“…pulmonary artery shunt. 73 The clinical conterpart to this is the patient with a tetralogy of Fallot who has too large a Blalock-Taussig shunt created.…”
Section: Right Ventriclementioning
confidence: 99%
“…In these studies of congestive heart failure secondary to acute marked pulmonary artery narrowing, increasing right ventricular blood flow via a cannula in the right coronary artery, partly occluding the descending aorta to raise aortic pressure, or raising aortic pressure with neosynephrine, reversed the congestive heart failure and restored right ventricular function without removing the pulmonary artery obstruction. Conversely, experimental right ventricular systolic hypertension secondary to pulmonic stenosis in which right ventricular function is well maintained may develop into congestive heart failure if the driving pressure is decreased further by opening systemic to pulmonary artery shunt . The clinical conterpart to this is the patient with a tetralogy of Fallot who has too large a Blalock‐Taussig shunt created.…”
Section: Indirect Measurement Of Supply:demand Ratiomentioning
confidence: 99%
“…Conversely, experimental right ventricular systolic hypertension secondary to pulmonic stenosis in which right ventricular function is well maintained may develop into congestive heart failure if the driving pressure is decreased further by opening systemic to pulmonary artery shunt. 73 The clinical conterpart to this is the patient with a tetralogy of Fallot who has too large a Blalock‐Taussig shunt created.…”
Section: Indirect Measurement Of Supply:demand Ratiomentioning
“…pulmonary artery shunt. 73 The clinical conterpart to this is the patient with a tetralogy of Fallot who has too large a Blalock-Taussig shunt created.…”
Section: Right Ventriclementioning
confidence: 99%
“…In these studies of congestive heart failure secondary to acute marked pulmonary artery narrowing, increasing right ventricular blood flow via a cannula in the right coronary artery, partly occluding the descending aorta to raise aortic pressure, or raising aortic pressure with neosynephrine, reversed the congestive heart failure and restored right ventricular function without removing the pulmonary artery obstruction. Conversely, experimental right ventricular systolic hypertension secondary to pulmonic stenosis in which right ventricular function is well maintained may develop into congestive heart failure if the driving pressure is decreased further by opening systemic to pulmonary artery shunt . The clinical conterpart to this is the patient with a tetralogy of Fallot who has too large a Blalock‐Taussig shunt created.…”
Section: Indirect Measurement Of Supply:demand Ratiomentioning
confidence: 99%
“…Conversely, experimental right ventricular systolic hypertension secondary to pulmonic stenosis in which right ventricular function is well maintained may develop into congestive heart failure if the driving pressure is decreased further by opening systemic to pulmonary artery shunt. 73 The clinical conterpart to this is the patient with a tetralogy of Fallot who has too large a Blalock‐Taussig shunt created.…”
Section: Indirect Measurement Of Supply:demand Ratiomentioning
“…The mechanism for this phenomenon is due to a fall in aortic diastolic pressure that consequently lowers coronary-driving pressure and has been well described. [2][3][4] Catecholamines constitute an important part of the therapy used to treat acute cardiac dysfunction. Others have studied the effects of isoproterenol, dopamine, and dobutamine in lambs with and without an SPS, but studies using epinephrine are lacking.…”
Section: Commentmentioning
confidence: 99%
“…The SPS can produce diastolic runoff from the coronaries by reducing aortic pressure and consequently decreasing coronary perfusion, which may result in cardiac dysfunction. [2][3][4] Catecholamines, particularly epinephrine, are frequently used to provide hemodynamic support during the acute phase of cardiac dysfunction. It increases heart rate, cardiac output, and blood pressure.…”
This study suggests that SPS decreases CBF, especially in the presence of a higher Qp/Qs and epinephrine. The mechanism is largely due to the decrease in diastolic pressure and the inability of the coronary arteries to compensate with vasodilation.
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