolic alkalosis by causing volume contraction, which leads to increased HCO­₃^- reabsorption, loss of H⁺/K⁺/Na⁺

§         Post-hypercapneic state (see previous clinical example)

o        Cl^- resistant (urinary Cl^- >20 mEq/L; cannot treat with normal saline)

§         Mineralocorticoid excess syndromes

·         In patients with metabolic alkalosis, the compensatory mechanism is mild hypoventilation, which leads to an increase in pCO₂

o        If compensated, a 0.3-0.5 mmHg increase in pCO₂ is expected for each 1 mEq/L increase in HCO₃^- 

Clinical Presentation of a Mixed Disturbance

·         4 y/o child consumes numerous aspirin tablets