Partial 6 - Acid-Base Disorders Flashcards
Hydrogen concentration in acidemia and alkalemia
Acidemia: H+ more than 45
Alkalemia: H+ less than 35
If pCO2 doubles while HCO3 remains constant
pH will drop by 0.3 units
If you reduce pCO2 by half
pH will rise by 0.3 units
If HCO3 doubles while pCO2 remains constant
pH will rise by 0.3 units
If you reduce HCO3 by half
pH will drop 0.3 units
Henderson hasselback equation states that
pH is equal to pK plus the log of the ratio of the concentration of a base to its related acid.
Normal concentration of bicarbonate
22-26 mmol/L
Normal concentration of CO2
35-45 mmHg
Normal concentration of hydrogen
40 nmol/L
What happens to the potassium concentration in acidemia and alkalemia and why?
Acidemia produces hyperkalemia, and alkalemia produces hypokalemia due to potassium being exchanged for hydrogen between the cell and extracellular fluid
Why can severe acidosis lead to osteodystrophy?
In severe acidosis the bones accept hydrogen and releases calcium
Anion gap
The measured ions are sodium (Na+), chloride (Cl-) and bicarbonate.
The formula goes like this: Na + UC = Cl + HCO3 + UA.
Unmeasured cations include
Potassium, calcium, and magnesium, and together these are 11 mEq/L.
Unmeasured anions include
Sulfates, phosphates, Albumin, Lactic acid, and organic acids which together are 23 mEq/L
Normal anion gap value
8-15
Causes of increased anion gap
Accumulation of organic acids (ketones, lactate)
Toxic ingestions (methanol, ethylene glycol, salicylates)
Reduced inorganic acid excretion (phosphates, sulfates)
Decrease in unmeasured cations (decreased in unmeasured cations leads to increased measured cation because the blood is electroneutral).
Increased anion gap value
more than 18
Decreased/Negative anion gap causes
Decreased proteins (mainly albumin); There is 2-2.5 mEq/liter drop in AG for every 1 g drop in albumin.
Other etiologies; High potassium, magnesium, calcium, increased globulins
Lithium, bromide or iodine intoxication
Increased globulins happens in which disease
Multiple myeloma
Increased lithium and bromide is also seen in multiple myeloma
Compensation in acid-base disorders are rarely complete. In which cases are they complete?
High altitude and pregnancy (chronic respiratory alkalosis)
Respiratory compensation to metabolic acidosis
Compensated by hyperventilation, called “kussmaul respiration” which is more deep than rapid, which means that it has high tidal volume
Respiratory compensation to metabolic alkalosis
Hypoventilation, and is this is restricted by hypoxemia
Metabolic compensation in acute hypercapnia
bicarbonate increases 1 mmol/L for each 10 mmHg increase in pCO2 more than 40
Metabolic compensation in chronic hypercapnia
Bicarbonate increases 3.5 mmol/L for each 10 mmHg increase in pCO2 more than 40
Metabolic compensation in acute hypocapnia
Bicarbonate decreases 2 mmol/L for every 10 mmHg decrease in pCO2 less than 40
Metabolic compensation in chronic hypocapnia
Bicarbonate decreases 5 mmol/L for every 10 mmHg decrease in pCO2 less than 40
Effects of metabolic acidosis
Vascular collapse Impaired cardiac contractility Increased pulmonary vascular resistance Inability to respond to catecholamines Decreased threshold for ventricular fibrillation Decreased hepatic and renal perfusion.
Effects of alkalemia
Generalized and cerebral vasoconstriction
Shift of oxyhemoglobin dissociation to left
Hypokalemia
Increased systemic vascular resistance
Decreased contractility
Cardiac arrhythmias refractory
Seizures.
Types of lactic acidosis
Type A (tissue hypoxia) Type B (normal oxygen, Paucity in NAD+, or excess NADH)
Causes of Type A lactic acidosis
(1) Toxins such as iron, isoniazid, CN, methgb, CO, HS, and toluene
(2) Shock states
(3) Profound anemia
(4) Massive catecholamines
(5) Hypoxia
(6) Anaerobic exertion, seizures, sprinting
(7) Beriberi, total parenteral nutrition, and alcoholics
Causes of Type B lactic acidosis
(1) Diabetes mellitus
(2) Liver failure
(3) renal failure
(4) Carcinoma
(5) Hypoglycemia
(6) EtOH ingestion and many others
Increased NADH leads to increased reduction of pyruvate to lactate.
Causes of ketoacidosis
It can be due to increase in FFA load to liver, or increased conversion of FFA to ketoacids. Increased conversion of FFA to ketoacids may occur in diabetic ketoacidosis, in alcoholism, and to a lesser degree in prolonged starvation or a high-fat diet
Causes of normal aniongap metabolic acidosis
(1) Loss of bicarbonate such as in chronic diarrhea, pancreatic fistulas, post-hypocapnia, uretroileostomy, acetazolamide
(2) Failure to excrete hydrogen such as in renal tubular acidosis and adrenal insufficiency
(3) Administration of hydrogen such as ammonium chloride, arginine hydrochloride, or aminoacidhydrochlorides
Types of renal tubular acidosis
RTA1 involves failure of distal tubules to excrete hydrogen properly, while RTA2 involves bicarbonate wasting in proximal tubules, and both lead to normal AG metabolic acidosis, with hypokalemia.
RTA4 is caused by lack of aldosterone and leads to hyperkalemia and acidemia.
Causes of metabolic alkalosis
Hypochloremia
Alkali ingestion
Massive transfusion
Causes of respiratory acidosis
Inadequate ventilation; (1) Head, chest, spinal cord trauma, (2) Sedative, hypnotics, (3) Neuropathy/myopathy, (4) Pulmonary disorder, (5) Airway obstruction, (6) Sleep apnea.
Increased dead space ventilation; (1) COPD.
Increased carbohydrate metabolism; (1) Total parenteral nutrition.
Causes of respiratory alkalosis
1) Salicylates (stimulate medullary chemoreceptor)
(2) increased intracranial pressure
(3) Liver failure (due to NH3)
(4) hypoxia, CHF, pericardial effusion, pulmonary embolus
(5) hyperthyroidism (due to increased metabolism and CO2)
(6) pregnancy (progesterone increases ventilation and lowers arterial pCO2 by as much as 5-10mmHG)
(7) Sympathomimetics (amphetamines, cocaine, and phencyclidine)
(8) Hyperventilation, in shock, sepsis, trauma/pain, psychogenic/anxiety
(9) CNS disease.
