Character

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The character of the apex beat is assessed in terms of its dynamicity; duration, and whether the impulse is single, double, or triple.

If the apical impulse cannot be felt or seen, it stands to reason that one cannot assess its character. This may be because of both cardiac and extracardiac factors. In fact, in patients with thick chest walls, obese patients, and patients with chronic obstructive pulmonary disease where one does not expect to be able to feel the apical impulse, mere palpability alone may indicate cardiomegaly.

Dynamicity

The normal apical impulse is generally felt as a short and quick outward movement, which is usually barely visible but often better felt than seen. Once the impulse is felt, it becomes easier to see the movement of the palpating finger along with the underlying chest wall in contrast to the surrounding area of the chest wall. Unless this method is followed, mistakes are often made, confusing a palpable loud heart sound in the apical area as the apical impulse. Sometimes beginners describe such palpable sounds as "diffuse apex beat." This term should never be used to describe the apical impulse in any circumstance because it does not convey any useful information.

When the movement of the apical impulse is exaggerated with large amplitude as well as being rapid, then the impulse is described as "hyperdynamic." Placing a stethoscope head on the area of the impulse and observing its movement can easily confirm this feature. In contrast to the normal, hyperdynamic apical impulse can be easily seen without having to palpate. In very thin-chested young adults, exaggerated amplitude may be present, but this should not be confused with hyperdynamicity.

A hyperdynamic apical impulse implies "volume overload' state of the ventricle involved. This usually results from a large stroke volume being ejected with increased force and velocity because of Starling mechanism. A hyperdynamic left ventricular impulse therefore suggests conditions that are associated with increased diastolic volumes (24,25). The conditions that cause this may be systemic or cardiac. The systemic causes are usually associated with increased cardiac output such as seen in anemia, thyrotoxicosis, Paget's disease, pregnancy, beriberi, and arteriovenous fistulae. The cardiac causes are usually not accompanied by high cardiac outputs. These include mitral regurgitation, aortic regurgitation, ventricular septal defect, and aorto-pulmonary communications (e.g., persistent ductus arteriosus). In these conditions the left ventricle receives extra volume of blood during diastole in addition to the normal pulmonary venous return (Fig. 8). (See also Apex Videofiles 2 and 3 under Precordial Pulsations on the Companion CD.)

If the apical impulse is right ventricular and is hyperdynamic, then volume overload of the right ventricle must be considered as in tricuspid regurgitation, atrial septal defect, and pulmonary regurgitation.

Duration

The duration of the apical impulse (how long the outward movement lasts during systole) can only be assessed properly by simultaneous auscultation during palpation of the apex beat. By relating the time at which the apical impulse moves away from the palpating hand to the timing of the second heart sound is heard, one can assess whether the duration of the apical impulse is normal or prolonged (17,18,23,24). The apical

Mitral Regurgitation Wave
Fig. 8. Apexcardiogram (Apex) of a patient with severe mitral regurgitation with a hyperdynamic left ventricular apical impulse. Prominent rapid filling wave (RFW) in early diastole and a corresponding S3 recorded on the phonocardiogram together with the systolic murmur of mitral regurgitation.

impulse with a prolonged duration is termed "sustained." The term "heave" should never be used to describe the apical impulse because it conveys no clear-cut meaning and is interpreted differently by different observers.

Normal apical impulse rises rather quickly and reaches a peak at the time of the first heart sound and moves away rapidly from the palpating hand so that the second heart sound is heard long after the apex beat has disappeared. If an apical impulse is not palpable in the supine position, it is crucial to repeat the examination in the left lateral decubitus position. In our experience this does not affect the duration of the impulse (24). In fact, we recommend that the duration of the apical impulse be determined in this position in all patients.

When the impulse is felt to recede from the palpating hand as the second heart sound is being heard, then the duration is prolonged and the apical impulse is sustained. Sustained left ventricular thrust during the second half of systole has been noted to be associated with an increase in left ventricular mass and volume (7,30,31). In addition, sustained apical impulse has been known to be associated with significant left ventricular dysfunction (6,7,17,31).

The sustained duration of the apical impulse implies that the wall tension in the ventricle forming the apex (usually the left ventricle) is maintained at a high level for the greater part of systole (17). This can occur as a result of increased pressure or increased volume being maintained throughout systole. This is contrary to the general belief and

Sustained Apical Impulse

Fig. 9. (A) Apexcardiogram of a patient with aortic stenosis with a sustained apical impulse. The fall occurs beginning with the second heart sound (S2). A prominent atrial kick and a corresponding S4 are noted. Also, S3 was heard in this patient with some early signs of heart failure. (Opposite page) (B) Simultaneous recordings of electrocardiogram (ECG), phono- (Phono), and apexcardiograms (Apex), with its first derivative (DD/dt) in a patient with aortic stenosis. The recording of the left ventricular (LV) and aortic pressures show the significant systolic gradient because of the obstruction. Also shown are the LV outlines in diastole and systole depicting the hypertrophied LV with normal systolic decrease in LV size. Note the atrial kick and the sustained apical impulse with the downstroke starting at the timing of S2. (C) Simultaneous recordings of electrocardiogram (ECG), phonocardiogram (Phono), and apexcardio-gram (Apex) and left ventricular (LV) pressure in a patient with coronary artery disease and left ventricular dysfunction. LV outlines in diastole and systole depict the lack of decrease in LV dimensions reflecting significant LV dysfunction and decreased EF. Apex recording shows sustained duration with the downstroke beginning close to S2. (Continued on page 128)

Fig. 9. (A) Apexcardiogram of a patient with aortic stenosis with a sustained apical impulse. The fall occurs beginning with the second heart sound (S2). A prominent atrial kick and a corresponding S4 are noted. Also, S3 was heard in this patient with some early signs of heart failure. (Opposite page) (B) Simultaneous recordings of electrocardiogram (ECG), phono- (Phono), and apexcardiograms (Apex), with its first derivative (DD/dt) in a patient with aortic stenosis. The recording of the left ventricular (LV) and aortic pressures show the significant systolic gradient because of the obstruction. Also shown are the LV outlines in diastole and systole depicting the hypertrophied LV with normal systolic decrease in LV size. Note the atrial kick and the sustained apical impulse with the downstroke starting at the timing of S2. (C) Simultaneous recordings of electrocardiogram (ECG), phonocardiogram (Phono), and apexcardio-gram (Apex) and left ventricular (LV) pressure in a patient with coronary artery disease and left ventricular dysfunction. LV outlines in diastole and systole depict the lack of decrease in LV dimensions reflecting significant LV dysfunction and decreased EF. Apex recording shows sustained duration with the downstroke beginning close to S2. (Continued on page 128)

teaching that sustained impulse results from a hypertrophied ventricle (18,22,23,25). If one relates wall tension according to Lame's modification of Laplace's formula, hypertrophy, if anything, should help normalize increased wall tension caused by either pressure or volume increase during systole. While the increased wall tension is a powerful stimulus for hypertrophy to occur, sometimes such hypertrophy may not fully normalize the wall tension.

The wall tension may be kept at a high level during systole by increased intraventricular systolic pressure. This is encountered in patients with significant outflow obstruction (e.g., aortic stenosis) or severe systemic hypertension. This can occur even when the ejection fraction (EF; the percentage of the diastolic ventricular volume that the ventricle ejects with each systole) is normal. The normal left ventricle ejects at least 60% of its contents with each systole. In other words, the normal EF is about 60% in these patients (Fig. 9A,B). Because there is increased impedance to ejection in such cases, the ventricle takes longer to eject its volume as opposed to normal, when most of the volume is ejected by the first third of systole.

Diagram Cardiac Physical Exam

Fig. 9. (Continued) (D) Sustained apex in a patient with ischemic heart disease and significant left ventricular dysfunction.

Fig. 9. (Continued) (D) Sustained apex in a patient with ischemic heart disease and significant left ventricular dysfunction.

In the absence of significant outflow obstruction and/or severe hypertension (systolic pressures >180 mmHg.), a sustained apical impulse would imply the second important cause of prolonged duration of elevated wall tension, which would result from poor systolic emptying. This is seen for instance in patients with left ventricular dysfunction (Grade III with EF of 30-49% and Grade IV with EF of <30%) (Fig. 9C,D) (17). The most important corollary of this is that a nonsustained apical impulse implies normal left ventricular ejection fraction (17).(See Apex Videofiles 3 and 4 under Precordial Pulsations on the Companion CD.)

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  • Calimero Panicucci
    WHAT IS DURATION OF APICAL IMPULSE?
    2 months ago

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