Changes In Left Atrial Pressure Research Articles

Effects of ritodrine infusion on hemodynamics and lung lymph in awake sheep

The effect of the β-agonist, ritodrine HCl, was studied on cardiac output (CO) and pulmonary lymph flow (Q L) in sheep. Increased CO is associated with an increase in pulmonary Q L in sheep during exercise. Isoproterenol increases CO but has not been shown to increase pulmonary Q L. Ritodrine HCl was chosen because of its association with pulmonary edema when used to halt premature labor in pregnant women. Unanesthetized sheep received an intravenous infusion of ritodrine in increasing doses over 4 h up to a maximum of 6.3 μg/kg/min. Pulmonary pressure increased 2 mmHg after 1 h and returned to baseline by hours 3 and 4 with no change in left atrial pressure or lymph to plasma protein ratio. Pulmonary Q L increased by 61% and CO by 80% at hour 3 of infusion (ritodrine dose 5.4 μg/kg/min) and remained at this level. Pulmonary Q L and CO (normalized to baseline) correlated, r = 0.72, p< 0.001, but there was no correlation between pulmonary Q L and calculated microvascular pressure. Although an increase in pulmonary microvascular endothelium permeability with concurrent pulmonary vasodilation can not be completely ruled out, it appears from this study that β-agonist theray with ritodrine increases pulmonary Q L by a CO related recruitment of microvessels.

Cardiac tamponade in left ventricular dysfunction.

Echocardiographic and hemodynamic data were measured in closed-chest dogs during graded cardiac tamponade (pericardial pressure 5, 10, and 15 mm Hg) before and after production of diffuse ischemic left ventricular dysfunction. Left ventricular dysfunction was produced by intracoronary injection of nonradioactive microspheres (54 +/- 3.9 mm diameter). Changes in left atrial pressure with cardiac tamponade were influenced by coexisting left ventricular dysfunction. Left atrial pressure increased with tamponade and was equal to pericardial pressure before left ventricular dysfunction was produced. However, after left ventricular dysfunction was produced, left atrial pressure was significantly higher than pericardial pressure before tamponade, but it fell toward pericardial pressure when tamponade was produced. Pulsus paradoxus (greater than 10 mm Hg) was present in all animals with cardiac tamponade before left ventricular dysfunction but in only one animal afterward. During each level of tamponade, the inspiratory fall of aortic systolic pressure was greater before than with left ventricular dysfunction. The slope of the linear regression between pericardial pressure and millimeters of mercury of inspiratory fall in aortic systolic pressure was significantly greater before than with left ventricular dysfunction (0.74 +/- 0.12 versus 0.32 +/- 0.12, p less than 0.05). Left ventricular dysfunction caused a leftward and upward shift of the pericardial pressure-volume relation. As a result, right atrial and ventricular collapse occurred with significantly smaller volumes of pericardial fluid after than before left ventricular dysfunction. We conclude that pulsus paradoxus may be absent in cardiac tamponade with coexisting left ventricular dysfunction and unequal filling pressures. Echocardiographic signs of cardiac tamponade may occur with small effusions in the presence of left ventricular dysfunction.

Effect of alteration in loading conditions on both normal and abnormal patterns of left ventricular filling in healthy individuals

Doppler analysis of mitral flow provides a means of analyzing left ventricular (LV) diastolic function. While experimental studies have suggested that changes in left atrial pressure may affect the normal pattern of early diastolic filling, the effect of such changes on abnormal patterns of filling is unknown. Accordingly, the Doppler pattern of LV filling was analyzed in 20 subjects with LV hypertrophy (mean age 59 ± 13 years, ± standard deviation), in 25 healthy normal subjects (29 ± 6 years) and in 11 elderly subjects (68 ± 5 years). All underwent Doppler examination of LV inflow at rest and immediately after postural changes. In all 3 groups, head-down positioning increased early diastolic flow velocity (E) (p < 0.001), and raised the E to late diastolic flow velocity (A) ratio (p < 0.01). However, an abnormal E A ratio never approached a normal resting value. Likewise, although E and the E A ratio decreased significantly in normal subjects with head-up positioning, it did not become abnormal. The magnitude of change in E, A and E A ratio did not differ among the 3 groups in response to postural changes. Thus, alterations of LV loading conditions alter the pattern of LV filling, whether normal or abnormal at baseline. The magnitude of change appears to be independent of the resting flow pattern. Although loading conditions may affect the Doppler pattern of filling, simple changes in venous return do not “normalize” an abnormal pattern, nor do they “abnormalize” a normal pattern.

Doppler echocardiographic-determined changes in left ventricular diastolic filling flow velocity during the lower body positive and negative pressure method

Changes in parameters of left ventricular (LV) diastolic filling flow obtained with Doppler echocardiography during the lower body positive and negative pressure method were analyzed in 15 patients (12 with coronary artery disease and 3 with dilated cardiomyopathy). Lower body pressure was altered at 5 steps (+20, +10, 0, −20 and −40 mm Hg vs atmospheric pressure). Pulmonary capillary wedge pressure measured with a ballon-tipped catheter was changed proportionally with lower body pressure during the procedures (p < 0.01). Mean systemic arterial pressure was changed slightly during lower body positive pressure and negative pressure of −40 mm Hg. Heart rate was almost unchanged except at lower body pressure of −40 mm Hg. The peak velocity of LV early diastolic filling flow was changed with pulmonary capillary wedge pressure in an almost parallel fashion during the procedures (p < 0.01). The peak velocity of LV late diastolic filling flow showed smaller changes than that of early diastolic filling flow. Changes in pulmonary capillary wedge pressure correlated positively with changes in the peak velocity of LV early diastolic filling flow (r = 0.759, p < 0.01), but not with changes in the peak velocity of LV late diastolic filling flow (r = 0.039, not significant) during lower body negative pressure of −20 mm Hg. These data suggest that left atrial pressure is one of the important determinants of LV early diastolic filling flow in this acute clinical setting and that LV late diastolic filling flow is less sensitive to changes in left atrial pressure than LV early diastolic filling flow.

Norepinephrine-induced atriopeptin release in conscious dogs is mediated by alterations in atrial pressure

This study was designed to determine whether the increase in atriopeptin secretion induced by an intravenous infusion of norepinephrine is mediated directly by adrenergic receptor stimulation or indirectly by the associated increase in atrial pressure. Norepinephrine was infused at 0.5 μg·kg t-1 ·min −1 for 30 min into both sham-operated (intact) and cardiac-denervated conscious dogs. The infusion increased mean arterial pressure all dogs. On the other hand, left atrial pressure increased from 5.0±0.7 to 9.6±1.6 mmHg (p < 0.01) in intact dogs, but decreased from 5.5±1.0 to 2.0±0.7(p < 0.01) in cardiac-denervated dogs. Right atrial pressure changes followed similar trends, but were not significant in the intact group. Plasma atriopeptin increased from 73±12 to 110±18 pg/ml (p < 0.01) as left atrial pressure increased in intact dogs and decreased from 79±15 to 54±10 pg/ml(p < 0.01) as left atrial pressure decreased in cardiac-denervated dogs. The changes in plasma atriopeptin correlated closely with the changes in left atrial pressure (r = 0.941, p < 0.001) and to a lesser extentent with the changes in right atrial pressure (r = 0.413, p < 0.05). These results suggest that the change in plasma atriopeptin induced by infusion of norepinephrine into conscious dogs in mediated by the ocncomitant change in atrial pressures.

Pulmonary venous flow determined by Doppler echocardiography in mitral stenosis

Recent studies have shown that pulmonary venous flow is normally biphasic. Both phases depend on changes in left atrial pressure that occur during the cardiac cycle. 1–3 The first phase corresponds to ventricular systole and is dependent on ventricular contraction and on a timed relaxation of the left atrium. The second phase occurs during diastole and follows the reduction in atrial pressure during the rapid transmitral flow and ventricular filling. In mitral stenosis (MS), flow rate across the mitral valve is reduced, as is the rate of left atrial pressure decay and left ventricular pressure rise. 4 These changes in left atrial hemodynamics may affect left atrial filling from the pulmonary veins. Moreover, many patients with MS have atrial fibrillation. This arrythmia results in a reduced systolic (J) phase of pulmonary venous flow. 1,5 The present study examines the pattern of pulmonary venous flow velocity in patients with MS.

Impaired atrial receptor modulation or renal nerve activity in dogs with chronic volume overload1

Left atrial receptors with vagal afferents are reset and become less sensitive in dogs with chronic high output congestive heart failure (Zucker et al J Clin Invst 1977;60:323). We determined if the normal reflex inhibition of renal sympathetic nerve activity (RNA) which occurs in response to left atrial distension is altered in dogs with chronic volume overload produced by an aorto-vena caval fistula (AVF). In addition, we examined the ability of the arterial baroreflex to alter RNA. In normal dogs, left atrial distension decreased RNA by 6.8 +/- 1.8% per mmHg change in left atrial pressure (LAP). After carotid sinus denervation (CSD), this inhibition was increased to 10.9 +/- 1.4% per mmHg change in RNA in response to left atrial distension. Vagotomy completely abolished any change in RNA in response to left atrial distension. In contrast, dogs with chronic AVF's demonstrated an increase in RNA in response to left atrial distension by 4.5 +/- 3.9% per mmHg change in LAP. The response of the AVF dogs was significantly different from the normal dogs (P less than 0.005). This was also the case after CSD. Loading and unloading of the arterial baroreceptors with norepinephrine and nitroprusside demonstrated that the modulation of RNA by arterial baroreceptors was similar in AVF dogs compared with normal dogs. The present study demonstrates that chronic volume overload results in a decrease in the peripheral sympathetic inhibitory effects of left atrial receptor stimulation at a time when arterial baroreceptor function is preserved.

Pulmonary venous flow pattern--its relationship to cardiac dynamics. A pulsed Doppler echocardiographic study.

We studied the physiology of pulmonary venous flow in 13 normal subjects and five patients with atrial rhythm disorders and atrioventricular conduction disturbances with pulsed Doppler and two-dimensional echocardiography. The left atrium, mitral valve, and pulmonary venous ostia were visualized through the apical four-chamber view. Mitral and pulmonary venous flows were obtained by placing the Doppler sample volume at the appropriate orifice. Pulmonary venous flow was biphasic: a rapid filling wave was observed during systole when the mitral valve was closed; a second wave was observed in diastole during the rapid ventricular filling phase of mitral flow, but was significantly delayed. In patients without atrial contraction (atrial fibrillation and sinoatrial standstill), the initial rapid filling was greatly diminished and only the second diastolic wave appeared to contribute to left atrial filling. In patients with high-grade atrioventricular block, each atrial contraction was followed by a surge in flow from the pulmonary veins. These results are consistent with data obtained from invasive measurements in both dogs and man, and confirm the validity of the use of pulsed Doppler echocardiography in the study of pulmonary venous flow. We suggest that pulmonary venous flow is influenced by dynamic changes in left atrial pressure created by contraction and relaxation of the atrium and ventricle. The initial peak in pulmonary venous flow occurs with atrial relaxation simultaneously with the reduction of left atrial pressure, and the second peak occurs with left ventricular relaxation and rapid transmitral filling of the ventricle.

Pulmonary lymphatic flow alterations during intracranial hypertension in sheep.

The role of intracranial hypertension in the genesis of neurogenic pulmonary edema was studied in 25 sheep; cardiopulmonary hemodynamics (aortic, pulmonary arterial, and left atrial pressures and cardiac output) and fluid and protein movement across the pulmonary capillary bed (efferent pulmonary lymph flow and lymph/plasma protein ratio) were monitored. Only when intracranial pressure was raised to equal the baseline mean systemic pressure (75 to 120 Torr) did we observe the expected Cushing response of increased aortic pressure, or any alteration in pulmonary hemodynamics or fluid movement. When pulmonary changes did occur, they included an increase in pulmonary arterial pressure of between 5 and 15 Torr without any notable rise in left atrial pressure, and a sustained doubling of the pulmonary lymph flow with no dilution of the lymph/plasma protein ratio. In 3 additional animals cerebral ischemia alone produced an elevation in systemic pressure (74 Torr over baseline) without change in pulmonary arterial pressure, left atrial pressure, or pulmonary lymph flow. Thus, intracranial hypertension and ischemia both affect systemic pressure, but only the elevated intracranial pressure is followed by changes in the pulmonary circuit. We suggest that these changes in pulmonary vascular pressure, independent of changes in left atrial pressure, produce increased pulmonary transcapillary fluid flux that may result in neurogenic pulmonary edema.

Pulmonary edema formation with myocardial infarction and left atrial hypertension: intravascular and extravascular pulmonary fluid volumes.

The response of pulmonary blood volume (PBV) and extravascular lung water (EVLW) was examined by indicator-dilution techniques in 14 "open chest" dogs, seven that underwent coronary occlusion (group 2) and seven that served as controls (group 1). Data were obtained in a control stage (control stage 1) 45 min after coronary ligation (control stage 2), and 90 min after the left atrial pressure had been increased to approximately 35 mm Hg with a left atrial balloon. In group 2 animals, EVLW increased after coronary ligation without a marked change in left atrial pressure (6.9 +/- 0.4 to 8.2 +/- 0.5 ml/kg mean +/- SD; p less than .05) and increased to 20.1 +/- 1.4 ml/kg after the production of left atrial hypertension (p less than .005 vs control and vs coronary ligation). In the control dogs, EVLW was unchanged 45 min after the initial data had been collected (7.1 +/- 0.7 to 7.0 +/- 0.8 ml/kg). After the production of left atrial hypertension in these dogs, EVLW rose (14.8 +/- 1.2 ml/kg; p less than .005 vs control stage 1 and control stage 2, p less than .01 vs group 2 dogs). PBV did not change significantly with ligation and increased similarly in both groups during left atrial hypertension. We conclude that coronary ligation can increase EVLW, independent of microvascular hydrostatic pressure. During the production of left atrial hypertension there was greater transcapillary fluid flux in group 2 dogs at matched levels of left atrial pressure elevation. This may be due to an alteration in the permeability of the pulmonary capillary membrane during myocardial infarction and provides a partial explanation for the occasional disparity between left heart dynamics and the chest radiograph in acute myocardial infarction.

Intravascular and extravascular pulmonary fluid volumes II. Response to rapid increases in left atrial pressure and the theoretical implications for pulmonary radiographic and radionuclide imaging.

Slutsky RA, Higgins CB. Intravascular and extravascular pulmonary fluid volumes II. Response to rapid increases in left atrial pressure and the theoretical implications for pulmonary radiographic and radionuclide imaging. The response of intravascular (pulmonary blood volume, PBV) and extravascular (extravascular lung water, EVLW) pulmonary fluid volume was examined using double indicator techniques (thermal-green dye) in 15 open-chest anesthetized dogs during the production of rapid left atrial (LA) hypertension by a LA balloon. In five dogs, the LA pressure was quickly increased from 1.0 ± 1.1 mm Hg to 10.6 ± 2.4 mm Hg (P < .01), associated with an increase in PBV (164 ± 76 ml to 223 ± 128 ml, P < .01) and an insignificant increase in EVLW (168 ± 84 ml to 181 ± 89 ml, P = not significant). In five dogs, the LA pressure was quickly increased from 1 ± 1 mm Hg to 17.3 ± 2.1 mm Hg (P < .01), with a marked increase in PBV (174.3 ± 81.1 ml to 262 ± 127 ml, P < .05) and a small change in EVLW (178 ± 101 to 204 ± 74 ml, P = not significant). In five dogs, LA pressure was increased from 1.0 ± 0.2 mm Hg to 32.2 ± 2.1 mm Hg (P < .001). In these dogs, PBV rose from 206 ± 99 ml to 342.8 ± 12.1 ml (P < .005, +66% over control), while the EVLW also rose significantly (230 ± 72 ml to 270 ± 69, P < .05) though slightly. With large rapid pressure rises, PBV rose in proportionately greater increments (δLA pressure 9.6 ± 1.4 mm Hg, δPBV 59 ± 8 ml; δLA pressure 16.4 ± 1.7 mm Hg,δPBV 87.7 ± 14.6; and δLA pressures of 31.3 ± 2.1 mm Hg, δPBV of 136.8 ± 31.2 ml). This study suggests that acute changes in LA pressure cause immediate increases in PBV and would presumably produce radiographically detectable pulmonary venous congestion. On the other hand, elevation in LA pressure even to levels above 30 mm Hg causes only a small immediate increase in EVLW. Because fluid transudes slowly into the extravascular space, prolonged elevation in LA pressure must occur before radioisotopes that measure EVLW could identify congestion. This study provides the physiologic basis for the proposed acute phase lag between pulmonary capillary wedge pressure and radiographic signs of pulmonary edema in acute cardiac disease states.

Mathematical simulation of the body fluid regulating system in dog.

Abstract A mathematical model of body fluid volume and osmolality regulation was developed which incorporated the major nonlinearities of fluid assimilation, exchange, distribution and excretion. The non-linear differential equations define compartmental material balances for water, urea, sodium, protein and antidiuretic hormone (ADH). The parameters of these equations were calculated using analytical solutions and available steady-state experimental data. The model was used to simulate the renal response to five input forcings: (1) intraesophageal water infusion; (2) water ingestion; (3) intravenous ADH injection; (4) intravenous water infusion; and (5) intermittent water loading. The model yielded continuous simulation curves which agreed reasonably well with the available transient and steady-state experimental data. The model predicted that stimulating volume receptors via changes in left atrial pressure accounts for only 15–20% of changes in ADH secretion rate, whereas stimulation of the osmotic receptors via changes in plasma osmolality accounts for the remaining 80–85% of changes. Thus, it appears that regulation of ADH secretion is largely dependent upon plasma osmolality during forcings which do not appreciably alter the cardiovascular blood volume.

Blood flow in pulmonary veins: II The influence of events transmitted from the right and left sides of the heart

The wave form of blood flow in the large extra parenchymal pulmonary veins has an inverse relationship to the pressure wave form in the left atrium during each cardiac cycle. However, when vein flow from the lungs is separated from the left atrium by diverting it into a constant pressure reservoir, its wave form then resembles a lung capillary flow pulse, though delayed from it in time and reduced in ampliture. The pulsatility of flow in pulmonary veins separated from the left atrium is further reduced when transcapillary pressure is elevated by lung inflation. However, in the intact state, the relation between the pattern of pulmonary vein flow and left atrial pressure remains unaffected by lung inflation. It is postulated that the thin walled extraperenchymal pulmonary veins together behave as a collapsible reservoir which enables outflow from them to be determined by changes in left atrial pressure, in spite of variations of pulsatile flow into them from the lungs.

Changes in the sensitivity of left atrial receptors following reversal of heart failure

Recordings were made from left atrial type B receptors in six mongrel dogs after recovery from the cardiac effects of a chronic AV fistula. All animals showed hemodynamic and clinical signs of congestive heart failure after 44.5 +/- 3.6 days with a patent Dacron shunt between the aorta and inferior vena cava below the level of the renal arteries. The stimulus-response curves of the left atrial stretch receptors (change in spikes/cardiac cycle or in spikes/minute vs. change in left atrial pressure) after 45.2 +/- 7.2 days of shunt closure were similar to those seen in sham-operated dogs from a previous study. However, the slope of the stimulus-response curve of the dogs in which the AV fistula was closed was significantly greater than the slope of the curve from the AV fistula dogs with heart failure. Radiographs indicated that after shunt closure, cardiac dilatation had regressed. This study incidates that a decrease in the sensitivity of left atrial receptors in dogs with congestive heart failure is a reversible phenomenon and that the initial depression is most likely related to the concomitant cardiac dilatation that accompanies the failure state.

Response of supraoptic neurosecretory cells to changes in left atrial distension

Acute studies were conducted in cats to determine the effects of small changes in left atrial pressure (LAP) on the activity of antidromically identified neurons in the supraoptic nucleus (SON). Inflation of left atrial balloons reproducibly altered the frequency of 15% of the SON neurons. More than half of these increased frequency, probably due to a simultaneous increase in arterial pressure. In a second series, the firing rates of 20% of the SON neurons tested were inversely related to changes in LAP produced by pumping blood into or out of the left atrium. A third series of experiments were conducted in which the left atrium was directly stretched by pulling on a suture placed in the atrial wall in addition to one of the above methods of changing LAP. Directly stretching the left atrium inhibited over 70% of the SON neurons; this included all the neurons that responded to changes in LAP. The results suggest that these SON neurons have differential sensitivities to inputs from left atrial receptors.

Reflex Inhibition of Renal Sympathetic Nerve Activity during Myocardial Ischemia Mediated by Left Ventricular Receptors with Vagal Afferents in Dogs

The major goal of this investigation was to determine if activation of cardiac receptors during coronary artery occlusion could inhibit efferent renal sympathetic nerve activity. In nine chloralose anesthetized dogs with only carotid (n = 3) or with sinoaortic (n = 6) baroreceptors operative, anterior descending coronary artery (LAD) occlusion resulted in a small decrease in mean arterial pressure (-9.8+/-5.1 mm Hg, NS) and in a significant (P < 0.05) increase in renal nerve activity (24.0+/-4.1%). In these dogs, circumflex coronary artery (Cx) occlusion resulted in greater hypotension (-18.4+/-4.0 mm Hg), and yet no change (1.1+/-9%) in renal nerve activity was noted. Changes in left atrial pressure during LAD and Cx occlusion were not different. In seven dogs with carotid sinus denervation, coronary occlusions resulted in decreases both in arterial pressure and in renal nerve activity which were consistently greater during Cx occlusion. The responses to coronary occlusion in six dogs after sinoaortic deafferentation were similar to those observed with only carotid sinuses denervated. In all experiments, vagotomy abolished the difference in the blood pressure responses and the decreases in renal sympathetic nerve activity during Cx occlusion. Vagotomy also abolished the decrease in nerve activity during LAD occlusion in dogs with carotid or sinoaortic denervation. These data show that Cx occlusion and, to a lesser degree, LAD occlusion resulted in reflex withdrawal of renal sympathetic nerve activity mediated by left ventricular receptors with vagal afferents. The reflex withdrawal of renal nerve activity during Cx occlusion occurred in spite of hypotension and the presence of functioning sinoaortic baroreceptors.

Pulmonary vascular effects of fat emulsion infusion in unanesthetized sheep. Prevention by indomethacin.

Pulmonary diffusing capacity and arterial blood Po(2) decrease in humans when 10% fat emulsion is infused. To study its effects on the pulmonary circulation and lung fluid balance, we infused 0.25 g/kg x h of a 10% fat emulsion (Intralipid, Cutter Laboratories, Inc., Berkeley, Calif.) into an awake sheep lung lymph preparation. The emulsion caused a sustained increase in pulmonary artery pressure to approximately twice base line with little change in left atrial pressure. Pa(O2) decreased an average 13 torr and lung lymph flow increased two- to threefold. Lymph/plasma total protein concentration fell as lymph flow increased; the magnitude of the lymph/plasma protein decrease was similar to that reported previously when lung vascular pressures were mechanically elevated. Heparin infusion (loading dose = 4,000 U, maintenance dose = 2,000 U/h) cleared the serum of triglycerides but did not alter the response to fat emulsion. Indomethacin infusion (loading dose = 5 mg/kg, maintenance dose = 3 mg/kg x h) blocked the rise in pulmonary artery pressure, the increase in lung lymph flow, and the fall in Pa(O2). Neither extravascular lung water nor [(14)C]urea lung vascular permeability surface area products were altered by fat emulsion infusion. We conclude that fat emulsion infusion in sheep increases lung microvascular filtration by increasing vascular pressures, but has no effect on vascular permeability. Since the effects are blocked by indomethacin, they may be prostaglandin mediated.

The effect of Swan-Ganz catheter height on the wedge pressure-left atrial pressure relationships in edema during positive-pressure ventilation.

We have studied the effect of the ventrical height of the pulmonary wedge catheter in the lung on the pulmonary wedge pressure-left atrial relationship during positive end-expiratory pressure ventilation in oleic acid-induced pulmonary edema. Pulmonary wedge catheters were placed above and below the left atrium in normal dogs and in dogs with oleic acid-induced edema. Wedge pressure and left atrial pressure were measured simultaneously during positive end-expiratory pressure ventilation (range, 0 to 30 cm H2O positive end-expiratory pressure). Pulmonary wedge catheters below the left atrium correctly recorded left atrial pressure and change in left atrial pressure at all positive end-expiratory pressures studied. Pulmonary wedge catheters above the atrium consistently recorded pressures higher than the normal left atrial pressure. They did not correctly respond to increases in left atrial pressure until it was increased to a value higher than the initial upper pulmonary wedge pressure. Pulmonary arterial catheters, when properly placed, should be reliable indicators of left atrial pressure during positive-pressure ventilation in normal and edematous lungs.

Influence of elevated pulmonary vascular resistance on the relationship between central venous pressure and pulmonary artery occluded pressure following cardiopulmonary bypass.

This study has demonstrated that CVP measurement is an unreliable index of left ventricular filling pressure in unselected patients undergoing A-C bypass procedures. The influence of altered PVR on the disparity between right and left ventricular filling pressures is not of prime importance. The inconsistent relationship between CVP and PAo is primarily a result of ventricular dysfunction and not altered PVR. This suggests that following A-C bypass surgery patients cannot be grouped with respect to altered PVR as the variable which determines whether CVP will be a reliable guide to changes in left atrial pressure. Routine use of Swan-Ganz catheters would improve the precision of monitoring and fluid administration in all patients following CPB. However, it would also increase the cost and complexity of routine care and add a very low incidence of complications to all patients having cardiac surgery. At present, we monitor high risk patients from the time of surgery and advocate early insertion of Swan-Ganz catheters in low risk patients if they are not responding to appropriate management.

The mechanism of adaptation of left atrial stretch receptors in dogs with chronic congestive heart failure.

Chronic congestive heart failure (CHF) was induced in dogs by the construction of an aorto-caval fistula below the level of the renal arteries. Aorto-caval fistula dogs showed signs of CHF which included ascites, hind limb edema, and pulmonary congestion. Ventricular catheterization indicated a significantly higher left ventricular end diastolic pressure and lower maximum velocity of left ventricular pressure development/left ventricular end diastolic pressure in CHF dogs when compared to sham-operated controls. Heart weight/body weight ratios were significantly higher in CHF dogs. Electrophysiological recordings from medullated left atrial type B receptors from the cervical vagus indicated a depressed sensitivity of these receptors in CHF dogs when compared to sham-operated control dogs. For any given change in left atrial pressure, the discharge of left atrial receptors was significantly reduced in CHF dogs compared with sham-operated controls. The mechanism for this depressed sensitivity was investigated. Sonomicrometry of the left atrial appendage indicated a decreased compliance of the left atrial appendage in the dogs with chronic CHF. In addition, microscope examination of the complex unencapsulated receptor endings taken from the left atrial endocardium indicated a marked alteration in receptor morphology. A loss of the end arborization was the most typical finding. It is concluded that chronic CHF brought about by an aorto-caval fistula results in a depressed left atrial stretch receptor response and that both decreased left atrial compliance and structural alterations in the receptor endings may account for this depressed sensitivity.