Warren G. Guntheroth

The hemodynamics of cardiac tamponade and constrictive pericarditis

Abstract This review of the hemodynamic alterations that accompany cardiac tamponade and constrictive pericarditis describes studies carried out in man and in experimental animals. Both constrictive pericarditis and cardiac tamponade increase pulmonary and systemic venous pressure and decrease cardiac output and stroke volume. In cardiac tamponade, the superior and inferior vena caval pressure record shows a single nadir, the x descent; this pressure event is accompanied by an increase in velocity of blood flow and, by inference, in quantity of blood flow. The y descent is absent from the vena caval and right atrial pressure curves, and no early diastolic dip appears in the right ventricular pressure tracing. During inspiration, blood flow velocity and, by inference, forward flow increase in the superior and inferior venae cavae and in the pulmonary artery. Pulsus paradoxus is almost invariably present. The major factors causing pulsus paradoxus are related to inspiratory augmentation of systemic venous return. The ensuing expansion of right-sided heart volume increases intrapericardial pressure, but does not increase systemic arterial pressure and flow until the subsequent expiration. In constrictive pericarditis a peak of blood flow velocity accompanies the x descent of superior vena caval pressure. A second flow velocity peak accompanies the y descent. Respiration fails to alter superior vena caval pressure or blood flow velocity, but during inspiration the velocity of pulmonary arterial blood flow increases. Pulsus paradoxus occurs much less often than in cardiac tamponade, and its mechanism is not well understood. Atrial fibrillation is common, and myocardial contractility is impaired.

Hemodynamic Effects of Intermittent Positive Pressure Respiration

The hemodynamic effects of intermittent positive pressure ventilation were studied in lightly anesthetized dogs following recovery from implantation of pulsed ultrasonic flow transducers on the aorta and vena cava. A partial rebreathing system was utilized to maintain constant PaCO. Data were obtained during spontaneous respiration and using a respirator, with peak airway pressures of 10, 20 and 30 cm. of water, inspiratory to expiratory ratios of 1:2, 1:1 and 2:1. Maximum values for stroke volume and cardiac output occurred during spontaneous breathing. Cardiac output and aortic stroke volume decreased with increasing airway pressure and increasing inspiratory to expiratory ratios. Venous return was inhibited by increasing pressure, and changes in vena caval flow were reflected in changes in aortic flow within the time of two heart beats. The circulatory effects of positive pressure breathing are related to the mean intrathoracic pressure and the effect on venous return.

Diagnosis of ventricular septal defect by pulsed Doppler echocardiography. Sensitivity, specificity and limitations.

SUMMARY The M-mode echocardiographic findings of ventricular septal defect (VSD) are nonspecific. A specific pulsed Doppler echocardiographic (PDE) diagnosis of VSD can be made by following the turbulent VSD jet through the septum. To assess the sensitivity, specificity and limitations of PDE diagnosis of VSD, 105 children undergoing cardiac catheterization were examined by PDE. These children had a variety of cardiac defects, and a PDE diagnosis of VSD was made in 46/51 (90%) who had VSD proven at catheterization. There was one false positive PDE diagnosis of VSD, for a specificity of 98%. Factors influencing the ability to diagnose VSD by PDE include the location of the defect, level of pulmonary vascular resistance and direction of blood flow through the VSD. The presence of additional defects did not interfere with PDE diagnosis of VSD. The PDE detection of additional defects may identify situations where M-mode echocardiographic estimation of dimensions may not be indicative of the size of the VSD shunt.

A Critical Review of the American College of Cardiology/American Heart Association Practice Guidelines on Bicuspid Aortic Valve With Dilated Ascending Aorta

The 2006 practice guidelines from the American College of Cardiology and the American Heart Association recommend prophylactic aortic replacement for even an asymptomatic patient with a bicuspid aortic valve (BAV) when the aortic dimensions exceed arbitrary ranges based on Marfan syndrome, without comparing risk estimates of aortic dissection with operative risks. In the International Registry of Acute Aortic Dissection, which includes >1,000 autopsied subjects, the average age is 63 years; BAVs are found in only 3%, compared with histories of hypertension in 72%. The risk for valve-sparing aortic replacement is 4% and that for late mortality is 10%, on the basis of 5 publications. The aortic dimensions are from guidelines for Marfan syndrome, with a proved genetic weakness of connective tissue, whereas no culprit genes have been demonstrated in BAV. Although cystic medial necrosis is seen in dilated aortas associated with Marfan syndrome and BAV, it is also seen in dilated aortas with other causes. There is no convincing proof that cystic medial necrosis causes dissection or is simply an effect of dilatation. BAV is not associated with dilatation of the pulmonary arteries, in contrast to Marfan syndrome. Hemodynamic explanations for dilatation of the ascending aorta have been largely ignored because of a belief that it requires severe aortic stenosis or regurgitation. In conclusion, vascular dilatation without a genetic weakness is caused by coarse periodic vibrations from even trivial valve disorders, demonstrated experimentally. There is a natural history of progressive deterioration of the BAV, including the valve left in a valve-sparing aortic replacement, that makes the operation ill advised, as opposed to valve replacement with aortic reinforcement.

Spontaneous closure of uncomplicated ventricular septal defect

The charts of 222 patients with a diagnosis of ventricular septal defect (VSD) were reviewed to determine the overall incidence, the prevalence of membranous and muscular defects and the rates of spontaneous VSD closure. VSD diagnosis and location were determined primarily from reports of 2-dimensional and pulsed Doppler echocardiograms. In a 5-year period, VSDs occurred in 3.85/1,000 live full-term births and 7.06/1,000 live premature births. The VSD closed spontaneously in 20 of 44 patients (45%) followed from birth (University Hospital group) during a mean follow-up of 12 months. Of 165 patients not followed from birth (referred group), the VSD closed spontaneously in 37 (22%). Overall, VSD location was determined in 101 of 209 patients (48%) and was distributed as follows: membranous 66 (65%), muscular 32 (32%) and subpulmonic 3 (3%). Rates of spontaneous closure for membranous and muscular VSDs were 37% and 50%, respectively, for the University Hospital group and 9% and 9%, respectively, for the referred group (no significant difference in either case). Surgical closure was required in 30 of 165 referred patients (18%) and only 1 of 44 University Hospital patients (2%). There was no significant difference in rate of closure for premature vs full-term infants or small vs larger defects. Data for patients followed from birth more likely reflect the true natural history of VSD.

Relationship of Pericardial to Pleural Pressure During Quiet Respiration and Cardiac Tamponade

Pericardial pressure was studied in chronic experiments on dogs with relation to intrathoracic pressure in the normal state and in cardiac tamponade. In the normal resting animal, the two pressures were in good agreement throughout the respiratory cycle. The cardiac cycle produced superimposed pressure fluctuations amounting to 30% of the respiratory swings. Adding saline to the pericardial sac produced sigmoid pressure-volume curves; tamponade required 100 to 330 ml of fluid. Although during tamponade the pericardial pressure greatly exceeded the intrathoracic pressure, the pericardial pressure invariably fell with inspiration, generally by the same amount as the intrathoracic pressure. The cardiac cycle produced greater pressure fluctuations (50% of the respiratory pressure fluctuations). The superior vena caval pressure always fell with inspiration in the normal state and during tamponade. Hypovolemia did not change the resting pericardial pressure, but decreased the slope of the pressure-volume curve measured during cardiac tamponade. Hypervolemia increased the resting pericardial pressure considerably, and increased the slope of the pericardial pressure-volume curve. The results suggest that pleural pressure is a reasonable approximation of the pericardial pressure in normal dogs. There appears to be no substantial evidence that pulsus paradoxus is due to failure of the pericardial sac to transmit inspiratory reductions of pleural pressure.

The Hemodynamic Effects of Changes in Blood Volume during Intermittent Positive-pressure Ventilation

The hemodynamic effects of changes in blood volume during intermittent positive-pressure ventilation (IPPV) were studied in lightly anesthetized dogs following recovery from implantation of pulsed ultrasonic flow transducers on vena cava and aorta. Alveolar ventilation was maintained in excess of no

Noninvasive detection of pulmonary hypertension in patent ductus arteriosus by pulsed Doppler echocardiography.

Twenty-five patients with proven patent ductus arteriosus were examined by pulsed Doppler echocardiography (PDE) before invasive assessment. Ten patients had normal pulmonary artery pressures, and by PDE, pandiastolic ductal flow. Fifteen patients had elevation of mean pulmonary artery pressure, and by PDE, all had abbreviations of diastolic ductal flow. PDE correctly distinguished between patients with normal pressure and those with evidence of pulmonary hypertension; the ECG did not allow such differentiation. Detection by PDE of pulmonary hypertension complicating patent ductus arteriosus appears to be clinically useful.

Effect of Respiration on Venous Return and Stroke Volume in Cardiac Tamponade

In 40 lightly anesthetized dogs, 5 to 30 days after surgical preparation, flow was measured simultaneously in the venae cavae, pulmonary artery, pulmonary vein, and aorta with ultrasonic flowmeters. Intrapleural and pericardial pressures were measured via silastic cannulas. Pulmonary vein diameter was monitored by miniature mutual inductance coils. In the resting animal with sinus arrhythmia, inspiration increased heart rate and flow in the vena cava, and to a lesser extent, in the pulmonary vein. Left ventricular stroke volume (LVSV) varied directly with the right ventricular stroke volume (RVSV) in dogs with slow heart rates. Cardiac tamponade invariably caused tachycardia and a marked decrease in cardiac output, arterial pressure, pulse pressure, and stroke volume; venous pressure and diameter increased. Pericardial pressure, although markedly elevated, fell with inspiration paralleling the fall in intrapleural pressure. Flow in the pulmonary vein rose or remained constant with inspiration. Pulmonary vein diameter frequently increased with inspiration during tamponade, but only after the pulmonary artery diameter increased with the inspiratory surge. LVSV did not decline sharply with inspiration, and actually increased within 2 beats of the increase in RVSV. The sum of LVSV plus RVSV increased markedly with inspiration, contradicting the concept of fixed intrapericardial volume. Almost all of the changes of pulsus paradoxus reflect the normal respiratory effects on the RVSV, delayed by transit through the pulmonary bed and exaggerated by the small LVSV in a vasoconstricted state.

Thermal Stress in Sudden Infant Death: Is There an Ambiguity With the Rebreathing Hypothesis?

Objective. To assess the role of thermal stress in the cause of sudden infant death syndrome (SIDS), and to compare risk factors with those of rebreathing. Methodology. Analysis of publications concerning the epidemiology and physiology of thermal stress in SIDS. Results. A strong association between thermal regulation and ventilatory control was found, specifically for prolonged apnea. Infections, excessive room heat and insulation, and prone sleeping produce significantly increased odds ratios for SIDS. Although some of the risk factors for rebreathing could be explained by the effects of thermal stress, several factors for thermal stress could not reasonably be explained by the rebreathing hypothesis. Conclusions. Although the risk of thermal stress is widely accepted abroad, it has received relatively little attention in the United States. The incidence of SIDS in the United States can likely be further reduced by educating the public against the dangers of overheating, as an integral part of the back-to-sleep campaign.