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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
Q

What are causes of hypoxia?

A
  • 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
Q

How does hypoventilation lead to type 2 respiratory failure?

A
  • 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
Q

What is the difference in treatment for acute and chronic hypoventilation ?

A

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
Q

What are causes of hypoventilation?

A
  • 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
Q

What are the effects of hypercapnia?

A
  • Respiratory acidosis
  • Impaired CNS function: drowsiness, confusion, coma, flapping 
tremors
  • Peripheral vasodilatation –warm hands, bounding pulse
  • Cerebral vasodilation – headache
30
Q

How is chronic hypercapnia compensated ?

A

Retention of HCO3- compensates for the respiratory acidosis

31
Q

How can treatment of hypoxia worsen hypercapnia?

A
  • 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
Q

What are the adjustments made to treat patients with severe COPD?

A
  • 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
Q

What are the effects of hypoxaemia?

A
  • Impaired CNS function, confusion, irritability
  • Cyanosis
  • Cardiac arrhythmia
  • Hypoxic vasoconstriction
34
Q

How is chronic hypoxaemia compensated?

A
  • Increased EPO secreted by kidney so raised Hb (Polycythaemia)
  • Increased 2,3, DPG to increase oxygen dissociation 

35
Q

How does the lung compensate for chronic hypoxemia?

A

Chronic hypoxic vasoconstriction of pulmonary vessels results in

  • Pulmonary hypertension
  • Right heart failure

  • Cor pulmonale
36
Q

What is the optimal V/Q ratio?

A

1

37
Q

What happens when V/Q ratio is <1?

A

-Alveolar pO2 falls and pCO2 rises

38
Q

What happens when pathology impairs ventilation in an area of the lung?

A
  • 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
Q

What is effect on an unaffected area of the lung when a pathology affects a region of the lungs?

A
  • 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
Q

How does a pulmonary embolus cause type 1 respiratory failure?

A
  • 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
Q

How can a diffusion defect lead to type 1 respiratory failure?

A
  • CO2 is more soluble
  • CO2 diffusion less affected than diffusion of O2 affected
  • pO2 low pCO2 normal or low Type 1 respiratory failure
42
Q

What are the causes of diffuse lung fibrosis?

A
  • Idiopathic fibrosing alveolitits
  • Asbestosis
  • Extrinsic allergic alveolitis
  • Pneumoconiosis

Kofi: Pure Clinical Sem 3 (44 decks)

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