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CV487 > Class 3 Respiratory > Flashcards

Class 3 Respiratory Flashcards

1
Q

Pulmonary vasculature

A

Goes around the alveoli; PEs get caught in the vasculature, not the alveoli

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2
Q

Neurochemical control of ventilation

A

-Respiratory center, central & peripheral chemoreceptors
-Mechanics of breathing
-Gas transport
-Control of pulmonary circulation

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3
Q

Neurochemical control of respiration

A

-Chemoreceptors monitor pH, PaCO2 and PaO2
-Located in medulla of the brain
-Monitor arterial blood by sensing changes in the CSF
-Respond to changes in CO2 which combines with H2O to form carbonic acid; hydrogen ions that are capable of stimulating the central chemoreceptors

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4
Q

Peripheral chemoreceptors

A

-In the carotid and aortic arch
-Respond to changes in PaO2 - activated when it drops below 60 mmHg
-Take over when central chemoreceptors are reset by chronic hypoventilation
-People with prolonged hypercapnia stop responding to CO2

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5
Q

Causes of hypercapnia

A

-Depression of the respiratory centre d/t medications
-Disease of the medulla, including CNS infections or trauma
-Spinal cord & thoracic cage abnormalities
-Airway obstruction
-Increased work of breathing

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6
Q

Hypoxemia

A

-Reduced oxygenation of arterial blood
-Caused by respiratory alterations:
-Issues with alveloar gas exchange (V/Q mismatch)
-Perfusion of pulmonary capillaries

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7
Q

Low V/Q

A

-Air is getting to the alveoli but it is constricted ie. Asthma
-Respiratory rate increases d/t bronchoconstriction

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8
Q

Shunt V/Q

A

-No gas exchange; less systemic oxygenated blood
-High respiratory rate d/t absent gas exchange

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9
Q

High V/Q

A

-Something wrong with the perfusion ie. PE, pulmonary HTN
-High respiratory rate because of reduced perfusion

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10
Q

Hypoxemia vs hypoxia

A

Hypoxemia is low O2 in the blood, hypoxic is low O2 in the tissue

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11
Q

Pediatric airway differences

A

-Obligate nasal breathing until 3-6 months
-Barrel chests
-Their neck is a bit extended

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12
Q

Continuation of airway

A

Large occiput-head flexes forward in infancy

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13
Q

LOC dictates

A

How much O2 is getting to the brain

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14
Q

In a pneumothorax

A

The chest wall expansion on the posterior side will be asymmetrical

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15
Q

Pediatric vs adut breathing

A

-6-8ml/kg/min children
-3-4ml/kg/min adults
-In paediatrics: Apnea, hypoxia, poor response to low O2 or high CO2, belly breathers, weak accessory muscles

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16
Q

Influenza pathophysiology

A

-Upper respiratory virus spread by poor hand hygiene
-Can lead to pneumonia or death

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17
Q

Manifestations of pneumonia

A

-Cough, fever, myalgia, headache and sore throat
-Mild symptoms similar to a common cold
-Dyspnea, diffuse crackles

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18
Q

Influenza assessment (neuro)

A

fever, headache, LOC, alert, orientated, lethargic, dizziness, lightheadedness

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19
Q

Influenza assessment (CV)

A

Hemodynamic status- pale, pink, gray, cyanotic, tachycardia, pulses, capillary refill

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20
Q

Influenza assessment (resp)

A

-Crackles, impaired gas exchange, tachypneic, cough

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21
Q

Influenza assessment (MSK)

A

Arthralgia

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22
Q

Lower respiratory conditions

A

-Disorders of the chest wall & pleura
-Restrictive lung diseases: Aspiration, atelectasis, pulmonary edema, ARDs
-Obstructive airway disorders
-Respiratory tract infections
-Pulmonary vascular disorders

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23
Q

Viral infections may not indicate a

A

Elevated WBC count

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24
Q

Cyanosis always means

A

Gas exchange issues

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25
Q

Pleural effusion pathophysiology

A

-Collection of fluid in the pleural space
-Sign of a serious disease

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26
Q

Transudative effusion (hydrothorax)

A

-Accumulation of protein and cell poor fluid and caused by:
-Increased hydrostatic pressure found in CHF *
-Decreased oncotic pressure (from hypoalbuminemia) found in chronic liver or renal disease
-Crackles outside of the lung

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27
Q

Exudative effusion

A

-Accumulation of fluid and cells from an area of inflammation
-Results in increased capillary permeability
-Occurs secondary to pulmonary malignancies, pulmonary infections, pulmonary embolization and GI disease

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28
Q

Empyema

A

-Pleural effusion that contains pus
-Caused by conditions such as pneumonia, TB, lung abscess and infection of surgical wounds of the chest

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29
Q

Pleural effusion manifestations

A

-Trapped lung can occur when the visceral pleura becomes encased; pulmonary restriction
-Progressive dyspnea and decreased movement of the chest wall on the affected side
-Fever, night sweats, cough and weight loss

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30
Q

Pleural effusion or thickening assessment

A

-Presence of fluid subdues all lung sounds
-Tachypnea, tachycardia, dyspnea, cyanosis, dry cough, abdominal distension
-Trachea shifts away from affected side, chest expansion decreased on the affected side
-Bronchial breath sounds heard over the fluid along with bronchophony, egophony, whispered pectoriloquy

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31
Q

Pneumothorax pathophysiology

A

-Pneumothorax & hemothorax can occur at the same time
-Presence of air in the pleural space that results in a complete or partial collapse of a lung
-Classified as either closed, open or tension pneumothorax

32
Q

Primary or spontaneous (closed) pneumothorax

A

-Spontaneous pneumothorax which is the accumulation of air in the pleural space without an apparent event (no external wound)
-Caused by rupture of small blebs on the visceral pleural space; underweight, male, cigarette smokers between 20-40 yrs old
-Line insertion can cause this

33
Q

Open pneumothorax

A

-Air enters the pleural space through an opening in the chest wall
-Penetrating chest wound is referred to as a sucking chest wound

34
Q

Tension pneumothorax

A

-Pneumothorax with a rapid accumulation of air in the pleural space causing high intrapleural pressures
-Occurs from either open or closed pneumothorax
-Air can enter but not escape
-May occur if chest tubes are clamped or become blocked with a patient who has a pneumo
-This is a medical emergency

35
Q

Hemothorax

A

-Accumulation of blood in the pleural space
-Causes include chest trauma, lung malignancy, complications of anticoagulant therapy, pulmonary embolism and tearing of pleural adhesions

36
Q

Chylothorax

A

-Presence of lymphatic fluid (chyle) that moves from lymphatic vessels into pleural space instead of passing from GI tract to thoracic duct
-Causes include trauma, surgical procedures and malignancy

37
Q

Pneumothorax is..

A

More serious than pleural effusion

38
Q

Manifestations of a pneumothorax

A

-Primary; sudden pleural plain, tachypnea, and dyspnea
-Absent or decreased breath sounds
-Tension pneumo; severe hypoxemia, tracheal deviation, and hypotension

39
Q

Assessment of a pneumothorax

A

-Absent breath sounds over the affected area
-If a tension pneumothorax develops, the patient may have severe respiratory distress, tachycardia and hypotension
-Mediastinal displacement occurs with tracheal shift
-Changes in BP, pulse, perfusion

40
Q

About pneumothorax’s

A

-Causes partial or complete lung collapse, usually unilateral; unequal chest expansion
-If pneumothorax is large, patients may have tachypnea, cyanosis, apprehension, bulging in interspaces
-Tracheal shift, tachycardia, decreased BP
-Decreased or absent breath sounds

41
Q

Aspiration

A

-May be related to aLOC, seizure disorders, CVA and neuromuscular disorders that cause dysphagia
-May cause severe pneumonitis
-Lung becomes still and noncompliant leading to edema and collapse

42
Q

Atelectasis

A

-Usually occurs after surgery
-Collapse of lung tissue
-Three types which are: compression atelectasis, absorption atelectasis and surfactant impairment

43
Q

Atelectasis manifestations

A

dyspnea, cough, fever and leukocytosis

44
Q

About atelectasis

A

-Collapsed shrunken section of alveoli, or an entire lung
-Cough, lag on expansion, increased respiratory & HR
-Assymetrical chest expansion, tracheal shift
-Diminished vesicular sounds, occasional fine crackles if the bronchus is patent

45
Q

Atelectasis causes

A

-Airway obstruction, the alveolar air beyond it is gradually absorbed by the pulmonary capillaries, and the alveolar walls cave
-Compression on the lung
-Lack of surfactant

46
Q

Pulmonary edema cause 1

A

-Valvular dysfunction, CAD, increased left atrial pressure & capillary hydrostatic pressure

47
Q

Pulmonary edema cause 2

A

-Injury to capillary endothelium; increased capillary permeability & disruption of surfactant production; movement of fluid & plasma proteins to the interstitial space and alveoli

48
Q

Pulmonary edema cause 3

A

-Lymphatic vessel blockage; inability to remove excess fluid from the interstitial space (fluid accumulates)

49
Q

Causes of pulmonary edema

A

-Commonly caused by left-sided heart disease
-Capillary injury that increases capillary permeability
-Lymphatic vessel obstruction

50
Q

Pulmonary edema manifestations

A

-Dyspnea, hypoxemia, increased work of breathing
-Fine inspiratory crackles
-V/Q mismatch leads to hypoxemia
-Pink, frothy sputum, hypoxemia worsens, hypoventilation with hypercapnia

51
Q

Pulmonary edema pathophysiology

A

-When hydrostatic pressure exceeds oncotic pressure fluid moves out into the interstitial space , when the flow of fluid out of the capillaries exceeds the lymphatic system’s ability to remove it, pulmonary edema develops

52
Q

Severe pulmonary illness/acute lung illness

A

-Stemmed from the CDC and FDA reports of severe pulmonary illness and deaths related to the use of vaping
-No specific device or substance has been linked to the illness but it is believed to be as a result of chemical exposure

53
Q

Bronchiolitis obliterans (popcorn lung)

A

Inflammatory obstruction of the airways

54
Q

Pathophysiology of acute lung illness (ABDIL)

A

-Bronchiolitis obliterans (popcorn lung)
-Acute eosinophilic pneumonia
-Diffuse alveolar damage; hemorrhage in alveolar
-Idiopathic interstitial pneumonia
-Lipoid pneumonia

55
Q

Lipoid pneumonia

A

Presence of lipids within alveolar space

56
Q

Idiopathic interstitial pneumonia

A

Inflammation and scarring in the alveoli

57
Q

Acute eosinophilic pneumonia

A

Inflammatory stimulus that recruits macrophages and neutrophils to lung tissue

58
Q

Manifestations of acute lung illness

A

-Cough, fever, malaise, fatigue and weight loss
-SOB & dry cough
-Tachycardia, tachypnea
-Potential to develop ARD
-Vomiting and diarrhea
-Scarring, chronic inflammation, cost to treat, addictions

59
Q

Acute Lung Injury (ALI)

A

Less severe form of lung inflammation

60
Q

Restrictive lung disease: ARDS

A

-Difficult for the lung to expand
-Characterized by acute lung inflammation and diffuse alveolar-capillary injury

61
Q

Common causes of ARDS

A

-Sepsis, inhalation of harmful substances, pneumonia, head chest or other major injury

62
Q

Pathophysiology of ARDS

A

-Inflammation injures the alveoli-capillary membrane causing pulmonary edema
-V/Q mismatching (shunting)
-Hypoxemia
-Endothelial damage initiates the complement cascade

63
Q

Endothelial damage initiates the complement cascade

A

-Toxic mediators such as tumor necrosis factor and interleukin 1 are released
-Alveoli and respiratory bronchioles fill with fluid or collapse
-Lungs stiffen increasing work of breathing, ventilation of alveoli decrease and hypercapnia causes acute respiratory failure

64
Q

Manifestation of ARDS

A

-Dyspnea, tachypnea, hypoxemia (unresponsive to O2)
-Lungs stiffen
-Alkalosis then acidosis

65
Q

ARDS progression

A

-Starts with dyspnea & hypoxemia
-Hyperventilation & respiratory alkalosis
-Decreased tissue perfusion, organ dysfunction, & metabolic acidosis
-Increased work of breathing, decreased tidal volume, & hypoventilation
-Respiratory acidosis & worsening hypoxemia
-Hypotension, decreased urine output, death

66
Q

About ARDS

A

-An acute pulmonary insult (trauma, gastric acid aspiration, shock, sepsis)
-Damages alveolar capillary membrane, leading to increased permeability of pulmonary capillaries and alveolar epithelium

67
Q

Subjective + ARDS

A

Acute onset of dyspnea, apprehension

68
Q

ARDS inspection

A

-Restlessness, rapid shallow breathing, thin & frothy sputum, retractions
-Decreased PaO2, blood gasses show respiratory alkalosis, radiographs show diffuse pulmonary infiltrates; a late sign is cyanosis

69
Q

ARDS palpation, auscultation & adventitious sounds

A

-Hypotension, tachycardia, crackles, rhonci

70
Q

Pathophysiology of COVID-19

A

-COV-2 binds to ACE2 receptor, viral RNA released
-ACE II expressed on type II cells
-RAS plays a significant role in COVID-19 infections

71
Q

COVID-19 assessment (neuro)

A

fever, headache, LOC, alert, orientated, lethargic, dizziness, lightheadedness

72
Q

COVID-19 assessment (resp)

A

-Crackles, gas exchange, tachypneic, cough, cyanosis, pleuritic chest pain

73
Q

COVID-19 lab values

A

-CBC: WBC (neutrophils, bands), platelets, hemoglobin
-Electrolytes: sodium, potassium, and BNP levels, creatinine, BUN, GFR, magnesium
-Clotting Factors: INR, PTT, D-Dimer (specific to clots); MISC: CRP, lactate, ABG

74
Q

COVID-19 pediatrics

A

-Multisystem Inflammatory Disease
-Increase in children with symptoms of Kawasaki disease

75
Q

Manifestations of COVID-19

A

-Fever, rash
-Abdominal & neck pain
-V/D
-Bloodshot eyes, feeling extra tired

CV487 (15 decks)

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