Pulmonic regurgitation pathophysiology: Difference between revisions
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The pulmonic regurgitation usually occurs by one of the following mechanisms:<ref>{{cite book | last = Khavandi | first = Ali | title = Essential revision notes for the cardiology KBA | publisher = Oxford University Press | location = Oxford | year = 2014 | isbn = 978-0199654901 }} </ref> | The pulmonic regurgitation usually occurs by one of the following mechanisms:<ref>{{cite book | last = Khavandi | first = Ali | title = Essential revision notes for the cardiology KBA | publisher = Oxford University Press | location = Oxford | year = 2014 | isbn = 978-0199654901 }} </ref> | ||
*'''[[Pulmonic valve]] ring dilatation''': | *'''[[Pulmonic valve]] ring dilatation''': | ||
*'''Acquired alteration in the valvular leaflet morphology''': | *'''Acquired alteration in the valvular leaflet morphology''':<ref name="CurtissMiller1983">{{cite journal|last1=Curtiss|first1=E I|last2=Miller|first2=T R|last3=Shapiro|first3=L S|title=Pulmonic regurgitation due to valvular tophi.|journal=Circulation|volume=67|issue=3|year=1983|pages=699–701|issn=0009-7322|doi=10.1161/01.CIR.67.3.699}}</ref> | ||
**The development of [[pulmonic regurgitation]] due to [[tophus]] valvular vegetations has been reported in a case. The patient reported had long-standing cyanotic [[congenital heart disease]] and developed [[hyperuricemia]] secondary to [[polycythemia]]. The possible mechanism of development of the [[vegetation]]s involved hemodynamic valvular trauma in the setting of sustained [[hyperuricemia]] and subsequent [[dystrophic calcification]] at primary [[tophus]] lesion. | |||
**On gross pathology vegetative lesions observed. | |||
**Polarized light microscopy of the material taken from the pulmonic valve demonstrated [[Gout diagnostic study of choice|negatively birefringent crystals]]. | |||
*'''Congenital absence or malformation of the valve''': | *'''Congenital absence or malformation of the valve''': | ||
*'''Increasing regurgitation causing [[right ventricle|right ventricular]] volume overload''': Patients with [[pulmonic regurgitation]] develop chronic [[right ventricular overload]] resulting in right [[ventricular remodelling]] and progressive decline in function.<ref name="pmid26430501">{{cite journal| author=Bigdelian H, Mardani D, Sedighi M| title=The Effect of Pulmonary Valve Replacement (PVR) Surgery on Hemodynamics of Patients Who Underwent Repair of Tetralogy of Fallot (TOF). | journal=J Cardiovasc Thorac Res | year= 2015 | volume= 7 | issue= 3 | pages= 122-5 | pmid=26430501 | doi=10.15171/jcvtr.2015.26 | pmc=4586599 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26430501 }} </ref> The rate of decline in right ventricular [[systolic function]] is affected by associated conditions such as peripheral [[pulmonary artery stenosis]] and [[pulmonary hypertension]] which further increase the severity of pulmonary regurgitation. In patients with increased [[pulmonary artery pressure]] from dysfunction of [[left ventricle]] or residual [[pulmonary artery stenosis]] increases the severity of [[pulmonary regurgitation]]. Progressive dilation of the [[right ventricle]] results in functional [[tricuspid regurgitation]] and increases the risk of developing [[arrhythmias]]. | *'''Increasing regurgitation causing [[right ventricle|right ventricular]] volume overload''': Patients with [[pulmonic regurgitation]] develop chronic [[right ventricular overload]] resulting in right [[ventricular remodelling]] and progressive decline in function.<ref name="pmid26430501">{{cite journal| author=Bigdelian H, Mardani D, Sedighi M| title=The Effect of Pulmonary Valve Replacement (PVR) Surgery on Hemodynamics of Patients Who Underwent Repair of Tetralogy of Fallot (TOF). | journal=J Cardiovasc Thorac Res | year= 2015 | volume= 7 | issue= 3 | pages= 122-5 | pmid=26430501 | doi=10.15171/jcvtr.2015.26 | pmc=4586599 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26430501 }} </ref> The rate of decline in right ventricular [[systolic function]] is affected by associated conditions such as peripheral [[pulmonary artery stenosis]] and [[pulmonary hypertension]] which further increase the severity of pulmonary regurgitation. In patients with increased [[pulmonary artery pressure]] from dysfunction of [[left ventricle]] or residual [[pulmonary artery stenosis]] increases the severity of [[pulmonary regurgitation]]. Progressive dilation of the [[right ventricle]] results in functional [[tricuspid regurgitation]] and increases the risk of developing [[arrhythmias]]. | ||
Revision as of 14:22, 28 July 2020
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Pulmonic regurgitation Microchapters |
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Diagnosis |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Aravind Kuchkuntla, M.B.B.S[2], Aysha Anwar, M.B.B.S[3]
Overview
Pathophysiologic mechanism of pulmonic regurgitation include right ventricular overload resulting in right ventricular remodelling and progressive decline in function. The rate of decline in right ventricular systolic function is affected by associated conditions such as peripheral pulmonary artery stenosis and pulmonary hypertension which further increase the severity of pulmonary regurgitation.
Pathophysiology
The pulmonic regurgitation usually occurs by one of the following mechanisms:[1]
- Pulmonic valve ring dilatation:
- Acquired alteration in the valvular leaflet morphology:[2]
- The development of pulmonic regurgitation due to tophus valvular vegetations has been reported in a case. The patient reported had long-standing cyanotic congenital heart disease and developed hyperuricemia secondary to polycythemia. The possible mechanism of development of the vegetations involved hemodynamic valvular trauma in the setting of sustained hyperuricemia and subsequent dystrophic calcification at primary tophus lesion.
- On gross pathology vegetative lesions observed.
- Polarized light microscopy of the material taken from the pulmonic valve demonstrated negatively birefringent crystals.
- Congenital absence or malformation of the valve:
- Increasing regurgitation causing right ventricular volume overload: Patients with pulmonic regurgitation develop chronic right ventricular overload resulting in right ventricular remodelling and progressive decline in function.[3] The rate of decline in right ventricular systolic function is affected by associated conditions such as peripheral pulmonary artery stenosis and pulmonary hypertension which further increase the severity of pulmonary regurgitation. In patients with increased pulmonary artery pressure from dysfunction of left ventricle or residual pulmonary artery stenosis increases the severity of pulmonary regurgitation. Progressive dilation of the right ventricle results in functional tricuspid regurgitation and increases the risk of developing arrhythmias.
- The diastolic pressure difference between right ventricle and pulmonary artery is usually very small and steers the pulmonic valve regurgitation. The right ventricular stiffness due to right ventricular hypertrophy (such as in Tetralogy of Fallot) and fibrosis, increases the ventricular diastolic pressure, decreasing the gradient thus causing regurge. A slight increase in the intrathoracic pressure (such as in ventilated patients) can accentuate the pulmonary regurgitation considerably.[4]
- The severity of regurgitant jet is dependent on:[3]
- Size of the regurgitant orifice
- Afterload of the right ventricle
- Right ventricle diastolic compliance
- Duration of right ventricular diastole
According to 2014, ACC/AHA valvular heart disease guidelines the stages of severe pulmonary regurgitation are described as follows:[5]
| Stage | Definition | Pulmonary Valve
Anatomy |
Valve Hemodynamics | Hemodynamic Consequences | Symptoms |
|---|---|---|---|---|---|
| C,D | Severe Pulmonary valve regurgitation |
|
|
|
None or variable and dependent on cause of pulmonary reguritation and right ventricular function |
References
- ↑ Khavandi, Ali (2014). Essential revision notes for the cardiology KBA. Oxford: Oxford University Press. ISBN 978-0199654901.
- ↑ Curtiss, E I; Miller, T R; Shapiro, L S (1983). "Pulmonic regurgitation due to valvular tophi". Circulation. 67 (3): 699–701. doi:10.1161/01.CIR.67.3.699. ISSN 0009-7322.
- ↑ 3.0 3.1 Bigdelian H, Mardani D, Sedighi M (2015). "The Effect of Pulmonary Valve Replacement (PVR) Surgery on Hemodynamics of Patients Who Underwent Repair of Tetralogy of Fallot (TOF)". J Cardiovasc Thorac Res. 7 (3): 122–5. doi:10.15171/jcvtr.2015.26. PMC 4586599. PMID 26430501.
- ↑ Chaturvedi RR, Redington AN (2007). "Pulmonary regurgitation in congenital heart disease". Heart. 93 (7): 880–9. doi:10.1136/hrt.2005.075234. PMC 1994453. PMID 17569817.
- ↑ Nishimura RA, Otto CM, Bonow RO, Carabello BA, Erwin JP, Guyton RA; et al. (2014). "2014 AHA/ACC guideline for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines". J Am Coll Cardiol. 63 (22): e57–185. doi:10.1016/j.jacc.2014.02.536. PMID 24603191.