New approaches to CPR. Four hands, a plunger, or a vest.
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Cardiopulmonary Resuscitation↗
Biomedical subjects
H R Halperin
Publications and source records attributed to H R Halperin.
Modeling the circulation with three-terminal electrical networks containing special nonlinear capacitors.
Development, first of analog and later of digital computers, as well as algorithms for analysis of electrical circuits, stimulated the use of electrical circuits for modeling the circulation. The networks used as building blocks for electrical models can provide accurate representation of the hydrodynamic equations relating the inflow and outflow of individual segments of the circulation. These networks, however, can contain connections in which voltages and currents have no analogues in the circulation. Problems arise because (a) electrical current must flow in closed loops, whereas no such constraints exist for hydraulic models; and (b) electrical capacitors have a number of characteristics that are not analogous to those of hydraulic compliant chambers. Disregarding these differences can lead to erroneous results and misinterpretation of phenomena. To ensure against these errors, we introduce an imaginary electrical element, the nonlinear residual-charge capacitor (NRCC), with characteristics equivalent to those of a compliant chamber. If one uses appropriate circuit connections and incorporates the residual-charge capacitor, then all voltages and currents in the model are proper analogues of pressures and flows in the circulation. It is shown that the capacitive current represents the rate of change of volume of blood inside the vessel, as well as the rate of the corresponding displacement of volume of the surrounding tissue.
Blood Circulation↗
Brain bioenergetics during cardiopulmonary resuscitation in dogs.
Cardiac arrest causes a rapid loss of cerebral adenosine triphosphate [corrected] (ATP) and a decrease in cerebral intracellular pH (pHi). Depending on the efficacy of cardiopulmonary resuscitation (CPR), cerebral blood flow levels (CBF) ranging from near zero to near normal have been reported experimentally. Using 31P magnetic resonance spectroscopy, the authors tested whether experimental CPR with normal levels of cerebral blood flow can rapidly restore cerebral ATP and pHi despite the progressive systemic acidemia associated with CPR. After 6 min of ventricular fibrillation in six dogs anesthetized with fentanyl and pentobarbital, ATP was reduced to undetectable concentrations and pHi decreased from 7.11 +/- 0.02 to 6.28 +/- 0.09 (+/- SE) as measured by 31P magnetic resonance spectroscopy. Application of cyclic chest compression by an inflatable vest placed around the thorax and infusion of epinephrine (40 micrograms/kg bolus plus 8 micrograms/kg/min, intravenously) maintained cerebral perfusion pressure greater than 70 mmHg for 50 min with the dog remaining in the magnet. Prearrest cerebral blood flows were generated. Cerebral pHi recovered to 7.03 +/- 0.03 by 35 min of CPR, whereas arterial pH decreased from 7.41 +/- 0.4 to 7.08 +/- 0.04 and cerebral venous pH decreased from 7.29 +/- 0.03 to 7.01 +/- 0.04. Cerebral ATP levels recovered to 86 +/- 7% (+/- SE) of prearrest concentration by 6 min of CPR. There was no further recovery of ATP, which remained significantly less than control. Therefore, in contrast to hyperemic reperfusion with spontaneous circulation and full ATP recovery, experimental CPR may not be able to restore ATP completely after 6 min of global ischemia despite restoration of CBF and brain pHi to prearrest levels.
Adenosine Triphosphate↗
Servo-controlled indenter for determining the transverse stiffness of ventricular muscle.
Regional ventricular wall stress is a critical determinant of cardiac function. There are, however, no validated methods for accurately estimating this stress. We have shown in the isolated ventricular septum that, during steady-state indentations, the transverse stiffness (the ratio of indentation stress [pressure acting on indenter face] to indentation strain [amount of indentation/nonindented thickness]) can be used as an estimate of the in-plane wall stress. Because of the long acquisition time for those transverse stiffness determinations, it was not possible to follow changes in wall stress over a single contraction. We recently developed a dynamic indentation system that can determine transverse stiffness in as little as 10 ms, allowing estimation of wall stress over a single contraction cycle. The apparatus consists of an indentation probe coupled to a linear motor. This indentation system was tested on two beating canine ventricular septa that were mounted in a biaxial system the could apply strains in the plane of the septa and measure the resulting in-plane stresses. The probe indented the septa with peak displacements of 0.1-0.5 mm at frequencies of 20 and 50 Hz. The transverse stiffness was calculated as the slope of the relation between the indentation stress and indentation strain during each high-frequency indentation. Consistent with earlier studies, the transverse stiffness was related to the inplane stress. In contrast to earlier studies, however, these dynamic transverse stiffness determinations could be made during a single contraction. Thus, dynamic transverse stiffness determinations allow estimation of wall stress in the isolated septa by minimal surface contact, and may lead to methods for estimating wall stress in the intact heart.
Animals↗
Optimization of the timing of skeletal to cardiac muscle contraction during dynamic cardiomyoplasty: analysis using a mathematical model.
Cardiomyoplasty, or the use of skeletal muscle to assist the failing heart, has been studied for many years but has enjoyed only minimal success. It has been suggested that a delay in the start of skeletal muscle contraction relative to the QRS complex would enhance aortic flow. To study the effects of simulated changes in the relative timing of skeletal muscle contraction, heart rate and skeletal muscle contraction duration, a mathematical model was used to predict the vascular pressures and flows during cardiomyoplasty. The vascular pressures and cardiac output generated by the model for both the normal and heart failure state were similar to previously published canine data. Skeletal muscle contraction synchronous with cardiac mechanical systole (i.e., delayed approximately 50-75 ms from the QRS) was able to provide improvements in cardiac output, arterial blood pressure and aortic flow velocity up to 40% over the baseline heart failure state. A delay in the start of skeletal muscle contraction, prolonged skeletal muscle contraction duration or an increase in the heart rate from 90 to 120/min reduced this benefit. Thus, mechanical synchrony of skeletal and cardiac muscle contraction optimizes hemodynamics during cardiomyoplasty.
Heart Failure↗
Vital organ perfusion during assisted circulation by manipulation of intrathoracic pressure.
BACKGROUND: We have previously shown, in dogs with severe cardiac depression, that modest cyclic increases in intrathoracic pressure, starting synchronously with left ventricular isovolumic contraction, significantly increase aortic flow and pressure. However, little is known of changes in vital organ perfusion during this technique of assisted circulation. METHODS AND RESULTS: We studied regional organ flow using radioactive labeled microspheres in 13 20-25-kg mongrel dogs. In the control group, after chemical induction of cardiac depression with verapamil and propranolol, coronary flow fell from 129.1 +/- 14.4 to 51.6 +/- 11.3 ml/100 g/min (p less than 0.005) and continued to decline over a 14-minute time period (flow was 32.2 +/- 11.5 ml/100 g/min at 7 minutes and 20.7 +/- 9.5 ml/100 g/min at 14 minutes [n = 6]; all p less than 0.05). In the intervention group, regional blood flow was evaluated before and after the induction of cardiac depression and also during assisted circulation using 400-msec, 20-25-mm Hg intrathoracic pressure increases delivered by a circumthoracic pneumatic vest, starting synchronously with left ventricular isovolumic contraction. In the intervention group, coronary flow fell from 119 +/- 26.7 to 47.9 +/- 13.1 ml/100 g/min 1 minute after the induction of cardiac depression (p less than 0.005). With the initiation of assisted circulation, coronary flow increased to 55.8 +/- 19.2 ml/100 g/min at 7 minutes and fell to 23.1 +/- 15.9 ml/100 g/min on termination of assisted circulation at 14 minutes (p less than 0.05 and p = NS versus control group flows at 1 and 14 minutes, respectively). During assisted circulation, cerebral, renal, and small intestinal flows also increased (all p less than 0.05 versus flows during myocardial depression). No significant increase in hepatic flow was observed. CONCLUSIONS: In the canine model, manipulation of intrathoracic pressure appears to be an effective, short-term, noninvasive means of not only increasing aortic pressure but also increasing vital organ perfusion during cardiogenic shock. Further studies are needed to assess the usefulness of this technique of assisted circulation in humans.
Animals↗
Observations of hemodynamics during human cardiopulmonary resuscitation.
To evaluate hemodynamics during human CPR, 32 patients with witnessed cardiac arrest were studied during manual and mechanical conventional CPR. In eight patients during manual conventional CPR, peak systolic radial artery, right atrial (RAP), and pulmonary artery pressures were found to be similar (59.8 +/- 4.3, 70.8 +/- 4.7, 71.2 +/- 8.2 mm Hg) and higher than external jugular venous pressure (33.8 +/- 1.9 mm Hg, p less than .0001). The diastolic radial artery to RAP gradient was found to be only 10.7 +/- 2.1 mm Hg. In four patients, maneuvers that avoid chest compression and thus obviate cardiac compression, i.e., rhythmic compression of the abdomen, yielded arterial pressures comparable to those generated by conventional CPR (48 +/- 6.4 vs. 52.8 +/- 3.4 mm Hg, NS). In 13 other patients during mechanical conventional CPR at constant chest compression force, radial artery pressure was higher during the first compression after ventilation as compared with subsequent chest compressions (67.5 +/- 5.0 vs. 61.9 +/- 4.8 mm Hg, p less than .007). These hemodynamic observations are similar to those reported in large dogs during CPR and support the generation of vascular pressures during CPR by an increase in intrathoracic pressure. They also suggest that despite anatomic differences, the similarity of hemodynamics in dogs and humans justifies the use of large dogs as a human model during acute resuscitation studies.
Arm↗
Manipulation of external pressure as a method to assist the failing heart.
The development and state of the art in circulatory assistance using external pressure variations is reviewed. All of these techniques use the principle that by cyclic external pressure waves properly timed to the cardiac cycle, hemodynamic energy can be noninvasively transmitted to assist the circulation. Cyclic pressure waves to the lower body require that the high pressure phase occurs in diastole in order to augment cardiac output or coronary flow. In contrast, pressure waves to the chest would optimally augment cardiac output if they begin at the onset of ventricular systole. Manipulation of lung pressure by synchronized ventilation may be also utilized to augment cardiac output. The above methods are discussed in detail in the manuscript with special emphasis on the pathophysiology and mechanisms of cardiac assistance.
Animals↗
System for mechanical measurements during cardiopulmonary resuscitation in humans.
Effective study of CPR requires measurement of the mechanical properties of the human chest and the resultant vascular pressures. A computer-based mobile data acquisition system was designed and built for this purpose. During manual CPR a short cylindrical module was placed between the rescuer's hands and the patient's chest. This module, which was attached to an easily manipulated position-sensing arm, measured force and acceleration at the sternum. Three-dimensional position and orientation of the module were measured, as well as the component of the applied force which was perpendicular to the sternum. The central venous and aortic pressures were measured by high fidelity pressure transducers. All transducer signals were recorded by digital computer. Real-time feedback of sternal force and displacement, and vascular pressures was provided to the rescue team via chart recordings. An audible signal was produced as an aid in maintaining desired compression rate and duration. The system's mobility permitted rapid implementation at any hospital location. In conclusion, this system was capable of measuring, recording, and displaying multiple physical quantities during manual CPR in humans.
Biomechanical Phenomena↗
Identification of dynamic mechanical parameters of the human chest during manual cardiopulmonary resuscitation.
Survival from cardiac arrest is dependent on timely cardiopulmonary resuscitation (CPR). Since CPR is often unsuccessful, the outcome may be improved by a better understanding of the relationship between force applied to the sternum and the resulting hemodynamic effects. The first step in this complex chain of interactions is the mechanical response of the chest wall to cyclical compression. We formulated a dynamic mechanical model of the chest response and developed a method of identification of the model parameters based on force, displacement, and acceleration data acquired during cyclical compressions. The elasticity, damping, and equivalent mass of the human chest were estimated with a constrained nonlinear least-mean-square identification technique. The method was validated on data acquired from a test apparatus built for this purpose. The model fit was measured with the normalized chi-square statistic on residuals obtained between recorded force and force predicted by the model. In the analysis of one human chest, the elasticity was found to be nonlinear and statistically different during compression and release. A considerable amount of damping was found, with no significant difference between compression and release. The equivalent mass was too small to be determined accurately. This method can be used to obtain the dynamic mechanical parameters of the human chest and may lead to a better understanding of CPR.
Biomechanical Phenomena↗
An improved video-based computer tracking system for soft biomaterials testing.
We present an improved video-based computer system for on-line tracking of small markers moving in a plane. The system consists of a CCD camera, a video monitor, a dedicated 80386/20 microcomputer, a video frame grabber, and custom software. Up to four markers can be tracked at the 30-Hz video frame rate using a two-step, correlation-based search procedure. We discuss the requisite hardware and software requirements and illustrate how this tracking system can be used to collect strain data during biaxial stretching tests on planar soft tissues. Operating at 30 Hz, this system is an improvement over those previously reported, which are either slower or yield less information.
Algorithms↗
Effect of wall stretch on coronary hemodynamics in isolated canine interventricular septum.
The effects of stretch on coronary pressure-flow relations are not well understood. To examine the role of wall stretch per se on coronary hemodynamics, we studied arterially perfused isolated canine interventricular septa in a noncontracting state with vasodilated vessels. We compared the hemodynamic parameters of zero-flow pressure and resistance during passive stretching in the circumferential and the base-to-apex directions alone as well as during simultaneous biaxial stretching in both directions. Even in the unloaded state the zero-flow pressure was positive. Any type of stretching significantly increased the zero-flow pressure and the resistance from their unloaded values. The pressure-flow responses also showed directional dependence. When stretches with matched strains or stresses in each direction were applied sequentially, the resistance increases corresponded to the direction of higher stress. Conversely, the zero-flow pressure response increase corresponded to the direction of greater strain. However, neither response correlated with a measure of global tissue stiffness. Thus there is a complex and tight mechanical interaction between the vessels and the surrounding tissue. These interactions, but not the tissue stiffness, are important determinants of coronary pressure-flow responses during stretch.
Animals↗
Vasoconstrictors during CPR. Are they used optimally?
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Epinephrine↗
Aortic diameter and pressure-flow sequence identify mechanism of blood flow during external chest compression in dogs.
Aortic flow and pressure relations and aortic diameter were examined during sinus rhythm, internal cardiac massage, vest cardiopulmonary resuscitation, conventional manual cardiopulmonary resuscitation and high impulse manual cardiopulmonary resuscitation in 14 anesthetized large dogs. During sinus rhythm and during internal cardiac massage, ascending aortic flow and pressure increased simultaneously and the rise in ascending aorta pressure preceded the rise in descending aortic pressure by (mean +/- SEM) 28 +/- 4 and 30 +/- 1 ms, respectively. In contrast, during vest, conventional and high impulse cardiopulmonary resuscitation, ascending aortic flow lagged behind the initial rise in aortic pressure by 40 +/- 4 to 46 +/- 4 ms and ascending and descending aortic pressure increased simultaneously (p less than 0.001 for each external compression mode versus sinus rhythm and internal massage). The ratio of pulse pressure to stroke volume increased by an order of magnitude during all modes of external chest compression (p less than 0.001 versus sinus rhythm and internal massage) and aortic diameter decreased during vest and high impulse cardiopulmonary resuscitation (p less than 0.05 versus sinus rhythm and internal massage). The hemodynamics of external chest compression depart from the normal physiologic sequence of stroke volume-induced increase in aortic pressure and diameter. The rise in aortic pressure precedes flow into the aorta, stroke volume does not fully account for pulse pressure, and aortic diameter decreases during chest compression. These data support the hypothesis that blood flow is due to fluctuations in intrathoracic pressure for high impulse as well as vest and conventional cardiopulmonary resuscitation.
Animals↗
Circulatory assistance by intrathoracic pressure variations: optimization and mechanisms studied by a mathematical model in relation to experimental data.
The hemodynamic effects of phasic variations in intrathoracic pressure (ITP) timed to the cardiac cycle were predicted by a mathematical model and were compared with data from canine experimental studies. The model was used to predict the hemodynamic effects of changing the onset of the ITP rise relative to the start of cardiac systole, as well as the hemodynamic effects of changes in the duration and amplitude of the ITP rise. The predictions of the model were compared with hemodynamic data from seven anesthetized dogs. Cardiac function was depressed with large doses of verapamil and propranolol, and the hearts were atrioventricular sequentially paced at a rate of 72 beats/min. Phasic ITP variations were generated by a perithoracic vest and were electronically timed to the cardiac cycle. The model predicted, and the experimental data confirmed, that phasic intrathoracic pressure variations generated by vest inflation, timed to the cardiac cycle, can augment both peak and mean aortic flow. The following predictions of the model were also confirmed by the experimental data: 1) Maximum flow augmentation occurs when the onset of the ITP rise is simultaneous with the onset of left ventricular isovolumic contraction, and the ITP rise has a duration of 400 msec. 2) The magnitude of the flow augmentation is a function of the amplitude of the ITP rise. The experimental data showed that there was little further flow augmentation when the ITP rise was greater than 30-40 mm Hg. 3) The magnitude of flow augmentation was inversely proportional to the peak left ventricular elastance (Emax). The best fit between the measured and predicted flow augmentations was obtained for an assumed Emax of 0.5 mm Hg/ml, while Emax measurements in three dogs, using a volume conductance catheter and transient vena caval occlusion, yielded values of 0.4-1.6 mm Hg/ml. Thus, both the mathematical model and canine experiments showed that relatively low-amplitude ITP variations, rising synchronously with the onset of cardiac systole and having an optimal duration, assist the failing heart by augmentation of aortic flow. The degree of cardiac assistance decreases if the ITP variations do not rise synchronously with the onset of systole, or if their duration is not optimal. Thus, properly applied ITP variations may be used as an efficient, noninvasive method to temporarily assist the failing heart.
Animals↗
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↗
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↗
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↗