acid-base Flashcards
What are the normal blood gas and acid-base values
pH 7.4; HCO3 20; PCO2 40; BE = 0
What specifically pCO2 a measure of
Carbon dioxide acts as an acid in the body because of its ability to ract with water to produce carbonic acid. With increases in PCO2, the ratio of bicarbonate to PCO2 is decreased, hence pH falls
What is the expected pO2 for a given FiO2
5 times the FiO2
What 3 values are used to evaluate the metabolic component of the acid-base status?
Bicarbonate, BE, -sig; BE- is not influenced by respiratory system like bicarbonate is
What is TCO2
is a measure of all the carbon dioxide in a blood sample, and the majority of th the carbon dioxide is carried as bicarbonate in the blood. TCO2 will be 1-2 mmol/L higher than the true bicarbonate in blood
What is a buffer?
Weak acids and their conjugate bases constitute the most effective buffer pairs in the body since they are more capable of accepting or donating H+ in the prescence of changes in H+ load than are strong acids which are highly dissociated in
Intracellular vs. extracellular buffers
Three primary chemical buffering systems within the body proteins (primary intracellular), PO4- and HCO3- (primary extracellular)
Bicarb
HCO3- roughly 20% of the total body buffer capacity Capable of responding to acute changes in H+ and its role in the carbonic anhydrase equation which allows changes in pH to be further modulated by changes in ventilation. – open system
How do we describe acid-base disturbances (there are 3 components)
Acidemia/alkilemia; Respiratory or metabolic; Compensated or mixed
Physiologically, how do you get a metabolic acidosis?
Normochloremic: lactic acidosis; ketoacidosis, toxins, renal failure
Hyyperchloremic causes: gastrointestinal losses, renal failure, renal tubular acidosis
Result from loss of bicarbonate or the gain of acid and the calculation of the AG may aid in determine which of these process is present.
- Physiologically how do you get metabolic alkalosis?
Chloride responsive: vomiting, direutic therapy, correction of respiratory acidosis
Chloride resistant causes: Primary hyperaldosteronism, hyperadrenocorticism, over administration of alkaline fluids
Acid loss or bicarb gain
Gastrointestinal obstructive process; nasogastic tube suction, renal acid loss due to loop diuretic (2Cl, Na, K co transporter), mineralocorticoid excess; nonresorbable ionons.
Hypokalemia can play a big role due to shifts
Physiologically, how do you get a respiratory acidosis
results from an imbalance of CO2 prodution via metabolism and alveolar minute ventilation in the lung PaCO2 ~ VCO2/Va; VCO2- production of CO2 by tissue and Va is alveolar ventilation rate Increased CO2 production or a decreased minute ventilation (most common).
Minute ventilation
Minute ventilation is respiratory x tidal volume; therefore most common causes cause a reduction of respiratory rate and tidal volume
Physiologically, how do you get a respiratory alkalosis
Iatrogenic, hypoxemia, pulmonary disease without hypoxemia, centrally mediated hyperventilation, pain/fear/anxiety
Decreased PCO2 is the result of increased Va; therefore increased respiratory rate or tital volume
Chemoreceptors located centrally and peripherally stimulate ventilation. Where, specifically, are these chemoreceptors located, and what are they sensing to affect ventilation
Medulla- brainstem
Afferent inputs include central chemoreceptors within the medulla and peripheral receptors in the carotic and aortic bodies, airway and lung receptis
Reach higher areas of cns such as pons where they affect the pattern of breathing and the correct where they contribute to voluntary control of breathing
Central chemoreceptos are responsible for approximately 85% of the respiratory response to carbon dioxide
Located on the ventral surface of the medullar in close proximity to the dorsal and ventral respiratory neurons
When do you need arterial samples, and when do you need venous blood gas samples
Arterial only when you are concerned about O2
