Lung resistance and Neonatal Respiratory Disease Flashcards

1
Q

What are volume and pressure changes?

A
  • Respiratory muscles initiate changes in the intraplueral pressure which sets up a partial pressure gradient enables air to flow
  • 1cm diaphragm movement creates a change in 3 cmH20 which is enough
  • The more muscular effort the more work
  • Ideally the lungs would be stretchy to allow inflation

Normal respiratory pressure around 1 L

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2
Q

What is Boyle’s Law?

A

The pressure of a given mass of a n ideal gas is inversely proportional to its volume at a constant temperature.

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3
Q

What are the two resistances that breathing effort work needs to overcome?

A
  • Elastic resistance ( Lungs and Chest wall = surface tension and surfactant) - contributes to 65% resistance (Static state)
  • Tissue - Lungs, Pleura
  • skeletal, muscular skin

Dynamic state - Tissue Viscous Resistance and Airway Resistance:
- 35% of resistance - tissue viscuous resistance and airway resistance
- 20% = Lungs, Ribs,, Diaphragm and organs
- Airways, Gas flow

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4
Q

What is compliance and specific compliance?

A

Compliance: Distensibility (stretch) of the lunge i.e. the change in lung volume that occurs with each unit change in transpulmonary pressure e.e. V/P i.e. for both lung by 200 mL.
- Specific compliance - the corrected for volume at that time e.e. compliance / V
- This standardises compliances for different volumes

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5
Q

What is Elastance?

A

-Property of resisting deformation (resistance) or desite to return to original shape
E = 1/C

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6
Q

What is the V/P (compliance) relationship (TP CHNAGES)?

A
  • Shows the capacity of the lungs to adapt to transpulmonary pressure changes
  • You need muscular effort so the work of breathing is the area in this loop plus the hatched area
  • Resistance are overcome
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7
Q

What is static resistance of the chest wall?

A
  • Stiffness of chest wall
  • Force of movement of chest wall is opposite that of lung
  • Chest wall has tendency to expand but held by negatove pleural pressure
  • Unopposed reaches 70% of TLC (resting position)
  • When thorax is intact, in equilibrium with the lungs, its restinf level is Functional Residual Capacity (FRC)
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8
Q

What are some causes of increased chest wall resistance?

A
  • Structural abnotmality - decreased flexibility/expansion
  • Deformities of thorax
  • Ossification of the costal cartilage
  • Paralysis of intercostal muscles
  • Chest trauma - paralysis, strain, pain
  • Loss of elasticity
  • Burns
  • Blockage of the smaller respiratory passages with mucus or fluid
  • Raised abdominal pressure
  • Obesity
  • Pregnancy
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9
Q

What is the static resistance of the lungs?

A

-Elastic recoil 0 the tendency of an elastic structure to oppose stretching
- The lungs naturally have a tendency to collapse because of elastic recoil
- Held open by the negative intraplueral pressure (established by lymphatic pumping of fluid)
- Collapse caused by :
- Elastin and collagen in lung tissues (1/3 of this)
- Surface tension (2/3 of this resistance)

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10
Q

Describe elastin and collagen in lung tissues

A
  • Interwoven in the lung parenchyma
  • Tendency to oppose stretching
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11
Q

What is surface tension in lungs?

A
  • Caused by an air-liquid interface
  • Small alveoli are unstable and have a greater tendency to collapse and empty its air into connected larger alveoli (i.e. atelectasis)
  • Reduction of ST forces allows interdependent/stability
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12
Q

What are the benefits of surfactant?

A
  • 3 X less transmural pressure needed to expamd lungs
  • Keeps alveoli dry - lowers the inwardly directed pressure which draws water into the alveoli
  • Maximises area for ventilation and perfusion
  • ST of small alveoli are reduced more than larger alveoli as syrfactant molecules crowd into the smaller space
  • Maintains ‘alveolar interdependence’
  • Aided by fibrous tissue seprtal and septal walls between alveoli of different sizes which act as additional splints
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13
Q

What are some disorders that influence surface tension?

A
  • Neonatal Respiratory Distress Syndrome (NRDS)- Alters or destroys surfactant
  • Adult respiratory distress syndrome
  • Oxygen toxicity
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14
Q

What is NRDS?

A
  • Increasing respiratory distress commencing at or shortly after birth. Increases in severity until progressive resolution occurs among survivors, usually around 2nd to 7th day . Caused by deficiency of surfactant
  • Can be primary or secondary
  • Mortality is 50% in infants <1 kg
  • Incidence and severity is inversely proportional to gestational
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15
Q

What are the symptoms of NRDS?

A

Cyanosis

Preterm birth

Tachypnea

Nasal flaring

Chest retractions and grunting

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16
Q

What are the causes and contributor factors of NRDS?

A
  • Fetal head injury during birth
  • Aspiration of blood or amniotic fluid
  • Excessive sedation of mother during birth
  • Maternal diabetes (excess insulin suppresses surfactant production)
  • Cold stress
  • Males
  • Genetic disorders (e.g. abnormalities in proteins B and C or transport proteins ABC transporter 3 (ABCA3)
17
Q

What is the pathogenesis of NRDS?

A

-Starts with immature and damaged Type II pneumocytes due to risk factor or specific cause
Low surfactant = increased Surface Tension = Lung collapse = Hypoxia = Pulmonary vasoconstriction and Alveolar epithelial damage TO fibrin hyaline membrane

18
Q

Compare normal vs hyaline membranes?

A

Hyaline:
-collapsed alveoli
- Wax layers of hyaline
- Bleeding and vascular congestion
- Fibrin, cell debris, erythrocytles, Neutrophils and macrophages

19
Q

What are consequences of NRDS?

A
  • Inflammation - neutrophils in lungs
  • Atelectasis
  • Leads to ventilation-perfusion mismatch (VQ)
  • Right to left shunting
  • Arterial hypoxaemia
  • Hyaline membrane
  • Epithelial necrosis
  • Decreases fluid absorption and lung oedema
  • May haemorrhage
  • Can lead to complications e.g. hypoxic related intracerebrral bleeding, GIT necrosis , failure to close the hole in the heart (i.e. ductus arteriosis, normally caused by oxygen) and also some fibrosis due to fibrin exudation
20
Q

How is NRDS treated?

A

In babies:
- Synthetic surfactant therapy (endotracheal)
- Application of surfactant to a preterm infant
- Surfactant therapy - effect on the flow loops
- Assisted ventilation
- Supportive care e.g., thermoregulation, fluid management and nutrition
- Pre-term mothers :
- I.v. betamethasone 26-28 weeks gestation
- Administered - single dose or repeated doses