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Hypertension in the setting of symptomatic congestive heart failure requires aggressive treatment. The optimal antihypertensive agent in such patients is one that effectively controls blood pressure without compromising the failing heart.
The prevalence of congestive heart failure (CHF), a debilitating condition associated with impaired quality of life and markedly shortened life expectancy, is increasing. The goals of therapy for CHF are reducing symptoms, improving functional capacity, and slowing the progression of the condition. In most cases, this is best achieved with a combination of diuretic and vasodilator therapy. Angiotensin-converting enzyme (ACE) inhibitors have several advantages over other vasodilatory agents and are becoming widely used for treating CHF. The most recently introduced ACE inhibitor, fosinopril, is at least as effective as enalapril, and its dual and compensatory route of excretion is particularly advantageous in patients with renal insufficiency. Fosinopril may also have particular benefits in the prevention of CHF, as it has beneficial effects on cardiac function that may help delay the onset of overt cardiac failure.
Congestive heart failure (CHF) from ischemic cardiomyopathy has emerged as an epidemic health problem. The pathogenesis of CHF is characterized by heightened activity of many neuroendocrine factors, including norepinephrine, angiotensin II, and arginine vasopressin, which lead to heightened systemic vascular resistance and further impedance of left ventricular ejection. Once CHF reaches New York Heart Association (NYHA) class III or IV with heightened activity of the many neurohumoral factors, it tends to be refractory to conventional therapy of vasodilators, inotropic agents, and diuretics. Treatment of refractory CHF appears to require a break in the neurohumoral hemodynamic vicious cycle, and ultrafiltration appears able to produce this interruption. Ultrafiltration has been shown to be successful in patients with NYHA class III to VI CHF and urine output less than 1,000 mL/d. It relieves pulmonary edema, reduces ascites and peripheral edema, and enhances the response to subsequent diuretic therapy. In patients with refractory CHF, the ability to provide adequate volume removal, thus improving overall volume status, normalizing filling pressures, and reducing clinical symptoms, offers an improvement in overall quality of life. Early results have shown that ongoing therapy actually may be associated with decreased hospital readmissions or, at the very least, shortened intensive care unit length of stay.
Congestive heart failure (CHF) is a significant health problem for women, particularly elderly women. The risk factors for heart failure appear to be different in women than in men, with hypertension and diabetes playing a greater role in women and ischaemic heart disease a greater role in men. The aim of this study was to describe, from a nurse's perspective, how female patients with CHF conceive their life situation. Interview questions were designed with a focus on five dimensions: biophysical, socio-cultural, emotional, intellectual and spiritual-existential. A qualitative method was used with a phenomenographic approach, as this approach examines aspects of the surroundings as they are conceived. Five categories emerged in the results: feeling content, feeling a sense of support, feeling a sense of limitation, feeling anxiety and feeling powerless. A sense of limitation regarding working capacity and being able to support those in their surroundings causes patients with CHF to experience anxiety due to feeling insecure about themselves and in relation to their surroundings. This may result in feelings of worthlessness in women with CHF, both concerning their own capacity and the fact that they feel they are a burden to those around them. Through nursing intervention, these patients can receive help to break this vicious circle of feeling limited and powerless. This can be done by encouraging them to verbalize their feelings and set realistic goals and expectations, and by increasing their knowledge and that of their families concerning CHF and its symptoms, with a focus on self-care and existing possibilities. These measures will make it easier for women with CHF to maintain a hopeful perspective and a sense of control, competence, and self-esteem.
In 30 individuals with class III congestive heart failure (CHF), negative feedback of 4 cardiac peptide hormones, ie, long-acting natriuretic peptide (LANP), vessel dilator, kaliuretic peptide, and atrial natriuretic factor (ANF) from the same 126-amino acid (aa) prohormone were studied with the infusion of 100 ng/kg body weight (BW) for 60 minutes of each of the 4 cardiac hormones and a saline control (n = 6 for each). LANP decreased the circulating concentrations of vessel dilator, kaliuretic peptide, and ANF by 24%, 55%, and 30%, respectively. Vessel dilator decreased the circulating concentrations of ANF, kaliuretic peptide, and LANP 27%, 12%, and 62%, respectively. Kaliuretic peptide decreased the circulating concentrations of LANP, ANF, and vessel dilator 89%, 67%, and 70%, respectively. ANF decreased the circulating concentrations of LANP, vessel dilator, and kaliuretic peptide 88%, 59%, and 98%, respectively. Infusion of each of these 4 cardiac hormones decreased the excretion of the other 3 hormones into the urine by 11% to 92%. These results suggest that the respective cardiac hormones inhibit the release of each other rather than their breakdown, which would have increased their urinary concentrations. The feedback regulation of these hormones found previously in healthy humans is, thus, preserved in persons with CHF despite their increased endogenous circulating concentrations.
Cognitive dysfunction, mainly memory impairment, characterizes congestive heart failure (CHF). Aim of this study was to verify whether: (1) CHF has differential effects on primary and secondary memory; (2) memory dysfunction can be diagnosed by a screening instrument. In a multicenter study we enrolled 369 patients with stable CHF who underwent a structured assessment of verbal memory mechanisms and selected cognitive functions. Performance on some verbal memory indexes (Recency, Rey's immediate and delayed recall, Learning efficiency) progressively decreased from II to IV New York Heart Association (NYHA) class. Rate of forgetting was uniformly high across NYHA classes II-IV. Verbal memory indexes were highly correlated with most nonverbal scores. The Mini Mental State Examination (MMSE) had poor sensitivity and specificity versus primary or secondary verbal memory dysfunction. Therefore, a deficit of both primary and secondary memory is relatively common in CHF but cannot be accurately recognized by a screening neuropsychological test.
This paper reviews the evidence that congestive heart failure is characterized by an increase in sympathetic nerve activity and that this may begin in an early symptomatic phase and progress with the severity of the disease. The sympathetic activation initially plays a compensatory role but eventually is outweighted by adverse consequences at both cardiac and vascular levels which may aggravate the clinical status and negatively affect prognosis. This is likely to depend on the fact that the sympathetic activation becomes excessive due to reduction in sensitivity of baroreflexes and cardiopulmonary reflexes restraining sympathetic tone (functional reflex denervation) and positive interactions between the sympathetic and the renin-angiotensin system. Therapeutic interventions may reduce the marked sympathetic activation which occurs in heart failure, and in some instances (particularly with digitalis compounds) may also improve the impaired sensitivity of reflex cardiovascular control.
Despite advances in medical therapy of congestive heart failure (CHF), morbidity and mortality for this disorder remain high. One factor that could contribute to the poor prognosis of CHF is Cheyne-Stokes respiration with central sleep apnea (CSR-CSA). This breathing disorder is a frequent complication of CHF, where it is associated with increased mortality. One reason for this higher mortality may be that apnea-related hypoxia and arousals from sleep can increase sympathetic nervous system activity (SNA), as manifested by increases in overnight urinary and daytime plasma norepinephrine concentrations ([UNE] and [PNE], respectively). Recently published randomized trials have demonstrated that nasal continuous positive airway pressure (CPAP), if applied nightly at high enough levels over periods of at least 1-3 months, can alleviate CSR-CSA in patients with CHF in association with hemodynamic improvement, as evidenced by increased left ventricular ejection fraction (LVEF) and inhibition of SNA, as manifest by reductions in [UNE] and [PNE]. These findings indicate a role for CPAP as a non-pharmacologic adjunctive therapy for CHF complicated by CSR-CSA. Longer-term trials of CPAP are needed to determine whether this intervention can provide long-lasting clinical benefit to patients with CHF and CSR-CSA.
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The Xe-133 ventilation pattern in congestive heart failure (CHF) was assessed using 24 inpatient ventilation/perfusion studies performed to rule out pulmonary embolism. Patients with histories of CHF, myocardial infarction (MI), and cardiomyopathy were included in the study. Frank pulmonary edema, pulmonary embolism, and other known lung diseases such as chronic obstructive lung disease, tumor, and pneumonia were excluded. Fifteen of the 24 patients had abnormal ventilation scans. Twelve of the 15 showed bilateral basal Xe-133 retention on washout; the remaining 3 showed diffuse, posterior regional retention. On perfusion scans, 14 of the 15 abnormal ventilation patients showed evidence of CHF such as inverted perfusion gradient, enlarged cardiac silhouette, or patchy perfusion, and all of them had a history of CHF or cardiac disease. Nine of the 24 patients had normal ventilation scans, including normal washout patterns. Seven of the nine had normal perfusion (p less than 0.01). Four of the nine normal ventilation patients had a history of cardiac disease or CHF but no recent acute MI. Bilateral basal regional Xe-133 retention, coupled with perfusion scan evidence of CHF such as inverted perfusion gradient, enlarged cardiac silhouette, and patchy perfusion pattern, appears to be a sensitive and characteristic ventilation/perfusion finding in mild or subclinical CHF.
This study compared elderly patients with congestive heart failure discharged from home healthcare to the home vs. those rehospitalized. The rate of rehospitalization in this sample of 117 was 27%. Significant predictors of rehospitalization included number of home healthcare days, number of previous hospitalizations, and the services of a home health aide. Implications include the timing and nature of home health visits.
PURPOSE: Functional limitation, often associated with congestive heart failure (CHF), is most accurately assessed with measurement of peak VO2 (VO2peak) during exercise testing. VO2peak strongly predicts survival in CHF patients and is used to triage patients for cardiac transplantation. However, the traditional mouthpiece/noseclip equipment used for gas exchange analysis is often cumbersome and uncomfortable. Several alternative facemask designs tested previously in healthy cohorts were inferior to the mouthpiece for measuring VO2peak. In this study, a series of facemasks designed specifically for VO2peak testing (Hans-Rudolph) was employed. Although previously validated in healthy young adults, this apparatus has not been validated in patients with severe CHF. METHODS: The Hans-Rudolph facemasks were compared with the mouthpiece apparatus in 30 patients with severe CHF. Each subject completed a cardiopulmonary exercise test with each device. Twelve subjects were randomized to evaluate a possible training effect. To enhance recruitment, 18 additional subjects were recruited after they had completed a test with the mouthpiece. RESULTS: There was no evidence of a training effect and no differences in gas exchange measurements were found between the two devices. The weight-adjusted VO2peak measurements were 17.1 +/- 5.3 ml O2/kg/min for the mouthpiece group and 17.3 +/- 5.6 ml O2/kg/min for the mask group (P = 0.54). CONCLUSIONS: The facemask was shown to be equivalent to the mouthpiece for measuring VO2peak in CHF patients. Concerns of hypoventilation and decreased VO2peak associated with previous facemask designs were not substantiated. Since successful exercise testing depends on maximal exertion, providing a choice of equipment may facilitate cooperation without sacrificing accuracy.
The majority of symptoms related to congestive heart failure (CHF) can be derived from the excessive accumulation of fluid in the body. The retention of fluid is the result of the activation of a complex system of compensatory mechanisms working on the kidneys and altering the hemodynamic situation in the body. The compensatory mechanisms are essentially the same as those activated in acute blood loss. The common denominator for CHF and acute blood loss is a decrease of the effective arterial blood volume (EABV), a parameter defined as blood volume in relation to vascular capacity. In the early stages of CHF there is an increased sympathoadrenergic tone, leading to a peripheral vasoconstriction and a decrease of blood flow to the kidneys. Due to a preferential constriction of the efferent arterioles, the filtration fraction is increased and the glomerular filtration rate remains unchanged. However, there is an increased colloid osmotic pressure and a decreased intravascular hydrostatic pressure in the peritubular capillaries. These alterations result in an increased reabsorption of sodium and water in the kidneys. Furthermore, the blood flow in the kidneys is rerouted from the cortical to the juxtamedullary nephrons, which have larger glomeruli and longer loops of Henle. This will further increase the retention of salt and water. The renin-angiotensin-aldosterone (R-A-A) system is also activated due to the decrease of EABV. Angiotensin II exerts about the same effects as norepinephrine--vasoconstriction, rerouting of blood within the kidney and preferential vasoconstriction of the efferent arterioles--all changes contributing to the retention of salt and water.(ABSTRACT TRUNCATED AT 250 WORDS)
Patients with congestive heart failure (CHF) need considerable education to enable them to provide effective self-care for their chronic illness. No information has been published about the learning needs of this population. The purpose of this study was to examine hospitalized CHF patients and their nurses' perceptions regarding the importance and realism of typical patient education content. An instrument to assess learning needs was developed and piloted for use in this study. Thirty hospitalized patients and 26 nurses were surveyed. Both nurses and patients rated all information as important to learn and realistic to learn during the patients' hospitalizations. Patients and nurses agreed that medication information was the most important to learn. Generally, patients rated information as more important than nurses rated the same information areas. Suggested nursing interventions and future research endeavours are addressed.
INTRODUCTION: The prognosis of women with congestive heart failure (CHF) is better than that for men, but the mechanisms underlying the female survival advantage are not well understood. CHF is characterized by profound abnormalities in cardiac autonomic control that contribute to progressive circulatory failure and influence survival. METHODS AND RESULTS: Time- and frequency-domain heart rate variability (HRV) indexes were obtained from 24-hour Holter recordings and compared to assess the role of gender in 131 men and 68 women with CHF (mean age 60 +/- 13.6 years, range 21 to 87; New York Heart Association Functional Class III [66%] and IV [34%]). Gender-related differences in HRV were observed only in the subset of patients with nonischemic heart failure (55 men and 39 women). Among the time-domain indexes, the SD of the RR intervals (76 +/- 5.3 msec vs 55.3 +/- 3.2 msec, P < 0.0001) and indexes denoting parasympathetic modulation, the percentage of RR intervals with >50 msec variation (4.0% +/- 1.0% vs 6.5% +/- 1.3%, P = 0.02), and the square root of mean squared differences of successive RR intervals (19.1 +/- 3.3 vs 28.4 +/- 3.8, P = 0.004) were higher in women. Among the frequency-domain indexes, the total power (7.5 +/- 0.13 ln-msec2 vs 8.3 +/- 0.14 ln-msec2, P = 0.0002), the ultralow-frequency power (7.2 +/- 0.11 ln-msec2 vs 8.0 +/- 0.14 In-msec2, P < 0.0001), the low-frequency power (3.8 +/- 0.25 ln-msec2 vs 4.8 +/- 0.28 ln-msec2, P = 0.006), and the high-frequency power (3.8 +/- 0.24 ln-msec2, vs 4.6 +/- 0.26 ln-msec2, P = 0.003) were greater in women than in men. CONCLUSION: Women with nonischemic CHF have an attenuated sympathetic activation and parasympathetic withdrawal compared with men. Gender-based differences in autonomic responses in the setting of CHF may be related to the female survival advantage.
We previously found that mice with congestive heart failure (CHF) were anemic, had decreased bone marrow haematopoiesis and functionally impaired neutrophilic granulocytes despite normal blood concentrations of these cells. We now asked if CHF-mice could mount an adequate immune response when challenged with an acute inflammation. A postinfarction heart failure was induced in mice. Six weeks later the mice had developed CHF. At that time a sterile peritonitis was induced by injection of a casein digest. Five hours after this injection a marked neutrophilia had developed. Specimens were then obtained from peritoneal washings, bone marrow and blood. Total bone marrow cell numbers were halved in CHF-peritonitis mice compared with sham-peritonitis mice. Bone marrow colony-forming cell numbers in CHF-peritonitis mice were only 14% of those in sham-peritonitis mice. The mobilization of leucocytes to the blood was much lower in CHF-peritonitis mice than in sham-peritonitis mice (5.6 vs. 8.1 million cells/mL), as was the peritoneal influx of these cells (1.6 vs. 4.1 million cells). A profound decline (>50%) in the functional activity, determined with various in vitro assays, was evident for both neutrophilic granulocytes and lymphocytes from CHF-peritonitis mice. Heart failure after myocardial infarction in mice may severely compromise their ability to combat an inflammatory challenge.
Treatment with captopril in resistant normotensive congestive heart failure is associated with a pronounced reduction in blood pressure, particularly after the first dose. The effects of this reduction on renal function were assessed in 10 patients at the beginning of and during chronic treatment (at one week and three months). Renal plasma flow and glomerular filtration rates were measured by isotope clearance during water diuresis. The first dose of captopril (25 mg) led to a pronounced fall in renal plasma flow and glomerular filtration rates together with a decrease in mean arterial pressure; this fall correlated with baseline plasma renin activity. These changes were paralleled by decreases in water and sodium excretion. In contrast, by the end of the first week of treatment a similar fall in mean arterial pressure occurred together with a pronounced increase in renal plasma flow; the glomerular filtration rate was maintained and there was no decrease in water and sodium excretion. This new response pattern recurred after three months of treatment. The difference in response at different stages of treatment may reflect the balance between the different mechanisms influencing kidney dynamics in heart failure and their alteration by converting enzyme inhibition. The sustained increase in renal plasma flow during chronic treatment with captopril may account for the continued control of heart failure in these patients.
The hypothesis that cellular hypertrophy in congestive heart failure (CHF) modulates mechanosensitive (ie, swelling- or stretch-activated) channels was tested. Digital video microscopy and amphotericin-perforated-patch voltage clamp were used to measure cell volume and ion currents in ventricular myocytes isolated from normal dogs and dogs with rapid ventricular pacing-induced CHF. In normal myocytes, osmotic swelling in 0.9x to 0.6x isosmotic solution (296 mOsm/L) was required to elicit an inwardly rectifying swelling-activated cation current (I(Cir,swell)) that reversed near -60 mV and was inhibited by 10 micromol/L Gd3+, a mechanosensitive channel blocker. Block of I(Cir,swell) by Gd3+ simultaneously reduced the volume of normal cells in hyposmotic solutions by up to approximately 10%, but Gd3+ had no effect on volume in isosmotic solution. In contrast, I(Cir,swell) was persistently activated under isosmotic conditions in CHF myocytes, and Gd3+ decreased cell volume by approximately 8%. Osmotic shrinkage in 1.1x to 1.5x isosmotic solution inhibited both I(Cir,swell) and Gd3+-induced cell shrinkage in CHF cells, whereas osmotic swelling only slightly increased I(Cir,swell). The K0.5 and Hill coefficient for Gd3+ block of I(Cir,swell) and Gd3+-induced cell shrinkage were estimated as approximately 2.0 micromol/L and approximately 1.9, respectively, for both normal and CHF cells. In both groups, the effects of Gd3+ on current and volume were blocked by replacing bath Na+ and K+ and were linearly related with varying Gd3+ concentration and the degree of cell swelling. CHF thus altered the set point for and caused persistent activation of I(Cir,swell). This current may contribute to dysrhythmias, hypertrophy, and altered contractile function in CHF and may be a novel target for therapy.