Cardiac Conditions Associated with Sudden Death

This course will help you identify heart sounds associated with conditions leading to sudden death. Before taking this course you should have completed the courses concerning heart sounds and murmurs and be comfortable with the material.

Using this course

Each lesson in this course includes text describing the heart or lung abnormality and a simulated torso indicating the stethoscope chestpiece location. An audio recording of the sound is provided. Phonocardiograms or waveforms are included with each lesson. These waveforms can be a highly useful aid in learning to recognize heart murmurs. In addition, short videos clips illustrate the heart's motion for each abnormality. These animations indicate the origin of each murmur. Blood flow is also animated. For lung sounds, the source (location) of the sound can be revealed.

After completing a lesson, use the lesson table of contents to navigate to another lesson.

When all lessons have been completed, we recommend using the auscultation practice exercises or quiz. In order to gain a certificate of achievement, please complete the course lessons and practice drill during one session. Most users complete the course in 30-45 minutes.

Click To Begin Training Module

Lessons

Lesson #1: Hypertrophic Cardiomyopathy - C30

An early peaking, harsh diamond shaped systolic murmur starts at the beginning of systole and ends well before the second heart sound. A fourth heart sound gallop is also present in diastole as you can readily see on the wave form tab. S1 is increased due to a hyperdynamic left ventricle. S2 is single. On the anatomy video you can see that the contraction of the left ventricle is strong and occurs in a reduced amount of time. Anatomically, the septal wall is very much thicker than the rest of the ventricle but this is not shown in the animation. The strong contraction of the left ventricle causes the anterior leaflet to be sucked into the ventricle, blocking the flow into the aorta and causing an aortic murmur. At the same time turbulent flow from the left ventricle to the left atrium causes a second murmur. Since the two murmurs occur at the same time you hear a single murmur. You can hear the difference between the two murmurs by moving the stethoscope head the aortic to the mitral valve area. First, you will hear the diamond shaped aortic murmur and later the rectangular pansystolic murmur.

Lesson #2: Aortic Stenosis - Severe #2 C30

In Severe Aortic Stenosis there is a diamond shaped systolic murmur which lasts throughout systole. The murmur is loud and higher pitched than the murmur of mild aortic stenosis. It is caused by calcification of the aortic valve leaflets. There is a fourth heart sound heard in late diastole (just before the first heart sound). This is caused by the increased left ventricular wall thickness and stiffness. S1 is normal. S2 is louder than normal. In fact, you are hearing only the accentuated pulmonic component of S2 due to heart failure on the left side. The aortic ejection click heard in mild cases of valvular aortic stenosis is gone. In the anatomy video you can see the greatly thickened left ventricular wall and the almost totally immobile aortic leaflets.

Lesson #3: Arrhythmogenic RV Dysplasia

This is an example of Arrhythmogenic RV Dysplasia heard at the tricuspid area. This is a familial abnormality which is associated with replacement of the right ventricle with fibro-fatty tissue. In this condition there is marked enlargement of the right ventricle with decreased vigor of contraction. The first and second heart sounds are normal. There is a pansystolic rectangular murmur caused by regurgitant turbulent flow from the right ventricle into the right ventricle.

Lesson #4: Mitral Valve Prolapse (Click - Late Systolic Murmur) C30

There is a medium-pitched diamond shaped murmur which begins right after a mid systolic click and runs to the end of systole. The intensity of the murmur increases and its starting point begins earlier in systole as left ventricular volume decreases (going from supine to standing). The intensity of the murmur and its starting position move later in systole as the volume increases (by raising the legs while in the supine position). The mid-systolic click also moves in tandem with the murmur. On the anatomy video you can see that the murmur is caused by the prolapse of the posterior mitral valve leaflet. The murmur is represented by turbulent flow from the left ventricle into the left atrium.

Lesson #5: Myocarditis

This is a simulation of Myocarditis taken at the apex. 1. The first heart sound is softer than normal because of decreased function of the left ventricle. 2. The second heart sound is normal at the mitral area. 3. There is a third heart sound caused by the failure of the left ventricle. 4. A rectangular, medium-pitched murmur of mild mitral regurgitation is caused by the incomplete closure of the mitral valve leaflets. In the anatomy video you can see the enlarged left ventricle with decreased vigor of contraction. You can see the regurgitant turbulent flow from the left ventricle into the left atrium which is responsible for the murmur. Myocarditis is often the result of a viral infection of the myocardium.

Lesson #6: Commotio Cordis

This is an example of commotio cordis as heard at the mitral valve area. This condition is caused by blunt force trauma to the chest such as a baseball batter being hit in the chest by a pitch. Severe damage to the right and left ventricles and mitral and tricuspid valves may result. In the example we are showing, the trauma is limited to the mitral valve leaflets. Rupture of a chordae tendinae has occurred resulting in a systolic murmur. The first half of the murmur is rectangular. It is followed by a decrescendo late systolic component. This is caused by rapid filling of the left atrium due to torrential mitral regurgitation.

Lesson #7: Ebstein's Anomaly - C30

This is an example of Ebstein's Anomaly as heard at the tricuspid area. The first heart sound is increased due to thickening of the tricuspid valve leaflets. The second heart sound is normal. A rectangular murmur of tricuspid regurgitation fills all of systole. An opening snap occurs 100 milliseconds into diastole followed by a decrescendo-crescendo murmur of mitral stenosis. These findings are all a manifestation of downward displacement of the tricuspid valve into the right ventricle In the anatomy video you can see the enlarged right atrium and the small right ventricle. The upward plume from the right ventricle to the right atrium represents the systolic murmur. The downward plume from the right atrium to the right ventricle represents the diastolic murmur. This abnormality is congenital in nature.

Authors and Reviewers

Heart sounds by Dr. Jonathan Keroes, MD and David Lieberman, Developer, Virtual Cardiac Patient.
Lung sounds provided by Diane Wrigley, PA
Heart sounds mentorship by W. Proctor Harvey, MD>
Reviewed by Dr. Barbara Erickson, PhD, RN, CCRN.
Last Update: 12/14/2022

Sources

Heart Sounds and Murmurs Across the Lifespan (with CD) by Dr Barbara Ann Erickson
Publisher: Mosby
ISBN-10: 0323020453; ISBN-13: 978-0323020459
Heart Sounds and Murmurs: A Practical Guide with Audio CD-ROM 3rd Edition
Elsevier-Health Sciences Division
Barbara A. Erickson, PhD, RN, CCRN
Heart Sounds Made Easy with CD-ROM: (with CD-ROM) 2nd Edition
Anthony P. Salmon
ISBN-13: 978-0443069079
NCBI Review of Heart Sounds and Murmurs: A Practical Guide
The Virtual Cardiac Patient: A Multimedia Guide to Heart Sounds And Murmurs Jonathan Keroes, David Lieberman
Publisher: Lippincott Williams & Wilkin)
ISBN-10: 0781784425; ISBN-13: 978-0781784429
Ventricular Function Curves in the Exercising Dog
JONATHAN KEROES , ROGER R. ECKER , and ELLIOT RAPAPORT
Circulation Research, Vol. 25, No. 5
Electrocardiographic changes associated with ritodrine-induced maternal tachycardia and hypokalemia American Journal of Obstetrics Gynecology, VOLUME 154, ISSUE 4, P921-923, APRIL 01, 1986
Susan K Hendricks, MD, Jonathan Keroes, MD, Michael Katz, MD
A Multimedia Guide to Heart Sounds and Murmurs
January 2007 JAMA The Journal of the American Medical Association 297(2):217-218
DOI:10.1001/jama.297.2.217. M. Saleem Seyal, MD, Reviewer
Clinical Heart Disease W Proctor Harvey, MD