Cardiovascular system
David A Lisle in Imaging for Students, 2012
Dyspnoea may have a variety of causes including cardiac and respiratory diseases, anaemia and anxiety states. Certain features in the clinical history may be helpful in diagnosis, such as whether dyspnoea is acute or chronic, worse at night, or accentuated by lying down (orthopnoea). Initial tests include full blood count, ECG and CXR, followed by pulmonary function tests when a respiratory cause such as emphysema or asthma is suspected. Congestive cardiac failure (CCF) is the most common cardiac cause of dyspnoea. CCF may be caused by systolic or diastolic dysfunction, or a combination of the two. Systolic dysfunction refers to reduction of the amount of blood pumped due to failure of ventricular contraction. Diastolic dysfunction refers to failure of ventricular relaxation between contractions leading to reduced filling of the ventricular chambers. The most common underlying cause of CCF is ischaemic heart disease. Other causes include valvular heart disease, hypertension, hypertrophic cadiomyopathy, infiltrative disorders like amyloidosis, pericardial effusion or thickening, or congenital heart disease. Imaging is performed to confirm that CCF is the cause of dyspnoea, to quantitate and classify cardiac dysfunction, and to search for underlying causes. CXR and echocardiography are the usual imaging tests employed for the initial assessment of CCF. Coronary artery imaging with CT or angiography is indicated where an ischaemic cause for CCF is suspected.
Venous flow is pulsatile
Dinker B. Rai in Mechanical Function of the Atrial Diastole, 2022
When the ventricle contracts it surges a volume of blood into the great arteries. The arteries expand as a result of this volume of blood which can be manually felt and visually observed. We have termed this phenomenon the arterial pulse. Historically, in the circulatory system the contraction of the heart or of the vessels was named “systole” and the dilatation or filling phase was called “diastole.”The term diastole was also applied to the pulsation of the arteries during that phase. Currently the terms systole and diastole are restricted to the description of the atria and ventricles of the heart. Dilatation or diastole of the artery is now termed “pulsation.”However, the age-old theory that the systole is the only active phase of the heart remains unchanged. The diastole is always considered to be the resting phase, wherein the supplying of the cardiac chambers with blood occurs during this phase. During ventricular systole there is a surge of blood into the arterial system which increases the flow and volume of the blood in the arteries. During the diastole of the ventricle the arteries do not completely collapse owing to the compliance in the wall of the artery. This helps the circulation in two ways. First if the arteries were to completely collapse during diastole then there would have been cessation of the flow of blood to the arteries. This would have resulted in the doubling of the workload on the consecutive ventricular systole. Second, compliance of the artery keeps the blood in motion during diastole, permitting the consecutive ventricular systole to take over the flow of blood in the already dilated arteries and resulting in a decrease of the workload of the ventricle by half. This observation of ventricular systole with active contraction of the muscles pushing the blood into the arteries and refilling itself during diastole without any interference in the flow of blood in the arteries has resulted in the popular inferences that systole is the only active function in the cardiac cycle of the heart and diastole, which is the filling phase, is the resting phase of the heart. This author has convincingly proved that both systole and diastole are equally active phases of the cardiac cycle and contribute equally to the function of the heart. This is because during both phases there are chemical, physical, and electrical changes taking place at the cellular level. This author has experimentally proved both contraction and dilatation of cardiac muscle as active phenomena and both are not the resting phase of the cardiac cycle.
Respiratory physiology
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal in Principles of Physiology for the Anaesthetist, 2015
Pressures in the pulmonary circulation are only 20% of systemic pressures, because the resistance of the former is much lower. Pulmonary artery systolic pressure is 25 mmHg and diastolic pressure is 10 mmHg, with a mean pulmonary artery pressure of 15 mmHg. Left atrial pressure is 5 mmHg, and the average pressure drop across the pulmonary circulation is therefore 10 mmHg. Pulmonary capillary flow is markedly pulsatile because the low pulmonary arteriolar resistance does not damp the pressure waveform produced in the pulmonary artery by the systolic output of the right ventricle. A value of 8 mmHg has been suggested for mean pulmonary capillary pressure.
Imaging assessment of left ventricular diastolic function: current and emerging methods
Published in Acta Cardiologica, 2016
Carmen C. Beladan, Adriana M. Iliesiu, Andreea C. Popescu, Ioan M. Coman, Carmen Ginghina, Bogdan A. Popescu
Left ventricular diastolic dysfunction (LVDD) plays a key role in the pathophysiology of heart failure with preserved ejection fraction and has prognostic implications even in the preclinical stage. The imaging assessment of left ventricular diastolic function is nowadays part of the routine clinical practice. Echocardiography is widely available, safe and versatile, and provides important structural and functional information relevant to diastolic function assessment. The currently used algorithms for LV diastolic function evaluation propose a variety of parameters that reflect different LV diastolic properties, each of them having potential limitations. Thus, there is still significant interobserver variability in classification of LVDD stage and estimation of LV filling pressure in a considerable proportion of studies. This review discusses the currently used methods for the assessment of LV diastolic function, higlighting their strengths and limitations. It also discusses some of the newer techniques with potential clinical impact, emphasizing their additional value and the current challenges inherent to their routine clinical use.
Interval training does not modulate diastolic function in heart transplant recipients
Published in Scandinavian Cardiovascular Journal, 2014
Tea Monk-Hansen, Christian H. Dall, Stefan B. Christensen, Martin Snoer, Finn Gustafsson, Hanne Rasmusen, Eva Prescott
Objectives. This study investigates the effect of aerobic interval training on diastolic function at rest and during exercise in stable heart transplant (HTx) recipients. Design. Twenty-three stable HTx recipients (74% males, mean age 50 ± 14.9 years) were recruited to a training programme. Intervention was 8 weeks intensive training or control in a randomized controlled design. Results. At baseline, participants had normal or mild diastolic dysfunction at rest. During exercise, mean E/e′ increased from 9.0 (± 2.8) to 12.8 (± 7.7) (p = 0.09), E/A increased from 2.1 (± 0.6) to 2.6 (± 0.7) (p = 0.02), and deceleration time decreased by over 50 ms, all markers of increased filling pressure. There were no correlations between diastolic function and VO2peak at baseline. After intervention VO2peak increased from 23.9 (± 4.5) to 28.3(± 6) ml/kg/min in the training group (difference between groups p = 0.0018). No consistent pattern of improvement in diastolic function at rest or during exercise was seen. Conclusion. The study does not support a role of diastolic dysfunction in the limited exercise capacity of HTx recipients and suggests that in these patients peripheral factors are of greater importance.
An elongation model of left ventricle deformation in diastole
Published in Computer Methods in Biomechanics and Biomedical Engineering, 2013
Yingying Hu, Liang Shi, Dongxing Du, Siva Parameswaran, Zhaoming He
A numerical method of the left ventricle (LV) deformation, an elongation model, was put forth for the study of LV fluid mechanics in diastole. The LV elongated only along the apical axis, and the motion was controlled by the intraventricular flow rate. Two other LV models, a fixed control volume model and a dilation model, were also used for model comparison and the study of LV fluid mechanics. For clinical sphere indices (SIs, between 1.0 and 2.0), the three models showed little difference in pressure and velocity distributions along the apical axis at E-peak. The energy dissipation was lower at a larger SI in that the jet and vortex development was less limited by the LV cavity in the apical direction. LV deformation of apical elongation may represent the primary feature of LV deformation in comparison with the secondary radial expansion. The elongation model of the LV deformation with an appropriate SI is a reasonable, simple method to study LV fluid mechanics in diastole.
Related Knowledge Centers
- Ventricle
- Heart
- Systole
- Myocardium
- Heart Ventricles
- Myocardial Contraction
- Muscle Relaxation