Student’s Corner-3

Explanation by Prof. Patnaik

With each ventricular systole the left lower costal cartilages along with the attached part of sternum get elevated due to the hypertrophied and dilated right ventricle. The inspection and palpation of this phenomenon in supine position has become a standard method of clinical cardiac evaluation.1 2 Appreciation of this lift/heave at the left parasternal area is not as precise as the cardiac apex3 however, clinicians have learned to roughly quantify the right ventricular systolic pressure and volume changes.

It is most conveniently graded (All India Institute of Medical Sciences [AIIMS] gradation) as follows:

• 1/3 (Grade 1): visible but not palpable

• 2/3 (Grade 2): visible and palpable but obliterable

• 3/3 (Grade 3): visible and palpable but not obliterable

In the presence of significant right ventricular pressure overload the palpation of the left parasternal area will reveal a sustained left parasternal lift.4 5 There may be associated prominent “a” wave in jugular venous pressure (JVP) and abnormal epigastric and subxiphoid pulsations. Common causes of raised right ventricle (RV) pressure are pulmonary hypertension and severe pulmonary stenosis. In RV volume overloaded states, the left parasternal impulse is appreciable but not sustained. Atrial septal defect (ASD) with significant left to right shunt can have an associated tricuspid mid-diastolic flow murmur. The ASD or severe tricuspid or pulmonary regurgitation cause RV volume overload.

Large left atrial enlargement in severe mitral regurgitation sometimes produces left parasternal lift but it is mostly confined to late systole. Similarly, a dilated left ventricle (LV) that is rotated counterclockwise in severe AR can also cause parasternal lift. In children and thin adults, a parasternal heave (PSH)–like chest motion may be appreciated without any heart disease.

Explanation by Prof. Dayasagar Rao

Parasternal Pulsations (Left)—Clinical Implications

In situs solitus state the most anterior structure of the heart is the right ventricle which is just below the anterior chest wall.

In patients with RV volume overload like ostium secundum ASD with large L–R shunt (and no pulmonary hypertension [PH]) or low pressure tricuspid regurgitation (TR) there will be vigorous pulsation in intercostal spaces (3rd, 4th, and 5th) of left parasternal region consequent to dilation of RV. These pulsations are present over RV inflow (5th space) and RV outflow (3rd and 4th interspace) but no significant, sustained lift of precordium.

In some clinical situations RV outflow pulsations without inflow pulsation are seen, classically in Ebstein’s anomaly of tricuspid valve (TV) where the inflow of RV is atrialized and in patients with RV and in endomyocardial fibrosis (EMF) where inflow is fibrosed plastering the posterior leaflet to TV.

In parasternal heave, unlike in the parasternal pulsation, precordium is lifted above the chest wall and sustained for significant time (>50% systole) and is characteristically seen in pressure overloaded RV, like in pulmonary hypertension and right ventricular outflow tract (RVOT) obstruction. The parasternal heave is graded (arbitrarily) as follows:.

• Grade I: visible, barely palpable

• Grade II: visible, palpable, but can be obliterated by counter-pressure of hand

• Grade III: parasternal heave that cannot be obliterated by counter-pressure (mild)

Occasionally in severe mitral regurgitation systolic expansile impulse of LA can be felt over left parasternal area even though LA is the most posterior structure (parasternal heave is a transmitted pulsation). This LA lift is better palpated in the upper parasternal area and occurs in later part of systole in contrast to early systolic lift of RV pressure overload.

Explanation by Prof. Patnaik

At the end of ejection of blood, that is, when the pressures in the ventricle and the great artery crossover), the semilunar valves are expected to close promptly. In reality, this mechanical event occurs with a slight time delay at point called the incisura. The hangout time is the interval between the end of ventricular ejection (when the ventricular pressure crosses over the pressure in the respective great artery) and the actual closure of the semilunar valve (Fig. 1). This term was coined by Shaver and associates who were convinced that it represents impedance of the vasculature. The hangout interval is longer in the pulmonary circulation (60–70 milliseconds) than in the systemic side (15–30 milliseconds). The compliance of aorta and the pulmonary artery also influence the hangout interval.6

Close

Fig. 1 Hangout interval in pulmonary circulation.

Export to PPT

Fig. 1 Hangout interval in pulmonary circulation.

Explanation by Prof. Dayasagar Rao

Hangout interval is time interval between the end of ventricular ejection and the closure of the semilunar valve, during which time, there is transient flow reversal in great vessels (aorta/pulmonary artery) facilitating closure of semilunar valves.

Timing of flow reversal is influenced by two factors—capacitance of circulation and resistance offered to forward flow (PVR–SVR) and compliance of great vessels. Normally pulmonary vascular resistance in much lower than systemic vascular resistance (PVR/SVR ratio: 0.25 or less), and PA is more compliant than aorta, both of which combine to have longer hangout interval (60–80 milliseconds) on right side, compared with left side (15–30 milliseconds). This difference in hangout interval contributes to degree of splitting of the second heart sound (A2–P2 intervals) as the electromechanical systole of both ventricles is nearly equal. Other hemodynamic factors that influence the A2–P2 interval are duration and difference in electromechanical systole of ventricles and ventricular systolic function.

In PH, the A2–P2 interval is short because hangout interval on right side is short due to increased PVR. The wide A2–P2 interval in idiopathic dilation of pulmonary artery (IDPA) is due to increase of hangout interval on right side, consequent to dilated and compliant main pulmonary artery (MPA). Persistent wide split second sound in ASD even after closure is explained by dilated PA causing increased hangout interval on right side.