Patent ductus arteriosus physical examination: Difference between revisions

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'''Assistant Editor-In-Chief:''' [[Kristin Feeney|Kristin Feeney, B.S.]] [[mailto:kfeeney@perfuse.org]]
'''Assistant Editor-In-Chief:''' [[Kristin Feeney|Kristin Feeney, B.S.]] [[mailto:kfeeney@perfuse.org]]


==Physical rxamination==
==Physical Examination==
Patients with a '''small PDA''' may have no symptoms. A '''large PDA''' can cause [[heart failure]] similar to a large [[ventricular septal defect]] [[VSD]],  wide [[pulse pressure]], and bounding arterial pulses. An apical heave may be observed, and a thrill may be heard at the second left intercostal space. The characteristic [[continuous murmur]] has been described as a '''machinery'''  or '''to and fro murmur''' heard in both [[systole]] and [[diastole]]. It can be less prominent or not heard at all in diastole in infants or in the patients with increased [[PVR]].<ref>Giuliani et al, Cardiology: Fundamentals and Practice, Second Edition, Mosby Year Book, Boston, 1991, pp. 1653-1663.</ref>  
Patients with a '''small PDA''' may have no symptoms. A '''large PDA''' can cause [[heart failure]] similar to a large [[ventricular septal defect]] [[VSD]],  wide [[pulse pressure]], and bounding arterial pulses. An apical heave may be observed, and a thrill may be heard at the second left intercostal space. The characteristic [[continuous murmur]] has been described as a '''machinery'''  or '''to and fro murmur''' heard in both [[systole]] and [[diastole]]. It can be less prominent or not heard at all in diastole in infants or in the patients with increased [[PVR]].<ref>Giuliani et al, Cardiology: Fundamentals and Practice, Second Edition, Mosby Year Book, Boston, 1991, pp. 1653-1663.</ref>  



Revision as of 17:49, 14 July 2011

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Associate Editor-In-Chief:Cafer Zorkun, M.D., Ph.D. [2]; Keri Shafer, M.D. [3] Priyamvada Singh, MBBS [[4]]

Assistant Editor-In-Chief: Kristin Feeney, B.S. [[5]]

Physical Examination

Patients with a small PDA may have no symptoms. A large PDA can cause heart failure similar to a large ventricular septal defect VSD, wide pulse pressure, and bounding arterial pulses. An apical heave may be observed, and a thrill may be heard at the second left intercostal space. The characteristic continuous murmur has been described as a machinery or to and fro murmur heard in both systole and diastole. It can be less prominent or not heard at all in diastole in infants or in the patients with increased PVR.[1]

In adults with a large PDA, Eisenmenger's Syndrome may develop with presents as cyanosis due to a right-to-left shunt. The inversion of the shunt is produced because of the progressive increase in pulmonary vascular resistance. Severe pulmonary vascular resistance results in reversal of flow through the ductus, and unoxygenated blood is shunted to the descending aorta, and the toes, but not the fingers, become cyanotic and clubbed, a finding termed differential cyanosis.

Small PDA

Rarely a continuous thrill in the first or second intercostal space. A continuous murmur is present underneath the left clavicle, soft and high in frequency. At the beginning of systole, the flow into the PA is chiefly from the RV rather than through the duct, through the course of systole the contribution from the ductus increases progressively, and then during diastole the flow is through the ductus alone and vanishes as the gradient decreases. During the neonatal period, the PVR is high, and flow across the ductus is reduced.

Medium-sized PDA

As a result of the runoff from the aorta, there are bounding pulses, and the pulse pressure widens. A continuous thrill may be present in the first or second left intercostal space. The continuous murmur is louder and more machinery murmur than for the small PDA. Due to increased left sided return, there is a middiastolic flow murmur and sometimes a third heart sound.

Large PDAs

If there is no reduction in the size of ductus, after age 2, progressive obstructive disease develops in these patients. Usually present in adolescence or adulthood with the physical findings of pulmonary hypertension associated with some right-to-left shunt. There is preferential cyanosis and clubbing of the lower extremities. The fingers of the left hand may be mildly cyanosed and clubbed. The JVP may be elevated due to RV failure. Prominent a wave due to diminished RV compliance and RVH. Loud pulmonic component of the second heart sound. As the pulmonary hypertension increases, left to right flow across the duct decreases and there is no audible murmur. A murmur of pulmonic insufficiency may be noted Graham Steell's murmur due to dilation of the pulmonic valve ring resulting from pulmonary hypertension. Flow into a dilated pulmonary trunk causes a pulmonic ejection sound and pulmonic ejection murmur. The second pulmonic heart sound is closely split or not split.

Assessment=

Small and medium-sized PDAs must be distinguished from other conditions with continuous murmurs:

  • Venous hum: frequently heard in children over the base of the neck, usually best on the right side. Louder in diastole and disappears in the supine position or with compression.
  • Mammary Souffle: heard during late pregnancy and the early postpartum period in lactating women. It is Thought to be arterial in origin and can be bilateral. Is louder, peaks in systole, vanishes in the upright position, and is abolished by local compression.
  • Aorticopulmonary Window: is a rare congenital opening between the aorta and the pulmonary trunk just above the aortic valve. It is associated with other abnormalities in approximately 1/2 the cases, such as anomalous origin of the coronary arteries from the pulmonary trunk and coarctation of the aorta. The murmur is lower and more medial in location. In adults is presented without a murmur and clinical features of the Eisenmenger's syndrome.
  • Rupture of the Sinus of Valsalva: It can rupture into a cardiac chamber. Almost always arise from the right or the noncoronary cusps and rupture into the RV and RA respectively. Occasionally is acquired as a result of endocarditis. Large acute perforations tend to occur between puberty and age 30 causing severe retrosternal chest pain, dyspnea related to the large left to right shunt. The murmur is louder in a lower parasternal position. People with VSDs and sudden development of chest pain have frequently experienced rupture of a coexistent sinus of valsalva aneurysm. A rupture of the sinus of valsalva can distort or compress the coronary arteries and cause an infarction, distort the conduction system, cause AV block, distort the aortic valve, and cause AS or AI. Patients with rupture of the sinus of valsalva, should undergo surgical correction because mortality is high within a year of rupture.
  • Fistulas of the coronary circulation': Generally a coronary artery that arises normally will communicate with the RV. Occasionally drain into the pulmonary trunk. The artery that forms the fistula is generally dilated, elongated, and tortuous. The left to right shunt is small. It may not be recognized radiographically. Patients with small fistula are generally asymptomatic. Therefore, no justification to repair it. On the other hand, if the shunt is extremely large, then failure may develop in the 4th, 5th or 6th decade of life. It can be treated with ligation.
  • Anomalous Origin of the Coronary Artery From the Pulmonary Trunk: Usually refers to the origin of the left coronary artery from the pulmonary trunk. Approximately, 80 to 90% of the patients die in their first year of life due to ischemia. Blood from the high pressure RCA flows to the low pressure left coronary artery and the pulmonary artery. Anomalous origin of the RCA from the PA is much rarer, but these patients stand a better chance of surviving into adulthood because it is less likely to cause ischemia early in life.
  • 'Pulmonary Arteriovenous Fistulas: Instead of being localized to the precordium, these murmurs are localized to the lung fields. Cyanosis is presented with a normal heart size. Seen in Rendu-Osler-Weber syndrome. A fistula causing cyanosis could be treated with lobectomy if it is confined to a single lobe.

References

  1. Giuliani et al, Cardiology: Fundamentals and Practice, Second Edition, Mosby Year Book, Boston, 1991, pp. 1653-1663.

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