Pathophysiology - Sinclair Flashcards

1
Q

How much Oxygen and Nitrogen is there in inspired air?

A

21% Oxygen

78% Nitrogen

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2
Q

How does ambient air differ once it enters the respiratory tract and becomes inspired air?
• how does this change calculations for PO2?

A

Ambient air is Rapidly warmed and saturated with 47mmHg of H2O

PO2 inspired = (Pb - Ph2o) x Fgas

*You must subtract 47mmHg from whatever the barometic pressure is

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3
Q

What is the formula for minute ventilation?

A

Ve = tidal volume x respiratory rate = Vt x f

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4
Q

If you take in 500mL of fresh air in a tidal breath, what is the volume of fresh air delivered to the alveoli?
• Why must we account for this?

A

Fresh Delivered air = 500mL - anatomic dead space

•Must account for this because alveolar gas remains in the anatomic dead space and re-enters the alveoli with the next breath

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5
Q

What causes Alveolar Dead Space?

A

• Alveoli that are ventilated but NOT perfused are useless in gas exchange

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6
Q

What is the physiologic dead space?

A

Vphysio = Vanatom + Valv

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7
Q

Differentiate Minute Ventilation and Alveolar Ventilation.

• what is Alveolar ventilation AKA?

A

Minute Ventilation:
• Vt•f

Alveolar Ventilation:
• (Vt - Vdphysio)•f

Alveolar Ventilation aka Effective Ventilation

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8
Q

What percentage of the Tidal Volume is physiologic dead space?

A

25-30% of Vt = dead space

typically this is 150-180mL

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9
Q

T or F: INCREASED Vdalv (alveolar dead space) is always pathologic

A

TRUE - paradigm example = pulmonary embolism

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10
Q

What happens to the alveolar dead space when you excercise and why?

A
  • Increased Tidal Volume

* massively INCREASED perfusion

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11
Q

What does alveolar gas equation tell us?

• what is the equation?

A

Tells us the PAO2 (we normally just estimate this as PaO2, but this may not be the case in lung pathology)
• Tells you if lung disease is due to hypoxemia or not

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12
Q

What is the only way we can remove CO2 from the body?

A

Ventillation

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13
Q

What is the Tissue O2 consumption?

A

~250ml/min

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14
Q
  • ***what is the COMPLETE ALVEOLAR GAS EQ?

* **What are the typical values in this equation?

A

PAO2 = PIO2 - (PaCO2/R)

OR

PAO2 = (Pb - Ph2o)•FiO2 - (PaCO2/R)

Typically:
• Alveolar O2 = 100mmHg
• Respiratory Exchange ratio is typically = 0.8
•Arterial CO2 = 40 mmHg

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15
Q

What defines Hyperventilation?

• how does this affect PAO2?

A
  • Breathing in O2 in excess of metabolic needs

* Increased Breathing increases PAO2

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16
Q

What is the A - a difference?
• how would you go about calculating this on the basis of obtainable values?
**What is a normal A-a difference

A

A - a difference = difference in O2 saturation in alveoli and in the blood
• Should be close to 0 if diffusion is happening efficiently

How to obtain:
• PaO2 obtained by direct measure
• Calculate PAO2 with eqn. = PAO2 = PiO2 - (PaCO2/R)

***A-a difference should usually be (Age+4)/4

17
Q

WHAT ARE THE 5 CAUSES OF HYPOXEMIA?
• break these down into categories
• what is the importance of this categorization?

A
  1. NORMAL A-a DIFFERENCE => No Lung Disease
    • Decreased PiO2
    • Hypoventilation
  2. WIDENED A-a DIFFERENCE => Lung Disease
    • Diffusion Limitation
    • R to L Shunt
    • Ventilation/Perfusion (V/Q) mismatch
18
Q

How does the A-a gradient change as you climb in altitude?

A

It’s unchanged because there is no lung disease, both the alveolar and arterial PO2 will decrease proportionally

19
Q

T or F: in someone who has overdosed on heroin, their arterial PO2 is a good predictor of alveolar PO2.

A

True, since there is no intrinsic lung disease PAO2 and PaO2 should be similar

20
Q

What is the least common cause of hypoxemia with increased A-a gradient?
• Can an abnormal Diffusion Capacity Test differentiate between the mechanisms of this disease?

A

Diffusion Limitation => anything that affects membrane Surface Area or Thickness

NO - abnormal diffusion capacity test will not differentiate what is causing this problem

21
Q

How far must the diffusion of O2 drop for it to become clinically relevant?

A
  1. 75s is the normal time an RBC spends inside a pulmonary capillary
  2. 25s is the normal time for equilibration

Therefore, diffusion must be decreased to 1/3 of normal for hypoxemia to result

CONVERSELY, if transit time increases by 3x you run the risk of hypoxemia

22
Q

Why do people with diffusion defects get out of breath when they start walking around, but are fine at rest?

A

Diffusion of Oxygen is limited (greater than 0.25 seconds needed for equilibration) THEN you get up and move and DECREASE transit time of RBCs and HYPOXEMIA results

23
Q

T or F: a DIFFUSION DEFECT can be corrected with 100% O2.

A

True

24
Q

Differentiate a Pulmonary and Cardiac Shunt.

• how does supplemental O2 affect patients with these problems?

A

Pulmonary:
• Perfused areas are NOT VENTILATED

Cardiac:
• ASD/VSD allows mixing of Right sided oxygenated blood with Left side deoxygenated blood

SUPPLEMENTAL O2 has NO EFFECT IN PATIENTS with this issue aka the A-a gradient will STILL BE HUGE

25
Q

If someone is put on 100% O2, how should their PaO2 change?

• how will this differ in a patient with shunting?

A

Normal:
• Low PaO2 ==> PaO2 ~ 600 mmHg

Shunting:
• Low PaO2 ==> PaO2 ~ 80 mmHg

26
Q

What is the respiratory exchange ratio in a patient that is on 100% oxygen?

A

Respiratory Exchange Ratio:

1.0 when on supplemental O2

27
Q

What Pulmonary Diseases are associated with a LOW V/Q mismatch?

A
  • COPD (asthma)
  • Pulmonary Edema
  • SHUNT = extreme case = 0
28
Q

What Pulmonary Diseases are associated with a HIGH V/Q mismatch?

A

• Pulmonary Embolism = infinity in DEAD SPACE

29
Q

WHAT IS THE MOST COMMON CAUSE OF HYPOXEMIA?

• does it correct with supplemental O2?

A

V/Q mismatch = most common cause

• YES, this corrects with O2