if ever the right ventricle, which is traditionally thought to be the somewhat weaker ventricle, was gonna expose itself as a weaker ventricle, it would be in the fontan circulation
if ever the right ventricle, which is traditionally thought to be the somewhat weaker ventricle, was gonna expose itself as a weaker ventricle, it would be in the fontan circulation
if ever the right ventricle, which is traditionally thought to be the somewhat weaker ventricle, was gonna expose itself as a weaker ventricle, it would be in the fontan circulation
if ever the right ventricle, which is traditionally thought to be the somewhat weaker ventricle, was gonna expose itself as a weaker ventricle, it would be in the fontan circulation
clinical40-50% of cardiac output at baseline in Fontan patients is driven directly by the work of breathing↗
▶Ep 2 · 2:43
clinical40-50% of cardiac output at baseline in Fontan patients is driven directly by the work of breathing↗
▶Ep 2 · 3:14
clinicalNegative mean airway pressure during normal ventilation draws blood into the Fontan circuit↗
▶Ep 2 · 3:14
clinicalNegative mean airway pressure during normal ventilation draws blood into the Fontan circuit↗
▶Ep 2 · 3:25
clinicalValsalva maneuver with mean airway pressure elevated to 20 cm H2O cuts off spontaneous respiratory flow, leaving only tiny flow with ventricular systole↗
▶Ep 2 · 3:25
clinicalValsalva maneuver with mean airway pressure elevated to 20 cm H2O cuts off spontaneous respiratory flow, leaving only tiny flow with ventricular systole↗
▶Ep 2 · 3:49
quotethe fontan circulation is one of the few situations where constipation can be fatal↗
▶Ep 2 · 3:49
quotethe fontan circulation is one of the few situations where constipation can be fatal↗
▶Ep 2 · 4:01
clinicalLow pulmonary vascular resistance is a prerequisite for good Fontan outcome↗
▶Ep 2 · 4:01
clinicalLow pulmonary vascular resistance is a prerequisite for good Fontan outcome↗
▶Ep 2 · 4:52
clinicalIn normal individuals, nitric oxide does not reduce pulmonary vascular resistance because the pulmonary vascular bed is maximally vasodilated↗
▶Ep 2 · 4:52
quotein you and I, if I give you nitric oxide, the pulmonary vascular resistance doesn't fall because we're maximally vasodilated in the pulmonary vascular bed↗
▶Ep 2 · 4:52
clinicalIn normal individuals, nitric oxide does not reduce pulmonary vascular resistance because the pulmonary vascular bed is maximally vasodilated↗
▶Ep 2 · 4:52
quotein you and I, if I give you nitric oxide, the pulmonary vascular resistance doesn't fall because we're maximally vasodilated in the pulmonary vascular bed↗
▶Ep 2 · 5:01
clinicalNitric oxide produced a statistically and physiologically significant fall in pulmonary vascular resistance of about 1 index wood unit in teenage Fontan patients↗
▶Ep 2 · 5:01
clinicalNitric oxide produced a statistically and physiologically significant fall in pulmonary vascular resistance of about 1 index wood unit in teenage Fontan patients↗
▶Ep 2 · 5:39
clinicalOnly half of teenage Fontan patients showed benefit from nitric oxide↗
▶Ep 2 · 5:39
clinicalOnly half of teenage Fontan patients showed benefit from nitric oxide↗
▶Ep 2 · 6:00
opinionIf only half of Fontan patients benefit from nitric oxide, they are unlikely to further benefit from PDE5 inhibitors↗
▶Ep 2 · 6:00
opinionIf only half of Fontan patients benefit from nitric oxide, they are unlikely to further benefit from PDE5 inhibitors↗
▶Ep 2 · 6:36
quoteif ever the right ventricle, which is traditionally thought to be the somewhat weaker ventricle, was gonna expose itself as a weaker ventricle, it would be in the fontan circulation↗
▶Ep 2 · 6:36
quoteif ever the right ventricle, which is traditionally thought to be the somewhat weaker ventricle, was gonna expose itself as a weaker ventricle, it would be in the fontan circulation↗
▶Ep 2 · 6:54
host_summaryCHOP data showed no difference in outcomes in the first 10 years after Fontan between hypoplastic left heart syndrome and systemic left ventricle patients↗
▶Ep 2 · 6:54
epidemiologicalCHOP data showed no difference in outcomes in the first 10 years after Fontan between hypoplastic left heart syndrome and systemic left ventricle patients↗
▶Ep 2 · 7:21
host_summaryBoston data showed patients born with systemic left ventricle with normally related great vessels or single right ventricle do better than all other diagnoses↗
▶Ep 2 · 7:21
epidemiologicalBoston data showed patients born with systemic left ventricle with normally related great vessels or single right ventricle do better than all other diagnoses↗
▶Ep 2 · 7:40
epidemiologicalMelbourne group data showed right ventricular dominance is a risk factor if present at birth, but after surviving the first couple of years post-Fontan, survival curves are essentially identical regardless of ventricular morphology↗
▶Ep 2 · 7:40
host_summaryMelbourne group data showed right ventricular dominance is a risk factor if present at birth, but after surviving the first couple of years post-Fontan, survival curves are essentially identical regardless of ventricular morphology↗
▶Ep 2 · 8:22
clinicalThe systemic ventricle in Fontan circulation is hypercontractile to match its increased afterload↗
▶Ep 2 · 8:22
clinicalThe systemic ventricle in Fontan circulation is hypercontractile to match its increased afterload↗
▶Ep 2 · 8:37
clinicalForce-frequency relationships in systemic right and left ventricles in univentricular circulation outperformed normal ventricles↗
▶Ep 2 · 8:37
host_summaryForce-frequency relationships in systemic right and left ventricles in univentricular circulation outperformed normal ventricles↗
▶Ep 2 · 9:03
host_summaryEnd-systolic elastance in Fontan patients is orders of magnitude higher than normals and even greater than in systemic right ventricle of Mustard patients↗
▶Ep 2 · 9:03
clinicalEnd-systolic elastance in Fontan patients is orders of magnitude higher than normals and even greater than in systemic right ventricle of Mustard patients↗
▶Ep 2 · 9:21
quotethese are strong ventricles that are pumping against, albeit a high resistance↗
▶Ep 2 · 9:21
quotethese are strong ventricles that are pumping against, albeit a high resistance↗
▶Ep 2 · 9:29
clinicalArterial elastance is high in Fontan patients but relatively well coupled to ventricular elastance↗
▶Ep 2 · 9:29
clinicalThe primary problem in Fontan ventricles is in diastole, not systole↗
▶Ep 2 · 9:29
clinicalArterial elastance is high in Fontan patients but relatively well coupled to ventricular elastance↗
▶Ep 2 · 9:29
clinicalThe primary problem in Fontan ventricles is in diastole, not systole↗
▶Ep 2 · 10:14
clinicalIn early post-Fontan course, it is early diastole (E wave) that is affected, not late diastole (A wave), with virtual abolishment of early rapid filling↗
▶Ep 2 · 10:14
clinicalIn early post-Fontan course, it is early diastole (E wave) that is affected, not late diastole (A wave), with virtual abolishment of early rapid filling↗
▶Ep 2 · 10:43
clinicalTime constant of relaxation and isovolumic relaxation time are prolonged in early post-Fontan patients, indicative of impaired relaxation↗
▶Ep 2 · 10:43
clinicalTime constant of relaxation and isovolumic relaxation time are prolonged in early post-Fontan patients, indicative of impaired relaxation↗
▶Ep 2 · 10:56
clinicalImpaired early relaxation is due to incoordinate wall motion during isovolumic relaxation, with post-systolic shortening of one part of the ventricle causing another part to move outward↗
▶Ep 2 · 10:56
clinicalImpaired early relaxation is due to incoordinate wall motion during isovolumic relaxation, with post-systolic shortening of one part of the ventricle causing another part to move outward↗
▶Ep 2 · 11:58
clinicalMRI tagging showed some segments of Fontan ventricular wall were 180 degrees out of phase with other parts, in systole when rest of ventricle was in diastole↗
▶Ep 2 · 11:58
host_summaryMRI tagging showed some segments of Fontan ventricular wall were 180 degrees out of phase with other parts, in systole when rest of ventricle was in diastole↗
▶Ep 2 · 12:23
clinicalLonger isovolumic relaxation time correlates with longer hospital stay immediately after Fontan operation↗
▶Ep 2 · 12:23
clinicalLonger isovolumic relaxation time correlates with longer hospital stay immediately after Fontan operation↗
▶Ep 2 · 13:03
clinicalLate post-Fontan patients can develop pseudonormalized filling pattern (E > A) due to rising left atrial pressure despite persistent incoordinate relaxation↗
▶Ep 2 · 13:03
clinicalLate post-Fontan patients can develop pseudonormalized filling pattern (E > A) due to rising left atrial pressure despite persistent incoordinate relaxation↗
▶Ep 2 · 13:36
clinicalIn normal individuals, left ventricular end-diastolic pressure rises by about 2 mmHg per decade after age 30↗
▶Ep 2 · 13:36
clinicalIn normal individuals, left ventricular end-diastolic pressure rises by about 2 mmHg per decade after age 30↗
▶Ep 2 · 14:18
host_summaryEight-year follow-up of Fontan patients showed maintained incoordinate relaxation, shortened IVRT suggesting rising left atrial pressure, and faster E wave deceleration suggesting falling compliance↗
▶Ep 2 · 14:18
clinicalEight-year follow-up of Fontan patients showed maintained incoordinate relaxation, shortened IVRT suggesting rising left atrial pressure, and faster E wave deceleration suggesting falling compliance↗
▶Ep 2 · 14:47
clinicalDiastolic compliance of Fontan ventricles (predominantly left ventricles) is highly abnormal, unlike Mustard systemic right ventricles where diastolic compliance is not a problem↗
▶Ep 2 · 14:47
host_summaryDiastolic compliance of Fontan ventricles (predominantly left ventricles) is highly abnormal, unlike Mustard systemic right ventricles where diastolic compliance is not a problem↗
▶Ep 2 · 15:06
quoteif you can't fill in early diastole and you can't fill in late diastole, you're not gonna fill at all and you have a low stroke volume and a low cardiac output↗
▶Ep 2 · 15:06
quoteif you can't fill in early diastole and you can't fill in late diastole, you're not gonna fill at all and you have a low stroke volume and a low cardiac output↗
▶Ep 2 · 15:33
clinicalFontan patients with high diastolic stiffness may have low end-diastolic pressure because reduced preload causes the ventricle to become smaller and pressure to fall down the pressure-volume curve↗
▶Ep 2 · 15:33
clinicalFontan patients with high diastolic stiffness may have low end-diastolic pressure because reduced preload causes the ventricle to become smaller and pressure to fall down the pressure-volume curve↗
▶Ep 2 · 15:41
quotein the presence of really profoundly abnormal ventricular compliance, these patients can have a normal left ventricular and diastolic pressure↗
▶Ep 2 · 15:41
quotein the presence of really profoundly abnormal ventricular compliance, these patients can have a normal left ventricular and diastolic pressure↗
▶Ep 2 · 17:37
clinicalBench pressing 500 pounds essentially cuts off pulmonary blood flow in Fontan patients↗
▶Ep 2 · 17:37
clinicalBench pressing 500 pounds essentially cuts off pulmonary blood flow in Fontan patients↗
▶Ep 2 · 18:13
opinionSustained Valsalva maneuvers may be particularly disadvantageous in old atrio-pulmonary Fontans due to direct effects on atrial stretch and potential for chronic atrial arrhythmias↗
▶Ep 2 · 18:13
opinionSustained Valsalva maneuvers may be particularly disadvantageous in old atrio-pulmonary Fontans due to direct effects on atrial stretch and potential for chronic atrial arrhythmias↗
▶Ep 2 · 20:04
host_summaryPHN data at 10-12 years post-Fontan showed systemic right ventricles had far more patients with increased E/E' ratio (indicating increased stiffness) compared to systemic left ventricles↗
▶Ep 2 · 20:04
clinicalPHN data at 10-12 years post-Fontan showed systemic right ventricles had far more patients with increased E/E' ratio (indicating increased stiffness) compared to systemic left ventricles↗
▶Ep 2 · 21:58
clinicalRise in end-diastolic pressure in normal individuals is more rapid with hypertension, diabetes, other risk factors, and ventricular volume load such as AV valve or aortic regurgitation↗
▶Ep 2 · 21:58
clinicalRise in end-diastolic pressure in normal individuals is more rapid with hypertension, diabetes, other risk factors, and ventricular volume load such as AV valve or aortic regurgitation↗
▶Ep 2 · 22:33
clinicalFontan patients frequently have some degree of volume load and have had volume load for the first few years of life↗
▶Ep 2 · 22:33
clinicalFontan patients frequently have some degree of volume load and have had volume load for the first few years of life↗
▶Ep 2 · 22:44
clinicalAll Fontan patients have very raised arterial impedance and systemic vascular resistance↗
▶Ep 2 · 22:44
clinicalAll Fontan patients have very raised arterial impedance and systemic vascular resistance↗
▶Ep 2 · 23:01
host_summaryRecent conductance catheter work from the Netherlands shows a tight relationship between arterial elastance and ventricular end-diastolic pressure↗
▶Ep 2 · 23:01
clinicalRecent conductance catheter work from the Netherlands shows a tight relationship between arterial elastance and ventricular end-diastolic pressure↗
▶Ep 2 · 23:18
opinionThere is no evidence-based role for ACE inhibition or arterial vasodilators in short-term Fontan management, as systemic vasodilation drops cardiac output↗
▶Ep 2 · 23:18
opinionThere is no evidence-based role for ACE inhibition or arterial vasodilators in short-term Fontan management, as systemic vasodilation drops cardiac output↗
▶Ep 2 · 23:38
opinionManagement of left ventricular end-diastolic pressure, fibrosis, and vascular biology have real potential as therapeutic targets in long-term Fontan management↗
▶Ep 2 · 23:38
opinionManagement of left ventricular end-diastolic pressure, fibrosis, and vascular biology have real potential as therapeutic targets in long-term Fontan management↗
▶Ep 2 · 23:58
opinionUnderstanding the impact of long-term therapies for diastolic dysfunction will require 10-20 years of follow-up↗
▶Ep 2 · 23:58
opinionUnderstanding the impact of long-term therapies for diastolic dysfunction will require 10-20 years of follow-up↗
clinical40-50% of cardiac output at baseline in Fontan patients is driven directly by the work of breathing↗
▶Ep 13 · 2:43
clinical40-50% of cardiac output at baseline in Fontan patients is driven directly by the work of breathing↗
▶Ep 13 · 3:14
clinicalNegative mean airway pressure during normal ventilation draws blood into the Fontan circuit↗
▶Ep 13 · 3:14
clinicalNegative mean airway pressure during normal ventilation draws blood into the Fontan circuit↗
▶Ep 13 · 3:25
clinicalValsalva maneuver with mean airway pressure elevated to 20 cm H2O cuts off spontaneous respiratory flow, leaving only tiny flow with ventricular systole↗
▶Ep 13 · 3:25
clinicalValsalva maneuver with mean airway pressure elevated to 20 cm H2O cuts off spontaneous respiratory flow, leaving only tiny flow with ventricular systole↗
▶Ep 13 · 3:49
quotethe fontan circulation is one of the few situations where constipation can be fatal↗
▶Ep 13 · 3:49
quotethe fontan circulation is one of the few situations where constipation can be fatal↗
▶Ep 13 · 4:01
clinicalLow pulmonary vascular resistance is a prerequisite for good Fontan outcome↗
▶Ep 13 · 4:01
clinicalLow pulmonary vascular resistance is a prerequisite for good Fontan outcome↗
▶Ep 13 · 4:52
clinicalIn normal individuals, nitric oxide does not reduce pulmonary vascular resistance because the pulmonary vascular bed is maximally vasodilated↗
▶Ep 13 · 4:52
quotein you and I, if I give you nitric oxide, the pulmonary vascular resistance doesn't fall because we're maximally vasodilated in the pulmonary vascular bed↗
▶Ep 13 · 4:52
quotein you and I, if I give you nitric oxide, the pulmonary vascular resistance doesn't fall because we're maximally vasodilated in the pulmonary vascular bed↗
▶Ep 13 · 4:52
clinicalIn normal individuals, nitric oxide does not reduce pulmonary vascular resistance because the pulmonary vascular bed is maximally vasodilated↗
▶Ep 13 · 5:01
clinicalNitric oxide produced a statistically and physiologically significant fall in pulmonary vascular resistance of about 1 index wood unit in teenage Fontan patients↗
▶Ep 13 · 5:01
clinicalNitric oxide produced a statistically and physiologically significant fall in pulmonary vascular resistance of about 1 index wood unit in teenage Fontan patients↗
▶Ep 13 · 5:39
clinicalOnly half of teenage Fontan patients showed benefit from nitric oxide↗
▶Ep 13 · 5:39
clinicalOnly half of teenage Fontan patients showed benefit from nitric oxide↗
▶Ep 13 · 6:00
opinionIf only half of Fontan patients benefit from nitric oxide, they are unlikely to further benefit from PDE5 inhibitors↗
▶Ep 13 · 6:00
opinionIf only half of Fontan patients benefit from nitric oxide, they are unlikely to further benefit from PDE5 inhibitors↗
▶Ep 13 · 6:36
quoteif ever the right ventricle, which is traditionally thought to be the somewhat weaker ventricle, was gonna expose itself as a weaker ventricle, it would be in the fontan circulation↗
▶Ep 13 · 6:36
quoteif ever the right ventricle, which is traditionally thought to be the somewhat weaker ventricle, was gonna expose itself as a weaker ventricle, it would be in the fontan circulation↗
▶Ep 13 · 6:54
host_summaryCHOP data showed no difference in outcomes in the first 10 years after Fontan between hypoplastic left heart syndrome and systemic left ventricle patients↗
▶Ep 13 · 6:54
epidemiologicalCHOP data showed no difference in outcomes in the first 10 years after Fontan between hypoplastic left heart syndrome and systemic left ventricle patients↗
▶Ep 13 · 7:21
epidemiologicalBoston data showed patients born with systemic left ventricle with normally related great vessels or single right ventricle do better than all other diagnoses↗
▶Ep 13 · 7:21
host_summaryBoston data showed patients born with systemic left ventricle with normally related great vessels or single right ventricle do better than all other diagnoses↗
▶Ep 13 · 7:40
epidemiologicalMelbourne group data showed right ventricular dominance is a risk factor if present at birth, but after surviving the first couple of years post-Fontan, survival curves are essentially identical regardless of ventricular morphology↗
▶Ep 13 · 7:40
host_summaryMelbourne group data showed right ventricular dominance is a risk factor if present at birth, but after surviving the first couple of years post-Fontan, survival curves are essentially identical regardless of ventricular morphology↗
▶Ep 13 · 8:22
clinicalThe systemic ventricle in Fontan circulation is hypercontractile to match its increased afterload↗
▶Ep 13 · 8:22
clinicalThe systemic ventricle in Fontan circulation is hypercontractile to match its increased afterload↗
▶Ep 13 · 8:37
host_summaryForce-frequency relationships in systemic right and left ventricles in univentricular circulation outperformed normal ventricles↗
▶Ep 13 · 8:37
clinicalForce-frequency relationships in systemic right and left ventricles in univentricular circulation outperformed normal ventricles↗
▶Ep 13 · 9:03
host_summaryEnd-systolic elastance in Fontan patients is orders of magnitude higher than normals and even greater than in systemic right ventricle of Mustard patients↗
▶Ep 13 · 9:03
clinicalEnd-systolic elastance in Fontan patients is orders of magnitude higher than normals and even greater than in systemic right ventricle of Mustard patients↗
▶Ep 13 · 9:21
quotethese are strong ventricles that are pumping against, albeit a high resistance↗
▶Ep 13 · 9:21
quotethese are strong ventricles that are pumping against, albeit a high resistance↗
▶Ep 13 · 9:29
clinicalThe primary problem in Fontan ventricles is in diastole, not systole↗
▶Ep 13 · 9:29
clinicalThe primary problem in Fontan ventricles is in diastole, not systole↗
▶Ep 13 · 9:29
clinicalArterial elastance is high in Fontan patients but relatively well coupled to ventricular elastance↗
▶Ep 13 · 9:29
clinicalArterial elastance is high in Fontan patients but relatively well coupled to ventricular elastance↗
▶Ep 13 · 10:14
clinicalIn early post-Fontan course, it is early diastole (E wave) that is affected, not late diastole (A wave), with virtual abolishment of early rapid filling↗
▶Ep 13 · 10:14
clinicalIn early post-Fontan course, it is early diastole (E wave) that is affected, not late diastole (A wave), with virtual abolishment of early rapid filling↗
▶Ep 13 · 10:43
clinicalTime constant of relaxation and isovolumic relaxation time are prolonged in early post-Fontan patients, indicative of impaired relaxation↗
▶Ep 13 · 10:43
clinicalTime constant of relaxation and isovolumic relaxation time are prolonged in early post-Fontan patients, indicative of impaired relaxation↗
▶Ep 13 · 10:56
clinicalImpaired early relaxation is due to incoordinate wall motion during isovolumic relaxation, with post-systolic shortening of one part of the ventricle causing another part to move outward↗
▶Ep 13 · 10:56
clinicalImpaired early relaxation is due to incoordinate wall motion during isovolumic relaxation, with post-systolic shortening of one part of the ventricle causing another part to move outward↗
▶Ep 13 · 11:58
host_summaryMRI tagging showed some segments of Fontan ventricular wall were 180 degrees out of phase with other parts, in systole when rest of ventricle was in diastole↗
▶Ep 13 · 11:58
clinicalMRI tagging showed some segments of Fontan ventricular wall were 180 degrees out of phase with other parts, in systole when rest of ventricle was in diastole↗
▶Ep 13 · 12:23
clinicalLonger isovolumic relaxation time correlates with longer hospital stay immediately after Fontan operation↗
▶Ep 13 · 12:23
clinicalLonger isovolumic relaxation time correlates with longer hospital stay immediately after Fontan operation↗
▶Ep 13 · 13:03
clinicalLate post-Fontan patients can develop pseudonormalized filling pattern (E > A) due to rising left atrial pressure despite persistent incoordinate relaxation↗
▶Ep 13 · 13:03
clinicalLate post-Fontan patients can develop pseudonormalized filling pattern (E > A) due to rising left atrial pressure despite persistent incoordinate relaxation↗
▶Ep 13 · 13:36
clinicalIn normal individuals, left ventricular end-diastolic pressure rises by about 2 mmHg per decade after age 30↗
▶Ep 13 · 13:36
clinicalIn normal individuals, left ventricular end-diastolic pressure rises by about 2 mmHg per decade after age 30↗
▶Ep 13 · 14:18
clinicalEight-year follow-up of Fontan patients showed maintained incoordinate relaxation, shortened IVRT suggesting rising left atrial pressure, and faster E wave deceleration suggesting falling compliance↗
▶Ep 13 · 14:18
host_summaryEight-year follow-up of Fontan patients showed maintained incoordinate relaxation, shortened IVRT suggesting rising left atrial pressure, and faster E wave deceleration suggesting falling compliance↗
▶Ep 13 · 14:47
clinicalDiastolic compliance of Fontan ventricles (predominantly left ventricles) is highly abnormal, unlike Mustard systemic right ventricles where diastolic compliance is not a problem↗
▶Ep 13 · 14:47
host_summaryDiastolic compliance of Fontan ventricles (predominantly left ventricles) is highly abnormal, unlike Mustard systemic right ventricles where diastolic compliance is not a problem↗
▶Ep 13 · 15:06
quoteif you can't fill in early diastole and you can't fill in late diastole, you're not gonna fill at all and you have a low stroke volume and a low cardiac output↗
▶Ep 13 · 15:06
quoteif you can't fill in early diastole and you can't fill in late diastole, you're not gonna fill at all and you have a low stroke volume and a low cardiac output↗
▶Ep 13 · 15:33
clinicalFontan patients with high diastolic stiffness may have low end-diastolic pressure because reduced preload causes the ventricle to become smaller and pressure to fall down the pressure-volume curve↗
▶Ep 13 · 15:33
clinicalFontan patients with high diastolic stiffness may have low end-diastolic pressure because reduced preload causes the ventricle to become smaller and pressure to fall down the pressure-volume curve↗
▶Ep 13 · 15:41
quotein the presence of really profoundly abnormal ventricular compliance, these patients can have a normal left ventricular and diastolic pressure↗
▶Ep 13 · 15:41
quotein the presence of really profoundly abnormal ventricular compliance, these patients can have a normal left ventricular and diastolic pressure↗
▶Ep 13 · 17:37
clinicalBench pressing 500 pounds essentially cuts off pulmonary blood flow in Fontan patients↗
▶Ep 13 · 17:37
clinicalBench pressing 500 pounds essentially cuts off pulmonary blood flow in Fontan patients↗
▶Ep 13 · 18:13
opinionSustained Valsalva maneuvers may be particularly disadvantageous in old atrio-pulmonary Fontans due to direct effects on atrial stretch and potential for chronic atrial arrhythmias↗
▶Ep 13 · 18:13
opinionSustained Valsalva maneuvers may be particularly disadvantageous in old atrio-pulmonary Fontans due to direct effects on atrial stretch and potential for chronic atrial arrhythmias↗
▶Ep 13 · 20:04
clinicalPHN data at 10-12 years post-Fontan showed systemic right ventricles had far more patients with increased E/E' ratio (indicating increased stiffness) compared to systemic left ventricles↗
▶Ep 13 · 20:04
host_summaryPHN data at 10-12 years post-Fontan showed systemic right ventricles had far more patients with increased E/E' ratio (indicating increased stiffness) compared to systemic left ventricles↗
▶Ep 13 · 21:58
clinicalRise in end-diastolic pressure in normal individuals is more rapid with hypertension, diabetes, other risk factors, and ventricular volume load such as AV valve or aortic regurgitation↗
▶Ep 13 · 21:58
clinicalRise in end-diastolic pressure in normal individuals is more rapid with hypertension, diabetes, other risk factors, and ventricular volume load such as AV valve or aortic regurgitation↗
▶Ep 13 · 22:33
clinicalFontan patients frequently have some degree of volume load and have had volume load for the first few years of life↗
▶Ep 13 · 22:33
clinicalFontan patients frequently have some degree of volume load and have had volume load for the first few years of life↗
▶Ep 13 · 22:44
clinicalAll Fontan patients have very raised arterial impedance and systemic vascular resistance↗
▶Ep 13 · 22:44
clinicalAll Fontan patients have very raised arterial impedance and systemic vascular resistance↗
▶Ep 13 · 23:01
host_summaryRecent conductance catheter work from the Netherlands shows a tight relationship between arterial elastance and ventricular end-diastolic pressure↗
▶Ep 13 · 23:01
clinicalRecent conductance catheter work from the Netherlands shows a tight relationship between arterial elastance and ventricular end-diastolic pressure↗
▶Ep 13 · 23:18
opinionThere is no evidence-based role for ACE inhibition or arterial vasodilators in short-term Fontan management, as systemic vasodilation drops cardiac output↗
▶Ep 13 · 23:18
opinionThere is no evidence-based role for ACE inhibition or arterial vasodilators in short-term Fontan management, as systemic vasodilation drops cardiac output↗
▶Ep 13 · 23:38
opinionManagement of left ventricular end-diastolic pressure, fibrosis, and vascular biology have real potential as therapeutic targets in long-term Fontan management↗
▶Ep 13 · 23:38
opinionManagement of left ventricular end-diastolic pressure, fibrosis, and vascular biology have real potential as therapeutic targets in long-term Fontan management↗
▶Ep 13 · 23:58
opinionUnderstanding the impact of long-term therapies for diastolic dysfunction will require 10-20 years of follow-up↗
▶Ep 13 · 23:58
opinionUnderstanding the impact of long-term therapies for diastolic dysfunction will require 10-20 years of follow-up↗