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O A Smiseth

Publications and source records attributed to O A Smiseth.

At least 19 recordsLinked to original sources
PubMed1999

Mechanisms of retarded apical filling in acute ischemic left ventricular failure.

BACKGROUND: We examined the hypothesis that retardation of apical filling as measured by color M-mode Doppler echocardiography in the diseased left ventricle (LV) reflects a decrease in the intraventricular mitral-to-apical pressure gradient. METHODS AND RESULTS: In 9 open-chest anesthetized dogs, micromanometers were placed near the mitral tip and in the apical region. From the color M-mode Doppler images, the time delay (TD) between peak velocity at the mitral tip and the apical region was determined as an index of LV flow propagation. Acute ischemic LV failure was induced by coronary microembolization. Induction of ischemia caused a marked increase in LV end-diastolic pressure and a decrease in LV ejection fraction. The time constant of LV isovolumic apical pressure decay (tau) increased from 31+/-8 to 49+/-16 ms (P<0.001). The peak early diastolic mitral-to-apical pressure gradient (DeltaPLVmitral-apex) decreased from 1.9+/-0.9 to 0.7+/-0.5 mm Hg (P<0.01), and TD increased from 5+/-3 to 57+/-26 ms (P<0.001). The slowing of flow propagation was limited to the apical portion of the LV cavity. The TD correlated with DeltaPLVmitral-apex (r=-0.94, P<0.01) and with tau (r=0.92, P<0.01). Before ischemia, the mitral-to-apical flow propagation velocity far exceeded the velocity of the individual blood cells, whereas during ischemia, flow propagation velocity approximated the blood velocity. CONCLUSIONS: Retardation of apical filling in acute ischemic failure was attributed to a decrease in the mitral-to-apical driving pressure, reflecting slowing of LV relaxation. The slowing of flow propagation appeared to represent a shift in apical filling from a pattern of column motion to a pattern dominated by convection.

Acute Disease↗
PubMed1998

Early diastolic intraventricular filling pattern in acute myocardial infarction by color M-mode Doppler echocardiography.

The aim of the present study was to investigate whether slowing of mitral-to-apical filling is present in patients with acute myocardial infarction (AMI). Twenty-eight patients with their first AMI were examined by color M-mode Doppler echocardiography. Twenty-eight age- and sex-matched healthy individuals served as control subjects. From the color M-mode Doppler images, we measured the time difference (TD) between occurrence of peak flow velocity at the mitral tip and in the apical region by a blinded analysis. The TD was increased in the AMI group compared with the control subjects (70 +/- 60 versus 40 +/- 30 msec, p = 0.02) and correlated with peak SGOT (r = 0.46, p = 0.02) and age (r = 0.57, p < 0.01). In the 15 patients with anterior AMI, the correlation between TD and SGOT was better (r = 0.68, p < 0.01). This study demonstrated slowing of early diastolic mitral-to-apical flow propagation in patients with AMI. Infarction size and age appear to be of importance for the retardation of mitral-to-apical flow propagation.

Adult↗
PubMed1998

Hepatic oxygen metabolism in porcine endotoxemia: the effect of nitric oxide synthase inhibition.

The role of endotoxin (lipopolysaccharide, LPS) and nitric oxide in hepatic oxygen metabolism was investigated in 36 pigs receiving 1) LPS (1.7 microgram. kg-1. h-1) for 7 h and NG-nitro-L-arginine methyl ester (L-NAME; 25 mg/kg) after 3 h, 2) LPS, 3) NaCl and L-NAME, and 4) NaCl. Infusion of LPS reduced hepatic oxygen delivery (DO2H) from 60 +/- 4 to 30 +/- 5 ml/min (P < 0.05) and increased the oxygen extraction ratio from 0.29 +/- 0.07 to 0.68 +/- 0.04 after 3 h (P < 0.05). Hepatic oxygen consumption (VO2H) was maintained (18 +/- 4 and 21 +/- 4 ml/min, change not significant), but acidosis developed. Administration of L-NAME during endotoxemia caused further reduction of DO2H from 30 +/- 3 to 13 +/- 2 ml/min (P < 0.05) and increased hepatic oxygen extraction ratio from 0.46 +/- 0.04 to 0.80 +/- 0.03 (P < 0.05). There was a decrease in VO2H from 13 +/- 2 to 9 +/- 2 ml/min that did not reach statistical significance, probably representing a type II error. Acidosis was aggravated. Administration of L-NAME in the absence of endotoxin also increased the hepatic oxygen extraction ratio, but no acidosis developed. In a different experiment, liver blood flow was mechanically reduced in the presence and absence of endotoxin, comparable to the flow reductions caused by L-NAME. The increase in hepatic oxygen extraction ratio (0.34) and maximum hepatic oxygen extraction ratio (approximately 0.90) was similar whether DO2H was reduced by occlusion or by L-NAME. We concluded that L-NAME has detrimental circulatory effects in this model. However, neither endotoxin nor L-NAME seemed to prevent the ability of the still circulated parts of the liver to increase hepatic oxygen extraction ratio to almost maximum when oxygen delivery was reduced. The effect of L-NAME on oxygen transport thus seems to be caused by a reduction in DO2H rather than by alterations in oxygen extraction capabilities.

Animals↗
PubMed1998

Mechanics of intraventricular filling: study of LV early diastolic pressure gradients and flow velocities.

This study investigates mechanisms of left ventricular (LV) intracavitary flow during early, rapid filling. In eight coronary artery disease patients with normal LV ejection fraction we recorded simultaneous LV apical and outflow tract pressures and intraventricular flow velocities by color M-mode Doppler echocardiography. In five anesthetized dogs we also recorded left atrial pressure and LV volume by sonomicrometry. In patients, as the early diastolic mitral-to-apical filling wave arrived at the apex, we observed an apex-outflow tract pressure gradient of 3.5 +/- 0.3 mmHg (mean +/- SE). This pressure gradient correlated with peak early apex-to-outflow tract flow velocity (r = 0.75, P < 0.05). The gradient was reproduced in the dog model and decreased from 3.1 +/- 0.3 to 1.7 +/- 0.5 mmHg (P < 0.05) with caval constriction and increased to 4.2 +/- 0.5 mmHg (P < 0.001) with volume loading. The pressure gradient correlated with peak early transmitral flow (expressed as time derivative of LV volume; r = 0.95) and stroke volume (r = 0.97). In conclusion, arrival of the early LV filling wave at the apex was associated with a substantial pressure gradient between apex and outflow tract. The pressure gradient was sensitive to changes in preload and correlated strongly with peak early transmitral flow. The significance of this gradient for intraventricular flow propagation in the normal and the diseased heart remains to be determined.

Adult↗
PubMed1998

ET-receptor antagonism, myocardial gene expression, and ventricular remodeling during CHF in rats.

Both myocardial and plasma endothelin-1 (ET-1) are elevated in congestive heart failure (CHF). However, the role played by endogenous ET-1 in the progression of CHF remains unknown. The aim of the present study was to investigate and correlate myocardial gene expression programs and left ventricular (LV) remodeling during chronic ET-receptor antagonism in CHF rats. After ligation of the left coronary artery, rats were randomized to oral treatment with a nonselective ET-receptor antagonist (bosentan, 100 mg . kg-1 . day-1, n = 11) or vehicle (saline, n = 13) for 15 days, starting 24 h after induction of myocardial infarction. Bosentan substantially attenuated LV dilatation during postinfarction failure as evaluated by echocardiography. Furthermore, bosentan decreased LV systolic and end-diastolic pressures and increased fractional shortening. Myocardial expression of preproET-1 mRNA and a fetal gene program characteristic of myocardial hypertrophy were increased in the CHF rats and were not affected by bosentan. Consistently, right ventricular-to-body weight ratios, diameters of cardiomyocytes, and echocardiographic analysis demonstrated a sustained hypertrophic response and a normalized relative wall thickness after intervention with bosentan. Thus the modest reduction of preload and afterload provided by bosentan substantially attenuates LV dilatation, causing improved pressure-volume relationships. However, the compensatory hypertrophic response was not altered by ET-receptor antagonism. Therefore, ET-1 does not appear to play a crucial role in the mechanisms of myocardial hypertrophy during the early phase of postinfarction failure.

Angiotensinogen↗
PubMed1997

Regulation of hepatic vascular volume: contributions from active and passive mechanisms during catecholamine and sodium nitroprusside infusion.

BACKGROUND: It is unclear how the liver contributes to regulation of cardiac filling. The aims of this study were to establish an animal model to quantify hepatic vascular capacitance and to determine the mechanisms whereby catecholamines and sodium nitroprusside modify hepatic blood volume. METHODS AND RESULTS: In 8 anesthetized pigs we measured hepatic and systemic pressures and flows. Liver vascular volume was measured by sonomicrometry calibrated against integrated hepatic inflow during outflow occlusion. Pressure-volume (P-V) curves were constructed during outflow occlusion. Sonomicrometry accurately reflected hepatic blood volume (r=.99+/-.001), and hepatic P-V curves were highly reproducible. Norepinephrine (0.3 and 0.7 microg x kg body weight (bwt)(-1) min(-1) intraportally) significantly reduced hepatic blood volume by 3.3+/-1 and 4.3+/-1 mL x kg bwt(-1), respectively. Nitroprusside (8 and 18 microg x kg bwt(-1) x min(-1) intraportally) increased hepatic blood volume by 1.1+/-0.2 and 1.9+/-0.3 mL x kg bwt(-1), respectively. Norepinephrine and nitroprusside parallel shifted the hepatic P-V curves, indicating reduced and increased unstressed blood volume, respectively. These curve shifts accounted for more than 90% of the respective blood volume changes. Compliance was unchanged. Phenylephrine but not isoprenaline yielded similar results as norepinephrine. CONCLUSIONS: The pig model used in this study, accurately quantified hepatic capacitance. Alpha-adrenergic stimulation decreased and nitroprusside increased capacitance by changing unstressed blood volume. These changes in capacitance correspond to expulsion of 300 mL and pooling of 130 mL of blood, respectively, in a 70-kg individual, reflecting that the liver is not only a passive blood reservoir but can respond actively and vigorously to pharmacological interventions.

Animals↗
PubMed1997

Increased cardiac expression of endothelin-1 mRNA in ischemic heart failure in rats.

OBJECTIVES: Plasma endothelin (ET) concentrations are increased in heart failure. The aims of the present study were to investigate to what extent cardiac ET mRNA expression is induced in ischemic heart failure and whether there may be compensatory downregulation of myocardial mRNA levels for the ETA and ETB receptor subtypes. METHODS: In rats with ischemic heart failure (left ventricular end-diastolic pressure > 15 mmHg) due to left coronary artery ligation. Northern blot analyses were performed on mRNA isolated from cardiac tissues. RESULTS: A substantial upregulation was revealed in all chambers of the failing hearts. Up to 27-fold upregulation (mean 10.6 +/- 4.0, P = 0.002) of left ventricular ET-1 mRNA levels was measured 1 week after myocardial infarction, whereas only a modest upregulation was detected after 6 weeks (mean 2.7 +/- 0.5, P < 0.05). Ribonuclease protection assay revealed 2.8 +/- 0.4-fold higher levels of ET-1 mRNA in the left ventricular area subjected to myocardial infarction compared to the non-infarcted tissue after 1 week. Left ventricular ET-1 mRNA correlated significantly with left ventricular end-diastolic pressure after 1 week (r2 = 0.86, P = 0.007). The ETA and ETB receptor mRNA levels tended to increase 1 week after myocardial infarction although these changes were not statistically significant. CONCLUSIONS: Cardiac ET-1 mRNA levels are increased in ischemic heart failure and correlate significantly with left ventricular end-diastolic pressure 1 week after myocardial infarction. The increase in cardiac ET-1 mRNA is not accompanied by a decrease in ET receptor mRNA.

Animals↗
PubMed1997

Transient, isopeptide-specific induction of myocardial endothelin-1 mRNA in congestive heart failure in rats.

Increased myocardial expression of preproendothelin-1 (ppET-1) mRNA has been associated with congestive heart failure (CHF) in rats. However, the time course and isoform pattern of ppET mRNA induction and the cellular localization of ET in failing hearts are unknown. Thus our aim was to investigate myocardial ppET mRNA expression in CHF rats during the first 6 wk after induction of myocardial infarction. Furthermore, performing immunohistochemical analysis, we also investigated the origin and localization of immunoreactive endothelin (ET) in different regions of the failing heart. Ribonuclease protection assays revealed a marked increase in ppET-1 mRNA levels in rat myocardial tissues during CHF. The induction of ppET-1 mRNA was isopeptide specific and transient. The most substantial upregulation was observed in the infarcted area, where maximal expression of ppET-1 mRNA was observed after 7 days (25-fold increase, P < 0.05). However, a marked and statistically significant induction of ppET-1 mRNA was also observed in the nonischemic myocardium. Immunohistochemical analysis revealed ET-1-like immunoreactivity in cardiomyocytes, vascular endothelial cells, macrophages, and proliferating fibroblasts. Thus immunohistochemistry revealed the structural basis for the dramatic upregulation of the myocardial ET system in the infarcted region, suggesting a role for ET in the healing process after myocardial infarction. However, the global upregulation of ppET-1 mRNA in the heart also suggests an autocrine/paracrine regulatory mechanism in the nonischemic myocardium during CHF.

Animals↗
PubMed1996

[Physicians' view on drug therapy for hypertension. A questionnaire in the county of Hordaland].

A questionnaire survey was conducted in Hordaland county to discover opinions on drug therapy for uncomplicated hypertensives with no other risk factors. The response rate was 66%; 179 general practitioners and 31 hospital doctors. The doctors were well informed about the documentation of the clinical benefit of various drugs. As regards the minimum blood pressure that was considered as warranting drug treatment, the majority of the doctors followed the recently issued national guidelines. For young patients the first choice drugs were beta-blockers (27%), ACE-inhibitors (25%) or calcium-blockers (20%). For older patients 65% of the doctors preferred diuretics or beta-blockers. The majority (80%) based their choice of drug primarily on documentation of clinical value or absence of side effects. The doctors underestimated the cost of the newer antihypertensive drugs.

Adult↗
PubMed1996

[Cardiology education in Norway--does it keep up with the needs?].

Despite an increase in the number of education positions for cardiologists in Norway in the late 1980s, there is felt to be a marked lack of sub-specialists in cardiology in most types of hospitals. A working group under the Norwegian Society of Cardiology has used a questionnaire in 1993, membership data from the Norwegian Society of Cardiology in 1994, a telephone query to all hospitals in the country, and data from the Norwegian Medical Association in 1995 to examine this apparent lack of specialists and the potentials for educating them. We were able to confirm a current lack of approximately 60 cardiologists. In addition, the capacity for education has been reduced and will not compensate for the predicted retirement of specialists from approximately year 2000. The capacity for educating cardiologists must be increased.

Cardiology↗
PubMed1996

A potential clinical method for calculating transmural left ventricular filling pressure during positive end-expiratory pressure ventilation: an intraoperative study in humans.

OBJECTIVES: This study sought to investigate whether right atrial pressure could be used to estimate pericardial pressure during positive end-expiratory pressure (PEEP). BACKGROUND: Because of elevated intrathoracic pressure during PEEP, pulmonary capillary wedge pressure may not accurately reflect left ventricular preload. An estimate of pericardial pressure during PEEP would allow assessment of transmural filling pressure. METHODS: In eight patients, at the start of cardiac surgery, pericardial and pleural pressures were recorded by balloon transducers placed over the anterolateral left ventricular wall. We also recorded intravascular pressures and left ventricular short-axis area by transesophageal echocardiography. RESULTS: A stepwise increase in PEEP from 0 to 15 cm H2O caused a linear increase in pleural pressure from 0.3 +/- 0.6 (mean +/- SEM) to 6.1 +/- 0.8 mm Hg (p < 0.01). Pericardial pressure increased from 2.3 +/- 0.5 to 5.9 +/- 0.6 mm Hg (p < 0.01). The correlation between right atrial (Pra) and pericardial pressure (Pperic) was good: Pra = 0.85 x Pperic + 1.8, r = 0.77. The correlation between changes in right atrial pressure and in pericardial pressure was better: delta Pra = 0.96 x delta Pperic -0.2, r = 0.97. Pulmonary capillary wedge pressure increased with PEEP (p < 0.05), whereas left ventricular area decreased (p < 0.05). However, there was a progressive reduction in transmural pressure, calculated as wedge pressure minus pericardial pressure (p < 0.05), and in transmural pressure, estimated as wedge pressure minus right atrial pressure (p < 0.05). The estimated transmural filling pressure correlated (r = 0.86) with end-diastolic area. CONCLUSIONS: The present observations suggest that right atrial pressure may be used to estimate changes in pericardial pressure with PEEP and that pulmonary capillary wedge pressure minus right atrial pressure is a potentially clinically useful approximation of transmural filling pressure.

Adult↗
PubMed1996

Nitric oxide synthase inhibition reduces venous return in porcine endotoxemia.

Mechanisms of circulatory effects induced by nitric oxide synthase inhibition in endotoxemia were investigated in 36 pigs randomized to 1) endotoxin infusion (1.7 micrograms.kg-1.h-1 iv) for 7 h and bolus NG-nitro-L-arginine methyl ester (L-NAME; 25 mg/kg iv) after 3 h; 2) endotoxin infusion for 7 h; 3) saline infusion for 7 h and L-NAME after 3 h; and 4) saline infusion for 7 h. Fifteen minutes after L-NAME injection during endotoxemia, reductions in cardiac output (41%, P < 0.05), portal venous flow (51%, P < 0.05), and hepatic artery flow (50%, P < 0.05) were observed. Systemic vascular resistance increased by 82% (P < 0.05), and the portocaval vascular resistance increased by 101% (P < 0.05). Despite marked vasoconstriction after L-NAME, left ventricular intracavitary filling pressure, central venous pressure, and arterial pressure remained unchanged. During endotoxemia, hematocrit increased from 38.4 +/- 1.4 to 41.9 +/- 1.2 after L-NAME, and blood volume (n = 3) was reduced by an average of 8.3 ml/kg body wt. These changes probably reflect transcapillary fluid loss as urine output was unchanged. In conclusion, L-NAME decreased intravascular blood volume and increased splanchnic venous resistance. These effects will tend to reduce venous return. Combined with a marked increase in left ventricular after-load, L-NAME may thus compromise cardiovascular function in endotoxemia.

Animals↗
PubMed1996

The NO donor sodium nitroprusside reverses the negative effects on hepatic arterial flow induced by endotoxin and the NO synthase inhibitor L-NAME.

In previous studies we have observed that the nitric oxide synthase inhibitor L-NAME induces a profound deterioration of liver circulation in experimental endotoxemia. Using the same porcine model we now have evaluated the possibility of modulating these effects with the nitric oxide donor sodium nitroprusside. Infusion of endotoxin led to a gradual deterioration of hemodynamic parameters, including liver blood flow. The decreases in portal blood flow paralleled and matched the decreases in cardiac output, and no compensatory increase in hepatic arterial flow occurred. L-NAME had detrimental effects on hemodynamics, including the liver circulation. The latter effects could, however, partially be reversed by sodium nitroprusside. Hepatic arterial flow increased from 1.9 to 7.2 ml/kg/min, with a concomitant decrease in hepatic arterial resistance from 5,364 to 1,746 dyn s/cm5 kg. A control group exhibited no significant change in either flow or resistance. The response to sodium nitroprusside was rapid and vigorous, and probably largely due to relaxation of the hepatic arterioles, and not to abatement of intrahepatic edema or plugging of the sinusoids. Furthermore, we conclude that the endotoxin-induced dysfunction of the hepatic arterial buffer response may be due to a selective inhibition of vascular endothelial function.

Animals↗
PubMed1995

Splanchnic venous pressure-volume relation during experimental acute ischemic heart failure. Differential effects of hydralazine, enalaprilat, and nitroglycerin.

BACKGROUND: Vasodilator drugs have variable effects on veins and arteries. However, direct measurements of their effects on the splanchnic veins, perhaps the most important volume reservoir, have not been reported. We assessed the effect of acute heart failure and the subsequent administration of hydralazine, enalaprilat, and nitroglycerin on the splanchnic venous pressure-volume relation in intact dogs. METHODS AND RESULTS: Experimental acute ischemic heart failure was induced in 19 splenectomized dogs by microsphere embolization of the left main coronary artery. Embolization was repeated until left ventricular end-diastolic pressure (LVEDP) reached 20 mm Hg and cardiac output decreased by 50%. The splanchnic vascular pressure-volume relation was determined by radionuclide plethysmography during the control stage, after acute heart failure had been established, and after administration of a vasodilator (hydralazine, enalaprilat, or nitroglycerin) at a dose sufficient to reduce mean aortic pressure by approximately 20%. Induction of acute heart failure was associated with a decrease in the splanchnic vascular volume from 100% to 86 +/- 2% and an increase in LVEDP from 6 +/- 1 to 21 +/- 1 mm Hg (P < .001). There was a parallel leftward shift of the splanchnic vascular pressure-volume curve. After the administration of hydralazine, enalaprilat, and nitroglycerin, the splanchnic vascular volumes increased from 86% to 88 +/- 3%, 96 +/- 3%, and 113 +/- 3%, respectively (P = NS, P < .01, and P < .001, respectively, versus heart failure). After drug administration, the LVEDPs were 18 +/- 2, 16 +/- 1, and 13 +/- 1 mm Hg (P = NS, P < .05, and P < .001, respectively, versus heart failure). CONCLUSIONS: Acute heart failure was associated with a parallel leftward shift of the splanchnic venous pressure-volume relation (venoconstriction). Splanchnic (systemic) venoconstriction may in part explain the increased LVEDP during acute heart failure by displacement of blood to the central compartment. Subsequently administered enalaprilat and, to a greater degree, nitroglycerin produced splanchnic venodilation, thereby lowering LVEDP. Hydralazine had no significant effect on the splanchnic veins and only a modest effect on LVEDP. In this model, splanchnic capacitance changes appear to modulate change in left ventricular preload.

Animals↗
PubMed1995

Measurement of intestinal vascular capacitance in dogs: an application of blood pool scintigraphy.

To define relative changes in intestinal vascular capacitance, we developed a model that allowed us to construct intestinal vascular pressure-volume relationships (PVR). Thirteen alpha-chloralose-anesthetized and splenectomized dogs were studied using a pneumatic constrictor and a small catheter to change and measure portal venous pressure. A small lead sheet was placed beneath the abdominal wall. Relative changes in intestinal blood volume (IBV) were determined by in vivo blood pool scintigraphy with 99mTc-labeled erythrocytes and were expressed as percentages corrected for specific activity and abdominal wall radioactivity. PVRs were constructed using data recorded during graded inflations of the portal venous constrictor. The abdominal wall contributed 32.4 +/- 7.7% (SD) of the total counts. During a 4-h control period, PVRs varied by no more than 6% (of IBV). In the isolated intestinal circulation, the change in IBV was precisely proportional to the volume of blood added, indicating that this method can detect very small changes in volume (< or = 5 ml). Nitroglycerin (25 micrograms.kg-1.min-1) increased capacitance by 20%. Although it measures only relative changes, the model is stable and sensitive, provides reproducible measurement of intestinal PVRs, and, with adaptation, may prove useful in patient studies.

Abdomen↗
PubMed1994

Juxtacardiac pleural pressure during positive end-expiratory pressure ventilation: an intraoperative study in patients with open pericardium.

OBJECTIVES: This study was conducted to measure the cardiac constraining effect of the lungs during positive end-expiratory pressure and relate extracardiac pleural pressure (radial stress) to airway pressure, right atrial pressure and left ventricular filling. BACKGROUND: During positive end-expiratory pressure ventilation, the extracardiac pressure is elevated, and therefore intracavitary filling pressure does not reflect ventricular preload. Estimates of this pressure might be useful clinically to assess left ventricular preload. METHODS: In eight patients who had undergone coronary or valvular surgery and whose pericardium was left widely open, a flat pleural balloon transducer was placed over the anterolateral left ventricular wall. We recorded pulmonary capillary wedge pressure, right atrial pressure and left ventricular short-axis end-diastolic area by transesophageal echocardiography. Incremental positive end-expiratory pressure was applied. RESULTS: Extracardiac pleural pressure increased (p < 0.01) from 0.6 +/- 1.8 (+/- SD) to 2.4 +/- 1.8, 5.3 +/- 1.5 and 8.2 +/- 1.5 mm Hg at a positive end-expiratory pressure of 5, 10 and 15 cm H2O, respectively. The slope relating extracardiac pleural pressure to positive end-expiratory pressure (in mm Hg) was 0.70 +/- 0.10, and the intercept was zero. Increasing extracardiac pleural pressure was associated with a progressive increase in pulmonary capillary wedge pressure and a decrease in left ventricular end-diastolic area. Consequently, although pulmonary capillary wedge pressure and left ventricular area changed in opposite directions, the value of pulmonary capillary wedge pressure minus extracardiac pleural pressure correlated positively with left ventricular area (r = 0.95, p < 0.001). Changes in right atrial pressure (Pra) correlated with changes in extracardiac pleural pressure (Ppleural): delta Pra = -0.3 + 0.56. delta Ppleural (r = 0.89, p < 0.001). CONCLUSIONS: In postoperative patients with open pericardium, pulmonary capillary wedge pressure minus extracardiac pleural pressure predicts left ventricular end-diastolic area during positive end-expiratory pressure. Further studies should be done to determine whether the observed relations between airway pressure and extracardiac pleural pressure and between right atrial pressure and extracardiac pleural pressure may give clinically useful estimates of left ventricular preload during positive end-expiratory pressure.

Aged↗
PubMed1994

Visual assessment of intra ventricular flow from colour M-mode Doppler images.

Left intra ventricular filling was studied by colour M-mode Doppler ultrasound to determine whether the flow pattern can be assessed visually, and explore its relation to left ventricular (LV) function. Patients with coronary artery disease (CAD) or dilated cardiomyopathy (DCM) were divided into three groups according to angiographically evaluated LV function. The groups were compared with a control group of 54 healthy volunteers. The mitral to apical delay of early diastolic flow was qualitatively assessed from printed colour M-mode images, twice by four independent observers blinded to the subject's status. The repeatability of the assessments as determined by the kappa statistic was good intra observer (kappa = 0.75) and moderate inter observer (kappa = 0.53). The CAD-group with angiographically normal LV function (n = 25) had flow patterns resembling those observed in the control group. The group with ejection fraction (EF) < 50% (n = 19) had flow patterns clearly different from the control group. Patients with regional wall motion abnormality (RWMA) but EF > 50% (n = 16) exhibited flow patterns intermediate between the control and the low EF group. Among the 50 CAD patients there was a negative correlation between EF and the presence of delay of apical peak velocity (Spearman's rs = -0.62, p < 0.0001). A visible delay of apical peak velocity had a sensitivity towards DCM of 83% and specificity of 75%. The sensitivity towards CAD with either RWMA or low EF was 55% and the specificity 75%. In conclusion, visual assessment of intra ventricular flow patterns was feasible and allowed discrimination between normal and diseased ventricles.

Adult↗