D . B A S E M E L S A I D E N A N Y
L E C T U R E R O F C A R D I O L O G Y
A I N S H A M S U N I V E R S I T Y
Acute Aortic regurge
ETIOLOGY
-Usually a medical emergency cardiogenic shock (no compensatory mechanisms)
-Endocarditis:
valve destruction, leaflet perforation
aortic perivalvular abscess may rupture into the left ventricle, resulting in AR, or into
the left atrium or right ventricular outflow tract, with a clinical presentation that
mimics acute aortic regurgitation.
-Aortic dissection:
Mechanisms:
Dilation of the sinuses with incomplete coaptation of the leaflets at the center of the
valve
involvement of a valve commissure resulting in inadequate leaflet support
Direct extension of the dissection into the base of a leaflet, resulting in a flail valve
leaflet
Prolapse of the dissection flap across the aortic valve into the left ventricular outflow
tract in diastole impeding leaflet closure.
-Rupture of a congenitally fenestrated cusp
-Traumatic rupture of the valve leaflets
-Iatrogenic : aortic balloon valvotomy or a failed surgical valve repair
-Acute mechanical valve regurgitation can be caused by valve thrombosis, IEC
PATHOPHYSIOLOGY
--Acute increase in left ventricular diastolic pressure
and a fall in forward cardiac output exacerbated by a
shortening of diastolic filling time {early closure of the
mitral valve (due to high end diastolic pressures) +
tachycardia (caused by a decrease in forward flow and
cardiac output)}.
The net effect is often profound hypotension and
cardiogenic shock.
--Elevated left ventricular end-diastolic pressure leads
to elevated left atrial and pulmonary venous pressures,
which can lead to pulmonary edema
CLINICAL PRESENTATION
--Sudden cardiovascular collapse.
--Other presenting symptoms are related to the cause
of acute AR (eg, signs and symptoms of endocarditis or
aortic dissection)
Physical examination
--Manifestations of cardiogenic shock  profound
hypotension, pallor, diaphoresis, occasional cyanosis, and
other signs of peripheral vasoconstriction.
--The pulse pressure is normal or may be reduced, but the
pulse is usually weak, thready, and rapid.
--If aortic dissection  inequality of pulses and blood
pressure between the left and right arms may be observed
{may not be appreciated in the setting of profound
hypotension}.
--The cardiac apex is generally not displaced and is not
hyperdynamic.
--peripheral manifestations of chronic AR are less apparent
or may be entirely absent (no wide pulse pressure)
Cardiac auscultation
--The early closure of the mitral valve generally produces a soft or
absent S1
--The aortic component of S2 is often soft, while P2 is usually
increased, reflecting pulmonary hypertension.
--An S3 is frequently heard but an S4 is absent.
--In contrast to the high pitched holodiastolic decrescendo murmur of
chronic AR, the murmur with acute AR is a low pitched early diastolic
murmur beginning after S2, may not be heard, especially when the
diastolic gradient between the aorta and left ventricle lessens.
--A systolic murmur resulting from the increased volume of blood
crossing the aortic valve may be heard, but is usually not loud.
--The combination of a soft systolic and a low-pitched diastolic
murmur often produces a "to-and-fro" murmur at the cardiac base in
acute AR.
Electrocardiogram
--No specific electrocardiographic changes.
--Nonspecific ST and T wave abnormalities are
common due to the markedly elevated left ventricular
pressures.
--If acute AR is due to aortic dissection, involvement of
the right coronary artery can result in ECG findings of
acute myocardial infarction
Chest radiograph
-Pulmonary edema redistribution of blood flow to
the upper lobes and an increase in size and amount of
the pulmonary vasculature
-The cardiac silhouette may be markedly enlarged due
to pericardial effusion
-Widened mediastinum may result from aortic root
dilation
Echocardiography
--Diagnostic in acute AR.{TOE more benefits}
--The cause of aortic regurgitation can be determined  aortic valve
endocarditis or aortic dissection
--Severe acute AR is based upon the following findings:
-A vena contracta width (narrowest segment of the color flow jet) >6
mm.
-For central severe jets, the jet width in the left ventricular outflow
tract is large (≥65 percent of the outflow tract width).
-For severe eccentric jets, the visualized jet width is variable.
-A dense continuous wave Doppler signal with a steep diastolic slope
(pressure half-time <200 msec).{rapid equalization of pressure
Ao.,LV}
-The presence of holodiastolic flow reversal in the descending thoracic
and proximal abdominal aorta.
--EF, pericardial effusion
Other imaging modalities
--CT imaging may help delineate the anatomy by
identifying the intimal flap, as well as the site and
extent of dissection and the possible involvement of
major branch arteries.
--Usually no time to perform cardiac catheterization or
contrast angiography. Emergency valve surgery should
not be delayed for coronary angiography if there is
severe acute AR with hemodynamic instability
TREATMENT
--Emergency aortic valve replacement or repair
--If delay  temporary stabilization : intravenous
vasodilators, such as nitroprusside, and possibly
inotropic agents such as dopamine or dobutamine in
an attempt to enhance forward flow and lower left
ventricular end-diastolic pressure.
--An intraaortic balloon pump is contraindicated
because inflation of the balloon in diastole will worsen
the severity of AR.
Acute mild or moderate AR
--Due to an aortic dissection aortic valve
resuspension along with graft replacement of the
ascending aorta often allows preservation of the native
valve with resolution of valve incompetence.
--Due to endocarditis, antibiotic therapy alone may be
sufficient unless the patient has another indication for
valve replacement
Thank you

acute Aortic regurge

  • 1.
    D . BA S E M E L S A I D E N A N Y L E C T U R E R O F C A R D I O L O G Y A I N S H A M S U N I V E R S I T Y Acute Aortic regurge
  • 2.
    ETIOLOGY -Usually a medicalemergency cardiogenic shock (no compensatory mechanisms) -Endocarditis: valve destruction, leaflet perforation aortic perivalvular abscess may rupture into the left ventricle, resulting in AR, or into the left atrium or right ventricular outflow tract, with a clinical presentation that mimics acute aortic regurgitation. -Aortic dissection: Mechanisms: Dilation of the sinuses with incomplete coaptation of the leaflets at the center of the valve involvement of a valve commissure resulting in inadequate leaflet support Direct extension of the dissection into the base of a leaflet, resulting in a flail valve leaflet Prolapse of the dissection flap across the aortic valve into the left ventricular outflow tract in diastole impeding leaflet closure. -Rupture of a congenitally fenestrated cusp -Traumatic rupture of the valve leaflets -Iatrogenic : aortic balloon valvotomy or a failed surgical valve repair -Acute mechanical valve regurgitation can be caused by valve thrombosis, IEC
  • 3.
    PATHOPHYSIOLOGY --Acute increase inleft ventricular diastolic pressure and a fall in forward cardiac output exacerbated by a shortening of diastolic filling time {early closure of the mitral valve (due to high end diastolic pressures) + tachycardia (caused by a decrease in forward flow and cardiac output)}. The net effect is often profound hypotension and cardiogenic shock. --Elevated left ventricular end-diastolic pressure leads to elevated left atrial and pulmonary venous pressures, which can lead to pulmonary edema
  • 4.
    CLINICAL PRESENTATION --Sudden cardiovascularcollapse. --Other presenting symptoms are related to the cause of acute AR (eg, signs and symptoms of endocarditis or aortic dissection)
  • 5.
    Physical examination --Manifestations ofcardiogenic shock  profound hypotension, pallor, diaphoresis, occasional cyanosis, and other signs of peripheral vasoconstriction. --The pulse pressure is normal or may be reduced, but the pulse is usually weak, thready, and rapid. --If aortic dissection  inequality of pulses and blood pressure between the left and right arms may be observed {may not be appreciated in the setting of profound hypotension}. --The cardiac apex is generally not displaced and is not hyperdynamic. --peripheral manifestations of chronic AR are less apparent or may be entirely absent (no wide pulse pressure)
  • 6.
    Cardiac auscultation --The earlyclosure of the mitral valve generally produces a soft or absent S1 --The aortic component of S2 is often soft, while P2 is usually increased, reflecting pulmonary hypertension. --An S3 is frequently heard but an S4 is absent. --In contrast to the high pitched holodiastolic decrescendo murmur of chronic AR, the murmur with acute AR is a low pitched early diastolic murmur beginning after S2, may not be heard, especially when the diastolic gradient between the aorta and left ventricle lessens. --A systolic murmur resulting from the increased volume of blood crossing the aortic valve may be heard, but is usually not loud. --The combination of a soft systolic and a low-pitched diastolic murmur often produces a "to-and-fro" murmur at the cardiac base in acute AR.
  • 7.
    Electrocardiogram --No specific electrocardiographicchanges. --Nonspecific ST and T wave abnormalities are common due to the markedly elevated left ventricular pressures. --If acute AR is due to aortic dissection, involvement of the right coronary artery can result in ECG findings of acute myocardial infarction
  • 8.
    Chest radiograph -Pulmonary edemaredistribution of blood flow to the upper lobes and an increase in size and amount of the pulmonary vasculature -The cardiac silhouette may be markedly enlarged due to pericardial effusion -Widened mediastinum may result from aortic root dilation
  • 9.
    Echocardiography --Diagnostic in acuteAR.{TOE more benefits} --The cause of aortic regurgitation can be determined  aortic valve endocarditis or aortic dissection --Severe acute AR is based upon the following findings: -A vena contracta width (narrowest segment of the color flow jet) >6 mm. -For central severe jets, the jet width in the left ventricular outflow tract is large (≥65 percent of the outflow tract width). -For severe eccentric jets, the visualized jet width is variable. -A dense continuous wave Doppler signal with a steep diastolic slope (pressure half-time <200 msec).{rapid equalization of pressure Ao.,LV} -The presence of holodiastolic flow reversal in the descending thoracic and proximal abdominal aorta. --EF, pericardial effusion
  • 10.
    Other imaging modalities --CTimaging may help delineate the anatomy by identifying the intimal flap, as well as the site and extent of dissection and the possible involvement of major branch arteries. --Usually no time to perform cardiac catheterization or contrast angiography. Emergency valve surgery should not be delayed for coronary angiography if there is severe acute AR with hemodynamic instability
  • 11.
    TREATMENT --Emergency aortic valvereplacement or repair --If delay  temporary stabilization : intravenous vasodilators, such as nitroprusside, and possibly inotropic agents such as dopamine or dobutamine in an attempt to enhance forward flow and lower left ventricular end-diastolic pressure. --An intraaortic balloon pump is contraindicated because inflation of the balloon in diastole will worsen the severity of AR.
  • 12.
    Acute mild ormoderate AR --Due to an aortic dissection aortic valve resuspension along with graft replacement of the ascending aorta often allows preservation of the native valve with resolution of valve incompetence. --Due to endocarditis, antibiotic therapy alone may be sufficient unless the patient has another indication for valve replacement
  • 13.