The response of right ventricular size, function, and pressure to supine exercise: a comparison of patients with chronic obstructive lung disease and normal subjects.
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Calculation of accurate stroke count ratios for the assessment of valvular regurgitation from equilibrium blood pool images has been difficult and did not permit computation of regurgitant fractions (RF) because of contamination of right ventricular (RV) stroke counts by right atrial activity. We describe a new approach to correct for this contamination by subtracting one half of the right atrial counts from the RV counts, assuming that in the standard or "modified" left anterior oblique projection commonly used about one half of the right atrial activity is superimposed to the RV. This new method was tested in 20 patients without valvular disease or shunts. Left ventricular (LV) to RV stroke count ratio approached unity (1.01 +/- 0.14). RV ejection fractions (EF) derived by this technique agreed well with those obtained by gated first-pass studies recorded in the right anterior oblique projection. In 9 normals and 17 patients with moderate severe or severe aortic (12 patients or mitral (7 patients) regurgitation, LVEF, RVEF, and RF were determined at rest and maximum exercise. In patients at rest, LVEF (56.0 +/- 6.4%) and RVEF (49.0 +/- 7.3%) did not differ significantly from LVEF (59.6 +/- 4.2%) and RVEF (52.5 +/- 6.4%) in normals. The calculated RF was negligible in normals (1.9 +/- 8.6%), but averaged 51.8 +/- 9.8% in patients with valvular disease. During exercise, LVEF fell significantly (p less than 0.001) to 44.1 +/- 7.2% in patients but increased to 70.5 +/- 3.8% in normals. RVEF increased in aortic regurgitation to 64.5 +/- 9.8% (NS to normals) but fell in mitral regurgitation to 36.6 +/- 5.9% (p greater than 0.001). In both patient subsets RF decreased with exercise to 25.4 +/- 15.0% in aortic and 39.1 +/- 12.7% in mitral regurgitation. The results indicate that this new approach permits assessment of RVEF and RF from gated equilibrium blood pool studies and is suitable to evaluate the hemodynamic response to physiologic and therapeutic interventions in patients with valvular regurgitation.
In valvular heart disease, there is a different radionuclide angiographic pattern in each of three left-sided valve abnormalities: pressure overload (aortic stenosis), volume overload (aortic or mitral regurgitation) and inflow obstruction (mitral stenosis). In pressure overload, the left ventricle is usually normal in size or minimally dilated. The ejection fraction may be normal, increased or decreased. In volume overload, there is left ventricular dilatation with a normal or reduced ejection fraction at rest. Scans may be performed during exercise to unmask abnormalities of ventricular function not evident at rest. In inflow obstruction, left ventricular function is usually normal but may be depressed. Right ventricular function may be abnormal secondary to pulmonary hypertension. Radionuclide angiography in valvular heart disease evaluates the impact of the valve abnormality on cardiac chamber size and function, which is useful in managing the patient, in determining the prognosis and in evaluating the success of valve surgery. Thallium-2-1 imaging evaluates regional myocardial blood flow and cell integrity and can be used to assess associated coronary artery disease.
Vasodilator therapy has not been effective in patients with pulmonary hypertension because most of the drugs that have been utilized in treating this disorder do not exert selective effects on the pulmonary circulation. Nonselective agents may cause predominant systemic vasodilation and lead to severe hypotension; they may elicit reflex activation of the sympathetic nervous system and further elevate pulmonary artery pressures; or they may exert depressant effects on right ventricular function and aggravate right-sided heart failure. Nitroglycerin has theoretic appeal as a vasodilator drug in patients with pulmonary hypertension because it exerts a direct effect on the pulmonary circulation in doses that do not affect systemic resistance vessels or the myocardium and do not activate neurohumoral reflexes. Furthermore, the drug uniquely reduces pulmonary artery pressures in addition to pulmonary vascular resistance due to its ability to dilate venous capacitance vessels. Preliminary studies with sublingual and intravenous nitroglycerin in patients with pulmonary hypertension have shown that the drug produces marked hemodynamic improvement and that clinical benefits follow long-term therapy with transcutaneous or oral nitrates. However, treatment may provoke hypotensive events in some patients and systemic hypoxemia in others; still others may fail to benefit because the pulmonary vasculature is unresponsive to any vasodilator stimulus. Further work is needed to define the benefits and risks of nitroglycerin therapy in patients with pulmonary hypertension.
In eligible patients, cardiac transplantation has become the definitive treatment for end-stage heart failure. The initial posttransplantation course is marked by many potential difficulties, including renal insufficiency, hemodynamic instability, and perioperative bleeding. It is important to prevent early rejection; calcineurin inhibitors, such as tacrolimus or cyclosporine, are integral parts of such management. However, these drugs are associated with renal toxicity in some patients. Previous work suggests that limiting the increase in tacrolimus levels is associated with less renal insufficiency. The hypothesis of the current study was that a combination of clinical or laboratory variables could identify patients at risk for rapid changes in tacrolimus target levels. No single variable was strongly associated with high resultant trough levels following a standard 1-mg oral "test dose" of tacrolimus. However, the combination of 2 indices of liver metabolism (alanine aminotransferase and total bilirubin) along with serum creatinine did identify patients who tended toward elevated levels of tacrolimus (> or =4.5 ng/dL). Other variables, such as demographics, and even functional variables, such as right ventricular function by echocardiography, did not enhance the predictive value of this simple scoring system.
OBJECTIVE: The purpose of this study was to quantify the magnitude of interaction between the right and left ventricles in conditions of heart failure. METHODS: Human hearts were taken from transplant recipients diagnosed with diluted cardiomyopathy at the time of transplantation and were restored to beating condition with use of an isolated perfusion circuit. Left ventricular-right ventricular interaction was determined by ramping volume in the left ventricle while holding right ventricular volume constant. Right ventricular pressure gain was plotted against left ventricular pressure and the slope of the linear regression determined the left ventricular-right ventricular interaction. A similar procedure was used to determine right ventricular-left ventricular interaction. Two normal hearts were obtained from transplant donors not suitable for cardiac donation to serve as control hearts. RESULTS: Mean left ventricular-right ventricular interaction was 0.22 in the hearts with dilated cardiomyopathy compared with 0.06 in the control hearts. Mean right ventricular-left ventricular interaction was 0.14 in the hearts with dilated cardiomyopathy compared with 0.09 in the control hearts. A marked increase in left ventricular-right ventricular interaction was noted in the hearts with dilated cardiomyopathy compared with control hearts. Although observed values of right ventricular-left ventricular interaction also correspond to previously published results, no significant increase was observed in the dilated cardiomyopathy condition. CONCLUSIONS: These studies confirm previously published values for systolic ventricular interaction obtained with animal models and demonstrate a marked increase in the dependence of the right ventricle on left ventricular function to maintain systolic pressure generation during conditions of dilated cardiomyopathy.
OBJECTIVES: To report the detection of a thrombus entrapped in a patent foramen ovale by echocardiography in a patient with recurrent pulmonary embolism. DESIGN: Case report. SETTING: Intensive care unit of a university hospital. PATIENT: A 62-yr-old man with initial deep venous thrombosis and recurrent minor pulmonary embolism followed by a severe embolic event with transitory hemiparesis 10 days after prostatectomy. INTERVENTION: Systemic anticoagulation, surgical removal of a crossing atrial thrombus, closure of a patent foramen ovale, and venous thrombectomy. MEASUREMENTS AND MAIN RESULTS: Transesophageal echocardiography revealed a large thrombus entrapped in a patent foramen ovale with portions in all four heart chambers. Intraoperatively, a 19-cm-long thrombus, shaped like the pelvic veins, was found. The patient was successfully weaned from cardiopulmonary bypass, requiring temporary positive inotropic support because of right ventricular dysfunction. Within 24 hrs of the operation, the patient was discharged to the intermediate care unit. CONCLUSIONS: Recurrent pulmonary embolism can potentially result in paradoxic embolism in patients with a patent foramen ovale. In such patients, it may be crucial to monitor right ventricular function and exclude right-to-left shunts by transesophageal echocardiography, regardless of clinical symptoms. The patent foramen ovale should be closed. This case emphasizes an important indication for transesophageal echocardiography in critically ill patients.
Oddly, Carl Wiggers (1883-1962), who is remembered for his work on the systemic circulation, may be considered the "American father of the pulmonary circulation." In nearly-20 papers published in the American Journal of Physiology between 1909 and 1925, he reported the first reliable pressure contours in the pulmonary artery, inquired into the relationship between respiration and pulmonary arterial pressure, examined right atrial and right ventricular function, and demonstrated how right and left heart dynamics relate to heart sounds. He also stimulated direct visualization of the lung microcirculation. Method and concept are inextricably linked in the progress of science. His contributions to the pulmonary circulation were based on his high-fidelity pressure and sound recording instruments, which he ultimately applied in the left heart. Wiggers' search for excellence in method brought him well-deserved fame in the systemic circulation, but the search began in the lung.
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Preoperative cardiac catheterization data of 21 patients requiring intraaortic balloon pumping (IABP) for weaning from cardiopulmonary bypass were analyzed and compared with similar data in 28 patients who underwent nearly similar operative procedures, but did not require IABP for weaning. Cardiac index (CI) and systemic vascular resistance (SVR) were found to have predictive value for the need of IABP for weaning from cardiopulmonary bypass and differentiated survival from non-survival. Left ventricular end diastolic pressure (LVEDP) was not found to be predictive. Ejection fraction (EF) was significantly lower in those who required IABP than those who did not; EF did not predict the outcome. Pulmonary capillary wedge pressure ([unk]), pulmonary artery pressure ([unk]) and pulmonary vascular resistance (PVR) were predictive of the need for IABP, but not the outcome. Left ventricular minute work index (LVMWI) was significantly lower in those requiring IABP, right ventricular minute work index (RVMWI) was predictive of survival with IABP. Together, LVMWI and RVMWI were predictive of the need for and outcome of IABP following cardiopulmonary bypass. Twenty-seven of 28 control RVMWI's were normal. No patient requiring IABP had depressed RVMWI's preoperatively. Elevated preoperative RVMWI's were associated with 80% survival with postcardiotomy IABP; normal RVMWI's were associated with a 56% survival with post-cardiotomy IABP. Elevated preoperative RVMWI's reflected moderate to maximal right ventricular compensatory capacity in response to depressed left ventricular function. Normal preoperative RVMWI's in the presence of depressed LVMWI's were indicative of decreased right ventricular compensatory capacity in post-cardiotomy IABP-support settings. Right ventricular function is as important as left ventricular function as a prognosticator for the need and outcome of IABP support of the failing post-cardiotomy circulation.
While operative approaches to postinfarction ventricular septal defect emphasize repair through the infarcted area, we present a case that illustrates the transatrial approach in an acute setting in which no discrete infarct or other abnormality of the free ventricular wall is apparent. In such a setting, transatrial repair of mid-muscular or posterior defects can avert unnecessary compromise of right ventricular function. Avoidance of a right ventriculotomy might also benefit patients with chronic defects complicated by severe lung disease or pulmonary hypertension. However, successful transatrial closure requires full visualization of the defect, avoidance of tricuspid valve damage, thorough débridement of necrotic tissue, and the taking of wide, deep sutures.
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The reversibility of right ventricular function in patients with mitral stenosis associated with secondary tricuspid regurgitation (TR) is as yet undetermined. We assessed the right ventricular systolic performance by cardiac catheterization before and 19 months after surgery in 18 patients who underwent DeVega's tricuspid annuloplasty plus mitral valve replacement (MS plus TR group) and in 9 with mitral valve replacement for isolated mitral stenosis (MS group). After surgery, the right ventricular systolic pressure decreased significantly in both groups (both p < 0.01). In the MS plus TR group, the postoperative right ventricular end-diastolic and end-systolic volume indices (RVEDVI and RVESVI, respectively) were significantly decreased compared with the respective preoperative values (both p < 0.001). No significant difference was noted between the groups with regard to the right ventricular peak-systolic pressure/end-systolic volume index ratio (RVPSP/ESVI) either before or after surgery. Various left ventricular indices were comparable between the groups both before and after surgery. Linear regression analysis revealed significant correlations between RVEDVI and the RVPSP/ESVI, and between RVPSP and the RVPSP/ESVI both before and after surgery. These results indicate that right ventricular systolic performance in patients with MS plus secondary TR became comparable to those that in patients with isolated MS after surgery, and that this was probably due to nearly equivalent right ventricular contractility before surgery.
UNLABELLED: Inhaled nitric oxide (iNO) is superior to i.v. vasodilators for treatment of pulmonary hypertension (PH) after cardiac surgery, but iNO is a potentially toxic gas, and patient subsets who benefit from iNO are not yet clearly defined. We administered iNO 40 ppm, prostaglandin E1 (PGE1) 0.1 microg x kg(-1) min(-1), and nitroglycerin (NTG) 3 to 5 microg x kg(-1) min(-1), in a randomized crossover study to 14 adult patients with severe PH after cardiac surgery. iNO, PGE1, and NTG were of similar efficacy in reducing pulmonary vascular resistance (P = 0.003). iNO induced selective pulmonary vasodilation, while PGE1 and NTG had significant concomitant systemic vasodilatory effects. iNO led to an increase in cardiac index (CI) (P = 0.012), and PGE1 increased CI (P = 0.006) and right ventricular (RV) ejection fraction (P = 0.015), while NTG had no effect on CI and RV performance. After study completion, patients continued with PGE1 administration with favorable in-hospital outcome. We conclude that PH per se, even if severe, does not necessarily imply postoperative RV dysfunction, and selective pulmonary vasodilation with iNO may not be superior to PGE1 with regard to CI and RV performance. IMPLICATIONS: In a prospective, randomized crossover study of inhaled nitric oxide (iNO) versus IV vasodilators, performed in adult patients with severe pulmonary hypertension but preserved right ventricular function after cardiac surgery, iNO was not superior to IV prostaglandin E1 with regard to cardiac index and right ventricular performance. Considering the potential toxicity of iNO, better definition of patient subsets with a positive benefit/risk ratio is warranted.