Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
20 Cards in this Set
- Front
- Back
|
Aortic regurgitation: acute vs chronic
|
chronic AR leads to eccentric LV hypertrophy and dilation
-LV compliance increases -able to handle the regurgitant volume without a drastic increase in diastolic pressure --less pressure impact on the LA --less problem with pulmonary edema, at least at rest Acute AR -just like acute MR – a drastic presentation with severe pulmonary edema --LV is not compliant |
|
|
Aortic regurgitation: "sneak up?"
|
it can “sneak up on you” like MR
-patient can be asymptomatic and yet already have irreversible LV damage -but this is less of a problem than in MR -again, certain measurements exist to guide intervention in asymptomatic patients in general, though: -primary reason to replace valve in AR is development of symptoms -fatigue, dyspnea… |
|
|
Aortic regurgitation: PE
|
diastolic “blowing” murmur
widened pulse pressure -difference between systolic and diastolic -because a bunch of blood is flowing backward into the LV -diastolic pressure is going to be pretty low -systolic pressure may be elevated – LV is pushing out a very big stroke volume -and using all the Starling forces it can find --large volume load = large preload: larger stroke volume |
|
|
Austin-Flint murmur
|
Low pitched rumbling murmur
Cardiac apex Mid-diastolic |
|
|
Aortic regurgitation: treatment
|
can’t slow progression, but can help a lot with symptoms
Vasodilators -encourage forward flow during systole -discourage backward flow during diastole --less systemic pressure to push blood back into the heart Rate slowing medications -not helpful if in sinus rhythm --think about it: the only real problem here is diastole that’s when the regurgitation occurs so it doesn’t help to increase the total time spent in diastole which is what happens when you slow the heart rate |
|
|
Aortic stenosis: hemodynamic curve
|
LV is generating extremely high pressures to force enough blood across the valve
LV systolic pressure >> Aortic systolic pressure Failure to generate high systolic pressure in aorta means low pulse pressure in aorta - Pulse Pressure = SBP – DBP Stroke volume will be normal in mild to moderate AS, but will be decreased in severe to critical AS -increased afterload -increased sympathetic tone (contractility) -LVH (decreased lusitropy) |
|
|
Aortic regurgitation (chronic): hemodynamic curve
|
Notice how the aortic pressure falls really low in diastole
-That’s because it’s leaking back into the heart during diastole High Pulse Pressure (SBP-DBP) in the aorta / arteries Huge stroke volume –that’s good, right? Problem: -most of that stroke volume pours back into the ventricle during diastole Also notice the ESPVR line has shifted – this is chronic AR: dilated LV with ↓contractility |
|
|
Mitral stenosis: hemodynamic curve
|
Notice the LA pressure tracing
LA must generate higher pressure to push across stenotic mitral valve And it’s still not enough ↓preload due to trouble filling LV ↓preload → ↓stroke volume The LV’s got it easy – not much work to do… |
|
|
Mitral regurgitation (chronic): hemodynamic curve
|
Notice the big V wave in LA tracing
Blood pouring back into LA during systole → ↑LA volume and pressure Acute MR would have a very big V wave Yay! Another huge stroke volume! No, sorry, a lot of that stroke volume is going backwards into the LA This is chronic MR as noted by the shift in the ESPVR |
|
|
Aortic regurgitation vs mitral regurgitation: hemodynamic curve
|
AR
Huge stroke volume -all of it is going forward into the aorta increased afterload -huge stroke volume – the aorta is compliant, but this is a bit much to handle… MR Huge stroke volume -lots of it is going backward into the LA very low afterload, considering the gigantic stroke volume |
|
|
Tricuspid stenosis
|
Rare
usually due to rheumatic fever -so almost certain to also have mitral stenosis |
|
|
Tricuspid regurgitation
|
usually not due to intrinsic valvular disease
usually due to too much RV pressure -which is usually due to too much pulmonary HTN -but could be due to pulmonic valve stenosis Carcinoid Syndrome -rare, but a great USMLE “zebra” |
|
|
Tricuspid valve surgery
|
operating on the tricuspid valve is not common
-not as important as the mitral valve --often not worth the morbidity of surgery --risk of thrombosis -frequently its problems are functional rather than structural (i.e. the problem is the pulmonary HTN, not the valve itself) --which you don’t fix by operating on the valve tricuspid valve annuloplasty -cinch it up with a ring to minimize regurgitation -not a stand-alone procedure – usually performed along with surgery on other valves |
|
|
Pulmonic stenosis
|
almost always congenital
-rarely caused by carcinoid syndrome balloon valvuloplasty -tear it open with a balloon -unlike aortic stenosis, this works pretty well --pulmonary pressures are much less than systemic pressures so causing pulmonic regurgitation is not as big of a problem as causing aortic regurgitation |
|
|
Pulmonic regurgitation
|
nearly always caused by severe pulmonary hypertension
-so the valve itself isn’t really the problem -not something you fix by operating on the valve |
|
|
Mechanical vs bioprosthetic valves
|
Mechanical:
durable -last longer than the patient -often preferred in younger patients require chronic anticoagulation -this is a big deal -especially mitral -stop anticoagulation for a few days – ↑risk of stroke -complicates all medical care Bioprosthetic: less durable -especially in mitral position -failure rate begins to increase after 10 years do not require chronic anticoagulation -this is a big deal -best for patients who are older, noncompliant, or at ↑risk for bleeding |
|
|
Tricuspid valve and inspiration
|
Inspiration
-lower intrathoracic pressure increases venous return to the RA -intensifies murmurs across the tricuspid valve --intensifies both TR and TS |
|
|
Maneuvers: basic principles
|
increase systemic afterload
-clench fists / handgrip increase venous return -inspiration -squat down decrease venous return -Valsalva maneuver -stand up |
|
|
Can't tell if MR or AS?
|
clench fists which ↑afterload
-MR gets louder --↑afterload increases the regurgitant fraction -AS doesn’t change |
|
|
S3 and S4
|
S3: “SLOSH ing in”
-S1 is the loudest part, so it’s in capital letters -S3 is "in" -Sloshing in emphasizes volume overload as etiology S4: “a STIFF wall” -S1 is the loudest part, so it’s in capital letters -S4 is "a" -Stiff wall emphasizes pressure overload as etiology |
