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Kofi: Pure Clinical Sem 3 > Respiratory: PE & Spirometry > Flashcards

Respiratory: PE & Spirometry Flashcards

1
Q

How can vital capacity be calculated?

A

Inspiratory capacity + expiratory reserve volume

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2
Q

What are the features of an obstructive disorder?

A
  • FEV1 is reduced
  • FVC may be reduced
  • FEV1/FVC is reduced
  • Shark peak peak flow
  • Scoopiness/Scalloped
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3
Q

What are the features of a restrictive disorder on spirogram?

A
  • FEV1 appropriate for FVC
  • FVC reduced
  • FEV1/FVC is normal
  • No Scoopiness/Scalloped
  • Straight
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4
Q

What are some quality control and practical aspects of spirometry?

A
  • Demostration and carful explanation
  • Person making the recordings is every bit as important as spirometer
  • Use of incentive spirometry
  • Observe the subject
  • Inspect raw data
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5
Q

When is extrathoracic abnormality evident?

A

On Inspiration

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6
Q

When is intrathoracic abnormality evident?

A

On Expiration

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7
Q

What is an embolism?

A

Movement of material from one part of circulation to another. Can be

  • Thrombus
  • Tumour
  • Air
  • Fat
  • Amniotic fluid
  • Bullet
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8
Q

What is the aetiology of a pulmonary embolism?

A
  • Thrombus entering the right side of the heart and pulmonary arteries in most cases
  • 90% arise from a DVT in the legs particularly in the popliteal vein and more proximal veins such as pelvic veins
  • However only 25% of patients with a PE have symptoms or signs of a DVT
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9
Q

What is the epidemiology of pulmonary embolism?

A
  • Third commoners cause of vascular death after myocardial infarction and stroke
  • Commonest cause of preventable death in hospital patient
  • Risk facts are age and incidence increase past 40
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10
Q

What are some risk factors for thromboembolism?

A
  • Surgery
  • Obesity
  • Cancer
  • Prolonged immobilisation
  • Previous thromboembolism
  • Heart failure
  • Contraceptive pill
  • Pregnancy
  • HRT
  • Long haul travel (>4hrs)
  • Thrombophilia
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11
Q

What are the outcomes of PE?

A
  • Sudden death

- Asymptomatic

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12
Q

What can a PE lead to that causes harm?

A
  • Right ventricular overload
  • Respiratory failure
  • Pulmonary infarction
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13
Q

How does right ventricular overload occur in PE?

A
  • Pulmonary artery pressure increase if more than 30% of total cross sectional area of peulmary arterial bed occluded.
  • Lead to right ventricle dilatation and strain
  • Inotropes released in attempt to maintain systemic BP which causes pulmonary vasoconstriction that further exacerbates the situation
  • This all leads to Right ventricular overload

-Right to left shunting through patent foramen ovale is present in 1/3 of patient and may lead to severe hypoxaemia and paradoxical embolisation and stroke

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14
Q

How does respiratory failure occur in PE?

A

-Due to areas of ventilation perfusion mismatch and low right ventricle output

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15
Q

How does pulmonary infarction occur in PE?

A
  • Small distal emboli may create areas of alveolar haemorrhage resulting in haemoptysis, pleuritis and small pleural effusion
  • Pleuritic pain is worse on inspiration
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16
Q

What are physical signs of PE?

A
  • Pleural rub in cases of pulmonary infarction

- Raised JVP

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17
Q

What are symptoms of PE?

A
  • Pleuritic chest pain
  • Haemoptysis
  • Dyspneoa
  • Cough
  • Fever
  • Syncope
  • Unilateral leg pain
  • Substernal chest pain
18
Q

What are investigations undertake for Pulmonary embolism?

A

CXR - Not useful as a primary diagnostic tool. Used to rule out other diagnoses

ECG - Right ventricular strain. S1 Q3 T3

Blood gas - Show hypoxaemia and hypocapcnia due to hyperventilation

D-dimer - Normal D-dimer rules out PE in those at low likelihood of having a PE. In those with high likelihood, the negative predictive value of D-dimer is too low to use

19
Q

What are D-dimers?

A
  • Fibrin degradation product.
  • Small protein fragment released into the blood when a thrombus is degraded by fibrinolysis.
  • Normally not present unless coagulation system has been activated
20
Q

What is the gold standard imaging technique for a PE?

A

-CT pulmonary angiography

21
Q

How is a pulmonary embolism treated?

A

-Immediate heparinisation

22
Q

How does immediate heparinaistion reduce mortality in a PE?

A
  • Stops thrombus propagation in the pulmonary and allows the body’s fibrinolytic system to lyse the thrombus
  • Stop thrombus propagation at the embolic source and reduced the frequency of further pulmonary embolism
23
Q

How are high risk PE patients treated?

A
  • Haemodynamic support
  • Respiratory support
  • Exogenous fibrinolytic (peripheral IV, delivered directly via percutaneous catheter into pulmonary arteries)
  • Percutaneous catheter directed thrombectomy
  • Surgical pulmonary embolectomy
24
Q

What happens after the initial heparinisation of the patients?

A

-Oral anticoagulants

3 months if identifiable temporary risk factor
Indefinitely if cancer or no identifiable risk factor

25
What are causes of hypoxia?
- Low inspired pO2 - Hypoventilation – (respiratory pump failure) - Ventilation/Perfusion mismatch - Diffusion defect – problems of the alveolar capillary membrane - Right to left shunt (eg. Cyanotic heart disease)
26
How does hypoventilation lead to type 2 respiratory failure?
- Alveolar ventilation is decreased - Amount of O2 entering the blood and CO2 leaving the blood remains unchanged at the start - Alveolar pO2 falls so arterial pO2 falls which leads to hypoxaemia - Alveolar pCO2 rises so arterial pCO2 increases which leads to hypercapnia
27
What is the difference in treatment for acute and chronic hypoventilation ?
Acute (Opiates, Head injury, Very severe acute asthma) -Need urgent treatment +/- artificial ventilation Chronic (Severe COPD) - Chronic hypoxia and Chronic hypercapnia - Slow onset and progression
 - Time for compensation - Therefore better tolerated
28
What are causes of hypoventilation?
- Brainstem (Opiates, Head injury) - Spinal cord (Trauma) - Phrenic and intercostal nerves (Guilain Barre syndrome) - Muscle of respiration (myopathy) - Neuromuscular junction (Myasthenia Gravis) - Chest wall (Severe Obesity, Kyphoscoliosis) - Pleural cavity (Pneumothorax, Large pleural effusions) - Poor lung compliance (Respiratory distress of newborn) - High airway resistance (very severe acute asthma, late stages of COPD) - Upper airway obstruction (Laryngeal oedema, Foreign body)
29
What are the effects of hypercapnia?
- Respiratory acidosis - Impaired CNS function: drowsiness, confusion, coma, flapping 
tremors - Peripheral vasodilatation –warm hands, bounding pulse - Cerebral vasodilation – headache
30
How is chronic hypercapnia compensated ?
Retention of HCO3- compensates for the respiratory acidosis
31
How can treatment of hypoxia worsen hypercapnia?
- O2 removes stimulus for the hypoxic respiratory drive
 - Alveolar Ventilation drops which causes worsening hypercapnia - Correction of hypoxia removes pulmonary hypoxic vasoconstriction which leads to increased perfusion of poorly ventilated alveoli, diverting blood away from better ventilated alveoli.
32
What are the adjustments made to treat patients with severe COPD?
- pO2 given but pCO2 needs to be monitored - Controlled oxygen therapy with a target saturation of 88-92% - If oxygen therapy causes rise in pCO2 - need ventilator support
33
What are the effects of hypoxaemia?
- Impaired CNS function, confusion, irritability - Cyanosis - Cardiac arrhythmia - Hypoxic vasoconstriction
34
How is chronic hypoxaemia compensated?
- Increased EPO secreted by kidney so raised Hb (Polycythaemia) - Increased 2,3, DPG to increase oxygen dissociation 

35
How does the lung compensate for chronic hypoxemia?
Chronic hypoxic vasoconstriction of pulmonary vessels results in - Pulmonary hypertension - Right heart failure
 - Cor pulmonale
36
What is the optimal V/Q ratio?
1
37
What happens when V/Q ratio is <1?
-Alveolar pO2 falls and pCO2 rises
38
What happens when pathology impairs ventilation in an area of the lung?
- V/Q < 1 in these alveoli - Hypoxic vasoconstriction occurs so this diverts some (but not all) blood to better ventilated areas - Blood from these alveoli will have low pO2 and high pCO2 mixed in the left atrium - Central and peripheral chemoreceptors are stimulated which causes hyperventilation - Affected area are still poorly ventilated due to the pathology
39
What is effect on an unaffected area of the lung when a pathology affects a region of the lungs?
- Unaffected segments have increased ventilation. V/Q > 1 - pO2 rises and pCO2 falls - Rise in pO2 leads to increased dissolved oxygen (very small amount) - But Hb is fully saturated above 10 kPa - Further increases in pO2 has no effect on Hb. - O2 content not significantly increased (only tiny amount of extra dissolved O2 - Insufficient to compensate for low pO2 from segments with V/Q <1 - Drop in pCO2 accompanied by reduction in total CO2 content in blood - Sufficient to compensate for CO2 retention from segments with V/Q <1 - Final result: low pO2 with normal (or low) pCO2 - Type 1 respiratory failure
40
How does a pulmonary embolus cause type 1 respiratory failure?
- The embolus results in redistribution of pulmonary blood flow - The blood is diverted to unaffected areas of the pulmonary circulation 
 - Leads to V/Q ratio < 1 if hyperventilation cannot match the increased perfusion which causes hypoxaemia. - Hyperventilation sufficient to get rid of CO2
41
How can a diffusion defect lead to type 1 respiratory failure?
- CO2 is more soluble - CO2 diffusion less affected than diffusion of O2 affected - pO2 low pCO2 normal or low Type 1 respiratory failure
42
What are the causes of diffuse lung fibrosis?
- Idiopathic fibrosing alveolitits - Asbestosis - Extrinsic allergic alveolitis - Pneumoconiosis

Kofi: Pure Clinical Sem 3 (44 decks)

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