Respiratory Disorders Flashcards

1
Q

What is Respiratory Failure?

A

“respiratory dysfunction resulting in abnormalities of oxygenation or ventilation (CO 2 elimination) severe enough to threaten the function of vital organs.” (Current 2024)

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2
Q

Type I vs Type II respiratory failure

A

● Type I Respiratory Failure is the inability to provide sufficient oxygen
à hypoxia
● Type II Respiratory Failure is the inability to remove carbon dioxide
à hypercapnia

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3
Q

Causes of Pulmonary edema

A

● Increased hydrostatic pressure
● LV dysfunction (eg, myocardial
ischemia, HF)
● Mitral regurgitation
● Left atrial outflow obstruction (eg,
mitral stenosis)
● Volume overload states
● Increased pulmonary capillary
permeability
● Acute respiratory distress syndrome

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4
Q

Parenchymal lung disorders

A

● Pneumonia
● Interstitial lung diseases
● Diffuse alveolar hemorrhage
syndromes
● Aspiration
● Lung contusion

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5
Q

Pulmonary vascular disorders

A

● Thromboembolism
● Air embolism
● Amniotic fluid embolism

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6
Q

Chest wall, diaphragm, and pleural
disorders

A

● Rib fracture
● Flail chest
● Pneumothorax
● Pleural effusion
● Massive ascites
● Abdominal distention and abdominal
compartment syndrome

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7
Q

Acute Resp Distress Syndrome

A

It is an acute hypoxemic respiratory failure following a systemic or pulmonary insult that results in fluid accumulation in the lungs without evidence of heart failure (cardiogenic pulmonary edema)

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8
Q

“Berlin” definition of ARDS:

A

1) acute onset,
2) bilateral pulmonary infiltrates on CXR/CT, and
3) poor oxygenation (PaO2/FiO2 <300 mmHGg)

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9
Q

Several disorders/conditions associated with ARDS, 75% are
found in one of three settings:

A

○ Sepsis (most common)
○ Severe multiple trauma
○ Aspiration of gastric contents

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10
Q

Pathophysiology of ARDS

A

○ Inflammatory response to the insult (whether primary or secondary)
○ large amounts of pro-inflammatory cytokines are released throughout the lungs
○ Widespread cytokine release triggers immense immune response, damaging the
pulmonary capillary epithelium
○ Damage to the capillary wall –>
○ marked increased capillary permeability, and
○ decreased surfactant production/activity

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11
Q

In ARDS, Damage to the capillary wall à
○ marked increased capillary permeability, and
○ decreased surfactant production/activity

A
  1. Interstitial edema
  2. Alveolar edema
  3. Alveolar collapse/noncompliance
  4. Profound hypoxemia
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12
Q

ARDS: Clinical Presentation

A

● Rapid onset of profound dyspnea.
■ Occurs 6-72 hours after precipitating event
■ Within 12-24 hrs à may see rapid deteriorationà intubate
○ Other signs and symptoms:
■ Tachypnea
■ Frothy pink/red sputum
■ Diffuse crackles
■ Retractions
■ Cyanosis with increasingly severe
hypoxemia (<90%) that is refractory to
oxygen administration

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13
Q

ARDS - Diagnosis

A

● Once symptoms set in, CXR becomes remarkable:
■ Diffuse or patchy bilateral infiltrates
● Infiltrates rapidly become confluent
● Characteristically spare the costophrenic angle
■ Pleural effusions are small or non-existent
■ Air bronchograms are seen in 80% of cases

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14
Q

CXR findings in ARDS

A

bilat pulmonary infiltrates
○ Generally normal cardiac silhouette

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15
Q

ABG findings in ARDS

A

○ PaO2 ↓ (<60 mmHg - always until ARDS resolves)
○ PaCO2 ↑ or normal

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16
Q

BNP findings in ARDS

A

BNP (helps differentiate ARDS from cardiopulmonary edema)
○ Obtain if enlarged pulmonary cardiac silhouette
■ High - points to cardiopulmonary edema
■ Low/normal - points to ARDS

17
Q

ABGs importance in ARDS = PaO2 & FiO2

A
  1. PaO2 = Measures partial pressure of oxygen in the blood
    a. Represents how well we are getting oxygen across the
    alveolus into the capillary
  2. FiO2 = fraction of oxygen that the patient is breathing
  3. PaCo2 = not an important measurement in ARDS
  4. With PEEP you adjust FiO2 in order to maintain the patient at >90%
    saturation
    Ratios between PaO2 and FiO2 give you a better idea of the severity of ARDS and contribute to the diagnosis of
    ARDS- however this is not the scope of this lecture and more advanced ICU respiratory medicine
18
Q

ARDS - Treatment Management

A
  1. Identification and aggressive treatment of the precipitating condition
  2. Focus on meticulous and aggressive supportive care.
    ○ Tracheal intubation
    ○ Positive pressure mechanical ventilation (PEEP)
    ■ Target of SaO2 > 88%
19
Q

Indications for intubation and ventilation include:

A

○ Hypoxemia despite delivery of supplemental oxygen
○ Upper airway obstruction (epiglottitis, for example)
○ Impaired airway protection (coma)
○ Inability to clear secretions
○ Severe respiratory acidosis
○ Progressive respiratory distress (ARDS, etc)
○ Apnea

20
Q

Complications of Mechanical Ventilation include:

A

○ NUMEROUS!
○ Atelectasis (partial or complete collapse of one lung)
○ Hyperinflation (usually of one side)
○ Pneumothorax
○ Ventilator-Acquired Lung Injury

21
Q

ARDS Prognosis:

A

○ Mortality rate associated with ARDS is 30-50%.
■ If the ARDS was secondary to sepsis (which is true of about one third of ARDS cases), mortality rate can reach 90%
■ Median survival is about 2 weeks
from onset of ARDS

22
Q

Infant Resp Distress Syndrome

A

● IRDS was previously known as Hyaline Membrane Disease.
○ It is the most common cause of respiratory distress in the preterm infant.
● It is caused by prematurity of
the lungs and deficiency in
pulmonary surfactant

23
Q

IRDS Pathophysiology

A

○ Without surfactant, alveoli collapse
and gas exchange is hindered.
○ Pulmonary edema and atelectasis can
occur, with hyaline membrane
formation worsening gas exchange

24
Q

IRDS Clinical Presentation

A

○ Typical signs of respiratory distress
in the newborn…
■ Dyspnea, retractions, hypoxia, etc

25
Q

IRDS - Diagnosis

A

● Chest X-ray:
■ Diffuse sign of interstitial and alveolar congestion in the newborn baby.
■ Air bronchograms.
■ Interstitial reticular pattern (linear-ground glass appearance)
● ABG will usually reveal:
■ Hypoxemia
■ Hypercapnia
■ Respiratory acidosis without compensation

26
Q

Lecithin-Sphingomyelin Ratio (aka L-S or L/S Ratio)

A
  1. Measures two substances:
    a. Lecithin (↑↑↑ as pregnancy progresses)
    b. Sphingomyelin (stays constant throughout all pregnancy)
  2. These substances are found in the amniotic fluid during pregnancy
  3. They are surfactants made by the lungs.
  4. Without surfactants the alveoli collapse (no O2 in the blood)
27
Q

What are some complications from IRDS

A

● Alveolar collapse (as already mentioned)
● Patent ductus arteriosus
● If you give too much oxygen supplementation
○ Retinopathy of prematurity
■ Abnormal vessel growth in the retina - can cause detachment
○ Bronchopulmonary dysplasia
■ Chronic lung disease from ventilation

28
Q

IRDS - Treatment and Management

A

● Intubation with mechanical ventilation or CPAP with nasal bubble is required.
● Aerosolized exogenous surfactant

29
Q

IRDS - Prevention

A

● If an expecting mother is showing signs of premature labor, glucocorticoids can be administered to help stimulate maturation of the baby’s lungs.
■ Prescribed if labor prior to 34 weeks gestation
● With current knowledge and treatment, mortality rate for babies born at 27 weeks gestation or later is at 10%