Lectures

Heart Sounds

by Carlo Raj, MD
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    Welcome to our cardiovascular heart sounds. Here is a lot to talk about, so let us get started. To begin with, what is the heart sound? Rememeber, heart sounds are only created by closure or opening? Closure, all of the time. Anytime that you have these valves are open, they don't ever create a heart sound. Is that clear? It must be understood for us to then continue. What then happens to a valve when it becomes narrowed? We will take a look at what may then happen if the valve becomes narrowed versus what happens when it becomes expanded. And each one is then going to give us different types of heart sounds and then eventually we are going to get into the different locations anatomically around our chest in which it's going to then give us clues as to diagnosis of our patient. And that will be fun, you will see. If the valve is expanded, the root of the valve, for example, we talk about congestive heart failure and tell me about their heart. When you're looking at this heart on x-ray, I want you to close your eyes and think about as such. There you have it. There's a chest x-ray and now you find the apex, which is laterally displaced and normally should be at the fifth intercostal space, midclavicular. But with congestive heart failure, you might find apex, which is now laterally displaced and maybe midaxillary. Not sign of good, that is a bad sign. With that expansion of that heart is it possible that the valves and the root then become expanded? Of course. And would it make any sense for it become smaller? And so, therefore, when you do have such expansion of the root, then you would have what kind of...

    About the Lecture

    The lecture Heart Sounds by Carlo Raj, MD is from the course Heart Sounds. It contains the following chapters:

    • Definitions
    • Heart Sounds: S1 and S2
    • Heart Sounds: S3 and S4
    • Dynamic Auscultation
    • Respiratory Variation in Heart Sounds
    • Auscultation Areas
    • Rapid Squatting

    Included Quiz Questions

    1. Closure of the aortic and pulmonic valves.
    2. Closure of the mitral and tricuspid valves.
    3. Closure of the aortic and mitral valves.
    4. Closure of the tricuspid and pulmonic valves.
    5. Closure of the aortic and tricuspid valves.
    1. SA node, AV node, bundle of His, left bundle branch, right bundle branch
    2. AV node, SA node, bundle of His, left bundle branch, right bundle branch
    3. right bundle branch, left bundle branch, bundle of His, AV node, SA node
    4. SA node, AV node, bundle of His, right bundle branch, left bundle branch
    5. SA node, AV node, left bundle branch, right bundle branch, bundle of His
    1. Mitral, Tricuspid, Aortic, Pulmonic
    2. Tricuspid, Aortic, Pulmonic, MItral
    3. Pulmonic, Aortic, Tricuspid, Mitral
    4. Mitral, Pulmonic, Aortic, Tricuspid
    5. Aortic, Pulmonic, MItral, Tricuspid
    1. Phase 0 - calcium channel
    2. Phase 4 - sodium channel
    3. Phase 3 - potassium channel
    4. Phase 0 - sodium channel
    5. Phase 4 - potassium channel
    1. S4
    2. S1
    3. S2
    4. S3
    5. S5
    1. 50 year old postmenopausal woman with a laterally displaced apex.
    2. 35 year old male marathon runner right after exercising.
    3. 25 year old G1P0 woman at 20 weeks gestation.
    4. 5 year old child with asthma.
    5. 20 year old woman with an apex at the 5th intercostal space, mid-clavicular line.
    1. Concentric hypertrophy due to parallel duplication of sarcomeres.
    2. Eccentric hypertrophy due to duplication of sarcomeres in series.
    3. Concentric hypertrophy due to duplication of sarcomeres in series.
    4. Eccentric hypertrophy due to duplication of sarcomeres in parallel.
    5. Congenital septal hypertrophy.
    1. Venodilation
    2. Increased venous return
    3. Venoconstriction
    4. Vasodilation
    5. Vasoconstriction
    1. Venodilation
    2. Vasoconstriction
    3. Aortic stenosis
    4. Coarctation of the aorta
    5. Increased total peripheral resistance
    1. Phase II Valsava.
    2. Decreased thoracic pressure.
    3. Increased abdominal pressure.
    4. Deep inspiration.
    5. Passive leg elevation.
    1. Decreased stretch sensed by carotid baroreceptor and transmitted via the glossopharyngeal nerve.
    2. Increased stretch sensed by carotid baroreceptors and transmitted via the vagus nerve.
    3. Decreased stretch sensed by aortic baroreceptors and transmitted via the glossopharyngeal nerve.
    4. Increased stretch sensed by aortic baroreceptors and transmitted via the glossopharyngeal nerve.
    5. Decreased stretch sensed by the carotid baroreceptors and transmitted via the vagus nerve.
    1. Increased total peripheral resistance permitting a reversal of the right to left shunt.
    2. Increased venous return by venoconstriction of lower extremity vessels.
    3. Decreasing afterload in order to ease arterial resistance.
    4. Decreasing preload in order to assist volume overloaded state.
    5. Increasing preload to improve cardiac output.
    1. Blood pressure is approximately normal due to a balance between venoconstriction and arterial vasodilation.
    2. Blood pressure increases due to a an increase in arterial vasoconstriction and a lesser degree of venodilation.
    3. Blood pressure decreases due to global arterial and venous vasodilation.
    4. Blood pressure is approximately normal due to a balance between venodilation and arterial vasoconstriction.
    5. Blood pressure increases due to arterial and venous vasoconstriction.
    1. ...physiologic splitting of S2
    2. ...fixed splitting of S2
    3. ...widened splitting of S2
    4. ...paradoxical splitting of S2
    5. ...disappearance of S2 splitting
    1. Delayed right ventricular emptying.
    2. Delayed conduction through the left bundle branch.
    3. Dilation of the aortic root.
    4. Asymmetrical septal hypertrophy.
    5. Defect between heart chambers.
    1. Left bundle branch block.
    2. Pulmonic stenosis.
    3. Atrial Septal Defect.
    4. Ventricular Septal Defect.
    5. Aortic regurgitation.
    1. ...left to right shunt causing increase blood flow to the right side of the heart.
    2. ...right to left shunt causing increased blood flow to the left side of the heart.
    3. ...delay in conduction to the left bundle branch.
    4. ...increased total peripheral resistance causing a reversal of a left to right shunt.
    5. ...decreased venous return reducing the amount of right ventricular filling.
    1. Pulmonic stenosis.
    2. Aortic stenosis.
    3. Aortic regurgitation.
    4. Mitral stenosis.
    5. Mitral regurgitation.
    1. Upper right parasternal border, 2nd intercostal space.
    2. Left Midclavicular line, 5th intercostal space.
    3. Left parasternal border, 2nd intercostal space.
    4. Left parasternal border, 4th intercostal space.
    5. Left parasternal border, 5th intercostal space.
    1. Systolic murmur that increases with respiration heard best at the 2nd intercostal space, left parasternal border.
    2. Systolic murmur that decreases with inspiration heard best at the 2nd intercostal space, right parasternal border.
    3. Diastolic murmur that decreases with inspiration heard best at the 5th intercostal space, midclavicular line.
    4. Diastolic murmur that increases with inspiration heard best at the 4th intercostal space, left parasternal.
    5. Diastolic murmur that decreases with inspiration heard best at the 3rd intercostal space, left parasternal.
    1. Aortic regurgitation.
    2. Aortic stenosis.
    3. Tricuspid regurgitation.
    4. Mitral stenosis.
    5. Ventricular septal defect.
    1. Hypertrophic obstructive cardiomyopathy.
    2. Atrial septal defect.
    3. Mitral regurgitation.
    4. Pulmonic stenosis.
    5. Aortic regurgitation.
    1. Diastolic murmur heard best at the 3rd intercostal space, left parasternal.
    2. Systolic murmur heard best at the 5th intercostal space, midclavicular line.
    3. Holosystolic murmur heard best at the 5th intercostal space, midclavicular line.
    4. Systolic murmur heard best at the 3rd intercostal space, left parasternal.
    5. Machine-like murmur heard best at the 2nd intercostal space, right parasternal border.
    1. IV drug abuse associated endocarditis.
    2. Aortic root dilation associated with ankylosing spondylitis.
    3. Narrowing of the aortic valve due to calcium deposition.
    4. Congenital infection with rubella virus.
    5. Patency of the connection between the aorta and pulmonary artery.
    1. Standing up.
    2. Deep inspiration.
    3. Passive leg raise.
    4. Supine position.
    5. 2nd phase of Valsava.
    1. Cyanosis is improved due to reversal of the left to right shunt.
    2. Increased venous return leads to improved cardiac output.
    3. Decreased peripheral resistance decreases afterload and improves cardiac output.
    4. Longer time to fill ventricle improves oxygenation.
    5. Outflow tract obstruction is improved by increased ventricular pressure.

    Author of lecture Heart Sounds

     Carlo Raj, MD

    Carlo Raj, MD


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    Very well done.
    By Jonathan K. on 13. May 2017 for Heart Sounds

    The best thing about how Dr. Raj presents is that he continually asks questions and brings the topics together. Keep being awesome, Doc.