Exam 3, L6 & Other Important Concept Connections Flashcards

(45 cards)

1
Q

How much oxygen is stored in the lungs at FRC in a healthy adult?

A

Approximately 395 mL (based on 13% O₂ in 3 L of FRC).

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2
Q

How much oxygen does a resting adult typically consume per minute?

A

Around 250 mL/min.

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3
Q

Why is the oxygen stored in FRC referred to as a buffer?

A

It acts as a reserve to maintain oxygenation between breaths or during apnea.

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4
Q

What is the alveolar PO₂ between breaths?

A

About 100 mmHg.

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5
Q

What determines the rate at which alveolar PO₂ falls during apnea?

A

The patient’s oxygen consumption rate and lung volume (FRC).

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6
Q

What factors reduce FRC and compromise oxygen buffering?

A

Anesthesia, supine position, muscle paralysis, abdominal pressure, and obesity.

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7
Q

How does anesthesia reduce FRC?

A

It causes loss of muscle tone, diaphragmatic elevation, and reduced chest wall compliance.

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8
Q

Why is preoxygenation important before induction of anesthesia?

A

It replaces nitrogen in the lungs with oxygen, maximizing the O₂ reservoir to delay desaturation during apnea.

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9
Q

How does preoxygenation affect alveolar composition?

A

It increases the fraction of O₂ in the alveoli to near 100%, eliminating nitrogen.

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10
Q

What happens to alveolar PO₂ if FRC drops and O₂ consumption remains constant?

A

Alveolar PO₂ falls more rapidly, increasing the risk of hypoxemia.

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11
Q

What is the primary stimulus for central respiratory drive under normal conditions?

A

Arterial CO₂ (PaCO₂) — detected by central chemoreceptors in the medulla.

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12
Q

What does the CO₂ response curve represent?

A

The relationship between PaCO₂ and minute ventilation.

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13
Q

What is the apneic threshold?

A

The PaCO₂ level below which spontaneous breathing ceases — usually around 32–34 mmHg.

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14
Q

How do opioids affect the CO₂ response curve?

A

They cause a right shift and decreased slope, meaning more CO₂ is required to stimulate ventilation, and the response is blunted.

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15
Q

How does hypoxemia affect the CO₂ response curve?

A

In moderate hypoxia, ventilation increases for a given PaCO₂ — steeper slope. In severe hypoxia, it may depress ventilation.

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16
Q

What causes a left shift in the CO₂ response curve?

A

Conditions like pregnancy, metabolic acidosis, or anxiety, which increase ventilatory drive.

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17
Q

How does gravity affect pulmonary perfusion?

A

Blood flow is highest at the base of the lung due to gravitational effects on hydrostatic pressure.

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18
Q

What are West’s Zones of the Lung based on?

A

The relationships between alveolar pressure, arterial pressure, and venous pressure.

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19
Q

Describe West Zone 1 physiology.

A

Alveolar pressure > arterial > venous → no perfusion (physiologic dead space).

20
Q

Describe West Zone 2 physiology.

A

Arterial > alveolar > venous → intermittent perfusion (‘waterfall’ effect).

21
Q

Describe West Zone 3 physiology.

A

Arterial > venous > alveolar → continuous perfusion — most normal gas exchange occurs here.

22
Q

What is hypoxic pulmonary vasoconstriction (HPV)?

A

A protective mechanism where pulmonary arterioles constrict in response to low alveolar PO₂ to redirect blood to better-ventilated areas.

23
Q

How do volatile anesthetics affect HPV?

A

They blunt HPV, leading to worsened V/Q mismatch under general anesthesia.

24
Q

Why do patients with fever desaturate more quickly?

A

Increased temperature causes a right shift of the O₂ curve → more unloading in tissues but faster depletion of O₂ stores.

25
Why do hypothermic patients retain O₂ in their blood longer?
Left shift from low temperature → increased affinity, less tissue unloading.
26
Why does a patient with carbon monoxide poisoning have normal SpO₂ but tissue hypoxia?
CO binds Hb with high affinity → falsely elevates pulse ox readings, reduces actual O₂ delivery.
27
What is the danger of anemia despite a normal PO₂ and O₂ sat?
Low hemoglobin concentration = reduced O₂ carrying capacity → low total O₂ content (CaO₂).
28
What causes a right shift of the O₂ dissociation curve?
↑CO₂, ↓pH, ↑Temperature, ↑2,3-BPG, exercise, acidosis — improves tissue unloading.
29
What causes a left shift?
↓CO₂, ↑pH, ↓Temp, ↓2,3-BPG, CO poisoning, fetal Hb — reduces unloading.
30
What is the equal pressure point (EPP)?
The point in the airway during forced expiration where airway pressure equals pleural pressure — beyond this, the airway collapses.
31
Where is the EPP located in healthy individuals?
In the larger, cartilaginous airways — which resist collapse.
32
What happens to the EPP in emphysema?
It shifts distally (toward smaller airways), which are not supported by cartilage → early airway collapse during expiration.
33
How does dynamic compression limit expiratory flow?
Once pleural pressure exceeds airway pressure, flow becomes effort-independent — pushing harder doesn't increase flow.
34
Why is FEV1 effort-independent in late expiration?
Because increased effort raises both alveolar and pleural pressure equally, not improving flow beyond the EPP.
35
How does this concept explain the scooped-out flow-volume loop in COPD?
Loss of elastic recoil shifts the EPP distally → small airway collapse → reduced flow in effort-independent phase.
36
How is Functional Residual Capacity (FRC) related to preoxygenation time during anesthesia?
FRC is the oxygen reservoir between breaths; higher FRC = longer time before desaturation during apnea.
37
How is flow-volume loop shape related to the equal pressure point (EPP) and elastic recoil?
In disease (e.g., emphysema), the EPP shifts distally due to lost recoil, causing early airway collapse and a scooped loop.
38
How does the CO₂ dissociation curve and Haldane effect connect to V/Q mismatch and ETCO₂ readings?
In V/Q mismatch or increased dead space, less CO₂ reaches alveoli, lowering ETCO₂ despite normal or high PaCO₂.
39
How do 2,3-BPG, pH, and temperature relate to oxygen delivery in exercise or anemia?
These cause a right shift of the O₂ dissociation curve → more O₂ released to tissues when metabolic demand is high or hemoglobin is low.
40
What is the connection between surfactant function and lung compliance?
Surfactant reduces surface tension, maintaining alveolar stability and preventing collapse → increases compliance, especially at low lung volumes.
41
How does diffusion-limited O₂ exchange connect to exercise, altitude, and pulmonary fibrosis?
In these conditions, gas exchange becomes limited by membrane thickness or time, not perfusion → O₂ fails to equilibrate.
42
What is the relationship between pleural pressure and alveolar stability during ventilation?
Negative pleural pressure keeps alveoli open; loss (e.g., pneumothorax) or inadequate positive pressure can lead to alveolar collapse.
43
How does understanding pulmonary compliance affect ventilator settings?
Low compliance (e.g., in ARDS) requires higher pressures to deliver volume → PEEP is needed to prevent atelectasis and improve V/Q matching.
44
How are Bohr and Haldane effects complementary in gas exchange?
Bohr effect: CO₂/H⁺ promotes O₂ unloading in tissues; Haldane effect: Deoxygenated Hb promotes CO₂ uptake in tissues and CO₂ unloading in lungs.
45
Why does ETCO₂ underestimate PaCO₂ in dead space ventilation?
Because non-perfused alveoli dilute exhaled CO₂, lowering ETCO₂ — the wider the gradient, the more dead space or V/Q mismatch is present.