lecture 8 Flashcards

1
Q

when someone is in acute asthma, what occurs in terms of their breathing

A
  • they have a decrease in maximum lung capacity

- they have a decrease in inspiration but prolonged expiration (wheezing)

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2
Q

what are the two components of therapeutic treatment for asthma

A
  • use of rescue reliever- bronchodilator
  • use of controller treatment that modify the asthmatic airway environment so that acute airway narrowing occurs less often
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3
Q

what are the 2 rescue treatments for asthma

A

b2 agonists- stimulate receptors to cause vasodilation

anticholinergics- decrease parasympathetic activity by binding to M3 receptors- vasodil

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4
Q

what are some of the controller treatments for asthma

A

inhaled corticosteroids- prevents inflammation
antileukotriences- decrease activity of inflame. mediators
long-acting beta2 agonists
theophylline-block phosphodiesterase activity in SM of bronchiole
systemic corticosteroids- no common- anti-inflammatory
anti-IgE treatment-against specific antigen

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5
Q

obstructive vs restrictive pulmonary disorder

A

obstructive- and restriction in airflow to the lungs
restrictive- decreased EXPANSION of the lungs due to alterations of the lung parenchyma, pleura, chest wall or neuromuscular function

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6
Q

what is ARDS

A
  • adult respiratory distress syndrome
  • damage to the alveolar-capillary membrane
  • get alveolar infiltrates with dyspnea
  • associated with- trauma, sepsis, aspiration of gastric acid, fat emboli, shock
  • ALWAYS PRESENT WITH SEVERE DECREASE IN PaO2 THAT IS UNMANAGEABLE WITH SUPPLEMENTAL O2 THERAPY-
  • mortality 30-60%
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7
Q

what are the three pathological features of ARDS

A
  • noncardiogenic pulmonary edema- because of damage to the capillary, not hydrostatic pressure
  • atelectasis associated with lack of surfactant (can be acute)
  • fibrosis (hyaline membranes) associated with inflammatory deposition of proteins
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8
Q

what are 5 common findings in ARDS

A

1) severe hypoxemia caused by intrapulmonary shunting of blood
2) decrease in lung compliance
3) decrease in functional residual capacity
4) diffuse, fluffy alveolar infiltrates on chest x-ray- WHITE OUT
5) non cardiogenic pulmonary edema

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9
Q

what is the treatment for ARDS

A
  • mostly supportive
  • enhance tissue oxygenation until inflammation resolves
  • identify and correct underlying cause
  • block inflammation
  • maintain electrolyte and fluid balance while avoiding overload
  • oxygenation in undamaged areas of the lungs
  • mechanical ventilation with positive end expiratory pressure (PEEP)- increases and prevents alveolar collapse at end of expiration and forces edema out of alveoli
  • high frequency jet ventilation- pulsating
  • inhaled NO- relax muscle/bronchioles
  • supplemental oxygen- >60% with fio2 decreased as fast as possible to avoid absorption atelectasis
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10
Q

what is absorption atelectasis

A
  • occurs when the FIO2 is too high for too long
  • normally we breath 21% oxygen and rest nitrogen. since we do not use the nitrogen it stays in our lungs as residual volume.- when you deliver too much oxygen for too long, we use the oxygen and there is not residual volume left
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