Papillary muscle rupture: Difference between revisions
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'''For patient information click [[Heart attack (patient information)|here]]''' | '''For patient information click [[Heart attack (patient information)|here]]''' | ||
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{{CMG}}; | {{CMG}}; {{AOEIC}} {{CZ}} | ||
==Overview== | ==Overview== | ||
Revision as of 01:14, 16 April 2012
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| Papillary Muscle Infarct with Rupture: Gross, an excellent example of ruptured papillary muscle. Image courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology |
For patient information click here
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Papillary muscle rupture Microchapters |
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Diagnosis |
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Treatment |
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Papillary muscle rupture On the Web |
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American Roentgen Ray Society Images of Papillary muscle rupture |
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Risk calculators and risk factors for Papillary muscle rupture |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]
Overview
Papillary muscle rupture is an infrequent mechanical complication of acute myocardial infarction. Early diagnosis is important so that surgical repair can be performed.
Pathophysiology
The vascularization of the papillary muscles shows many individual variations and depends in part on coronary artery anatomy and dominance. However, the posterior papillary muscle is vascularized by posterior left ventricular branches that may have origin in the right, left or both coronary arteries. The anterior papillary muscle is vascularized by branches from diagonal, circumflex or even acute marginal branches of the left coronary artery. Papillary muscle ischemia occurs along with ischemia of the adjacent ventricular wall.
- Acute mitral regurgitation (as may occur due to the sudden rupture of a chordae tendineae or papillary muscle) causes a sudden volume overload of both the left atrium and the left ventricle.
- The left ventricle develops volume overload because with every contraction it now has to pump out not only the volume of blood that goes into the aorta (the forward cardiac output or forward stroke volume), but also the additional blood that regurgitated into the left atrium (the regurgitant volume).
- The combination of the forward stroke volume and the regurgitant volume is known as the total stroke volume of the left ventricle.
- In the acute setting, the total stroke volume (i.e. the forward plus the regurgitant volume) is increased, but the forward cardiac output into the aorta is decreased because a proportion of the blood is going backward into the left atrium. The mechanism by which the total stroke volume is increased as a result of increased left ventricular filling is known as the Frank-Starling mechanism.
The regurgitant volume causes acute volume overload and pressure overload of the left atrium as shown in the figure below. The sudden increase in pressure in the left atrium is transmitted backward into the pulmonary vein which in turn reduces drainage of blood from the lungs via the pulmonary veins and raises the pulmonary capillary sedge pressure. This causes pulmonary congestion.
Pathological Findings
Images shown below are courtesy of Professor Peter Anderson DVM PhD and published with permission. © PEIR, University of Alabama at Birmingham, Department of Pathology
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Papillary Muscle Infarct with Rupture: Gross, left ventricle opened partially to show infarct and ruptured muscle, an excellent example
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Papillary Muscle Infarct with Rupture: Gross, very good example
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Papillary Muscle Infarct: Gross, an excellent example
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Papillary Muscle Infarct: Gross, an excellent example
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Papillary Muscle Infarct with Rupture: Gross, horizontal section of left ventricle looking toward base of heart, a very good example with lateral wall transmural infarct and ruptured papillary muscle
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Papillary Muscle Infarct with Rupture: Gross, an excellent example of ruptured papillary muscle
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Papillary Muscle Infarct with Rupture
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Papillary Muscle Infarct with Rupture: Gross, natural color, close-up, well shown
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Papillary Muscle Infarct: Gross fixed tissue very well shown and typical papillary muscle infarct
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Papillary Muscle Infarct: Gross, natural color, close-up view of longitudinally section. Papillary muscle with obvious infarct, a very good example. There is a large old infarct with aneurysm in the anterior wall. The infarcted papillary muscle is the posterior one.
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Papillary Muscle Thinning: Gross, natural color, band-like anterior papillary muscles secondary to healed infarct which is present in picture (but not easily seen). An excellent example for papillary muscle change
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Mitral Valve Prosthesis and Large Apical Infarct: Gross, natural color, caged plastic ball with complete steel struts. A large recent infarct at apex of heart, at base of posterior papillary muscles. Etiology not completely clear but looks like an iatrogenic lesion (good illustration)
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Myocardial Hemorrhage Following Mitral Valve Replacement: Gross, natural color, horizontal section of left ventricle showing a large area of mural hemorrhage extending from anterior papillary muscle
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Papillary Muscle Infarct with Rupture: Gross, natural color, a close-up view (very good example)
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Papillary Muscle Infarct with Rupture: Gross, fixed tissue, a close-up view (quite good example)
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Papillary Muscle Infarct with Rupture: Gross, fixed tissue, but good color. Horizontal slice of LV with posterior infarct that appears old and a ruptured papillary muscle head.
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Papillary Muscle Infarct with Rupture: Gross, fixed tissue, but good color. An outstanding photo of ruptured head of posterior papillary muscle with entangled chordae
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Papillary Muscle Infarct with Rupture: Gross, fixed tissue, but good color. An outstanding photo of ruptured head of posterior papillary muscle with entwined chordae
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Papillary Muscle Infarct with Rupture: Gross, fixed tissue, but good color. An outstanding photo of ruptured head of posterior papillary muscle with entwined chordae
Diagnosis
Symptoms
The symptoms of an acutely elevated wedge pressure due to papillary muscle rupture include dyspnea, PND, and orthopnea.
Physical Examination
Vitals
Tachycardia and hypotension are often present
Heart
- A palpable thrill may be present
- A harsh, not a blowing murmur is often present throughout the precordium
Lungs
Rales may be present
Echocardiographic Findings of Ruptured Papillary Muscle and Severe MR
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Chest X Ray
Pulmonary edema is present without enlargement of the heart.
Treatment
Acute mitral regurgitation secondary to left ventricular papillary muscle rupture or chordae tendineae rupture, is a medical and surgical emergency. Patients may present with acute pulmonary edema or cardiogenic shock and most often the required and definitive treatment is valvular surgery. However, medical therapy may be needed to stabilize the patient until surgery can be performed.
Medical Therapy
Normotensive patients
Vasodilators may be of use to decrease the afterload and thereby decrease the regurgitant fraction. The vasodilator most commonly used is nitroprusside [1][2]. ACE inhibitors may be useful as oral therapy.
Hypotensive patients
Prior to the surgical procedure, an intra-aortic balloon pump may be placed in order to improve perfusion of the organs and to reduce afterload and thereby decrease the degree of mitral regurgitation [3].
In patients with acute mitral regurgitation secondary to myocardial ischemia/infarction, early coronary revascularization should be performed.
Surgical approach
Patients with rupture of the chordae tendineae or papillary muscle should undergo early mitral valve repair if possible which results in a better preservation of left ventricular function and long term survival in comparison to mitral valve replacement [4].
References
- ↑ Chatterjee K, Parmley WW, Swan HJ, Berman G, Forrester J, Marcus HS (1973). "Beneficial effects of vasodilator agents in severe mitral regurgitation due to dysfunction of subvalvar apparatus". Circulation. 48 (4): 684–90. PMID 4744778. Retrieved 2011-03-18. Unknown parameter
|month=ignored (help) - ↑ Harshaw CW, Grossman W, Munro AB, McLaurin LP (1975). "Reduced systemic vascular resistance as therapy for severe mitral regurgitation of valvular origin". Annals of Internal Medicine. 83 (3): 312–6. PMID 1180426. Unknown parameter
|month=ignored (help);|access-date=requires|url=(help) - ↑ Bonow RO, Carabello BA, Chatterjee K, de Leon AC, Faxon DP, Freed MD, Gaasch WH, Lytle BW, Nishimura RA, O'Gara PT, O'Rourke RA, Otto CM, Shah PM, Shanewise JS (2008). "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". Circulation. 118 (15): e523–661. doi:10.1161/CIRCULATIONAHA.108.190748. PMID 18820172. Retrieved 2011-03-18. Unknown parameter
|month=ignored (help) - ↑ Society of Thoracic Surgeons National Cardiac Surgery Database. Available at : http://www.sts.org/documents/pdf/STSExecutiveSummaryFall2005.pdf. Accessed November 2005