2
edits
Changes
Ruptured chordae tendinae (view source)
Revision as of 18:23, 8 February 2021
, 18:23, 8 February 2021no edit summary
Introduction
== Introduction ==
Chordae tendinae (tendinous chords) are fibrous structures of connective tissue that attach the cusps of the mitral and tricuspid valvular leaflets to the papillary muscles of the ventricular walls of the cardiac muscle. Their function is to support the leaflets of the atrioventricular valves and prevent the leaflets from everting and prolapsing.
In atrial systole, blood flows from the atria to the ventricles passively down the pressure gradient, and the chordae tendinae are relaxed because the valve leaflets are open at this time. During ventricular systole, the increased blood pressure in both ventricles push the atrioventricular valves to close simultaneously preventing back flow of blood to the atria, and the contraction of thick muscular walls of the ventricles help to support that. Since the blood pressure in the atria is lower than the pressure in the ventricles, the valve leaflets are sucked into the atria during ventricular systole. The chordae tendinae prevent the prolapse of the valves into the atria by the tensing of the papillary muscles which pull on the chords, thus holding the atrioventricular valves in a closed position for the duration of ventricular systole.
Chordae tendineae are comprised of approximately 80% collagen and 20% elastin and endothelial cells.
There are three groups of chordae tendinae: primary, secondary and tertiary, with different inserts into the valvular leaflets and papillary muscle.
* Primary chordae (marginal chordae) insert onto the free margin of the leaflet and are the main support to prevent prolapse of the leaflet
* Secondary chordae (intermediate chordae) insert onto the ventricular surface of the leaflet and function to relieve excess tension on the valvular tissue.
* Tertiary chordae (basal chordae) are limited to the posterior leaflet and connect the leaflet base and mitral annulus to the papillary muscle.
== Clinical Presentation ==
Rupture of the chordae tendinae: Inflammatory and degenerative changes in the chordae as a primary or secondary disease entity.
'''Causes''': Valvular endocardiosis (myxomatous degeneration), bacterial endocarditis, myocardial necrosis, indirect trauma, severe physical exertion, heartworms, and idiopathy have been implicated as possible aetiologies.
In dogs the primary cause is myxomatous degeneration of the valvular leaflets, and primarily seen in the mitral valve. In horses valvular degeneration and subsequent insufficiency secondary to endocarditis and endocardiosis, as well as spontaneous rupture are implicated as possible causes of rupture.
'''Pathophysiology''': Valvular degeneration leads to valvular incompetency and then subsequent rupture of chordae tendinae. The degeneration can be due to any cause, and causes regurgitation of that valve and prolapse during ventricular systole. An increased systolic pressure gradient across the incompetent valve can then be exacerbated by exertion or thoracic trauma. Due to that increased pressure, one of the groups of chordae tendinae may rupture. This leads to an increase in the severity of the valvular regurgitation, and depending on which group of tendinae are ruptured and which valve is regurgitating will affect the clinical signs and prognosis.
Mitral valve tendinae rupture --> Sudden increase in left atrial/left ventricular volume causes overload, which cannot be compensated for by dilatation of the left atrium and ventricle in an acute rupture. This leads to increase in left atrial and left ventricular end-diastolic pressures. This then leads to pulmonary oedema, causing hypoxic vasoconstriction, then leading to pulmonary hypertension causing secondary right ventricular failure.
Tricuspid valve tendinae rupture --> Rupture of tendinae causes valvular prolapse and tricuspid regurgitation. This causes an increase in right atrial/right ventricular volume but unlike the left side regurgitation is well tolerated. Will eventually lead to pulmonary hypertension.
'''Signs''': Dyspnoea, tachycardia, heart murmurs (depending on which valve affected), exercise intolerance, arrhythmia, sudden death if acute primary chord rupture, expectoration of pulmonary surfactant - frothy fluid if pulmonary oedema, congestive heart failure, jugular vein distention, pale mucous membranes, weak pulses, high CRT, cold extremities, fainting. Onset and severity depending on which valve affected, underlying aetiology and which group of tendinae are ruptured.
'''Diagnosis''': Prior to diagnostic workup patient must be stabilized as readily decompensates.
Radiography: Thoracic radiography, showing variable signs of endocardiosis and heart failure. Can see atrial and ventricular enlargement, and pulmonary venous congestion. Air bronchograms may be observed with pulmonary oedema.
Ultrasonography: Can use a doppler or 2-D ultrasound. Observe enlargement of the atria and ventricle, dilation of pulmonary veins, flail of the valve - part of the leaflet or distal part of ruptured chord flails into the atrium. For the doppler can observe severe jet regurgitation originating at site of the flail of the leaflet.
Echocardiography: May observe ruptured chords. Will observe enlargement.
ECG for arrhythmias.
'''Treatment''': For acute primary chord rupture treat as an emergency patient and stabilize as for severe mitral valve degeneration and congestive heart failure. Treat and stabilize the arrhythmia. Manage after stabilized as a heart failure case.
'''Prognosis''': High mortality rate for affected animals. Poor long term survival and exercise capacity and quality of life poor. Dependent on which valve affected and which chords ruptured.