Shortness of Breath - Part 2 Flashcards
Heart failure - symptom explanation: SOB
heart can’t pump enough blood out, especially if venous return is increased (exercise, lying down)
◦ Get back pressure into lungs: pulmonary oedema
◦ Decreased gas exchange and lung compliance
Heart failure - symptom explanation: Orthopnea and displaced apex beat
- Orthopnea: lying down increases venous return to heart, increasing congestion in pulmonary vessels
- Displaced Apex beat: heart becomes dilated and volume overloaded
Heart failure - symptom explanation: Crackles in the lungs and peripheral oedema
Crackles in lungs: increased hydrostatic pressure in vasculature pushes fluid into alveoli. Interstitial fluid dilutes surfactant and increases alveolar surface tension = collapse of alveoli. Crackle is popping open of alveoli
Peripheral oedema: back pressure in venous system + inappropriate stimulation of RAAS system
Rx
SOB brought on by ischaemic heart disease/HF: symptomatic relief for pulmonary oedema
◦ Acute pulmonary oedema: sit upright, O2 and reduce cardiac pre-load with vasodilators —> morphine, nitrates and furosemide
◦ Chronic pulmonary oedema: loop diuretic (furosemide) and K+ sparing spironolactone
*If patient continues to deteriorate then consider starting NIV
Rx
SOB brought on by ischaemic heart disease/HF: Rx for LVF
◦ Reduce demand on heart: Beta blocker
◦ Inhibit RAAS: ACE inhibitors or ARBs (spironolactone
Rx
SOB brought on by ischaemic heart disease/HF: Rx for underlying cause (which is atherosclerosis)
◦ Statins: reduce cholestone
◦ Aspiring: reduces risk of thrombosis
◦ DM medication: hyperglycaemia accelerates atherosclerosis
Rx
SOB brought on by ischaemic heart disease/HF: Rx for advanced HF
- digoxin
- cardiac resynchroniation therapy (biventricular)
- implantable cardioversion devices (ICD)
The notes of a patient you are asked to see state that his past medical history is of ‘asthma/COPD’. Is such a diagnosis possible?
It is obviously possible to have both COPD and asthma at the same time, but it is much more likely that a clear diagnosis has simply not been made. Asthma and COPD are very different diseases and should not be confused:
• Asthma is a reversible and transient obstruction of the airways caused by excessive mucus production, airway inflammation, and constriction of the bronchi. Flow spirometry shows only obstructive changes (i.e. drop in FEV1 <70% but normal FVC, that is, a reduced rate of air flow but a normal lung capacity). It is usually accompanied by a cough and is often worse at night. It is often linked to triggers such as pollen, dust mites, or cold air and is common in patients who are atopic (i.e. who suffer from multiple diseases caused by excessive IgE-mediated hypersensitivity, such as eczema, hayfever, or urticaria).
• COPD is an irreversible and progressive obstruction of the airways. There is a history of chronic bronchitis and/or emphysema. Flow spirometry shows obstructive changes (i.e. drop in FEV1 <70%) but often also a degree of restrictive change (i.e. FVC <70%). Patients are usually older and have a smoking history of >20 pack years.
Which different classes of inhaled drugs are used in obstructive airways disease (asthma and/or COPD)? What is the mechanism of action of each drug?
1) Short-acting bronchodilators
− Salbutamol (UK: blue, ‘Ventolin’): selective β2-agonist. Acts on a G-protein-coupled receptor, activating adenylate cyclase and increasing the formation of cAMP, leading to relaxation of the smooth
muscle lining the airways.
− Ipratropium (UK: white + green, ‘Atrovent’): antimuscarinic/cholinergic. Antagonizes muscarinic acetylcholine receptors in the airways, preventing parasympathetic-mediated smooth muscle contrac-
tion. Often used in COPD, but less often in asthma.
− Salbutamol + ipratropium (UK: white + orange, ‘Combivent’).
2) Inhaled steroids − For example beclometasone, budesonide (UK: brown inhalers), fluticasone (UK: orange inhaler). Work by affecting intracellular transcription of various proteins to reduce inflammation in the airways. Used in asthma and COPD as second-line treatment.
3) Long-acting bronchodilators
− Salmeterol, formoterol: long-acting β2-agonist (LABA). Mechanism like the short-acting variant.
− Tiotropium: long-acting anticholinergic (LACA). Mechanism like the short-acting variant. Used in
COPD but not asthma.
− Long-acting bronchodilators can also be combined with inhaled steroids, e.g. budesonide + formoterol
(UK: red, ‘Symbicort’) or fluticasone + salmeterol (UK: purple, ‘Seretide’).
there has been a large decrease in the incidence of epiglottitis in recent years, particularly in children. How can you explain this?
Answer: Historically, epiglottitis primarily affected children and was a severe, sometimes fatal, condition. It is nearly always due to bacterial infection by Haemophilus influenzae B (HiB). The development and introduction of a HiB vaccine into the UK vaccination schedule in the mid-1990s has led to a decrease in both meningitis (another condition often caused by HiB) and epiglottitis.
- Question: What is the difference between type I and type II respiratory failure? What are some of the causes?
Answer: Respiratory failure is defined as impairment of pulmonary gas exchange sufficient to result in hypoxaemia (PaO2 <8 kPa or 60 mmHg) and/or hypercapnia (PaCO2 >6 kPa or 45 mmHg). It is divided into two types depend- ing on whether CO2 is expelled (and therefore normal or low) or retained (and therefore raised):
Type I respiratory failure
• Pathology: this is a problem with one gas (oxygen), i.e. hypoxaemic respiratory failure. It is caused by a ventilation–perfusion mismatch in the lungs, with ventilation of the unaffected alveoli normal. Compensatory hyperventilation increases CO2 removal but not O2 saturation as blood leaving the unaffected alveoli is already saturated.
• Causes: any lung disease, e.g. asthma, COPD, pneumonia, pulmonary fibrosis, pulmonary oedema.
Type II respiratory failure
• Pathology: this is a problem with two gases (oxygen and carbon dioxide), i.e. hypercapnic respiratory failure (low PaO2 and a raised PaCO2). This is caused by ventilatory failure, i.e. impairment of the respira- tory ‘bellows’, resulting in alveolar hypoventilation.
• Causes:
− Decreased respiratory drive, e.g. opiates, central neurological damage (stroke, head trauma)
− Impaired lung movements, e.g. chest wall deformity (as in Duchenne’s muscular dystrophy for
example), neuromuscular impairment (as in motor neuron disease) − Lung pathology, e.g. long-standing COPD, pulmonary fibrosis.
What is Eisenmenger’s syndrome?
Answer: Eisenmenger’s syndrome describes the situation where a left to right cardiac shunt becomes a right to left (or bidirectional) shunt. It follows a sequence of events beginning with a left to right cardiac shunt, due to, for example, a ventricular and/or atrial septal defect, patent ductus arteriosus. Over time this causes progres- sive pulmonary hypertension as the delicate pulmonary vasculature is subjected to blood emerging from the left ventricle, via the shunt, at greater pressures than normal pulmonary pressures. Eventually the pulmonary hypertension provides enough resistance to reverse the direction of the shunt.
Ultimately it leads to heart failure and can only be cured by heart–lung transplant. Women of childbearing age must be warned about the increased mortality in pregnancy (over 50%) and strongly advised against it. This condition has become relatively rare in the UK due to early surgical correction of cardiac defects (indeed this is the rationale behind early correction of such defects
What is the differential diagnosis for bibasal creps?
Which features in Hx and examination will help you distinguish them?
- Pulmonary oedema: displaced apex, raised JVP, ankle oedema
- Pulmonary fibrosis: reduced expansion, clubbing, creps that don’t vary with cough
- Bronchiectasis: chronic productive cough, wheeze, clubbing, creps that vary with cough
- Pneumonia: acute productive cough, fever, chest pain, bronchial breathing, dull percussion
