The medical students were asked to examine the cardiovascular system.
The patient was an elderly man who was propped up in bed and had an oxygen mask on. He was of average height but looked underweight.
The students were asked for their impression at this point and they remarked that the patient looked breathless. As they had been asked to examine the cardiovascular system it was likely the breathlessness was related to the cardiovascular system and hence they concluded that the patient probably had left ventricular failure.
On examination of the head they noticed flaring of the alae nasi, further evidence of respiratory distress and giving further weight to the idea that the patient had left ventricular failure.
On examination of his hands there was no gross abnormality. His pulse rate was 90 beats per minute, regular in rhythm good volume and normal character. There was no radio-radial or radio-femoral delay. This did not help us any further in our diagnosis.
When the students began to examine the neck they were asked what they would expect to find in this patient. They replied that his JVP (jugular venous pressure) was likely to be elevated. Indeed this was the case and the JVP was elevated 6 cms above the manubriosternal angle. There was no dominant wave. The trachea was in the midline the carotids were normal.
On examination of the chest, the apex beat was felt in the 5th left intercostal space at the midclavicular line. It was a diffuse impulse. This did not give any further clues to the diagnosis. There was no parasternal heave and no palpable heart sounds or thrills.
On auscultation, the first heart sound was soft. This indicated that the mitral valve was not competent. Hence the students quite correctly suspected mitral regurgitation.
The second sound was of normal intensity signifying that the aortic valve was probably normal and that there was no pulmonary hypertension.
There was a blowing pan systolic murmur best heard at the apex. More evidence in favour of mitral regurgitation. The murmur increased in expiration; mitral regurgitation. The murmur radiated to the axilla; mitral regurgitation.
There were no added sounds or extra-cardiac sounds
On examination of the back of the chest there were fine late inspiratory crepitations at both bases, more marked on the right hand side, confirming our initial suspicion that the patient had left ventricular failure. There was no sacral oedema
Diagnosis: Mitral regurgitation, left ventricular failure
We next went through the causes of mitral regurgitation and discussed how to work out the causes of mitral regurgitation by drawing a diagram of the mitral valve apparatus and working out what could go wrong with each component of it.
Saturday, December 16, 2006
Sunday, December 10, 2006
Cardiovascular Examination (MRCP PACES)
The patient was a middle-aged lady seated up in bed. She had an oxygen mask on.
At this point we thought that as it was a cardiovascular examination the patient was likely to have left ventricular failure.
She was of average height and weight.
On examination of her head we noticed that she had a high arched palate.
There was no abnormality detected on examination of her hands. Her pulse rate was 55 beats per minute, regular in rhythm. It was low in volume and slow rising in character. At this point the diagnosis of aortic stenosis came to mind.
There was no brachio-radial delay.
On examination of the neck we noticed that her JVP was elevated 6 cms above the manubriosternal angle. This made us think that the initial impression that she had heart failure was correct.
On examination of her chest, the apex beat was at the 5th intercostal space just medial to the mid-clavicular line. There was no appreciable variation in character. No parasternal heave, no palpable heart sounds or thrills.
On auscultation the first heart sound was normal, the second heart sound was soft and single (further evidence in favour of aortic stenosis)
There was an ejection systolic murmur best heard at the aortic area and this murmur radiated to the neck (in keeping with aortic stenosis)
There were fine late inspiratory crepitations at both lung bases (in keeping with left ventricular failure)
Diagnosis: aortic stenosis with left ventricular failure
At this point we thought that as it was a cardiovascular examination the patient was likely to have left ventricular failure.
She was of average height and weight.
On examination of her head we noticed that she had a high arched palate.
There was no abnormality detected on examination of her hands. Her pulse rate was 55 beats per minute, regular in rhythm. It was low in volume and slow rising in character. At this point the diagnosis of aortic stenosis came to mind.
There was no brachio-radial delay.
On examination of the neck we noticed that her JVP was elevated 6 cms above the manubriosternal angle. This made us think that the initial impression that she had heart failure was correct.
On examination of her chest, the apex beat was at the 5th intercostal space just medial to the mid-clavicular line. There was no appreciable variation in character. No parasternal heave, no palpable heart sounds or thrills.
On auscultation the first heart sound was normal, the second heart sound was soft and single (further evidence in favour of aortic stenosis)
There was an ejection systolic murmur best heard at the aortic area and this murmur radiated to the neck (in keeping with aortic stenosis)
There were fine late inspiratory crepitations at both lung bases (in keeping with left ventricular failure)
Diagnosis: aortic stenosis with left ventricular failure
Chest Examination
We asked the medical students to examine a patient.
The patient was seated next to his bed and had an oxygen mask on. The students concluded that this patient must be suffering from a condition that would cause respiratory distress.
He was of average height but looked thin. This made them think that it must be a chronic condition that could cause cachexia or a malignancy.
They also noticed that he had a productive cough and that the sputum pot on his bedside table was almost half full. This made them think that it was a chronic respiratory condition that caused a productive cough. They suggested chronic bronchitis or bronchiectasis. The patient did not look a “blue-bloater”. This left the possibility of bronchiectasis.
On examination of his head we noticed that his face looked very thin, his alae nasi were flaring (further evidence of respiratory distress) and he had pursed lip breathing (suggesting chronic distal obstruction).
On examination of his hands we noticed that his fingers were clubbed. This more or less made the diagnosis of bronchiectasis secure.
His fingers were also very severely tar stained. This made us think of the possibility of bronchial cancer as a consequence of prolonged cigarette smoking.
On examination of his neck we notice that it was thin and that the crico-sternal distance was reduced (further evidence of chronic obstructive pulmonary disease).
His chest looked hyperinflated and thin, there was a scar in the right subclavian region, which looked like a long line had been inserted (either as an emergency or for feeding, which was unlikely as he presumably had a working gut, or for chemotherapy, bringing up the possibility of bronchial cancer).
The respiratory rate was 26 per minute, the apex was difficult to palpate, respiratory movements were equal, vocal fremitus was equal on the two sides but reduced.
Percussion note was resonant, with reduced cardiac and liver dullness further evidence of chronic obstructive pulmonary disease.
Breath sounds were vesicular, reduced in intensity and there were coarse crepitations mainly at the right base (in keeping with bronchiectasis)
Diagnosis: bronchiectasis
We needed to think of bronchial cancer in view of our other findings.
The patient had been on chemotherapy but this was for oesophageal cancer, which was not resectable.
The patient was seated next to his bed and had an oxygen mask on. The students concluded that this patient must be suffering from a condition that would cause respiratory distress.
He was of average height but looked thin. This made them think that it must be a chronic condition that could cause cachexia or a malignancy.
They also noticed that he had a productive cough and that the sputum pot on his bedside table was almost half full. This made them think that it was a chronic respiratory condition that caused a productive cough. They suggested chronic bronchitis or bronchiectasis. The patient did not look a “blue-bloater”. This left the possibility of bronchiectasis.
On examination of his head we noticed that his face looked very thin, his alae nasi were flaring (further evidence of respiratory distress) and he had pursed lip breathing (suggesting chronic distal obstruction).
On examination of his hands we noticed that his fingers were clubbed. This more or less made the diagnosis of bronchiectasis secure.
His fingers were also very severely tar stained. This made us think of the possibility of bronchial cancer as a consequence of prolonged cigarette smoking.
On examination of his neck we notice that it was thin and that the crico-sternal distance was reduced (further evidence of chronic obstructive pulmonary disease).
His chest looked hyperinflated and thin, there was a scar in the right subclavian region, which looked like a long line had been inserted (either as an emergency or for feeding, which was unlikely as he presumably had a working gut, or for chemotherapy, bringing up the possibility of bronchial cancer).
The respiratory rate was 26 per minute, the apex was difficult to palpate, respiratory movements were equal, vocal fremitus was equal on the two sides but reduced.
Percussion note was resonant, with reduced cardiac and liver dullness further evidence of chronic obstructive pulmonary disease.
Breath sounds were vesicular, reduced in intensity and there were coarse crepitations mainly at the right base (in keeping with bronchiectasis)
Diagnosis: bronchiectasis
We needed to think of bronchial cancer in view of our other findings.
The patient had been on chemotherapy but this was for oesophageal cancer, which was not resectable.
Saturday, December 02, 2006
COPD
The medical students examined a patient who had been admitted to the medical admissions unit.
On approaching the patient they noticed that the patient was dressed in hospital pyjamas. I asked them whether this was significant. We worked out that this would mean that the patient was admitted as an emergency and did not have time to pack a bag to bring in to hospital. Thus we concluded that this was an acute illness or acute exacerbation of a chronic illness.
The patient was seated up in bed with an oxygen mask on and did not appear perfectly comfortable. This was evidence of respiratory distress.
On examination of his head we noticed flaring of his alae nasi, further evidence of compromised respiratory function.
On examination of his hands there was no definite abnormality in particular no clubbing and no flapping tremor. His pulse rate was 100 per minute.
On examination of his neck we noticed that the trachea was in the midline but the cricosternal distance was reduced. The students correctly interpreted this as evidence of a hyper inflated chest and therefore airways obstruction.
We now knew that this patient had airways obstruction and respiratory distress as a consequence of this.
The students then proceeded to the foot end of the bed and looked at the patient’s chest. They noticed that it was barrel shaped; further evidence of obstructed airways and the fact that a change in shape had occurred would mean that this obstruction was chronic.
The diagnosis at this point was chronic obstructive airways (pulmonary) disease with and acute exacerbation.
We had noticed by this point that the patient had a productive cough and thus we inferred that the likely cause of the exacerbation of airways obstruction was an infection of the chest.
Vocal fremitus was reduced but equal
Respiratory movements by palpation were equal
Percussion note was hyper-resonant with decreased cardiac and liver dullness (further evidence in favour of airways obstruction)
Breath sounds were vesicular but reduced in intensity (indicating a degree of emphysema)
There were no added sounds
Diagnosis: acute exacerbation of chronic obstructive pulmonary disease probably caused by a chest infection
On approaching the patient they noticed that the patient was dressed in hospital pyjamas. I asked them whether this was significant. We worked out that this would mean that the patient was admitted as an emergency and did not have time to pack a bag to bring in to hospital. Thus we concluded that this was an acute illness or acute exacerbation of a chronic illness.
The patient was seated up in bed with an oxygen mask on and did not appear perfectly comfortable. This was evidence of respiratory distress.
On examination of his head we noticed flaring of his alae nasi, further evidence of compromised respiratory function.
On examination of his hands there was no definite abnormality in particular no clubbing and no flapping tremor. His pulse rate was 100 per minute.
On examination of his neck we noticed that the trachea was in the midline but the cricosternal distance was reduced. The students correctly interpreted this as evidence of a hyper inflated chest and therefore airways obstruction.
We now knew that this patient had airways obstruction and respiratory distress as a consequence of this.
The students then proceeded to the foot end of the bed and looked at the patient’s chest. They noticed that it was barrel shaped; further evidence of obstructed airways and the fact that a change in shape had occurred would mean that this obstruction was chronic.
The diagnosis at this point was chronic obstructive airways (pulmonary) disease with and acute exacerbation.
We had noticed by this point that the patient had a productive cough and thus we inferred that the likely cause of the exacerbation of airways obstruction was an infection of the chest.
Vocal fremitus was reduced but equal
Respiratory movements by palpation were equal
Percussion note was hyper-resonant with decreased cardiac and liver dullness (further evidence in favour of airways obstruction)
Breath sounds were vesicular but reduced in intensity (indicating a degree of emphysema)
There were no added sounds
Diagnosis: acute exacerbation of chronic obstructive pulmonary disease probably caused by a chest infection
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