Ludzkie koronawirusy - autor: Krzysztof Pyrć z Zakładu Mikrobiologii, Wydział Biochemii, Biofizyki i Biotechnologii, Uniwersytet Jagielloński, Kraków

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© Borgis - New Medicine 1/2007, s. 15-19
*Robert Skalik1, 2, Ludmiła Borodulin-Nadzieja1, Anna Janocha1, Wojciech Woźniak1
Physiology of heart and echocardiography – do physicians always combine them in clinical practice?
1Department of Physiology, Medical University of Wrocław, Poland
2Echocardiography Laboratory, Department of Internal Medicine, County Hospital, Oleśnica, Poland
Summary
Summary
This article demonstrates the clinical utility of implementation of cardiovascular physiology in a routine bedside echocardiographic examination for better understanding of clinical status of a patient and optimalization of treatment strategy. Relying on the fundamental physiological laws and interactions, the authors of the article try to show usefulness of application of some standard and sophisticated echocardiographic techniques to noninvasive estimation and monitoring of heart hemodynamics in the clinical milieu.
There are still many controversial opinions on practical link between preclinical theoretic knowledge and clinical practice. Some of young medical graduates or even experienced doctors are not able to find a necessary reason to use fundamentals of cardiovascular physiology in clinical practice or ignore its potentially powerful tools. However, the milieu of intensive care unit is the unique example of how the physiological theory joins together with good everyday clinical practice. The simple hemodynamic parameters such as cardiac output, stroke volume, left ventricular filling pressure, cardiac index and many others as measured by very sophisticated, invasive equipment allow for insight into circulatory homeostasis. However, in this context it is often forgotten that echocardiography as a simple, noninvasive and reliable diagnostic tool for evaluation of heart hemodynamics could be really helpful. Kitabatake was the first to relate the phenomenon of early and late diastolic LV filling in the physiological heart cycle to E and A velocity as measured with conventional doppler echocardiography [1]. Further progress in echocardiographic techniques including Tissue Doppler Echocardiography allowed for measurements of long and short axis myocardial fibers shortening in the clinical setting, which was previously demonstrated only on the animal experimental models by Rushmer and Rankin [2, 3, 4]. At present, more and more intensivists and cardiac anaesthesiologists become aware of significance of intra- and peri-operative implementation of modern echocardiographic modalities for monitoring of heart function. The application of apparently fundamental rules and laws of cardiovascular physiology during conventional echocardiographic interrogation may broaden the portfolio of information about hemodynamics of left ventricle and thus facilitate the decision-making process with its medical and economic consequences [5]. However, often observed omitting of heart physiology during echocardiographic interrogation can make this diagnostic tool useless or even detrimental to critically ill patient. Hence, this article demonstrates the most relevant examples of clinical utility of physiology-echocardiography interactions that certainly give a better insight into pathophysiology of circulatory diseases and allow for optimalization of treatment strategy.
Estimation of left ventricular systolic function
Cardiac output as basic physiological parameter of heart function generally used for estimation of circulatory haemodynamics in intensive care unit (ICU) is a resultant of heart rate and stroke volume [6]. Unfortunately, the close physiological relationship between cardiac output and heart rate can bias the invasive assessment of factual hemodynamic status of critical care patients. The significant compensatory increase in heart rate in course of left ventricular hemodynamic collapse (acute postmyocardial heart failure, post-CABG myocardial stunning) may mask actual hemodynamic conditions in patients with severe myocardial damage and subsequent poor stroke volume. On the other hand, this confounding factor can be omitted by using conventional doppler echocardiography. Continuous Wave Doppler sample volume placed in the left ventricular outflow tract (LVOT) allows for visualization of aortic ejection spectrum and further calculation of Velocity Time Integral (VTI) that depicts velocity of blood flow in LVOT in the designated time span [5]. This easy to measure parameter even in critically ill patients with poor "acoustic window” reliably reflects global left ventricular (LV) systolic function. VTI is useful for calculation of stroke volume, which is a resultant of VTI value and cross sectional area of LVOT (CSA). Nonetheless, it must be remembered that a big variability of beat-to-beat measurements of LVOT dimensions accompanied by often volatile heart rate in ICU patients may significantly influence accuracy of Doppler estimation of cardiac output (cardiac output = VTI x CSA x heart rate) [5]. Hence, it is more advisable and practical to monitor LV hemodynamics by calculating only VTI. The average value of VTI between 12.6 and 22.5 cm usually indicates at normal global LV systolic function [5]. However, it must be remembered that puristic Doppler approach without considering other hemodynamically important measurable parameters and dynamics of heart physiology may be clinically counterproductive. The often ignored physiological phenomenon of post-extrasystolic potentiation of left ventricular contraction during echocardiographic interrogation of VTI and LV stroke volume may cause overestimation of factual global systolic function even in patients with severe chronic heart failure [6]. According to the rules of physiology, the premature ventricular extrasystole changes the pace of rhythm producing long post-extrasystolic interval. Subsequently, the normal heart beat that originates from sinus node soon after the premature contracture becomes significantly strengthened, which also may be reflected in the higher value of VTI and stroke volume irrespective of factual contractile LV function [7]. On the other hand, the post-extrasystolic potentiation-induced increase in stroke volume may facilitate interrogation of severity of aortic stenosis in patients with poor LV ejection fraction. These patients are sometimes problematic, because significantly impaired contractile LV function does not allow for generation of proper stroke volume and further aortic transvalvular pressure gradient [8]. Hence, the coincidental premature ventricular contracture transiently increases LV contraction force thus producing factual aortic gradient [9].
The accuracy and repeatability of obtained measurements of stroke volume can be lowered if the physiological respiration-stroke volume interaction is ignored, too [6]. According to heart-lung physiology, stroke volume normally decreases during inspiration. Inspiration decreases the intrathoracic pressure causing an increase in systemic venous return and in right ventricular volume, which itself reduces left ventricular end-diastolic volume via diastolic ventricular interdependence. Furthermore, inspiration increases the left ventricular afterload thus reducing the left ventricular stroke volume. These different mechanisms join together to produce a decrease in end-diastolic left ventricular dimensions with no change in end-systolic dimensions and a fall in stroke volume. Hence, determination of stroke volume at end-expiration during echocardiographic interrogation is always recommended [10].
Evaluation of LV contractile synchronicity that consists in qualification for resynchronization therapy in patients with severe chronic heart failure is another interesting practical aspect of physiology – echocardiography interaction. Relatively synchronic contraction of LV wall segments is an indispensable condition for maintenance of effective stroke volume and circulatory homeostasis. Patients with ischemic heart disease or especially severe heart failure (CHF) may demonstrate significant regional contractile dyssynchrony that is partially responsible for poor stroke volume and severity of clinical symptoms of heart failure [11]. The regional contractile asynchrony in patients with CHF results from significant differences between segmental contraction times of particular LV wall segments as measured with tissue Doppler echocardiography [12]. As it is known from heart´s physiology, global isovolumic contraction time (IVCT) reflects contraction of left ventricle while the volume of LV does not become changed. IVCT precedes aortic valve opening and LV ejection phase [6]. However, it must be stressed that IVCT of physiological cardiac cycle is a resultant of regional isovolumic contraction times of particular segments of LV walls that can be measured only by tissue Doppler echocardiography in the clinical setting [9]. The severe impairment of LV systolic function may disturb synchronic contraction of left ventricular segments thus reducing stroke volume and cardiac output [9]. In order to make the issue of contractile dyssynchrony more complicated it must be remembered that regional contractile left ventricular asynchrony is to some degree a physiological phenomenon [2]. It was demonstrated that the physiological contracture of left ventricle is not completely uniform, i.e. there are some slight differences in contraction times of particular LV segments [6]. However, the physiological contractile LV asynergy must be separated from severe heart failure-related pathological dyssynchrony that can be established by sophisticated echocardiographic techniques. Thus, the in-depth echocardiographic analysis of significant delays in contraction times of left ventricular segments allows for both selection of these patients with chronic heart failure, who present significant asynchrony and will really benefit from resynchronization procedure [13, 14].
Afterload fluctuations versus reliability of estimation of mitral regurgitation and LV Ejection Fraction

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Piśmiennictwo
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Adres do korespondencji:
*Robert Skalik, MD, PhD
Department of Physiology, Medical University of Wrocław, Poland
Chałubińskiego Str. 10
e-mail: rskalik@fizjo.am.wroc.pl

New Medicine 1/2007
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