Valvular Heart Disease: Aortic Stenosis

by Carlo Raj, MD

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    Valvular heart diseases. Where are we and what are we doing? My goodness. There is so much to discuss here, but approaches one valve at a time. And as we do so, we will dissect every single aspect of that valvular heart disease so that by the time you have gone through this, you know who your patient is, what they are presenting with and understand the pathogenesis of what guide is here in the first place. Let us begin. Here once again is the chest. How important is this chest? Quite. We talked about the aortic area. I want you to point to it. Where am I? Right parasternal second intercostal space. Why? Because in anatomy of your aorta, take a look at the arch and so therefore, that is where you normally would hear your aortic valve. If you are dealing with a systolic murmur, take a look at aortic stenosis and I told you about that patient thus feeling tired, fatigue, maybe a little bit of chest pain with exertion. Let us talk about that for one second here. If it is aortic stenosis, what is causing this chest pain? It is not myocardial infarction, but it is the fact that with aortic stenosis, the left ventricle is having a hard time kicking against that increased afterload and so therefore the left ventricle is lifting weights. Once upon a time, when I was younger and I was lifting weights, I was undergoing hypertorphy of my biceps. Nowadays it is more about atrophy. But as far as the left ventricle is concerned, it is also lifting weights. What are the weights in this environment? The stenotic aortic valve. So what is the hypertrophy that we were referring to in the left ventricle? It is the fact that it...

    About the Lecture

    The lecture Valvular Heart Disease: Aortic Stenosis by Carlo Raj, MD is from the course Valvular Heart Disease. It contains the following chapters:

    • Aortic Stenosis
    • Pathogenesis
    • Visualisation
    • Signs & Symptoms
    • Diagnosis

    Included Quiz Questions

    1. Increased afterload.
    2. Decreased afterload.
    3. Increased preload.
    4. Decreased preload.
    5. Increase in preload and decrease in afterload.
    1. 2nd intercostal space, left parasternal AND 5th intercostal space, left parasternal
    2. 2nd intercostal space right parasternal, AND carotids
    3. 5th intercostal space, midclavicular line AND 5th intercostal space, midaxillary line
    4. 4th intercostal space left parasternal AND 2nd intercostal space left parasternal
    5. 2nd intercostal space left parasternal AND 2nd intercostal space right parasternal
    1. Demand ischemia.
    2. Coronary atherosclerosis.
    3. Insufficient treatment of streptococcus infection.
    4. Sequelae of aortic regurgitation.
    5. Hypotension.
    1. ...aortic regurgitation.
    2. ...left ventricular hypertrophy.
    3. ...left axis deviation.
    4. ...hypertension.
    5. ...congenital bicuspid aortic valve.
    1. 10 year old girl recently immigrated from Chile with untreated impetigo caused by streptococcus pyogenes.
    2. 10 year old boy born in WIsconsin with untreated impetigo caused by staph infection.
    3. 15 year old boy with Down syndrome and a tricuspid aortic valve.
    4. 40 year old man with longstanding hypertension.
    5. 12 year old boy born from Dallas with successfully treated strep A pharyngitis.
    1. Reduced left ventricular chamber size.
    2. Heart pump failure.
    3. Coagulative necrosis of a region of myocardium.
    4. Coronary artery narrowing.
    5. Endocarditis.
    1. Left ventricle to the aorta.
    2. Aorta to the peripheral circulation.
    3. Pulmonary vasculature to the right atrium.
    4. Left atrium to the left ventricle.
    5. Aorta to the pulmonary artery.
    1. Increased end systolic volume.
    2. Increased stroke volume.
    3. Decreased end diastolic pressure.
    4. Decreased end systolic volume.
    5. Increased end diastolic volume.
    1. Concentric hypertrophy of the left ventricle
    2. Eccentric hypertrophy of the left ventricle
    3. Dilation of the right ventricle
    4. Global atrophy of the heart
    5. Moderate atherosclerosis of the proximal aorta
    1. Delayed closure of mitral valve.
    2. Decreased chamber size due to left ventricular hypertrophy.
    3. Delay opening of aortic valve.
    4. Increase in end systolic volume.
    5. Increased ventricular pressure required to open aortic valve.
    1. Isovolumetric contraction.
    2. Isovolumetric relaxation.
    3. Mitral valve closure.
    4. Diastolic filling.
    5. Systolic Ejection.
    1. Dilated aortic root.
    2. Senile dystrophic calcification.
    3. Bicuspid aortic valve.
    4. Sequelae of untreated strep pharyngitis.
    5. Sequelae of untreated strep impetigo.
    1. FIxed splitting of S2.
    2. Paradoxical splitting of S2.
    3. Pulsus parvus et tardus.
    4. Hyperdynamic and enlarged left ventricle.
    5. Syncope.
    1. Left axis deviation.
    2. Left atrial enlargement.
    3. AV nodal blocks.
    4. Right axis deviation.
    5. Left bundle branch block.
    1. Pulmonic valve closure prior to aortic valve closure.
    2. Fixed splitting of S2, with no variation with inspiration.
    3. Widened S2 split with aortic valve closing prior to pulmonic valve.
    4. Physiologic splitting of S2.
    5. No splitting of S2.
    1. Decrease afterload.
    2. Increase preload.
    3. Decrease preload.
    4. Increase total peripheral resistance.
    5. Increase venous return.
    1. Heart failure with reduced ejection fraction.
    2. Heart failure with preserved ejection fraction.
    3. Patient with angina on exertion.
    4. Patient with syncope.
    5. Patient with paradoxical splitting of S2.
    1. Positive deflection in lead I and negative deflection in lead aVF
    2. Positive deflection in lead I and positive deflection in lead aVF.
    3. Negative deflection in lead I and negative deflection in lead aVF.
    4. Negative deflection in lead I and positive deflection in lead aVF.

    Author of lecture Valvular Heart Disease: Aortic Stenosis

     Carlo Raj, MD

    Carlo Raj, MD

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    More Management Discussions Needed
    By Hamed S. on 18. February 2017 for Valvular Heart Disease: Aortic Stenosis

    This was a well explained lecture but a trend I have noticed with these videos so far is the immense focus on physiology at the expense of diagnosis and management which is important for step 2. The avoidance of vasodilators, ACE-Inhibitors etc was glossed over. Moreover, a discussion of surgical options including valvuloplasty and percutaneous valve replacement was omitted. Common on guys if you are serious about step-2 and want people to transition from established providers like Kaplan then you need to focus more on management. I'm beginning to lose faith in these videos