Module 3: ABGs Flashcards by M R

why do we obtain an ABG?

to get info about a pt’s ventilation, alveolar gas exchange and acid-base balance
to confirm/expand our understanding of a pt’s comprehensive ax
to help with dx of certain medical conditions
to evaluate the effectiveness of interventions

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what does pH measure and what is its determinant of O2 supply and demand?

how acidic or basic a solution is
overall acid-base balance in the body

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what does PaCO2 measure and what is its determinant of O2 supply and demand?

partial pressure of dissolved CO2
ventilation

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what does HCO3 measure and what is its determinant of O2 supply and demand?

calculated bicarb level
ventilation

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what does PaO2 measure and what is its determinant of O2 supply and demand?

partial pressure of dissolved O2
gas exchange

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what does SaO2 measure and what is its determinant of O2 supply and demand?

% of Hgb saturated with oxygen
gas exchange

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compare SpO2 and SaO2

SaO2 = obtained from ABG sample
SpO2 = obtained from pulse oximetry

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what are factors impacting SpO2 levels?

increased levels of Hgb increasing SpO2
vascular dyes = falsely low
poor tissue perfusion = loss of pulsatile flow and signal failure
poor probe placement

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compensatory mechanisms

when alveolar gas exchange is decreased
when ventilation is decreased
when O2 transport is decreased

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when alveolar gas exchange is decreased….

1) peripheral chemoreceptors located in the aortic arch and carotid sinuses detect drops in PaO2 below 60mmHg

2) resp centre in brain is triggered to increase RR and TV in order to bring more O2 to a-c membrane, increasing O2 available for diffusion

3) for hypoxemic patients: high RR causes exhalation of more than normal amounts of CO2, causes drop in PaCO2 (= hyperventilation). but once pt tires, they can’t hyperventilate anymore = TV decrease, PaCO2 rises

*hypoxemia also triggers SNS to increase HR to better circulate O2

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which type of patients is the alveolar gas exchange mechanism seen in?

patients who suffer from hypoxemia (like from pneumonia)

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a disruption in alveolar gas exchange is reflected by…

a drop in PaO2

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when ventilation is decreased…

1) As CO2 levels in the blood and CSF increase, the central chemoreceptors detect these changes and stimulate the nearby respiratory centre
2) respiratory centre’s response to chemoreceptor stimulation (increased RR and depth) results in an increased respiratory workload
3) chemoreceptor stimulation is often triggered by respiratory pathophysiology

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central chemoreceptors

in the medulla of the brain and in contact with CSF, which enhances their effectiveness in responding to CO2 changes
are highly sensitive to even slight changes in PaCO2 and adjust ventilation accordingly

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normal PaCO2 range

35-45mmHg

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when oxygen transport is decreased…

1) When hemoglobin levels fall, less oxygen is transported in the blood to the cells
2) there’s an increase in HR and contractility, which is mediated by the SNS
3) increase in CO means that blood is circulated through the body more rapidly, maximizing the use of existing hemoglobin to carry more “loads” of O2 over a given time period

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how does physiological demand become increased by SNS is activated?

due to increased respiratory rate and depth (increased WOB), elevated heart rate (increased myocardial demand), and the release of stress hormones that enhance focus and awareness
important to TREAT UNDERLYING CAUSE not symptoms

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7.35-7.45
above 7.45 = base
below 7.35 = acid

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PaCO2

35-45
above 45 = acid
below 35 = base

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HCO3

22-26
above 26 = base
below 22 = acid

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how to determine an ABG

1) Acid or Base? look at pH
2) metabolic or resp? bicarb = base, metabolic; CO2 = acid, resp
3) compensation? if pH is not normal, its partial. if pH is normal, its full. if either HCO3 or PaCO2 is normal, its uncompensated.

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how to determine ABG if pH is normal

1) look at pt’s dx
2) what is pH closer to? acidic or alkalotic?

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what is HCO3 regulated by?

kidneys = metabolic = base

what is PaCO2 regulated by?

lungs = respiratory = acid

when does a mixed or combined pH imbalance occur?

when has person has more than one acid-base disorder at the same time

PaO2

>80mHg

mild hypoxemia

> 60 and < 80 mmHg

moderate hypoxemia

> 40 and < 60 mmHg

severe hypoxemia

< 40 mmHg

SaO2

> 93%

where are ABG samples generally obtained from?

radial artery or arterial catheter; b/c it is easy to get at and can be compressed against the wrist ligaments afterwards to reduce hematoma

what errors in sampling can occur and what will it cause?

shaking to mix the specimen, or failure to expel air bubbles or to record the use of supplemental O2, can cause unrepresentative or false O2, CO2 and pH results; anxiety, pain, exercise

complications following ABG sampling

fainting, arteriospasm, hematoma, thrombus/embolism (smaller arteries more at risk)

analysis of results should be approached in 2 phases which are:

1) ax of pulmonary gas exchange 2) ax of acid-base status

what does PaO2 and CO2 mean?

pressure of O2/CO2 dissolved in plasma in arterial blood

how can pressure of CO2 in alveoli be altered?

if residual and dead space air volumes are increased or decreased

larger breaths (increased TV) and increased RR will?

flush CO2 out of the alveoli; decreased resp effort will cause CO2 levels to rise

if amount of alveolar CO2 rises, then...

PaO2 will also increase

hypoxemia vs hypoxia

hypoxemia = reduced O2 content in blood hypoxia = lack of O2 in tissues

3 causes of hypoxemia

1) impaired diffusion of O2 across the alveoli 2) shunt and inequality between ventilation and perfusion of lung regions 3) hypoventilation

what does a V/Q mismatch normally trigger?

increase in ventilation (RR and TV) maintaining normal or even slightly lower PaO2

what will likely cause hypercapnia?

reduction in RR and TV

type 1 resp failure

- PaO2 is decreased but PaCO2 is normal or low - impaired oxygenation but adequate ventilation since CO2 is excreted - causes: pneumonia, acute asthma, PE, pulm edema, COAD

type 2 resp failure

- increase in PaCO2 due to inadequate ventilation - PaO2 may be low or normal - may see signs of hypercapnia and acidosis

acid

substance that releases H+ ions when dissolved in a solution

base

substance that mops up H+ ions in solution, thus decreasing the concentration of H+ ions and increasing pH

when will respiratory acidosis occur?

when ventilation is impaired; produces an increase in PaCO2 levels

when will respiratory alkalosis occur?

when too much CO2 is removed through hyperventilation

what causes metabolic acidosis?

Any condition, other than a rise in PaCO2, that causes a decrease in plasma pH

common causes of metabolic acidosis

1) Excess ingestion of acids 2) Excess production of acids (DKA, lactic acid in shock) 3) Decreased excretion of acids (ARF) 4) Increased loss of alkaline secretions (diarrhea)

what is the main symptom of metabolic acidosis?

Kussmaul’s respirations – deep rapid respirations triggered by increased PaCO2 as the plasma attempts to buffer the decrease in pH

what are early symptoms of metabolic acidosis?

headache, lethargy, n/v, diarrhea

when does metabolic alkalosis most commonly occur?

when there is excess loss of acids from the body, ie.) in prolonged vomiting or excess GI suctioning, diuretic therapy causing low Cl and K+

metabolic alkalosis

any condition, apart from a decrease in PaCO2, that causes an increase in plasma pH

symptoms of metabolic alkalosis

cardiac dysrhythmias, confusion, convulsions, muscle cramp and tetany; breaths may be slow and shallow to increase PaCO2 and there is impaired oxygenation of the tissues