© 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
The afterload and LV systolic stress interdependence, which is often ignored by echocardiographers during interrogation of mitral regurgitation and LV ejection fraction in turmoil of everyday routine in-hospital practice, is another clinically relevant physiological phenomenon. The significant increase in afterload caused by increase in arterial blood pressure in aorta obviously produces a bigger workload for contracting left ventricle. Hence, the LV contraction force and subsequently intraventricular pressure must rise properly during systole to be a respectable counterpoise for increased afterload. In patients with normal subvalvular and valvular mitral apparatus this physiological intracavitary pressure overload will not have a significant impact on blood flow through heart cavities. However, the meaningful rise in afterload in patients with postinfarctous LV dysfunction with mitral apparatus engagement may change the course of mitral regurgitation as interrogated with echocardiography causing the clinical and treatment strategy consequences [5, 6]. The significantly elevated intraventricular systolic workload caused by increase in blood pressure in aorta (e.g. hypertensive crisis, significant peripheral vessel constriction induced by intravenous catecholamines infusion) may affect the pressure gradient between left atrium (LA) and left ventricle thus producing significant backflow of blood into LA through even slightly impaired mitral apparatus. Then, preoperative echocardiographic interrogation of mitral regurgitation without pre-considering the actual systolic blood pressure may cause over- or under-estimation of its severity and further wrong treatment strategy. What is more, deterioration of mitral regurgitation induced by volatile hemodynamic conditions may also cause overestimation of left ventricular ejection fraction. LV ejection fraction is strictly dependent on local LV contractility, but also changing loading conditions. Hence, the apparent unexpected increase in ejection fraction, which is sometimes observed in patients with obviously impaired LV regional contractile function, will be caused by decrease in end-systolic volume of left ventricle following significant backflow of blood from left ventricle into LA during systole (phenomenon of unloading left ventricle during LV contraction phase through insufficient mitral valve). Then, echocardiographic interrogation of left ventricular hemodynamics must be supplemented with cautious monitoring of actual blood pressure either in echocardiography laboratory or in the milieu of intensive care unit. This rule should be also obeyed during the intraoperative evaluation of the degree of residual mitral valve leakage after mitral valve plasty. The premature intraoperative echocardiographic estimation of post mitral valve repair leakage in persistent hypovolemic conditions (soon after switching off the extracorporeal circulation) may underestimate the factual volume of residual mitral regurgitation and thus discourage a surgeon from necessary intraoperative reintervention. The significantly reduced preload soon after weaning off the cardiopulmonary bypass hinders left ventricle from generating proper systolic intracavitary pressure and subsequent respectable LA-LV pressure gradient. Thus, the intravetricular pressure against mitral valve apparatus is too low to allow for echocardiographic visualization of factual volume of blood backflow through the repaired valve even though the postoperative contractile LV function is normal (volemia – precontraction myocardial fiber stretching interdependence). So, the intraoperative echocardiographic evaluation of the outcome of mitral valve repair is recommended when the intracavitary systolic blood pressure generated by left ventricle reaches at least 120 mmHg [15].
Hypovolemia – tachycardia syndrome
The strong relationship between stroke volume and loading conditions can be spectacularly exemplified by hypovolemia-tachycardia syndrome. Stroke volume is dependent on both LV contractile function and LV filling conditions. The cardiac muscle contraction without proper LV filling from left atrium in the preceding diastolic phase and further proper LV distension will not guarantee satisfactory contraction force and stroke volume [6]. Unfortunately, this seemingly obvious and well-known physiological is often ignored by cardiologists, internists and especially cardiac intensivists. The volemia – LV stroke volume interaction well known to physiologists as a fundament for understanding Starling law consists in pathophysiology of hypovolemia – tachycardia syndrome. This pathological state is sometimes observed in post cardiac surgery patients in the perioperative period. Patients affected by this syndrome present significant increase in pulmonary capillary wedge pressure (PCWP) and heart rate with concomitant decrease in cardiac output as measured invasively with Swan Ganz catheter [16]. Such constellation of hemodynamic parameters can be usually suggestive of postoperative LV contractile dysfunction caused by either perioperative myocardial infarction or myocardial stunning. However, the elevation of PCWP found in patients with hypovolemia-tachycardia syndrome does not result from depressed LV contractile function and subsequent increase in LV filling conditions, but is factually related to significant tachycardia. It is known that meaningful increase in heart rate lowers accuracy of invasive Swan-Ganz catheter measurements [17]. In turn, accelerated heart rate and lowered cardiac output observed in this syndrome are surprisingly caused by obvious hypovolemia instead of LV acute systolic dysfunction. Relying only on invasively measured parameters of heart hemodynamics it can be sometimes difficult to discriminate between acute LV contractile failure and poor volemia. Moreover, the significant tricuspid regurgitation often present in the perioperative period after cardiac surgery (impairment of tricuspid leaflets coaptation by temporal or permanent pacing electrode or Swan-Ganz catheter placed in the right heart) overestimates central venous pressure, i.e. the invasive marker of actual loading conditions and volemia. The significant decrease in LV diastolic volume as found with 2-D postoperative transesophageal echocardiography in patients with hypovolemia – tachycardia syndrome confirms hypovolemia as a cause of increase in heart rate and decrease in cardiac output [16]. This prompt information from bedside echocardiographic interrogation in ICU is also an obvious answer on how to treat the patient effectively. In this case, the fluid replenishment instead of cardiac beta-receptors stimulation will guarantee better filling of left ventricle in diastole and subsequently (according to Starling law) strengthen LV contractile force, cause increase in cardiac output and subsequently allow for lowering heart rate and oxygen consumption by cardiac muscle. On the contrary, the use of beta-mimetics in this situation will be counterproductive and enhance the viscious circle of pathological events, i.e. further increase in heart rate, decrease in systolic blood pressure and cardiac output, increase in oxygen consumption by cardiomyocytes with all possible adverse effects such like acute myocardial ischaemia, malignant arrhythmias and deterioration of hemodynamic instability.
Left ventricular filling pressure
Echocardiography also may promptly provide useful bedside information on actual hemodynamic status of patients with decompensated systolic heart failure or facilitate recognition of often misdiagnosed acute isolated diastolic heart failure manifested by acute pulmonary oedema in presence of normal global LV systolic function [18, 19]. Tissue Doppler echocardiography (TDE) is an easy to use and repeatable diagnostic tool in this respect [20, 21]. The estimation of early diastolic movement of mitral annulus (Em) with TDE when combined with measurement of maximal velocity of early phase of LV filling (E velocity) by means of conventional Doppler (E/Em ratio) accurately reflects actual LV filling pressure irrespective of heart rate and degree of LV contractile dysfunction [22]. Unlike invasive measurements of LV filling conditions the estimation of E/Em ratio is poorly dependent on increase in heart rate, which makes this method really useful and reliable in patients with decompensated systolic or diastolic heart failure. Furthermore, the E/Em doppler index can be also used as an adjunct to the diagnostics of hypovolemia-tachycardia syndrome. As mentioned before, this syndrome results from poor volemia and subsequently reduced LV filling. Then, low E/Em ratio as measured with echocardiography may accessorily confirm reduced preload as a cause of low LV filling pressure and significant tachycardia. Some authors argue that Em as itself can be an independent marker of LV relaxation that becomes gradually reduced while the LV filling pressure rises irrespective of actual preload and afterload. According to Stevenson, evaluation of hemodynamic status only on the basis of clinical symptoms and signs in physical examination identifies patients with high LV filling pressure only with 60% sensitivity [23]. Hence, E/Em ratio can be smoothly and reliably implemented for discrimination between non – cardiac and cardiac origin of dyspnoea [18].
Pulmonary Vessel Resistance
There is another interesting application of Doppler modalities, rarely used by clinicians, which may respectably contribute to the diagnostics of elevated pulmonary vessel resistance [5]. As it is known from clinical cardiology, the accurate measurement of pulmonary vessel resistance is extremely significant to qualification process for cardiac transplantation, cardiac surgery of septal defects and perioperative cardiac ICU monitoring. The predominant number of cardiologists resort only to invasive cardiology and catheterization of right heart in this respect. However, pulmonary vessel resistance can be reliably estimated in patients with slight to severe tricuspid regurgitation often observed in course of chronic heart failure or septal heart defects. The maximal velocity of the tricuspid regurgitation (TRV), i.e. systolic pulmonary pressure, divided by velocity time integral in the right ventricular outflow tract (VTI rvot, right ventricular stroke volume) as measured with conventional doppler echocardiography reflects pulmonary vessel resistance (PVR) [5]. The validation of this method relies upon the physiological interaction between pulmonary blood flow and pressure difference between the right heart and pulmonary circulation. The systolic pulmonary pressure as measured from TRV reflects the flow through the right heart and VTI rvot characterizes the right ventricular stroke volume and pulmonary flow [5]. Then, pulmonary vessel resistance is always proportional to the systolic pulmonary pressure and inversely related to the pulmonary blood flow (PVR = TRV/VTI rvot x 10 + 0, 16). Hence, the higher TRV/VTI rvot ratio, i.e. the higher systolic pulmonary artery pressure and the lower VTI rvot, the higher PVR can be expected. The very high systolic pulmonary pressure as calculated from maximal velocity of tricuspid regurgitation combined with low VTI rvot, i.e. poor flow through pulmonary valve, is parallel to increase in pulmonary resistance. On the other hand, the very high systolic pulmonary pressure concomitant with high VTI rvot is only associated with enhanced pulmonary flow. In this case, despite the high systolic pulmonary pressure pulmonary vessel resistance still remains low. The reliability of the above mentioned mathematical formula was confirmed by parallel invasive measurements of pulmonary vessel resistance that highly agreed with non-invasive echocardiographic calculations [5].
According to the father of modern echocardiography Harvey Feigenbaum, today understanding of cardiological problems is impossible without regard to echocardiographic examination [5]. Hence, this review article is to be a prelude to more thorough approach to echocardiography, which in fact allows for calculation of a whole gamut of clinically important indicators (not mentioned here) when applied by doctors aware of interactions between physiology laws, clinical echocardiography and clinical status of a patient.
Piśmiennictwo
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