nyimalay
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Phenylepherine and hand grip increase systemic resistance.
-decrease the gradient across aortic valve in AS and HOC
-increase LV end-systolic volume that increase gradient across Mitral valve and VSD
Amyl nitrite - venodilatation,less venous return, decreased ventricular end-diastolic volume
-this provoke more obstruction in HOC (I don't know the mechanism for AS)
-less gradient across Mitral valve and VSD
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| farnsworth
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Heart murmur are caused by turbulent flow. If you know this, all the murmurs and their pathophysiology is self-explanatory.
Aortic stenosis, HOCM: decreasing the afterload (by lowering the systemic vascular resistance, SVR) -> the pressure gradient across the valve increases, the flow becomes more turbulent -> the intensity of the murmur increases. Amyl nitrite acts on vascular smooth muscles predominantly, leading to a decrease in preload (venous pooling), as well as to a dimished left ventricular afterload (arterial relaxation, SVR decreases).
The decreased afterload after administration of amyl nitrite leads to a more turbulent flow across the aortic valve = increased intensity of systolic murmur.
The decrease in intensity of the murmur in VSD and mitral valve insufficiency upon infusion of amyl nitrite is not solely created by the decrease in left ventricular preload (filling), but also by the decrease in afterload (SVR): during systole the blood fraction of blood pumped out of the heart is increased by the decrease in SVR, thus less blood flows across the VSD (or the incompetent mitral valve).
The fact that murmurs are caused by turbulent flow also explains why you cannot detect a very large VSD (or mitral valve insufficiency): the defect is large enough to create laminar flow! So I cannot recommend to relay on auscultatory findings in patient where heart defects are already known or suspected (echocardiography is the gold standard!!!).
Example from the 'real life': a 42 y/o patient w/ fever, mailaise, elevated levels of Il-6 and ESR was suspected to have a thoracic vertebral discitis, the pre-operative CXR showed a small pleural effusion on the right side, normal heart configuration, no pulmonary congestion, no infiltrated, small region of atelectasis on the right side. ECG: sinus rhythm, tachycardic (104 bpm), otherwise unconspicuous. Lab values: Il-6 elevation, leukocytosis, slightly elevated AST, ALT, coagulation parameters normal. The patient was able to climb 3 flights of stairs without pausing, but at a slower pace than usual. Auscultation: no rubs, no murmurs, no gallop, audible S1/S2, no S3 or S4. So the patient was scheduled to neurosurgery to get a biopsy from the vertrebral disc (and to remove the potential inflammatory focus).
Induction of anesthesia was uneventful, patient was intubated, chest movements bilaterally equal. Mean arterial pressure was around 70mmHg in supine position and declined to 60 in prone position (required for this type of surgery). In the course of the procedure, the MAP steadily declined to 55-50 over 30mins, the anesthesiologist decided to give some fluids (1L acetated Ringer's, 1L of gelatin and 1L of HES 130/0.45), which was infused over the next 30min. Rationale: the patient was hospitalized for a couple of days, had fever (T=38.9C), was possibly septic, so a volume deficit was suspected. The MAP went up to 55-60mmHg, the anesthesiologist decided to add inotropic support (norepinephrine, 2-4micg/min) to keep the MAP>60mmHg. During the procedure the patient was on PCB (FiO2=.4, PEEP 6mbar, Pinsp=18mbar, I:E=1:1, RR=12, resulting VT=450mL, SpO2=99%).
The patient was extubated at the end of the procedure after returning him into supine position. The patient received oxygen insufflation via nasal prong, because SpO2 dropped to 84% after extubation, but returned to 96% w/ 6L/min O2. The patient received 0.15mg/kg Cisatracurium for intubation, no repetive doses given, the neuromuscular monitoring showed complete recover 60min after induction (TOF>90%), so residual relaxation was excluded. Auscultation show slightly diminished breath sound a the right lung base, and coarse crackles at the left lower regions. A CXR done in the revovery room showed: small right sided pleural effusion, slightly enlarged heart, pulmonary edema, small atelectatic region in the right lower lung. The patient was transfered to the neurosurgical ICU.
Six weeks later the patient is scheduled for a neurosurgical procedure again (the microbiological specimen proved an inflamed vertebral disc, an recent MRI showed still some remaining inflamed tissue that has to be removed). By chance, the same anesthesiologist is scheduled for performing anesthesia on this patient. He noticed that the patient has a fresh, huge thoracic scar over his sternum.
Guess the diagnosis!
Edited by farnsworth on 02/18/08 - 07:24 AM
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| nyimalay
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Thanks for you explanation regarding murmurs.
I couldn't find any clue from the real case.
Was that inflammatory thoracic aortic aneurysm? Let me guess.
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| Sayulita
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cool posting
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| simi
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nyimalay n farnsworth thanks....
farnsworth very nice explanation but not sure of the diagnosis
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| farnsworth
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inflammatory aortic aneurysm is not a bad guess, but it would not explain pulmonary edema and the need for the fluid and vasopressor requirements intraoperatively.
The anesthesiologist was thinking about sepsis, hence the fluid and vasopressor therapy. The next thing he was thinking of, was septic cardiomyopathy (yes, yes. Everybody was talking about the toll-like receptor at that time and its role in septic cardiomyopathy). But in the end it turned out, that the patient had a 3rd to 4th grade mitral valve insufficiency! The defect was large enough to prevent the flow becoming turbulent, thus it was not noticed during auscultation. The patient was scheduled to mitral valve replacement, which showed an inflamed and destroyed mitral valve, hence the scar over the sternum.
The epinephrine dosage was low, so a the anesthesiologist did not use a TEE intraoperatively (challinging, in a patient in prone position), but if he did, he would have seen the MVI. It would have change the management in a way, that he would have avoided the use or norepinephrine, but used low dose dobutamine instead. Rationale: keep the left ventricle filled and fast. MVI is one of the worst conditions. Why? Because the mitral valves is one of the main determinants of the direction of the blood flow within the heart! If the systemic vascular resistance (SVI) increases, e. g. by norepinephrine infusion or endogenous catecholamines, the reflux over the mitral valve increases -> pulmonary edema (worst case: right heart failure).
In this case it remained unclear, if septic emboli from a damaged mitral valve (endocarditis) could have caused the discitis, or if the discitis preceded the mitral valve destruction.
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