Respiratory Flashcards

1
Q

What is type 1 respiratory failure?

A

Type I (hypoxaemic) resp failure
PaO2< 60 mm Hg with a normal or low PaCO2
VQ mismatch (eg alveoli collapse/fluid filled)
eg pulmonary oedema, pneumonia

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2
Q

What is type 2 respiratory failure?

A

Hypercapnic
Ventilation failure
PaCO2>50mm Hg
eg drug overdose, neuromuscular disease, chest wall abnormalities

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3
Q

What is CPAP?

A

CPAP: continuous positive airway pressure
Prevents alveoli collapsing at end of respiration
Reduces shunting
Used in type 1 respiratory failure

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4
Q

What is BIPAP?

A

Bilevel positive airway pressure
Increases tidal volume by changing pressure
Helps blow off CO2
Reduces shunting and increases oxygenation
Used in type 2 resp failure

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5
Q

Explain the numbers in BIPAP

A

eg 12/4
Numbers show the changing pressure, eg inspiration 12cmH2O, expiration 4cmH2O
In compliant lungs, only small differences are needed

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6
Q

If pt is hypoxic at 12/4, what would you change on the BIPAP machine?

A

Increase bottom number but keep difference the same (eg 13/5)

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7
Q

If pt is hypercapnic at 12/4, what would you change on the BiPAP machine?

A

Increase difference between pressures

eg 14/4

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8
Q

What is PPV?

A

Positive pressure ventilation

On a ventilator in ITU

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9
Q

What is the most common food to be aspirated?

A

Peanuts

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10
Q

Where do things go when aspirated?

A

Right main bronchus or trachea if larger

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11
Q

What are the phases of aspiration?

A
  • Initial phase - Choking and gasping, coughing, or airway obstruction at the time of aspiration
  • Asymptomatic phase - Subsequent lodging of the object with relaxation of reflexes that often results in a reduction or cessation of symptoms, lasting hours to weeks
  • Complications phase - Foreign body producing erosion or obstruction leading to pneumonia, atelectasis, or abscess
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12
Q

How can you work out where the aspirated item is lodged from clinical signs?

A

Hoarseness/aphonia, stridor: laryngeal
Wheezing: tracheal
Bronchial: coughing, unilateral wheezing, decreased breath sounds

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13
Q

Treatment of aspiration

A

Rigid bronchoscopy if witnessed/radiologically confirmed/classic triad
Heimlich manoeuvre if complete obstruction

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14
Q

Types of stridor and cause

A
  • Inspiratory stridor suggests a laryngeal obstruction
  • Expiratory stridor implies tracheobronchial obstruction
  • Biphasic stridor suggests a subglottic or glottic anomaly
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15
Q

Name 8 causes of acute stridor

A
Laryngotracheobronchitis
Aspiration of foreign body
Bacterial tracheitis
Retropharyngeal abscess
Peritonsillar abscess
Spasmodic croup
Allergic reaction
Epiglottitis
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16
Q

Name the categories used for classifying chronic causes of stridor

A

External

Internal

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17
Q

Name 6 internal causes of stridor

A
  • Laryngomalacia
  • Vocal cord dysfunction
  • Laryngeal dyskinesia
  • Laryngeal webs in neonates
  • Laryngeal cysts
  • Haemangiomas
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18
Q

Name 3 external causes of stridor

A
  • Vascular rings
  • Double aortic arch
  • Tumour
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19
Q

What is the difference in pH in acute versus chronic hypercapnic respiratory failure?

A

Acute hypercapnic respiratory failure develops over minutes to hours; therefore, pH is less than 7.3. Chronic respiratory failure develops over several days or longer, allowing time for renal compensation and an increase in bicarbonate concentration. Therefore, the pH usually is only slightly decreased.

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20
Q

What is the alveolar gas equation?

A

PAO2 = FiO2 × (PB – PH2 O) – PACO2/R
where PA O2 is alveolar PO2, FiO2 is fractional concentration of oxygen in inspired gas, PB is barometric pressure, PH2O is water vapour pressure at 37°C, PACO2 is alveolar PCO2 (assumed to be equal to PaCO2), and R is respiratory exchange ratio. R depends on oxygen consumption and carbon dioxide production. At rest, the ratio of VCO2 to oxygen ventilation (VO2) is approximately 0.8.

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21
Q

What does an increase in the alveolar-arterial PO2 gradient above 15-20 mm Hg indicate?

A

An increase in the alveolar-arterial PO2 gradient above 15-20 mm Hg indicates pulmonary disease as the cause of hypoxemia.

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22
Q

Define shunt

A

Shunt is defined as the persistence of hypoxemia despite 100% oxygen inhalation. The deoxygenated blood (mixed venous blood) bypasses the ventilated alveoli and mixes with oxygenated blood that has flowed through the ventilated alveoli, consequently leading to a reduction in arterial blood content. ie. Ventilation fails.
Anatomic shunt exists in normal lungs because of the bronchial and thebesian circulations, which account for 2-3% of shunt.

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23
Q

Define dead space

A

Dead Space is when there is ventilation but no perfusion. This is seen physiologically as the trachea and bronchi have ventilation but no semi permeable membrane and perfusion to transfer oxygen.

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24
Q

Signs of respiratory failure?

A
  • Asterixis may be observed with severe hypercapnia. Tachycardia and a variety of arrhythmias may result from hypoxemia and acidosis.
  • Cyanosis, a bluish colour of skin and mucous membranes, indicates hypoxemia. Visible cyanosis typically is present when the concentration of deoxygenated haemoglobin in the capillaries or tissues is at least 5 g/dL.
  • Dyspnoea, an uncomfortable sensation of breathing, often accompanies respiratory failure. Excessive respiratory effort, vagal receptors, and chemical stimuli (hypoxemia and/or hypercapnia) all may contribute to the sensation of dyspnoea.
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25
Q

Investigations needed in respiratory failure

A
  • ABG
  • FBC (polycythaemia versus anaemia)
  • Electrolytes (may exacerbate pulmonary dysfunction)
  • Troponin (MI?)
  • Chest radiography is essential
  • Echocardiography is not routinely done but is sometimes useful
  • Pulmonary functions tests (PFTs), if feasible, may be helpful, although more useful in terms of defining recovery potential
  • ECG should be performed to evaluate the possibility of a cardiovascular cause of respiratory failure; it also may detect dysrhythmias resulting from severe hypoxemia or acidosis
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26
Q

What is the score done for community acquired pneumonia to assess severity?

A
CURB-65
Confusion of new onset
Urea>7mmol/L
Resp rate>30
Blood pressure<90mmHg or diastolic<60
Age 65 or older
27
Q

What does a CURB 65 score of 3 or more mean?

A

> 40% risk of death

28
Q

Signs of pneumonia

A
  • Fever, Rigors
  • Malaise, anorexia
  • Dyspnoea, cyanosis
  • Cough with purulent sputum
  • Haemoptysis
  • Pleuritic chest pain
  • Tachypnoea, tachycardia, hypotension
  • Diminished expansion, consolidation
  • Pleural effusion? Empyema?
29
Q

Common viral pathogens in pneumonia?

A

Influenza
RSV
Adenovirus
Rhinovirus

30
Q

Common fungal causes of pneumonia?

A

All fungal are rare
Aspergillus fumigatus
Pneumocystitis carinii

31
Q

Common community acquired causes of pneumonia

A
  • Strep. pneumoniae
  • Haemophilus influenza
  • Mycoplasma pneumoniae
  • Chlamydophila pneumophila
32
Q

What are the most common causes of pneumonia in the elderly?

A

E.coli

Klebsiella pneumoniae

33
Q

Common causes of pneumonia in infants

A

Group B strep

Listeria monocytogenes

34
Q

Common hospital acquired pneumonia pathogens

A
  • Strep. pneumoniae
  • Coliforms
  • Staph aureus
  • Pseudomonas aeruginosa
35
Q

What organisms causes pneumonia in immunocompromised individuals?

A
  • Strep. pneumoniae
  • Haemophilus influenzae
  • Mycoplasma pneumoniae
  • Pneumocystis jiroveci (PCP)
  • CMV, HSV
  • Mycobacteria
36
Q

Management of pneumonia

A
  • Assess ABC
  • Resp failure? O2 therapy/NIV/ventilation
  • Blood cultures, sputum culture
  • Serum transaminase, serum sodium, serum ferritin, serum phosphorus, and creatine phosphokinase (CPK) levels may provide evidence supporting a particular pathogen, such as Legionella
  • C-reactive protein (CRP) levels and procalcitonin may help predict the likelihood of a bacterial origin for pneumonia
  • Serum lactic acid, WCC, urea nitrogen, and creatinine may be used in categorising severity
  • PCR for viruses/atypicals
  • CXR
  • Bronchoscopy with bronchoalveolar lavage when pneumocystis, mycobacteria, or fungal pathogens are likely
  • Antibiotics (flucloxicillin)
37
Q

What are the 2 main causes of pulmonary oedema

A

Cardiogenic

Non cardiogenic

38
Q

How does cardiogenic pulmonary oedema occur?

A
  • Imbalance of Starling forces - ie, increased pulmonary capillary pressure, decreased plasma oncotic pressure, increased negative interstitial pressure
  • Damage to the alveolar-capillary barrier
  • Lymphatic obstruction/ cap pressure rises without rise in lymphatic drainage
39
Q

Give examples of cardiogenic causes of pulmonary oedema

A
  • LV volume overload (aortic insufficiency/septal rupture/mitral regurgitation)
  • Pulmonary venous outflow obstruction (mitral stenosis)
  • LV failure (eg in CCF or cardiomyopathy)
40
Q

Give 9 non cardiogenic causes of pulmonary oedema

A
•	Drowning
•	Acute glomerulonephritis
•	Fluid overload (renal)
•	Aspiration
•	Inhalation injury
•	Neurogenic pulmonary oedema
•	Allergic reaction
•	Adult respiratory distress syndrome (ARDS)
High altitude (hypoxia->pulmonary arterial vasoconstriction-> leak of capillary membranes + ADH excess)
41
Q

Signs and symptoms of pulmonary oedema

A
  • Feeling of drowning
  • Extreme breathlessness (esp when lying flat)
  • Anxiety
  • Cough w/pink frothy sputum
  • Hoarse voice (due to compression of recurrent laryngeal nerve w/mitral stenosis causing an enlarged left atrium)
  • Hypoxia
  • Increased sympathetic tone (tachypnoea, tachycardia, hypertension)
  • Cardiogenic shock?
  • Murmurs?
  • Fine creps in lung bases
42
Q

Treatment of pulmonary oedema

A
  • Sit patient up
  • O2 high flow
  • IV access and monitor ECG
  • Morphine + metoclopramide
  • Furosemide
  • GTN
  • Consider CPAP, dialysis, inotropes
43
Q

Further management of pulmonary oedema

A
  • Daily weights
  • DVT prophylaxis
  • Repeat CXR
  • Oral furosemide ?spironolactone
  • ACEi & ß-blocker if heart failure
44
Q

What does pulmonary oedema look like on CXR?

A

Indistinct hila
Alveolar infiltrates
Kerley B lines of interlobular septa

45
Q

Define pleural effusion

A

Abnormal collection of fluid in the pleural space resulting from excess fluid production or decreased absorption or both.

46
Q

Describe the pleura

A

The pleural space is bordered by the parietal and visceral pleurae.
The parietal pleura covers the inner surface of the thoracic cavity, including the mediastinum, diaphragm, and ribs.
The visceral pleura envelops all lung surfaces, including the interlobar fissures.
The right and left pleural spaces are separated by the mediastinum.

47
Q

Is fluid in the pleural space normal?

A

A small volume of pleural fluid (0.13 mL/kg of body weight under normal circumstances), serves as a lubricant to facilitate movement of the pleural surfaces against each other in the course of respirations.
This small volume of fluid is maintained through the balance of hydrostatic and oncotic pressure and lymphatic drainage, a disturbance of which may lead to pathology.

48
Q

How are pleural effusions classified?

A
  • Pleural effusions are generally classified as transudates or exudates, based on the mechanism of fluid formation and pleural fluid chemistry.
  • Transudates result from an imbalance in oncotic and hydrostatic pressures (ultrafiltrates of plasma)
  • Exudates are the result of inflammation of the pleura or decreased lymphatic drainage
49
Q

Explain the pathophysiology and causes of exudates

A
  • Altered permeability of the pleural membranes (eg, inflammation, malignancy, pulmonary embolus)
  • Increased capillary permeability or vascular disruption (eg, trauma, malignancy, inflammation, infection, pulmonary infarction, drug hypersensitivity, uremia, pancreatitis, SLE, rheumatoid, TB)
  • Decreased lymphatic drainage or complete blockage, including thoracic duct obstruction or rupture (malignancy, trauma)
  • Movement of fluid from pulmonary edema across the visceral pleura
  • Persistent increase in pleural fluid oncotic pressure from an existing pleural effusion, causing further fluid accumulation
  • Reduction of pressure in the pleural space, due to inability of the lung to fully expand during inspiration, known as “trapped lung” (eg, extensive atelectasis due to obstructed bronchus or contraction from fibrosis)
50
Q

Explain the pathophysiology and causes of transudates

A
  • Reduction in intravascular oncotic pressure (eg, hypoalbuminemia due to nephrotic syndrome or cirrhosis)
  • Increased capillary hydrostatic pressure in the systemic and/or pulmonary circulation (CHF, superior vena cava syndrome)
  • Increased peritoneal fluid, with migration across the diaphragm via the lymphatics or structural defect (eg, cirrhosis, peritoneal dialysis)
  • CSF leak/duropleural fistula
  • Extravascular migration of central venous catheter
  • Atelectasis
51
Q

Signs and symptoms of pleural effusion and what other symptoms would indicate as cause

A
  • Dyspnoea
  • Cough (mild, unproductive)
  • Chest pain-> exudative? Sharp, stabbing, worse with deep inspiration
  • Ankle oedema, orthopnea -> CHF?
  • Night sweat, weight loss, fever-> TB
  • Haemoptysis-> malignancy
  • Acute febrile episode, purulent sputum production, pleuritic chest pain-> pneumonia
  • Dullness to percussion
  • Decreased tactile fremitus
  • Asymmetrical chest expansion, with diminished or delayed expansion on the side of the effusion
52
Q

Describe interpretation of the results of a thoracocentesis

A
  • Frankly purulent fluid indicates an empyema
  • A putrid odour suggests an anaerobic empyema
  • A milky, opalescent fluid suggests a chylothorax, resulting most often from lymphatic obstruction by malignancy or thoracic duct injury by trauma or surgical procedure
  • Grossly bloody fluid may result from trauma, malignancy, postpericardiotomy syndrome, or asbestos-related effusion and indicates the need for a spun haematocrit test of the sample. A pleural fluid haematocrit level of more than 50% of the peripheral haematocrit level defines a haemothorax, which often requires tube thoracostomy
  • Black pleural fluid suggests a limited number of diseases, including infection with Aspergillus niger or Rizopus oryzae, malignant melanoma, non-small cell lung cancer or ruptured pancreatic pseudocyst, or charcoal-containing empyema
  • MC&S, TB culture, cytology, immunology
  • pH: low= infective
  • Cytology: malignancy
  • Protein: <30g/l = transudate
  • Protein: >30g/l = exudate
  • If too close, compare effusion protein conc/serum protein conc. >0.5 = exudate
53
Q

If pleural effusion is seen on a CXR, how big is it?

A

At least 500ml

54
Q

Define pneumothorax

A

An abnormal collection of air/gas in the pleural space that causes an uncoupling of the lung from the chest wall

55
Q

Name 8 causes of pneumothorax

A
  • Spontaneous (esp in young, thin men) due to rupture of a sub-pleural bulla
  • Asthma, COPD, emphysema
  • TB, pneumonia
  • Lung abscess, carcinoma
  • CF, lung fibrosis
  • Sarcoidosis, CT disorder (Marfan’s)
  • Trauma
  • Iatrogenic (pleural aspiration/biopsy, percutaneous liver sampling)
56
Q

Signs and symptoms of pneumothorax

A
  • No symptoms
  • Sudden onset of dyspnoea
  • Pleuritic chest pain
  • Sudden deterioration in asthma & COPD patients
  • Decreased expansion
  • Hyper-resonance
  • Decreased breath sounds
  • Trachea deviated away from affected side? (tension)
57
Q

Management of pnuemothorax

A

• Due to trauma/mechanical ventilation? -> chest drain
• Aspiration of a pneumothorax
• Tension pneumothorax? Insert a large bore cannula/needle with a syringe partially filled with 0.9% saline into 2nd intercostal space, midclavicular line on side of suspected pneumothorax
Remove plunger, saline acts as seal, air bubbles out

58
Q

Define PE

A

Pulmonary embolism

Blockage in the pulmonary artery system

59
Q

6 causes of PE

A
  • VTE in pelvis/legs-> pulmonary artery
  • Right ventricular thrombus (post MI)
  • Septic emboli (right sided endocarditis)
  • Fat, air, amniotic fluid embolism
  • Neoplastic cells
  • Parasites
60
Q

Risk factors for PE (11)

A
  • Recent surgery
  • Hypercoagulability (eg antiphospholipid syndrome)
  • Leg fracture
  • Prolonged bed rest/reduced mobility
  • Malignancy/cancer treatment
  • Pregnancy/post partum
  • Pill/HRT
  • Previous DVT/PE (esp if unprovoked)
  • Varicose veins
  • Obesity
  • Old age
61
Q

Signs and symptoms of PE

A
  • Acute dyspnoea, tachypnoea
  • Pleuritic chest pain
  • Haemoptysis
  • Dizziness, syncope
  • Pyrexia
  • Cyanosis (hypoxia due to decreased gas exchange of affected lung tissue)
  • Tachycardia
  • Raised JVP
  • Hypotension
  • DVT?
62
Q

Investigations for PE

A
  • ABG (type 1 resp failure, both Co2 and O2 are low)
  • Chest xray: dilated pulmonary artery, linear collapse of lung, wedge shaped opacities
  • CTPA: dilated pulmonary artery, blockage?
63
Q

Treatment of PE

A
  • Anticoagulate (LMWH)
  • Warfarin/NOAC (apixiban)
  • Thrombolysis if massive PE (ALTEPLASE)
  • Vena caval filter (if still developing clots/can’t anticoagulate)
64
Q

Prevention of PE

A
  • Heparin for all immobile patients
  • Compression stockings (TEDs)
  • Early mobilisation
  • Stop pill/HRT pre op
  • FH? Investigate thrombophilia/cancer