Ch 7.2: Acid-Base Disorders Flashcards
Acid
Substance that donates hydrogen ions (H+)
Base
Substance that accepts or combines with hydrogen ions
pH
Free H+ concentration that determines the acidity of body fluids
An increase in hydrogen ions → _ _ _ in pH
A decrease in hydrogen ions → _ _ _ in pH
An increase in hydrogen ions → decrease in pH
A decrease in hydrogen ions → increase in pH
Arterial blood pH range
7.35 to 7.45
“-emia”
Acidemia, Alkalemia
Refers to the measurement of pH in the blood
* Acidemia: pH below 7.35
* Alkalemia: pH above 7.45
“-osis”
Acidosis, Alkalosis
Refers to the clinical condition associated with the blood pH
* Acidosis: processes that raise H+ concentration
* Alkalosis: processes that lower H+ concentration
Mixed Acid-Base Disorders
disorders where acidotic and alkalotic processes may coexist
Body’s regulation of acid-base via 3 mechanisms
- Chemical buffering by extracellular (ECF) and intracellular (ICF) mechanisms
- Control of the partial pressure of CO2 (PCO2) in the blood by alterations in the rate and depth of ventilation
- Control of the serum bicarbonate (HCO3-) concentration by changes in renal H+ excretion and HCO3- reabsorption
Buffers
Prevent large changes in H+ concentration in the body
Buffers reversibly consume or release [H+] to maintain normal pH
Most abundant ECF buffer
& other buffer systems:
Carbonic acid/bicarbonate system
Others: plasma proteins, hemoglobin, phosphates
Lungs
- Regulate the pressure excreted by CO2 gas in the blood (PCO2)
- Begins to compensate for acid-base disturbances from diet/metabolism within minutes
- Conditions that impair respiratory system function (opiate overdose can cause acid-base imbalances
Respiratory Acidosis/Alkalosis
pH and PCO2 levels
Respiratory Acidosis: ↓ pH ↑ PCO2
Respiratory Alkalosis: ↑ pH ↓ PCO2
Opposites
Metabolic Acidosis/Alkalosis
pH and PCO2 levels
Metabolic Acidosis: ↓ pH ↓ PCO2
Metabolic Alkalosis: ↑ pH ↑ PCO2
The same
Kidneys
- Alterations in renal H+ excretion
- Slowest mechanism to maintain acid-base balance
Two processes involved to achieve this:
1) Reabsorption of filtered HCO3 (bicarbonate)
2) Excretion of H+ produced daily as a result of protein metabolism
Only the kidneys can regulate alkaline substances in the blood and eliminate metabolic acids
Arterial blood gas (ABG)
reflect the ability of lungs to oxygenate blood
Venous blood gas (VBG)
reflect tissue oxygenation
PCO2
The acid component
Lung’s ability to excrete CO2
* Increases in PCO2 = acidosis
* Decreases in PCO2 = alkalosis
PO2
Ability of Hgb to carry oxygen
* Higher PO2 = more saturated Hgb is with oxygen
HCO3: bicarbonate
the base component
Changes are associated with metabolic processes that can lead to acid-base disorders
* Increases in HCO3 = alkalosis
* Decreases in HCO3 = acidosis
Steps to evaluate acid-base disorders
1) Assess the pH of blood
* Acidemic: pH <7.4
* Alkalemic: pH >7.4
* pH 7.4 = possible mixed acid-base disorder
2) Assess PCO2 to determine whether respiratory process is contributing to acid-base disorder
* High PCO2 = respiratory acidosis
* Low PCO2 = respiratory alkalosis
3) Assess serum HCO3 to determine whether a metabolic process may be contributing to an acid-base disorder
* High HCO3 = metabolic alkalosis
* Low HCO3 = metabolic acidosis
4) Calculate the anion gap to determine whether metabolic acidosis is present
* Critical in determining the etiology and treatment of the acid-base disorder
5) Determine whether the acid-base disorder is acute or chronic
* If compensation is not appropriate, the patient has a mixed acid-base disorder
Compensatory Response
For respiratory disorders
- Kidneys regulate HCO3- via alterations in renal HCO3- excretion
- Compensation fully activated in 2 – 3 days
Compensatory Response
For metabolic disorders
- Lungs regulate PCO2 by altering the rate and depth of ventilation to allow for excretion of CO2 generated by diet and cellular metabolism
- Compensation starts within minutes
Respiratory Acidosis
Almost always results from decreased effective alveolar ventilation, NOT an increase in CO2 production
Hypoventilation
Respiratory Acidosis
Acute Causes
Acute airway disorders
* Airway obstruction
* Asthma/COPD exacerbation
Acute central nervous system depression
* Drug overdose
* Head trauma
* Stroke
* Infections
Acute neuromuscular disorders
* Guillain-Barre
* Spinal cord injury
* Neuromuscular blocking agents
Acute respiratory disorder
* Pneumonia
* Pulmonary edema
* Pulmonary embolus
* Hemothorax
* Pneumothorax
Parenteral or enteral nutrition overfeeding
* Excess CHO calories in PN solutions can lead to increased CO2 production and potential difficulty in weaning from respirators
In setting of hypoventilation = retaining CO2 (acid)
Respiratory Acidosis
Chronic Causes
acute & chronic
- Asthma
- COPD, emphysema
- Obstructive sleep apnea
- Hypoventilation syndromes
- Diaphragmatic paralysis
- Myasthenia gravis
- Amyotrophic lateral sclerosis (ALS)
- Spinal cord injury
- Multiple sclerosis
- Muscular dystrophy
- Poliomyelitis
- Kyphoscoliosis
- Hypothyroidism
In setting of hypoventilation = retaining CO2 (acid)
Respiratory Alkalosis
Occurs when effective alveolar ventilation is increased beyond the level necessary to eliminate metabolically produced CO2
Hyperventilation
Disease in which, due to reduced oxygen in blood (hypoxemia), the respiratory center is stimulated can result in respiratory alkalosis.
Respiratory Alkalosis - Causes
- Central nervous system disorders (anxiety, pain, infections, head trauma, malignancy, cerebrovascular disease)
- Hypoxia, high altitudes
- Lung disorder (Pneumonia, pulmonary edema, pulmonary embolism, asthma, hyperventilation, interstitial fibrosis)
- Mechanical ventilation
- Pregnancy
- Sepsis
- Medications (Xanthine derivatives, nicotine, catecholamines, salicylates)
- Hepatic encephalopathy / cirrhosis
In setting of hyperventilation = blowing off CO2 (acid)
Anion gap formula
= Na – (Cl + HCO3)
Decreased AG = decreased unmeasured anions (e.g., Albumin)
_ _ _ can falsely decrease the anion gap
What is the formula to correct AG?
- Hypoalbuminemia
- = AG + 2.5 x (4.5 – measured albumin)
For 1g/dL decrease of Alb, 2.5 mEq/L must be added to the anion gap
Anion gap
Used to differentiate the 2 main types of metabolic acidosis
- Normal anion gap acidosis (hyperchloremic acidosis)
- Elevated anion gap acidosis
Normal anion gap acidosis (hyperchloremic acidosis)
- mEq for mEq replacement of extracellular HCO3 by Cl
- the anion gap doesn’t change because the sum of major anions remains constant
Causes of normal anion gap acidosis (hyperchloremic acidosis)
USEDCAR
- GI bicarb losses – diarrhea, pancreatic or SB fistula
- Renal bicarb losses – type 2 renal tubular acidosis, hyperparathyroidism, hypoaldosteronism
- Ingestion of ammonium chloride or PN containing chloride salts
USEDCAR
* Ureteroenterostomy (urinary diversion)
* Small bowel (pancreatic / biliary) fistula
* Excessive chloride salts (IVF / parenteral nutrition)
* Diarrhea
* Carbonic anhydrase inhibitors (acetazolamide) / chronic kidney disease
* Adrenal insufficiency / aldosterone deficiency / ammonium chloride
* Renal tubular acidosis
Elevated anion gap acidosis
Accumulation of unmeasured anions → elevation in the anion gap
Causes of elevated anion gap acidosis
GOLDMARK
- Increased production of endogenous acids (lactic acidosis; ketoacidosis - diabetic, starvation, ETOH; inborn errors of metabolism)
- Failure to excrete acids (renal failure)
- Ingestion of exogenous acid (salicylates, methanol, ethanol)
GOLDMARK
* Glycols – ethylene and propylene
* Oxoproline (acetaminophen)
* Lactic acidosis
* D-lactate acidosis (small bowel bacterial overgrowth)
* Methanol
* Aspirin
* Renal failure
* Ketoacidosis – diabetic and starvation
What should a PN formulation for a high-output ileostomy contain?
- Maximum amounts of acetate salts to prevent or correct a hyperchloremic metabolic acidosis
- The sodium concentration should be ~normal saline to approximate sodium concentration of the ileostomy fluid
Metabolic Acidosis
- Characterized by reduced pH, reduced HCO3
- Compensatory hyperventilation → decreased PCO2 (acid)
Metabolic Acidosis can be induced by 2 mechanisms:
- Inability of kidneys to excrete dietary H+ load
- Increase in the generation of H+ – either by addition of H+ or loss of HCO3
Causes/examples in Metabolic Acidosis
Lactic acidosis (all cells produce lactic acid if deficient of oxygen; increased lactic acid production and resulting metabolic acidosis occur in any condition in which oxygen delivery to the tissues is severely compromised
* Cardiac arrest
* Any condition associated with hypovolemic shock (e.g. massive fluid loss)
* Liver failure – the liver plays a major role in removing the small amount of lactic acid that is produced during normal cell metabolism, so that lactic acidosis can be a feature of liver failure
Diabetic ketoacidosis (abnormally high blood concentrations of keto-acids)
Diarrhea – abnormal loss of bicarbonate from the body
Renal failure – failure to regenerate bicarbonate and excrete hydrogen ions
Metabolic Alkalosis
Characterized by elevated pH, increased HCO3
* Compensatory hypoventilation → rise in PCO2
Causes/examples in Metabolic Alkalosis
- Loss of gastric acid (vomiting, NG suction)
- Loss of intravascular volume and chloride 2/2 diuretic use
- In hospital setting: overzealous treatment of metabolic acidosis with bicarb or an excess of acetate in the PN
- Transcellular shift of H+ that occurs with severe hypokalemia
How can severe potassium depletion cause metabolic alkalosis?
Due to the reciprocal relationship between hydrogen and potassium ions
In normal circumstances, the kidneys can correct by …
excreting the excess HCO3 in the urine
Urine chloride concentration:
is useful in differential diagnosis of metabolic alkalosis and predicts those who will respond to volume repletion
Mechanisms to sustain metabolic alkalosis:
Volume-mediated processes (saline responsive)
- Urine chloride level
- Treatment
- Causes
Urine chloride <20 mEq/L
Treatment: administration of half-isotonic or isotonic (0.9%) saline
* Will not reverse metabolic alkalosis r/t moderate to severe hypokalemia – only KCl administration will correct this disorder
Causes: GI loss, vomiting, NG suction, renal loss, diuretics, excessive bicarb administration, rapid correction of hypocapnia
Mechanisms to sustain metabolic alkalosis:
Volume-independent processes (saline unresponsive)
- Urine chloride level
- Treatment
- Causes
Urine chloride >20 mEq/L
High urinary chloride concentration
Typically associated with hyperaldosteronism
Treatment: management of underlying cause of mineralocorticoid (a class of steroid hormones that regulate salt and water balances) excess
* Aggressive potassium repletion with hypokalemia in setting of primary aldosteronism
Causes: excess mineralocorticoids, cushing’s syndrome, hyperaldosteronism, profound hypokalemia (<2mEq/L), excessive licorice ingestion (ex: from chewing tobacco)
Mixed
Examples of Mixed Acid-Base Disorders
- High output fistula presenting with respiratory failure
- Diabetic ketoacidosis (DKA) presenting with pneumonia
A patient presents with a metabolic acidosis. Which ABG pattern fits this disorder?
A. Decreased pH, decreased HCO3-
B. Decreased pH, increased PCO2
C. Increased pH, increased HCO3-
D. Increased pH, decreased PCO2
Nutr Fundamentals - Acid Base ppt
For a patient with metabolic acidosis, what is the appropriate method of compensation seen on an ABG?
A. Hyperventilation leading to an increase in pCO2
B. Hyperventilation leading to a decrease in pCO2
C. Hypoventilation leading to an increase in pCO2
D. Hypoventilation leading to an increase in pCO2
Nutr Fundamentals - Acid Base ppt
Which of the following can lead to metabolic alkalosis?
A. Pulmonary embolism
B. Septic shock
C. High nasogastric output
D. Morphine overdose
Nutr Fundamentals - Acid Base ppt
