Correlations between changes of the right and left atrial pressures and systemic hemodynamics parameters following catecholamines intravenous injections in cats

In acute experiments on anesthetized cats, intravenous injection of epinephrine and norepinephrine caused different changes of right and left artrial pressures. These shifts mostly (82%) had similar directions: in these experiments, both right and left atrial pressures could be decreased (I group of animals) or increased (II group). The number of animals in these groups was equal. However, in 18% of the experiments, right atrial pressure was decreased, while left atrial pressure was increased. The changes of the left atrial pressure was, as a rule, more significant as compared with right atrial pressure shifts. In the I group of animals, systolic right atrial pressure was not changed, and systolic left atrial pressure was decreased. In the II group of animals, systolic pressure in both atria was augmented. Diastolic pressure was decreased in both atria in all the animals. When the atrial pressures were decreased, the increases of the superior and inferior vena cava flows, venous return and cardiac output were more significant as compared with animals in which the atrial pressures had been elevated. The changes of the superior and inferior vena cava flows were more obvious in animals following epinephrine injection as compared with animals in which norepinephrine was injected. The right atrial pressure returned to the initial level more rapidly than the left atrial pressure, and the time dynamics of the shifts of the right atrial pressure was similar to that of the superior vena cava flow. The temporal changes of the left atrial pressure were identical to the time changes of the cardiac output. We concluded that character of changes of the mean, systolic, and diastolic right and left atrial pressures following catecholamines injections was not correlated with the direction of venous return and cardiac output shifts, and was depending on intracardiac hemodynamics.     

The role of vagus nerves in different changes of the right atrial pressure following intravenous injection of pressor vasoactive drugs

In acute experiments on anesthetized cats, intravenous injection of the norepinephrine and angiotensin caused different changes of right atrial pressure in intact animals (decreasing--I group, of animals, and increasing--II group). After right and left vagus nerves had been cut, the right atrial pressure in the I group of animals decreased, but its changes were lesser than in intact animals due to slowing down of the increase of the right ventricular myocardial contractility and venous return. The latter was the result of severe diminution of the increase of the superior vena cava flow compared with the intact animals, meanwhile the value of the inferior vena cava flow did not change. In the II group animals after vagotomy and intravenous injection of the noripinephrine and angiotensin the sign of the right atrial pressure became negative, i. e. the direction of its shifts changed to the opposite, compared with intact animals. In this case, the changes of the sign of the right atrial pressure was caused by the removal of the reflectory inhibitory vagal influences on the heart, because the values of the right ventricular myocardial contractility and venous return were the same as in intact animals of the group, due to decreasing of the value of the superior vena cava flow and increasing of the shifts of the inferior vena cava flow. The vagotomy alone caused also different changes (decreasing or increasing) of right atrial pressure following increasing of the right ventricular myocardial contractility, meanwhile the changes of the venous return were insignificant. Direct electrical stimulation of both the right and the left vagus nerves caused the increasing of the right atrial pressure and decreasing of the right ventricular myocardial contractility and venous return. Thus we concluded, that different changes of the right atrial pressure in animals following intravenous injection of the pressor vasoactive drugs could be the result of different manifestations of the vagal afferent impulsation, which has influence on the sympathetic tonic discharges on the vessels of the regions of the superior and inferior vena cava, and the vagal reflectory inhibitory influences on the heart.     

Hemodynamic mechanisms of the pulmonary artery pressure and blood flow changes following vasoactive pressor drugs injection

The character and values of changes of the pulmonary and systemic hemodynamics following epinephrine, norepinephrine and angiotensin intravenous injection were studied in acute experiments on the anesthetized cats. After catecholamines injection pulmonary blood flow was always increased, meanwhile pulmonary artery pressure can be elevated (in the most observations) or decreased. In the cases of angiotensin administration the pulmonary blood flow could be augmented or decreased; pulmonary artery pressure had been increased or decreased independently from the character of changes of pulmonary flow. Thus, linear correlation between shifts of the pulmonary artery pressure and pulmonary blood flow had not been revealed. The changes of the pulmonary artery pressure were not correlated with the pulmonary vascular resistance ones; however they had strong relationship with the changes of the left atrial pressure. If the left atrial pressure was decreased the pulmonary artery pressure elevation was less, comparing with its values in experiments, where the left atrial pressure was increased; in the case of depressor shifts of pulmonary artery pressure, the left atrial pressure was also decreased. The character and values of the pulmonary blood flow changes were strongly correlated with the changes of the venous return; however they had no linear correlations with the right and left atrial pressures and pulmonary vascular resistance changes. Thus we concluded, that hemodynanics mechanisms of the pulmonary artery pressure and flow changes following vasoactive pressor drugs injection changes are different.     

Hemodynamics mechanisms of changes in the right atrial pressure following intravenous injection of the depressor drugs

Changes of the right atrial pressure, superior and inferior vena cava flows, right ventricular myocardial contractility (first derivate of right ventricular pressure, dP/dt max) following i.v. injection of acetylcholine, histamine and isoproterenol, were studied in acute experiments on anaesthetized mongrel cats with artificial lung ventilation and opened chest. The right atrial pressure in those cases could be increased (I group of animals) or decreased (II group). In maximal shifts of right atrial pressure following acetylcholine injection, the superior vena cava flow increased but the inferior vena cava flow decreased in equal proportion. When the right ventricular myocardial contractility decreased more than the right atrial pressure was augmented, and when the cardiac negative inotropic effect was weak, the right atrial pressure was reduced. After histamine injection in both groups of animals, right ventricular myocardial contractility was increased on the same level, and changes of the inferior vena cava flow were insignificant. The right atrial pressure was elevated following greater increase of superior vena cava flow. Isoproterenol caused the positive cardiac inotropic effect and augmenting of the superior vena cava flow in both groups of animals. The right atrial pressure was elevated if the inferior vena cava flow increased and, on the other hand, when the inferior vena cava flow decreased the right atrial pressure was reduced. Thus different maximal changes of the right atrial pressure following i.v. injection of acetylcholine, histamine and isoproterenol could be explained by different hemodynamic mechanisms of the interaction between superior and inferior vena cava flow shifts and changes of the right ventricular myocardial contractility.     

Hemodynamic mechanisms of the pulmonary artery pressure and blood flow changes following vasoactive depressor drugs injection

The character and values of changes of the pulmonary hemodynamics and venous return following acetylcholine, histamine and isoproterenol intravenous injection were studied in acute experiments on the anesthetized cats. After depressor drugs injection the character and values of changes of pulmonary artery pressure and flow were different. In 67% cases the pulmonary artery pressure was decreased, and in 33%--it was elevated, meanwhile the pulmonary artery flow was decreased in 48% cases and it was increased in 52%, i.e., in the equal number of observations. Thus, following depressor drugs intravenous injection, hemodynamic mechanisms of the changes of pulmonary artery pressure and flow are different. The character and values of changes of the pulmonary artery pressure are correlated with the changes of pulmonary vascular resistance and are not dependent with the left atrial pressure shifts. The changes of the pulmonary artery blood flow are caused by the changes of the venous return and are not correlated with the changes of the right and left atrial pressure.     

Changes in the venous vessels capacitance in the cat forepaw in response to neurohumoral stimuli

The trend in changes of the cat forepaw vessels' capacity was found to practically not differ from the trend in shifts in the vena cava anterior basin's capacity: in both areas the capacity decreases in response to pressor neurogenic stimuli and decreases or increases under the effects of pressor and depressor humoral stimuli. The data obtained suggest that the trend in shifts of the vena cava anterior basin's capacity under the effects of pressor humoral stimuli mainly depends on the skin-muscular area's vessels, whereas the trend in shifts of the vena cava anterior basin's capacity under the effects of depressor humoral stimuli depends, apparently, on the shifts in the brain vessels' capacity function.     

Experimental cardiac tamponade: correlation of pressure, flow velocity, and echocardiographic changes

Seven episodes of experimental cardiac tamponade were induced in five anesthetized closed-chest dogs. Simultaneous pericardial and intracavitary pressures were synchronized with superior vena caval and transvalvular pulsed-Doppler flow tracings. The earliest indication of tamponade was the development of a negative transmural right atrial pressure that occurred during early ventricular diastole and was associated with echocardiographic evidence of right atrial collapse. This was also associated with reversal of diastolic flow in the superior vena cava and with diminished early diastolic flow velocity across the tricuspid as well as the mitral valve. During more advanced cardiac tamponade, the transmural right atrial pressure became negative during both early and late ventricular diastole as well as during isovolumic ventricular systole. This was associated with a disappearance of early diastolic ventricular filling and right ventricular diastolic collapse as observed on two-dimensional echocardiography. In hypotensive cardiac tamponade (cardiac output diminished by 70%), the decreased transmural right atrial pressure that developed during ventricular systole was accompanied by diminished antegrade flow in the superior vena cava. In advanced and hypotensive tamponade, ventricular filling occurred mainly during atrial contraction.     

Responses of the rat cardiovascular system to substance P,neurotensin and bombesin

The carotid arterial blood pressure and heart rate responses to intravenous injections of substance P, neurotensin and bombesin were compared in anaesthetized rats. In rats anaesthetized with urethane neurotensin produced only a fall in blood pressure but in rats anaesthetized with sodium thiobutabarbitone, the fall was preceded by a transient rise in blood pressure. The reason for the different responses to neurotensin with the two anaesthetics was not investigated. The hypotensive effect of neurotensin observed with both anaesthetics was abolished by mepyramine and therefore appeared to be mediated by action on H₁ receptors either of neurotensin directly or of histamine released. On the other hand, catecholamines might be implicated in the pressor response to neurotensin observed in rats anaesthetized with sodium thiobutabarbitone since it was reduced by phentolamine and hexamethonium. Low doses of substance P produced a depressor response which was not inhibited by the antagonists tested. At higher doses marked tachycardia occurred and the depressor response was less and was often followed by a pressor response. The tachycardia was abolished by propranolol but not by cervical cord section or by hexamethonium. Bombesin produced a pressor response which was unaffected by hexamethonium but was reversed to depressor by phentolamine. This depressor response to bombesin was abolished by propranolol. It was concluded that substance P produced a depressor response by action on its own specific receptors and tachycardia by catecholamine release whereas neurotensin and bombesin produced cardiovascular actions which were mediated entirely by amine release.     

Haemodynamic mechanism of the variety of changes in the right atrial pressure following catecholamines administration

Changes of the right atrial pressure and systemic haemodynamics following action of catecholamines (epinephrine and norepinephrine) were studied in acute experiments on anaesthetised mongrel cats with artificial lung ventilation and opened chest. Maximal changes of the right atrial pressure took place on the 12th-16th second following catecholamine administration. In that case, the atrial pressure could be decreased or increased. At the moment of maximal changes of the right atrial pressure, the venous return and the right ventricular myocardial contractility (the first derivative of the right atrial pressure, dP/dt max) increased more if the right atrial pressure decreased, as compared with the animals whose right atrial pressure augmented. The findings suggest that at the time of the maximal changes of the right atrial pressure following action of catecholamines, there may be a direct connection of the right atrial pressure with interrelation of venous return and the right ventricular contractility. The right atrial pressure, however, is a dependent parameter but it does not determine the venous return.     

ISOLATED ANOMALOUS INFERIOR VENA CAVA CONNECTION TO THE LEFT ATRIUM: REPORT OF A SUCCESSFUL SURGICAL CASE AND REVIEW OF THE LITERATURE

This report describes a rare case of isolated anomalous connection of the inferior vena cava to the left atrium. Patching of a surgically-created atrial septal defect and rerouting of caval drainage ino the right atrium effected a successful correction. This case brings to 18 the total number of reported cases in the literature in which the inferior vena cava was connected to the left atrium.     

HEMIAZYGOS CONTINUATION TO CORONARY SINUS WITH NORMAL LEFT INNOMINATE VEIN

A case is described of absent hepatic segment of the inferior vena cava with hemiazygos continuation and drainage into the coronary sinus with associated atrial septal defect and patent ductus arteriosus. In all previously reported cases of inferior vena caval anomalies with persistent hemiazygos, the hemiazygos joined the homolateral superior vena cava. To our knowledge this is the first case to be reported of a patient who had hemiazygos continuation to the coronary sinus with a normal left innominate vein and a single right superior vena cava.     

Relations between changes of the pulmonary and systemic hemodynamics following neurogenic stimuli

The character and values of changes of the pulmonary and systemic hemodynamics following neurogenic stimuli application on the cardiovascular system were studied in acute experiments on the anesthetized cats. Vagus nerve stimulation reduced the heart rate and decreased myocardial contractility in result, right and left atrial pressure increased, whereas pulmonary pressure and flow, venous return, cardiac output and venous return decreased. Pulmonary pressure reached maximal level and returned to the initial value earlier than the pulmonary flow. On the contrary, pulmonary pressure, following neurogenic pressor stimuli, reached maximal level and returned to the initial value later than the pulmonary flow; the sign of the changes of the pulmonary pressure could be positive or negative, whereas pulmonary flow were always increased. The venous return did not change, and for this reason it could not cause the increasing of pulmonary flow which was elevated following increasing of the heart rate and myocardial contractility. The shifts of the pulmonary pressure were correlated with the pulmonary resistance those, which were increased after the stellate ganglion stimulation and decreased following carotid reflex; they did not change in case of sciatic nerve stimulation. The shifts of the pulmonary pressure did not depended on the decreased right and left atrial pressures. When the pulmonary flow was always increased, the cardiac output following electrical stimulation of the stellate ganglion and sciatic nerve was elevated, and it was decreased following carotid reflex, i. e. linear correlation between these parameters were not found. Pulmonary and systemic arterial pressure changes were more obvious in case of direct neurogenic stimuli application comparing with reflectory ones; in both cases, the positive chrono- and inotropic cardiac effects were similar.     

Participation of the cava vein blood flow in forming the total venous return under influence of different modality stimuli on the circulation system

Participation of the anterior and posterior veins cava in forming the total venous return under pressor and depressor effects, stimulation of depressing foci of the medulla's ventral part, enhancement of pulmonary ventilation, hypoxia, hypothermia, administration of acetylcholine, histamine, corinfar, was shown to depend on the blood flow shift direction in each of the veins cava, dynamics of shifts' development in time, and intensity of the stimulus. In systemic responses, the blood flow shifts in the vena cava anterior much contribute to the total venous return at the maximum of the systemic arterial pressure rise (r = 0.87) whereas contribution of the vena cava posterior is the greatest during a later occurring increase in the venous return (r = 0.84). Along with increase in the stimulus intensity the vena cava anterior's part in forming the venous return becomes more limited whereas that of the vena cava posterior is enhanced.     

Effective vascular compliance of dogs in acute heart failure.

Effective vascular compliance was measured repeatedly in dogs without circulatory arrest utilizing a closed-circuit venous bypass system and constant cardiac output. Compliance, determined by the delta V/delta P relationship at the end of a 1-min infusion of 5% of the circulating volume into the inferior vena cava, was independent of the initial venous pressure, total circulating volume and systemic arterial pressure. It remained constant over a 3 h experimental period at 1.55 plus or minus 0.05 ml (mm Hg)-1-kb-1 body weight. Elevation of mean left atrial pressure and mean pulmonary arterial pressure by gradual aortic constriction was associated with a large and significant reduction in vascular compliance to a value of 1.14 plus or minus 0.06 ml (mm Hg)-1-kg-1 after 2 h. This reduction was independent of the initial venous pressure and total circulating volume but was associated with the changes in left atrial and pulmonary artery pressures and an increase in plasma catecholamine concentrations. The mechanism responsible for the reduction in effective compliance is not clear from the present experiments. Increased circulating catecholamines and sympathetic nerve traffic resulting from baro- and volume receptor stimulation in the vascular tree may be the causative mechanism.     

Plasma alpha natriuretic peptide in cardiac impairment.

Regional plasma alpha human atrial natriuretic peptide concentrations were measured, and their relation to intracardiac pressures assessed, in an unselected series of 45 patients undergoing diagnostic cardiac catheterisation. Arteriovenous gradients in plasma concentrations of alpha human atrial natriuretic peptide were consistent with its cardiac secretion and its clearance by the liver and kidneys. Plasma concentrations of the peptide in the pulmonary artery, aorta, and superior vena cava correlated closely with the mean right atrial and pulmonary arterial pressures, and similar, though weaker, positive relations were seen with the left ventricular end diastolic and pulmonary artery wedge pressures. Concentrations of both atrial natriuretic peptide and renin showed significant inverse relations with serum sodium concentrations. Plasma concentrations of alpha human atrial natriuretic peptide are an additional objective indicator of the severity of haemodynamic compromise in patients with cardiac impairment.     

Conduction left-to-right and right-to-left across the crista terminalis

A line of block between the vena cava and the crista terminalis (CT) region is important for atrial flutter (AFL), but whether it is fixed or functional is controversial. To test the hypothesis that conduction across the CT normally occurs, but when block occurs in this region it is functional, we analyzed atrial activation during right and left atrial pacing (cycle lengths of 500--130 ms), AFL, and atrial fibrillation in 15 dogs with sterile pericarditis and 7 normal dogs. Electrograms from 396 right, left, and septal atrial sites were simultaneously recorded. Activation across the CT occurred during atrial pacing, AFL, and atrial fibrillation. Activation wave fronts from the right to the left atrium and vice versa traveled over several routes, including Bachmann's bundle and inferior to the inferior vena cava, as well as across the CT. In these models, there is no fixed conduction block across the CT, and when block in the CT region occurs, as during AFL, it is functional.     

Implantation of a resynchronization implantable cardioverter defibrillator in a patient with persistent left superior vena cava

Implantation of resynchronization implantable cardioverter defibrillator was performed in a patient with persistent left superior vena cava. A dual coil defibrillation lead was inserted in the right ventricle apex via a small innominate vein. Left ventricular and atrial leads were implanted through persistent left superior vena cava. Left ventricular lead was easily implanted into the postero lateral vein. Pacing thresholds and sensing values were excellent and remained stable at 18 months follow-up.Presence of persistent left superior vena cava generally makes transvenous lead implantation difficult. However when a favorable coronary sinus anatomy is also present, it may facilitate left ventricular lead positioning in the coronary sinus branches.     

Plasma vasopressin and atrial natriuretic factor in response to blood volume changes in the anaesthetized rabbit

The influence of aortic baroreceptors and vagal afferent nerves on the release of immunoreactive vasopressin (iVP) and immunoreactive atrial natriuretic factor (iANF) was examined in anaesthetized rabbits. Changes in plasma concentrations of iVP and iANF, heart rate, mean arterial pressure, and right atrial pressure were measured in response to blood volume changes (+20, +10, -10, -20%). Carotid sinus pressure was maintained at 100 mmHg (1 mmHg = 133.3 Pa), and blood volume changes were performed before and after bilateral vagotomy (VNX) in all experiments. Two experimental groups were studied: rabbits with aortic depressor nerves intact (ADNI) and those with aortic depressor nerves sectioned (ADNX). Mean arterial and right atrial pressures decreased during haemorrhage and increased in response to volume expansion. Plasma iVP concentrations increased with haemorrhage and decreased with volume expansion in the ADNI group. Plasma iANF, however, decreased with haemorrhage and increased during volume expansion in both ADNI and ADNX groups. Vagotomy caused an increase in baseline plasma iANF in the ADNX group. The responses of iANF to blood volume changes were augmented after VNX and ADNX. The results show that neither the aortic baroreceptor nor the vagal afferent input are needed for the iANF response to changes in blood volume, over the range of +/- 20%. In contrast, intact aortic baroreceptors are essential for changes in circulating iVP in this preparation.     

Respiratory effects of pressor and depressor agents in conscious rats

We hypothesized that the respiratory baroreflex in conscious rats is either more transient, or has a higher pressure threshold than in other species. To characterize the effect of arterial pressure changes on respiration in conscious rats, ventilation (V) was measured by the plethysmographic technique during injections, or infusions, of pressor and depressor agents. Bolus injections of angiotensin II (Ang II) or arginine vasopressin (AVP), transiently increased mean arterial pressure (MAP; mean +/- SE) 43+/-6 and 28+/-5 mm Hg (1 mm Hg = 133.3 Pa), respectively, and immediately reduced tidal volume (Vt) and, in the case of AVP, V. In contrast, by 10 min of a sustained elevation of MAP (40+/-3 mm Hg) with infusion of Ang II, Vt, f, and V were not different from control levels. Bolus injection of sodium nitroprusside (SNP) to lower MAP (-28+/-3 mm Hg) immediately increased breathing frequency (f) and V, whereas sustained infusion of SNP to lower MAP (-21+/-3 mm Hg) did not change for V at 10 and 20 min. In conscious rats, both injection and infusion of the pressor agent PE (+40 to 50 mm Hg) stimulated f and V; this contrasted with anesthetized rats where PE inhibited f and V, as reported by others. In conscious rats, respiratory responses associated with baroreflexes adapt rapidly and, in the case of PE, can be overridden by some other mechanism.     

Isolation of persistent left superior vena cava during atrial fibrillation ablation

Persistent left superior vena cava is a rarely seen anomaly but it may be an arrhythmogenic source for paroxysmal atrial fibrillation. Furthermore, the complex anatomicregion between the left superior vena cava and the pulmonary veins may leads to misinterpretation of the pulmonary vein recordings during atrial fibrillation ablation. Approaches that might be helpful to overcome these problems are discussed in this case report.