Meaning and centrality of caring activities among older women.

This article explores the meaning and conditions of caring activities for older women. Taped, in-person interviews were conducted with 53 ethnically and economically diverse women, 55-84 years old. The interview guide contained open-ended questions regarding the process of taking on caring activities and the centrality of care to personal identity. Past activities were automatically assumed, in contrast to the present experience of choice. Caring activities provided meaning and continuity throughout the life course. Participants reported becoming more self-protective over the life course and offered seven explanations for their increased ability to be self-protective.

Family relationships during serious illness.

Serious illness can have a profound effect on patients and their families, whose attempts to protect each other often mean they have to deal with their fears and anxieties on their own when they are most in need of mutual support. And this can affect the way in which they relate to the nursing staff they depend on. Talking to patients about their families can help them to maintain their identities, both as patients and as family members.

Right ventricular-vascular interaction in congestive heart failure. Importance of low-frequency impedance.

BACKGROUND: Vasodilator agents are widely used in congestive heart failure. These agents may have important effects on the pulsatile aspects of right ventricular hydraulic load. METHODS AND RESULTS: Fifteen patients with severe congestive heart failure were studied during cardiac catheterization by use of high-fidelity pressure transducers and a catheter-mounted flow velocity probe. Three graded doses of nitroprusside were infused as pulmonary artery (PA) pressure and flow were continuously recorded. From Fourier transforms of signal-averaged waves, PA impedance, hydraulic power, and wave reflection indices were derived. At the highest dose of nitroprusside (66 +/- 41 micrograms/min), cardiac output was significantly improved, whereas PA mean and wedge pressure, resistance, impedance at the first harmonic, characteristic impedance, and wave reflection amplitude were all reduced. At the dose (32 +/- 20 micrograms/min) at which cardiac output first showed improvement, only PA mean pressure and first-harmonic impedance were significantly reduced. Hydraulic power cost per unit of forward flow was also lowered at this dose, despite lack of significant change in pulmonary vascular resistance. At the lowest dose of nitroprusside (11 +/- 4 micrograms/min), six patients experienced a decrease in stroke volume, whereas the other nine were either unchanged (n = 1) or showed an increase (n = 8). Multiple regression revealed that only the change in first-harmonic impedance correlated with this effect, increasing when stroke volume decreased and decreasing when stroke volume increased (P = .02). The change in first-harmonic impedance at this dose appeared to be caused by alterations in the amplitude of PA wave reflections. At higher doses, changes in mean PA pressure (but not in pulmonary vascular resistance) correlated with changes in stroke volume. CONCLUSIONS: Nitroprusside vasodilation at low doses alters PA hemodynamics in congestive heart failure primarily through changes in low-frequency impedance. In some patients, this effect is associated with decreased stroke output. At higher doses, favorable alterations in resistance, low- and high-frequency impedance, and wave reflections all contribute to increased forward flow and decreased power requirement per unit forward flow. These findings show that ventricular-vascular interaction is importantly affected by pulmonary vasodilation and that appreciation of pulsatile properties is required to understand the effects of pulmonary vasodilation on cardiac output.

Pulmonary impedance and right ventricular-vascular coupling during coronary angioplasty.

Right ventricular ejection may be modified by alterations in pulmonary vascular properties during acute pulmonary hypertension. Pulmonary artery impedance and reflection properties were analyzed during coronary angioplasty in nine patients with single-vessel disease involving the left anterior descending artery by use of high-fidelity catheter recordings of pulmonary pressure and flow made before angioplasty balloon inflation and at peak ischemia. Acute pulmonary hypertension in this resting model resulted in a significant decrease in pulmonary vascular resistance (142 +/- 54 to 92 +/- 64 dyn.s.cm-5, P < 0.05), increase in low-frequency impedance (67 +/- 36 to 101 +/- 43 dyn.s.cm-5, P < 0.05), and no change in high-frequency (characteristic) impedance (38 +/- 14 to 41 +/- 13 dyn.s.cm-5). Pulmonary wave reflection amplitudes were increased, and the amount of hydraulic power expended per unit of net forward flow significantly increased (3.1 +/- 0.7 to 4.3 +/- 0.7 mW.ml-1.s-1, P < 0.001). These findings indicate that, during acute pulmonary hypertension in humans, 1) recruitment of additional resistance vessels can occur, 2) pulsatile pulmonary artery properties are significantly altered, and 3) right ventricular power output requirements are increased. Because episodic pulmonary hypertension occurs frequently in coronary artery disease, these changes may help explain eventual right ventricular hypertrophy or failure.

Effects of pacing tachycardia and balloon valvuloplasty on pulmonary artery impedance and hydraulic power in mitral stenosis.

BACKGROUND: Mitral stenosis is characterized by progressive pulmonary hypertension and eventual right ventricular failure. However, the correlation between right ventricular failure and the level of pulmonary hypertension is poor, suggesting that factors other than those recognized from nonpulsatile hemodynamic parameters may contribute to impaired right ventricular performance in this condition. METHODS AND RESULTS: We studied 16 patients with severe mitral stenosis (mean valve area, 1.0 +/- 0.2 cm2) at supine rest and during pacing tachycardia using high-fidelity catheter recordings of pulmonary artery (PA) pressure and flow velocity. Pulmonary impedance spectra, wave reflection properties, and hydraulic power data were derived from Fourier analysis of signal-averaged data. Pacing tachycardia (baseline heart rate, 81 +/- 11 beats per minute; pacing, 132 +/- 11 beats per minute) significantly raised pulmonary wedge and mean PA pressures. There was no change in pulmonary vascular resistance (209 +/- 144 to 232 +/- 164 dyne-sec/cm5) or PA characteristic impedance (62 +/- 25 to 55 +/- 28 dyne-sec/cm5). However, first harmonic impedance (Z1) significantly decreased (134 +/- 71 to 100 +/- 68 dyne-sec/cm5; p < 0.001). Accordingly, oscillatory and total dissipated hydraulic power per unit forward flow (WT/CO) fell during tachycardia (2.6 +/- 1.6 to 2.3 +/- 1.4 mW/ml.sec-1; p = 0.06) despite acute pulmonary hypertension. Reflected pressure waves returned earlier to the proximal PA, suggesting increased vessel stiffness. Immediately after percutaneous balloon mitral valvuloplasty (PBV) in eight of the patients, baseline and pacing data were again recorded. Compared with the pre-PBV baseline state, post-PBV resting data demonstrated no change in resistance or characteristic impedance, but there was a significant fall in Z1 (166 +/- 75 to 103 +/- 45 dyne-sec/cm5; p < 0.05) and in the magnitude of pulmonary wave reflections. WT/CO tended to decrease after PBV, and pacing after PBV produced a further decrease in WT/CO, again in association with lower Z1. CONCLUSIONS: These data demonstrate that 1) increased pulmonary characteristic impedance, although a feature of mitral stenosis, is not exacerbated by the acute effects of increased distending pressure; 2) pacing tachycardia in mitral stenosis causes little change in the pulmonary impedance spectrum except at low frequencies, where decreased impedance lowers power requirements per unit flow; and 3) relief of mitral stenosis produces immediate improvement in low-frequency impedance and in hydraulic power requirements. These findings suggest that although characteristic impedance may be a measure of the long-term effects of pulmonary hypertension on the pulmonary circulation, acute increases and decreases in PA pressure produce effects on right ventricular load that are best described in terms of the low-frequency properties of the PA system. Improvement in low-frequency impedance diminishes hydraulic power requirements and thus reflects improved ventricular-vascular coupling, irrespective of distending PA pressure. Efforts to treat or prevent right heart failure in the presence of pulmonary hypertension should take account of the potential benefit of changes in low-frequency impedance characteristics of the pulmonary vascular bed.