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Table 3.1 addresses causes of ↑ and ↓ pulses.
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See the Child and Adolescent Medicine chapter for a discussion of heart murmurs. Sites for auscultation of the heart are shown in Figure 3.1.
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S1: Closure of the mitral and tricuspid valves. ↓ with LV systolic dysfunction and mitral regurgitation. See Figure 3.2 for the relation of heart sounds to other parts of the cardiac cycle.
S2: Closure of the aortic and pulmonary valves. Normally, the aortic component (A2) precedes the pulmonic component (P2).
Physiologic splitting: ↑ time between A2 and P2 with inspiration. P2 is delayed during inspiration as negative intrathoracic pressure pulls more blood volume into right side of the heart. Normalizes when the breath is held.
Wide splitting: Early closing of A2 or delayed P2. Causes include right bundle branch block (RBBB), pulmonic stenosis, pulmonary embolism (PE), or pulmonary hypertension (HTN).
Paradoxical splitting: A2 comes after P2 so ↑ splitting with expiration. Causes include aortic stenosis (AS), left bundle branch block (LBBB), use of a pacemaker, and left ventricular (LV) systolic dysfunction.
Fixed splitting: Time between A2 and P2 does not vary with breath. Caused by atrial septal defect (ASD).
S3: Low-pitched sound after S2 as ↑ blood volume flows into dilated ventricle. Best heard with the bell at the apex. Suggests ventricular enlargement and LV systolic dysfunction such as heart failure (HF) and dilated cardiomyopathy.
S4: Low-pitched sound preceding S1 as atrial contraction forces blood into a stiff ventricle.
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The key elements of an ECG are shown in Figure 3.3.
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