Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

VTS(ECC) Preparation > Respiratory system, respiratory emergencies & ventilation > Flashcards

Respiratory system, respiratory emergencies & ventilation Flashcards

1
Q

The tidal volume for a 65^lb (29kg) dog is approximately:
a. 100–200^mL
b. 300–600^mL
c. 700–1000^mL
d. 1.5–2^L

A

B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Which is the most common cause of hypoxemia in cats and dogs?
a. Hypoventilation
b. Diffusion impairment
c. Ventilation/perfusion mismatch
d. Decreased fractional inspired oxygen concentrations

A

C

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

When listening to lung sounds, wheezing is indicative of what disorder?
a. Narrowed respiratory passages
b. Upper airway obstruction
c. Pulmonary edema
d. Diaphragmatic hernia

A

A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

An increase in which of the following will stimulate ventilation?
a. pH
b. H+
c. K+
d. SpO2

A

B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Which of the following conditions can cause a patient to have a normal PaO2 value but have impaired delivery of oxygen to tissues?
a. IMHA
b. Pneumonia
c. Laryngeal paralysis
d. Diaphragmatic hernia

A

A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Which of the following is considered a lung-protective strategy in mechanical ventilation?
a. Low PEEP
b. Low tidal volume
c. Low respiratory rate
d. Low ETCO2

A

B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Which value represents a normal PF ratio?
a. 144
b. 217
c. 301
d. 517

A

D

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Which of the following would be responsible for a right shift in the oxyhemoglobin dissociation curve?
a. Hypocarbia
b. Acidosis
c. Hypothermia
d. Alkalosis

A

B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

The inequality of regional ventilation and blood flow within the lung is referred to as:
a. V/Q mismatch
b. diffusion defect
c. right-to-left shunting
d. hypoxemia

A

A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

An effusion that has a total solids value of 2.9^g/dL would be classified as what type of effusion?
a. Transudate
b. Modified transudate
c. Exudate
d. Modified exudate

A

B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Which of the following can help reduce the chances of ventilator-associated pneumonia for a patient receiving mechanical ventilation?
a. Appropriate oral care
b. Decreasing PEEP
c. Lung protective tidal volumes
d. All of the above

A

A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Lung compliance in mechanically ventilated patients can be evaluated using which method?
a. CPAP
b. Pressure volume loop
c. PEEP
d. Flow waveform

A

B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Respiratory rate, tidal volume, and dead space will all determine which parameter?
a. FiO2
b. PaO2
c. PaCO2
d. A-a gradient

A

C

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Mechanical ventilation is indicated by all of the following, except:
a. severe hypoxemia in the face of oxygen supplementation
b. severe hypercapnia despite therapy
c. excessive respiratory effort and risk of fatigue or arrest
d. severe hyperventilation

A

D

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Barring occlusion, the endotracheal tube for a patient receiving mechanical ventilation should be changed:
a. every hour
b. every 8 hours
c. every 24 hours
d. only when signs of occlusion are present

A

C

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Which is not a benefit of airway humidification?
a. Maintaining airway patency
b. Reduction of tracheal inflammation
c. Ability to decrease PEEP
d. Promote ciliary function

A

C

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

n which ventilator mode is the patient unable to take spontaneous breaths?
a. CMV
b. IMV
c. Manual PPV
d. SIMV

A

A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

According to human literature, during mechanical ventilation, suction of endotracheal tubes should be performed:
a. every 4 hours
b. every 12 hours
c. every 24 hours
d. when secretions are present

A

D

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Heat and moisture exchange filters should be replaced after:
a. 4 hours
b. 12 hours
c. 24 hours
d. 72 hours

A

C

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

During mechanical ventilation, corneal ulceration is most commonly see within the first:
a. 12 hours
b. 24 hours
c. 48 hours
d. 72 hours

A

D

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the main function of the respiratory system?

A

Supply the body with a continuous source of gas exchange between the inspired environment and the circulatory system.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Where does gas exchange occur? How does normal gas exchange occur?

A

Occurs in the ‘respiratory zones’ or the alveolar-capillary membrane and occurs via passive diffusion of gasses (O2 and CO2) from an area of high concentration to low concentration.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the space between the lungs and the thoracic cavity called?

A

Pleural space

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the purpose of the pleural space and what pressure is it normally kept at?

A

Lubrication as the lungs expand, it is kept usually at a negative pressure of 5cmH20.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How is a breath generated?

A

On inspiration air is sucked into the lungs and alveoli causing the thoracic cavity to become more negative (approx. 10cmH20) as the diaphragm flattens. On expiration the lungs and chest wall passively return to their original place and air is pushed out of the lungs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is tidal volume (Vt)? What is considered normal?

A

The volume of gas normally inspired within a given breath
Vt = Va + Vd
Normal 10-20ml/kg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the fuctional residual capacity (FRC)?

A

The volume of air that remains in the lung always or the lung will collapse.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is minute ventilation (Ve)?

A

The volume of gas that is ventilated per minute
Ve = Vt X RR
Normal 150-250mL/kg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Breathing….

A

Is an intrinsic, automated and unconscious process that originates from the brainstem and the central pattern generator in the medulla of the brainstem controls inspiration & expiration.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

The pneumotaxic centre….

A

Located in the upper pons and is responsible for regulating the volume and rate of ventilation. Sends inhibitory impulses to the inspiratory centre to terminate inspiration and regulates inspiratory volume and respiratory rate.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

The limbic system….

A

Regulates breathing pattern.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Central chemoreceptors….

A

Respond to changes in ECF hydrogen (H+) concentrations and are located in the brain, carotid & aortic arteries. They are responsible for 85% of the respiratory response to CO2.
Increased H ions = increased ventilation (increased CO2)
Decreased H ions = decreased ventilation (decreased CO2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Pulmonary stretch receptors….

A

Located in airway smooth muscles and respond when the lung is distended - brief drop in respiration/apnoea. Send action potentials through myelinated fibres of the vagus nerve to inspiratory area and apneustic centre to inhibit inspiratory discharge.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Hering-breuer reflex….

A

What keeps the lungs from over-inflating with inspired air.
Pulmonary stretch receptors respond to excessive stretching of the lung during large inspirations. Once activated they send action potentials through large myelinated fibres of the vagus nerve to the inspiratory area in the medulla and apneustic center of the pons. In response, the inspiratory area is inhibited directly and the apneustic center is inhibited from activating the inspiratory area. This inhibits inspiration, allowing expiration to occur.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Irritant receptors….

A

Located between airway epithelial cells and when stimulated cause rapid bronchoconstriction and hyperpnoea.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Normal respiration….

A

Air enters the lungs reaching the alveoli and O2 passively diffuses through alveolar-capillary membranes where it binds with haemoglobin (Hb) forming oxyhaemoglobin (HbO2). This displaces CO2 and aids in its secretion. Oxygenated blood is delivered to the body and CO2 is exhaled.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

1 Hb can carry ____ oxygen molecules?

A

4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

__% of O2 diffused into the cell is utilised by mitochondria during the production of ATP

A

80-90

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

____ is the major by-product of internal respiration within the cell

A

CO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

CO2 combines with H2O forming _________ which dissolves into _____ + _____ ions. _____ is directly affected by the ratio of these ions.

A

a) carbonic acid
b) H+
c) HCO3-
d) pH
CO2 + H20 < – > H2CO3 < – > HCO3- + H+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What are the 5 types of hypoxia?

A
  1. Hypoxaemic-hypoxia i.e. inadequate CaO2 due to hypoxaemia
  2. Hypaemic-hypoxia i.e. aneamia resulting in decreased Hb
  3. Stagnant/circulatory hypoxia i.e. reduced CO or poor perfusion
  4. Histotoxic-hypoxia i.e. O2 extraction disorder
  5. Metabolic hypoxia i.e. increased VO2
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Carbon monoxide….

A

220X affinity for Hb and will bind to Hb rendering it non-functional
“carboxyhaemoglobin”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Methaemoglobin….

A

May result from acetominophen toxicity in cats, nitrate toxicity, phenol toxicity, sulfites and napthalene.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

CO2 is ___% more soluble than O2?

A

20

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What are the 5 general causes of hypoxaemia?

A
  1. VQ mismatch
  2. Low FiO2
  3. Diffusion impairment
  4. R - L shunting
  5. Hypoventilation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

VQ mismatch….

A

There is inequailty between regional ventilation and blood flow within the lung (ventilation v. perfusion). The lung can be adequately perfused but inappropriately ventilated or vice versa.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Treatment to improve lung ventilation and maximise perfusion

A

Oxygen
- improve MV
- PEEP
- alveolar recruitment maneuvers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Cyanosis present when

A

Hb <5g/dL and deoxyhaemoglobin >5g/dL which is the equivalent of HbO2 dropping between 50-70%.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What can auscultating crackles indicate?

A

Pulmonary oedema, pneumonia, fluid in the alveoli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What may audible wheezing indicate?

A

Narrowed respiratory passages, obstructive diseases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Absent or muffled heart sounds indicate?

A

Pleural space disease, pericardial disease, pneumothorax, diaphragmatic hernia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What may inspiratory stridor indicate?

A

Obstructive airway disease i.e. laryngeal paralysis, BOAS, collapsing trachea.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Inspiratory effort visualised….

A

likely upper airway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Expiratory effort visualised….

A

likely lower airway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Rapid, shallow breathing….

A

pleural space disease, pneumothorax

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Cheyne-stokes respiratory pattern….

A

Brief periods of apnoea followed by brief hyperventilation.
Commonly seen in severe intracranial disease, cardiac abnormalities and hypoxaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Kussmal respiratory pattern….

A

Sustained increase in depth of respiration commonly seen in patients with significant metabolic acidosis i.e. DKA, CKD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Apneustic breathing pattern….

A

Deep respirations with pause at full inspiration followed by brief expiration.
Commonly seen secondary to ketamine administration in Cats, central neurological disease and TBI.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

PaO2 is a good indicator of?

A

Oxygen status
Patient can however have normal PaO2 and have decreased DO2 i.e. anaemia, reduced CO, toxicities.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

The PaO2 of a healthy patient should be?

A

5 X FiO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Alveolar partial pressure of O2/Alveolar gas equation

A

PAO2 = FiO2 (Patm - Ph) - PaCO2/RQ
On room air @ sea level PAO2=150-PaCO2/0.8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

The difference between PAO2 and PaO2 should be?

A

A-a gradient
PAO2 - PaO2
Normal 5-15mmHg
ARDS >30mmHg
Negative = shunting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What does a high A-a gradient indicate?

A

The O2 in the alveoli struggles to diffuse into the blood i.e. VQ mismatch, diffusion impairment, R-L shunting, increasing age.
- Indicates pulmonary issue for hypoxaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

P:F ratio….

A

P:F = PaO2/FiO2
Indicator of inappropriate oxygenation and is reliable for any FiO2 but can be unreliable in shunting.
Normal: 500
<200 indicative of ARDS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Laryngeal paralysis….

A

Complete or partial failure of the aryntenoid cartilages to abduct during inspiration and adduct in expiration. It is generally idiopathic but may be due to a neuromuscular disease i.e. polyneuropathy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Signs of laryngeal paralysis

A

Stridorous breathing, inspiratory effort
Narrowed laryngeal lumen, increased airway resistance
Increased WOB
Airway obstruction
Dysphonia
Gagging/retching especially after eating and drinking
Heat intolerance, hyperthermia
NCPO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What are 2 common complications of laryngeal paralysis?

A

Pneumonitis and aspiration pneumonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

How is laryngeal paralysis treated?

A

Can medically manage with anxiolytics, oxygen, active cooling and weight reduction however surgery almost always indicated and has excellent prognosis (laryngeal tie back).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Collapsing trachea….

A

Degeneration of the tracheal cartilage that results in increased collapsibility of the trachea, trahceal flattening and tracheal narrowing. The upper portion of the trachea collapses on inspiration and the lower portion collapses on expiration.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What breeds are at higher risk of tracheal collapse?

A

Miniature & toy breeds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Clinical signs of collapsing trachea

A

Moderate to severe respiratory distress
Inspiratory stridor
Exercise intolerance
“goose-honk”, wheezing, hacking, coughing
Orthopnoea
Syncope

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What are 4 anatomical features of brachycephalic airway syndrome?

A
  1. Stenotic nares
  2. Everted laryngeal saccules
  3. Hypoplastic trachea
  4. elongated soft palate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Pulmonary contusions….

A

Damage to the pulmonary capillaries - usually after blunt force trauma - which causes haemorrhage to the alveoli and broncheoli. This impairs gas exchange due to a physical barrier a the alveolar-capillary membrane, and there is VQ mismatch and hypoxaemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Clinical signs and diagnosis of pulmonary contusions

A

Thoracic pain, coughing, haemoptysis, mild to severe dyspnoea, cyanosis, increased/crackly bronchovesicular sounds.
Diagnosis with radiographs and history of blunt force trauma (radiographic evidence may not be present until 36h after event).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

How are pulmonary contusions treated?

A

Supportive - oxygen, fluids, analgesia, decreased WOB (encourage rest).

  • Diuretics, AB’s and corticosteroids unlikely to be beneficial
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Feline asthma….

A

Hypersensitivity reaction characterised by bronchoconstriction, eosinophilic airway inflammation and airway oedema. It can range from mild to severe and is diagnosed via airway imaging. Reoccurrence is common.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

How is feline asthma treated?

A

Environmental modification, corticosteroids (terbutaline, aminophylline, dexamethasone/prednisone).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Pneumonia….

A

Inflammation of the pulmonary parenchyma that results in exudate infiltration of the alveoli secondary to infection. Bacterial pathogens are the #1 cause but other pathogens such as viruses, fungi, parasites and protozoa may also induce.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Pneumonitis….

A

Inflammation of the pulmonary parenchyma that has no infectious cause and usually occurs secondary to aspiration of gastric contents, chemical irritants and smoke inhalation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Clinical signs of pneumonia & pneumonitis

A

Lethargy
Moist cough
Tracheal irritation
Anorexia/Inappetant
Dehydration
Hypoxaemia
Increased, decreased or absent bronchovesicular sounds
+- pyrexia
Dyspnoea (often rapid, shallow)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Treatment for pneumonia & pneumonitis

A

Oxygen therapy
Antimicrobials
IVFT
Nebulisation +- coupage
Regular walks (facilitate in loosening secretions)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

ARDS….

A

Acute, diffuse inflammation lung injury that leads to increased pulmonary vascular permeability, increased lung weight and loss of aerated lung tissue with hypoxaemia and bilateral radiographic opacities. It can be induced directly by the lungs or occur secondary to systemic diseases (pancreatitis, TRALI, severe burns, TBI).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Criteria for ARDS

A
  1. Must be acute onset
  2. Bilateral opacities consistent with pulmonary oedema
  3. P:F <300
  4. Signs cannot be attributed to cardiac failure or fluid overload.

ARDS most often occurs whilst a patient is hospitalised

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Mild, moderate, severe ARDS

A

Mild 200-300
Moderate 100-200
Severe <100

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Clinical signs of ARDS

A

Bilateral increased bronchovesicular sounds
Increased respiratory rate & effort
Severe dyspnoea
Cough
Cyanosis
Profound hypoxaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Treatment of ARDS

A

Oxygen - HFNO, ventilation (lung protective), CPAP
IVFT
Neuromuscular blockers (ventilated patients)

  • corticosteroids, diuretics & bronchodilators not recommended
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Pneumothorax….

A

Accumulation of air in the pleural space in a sufficient quantity that increases pressure within the pleural space impeding the ability of the lungs to expand, and participate in gas exchange.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Clinical signs of pneumothorax

A

Dyspnoea
Decreased/absent lung sounds
Rapid, shallow ‘restrictive’ breathing
Hypoxaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Treatment of pneumothorax

A

Oxygen
Thoracocentesis
Analgesia, anxiolysis
Chest tube placement
Immediate sterile dressing is open-pneumothorax
Surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Pleural effusion….

A

Accumulation of fluid in the pleural space and it occurs when the rate of fluid accumulation exceeds the rate of fluid absorption. This leads to an increase in pleural space pressure, inability of the lung to expand which impairs oxygenation and ventilation.
- Haemothorax
- Chylothorax
- Pyothorax

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Causes of pleural effusion

A

Neoplasia
Hypoalbuminaemia
RHS and/or LHS heart failure
Infection
Coagulopathy
Diaphragmatic hernia
Lung lobe torsion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Clinical signs of pleural effusion

A

Restrictive breathing pattern
Respiratory distress
Anorexia
Muffled heart/lung sounds
Lethargy
Exercise intolerance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Treatment of pleural effusion

A

Thoracocentesis
Chest drain placement
Surgery
Anxiolysis
Pain relief
Oxygen
Treat underlying cause
Antibiotics where indicated
Diet alteration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Pure transudate….

A

Low protein <2.5g/dL
Low cell count <1000cells/uL

Due to low oncotic pressure i.e. low albumin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Modified transudate….

A

Protein 2.5-3.5g/dL
Cell count <1000-5000cells/uL

Due to congestion (increased hydrostatic pressure) i.e. HF, neoplasia, lung lobe torsion, lymphoma etc

96
Q

Exudate….

A

Protein >3.5g/dL
Cell count >5000cells/uL (degenerate neutrophils)

Due to altered membrane permeability i.e. haemothorax, chylothorax, pyothorax

97
Q

Rib fractures/flail chest….

A

Occurs after trauma where multiple adjacent ribs fracture in multiple spots causing a ‘flail’ segment. Negative pressure pulls the flail segment inwards whilst the chest wall moves outward during inspiration.

98
Q

Treatment of rib fractures/flail chest

A

Oxygen therapy
Place affected side down or in sternal recumbency
Analgesia
Surgery

  • No chest wraps
99
Q

Diaphragmatic hernia….

A

Entrapment of abdominal organs in the thoracic cavity and can be acutely identified (after trauma) or chronic with an acute onset of clinical signs. It prevents normal lung expansion and over time compression atelectasis, collapse of the lung and adhesions within the pleural space. Blood flow to the entrapped organs is compromised which leads to ischaemia and necrosis of affected organs.

100
Q

Clinical signs of diaphragmatic hernia

A

Restrictive breathing pattern
Cardiac arrhythmias
Muffled chest and heart sounds
palpable empty abdomen

101
Q

Treatment of diaphragmatic hernia

A

Pain relief
Anxiolysis
IVFT
Oxygen
Surgery
+- blood products

102
Q

Hypoxaemia ranges

A

PaO2 <80mmHg or SaO2/SpO2 of <95%
Severe if PaO2 <60mmHg or SaO2/SpO2 <90%

103
Q

Small changes in SpO2 can be _______ changes in PaO2

A

Large

104
Q

Cyanosis is a _______ sign of hypoxaemia and corresponds to a PaO2 of ______ and a Hb of ________.

A

Late
37mmHg
15g/dL

105
Q

What are the 4 main mechanisms of hypoxaemia?

A
  1. Low FiO2
  2. Hypoventilation
  3. Venous admixture
  4. Low venous O2 content
106
Q

Venous admixture….

A

How venous blood gets from RHS to LHS of circulation without being properly oxygenated. Net PaO2 is decreased and can be due to diffusion impairment, pulmonary oedema, shunt membrane impairment.
Normally admixture is approximately of 5%

107
Q

Ventilated but under perfused lung….

A

No blood flow to or from affected regions i.e. PTE

108
Q

Higher than average VQ ratio….

A

Regional hyperventilation (low CO2) i.e. hypovolaemia, increased Vt

109
Q

Lower than average VQ ration….

A

Regional hypoventilation (high CO2) i.e. lower airway disease, small airway narrowing.
- Oxygen responsive

110
Q

Not ventilated but perfused lung….

A

physiologic shunt with decreased PaO2 i.e. small airway collapse, alveolar collapse
- Not O2 responsive but responsive to PPV

111
Q

The 120 rule

A

Normal PaCO2 = approx. 40, Normal PaO2 = approx. 80
PaCO2 + PaO2 = 120

<120 = venous admixture, lung dysfunction (the larger the deviation the worse the lung dysfunction)
* can only be used on room air and at sea level

112
Q

Dead space….

A

Areas of the airway that don’t participate in gas exchange and can be physiological, anatomical or alveolar. Where there is increased dead space ventilation there is reduced alveolar ventilation. Thus PCO2 is a measurement of the ventilatory status of a patient.

113
Q

Apneustic centre….

A

Controls the speed of inhalation and exhalation which can be overridden by signals from pneumotaxic centre to terminate inspiration.

114
Q

Peripheral chemoreceptors….

A

Sense changes in arterial blood gas tensions to increase ventilation when there is decreased pH, increased CO2 and decreased PaO2.

115
Q

Clinical signs of hypoventilation

A

Elevated CO2
Shallow, rapid breathing
Deep slow breathing
Dyspnoea
Vasodilation
AKI

116
Q

Treatment of hypoventilation

A

Oxygen
PPV
Ventilation
Bicarbonate
Respiratory stimulant

117
Q

Clinical signs of upper airway disease

A

Nasal discharge
Reverse sneezing, sneezing
Inspiratory stridor, snoring
Stertorous breathing
Loud URN
Long inspiratory phase
Dyspnoea
Gagging/coughing
Heat intolerance
* as continues can be self-perpetuating causing oedema and inflammation, narrowing of the airway, increased effort, worsened obstruction.

118
Q

Nasopharyngeal polyps….

A

Common UAO in cats (28%) that have nasopharyngeal disease. They are usually benign inflammatory lesions that arise from the mucosa of auditory tube or middle ear and grow into nasopharynx or external ear canal. Surgical removal required.

119
Q

Tracheal stenosis/stricture….

A

Full thickness tracheal tears can result in circumferential tracheal stricture and ultimately tracheal narrowing leading to UAO.

120
Q

Pathophysiology of BAS

A

Altered craniofacial and tracheal anatomy increases resistance to airflow on inspiration which the patient must overcome to adequately ventilated and oxygenate.

121
Q

Consequences of chronic UAO in brachycephalic’s

A

Generate greater subatmospheric pleural pressures on inspiration in order to overcome an increase in UA resistance.
- increased PCV due to CIH
- bronchial collapse
- pulmonary oedema due to repetitive airway obstruction
- habituation: tolerate lower PaO2 and increased PaCO2 without increasing MV
- regurgitation and oesophageal dysfunction
- aspiration pneumonia
- hypertension

122
Q

What is the pathogenesis of allergic airway disease?

A

Increased eosinophils in the airway, hyperinflation of the lungs and thickening of the bronchi & bronchioles.
- mucosal oedema
- airway smooth muscle hypertrophy
- constriction
- excessive airway secretions

123
Q

How is allergic airway disease treated?

A

Inhalant steroids
Oxygen

124
Q

________ is the main determinant of fluid extravasation and oedema formation in the lungs.

A

Hydrostatic pressure

125
Q

High pressure oedema occurs when

A

There is an increase in pulmonary capillary pressures causing fluid extravasation overwhelming lymphatic removal. Fluid builds up in the airspaces at the junction of alveolar and airway epithelia.

126
Q

Clinical presentation of pulmonary oedema

A

Hypoxaemia
+- paradoxical breathing
Respiratory distress
Crackles/coarse lung sounds

127
Q

Treatment of pulmonary oedema

A

Diuretics (cardiogenic PO)
Oxygen
Ventilation
Nitric oxide donors
B2 agonism
IVFT (NCPO)
a-adrenergic antagonism

128
Q

Radiographic findings of pneumonia

A

Alveolar opacification
Air bronchograms
Silhouette of lungs and heart
Interstitial pattern

129
Q

What are some blood smear findings in patients with pneumonia?

A

May be unremarkable
Leukocytosis with neutrophilia
+- left shift
+- monocytosis
+- eosinophilic

130
Q

Pathophysiology of pneumonia

A

Particles <3um bypass URT and deposit in alveoli. Increased number of organisms/high virulence organisms enter lower airway surfactant and alveolar macrophages are overwhelmed. Bronchoalveolar inflammation (vulnerable to damage) occurs. VQ mismatch, shunting and impaired diffusion lead to hypoxaemia.
Severe and chronic pneumonia lead to destruction of the alveolar walls increasing pulmonary vascular permeability and putting the patient at risk for ALI or ARDS. Can have systemic consequences (SIRS, sepsis, MODS)

131
Q

Treatment for pneumonia

A

Antimicrobials
Oxygen
Ventilation
Treat underlying disorder
Glucocorticoids
B agonists
Mucolytics
+- NAC
Nebulising +- coupage

132
Q

When does aspiration pneumonitis & pneumonia occur?

A

After chemical injury to the lungs and causes an inflammatory cascade that impairs respiratory function,

133
Q

Pathophysiology of aspiration pneumonitis/penumonia

A

Acid damages bronchial & alveolar epithelium as well as the pulmonary capillary endothelium stimulating tracheobronchial substance P immunoreactive neurons which control smooth muscle tone and vascular permeability. This induces tachykinin neuropeptide release leading to neurogenic inflammation which causes bronchoconstriction, vasodilation & increased vascular permeability (peaking 1-2 hours after event). First-phase damage causes epithelial & endothelial degeneration, necrosis of type I alveolar cells and intra-alveolar haemorrhage. After this, second-phase damage (4-6h after event) occurs increasing permeaability and protein extravasation leading to compromised gas exchange, VQ mismatch and reduced lung compliance. Chemotactic mediators are then released by macrophages attracting neutrophils causing a local proinflammatory state.

134
Q

Criteria for ALI/ARDS

A

Timing: <1wk clinical insult or worsening of resp symptoms
Imaging: bilateral opacities that can’t be explained by effusions, lobar/lung collapse or nodules
Origin of oedema: not explained by cardiac disease or fluid overload
Oxygenation: mild - PF 200-300 with PEEP >5; moderate - PF 100-200 with PEEP 5; severe <100 with PEEP >5

135
Q

Pathophysiology of ALI/ARDS

A
  1. Initial insult causes haemorrhage and pulmonary oedema (damaged type I pneumocytes) in alveoli - day 0-6
  2. Proliferation phase involves decreased oedema, hyaline membrane formation, and interstitial fibrosis (type II pneumocytes) - day 4-10
  3. Fibrosis phase is where there is obliterate areas of lungs - day 8 onwards
  4. Recovery (rare) - mortality 99%
136
Q

Common features ALI/ARDS

A

Pronounced microvascular permeability
Leukocyte activation (neutrophils, macrophages)
Altered cytokine production
Arterial hypoxaemia

137
Q

Incomplete resolution of ALI/ARDS….

A

Persistent deficiencies in lung function. Healing takes <1 year and QOL can be good but ongoing therapy may be required.

138
Q

Treatment of ALI/ARDS

A

Mostly supportive
- oxygen
- ventilation (lung protecctive)
- +- nitrous oxide & surfactant therapy (may not be beneficial)
- cytokine blocking agents
- avoid positive fluid balance

139
Q

How do pulmonary contusions/haemorrhage occur

A

Acute compression then expansion lead to transmission of mechanical forces and energy to the pulmonary parenchyma.
‘spalling effect’ - shearing or bursting at gas-fluid interfaces disrupting alveoli when shock waves occur. ‘inertial effect’ - alveolar tissue stripped from hilar structures as they accelerate at different rates . ‘implosion effect’ - rebound or overexpansion of gas bubbles after the pressure wave passes leading to tearing of the pulmonary parenchyma from excess dilation.
Subsequent haemorrhage results in bronchospasm, increased mucous production, and alveolar collapse as a result of reduced surfactant. VQ mismatch occurs as lungs flood with blood and underventilated, protein-rich oedema accumulates as there is decreased lung compliance.

140
Q

Resolution of pulmonary contusions/haemorrhage occurs

A

within 3-7 days

141
Q

Brief pathophysiology of pulmonary contusions/haemorrhage

A

Immediate interstitial haemorrhage is followed by interstitial oedema and infiltration of monocytes and neutrophils during the first few hours of injury. 24h after insult the alveoli and smaller airways are filled with protein, RBC and inflammatory cells causing loss of normal architecture. Alveoli surrounding the affected area may be normally perfused but will be less compliant because of the oedema and disruption of the surfactant layer therefore increased VQ mismatch is present. 48h after injury healing has started and the lymphatic vessels are dilated and filled with protein. After 7-10 days lungs a generally completely healed with little scarring.

142
Q

Treatment of pulmonary contusions/haemmorhage

A

Mostly supportive
- oxygen (PPV, HFNO)
- fluid therapy
- analgesia
-dexmedetomidine

  • most don’t have bacterial infections so don’t need antimicrobials
  • avoid glucocorticoids
143
Q

Pulmonary thromboembolism….

A

Obstruction of pulmonary vascular bed due to fat, septic emboli, metastatic neoplasia, parasites or blood clots. Embolism causes both a mechanical obstruction and reactive vasoconstriction (serotonin mediates) due to the release of vasoactive mediators (platelet aggregation) increasing pulmonary vascular resistance and increased pulmonary arterial pressure. This causes hypoxaemia, shunting and reduced arterial oxygen content.

144
Q

Treatment of PTE

A

Oxygen
Thrombolysis (tPA)
Anticoagulants (dalteparin)

145
Q

Diagnosis of chest wall disease

A

Paradoxical breathing
Radiographs
Hypoventilation (evident on ABG)

146
Q

Diseases of the chest wall

A

Neoplasia
Rib fractures
Congenital
Penetrating wounds
Cervical spine disease
Neuromuscular disease

147
Q

Clinical signs of pleural space disease

A

Tachypnoea
Orthopnoea, open-mouth breathing
Coughing
Cyanosis
Abdominal breathing, paradoxical breathing
Muffled heart sounds
Short, shallow breathing

148
Q

Pyothorax….

A

Accumulation of purulent exudate in the thoracic cavity and is usually caused by anaerobic bacteria including pasteurella and E.coli
- treated with supportive care
- 63-66% survival rate

149
Q

Chylothorax….

A

Fatty, opaque/whit/pink effusion that may require thoracocentesis, or surgery to ligate the thoracic duct or pleuroports if reoccurring.

150
Q

Non-respiratory lookalikes

A

Metabolic acidosis i.e. DKA
Drug therapy
Neurological disease
Hypovolaemia/hypotension i.e. anaemia, CKD
Pain
Anxiety

151
Q

Indications for thoracocentesis

A

Suspicion of pneumothorax and pleural effusion
Air or fluid accumulation is contributing to respiratory distress
Sample of fluid will aid in diagnosis

152
Q

Contraindications for thoracocentesis

A

Coagulopathy
Pleural space diseases that can’t be treated with thoracocentesis
Pneumomediastinum
Diaphragmatic hernia with fluid accumulation
Pleural masses
Large bullae

153
Q

Location of thoracocentesis

A

7th-9th intercostal spaces
Air = mid to upper thorax
Fluid = lower third of thorax
* avoid thoracic arteries - few cm either side of sternum ventrally

154
Q

Indications for thoracostomy tube placement

A

Tension pneumothorax
Repeated thoracocentesis
Thoracic surgery
Penetrating chest injury
pleurodesis
Pyothorax

155
Q

Contraindications for thoracostomy tube placement

A

Coagulopathies
Pleural adhesions

156
Q

Fick’s law

A

A decrease in lung surface area will mean less gas exchange
Q = VO2 / CaO2 - CmvO2
“ the rate of diffusion is directly proportional to both the surface area and concentration difference and is inversely proportional to the thickness of the membrane “

157
Q

Respiratory system functions

A

Physical defence againsts inhaled particles/pathogens
Immune function
Metabolising compounds
Dissipating heat
Reservoir for blood

158
Q

What can be assessed using capnography?

A

Adequacy of ventilation
Systemic metabolism
Circulation

159
Q

Normal EtCO2

A

35-45mmHg
>50mmHg indicates inadequate ventilation and highest permissible limit is 60mmHg

160
Q

What forms does CO2 transport around the body?

A
  1. 60-70% bicarbonate ion
  2. 20-30% bound to proteins
  3. 5-10% dissolved in plasma *measured in blood gas analysis (PaCO2)
161
Q

What is the difference between PaCO2 and EtCO2

A

2-5mmHg

162
Q

EtCO2 is a product of 3 major determinants

A
  1. Rate of CO2 production by the tissues
  2. Rate of CO2 exchange from the blood to the alveoli
  3. Rate of CO2 removal by alveolar ventilation
163
Q

How do most clinical capnographs work?

A

Infrared absorption spectroscopy. Infrared light at wavelengths absorbed by CO2 passes over expired gas and the concentration is determined according to the beer-lambert law (relationship between the absorption of light and properties of a solution).
A = εbC

164
Q

Phases of a capnogram

A

I: Inspiration. End of phase one expiration starts (anatomic dead space)
II: Exhalation of alveolar gas and mixes with gas from the anatomical dead space.
III: Plateau. PCO2 is almost as constant as alveolar gas is exhaled. Expiration ends partway through this phase and followed by pause.
IV: Rapid downstroke that corresponds with inspiration.

165
Q

Abnormal phase I on capnogram

A

No return to baseline indicates rebreathing of CO2 (bain circuits, circle systems, malfunctioning inspiratory valves)

166
Q

Abnormal phase II on capnogram

A

Delayed equipment response time (particularly sidestream)
Slow expiration

167
Q

Abnormal phase III on capnogram

A

Hypoventilation or hyperventilation
Equipment failure
‘cleft’ - patient effort during whilst in mandaotry ventilation
Cardiac oscillations

168
Q

Abnormal phase IV on capnogram

A

Malfunctioning inspiratory valve (rebreathing system)
Obstruction etc

169
Q

Pulse oximetry wavelengths

A

660 & 940nm

170
Q

Primary physiological causes of hypoxaemia

A
  1. Low FiO2
  2. Hypoventilation
  3. Venous Admixture
171
Q

Venous admixture

A

All the ways venous blood can get from the RHS to the LHS of circulation without being oxygenated.
- Low VQ regions
- No VQ regions
- Diffusion defects
- R-L shunting

172
Q

Pulmonary oedema results in

A

Reduced oxygenation so patients have signs of hypoxaemia and respiratory distress

173
Q

Increased permeability oedema

A

Injury to the microvascular barrier that allows protein-rich fluid to leak into the pulmonary parenchyma (alveolar flooding)

173
Q

Major site of small particle deposition

A

Bronchoalveolar junctions

174
Q

Difference between aspiration pneumonitis & aspiration pneumonia

A

Pneumonitis: ALI due to irritant
Pneumonia: pulmonary infection developing after an aspiration event

175
Q

Magnitude of lung injury depends on

A

pH
Osmolality
Presence or absence of particulate matter

176
Q

Pathophysiology of aspiration pneumonitis or pneumonia

A

direct caustic damage to alveolar and bronchial epithelium as well as the pulmonary capillary endothelium > Tachykinin release leading to necrosis of type I alveolar cells and intraaveolar damage > increase in pulmonary permeability and protein extravasation > extensive oedema formation and compromised gas exchange > VQ mismatch and reduced lung compliance > inflammatory response (activated neutrophils) > proinflammatory state > clinical signs

177
Q

Physiologic shunt occurs when

A

Venous blood passes over flooded or collapsed alveoli and never participates in gas exchange.`

178
Q

Hallmark of ARDS

A

Lowered compliance (P-V curve)
* Higher pressures required to achieve adequate TV

179
Q

Virchow’s triad (relative to PTE)

A

Hypercoagulable state in citing cause
1. Hypercoagulability
2. Blood stasis
3. Endothelial damage

180
Q

What happens in PTE

A

Altered haemodynamics, increased pulmonary vascular resistance, abnormal gas exchange, altered ventilatory control, altered pulmonary dynamics (mechanical obstruction and vasoactive vasoconstriction).

  • hypoxaemia due to low VQ regions
181
Q

2 blood test findings associated with hypercoagulobility

A

Low albumin (antithrombin III loss) and low Vit B12

182
Q

Brief pathopysiology of acute idiopathic polyradiculoneuritis

A

Immune mediated demyelination of axons of ventral roots & spinal nerves (blockade motor signals from brain to muscle)

183
Q

Brief pathophysiology of myasthenia gravis

A

Autoimmune blockade or congenital alteration/destruction of acetylcholine receptors at the neuromuscular junctions

  • Treated with anticholinergistics
184
Q

Hypoxaemia - not CO2 - becomes the driver for ventilation when

A

PaO2 drops below 50mmHg

185
Q

Metabolic acidosis has what effect on ventilation

A

Increased rate and depth of respiration
Every 0.7mmHg drop in CO2 results in approx. 1mEq/L drop in HCO3-

186
Q

Three electrolyte changes that result in altered respiration

A

Glucose, potassium and calcium

187
Q

Oxygenation

A

Movement of air from the alveoli to pulmonary capillaries

188
Q

Ventilation

A

Removal of CO2 and is dependent on fresh gas movement into alveoli

189
Q

Compliance

A

Distensibility of the lungs and is the change of volume for a given change in pressure

190
Q

High compliance

A

large increase in volume for a small change in pressure

191
Q

Low compliance

A

large pressures required for a small increase in volume

192
Q

Ventilator breaths

A

Spontaneous: patient dictates RR and TV
Assisted: patient dictates RR but TV determined by ventilator
Controlled: ventilator dictates RR and TV

193
Q

Suggested ventilator settings for a patient with normal lung function

A

FiO2 100%
RR 10-20
TV 10-20ml/kg
MV 150-250ml/kg
Pressure above PEEP 8-12 cmH2O
PEEP 0-4 cmH2O
Insp flow rate 40-60
Inspiratory time 0.8-1 sec
Rise time0.1-0.5
I:E 1:2
Trigger 1-2L/min

194
Q

Suggested ventilator settings for a patient with diseased lungs

A

FiO2 100%
RR 15-30
TV 6-8ml/kg
MV 100-250ml/kg
Pressure above PEEP 10-15 cmH2O
PEEP 4-8 cmH2O
Insp flow rate 40-60
Inspiratory time 0.8-1 sec
Rise time0.1-0.5
I:E 1:2
Trigger 1-2L/min

195
Q

Indications for ventilation

A
  1. Hypoxaemia despite oxygen therapy (PaO2 <80mmHg)
  2. Hypoventilation despite therapy (PaCO2 >60mmHg)
  3. Respiratory fatigue or failure

Other: ROSC, refractory seizures, refractory severe haemodynamic compromise

196
Q

What pressure should an ETT cuff not exceed

A

25mmHg

197
Q

Goals of ventilation

A

PaO2 80-120mmHg
PaCO2 35-50mmHg

On lowest ventilator settings possible

198
Q

Complications of ventilation

A

Volutrauma
Barotrauma
Pneumothorax
Infection
Asynchrony

199
Q

Causes of ventilator-patient asynchrony

A

Hypoxaemia
Hypercapnoea
Pneumothorax
Hyperthermia
Inappropriate settings
Inappropriate anaesthesia and analgesia
Full bladder/colon

200
Q

Causes of hypercapnoea on a ventilator

A

Pneumothorax
Bronchoconstriction
Obstruction ETT
Increased dead space
Inadequate ventilator settings
Incorrect circuit set up

201
Q

Causes of decreased oxygenation on a ventilator

A

Machine or circuit error
loss of O2 supply
Deterioration of disease
Development of new pulmonary disease

202
Q

Volume-controlled breath

A

Flow and TV are set and inspiration ends when the volume target has been reached

203
Q

Volume-controlled breath

A

Flow and TV are set and inspiration ends when the volume target has been reached

203
Q

Pressure-controlled breathing

A

Ventilator maintains airway pressure and inspiration ends once target pressure is reached.

204
Q

Pressure-controlled breathing

A

Ventilator maintains airway pressure and inspiration ends once target pressure is reached.

205
Q

Trigger variable (respiration & ventilation)

A

When to start inspiration
No patient effort = time
Patient effort = pressure or flow

206
Q

Cycle variable

A

When to start expiration
I:E

207
Q

Limit variable (respiration & ventilation)

A

What a breath can’t exceed on inspiration

208
Q

Baseline variable

A

Point reached in Expiration (baseline)
PEEP

208
Q

Limit variable

A

What a breath can’t exceed on inspiration

209
Q

Baseline variable

A

Point reached in Expiration (baseline)
PEEP

210
Q

Ideal combination for TIVA of ventilated patients

A

Propofol, benzodiazepine and opiate (avoid propofol in cats)

211
Q

Propofol handling

A

Draw up 6hrs and change line every 24hrs
Avoid in cats over 24h due to formation of heinz body anaemia

212
Q

When to discontinue ventilation

A
  1. Adequate gas exchange with least aggressive settings
  2. Appropriate ventilatory drive
  3. Recovery from underlying condition
213
Q

Failure of SBT

A

Tachypnoea>50
Tachycardia
Hypertension
Temp increase over 1

214
Q

Failure of SBT

A

Tachypnoea>50
Tachycardia
Hypertension
Temp increase over 1
PaO2 <60
SpO2 <90%
PaCO2 >55-60
TV <7
Anxiety

214
Q

Stretch injury

A

High end inspiratory volume, overstretching of alveoli

215
Q

Shear injury

A

Repetitive opening and closing of the small airways leading to repetitive alveolar collapse, alveolar flooding and increased permeability etc (PEEP at least 5cmH2O to avoid)

216
Q

Biotrauma

A

two hit theory
1. Volutrauma/atelectrauma
2. Biotrauma (increased circulating cytokines and increased infection risk)

217
Q

Preventative VILI strategies

A

TV 6-10ml/kg
PEEP at least 5cmH2O
Permissive hypoxaemia
Permissive hypercapnoea
P-V to guide PEEP & PIP
Avoid asynchrony
Recruitment maneuvers
Limit oedema
PIP <30cmH2O

218
Q

VAP

A

Ventilator associated pneumonia
- >48h of ET intubation that wasn’t present prior to intubation

219
Q

2 major pathological mechanisms behind VAP

A

Microaspiration past the ETT cuff
Biofilm development in ETT

220
Q

Diagnosis of VAP

A

Have to have had ETT in place over 48hrs abd have radiographic, systemic and pulmonary criteria met
- leukocytosis/leukopaenia
- fever
- New onset purulent sputum
- worsening gas exchange
- Crackles/increased bronchial sounds
- New or progressive consolidation

221
Q

Prevention of VAP

A

Hand hygiene
Oral/mouth care with dilute chlorhexidine
ETT cuff equal or >25mmHg
Minimise intubation time
Avoid prophylactically increasing gastric pH
Don’t change circuit unless contaminated

222
Q

Maintaining thoracostomy tubes

A

E-collars
Inspect site daily
Draining q4-PRN to maintain negative pressure
Keep in until 1-2ml/kg/day output
Sterile handling

223
Q

Overall complication rates and causes for thoracotomy

A

Overall mortality of 11-44% with a complication rate of 36-47%
#1 surgical approach
#2 thoracotomy tube
#3 surgery itself (anaesthesia)
#4 related to the primary disease

224
Q

Hypovolaemia after thoracotomy

A

Can be directly due to blood loss or reduced venous return, collapse of the large veins, loss of negative pressure or evaporative losses
* watch perfusion parameters

225
Q

Changes in respiration in patients recovering from thoracotomy and chest drain placement

A

Immediate imaging and listen to chest sounds
SpO2 and PaO2 might be helpful
Administer more pain relief
Drain chest
Give oxygen

226
Q

Best analgesic strategy for post thoracotomy

A

1) neuronal blockade
2) IV opiates
3) NSAIDs
4) ketamine, lidocaine, dexmedetomidine

  • avoid allodynia and PTPS by good analgesia particularly in first 24h after surgery
227
Q

Lung function in post thoracotomy patients

A

<50% reduced compliance
>200% increase in WOB
>400% increase in resistance

Low PaO2, arterial pH and SaO2, increased PaCO2

228
Q

Intrapleural bupivacaine administration

A

1) 1.5mg/kg or 0.3ml/kg (0.5% solution)
2) administer slowly and let absorb over 20min with incision side down
3) repeat q4-6 max of 9mg/kg/day

  • will not be effective for patients with effusive pleural space disease
229
Q

Pain in post op thoracotomy

A

Will impair ventilation
Will increase catecholamines and likely impair coagulation and stress response
Put patient at risk for PTPS

230
Q

Immediate post-thoracotomy surgery

A

PCV/TS, ABG, BP, SpO2, lactate, UOP, HR/ECG
Quantify drain output

231
Q

Elevated CO2

A

Potent vasodilator that can induce increased cardiac output and heart rate if elevated also; acidaemia, met alkalosis, narcosis,electrolyte abnormalities, hypertension and neurological dysfunction
Considered severely elevated above >60mmHg

232
Q

Delivery of carbon dioxide to the lungs requires

A

Blood flow

VTS(ECC) Preparation (21 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions