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NUR4630 > Week 2: Disorders of Ventilation > Flashcards

Week 2: Disorders of Ventilation Flashcards

1
Q

the volume of air contained in the lungs at the end of maximum inspiration. Total volume of the lungs.

6.0: IRV+TV+ERV

A

total lung capacity

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2
Q

The volume of air that can be expelled from the lungs after a complete maximum inspiration

4.6: IRV+TV+ERV

A

vital capacity

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3
Q

the volume of air breathed in or out of the lungs during normal respiration

0.5

A

Tidal volume

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4
Q

the volume of air left in the lungs after a maximum exhalation

1.2

A

residual volume

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5
Q

the volume of air that stays in the lungs during normal breathing

2.4: ERV+RV

A

functional residual capacity

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6
Q

the maximum volume of air that can be inspired into the lungs in addition to tidal volume

3.0: VC- (TV+ERV)

A

inspiratory reserve volume

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7
Q

the maximum volume of air that can be inspired into the lungs following a normal expiration

3.5: TV+IRV

A

inspiratory capacity

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8
Q

the volume of air that can be expelled from the lungs after the expiration of a normal breath

1.2

A

Expiratory reserve volume

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9
Q

normal tidal volume

A

500 ml

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10
Q

need to breath is in?

A

brain stem and cerebral cortex

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11
Q

normal expiratory reserve volume

A

1200ml

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12
Q
  • Respond to hydrogen ion levels of the blood (central)
  • Respond to the oxygen , carbon dioxide, and hydrogen ion in the blood (peripheral)
A

chemoreceptors

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13
Q

The Ventilation-Perfusion (V/Q) ratio (normal?)

A

The V/Q ratio is the ratio between the amount of air getting to the alveoli (the alveolar ventilation, V, in ml/min) and the amount of blood being sent to the lungs (the cardiac output or Q - also in ml/min).
V/Q = (4 l/min)/(5 l/min)
V/Q = 0.8

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14
Q

Inadequate ventilation to an alveolus
Example: Pneumonia

A

Shunt Unit

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15
Q

Alveolar cluster where perfusion fails
Example: Pulmonary embolism

A

Dead Space Unit-

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16
Q

Both ventilation and perfusion fail
Example: Acute Respiratory Distress Syndrome

A

silent shunt

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17
Q

Normal ABG’s

A
  • PaO2: 80-100
  • SaO2: 93-99
  • pH: 7.35-7.45
  • PaCO2: 35-45
  • HCO3: 22-26
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18
Q

PzCO2 up, pH down

A

respiratory acidosis

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19
Q

PaCO2 down, pH up

A

respiratory alkalosis

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20
Q

HCO3 down, pH down

A

metabolic acidosis

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21
Q

HCO3 up, pH up

A

Metabolic Alkalosis

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22
Q

The Oxyhemoglobin dissociation curve

A

non-linear tendency for oxygen to bind to hemoglobin: below a SaO2 of 90%, small differences in hemoglobin saturation reflect large changes in PaO2

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23
Q

Type?

Impaired Gas Exchange

  • Pneumonia
  • Pulmonary edema
  • ARDS
  • Atelectasis

Nursing Interventions?

A

Type I- Hypoxemic

Nursing Interventions:

  • Cough and deep breathe
  • HOB elevated
  • administering of meds such as diuretics
  • Add some ventilator peep
  • incentive spirometry
  • Get up to allow lung expantion
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24
Q

Ineffective Breathing Pattern

  • COPD
  • Neurological Respiratory Failure
  • Muscular Failure

Type?
Nursing Interventions?

A

Type II- Hypercapneic

Nursing interventions:

  • Bipap
  • ventilate them and change inspiratory expiratory ratio to allow more time to breathe in (add paralytics)
  • mechanical ventilation
  • change position Q2
  • HOB elevated
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25
Q

Continuous Positive Airway Pressure

  • for patients who need continuous low pressure to keep lungs open
A

CPAP

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26
Q

Bilevel Positive Airway Pressure

  • can assist with low level pressure at inspiration and expiration to help lungs stay open
A

BIPAP

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27
Q

Indications for Mechanical Ventilation

A
  • Airway
  • – Ventilation failure
  • (CO2)
  • – Hypoxia
  • – Combination
  • • Airway obstruction
  • • Inability to protect
  • airway
  • • Hypoxia (PaO2 < 50)
  • • Hypercapnia (PaCO2
  • > 50)
  • • Respiratory distress
  • (RR > 30, use of
  • accessory muscles)
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28
Q

controlling the volume on the ventilator

A

Volume Control

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29
Q

delivers volume until a certain pressure is acheived

A

pressure control

30
Q

a little bit of both. Ensure a certain amount of volume, but if you reach a certain pressure, it will stop

A

pressure-regulated volume control

31
Q

Every breath is assisted. pt gets a certain number of breaths per minute plus they can breathe on their own on top of that

A

assist control

32
Q

on the breaths that the ventilator is going to deliver, it will deliver the settings. Won’t assist on their own breaths

A

synchronized intermitted mandatory ventilation

33
Q

cpap on vent

A

use positive end-expiratory pressure

34
Q

a little pressure on the inhalation on the vent (similar to bipap)

A

pressure support

35
Q
A
  • PEEP: set at 5.0
  • I:E : 1:2.8 (normal is 1:2-1:3)
  • mode: IMV
  • FIO2: 40%
  • Tidal volume:429ml/breath
  • Rate: 16
  • Sensitivity
  • High Pressure Limit: when you get to that point, it will stop delivering the breath
  • Pressure support: 2
36
Q

Naso/oral endotracheal intubation &
Tracheostomy tubes nursing care

A
  • Oral care every 2 hours
  • Check placement of tube at lip line for endotracheal tubes
  • Verify size
  • _Have emergency equipment ready: _Ambu Bag
  • Obturator, Suction Equipment, Extra Tubes
37
Q

if the trach tube comes out and you don’t have another, what do you do?

A

put the old trach tube back in

38
Q

what do you do for a wean?

A
  • sedation vacation
  • assess for alertness, assistance of vent, vital signs
  • underlying cause of intabation should be stabilizing
  • ability to follow directions
39
Q

ECMO

A
  • extracorporeal life support
  • De-saturated blood is drained via a venous cannula, CO2 is removed, O2 added through an “extracorporal” device (often misnamed an oxygenator), and the blood is then returned to systemic circulation via another vein (VV ECMO) or artery (VA ECMO)
40
Q

ECMO indications

A
  • Acute, potentially reversible respiratory (and/or cardiovascular) disease unresponsive to conventional/alternative arrangement
  • Oxygenation index >40 x 2 hours
  • Barotrauma
  • P/F ratio <200
41
Q

Acute Lung Injury/ ARDS

  • common causes
A
  • The most common causes of ARDS are pneumonia, sepsis, aspiration, and trauma.
42
Q

Patho of ALI/ARDS phases

A
  • Phase 1: (inflammation and exudation) Capillary membranes are compromised and alveoli begin to fill with protein rich fluid. Type I alveolar cells are destroyed. Hyaline membranes are formed.
  • Phase 2: (proliferation) Type II alveolar cells are damaged & surfactant production declines. Inspiratory pressures increase as compliance decreases resulting in a ventilation/perfusion mismatch.
  • Phase 3: (resolution) Fibrotic tissue develops resulting in increased pulmonary pressures and ventilation dead space.
43
Q
  • severe hypoxia coupled with bilateral infiltrates in the lung fields that is not related to cardiogenic reasons
  • classic signs: tachypenia, tachycardia, bilateral infiltrates, hypoxia
A

Acute lung injury/ARDS clinical manifestations

44
Q

NON-PHARMACOLOGICAL interventions for ALI/ARDS

A
  • Nutrition Support
  • Prone positioning: Guérin et al (2013) found early prone positioning decreased 30 & 90 day mortality
  • Mechanical Ventilation: Low VT and high PEEP,FiO2 below 60%, High Frequency Oscillation
  • Extracorporeal Life Support (ECLS): Lung bypass, ECMO
45
Q

Pharmacological interventions for ARDS/ALI

A
  • Anti-Inflammatories: Cases of hypoxia >7Days & started before Day 14
  • Vasodilators
  • Surfactant
  • B-Agonists
  • Cytokine Inhibitors
  • Colloids
  • Paralytics
  • Oxygen
46
Q
  • Occurs in nose, sinuses, larynx (occasionally also in lower airways
  • Associated with human papilloma virus types 6 and 11
  • Laryngeal lesions common in children – can occlude airway
A

Papilloma

47
Q

High Frequency Oscillation

A
  • mean airway pressure with fluctuating tidal volumes being delivered at 900 fluctuations a minute. This creates waves of oxygen/volume being pushed in
48
Q

Benign non-neoplastic nodules in smokers and those putting strain on vocal cords “singers nodules”

A

Vocal cord polyps

49
Q
  • Great geographical variation in incidence
  • Asia (Far East)
  • Africa
  • Sporadically elsewhere
A

Nasopharyngeal carcinoma

50
Q
  • Epstein-Barr virus (detectable in tumour)
  • Other factors – diet smoking
  • Present with neck node enlargement and/or nasal symptoms
  • Spreads to lymph nodes
  • Very sensitive to radiotherapy
A

Nasopharyngeal carcinoma

51
Q
  • Smoking related
  • Usually on the vocal cord
  • Squamous cell carcinomas
  • Effects by local tissue destruction (loss of voice)
  • Neck node metastases
A

Laryngeal carcinoma

52
Q
  • Leading cause of cancer deaths in the US
  • Main Types: SCLC, NSCLC (small cell: agressive & paliate care starts at the begginning, nonsmall cell is the other)
A

Lung Cancer

53
Q

Treatment options for lung cancer

A
  • Proton therapy —A type of radiation that uses high energy beams.
  • Chemotherapy —The most commonly used drugs to treat small cell lung cancer are cisplatin or carboplatin with etoposide.
  • Brachytherapy —radiation beads or rods are inserted at the cancer site.
54
Q
  • One of the most common congenital abnormalities
  • Incidence 1 in 2000 to 5000 births
  • One third of infants with this are stillborn, usually due to associated fatal anomalies like neural tube defects and cardiac defects
  • Defects are common on left side (80%) compared to right (20%)
  • expected risk in a 1st degree relative is 1 in 45
  • combo with karyotype is associated with poor outcome
  • Bilateral is very rare
A

Congenital Diaphragmatic Hernias (CDH

55
Q

cause of cdh

A
  • unknown, might be some genetic and environmental predisposition
56
Q

two main CDH

A

Bochdalek: most common

Morgani: much less common

57
Q

Diaphragmatic eventration

A

diaphragm itself is mishapen

58
Q
  • Right lobe of liver can occupy most of hemithorax in rt side defect
  • Hepatic veins may drain ectopically into right atrium
  • Lung and liver may be fused
  • In?
A

CDH

59
Q

Pathophysiology CDH

A
  • Pulmonary parenchymal compression by herniated organs and its effect on growth and maturation of lung
  • Unilateral hernia is associated with bilateral abnormal pulmonary development (severe on ipsilateral side)
  • Lung is smaller, pulmonary vascular bed is abnormal on affected side in pts with CDH
  • The musculature isn’t developed properly causing compromised arterioles, pulm htn which is associated with level of hypoxia, stress state, temp
60
Q

How to diagnose/treat CDH

A
  • CXR showing displaced organs into the chest cavity
  • diagnosed with ultrasound usually in utero, can be diagnosed 1st day of life
  • EKG shows stress to heart
  • surgical treatment: Laparotomy, thoracotomy, laparoscopy and thoracoscopy. When diaphragmatic tissue is adequate, primary repair with nonabsorbable suture can be done. If the defect is too large, prosthetic material can be used for a tension-free repair
  • Meds: nitros oxide in lung and htn medicine
61
Q

problems for survivors of CDH

A
  • In the survivors, long term problems include chronic lung disease, developmental delay, nutritional and growth related problems
  • Major predictor of survival is resolution of pulmonary HTN
62
Q

Fetal Lung Characteristics

A
  • Decreased blood flow: caused by compression of the pulmonary capillaries by fetal lung fluid
  • _Pulmonary arterie_s: thick muscular layer present, very reactive to hypoxemia
  • Lung fluid secretion: fetal lungs secrete fluid, adequate lung volume is necessary for fetal development
  • Fetal breathing: contributes to fetal lung development, moves fluid in and out of fetal lung
  • Surfactant: necessary amount to support breathing after birth, present after ~ 34 weeks gestation
63
Q
  • Disease of surfactant deficiency
  • Surfactant decreases surface tension and improves lung compliance
  • Surface tension: intrinsic tendency for alveoli to collapse
A

Respiratory Distress Syndrome

64
Q

when does surfactant start to develop?

A

34 weeks

65
Q
  • Develops in ~ 50% of infants born between 28-32 weeks gestation
  • Inversely related to prematurity
  • Males
  • Second born twins
  • C-section
  • Caucasian race

Risk factors for?

A

RSD risk factors

66
Q

Secondary surfactant deficiency risk factors?

A
  • Maternal diabetes
  • Asphyxia
  • Pneumonia
  • Pulmonary hemorrhage
  • Meconium aspiration
  • Oxygen toxicity
67
Q

Non-specific findings of respiratory distress

A
  • Grunting
  • Flaring
  • Retracting
  • *O2 requirement*
68
Q
  • Diffuse reticular granular or “ground glass”pattern
  • Air bronchograms (bronchi visible)
  • Underaeration
A

alveolar disease

69
Q

RDS: Treatment

A
  • Maintain FRC (CPAP vs. intubation)
  • Surfactant replacement (with temporary intubation)
  • Exogenous surfactants (if they don’t have any)
  • Survanta 4cc/kg
  • Infasurf 3cc/kg
70
Q

Meconium Aspiration Syndrome

A
  • Be very concerned about pulmonary hypertension, as this is also a fetal response to asphyxia
  • Meconium contains epithelial cells and bile salts
  • Released with intrauterine stress or asphyxia
  • Present in 15% of all newborns.
  • Only 5-10% develop MAS
  • Airway plugging, with air trapping
  • Inflammation, leading to inactivation of surfactant
  • Surfactant inactivation leads to decreased compliance, and alveolar collapse
  • Alveolar collapse = loss of FRC
  • Loss of FRC = V/Q mismatch
  • V/Q mismatch = desaturation
71
Q

Areas of hyperexpansion mixed with patchy densities and atelectasis

A

meconium aspiration xray

72
Q

treating meconium aspiration

A
  • ventilation
  • antibiotics
  • surfactants
  • nitrous oxide (allows for the vasodilation which helps decrease pulmonary pressures)
  • ecmo, or high frequency oscillatory ventilation

NUR4630 (34 decks)

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