Today's case is a time to consider reviewing common murmurs and how to identify a pleural effusion in a patient with heart failure.
This is a real case but I have as always anonymised the case. All pictures are self drawn so please excuse my poor artistic skills!
This elderly patient presented to another hospital with symptoms of fatigue, appetite loss and dyspnoea occurring over 4 days.
She was normally quite well and had just been on a recent trip within Japan. However, the patient began to feel weak and had difficulty walking far, needing to frequently rest. She also began to lose her appetite and prior to admission the patient was noticed to have difficulty breathing although the patient denied being breathless.
When seen, the patient admitted to being only able to walk no more than 100 metres before needing to rest. She rested normally for up to 2 minutes but had no chest pains. The patient had recently needed to prop herself up in bed with pillows to feel comfortable. Again, the patient denied being breathless!
The patient denied having a fever, cough, sputum, haemoptysis. There was no recent history of a common cold. Although the patient's spouse had said the patient had lost her appetite, the patient said there was no problem!
There was no history of any abdominal problem. No Genitourinary problems.
The patient was known to have Sick Sinus Syndrome for which the patient had a biventricular pacemaker, some mild dementia, and type 2 diabetes mellitus for which she took insulin.
Drugs included warfarin, digoxin 125mcg, donezapil and insulin.
There was a history of heavy alcohol use in the past but the patient had stopped drinking several years before and she still smoked 12 cigarettes per day.
When examined, the following findings were seen:
On inspection the patient looked relatively well.
BP 159/95, pulse 76 regular, Afebrile, Sats 97% on room air, Resp rate 30/min.
Hands showed some fine tremor and there were red palms. There was some early clubbing and no Quinke's Sign. There was no liver/ CO2 flap [asterixis]. Sclerae looked yellow. The tongue was blue tinged consistent with central cyanosis.
JVP was pulsatile and raised above 4cm. The Carotid was evident at the neck and pulsatile (Corrigan's Sign). Precordial examination revealed a left parasternal heave consistent with RV hypertrophy. Aortic area revealed a grade 2/6 systolic murmur with no diatolic component audible radiating to the carotids in the neck (aortic systolic murmur; probable aortic stenosis). The Apex revealed a 3/6 mitral pansystolic murmur radiating to the left axilla. Both murmurs increased in loudness on expiration.
Interestingly, there was a murmur in the tricuspid area (right side of the xiphoid process) and with slight radiation over the liver area consistent with tricuspid regurgitation. There was no pulsatility of liver as can be sometimes seen in TR (please see diagram 2).
Respiratory examination revealed 'stony' dullness at the left base. Vocal Resonance was reduced compared to the right side [ask patient to say 'hitotsu' whilst listening over the area of dullness and compare to the normal side; in effusion the sound decreases; in consolidation the sound increases] and the breath sounds were decreased over the area of dullness. These findings were consistent with a pleural effusion. There were also crackles on the surface of the effusion and at the right base (see diagram 3)
Abdominal examination was normal.
Lower limb examination revealed no oedema or evidence of deep vein thrombosis.
Clinical Impression:
1) Congestive Heart Failure
2) Mixed Valvular Disease (Mixed AS and AR, TR and MR)
3) Right Ventricular Hypertrophy
4) Left sided Pleural Effusion
5) Possible thyrotoxicosis / liver disease (tremor and red palms)
6) Possible recent MI (decompensated Heart Failure and possible silent event due to diabetes)
7) Possible alcholic cardiomyopathy (history of heavy alcohol use)
Chest Xray (diagram 1) revealed severe cardiomegally and upper lobe diversion (bat's wings or Butterfly shadow) and fluid in the horizontal fissure on the right. The left costophrenic angle was obscured [please don't refer to it as 'dull'; dull is a sound not the description of an X-ray shadow!! Pictures don't make sounds]
The ventricular pacing leads did not reach the apex suggesting that either the heart was normal size and surrounded by a large pericardial effusion, or the heart has enlarged significantly in the 15 years since the pacemaker was put into the patient.
ECG showed a single pacing spike and a wide QRS complex consistent with being paced.
Bloods showed a normal Neutrophil Count, Normal Haemoglobin, Slightly raised BUN but normal creatinine. Liver Function was normal. INR was 1.29 and therefore subtherapeutic. CK was 66 and troponin T was Negative. CRP was raised at 2.1 and monocytes were mildly raised making me suspicious of a possible viral aetiology for his decompensated cardiovascular status.
Blood gas revealed a respiratory alkalosis and hypoxaemia.
Hence, AMI had been ruled out here but not thyroid disease.
Echocardiogram revealed an ejection fraction of 29%, severely thinned LV wall, hypokinesis, 3rd degree TR and MR. There was 1st degree AR but no Aortic stenosis component. There was no pericardial effusion.
Sometimes the increased cardiac output associated with AR can cause a Flow Murmur that can be easily confused with AS as in this situation.
Hence the diagnosis here from history and physical was not altered significantly by other tests.
It was decided not to attempt removing the pleural effusion on the left as firstly it was relatively small, the patient had not had a long challenge with diuretic therapy, the patient was taking warfarin and the patient's heart was so large there was a risk of puncturing the ventricle.
The treatment suggested was 1) Furosemide 2) ACE inhibitor therapy
ACE-I therapy improves cardiac function by remodelling the myocardium and reduding hypertension, and it is also known to reduce hospital admissions. It is also protective of the patient's kidneys especially as she is diabetic. However, always be cautious with ACE-I / ARB / Aldactone therapy as it can worsen creatinine and cause hyperkalaemia. On starting an ACE-1 /ARB it is acceptable to see a rise in creatinine of up to 30%.
The funny thing was that I have NEVER done a CT scan for someone who presented with pure heart failure as history, examination and a simple chest Xray usually suffice. If an effusion is considered then an ultrasound is sought or even a diagnostic needle aspiration.
The CT showed all the features already found by other methods but two metallic objects were noted which were the pacing leads causing interference of the image on the CT scan!!
This is a real case but I have as always anonymised the case. All pictures are self drawn so please excuse my poor artistic skills!
This elderly patient presented to another hospital with symptoms of fatigue, appetite loss and dyspnoea occurring over 4 days.
She was normally quite well and had just been on a recent trip within Japan. However, the patient began to feel weak and had difficulty walking far, needing to frequently rest. She also began to lose her appetite and prior to admission the patient was noticed to have difficulty breathing although the patient denied being breathless.
When seen, the patient admitted to being only able to walk no more than 100 metres before needing to rest. She rested normally for up to 2 minutes but had no chest pains. The patient had recently needed to prop herself up in bed with pillows to feel comfortable. Again, the patient denied being breathless!
The patient denied having a fever, cough, sputum, haemoptysis. There was no recent history of a common cold. Although the patient's spouse had said the patient had lost her appetite, the patient said there was no problem!
There was no history of any abdominal problem. No Genitourinary problems.
The patient was known to have Sick Sinus Syndrome for which the patient had a biventricular pacemaker, some mild dementia, and type 2 diabetes mellitus for which she took insulin.
Drugs included warfarin, digoxin 125mcg, donezapil and insulin.
There was a history of heavy alcohol use in the past but the patient had stopped drinking several years before and she still smoked 12 cigarettes per day.
When examined, the following findings were seen:
On inspection the patient looked relatively well.
BP 159/95, pulse 76 regular, Afebrile, Sats 97% on room air, Resp rate 30/min.
Hands showed some fine tremor and there were red palms. There was some early clubbing and no Quinke's Sign. There was no liver/ CO2 flap [asterixis]. Sclerae looked yellow. The tongue was blue tinged consistent with central cyanosis.
JVP was pulsatile and raised above 4cm. The Carotid was evident at the neck and pulsatile (Corrigan's Sign). Precordial examination revealed a left parasternal heave consistent with RV hypertrophy. Aortic area revealed a grade 2/6 systolic murmur with no diatolic component audible radiating to the carotids in the neck (aortic systolic murmur; probable aortic stenosis). The Apex revealed a 3/6 mitral pansystolic murmur radiating to the left axilla. Both murmurs increased in loudness on expiration.
Interestingly, there was a murmur in the tricuspid area (right side of the xiphoid process) and with slight radiation over the liver area consistent with tricuspid regurgitation. There was no pulsatility of liver as can be sometimes seen in TR (please see diagram 2).
Respiratory examination revealed 'stony' dullness at the left base. Vocal Resonance was reduced compared to the right side [ask patient to say 'hitotsu' whilst listening over the area of dullness and compare to the normal side; in effusion the sound decreases; in consolidation the sound increases] and the breath sounds were decreased over the area of dullness. These findings were consistent with a pleural effusion. There were also crackles on the surface of the effusion and at the right base (see diagram 3)
Abdominal examination was normal.
Lower limb examination revealed no oedema or evidence of deep vein thrombosis.
Clinical Impression:
1) Congestive Heart Failure
2) Mixed Valvular Disease (Mixed AS and AR, TR and MR)
3) Right Ventricular Hypertrophy
4) Left sided Pleural Effusion
5) Possible thyrotoxicosis / liver disease (tremor and red palms)
6) Possible recent MI (decompensated Heart Failure and possible silent event due to diabetes)
7) Possible alcholic cardiomyopathy (history of heavy alcohol use)
Chest Xray (diagram 1) revealed severe cardiomegally and upper lobe diversion (bat's wings or Butterfly shadow) and fluid in the horizontal fissure on the right. The left costophrenic angle was obscured [please don't refer to it as 'dull'; dull is a sound not the description of an X-ray shadow!! Pictures don't make sounds]
The ventricular pacing leads did not reach the apex suggesting that either the heart was normal size and surrounded by a large pericardial effusion, or the heart has enlarged significantly in the 15 years since the pacemaker was put into the patient.
ECG showed a single pacing spike and a wide QRS complex consistent with being paced.
Bloods showed a normal Neutrophil Count, Normal Haemoglobin, Slightly raised BUN but normal creatinine. Liver Function was normal. INR was 1.29 and therefore subtherapeutic. CK was 66 and troponin T was Negative. CRP was raised at 2.1 and monocytes were mildly raised making me suspicious of a possible viral aetiology for his decompensated cardiovascular status.
Blood gas revealed a respiratory alkalosis and hypoxaemia.
Hence, AMI had been ruled out here but not thyroid disease.
Echocardiogram revealed an ejection fraction of 29%, severely thinned LV wall, hypokinesis, 3rd degree TR and MR. There was 1st degree AR but no Aortic stenosis component. There was no pericardial effusion.
Sometimes the increased cardiac output associated with AR can cause a Flow Murmur that can be easily confused with AS as in this situation.
Hence the diagnosis here from history and physical was not altered significantly by other tests.
It was decided not to attempt removing the pleural effusion on the left as firstly it was relatively small, the patient had not had a long challenge with diuretic therapy, the patient was taking warfarin and the patient's heart was so large there was a risk of puncturing the ventricle.
The treatment suggested was 1) Furosemide 2) ACE inhibitor therapy
ACE-I therapy improves cardiac function by remodelling the myocardium and reduding hypertension, and it is also known to reduce hospital admissions. It is also protective of the patient's kidneys especially as she is diabetic. However, always be cautious with ACE-I / ARB / Aldactone therapy as it can worsen creatinine and cause hyperkalaemia. On starting an ACE-1 /ARB it is acceptable to see a rise in creatinine of up to 30%.
The funny thing was that I have NEVER done a CT scan for someone who presented with pure heart failure as history, examination and a simple chest Xray usually suffice. If an effusion is considered then an ultrasound is sought or even a diagnostic needle aspiration.
The CT showed all the features already found by other methods but two metallic objects were noted which were the pacing leads causing interference of the image on the CT scan!!
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