Left ventricular diastolic dysfunction plays an important role in congestive heart failure. Although once thought to be lower, the mortality of diastolic heart failure may be as high as that of systolic heart failure. Diastolic heart failure is a clinical syndrome characterized by signs and symptoms of heart failure with preserved ejection fraction (0.50) and abnormal diastolic function. One of the earliest indications of diastolic heart failure is exercise intolerance followed by fatigue and, possibly, chest pain. Other clinical signs may include distended neck veins, atrial arrhythmias, and the presence of third and fourth heart sounds. Diastolic dysfunction is difficult to differentiate from systolic dysfunction on the basis of history, physical examination, and electrocardiographic and chest radiographic findings. Therefore, objective diagnostic testing with cardiac catheterization, Doppler echocardiography, and possibly measurement of serum levels of B-type natriuretic peptide is often required. Three stages of diastolic dysfunction are recognized. Stage I is characterized by reduced left ventricular filling in early diastole with normal left ventricular and left atrial pressures and normal compliance. Stage II or pseudonormalization is characterized by a normal Doppler echocardiographic transmitral flow pattern because of an opposing increase in left atrial pressures. This normalization pattern is a concern because marked diastolic dysfunction can easily be missed. Stage III, the final, most severe stage, is characterized by severe restrictive diastolic filling with a marked decrease in left ventricular compliance. Pharmacological therapy is tailored to the cause and type of diastolic dysfunction.

Seizures are common neurologic complications of cancer and can occur at any point in the disease trajectory. Despite this, the exact pathophysiologic basis of seizures related to cancer is not known. The etiology of seizures is thought to be multifactorial, including the presence of tumors within the cranial cavity, metabolic derangements, and the direct effect of medications on the central nervous system. Seizure management often employs anticonvulsant medications and interventions to promote patient safety. Oncology nurses must be aware of the potential seriousness of this complication and implement appropriate strategies to assist patients in maintaining safety and quality of life.

Left ventricular diastolic function plays an important role in cardiac physiology. Lusitropy, the ability of the cardiac myocytes to relax, is affected by both biochemical events within the myocyte and biomechanical events in the left ventricle. β-Adrenergic stimulation alters diastole by enhancing the phosphorylation of phospholamban, a substrate within the myocyte that increases the uptake of calcium ions into the sarcoplasmic reticulum, increasing the rate of relaxation. Troponin I, a regulatory protein involved in the coupling of excitation to contraction, is vital to maintaining the diastolic state; depletion of troponin I can produce diastolic dysfunction. Other biochemical events, such as defects in the voltage-sensitive release mechanism or in inositol triphosphate calcium release channels, have also been implicated in altering diastolic tone. Extracellular collagen determines myocardial stiffness; impaired glucose tolerance can induce an increase in collagen cross-linking and lead to higher end-diastolic pressures. The passive properties of the left ventricle are most accurately measured during the diastasis and atrial contraction phases of diastole. These phases of the cardiac cycle are the least affected by volume status, afterload, inherent viscoelasticity, and the inotropic state of the myocardium. Diastolic abnormalities can be conceptualized by using pressure-volume loops that illustrate myocardial work and both diastolic and systolic pressure-volume relationships. The pressure-volume model is an educational tool that can be used to demonstrate isolated changes in preload, afterload, inotropy, and lusitropy and their interaction.

The purpose of this study was to compare the cardiopulmonary effects of expiratory positive airway pressure (EPAP) and continuous positive airway pressure (CPAP) in conscious, spontaneously breathing dogs. Nine conscious dogs with electromagnetic flow probes on their pulmonary arteries, catheters in their left atria and pulmonary arteries, and chronic tracheostomies, stood partially supported by slings, and breathed 100% oxygen through endotracheal tubes, pneumotachographs, and nonrebreathing valves which were part of either an EPAP or CPAP system. The effects of EPAP only were studied on four dogs while five were exposed to both EPAP and CPAP. After a 20-min control period, they breathed through either the EPAP or CPAP system for 10 min each under 5-, lo-, 1 5 , and 20-cm H,O airway pressure. The mean pulmonary artery pressure, mean left atrial pressure, pulmonary vascular resistance, and minute ventilation were found to be significantly higher in the CPAP-treated group. Stroke volume and cardiac output were significantly higher in the EPAP-treated group. Both groups showed a significant carbon dioxide retention. 47 0037-9727/82/0 lOO47-07$01 .OO/O