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HMS Homeostasis I > Respiratory Failure > Flashcards

Respiratory Failure Flashcards

1
Q

Respiratory failure

A

When the respiratory system can no longer function to keep gas exchange at an acceptable level

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2
Q

General evidence of respiratory failure

A

arterial Po2 less than 60 mm Hg or Pco2 greater than 50 mm Hg

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3
Q

“Categories” of respiratory failure

A
  • Hypoxemic type: Hypoxemia in absence of hypercapnia
  • Hypoxemic/Hypercapnic type: Hypercapnia in addition to hypoxemia, associated with renal metabolic compensation for pH. aka acute-on-chronic respiratory failure
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4
Q

Causes of hypercapnic/ hypoxemic respiratory failure are:

A
  • Depression of CNS/nervous control of respiratory pump
  • Disease of respiratory bellows
  • COPD
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5
Q

Examples of hypoxemic respiratory failure are:

A
  • Severe pneumonia
  • ARDS
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6
Q

Clinical presentation with respiratory failure consists of:

A
    1. Dyspnea
    1. Impaired mental status
    1. Headache
    1. Tachycardia
    1. Papilledema (with ↑ PCO2)
    1. Variable findings on lung examination
    1. Cyanosis (with severe hypoxemia)
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7
Q

Papilledema

A

swelling and elevation of the optic disk

Results from hypercapnia

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8
Q

Major mechanism of gas exchange interferrence in hypoxemic respiratory failure

A
  • V/Q mismatch
  • Shunt
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9
Q

Major mechanism of gas exchange interferrence in hypercapnic respiratory failure

A
  • Hypoventilation (primarily)
  • V/Q mismatch (often accompanying)
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10
Q

Factors that may decrease alveolar ventilation

A
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11
Q

Therapeutic approach to hypercapnic respiratory failure

A
  1. Support gas exchange
  2. Treat acute precipitating event
  3. Treat underlying pulmonary disease
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12
Q

Indications for mechanical ventilation in hypercapnic respiratory failure patients

A
  • Acidemia
  • Changes in mental status
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13
Q

Berlin definition of ARDS

A
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14
Q

Essential physiology of ARDS

A

A disturbance in the normal barrier that limits leakage of fluid out of the pulmonary capillaries and into the pulmonary parenchyma

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15
Q

Two major mechanisms of fluid accumulation in ARDS

A
  • Increased pulmonary capillary pressure - cardiogenic or hydrostatic – transudate
  • Increased pulmonary capillary permeability - noncardiogenic – exudate
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16
Q

Causes of ARDS

A
  • Inhaled injurious agents (gastric contents, salt or fresh water, hydrocarbons, gases in combustion smoke, pure oxygen, microorganisms like pneumocystis jirovecii in AIDS patients)
  • Injury via pulmonary circulation (sepsis, blood tranfusions causing inflammation, DIC, fat, amniotic fluid, heroin and other narcotics, pancreatitis)
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17
Q

Pathologic features of ARDS

A
  1. Damage to alveolar type I epithelial cells
  2. Interstitial and alveolar fluid
  3. Areas of alveolar collapse
  4. Inflammatory cell infiltrate
  5. Hyperplasia of alveolar type II epithelial cells

6. Hyaline membranes

  1. Fibrosis
  2. Pulmonary vascular changes
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18
Q

Hyaline membrane

A

These membranes are believed to represent the protein-rich edema fluid that has filled the alveoli. The membranes are composed of a combination of fibrin, cellular debris, and plasma proteins that are deposited on the alveolar surface.

Their presence suggests that alveolar injury and a permeability problem, rather than elevated hydrostatic pressures, are the cause of pulmonary edema.

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19
Q

Proliferative phase

A

After approximately 1 to 2 weeks (post-exudative phase)

Alveolar type II epithelial cells replicate in an attempt to replace the damaged type I epithelial cells. Hyperplastic type II epithelial cells often figure quite prominently in the pathologic picture of ARDS. Accumulation of fibroblasts as well.

20
Q

Exudative phase

A

First 1-2 weeks of ARDS

Fluid can be seen in the interstitial space of the alveolar septum as well as in the alveolar lumen. Scattered bleeding and regions of alveolar collapse. Protein-rich alveolar exudates inactivate surfactant.

21
Q

Pathophysiologic features of ARDS

A
  1. Shunting and V/Q mismatch
  2. Secondary alterations in function of surfactant
  3. Increased pulmonary vascular resistance
  4. Decreased pulmonary compliance
  5. Decreased FRC
22
Q

Alveolar flooding

A

Present in ARDS. Effectively prevents ventilation of affected alveoli even though perfusion may be relatively preserved. Shunt physiology.

23
Q

Changes in pulmonary vasculature in ARDS

A
  • Elevated pulmonary vascular resistance
  • Blood flow preferentially to low resistance areas, not necessarily those receiving best ventilation
  • Exacerbation of V/Q mismatch
24
Q

Effects of ARDS on mechanical properties of lung

A
  • Alveoli are not diffusely and relatively homogeneously stiffened, thus some regions ventilate poorly and some well. Fewer ‘functional’ alveoli
  • Decreased compliance of lung
  • Decreased FRC, though not uniformly
  • Breathe at a much lower overall lung volume than normal, preferentially ventilating those alveoli that are relatively preserved
  • This type of breathing demands increased work of breathing
25
Q

Clinical features of ARDS

A
  • Dyspnea
  • Tachypnea
  • Rales
  • ↓ PO2, normal or ↓ PCO2, ↑ AaDO2
  • . Radiographic findings of interstitial and alveolar edema
26
Q

Diagnosis of ARDS

A
  • Combination of clinical, radiological, and ABG labs
    *
27
Q

Treatment of ARDS

A
  • Treatment of precipitating disorder
  • Interruption of interference with the pathogenetic sequence of events involved in the development of capillary leak
  • support of gas exchange until the pulmonary process improves
28
Q

Almost all patients with ARDS require ___.

A

Almost all patients with ARDS require mechanical ventillation.

29
Q

Why do we mechanically ventilate at low lung volumes?

A

It is hypothesized that ventilating the lungs at lower lung volumes avoids overdistention of alveoli and a consequent deleterious release of inflammatory mediators

30
Q

Peak pressure on mechanical ventilation

A

Maximal pressure during mechanical inspiration. Represents the pressure necessary to overcome the resistance of lung tissue in addition to its elastic forces.

31
Q

Plateau pressure on mechanical ventilation

A

Pressure during mechanical inspiration following the initial descent from maximal pressure as flow stops. Represents the pressure necessary to overcome only the elastic forces of hte lung tissue.

32
Q

Peak pressure - plateau pressure

A

Represents the resistive forces of the lung tissue. Ordinarily less than 10 cm H2O, but may be elevated in patients with compressed airways, like an asthma patient or chronic bronchitis patient.

33
Q

Mechanical ventilation pressure-time plot

A
34
Q

Ways to set up a ventilator

A
  • Define a pressure -> tidal volume becomes dependent variable
  • Define a tidal volume -> pressure becomes dependent variable
35
Q

Static Compliance

A

Compliance measured under static conditions (no flow); ΔP taken as the difference between the pressure at the beginning and end of the inhalation when there is no flow.

Reflects only the recoil forces of the lungs and chest wall.

Measured with plateau pressure

36
Q

Dynamic Compliance

A

Compliance measured under dynamic conditions (when air is flowing into the lungs); since this measurement is done while gas is flowing into the lung, we must account for resistive forces as well.

Measured with peak pressure

37
Q

Positive End Expiratory Pressure (PEEP)

A

With the ventilator, one can prevent airway pressure during exhalation from going back down to zero, aka FRC. One can use PEEP to prevent the patient from exhaling to FRC and, thereby, prevent alveolar collapse

The end-expiratory lung volume or EELV is higher with PEEP than when the alveolar pressure reaches 0 at the end of a normal exhalation. This is the mechanical ventilation equivalent of dynamic hyperinflation.

38
Q

If the machine is set for PEEP, to calculate compliance, one. . .

A

. . . subtracts the PEEP from the peak or plateau pressure to determine the “driving pressure” for the breath or the ΔP in the compliance equation.

The PEEP is the pressure at the end of exhalation, which is also the pressure at the beginning of the next inhalation.

39
Q

auto-PEEP or intrinsic PEEP

A

In patients with severe airflow obstruction with decreased expiratory flow, the lung volume may not return to FRC before the ventilator initiates the next breath. In these cases, there is still positive pressure in the airways at the onset of inspiration.

This is really a form of dynamic hyperinflation

40
Q

If the pleural pressure (Ppl) is positive, then, on mechanical ventilation, . . .

A

. . . the size of the alveolus will be smaller for any given Palv than when Ppl=0. Remember, it is the transalveolar pressure that determines lung size and therefore ventilation.

This can happen due to a stiff or heavy chest wall.

41
Q

Esophageal pressure

A

An approximation of Ppl by placing a balloon (connected to catheter) in the esophagus

42
Q

When a patient is breathing with positive pressure ventilation, the intra-thoracic pressure . . .

A

. . .is always positive!

Positive pressure in the thorax reduces the pressure gradient for movement of blood from extrathoracic veins into the right atrium – i.e., venous return is reduced. For any given central venous pressure (CVP), the volume of the right atrium will be less if the Ppl is positive

43
Q

To determine the “true filling pressure” of someone on PEEP, you must. . .

A

. . . subtract the Ppl from the intra-vein or intra-cardiac pressure.

This enables us to determine the approximate location of the patient on his/her Starling Curve. This information is critical for determining how to treat a patient who is receiving positive pressure ventilation and who is hypotensive.

44
Q

ARDS capillaries

A

Capillaries are injured by cytokine storm, resulting in exudative process characteristic of ARDS.

So when you think high protein pulmonary edema, think ARDS.

45
Q

What is the fundamental reason why PEEP works?

A

It holds alveoli and airways open to improve ventilation.

46
Q

You should think of ARDS patients as having lungs that are. . .

A

. . . stiff (poor surfactant function) and small (collapsed)

HMS Homeostasis I (62 decks)

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