How To Repair A Mitral Valve Surgically

Continuing Instruction Activeness

Mitral valve repair is usually used to treat mitral valve pathology due to mitral regurgitation. Mitral regurgitation (MR) is classified as primary or secondary, depending on whether the lesion is located at the mitral valve apparatus or due to left ventricular changes. This action reviews and highlights the role of an interprofessional care team in managing patients who undergo mitral valve repair.

Objectives:

• Identify the relevant beefcake, indications, and contraindications for mitral valve repair.

• Describe the equipment, personnel, preparation, and technique in regards to mitral valve repair.

• Review appropriate evaluation of the potential complications and clinical significance of mitral valve repair.

• Summarize interprofessional team strategies for improving care coordination and communication to advance mitral valve repair and improve outcomes.

Access complimentary multiple choice questions on this topic.

Introduction

Although the standard of care for mitral valve (MV) pathology due to degenerative changes is surgical repair, patient outcomes depend on multiple factors including pre-operative condition, the severity of mitral regurgitation (MR), the technique of repair and surgeon and center experience. If MV repair is carried out in a timely mode, the operative take a chance is low, and life expectancy is close to that of similar sex-aged matched controls. In loftier-risk patients, the pick amongst surgical, percutaneous, and conservative approaches can exist challenging but should accept as its footing patient comorbidities and surgical expertise. Mitral valve repair (MVr) surgery has some advantages over mitral valve replacement (MVR), although patient-specific factors must exist taken into consideration. Of note, close to 50% of patients with astringent mitral valve pathology are not candidates for surgical intervention due to historic period or other comorbidities.[1]

Up to 2 to three% of adults in the Usa are afflicted with degenerative mitral valve affliction.[2] Patients with degenerative MV pathology who develop symptoms of MR accept a poor prognosis, with annual bloodshed rates of up to 34%.[3] Mitral stenosis (MS), primarily caused by rheumatic center disease (RHD), is commonly treated past percutaneous airship mitral valvuloplasty or MVR. Repair is usually not viable in these patients with rheumatic mitral disease. MR is classified every bit primary or secondary, depending on whether the lesion is located at the mitral valve apparatus or due to left ventricular changes, respectively. While severe primary MR all the same receives treatment with surgical intervention, percutaneous techniques for repair and replacement are besides gaining traction. MVR may be considered in patients with MR caused past papillary muscle rupture, degenerative and ischemic MR, or in patients with a failed repair undergoing reoperation.[4]

Beefcake and Physiology

The mitral valve apparatus has a complex anatomy, including an annulus, 2 leaflets, 3 types of chordae tendinae, and 2 papillary muscles.  The MV annulus is a saddle-shaped structure in continuity with the aortic valve. The annulus is near vulnerable to dilatation at its insertion on the posterior leaflet considering it is the thinnest at this junction. There are two MV leaflets; the inductive is tall and narrow, and the posterior is shorter and broader. These two leaflets meet at their respective commissures, known equally the anterolateral and posteromedial commissures. Each leaflet divides into iii scallops, one to 3, from lateral to medial, and are designated A1, A2, A3 (anterior) and P1, P2, P3 (posterior).[5] The anterior leaflet occupies two-thirds of the valvular area and one-third of the annular expanse, whereas the posterior leaflet comprises 2-thirds of the annular circumference. The leaflets have a normal line of coaptation from seven to 9 mm, allowing for a range of normal physiologic pressures and volumes. The posterior, or mural leaflet, is more vulnerable to prolapse considering it is fastened to the free wall of the ventricle, leaving it exposed to the recurrent stress of ventricular contraction.[6]

Fibrous structures, known as the chordae tendinae, attach the MV leaflets to the papillary muscles. In that location are 3 types of chordae based on their level of insertion: master, secondary, and tertiary. Primary chordae insert on the leaflet'southward free margin and aid in the prevention of leaflet prolapse.  Secondary chordae insert on the leaflet's rugged surface, and tertiary on the basal portion of the leaflet. There are 2 papillary muscles known equally anterolateral and posteromedial. The posteromedial muscle receives vascular supply solely by the posterior descending artery, while the supply to anterolateral is by both the left anterior descending avenue and the left circumflex artery.[5] The same elements of the mitral valve apparatus piece of work in concert to maintain valvular competence and enable proper blood flow from the left atrium (LA) to the left ventricle (LV). A normal MV area is 4 to six cm. In MR patients, the LV is normally thin, dilated, dysfunctional, and arrhythmogenic.

Indications

Rheumatic heart illness usually causes MS, idea to be related to an exaggerated immune response secondary to cross-reactivity between streptococcal antigen and MV tissue.[vii] Changes associated with rheumatic mitral disease include a "fish-mouth" appearance of the MV orifice, commissural fusion, leaflet thickening, and shortening and fusion of chordae tendinae. These changes lead to the subsequent hockey-stick appearance of the anterior leaflet on echocardiography. Other etiologies of MS include mitral annular calcification (MAC) common in elderly patients or those with avant-garde renal illness, radiation valvulitis, systemic inflammatory disorders, obstructing lesions, infectious vegetations, and congenital valvular abnormalities.[eight] Progressive MS, especially a valve area less than 2 cm, leads to a diastolic pressure gradient between the LA and LV, increasing LA pressures and potentially reducing forward flow. Tachycardia should exist avoided in patients with MS, every bit it reduces diastolic filling time, leading to an increased transmitral gradient. Increased LA pressures tin can atomic number 82 to atrial enlargement with increased risk of thromboembolism and arrhythmias, most ordinarily atrial fibrillation (AF). Elevated pulmonary dorsum pressure can subsequently cause pulmonary edema and hypertension, precipitating correct ventricular (RV) failure and possible tricuspid regurgitation. Decreased forwards period can produce poor LV filling and reduced cardiac output (CO).

Clinicians can all-time accomplish quantification of MS with echocardiography, based on mean diastolic transmitral pressure gradient, MV expanse, and LA and right-sided bedchamber sizes and pressures.[9] The mean diastolic force per unit area gradient gets calculated with continuous-moving ridge Doppler from an apical four-chamber view. The Doppler reveals diastolic transmitral menstruation via a velocity measurement, which then converts into a pressure with Bernoulli'south simplified equation to discern the mean MV gradient. The definition of severe MS is a mean gradient over ten mmHg, moderate MS is 5 to 10 mmHg, and mild MS is below v mmHg. The transmitral gradient is under strong influence from center rate and forrard blood flow. According to the 2014 valvular middle illness guidelines and the 2017 guideline update, they consider MS to be very severe if MVA less than or equal to 1 cm squared, and severe if it is less than or equal to one.five cm squared.

MR tin can be defined as primary or secondary depending on whether the aberration is located at the level of the mitral valve apparatus or the left ventricle, respectively. In developing countries, mitral valve prolapse is the most mutual crusade of MR requiring surgical repair, while degenerative disease is virtually common in the United States.[10] Mitral valve prolapse is a systolic leaflet displacement of greater than or equal to two mm in a higher place the mitral annulus aeroplane in a long-axis view. Barlow's disease results in abnormal accumulation of mucopolysaccharides and fibroelastic deficiency, leading to loss of mechanical integrity of the MV. Primary MR can also outcome from infective endocarditis, MAC, RHD, connective tissue disorders, congenital malformations, and drug apply. Secondary MR, also known equally functional MR, is due to LV remodeling or dyssynchrony, mitral annular dilatation, and impaired LV contractility. Secondary causes of MR can subdivide into ischemic and non-ischemic. Ischemic MR is caused past LV dysfunction secondary to coronary artery disease (CAD) and foreshadows a poor prognosis in terms of survival and development of heart failure. Non-ischemic MR results from the diverse cardiomyopathies (dilated, restrictive, and hypertrophic) likewise as secondary to AF with subsequent annular dilatation.

MR leads to LA and LV book overload, depending on the time course of the MR (acute vs. chronic) and the magnitude of the regurgitant volume. Acute MR leads to a sudden increase in preload and LV filling pressures that can cause pulmonary edema. Cardiac output as well becomes reduced since blood period now gets directed to the LA, which can precipitate cardiogenic daze; this is a mutual presentation in patients with infective endocarditis, chordae tendinae rupture, or papillary muscle rupture following myocardial infarction (MI). Chronic MR divides into three stages: a compensated phase where well-nigh patients are asymptomatic, a transitional stage with LV remodeling, and a decompensated phase marked past insidious symptom development. Chronic MR also leads to LA enlargement, which increases the risk for atrial arrhythmias and thromboemboli. Carpentier developed a functional classification of MR based on leaflet motility.[xi]

Echocardiography is the modality of choice for the categorization of MR. Color Doppler is useful in assessing the jet area, as well as its ratio to the LA area. A jet over forty% of the LA surface area suggests severe MR. In severe MR, measured peak mitral arrival velocity is usually more 120 cm/sec, and diastolic reversal of pulmonary venous menstruation is nowadays.[11] Worsening MR leads to systolic flow reversal forth with a blunting of the systolic component. In patients with astringent MR and preserved EF, prompt surgical intervention is paramount to prevent adverse LV remodeling. Beta natriuretic peptide (BNP), global longitudinal strain, do capacity, and right ventricular systolic pressure are important prognostic indicators in such patients.[12] Co-ordinate to the American Higher of Cardiology/American Heart Association (ACC/AHA) guidelines, the post-obit are indications for surgery in astringent master MR: chronic severe primary MR, with repair preferable over replacement if durable repair can be achieved (class I).[xiii]

Contraindications

Patients with severe MR must be evaluated by a cardiac surgeon with experience in mitral valve surgery. The standard pre-operative evaluation must be undertaken to decide surgical candidacy, including cess of coronary arteries, medical co-morbidities, and prior surgical history. Patients with aortic calcification, RV dysfunction, or astringent MAC are considered relative contraindications. Lodge of Thoracic Surgeons (STS) risk calculation tin can be performed to assist with conclusion of surgical risk, including that of bloodshed and major morbidity. Astringent LV dysfunction is also a relatively contraindication as repair of the mitral valve leads to a competent valve, thereby increasing afterload on the LV. Thus, the pre-operative LV function and ejection fraction usually overestimates the true left ventricular function in cases of severe MR since the regurgitant valve acts as a "pop-off" valve. Severe emphysema, restrictive lung disease, and pulmonary hypertension (PHT) are also commonly seen comorbidities with severe longstanding MR and pose relative contraindication to surgery.[xiv]

Equipment

MVr requires cardiopulmonary bypass and, in the vast majority of cases, requires full cardiac arrest. Standard equipment volition include instrumentations necessary for open cardiac operations. Transesophageal echocardiography is mandatory for intraoperative evaluation of repair and ventricular role.

Personnel

MVr requires standard open cardiac surgical staff, which includes at a minimum: cardiac surgeon experienced in mitral valve surgery, cardiac anethesiologist, perfusionist, surgical banana, surgical scrub nurse or technician, and circulating nurse. Postoperatively, care of these patients requires a critical care intensivist, cardiologist, intensive intendance and ward nursing, physical therapy, and social workers.

Preparation

Preoperative assessment of patients before cardiac surgery requires an appraisement of the patient and procedural risks, including a thorough history, focused physical examination, and review of diagnostic studies and pertinent consultant preoperative evaluations. Pregnant cardiovascular risk factors include myocardial ischemia, ventricular dysfunction with eye failure, and atherosclerotic illness of the carotid arteries or proximal aorta. The etiology of ventricular dysfunction is essential to establish optimal perioperative hemodynamic parameters. Patients can exist stratified into depression, intermediate, or loftier take a chance depending on their presentation. Low-risk patients are those with angina without evidence of preoperative MI scheduled for elective surgery. Intermediate risk patients are those with an acute MI who are hemodynamically stable but are usually hospitalized and might be receiving heparin and antiplatelet medications. Loftier-risk patients are those with the highest risk of morbidity and bloodshed, presenting as hemodynamically unstable following an acute MI.[15] Preoperative risk evaluation of patients with CHF includes cess of LV and RV dysfunction. An anesthetic programme should consist of appropriate intraoperative monitoring modalities, optimal coldhearted induction agents, vasoactive infusions, and the need for mechanical support. Pulmonary hypertension, defined as mean pulmonary avenue pressure (PAP) greater than 25 mmHg at rest, significantly increases morbidity and mortality gamble.[fifteen]

Perioperative stroke is common in patients with severe atherosclerosis of the proximal aorta or the carotid arteries. Other comorbidities that require investigation include diabetes, hypertension, previous cerebrovascular event, peripheral vascular disease, and history of smoking-related pulmonary pathology. Perioperative stroke risk is reducible past ensuring that the patient is accordingly taking aspirin, beta-blockers, and statins. Patients with a very high stroke hazard should have an evaluation by a peripheral vascular surgeon before surgery. During cardiac surgery, thrombi or atheromatous debris tin dislodge from aortic plaques during clamping and unclamping of the aorta, or past turbulent high-velocity blood flow via cannulae.[16]

Noncardiac risk factors that cannot be modified include female gender, advanced age, NYHA Iv functional status, preexisting renal insufficiency, prior transient ischemic assail (TIA), anemia, and tobacco use. Preexisting renal insufficiency tin can lead to acute kidney injury (AKI) in about 1 to 2% of patients, which significantly increases mortality.[17] These patients should avoid exposure to nephrotoxic agents, and have their volume status optimized. Reduced cardiac output or hypotension needs to promptly treated. Anemia is a common perioperative finding in cardiac surgical patients and is independently associated with increased transfusion risk.[17] In diabetic patients, hypoglycemia and marked hyperglycemia should exist strictly avoided to prevent perioperative complications. Hypertensive patients should accept chronically administered oral antihypertensive agents continued up to the fourth dimension of surgery, excluding angiotensin-converting enzyme (ACE) inhibitors and angiotensin Two receptor blockers (ARBs).

Patients with chronic obstructive pulmonary illness (COPD) should be at their optimal baseline level of pulmonary office before the intervention. Smokers should receive counsel most preoperative cessation.[18] Ensuring optical preoperative nutrition and postoperative rehabilitation programs has improved functional capacity in elderly patients. For elective surgical procedures, prolonged aortic cross-clamp time and total CPB fourth dimension confer a higher risk. The bloodshed risk also directly correlates with the procedural volume or experience of both the hospital and the cardiac surgeon.[19] Medical direction of MV pathology includes diuretics and charge per unit-controlling agents, such as beta-blockers, for symptomatic relief. Patients with AF should receive anticoagulation with warfarin. Vasodilators are frequently used to reduce arterial resistance and meliorate CO, which increases the MV endmost strength and reduces backflow. Although acute MR reduction is effective with vasodilators, sustained comeback can be challenging.

Technique

Standard MVr is performed utilizing full cardiopulmonary bypass (CPB) and ischemic arrest. At that place are numerous possible surgical approaches, including median sternotomy, right thoracotomy, and robot-assisted. Regardless of incisional approach taken, the cadre principles of mitral valve repair remain the same: the goal is to create a competent mitral valve with skilful coaptation depth, ring annuloplasty, and avoidance of systolic inductive motion. We describe here the surgical techniques for MVr via median sternotomy. This approach is necessary for patients requiring additional concomitant procedures including coronary artery bypass grafting (CABG), ascending aortic intervention, or additional/multiple valve intervention.

Cannulation for CPB is achieved via the ascending aorta and bicaval venous cannulation. Cardioplegic arrest is accomplished via the antegrade and retrograde routes. After aortic crossclamping and acceptable diastolic cardioplegic arrest, the interatrial groove (Sondergaard's or Waterston's) is exposed. Left atriotomy is created away from the pulmonary veins. Alternatively, a transseptal approach can be performed by right atriotomy and incising the septum by the fossa ovalis. Advisable retractors are placed for exposure. The valve is so inspected systematically using saline injection also as visual inspection of each segment. Repair technique will depend on findings of valve pathology. Isolated P2 prolapse, for instance, tin be repaired either past triangular vs. quadrangular resection and ring annuloplasty, or by creating neo-chordae to the appropriate papillary muscle. Nosotros recommend ring annuloplasty for all repairs. Annuloplasty sutures are placed effectually the annulus, and the anterior leaflet height is sized. Depending on MR pathology (primary vs. secondary, ischemic vs. non-ischemic), the ring tin can be truthful-sized or undersized. It is of import to exam the valve for coaptation depth with the ideal depth being about 1 cm. It is also important to avert excessive undersizing of the band as this may cause systolic anterior motion (SAM).

Alain Carpentier's technique for correction of MR includes leaflet repair with quadrangular resection and rigid annuloplasty to correct annular dilatation, adult through dissection and pathology studies of the MV.[20] Lawrie et al. described a functional correction of MR, which spares valve leaflets and chordae during the repair.[26] A flexible annuloplasty ring corrects annular dilatation, and proprietary cloth artificial chordae are used to repair prolapse and realign leaflets.[21] In patients with degenerative MR, the MV annulus can double in size leading to flattening of the valvular orifice and reduced leaflet edge apposition. With inadequate leaflet coaptation, ventricular systole adds additional stress to the leaflet bodies and marginal chordae, leading to further dysfunction and failure.

With Lawrie's technique, avoidance of reoperation and significant recurrent MR as assessed by echocardiography at ten years is 90.1% and 93.9%, respectively, according to reports. Likewise, if the ventricular filling gets optimized through adequate preload and afterload, atrioventricular dyssynchrony is avoided, and hypercontractility is express, at that place is nigh no postoperative systolic anterior movement (SAM).[22] Braunberger et al.reported long-term results of valve repair in nonrheumatic MR.[29] In patients with isolated posterior leaflet prolapse, 10- and twenty-year freedom from reoperation was 98.5% and 96.9%, respectively. In patients with isolated anterior prolapse, it was 86.2% and 82.2%, respectively. In patients with bileaflet prolapse, freedom from reoperation was 88.1% and 82.6%, respectively. These information confirm the results of Carpentier's repair and its stability over an extended period.

Minimally invasive mitral valve surgery (MIMVS) tin exist divided into two groups: fractional sternotomy and right thoracotomy, including the open up and video-assisted methods, with or without robotic help.[27][28] MIMVS has been shown to reduce surgical trauma past avoidance of a total sternotomy incision. MIMVS approaches will require dissimilar cannulation techniques, generally involving the femoral vessels. Sündermann et al. showed equivalent short-term and mid-term outcomes with MIMVS, every bit compared to conventional surgery, regarding the incidence of stroke, mortality, and immovability of repair.[30] Patients who undergo MIMVS accept reduced blood loss, need for blood transfusion, mechanical ventilation time, and intensive care unit stay, equally well every bit a quicker resumption of regular action.[23] Iribarne et al. reported that MIMVS is associated with lower infirmary costs.[32] Due to these highly optimistic results, there has been an increase in the proportion of MIMVS from 10% in 2004 to xx% in 2008. The least invasive approach for MIMVS is robotically assisted, without thoracotomy or meaning rib spreading, simply it also has higher operative costs. This method allows excellent three-dimensional visualization of the valvular and subvalvular appliance via EndoWrist engineering, which permits complex surgical maneuvers.

An innovative approach for the treatment of degenerative MV affliction due to posterior leaflet prolapse is trans-apical chirapsia eye MV repair with polytetrafluoroethylene (PTFE) chordae implantation. CPB is avoided as a small left anterolateral thoracotomy incision is made at the 4th or fifth intercostal space to access the cardiac apex. The Neochordae device used for this procedure allows the md to grasp and pierce the leaflet while pulling the PTFE cord through the prolapsing segment. The neochordae go externalized at the level of the cardiac apex and titrated to maximal coaptation on echocardiography with the resolution of MR. Most patients were found to exist stable at early on follow-up. This technique is utilized to treat MR due to prolapsing lesions early in the history of the illness, with little or no annular dilatation and limited LV remodeling.[24] Trans-catheter techniques are utilized in the presence of prolapse to target both the leaflets and the annulus to achieve favorable long-term results. Excluding ring annuloplasty correlates with poor long term outcomes. Transcatheter methods should exist utilized merely in patients that are appropriate for such interventions.

Complications

Recurrent MR is the most mutual complication following main MVr. Intraoperative assessment via TEE of the repaired valve is crucial, as it can assistance in immediate assessment of the valve. If in that location is persistent mild or greater MR, the valve must be re-explored and either re-repaired or replaced. This decision is critical in cases of impaired LV office, as these patients may non tolerated a long repeat ischemic/abort menstruation. MVr long term durability is more difficult to predict. Flameng et al. [25] reported that only 50% of patients remain free from MV incompetence 7 years following repair. A study by Chikwe et al. [26] demonstrated that mitral valve repair did not confer a long term survival benefit in patients over the historic period of 60 who required concomitant CABG surgery. 50-nine octogenarians undergoing MV surgery for nonrheumatic disease demonstrated similar outcomes between repair and replacement.[27] A Order for Thoracic Surgeons (STS) national database analysis included 8523 MVrs and 3520 MVRs and concluded that there was operative mortality reduction in the MVr cohort equally compared to MVR with and without chordal preservation.[28]

Following successful repair, patients with PHT/AF accept worse long-term survival and event-free survival, as well as increased compromise of MV repair.[29] Based on findings by the Mayo Clinic group, postoperative AF occurs in upwards to 24% of patients previously in sinus rhythm, especially those with LA enlargement, and is associated with increased mortality.[30] To aid with this complication, there has been a contempo trend to perform surgical ablation of AF during mitral valve repair. Up to 32.two% of patients presenting for repair have AF, and concomitant AF ablation took identify in 61.v% of patients according to the STS database.[31] Gillinov et al. reported that the addition of AF ablation to MV surgery increased the rate of liberty from AF at one twelvemonth (63.2% vs. 39.4%) with like mortality in both groups. Still, pacemaker implantation increased in the ablation group.[32]

SAM of the mitral valve can result if there is a discrepancy between the annular surface area and leaflet tissue following repair. SAM is the result of inductive MVP into the left ventricular outflow tract (LVOT) during systole. It most commonly occurs with an undersized annuloplasty ring or excess leaflet tissue.[33] SAM can atomic number 82 to residual MR and LVOT obstacle, both of which are observable on intraoperative transesophageal echocardiography (TEE). If SAM is seen intraoperatively following the repair, the ventricular filling should immediately be optimized, atrioventricular pacing should exist implemented to improve atrioventricular synchrony, and ventricular hypercontractility should lessen. Postoperative beta-blockers are useful in this regard. David and colleagues report freedom from MR ranging from 65 to 80% at 12 years postoperatively, depending on which MV leaflet suffered prolapse.[34] In patients with Barlow disease, Jouan et al. describe a nine.8% recurrence charge per unit of moderate or severe MR.[35]

Clinical Significance

With advanced historic period, degenerative MV affliction is the nigh common cause of MR. MVr is the gold standard for degenerative MR and is the recommendation of the current guidelines for the management of valvular heart disease. The ACC/AHA guidelines recommend that surgery accept identify before LV dysfunction (grade IIa) in experienced centers. Mitral regurgitation imposes significant book overload on the LV, leading to permanent structural and functional deterioration of the myocardium and subsequent centre failure. Timely correction of MR is paramount to the preservation of cardiac function. MIMVS and transcatheter MVr technologies have been instrumental in allowing repair of MV pathology in high-adventure patients who are non appropriate for open-heart surgery.

Enhancing Healthcare Team Outcomes

MR is the second most common valvular center disease after aortic stenosis in the general population and requires an interprofessional healthcare team for management. In industrialized countries, the virtually mutual etiology is degenerative MV affliction leading to prolapse caused by either myxomatous degeneration or fibroelastic deficiency. MVr is preferred over MVR if complete and durable repair tin can exist achieved. While the natural history of this valvular pathology is poor, leading to eventual LV decompensation, an advisable and timely repair can exist lifesaving and prolongs life expectancy to that of the healthy age-matched population. Mortality is increased in patients with symptoms of CHF and reduced EF. Transcatheter techniques may exist challenging in patients with certain anatomical limitations, including calcified leaflets and avant-garde disease. Repair is not e'er effective, and patient option is imperative to prevent the recurrence of MR.

The success of repair depends partially on the centre and the surgeon'southward level of experience. Intraoperative collaboration with cardiac anesthesia and TEE is critical. Current guidelines advise that these procedures should take identify at "Heart Valve Centers of Excellence" (HVCE) that offering comprehensive options for diagnosis and direction of the valvular illness.[36] An HVCE should deliver superior quality of intendance due to a larger book of repair procedures, avant-garde imaging techniques, and greater transparency regarding patient outcomes.[37] An annual surgical volume of fewer than 25 cases per year correlates with lower repair rate, increased one-twelvemonth mortality, and a higher incidence of subsequent reoperation.[38]

An interprofessional team dedicated to these patients should include cardiologists, anesthesiologists, nurse anesthetists, and intensivists. Cardiology specialty nursing should be available to assistance at every step, both perioperatively as well equally during the procedures, working in collaboration with the clinicians and specialists to provide monitoring and patient and family unit education. Perioperative evaluation should consist of high-quality TEE with 3-dimensional technology. Goals for repair should include below 1% mortality for isolated repair, a near 100% repair charge per unit, and less than v% repair failure at a five-twelvemonth follow-up. Centers should be involved in research and innovation of techniques for procedural improvement. A successful HVCE should adhere to international guidelines, engage in the appropriate and timely referral of patients, partake in evaluation and enhancement of patient outcomes, and participate in regional or national upshot registries. With an interprofessional team approach, including specialists, clinicians, nurses, and pharmacists, patient results tin amend, and agin events kept to a minimum, resulting in a improve quality of life and improve outcomes. [Level 5]

Nursing, Allied Wellness, and Interprofessional Team Interventions

The role of the nurse is limited to the care of the postoperative patient. This includes:

• Educating the patient on the grade of the illness

• Encourage incentive spirometry

• Ambulate

• Eat a good for you nutrition

• Remain compliant to medications-esp if an oral anticoagulant has been prescribed

• Maintain a salubrious body weight

• Exist aware of antibiotic precautions when undergoing invasive tests or procedures

Nursing, Allied Wellness, and Interprofessional Team Monitoring

After surgery, the nursing responsibilities include:

• Monitor vital signs

• Monitor Ins and Outs

• Cheque daily labs and x-ray

• Monitor output from the mediastinal tubes

• Assess neurovitals

• Check and clean the wounds

• Dispense medications every bit ordered

Review Questions

Figure

Bereft mitral valve (the valve no longer closes). Contributed by Bruno Bordoni, PhD.

Figure

Mitral Valve, Repair Tabular array 01. Contributed by Irim Salik, Doctor

Effigy

Mitral Valve, Repair Table 02. Contributed by Irim Salik, Physician

Figure

Mitral valve beefcake. Image courtesy S Bhimji MD

Effigy

Mitral valve anatomy. Image courtesy Due south Bhimji Md

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Source: https://www.ncbi.nlm.nih.gov/books/NBK549879/

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