Auscultation

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Heart Sounds:

Heart sounds and implications of these sounds

1) Normal heart sounds: These consist of two sharp sounds, S1 and S2, which diffreciate systole from diastole and no other significant sounds will be heard. A systole occurs when the ventricles fill with blood and the heart contracts. The sudden closure of the tricuspid valves and AV valves is caused by a decrease in pressure in the atria and a sharp increase in the intraventricular pressure which exceeds the pressure of the atria. This is the S1 sound. The ventricles continue to contract throughout systole forcing blood through the aortic and pulmonary semilunar valves. S2 is formed at the end of systole when the ventricles begin to relax and the pressure in the aorta and pulmonary artery begin to exceed the intraventricular pressure. When this happens there is a slight backflow of blood into the heart which causes the semilunar valves to snap shut, producing S2. These two sounds are to be considered single and instantaneous, indicating a normal healthy heart.

2) Aortic Stenosis: This is a systolic murmur that indicates a physiological defect. The word stenosis refers to the abnormal turbulent flow of blood due to a narrow damaged blood vessel. Stenosis in the aorta results in this murmur sound which occurs between S1 and S2. In addition to this other sounds may be heard such as S4 which results from the heavy work required by the left ventricle to pump the blood though the stenotic valve. Also because S2 is caused by the sudden closing of the aortic valve ,a weaken poorly functioning stenotic valve may cause S2 to be very discreet or even inaudible. This murmur is usually best heard over the aortic area.it is important to note that this is a sharp murmur with notable start and finishing points within a systole. We can usually tell how serious the stenosis is by listening to the timing of the murmur. An early peaking murmur is usually a less serious case of stenosis , while a late peaking murmur indicates more serious stenosis, because the stenotic valve is quite weak and the ventricle takes a lot more time to build the strength to pump the blood out of the heart.
3) Mitral valve prolapse: This sound is thought to e caused by the failure of the papillary muscles and/or chordae to maintain tension during the late systole. As the left ventricle decreases in size the papillary muscles and/or the chordae don’t tether the valve resulting in the mitral valve remaining slightly open and a slight regurgitation period into the atium. The sound is formed during systole just when the valve prolapses and consists of a mid-systolic click just after a normal S1 sound. This sound alone is enough for diagnosis, however MVP is often followed by a murmur best heard at the apex of the heart. In addition to this ,it can be enhanced or decreased by certain maneuvers. Standing the patient up will decrease the volume of the left ventricle and cause the MVP to occur more frequently. If the patients squats the opposite effect is seen ,the ventricle volume is increased and more tension is put on the papillary muscles and chordae which help close the valve. This condition is common in young adult women and causes symptoms of light-headednesss, anxiety and palpitation attacks. Symptoms are usually mild but patients with evidence of the MVP should be given antibiotic prophylaxis when undergoing any invasive procedures to help avoid the risk of bacterial endocarditis.
4) Pulmonary Stenosis: This is similar to aortic stenosis in that it takes longer for the right ventricle to pump the blood out of the heart through the stenotic pulmonary valve. This results in a delay in the valve closing and causes a split in S2. This splitting of S2 is heard because the aortic valve shuts before the stenotic pulmonary valve at the end of the systole. T he splitting is best heard in the pulmonic area, the second intercostal space along the left sternal border. Maneuvers such as a heavy inspiration can increase the intensity of this murmur
Heart sounds and implications of these sounds

References:

http://www.med.ucla.edu/wilkes/intro.html