Mitral regurgitation and Mitral Valve Prolapse Flashcards
A holosystolic murmur heard at the apex, radiating to the axilla is due to what underlying condition?
Mitral regurgitation. This is caused by the backflow of blood from the left ventricle into the left atrium during systole due to mitral valve incompetence. MR is a holosystolic murmur best heard at the apex, radiating to the axilla.
What are the primary causes of mitral regurgitation?
The primary causes of mitral regurgitation result from a disruption of the mitral valve apparatus itself:
- Degenerative valve disease (e.g., mitral valve prolapse, myxomatous degeneration).
- Dysfunction from valve leaflets or chordae tendineae.
- Endocarditis.
- Rheumatic valve disease.
What is the most common primary cause of mitral regurgitation?
Mitral valve prolapse (MVP) secondary to myxomatous degeneration.
Why does endocarditis lead to mitral regurgitation?
Infective endocarditis involving the mitral valve can lead to acute mitral regurgitation due to inadequate leaflet coaptation, leaflet perforation, or papillary muscle involvement.
What is the most common cause of rheumatic valve disease?
Acute rheumatic fever is an inflammatory condition most often seen following group A streptococcal infection. Major manifestations are migratory arthritis, carditis or valvulitis, central nervous system involvement with Sydenham chorea, erythema marginatum, and subcutaneous nodules. Sequelae of acute rheumatic fever is Post-Streptococcal Autoimmune Reaction. It is important to note that antibiotics play a crucial role in preventing rheumatic heart disease (RHD) by targeting group A Streptococcus (GAS) infections, which are the underlying cause of acute rheumatic fever (ARF) and its progression to RHD. However, antibiotics do not reliably prevent post-streptococcal glomerulonephritis (PSGN), even if the group A Streptococcal (GAS) infection is treated promptly.
What is the most common secondary cause of mitral regurgitation?
Mitral regurgitation can also be secondary, resulting from heart disease, such as left ventricular dilation in the setting of dilated cardiomyopathy. Other secondary causes of mitral regurgitation that involve left ventricular dysfunction leading to poor mitral valve leaflet closure are papillary muscle rupture, functional heart failure, and hypertrophic cardiomyopathy (SAM).
What causes mitral regurgitation to increase in intensity over time?
Chronic MR is primarily driven by LV dilation (ischemic or non-ischemic) leading to progressive heart failure symptoms. In chronic MR, the left atrium becomes more compliant and the lower left atrial pressures facilitate greater regurgitant flow.
What are the features of chronic mitral regurgitation?
Progressive symptoms of left-sided heart failure, such as exertional dyspnea, fatigue, and atrial fibrillation.
Is the murmur that is associated with mitral regurgitation (MR) High or Low pitched?
The murmur of mitral regurgitation (MR) is a high-pitched, blowing, holosystolic murmur best heard at the apex with the diaphragm of the stethoscope. Since MR is a left-sided murmur, its intensity changes based on preload, afterload, and contractility.
Where does the murmur from mitral regurgitation radiate?
Axilla.
What are the maneuvers that will increase the intensity of mitral regurgitation?
- The intensity is increased preload (leg raise or squat)
- The intensity is increased afterload (handgrip)
A physiologic break-down of blood flow in mitral regurgitation:
In patients with MR, some of the blood in the left ventricle is pumped forward through the aortic valve (forward stroke volume), and some is forced backward through the incompetent mitral valve (regurgitant stroke volume). The amount of blood flowing down each pathway is determined by the relative contribution of the resistance of each pathway to the total left ventricular afterload. Resistance to forward flow is primarily determined by the pressure in the aorta (systolic blood pressure). Resistance to regurgitant flow is determined by the mitral valve orifice size during systole and the degree of left atrial compliance. A reduction in systemic vascular resistance leads to reduced systemic blood pressure and an increase in the ratio of forward to regurgitant blood flow. Pharmacologic vasodilators (eg, nitroprusside) therefore help to increase forward cardiac output and reduce pulmonary congestion in patients with MR. A decrease in heart rate leads to an increase in venous return to the left ventricle (preload) due to increased diastolic filling time. This causes an absolute increase in both forward and regurgitant blood flow (stroke volume increases in accordance with the Frank-Starling mechanism), but the ratio of forward to regurgitant flow is unlikely to significantly change. A reduction in venous return to the left ventricle decreases stroke volume with absolute reductions in both forward and regurgitant flow, but is unlikely to significantly affect the ratio of forward to regurgitant flow. An increase in left ventricular contractility increases stroke volume and leads to an increase in both forward and regurgitant blood flow. However again, as the relative resistance of each pathway is unchanged, the ratio of forward to regurgitant blood flow remains essentially the same.
During what phase in the respiratory cycle is mitral regurgitation more intense?
Expiration increases blood flow to the left heart → More regurgitation → Louder murmur.
Could positioning of the patient enhance the sound of mitral regurgitation?
Left lateral decubitus position enhances mitral sounds.
What would lessen the intensity of mitral regurgitation?
- Inspiration
- Decrease in afterload
- Decrease in preload
A physiologic break-down of blood flow in mitral regurgitation:
In patients with MR, some of the blood in the left ventricle is pumped forward through the aortic valve (forward stroke volume), and some is forced backward through the incompetent mitral valve (regurgitant stroke volume). The amount of blood flowing down each pathway is determined by the relative contribution of the resistance of each pathway to the total left ventricular afterload. Resistance to forward flow is primarily determined by the pressure in the aorta (systolic blood pressure). Resistance to regurgitant flow is determined by the mitral valve orifice size during systole and the degree of left atrial compliance. A reduction in systemic vascular resistance leads to reduced systemic blood pressure and an increase in the ratio of forward to regurgitant blood flow. Pharmacologic vasodilators (eg, nitroprusside) therefore help to increase forward cardiac output and reduce pulmonary congestion in patients with MR. A decrease in heart rate leads to an increase in venous return to the left ventricle (preload) due to increased diastolic filling time. This causes an absolute increase in both forward and regurgitant blood flow (stroke volume increases in accordance with the Frank-Starling mechanism), but the ratio of forward to regurgitant flow is unlikely to significantly change. A reduction in venous return to the left ventricle decreases stroke volume with absolute reductions in both forward and regurgitant flow, but is unlikely to significantly affect the ratio of forward to regurgitant flow. An increase in left ventricular contractility increases stroke volume and leads to an increase in both forward and regurgitant blood flow. However again, as the relative resistance of each pathway is unchanged, the ratio of forward to regurgitant blood flow remains essentially the same.
What phase of the respiratory cycle would decrease the intensity of mitral regurgitation?
- Inspiration (decreases preload).
What might be seen clinically as a result of the manifestations that are secondary to mitral regurgitation?
Symptoms range from asymptomatic to left-sided heart failure:
- Fatigue
- Dyspnea
- Orthopnea
- Crackles on lung auscultation (due to decompensated left-sided heart failure).
What specific murmur is associated with mitral valve prolapse (MVP)?
Cardiac auscultation in patients with mitral valve prolapse (MVP) typically reveals a nonejection click due to snapping of the mitral chordae as the valve cusps extend into the atrium during systole, followed by a systolic murmur of mitral regurgitation. It is best heard in the left lateral decubitus position at the cardiac apex.
Would Valsalva standing increase or decrease the intensity of the murmur associated with mitral valve prolapse?
Increase (less preload = less blood = more murmur).
How would the intensity of the murmur associated with mitral valve prolapse change with squatting, leg raise, or hand grip?
The intensity of the murmur would decrease.
What dictates the intensity of murmur for mitral valve prolapse?
In each patient with MVP there is a critical left ventricular size at which prolapse occurs during ventricular contraction; therefore, the timing of the click and murmur during systole varies depending on left ventricular end-diastolic volume (LVEDV). Patients with mitral valve prolapse (MVP) typically have single or multiple (mid-systolic) non-ejection clicks and/or mid to late systolic murmur of mitral regurgitation that is best heard at or just medial to the cardiac apex. The systolic murmur of MVP starts earlier (and is longer and softer) with standing, Valsalva, and inhalation of amyl nitrate. Conversely, it is delayed in onset (and shorter in duration) with squatting, leg elevation, and handgrip.
What are the common causes for degenerative valve disease leading to mitral valve prolapse?
- Primary: idiopathic or familial.
- Secondary: connective tissue disease diseases such as Ehlers-Danlos syndrome and Marfan syndrome.
Patients with mitral valve prolapse, especially when it is related to underlying connective tissue disease (eg, Marfan syndrome, Ehlers-Danlos syndrome), are at risk for mitral chordae tendineae rupture, leading to a flail leaflet and acute MR.
What dangerous condition does the most common cause of mitral regurgitation predispose patients to in terms of onset of mitral valve regurgitation?
myxomatous degeneration (MVP) predisposes patients to acute mitral valve regurgitation.
What are the features of acute mitral regurgitation?
Sudden onset of severe symptoms such as pulmonary edema and cardiogenic shock. Common causes include papillary muscle or chordae rupture. Patients have acute heart failure due to acute mitral valve regurgitation (MR). Acute mitral valve regurgitation can occur due to papillary muscle rupture, typically in the setting of myocardial infarction (MI), or due to rupture of the mitral chordae tendineae. Patients with mitral valve prolapse, especially when it is related to underlying connective tissue disease (eg, Marfan syndrome, Ehlers-Danlos syndrome), are at risk for mitral chordae tendineae rupture, leading to a flail leaflet and acute mitral valve regurgitation. Patients with acute mitral valve regurgitation typically have a dramatic presentation (due to lack of time for left heart adaptation) compared to those with chronic MR. They often present with sudden-onset hypotension and can rapidly progress to cardiogenic shock with poor tissue perfusion and peripheral vasoconstriction. Cardiac examination reveals a hyperdynamic precordium from equalization of left atrial and left ventricular pressures and a decrescendo holosystolic murmur at the cardiac apex, but up to 50% (especially with ischemic MR) may have no audible murmur (silent MR). The diagnosis is typically confirmed by rapid bedside echocardiography.
Spontaneous papillary muscle rupture tends to occur … ?
Papillary muscle rupture typically 3-5 days after an infarct of the myocardium. This presents with with acute, severe MR and is a life-threatening mechanical complication of acute MI, leading to cardiogenic shock. When there are acute findings of cardiogenic shock along with the absence of ischemia on ECG in a younger patient, the cause is more likely from dysfunction or rupture of mitral chordae tendineae, rather than sequelae from a myocardial infarction.
What is the test of choice for diagnosing mitral regurgitation?
Transthoracic echocardiography (TTE) to assess regurgitation severity and left atrial/ventricular dilation.
What echocardiographic findings are associated with mitral regurgitation?
Regurgitation into the left atrium and left atrial dilation.
What is the management of acute mitral regurgitation?
Emergent valve repair or replacement.
What is the management of chronic mitral regurgitation?
Medical therapy for heart failure (e.g., diuretics, ACE inhibitors) and surgery if severe or symptomatic.
What are potential complications of untreated mitral regurgitation?
Left-sided heart failure, pulmonary hypertension, and atrial fibrillation.
What are the indications for valve replacement in mitral regurgitation (MR)?
Once primary MR becomes severe, close monitoring is required to determine the optimal timing of surgical valve repair/replacement to prevent irreversible LV dysfunction. In patients with severe primary MR and associated symptoms, prompt valve surgery is indicated. In addition, prompt valve surgery is indicated in all patients regardless of symptoms with severe LV dilation or a LV ejection fraction (LVEF) ≤ 60%, which is relatively high LVEF cutoff because severe MR allows for a large portion of the LVEF to flow backward through a low-resistance pathway into the left atrium rather than forward into the aorta. Given this limitation of forward ejection fraction, the expected LVEF in severe MR is substantially higher than normal. In other words, in severe mitral regurgitation (MR), a substantial portion of the left ventricular stroke volume is ejected backward into the low-resistance left atrium instead of forward into the high-resistance aorta. This artificially inflates the left ventricular ejection fraction (LVEF) because the heart is still ejecting a large proportion of its volume, just in the wrong direction. Whenever possible, surgical mitral valve repair is favored over prosthetic valve replacement because prosthetic mitral valve replacement necessitates life-long anticoagulation and creates increased risk of infective endocarditis.
