Pulsus paradoxus in asthmatic children.

Pulsus paradoxus is a useful physical sign in the assessment of the severity of asthma in adults. Whether this is also true for asthmatic children was determined by measuring respiratory fluctuations in systolic blood pressure during attacks of asthma in 24 children. A decrease in systolic pressure during inspiration exceeding 15 mm Hg was found only when the 1-second forced expiratory volume was less tha 60 percent of the predicted value. There was a highly significant (P smaller than 0.001) correlation between the degree of pulsus paradoxus and the severity of airway obstruction. In nonasthmatic children the systolic pressure was found to fluctuate by as much as 7 mm Hg during the respiratory cycle. It is concluded that, as in adults, the presence of pulsus paradoxus (larger than or equal to 15 mm Hg) in children indicates that their asthma is very severe.     

Relation between pulsus paradoxus and pulmonary function in patients with chronic airways obstruction.

The relation of pulsus paradoxus to chronic, stable obstructive disease of the airways has not previously been described. Pulsus paradoxus was observed in 66% of 68 patients with such disease but in none of 14 healthy individuals. There was a significant correlation between the degree of pulsus paradoxus and the forced expiratory volume in 1 second (FEV1) in the subgroup of patients with bronchial asthma but not in the subgroup with chronic bronchitis or emphysema, or both. There was no correlation between the degree of pulsus paradoxus and the degree of hyperinflation in either group. Hence factors other than hyperinflation contribute importantly to the decrease in systolic pressure that occurs at full inflation of the lungs.     

Effect of lung inflation on lung blood volume and pulmonary venous flow

Phasic changes in lung blood volume (LBV) during the respiratory cycle may play an important role in the genesis of the respiratory wave in arterial pressure, or pulsus paradoxus. To better understand the effects of lung inflation on LBV, we studied the effect of changes in transpulmonary pressure (delta Ptp) on pulmonary venous flow (Qv) in eight isolated canine lungs with constant inflow. Inflation when the zone 2 condition was predominant resulted in transient decreases in Qv associated with increases in LBV. In contrast, inflation when the zone 3 condition was predominant resulted in transient increases in Qv associated with decreases in LBV. These findings are consistent with a model of the pulmonary vasculature that consists of alveolar and extra-alveolar vessels. Blood may be expelled from alveolar vessels but is retained in extra-alveolar vessels with each inflation. The net effect on LBV and thus on Qv is dependent on the zone conditions that predominate during inflation, with alveolar or extra-alveolar effects being greater when the zone 3 or zone 2 conditions predominate, respectively. Lung inflation may therefore result in either transiently augmented or diminished Qv. Phasic changes in left ventricular preload may therefore depend on the zone conditions of the lungs during the respiratory cycle. This may be an important modulator of respiratory variations in cardiac output and blood pressure.     

Transmural pressure in the right atrium during positive pressure respiration in cats

The influence of continuous positive pressure breathing (cm H2O) on the breathing mechanics, central venous pressure, and transmural pressure in the right atrium, were studied in anaesthetised cats separately during inspiration and expiration. It's shown that hemodynamics effects are directly connected with the influence of increased intrathoracic pressure during whole breathing cycles in contrast with the phase changes in natural expiration and inspiration. The inversion of relation of intrathoracic and central venous pressure due to displacement of the mechanical respiratory characteristics became the factors defining the fall of the right atrium filling pressure.     

Images in cardiovascular medicine: Transkei heart

A 16-year-old student from the rural Eastern Cape (former Transkei) was referred to Capetown for cardiovascular evaluation because of a four-month history of progressive dyspnoea and cardiomegaly reported on the chest-X ray. At physical assessment he appeared chronically ill, the blood pressure was 110/ 70 mmHg, the resting pulse rate 114 beats/minute, regular and equal, with pulsus paradoxus of 14 mmHg, and the central venous pressure was raised with a positive Kussmaul’s sign. His lungs were clear, the heart sounds muffled, without a pericardial rub or knock, and the liver was palpable 2 cm below the costal margin.     

Using a human cardiovascular-respiratory model to characterize cardiac tamponade and pulsus paradoxus

Background  

Cardiac tamponade is a condition whereby fluid accumulation in the pericardial sac surrounding the heart causes elevation and equilibration of pericardial and cardiac chamber pressures, reduced cardiac output, changes in hemodynamics, partial chamber collapse, pulsus paradoxus, and arterio-venous acid-base disparity. Our large-scale model of the human cardiovascular-respiratory system (H-CRS) is employed to study mechanisms underlying cardiac tamponade and pulsus paradoxus. The model integrates hemodynamics, whole-body gas exchange, and autonomic nervous system control to simulate pressure, volume, and blood flow.     

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.     

Understanding Guyton's venous return curves

Based on observations that as cardiac output (as determined by an artificial pump) was experimentally increased the right atrial pressure decreased, Arthur Guyton and coworkers proposed an interpretation that right atrial pressure represents a back pressure restricting venous return (equal to cardiac output in steady state). The idea that right atrial pressure is a back pressure limiting cardiac output and the associated idea that "venous recoil" does work to produce flow have confused physiologists and clinicians for decades because Guyton's interpretation interchanges independent and dependent variables. Here Guyton's model and data are reanalyzed to clarify the role of arterial and right atrial pressures and cardiac output and to clearly delineate that cardiac output is the independent (causal) variable in the experiments. Guyton's original mathematical model is used with his data to show that a simultaneous increase in arterial pressure and decrease in right atrial pressure with increasing cardiac output is due to a blood volume shift into the systemic arterial circulation from the systemic venous circulation. This is because Guyton's model assumes a constant blood volume in the systemic circulation. The increase in right atrial pressure observed when cardiac output decreases in a closed circulation with constant resistance and capacitance is due to the redistribution of blood volume and not because right atrial pressure limits venous return. Because Guyton's venous return curves have generated much confusion and little clarity, we suggest that the concept and previous interpretations of venous return be removed from educational materials.     

Extracorporeal circulation in the isolated in situ lamb placenta: hemodynamic characteristics.

Decreased placental perfusion and respiratory gas exchange have been observed after experimental fetal cardiopulmonary bypass (CPB). To better characterize placental hemodynamics during CPB, seven isolated in situ lamb placentas were placed on a CPB circuit by use of umbilical arterial and venous cannulation. Measures were taken to simulate normal placental hemodynamics. Perfusion flow rates were varied from 15 to 300 ml.min-1.kg fetal wt-1 during normothermia and hypothermia. Placental vascular resistance (PVR) remained constant when perfusion pressure and flow were varied above 40 mmHg and 150 ml.min-1.kg-1, respectively. Below these values, PVR varied inversely. This increase in PVR was more marked when CPB was performed with hypothermia than with normothermia. The clinical implication is that decreased placental flow and pressure on CPB may lead to a vicious cycle, resulting in further impairment of placental perfusion and respiratory gas exchange. Hypothermia promotes this impairment.     

Parasympathetic control of the heart. I. An interventriculo-septal ganglion is the major source of the vagal intracardiac innervation of the ventricles.

The locations, projections, and functions of the intracardiac ganglia are incompletely understood. Immunocytochemical labeling with the general neuronal marker protein gene product 9.5 (PGP 9.5) was used to determine the distribution of intracardiac neurons throughout the cat atria and ventricles. Fluorescence microscopy was used to determine the number of neurons within these ganglia. There are eight regions of the cat heart that contain intracardiac ganglia. The numbers of neurons found within these intracardiac ganglia vary dramatically. The total number of neurons found in the heart (6,274 +/- 1,061) is almost evenly divided between the atria and the ventricles. The largest ganglion is found in the interventricular septum (IVS). Retrogradely labeled fluorescent tracer studies indicated that the vagal intracardiac innervation of the anterior surface of the right ventricle originates predominantly in the IVS ganglion. A cranioventricular (CV) ganglion was retrogradely labeled from the anterior surface of the left ventricle but not from the anterior surface of the right ventricle. These new neuroanatomic data support the prior physiological hypothesis that the CV ganglion in the cat exerts a negative inotropic effect on the left ventricle. A total of three separate intracardiac ganglia innervate the left ventricle, i.e., the CV, IVS, and a second left ventricular (LV2) ganglion. However, the IVS ganglion provides the major source of innervation to both the left and right ventricles. This dual innervation pattern may help to coordinate or segregate vagal effects on left and right ventricular performance.     

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.     

Effects of static and fluctuating airway pressure on intact pulmonary circulation

The direct effects on the pulmonary circulation of static and fluctuation airway pressure were compared in intact close-chest infant lambs with reactive pulmonary vasculature under alpha-chloralose anesthesia. A preparation developed to permit independent ventilation of right and left lungs and independent measurement of right and left lung blood flow was employed to separate direct from indirect effects of unilateral airway pressure changes on pulmonary vascular resistance (PVR). Both static and fluctuating unilateral airway pressure interventions directly elevated ipsilateral PVR. For purposes of comparison mean alveolar pressure (PA) was estimated for both static and fluctuating trials. Fluctuating interventions increased PVR more than did static trials at comparable levels of PA. Substantially less PA was needed to double ipsilateral PVR by fluctuating than by static interventions (16 vs. 26 mmHg, respectively). These data indicate that, in the intact animal with reactive pulmonary vasculature, both PA and the waveform of airway pressure applied can influence PVR.     

Dynamic components of interrelation among the parameters of heart preload, venous return and central venous pressure

In acute experiments on cats, in applying of original methodical approach--control of systemic circulation by the aid of computerized negative feedback loop changing the volume of circulating blood (method of biological feedback)--first were experimentally measured and analyzed the dynamic characteristics of relationship between central venous pressure and venous return of blood to the right heart. The following positions are offered and validated in the work. (1) It is shown that the passive component (mechanical compliance) is more important than active one (active myogenic component) in the small circle of circulation being compared to large one. (2) Venous return plays the leading role in forming the shifts of central venous pressure directly during developing of the transition processes of systemic circulation caused by the norepinephrine injection and the linear type of this link is proved directly during the development of the cardiovascular shift. (3) The dynamic characteristics of relationship between venous return and central venous pressure during the geodynamical reaction caused by the shifts of intravascular blood volume are experimentally measured and mathematically analyzed. It is revealed that dynamic summands of this link may overbalance the static ones known before in influence on the total shifts in developing of the systemic reaction of circulation and this influence increases when the velocity of changes in studied parameters of circulation becomes more.     

Sildenafil is more selective pulmonary vasodilator than prostaglandin E1 in patients with pulmonary hypertension due to heart failure

In some patients, heart failure (HF) is associated with increased pulmonary vascular resistance (PVR). The magnitude and the reversibility of PVR elevation affect the HF management. Sildenafil has been recently recognized as potent PVR-lowering drug in HF. The aim of the study was to compare hemodynamic effects and pulmonary selectivity of sildenafil to prostaglandin E(1) (PGE(1)). Right-heart catheterization was performed in 13 euvolemic advanced HF patients with elevated PVR (6.3+/-2 Wood's units). Hemodynamic parameters were measured at the baseline, during i.v. infusion of PGE1 (alprostadil 200 ng · kg(-1) · min(-1)) and after 40 mg oral dose of sildenafil. Both drugs similarly reduced systemic vascular resistance (SVR), but sildenafil had higher effect on PVR (-28 % vs. -49 %, p = 0.05) and transpulmonary pressure gradient than PGE(1). The PVR/SVR ratio--an index of pulmonary selectivity, did not change after PGE(1) (p = 0.7) but it decreased by -32 % (p = 0.004) after sildenafil. Both drugs similarly reduced pulmonary artery mean and wedge pressures and increased cardiac index (+27 % and +28 %). Sildenafil led more often to transplant-acceptable PVR while causing smaller drop of mean systemic pressure than PGE(1). In conclusion, vasodilatatory effects of sildenafil in patients with heart failure are more pronounced in pulmonary than in systemic circulation.     

Effect of NO synthase inhibition on cardiovascular and pulmonary dysfunction in a porcine short-term model of endotoxic shock

In a porcine model of endotoxic shock, we evaluated the circulatory and respiratory effects of NO synthase (NOS) blockade. Twenty anaesthetised pigs were divided into three groups and studied for 240 min after induction of endotoxic shock with lipopolysaccharides of Escherichia coli (LPS). After 180 min of endotoxic shock, one group (n = 6) received aminoguanidine, another group (n = 6) received N(G)-nitro-L -arginine methyl ester (L -NAME) and a third group (n = 8) received only LPS. A sham group (n = 3) was also studied. LPS decreased systemic arterial pressure and cardiac output (CO) and increased mean pulmonary arterial pressure (MPAP), pulmonary vascular resistance (PVR) and heart rate. Significant changes were also observed in compliance (-18.4%) and resistance (+33.6%) of the respiratory system. Aminoguanidine did not modify LPS-dependent effects, while, after L -NAME, a significant increase in MPAP, PVR and SVR and a decrease in CO were observed. In conclusion, aminoguanidine does not play a significant cardiocirculatory and pulmonary role in the short-term dysfunction of endotoxic shock, while L -NAME has a detrimental effect on haemodynamics, suggesting a protective role of constitutive NO production at vascular level during the early stages of endotoxaemia.     

Volume loading reduces pulmonary vascular resistance in ventilated animals with acute lung injury: evaluation of RV afterload

During mechanical ventilation, increased pulmonary vascular resistance (PVR) may decrease right ventricular (RV) performance. We hypothesized that volume loading, by reducing PVR, and, therefore, RV afterload, can limit this effect. Deep anesthesia was induced in 16 mongrel dogs (8 oleic acid-induced acute lung injury and 8 controls). We measured ventricular pressures, dimensions, and stroke volumes during positive end-expiratory pressures of 0, 6, 12, and 18 cmH(2)O at three left ventricular (LV) end-diastolic pressures (5, 12, and 18 mmHg). Oleic acid infusion (0.07 ml/kg) increased PVR and reduced respiratory system compliance (P < 0.05). With positive end-expiratory pressure, PVR was greater at a lower LV end-diastolic pressure. Increased PVR was associated with a decreased transseptal pressure gradient, suggesting that leftward septal shift contributed to decreased LV preload, in addition to that caused by external constraint. Volume loading reduced PVR; this was associated with improved RV output and an increased transseptal pressure gradient, which suggests that rightward septal shift contributed to the increased LV preload. If PVR is used to reflect RV afterload, volume loading appeared to reduce PVR, thereby improving RV and LV performance. The improvement in cardiac output was also associated with reduced external constraint to LV filling; since calculated PVR is inversely related to cardiac output, increased LV output would reduce PVR. In conclusion, our results, which suggest that PVR is an independent determinant of cardiac performance, but is also dependent on cardiac output, improve our understanding of the hemodynamic effects of volume loading in acute lung injury.     

Atrial natriuretic factor attenuates the pulmonary pressor response to hypoxia

The influence of endogenous and exogenous atrial natriuretic factor (ANF) on pulmonary hemodynamics was investigated in anesthetized pigs during both normoxia and hypoxia. Continuous hypoxic ventilation with 11% O2 was associated with a uniform but transient increase of plasma immunoreactive (ir) ANF that peaked at 15 min. Plasma irANF was inversely related to pulmonary arterial pressure (Ppa; r = -0.66, P less than 0.01) and pulmonary vascular resistance (PVR; r = -0.56, P less than 0.05) at 30 min of hypoxia in 14 animals; no such relationship was found during normoxia. ANF infusion after 60 min of hypoxia in seven pigs reduced the 156 +/- 20% increase in PVR to 124 +/- 18% (P less than 0.01) at 0.01 microgram.kg-1.min-1 and to 101 +/- 15% (P less than 0.001) at 0.05 microgram.kg-1.min-1. Cardiac output (CO) and systemic arterial pressure (Psa) remained unchanged, whereas mean Ppa decreased from 25.5 +/- 1.5 to 20.5 +/- 15 mmHg (P less than 0.001) and plasma irANF increased two- to nine-fold. ANF infused at 0.1 microgram.kg-1.min-1 (resulting in a 50-fold plasma irANF increase) decreased Psa (-14%) and reduced CO (-10%); systemic vascular resistance (SVR) was not changed, nor was a further decrease in PVR induced. No change in PVR or SVR occurred in normoxic animals at any ANF infusion rate. These results suggest that ANF may act as an endogenous pulmonary vasodilator that could modulate the pulmonary pressor response to hypoxia.     

Down syndrome associated with hypothyroidism and chronic pericardial effusion: echocardiographic follow-up

We present a 39-year-old male patient with Down syndrome who was evaluated for fatigue, palpitations and bouts of cyanosis. Physical examination showed features of trisomy-21(Down syndrome), with a slow pulse rate, distant cardiac sounds and absent apex beat. He had normal jugular venous pressure without pulsus paradoxus. The ECG showed QRS microvoltage and flattened P and T segments. The 48-hour ambulatory ECG depicted normal sinus rhythm with intermittent short PR interval without tachyarrhythmias. The chest Xray revealed cardiomegaly without pulmonary venous congestion. Although serial transthoracic echocardiographic examination demonstrated pericardial effusion with features of tamponade, there were no overt signs of clinical cardiac tamponade. Biochemically, the serum thyroxine of 3 pmol/l (normal 10 to 25) and thyroid-stimulating hormone of 160 mU/l (normal 0.20 to 4.20)) were compatible with hypothyroidism. The patient was treated with L-thyroxine sodium daily, which was gradually increased to 0.125 mg daily. Within a few months he lost weight and became more alert; furthermore, the symptoms of hypothyroidism and the pericardial effusion resolved. It can be concluded that Down syndrome may be associated with hypothyroidism and pericardial effusion. These were alleviated following hormone replacement. Regular evaluation of thyroid function tests is important in Down syndrome. (Neth Heart J 2007;15:67-70.)     

RV filling modulates LV function by direct ventricular interaction during mechanical ventilation

During mechanical ventilation, phasic changes in systemic venous return modulate right ventricular output but may also affect left ventricular function by direct ventricular interaction. In 13 anesthetized, closed-chest, normal dogs, we measured inferior vena cava flow and left and right ventricular dimensions and output during mechanical ventilation, during an inspiratory hold, and (during apnea) vena caval constriction and abdominal compression. During a single ventilation cycle preceded by apnea, positive pressure inspiration decreased caval flow and right ventricular dimension; the transseptal pressure gradient increased, the septum shifted rightward, reflecting an increased left ventricular volume (the anteroposterior diameter did not change); and stroke volume increased. The opposite occurred during expiration. Similarly, the maneuvers that decreased venous return shifted the septum rightward, and left ventricular volume and stroke volume increased. Increased venous return had opposite effects. Changes in left ventricular function caused by changes in venous return alone were similar to those during mechanical ventilation except for minor quantitative differences. We conclude that phasic changes in systemic venous return during mechanical ventilation modulate left ventricular function by direct ventricular interaction.