Impedance cardiography

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Impedance cardiography
MeSH D002307

Impedance cardiography (ICG) is a non-invasive technology measuring total electrical conductivity of the thorax and its changes in time to process continuously a number of cardiodynamic parameters, such as stroke volume (SV), heart rate (HR), cardiac output (CO), ventricular ejection time (VET), pre-ejection period and used to detect the impedance changes caused by a high-frequency, low magnitude current flowing through the thorax between additional two pairs of electrodes located outside of the measured segment. The sensing electrodes also detect the ECG signal, which is used as a timing clock of the system. [1] [2]

Contents

Introduction

Impedance cardiography (ICG), also referred to as electrical impedance plethysmography (EIP) or Thoracic Electrical Bioimpedance (TEB) has been researched since the 1940s. NASA helped develop the technology in the 1960s. [3] [4] The use of impedance cardiography in psychophysiological research was pioneered by the publication of an article by Miller and Horvath in 1978. [5] Subsequently, the recommendations of Miller and Horvath were confirmed by a standards group in 1990. [6] A comprehensive list of references is available at ICG Publications. With ICG, the placement of four dual disposable sensors on the neck and chest are used to transmit and detect electrical and impedance changes in the thorax, which are used to measure and calculate cardiodynamic parameters.[ citation needed ]

Process

Hemodynamics

Hemodynamics is a subchapter of cardiovascular physiology, which is concerned with the forces generated by the heart and the resulting motion of blood through the cardiovascular system. [7] These forces demonstrate themselves to the clinician as paired values of blood flow and blood pressure measured simultaneously at the output node of the left heart. Hemodynamics is a fluidic counterpart to the Ohm's law in electronics: pressure is equivalent to voltage, flow to current, vascular resistance to electrical resistance and myocardial work to power.

Fig.1: Aortic blood pressure and aortic blood flow over one heartbeat interval: S = Systolic blood pressure; D = Diastolic blood pressure; MAP = Mean Arterial Pressure; SV = Stroke Volume; DN = dicrotic notch (aortic valve closure) Relationship between Aortic Blood Pressure and Aortic Blood flow.png
Fig.1: Aortic blood pressure and aortic blood flow over one heartbeat interval: S = Systolic blood pressure; D = Diastolic blood pressure; MAP = Mean Arterial Pressure; SV = Stroke Volume; DN = dicrotic notch (aortic valve closure)

The relationship between the instantaneous values of aortic blood pressure and blood flow through the aortic valve over one heartbeat interval and their mean values are depicted in Fig.1. Their instantaneous values may be used in research; in clinical practice, their mean values, MAP and SV, are adequate.[ citation needed ]

Blood flow parameters

Systemic (global) blood flow parameters are (a) the blood flow per heartbeat, the Stroke Volume, SV [ml/beat], and (b) the blood flow per minute, the Cardiac Output, CO [l/min]. There is clear relationship between these blood flow parameters:

CO[l/min]= (SV[ml]× HR[bpm])/1000    {Eq.1}

where HR is the Heart Rate frequency (beats per minute, bpm).

Since the normal value of CO is proportional to body mass it has to perfuse, one "normal" value of SV and CO for all adults cannot exist. All blood flow parameters have to be indexed. The accepted convention is to index them by the Body Surface Area, BSA [m2], by DuBois & DuBois Formula, a function of height and weight:

BSA[m2]=W0.425[kg]×H0.725[cm]×0.007184     {Eq.2}

The resulting indexed parameters are Stroke Index, SI (ml/beat/m2) defined as

SI[ml/beat/m2]= SV[ml]/BSA[m2]         {Eq.3}

and Cardiac Index, CI (l/min/m2), defined as 

CI[l/min/m2]= CO[l/min]/BSA[m2]         {Eq.4}

These indexed blood flow parameters exhibit typical ranges:

For the Stroke Index: 35 < SItypical < 65 ml/beat/m2; for the Cardiac Index:2.8 < CItypical < 4.2 l/min/m2.

Eq.1 for indexed parameters then changes to

CI[l/min/m2]= (SI[ml/beat/m2]× HR[bpm])/1000       {Eq.1a}

Oxygen transport

The primary function of the cardiovascular system is transport of oxygen: blood is the vehicle, oxygen is the cargo. The task of the healthy cardiovascular system is to provide adequate perfusion to all organs and to maintain a dynamic equilibrium between oxygen demand and oxygen delivery. In a healthy person, the cardiovascular system always increases blood flow in response to increased oxygen demand. In a hemodynamically compromised person, when the system is unable to satisfy increased oxygen demand, the blood flow to organs lower on the oxygen delivery priority list is reduced and these organs may, eventually, fail. Digestive disorders, male impotence, tiredness, sleepwalking, environmental temperature intolerance, are classic examples of a low-flow-state, resulting in reduced blood flow.[ citation needed ]

Modulators

SI variability and MAP variability are accomplished through activity of hemodynamic modulators.

Fig.5: The Frank-Starling Law and Inotropy: Three Frank-Starling curves shown for normoinotropy, hyperinotropy and hypoinotropy. A patient, who is normovolemic and normoinotropic, exhibits normal level of Ejection Phase Contractility (EPC). However, a patient who is hypovolemic can exhibit the same normal level of EPC if given positive inotropes, and a patient who is volume overloaded (hypervolemic) can also have normal level of EPC if given negative inotropes Frank-Starling Law and Inotropy.png
Fig.5: The Frank-Starling Law and Inotropy: Three Frank-Starling curves shown for normoinotropy, hyperinotropy and hypoinotropy. A patient, who is normovolemic and normoinotropic, exhibits normal level of Ejection Phase Contractility (EPC). However, a patient who is hypovolemic can exhibit the same normal level of EPC if given positive inotropes, and a patient who is volume overloaded (hypervolemic) can also have normal level of EPC if given negative inotropes

The conventional cardiovascular physiology terms for the hemodynamic modulators are preload, contractility and afterload. They deal with (a) the inertial filling forces of blood return into the atrium (preload), which stretch the myocardial fibers, thus storing energy in them, (b) the force by which the heart muscle fibers shorten thus releasing the energy stored in them in order to expel part of blood in the ventricle into the vasculature (contractility), and (c) the forces the pump has to overcome in order to deliver a bolus of blood into the aorta per each contraction (afterload). The level of preload is currently assessed either from the PAOP (pulmonary artery occluded pressure) in a catheterized patient, or from EDI (end-diastolic index) by use of ultrasound. Contractility is not routinely assessed; quite often inotropy and contractility are interchanged as equal terms. Afterload is assessed from the SVRI value.

Fig.6: Timing considerations of working effects of preload, contractility (pharmacological = inotropes, and mechanical = Frank-Starling mechanism, i.e., effects of intravascular volume) and afterload in respect to Systolic and Diastolic Time Intervals: Diastole => Starts at S2-time, ends at Q-time. Systole => Isovolumic phase starts at Q-time, ends at AVO-time; Ejection phase starts at AVO-time, ends at S2-time. (S2 = 2nd heart sound = aortic valve closure; AVO = aortic valve opening) Timing considerations of hemodynamic modulation.png
Fig.6: Timing considerations of working effects of preload, contractility (pharmacological = inotropes, and mechanical = Frank-Starling mechanism, i.e., effects of intravascular volume) and afterload in respect to Systolic and Diastolic Time Intervals: Diastole => Starts at S2-time, ends at Q-time. Systole => Isovolumic phase starts at Q-time, ends at AVO-time; Ejection phase starts at AVO-time, ends at S2-time. (S2 = 2nd heart sound = aortic valve closure; AVO = aortic valve opening)

Rather than using the terms preload, contractility and afterload, the preferential terminology and methodology in per-beat hemodynamics is to use the terms for actual hemodynamic modulating tools, which either the body utilizes or the clinician has in his toolbox to control the hemodynamic state:

The preload and the Frank-Starling (mechanically)-induced level of contractility is modulated by variation of intravascular volume (volume expansion or volume reduction/diuresis).

Pharmacological modulation of contractility is performed with cardioactive inotropic agents (positive or negative inotropes) being present in the blood stream and affecting the rate of contraction of myocardial fibers.

The afterload is modulated by varying the caliber of sphincters at the input and output of each organ, thus the vascular resistance, with the vasoactive pharmacological agents (vasoconstrictors or vasodilators and/or ACE Inhibitors and/or ARBs)(ACE = Angiotensin-converting-enzyme; ARB = Angiotensin-receptor-blocker). Afterload also increases with increasing blood viscosity, however, with the exception of extremely hemodiluted or hemoconcentrated patients, this parameter is not routinely considered in clinical practice.

With the exception of volume expansion, which can be accomplished only by physical means (intravenous or oral intake of fluids), all other hemodynamic modulating tools are pharmacological, cardioactive or vasoactive agents.

The measurement of CI and its derivatives allow clinicians to make timely patient assessment, diagnosis, prognosis, and treatment decisions. It has been well established that both trained and untrained physicians alike are unable to estimate cardiac output through physical assessment alone.

Invasive monitoring

Clinical measurement of cardiac output has been available since the 1970s. However, this blood flow measurement is highly invasive, utilizing a flow-directed, thermodilution catheter (also known as the Swan-Ganz catheter), which represents significant risks to the patient. In addition, this technique is costly (several hundred dollars per procedure) and requires a skilled physician and a sterile environment for catheter insertion. As a result, it has been used only in very narrow strata (less than 2%) of critically ill and high-risk patients in whom the knowledge of blood flow and oxygen transport outweighed the risks of the method. In the United States, it is estimated that at least two million pulmonary artery catheter monitoring procedures are performed annually, most often in peri-operative cardiac and vascular surgical patients, decompensated heart failure, multi-organ failure, and trauma.[ citation needed ]

Noninvasive monitoring

In theory, a noninvasive way to monitor hemodynamics would provide exceptional clinical value because data similar to invasive hemodynamic monitoring methods could be obtained with much lower cost and no risk. While noninvasive hemodynamic monitoring can be used in patients who previously required an invasive procedure, the largest impact can be made in patients and care environments where invasive hemodynamic monitoring was neither possible nor worth the risk or cost. Because of its safety and low cost, the applicability of vital hemodynamic measurements could be extended to significantly more patients, including outpatients with chronic diseases. ICG has even been used in extreme conditions such as outer space and a Mt. Everest expedition. [8] Heart failure, hypertension, pacemaker, and dyspnea patients are four conditions in which outpatient noninvasive hemodynamic monitoring can play an important role in the assessment, diagnosis, prognosis, and treatment. Some studies have shown ICG cardiac output is accurate, [9] [10] while other studies have shown it is inaccurate. [11] Use of ICG has been shown to improve blood pressure control in resistant hypertension when used by both specialists [12] and general practitioners. [13] ICG has also been shown to predict worsening status in heart failure. [14]

ICG Parameters

The electrical and impedance signals are processed to determine fiducial points, which are then utilized to measure and calculate hemodynamic parameters, such as cardiac output, stroke volume, systemic vascular resistance, thoracic fluid content, acceleration index, and systolic time ratio.

ParameterDefinition
Heart RateNumber of heart beats each minute
Cardiac OutputAmount of blood pumped by the left ventricle each minute
Cardiac IndexCardiac output normalized for body surface area
Stroke VolumeAmount of blood pumped by the left ventricle each heartbeat
Stroke IndexStroke volume normalized for body surface area
Systemic Vascular ResistanceThe resistance to the flow of blood in the vasculature (often referred to as "Afterload")
Systemic Vascular Resistance IndexSystemic vascular resistance normalized for body surface area
Acceleration IndexPeak acceleration of blood flow in the aorta
Velocity IndexPeak velocity of blood flow in the aorta
Thoracic Fluid ContentThe electrical conductivity of the chest cavity, which is primarily determined by the intravascular, intraalveolar, and interstitial fluids in the thorax
Left Cardiac WorkAn indicator of the amount of work the left ventricle must perform to pump blood each minute
Left Cardiac Work IndexLeft cardiac work normalized for body surface area
Systolic Time RatioThe ratio of the electrical and mechanical systole
Pre Ejection PeriodThe time interval from the beginning of electrical stimulation of the ventricles to the opening of the aortic valve (electrical systole)
Left Ventricular Ejection TimeThe time interval from the opening to the closing of the aortic valve (mechanical systole)

Related Research Articles

<span class="mw-page-title-main">Blood pressure</span> Pressure exerted by circulating blood upon the walls of arteries

Blood pressure (BP) is the pressure of circulating blood against the walls of blood vessels. Most of this pressure results from the heart pumping blood through the circulatory system. When used without qualification, the term "blood pressure" refers to the pressure in a brachial artery, where it is most commonly measured. Blood pressure is usually expressed in terms of the systolic pressure over diastolic pressure in the cardiac cycle. It is measured in millimeters of mercury (mmHg) above the surrounding atmospheric pressure, or in kilopascals (kPa).

<span class="mw-page-title-main">Cardiac output</span> Measurement of blood pumped by the heart

In cardiac physiology, cardiac output (CO), also known as heart output and often denoted by the symbols , , or , is the volumetric flow rate of the heart's pumping output: that is, the volume of blood being pumped by a single ventricle of the heart, per unit time. Cardiac output (CO) is the product of the heart rate (HR), i.e. the number of heartbeats per minute (bpm), and the stroke volume (SV), which is the volume of blood pumped from the left ventricle per beat; thus giving the formula:

Hemodynamics or haemodynamics are the dynamics of blood flow. The circulatory system is controlled by homeostatic mechanisms of autoregulation, just as hydraulic circuits are controlled by control systems. The hemodynamic response continuously monitors and adjusts to conditions in the body and its environment. Hemodynamics explains the physical laws that govern the flow of blood in the blood vessels.

In cardiovascular physiology, stroke volume (SV) is the volume of blood pumped from the left ventricle per beat. Stroke volume is calculated using measurements of ventricle volumes from an echocardiogram and subtracting the volume of the blood in the ventricle at the end of a beat from the volume of blood just prior to the beat. The term stroke volume can apply to each of the two ventricles of the heart, although it usually refers to the left ventricle. The stroke volumes for each ventricle are generally equal, both being approximately 70 mL in a healthy 70-kg man.

End-systolic volume (ESV) is the volume of blood in a ventricle at the end of contraction, or systole, and the beginning of filling, or diastole.

<span class="mw-page-title-main">Afterload</span> Pressure in the wall of the left ventricle during ejection

Afterload is the pressure that the heart must work against to eject blood during systole. Afterload is proportional to the average arterial pressure. As aortic and pulmonary pressures increase, the afterload increases on the left and right ventricles respectively. Afterload changes to adapt to the continually changing demands on an animal's cardiovascular system. Afterload is proportional to mean systolic blood pressure and is measured in millimeters of mercury.

<span class="mw-page-title-main">Cardiac catheterization</span> Insertion of a catheter into a chamber or vessel of the heart

Cardiac catheterization is the insertion of a catheter into a chamber or vessel of the heart. This is done both for diagnostic and interventional purposes.

<span class="mw-page-title-main">Pulmonary artery catheter</span> Catheter for insertion into a pulmonary artery

A pulmonary artery catheter (PAC), also known as a Swan-Ganz catheter or right heart catheter, is a balloon-tipped catheter that is inserted into a pulmonary artery in a procedure known as pulmonary artery catheterization or right heart catheterization. Pulmonary artery catheterization is a useful measure of the overall function of the heart particularly in those with complications from heart failure, heart attack, arrythmias or pulmonary embolism. It is also a good measure for those needing intravenous fluid therapy, for instance post heart surgery, shock, and severe burns. The procedure can also be used to measure pressures in the heart chambers.

<span class="mw-page-title-main">Arteriovenous fistula</span> Medical condition

An arteriovenous fistula is an abnormal connection or passageway between an artery and a vein. It may be congenital, surgically created for hemodialysis treatments, or acquired due to pathologic process, such as trauma or erosion of an arterial aneurysm.

Central venous pressure (CVP) is the blood pressure in the venae cavae, near the right atrium of the heart. CVP reflects the amount of blood returning to the heart and the ability of the heart to pump the blood back into the arterial system. CVP is often a good approximation of right atrial pressure (RAP), although the two terms are not identical, as a pressure differential can sometimes exist between the venae cavae and the right atrium. CVP and RAP can differ when arterial tone is altered. This can be graphically depicted as changes in the slope of the venous return plotted against right atrial pressure.

Arterial stiffness occurs as a consequence of biological aging and arteriosclerosis. Inflammation plays a major role in arteriosclerosis development, and consequently it is a major contributor in large arteries stiffening. Increased arterial stiffness is associated with an increased risk of cardiovascular events such as myocardial infarction, hypertension, heart failure and stroke, the two leading causes of death in the developed world. The World Health Organization predicts that in 2010, cardiovascular disease will also be the leading killer in the developing world and represents a major global health problem.

Cardiac index (CI) is a haemodynamic parameter that relates the cardiac output (CO) from left ventricle in one minute to body surface area (BSA), thus relating heart performance to the size of the individual. The unit of measurement is litres per minute per square metre (L/min/m2).

Early goal-directed therapy was introduced by Emanuel P. Rivers in The New England Journal of Medicine in 2001 and is a technique used in critical care medicine involving intensive monitoring and aggressive management of perioperative hemodynamics in patients with a high risk of morbidity and mortality. In cardiac surgery, goal-directed therapy has proved effective when commenced after surgery. The combination of GDT and Point-of-Care Testing has demonstrated a marked decrease in mortality for patients undergoing congenital heart surgery. Furthermore, a reduction in morbidity and mortality has been associated with GDT techniques when used in conjunction with an electronic medical record.

Electrical cardiometry is a method based on the model of Electrical Velocimetry, and non-invasively measures stroke volume (SV), cardiac output (CO), and other hemodynamic parameters through the use of 4 surface ECG electrodes. Electrical cardiometry is a method trademarked by Cardiotronic, Inc., and is U.S. FDA approved for use on adults, children, and neonates.

Cardiac physiology or heart function is the study of healthy, unimpaired function of the heart: involving blood flow; myocardium structure; the electrical conduction system of the heart; the cardiac cycle and cardiac output and how these interact and depend on one another.

A plot of a system's pressure versus volume has long been used to measure the work done by the system and its efficiency. This analysis can be applied to heat engines and pumps, including the heart. A considerable amount of information on cardiac performance can be determined from the pressure vs. volume plot. A number of methods have been determined for measuring PV-loop values experimentally.

<span class="mw-page-title-main">Heart failure with preserved ejection fraction</span> Medical condition

Heart failure with preserved ejection fraction (HFpEF) is a form of heart failure in which the ejection fraction – the percentage of the volume of blood ejected from the left ventricle with each heartbeat divided by the volume of blood when the left ventricle is maximally filled – is normal, defined as greater than 50%; this may be measured by echocardiography or cardiac catheterization. Approximately half of people with heart failure have preserved ejection fraction, while the other half have a reduction in ejection fraction, called heart failure with reduced ejection fraction (HFrEF).

Continuous noninvasive arterial pressure (CNAP) is the method of measuring beat-to-beat arterial blood pressure in real-time without any interruptions (continuously) and without cannulating the human body (noninvasive).

quantium Medical Cardiac Output (qCO) uses impedance cardiography in a simple, continuous, and non-invasive way to estimate the cardiac output (CO) and other hemodynamic parameters such as the stroke volume (SV) and cardiac index (CI). The CO estimated by the qCO monitor is referred to as the "qCO". The impedance plethysmography allows determining changes in volume of the body tissues based on the measurement of the electric impedance at the body surface.

<span class="mw-page-title-main">Acute cardiac unloading</span>

Acute cardiac unloading is any maneuver, therapy, or intervention that decreases the power expenditure of the ventricle and limits the hemodynamic forces that lead to ventricular remodeling after insult or injury to the heart. This technique is being investigated as a therapeutic to aid after damage has occurred to the heart, such as after a heart attack. The theory behind this approach is that by simultaneously limiting the oxygen demand and maximizing oxygen delivery to the heart after damage has occurred, the heart is more fully able to recover. This is primarily achieved by using temporary minimally invasive mechanical circulatory support to supplant the pumping of blood by the heart. Using mechanical support decreases the workload of the heart, or unloads it.

References

  1. 1 2 "What is TEB and how it works". Archived from the original on 2016-07-03. Retrieved 2015-05-01.
  2. ↑ "25. Impedance Plethysmography". www.bem.fi.
  3. ↑ Kubicek W.G., Witsoe, D.A., Patterson, R.P., Mosharrata, M.A., Karnegis, J.N., From, A.H.L. (1967). Significant improvements of its clinical accuracy took place in the '80s at BoMed Medical Manufacturing LTD under B. Bo Sramek with the product NCCOM3. in 1992 the company was renamed to CDIC and product renamed to BioZ. Development and evaluation of an impedance cardiographic system to measure cardiac output and development of an oxygen consumption rate computing system utilizing a quadrupole mass spectrometer. NASA-CR-92220, N68-32973.
  4. ↑ "Technology Transfer". 2016-09-15. Archived from the original on 2002-06-13.
  5. ↑ Miller, J. C., & Horvath, S. M. (1978). Impedance cardiography. Psychophysiology, 15(1), 80–91.
  6. ↑ Sherwood, A., Allen, M. T., Fahrenberg, J., Kelsey, R. M., Lovallo, W. R., & van Doornen, L. J. (1990). Methodological guidelines for impedance cardiography. Psychophysiology, 27(1), 1–23.
  7. ↑ WR Milnor: Hemodynamics, Williams & Wilkins, 1982
  8. ↑ "Local Biomed Device Aiding NASA". 9 January 2000.
  9. ↑ Van De Water, Joseph M.; Miller, Timothy W.; Vogel, Robert L.; Mount, Bruce E.; Dalton, Martin L. (2003). "Impedance Cardiographya". Chest. 123 (6): 2028–2033. doi:10.1378/chest.123.6.2028. PMID   12796185.
  10. ↑ Albert, Nancy M.; Hail, Melanie D.; Li, Jianbo; Young, James B. (2004). "Equivalence of the Bioimpedance and Thermodilution Methods in Measuring Cardiac Output in Hospitalized Patients with Advanced, Decompensated Chronic Heart Failure". American Journal of Critical Care. 13 (6): 469–479. doi:10.4037/ajcc2004.13.6.469. PMID   15568652.
  11. ↑ Kamath SA, Drazner MH, Tasissa G, Rogers JG, Stevenson LW, Yancy CW (August 2009). "Correlation of impedance cardiography with invasive hemodynamic measurements in patients with advanced heart failure: the BioImpedance CardioGraphy (BIG) substudy of the Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheterization Effectiveness (ESCAPE) Trial". Am. Heart J. 158 (2): 217–23. doi:10.1016/j.ahj.2009.06.002. PMC   2720805 . PMID   19619697.
  12. ↑ Taler, Sandra J.; Textor, Stephen C.; Augustine, Jo Ellen (2002). "Resistant Hypertension". Hypertension. 39 (5): 982–988. doi: 10.1161/01.HYP.0000016176.16042.2F . PMID   12019280.
  13. ↑ Smith, Ronald D.; Levy, Pavel; Ferrario, Carlos M. (2006). "Value of Noninvasive Hemodynamics to Achieve Blood Pressure Control in Hypertensive Subjects". Hypertension. 47 (4): 771–777. doi: 10.1161/01.HYP.0000209642.11448.e0 . PMID   16520405.
  14. ↑ Packer, Milton; Abraham, William T.; Mehra, Mandeep R.; Yancy, Clyde W.; Lawless, Christine E.; Mitchell, Judith E.; Smart, Frank W.; Bijou, Rachel; o'Connor, Christopher M.; Massie, Barry M.; Pina, Ileana L.; Greenberg, Barry H.; Young, James B.; Fishbein, Daniel P.; Hauptman, Paul J.; Bourge, Robert C.; Strobeck, John E.; Murali, Srinvivas; Schocken, Douglas; Teerlink, John R.; Levy, Wayne C.; Trupp, Robin J.; Silver, Marc A.; Prospective Evaluation Identification of Cardiac Decompensation by ICG Test (PREDICT) Study Investigators Coordinators (2006). "Utility of Impedance Cardiography for the Identification of Short-Term Risk of Clinical Decompensation in Stable Patients with Chronic Heart Failure". Journal of the American College of Cardiology. 47 (11): 2245–2252. doi:10.1016/j.jacc.2005.12.071. PMID   16750691.
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