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HANDBOOK OF PHYSIOLOGY 



CIRCULATION I 



effect, but in others there will be an opposite effect 

 which may tend to cancel out or even overbalance 

 the primary effect. For example, in the effect of the 

 decrease in vascular resistance on murmurs produced 

 at the semilunar \alve, the primary effect of lowering 

 on-going resistance and great vessel pressure tended 

 to increase the systolic murmur and decrease the 

 diastolic murmur. The compensatory phenomenon of 

 an increased stroke output acts in the same direction 

 for the systolic murmur and, if anything, tends to 

 accentuate its increase. However, so far as the diastolic 

 murmur is concerned an increased stroke output 

 makes more blood available for regiu'gitation, and 

 this tends to act in the opposite direction on murmur 

 intensity. 



When the action of pharmacological agents is con- 

 sidered in reference to shunt murmurs, the important 

 consideration is the effect of the agent on the balance 

 between systemic and pulmonary vascular resistance. 

 The direction and magnitude of the shunt depends on 

 systemic vascular resistance, pulmonary vascular re- 

 sistance, and the resistance imposed by the communi- 

 cation itself. Since this last is constant in this situation 

 any alteration in the vascular resistance of either bed 

 will result in a change in shunt flow. From this con- 

 sideration one can reasonably predict the effects. For 

 left-to-right shunts an increase in systemic resistance 

 and/or a decrease in pulmonary resistance will in- 

 crease the shunt flow and the murmur. Conversely, a 

 decrease in systemic resistance and/or an increase in 

 pulmonary resistance will decrease murmur intensity. 

 For example, mephentermine, which increases pri- 

 marily the systemic resistance, increases the intensity 

 of the murmur of patent ductus arteriosus. Such an 

 effect is of greatest clinical assistance when a part of 

 the murmur is inaudible on the thorax. Here the 

 increase in intensity produced may raise this in- 

 audible segment to the level of audibility thus con- 

 verting it from an "atypical" murmur to a "typical" 

 murmur. We have discussed above the observation 

 that partial balloon occlusion of the pulmonary artery 

 could be made to abolish the murmur of ventricular 

 septal defect. Alterations in vascular resistances in the 

 presence of right-to-left shunts have been carried out 

 mainly to demonstrate the effect upon arterial oxygen 

 saturation (i6). The effect on the acoustic events has 

 been less well studied. However, the observations on 

 left-to-right shunts suggest that one might be able to 

 predict the effect on the murmurs due to these shunts. 

 This deserves careful analysis, since often such mur- 

 murs as are present may be due to relative changes in 



flow through normal channels rather than flow 

 through the shunt itself. 



Occasionalh', agents employed primarily to change 

 vascular resistance will produce side effects that may 

 be used to obtain information on the acoustic events. 

 For example, certain agents at times will produce 

 premature ventricular contractions. These may also 

 occur spontaneously. Although numbers of these can 

 be considered troublesome, an occasional one can be 

 helpful. Consider the effect of a premature \entricular 

 contraction on the intravascular pressures. Due mainly 

 to the smaller diastolic volume, but perhaps to other 

 factors as well, the systolic pressure produced by the 

 premature ventricular contraction is less than normal. 

 The great vessel pressure will also be less, since the 

 energy supplied bv the ventricle is less. The atrial 

 pressure during the premature systole will rise, since 

 at the beginning of the premature contraction the 

 atrium was left with a more than normal volume of 

 blood. Consider now the effect that this would ha\'e 

 on systolic murmurs of valvular origin. The pre- 

 mature contraction would decrease the gradient of 

 pressure across the semilunar valve, and since ven- 

 tricular pressure is lower and atrial pressure is liigher, 

 the .systolic gradient across the atrio\entricuIar valve 

 would also be decreased. Both would result in a 

 decrease in murmur intensity. However, since the 

 ventricular pressure must rise to a reasonably high 

 level to open the semilunar valve, the effect on the 

 gradient across the semilunar valve would be expected 

 to be much greater than that across the atrioven- 

 tricular valve (fig. lo). The result is that, whereas the 

 intensity of both murmurs will move in the direction 

 of a decrease, the decrease is much greater for the 

 semilunar murmur than for the atrioventricular 

 murmur. So that on auscultation premature ven- 

 tricular contractions can be expected to produce quite 

 easily recognizable changes in the intensity of semi- 

 lunar ejection type systolic murmurs, and less readily 

 recognizable changes in atrioventricular regurgitant 

 type systolic murmurs. 



Premature ventricular contractions can also be used 

 to help identif\- the site of origin of heart sounds. This 

 has been di.scussed by Hartman (37) and deserves 

 further application. The basis for the application to 

 sound identification resides in the fact that if the 

 ventricle from which the premature contraction origi- 

 nates can be identified (e.g., from the electrocardio- 

 gram), then advantage can be taken of the fact that 

 the opposite ventricle will be delayed in the onset of 

 its mechanical activitw Bv combining sound re- 



