Andrew Reddington

154 statements · 2 topics · summaries given as host listed separately

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if 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
in 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
in the presence of really profoundly abnormal ventricular compliance, these patients can have a normal left ventricular and diastolic pressure
the fontan circulation is one of the few situations where constipation can be fatal

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Andrew's statements about Hypoplastic Left Heart Syndrome 77 statements

Open the Hypoplastic Left Heart Syndrome collection →

How Does the Blood Go Round in Single Ventricles and Fontans? New Horizons in...

Quotation how does the blood go round? Open
Quotation breathing makes the blood go round Open
Quotation breathing makes the blood go round Open
Statement 40-50% of cardiac output at baseline in Fontan patients is driven directly by the work of breathing Open
Statement 40-50% of cardiac output at baseline in Fontan patients is driven directly by the work of breathing Open
Statement Negative mean airway pressure during normal ventilation draws blood into the Fontan circuit Open
Statement Negative mean airway pressure during normal ventilation draws blood into the Fontan circuit Open
Statement Valsalva maneuver with mean airway pressure elevated to 20 cm H2O cuts off spontaneous respiratory flow, leaving only tiny flow with ventricular systole Open
Statement Valsalva maneuver with mean airway pressure elevated to 20 cm H2O cuts off spontaneous respiratory flow, leaving only tiny flow with ventricular systole Open
Quotation the fontan circulation is one of the few situations where constipation can be fatal Open
Quotation the fontan circulation is one of the few situations where constipation can be fatal Open
Statement Low pulmonary vascular resistance is a prerequisite for good Fontan outcome Open
Statement Low pulmonary vascular resistance is a prerequisite for good Fontan outcome Open
Statement In normal individuals, nitric oxide does not reduce pulmonary vascular resistance because the pulmonary vascular bed is maximally vasodilated Open
Quotation in 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 Open
Statement In normal individuals, nitric oxide does not reduce pulmonary vascular resistance because the pulmonary vascular bed is maximally vasodilated Open
Quotation in 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 Open
Statement Nitric oxide produced a statistically and physiologically significant fall in pulmonary vascular resistance of about 1 index wood unit in teenage Fontan patients Open
Statement Nitric oxide produced a statistically and physiologically significant fall in pulmonary vascular resistance of about 1 index wood unit in teenage Fontan patients Open
Statement Only half of teenage Fontan patients showed benefit from nitric oxide Open
Statement Only half of teenage Fontan patients showed benefit from nitric oxide Open
Statement If only half of Fontan patients benefit from nitric oxide, they are unlikely to further benefit from PDE5 inhibitors Open
Statement If only half of Fontan patients benefit from nitric oxide, they are unlikely to further benefit from PDE5 inhibitors Open
Quotation 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 Open
Quotation 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 Open
Statement CHOP data showed no difference in outcomes in the first 10 years after Fontan between hypoplastic left heart syndrome and systemic left ventricle patients Open
Statement Boston data showed patients born with systemic left ventricle with normally related great vessels or single right ventricle do better than all other diagnoses Open
Statement Melbourne 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 Open
Statement The systemic ventricle in Fontan circulation is hypercontractile to match its increased afterload Open
Statement The systemic ventricle in Fontan circulation is hypercontractile to match its increased afterload Open
Statement Force-frequency relationships in systemic right and left ventricles in univentricular circulation outperformed normal ventricles Open
Statement End-systolic elastance in Fontan patients is orders of magnitude higher than normals and even greater than in systemic right ventricle of Mustard patients Open
Quotation these are strong ventricles that are pumping against, albeit a high resistance Open
Quotation these are strong ventricles that are pumping against, albeit a high resistance Open
Statement The primary problem in Fontan ventricles is in diastole, not systole Open
Statement Arterial elastance is high in Fontan patients but relatively well coupled to ventricular elastance Open
Statement The primary problem in Fontan ventricles is in diastole, not systole Open
Statement Arterial elastance is high in Fontan patients but relatively well coupled to ventricular elastance Open
Statement In 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 Open
Statement In 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 Open
Statement Time constant of relaxation and isovolumic relaxation time are prolonged in early post-Fontan patients, indicative of impaired relaxation Open
Statement Time constant of relaxation and isovolumic relaxation time are prolonged in early post-Fontan patients, indicative of impaired relaxation Open
Statement Impaired 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 Open
Statement Impaired 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 Open
Statement MRI 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 Open
Statement Longer isovolumic relaxation time correlates with longer hospital stay immediately after Fontan operation Open
Statement Longer isovolumic relaxation time correlates with longer hospital stay immediately after Fontan operation Open
Statement Late post-Fontan patients can develop pseudonormalized filling pattern (E > A) due to rising left atrial pressure despite persistent incoordinate relaxation Open
Statement Late post-Fontan patients can develop pseudonormalized filling pattern (E > A) due to rising left atrial pressure despite persistent incoordinate relaxation Open
Statement In normal individuals, left ventricular end-diastolic pressure rises by about 2 mmHg per decade after age 30 Open
Statement In normal individuals, left ventricular end-diastolic pressure rises by about 2 mmHg per decade after age 30 Open
Statement Eight-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 Open
Statement Diastolic compliance of Fontan ventricles (predominantly left ventricles) is highly abnormal, unlike Mustard systemic right ventricles where diastolic compliance is not a problem Open
Quotation if 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 Open
Quotation if 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 Open
Statement Fontan 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 Open
Statement Fontan 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 Open
Quotation in the presence of really profoundly abnormal ventricular compliance, these patients can have a normal left ventricular and diastolic pressure Open
Quotation in the presence of really profoundly abnormal ventricular compliance, these patients can have a normal left ventricular and diastolic pressure Open
Statement Bench pressing 500 pounds essentially cuts off pulmonary blood flow in Fontan patients Open
Statement Bench pressing 500 pounds essentially cuts off pulmonary blood flow in Fontan patients Open
Statement Sustained Valsalva maneuvers may be particularly disadvantageous in old atrio-pulmonary Fontans due to direct effects on atrial stretch and potential for chronic atrial arrhythmias Open
Statement Sustained Valsalva maneuvers may be particularly disadvantageous in old atrio-pulmonary Fontans due to direct effects on atrial stretch and potential for chronic atrial arrhythmias Open
Statement PHN 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 Open
Statement Rise 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 Open
Statement Rise 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 Open
Statement Fontan patients frequently have some degree of volume load and have had volume load for the first few years of life Open
Statement Fontan patients frequently have some degree of volume load and have had volume load for the first few years of life Open
Statement All Fontan patients have very raised arterial impedance and systemic vascular resistance Open
Statement All Fontan patients have very raised arterial impedance and systemic vascular resistance Open
Statement Recent conductance catheter work from the Netherlands shows a tight relationship between arterial elastance and ventricular end-diastolic pressure Open
Statement There is no evidence-based role for ACE inhibition or arterial vasodilators in short-term Fontan management, as systemic vasodilation drops cardiac output Open
Statement There is no evidence-based role for ACE inhibition or arterial vasodilators in short-term Fontan management, as systemic vasodilation drops cardiac output Open
Statement Management of left ventricular end-diastolic pressure, fibrosis, and vascular biology have real potential as therapeutic targets in long-term Fontan management Open
Statement Management of left ventricular end-diastolic pressure, fibrosis, and vascular biology have real potential as therapeutic targets in long-term Fontan management Open
Statement Understanding the impact of long-term therapies for diastolic dysfunction will require 10-20 years of follow-up Open
Statement Understanding the impact of long-term therapies for diastolic dysfunction will require 10-20 years of follow-up Open
Andrew's statements about Single Ventricle / HLHS 77 statements

Open the Single Ventricle / HLHS collection →

How Does the Blood Go Round in Single Ventricles and Fontans? New Horizons in...

Quotation how does the blood go round? Open
Quotation breathing makes the blood go round Open
Quotation breathing makes the blood go round Open
Statement 40-50% of cardiac output at baseline in Fontan patients is driven directly by the work of breathing Open
Statement 40-50% of cardiac output at baseline in Fontan patients is driven directly by the work of breathing Open
Statement Negative mean airway pressure during normal ventilation draws blood into the Fontan circuit Open
Statement Negative mean airway pressure during normal ventilation draws blood into the Fontan circuit Open
Statement Valsalva maneuver with mean airway pressure elevated to 20 cm H2O cuts off spontaneous respiratory flow, leaving only tiny flow with ventricular systole Open
Statement Valsalva maneuver with mean airway pressure elevated to 20 cm H2O cuts off spontaneous respiratory flow, leaving only tiny flow with ventricular systole Open
Quotation the fontan circulation is one of the few situations where constipation can be fatal Open
Quotation the fontan circulation is one of the few situations where constipation can be fatal Open
Statement Low pulmonary vascular resistance is a prerequisite for good Fontan outcome Open
Statement Low pulmonary vascular resistance is a prerequisite for good Fontan outcome Open
Quotation in 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 Open
Quotation in 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 Open
Statement In normal individuals, nitric oxide does not reduce pulmonary vascular resistance because the pulmonary vascular bed is maximally vasodilated Open
Statement In normal individuals, nitric oxide does not reduce pulmonary vascular resistance because the pulmonary vascular bed is maximally vasodilated Open
Statement Nitric oxide produced a statistically and physiologically significant fall in pulmonary vascular resistance of about 1 index wood unit in teenage Fontan patients Open
Statement Nitric oxide produced a statistically and physiologically significant fall in pulmonary vascular resistance of about 1 index wood unit in teenage Fontan patients Open
Statement Only half of teenage Fontan patients showed benefit from nitric oxide Open
Statement Only half of teenage Fontan patients showed benefit from nitric oxide Open
Statement If only half of Fontan patients benefit from nitric oxide, they are unlikely to further benefit from PDE5 inhibitors Open
Statement If only half of Fontan patients benefit from nitric oxide, they are unlikely to further benefit from PDE5 inhibitors Open
Quotation 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 Open
Quotation 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 Open
Statement CHOP data showed no difference in outcomes in the first 10 years after Fontan between hypoplastic left heart syndrome and systemic left ventricle patients Open
Statement Boston data showed patients born with systemic left ventricle with normally related great vessels or single right ventricle do better than all other diagnoses Open
Statement Melbourne 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 Open
Statement The systemic ventricle in Fontan circulation is hypercontractile to match its increased afterload Open
Statement The systemic ventricle in Fontan circulation is hypercontractile to match its increased afterload Open
Statement Force-frequency relationships in systemic right and left ventricles in univentricular circulation outperformed normal ventricles Open
Statement End-systolic elastance in Fontan patients is orders of magnitude higher than normals and even greater than in systemic right ventricle of Mustard patients Open
Quotation these are strong ventricles that are pumping against, albeit a high resistance Open
Quotation these are strong ventricles that are pumping against, albeit a high resistance Open
Statement The primary problem in Fontan ventricles is in diastole, not systole Open
Statement Arterial elastance is high in Fontan patients but relatively well coupled to ventricular elastance Open
Statement Arterial elastance is high in Fontan patients but relatively well coupled to ventricular elastance Open
Statement The primary problem in Fontan ventricles is in diastole, not systole Open
Statement In 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 Open
Statement In 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 Open
Statement Time constant of relaxation and isovolumic relaxation time are prolonged in early post-Fontan patients, indicative of impaired relaxation Open
Statement Time constant of relaxation and isovolumic relaxation time are prolonged in early post-Fontan patients, indicative of impaired relaxation Open
Statement Impaired 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 Open
Statement Impaired 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 Open
Statement MRI 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 Open
Statement Longer isovolumic relaxation time correlates with longer hospital stay immediately after Fontan operation Open
Statement Longer isovolumic relaxation time correlates with longer hospital stay immediately after Fontan operation Open
Statement Late post-Fontan patients can develop pseudonormalized filling pattern (E > A) due to rising left atrial pressure despite persistent incoordinate relaxation Open
Statement Late post-Fontan patients can develop pseudonormalized filling pattern (E > A) due to rising left atrial pressure despite persistent incoordinate relaxation Open
Statement In normal individuals, left ventricular end-diastolic pressure rises by about 2 mmHg per decade after age 30 Open
Statement In normal individuals, left ventricular end-diastolic pressure rises by about 2 mmHg per decade after age 30 Open
Statement Eight-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 Open
Statement Diastolic compliance of Fontan ventricles (predominantly left ventricles) is highly abnormal, unlike Mustard systemic right ventricles where diastolic compliance is not a problem Open
Quotation if 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 Open
Quotation if 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 Open
Statement Fontan 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 Open
Statement Fontan 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 Open
Quotation in the presence of really profoundly abnormal ventricular compliance, these patients can have a normal left ventricular and diastolic pressure Open
Quotation in the presence of really profoundly abnormal ventricular compliance, these patients can have a normal left ventricular and diastolic pressure Open
Statement Bench pressing 500 pounds essentially cuts off pulmonary blood flow in Fontan patients Open
Statement Bench pressing 500 pounds essentially cuts off pulmonary blood flow in Fontan patients Open
Statement Sustained Valsalva maneuvers may be particularly disadvantageous in old atrio-pulmonary Fontans due to direct effects on atrial stretch and potential for chronic atrial arrhythmias Open
Statement Sustained Valsalva maneuvers may be particularly disadvantageous in old atrio-pulmonary Fontans due to direct effects on atrial stretch and potential for chronic atrial arrhythmias Open
Statement PHN 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 Open
Statement Rise 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 Open
Statement Rise 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 Open
Statement Fontan patients frequently have some degree of volume load and have had volume load for the first few years of life Open
Statement Fontan patients frequently have some degree of volume load and have had volume load for the first few years of life Open
Statement All Fontan patients have very raised arterial impedance and systemic vascular resistance Open
Statement All Fontan patients have very raised arterial impedance and systemic vascular resistance Open
Statement Recent conductance catheter work from the Netherlands shows a tight relationship between arterial elastance and ventricular end-diastolic pressure Open
Statement There is no evidence-based role for ACE inhibition or arterial vasodilators in short-term Fontan management, as systemic vasodilation drops cardiac output Open
Statement There is no evidence-based role for ACE inhibition or arterial vasodilators in short-term Fontan management, as systemic vasodilation drops cardiac output Open
Statement Management of left ventricular end-diastolic pressure, fibrosis, and vascular biology have real potential as therapeutic targets in long-term Fontan management Open
Statement Management of left ventricular end-diastolic pressure, fibrosis, and vascular biology have real potential as therapeutic targets in long-term Fontan management Open
Statement Understanding the impact of long-term therapies for diastolic dysfunction will require 10-20 years of follow-up Open
Statement Understanding the impact of long-term therapies for diastolic dysfunction will require 10-20 years of follow-up Open

Summaries Andrew gave as host · 22 summaries

Recaps of other experts' statements, not Andrew's own clinical position.

Summaries Andrew gave as host · Hypoplastic Left Heart Syndrome 11 summaries

Open the Hypoplastic Left Heart Syndrome collection →

How Does the Blood Go Round in Single Ventricles and Fontans? New Horizons in...

Host summary Andrew Reddington summarizing the discussion: how does the blood go round? Open
Host summary Andrew Reddington summarizing the discussion: CHOP data showed no difference in outcomes in the first 10 years after Fontan between hypoplastic left heart syndrome and systemic left ventricle patients Open
Host summary Andrew Reddington summarizing the discussion: Boston data showed patients born with systemic left ventricle with normally related great vessels or single right ventricle do better than all other diagnoses Open
Host summary Andrew Reddington summarizing the discussion: Melbourne 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 Open
Host summary Andrew Reddington summarizing the discussion: Force-frequency relationships in systemic right and left ventricles in univentricular circulation outperformed normal ventricles Open
Host summary Andrew Reddington summarizing the discussion: End-systolic elastance in Fontan patients is orders of magnitude higher than normals and even greater than in systemic right ventricle of Mustard patients Open
Host summary Andrew Reddington summarizing the discussion: MRI 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 Open
Host summary Andrew Reddington summarizing the discussion: Eight-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 Open
Host summary Andrew Reddington summarizing the discussion: Diastolic compliance of Fontan ventricles (predominantly left ventricles) is highly abnormal, unlike Mustard systemic right ventricles where diastolic compliance is not a problem Open
Host summary Andrew Reddington summarizing the discussion: PHN 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 Open
Host summary Andrew Reddington summarizing the discussion: Recent conductance catheter work from the Netherlands shows a tight relationship between arterial elastance and ventricular end-diastolic pressure Open
Summaries Andrew gave as host · Single Ventricle / HLHS 11 summaries

Open the Single Ventricle / HLHS collection →

How Does the Blood Go Round in Single Ventricles and Fontans? New Horizons in...

Host summary Andrew Reddington summarizing the discussion: how does the blood go round? Open
Host summary Andrew Reddington summarizing the discussion: CHOP data showed no difference in outcomes in the first 10 years after Fontan between hypoplastic left heart syndrome and systemic left ventricle patients Open
Host summary Andrew Reddington summarizing the discussion: Boston data showed patients born with systemic left ventricle with normally related great vessels or single right ventricle do better than all other diagnoses Open
Host summary Andrew Reddington summarizing the discussion: Melbourne 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 Open
Host summary Andrew Reddington summarizing the discussion: Force-frequency relationships in systemic right and left ventricles in univentricular circulation outperformed normal ventricles Open
Host summary Andrew Reddington summarizing the discussion: End-systolic elastance in Fontan patients is orders of magnitude higher than normals and even greater than in systemic right ventricle of Mustard patients Open
Host summary Andrew Reddington summarizing the discussion: MRI 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 Open
Host summary Andrew Reddington summarizing the discussion: Eight-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 Open
Host summary Andrew Reddington summarizing the discussion: Diastolic compliance of Fontan ventricles (predominantly left ventricles) is highly abnormal, unlike Mustard systemic right ventricles where diastolic compliance is not a problem Open
Host summary Andrew Reddington summarizing the discussion: PHN 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 Open
Host summary Andrew Reddington summarizing the discussion: Recent conductance catheter work from the Netherlands shows a tight relationship between arterial elastance and ventricular end-diastolic pressure Open