Aortic Pulse Contour Research Articles

P232 EXERTIONAL BREATHLESSNESS IN HYPERTROPHIC CARDIOMYOPATHY: OBSTRUCTION–INDEPENDENT SYMPTOMS IN A “PARADOXICAL” RESPONSE TO EXERCISE

Abstract A 66–y.o. man with hypertrophic cardiomyopathy presented with residual exertional dyspnea NYHA III a few years after surgical myectomy, mitral valve repair and ICD implantation. Echocardiography showed residual mild septal hypertrophy and mitral regurgitation (MR), and a variable obstruction of left ventricular outflow tract (LVOT), witnessed by a pressure gradient ranging from 15 to 50–70 mmHg (Figure 1). Exercise echocardiography did not suggest exercise–induced LVOT obstruction (LVOTO) or functional MR. We thus performed a thorough invasive hemodynamic evaluation at rest and during exercise. LVOTO was present at rest, with a maximum pressure gradient of 90–100 mmHg and typical “spike–and–dome” configuration of the aortic pulse contour (Figure 2), with LV end–diastolic pressure (LVEDP) at the upper limit of normal (15 mmHg) and normal pulmonary hemodynamics. During exercise, we observed a paradoxical reduction of the LVOTO (30–40 mmHg at peak, Figure 2). Pulmonary hypertension developed during exercise, due to LV diastolic dysfunction, witnessed by a marked increase in pulmonary artery wedge pressure and LVEDP (up to 25 mmHg and 30 mmHg at peak, respectively). Cardiac output (CO) reserve was at the lower limits of normal, mainly due to chronotropic incompetence, responsible for a mildly reduced exercise capacity (peak oxygen consumption was 20 mL/Kg/min, 75% of predicted). Thus, cardiac catheterization confirmed the presence of a relevant LVOTO at rest, that was not directly related to exertional symptoms. These latter were mainly attributable to LV diastolic dysfunction and reduced CO reserve. These findings helped us driving treatment decision in a tailored way: beta–blockers were not uptitrated, because of their negative inotropic effect, and high–risk septal reduction therapies were excluded, since exertional symptoms were unrelated to LVOTO. However, an attempt to reduce LVOTO was done by DDD sequential pacing through the ICD. Pacing could induce mechanical dyssynchrony and reduce LVOTO by increasing the end–systolic LVOT diameter. The simultaneous echocardiographic monitoring highlighted an acute reduction of LVOT gradient from 50–70 mmHg to 20–30 mmHg (Figure 3). This case suggests that, in well–selected cases, patients’ management based on pathophysiological reasoning may help to define the etiopathogenetic mechanism underlying symptoms, and to drive treatment decision in a patient–centered way.

Aortic stenosis and the pulse contour: A true marker of severity?

The aortic pulse contour displays characteristic changes associated with the progression of aortic stenosis (AS). A diminished and delayed aortic pulse contour is indicative of significant AS, but the aortic contour may also be affected by factors including aging, hypertension and increased peripheral arterial elastance. This review describes the components of the aortic pulse contour in AS and how it can be affected by different conditions and interventions.

Prediction of aortic augmentation index using radial pulse transmission-wave analysis

Current arterial transfer functions have low capability in predicting aortic augmentation index (AIx) from radial pulse contour (RPC), because of the difficulty in accurately identifying the merging point (inflection point) in the derived aortic pulse contour (APC). We hypothesize that the formation time between each characteristic wave in APC is about one-third of ejection duration (ED/3). We sought to assess the accuracy of ED/3 in identifying the merging point in APC as compared to the conventional differential method. In addition, we sought to derive the AIx from RPC based on an arterial transfer function and the ED/3 method. APC and RPC sequences were measured digitally and simultaneously in 60 subjects (37 males; aged 60 +/- 10 years). An ensemble-averaged RPC-to-APC transfer function was determined from 30 randomly selected subjects and was used to derive APC sequences in the 30 additional subjects. The accuracy of AIx predicted from RPC was determined. In patients with a clearly identifiable merging point in APC, the ED/3 method identified the merging point of measured APC within 1.97 +/- 0.60 ms of that identified by the conventional differential method, with identical AIx. The AIx and merging point of derived APC using the ED/3 method were also within 0.22 +/- 1.01% and 1.81 +/- 1.64 ms, respectively, of those of the measured APC using the conventional differential method. The accuracy of the predicted AIx was independent of age, sex, body-mass index and presence of hypertension. In a quiet resting state, the ED/3 is an alternative method for identifying the merging point in APC. In conjunction with transfer-function technique, AIx can be derived accurately from RPC.

Practice Corner: Taking evidence in hand

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Implantation of the Jarvik 2000 heart

Implantation of the Jarvik 2000 heart

Implantation of the Jarvik 2000 Heart

The axial-flow cardiac assist pump is an innovative type of iml)lautable left ventricular assist system (LVAS) that offers a numl)cr of advantages over conventional, pulsatilc systems. The axial-flow pure I) is significantly smaller than coral)arable l)ulsatile iml)lantable pumps and requires no valvular mechanism. The constant flow of blood through the I)um I) mininfizes stasis anti continuously washes the inorganic surfaces, reducing the likelihood of device thrombosis. The constant flow also obviates the need for a coml)liance chamber, so venting is unnecessary. Because the axialflow immp is nonl)ulsatile, trauma related to movement of the drivelinc (an important potential source of infection) is significantly reduced. Whereas traditional LVASs necessitate a fairly extensive implant oI)eration, the axial-flow llUml ) is easier to implant, hcll)ing to minimize operative complications. As this LVAS has only 1 movable component, device reliability and durability are enhanced. The pump can be used to support chihlrcn and smaller aduhs, as well as adults of usual size. In contrast to conventional, 1)ulsatile LVASs, which are intended to capture the entire left ventricular outi)ut and, therefore, to serve as vcntricnlar rel)laccmcnt devices, the axial-flow pnm I) is best used as a true assist device. This article focuses on the Jarvik 2000 Heart (Jarvik Heart, Inc., New York, NY), an electrically I)owered LVAS that provides continuous flow from tlle left ventricle to tlle descending thoracic aorta. This pump is unique in that it can be placed within the left ventricle, thereby avoiding the rheologic problems (negative pressure stasis) associated with an inflow conduit. The Jarvik 2000 system, which has been described elsewhere FIG I. The Jarvik 2000 left ventricular assist system.

Beat to beat analysis of left ventricular volume and stroke volume by conductance catheter and aortic pulse contour in cardiomyoplasty patients

Beat to beat analysis of left ventricular volume and stroke volume by conductance catheter and aortic pulse contour in cardiomyoplasty patients

Negative effect of insufflation on cardiac output and pulmonary blood volume

In 14 anaesthetized young pigs the changes in pulmonary blood flow and pulmonary blood volume (Qp) during mechanical ventilation were quantified. Ventilation was performed at 10 cycles per min and tidal volume (VT) was adjusted to an arterial PCO2 of about 40 mmHg (5.3 kPa). In 4 animals, 7 ventilatory cycles with an inspiratory pause (IP) of 7.2 s but different tidal volumes were inserted at intervals of 5 min to determine the decrease in Qp (delta Qp) from the differences between right ventricular (Qs,rv) and left ventricular (Qs,lv) stroke volume, and to relate delta Qp to VT. We measured pressure in the aorta (Pao), central veins (Pcv), right and left ventricles (Prv, Plv) pericardium (Pit), and trachea (PT). Blood flow was measured electromagnetically (EM) in the pulmonary artery (Q'pa) and aorta (Q'ao). Stroke volumes were derived from the EM-flow curves. In the other 10 experiments, Qs,lv was derived from the aortic pulse contour. Beat-to-beat analyses of Qs,rv and Qs,lv and blood pressures during the normal ventilatory cycles and those with an IP revealed the following: 1) The end-expiratory RV output and LV output were constant and were defined as baseline values. 2) The accumulated decrease in Qs,rv during insufflation caused a mean deficit in cardiac output of 10.3 +/- 3.2% (s.d.), n = 135; the same was found for Qs,lv, indicating the pulse contour as a useful method to estimate the variations in cardiac output during a ventilatory cycle.(ABSTRACT TRUNCATED AT 250 WORDS)

Mechanics of the aorta in vivo. A radiographic approach.

The hydraulic properties of the unexposed thoracic aorta were studied in five cats by angiography. Repeated measurements of pressure and diameter were obtained at various distances from the aortic root, and it became obvious that the unexposed aorta in cats was more than twice as distensible as the exposed aorta. Diameter of the aortic root, for example, varied by about 20% over a physiologic pulse pressure (40 mm Hg); even in the lower thoracic aorta variations exceeded 15%. When plotted as a function of distance from the root, aortic diameter and distensibility both decreased, and the calculated impedance increased. Despite these changes, however, the calculated reflection coefficients were quite small. It was concluded that geometric and elastic inhomogeneities in the thoracic aorta tend to balance one another, keeping the reflection coefficient quite low and helping to "decouple" the oscillatory left ventricular pump from the static peripheral vasculature. Since the aortic pulse contour is reflection-free during the first 50 msec following the onset of ventricular ejection, it may reliably indicate left ventricular properties and their changes with stress. In several animals, norepinephrine infusion was used to elevate the aortic pressure to hypertensive levels. When compared to hypertension induced by carotid reflex stimulation or mechanical occlusion of the aorta, however, aortic wall properties were essentially the same, suggesting that this agent has no important direct effect on the aortic wall.

Aortic pulse contour and cardiac output : C. L. Graves and T. S. Underwood. Anesthesiology 29:580–584 (May–June) 1968

Aortic pulse contour and cardiac output : C. L. Graves and T. S. Underwood. Anesthesiology 29:580–584 (May–June) 1968

Aortic pulse contour calculation of cardiac output.

Aortic pulse contour calculation of cardiac output.

Contour changes of the aortic pulse during propagation.

Changes in aortic pulse contour were mapped by moving a recording sound through the aorta of lightly anesthetized dogs. The initial anacrotic slope of the ascending aortic (root) pulse usually traverses the arch and the thoracic aorta unchanged, but is often steepened in the abdominal aorta. The break in this slope occurs at a progressively higher pressure level as the pulse moves outward. Starting in the descending arch, a new wave, not seen in the root pulse, rises from the broad top of the systolic portion of the pulse. As the pulse moves peripherad, the peak of this wave moves progressively earlier until finally it may merge with the anacrotic slope itself. Hence the peaks are approximately simultaneous for all parts of the aorta beyond the arch, i.e. they are ‘standing waves.’ In a few cases, the root pulse shows a small but clear negative trough coincident with this peripheral pulse peak. In late systole or early diastole, the root pulse shows a pressure plateau or even a rise, while the pressure in the peripheral pulses is falling sharply to make a trough. Following this, there may be one or more reciprocal oscillations between the root and a peripheral aortic pulse. While standing waves are commonly seen in the dog, they are not developed in some cases, but the pulse pressure may still show an augmentation.

Quantitation of beat-to-beat changes in stroke volume from the aortic pulse contour in man.

Quantitation of beat-to-beat changes in stroke volume from the aortic pulse contour in man.

Can experimental shock be induced by coronary occlusion?

Summary and ConclusionsThe left ramus descendens anterior of the exposed hearts of dogs was ligated, arrhythmia was prevented by use of small doses of quinidine, and records of aortic, left atrial and right atrial pressures were repeatedly recorded by calibrated Greggtype manometers for 5 to 7 hours. Blood volume and cardiac output determinations were made in some animals. The results indicate that up to 7 hours there is no evidence, on the basis of an analysis of cardiac output, blood volume and pressure pulses, that circulatory failure of peripheral origin supervenes in dogs after ligation of a major coronary branch.Comparison of cardiac output data obtained by the Fick method and the aortic pulse contour method showed sufficient disagreement to indicate that the latter method is not sufficiently accurate for quantitative evaluation of cardiac output, even when pressure pulses of normal contour and normal aortic pressures prevail.