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Step I Breath sounds?
Started by Divine Furor
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I haven't taken the test yet, but I haven't heard anyone say they had breath sounds.
On a related note, could someone explain the significance of fremitus, rales, rhonchi, crackles, etc?
On a related note, could someone explain the significance of fremitus, rales, rhonchi, crackles, etc?
I've heard several people say they had heart sounds on their exam too, but that the quality was super bad and you obviously can't ask the patient do turn to one side or another or ask them to inhale/exhale etc. Did it seem to you that the question stems had enough information to determine what the heart sounds were (i.e. "accentuated on inspiration" "radiates to the carotids",etc) or do you actually need to be able to tell from the audio? The other reason I ask is because I can't time S1/S2 reliably yet on normal patients w/o feeling their carotid pulse at the same time as listening to their heart (which is the way I was taught by my MS1 preceptor who is a super-specialied cardiologistt)
I had 3 or 4 questions on my test with heart sounds, but they were all easy/classic to distinguish and all contained info in the stem about radiation/loudest point (which are almost dead givaways, though they try to trick with you lower left sternal border murmurs). I don't link you're going to get any "low humbling diastolic murmurs" on your test. Think more along the lines of the classic crescendo-decresendo systolic ejection murmur, the fixed split S2 of an ASD, the machinery murmur of a VSD, etc. Distinguishing the murmur isn't supposed to be the part that trips you up, I believe, as I didn't have a single question saying "what does this murmur indicate?" All the questions I had wanted to know something about the association of the murmur (i.e. indomethacin to close a PDA, ASD is associated with Down's, etc).
Didn't have any A/V questions with respiratory findings, and didn't encounter any in any NBMEs. But I did have several questions with written respiratory findings and CXRs (resonance on percussion, tactile fremitus, egophany, bronchial breath sounds, crackles, trachial deciation, etc). There's a table in the Respiratory section of FA with the rundown on these. Memorize the "classic" cases like spontaneous pneumothorax, tension pneumothorax, consolidative pneumonia, obstruction, effusion. You WILL have a question on pulmonary edema, I can almost guarantee it, since its an integrative point between CV and Respiratory pathophys and CV is often heavily represented on exams. So know the classic findings of pulmonary edema (symptoms, CXR findings, PE findings, what happens to pressures in the L and R side of the heart, and such)
Didn't have any A/V questions with respiratory findings, and didn't encounter any in any NBMEs. But I did have several questions with written respiratory findings and CXRs (resonance on percussion, tactile fremitus, egophany, bronchial breath sounds, crackles, trachial deciation, etc). There's a table in the Respiratory section of FA with the rundown on these. Memorize the "classic" cases like spontaneous pneumothorax, tension pneumothorax, consolidative pneumonia, obstruction, effusion. You WILL have a question on pulmonary edema, I can almost guarantee it, since its an integrative point between CV and Respiratory pathophys and CV is often heavily represented on exams. So know the classic findings of pulmonary edema (symptoms, CXR findings, PE findings, what happens to pressures in the L and R side of the heart, and such)
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I thought ASD was associated with Down Syndrome?
Can you tell us what they are?
My mistake, you're correct. My brain has already started purge mode.
Pulomonary edema is either doing to be a transudate or an exudate. If its an exudate, its due to injury in the lung itself. Sepsis, pneumonia, shock, etc. If its a transudate, it has to be due to only one of two reasons: 1. Decreased oncotic pressure (can't hold water in the vascular space) or 2. Increased hydrostatic pressure (water is being pushed out of the vascular space).
Decreased oncotic pressure is always going to be in the scenario of low albumin, either due to nephrotic syndrome or end stage liver disease. Heart pressures will be in the normal range, and the patient is at risk of developing HIGH OUTPUT cardiac failure (trying to maintain cardiac output without enough blood coming through since fluid is leaving the vascular space).
Increased hydrostatic pressure is going to be either due to left-sided heart failure or mitral stenosis. You can reason the pressures out for each:
-In mitral stenosis, the left ventricle is not getting enough blood from the atrium. As a result, LV pressure will be low-to-normal. Left atrial pressure will be increased since you can't get enough blood through the stenotic valve, and that increased pressure backs up into the lungs.
-In LHF, the ventricle is sick and can't pump out enough blood to maintain cardiac output. This can either be due to SYSTOLIC failure (decrease in contractility, due to ischemia, fibrosis, etc) or DIASTOLIC failure (decreased in filling due to concentric hypertrophy or muscle infiltration i.e. stiff ventricle). In systolic failure, the sick ventricle results in decreased CO which activates the Frank-Starling heart mechanism and preload goes up to try to compensate (left ventricular end diastolic volume/pressure). In diastolic function, the stiff ventricle increases pressures just by the nature of it losing compliance. Regardless of the cause, the result is still the same: the left ventricular pressures go up. These pressures back up into the left atrium and ultimately the pulmonary circulation, increasing hydrostatic pressure and causing a transudative pulmonary edema.
Both mitral stenosis and LHF can result in ultimate right-sided heart failure if the pressures back up through the pulmonary circulation into the right side of the heart. So the right side of the heart can have either normal or elevated pressures with pulmonary edema. But the key is the left side of the heart. The only tricky point here is that pulmonary hypertension/cor pulmonale can ALSO cause right sided heart failure. However, you will not see pulmonary edema with pulmonary HTN as its not a pressures problem, its a total vascular resistance problem.
Zagdoc,
Thank you, and thank you for the detailed response -- that correlates nicely with my own experiences and the general emphasis on heart sounds in general.
Thank you, and thank you for the detailed response -- that correlates nicely with my own experiences and the general emphasis on heart sounds in general.
