ABGs Flashcards
Arteries to get ABGs from?
- radial artery should be 1st choice: superficial, easily compressed
- other arteries: femoral and brachial
What can acidosis cause?
- decreased force of cardiac contraction
- decreased vascular response to catecholamines
- decreased response to effects and action of certain meds
What can alkalosis interfere w/?
- tissue O2
- neuro and muscle fxn
O2-Hgb dissociation?
- Bohr effect: increased CO2 = decreased pH
- when pH changes - that changes binding of O2
- lower the pH the curve moves right, allows O2 to dissociate easier
- left shift (alkalosis): O2 doesn’t unload as well
What controls the pH?
- diet
- metabolic prod of CO2
- regulation through GI tract
- influence of other lytes
- buffers
3 systems that maintain pH?
- chemical buffering: carbonic acid (main buffer) - CO2 is best transported as HCO3- (as CO2 increases so does H+) phosphate plasma proteins - resp center - kidneys
How does resp buffer work?
- conc. of CO2, carbonic acid, and HCO3 will trigger resp center
- RR and tidal vol will be altered to either increase or decrease ventilation
- response occurs in 1-3 min
How does renal buffer work?
- kidneys can excrete either acid or alkaline urine, thereby adjusting pH of blood:
excrete or retain HCO3- and H+
if blood pH decreases then bicarb would be retained to balance out acidity) - response takes over hours or even days, but represents a more powerful regulatory system
Onset of action of buffer systems?
- chemical buffer systems occur almost immediately
- respiratory and renal systems act more slowly than chemical buffers, have more capacity than chemical buffers
Causes of resp acidosis?
- CNS depression: meds - narcotics, sedatives, anesthesia
- impaired muscle fxn: spinal cord injury, neuromuscular diseases, or neuromuscular blocking drugs
- pulm disorders: atelectasis, pneumonia, pneumothorax, pulmonary edema, bronchial obstruction
- massive PE
- hypoventilation due to pain, chest wall injury, or abdominal pain
S/S of resp acidosis?
- resp: dyspnea, resp distress, and/or shallow respiration
- nervous: HA, restlessness and confusion: if CO2 level extremely high drowsiness and unresponsiveness may be noted (hypoxic)
- CVS: tachycardia and dysrhythmias
Management of respiratory acidosis?
- increase ventilation
- causes that can be tx rapidly: pneumo, pain and CNS depression due to med
- if cause can’tbe readily resolved then will reqr mechanical ventilation
Causes of resp alkalosis?
- psych responses, anxiety or fear
- pain
- increased metabolic demads: fever, sepsis, preg, or thyrotoxicosis
- meds: resp stimulants
- CNS lesions
S/S of resp alkalosis?
- CNS: light headedness, numbness, tingling, confusion, inability to concentrate and blurred vision
- dysrhythmias and palpations
- dry mouth, diaphoresis and tetanic spasms of arms and legs
Management of resp alkalosis?
- resolve underlying problem
- monitor for resp muscle fatigue
- when resp muscles become exhausted, acute resp failure may ensue
Causes of metabolic acidosis?
- renal failure
- DKA
- anaerobic metabolism (tissue death, lactic acidosis)
- starvation
- salicylate intoxication
- sepsis
MUDPILES?
increased anion gap metabolic acidosis
- M: methanol intoxication
- U: uremia
- D: diabetic or alcoholic ketoacidosis
- P: paraldehyde
- I: isoniazide or Fe overdose
- L: lactic acid
- E: ethylene glycol intoxication
- S: salicylate overdose
USED CAR?
non-anion gap metabolic acidosis:
- U: ureteral - sigmoid diversions - reabsorb Cl-, H2O in intestine - secrete bicarb in intestine
- S: small bowel fistula, saline admin
- E: endocrinopathies: addison’s, hyperparathyroidism
- D: diarrhea
- C: carbonic anhydrase inhibitors
- A: hyperalimentation (tPA)
- R: renal tubular acidosis
S/S of metabolic acidosis?
- CNS: HA, confusion, restlessness progressing to lethargy, stupor or coma
- CVS: dysrhythmias
- KUssmaul’s respirations (big deep fast resp)
- warm, flushed skin as well as nausea and vomiting
Tx of metabolic acidosis?
- tx cause
- hypoxia of any tissue bed will produce metabolic acids as result of anaerobic metabolism even if paO2 is normal
- restore tissue perfusion to hypoxic tissues
- use of bicarb is indicated
- hydration
Causes of metabolic alkalosis?
- ingestion of excess antacids, excess use of bicarb, or use of lactate in dialysis
- protracted vomiting, gastric suction, hypochloremia, excess use of diuretics or high level of aldosterone
S/S of metabolic alkalosis?
- CNS: dizziness, lethargy, disorientation, seizures, and coma
- M/S: weakness, muscle twitching, muscle cramps and tetany
- nausea, vomiting, resp depression
- diff to tx
Base excess?
- amt of excess or insufficient level of bicarb:
- 2 to +2 mEq/L
- negative base excess indicates a base deficit in blood
- it is an est of amt of strong acid or base needed to correct metabolic component of acid base disorder
Major anion in ECF?
- Cl: it helps maintain osmotic pressure of blood
- when acidosis occurs, fewer Cl- are reabsorbed
- other anions have transport maximums and excesses are excreted in urine
What is the anion gap?
- unmeasured anions = proteins, phosphates, citrate, sulfate
- normal is equal to 12
pt admitted for severe asthma attack, been having increasing SOB since admission 3 hrs ago ABGs: pH 7.22 paCO2: 55 HCO3: 25 DX? Tx?
- resp acidosis
- need to improve ventilation and O2 by admin bronchodilators, O2, possible mechanical ventilation
55 admitted w/ recurring bowel obstruction has been experiencing intractable vomiting for last several hours: pH: 7.5 paCO2: 42 HCO3: 33 Dx? Tx?
- metabolic alkalosis
- tx: IV fluids, measures to reduce excess base
When does compensation occur in primary resp acidosis?
- when kidneys retain HCO3
Pt on hemodialysis and has missed her last 2 appts ABG: pH 7.32 paCO2 32 HCO3 18 paO2 88 Dx?
- partially compensated metabolic acidosis
Pt w/ hx of COPD presents for resting ABG prior to PFTs: pH 7.35 paCO2 48 HCO3 28 PaO2 90 Dx?
fully compensated resp acidosis
pH 7.51 PaCo2 50 HCO3 40 PaO2 40 (21% O2) Dx?
- metabolic alkalosis w/ partial resp compensation