Users Online: 1283 Home Print this page Email this page Small font sizeDefault font sizeIncrease font size  
Home | About us | Editorial board | Search | Ahead of print | Current issue | Archives | Submit article | Instructions | Subscribe | Contacts | Login 


RSACP wishes to inform that it shall be discontinuing the dispatch of print copy of JOACP to it's Life members. The print copy of JOACP will be posted only to those life members who send us a written confirmation for continuation of print copy.
Kindly email your affirmation for print copies to dranjugrewal@gmail.com preferably by 30th June 2019.

 

 
Table of Contents
LETTER TO EDITOR
Year : 2012  |  Volume : 28  |  Issue : 2  |  Page : 261-262

Pulmonary artery hypertension in mitral stenosis: Role of right ventricular stroke volume, atrio-ventricular compliance, and pulmonary venous compliance


Department of Anaesthesiology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Thiruvananthapuram, Kerala, India

Date of Web Publication11-Apr-2012

Correspondence Address:
Praveen Kumar Neema
Department of Anaesthesiology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Thiruvananthapuram, Kerala
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0970-9185.94916

Rights and Permissions

How to cite this article:
Neema PK, Rathod RC. Pulmonary artery hypertension in mitral stenosis: Role of right ventricular stroke volume, atrio-ventricular compliance, and pulmonary venous compliance. J Anaesthesiol Clin Pharmacol 2012;28:261-2

How to cite this URL:
Neema PK, Rathod RC. Pulmonary artery hypertension in mitral stenosis: Role of right ventricular stroke volume, atrio-ventricular compliance, and pulmonary venous compliance. J Anaesthesiol Clin Pharmacol [serial online] 2012 [cited 2020 Jul 5];28:261-2. Available from: http://www.joacp.org/text.asp?2012/28/2/261/94916

Sir,

The normal mitral valve area (MVA) is approximately 4-6 cm 2 . At a MVA below 1 cm 2 (severe mitral stenosis [MS]) patients usually become symptomatic even at rest. [1] In patients of severe MS, a substantial increase in left atrial pressure (LAP) occurs and a gradient develops across the MV to accomplish left ventricular (LV) filling. The increased LAP passively elevates pulmonary venous and pulmonary capillary pressures and cause symptoms of pulmonary congestion. [2] When the MVA is reduced to 1 cm 2 , a mean gradient of 20 mmHg across the stenosed MV is required to maintain normal cardiac output at rest. [3] The persistently raised LAP results in left atrial (LA) dilatation, atrial fibrillation, pulmonary venous hypertension, reflex pulmonary arteriolar constriction, obliterative changes in pulmonary vascular bed, pulmonary artery hypertension (PAH), right ventricular (RV) hypertrophy, its dilatation, tricuspid valve dysfunction, systemic venous congestion, compromised LV filling, and a state of subnormal cardiac output. [4] The pulmonary arterioles may react with vasoconstriction, intimal hyperplasia, and medial hypertrophy, which further increases PAH. [5]

We discuss role of RV stroke volume, atrio-ventricular compliance, and pulmonary venous compliance in the development of PAH in MS. A close scrutiny of causes of increased LAP is necessary to understand genesis of PAH. The pressure in a relatively thin-walled chamber like left atrium depends on several factors such as its stiffness, mechanical effects of its rhythmic contraction and relaxation, diastolic period, the quantity of blood entering and exiting it, and the net atrio-ventricular compliance which include compliance of LA and LV, and compliance of the pulmonary venous system. For the increase in LAP to be substantial that develops in severe MS, the compliance of LA and pulmonary venous system should be low else the effect of damming of blood will dissipate in left atrium and pulmonary vascular bed and a substantial increase in LAP will not occur. In a study of 20 patients, a subgroup of patients was found who responded to exercise by a significant increase in PA pressure, in that subgroup the net atrio-ventricular compliance was found significantly low. [6] Apparently, in patients of MS a wide spectrum of atrio-ventricular compliance exist - patients with low compliance and patients with normal compliance. Patients with low compliance develop significant PAH, severe increase in LAP and symptoms of MS on exercise or in situations of increased cardiac output, whereas patients with normal compliance remain asymptomatic in situations of increased cardiac output as the increased RV stroke volume is accommodated in the compliant pulmonary venous bed [Figure 1].
Figure 1: Schematic diagram to show effect of increasing right ventricular (RV) stroke volume on pulmonary artery pressure in presence of low pulmonary venous and/or low atrio-ventricular compliance and normal pulmonary venous and normal atrio-ventricular compliance

Click here to view


Atleast two more factors should be considered in the genesis of raised LAP, the effect of LV relaxation on transmitral flow and the role of RV stroke volume. The flow across MV during early diastole is described passive; however, it is well established that the flow across the MV is augmented by suction effect generated by LV relaxation during early diastole and by LA systole during late diastole. [7] Conceivably, in presence of MS, the suction augmentation of early diastolic flow will be reduced and/or ineffective. Arguably, to generate flow across the stenosed MV, the LA has to be pressurised, it is intuitive that RV stroke volume generated during systole pressurises LA and pulmonary vascular system which raises the mean pulmonary artery (PA) pressure and LAP, and serve as potential energy to achieve transmitral flow during diastole. The RV stroke volume raises the mean pulmonary vascular system filling pressure and drives the flow across the mitral valve during diastole; the concept is similar to mean systemic filling pressure .[8] However, over a period, reflex protective pulmonary vasoconstriction and pulmonary arteriolar obliteration sets in, which further increases PA pressure and result in remodelling of the RV to overcome raised pulmonary vascular resistance. Apparently, the PAH in MS is benign and mechanical in the beginning and develops as a compensatory mechanism to overcome resistance offered by the stenosed mitral valve; later, it progresses secondary to pulmonary vasoconstriction and pulmonary arteriolar obliteration. However, in a given patient it is not possible to know the contribution of each of these factors in the genesis of PAH. Apparently, the PAH in MS is not only due to raised LAP and raised pulmonary vascular resistance secondary to pulmonary vasoconstriction and obliterative changes in pulmonary vascular bed, but it also depends on contribution of net atrio-ventricular compliance, pulmonary venous compliance, and RV stroke volume; an increased RV stroke volume and low net atrio-ventricular compliance and pulmonary venous compliance results in severe increase in PA pressure and symptoms of pulmonary congestion.

It is intuitive from the above discussion that in patients of MS sustained RV performance and persistently maintained PA pressure is essential for achieving transmitral flow, LV filling, and LV stroke output. The clinical situations that decrease RV performance can result in low cardiac output, whereas situations where RV performance remains unaffected or increases in response to pathophysiological stimulation might result in increased LAP, pulmonary congestion, edema, but sustained cardiac output. Apparently, in patients of MS, RV performance in response to varying clinical demands and basal atrio-ventricular and pulmonary venous compliance decides the clinical features. This could be the mechanism that explains varying clinical presentation of similar degree of tachycardia in patients having similar degree of MS. Apparently, patients who can mount RV performance and increase or maintain PA pressure in response to pathophysiologic challenges maintain cardiac output but are likely to develop pulmonary congestion and edema, whereas those who develop RV decompensation and cannot sustain PA pressure develop low cardiac output and possibility of acute cardio vascular collapse. Arguably, while anesthetising these patients, it is important to sustain RV function else the patient may develop cardiovascular decompensation.

 
  References Top

1.Maganti K, Rigolin VH, Sarano ME, Bonow RO. Valvular heart disease: Diagnosis and management. Mayo Clin Proc 2010;85:483- 500.   Back to cited text no. 1
[PUBMED]  [FULLTEXT]  
2.Mittnacht AJ, Fanshawe M, Konstadt S. Anesthetic considerations in the patient with valvular heart disease undergoing noncardiac surgery. Semin Cardiothorac Vasc Anesth 2008;12:33-59.  Back to cited text no. 2
[PUBMED]  [FULLTEXT]  
3.Rahimtoola SH, Durairaj A, Mehra A, Nuno I. Current evaluation and management of patients with mitral stenosis. Circulation 2002;106:1183-8.  Back to cited text no. 3
[PUBMED]  [FULLTEXT]  
4.Hugenholtz PG, Ryan TJ, Stein SW, Belmann WH. The spectrum of pure mitral stenosis: hemodynamic studies in relation to clinical disability. Am J Cardiol 1962;10:773-84.  Back to cited text no. 4
[PUBMED]    
5.Bonow RO, Carabello BA, Chatterjee K, de Leon AC Jr, Faxon DP, Freed MD, et al; American College of Cardiology/American Heart Association Task Force on Practice Guidelines. 2008 focused update incorporated into the ACC/AHA 2006 guidelines 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 (Writing Committee to revise the 1998 guidelines for the management of patients with valvular heart disease). Endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. J Am Coll Cardiol 2008;52:e1-142.  Back to cited text no. 5
[PUBMED]  [FULLTEXT]  
6.Schwammenthal E, Vered Z, Agranat O, Kaplinsky E, Rabinowitz B, Feinberg MS: Impact of atrioventricular compliance on pulmonary artery pressure in mitral stenosis: An exercise echocardiographic study. Circulation 2000;102:2378-84.  Back to cited text no. 6
    
7.Nishimura RA, Tajik AJ. Evaluation of diastolic filling of left ventricle in health and disease: Doppler echocardiography is the clinician's Rosetta Stone. J Am Coll Cardiol 1997;30:8-18.  Back to cited text no. 7
[PUBMED]  [FULLTEXT]  
8.Guyton and Hall: Cardiac output, venous return, and their regulation in text book of medical physiology. 10th (ed), WB Saunders company, Noida, page 210-222  Back to cited text no. 8
    


    Figures

  [Figure 1]


This article has been cited by
1 Computed Tomography in the Evaluation of Pulmonary Hypertension
Seth Kligerman,Lewis Hahn,Elizabeth Weihe
Advances in Clinical Radiology. 2020;
[Pubmed] | [DOI]
2 Left Atrial Volume Index (LAVI) as an Indicator of Severity and Pulmonary Hypertension in Mitral Stenosis
G M Rahman,A Subagjo
IOP Conference Series: Earth and Environmental Science. 2020; 441: 012173
[Pubmed] | [DOI]
3 Mitral Intervention with LVAD: Preparing for Recovery
Cory Maxwell,George Whitener
Seminars in Cardiothoracic and Vascular Anesthesia. 2019; 23(1): 134
[Pubmed] | [DOI]
4 Pulmonary hypertension in rheumatic mitral stenosis revisited
L. Pourafkari,S. Ghaffari,M. Ahmadi,A. Tajlil,N. Aslanabadi,N. D. Nader
Herz. 2016;
[Pubmed] | [DOI]



 

Top
 
  Search
 
    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
    Access Statistics
    Email Alert *
    Add to My List *
* Registration required (free)  

 
  In this article
   References
   Article Figures

 Article Access Statistics
    Viewed2116    
    Printed83    
    Emailed1    
    PDF Downloaded439    
    Comments [Add]    
    Cited by others 4    

Recommend this journal