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.

Turning critically ill, mechanically ventilated patients every 2 hours is a fundamental nursing intervention to reduce the negative impact of prolonged immobility from preventable pulmonary complications such as ventilator-associated pneumonia and atelectasis. Unfortunately, when coupled with positive pressure ventilation, the benefits of turning may come at the expense of cardiovascular function. Clinicians should closely monitor the hemodynamic response to turning mechanically ventilated patients, and if compromise is observed, the degree and duration of compromise may provide guidance to the appropriate intervention.

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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.

Mechanically ventilated patients in the intensive care unit (ICU) are typically turned manually by nursing staff to reduce the risk of developing ventilator associated pneumonia and other problems in the lungs. However, turning can induce changes in the heart rate and blood pressure that can at times have a destabilizing effect. We report here on the early stage of a study that has been undertaken to measure the cardiovascular impact of manual turning, and compare it to changes induced when patients lie on automated beds that turn continuously. Heart rate and blood pressure data were analyzed over ensembles of turns with autoregressive models for comparing baseline level to the dynamic response. Manual turning stimulated a response in the heart rate that lasted for a median of 20 minutes and was of magnitude 5 to 13 bpm. The corresponding response in mean arterial pressure was 11 to 19 mm Hg, lasting for 8 to 21 minutes. There was no discernible response of either variable to automated turns.

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In this article, we illustrate a new method for random selection and random assignment that we developed in a pilot study for a randomized clinical trial. The randomization database is supported by a commonly available spreadsheet. Formulas were written for randomizing participants and for creating a "shadow" system to verify integrity of the randomization. Advantages of this method are that it is easy to use, effective, and portable, allowing it to be shared among multiple investigators at multiple study sites. Clinical researchers may find the method useful for research projects that are pilot studies or conducted with limited funding.