Lecture 7 Acid/Base Disorders Flashcards
(17 cards)
Where is blood drawn from to get things like pH, pCO2, pO2, etc?
arterial blood gas (ABG)
drawn from an artery rather than a vein which gives accurate measure of pO2 and pCO2
What is physiologic buffers when it comes to compensatory mechanisms for blood pH?
primary elimination through the carbonic (H2CO3) buffer system
other ones include phosphate buffers, protein buffers (Hgb, albumin)
Preview
What role can the lungs play when it comes to buffering systems?
respiratory regulation: increase CO2 (decrease resp rate) - more acidic environment
decrease CO2 (increase respiratory rate) - more basic environment
chemoreceptors are responsible for these ventilation responses
What role can the kidneys play in buffering systems?
slow onset (> 48 hours)
metabolic regulation: increase HCO3- (reabsorbs or produces HCO3-) - more basic environment
decrease HCO3- (excreting HCO3-) - more acidic environment
What are the four main types of primary acid base disorders and what do they involve?
- Respiratory acidosis (CO2 retention)
- Respiratory alkalosis (CO2 loss)
- Metabolic acidosis (H+ accumulation/HCO3)
- Metabolic alkalosis (H+ loss/HCO3 retention).
What is primary respiratory alkalosis, S&S, causes?
defined by pH > 7.4 and pCO2 < 40 mmHg
S&S: mostly CNS effects, usually mild - dizziness, lightheadedness, paresthesia ⇒ can progress to serious signs like confusion, seizures
Causes: 1. Hyperventilation - drug induced (ex. nicotine), anxiety, infection
- Hypoxia - high altitudes
What is primary respiratory acidosis, S&S, causes?
defined by pH < 7.4 and pCO2 > 40 mmHg
S&S: H/A, delirium, coma, tachycardia, hypotensive sx (ex. lightheaded, dizziness, etc), arrythmias
Causes: 1. Hypoventilation - drug induced, neuromuscular dysfunction, head injury
- Airway obstruction - pneumonia, COPD, pulmonary edema
- Hypermetabolic states
What is primary metabolic alkalosis, S&S, causes?
defined by pH > 7.4 and HCO3- > 28 mEq/L
S&S: CNS - lethargy, confusion, muscle weakness, hypoventilation (decrease RR), hypokalemia, cardiac effects (tachycardia, arrhythmias)
Causes: 1. intake of excess alkali (excess bicarbonate) - ex. excessive antacid usage
- severely decreased renal fxn - leads to retention of HCO3- because it can’t get rid of excess properly
- loss of excess H+ - ex. vomiting, diuretics
What is primary metabolic acidosis, S&S, causes?
defined by pH < 7.4 and HCO3- < 22 mEq/L
S&S: hyperventilation (increase in RR), CNS effects - lethargy, confusion, coma
hyperkalemia, insulin resistance, N/V
Causes: need to calculate an anion gap
What is an anion gap (AG), value ranges?
represents difference between unmeasured cations and anions
this = unmeasured anions - unmeasured cations OR [Na+] - [Cl-] - [HCO3-], normally = 12 mmol/L (Range: 8-14 mmol/L)
includes positively charged proteins, Ca2+, Mg2+, negatively charged proteins (ex. albumin), non-carbonic acids (ex. lactate, phosphates, ketones)
this = 12 - acidosis is not being caused by unmeasured cations/anions
this > 14 mmol/L - likely an excess of unmeasured anions that factor into acidosis
this < 8 mmol/L - likely lack of unmeasured anions that factor into acidosis
What is normal anion gap metabolic acidosis, causes?
this is around 12 mmol/L
bicarbonate loss due to: diarrhea, drugs (ex. acetazolamide, amphotericin B), excessive fluid admin (ex. normal saline)
reduced kidney fxn - inability to eliminate H+ or retain HCO3-
body is compensating with increasing the amount of Cl-
Causes: HARDUP - Hyperalimentation, Acetazolamide, Renal tubular acidosis, Diarrhea/dilutional (rapid saline admin), Ureteral diversion, Pancreatic fistula
Preview
What is increased anion gap metabolic acidosis, causes?
this is > 14 mmol/L
overproduction of various acids (ex. lactic acidosis, diabetic ketoacidosis), large ingestion of various chemicals (ex. methanol, ethanol, ethylene glycol), drugs (ex. metformin, propofol, salicylates, iron), severe renal failure - leads to loss or retention of those unmeasurable anions/cations
Causes: MUDPILES - Methanol/metformin, Uremia, Diabetic ketoacidosis, Propofol/paraldehyde, Iron/isoniazid, Lactate/linezolid, Ethylene glycol, Salicylates/starvation
What is decreased anion gap metabolic acidosis, causes?
this is < 8 mmol/L
uncommon, generally associated with hypoalbuminemia, low albumin levels leads to lower anion gap (albumin is unmeasured anion)
Tx of primary respiratory alkalosis?
physiologic compensation (secondary): 1. instant buffer mechs, 2. lungs: can’t use, part of problem, 3. kidneys: retain acid and excrete base to lower pH - takes awhile to adjust, will see HCO3- of <22 mEq/L
HCP interventions: identify and correct underlying cause, monitor ABGs and RR
Tx of primary respiratory acidosis?
physiologic compensation (secondary): 1. instant buffer mechs, 2. lungs: can’t use, part of problem, 3. excrete acid and retain base to increase pH - takes awhile to adjust, will generally see HCO3- of >28 mEq/L
HCP interventions: identify and correct underlying cause, monitor ABGs and RR
Tx of primary metabolic alkalosis?
physiologic compensation (secondary): 1. instant buffer mechs, 2. lungs: RR decreases to increase CO2 and lower pH, will see CO2 > 40 mmHg, 3. kidneys: can’t use, part of problem
HCP intervention: identify and correct underlying, correct fluid/electrolyte abnormalities
Tx of primary metabolic acidosis?
physiologic compensation (secondary): 1. instant buffer mechs, 2. lungs: RR increases to reduce CO2 and increase pH, will see CO2 < 40 mmHg, 3. kidneys: can’t use, part of problem
HCP intervention: identify and correct underlying, consider admin depending on severity sodium bicarbonate (PO/IV)
