S1 (first sound) is the closure of the mitral and tricuspid valves. Heard best at the apex, but is identified in the whole chest area. Identified as noise that begins in systole, at the end of diastole is longer. When there is tachycardia, diastole is shortened and is similar to the duration of systole, in these cases, it is felt concomitantly the cardiac apex or a peripheral pulse since S 1 coincides with the onset of beating. Usually noise is heard as a single, but sometimes split is perceived, especially in the tricuspid focus on deep inspiration. At the apex, S 1 is heard more intense than S 2, but instead at the base of the heart, S 2 is heard louder. Variations that can occur are:
- S1 more intense: Tachycardia, cardiac conditions associated with high (eg, anemia, exercise, hyperthyroidism), mitral stenosis.
- S1 less intense: Atrioventricular block first degree (the leaflets of the valves have had time to go back after atrial contraction), mitral regurgitation, heart disease associated with decreased myocardial contractility (eg, congestive heart failure)
- S1 varies in intensity: Arrhythmias such as atrial fibrillation or complete atrioventricular block (at the time of occurring each systole, the leaflets are in varying degrees of openness by the dissociation between the activity of the atria and ventricles)
- S1 split: usually listening could slightly split in the lower left sternal border (tricuspid component is weaker), the split is unusual in situations like complete blockage of the right branch and premature ventricular contractions.
S2 (second sound) is caused by aortic valve closure (A 2) and pulmonary (P 2). The aortic component (A 2) is stronger and is heard throughout the precordium, since the 2 nd right parasternal area to the apex. The pulmonary component (P 2) is weaker and, under normal conditions, is heard in the 2 nd or 3 rd left parasternal space, can be heard at the apex or aortic area.
Variations of the second sound is found in the following situations:
- A 2 more intense: in hypertension.
- A 2 less intense or not heard: In aortic stenosis, aortic insufficiency or sharp, calcified aortic leaflets; disorders associated with lower transmission of heart sounds (obesity, emphysema, cardiac tamponade), lower myocardial contractility (cardiogenic shock).
- P 2 more intense (becoming of equal or greater intensity than A 2): pulmonary hypertension. When you hear the second sound split at the apex or second right parasternal space, P 2 is pronounced.
- P 2 less intense or not heard, in severe stenosis of the pulmonary valve. Heard weak conditions under which transmit less noise (obesity, emphysema).
Physiological splitting of the second sound: On expiration, A 2 and P 2 are heard usually forming a single noise on inspiration, P 2 is delayed (due to increased arrival of the right heart blood) and there is a splitting of second sound . Is heard in the 2 nd or 3 rd left parasternal space. At the apex and aortic area only heard the aortic component (A 2).
Fixed splitting of second sound: When two components are heard with a separation that does not vary with breathing. It is located in the atrial septal defect with left to right shunt and increased blood flow through the pulmonary valve.
Wide splitting of the second sound: (with some variation in inspiration and expiration, but always present throughout the respiratory cycle). This may be due to delayed closure of the pulmonary valve (eg, pulmonary stenosis, complete blockage of the right branch) or an earlier closure of the aortic valve (eg, mitral insufficiency).
Paradoxical or reversed splitting of second sound: Unlike the previous split, in this case the aortic component (A 2) is delayed and occurs after P 2 at the end of expiration. During inspiration, the splitting disappears and the normal delay that occurs in P 2 and A 2 that closes a little earlier. Seen in severe aortic stenosis and left bundle branch block.
S3 (third sound) is related to the rapid filling of the ventricles (ventricular passive filling phase) after they have opened the atrioventricular valves, is caused by distention of the ventricular walls. Must be differentiated from an initial noise and a split opening snap (keep in mind that mitral or tricuspid stenosis there is no third sound by limiting the flow). Low tone is heard best with the bell of the stethoscope applied with gentle pressure. Where it originates from the left ventricle is best heard at the apex, left semi-lateral decubitus; if it originates from the right ventricle should be sought in the lower left sternal border with the patient supine and with the inspiration may increase. Boxes found in heart failure and mitral or tricuspid regurgitation. In these cases, especially if associated with tachycardia, acquires a gallop rhythm. Can be found in physiological conditions many children, young adults and in the third trimester of pregnancy.
S4 (fourth sound) is due to the contraction of the atrium to the ventricle emptied into a relaxed (active ventricular filling phase) is related to vibrations of the valves, the papillary muscles and ventricular walls. Occurs at the end of diastole, just prior to S 1. Low tone is heard best with the bell of the stethoscope. When it originates in the left heart can be heard at the apex and left semi-lateral decubitus found in hypertension, aortic stenosis, hypertrophic cardiomyopathy, coronary artery disease. If it originates from the right heart, which is less common, is heard in the lower left sternal border and increases with inspiration and is found in pulmonary hypertension and pulmonary valve stenosis. A distinction should be a split first sound. Along with S 1 and S 2, can give a gallop rhythm, if it coexists with S 3, a gallop may be heard four times, if there is tachycardia, S 3 and S 4 can melt and produce a summation gallop. Occasionally you can hear a S4 in normal conditions or in older athletes. If an atrial fibrillation, you can not find a room noise.
Opening snap: Is due to the opening of an atrioventricular valve and are thick. It is more common to find mitral stenosis. Tone is high and occurs in early diastole, after the second sound. Is heard just medial to the apex and lower left sternal border, if very intense radiating to the apex and the lung area. It is often followed by a decrescendo murmur.
Click systolic, aortic, pulmonary or mitral valve prolapse:
- Aortic ejection click, is loud and is heard with the diaphragm of the stethoscope. You hear both the base of the heart as the apex (it may even be more intense in the apex). In general, does not vary with breathing. Can be found in aortic valve stenosis, bicuspid valve, dilation of the aorta.
- Pulmonary ejection click, is heard in the 2 nd or 3 rd right parasternal space. It is loud and can be confusing to a first noise in this location. Its intensity decreases with inspiration. Can be found in pulmonary valve stenosis, pulmonary hypertension or pulmonary artery dilation.
- Click meso or systolic, is due to a veil prolapse of the mitral valve (usually later). It is more common in women. Heard best at the apex or lower left parasternal edge. It is loud and is heard with the diaphragm of the stethoscope. Usually follow a regurgitant systolic murmur in crescendo, until the second sound.
Pericardial Rub: They are harsh noises that are due to rubbing of the inflamed pericardium sheets and overlap with normal sounds. It auscultation with the patient in expiratory apnea, sitting up and leaning forward. It is recommended to apply some pressure with the stethoscope. The sounds can be auscultated in systole and diastole, when it is located only in systole can be confused with a murmur. The location is variable, but are best heard in the 3 rd intercostal space to the left of the sternum. Could be felt a thrill
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