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The AHA Committee on Emergency Cardiac Care recommends that all communities strengthen the four links in the chain of survival: Early Access: Install an enhanced 911 emergency dispatch system. Provide certification training to all emergency medical dispatchers. Develop community-wide education and publicity programs that focus on cardiac emergencies and a proper response by citizens. Early CPR: Implement and support community CPR training programs. In these programs emphasize early recognition, early telephone contact with the EMS system, and early defibrillation. Use training methods that will increase the likelihood that citizens will start CPR. Adopt targeted CPR programs. Implement programs for dispatcher-assisted CPR. Early Defibrillation: Adopt the principle of early defibrillation. Train all emergency personnel who perform basic CPR to operate an automated external defibrillator. Implement more widespread use of automated external defibrillators by community responders and allied health responders. Early Advanced Life Support: Coordinate advanced life support units with first-response units that provide early defibrillation. Develop procedures that combine rapid defibrillation by first-response units with rapid intubation and intravenous medications by the advanced life support units.
Heart Dis Stroke
PMID:The "chain of survival" concept: how it can save lives. 134 85

Cardiovascular reflexes were studied during immersion in water to the chest. Cardiac output (CO) was determined by acetylene rebreathing; forearm muscle and subcutaneous blood flow by 133Xe-clearance; and cutaneous blood flow by laser Doppler. Measurements were taken in a) control situation (CTR) (subject sitting dry); b) immersed in thermoneutral (NWI); c) in cold (CWI); and d) in hot water (HWI). The overall trend was that water immersion per se increased stroke volume (SV), but mostly during NWI and CWI, where heart rate (HR) was decreased by 15%; during HWI, HR increased by 32%, the temperature effect evidently overriding the immersion effect. Insignificant increases in CO were seen in NWI and HWI (18% and 44%), and no effect in CWI. Arterial pressure and total peripheral resistance (TPR) increased significantly in CWI due to an increase in peripheral vascular resistance, while significant decreases in TPR and CPR were observed in HWI and tendencies to decreases were found in NWI.
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PMID:Peripheral and central blood flow in man during cold, thermoneutral, and hot water immersion. 159 79

Using a standardized porcine CPR-model (3 min of cardiac arrest induced by ventricular fibrillation) the effects of epinephrine (10 micrograms/kg iv, 50 micrograms/kg iv, 100 micrograms/kg endobronchially, eb) and norepinephrine (10 micrograms/kg iv, 100 micrograms/kg eb) on resuscitability and early post-resuscitation haemodynamics were compared. Success rate was 100% after epinephrine 10 micrograms/kg iv and 100 micrograms/kg eb, 75% after epinephrine 50 micrograms/kg iv, 80% after norepinephrine iv and 60% after norepinephrine eb. In an unmedicated control group 50% of all animals were successfully resuscitated. Early post-resuscitation haemodynamics in the high dose epinephrine group were characterized by tachycardia and progredient myocardial failure, while in the norepinephrine groups a low cardiac output was accompanied by small cardiac stroke volumes and an increased vascular resistance. It is concluded that iv or eb epinephrine given in standard doses has still to be considered as the drug therapy of choice after short term cardiac arrest or in the presence of ventricular fibrillation. Before different drugs or dosing strategies can be recommended, further experimental and clinical validation is required.
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PMID:[New standards for catecholamine therapy in cardiopulmonary resuscitation? Results of a modified application in a resuscitation model]. 163 6

The empiric administration of 50% dextrose to all patients presenting to the ED with altered mental status is a standard of care predicated on the assumption that glucose administration is harmless to nonhypoglycemic patients. Considerable evidence now disputes this assumption. Glucose administration before complete cerebral ischemia in experimental animals worsens neurologic and histologic outcome. Administration of glucose during severe incomplete ischemia has a similar detrimental effect. The translation of these experimental findings into clinical practice has been slow, perhaps hindered by the frequent use of rodent models and large bolus doses of glucose. However, evidence is now provided by primate and human studies and by experimental designs using clinically relevant doses of glucose. These clinical and experimental findings in conjunction with the wide availability of a rapid bedside screen for hypoglycemia provide the rationale for an alteration in the standard of care. The empiric administration of glucose should be avoided in patients at risk of cerebral ischemia, such as those with acute stroke, impending cardiac arrest, or severe hypotension or receiving CPR. A bedside fingerstick blood glucose estimation should be performed immediately on all patients presenting with altered mental status. The administration of 50% dextrose should be reserved for those patients in whom hypoglycemia is demonstrated; this practice will uphold Hippocrates' most basic principle of clinical medicine, "The physician must...do no harm."
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PMID:50% dextrose: antidote or toxin? 212 May 1

The empiric administration of 50% dextrose to all patients presenting to the ED with altered mental status is a standard of care predicated on the assumption that glucose administration is harmless to non-hypoglycemic patients. Considerable evidence now disputes this assumption. Glucose administration before complete cerebral ischemia in experimental animals worsens neurologic and histologic outcome. Administration of glucose during severe incomplete ischemia has a similar detrimental effect. The translation of these experimental findings into clinical practice has been slow, perhaps hindered by the frequent use of rodent models and large bolus doses of glucose. However, evidence is now provided by primate and human studies and by experimental designs using clinically relevant doses of glucose. These clinical and experimental findings in conjunction with the wide availability of a rapid bedside screen for hypoglycemia provide the rationale for an alteration in the standard of care. The empiric administration of glucose should be avoided in patients at risk for cerebral ischemia, such as those with acute stroke, impending cardiac arrest, or severe hypotension or receiving CPR. A bedside fingerstick blood glucose estimation should be performed immediately on all patients presenting with altered mental status. The administration of 50% dextrose should be reserved for those patients in whom hypoglycemia is demonstrated; this practice will uphold Hippocrates' most basic principle of clinical medicine, "The physician must ... do no harm."
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PMID:50% dextrose: antidote or toxin? 218 38

Heat stroke and other hyperthermia-related crises are serious clinical problems in childhood and adolescence. Rapid cooling is required to reduce morbidity and mortality. A variety of effective cooling methods exist, and some may interfere with monitoring and resuscitation or are not readily available. We studied in 12 pigtail monkeys the pathophysiology of immersion hyperthermia (42 degrees C) to cardiac arrest (1 min no flow) and CPR plus cooling to normothermia for restoration and stabilization of spontaneous normotension. This was followed by intractable shock and secondary arrest. These studies gave us the opportunity to compare two simple cooling methods applied during and after CPR: group I (n = 6) received application of ice bags to the groins, axillae, and neck. Group II (n = 6) received ice bags plus cold water wetting (sponging) over the entire anterior surface of trunk and extremities, plus fanning. CPR restored spontaneous circulation in four of six in each group, after CPR of 1.5-16 min (NS between groups). Speed of cooling correlated with speed of stabilization of spontaneous normotension. After cardiac arrest and during and after CPR, rectal temperature had declined from a lethal level of 42.2 degrees C to a safe level of 38.5 degrees C within 45 +/- 6 (38-53) min in group I, and within 28 +/- 4 (23-32) min in group II (p less than 0.05). Epidural and esophageal temperatures declined more rapidly than rectal temperature. For critical hyperthermia, we recommend immediate application of ice bags, cold water wetting (sponging), fanning, and head cooling combined when invasive blood cooling (the most effective method) is not immediately available.
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PMID:Evaporative cooling as an adjunct to ice bag use after resuscitation from heat-induced arrest in a primate model. 232 Mar 92

Current research on the efficacy of CPR in specific patient groups may lead to the withholding of CPR in groups that statistically show minimal success. Prognosticative factors that indicate minimal-at-best success with CPR include age greater than 70, dysrhythmias such as asystole and electromechanical dissociation, sepsis, metastatic cancer, GI hemorrhage, and acute stroke. Although physicians are under no legal or ethical obligation to provide futile treatments, how one defines a treatment as "futile" is unclear. As a patient advocate, the nurse acts to ensure the autonomous patient is fully informed, freely consenting, and actively directing his/her own health care. End-of-life decisions regarding health care must be based on the patient's goals, which will be revealed through the moral discourse among health care professionals, patients, and their loved ones.
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PMID:Limiting care: is CPR for everyone? 235 36

The following parameters were monitored simultaneously in 15 dogs, in order to evaluate the efficacy of conventional CPR (C-CPR), new CPR (N-CPR), and open-chest CPR (O-CPR) on cerebral perfusion: arterial blood pressure (BP), central venous pressure (CVP), intrathoracic airway pressure, blood flow in carotid artery, intracranial pressure (ICP), sagittal sinus blood flow (sinus BF) and pressure (sinus P), and blood flow in cerebral cortex (cortical BF). The sinus blood flow was measured by the direct-method and with a cannulating electromagnetic flowmeter. The cortical blood flow was measured with a termocouple tissue flowmeter. Intracranial pressure was obtained by measuring subarachnoid cerebrospinal fluid pressure. Ventricular fibrillation was induced electrically. Chest compression and ventilation were always done manually in all cardiopulmonary resuscitation. The mean blood pressures during C-CPR, N-CPR and O-CPR were 52, 68 and 95 mmHg, respectively, and mean carotid blood flows per stroke were 36, 71 and 131% of the control values, respectively. The intracranial pressures were 30, 42 and 36 mmHg, respectively, giving the calculated cerebral perfusion pressures (BP-ICP) of 22, 27 and 60 mmHg, respectively. This should have been reflected in cerebral blood flow. Sinus blood flows/min were 18, 18 and 42%, and sinus blood flows per stroke were 55, 45 and 127% of control values, respectively; the differences between C-CPR and N-CPR were not significant. This was also true for cortical blood flow. From this we conclude that, firstly, N-CPR is not significantly better than C-CPR in cerebral perfusion because of its accompanying high intracranial pressure, secondly, O-CPR is far superior to the other two methods in respect of cerebral perfusion.
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PMID:Cerebral blood flow during conventional, new and open-chest cardio-pulmonary resuscitation in dogs. 609 Dec 3

It has been generally accepted that enhanced blood flow during closed-chest CPR is generated from compression of the heart between the sternum and the spine. To visualize the heart during closed-chest massage, we performed two-dimensional echocardiography (2DE) during resuscitation efforts in four patients who had cardiac arrest. 2DE analysis showed that (1) the LV internal dimensions did not change appreciably with chest compression; (2) the mitral and aortic valves were open simultaneously during the compression phase; (3) blood flow into the right heart, as evidenced by saline bubble contrast, occurred during the relaxation phase; and (4) compression of the right ventricle and LA occurred in varying amounts in all patients. We conclude that stroke volume from the heart during CPR does not result from compression of the LV. Rather, CPR-induced improved cardiocirculatory dynamics appear to be principally the result of changes in intrathoracic pressure created by sternal compression.
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PMID:Clinical assessment of heart chamber size and valve motion during cardiopulmonary resuscitation by two-dimensional echocardiography. 727 Mar 85

Based upon an anecdotal report of successful resuscitation using a toilet plunger, Cohen and co-workers have developed and investigated a hand-held suction cup as an adjunct to standard manual CPR. This new method, called active compression-decompression cardiopulmonary resuscitation, utilizes a device which is placed over the mid-sternum, approximately 1-2 inches above the lower rib cage border. Active compression-decompression cardiopulmonary resuscitation is then performed in accordance with American Heart Association guidelines at a rate equal to 80-100/min using a 50% duty cycle and compression depth of 1.5-2.0 inches. Initial studies using the ACD device in both models and human subjects late after cardiac arrest have demonstrated improved cardiopulmonary hemodynamics when compared to standard manual CPR. Transophageal echocardiographic studies in human subjects have shown increased left ventricular filling during active decompression suggesting that active chest decompression improves venous return to the heart thus increasing left ventricular volume and stroke volume. Improved resuscitation success has also been documented in human subjects after in-hospital and pre-hospital cardiac arrest. Active compression-decompression cardiopulmonary resuscitation is a simple method which utilizes a hand held suction cup as an interface between rescuer and victim during closed chest circulatory support. This method allows for standard manual cardiopulmonary resuscitation with the addition of active chest wall decompression and appears to be a beneficial adjunct to standard manual cardiopulmonary resuscitation.
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PMID:Clinical and laboratory investigations of active compression-decompression cardiopulmonary resuscitation. 780 80


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