arterial blood gases and acid-base balance

normal range for pH

7.35-7.45

PaCO2 range

35-45

paCO2 what is associated with

respiratory/lungs

paO2 range

80-100 mmHg

what is HCO3 range

22-26

what is HCO3 associated with

metabolic/kidneys

what happens to BE as bicarb decreases

BE more negative

what happens to BE (base excess) as hco increases

BE becomes more positive

what is equation for PaCO2

see equation

what does hypoventilation do to co2

elevated CO2

what does hyperventilation do to CO2

decrease— drives rxn to the left

what are factors that affect PaO2

ventiliation (breath depth and rate)

lung capacity

oxyhemoglobin dissociation curve (the higher on the curve, the more o2 there is to bind to Hbg)

what are key takeways from oxyhemoglobin dissociation curve

• once o2 binds one heme, its easier to bind the next

• normal half sat is at 26 mmHg

  • shifting to left means Hb has higher affinity (need a lower half sat to get 50% Hb bound to o2), right shift means half sat increase or Hb has lower affinity

can body handle acid or base better

acidosis a bit better

where is half sat lower (left shift) /higher Hbg affinity?

lung capillaries— hang on to that O2

• area of high O2 content

where is O2 low/lower affinity of Hgb of O2

tissues, organs

what is FiO2

fractional percent of oxygen in air

what is PF ratio

ratio of PaO2 to FiO2

• normal is 400 to 500, mild resp distress is 300

what is normal FiO2

21%

how is arterial bicarb calculated

using H-H equation- measured pH and PaCO2

• should be close to serum bicarb on the BMP

what does elevated serum bicarb mean

alkalosisw

what does decreased serum bicarb mean

acidemia

what does raised anion gap mean

anion accumulation

• too much acid in body— lactic acidosis, ketoacidosis

  • the acid is sequestered by bicarb but the anions acculmulate

what is venous oxygen saturation used to measure

oxygen delivery/uptake by tisues

• can compare with arterial sat— if SaO2 and SvO2 are good then lungs AND heart ok

what is O2 sat ? what is normla value?

oxygen sat of hemoglobin

• >95%

why are arterial samples pref over venous blood gas samples

• venous only represents local tissue perfusion

• venous tissue can’t show why gas levels abnormal

• ABG show if lung, heart or tissue failing

  • PaO2 show how well lungs got oxygen in

  • PaCO2 show how well lungs removed CO2

    • arterial blood is same everywhere in the body

how is CO2 produced in the body

carb/fat metabolism— produces waaaay more

protein/tissue metabolism

what does high serum lactate show

anaerobic metabolism— there ia problem going on

what are buffers for acid-base homeostasis

• bicarb.carbonic acid system

• phosphates

• proteins

resp regulation

rate/depth of breathing

renal regulation

bicarb filtration by glomerulus and reabsorption

excretion of nonvolatile acids

distal tubular hydrogen ion secretion

what is acidosis vs acidemia

acidosis is process LEADING TO acidemia (which is the state of having low blood pH)

what are two main cuases of acidemia

resp (hanging on to CO2)

metabolic (decreased serum HCO3)

what are two causes of alkalosis

resp (excessive loss of CO2)

metabolic (rention of bicarb)

what disorder is pCO2 under 35

resp alkalosis

what is quick acting buffer

bicarb/carbonic acid system

what oes pCO2 over 45 mean

resp acidosis

what does HCO3 under 22 mean

metabolic acidosis

what does hco3 over 26 mean

metabolic alkalosis

how is resp alkalosis compensated for (means too little CO2)

decreasing bicarb

how is resp acidosis (too much co2) compensated for

increasing bicarb

how is metabolic acidosis (too little bicarb) compensated for

decrease Co2

how is metabolic alkalosis (too much bicarb) compensated for

increase pCO2

what is dif between acute and chronic a/b disorder

acute means the body is in the process of compensation and pH is returnING to normal.

chronic means pH is normal but the compensation is ongoing

what is correction vs compensation

correction is where the dysfunctional organ can self-correct— ex with resp alkalosis, able ot increase pCO2.

compensation is when the other organ has to help restore pH, so in resp alkalosis hte kidneys have to decrease bicarb

how long for resp compensation of metabolic disorders to take affet

hours

how long metabolic compensation of resp problems to take affect

3-5 days

what is an example of chronic disorder

COPD

• always have high pCO2, kidneys ALWAYS working

  • so pH is normal but not normal phys

what does AG over 20 mM/L mean regardless of pH or HCO3

priamary metabolic acidosis

what does MUDPILES stand for in regards to causes of anion gap

methanol (tox)

uremia (renal fail)

diabetic ketoacidosis

prop glycol/paraldehyde (tox)

Intoxication (alcohol)

Lactic acidosis

Ethl glycol (tox)

Salicylates (tox)

more bc acid is ADDED to the blood

what are causes of nonanion gap metabolic acidosis

Gi bicarb loss (d, pancreatic fluid drainage, ileostomy— intestines removed and bag to collect feces, its like diarrhea when high output)

renal bicarb loss (carb anhydrase inhibitors)

impaired adrenal acid excretion

Iatrogenic (HCl given in excess, poor TPN, excess NaCl)

post hypocapnia (hyperventiliating— lungs correct hyperventilation so more CO2, but means there is a time where kidneys not normalized yet so still acidic)

more because of LOSS of bicarb lost

what disorder does chloride responsive vs resistant represent

metabolic alkalosis

what is dif between Cl resistance vs responsive

responsive— chloride fixes kidney inability to excrete bicarb

• the body reabsorbs Na with another anion besides Cl if defic— so means HCO3 will be reabsorbed

why is hypokalemia also associated with metabolic alkalosis

bc can’t retain Na, so use bicarb to pump back into stomach

what are chloride responsive metabolic alkalosis conditions

GI losses— vommitting, nasogastic sunction, Cl loss in diarrhea

diuertics

excess bicarb (TPN, PO, IV— iatrogenic)

post hypercapnia

chloride resistance conditions

mineralocortiod excess (hyperaldosteronism— hang onto Na no matter waht, cuhsing, exogenous mineralocort)

severe hypokalemia, hypomag (mag important to K transport)

bartters or gitelman’s syndrome

cauese of respi acidosis (not breathing fast— more CO2)

CNS— stroke

drugs—opiatives, sedatives

pulmonary— asthma/copd, pneumonia

neuromsuclar— brainstem injury, neuromuscular blocking drugs, myasthenia gravis

causes of resp alkalosis (hyperventilation— not enough CO2)

CNS— resp stim— anxiety/pain, fever, salicylate, stimulants

pulomary— embolus (not enough perfusion), asthma

preg— hypoxemia

why mineralcortiocoids cause metabolic alkalosis