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S Rubertsson

Publications and source records attributed to S Rubertsson.

29 records · Page 2Linked to original sources

Systemic oxygen uptake during experimental closed-chest cardiopulmonary resuscitation using air or pure oxygen ventilation.

BACKGROUND: Although clinical cardiopulmonary resuscitation always includes ventilation with pure oxygen, this kind of ventilation has been reported to be associated with worse neurological outcome than ventilation with air in experimental cardiopulmonary resuscitation (CPR). The aim of the present investigation was to compare the systemic oxygen uptake during experimental closed-chest CPR including ventilation with pure oxygen or ambient air and, furthermore, to elucidate possible mechanisms of action in the regulation of pulmonary gas exchange. METHODS: In 24 anesthetized piglets, 2 min of induced ventricular fibrillation and no ventilation was followed by 10 min of closed-chest CPR including i.v. administration of 0.5 mg adrenaline (at 8 min), and in one of the experimental groups alkaline buffer (at 5 min). The piglets were randomly divided into 3 groups: air ventilation during the entire CPR period with saline administration (n=8), air ventilation during the entire CPR period plus tris buffer mixture (n=8), and air ventilation for 3 min followed by 100% oxygen with saline administration (n= 8). RESULTS: In the group ventilated with air and treated with tris buffer mixture, cardiac output was significantly greater than in the group ventilated with pure oxygen. The arterial-mixed venous oxygen content difference was approximately 25% greater with pure oxygen than with air ventilation; however, there was no difference in systemic oxygen uptake. Systemic oxygen uptake increased after administration of tris buffer mixture in the group ventilated with air. CONCLUSIONS: Pulmonary hypoxic vasoconstriction appeared to be abolished during CPR including pure oxygen ventilation. Blood flow, not ventilation or pulmonary gas exchange, is the limiting factor during experimental closed-chest CPR.

Adrenergic Agonists↗

Future directions for resuscitation research. V. Ultra-advanced life support.

Standard external cardiopulmonary resuscitation (SECPR) frequently produces very low perfusion pressures, which are inadequate to achieve restoration of spontaneous circulation (ROSC) and intact survival, particularly when the heart is diseased. Ultra-advanced life support (UALS) techniques may allow support of vital organ systems until either the heart recovers or cardiac repair or replacement is performed. Closed-chest emergency cardiopulmonary bypass (CPB) provides control of blood flow, pressure, composition and temperature, but has so far been applied relatively late. This additional low-flow time may preclude conscious survival. An easy, quick method for vessel access and a small preprimed system that could be taken into the field are needed. Open-chest CPR (OCCPR) is physiologically superior to SECPR, but has also been initiated too late in prior studies. Its application in the field has recently proven feasible. Variations of OCCPR, which deserve clinical trials inside and outside hospitals, include 'minimally invasive direct cardiac massage' (MIDCM), using a pocket-size plunger-like device inserted via a small incision and 'direct mechanical ventricular actuation' (DMVA), using a machine that pneumatically drives a cup placed around the heart. Other novel UALS approaches for further research include the use of an aortic balloon catheter to improve coronary and cerebral blood flow during SECPR, aortic flush techniques and a double-balloon aortic catheter that could allow separate perfusion (and cooling) of the heart, brain and viscera for optimal resuscitation of each. Decision-making, initiation of UALS methods and diagnostic evaluations must be rapid to maximize the potential for ROSC and facilitate decision-making regarding long-term circulatory support versus withdrawal of life support for hopeless cases. Research and development of UALS techniques needs to be coordinated with cerebral resuscitation research.

Cardiopulmonary Resuscitation↗

Response of myocardial cellular energy metabolism to variation of buffer composition during open-chest experimental cardiopulmonary resuscitation in the pig.

The aim of the present study was to investigate possible relationships in piglets between myocardial energy-related metabolites and intracellular electrolytes during open-chest cardiopulmonary resuscitation (OCCPR) supplemented by the administration of alkaline buffers with varying sodium content. Our hypothesis was that an increasing myocardial intracellular sodium content would decrease the intracellular energy stores. In addition to haemodynamics, acid-base and blood gas variables were analysed, and myocardial biopsies were collected before and during OCCPR as well as after the return of spontaneous circulation. After a period of 4 min of untreated ventricular fibrillation (VF). 25 piglets were randomly allocated to one of four groups: OCCPR with normal saline (n = 5); OCCPR with sodium bicarbonate (SB) (n = 7); OCCPR with Tris buffer mixture (TBM) (n = 7); and a totally untreated control group (n = 6). The results showed that 4 min of untreated VF almost eradicated creatine phosphate (CrP) and that the ATP/ADP ratio decreased to 1.5-2.0. During OCCPR with normal saline, the myocardial content of CrP increased, whereas lactate, ATP and ADP levelled off and AMP decreased, causing an increased ATP/ADP ratio. The adenosine and inosine contents increased, whereas inosine monophosphate was unchanged at a low level, the adenosine and inosine contents being inversely correlated with the total content of adenine nucleotides. In both buffered groups, the increase in most energy-related metabolites (CrP, ATP, ADP, AMP and the ATP/ADP quotient) was less and in lactate more pronounced than in the group not being buffered, with no difference between the groups receiving SB or TBM. Although the intracellular potassium content was unaltered, the sodium, chloride and calcium concentration increased, more so in the group receiving SB. The intracellular content of sodium was correlated with that of calcium. Thus, buffering increased the myocardial AMP degradation during OCCPR by increasing the flux via the 5'-nucleotidase reaction, and SB increased the intracellular contents of sodium and calcium to a greater extent than did TBM.

Adenosine Diphosphate↗

Effects of intra-aortic balloon occlusion on hemodynamics during, and survival after cardiopulmonary resuscitation in dogs.

OBJECTIVE: To evaluate the effect of balloon occlusion of the proximal descending aorta during cardiopulmonary resuscitation (CPR) on hemodynamics, restoration of spontaneous circulation, and 24-hr survival. DESIGN: Prospective, randomized, controlled trial. SETTING: Experimental laboratory in a university hospital. SUBJECTS: Eighteen anesthetized dogs. INTERVENTIONS; Catheters were placed for hemodynamic and blood gas monitoring. An aortic balloon catheter was placed with its tip just distal to the left subclavian artery. After 10 mins of ventricular fibrillation without CPR, 3 mins of Basic Life Support (chest compressions and ventilation with 100% oxygen) was followed by up to 30 mins of Advanced Cardiac Life Support with canine drug dosages. In the treatment group (n = 8), the intra-aortic balloon was inflated when Advanced Cardiac Life Support started and not deflated until shortly after restoration of spontaneous circulation. The control animals (n = 10) were treated with an identical resuscitation but without intra-aortic balloon occlusion. MEASUREMENTS AND MAIN RESULTS: In the treatment group, coronary perfusion pressure was greater during Advanced Cardiac Life Support (p = .026). Restoration of spontaneous circulation was more frequent (7/8 dogs) as compared with the control group (3/10 dogs) (p = .025). There was a trend toward greater 24-hr survival in the treatment group (5/8 dogs) than in the control group (3/10 dogs). CONCLUSIONS: Balloon occlusion of the proximal descending aorta during experimental CPR improves restoration of spontaneous circulation. Further laboratory and human studies are needed to determine the clinical efficacy of this technique.

Animals↗

Future directions for resuscitation research. III. External cardiopulmonary resuscitation advanced life support.

This discussion about advanced cardiac life support (ACLS) reflects disappointment with the over 50% of out-of-hospital cardiopulmonary resuscitation (CPR) attempts that fail to achieve restoration of spontaneous circulation (ROSC). Hospital discharge rates are equally poor for in-hospital CPR attempts outside special care units. Early bystander CPR and early defibrillation (manual, semi-automatic or automatic) are the most effective methods for achieving ROSC from ventricular fibrillation (VF). Automated external defibrillation (AED), which is effective in the hands of first responders in the out-of-hospital setting, should also be used and evaluated in hospitals, inside and outside of special care units. The first countershock is most important. Biphasic waveforms seem to have advantages over monophasic ones. Tracheal intubation has obvious efficacy when the airway is threatened. Scientific documentation of specific types, doses, and timing of drug treatments (epinephrine, bicarbonate, lidocaine, bretylium) are weak. Clinical trials have failed so far to document anything statistically but a breakthrough effect. Interactions between catecholamines and buffers need further exploration. A major cause of unsuccessful attempts at ROSC is the underlying disease, which present ACLS guidelines do not consider adequately. Early thrombolysis and early coronary revascularization procedures should also be considered for selected victims of sudden cardiac death. Emergency cardiopulmonary bypass (CPB) could be a breakthrough measure, but cannot be initiated rapidly enough in the field due to technical limitations. Open-chest CPR by ambulance physicians deserves further trials. In searches for causes of VF, neurocardiology gives clues for new directions. Fibrillation and defibrillation thresholds are influenced by the peripheral sympathetic and parasympathetic nervous systems and impulses from the frontal cerebral cortex. CPR for cardiac arrest of the mother in advanced pregnancy requires modifications and outcome data. Until more recognizable critical factors for ROSC are identified, titrated sequencing of ACLS measures, based on physiologic rationale and sound judgement, rather than rigid standards, gives the best chance for achieving survival with good cerebral function.

Animals↗

Blood flow and perfusion pressure during open-chest versus closed-chest cardiopulmonary resuscitation in pigs.

OBJECTIVE: To evaluate the blood flow and perfusion pressure differences observed during open- vs. closed-chest cardiopulmonary resuscitation (CPR), including the effects of epinephrine and sodium bicarbonate administration. DESIGN: Prospective, randomized, controlled trial. SETTING: Experimental animal laboratory in a university hospital. SUBJECTS: A total of 35 anesthetized piglets. INTERVENTIONS: After tracheostomy and insertion of arterial, right atrial, and pulmonary arterial catheters, thoracotomy was performed with placement of a pulmonary arterial flow probe and left atrial catheter. Ventricular fibrillation was induced and followed by 15 mins of either open-chest (n = 14) or closed-chest (n = 21) CPR. A 4-min infusion of 50 mmol of sodium bicarbonate or saline was added at the start of CPR. After 8 mins of CPR, 0.5 mg of epinephrine was given intravenously, and after 15 mins, direct current (DC) shocks were used to revert the heart to sinus rhythm. MEASUREMENTS AND MAIN RESULTS: Blood flow was studied using transit-time ultrasound flowmetry. In an extended group, intrathoracic pressure was measured for calculation of transmural pressure. Before epinephrine administration, mean pulmonary arterial flow (cardiac output) was reduced: a) during closed-chest CPR relatively more than pulmonary perfusion pressure but in proportion to systemic perfusion pressure; b) during open-chest CPR relatively less than pulmonary perfusion pressure but still in proportion to systemic perfusion pressure. Epinephrine administration temporarily increased systemic perfusion pressure during both closed- and open-chest CPR but temporarily decreased pulmonary perfusion pressure only during closed-chest CPR. After epinephrine administration, cardiac output temporarily decreased during both closed-and open-chest CPR. CONCLUSIONS: Open-chest CPR resulted in better cardiac output and systemic perfusion pressure than closed-chest CPR. However, cardiac output values obtained with both methods were much lower than previously reported. After epinephrine administration, cardiac output became extremely low with both methods.

Animals↗

Systemic perfusion pressure and blood flow before and after administration of epinephrine during experimental cardiopulmonary resuscitation.

OBJECTIVES: To evaluate instantaneous blood flow variations in the compression and relaxation phases of cardiopulmonary resuscitation (CPR) and the effect of epinephrine administration. DESIGN: Prospective, randomized, controlled trial. SETTING: Experimental laboratory in a university hospital. SUBJECTS: Twenty-two anesthetized piglets. INTERVENTIONS: A tracheostomy was performed and arterial, central venous, and pulmonary arterial catheters were inserted, followed by thoracotomy with placement of pulmonary arterial, aortic, and left anterior descending coronary arterial (extended study group) flow probes and a left atrial catheter. Ventricular fibrillation for 2 mins was followed by 10 mins of either open-chest (n = 10) or closed-chest (n = 12) CPR. Seven minutes after the initiation of CPR, all piglets received 0.5 mg of epinephrine iv; at 12 mins, direct current shocks were applied. MEASUREMENTS AND MAIN RESULTS: Open-chest CPR generated greater systemic perfusion pressure than closed-chest CPR, especially during the relaxation phase, resulting in greater mean blood flow. With both open- and closed-chest CPR, antegrade pulmonary arterial and aortic blood flow occurred during compression, whereas antegrade left anterior descending coronary arterial blood flow occurred during relaxation. During relaxation, retrograde flow was found in the pulmonary artery and aorta. During compression, retrograde flow was found in the left anterior descending coronary artery. The administration of epinephrine had the following effects: a) increased the systemic perfusion pressure more during open- than closed-chest CPR; b) increased the systemic relaxation perfusion pressure more than the compression perfusion pressure; c) decreased mean pulmonary arterial and aortic blood flow, but substantially increased the mean left anterior descending coronary artery blood flow; and d) reduced the retrograde flow in the left anterior descending coronary artery. CONCLUSIONS: Open-chest CPR generated greater systemic perfusion pressure and blood flow than closed-chest CPR. Epinephrine increased left anterior descending coronary artery blood flow but decreased total cardiac output, such that cerebral perfusion might be endangered. This problem will be studied separately.

Animals↗

Hemodynamic effects of epinephrine in combination with different alkaline buffers during experimental, open-chest, cardiopulmonary resuscitation.

OBJECTIVE: To evaluate the hemodynamic actions of epinephrine combined with different alkaline buffers during experimental, open-chest, cardiopulmonary resuscitation (CPR). DESIGN: Prospective, randomized, controlled trial. SETTING: Experimental animal laboratory in a university hospital. SUBJECTS: A total of 28 anesthetized piglets. INTERVENTIONS: After catheterization and application of a pulmonary artery flow probe (transit-time ultrasound flowmetry), the animals were stabilized. Induction of ventricular fibrillation was followed by a 15-min period of CPR, including manual heart compressions and mechanical ventilation with pure oxygen. On commencement of CPR, a 4-min alkaline buffer infusion began, with 50 mmol of sodium bicarbonate (n = 7), tris buffer mixture (n = 7), or tris buffer (n = 7), or, as a control (n = 7), the same volume of normal saline. After 8 mins of CPR, 0.5 mg of epinephrine was given intravenously; after 15 mins, direct current shocks were used to revert the heart to sinus rhythm. MEASUREMENTS AND MAIN RESULTS: Blood flow measured in the pulmonary artery during open-chest CPR was approximately 20% of normal cardiac output. Administration of epinephrine reduced pulmonary artery flow irrespective of buffer. Sodium bicarbonate alone resulted in higher systemic blood pressure than pure tris: tris buffer mixture and normal saline were intermediate. Sodium bicarbonate combined with epinephrine tended to produce lower systemic blood pressure than other combinations. CONCLUSIONS: Experimental open-chest CPR generates pulmonary artery blood flows (20% of normal cardiac output) that are at best at the lower level of those blood flow rates previously reported (25% to 40% of normal cardiac output) from studies of closed-chest CPR. Different alkaline buffers influence circulatory and acid-base parameters differently before and after administration of epinephrine.

Animals↗

Gas exchange as monitored in mixed venous and arterial blood during experimental cardiopulmonary resuscitation.

Nineteen anaesthetized piglets were investigated. After catheterization and a stabilization period, ventricular fibrillation was induced with a transthoracic DC shock, after which a 10-min period of cardiopulmonary resuscitation (CPR) took place. CPR included manual chest compression and mechanical ventilation with pure oxygen. After 1 min of CPR, an infusion of alkaline buffer was begun and completed within 5 min. A total of 50 mmol of either sodium bicarbonate (n = 6) or tris buffer mixture (n = 7) were given. These two groups were compared with a third control group (n = 6) receiving the same volume of normal saline. After 8 min of CPR all animals were given 0.5 mg adrenaline i.v., and after 10 min DC shocks were used to revert the heart back to normal sinus rhythm. Our results demonstrate that blood flow and not ventilation is the limiting factor for the efficient disposal of CO2 during CPR. This also applied when the demand for CO2 transport was increased by administration of sodium bicarbonate. The respiratory exchange ratio increased 1.9-fold, indicating that the transport of carbon dioxide was less affected than that of oxygen. The estimated alveolo-arterial oxygen tension difference, shunt, and overall ventilation/perfusion ratio increased, creating an inverse hyperbolic relationship between arterial PCO2 and PO2. The difference between mixed venous and arterial PCO2 correlated well to the mixed venous PCO2, implying more efficient pulmonary elimination of PCO2 when the mixed venous PCO2 was high. Pulmonary gas exchange during CPR appears to be independent of alkaline buffer therapy in the form of sodium bicarbonate or tris buffer mixture.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Kinetics of carbon dioxide during cardiopulmonary resuscitation.

CO2 kinetics during CPR was investigated in 15 anesthetized piglets. BP, blood gases, and acid-base balance were monitored through catheters in the carotid artery and a central vein, as well as in cerebrospinal fluid. Cardiac arrest was induced by a transthoracic direct current shock. CPR was begun immediately by artificial ventilation and simultaneous external chest compressions. Epinephrine was administered after 8 min of CPR. One group (n = 5) of animals received no buffer treatment while another (n = 5) received an infusion of 75 mmol sodium bicarbonate and a third group (n = 5) received an equivalent amount of tris-buffer mixture. The results of these experiments, as well as previously described circulatory variables during CPR, were analyzed using a computer model describing the CO2 kinetics of the pig. Our main finding was that PaCO2 was positively correlated to cardiac output during CPR; improved cardiac output during CPR resulted in more efficient tissue CO2 elimination and was associated with increased survival rates. PaCO2 was also somewhat reduced by efficient alveolar hyperventilation. The arterial PCO2 and pH did not reflect the acid-base balance in peripheral tissues. During CPR, bicarbonate and tris-buffer mixture both quickly passed through the blood-brain barrier. When buffer treatment is indicated during CPR, a buffer which does not increase tissue PCO2 may be the drug of choice.

Acid-Base Equilibrium↗

Improved haemodynamics and restoration of spontaneous circulation with constant aortic occlusion during experimental cardiopulmonary resuscitation.

Continuous balloon occlusion of the descending aorta is an experimental method that may improve blood flow to the myocardium and the brain during cardiopulmonary resuscitation (CPR). The aim of the present investigation was to evaluate the effects of this intervention on haemodynamics and the frequency of restoration of spontaneous circulation. Ventricular fibrillation was induced in 39 anaesthetised piglets, followed by an 8-min non-intervention interval. In a haemodynamic study (n = 10), closed chest CPR was performed for 7 min before the intra-aortic balloon was inflated. This intervention increased mean arterial blood pressure by 20%, reduced cardiac output by 33%, increased coronary artery blood flow by 86%, and increased common carotid artery blood flow by 62%. All these changes were statistically significant. Administration of epinephrine further increased mean arterial blood pressure and coronary artery blood flow, while cardiac output and common carotid artery blood flow decreased. In a study of short-term survival, nine out of 13 animals (69%) in the balloon group and in three out of 13 animals (23%) in the control group had spontaneous circulation restored. The difference between these two proportions was 0.46, which was statistically significant with a 95% confidence interval from 0.12 to 0.80. In conclusion, balloon occlusion of the descending aorta increased coronary and common carotid artery blood flow and the frequency of restoration of spontaneous circulation. It was also noted that epinephrine appears to augment the redistribution of blood flow caused by the aortic occlusion.

Adrenergic Agonists↗