Equations & Physiology Flashcards

1
Q

Normal PaO2, PaCO2, Vt, Vd

A

PaO2 > 80mmHg
PaCO2 = 40mmHg
Vt = 500 mL
Vd = 150 mL

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2
Q

RQ Equation

A

RQ = VCO2/VO2
Based on diet/metabolism
Normal 0.8

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3
Q

Alveolar Gas Equation (Oxygen)

A

PAO2 = PiO2 - (PaCO2/RQ)

where PiO2 = (PB - PH2O)*FiO2

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4
Q

Alveolar Ventilation Equation (CO2)

A

PACO2 = 863mmHg*(VCO2/VA)

where VA = (RRVt)(1-(Vd/Vt))
and PACO2 = PaCO2 due to blood saturation curve not plateaued

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5
Q

Oxygen Content Equation

A

C(O2) = (%O2,sat * 1.34 (mL O2/gm Hb) * [Hb]) + 0.003*PaO2

Normal [Hb] = 15gm/dL

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6
Q

List the 3 key points on the O2-Hb Dissociation Curve

A

Normal: PO2 = 95mmHg, Hb-sat = 97%
Knee: PO2 = 60mmHg, Hb-sat = 90%
Mixed Venous: PO2 = 40mmHg, Hb-sat = 75%

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7
Q

Normal A-a Difference and P-F ratio

A

A-a: PAO2:PaO2 - normal <10mmHg

P-F: PaO2/FiO2 > 300 (for when on supplemental O2/ventilation) bad if lower

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8
Q

Criteria for ARDS (Timing, Imaging, Origin, Oxygenation, Pathophys, Histopath)

A
Timing: <1 week
Imaging: bilateral alveolar opacities
Origin: Non-cardiogenic 
Oxy: PaO2/FiO2 < 300
Pathophys: Injury to alveolar-capillary barrier, influx of protein-rich, low-pressure edema
Histopath: Diffuse Alveolar Damage (DAD)
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9
Q

8 Causes of Hypoxemia

A
Low PAO2
1. Low PB (elevation)
2. Low FiO2 (smoke)
3. High PaCO2 (hypoventilation)
4. Low RQ
High A-a Difference
1. Shunt (V/Q = 0) (R->L Heart, BPWA)
2. V/Q mismatch (COPD, PE)
3. Diffusion Limitation (ILD, Emphysema)
4. Low mixed venous sat (low CO, Anemia, Hypoxemia, high VO2 - metabolism/exercise)
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10
Q

Equation for mixed venous sat

A

MvO2 or SvO2 = delivered - lost
(CO* C(O2)) - VO2

Where C(O2) = (%O2,sat * 1.34 * [Hb] + 0.003 * PaO2); and [Hb] = 15

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11
Q

Determining Primary Respiratory and Metabolic Acid Disturbances

A

Respiratory: pH and PCO2 move in opposite directions
R. Acid: low pH and high PCO2
R. Alka: high pH and low PCO2

Metabolic: pH and PCO2 move in same direction
M. Acid: low pH and low PCO2
M. Alka: high pH and high PCO2

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12
Q

In Metabolic Disturbances, does bicarb change more or less than pH?

In Respiratory Disturbances, does bicarb change more or less than pH?

A

Bicarb changes less due to isohydric buffering - pH change reduced by other buffers

Bicarb changes more than pH because extra H+ are taken up by other buffers

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13
Q

What is the buffer line? How is it determined?

A

Slope of where along PCO2 isobar the patient’s pH and HCO3- is
Based on the amount of non-bicarb buffer! More non-bicarb buffer = steeper slope (greater change in bicarb with pH)
No non-bicarb buffer - buffer line is flat - change in bicarb is 1:1 with H+ ions - negligible amount in blood

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14
Q

How to calculate anion gap?

What does acid accumulation do to AG?

A

Na+ - (Cl- + HCO3-)
Normal: 10 +/- 2 mEq/L

Acid accumulation = increase in unmeasured anions (decrease in bicarb) = increases anion gap

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15
Q

3 big causes of respiratory acidosis

A
  1. CNS Drugs (opioids, sedatives)
  2. SEVERE respiratory conditions
  3. Acute neuromuscular problems
    ALL CAUSE HYPOVENTILATION
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16
Q

Causes of Respiratory Alkalosis

A

ALL CAUSE HYPERVENTILATION
fear, anxiety, pain, fear
pregnancy
early sepsis
hyperthyroidism
drugs (stimulants) - cocaine, PCP, aspirin OD
MILD respiratory conditions (early stages)

17
Q

How does the body respond to respiratory acid-base disturbances? How long does this take

A

Kidney
Alkalosis: Secrete more bicarb to lower pH
Acidosis: Resorb more bicarb to increase pH
takes three days for full compensation

18
Q

How does the body respond to metabolic acid-base disturbances? How long does this take? How do you calculate this?

A
Lungs
Occurs immediately through ventilation changes
Winter's Formula:
1.5x[HCO3-] + 8 = PaCO2 (~+/-2)
OR decimals of pH ~ PaCO2
19
Q

Types of metabolic acidosis

A
AG elevated (MUDPILES)
non AG Elevated (USEDCARS)
20
Q

Types of AG elevated metabolic acidosis

A
Acid Accumulation
M - methanol (formic acid)
U - uremia (kidney)
D - diabetic ketoacidosis (or other ketoacids)
P - propylene glycol (antifreeze)
I - isoniazid (TB)
L - lactic acidosis
E - ethylene glycol (antifreeze)
S - salicyclic acid (asprin OD)
21
Q

Types of non-AG elevated Metabolic Acidosis

A
Bicarbonate Loss
U - uretero-enterostomy
S - saline (hyperchlorinemia)
E - endocrinopathies, adrenal insufficiency
D - diarrhea
C - carbonic anhydrase inhibitor
A - ammonium chloride (old cough syrup)
R - renal tubular acidosis
S - spironolactone
22
Q

Delta-Delta Analysis: how to do it, and what the results show

A

Determine if change in AG = change in bicarb

If you get a higher than normal bicarb –> concurrent metabolic alkalosis

If you get a lower than normal bicarb –> concurrent non-elevated metabolic acidosis (bicarb wasting)

23
Q

Types of Metabolic Alkalosis (and subtypes of those)

A

Need urinalysis

Chloride Responsive: Vomiting, NG Tube Suction, Over Diuresis (low Na/Cl in urine, low urine output)

Chloride Unresponsive: Hypokalemia, hyperaldosteronism

24
Q

What happens to the following in obstructive lung disease?
FEV1, FVC, FEV1/FVC
TLC, FRC, RV, PEF,
DLCO, Isovolume Flow

A

OBSTRUCTIVE (scoop shaped Q-V diagram)
FEV1 = down
FVC = normal
FEV1/FVC = down (defined by less than 0.7)
TLC/FRC/RV = up
PEF = down
DLCO = low (emphysema), normal/high (asthma with airway remodeling)
Isovolume Flow = low (lungs more compliant)

25
Q

What happens to the following in restrictive lung disease?
FEV1, FVC, FEV1/FVC
TLC, FRC, RV, PEF,
DLCO, Isovolume Flow

A
RESTRICTIVE (witch hat shaped Q-V diagram)
FEV1 = down
FVC = down
FEV1/FVC = up
TLC/FRC/RV = down
PEF = down
DLCO = low
Isovolume Flow = high (lungs less compliant)