Internal Cardiac Massage Research Articles

The physiology of cerebral blood flow during cardiopulmonary resuscitation.

For decades after Kouwenhoven'z original description of cardiopulmonary resuscitation (CPR), I antegrade blood flow during was generally assumed to result from the direct compression of the heart between the sternum and the vertebral column, thereby forcing blood out of the ventricle cardiac mechanism of blood flow. If this hypothesis is correct, the fotlowing haemodynamie findings and flow events would be expected. During chest compression or systole, a ventricular-atrial pressure gradient should develop that would close the atrioventricular valves. Synchronous left and right ventricular ejection would be associated with a reduction in ventricular volume. During chest relaxation or diastole ventricular pressure would fall below atrial pressure with subsequent atrioventricnlar valve opening and ventricular filling. Such a mechanism of blood flow generation is obviously operative during open-chest, internal cardiac massage. Several observations of early investigators, however, did not support the cardiac pump hypothesis of antegrade blood flow. Weale and Rothwel]-Jackson 2 measured equivalent elevations in arterial and right atrial pressures with external chest compression and Gall et al. using a cardioscope demonstrated that the mitral valve is open during chest compression. Other clinical observations also raised questions about direct cardiac compression as a sole mechanism of blood flow. has certainly been successful in resuscitating either extremely large individuals or patients with severe emphysema. Nevertheless, in these patients it is physically impossible to depress the sternum enough to squeeze the heart against the sternum. External is frequently ineffective in patients with flail chests, a situation that should more readily permit direct cardiac compression. 3 Furthermore, a knowledge of anatomy would reveal that it is the right ventricle that is placed below the sternum and that the left ventricle is laterally placed and less likely to be squeezed by chest compression. Despite these observations, it was not until the dramatic observations of Criley in 1976, 4,s that Kouwenhoven's cardiac compression hypothesis was seriously ques tinned. Criley reported that several patients who developed ventricular fibrillation during cardiac eatheterization maintain a cardiac output adequate to maintain consciousness by repetitive coughing and phasically elevating intrathoracic pressure. This observation of cough CPR focused research on whether either direct cardiac compression or large fluctuations in intrathoracic pressure was the mechanism for forward blood flow during CPR. In 1980, the demonstration that manoeuvres that increased intrathoracic pressure with chest compression, increased aortic pressure and carotid blood flow during CPR, led to a new theory accotmting for forward blood flow during CPR. 6'7 This hypothesis proposed that blood flow produced by external chest compression could be generated by phasle changes in intrathoraeic pressure without the direct compression of the heart. According to this model, external chest compression produced a generalized elevation of intrathoracic pressure, that was transmitted equally to all cardiac chambers and intrathoracic vascular structures. This increase in intravascular pressure was transmitted from the intrathoracic to extrathoracic arteries but not to extrathoracic veins because of the presence of venous valves, a compliant exttalhoracic venous system and easily collapsible veins but not arteries at the thoracic inlet. The difference in pressure between the intrathoracic arteries and extratboracic veins caused blood to move from the chest into the extrathoracic vascular system. 67 The mechanism implies that with chest compression-systole blood flows from the lungs through the left atrium, and an open mitral valve, left ventricle and aorta into the systemic circulation. During the release of chest compression-diastole intrathuracic pressure falls below that of the extrathoracic venous pressure and blood returns to the lungs. With this

Lactic acidosis during closed-chest CPR in dogs

Survival after out-of-hospital cardiac arrest is intimately related to the time from cardiovascular collapse to the initiation of CPR, or downtime. Furthermore, the reperfusion technique that optimizes coronary and cerebral blood flow after cardiac arrest may also be dependent on downtime. Peak blood lactate levels have been shown to be unchanged throughout resuscitation and predictive of downtime in dogs subjected to cardiopulmonary arrest and open cardiac massage. The purpose of this study was to determine the course of arterial lactate levels in dogs subjected to a fibrillatory cardiopulmonary arrest and conventional closed-chest CPR (CCPR). Fourteen dogs were subjected to five minutes of cardiopulmonary arrest and 30 minutes of CCPR. Resuscitation was performed according to a standardized protocol. Arterial lactic acid samples were collected at timed intervals throughout the experiment. Mean arterial lactic acid levels increased significantly with each sampling interval during 30 minutes of CCPR (overall P less than .05). In nine dogs successfully resuscitated, there were no significant differences in mean arterial lactic acid levels after the return of spontaneous circulation (ROSC). Open-chest resuscitation after five minutes of ventricular fibrillation in dogs results in peak lactic acid levels that do not change significantly once internal cardiac massage is initiated. In contrast, CCPR in similarly arrested dogs does not appear to provide adequate tissue oxygenation and/or perfusion to prevent continuous lactic acid accumulation.

Natural course of iron delocalization and lipid peroxidation during the first eight hours following a 15-minute cardiac arrest in dogs

Lipid peroxidation is thought to be a major contributing factor in neurological injury following cardiac arrest. Because iron availability is a prerequisite for lipid peroxidation, this experiment was designed to examine the natural time course of iron release, lipid peroxidation, and cerebral polyunsaturated fatty acid content following a 15-minute cardiac arrest in dogs. Large mongrel dogs were anesthetized with ketamine and halothane and divided into three groups of five each. In two groups, cardiac arrest was induced with KCl. After 15 minutes of cardiac arrest, the dogs were resuscitated by five minutes of internal cardiac massage, epinephrine, bicarbonate, and internal defibrillation. All ten dogs were resuscitated and supported by a standard intensive care protocol until tissue harvest. A 3-g portion of parietal cerebral cortex was obtained from the nonischemic dogs (n = 5), or at two hours (n = 5), or eight hours (n = 5) after resuscitation. Total tissue iron was measured by an atomic emission spectrometer; low molecular weight species (LMWS) iron by the o-phenanthroline test on an ultrafiltered sample; and lipid peroxidation by both the thiobarbituric acid test (TBARS) and determination of the tissue content of lipid double bonds, calculated by first fractionating the lipids by gas-liquid chromatography and then measuring the double bonds in each fraction by spectrometry and summing the results. Univariate ANOVA demonstrated all variables except total tissue iron to have significance at P less than .02. At two hours of reperfusion, LMWS iron and TBARS were significantly elevated above nonischemic control levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Arrêt circulatoire par luxation extrapéricardique du cœur

A case is reported of a 33-year-old multiple injured patient with closed chest trauma and an unknown rupture of left pericardium and hemidiaphragm. A peroperative cardiac arrest, one year later, was related to dislocation of the heart. Thoracotomy for internal cardiac massage was responsible for a successful outcome.

Cardiac arrest and resuscitation: Brain iron delocalization during reperfusion

We hypothesize that brain injury from cardiac arrest occurs during reperfusion and is in part mediated by iron-dependent lipid peroxidation. We conducted a study to examine the time course of brain iron delocalization and lipid peroxidation in an animal model of cardiac arrest and resuscitation. Assays for brain tissue iron in low-molecular-weight species (LMWS iron) used the o-phenanthroline test on an ultrafiltered (molecular weight less than 30,000) tissue sample; malondialdehyde (MDA), a product of lipid peroxidation, in brain tissue was assayed by the thiobarbituric acid test (TBA). Samples of the parietal cortex from 11 nonischemic control dogs (Group 1) had LMWS iron levels of 9.6 +/- 4.9 nmol/100 mg tissue and MDA levels of 7.7 +/- 2.0 nmol/100 mg tissue. Samples from the parietal cortex taken from five dogs after 15 minutes of cardiac arrest (Group 2) had LMWS iron levels of 9.3 +/- 3.1 nmol/100 mg tissue and MDA levels of 6.1 +/- 1.0 nmol/100 mg tissue. Samples from the parietal cortex taken from five dogs after 45 minutes of cardiac arrest (Group 3) had LMWS iron levels of 6.7 +/- 3.3 nmol/100 mg tissue and MDA levels of 5.6 +/- 0.4 nmol/100 mg tissue. There was no significant difference among the three groups for either LMWS iron or MDA. Five dogs were subjected to 15 minutes of cardiac arrest and definitive resuscitation by internal cardiac massage and defibrillation (Group 4). Following resuscitation the chest was closed and the dogs were given intensive care for two hours.(ABSTRACT TRUNCATED AT 250 WORDS)

Prolonged cardiac arrest and resuscitation in dogs: Brain mitochondrial function with different artificial perfusion methods

Clinical techniques for artificial perfusion have not previously been examined directly for their effects on brain high-energy metabolism. Our study involved 24 large mongrel dogs that were anesthetized, instrumented for central venous intravenous access, and subjected to craniotomy to expose the dura and underlying parietal cortex. The animals were divided into the following six experimental groups of four animals each: nonischemic controls; 15-minute cardiac arrest without resuscitation; 45-minute cardiac arrest without resuscitation; 15-minute cardiac arrest plus 30 minutes resuscitation with conventional cardiopulmonary resuscitation (CPR); 15-minute cardiac arrest plus 30 minutes resuscitation with interposed abdominal compression (IAC) CPR; and 15-minute cardiac arrest plus 30 minutes resuscitation with internal cardiac massage. Cardiac arrest was induced by central venous injection of KCl 0.6 mEq/kg, and it was confirmed by continuous ECG monitoring. The three active resuscitation models included administration of NaHCO3 and epinephrine, but no attempt was made to restart the heart by defibrillation during resuscitation. At the indicated time in each group, a 4- to 5-g sample of brain was removed through the craniotomy, immediately cooled to 0 C and processed for isolation of mitochondria. The mitochondria were studied for their content of superoxide dismutase and for quantitative oxygen consumption with glutamate/malate substrate during resting and ADP-stimulated respiration. Our results show a significant drop in brain mitochondrial superoxide dismutase activity during the first 15 minutes of cardiac arrest. There is minimal injury to brain mitochondrial oxygen consumption during both 15 and 45 minutes of complete ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Advantages of Open Chest Cardiopulmonary Resuscitation (OCCPR)

Introduction: Although the hemodynamic superiority of open chest cardiopulmonary resuscitation has long been recognized, its advantages with respect to the brain have only recently been investigated. Yashon demonstrated the ability of open chest CPR to maintain EEG activity during prolonged resuscitation. Alifimoff showed improved cerebral reco-very in dogs after open chest CPR. Byrne has demonstrated that internal cardiac massage can provide nearly normal cerebral blood flow in dogs as opposed to the 30% of normal seen during standard CPR, which consists of 60 chest compressions per min with a ventilation interposed after every fifth compression and 50% compression duration.

Improved resuscitation from cardiac arrest with open-chest massage

A study was done to assess the effect of open-chest massage on resuscitation from cardiac arrest. Ten mongrel dogs weighing 20.3 +/- 3.2 kg were fibrillated electrically. Cardiopulmonary resuscitation (CPR) was initiated and continued for 15 minutes. Half the dogs with coronary perfusion pressures less than 30 mm Hg underwent thoracotomy and internal cardiac massage for three minutes. Closed-chest massage was continued with the other dogs. All dogs were defibrillated at 19 minutes, and resuscitation was determined at 20 minutes after defibrillation. None of the dogs in the closed-chest massage group was resuscitated successfully. Four of the five dogs that underwent open cardiac massage were resuscitated. Significant differences in aortic pressures and coronary perfusion pressures were noted for the first two minutes of open-chest massage (P less than .05). The results of this study indicate that resuscitation may be improved using open-chest massage when closed-chest massage fails to produce an adequate coronary perfusion pressure.

Efficacy of absorption of sublingual and intravenous cardio-green

To simulate the effect of sublingual injections on pediatric patients, open-chested kid goats were injected sublingually or peripherally with Cardio-Green while being supported by internal cardiac massage. Our study demonstrates that there is statistically a ten-fold lower central blood level after sublingual injection compared to that after use of the peripheral intravenous route. Our experiment casts doubt on whether absorption through the sublingual route is adequate, and shows that if a peripheral intravenous line cannot be started, vigorous attempts should be made to obtain a central line rather than taking valuable time to inject sublingual drugs. Further studies must be done before these results can be applied to clinical situations.

Resuscitation of the Multiply Injured Patient

The resuscitation of the traumatized patient with multisystem injuries begins on the scene of the incident, continues into the emergency department, and finally includes the surgeon and the operating room. Treatment of the traumatized patient requires a systematic approach to best utilize all facilities and personnel while limiting duplication of service. The patient must go to the facility that best meets his or her needs. Stabilization in the emergency department should proceed in an orderly and organized fashion. Care must be taken when establishing the airway to protect the cervical spine. Massive hemothorax, tension pneumothorax, cardiac tamponade, intraabdominal bleeding, and retroperitoneal bleeding, as well as flail chest, must be remedied before stabilization and resuscitation can come to a successful outcome. Internal cardiac massage may need to be done for cardiac tamponade or when resuscitation has failed. Fluid repletion must be vigorous and aggressive. Albumin is probably of no benefit to the patient and, in fact, may be deleterious. Hetastarch may turn out to be a valuable addition to the fluid management of these patients. The patient is entitled to one physician who can call the consultants together. In addition, there should be a single physician for the patient who can control the timing of operative intervention as well as coordinate the overall management by the consultants.

Improved survival from cardiac arrest with open chest massage

Improved survival from cardiac arrest with open chest massage

Cerebral cortical perfusion during and following resuscitation from cardiac arrest in dogs

Perfusion of the cerebral cortex during closed chest CPR in dogs, generating systolic pressures of 60 to 70 mmHg, is only 10% of pre-arrest blood flow. In contrast, internal cardiac massage produces normal cortical perfusion rates. Following a 20-min perfusion arrest, during pressure controlled reperfusion, cortical flow rates decay to less than 20% normal after 90 min of reperfusion. This appears to be due to increasing cerebral vascular resistance, and is not due to rising intracranial pressure. The post-arrest cortical hypoperfusion syndrome is prolonged with cortical flow remaining below 20% normal up to 18 hr post arrest. The use of a variety of calcium antagonists, including flunarizine, lidoflazine, verapamil, and Mg 2+, immediately post-resuscitation maintains cerebral vascular resistance and cortical perfusion at normal levels. A prospective blind trial of the calcium antagonist lidoflazine following a 15-min cardiac arrest in dogs and resuscitation by internal massage, demonstrates amelioration of neurologic deficit in the early post-resuscitation period.

Contrasts between intrathoracic pressures during external chest compression and cardiac massage.

Pressures were measured in the right atrium, thoracic aorta, and pleural space during conventional cardiopulmonary resuscitation (CPR) and simultaneous ventilation compression cardiopulmonary resuscitation (SVC-CPR) in dogs, pigs, and a baboon. During both forms of closed chest resuscitation, the changes in atrial and aortic pressures were virtually identical over a range of 0-90 mm Hg and essentially equaled the change in pleural pressure measured at the most lateral portion of the chest cavity. During internal cardiac massage, there was no consistent relationship between right atrial and aortic pressures. However, even after the chest had been opened, the hemodynamics of external chest compression could be restored by the creation of a closed, air filled cavity surrounding the heart and great vessels. Thus, elevation of intrathoracic pressure, not direct cardiac compression, is essential to and determine circulation of blood during CPR.

Penetrating left ventricular stab wound: a method of control during resuscitation and prior to repair

A 34-year-old man with left ventricular stab wounds, suffered cardiac arrest soon after arriving in the Intensive Care Unit from the Accident and Emergency Department. He had cardiac tamponade without elevation of his central venous pressure; this was because of exsanguination into his left hemithorax. Immediate thoracotomy while still in his bed confirmed tamponade and revealed two large left ventricular stab wounds, one anterior and one posterior; the heart was in ventricular fibrillation. As he had already been anoxic for some time, no effort could be made to repair the stab wounds before resuscitating him. It was neccessary to control bleeding from two separate injuries while replacing volume, continuing with intracardiac drugs, internal cardiac massage and internal defibrillation. This was achieved by inserting a Foley catheter into each wound, inflating the balloons, clamping the catheters and having the assistant gently retracting the catheters against each other while the operator continued with the resuscitation. When the circulation was restored, pledgeted horizontal mattress sutures were inserted on either side of each Foley catheter, which was with-drawn immediately before tying the suture. The patient was discharged home 12 days later without any complications.

Physiology of cardiopulmonary resuscitation.

.,7410Myron L. Weisfeldt, M. D. and Nisha Chandra, M. D.,Peter Belfer Laboratory for Myocardial Research and the Cardiology Division,The Johns Hopkins Medical Institutions, Baltimore, Maryland 21205INTRODUCTIONFor 20 years sternal compression has been used to create artificialcirculation in patients following cardiac arrest (15), and the mechanism forthe resulting movement of blood to the brain was thought to be understood.The arrested heart was viewed as a rubber ball filled with fluid with one-wayvalves at its entrance and exit. The heart is situated between the sternumand the vertebral column, thus chest compression moves the ster-num and was thought to compress the heart against the vertebral col-umn. Such compression, like internal cardiac massage, moved blood fromthe left ventricle into the aorta as the aortic valve opened. Retrograde flowwas prevented by mitral valve closure. Following the period of compressionthe left ventricle filled with blood when the mitral valve opened.This widely held concept appeared inconsistent with a number of obser-vations in animal models (21) and man (17), but no alternative mechanismsfor the movement of blood were suggested. In the dog arterial and venouspressures during chest compression were similar if not identical (21). fact, the high intrathoracic venous pressure was considered by some (17, 21 to point to an important injurious effect of external massage. It wasassumed that the very high intrathoracic venous pressures were transmittedperipherally to the brain and caused brain injury.Only recently did it become clear that other mechanisms beside cardiaccompression operate during chest compression. These new suggestions (20)

A comparison of standard, "MAST"-augmented, and open-chest CPR in dogs. A preliminary investigation.

Hemodynamic, respiratory, and cerebral variables during 2 h of standard external CPR were studied in 5 dogs. In an additional 12 dogs, possible augmentation of these variables by Military Anti-Shock Trousers (MAST) was evaluated. In 9 dogs, external and internal cardiac massage were compared. During ventricular fibrillation (VF) and after 2 min of circulatory arrest, standard CPR basic life support (without drug support) could sustain only borderline values: systolic arterial pressure (SAP) remained at 70--80 mm Hg and mean arterial pressure (MAP) at 35--45 mm Hg. Sternal compressions increased central venous pressure (CVP) to near SAP, and also increased intracranial pressure (ICP), but less than CVP. Thus, systemic perfusion pressures (SPP, i.e., MAP-mean CVP) control value 130 mm Hg) were only 11--15 mm Hg; and cerebral perfusion pressures (CPP, i.e., MAP-ICP) were 20--32 mm Hg during CPR. Common carotid arterial blood flow (CCABF) remained at an average of 8--20% of control values. Normalization of aerobic metabolism proved impossible (final pHa of 7.1). During external CPR, MAST inflation moderately increased MAP, SAP, SPP, and CPP; and significantly increased CCABF from 6.8 to 13.2% of prearrest control. The MAST failed to improve cerebral venous PO2, pupil signs, and EEG activity. With fixed pressure IPPV/100% O2, the MAST decreased tidal volumes and PaO2 (increased shunting); and increased PaCO2 and acidemia. Epinephrine 1 mg iv improved arterial pressures but not flows. A switch to open-chest (internal) cardiac massage (OCCM) after 2 h of external CPR significantly increased arterial and perfusion pressures (decreased venous pressures) and more than doubled CCABF; and resulted in a return of EEG activity and pupillary constriction. Prolonged standard CPR, and to a lesser extent MAST-augmented CPR, seem unlikely to maintain adequate oxygen transport for vital organ systems viability, particularly the brain. OCCM might better sustain viability.

A simple method of resuscitation and short-term preservation of the canine cadaver heart

A simple technique of resuscitation of the canine cadaver heart is described. The method includes internal manual cardiac massage and positive-pressure ventilation of the lungs after isolation of the heart-lung preparation from the rest of the systemic circulation. This techniqle proved successful in 20 of 25 cases after periods of anoxic cardiac arrest ranging from 15 to 128 minutes (average 35 minutes). An evaluation of the state of the myocardium in the postresuscitation period was made by a number of hemodynamic, electrocardiographic, blood chemistry, and histopathological observations, with particular note being taken of those relating to left ventricular contractility and to hematoxylin-basic fuchsin-picric acid (HBFP) staining.

Aortocoronary Artery Graft During Early and Late Phases of Acute Myocardial Infarction

From April, 1968, to August, 1972, 30 patients received one to three emergency saphenous vein grafts during acute myocardial infarction. In all but 1 patient, acute myocardial infarction occurred while the patients were in the hospital awaiting coronary angiography or myocardial revascularization. The patients were divided into two groups: those in the early and those in the late phases of acute myocardial infarction, depending on the time interval between the onset of chest pain and operation. Twenty-four patients (early phase) received grafts within 10 hours after the onset of infarction, and 18 of these 24 patients underwent operation within 4 hours after infarction. Two patients included in this group sustained myocardial infarctions in the operating room during elective myocardial revascularization procedures; another patient was brought to the operating room following cardiac arrest and was supported by internal cardiac massage throughout the opening of the chest and cardiac cannulation. Six patients (late phase) received grafts from three to fourteen days after acute infarction because of postinfarction angina. Only 1 patient was in cardiogenic shock prior to operation. Two patients, both from the early phase group, died in the postoperative period; and 1 patient died seven months postoperatively from a noncardiac cause. Twenty-five of 27 surviving patients became asymptomatic, and 2 patients continue to have mild angina (Functional Class II). Sixteen patients with 24 grafts were restudied in the postoperative period, and 22 of the grafts were found to be patent. This experience suggests that early operative intervention in acute myocardial infarction by the saphenous vein graft technique is beneficial to the patient. The rationale of revascularization in the early phase of acute myocardial infarction is to minimize the area of muscle necrosis by increasing perfusion to the ischemic myocardium around the infarct.

A Method of Augmenting Coronary Perfusion during Internal Cardiac Massage

A method of open cardiac massage employing alternate manual compression of the heart and the ascending aorta is described. Coronary sinus blood flows were measured and compared during ventricular fibrillation in ten dogs while circulation was maintained either by cardiac massage and aortic countercompression or by conventional massage alone. The results of 90 sets of comparisons show that coronary sinus blood flow was significantly greater during massage and aortic countercompression than during massage alone. This method offers an easily applied means of selective diastolic augmentation to increase coronary flow during internal cardiac massage.

Technique of Compression in Closed-Chest Cardiac Massage

THE SUCCESSFUL reversal of cardiac arrest by cardiopulmonary resuscitation has been well documented. The controversal question of whether external or internal cardiac massage is more effective has still not been solved. Recent evidence favors the use of open-chest cardiac massage if appropriaate facilities are available and the patient has not responded to 10 to 15 minutes of closed-chest massage.¹Higher cardiac output with open-chest resuscitation has been shown in animals²as well as man.³The difference in part may be due to the lower mean arterial pressure obtained with external cardiac massage. With cardiac arrest and cessation of circulation, there is a sudden rise of venous pressure and a similar fall in arterial pressure so that the two equilibrate at 20 to 25 mm Hg.¹If cardiac output is to follow traditional pressure flow relationships (flow = pressure/resistance) the mean arterial pressure must be higher than 25