Viral encephalitis associated with reversible asystole due to sinoatrial arrest.

We report a case of sinoatrial node block associated with syncopal episodes that required a temporary pacemaker. Magnetic resonance imaging (MRI) of the brain showed lesions of both temporal lobes consistent with viral encephalitis, presumably due to herpes simplex virus (HSV). The patient quickly recovered with intravenous acyclovir (Zovirax) therapy. Patients with presumed encephalitis might benefit from cardiac monitoring for possible associated cardiac arrhythmia. A permanent pacemaker is rarely required, since recovery is spontaneous in the majority of these cases.

The technique of inserting a Swan-Ganz catheter. Selecting the equipment; positioning the catheter properly.

Before hemodynamic monitoring, carefully select and test the appropriate equipment and calibrate all monitors. To insert the catheter, use strict aseptic technique and, whenever possible, fluoroscopic guidance. The internal jugular vein is generally preferred for cannulation, but cutdown of an antecubital vein may be better for patients receiving anticoagulants or thrombolytics. The balloon remains deflated until the catheter tip is in the right atrium. Characteristic pressure wave forms signal the catheter's passage through each heart chamber. In most patients, advancement from the right atrium to wedge position is completed within 20 to 30 seconds.

Deciding when hemodynamic monitoring is appropriate. How will the data affect your diagnostic or therapeutic approach?

Hemodynamic data can be used to differentiate a variety of cardiopulmonary disorders, including right ventricular dysfunction, massive pulmonary embolism, and precapillary pulmonary hypertension. In patients with acute pulmonary edema, low-output states, or shock, hemodynamic measurements can help guide therapy; they also provide a precise estimate of a patient's response to vasoactive or inotropic drugs. Consider a flotation catheter for patients with complicated MIs, critically ill patients with multiorgan or major organ dysfunction, and high-risk cardiac patients undergoing surgery.

Does nitroglycerin induce heparin resistance?

We studied the possibility that intravenous nitroglycerin may produce heparin resistance both in vitro and prospectively in a group of 10 patients following coronary angioplasty. Nitroglycerin in physiologic to pharmacologic concentrations (41-250 micrograms/ml) did not produce heparin resistance in vitro as measured by activated partial thromboplastin time and thrombin time. The maximum reduction in activated partial thromboplastin time was 7%. In patient studies, the activated partial thromboplastin time at baseline on heparin alone (93 + 22 s) was not significantly different (p = 0.61) from activated partial thromboplastin measured upon addition of nitroglycerin (94 +/- 27 s) or 30 min following cessation of the nitroglycerin infusion while continuing the same dose of heparin (91 +/- 24 s). We conclude that intravenous nitroglycerin does not induce heparin resistance in vitro or in patients during short-term administration.

Regional distribution of lung perfusion and ventilation in patients with chronic congestive heart failure and its relationship to cardiopulmonary hemodynamics.

To study the relationship between the distribution of pulmonary blood flow, pulmonary ventilation, and pulmonary capillary wedge pressure, we studied six patients with chronic congestive heart failure (CHF) (New York Heart Association classes II and III) at rest and during exercise. We used krypton 81m (81mKr) and technetium 99m (99mTc) to assess lung ventilation and perfusion at rest and during exercise. Hemodynamic measurements were obtained with a balloon floatation thermodilution catheter. At rest, the upper lung zones of patients with CHF received significantly higher proportions of the blood flow compared with previously published data in normal volunteers. During exercise, however, the fractional perfusion to apices did not change, which suggests that apical flow redistribution is already maximized at rest. Measured pulmonary capillary wedge pressure failed to correlate with the upper zone or the ratio of upper-to-lower zone perfusion counts. Our findings suggest that upper zone flow redistribution may be associated with high, normal, or low capillary wedge pressure and therefore does not correlate with the pulmonary capillary wedge pressure in patients with chronic CHF.

Hemodynamic effects of lisinopril after long-term administration in congestive heart failure.

To determine whether acute effects of the angiotensin converting enzyme inhibitor lisinopril are maintained during long-term therapy, 19 patients were studied using right-sided heart catheterization before an initial randomized dose of lisinopril and again after 12 weeks of maintenance lisinopril therapy. During initial evaluation, lisinopril produced significant decreases in mean systemic arterial pressure, pulmonary artery wedge pressure, systemic vascular resistance, mean pulmonary arterial pressure, mean right atrial pressure and pulmonary vascular resistance, and concomitant increases in cardiac index and stroke volume index. After 12 weeks of therapy with lisinopril, the dosage of which was titrated to produce optimal relief of symptoms of congestive heart failure (CHF), repeat hemodynamic studies revealed persistent significant reductions in baseline systemic arterial pressure, pulmonary artery wedge pressure, mean pulmonary arterial pressure and systemic vascular resistance. However, the increases in cardiac index and stroke volume index were not statistically significant. To determine if further acute hemodynamic changes occur during long-term therapy, the patients were readministered a dose of lisinopril. This caused further decreases in systemic arterial pressure, mean pulmonary arterial pressure, pulmonary artery wedge pressure, systemic vascular resistance and mean right atrial pressure, and an increase in cardiac index. Lisinopril did not change stroke work index at either initial or rechallenge study. This study indicates that in patients with CHF treated with lisinopril, acute hemodynamic effects persist after 12 weeks of therapy, and acute hemodynamic response continues to occur upon drug readministration.

Acute myocardial infarction during streptokinase therapy.

A 45-year-old man developed sequential inferolateral and anterior myocardial infarctions within 10 hours of a possible allergic reaction to oral penicillin. The anterior myocardial infarction occurred during apparently successful streptokinase therapy for the initial inferolateral infarction. Subsequent coronary arteriography confirmed a subtotal stenosis of the left circumflex coronary artery and a complete thrombotic occlusion of the left anterior descending artery. This case documents the occurrence of three rare clinical phenomena; first, the occurrence of sequential acute myocardial infarctions in close temporal proximity; second, the occurrence of myocardial infarction during thrombolytic therapy; and third, the association of myocardial infarction with a possible allergic reaction.

Comparative acute hemodynamic effects of intravenous sodium nitroprusside and MDL-17,043, a new inotropic drug with vasodilator effects, in refractory congestive heart failure.

We compared the acute hemodynamic effects of intravenous nitroprusside (NTP), a pure vasodilator, to those of intravenous MDL-17,043 (MDL), a phosphodiesterase inhibitor with inotropic and vasodilator effects, in 12 patients with chronic refractory congestive heart failure (CHF). Intravenous NTP was infused and titrated to achieve optimal hemodynamic effects, whereas MDL was given intravenously in 0.5 mg/kg increments every 10 to 15 minutes until no further increase occurred in cardiac output or until a maximum cumulative dose of 4.5 mg/kg had been given. Both NTP and MDL reduced pulmonary capillary wedge pressure (27 +/- 5 to 15 +/- 6 and 29 +/- 3 to 15 +/- 7 mm Hg, respectively; both p less than 0.0001), systemic vascular resistance (2173 +/- 1137 to 1118 +/- 306 and 1805 +/- 425 to 956 +/- 235 dynes-sec-cm-5, respectively; both p less than 0.0002), mean arterial pressure (85 +/- 18 to 69 +/- 14 and 83 +/- 15 to 75 +/- 16 mm Hg respectively; both p less than 0.05), and increased cardiac index (1.7 +/- 0.4 to 2.6 +/- 0.4 and 1.8 +/- 0.2 to 3.3 +/- 0.5 L/minute/m2, respectively; both p less than 0.05) without an overall significant change in heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)

Inotropic therapy for refractory congestive heart failure with oral fenoximone (MDL-17,043): poor long-term results despite early hemodynamic and clinical improvement.

Thirteen male patients with NYHA class IV congestive heart failure refractory to conventional therapy were treated with oral fenoximone, a new imidazole compound with inotropic and vasodilator effects, for a mean duration of 11 weeks (range 2 to 34). On initial hemodynamic evaluation, the effects of oral fenoximone were comparable to those of the intravenous form and included a significant (p = .0001) increase in cardiac index (mean +/- SD) (1.7 +/- 0.4 to 3.0 +/- 0.7 liters/min/m2) and a significant (p = .0001) but modest decrease in pulmonary capillary wedge pressure (27 +/- 6 to 23 +/- 6 mm Hg), with only minor overall changes in heart rate and arterial blood pressure. Symptomatic improvement by at least one NYHA class was observed in all patients during the first week of therapy with fenoximone; however, severe and symptomatic congestive heart failure recurred in seven patients within an average of 8 weeks after initiation of therapy, resulting in death in all seven. Of the remaining six patients, two died suddenly at home within 3 weeks of initiation of therapy, one died from ventricular fibrillation in the hospital 7 weeks after initiation of therapy, and two died from noncardiac causes. One patient is currently alive with NYHA class II heart failure 21 weeks after the initiation of therapy. Partial or complete attenuation of hemodynamic efficacy of oral fenoximone during long-term administration was demonstrated during repeat hemodynamic evaluation in six of eight patients. We conclude that despite short-term hemodynamic and clinical benefits, oral fenoximone therapy in patients with NYHA class IV congestive heart failure does not produce sustained clinical or hemodynamic benefit and is associated with a high mortality.

Comparative hemodynamic effects of intravenous dobutamine and MDL-17,043, a new cardioactive drug, in severe congestive heart failure.

In 14 patients with severe congestive heart failure (CHF) due to ischemic heart disease or idiopathic dilated cardiomyopathy, the hemodynamic response to intravenous infusion of dobutamine (D) was compared to that of a new non-catechol, non-glycoside, inotropic and vasodilator agent, MDL-17,043 (MDL) administered in incremental intravenous doses. D and MDL produced comparable increases in cardiac index (L/min/m2) (1.8 +/- 0.4 to 2.9 +/- 0.8 and 1.7 +/- 0.3 to 3.3 +/- 0.6, respectively; both p = 0.001) and stroke volume index (ml/beat/m2) (24 +/- 8 to 35 +/- 9 and 22 +/- 7 to 39 +/- 11, respectively; both p = 0.001). Both D and MDL reduced left ventricular filling pressure (29 +/- 5 to 24 +/- 5 and 29 +/- 6 to 17 +2- 6 mm Hg, respectively; both p less than 0.05), and mean right atrial pressure (11 +/- 4 to 8 +/- 4 and 13 +/- 5 to 6 +/- 4 mm Hg, respectively; both p = 0.001). The overall changes in heart rate and mean arterial pressure were small with both D and MDL. However, MDL in comparison to D resulted in a significantly lower left ventricular filling pressure (p = 0.001), mean pulmonary arterial pressure (p = 0.001), and mean arterial pressure (p less than 0.05). The salutary hemodynamic effects of MDL on cardiac index and left ventricular filling pressure were sustained for an average of 9.6 hours, whereas the effects of D dissipated within 30 minutes of stopping the infusion. No serious adverse effects were noted during acute administration with either drug. Therefore, intravenous MDL may be a useful substitute for D in the acute therapy of severe CHF.

Myocardial metabolic and hemodynamic effects of intravenous MDL-17,043, a new cardiotonic drug, in patients with chronic severe heart failure.

MDL-17,043, a new inotropic drug with vasodilator properties, has been shown to produce salutary hemodynamic effects in severe heart failure, but its effects on myocardial metabolism are unknown. To determine whether such hemodynamic effects are associated with adverse effects on the myocardial oxygen demand and supply relationship, we evaluated the effects of intravenous MDL-17,043 given in incremental doses to a mean maximum dose of 2.1 mg/kg, in nine patients with severe chronic heart failure. Overall cardiac pump performance was significantly improved by MDL-17,043, as reflected by an 88% increase in stroke work index (17 +/- 11 to 32 +/- 19 gm-m/m2; p less than 0.001), a 43% reduction in left ventricular filling pressure (28 +/- 4 to 16 +/- 5 mm Hg; p less than 0.0001), a 49% reduction in systemic vascular resistance (1832 +/- 490 to 937 +/- 296 dynes-sec-cm-5; p less than 0.0001) with a slight (11%) decrease in mean arterial pressure (86 +/- 17 to 76 +/- 19 mm Hg; p = 0.005) and without significant changes in heart rate (88 +/- 14 to 91 +/- 12 bpm; p = NS). These hemodynamic effects were associated with an 18% reduction in myocardial oxygen consumption (17 +/- 5 to 14 +/- 5 ml/min p = 0.01), a 17% reduction in myocardial arteriovenous oxygen difference (13.2 +/- 2.4 to 10.9 +/- 1.8 volumes %; p = 0.01), and a 120% improvement in external myocardial efficiency (stroke work index/oxygen consumption) (1.0 +/- 0.6 to 2.2 +/- 0.9; p less than 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)