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Boards Review > Respiratory Recap > Flashcards

Respiratory Recap Flashcards

1
Q

What is the anatomic dead space?

A

The volume of the conducting airways (not involved in gas exchange)

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2
Q

Label the lung volume diagram:

A

A: Inspiratory reserve volume
B: Tidal volume
C: Expiratory reserve volume
D: Residual volume
E: Inspiratory capacity
F: Functional residual capacity
G: Vital capacity
H: Total Lung Capacity

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3
Q

Explain Fick’s Law of diffusion

A

Rate of transfer of a gas through a sheet of tissue.

= A x D X (P1-P2)/T

D = diffusion constant = solubility / √MW
A = area
P1-P2 = Pressure difference
T = thickness
MW = molecular weight

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4
Q

Which diffuses more easily- O2 or CO2? Why?

A

CO2- MUCH more soluble, only slightly higher MW

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5
Q

Define compliance.

A

Compliance is the volume change per unit of pressure of the lung (ΔV/ΔP)- “stretchiness”, “how easy it is to blow up the balloon”

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6
Q

Give examples of situations where compliance is higher than normal.

A

Increased compliance (easier to blow up): pulmonary emphysema, lung engorged with blood

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7
Q

Give examples of situations where compliance is lower than normal.

A

Decreased compliance (harder to blow up): pulmonary edema, pulmonary fibrosis, atelectasis

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8
Q

Where is surfactant made and what does it do?

A

Made by type II alveolar epithelial cells

Lowers surface tension of the alveoli → increased compliance (decreased work to expand), helps prevent pulmonary edema

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9
Q

What is the equation for determining resistance to flow in a tube (ie airway)?

A

R = 8 nL/ πR4

N= viscosity
L= length
R = radius

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10
Q

What is the normal “O2 cost” of quiet breathing (as a percent of normal oxygen consumption)? What can it go up to with dyspnea?

A

5% → 30%

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11
Q

Where is the main control of respiration in the brain? What influences this?

A

Medullary respiratory center in medulla.

Influenced by apneustic center in the pons (excitatory effect) and pneumotaxic center in the pons (inhibitory effect).

The cortex can also override the brainstem.

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12
Q

List causes of hypoventilation:

A
  1. Brain disease
  2. Cervical disease (above C5)
  3. Respiratory depressive drugs
  4. Lower motor neuron diseases
  5. Metabolic alkalosis
  6. Abnormal respiratory mechanics (fatigue, pickwickian syndrome, pleural space disease, chest wall abnormalities, or chest wall pain
  7. Upper airway obstruction
  8. Bronchoconstriction
  9. Increased dead space (poor cardiac output/shock, PTE, anesthetic circuit)
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13
Q

What is the normal response of pulmonary blood vessels to alveolar hypoxia?
Why does this occur?
How can this be harmful?

A

Vasoconstriction to decrease blood flow to the area.

This helps to prevent V/Q mismatch (avoid perfusing unventilated areas of lung).

When a large portion of lung is hypoxic, this causes pulmonary hypertension, further decreasing the ability to oxygenate.

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14
Q

How is the water balance of the lung different from the systemic circulation (ie Starling’s law stuff)?

A
  • Pulmonary capillaries are more leaky than systemic (fluid out of vessel)
  • Colloid osmotic pressure of pulmonary interstitium is higher compared to systemic (fluid out of vessel)
  • More lymph drainage from the interstitium compared to systemic (aided by rhythmic compression of ventilation) (fluid away from lungs)
  • Hydrostatic pressure of pulmonary capillaries is lower than systemic (fluid stays in vessel)
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15
Q

What are the 2 main categories of pulmonary edema?

A

High pressure edema
Increased permeability edema (leaky vessels)

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16
Q

Define hypoxemia

A

Low PaO2

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17
Q

List the possible causes of hypoxemia.
Star the ones that can be helped significantly with supplemental oxygen.
Which is the most common?

A
  1. Hypoventilation *
  2. Diffusion impairment *
  3. Shunt
  4. Ventilation perfusion mismatch * MOST COMMON
  5. Low inspired O2 content *
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18
Q

Define hypoxia

A

Low oxygen level in the tissues.

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19
Q

List possible causes of hypoxia.

A
  1. Low PaO2
  2. Anemia
  3. Dyshemoglobinemias (Hb can’t carry O2)- CO poisoning or metHb
  4. Decreased tissue blood flow (circulatory)
  5. Mitochondrial dysfuction, cyanide poisoning preventing tissue use of O2
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20
Q

How is oxygen carried in blood?
Use this to write out the equation for arterial oxygen content (CaO2).

A

Dissolved in blood (small) or combined with hemoglobin (most)

CaO2 (arterial oxygen content) = [1.34 x SaO2 x hemoglobin] + [PaO2 x 0.003]
= bound O2 + unbound (dissolved) O2

21
Q

Draw the O2/Hb dissociation curve.

A
22
Q

What does a “right shift” of the O2/Hb dissociation curve mean? What causes this?

A

Easier unloading, reduced O2 affinity of Hb

Causes:
- increased H+
- increased PCO2 (Bohr effect)
increased temp
- increased 2,3-DPG in RBCs (elevation)
- “High, Hot, Acid”

23
Q

How is CO2 carried in blood?

A

Dissolved (10%), as bicarbonate (MOST), or as carbamino compounds (esp with Hb)

24
Q

How does a pulse oximeter work?

A
  • Emits light with 660nm (red light) and 940nm (infrared) wavelengths from the light emitting diode (LED)
  • Receives light back, either by reflecting off the tissue (ie rectal probe) or transmission to the receiving end of the probe (ie tongue clip SpO2 monitor)
  • Determines SpO2 by the amount/types of light absorbed
    — Oxyhemoglobin: absorbs 940nm light
    — Deoxyhemoglobin: absorbs 660nm light
    — Methemoglobin: absorbs light at 660 and 990 nm (so always reports SpO2 of 80-85%)
    — Carboxyhemoglobin: absorbs 990nm light (so gives a false elevation to SpO2)
  • Only reads “pulsatile flow” because some static tissues can absorb light
25
Q

What would you expect to be the difference in PCO2 between a venous and arterial blood gas?

A

5mmHg higher in venous

26
Q

Write out the full equation for A-a gradient.

A

A-A gradient = PAO2 – PaO2

PAO2 = FiO2 decimal (barometric pressure– 50) – (PaCO2 x 1.1)

Sea level barometric pressure = 760 (so short formula = 150 – PaCO2 x 1.1)

Normal A-A gradient = <15 (on room air), <150mmHg (100% O2)

27
Q

What does the A-a gradient tell you?

A

Tells you whether hypoxia is due to hypoventilation or pulmonary dysfunction.
Can be used to track progress of disease.
Not able to use if FiO2 not 21 or 100%

28
Q

What is a normal PaO2/FiO2 ratio?

A

500 is normal (PaO2 = 5x FiO2)

29
Q

What are criteria for ALI and ARDS?
(PaO2/FiO2 ratio)

A

ALI = 200-300
ARDS = <200

30
Q

Explain the capnogram below:

A
  • Phase I: CO2 free phase- inspiration is occurring during the beginning of the phase, then expiration is starting at the end (gas from anatomic dead space so has no CO2)
  • Phase II: Upstroke- expiration of mixture of alveolar gas and gas from dead space
  • Phase III: Plateau- expiration of pure alveolar gas + pause at end of expiration
  • Phase IV: Downstroke- beginning of inspiration
  • Alpha angle: at C
  • Beta angle: at D
31
Q

What are the possible underlying pathophysiologies for “non-cardiogenic” pulmonary edema?

A
  • Neurogenic pulmonary edema: massive sympathetic activity → sudden increase in hydrostatic pressure
  • Negative pressure pulmonary edema (choking): massive increase in negative intrathoracic pressure 🡪 damaged endothelium and transiently increased hydrostatic pressure
32
Q

What are the 5 classes of pulmonary hypertension and examples of each?

A
  1. Arterial disease (ie idiopathic, congenital shunt 🡪 increased pulmonary blood flow, HW disease
  2. Venous hypertension (L CHF)
  3. Pulmonary disease: chronic hypoxia, chronic lower airway disease
  4. Thromboembolic event
  5. Miscellaneous: polycythemia vera, neoplasia causing vascular compression
33
Q

What are echo findings supportive of pulmonary hypertension?

A
  • Tricuspid regurgitation velocity: (4 x V2 ) + RA pressure
  • RA dilation
  • RV thickening and dilation
  • Flattening of interventricular septum
  • Paradoxical movement of septal wall
  • LA dilation (if left sided disease contributing)
  • Main pulmonary artery dilation
  • Thrombus or HW in PA
34
Q

List the indications for mechanical ventilation

A

Severe hypoxemia despite therapy (PaO2 <60, SpO2 <90)

Severe hypoventilation despite therapy (PCO2 >60)

Excessive respiratory effort

Cardiovascular support (CHF, sepsis)

35
Q

Explain assist control ventilation ventilator mode:

A

Minimum respiratory rate is set, ventilator breaths are given at that rate, additional assisted breaths can also be triggered

36
Q

Explain SIMV ventilator mode:

A

Ventilator delivers a set number of mandatory breaths, patient can trigger additional breaths which may or may not be assisted, machine attempts to synchronize mandatory breaths with patient efforts

37
Q

Explain pressure support ventilation ventilator mode:

A

All breaths are patient triggered, but a set amount of positive pressure is given during inspiration only

38
Q

Explain CPAP ventilator mode:

A

constant level of positive pressure is applied during inspiration and expiration (PEEP), does not augment inspiration, just helps to prevent alveolar collapse

39
Q

List the benefits of PEEP

A

Increases the oxygenating efficiency of diseased lungs by recruiting previously collapsed alveoli, preventing further alveolar collapse.

Reducing ventilator-induced lung injury by reducing the shear injury associated with re-opening of alveoli

Improves compliance

Decreases work of breathing

40
Q

List the possible detrimental effects of PEEP

A

overdistension of healthier alveoli

can reduce cardiac output/blood pressure by impairing venous return during expiration

41
Q

What are the 5 different mechanisms of ventilator associated lung injury?
Which is most important?

A
  1. Volutrauma Most important
  2. Barotrauma
  3. Biotrauma (general inflammatory mediators induced by ventilation + VAP)
  4. Atelectotrauma (aka shearing injury)
    5 .Oxygen toxicity
42
Q

What are the best ways to “protect” the lungs from injury during ventilation (particularly with ARDS)?

A
  • Use lower tidal volumes (4-8ml/kg): fewer aerated lung regions, so lung volume is actually decreased- normal tidal volumes would cause overdistension of normal areas
  • Moderate to high PEEP
  • Limited peak inspiratory pressure (no higher than 30cm H20)
  • Permissive hypercapnia: low tidal volume ventilation can cause elevations in PCO2 which is permitted in some patients. Often need heavier sedation (due to increased respiratory drive). Can lead to acidemia.
  • Permissive hypoxia: allow mild hypoxia so that ventilator settings can be less aggressive
  • Ventilate below the UIP and above the LIP on the pressure/volume loop
  • Appropriate nursing care, etc to minimize VAP
43
Q

Draw All 3 Scalars for mandatory volume control ventilation

A
44
Q

Draw All 3 Scalars for pressure control ventilation

A
45
Q

Draw Appearance of a “patient triggered breath” on both the pressure time scalar and the pressure volume loop

A
46
Q

Draw Appearance of PEEP on both the pressure time scalar and the pressure volume loop.

A
47
Q

Draw Change in compliance using the pertinent waveform

A
48
Q

Draw A normal flow-volume loop- spontaneous and ventilated

A
49
Q

Draw Appearance of a leak on flow-volume loop, PV loop, and volume-time scalar

A

Boards Review (14 decks)

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