scholarly journals Impedance cardiography: Pulsatile blood flow and the biophysical and electrodynamic basis for the stroke volume equations

2019 ◽  
Vol 1 (1) ◽  
pp. 2-17 ◽  
Author(s):  
Donald P. Bernstein
Keyword(s):  
Blood Flow ◽  
Stroke Volume ◽  
Impedance Cardiography ◽  
Left Ventricular ◽  
Square Root ◽  
Pulsatile Blood Flow ◽  
Mean Flow ◽  
Current Field ◽  
Blood Resistivity ◽  
Resistivity Variation

Abstract Impedance cardiography (ICG) is a branch of bioimpedance primarily concerned with the determination of left ventricular stroke volume (SV). As implemented, using the transthoracic approach, the technique involves applying a current field longitudinally across a segment of thorax by means of a constant magnitude, high frequency, low amplitude alternating current (AC). By Ohm’s Law, the voltage difference measured within the current field is proportional to the electrical impedance Z (Ω). Without ventilatory or cardiac activity, Z is known as the transthoracic, static base impedance Z0. Upon ventricular ejection, a characteristic time dependent cardiac-synchronous pulsatile impedance change is obtained, ΔZ(t), which, when placed electrically in parallel with Z0, constitutes the time-variable total transthoracic impedance Z(t). ΔZ(t) represents a dual-element composite waveform, which comprises both the radially-oriented volumetric expansion of and axially-directed forward blood flow within both great thoracic arteries. In its majority, however, ΔZ(t) is known to primarily emanate from the ascending aorta. Conceptually, commonly implemented methods assume a volumetric origin for the peak systolic upslope of ΔZ(t), (i.e. dZ/dtmax), with the presumed units of Ω·s–1. A recently introduced method assumes the rapid ejection of forward flowing blood in earliest systole causes significant changes in the velocity-induced blood resistivity variation (Δρb(t), Ωcm·s–1), and it is the peak rate of change of the blood resistivity variation dρb(t)/dtmax (Ωcm·s–2) that is the origin of dZ/dtmax. As a consequence of dZ/dtmax peaking in the time domain of peak aortic blood acceleration, dv/dtmax (cm·s–2), it is suggested that dZ/dtmax is an ohmic mean acceleration analog (Ω·s–2) and not a mean flow or velocity surrogate as generally assumed. As conceptualized, the normalized value, dZ/dtmax/Z0, is a dimensionless ohmic mean acceleration equivalent (s–2), and more precisely, the electrodynamic equivalent of peak aortic reduced average blood acceleration (PARABA, d<v>/dtmax/R, s–2). As necessary for stroke volume calculation, dZ/dtmax/Z0 must undergo square root transformation to yield an ohmic mean flow velocity equivalent. To compute SV, the square root of the dimensionless ohmic mean acceleration equivalent ([dZ/dtmax/Z0]0.5, s–1) is multiplied by a volume of electrically participating thoracic tissue (VEPT, mL) and left ventricular ejection time (TLVE, s). To find the bulk volume of the thoracic contents (i.e. VEPT), established methods implement exponential functions of measured thoracic length (L(cm)n) or height-based thoracic length equivalents (0.01×%H(cm)n). The new method conceptualizes VEPT as the intrathoracic blood volume (ITBV, mL), which is approximated through allometric equivalents of body mass (aMb). In contrast to the classical two-element parallel conduction model, the new method comprises a three-compartment model, which incorporates excess extra-vascular lung water (EVLW) as a component of both Z0 and VEPT. To fully appreciate the evolution and analytical justification for impedance-derived SV equations, a review of the basics of pulsatile blood flow is in order.

Pattern of blood flow in the pulmonary veins of the dog

1965 ◽  
Vol 20 (6) ◽  
pp. 1118-1128 ◽  
Author(s):  
Eugene Morkin ◽  
John A. Collins ◽  
Harold S. Goldman ◽  
Alfred P. Fishman
Keyword(s):  
Blood Flow ◽  
Pulmonary Circulation ◽  
Pulmonary Veins ◽  
Electromagnetic Flowmeter ◽  
Sine Wave ◽  
Left Ventricular ◽  
Mean Flow ◽  
Venous Flow ◽  
Pulmonary Venous Flow ◽  
Atrial Contraction

The pattern of blood flow in the large pulmonary veins was studied in dogs by chronic implantation of sine-wave electromagnetic flowmeters and cineangiographic observations. These revealed that: 1) pulmonary venous flow is continuous and pulsatile with peak rate of flow of approximately twice the mean flow; 2) the initial rapid increase in venous flow occurs 0.10 sec after the onset of ventricular systole, reaching a peak at the time of closure of the A-V valves; 3) left atrial contraction produces a fleeting slowing or reversal of flow; and 4) respiratory variations in pulmonary venous flow follow those in pulmonary arterial flow, beat by beat. The genesis of phasic pulmonary venous flow was investigated by analysis of pressure and flow curves from the two sides of the heart, by consideration of the energy required for left ventricular filling, and by reconstruction of the pulmonary venous flow pulse using a mathematical model of the pulmonary circulation. These three lines of evidence are consistent in indicating that the transmitted right ventricular pressure is the major determinant of the pulmonary venous flow pattern in the dog. pulsatile pulmonary venous flow; pulmonary venous flow; pulmonary circulation; ventricular suction; respiration on pulmonary circulation; pulmonary venous angiography; pulmonary veno-atrial junctions; electromagnetic flowmeter; cineangiography Submitted on November 16, 1964

Function of mature coronary collateral vessels and cardiac performance in the exercising dog

1985 ◽  
Vol 59 (2) ◽  
pp. 392-400 ◽  
Author(s):  
J. C. Longhurst ◽  
S. Motohara ◽  
J. M. Atkins ◽  
G. A. Ordway
Keyword(s):  
Blood Flow ◽  
Stroke Volume ◽  
Myocardial Blood Flow ◽  
Left Ventricular ◽  
Functional Responses ◽  
Circumflex Artery ◽  
Ventricular Performance ◽  
Left Circumflex Artery ◽  
Severe Exercise ◽  
Collateral Vessels

Formation of extensive collateral vessels after chronic constriction of a coronary artery in dogs can provide for similar increases in blood flow to native and collateralized regions of myocardium during exertion. Previous investigations have not compared myocardial blood flow and cardiac functional responses during exercise in constricted and nonconstricted (sham) animals. Thus we evaluated left ventricular performance and myocardial blood flow at rest and during mild, moderate, and severe exertion in sham-operated dogs and in dogs 2–3 mo after placement of an Ameroid occluder around the proximal left circumflex artery. Changes in double product, maximal left ventricular dP/dt, and pressure-work index were similar in both groups for each level of exertion. Despite similar increases in estimated myocardial O2 demand and similar diastolic perfusion pressures, average transmural myocardial blood flow increased less in the constrictor animals, particularly during severe exercise (2.74 +/- 0.22 vs. 1.45 +/- 0.29 ml X min-1 X g-1). The smaller increases in blood flow occurred equally in native and collateralized regions as well as in the papillary muscles and boundary areas between the native and collateralized regions. The differences in flow in the native and collateralized regions were uniform across the wall of the myocardium. We also observed smaller increases in stroke volume and cardiac output in the constrictor group, disparities which increased with increasing exertion (stroke volume, severe exercise = 0.92 +/- 0.13 vs. 0.53 +/- 0.09 ml/kg). We postulate that myocardial active hyperemia is limited either because the coronary vessels remaining after chronic circumflex occlusion cannot dilate sufficiently or that there is inappropriate active vasoconstriction during severe exertion.

Effect of tachycardia on left ventricular blood flow distribution during coronary occlusion

1976 ◽  
Vol 230 (4) ◽  
pp. 1072-1077 ◽  
Author(s):  
L Becker
Keyword(s):  
Blood Flow ◽  
Harmful Effect ◽  
Flow Distribution ◽  
Left Ventricular ◽  
Coronary Artery Ligation ◽  
Base Line ◽  
Atrial Pacing ◽  
Mean Flow ◽  
Artery Ligation ◽  
St Segment Elevation

The effect of heart rate on the amount and distribution of collateral blood flow was determine in open-chested dogs 1 h after coronary artery ligation. Flows to ischemic and nonischemic regions of left ventricle were measured with 7- to 10- mum diam radioactive microspheres during base-line conditions (118 +/- 6 beats/min) and again during atrial pacing at rates 20 and 40% above control (141 +/- 7 and 165 +/- 9 beats/min). During pacing aortic and left atrial pressures and cardiac output did not change significantly, whereas ST segment elevation in epicardial electrograms increased markedly. In nonischemic myocardium, mean flow increased approximately in proportion to the increase in rate, but subepicardial (EPI) flow increased somewhat more than subendocardial (ENDO) flow. In ischemic myocardium, overall flow did not change significantly, but a redistribution from ENDO to EPO was seen. At the faster rate ENDO flow fell 25% (P less than 0.02), EPI flow increased slightly, and ENDO/EPI fell in 8/9 animals (mean 0.54-0.43, P less than 0.01). The ENDO/EPI maldistribution present in ischemic muscle is thus accentuated by tachycardia; this may account for part of the harmful effect of tachycardia in acute myocardial infarction and may help explain the disproportionate ENDO ischemia seen in angina pectoris.

Hemodynamic and Energetic Assessment of Calves Implanted with a Left Ventricular Assist Device (LVAD)

1988 ◽  
Vol 11 (2) ◽  
pp. 119-126 ◽  
Author(s):  
G.M. Pantalos ◽  
J.D. Marks ◽  
J.B. Riebman ◽  
N.A. Burton ◽  
R. Depaulis ◽  
...  
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Left Ventricular ◽  
Control Mode ◽  
Mean Flow ◽  
Assist Device ◽  
Ventricular Assist ◽  
Intramyocardial Pressure ◽  
Ventricular Assistance ◽  
Left Ventricular Assistance

Hemodynamic and ventricular energetic parameters were measured in calves implanted with the air driven Utah Ventricular Assist Device (UVAD). Uptake site was varied to determine the effect of control mode and vacuum augmentation of filling. Uptake was drawn solely from the left atrium or combined with a left ventricular apical vent. LVAD outflow returned to the descending, thoracic aorta. Control modes examined included asynchronous pumping as well as 1:1 and 1:2 synchronous diastolic counterpulsation. The 85cc LVAD, vacuum formed from PELLETHANE®, was implanted acutely in four animals and chronically in six (7, 49 and 116 days paracorporeally, 1, 28 and 32 days intrathoracically). Instantaneous blood pressures, intramyocardial pressure, aortic outflow, oxygen consumption, LVAD output and drive parameters were recorded. LVAD output was independent of control mode when the natural heart rate was ≥ 80 beats per minute. Intrathoracically positioned LVADs pumped a mean flow of ≈5 liters/min without vacuum augmentation of filling. Paracorporeally positioned LVADs pumped ≈3 liters/min mean flow without vacuum augmentation and up to ≈6 liters/min with 38 mm Hg of vacuum augmentation of filling. Instantaneous ascending aortic pressure and flow showed distinct beat-to-beat variation depending on LVAD control mode. Lower average ventricular afterload was observed when pumping the LVAD asynchronously or 1:2 synchronously. In one acute preparation, left ventricular myocardial oxygen consumption was reduced from the unassisted average control level by 37% for the asynchronous and 1:1 synchronous control modes with left atrial uptake. With combined uptake, oxygen consumption was reduced an additional 30% during asynchronous control or 11% during 1:1 synchronous control without any change in LVAD output. Endocardial/epicardial blood flow ratio was similar and ≥1.12 for all test conditions. Renal and brain blood flow was maintained, or slightly elevated during ventricular assistance. Intramyocardial pressures were monitored using Millar catheter tip transducers. In an acute preparation, left ventricular assistance reduced peak intramyocardial pressure. Changing from atrial to combined uptake cannulation further reduced peak intramyocardial pressure for asynchronous and 1:1 synchronous LVAD control. Reduced end-diastolic intramyocardial pressures were seen with all modes of LVAD control. These data demonstrate excellent UVAD pumping function and suggest that left ventricular assistance does not compromise endocardial blood flow while sustaining blood flow to other major organs. Regardless of the uptake site, asynchronous or 1:2 synchronous LVAD control may be clinically preferable for effective reduction of left ventricular myocardial oxygen consumption.

Hemodynamics during pregnancy and sex steroid administration in guinea pigs

1985 ◽  
Vol 249 (2) ◽  
pp. R179-R185 ◽  
Author(s):  
M. V. Hart ◽  
J. D. Hosenpud ◽  
A. R. Hohimer ◽  
M. J. Morton
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Guinea Pigs ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Sex Steroid ◽  
Uterine Blood Flow ◽  
Steroid Administration

We investigated the time course and possible mechanisms by which the maternal cardiovascular system adapts to the demands of pregnancy. Control, 20-, 40-, and 60-day gestation guinea pigs (total 68 days) and nonpregnant virgin female guinea pigs chronically dosed with cholesterol (control), estrogen (17beta-estradiol), progesterone, and estrogen plus progesterone were studied. In vivo heart rates, pressures, cardiac outputs, blood volumes, and in vitro left ventricular pressure-volume relations were measured. There was no difference in heart rate, mean arterial, right atrial, or left ventricular end-diastolic pressures, or left ventricular weights between the various pregnant animals or hormone-dosed animals and their respective controls. By 20 days gestation blood volume (24%, P less than 0.005), cardiac output (22%, P less than 0.005), and stroke volume (22%, P less than 0.05) were increased, whereas uterine blood flow was unchanged. Chronic estrogen administration resulted in similar increases in cardiac output (24%, P less than 0.05), stroke volume (31%, P less than 0.05), and blood volume (13%, P less than 0.05). In vitro left ventricular pressure-volume relations were shifted to the right in all pregnant and hormone-dosed groups. Increases in left ventricular size and output occur before changes in uterine blood flow in guinea pig pregnancy, and these adaptations can be elicited by chronic sex steroid administration.

scholarly journals Distinct hemodynamic responses to (pyr)apelin-13 in large animal models

2020 ◽  
Vol 318 (4) ◽  
pp. H747-H755
Author(s):  
Johnathan D. Tune ◽  
Hana E. Baker ◽  
Zachary Berwick ◽  
Steven P. Moberly ◽  
Eli D. Casalini ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Stroke Volume ◽  
Coronary Blood Flow ◽  
Myocardial Contractility ◽  
Left Ventricular ◽  
Large Animal ◽  
Hemodynamic Responses ◽  
End Diastolic Volume

This study tested the hypothesis that (pyr)apelin-13 dose-dependently augments myocardial contractility and coronary blood flow, irrespective of changes in systemic hemodynamics. Acute effects of intravenous (pyr)apelin-13 administration (10 to 1,000 nM) on blood pressure, heart rate, left ventricular pressure and volume, and coronary parameters were measured in dogs and pigs. Administration of (pyr)apelin-13 did not influence blood pressure ( P = 0.59), dP/d tmax ( P = 0.26), or dP/d tmin ( P = 0.85) in dogs. However, heart rate dose-dependently increased > 70% ( P < 0.01), which was accompanied by a significant increase in coronary blood flow ( P < 0.05) and reductions in left ventricular end-diastolic volume and stroke volume ( P < 0.001). In contrast, (pyr)apelin-13 did not significantly affect hemodynamics, coronary blood flow, or indexes of contractile function in pigs. Furthermore, swine studies found no effect of intracoronary (pyr)apelin-13 administration on coronary blood flow ( P = 0.83) or vasorelaxation in isolated, endothelium-intact ( P = 0.89) or denuded ( P = 0.38) coronary artery rings. Examination of all data across (pyr)apelin-13 concentrations revealed an exponential increase in cardiac output as peripheral resistance decreased across pigs and dogs ( P < 0.001; R2 = 0.78). Assessment of the Frank-Starling relationship demonstrated a significant linear relationship between left ventricular end-diastolic volume and stroke volume across species ( P < 0.001; R2 = 0.70). Taken together, these findings demonstrate that (pyr)apelin-13 does not directly influence myocardial contractility or coronary blood flow in either dogs or pigs. NEW & NOTEWORTHY Our findings provide much needed insight regarding the pharmacological cardiac and coronary effects of (pyr)apelin-13 in larger animal preparations. In particular, data highlight distinct hemodynamic responses of apelin across species, which are independent of any direct effect on myocardial contractility or perfusion.

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