PubMed Health⌕ Search

Biomedical subjects

H R Halperin

Publications and source records attributed to H R Halperin.

At least 55 records · Page 3Linked to original sources
PubMed1989

Intermittent coronary sinus occlusion after coronary arterial ligation results in venous retroperfusion.

Coronary sinus occlusion retards necrosis of ischemic myocardium. To test the hypothesis that coronary sinus occlusion induces retrograde venoarterial flow, the coronary arteriovenous pressure gradient and the coronary arterial oxygen saturation were measured distal to a left anterior descending coronary artery ligature in dogs. In parallel, we constructed a mathematical model of known coronary physiology to characterize pressure and flow patterns during coronary sinus occlusion. In dogs, coronary sinus occlusion produced a systolic pressure gradient between the coronary artery and the coronary sinus of -20 +/- 9 mm Hg (higher venous pressure, p less than 0.0001) and a positive diastolic gradient of 3 +/- 5 mm Hg (lower venous pressure p less than 0.01). An average reduction in the oxygen saturation in the ligated coronary artery of 20 +/- 13% was also observed (p less than 0.005) consequent to admixture of venous (desaturated) blood. By graded inflation of the coronary sinus balloon, it was demonstrated that desaturation of arterial blood typically occurs above a coronary sinus systolic pressure of 40-50 mm Hg. The mathematical model indicates the possibility of venoarterial pressure gradients and reversal of flow at the microcirculatory level during coronary sinus occlusion. These studies provide evidence that retrograde flow into the ischemic zone occurs in association with intermittent coronary sinus occlusion. Thus, alternating flow over the ischemic territory may be the mechanism of myocardial salvage during intermittent coronary sinus occlusion.

Animals↗
PubMed1989

Air trapping in the lungs during cardiopulmonary resuscitation in dogs. A mechanism for generating changes in intrathoracic pressure.

To test the hypothesis that during cardiopulmonary resuscitation, chest compression with an unobstructed trachea raises and maintains intrathoracic pressure by collapsing airways and trapping air in the lung, we studied 11 dogs (20-32 kg). An inflatable vest compressed the thorax after induction of ventricular fibrillation. First, tracheal airflow was measured by a pneumotachometer during vest inflation and deflation in nine of the dogs. As expected, during the initial phase of vest inflation of cycles after ventilation, air moved out of the lungs, but then airflow stopped. After vest deflation, however, more air moved out of the lungs in eight of the nine dogs; this occurrence indicated that a portion of the inspired tidal volume was trapped during vest inflation. During cycles without prior ventilation, the amount of air expired by chest compression decreased, paradoxically, at higher peak vest pressure (p less than 0.002); this occurrence indicated that air was trapped at the higher vest pressures. The change in right atrial pressure was higher on cycles after ventilation than on cycles without prior ventilation (79 +/- 12 vs. 67 +/- 12 mm Hg [mean +/- SEM], p less than 0.005), and lung volume was higher on cycles after ventilation (p less than 0.001). Next, a 5-Fr micromanometer was advanced down the airway in eight of the dogs. With the tip of the micromanometer 5-8 cm distal to the carina, a zone of high pressure was noted in seven dogs; this high pressure suggested a zone of airway collapse distal to the carina.(ABSTRACT TRUNCATED AT 250 WORDS)

Air↗
PubMed1988

Correlation of transconjunctival PO2 with cerebral oxygen delivery during cardiopulmonary resuscitation in dogs.

The relationship between transconjunctival PO2 (PcjO2) and cerebral oxygen delivery (DO2) was examined in dogs during sinus rhythm and CPR with an inflatable vest. Microsphere-determined cerebral blood flow (CBF), DO2, and PcjO2 readings were normal during sinus rhythm. During CPR, with carotid pressure of 82 +/- 11/25 +/- 5 (SEM) mm Hg, cerebral perfusion and DO2 fell by 53% and 57%, respectively, while PcjO2 fell by 87%. After epinephrine administration, carotid pressure increased to 128 +/- 13/48 +/- 9 mm Hg, and CBF and DO2 rose to 130% and 115% of pre-arrest levels, respectively, but PcjO2 readings remained at 11% of control values. Thus, PcjO2 failed to reflect accurately either CBF or DO2 during CPR. In the presence of epinephrine, PcjO2 does not seem to provide an accurate index of the effectiveness of CPR.

Animals↗
PubMed1988

Cyclic elevation of intrathoracic pressure can close the mitral valve during cardiac arrest in dogs.

Mitral valve closure during cardiopulmonary resuscitation may result from direct cardiac compression. An alternative hypothesis is that with a rise in intrathoracic pressure, mitral valve closure can occur but may be influenced by whether the lungs are inflated or deflated. To test this hypothesis, we placed a large-bore cannula into the thoraces of 11 dogs. Intrathoracic pressure was changed by inflating and deflating the thorax through the cannula while the airway was open, as well as by inflating and deflating the lungs with the thoracic cannula clamped. Mitral valve motion was observed with two-dimensional echocardiography from the right chest wall or esophagus in eight of the dogs. With a rise in intrathoracic pressure from thoracic inflation, all eight dogs showed closure of the mitral valve, while with thoracic deflation, all showed mitral valve opening. With lung inflation and deflation alone, however, the mitral valve remained open throughout the cycle. In seven dogs, with thoracic inflation, the peak gradient from the left ventricle to the left atrium was (mean +/- SEM) 18 +/- 4 mm Hg and the average gradient was 7 +/- 3 mm Hg, while with lung inflation alone, the average gradient was -1 +/- 1 mm Hg (p less than 0.01 vs. thoracic inflation). Thus, mitral valve closure, with concomitant retrograde pressure gradients, can be produced by intrathoracic pressure changes with accompanying lung deflation. With lung inflation alone, however, the mitral valve remains open, and there are no significant transmitral pressure gradients. We conclude that intrathoracic pressure changes can cause the mitral valve to close or to remain open, depending on how intrathoracic pressure is generated.

Animals↗
PubMed1987

Augmentation of pressure in a vessel indenting the surface of the lung.

The lungs and intrathoracic cardiovascular structures compete for space within the thorax, interacting through their adjacent surfaces via the pleural space. Theoretical analysis and in vitro model studies (detailed here) established that when a vessel indents the lung surface, the increase in intravascular pressure with positive pressure lung inflation can be greater than the change in the pleural surface pressure measured outside of the interaction area. We define this phenomenon as intravessel pressure augmentation. We determined the average intravessel pressure gain as the slope of the linear regression of the pressure in a vascular structure or balloon indenting the lung on the pleural surface pressure measured by a flat disk-shaped device (disk). The analysis showed that the disk pressure overestimates the pleural pressure. Therefore, the derived pressure gain underestimated the pressure augmentation. In five dogs, the disk and a 2-ml balloon were placed in the lateral pleural space, and a segment of IVC was ligated at both ends and filled with saline. The dogs were ventilated with fixed tidal volumes, while the positive end-expiratory pressure was changed. The pressures were compared at the end of expiration. For the IVC segment, the pressure gains under four different tidal volumes were significantly greater than one [95% confidence interval of mean value (CIM) = 1.57 +/- 0.16, P less than 10(-4)], and for the small balloon, this was the case for three of four tidal volumes (95% CIM for all four volumes 1.13 +/- 0.04, P less than 10(-4)). We conclude that the surface interaction of the lungs with adjacent cardiovascular structures causes appreciable pressure augmentation in those structures during ventilation with the positive end-expiratory pressure.

Animals↗
PubMed1987

Intrathoracic pressure fluctuations move blood during CPR: comparison of hemodynamic data with predictions from a mathematical model.

Whether blood flow during cardiopulmonary resuscitation (CPR) results from intrathoracic pressure fluctuations or direct cardiac compression remains controversial. We developed a mathematical model that predicts that blood flow due to intrathoracic pressure fluctuations should be insensitive to compression rate over a wide range but dependent on the applied force and compression duration. If direct compression of the heart plays a major role, however, the model predicts that flow should be dependent on compression rate and force, but above a threshold, insensitive to compression duration. These differences in hemodynamics produced by changes in rate and duration form a basis for determining whether blood flow during CPR results from intrathoracic pressure fluctuations or from direct cardiac compression. The model was validated for direct cardiac compression by studying the hemodynamics of cyclic cardiac deformation following thoracotomy in four anesthetized, 21-32-kg dogs. As predicted by the model, there was no change in myocardial or cerebral perfusion pressures when the duration of compression was increased from 15% to 45% of the cycle at a constant rate of 60/min. There was, however, a significant increase in perfusion pressures when rate was increased from 60 to 150/min at a constant duration of 45%. The model was validated for intrathoracic pressure changes by studying the hemodynamics produced by a thoracic vest (vest CPR) in eight dogs. The vest contained a bladder that was inflated and deflated. Vest CPR changed intrathoracic pressure without direct cardiac compression, since sternal displacement was less than 0.8 cm. As predicted by the model and opposite to direct cardiac compression, there was no change in perfusion pressures when the rate was increased from 60 to 150/min at a constant duration of 45% of the cycle. Manual CPR was then studied in eight dogs. There was no surgical manipulation of the chest. Myocardial and cerebral blood flows were determined with radioactive microspheres and behaved as predicted from the model of intrathoracic pressure, not direct cardiac compression. At nearly constant peak sternal force (378-426 N), flow was significantly increased when the duration of compression was increased from short (13%-19% of the cycle) to long (40%-47%), at a rate of 60/min. Flow was unchanged, however, for an increase in rate from 60 to 150/min at constant compression duration. In addition, myocardial and cerebral flow correlated with their respective perfusion pressures.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1987

Interaction between cardiac chambers and thoracic pressure in intact circulation.

A comprehensive model that describes the interaction between the cardiovascular system (CVS) and the intrathoracic pressure (ITP) based on a lumped parameter vascular representation and a time-varying elastance concept for the four cardiac chambers is presented. Special attention is given to two possible mechanisms of interventricular interaction; the constraining effects of the pericardium and direct interventricular interaction that results from the fact that the two ventricles share a common interventricular septum. The response of the CVS to positive and negative perturbations in the ITP and to injection of fluid into the pericardium was simulated and compared with experimental literature data. The results show that 1) the total heart volume is relatively constant throughout the cycle both for ITP of 0 and +15 mmHg, which is consistent with experimental data in dogs, thus suggesting that intrinsic properties of the cardiac chambers rather than a restricting pericardium is the mechanism for that observation. 2) The pericardium has a major role in modifying the transient and steady-state response to a step decrease in the ITP with a transient decrease in left ventricle (LV) end-diastolic volume followed by gradual increase afterwards. 3) The response to sudden injection of fluid into the pericardial space is a larger transient decrease in right ventricle than LV volume, which is consistent with experimental data. 4) Transmission across the septum has a relatively minor role in modifying the response of the CVS to negative pressure. Thus the model reasonably predicts the effects of intrathoracic and pericardial pressures on the circulation in a reflex-blocked animal and provides a means for placing multiple potential mechanisms in proper hierarchial order with regard to contributions to LV and overall CVS function.

Cardiovascular Physiological Phenomena↗
PubMed1987

Transverse stiffness: a method for estimation of myocardial wall stress.

Determination of regional ventricular wall stress would allow quantification of both regional contractile state and its interplay with global function. Current methods for quantifying regional stress include mathematical modelling and measurements with strain gauges. Both methods are difficult to validate. We hypothesized that transverse stiffness (i.e., the ratio of indentation stress to strain as the ventricular wall is indented in the direction perpendicular to the wall) would be proportional to the stresses in the plane of the wall and could be used to estimate the latter. To test this hypothesis, 6 arterially perfused canine ventricular septa were mounted in an apparatus that could exert biaxial load in the plane of the wall. A servo system maintained the central third of the septa isometric during active contractions while the septa were paced at 30-60 pulses/min. In the center of the isometric region, a probe of 7 mm diameter indented the septa while the transverse indentation stress and strain were measured. For values of peak systolic in-plane stress from 0.56 to 2.6 g/mm2, the transverse stiffness varied from 1.2 to 11.7 g/mm2 and was linearly related to the in-plane wall stress in each septum (p less than 0.001, ANOVA). After cardioplegia, the transverse stiffness also correlated with passively applied wall stress for each dog (p less than 0.001). The slopes of the individual relations between transverse stiffness and wall stress from active contractions were similar to those from passively applied stress (mean +/- SEM; 1.82 +/- 0.36 versus 1.45 +/- 0.31, NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Relationship between canine transthoracic impedance and defibrillation threshold. Evidence for current-based defibrillation.

The electrical parameter used to define defibrillation strength is energy. Peak current, however, may more accurately reflect the field quantities (i.e., electric field strength and current density) that mediate defibrillation and therefore should be a better clinical descriptor of threshold than energy. Though transthoracic impedance is a major determinant of energy-based threshold and is sensitive to operator-dependent changes in impedance (electrode-subject interface), an ideal threshold descriptor should be invariant with respect to these changes in impedance. We therefore compared the relative invariance of energy- and current-based thresholds when transthoracic impedance was altered by one of two methods: (a) change in electrode size (protocol A) or (b) change in electrode force (protocol B). In protocol A, impedance was altered in each dog by a mean of 95%. Energy thresholds determined at both low and high impedance were 44 +/- 21 J (mean +/- SD) and 105 +/- 35 J, respectively, P less than 0.0001. In contrast, peak current (A) thresholds were independent of transthoracic impedance, 22 +/- 5 A (low impedance) vs. 24 +/- 6 A (high impedance), P = NS. Energy and current thresholds showed a similar relationship for animals tested in protocol B. Therefore, current-based thresholds, in contrast to energy thresholds are independent of operator-dependent variables of transthoracic impedance and are invariant for a given animal. These results suggest that redefining defibrillation threshold in terms of peak current rather than energy provides a superior method of defibrillation.

Animals↗
PubMed1986

The characterization of human transmyocardial impedance during implantation of the automatic internal cardioverter defibrillator.

We set out to determine in a prospective fashion the characteristics of energy delivery related to defibrillation in a population of patients receiving the AICD. Specifically, we examined the characteristics of the delivered current, transmyocardial voltage, and transmyocardial impedance. Secondly, we determined the relationship between the energy delivered, the impedance encountered and the defibrillation threshold. Since the AICD will deliver a succession of shocks if the initial shock does not cardiovert, the effects of consecutive shocks at different energy levels on the transmyocardial impedance were also assessed.

Cardiac Surgical Procedures↗
PubMed1986

Determinants of blood flow to vital organs during cardiopulmonary resuscitation in dogs.

Whether blood flow during cardiopulmonary resuscitation (CPR) results from intrathoracic pressure fluctuations or direct cardiac compression remains controversial. From modeling considerations, blood flow due to intrathoracic pressure fluctuations should be insensitive to compression rate over a wide range, but dependent on the applied force and compression duration. If direct compression of the heart plays a major role, however, flow should be dependent on compression rate and force, but above a threshold, insensitive to compression duration. These differences in hemodynamics produced by changes in rate and duration form a basis for determining whether blood flow during CPR results from intrathoracic pressure fluctuations or from direct cardiac compression. Manual CPR was studied in eight anesthetized, 21 to 32 kg dogs after induction of ventricular fibrillation. There was no surgical manipulation of the chest. Myocardial and cerebral blood flows were determined with radioactive microspheres. At nearly constant peak sternal force (378 to 426 newtons), flow was significantly increased when the duration of compression was increased from 14 +/- 1% to 46 +/- 3% of the cycle at a rate of 60/min. Flow was unchanged, however, after an increase in rate from 60 to 150/min at constant compression duration. The hemodynamics of manual CPR were next compared with those produced by vest inflation with simultaneous ventilation (vest CPR) in eight other dogs. Vest CPR changed intrathoracic pressure without direct cardiac compression, since sternal displacement was less than 0.8 cm. At a rate of 150/min, with similar duration and right atrial peak pressure, manual and vest CPR produced similar flow and perfusion pressures. Finally, the hemodynamics of manual CPR were compared with the hemodynamics of direct cardiac compression after thoracotomy. Cardiac deformation was measured and held nearly constant during changes in rate and duration. As opposed to changes accompanying manual CPR, there was no change in perfusion pressures when duration was increased from 15% to 45% of the cycle at a constant rate of 60/min. There was, however, a significant increase in perfusion pressures when rate was increased from 60 to 150/min at a constant duration of 45%. Thus, vital organ perfusion pressures and flow during manual external chest compression are dependent on the duration of compression, but not on rates of 60 or 150/min. These data are similar to those observed for vest CPR, where intrathoracic pressure is manipulated without sternal displacement, but opposite of those observed for direct cardiac compression.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1986

Vest inflation without simultaneous ventilation during cardiac arrest in dogs: improved survival from prolonged cardiopulmonary resuscitation.

Myocardial and cerebral blood flow can be generated during cardiac arrest by techniques that manipulate intrathoracic pressure. Augmentation of intrathoracic pressure by high-pressure ventilation simultaneous with compression of the chest in dogs has been shown to produce higher flows to the heart and brain, but has limited usefulness because of the requirement for endotracheal intubation and complex devices. A system was developed that can produce high intrathoracic pressure without simultaneous ventilation by use of a pneumatically cycled vest placed around the thorax (vest cardiopulmonary resuscitation [CPR]). The system was first tested in a short-term study of the maximum achievable flows during arrest. Peak vest pressures up to 380 mm Hg were used on eight 21 to 30 kg dogs after induction of ventricular fibrillation and administration of epinephrine. Microsphere-determined myocardial blood flow was 108 +/- 17 ml/min/100 g (100 +/- 16% of prearrest flow) and cerebral flow was 51 +/- 12 ml/min/100 g (165 +/- 39% of prearrest). Severe lung or liver trauma was noted in three of eight dogs. If peak vest pressure was limited to 280 mm Hg, however, severe trauma was no longer observed. A study of the hemodynamics during and survival from prolonged resuscitation was then performed on three groups of seven dogs. Vest CPR was compared with manual CPR with either conventional (300 newtons) or high (430 newtons) sternal force. After induction of ventricular fibrillation, each technique was performed for 26 min. Defibrillation was then performed.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Failure of sodium bicarbonate to improve resuscitation from ventricular fibrillation in dogs.

To determine the value of sodium bicarbonate in resuscitation from ventricular fibrillation and the prevention of spontaneous refibrillation, sodium bicarbonate (1 meq/kg) or placebo was administered on a random basis to 16 pentobarbital-anesthetized dogs 18 min after the induction of ventricular fibrillation and cardiopulmonary resuscitation. Defibrillation was attempted 2 min after the administration of bicarbonate or placebo. All animals were successfully defibrillated, but three of eight bicarbonate-treated and two of eight control animals died in electromechanical dissociation (p = NS). Spontaneous refibrillation occurred in three animals in each group (p = NS). Successful resuscitation was not dependent on treatment, arterial or mixed venous Pco2, or arterial or mixed venous pH but correlated strongly with coronary perfusion pressure (p less than .003). Spontaneous refibrillation occurred without relation to any identifiable variable. The gradient between diastolic aortic and right atrial pressures was 24 +/- 2 mm Hg in controls and 23 +/- 2 mm Hg in treated animals over the entire 20 min of cardiopulmonary resuscitation (p = NS). However, among animals successfully resuscitated, mean diastolic coronary perfusion pressure averaged 27 +/- 2 mm Hg compared with 20 +/- 1 mm Hg among those dying in electromechanical dissociation (p less than .02). For the final 2 min of resuscitation, after drug administration, these gradients were 31 +/- 2 and 23 +/- 2 mm Hg, respectively (p less than .01). Microsphere determined myocardial perfusion correlated with the diastolic aortic-right atrial perfusion pressure gradient (r = .86) and was 0.43 +/- 0.03 ml/min/g in survivors and 0.22 +/- 0.01 ml/min/g in nonsurvivors (p less than .01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Elastic properties of the human chest during cardiopulmonary resuscitation.

Sternal displacement during CPR was measured in 11 adults and 2 manikins (Recording Resusci Anne) while the chest was compressed with variable maximum pulse compression force at a rate of 60/min with compression duration of 0.5-0.6 sec. In 10 patients, the pulsatile sternal elastic characteristic can be satisfactorily described with a 2nd degree polynomial F = beta Ds + gamma D2s, where beta = 54.9 +/- 29.4 (mean +/- SD) N/cm is the pulsatile initial elasticity and gamma = 10.8 +/- 4.1 N/cm2 is the posterior resiliency. The sternal characteristics of manikins were linear F = kDs with high elasticity constants, k = 131 and 142 N/cm. Therefore, the manikins tested differ significantly in elasticity characteristics from the human chest during resuscitation. In general, the manikin: (1) has markedly greater stiffness at the onset of compression, and (2) maintains a linear stiffness throughout the usual range of displacement, rather than becoming stiffer with greater chest displacement.

Adolescent↗
PubMedDate not supplied

Hand-held, dynamic indentation system for measuring myocardial transverse stiffness.

Primary muscle abnormalities and/or alterations in regional loading may be critical in myocardial infarct expansion and remodeling, cardiomyopathy progression, and arrhythmia generation. To differentiate muscle abnormalities from loading abnormalities, an estimation of regional wall stress is needed. Researchers have previously relied on geometric models and finite element analysis to estimate wall stress, but these estimations have not been validated. It has been shown that the transverse stiffness (the ratio of indentation stress to indentation strain during transverse indentations) of a cardiac muscle can be used to estimate the myocardial wall stress. The authors designed and tested a hand-held dynamic indentation system that can determine the regional transverse stiffness of an intact heart in as little as 15 milliseconds, allowing multiple estimations of wall stress over a single contraction cycle. The sensor was validated with a finite-element analysis of the indentation process, as well as with direct measurements on isolated heart muscle, and on soft, nonbiologic materials. The validations confirmed that the dynamic indentation system does accurately estimate myocardial wall stress. This regional-wall-stress sensor could help to enhance the understanding of cardiac pathophysiology, guide therapy, and assist surgeons in planning cardiac surgeries.

Cardiac Surgical Procedures↗