Pulmonic regurgitation pathophysiology: Difference between revisions
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**RV diastolic complaince | **RV diastolic complaince | ||
**Duration of RV diastole | **Duration of RV diastole | ||
==== According to 2014, ACC/AHA valvular heart disease guidelines the stages of severe pulmonary regurgitation are described as follows:<ref name="pmid24603191">{{cite journal| author=Nishimura RA, Otto CM, Bonow RO, Carabello BA, Erwin JP, Guyton RA et al.| title=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. | journal=J Am Coll Cardiol | year= 2014 | volume= 63 | issue= 22 | pages= e57-185 | pmid=24603191 | doi=10.1016/j.jacc.2014.02.536 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24603191 }} </ref> ==== | |||
{| class="wikitable" | |||
!Stage | |||
!Definition | |||
!Pulmonary Valve | |||
Anatomy | |||
!Valve Hemodynamics | |||
!Hemodynamic Consequences | |||
!Symptoms | |||
|- | |||
|C,D | |||
|Severe PR | |||
| | |||
*Distorted or absent leaflets | |||
*Annular dilation | |||
| | |||
*Color jet fills RVOT | |||
*CW jet density and contour: dense laminar flow with steep deceleration slope; may terminate abruptly | |||
| | |||
*Paradoxical septal motion (volume overload pattern) | |||
* RV enlargement | |||
|None or variable and dependent on cause of PR and RV function | |||
|} | |||
==References== | ==References== | ||
{{Reflist}} | {{Reflist}} | ||
Revision as of 19:48, 30 December 2016
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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.[1]
Pathophysiology
Pathophysiologic mechanism of pulmonic regurgitation may include the following steps:
- Patients with PR develop chronic right ventricular overload resulting in right ventricular remodelling and progressive decline in function.[1]
- Progressive dilation of the right ventricle results in functional tricuspid regurgitation and increases the risk of developing arrhythmias.
- 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 LV or residual pulmonary artery stenosis increases the severity of PR.
- The severity of regurgitant jet is dependent on:[1]
- Size of the regurgitant orifice
- Afterload of the RV
- RV diastolic complaince
- Duration of RV diastole
According to 2014, ACC/AHA valvular heart disease guidelines the stages of severe pulmonary regurgitation are described as follows:[2]
| Stage | Definition | Pulmonary Valve
Anatomy |
Valve Hemodynamics | Hemodynamic Consequences | Symptoms |
|---|---|---|---|---|---|
| C,D | Severe PR |
|
|
|
None or variable and dependent on cause of PR and RV function |
References
- ↑ 1.0 1.1 1.2 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.
- ↑ 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.