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March 23, 2007
Today I had my respiratory clinical skills session at the Walsgrave hospital, and I learned a couple of valuable things.
The first patient, Mr R, was a 69 year old male, currently retired, who worked for 35 years as a coal miner. Mr R had been in hospital for 4 weeks with shortness of breath which began 3 weeks prior to his admission to hospital. He also reported a dry (not ‘painful’ but ‘dry’) cough which produced an eggcup of green sputum per day, in the recent 24 hours the sputum production had doubled.
Mr R suffers from rheumatoid arthritis of the lower back, which had progressed from osteoarthritis some years earlier, probably due to him having worked as a coal miner. There was a fairly strong family history of heart disease, and Mr R himself suffers from left heart failure though this is likely to be secondary to his concurrent diagnosis of pernicious anaemia – the increased cardiac output induced by anaemia put extra strain on his left heart.
It was particularly interesting to talk with Mr R as he presented a bit of a challenge in that due to his dyspnoea he was on oxygen and could not talk for very long. This meant that some parts of my history had to be phrased such that he could answer with a ‘yes’ or ‘no’, though he did make an excellent effort to talk with me and even got carried away in parts.
Upon inspection Mr R had peripheral and central cyanosis and finger clubbing, all things I had only previously seen in textbooks! I couldn’t feel his pulse (nor did I make the mistake of telling him this), but I established that his respiratory rate was 40 breaths per minute – very high. Pallor was evident on his palms and ocular mucous membranes, this is consistent with his anaemia.
When I percussed Mr R’s chest, anteriorly I found dull areas over the left and right upper lobes approximately at the 4th intercostal spaces, this dullness was particularly pronounced on the left side.
Auscultation was particularly interesting with this patient. For the first time yet I heard crepitations over the patient’s lungs, and funnily enough the crepitations were more pronounced in the areas which were dull on percussion, and particularly on the 4th intercostal space on the left side. I would describe these crepitations as the sound of a grainy old vinyl record player with the crackling being a background noise which was present between the patient’s breaths. The crackling did however become louder and more chaotic during inspiration and expiration.
During the rest of my auscultation I think I heard what all the textbooks and doctors refer to as ‘bronchial breathing’, and it is fascinating to consider this in the light of the pathophysiology of Mr R’s current diagnoses. When auscultating over Mr R’s lower lung lobes (posterior chest) I identified that his breath sounds were in separate distinct inspiratory and expiratory ‘packets’, with a gap in between them – a sound which can be imitated by breathing through ones open mouth with your tongue pressed against the roof of your mouth. This is the sound of bronchial breathing.
By comparison, vesicular breathing (the sound you should hear over the lungs) has a rustling quality which builds up from the onset of inspiration to expiration, where it tails off such that it is not heard in the latter half of expiration. The important difference is that with vesicular breath sounds there is no gap between inspiration and expiration, I’ve attempted to explain this below.
I think the concepts of bronchial and vesicular breathing are quite difficult to grasp, but I found it so much easier when I considered this alongside Mr R’s diagnoses, so I will begin with these.
Mr R has suffered from pulmonary oedema (secondary to his left heart failure, which is secondary to his pernicious anaemia) in the past, and I suspect that he was suffering from it when I examined him. The cyanosis I observed, and crepitations I heard on auscultation are consistent with this.
Furthermore, Mr R has been diagnosed with pulmonary fibrosis (working as a coal miner and smoking 26 pack years are both risk factors for this) which is a condition resulting in fibrosis of the lungs, this essentially means that his bronchioles and alveoli have a significantly reduced compliance.
This is the pathology which underlies his presentation with bronchial breathing, and I’ll have a go at explaining it now…
Bronchial breathing is the sound which can be heard when one auscultates over the trachea, as aforementioned bronchial breathing consists of discrete inspiratory and expiratory breath ‘packets’ separated by a silent gap.
This silent gap can be equated to the split second moment of inertia when you throw a ball up in the air, the moment between the upwards journey (i.e. inspiration) and the downwards journey (i.e. expiration). It is also useful to consider this in analogy with the heartbeat, and imagine the heart is pumping into a rigid tube with little compliance (like the trachea!). If the heart beats into a rigid tube, then the blood flow is in discrete packets, which coincide with systole, and between the beats there would be absolutely no blood flow (the diastole, or ‘silence’). In principle this is how bronchial breathing works, with each systole representing the airflow heard in inspiration/expiration, and the diastole representing the moment of silence where breath direction is reversed between inspiration and expiration.
Vesicular breathing on the other hand is the ‘attenuated’ form of bronchial breathing, heard at the lung surface. It has been attenuated by passing through the moist and compliant bronchioles and alveoli, which dampen down its ‘pulsatility’ – exactly the same as how the elasticity of the aorta and arteries help to dampen down the pulsatility of blood flow. In the circulatory system, the result of this dampening of ‘pulsatility’ is that blood flow persists between heartbeats, albeit at a lower rate. In the respiratory system exactly the same principle applies – the end result is that the breath sounds (vesicular breath sounds) persist between inspiration and expiration, and then tail off until the next inspiration. I think the reason that the vesicular breath sounds tail off in the latter half of expiration is because the alveoli collapse in the latter half of expiration, and thus no air can be heard travelling through them.
SO, the reason Mr R had bronchial breath sounds at his lung surfaces is because the lung fibrosis reduced the compliance of his bronchioles and alveoli – this locks them in a half open state wherein, due to their lack of movement, they conduct the bronchial breath sounds from their origin (the trachea) to the lung surfaces unattenuated. The reason we can hear the full expiratory sound is because the alveoli are ‘locked open’ due to the fibrosis, and they therefore conduct the sound of the air leaving the lungs throughout expiration.