The trainee was asked to examine the patient's cardiovascular system. He carried out the examination and he was then asked to present his findings.
The presentation was as follows:
The patient is an elderly gentleman who is of average height and weight. There are no signs of bacterial endocarditis. Pulse 80 beats per minute regular, no collapse.
No cyanosis.
JVP not elevated
Apex 5th left intercostal space, medial to the mid-clavicular line
First heart sound was soft. There was a pan systolic murmur best heard at the apex with radiation to the axilla. The murmur increased in intensity during expiration.
He was then asked the diagnosis and replied that the patient had mitral regurgitation.
We then thought we would go through the patient again. This time we went more slowly, following the method (ACES for PACES pages 157-171), we meticulously went though each step and analysed one step at a time
We started with a general examination.
The patient was an elderly gentleman of average height and weight. He was lying propped up in bed and appeared tachypnoeic. We paused to think what this would indicate and decided that on this information and the fact that we were examining the cardiovascular system, the patient must have heart failure.
We looked at his head, quickly went though the general examination and then looked at his nose. His alae nasi were flaring; in keeping with the suspicion that the patient had heart failure.
On examination of his mouth we noticed that the patient had a high arched palate.
On examination of his hands, there was no abnormality of his nails but on examination of the skin we noted multiple bruises. In the context of the cardiovascular system this could indicate that the patient was being treated with an anticoagulant.
His pulse rate was 80 beats per minute, regular in rhythm and volume no collapse, normal character, no radio-radial, radio-femoral or brachio-radial delay.
We asked the patient to stretch his palms out, there was no tremor. We asked him to spread his finger wide apart and cock his wrists back and noted that the patient had a flapping tremor. We thought about the causes of a flapping tremor and decided that of the many causes pf a flapping tremor; this patent’s tremor was most likely to be due to heart failure (see ACES for PACES page 446 causes of flapping tremor)
On examination of his neck there were no abnormalities on general examination, no goitre, muscles normal. His JVP was elevated to his ear lobe. The trainee remarked that he had noted the pulsation in the patient's neck but thought that this was carotid pulsation. We then went through how to differentiate pulsations in the neck (see ACES for PACES page 162)
The predominant wave in the JVP was a systolic wave, which was expansile, a V wave, and this suggested that the patient had tricuspid regurgitation.
The carotids were normal; the trachea was in the midline.
There was no structural abnormality of his praecordium, skin was normal and there were no visible pulsations.
The apex beat was in the 5th left intercostal space just medial to the mid-clavicular line and it was diffuse in nature. There was no left parasternal heave.
The heart sounds were regular in rhythm 80 beats per minute. The 1st heart sound was soft. This made us think that the patient had mitral regurgitation.
The 2nd heart sound was normal in intensity and not split.
There was a pan systolic murmur at the apex and this murmur radiated to the axilla. The murmur increased in expiration. This was in keeping with the earlier suspicion that the patient had mitral regurgitation.
There was a pan systolic murmur at the left sternal edge. It was difficult to say whether this murmur increased in inspiration. The murmurs were in keeping with mitral and tricuspid regurgitation, which we suspected from our earlier findings.
On examination of the back we looked at the neck and spine and traced our fingers down the spine as recommended in the method and this enabled us to readily observe that the patient had sacral oedema, in keeping with our suspicion that the patient had heart failure.
On auscultation of the lung bases we noted that the patient had fine bilateral basal crepitations. Further evidence in favour of our suspicion that the patient had heart failure.
Diagnosis:
Mitral and tricuspid regurgitation
Sinus rhythm
Congestive cardiac failure
We discussed the differences in the amount of information obtained and came to the conclusion that following the method and concentrating on one step at a time enabled us to obtain much more information.
The recommendation to the trainee was to read the method over and over again and practice over and over again until the method became second nature to him. Read, practice, read again ad infinutm.
Further questions:
What is the cause of the mitral regurgitation? (See causes of mitral regurgitation ACES for PACES page)
Advanced level question:
Is it primary valvular disease or regurgitation secondary to cardiac dilatation?
The absence of a loud 2nd heart sound makes it unlikely that the patient has developed pulmonary hypertension and further the absence of left parasternal heave makes it unlikely that that patient had developed right heart failure secondary to chronic left heart failure and pulmonary hypertension.
Hence, the valvular regurgitation was more likely to be due to heart failure and cardiac dilatation.
Notes on mitral regurgitation :
http://www.medicalrevision.org/mitral_regurgitation.htm
