Catheter-tip Manometer Research Articles

Mechanism of augmented left atrial pump function in myocardial infarction and essential hypertension evaluated by left atrial pressure-dimension relation

To analyze left atrial (LA) pump function in normal subjects, in patients with essential hypertension and in patients with a healed myocardial infarction, LA dimension (aortic-root echogram) and pressure (catheter-tip manometer) were simultaneously recorded in 25 patients (8 normal subjects, 7 with hypertension and 10 with myocardial infarction). The pressure-dimension relation of the left atrium was composed of 2 loops: the A loop (expressing the pump function of the left atrium) and the V loop. LA dimension at the beginning of active LA shortening was significantly greater in hypertensive subjects (33 ± 3 mm) and in those with myocardial infarction (32 ± 4 mm) than in normal subjects (28 ± 3 mm) (p < 0.01, p < 0.05, respectively). The area of the A loop significantly increased in subjects with hypertension (48 ± 3 mm Hg · mm, p < 0.01) and in subjects with myocardial infarction (29 ± 10 mm Hg · mm, p < 0.05), compared with normal subjects (20 ± 8 mm Hg · mm). The mean fractional shortening velocity of the left atrium significantly increased in subjects with hypertension, compared with normal subjects and those with myocardial infarction (p < 0.05 for both). LA peak wall tension during the LA active contraction period significantly increased with hypertension and with myocardial infarction, compared with normal subjects (p < 0.01, p < 0.05, respectively). The area of the A loop was directly proportional to the LA dimension at the beginning of active LA shortening (r = 0.53), p < 0.01). The mean fractional shortening velocity of the left atrium was inversely correlated with the LA peak wall tension during the LA active contraction period (r = −0.44, p < 0.05). With hypertension, the relation between the mean shortening velocity and the peak wall tension of the left atrium shifted up and rightward. It is concluded that the augmented pump function of the left atrium in patients with a healed myocardial infarction is attributed to Starling's mechanism, whereas with hypertension the increased pump function of the left atrium may be attributed not only to Starling's effect, but also to the enhanced inotropic state of the left atrium.

Significance of the Subvalvular Apparatus for Left-Ventricular Dimensions and Systolic Function: Experimental Replacement of the Mitral Valve

To study the significance of the subvalvular apparatus for left-ventricular performance in mitral valve replacement, a new experimental model was developed. In 21 dogs St. Jude prostheses were implanted in the mitral position preserving the chordae tendineae and the papillary muscles by plicating and fixing the mitral leaflets with the prosthesis on the valvular annulus. Flexible steel wires were slung around the chordae tendineae of the anterior and the posterior papillary muscle separately and passed through the left ventricular wall via insulating plastic cannulas. Left-ventricular dimensions and global systolic function were measured during volume loading with blood before and after severance of the chordae tendineae by external application of electrocautery to the steel wires. Thus the heart continued beating without any interference following loss of the subvalvular apparatus. The external left ventricular diameters in the major and minor axis were determined by sonomicrometry. Left-ventricular systolic and diastolic pressures were measured by catheter tip manometers, stroke volume by electromagnetic measurements of flow in the ascending aorta. When the chordae tendineae had been cut, left-ventricular end-diastolic diameters in the major axis were increased ( + 2%), in the minor axis decreased (-1%) at any left-ventricular end-diastolic pressure. Systolic shortening of the major axis diameter was considerably reduced (20-27%) at any left-ventricular end-diastolic pressure following severance of the chordae tendineae. Significant increase of the systolic shortening in the minor axis diameter occurred at preload levels of 3-6 mmHg (15-8%), while at higher left-ventricular end-diastolic pressure of 7-8 mmHg no significant changes were present.(ABSTRACT TRUNCATED AT 250 WORDS)

Responses to changes in filling and contractility of indices of human left ventricular mechanical performance.

1. Beat-by-beat indices of contractility for assessment of inotropic effects in a given subject were studied using pacing with beta-adrenergic blockade, in eight patients undergoing routine left heart catheterization. A catheter-tip manometer was sited in the left ventricle and an electromagnetic velocity transducer was mounted further back on the same catheter so that it was sited in the ascending aorta. 2. The maximum rate of rise of left ventricular pressure (dPLV/dtmax), and of aortic velocity (maximum acceleration, MA) and stroke volume (SV) were all obtained with this catheter. Filling effects were assessed by head-up to head-down tilt, inotropic effects by paced post-extrasystolic potentiation. 3. Tilt produced a mean increase in left ventricular end-diastolic pressure (PLVED) of 8.1 mmHg (P less than 0.05), dPLV/dtmax decreased 4.3% (n.s.), peak velocity (PV) increased 23% (P less than 0.05), MA increased 5.4% (n.s.), and SV increased 17.5% (P less than 0.05). Post-extrasystolic potentiation produced a mean decrease in PLVED of 2.8 mmHg (n.s.), dPLV/dtmax increased 35% (P less than 0.05), PV increased 14% (P less than 0.05), MA increased 55% (P less than 0.05), and SV increased 8.7% (n.s.). 4. There was no difference in response between patients with normal and patients with impaired left ventricular ejection fraction. 5. It is concluded that increased left ventricular filling increases stroke volume greatly (Starling effect) but does not affect dPLV/dtmax, which (together with MA) nevertheless responds markedly to increased contractility. dPLV/dtmax appears to be a volume-insensitive index of contractility in the intact human, whether ejection fraction is normal or impaired.

Left ventricular systolic and diastolic function in the hypertrophied ventricle.

To investigate left ventricular (LV) systolic and diastolic function in cardiac hypertrophy, we analysed LV pressure (catheter tip-manometer) and simultaneously performed cineangiography in 24 patients with systemic hypertension (HT), 25 patients with hypertrophic cardiomyopathy (HCM) and 25 normal subjects. We digitized LV cineangiograms frame by frame and computed volume and its derivatives, wall thickness and circumferential wall stress. LV systolic pump function was normal or supernormal in HT and HCM. However, myocardial contractility assessed by end-systolic wall stress-volume relation was depressed in HCM whereas it is normally maintained in HT. LV diastolic function was also impaired in HCM and even in HT despite normal systolic function. The LV hypertrophy group showed significantly prolonged time constant of isovolumic relaxation, increased time from end-systole to the peak filling rate, and upward shift of the diastolic pressure-volume relationship. The characteristic findings of LV diastolic function in LV hypertrophy, therefore, can be summarized as impaired isovolumic relaxation, delayed early diastolic filling and decreased diastolic distensibility. The mechanisms of abnormal systolic and diastolic function may include myocardial ischemia and/or calcium overload in hypertrophied myocardium, but further study will be needed to clarify these problems.

Segmental volume distensibility of the canine thoracic aorta in vivo.

Segments of the canine ascending aorta, upper descending thoracic aorta, and middle descending thoracic aorta were instrumented with ultrasonic dimension gauges and a cathetertip manometer simultaneously to measure changes in segment diameter, length, and intravascular pressure. Volume distensibility (EV) was calculated as the sum of circumferential extensibility (EC), longitudinal extensibility (EL), and high order extensibilities (EK) for each segment. The EC and EL were linear expressions that represented percentage volume changes per mmHg pulse pressure due to circumferential and longitudinal dimensional changes. The high order extensibilities (second and third order) accounted for the percentage volume changes per mmHg pulse pressure due to the interactions between circumferential and longitudinal dimensional changes. Mean(SEM) EV values from six dogs were 1.62(0.31), 0.84(0.08), and 0.62(0.08)% delta V/mmHg delta P for the ascending aorta, upper descending thoracic aorta, and middle descending thoracic aorta segments respectively. The EV, EL, and EK of the ascending aorta segment were significantly greater than those of the upper descending thoracic aorta and middle descending thoracic aorta segments, whereas EC was significantly less in the ascending aorta than in both the upper descending thoracic aorta and middle descending thoracic aorta segments. It is concluded that there are regional differences in aortic distensibility and its components in vivo. Longitudinal wall motion is an important determinant of these aortic mechanical properties.

Problem of measuring the positive inotropic property of a vasodilating drug: an illustration using felodipine.

A study was undertaken to determine the presence or absence in patients of positive inotropic activity in a vasodilator drug that improves cardiac output by virtue of that vasodilatation. Felodipine is a dihydropyridine calcium antagonist that has a positive inotropic effect at low concentration in the dog in vivo. In nine patients undergoing coronary angiography in whom heart rate was kept constant by atrial pacing the solvent for the intravenous administration of the drug was infused followed by the active solution. Haemodynamic variables were measured with the Mills combined left ventricular cathetertip manometer and aortic electromagnetic blood velocity transducer. Reflex positive inotropic effects were blocked with the beta adrenergic blocking drug atenolol. An index of contractility was used to assess inotropic effects--the maximum rate of rise of left ventricular pressure measured by cathetertip micromanometry; this was an isovolumic event and therefore not sensitive to arterial pressure change, and it was unaffected by changes in left ventricular end diastolic pressure. In all patients peripheral vasodilatation was observed in the plasma felodipine concentration range of 2-40 nmol.litre-1. In eight patients this was accompanied by an 11-36% increase in maximum rate of rise of left ventricular pressure, indicating a small positive inotropic effect. Felodipine appears to show both agonist and antagonist properties in man as well as in the dog.

The effects of felodipine on left ventricular function in beta-blocked patients.

Felodipine is a dihydropyridine calcium antagonist which has a positive inotropic effect in the dog in vivo. However to date, no inotropic effects have been described in man. Thus, the solvent for the intravenous administration of the drug was infused, followed by the active solution, in 9 beta-blocked patients undergoing coronary angiography; heart rate was held constant by atrial pacing. Haemodynamic variables were measured with the Mills combined left ventricular catheter-tip manometer and aortic electromagnetic blood velocity transducer. In all patients, peripheral vasodilatation was observed. In 8 patients, this was accompanied by a 9 to 50% increase in maximum rate of rise of left ventricular pressure indicating a small positive inotropic effect.

Assessment of slope of end-systolic pressure-volume line of in situ dog heart

The purpose of this study was to establish a new method of assessment of the slope (Emax) of the end-systolic pressure-volume line (ESPVL) of the in situ heart. In anesthetized open-chest dogs, an isovolumic contraction was produced by an aortic occlusion after steady-state ejecting contractions in the left ventricle. We plotted ventricular pressure measured with a catheter-tip manometer against time integral of aortic flow measured with an electromagnetic flowmeter of the last ejecting and the first isovolumic contraction, assuming the same end-diastolic volume. ESPVL was drawn from the peak isovolumic pressure-volume point tangential to the left upper corner of the +/- 3.0 (SE) mmHg/ml (n = 9 dogs) in control run and was increased by 59 +/- 19% under isoproterenol and decreased by 47 +/- 9% after propranolol. Emax was little changed by atrial pacing. We conclude that Emax by this aortic occlusion method is useful for assessment of left ventricular contractility of the in situ dog heart.

Hemodynamic correlates of arterial compliance.

There is at present no good understanding of the exact clinical correlates of arterial compliance. The purpose of this study was to establish which hemodynamic variables are most strongly associated with compliance. Hemodynamic measurements were performed on 41 patients undergoing diagnostic cardiac catheterization. Cardiac outputs were determined by thermodilution, and pressures were measured in the ascending aorta with a catheter-tip manometer. Compliance was calculated from a mono-exponential fit of diastolic decay pressures. Pulse pressure(PP), stroke volume(SV), age, systolic blood pressure(SBP), and cardiac output(CO) were significantly related to compliance. The quotient SV/PP was a good estimate of compliance, as was a first-order function of both SV and PP. There appear to be specific clinical correlates of arterial compliance, as well as ways to estimate arterial compliance on the basis of conventional hemodynamic measurements when direct calculations are not possible.

Impulse propagation in rubber-tube analogues of arterial stenoses and aneurysms.

Analogues of arterial stenoses and aneurysms were constructed from latex tubing containing inserts of various lengths, and with diameters and elastic properties that differed from those of the surrounding tube. A pressure impulse (duration <10ms). was generated at one end of the tube and its transmission and reflection were monitored at various points within the system using a catheter-tip manometer. The complex waveforms produced by multiple reflections from either end of the insert were analysed and compared with those generated by a numerical model in which the reflection sites were regarded as isolated junctions between two tubes of infinite length. There was close agreement between the synthesised and measured waveforms.

Systemic compliance: does it play a role in the genesis of essential hypertension?

Arterial compliance is part of the load faced by the heart. Decreased compliance increases this load. We have studied the cardiovascular consequences of decreased systemic compliance in six closed chest anaesthetised dogs where ascending aortic flow transducers and left ventricular crystals had previously been implanted. A stiff tube was put into the abdominal aorta from the left flank and moved to the ascending aorta. Inflation of a cuff on the proximal end of the tube forced the heart to eject into a non-compliant outflow conduit. The distal end of the tube was connected to the distal aorta and, via a pump, to a carotid artery where mean pressure was kept above 80 mmHg. We measured systemic pressures (catheter-tip manometer), cardiac output (electromagnetic flowmeter) and either left ventricular end-diastolic pressure (fluid filled catheter, Statham P23Db) or left ventricular diameter (ultrasound transit time method). From these variables we calculated systemic compliance and input impedance. A 35% decrease in compliance caused a 12% increase in systolic, and a 12% decrease in diastolic pressure while mean pressure and cardiac output did not change significantly. With a decrease in compliance of 63% systolic pressure increased by 18%, while diastolic pressure decreased by 24%. Mean pressure did not change significantly but cardiac output fell by 21%. In both groups of altered compliance peripheral resistance rose slightly but this was not significant. Decreased compliance mainly caused changes in the low frequency range of the input impedance: moduli increased and phase angles became more negative.(ABSTRACT TRUNCATED AT 250 WORDS)

Measurement of left ventricular hemodynamic parameters in closed-chest rats under control and various pathophysiologic conditions.

A prototype of a recently developed mikro-tip pressure transducer catheter (3 French) was inserted into the left ventricle of closed-chest rats via the right carotid artery. In thiobutabarbital-sodium anesthesia, heart rate (409 +/- 7 beats/min), left ventricular systolic pressure (LVSP: 142 +/- 4 mm Hg) and the maximal rate of rise of left ventricular pressure (LV dP/dtmax: 6073 +/- 187 mm Hg/sec, mean values +/- SEM, n = 19) were measured. The baroreceptor reflex was intact under these experimental conditions. In closed-chest guinea pigs, all functional parameters determined were lower (heart rate: 271 +/- 11 beats/min; LVSP: 94 +/- 6 mm Hg; LV dP/dtmax: 3248 +/- 295 mm Hg/sec, mean values +/- SEM, n = 9). To test the applicability of the new catheter tip manometer, cardiac hemodynamic parameters were determined in rats under various pathophysiologic conditions: Several periods of asphyxia were followed by progressive depressions in heart rate, LVSP and LV dP/dtmax, and acute as well as chronic stimulation with catecholamines (noradrenaline and isoproterenol) and with triiodothyronine was characterized by a pronounced positive inotropic and chronotropic effect. The technique described has many potential applications in cardiovascular studies on intact small laboratory animals.

Cardiovascular and biochemical changes in dogs during etomidate-nitrous oxide anaesthesia.

Etomidate was infused in dogs to test whether the drug could be used for long-lasting stable anaesthesia. In six dogs anaesthesia was induced with pentothal (20 mg·kg−1) and continued with a constant infusion of etomidate (4 mg·kg−1·h−1). The animals were ventilated with a mixture of O2 and N2O (1:2). Several haemodynamic (heart rate, arterial pressure, central venous pressure, pulmonary artery pressure, left ventricular end-diastolic pressure, dP/dtLV, cardiac output, systemic vascular resistance) and biochemical (pO2, pCO2, pH, O2 content, lactate, glucose) variables together with the distribution of cardiac output (radioactive microsphere method) were studied for four and a half hours. In the course of the experiment cardiac output (thermodilution), stroke volume and dP/dtLV (catheter tip manometer) decreased by 38, 40 and 25% respectively while systemic vascular resistance increased (38%); the pH in mixed venous blood fell from 7.31 to 7.26. Blood flow to gastrointestinal tract, pancreas, skin and muscle decreased in proportion with the fall in cardiac output. Myocardial, renal, adrenal and splenic blood flow did not change. Hepatic artery flow decreased (67%). Liver perfusion was thus severely affected since portal blood flow also decreased. Oxygen consumption in the systemic, myocardial and splanchnic bed was not affected. In four other dogs blood etomidate levels were also measured. They rose gradually in the course of the experiment even though concentration and infusion rate of etomidate were kept constant throughout the four and a half hour experiment in these and all other dogs. Etomidate thus caused cardiovascular depression when it was used as long-lasting anaesthetic. Insufficient clearance of etomidate by the liver through deficient hepatic blood flow may be a causative factor.

Pulse wave reflection: can it explain the differences between systemic and pulmonary pressure and flow waves? A study in dogs.

We have studied the effect of changes in pulse wave reflection on the configurations of pressure and flow in systemic and pulmonary circulation. Electromagnetic flow transducers, atrial catheters, and pacing leads were implanted in 10 dogs. In four animals, the flow transducer was placed on the pulmonary artery, in another four on the ascending aorta, and in two additional dogs on both vessels. One week later, ascending aortic and/or pulmonary artery flow and pressure (catheter tip manometer) were measured under general anesthesia (Nembutal, 30 mg/kg, iv). When the pulmonary circulation was studied (six dogs), measurements were made before and during serotonin infusion (0.5-0.75 mg/min). When the systemic circulation was studied (six dogs), measurements were made before and during nitroprusside infusion (50-200 micrograms/min). To quantify the arterial load, we calculated pulmonary and systemic input impedances. To estimate the amount of reflection, we used a reflection index which we defined as the amplitude ratio of reflected and forward wave. Nitroprusside decreased total peripheral resistance, increased total arterial compliance, and decreased the reflection index; similarity between aortic pressure and flow wave shapes increased, and they looked more like their pulmonary counterparts. Serotonin increased pulmonary vascular resistance, decreased pulmonary arterial compliance, and increased the reflection index. Resemblance of pressure and flow waves decreased. The differences in wave shapes can thus be explained by the amount of reflection: the less reflection the more pressure and flow resemble each other.

Left ventricular diastolic capacity in man.

Plasma volume expansion with 500 ml of low-molecular-weight dextran was used in 27 patients (nine normal subjects, 13 patients with ischemic heart disease, four with aortic stenosis and one with cardiomyopathy) to increase left ventricular end-diastolic pressure (LVEDP) from a control value of 12.4 +/- 7.0 mm Hg (mean +/- SD) to 23.3 +/- 7.0 mm Hg and end-diastolic volume (EDV) from 84.0 +/- 23.8 ml/m2 to 97.6 +/- 22.9 ml/m2. EDV-LVEDP curves constructed for 12 patients from multiple angiograms at progressively increasing LVEDPs during plasma volume expansion showed an initial part where EDV increased in parallel with LVEDP and a final steep or perpendicular part where EDV increased minimally or not at all as LVEDP exceeded 20 mm Hg. Exponential equations were used to fit diastolic volume-pressure data obtained with catheter-tip manometers in seven patients: the exponential constant, k, was 0.012-0.044 ml-1 and was inversely related to EDV (Spearman's rank correlation coefficient = -1). For comparable EDV, there were no differences in k values between normal subjects and patients with a variety of heart diseases.

The relationship between the strength of the human heart beat and the interval between beats.

In 15 patients undergoing cardiac catheterization and pacing tests, the left ventricular (LV) pressure and its maximum rate of rise (LV dP/dt max) were measured with catheter-tip manometers. Atrial or ventricular pacing at a single steady frequency (the priming frequency) was followed by a test pulse at a varying interval (test pulse interval). In 14 subjects in whom it was examined, the contractile response after the test pulse increased with test pulse interval to reach a maximum plateau value--the optimum contractile response (OCR). In five cases, further prolongation of the test pulse interval decreased the contractile response. The optimum test pulse interval occurred at 800-900 msec. An increase in the priming frequency before the introduction of the test pulse caused a progressive increase in OCR, in contrast to the minor effects on LV dP/dt max of the control beats. Similar results were recorded in four other patients in whom contractile response was assessed from the rate of rise of right ventricular pressure. These results indicate that with tachycardia, the interval between beats is insufficient to allow maximum contractile performance (presumed to be activated by calcium ions) to develop. The true effect of increasing heart rate is only revealed by the relationship between OCR and the preceding frequency of contraction.

Constriction of the epicardial coronary artery induced by alpha-adrenergic stimulation.

Effects of alpha adrenergic stimulation on diameter change of the epicardial coronary artery were studied in in-situ canine heart. The diameter of the left circumflex coronary artery (LCX) was continuously measured by 10 MHz PZT crystals applied to the external wall of the LCX. Aortic pressure was measured using high fidelity catheter-tip manometer. Enhanced activity of alpha adrenergic receptor by humoral and/or somatic nerve stimulations caused a reduction of the LCX diameter despite of the systemic pressure rise.

Effects of high-frequency harmonics on cardiac relaxation indices.

This study was designed to determine the degree to which the systematic distortions in the pressure curve due to recording and filtering systems influence the relaxation indices. The purposes are 1) to analyze the dependency on the high frequencies of the relaxation and contractility parameters, 2) to determine the degree to which the catheter recordings modify those parameters, and 3) to test the monoexponential hypothesis in which the T index is based (Weiss, Frederiksen, and Weisfeldt, J. Clin. Invest. 58: 751-760, 1976). In 17 open-chest dogs, the left ventricular pressure (LVP) was recorded in four different ways: 1) with a large-bored metal cannula, 2) with a catheter-tip manometer, 3) with a Cournand catheter, and 4) with a pigtail catheter. The ECG and LVP were digitized by a computer. A Fourier analysis was performed, and the LVP waves were resynthesized with different numbers of harmonics. We conclude that 1) the catheter recordings are not recommended to calculate relaxation indices, 2) relaxation parameters present more sources of errors than contractility parameters, 3) the monoexponential hypothesis of T is fulfilled if the isovolumic relaxation is considered to end at the time the LVP is 10 mmHg more than left ventricular end-diastolic pressure level, 4) the dependency on higher harmonics of T index and +dP/dtmax is similar, and 5) -dP/dtmax is much more high-frequency dependent than T index.

Impulse propagation in normal and stenosed vessels.

The propagation of a transient pressure impulse in a viscoelastic medium was investigated by experiments using water-filled latex rubber tubing and the aorta of anaesthetised dogs. A 5 ms pressure impulse was produced by the impact of a solenoid driven hammer. The propagation characteristics of the impulse (attenuation and propagation velocity) along the vessel were determined by means of a catheter-tip pressure manometer placed at various distances distal to the impulse generator. The presence of stenoses of varying degrees of severity resulted in reflection of the impulse and the appearance of reflected pulses whose magnitude depended on the stenotic severity. The experiments suggest that for the technique to be used in the detection of local reflecting sites such as might result from vascular occlusive disease, the lesions should occlude at least 70% of the lumen and should be no more than 0.20 m distal to the impulse generator.

Pressure-diameter relationships in the coronary artery of intact, awake calves

We have developed a method for simultaneously measuring coronary artery pressure and diameter in intact, awake animals. Cattle were chronically instrumented with ultrasonic dimension gauges on the left common coronary artery. A high fidelity catheter-tip manometer was placed in the same vessel. Along with the coronary pressure-diameter measurements, simultaneous measurements of ECG, aortic pressure, left ventricular pressure, intrathoracic pressure, and the right atrial pressure were made in 5 calves and 1 dwarf cow. After the arteries had some time to recover from the trauma of the surgical intervention and instrumentation, we measured the pressure-diameter relationships at various post-operative time intervals. Control measurements were followed by measurements made after pharmacologic interventions in two of the animals. The various pressure-diameter curves are illustrated in this paper. In addition an empirical parameter of vessel wall stiffness, the pressure elastic modulus, ( E p ), was calculated. The average value of E p for the left coronary artery 24 h after surgery for the control state was 1.56 (±0.19 SEM) × 10 6 dyn/cm 2.