Acute aortic and mitral regurgitation: Causes, Diagnosis, Management, by Nursesnote

 Acute Aortic and Mitral Regurgitation 

Acute Aortic 

• Sudden, severe aortic regurgitation (AR) presents as cardiogenic shock and acute pulmonary edema. 
• The hemodynamic changes are markedly different from those seen in chronic AR.  The previous normal-sized LV results in a smaller effective forward flow and higher LVEDP for the same degree of AR. 
• Patients are often extremely unstable, tachycardic, and peripherally vasoconstricted and often have pulmonary edema. Unlike chronic AR,  pulse pressure may be near normal. 
• If available, ask about history of previous valvular heart disease, hypertension, features of Marfan's syndrome (family history), and risk factors for infective endocarditis. 
• Physical signs of severe AR include a quit aortic closure sound (S2); high-pitched and short, early diastolic murmur  (AR); quiet S1 ( premature closure of the mitral valve )
• Examine specifically for signs of an underlying cause. 
• Where there is no obvious underlying cause (e.g.  acute MI ) assume infective endocarditis until proven otherwise. 

Causes 

• Infective endocarditis 
• Ascending aortic dissection 
• Collagen vascular disorders  ( e.g.Marfan's )
• Connective tissue disease (large - and medium - vessel arteries )
• Trauma 
• Dehiscence of a prosthetic valve 

Diagnosis 

Diagnosis is based on a combination of clinical features and transthoracic and transesophageal ECHO.

Management 

Acute AR is a surgical emergency and all other management measures are only aimed at stabilizing the patient until urgent aortic valve replacement (AVR) can take place. The patients clinical condition will determine the urgency of surgery ( and risk of mortality ).

General Measures 

• Admit the patient to intensive care unit (ICU)
• Give oxygen and begin treating any pulmonary edema with diuretics. 
• Monitor blood gases; mechanical ventilation may be necessary. 
• Serial ECG: watch for developing atrioventricular (AV) block or conduction defects endocarditis. 

Specific measures 

• Every patient must be discussed with a cardiothoracic surgeon.
• In the context of good systematic BP, vasodilators such as sodium nitroprusside or hydralazine may temporarily improve forward flow and relive pulmonary edema.
• Inotropic support may be necessary if the patient is hypotensive. However, inotropes are best avoided as any increase in systematic pressures and peripheral vasoconstriction may worsen AR.
• All patient with hemodynamic compromise should have immediate or urgent AVR.
• Infective endocarditis
• Intra-aortic balloon pump (IABP) must be avoided,  as it will worsen AR.

Acute Mitral regurgitation 

• Patients most commonly present with acute shortness of breath and severe pulmonary edema. Symptoms may be less severe, or spontaneously improve as left atrial compliance increases. There may be a history of previous murmur, angina, or myocardial infarction.
• The signs are different from those seen in chronic MR  because of the presence of a nondilated and relatively noncompliant LA, Acute MR results in a large LA systolic pressure wave ( v wave) and hence pulmonary edema.
• Patients may be actually ill with tachycardia, hypotension, peripheral vasoconstriction, and pulmonary edema, and a pan-systolic murmur of MR.
• Later in the illness, probably because of sustained high left atrial and pulmonary venous pressure, right heart failure develops.

Causes of acute mitral regurgitation 

• Infective endocarditis 
• Papillary muscle dysfunction or rupture (post-MI).
• Rupture of chordae tendinae ( e.g. infection, myxomatous degeneration, systemic lupus erythematosus)
• Trauma ( to leaflets, papillary muscle, or chordae)
• Prosthetic valve malfunction ( e.g.secondary to infection )
• Left atrial myxoma
• Acute rheumatic fever
• Collagen vascular disorders 
• Connective tissue disease 

Diagnosis 

Diagnosis is based on a combination of clinical features and ECHO. Transthoracic echocardiography (TTE) can be used to readily diagnose and quantify MR. It also provides information on LV status ( in particular regional wall motion abnormalities that can give rise to MR).

 TEE can provide specific information about etiology of valve dysfunction, including papillary muscle rupture and MV leaflet  (anterior and posterior ) structural abnormalities. This information will be vital for a decision regarding definitive management. The important differential diagnosis is a VSD.

TTE and doppler studies can readily differentiate between the two conditions. Alternatively, if ECHO is not available, pulmonary artery catheterization in acute MR will exclude the presence of a left-right shunt and the pulmonary capillary wedge pressure (PCWP) trace will demonstrate a large v-wave.

General measures 

• Admit patient to ICU. 
• Give oxygen and begin treating any pulmonary edema with diuretics. 
• Monitor blood gases: mechanical ventilation may be necessary. 
• If present, MI should be treated in the standard manner. 

Specific measures 

Pulmonary edema may be very resistant to treatment. 

• In the presence of good BP, reduction in preload ( nitroglycerin infusion ) and afterload, especially with ACE inhibitors, in important. Systemic vasodilators such as hydralazine (12.5-100 mg tid) can also be added. 
• An IABP will help decrease LVEDP and increase coronary blood flow. 
• Patients may require inotropic support. There are multiple combinations and etiologies of MR and hemodynamic status, and local policy and expertise should dictate choice of agent. 
• CPAP and incubation and positive-pressure ventilation are extremely useful and must be considered in all severe and resistant cases. 
• Hemodynamic disturbance and severe pulmonary edema in the context of acute MR is a surgical emergency. 
• Infective endocarditis 
• Post-infract MR: management depends on the patient's condition following resuscitation. Patients who are stabilized may have mitral valve replacement (MVR) deferred because of risk of surgery in the post-infarct patient. Preoperative management should consist of diuretics and vasodilators, including ACE inhibitors if tolerated. Opening the infarct-related artery (angioplasty ) may improve active MR.