acid base balance

carbon dioxide in the blood is normally

35-45mmHg

70% of CO2 is transported as

bicarbonate by conversion via carbonic anyhydrase

normal pH

7.35-7.45

acidosis pH

<7.35

alkalosis pH

>7.45

buffer system

any system that can reversibly bind a H+

role of the lungs

control how much CO2 is in our blood based on amount of H+

is there is high CO2

more acidic, lower pH, make H+

if there is low CO2

more basic, higher pH, pulls H+ out of blood

CO2 is essentially

an acid

bicarbonate normal levels (HCO3-)

22-26mEq/L

HCO3- is essentially

a base

alkalosis can be caused by

too much HCO3- or too little CO2

acidosis can be caused by

too much CO2 or too little HCO3-

if the CO2 is responsible for putting the pH off balance (either alkalosis or acidosis)

the cause is respiratory

if the HCO3- is responsible for putting the pH off balance (either alkalosis or acidosis)

the cause is metabolic (kidneys ridding waste in urine)

if both CO2 and HCO3- are out of range, but pH is normal

the body has fully compensated

partial compensation

when kidneys or lungs are trying to restore pH levels but havent reached a level high enough to do so

uncompensated

CO2 or HCO3- normal (not modulated by kidneys or lungs at all in efforts to fix pH)

common cause of respiratory acidosis

hypoventilation, over-sedation, re-breathing exhaled CO2

hypoventilation causes acidosis because

you aren't breathing fast enough to clear CO2 from lungs

acidosis of respiratory cause could present with

cognitive effects and altered mental status

respiratory origin alkalosis common cause

hyperventilation, anxiety attack, hypoxia (large exertions of CO2)

pulmonary fibrosis is an example of

respiratory alkalosis

clinical presentations of alkalosis

tachypnea, dizziness, anxiety, difficulty concentrating, blurred vision, diaphoresis, muscle cramps, arrhythmias

metabolic acidosis

body produces too much acid to kidney fails to remove acid, insufficient bicarbonate

metabolic acidosis clinical presentation

compensatory hyperventilation, weakness, muscle twitching, malaise, nausea, vomiting, diarrhea, headache, dry skin/mucus membranes, poor skin turgor

metabolic alkalosis

loss of acid from the body, increase bicarbonate

clinical presentation of metabolic alkalosis

compensatory hypoventilation, dysrhythmias, prolonged vomiting, diarrhea, weakness, muscle twitching, irritability, agitations, coma

in order to get arterial blood gas values you have to

draw arterial blood - painful without lines

PaO2

80-100mmHg

PaCO2

35-45mmHg

SpO2

95-100%

pH

7.35-7.45

HCO3

22-26mEq/L

base excess

-2 to +2 mEq/L

SpO2 is a good surrogate for measuring

PaO2 with a pulse ox monitor

limitations of SpO2 measurment

only tells you % of saturation based on the amount of RBCs you have - could have low RBC count initially and risk O2 deficit with therapy

pulmonary fibrosis changes in ABCs

poor diffusion, hard to get air in - low PaO2, hyperventilators causing low PaCO2

emphysema changes in ABCs

patchy, some healthy areas - breath quickly and make way to normal blood gases

chronic bronchitis changes in ABCs

brain stops responding to increased CO2, hypoxic breathers and dont get stimulus to breath until O2 is low enough, hypoventilators despite low PaO2 and high PaCO2

with chronic bronchitis, its important to follow O2 prescription to

maintain stimulus to breath (need that O2 level to get low)