Lester T. Proctor

Part 13: Pediatric Basic Life Support 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care

In contrast to adults, cardiac arrest in infants and children does not usually result from a primary cardiac cause. More often it is the terminal result of progressive respiratory failure or shock, also called an asphyxial arrest. Asphyxia begins with a variable period of systemic hypoxemia, hypercapnea, and acidosis, progresses to bradycardia and hypotension, and culminates with cardiac arrest.1 Another mechanism of cardiac arrest, ventricular fibrillation (VF) or pulseless ventricular tachycardia (VT), is the initial cardiac rhythm in approximately 5% to 15% of pediatric in-hospital and out-of-hospital cardiac arrests;2,–,9 it is reported in up to 27% of pediatric in-hospital arrests at some point during the resuscitation.6 The incidence of VF/pulseless VT cardiac arrest rises with age.2,4 Increasing evidence suggests that sudden unexpected death in young people can be associated with genetic abnormalities in myocyte ion channels resulting in abnormalities in ion flow (see “Sudden Unexplained Deaths,” below). Since 2010 marks the 50th anniversary of the introduction of cardiopulmonary resuscitation (CPR),10 it seems appropriate to review the progressive improvement in outcome of pediatric resuscitation from cardiac arrest. Survival from in-hospital cardiac arrest in infants and children in the 1980s was around 9%.11,12 Approximately 20 years later, that figure had increased to 17%,13,14 and by 2006, to 27%.15,–,17 In contrast to those favorable results from in-hospital cardiac arrest, overall survival to discharge from out-of-hospital cardiac arrest in infants and children has not changed substantially in 20 years and remains at about 6% (3% for infants and 9% for children and adolescents).7,9 It is unclear why the improvement in outcome from in-hospital cardiac arrest has occurred, although earlier recognition and management of at-risk patients on general inpatient units …

2005 American Heart Association (AHA) guidelines for cardiopulmonary resuscitation (CPR) and emergency cardiovascular care (ECC) of pediatric and neonatal patients: Pediatric advanced life support

This publication presents the 2005 American Heart Association (AHA) guidelines for cardiopulmonary resuscitation (CPR) and emergency cardiovascular care (ECC) of the pediatric patient and the 2005 American Academy of Pediatrics/AHA guidelines for CPR and ECC of the neonate. The guidelines are based on the evidence evaluation from the 2005 International Consensus Conference on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations, hosted by the American Heart Association in Dallas, Texas, January 23–30, 2005. The “2005 AHA Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care” contain recommendations designed to improve survival from sudden cardiac arrest and acute life-threatening cardiopulmonary problems. The evidence evaluation process that was the basis for these guidelines was accomplished in collaboration with the International Liaison Committee on Resuscitation (ILCOR). The ILCOR process is described in more detail in the “International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations.” The recommendations in the “2005 AHA Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care” confirm the safety and effectiveness of many approaches, acknowledge that other approaches may not be optimal, and recommend new treatments that have undergone evidence evaluation. These new recommendations do not imply that care involving the use of earlier guidelines is unsafe. In addition, it is important to note that these guidelines will not apply to all rescuers and all victims in all situations. The leader of a resuscitation attempt may need to adapt application of the guidelines to unique circumstances. The following are the major pediatric advanced life support changes in the 2005 guidelines: There is further caution about the use of endotracheal tubes. Laryngeal mask airways are acceptable when used by experienced providers. Cuffed endotracheal tubes may be used in infants (except newborns) and children in in-hospital settings provided that cuff inflation pressure is kept <20 cm H2O. Confirmation of tube placement requires clinical assessment and assessment of exhaled carbon dioxide (CO2); esophageal detector devices may be considered for use in children weighing >20 kg who have a perfusing rhythm. Correct placement must be verified when the tube is inserted, during transport, and whenever the patient is moved. During CPR with an advanced airway in place, rescuers will no longer perform “cycles” of CPR. Instead, the rescuer performing chest compressions will perform them continuously at a rate of 100/minute without pauses for ventilation. The rescuer providing ventilation will deliver 8 to 10 breaths per minute (1 breath approximately every 6–8 seconds). Timing of 1 shock, CPR, and drug administration during pulseless arrest has changed and now is identical to that for advanced cardiac life support. Routine use of high-dose epinephrine is not recommended. Lidocaine is de-emphasized, but it can be used for treatment of ventricular fibrillation/pulseless ventricular tachycardia if amiodarone is not available. Induced hypothermia (32–34°C for 12–24 hours) may be considered if the child remains comatose after resuscitation. Indications for the use of inodilators are mentioned in the postresuscitation section. Termination of resuscitative efforts is discussed. It is noted that intact survival has been reported following prolonged resuscitation and absence of spontaneous circulation despite 2 doses of epinephrine. The following are the major neonatal resuscitation changes in the 2005 guidelines: Supplementary oxygen is recommended whenever positive-pressure ventilation is indicated for resuscitation; free-flow oxygen should be administered to infants who are breathing but have central cyanosis. Although the standard approach to resuscitation is to use 100% oxygen, it is reasonable to begin resuscitation with an oxygen concentration of less than 100% or to start with no supplementary oxygen (ie, start with room air). If the clinician begins resuscitation with room air, it is recommended that supplementary oxygen be available to use if there is no appreciable improvement within 90 seconds after birth. In situations where supplementary oxygen is not readily available, positive-pressure ventilation should be administered with room air. Current recommendations no longer advise routine intrapartum oropharyngeal and nasopharyngeal suctioning for infants born to mothers with meconium staining of amniotic fluid. Endotracheal suctioning for infants who are not vigorous should be performed immediately after birth. A self-inflating bag, a flow-inflating bag, or a T-piece (a valved mechanical device designed to regulate pressure and limit flow) can be used to ventilate a newborn. An increase in heart rate is the primary sign of improved ventilation during resuscitation. Exhaled CO2 detection is the recommended primary technique to confirm correct endotracheal tube placement when a prompt increase in heart rate does not occur after intubation. The recommended intravenous (IV) epinephrine dose is 0.01 to 0.03 mg/kg per dose. Higher IV doses are not recommended, and IV administration is the preferred route. Although access is being obtained, administration of a higher dose (up to 0.1 mg/kg) through the endotracheal tube may be considered. It is possible to identify conditions associated with high mortality and poor outcome in which withholding resuscitative efforts may be considered reasonable, particularly when there has been the opportunity for parental agreement. The following guidelines must be interpreted according to current regional outcomes: When gestation, birth weight, or congenital anomalies are associated with almost certain early death and when unacceptably high morbidity is likely among the rare survivors, resuscitation is not indicated. Examples are provided in the guidelines. In conditions associated with a high rate of survival and acceptable morbidity, resuscitation is nearly always indicated. In conditions associated with uncertain prognosis in which survival is borderline, the morbidity rate is relatively high, and the anticipated burden to the child is high, parental desires concerning initiation of resuscitation should be supported. Infants without signs of life (no heartbeat and no respiratory effort) after 10 minutes of resuscitation show either a high mortality rate or severe neurodevelopmental disability. After 10 minutes of continuous and adequate resuscitative efforts, discontinuation of resuscitation may be justified if there are no signs of life.

Opioid‐mediated muscle afferents inhibit central motor drive and limit peripheral muscle fatigue development in humans

We investigated the role of somatosensory feedback from locomotor muscles on central motor drive (CMD) and the development of peripheral fatigue during high‐intensity endurance exercise. In a double‐blind, placebo‐controlled design, eight cyclists randomly performed three 5 km time trials: control, interspinous ligament injection of saline (5KPlac, L3–L4) or intrathecal fentanyl (5KFent, L3–L4) to impair cortical projection of opioid‐mediated muscle afferents. Peripheral quadriceps fatigue was assessed via changes in force output pre‐ versus postexercise in response to supramaximal magnetic femoral nerve stimulation (ΔQtw). The CMD during the time trials was estimated via quadriceps electromyogram (iEMG). Fentanyl had no effect on quadriceps strength. Impairment of neural feedback from the locomotor muscles increased iEMG during the first 2.5 km of 5KFentversus 5KPlac by 12 ± 3% (P < 0.05); during the second 2.5 km, iEMG was similar between trials. Power output was also 6 ± 2% higher during the first and 11 ± 2% lower during the second 2.5 km of 5KFentversus 5KPlac (both P < 0.05). Capillary blood lactate was higher (16.3 ± 0.5 versus 12.6 ± 1.0%) and arterial haemoglobin O2 saturation was lower (89 ± 1 versus 94 ± 1%) during 5KFentversus 5KPlac. Exercise‐induced ΔQtw was greater following 5KFentversus 5KPlac (−46 ± 2 versus−33 ± 2%, P < 0.001). Our results emphasize the critical role of somatosensory feedback from working muscles on the centrally mediated determination of CMD. Attenuated afferent feedback from exercising locomotor muscles results in an overshoot in CMD and power output normally chosen by the athlete, thereby causing a greater rate of accumulation of muscle metabolites and excessive development of peripheral muscle fatigue.

Group III and IV muscle afferents contribute to ventilatory and cardiovascular response to rhythmic exercise in humans

We investigated the role of somatosensory feedback on cardioventilatory responses to rhythmic exercise in five men. In a double-blind, placebo-controlled design, subjects performed the same leg cycling exercise (50/100/150/325 ± 19 W, 3 min each) under placebo conditions (interspinous saline, L(3)-L(4)) and with lumbar intrathecal fentanyl impairing central projection of spinal opioid receptor-sensitive muscle afferents. Quadriceps strength was similar before and after fentanyl administration. To evaluate whether a cephalad migration of fentanyl affected cardioventilatory control centers in the brain stem, we compared resting ventilatory responses to hypercapnia (HCVR) and cardioventilatory responses to arm vs. leg cycling exercise after each injection. Similar HCVR and minor effects of fentanyl on cardioventilatory responses to arm exercise excluded direct medullary effects of fentanyl. Central command during leg exercise was estimated via quadriceps electromyogram. No differences between conditions were found in resting heart rate (HR), ventilation [minute ventilation (VE)], or mean arterial pressure (MAP). Quadriceps electromyogram, O(2) consumption (VO(2)), and plasma lactate were similar in both conditions at the four steady-state workloads. Compared with placebo, a substantial hypoventilation during fentanyl exercise was indicated by the 8-17% reduction in VE/CO(2) production (VCO(2)) secondary to a reduced breathing frequency, leading to average increases of 4-7 Torr in end-tidal PCO(2) (P < 0.001) and a reduced hemoglobin saturation (-3 ± 1%; P < 0.05) at the heaviest workload (∼90% maximal VO(2)) with fentanyl. HR was reduced 2-8%, MAP 8-13%, and ratings of perceived exertion by 13% during fentanyl vs. placebo exercise (P < 0.05). These findings demonstrate the essential contribution of muscle afferent feedback to the ventilatory, cardiovascular, and perceptual responses to rhythmic exercise in humans, even in the presence of unaltered contributions from other major inputs to cardioventilatory control.

Pediatric Advanced Life Support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care

For best survival and quality of life, pediatric basic life support (BLS) should be part of a community effort that includes prevention, early cardiopulmonary resuscitation (CPR), prompt access to the emergency response system, and rapid pediatric advanced life support (PALS), followed by integrated post–cardiac arrest care. These 5 links form the American Heart Association (AHA) pediatric Chain of Survival (Figure 1), the first 3 links of which constitute pediatric BLS. FIGURE 1. Pediatric Chain of Survival. Rapid and effective bystander CPR can be associated with successful return of spontaneous circulation (ROSC) and neurologically intact survival in children following out-of-hospital cardiac arrest.1,–,3 Bystander resuscitation may have the greatest impact for out-of-hospital respiratory arrest,4 because survival rates >70% have been reported with good neurologic outcome.5,6 Bystander resuscitation may also have substantial impact on survival from primary ventricular fibrillation (VF), because survival rates of 20% to 30% have been documented in children with sudden out-of-hospital witnessed VF.7 Overall about 6%8 of children who suffer an out-of-hospital cardiac arrest and 8% of those who receive prehospital emergency response resuscitation survive, but many suffer serious permanent brain injury as a result of their arrest.7,9,–,14 Out-of-hospital survival rates and neurological outcome can be improved with prompt bystander CPR,3,6,15,–,17 but only about one third to one half of infants and children who suffer cardiac arrest receive bystander CPR.3,9,12,18 Infants are less likely to survive out-of-hospital cardiac arrest (4%) than children (10%) or adolescents (13%), presumably because many infants included in the arrest figure are found dead after a substantial period of time, most from sudden infant death syndrome (SIDS).8 As in adults, survival is …

Implications of group III and IV muscle afferents for high‐intensity endurance exercise performance in humans

Non‐Technical Summary  We investigated the influence of group III/IV muscle afferents on central motor drive, the development of peripheral locomotor muscle fatigue, and endurance performance time during high‐intensity constant‐load cycling exercise to exhaustion. Our findings suggest that, on the one hand, afferent feedback ensures adequate circulatory and ventilatory responses to exercise which optimizes muscle O2 transport and thereby facilitates exercise performance by preventing premature peripheral fatigue. On the other hand, afferent feedback inhibits central motor drive, which is reflected in the restriction of the neural excitation of the locomotor musculature and the reduced tolerance for peripheral muscle fatigue, and thereby limits exercise performance. Taken together, the current investigation revealed the net effects of sensory afferent feedback on time to exhaustion during high‐intensity constant‐load cycling exercise and showed that intact group III/IV muscle afferent feedback is a vital component in achieving optimal endurance performance.

Somatosensory feedback from the limbs exerts inhibitory influences on central neural drive during whole body endurance exercise

We investigated whether somatosensory feedback from contracting limb muscles exerts an inhibitory influence on the determination of central command during closed-loop cycling exercise in which the subject voluntarily determines his second-by-second central motor drive. Eight trained cyclists performed two 5-km time trials either without (5K(Ctrl)) or with lumbar epidural anesthesia (5K(Epi); 24 ml of 0.5% lidocaine, vertebral interspace L(3)-L(4)). Percent voluntary quadriceps muscle activation was determined at rest using a superimposed twitch technique. Epidural lidocaine reduced pretime trial maximal voluntary quadriceps strength (553 +/- 45 N) by 22 +/- 3%. Percent voluntary quadriceps activation was also reduced from 97 +/- 1% to 81 +/- 3% via epidural lidocaine, and this was unchanged following the 5K(Epi), indicating the presence of a sustained level of neural impairment throughout the trial. Power output was reduced by 9 +/- 2% throughout the race (P < 0.05). We found three types of significant effects of epidural lidocaine that supported a substantial role for somatosensory feedback from the exercising limbs as a determinant of central command throughout high-intensity closed-loop cycling exercise: 1) significantly increased relative integrated EMG of the vastus lateralis; 2) similar pedal forces despite the reduced number of fast-twitch muscle fibers available for activation; 3) and increased ventilation out of proportion to a reduced carbon dioxide production and heart rate and increased blood pressure out of proportion to power output and oxygen consumption. These findings demonstrate the inhibitory influence of somatosensory feedback from contracting locomotor muscles on the conscious and/or subconscious determination of the magnitude of central motor drive during high intensity closed-loop endurance exercise.

Influence of desflurane, isoflurane and halothane on regional tissue perfusion in dogs

The actions of desflurane, isoflurane and halothane on regional tissue perfusion were studied using radioactive microspheres in dogs chronically instrumented for measurement of arterial and left ventricular pressure, global (left ventricular dP/dtmax) and regional (percent segment shortening) contractile function, and diastolic coronary blood flow velocity. Systemic and coronary haemodynamics and regional tissue perfusion were measured in the conscious state and during anaesthesia with equihypotensive concentrations of desflurane, isoflurane, and halothane. All three volatile anaesthetics (P < 0.05) increased heart rate and decreased mean arterial pressure, left ventricular systolic pressure, and left ventricular dP/dtmax Myocardial perfusion was unchanged in subendocardial, midmyocardial, andsubepicardial regions by the administration of either dose of desflurane. No redistribution of intramyocardial blood flow (endo/epi ratio) was observed during desflurane anaesthesia. Although regional myocardial perfusion was reduced (P < 0.05) in a doserelated fashion by halothane and by isoflurane at high concentrations, redistribution of intramyocardial blood flow was not observed during halothane or isoflurane anaesthesia. All three volatile anaesthetics reduced blood flow to the renal cortex, but only desflurane produced a decrease in renal cortical vascular resistance. Hepatic blood flow decreased in response to halothane but not desflurane or isoflurane. Concomitant decreases in hepatic resistance were observed during administration of desflurane and isoflurane. Doserelated decreases in intestinal and skeletal muscle blood flow were observed during halothane and isoflurane but not desflurane anaesthesia. The results suggest that desflurane maintains myocardial, hepatic, intestinal, and skeletal muscle blood flow while halothane and isoflurane decrease regional tissue perfusion in these vascular beds to varying degrees during systemic hypotension in the chronically instrumented dog.RésuméCe travail étudie les effets du desflurane, de l’isoflurane et de l’halothane sur la perfusion régionale à l’aide de microsphères radioactives sur des chiens préparés à demeure pour mesures itératives de la tension artérielle et ventriculaire gauche, de la contractilité globale (dP/dtmax ventriculaire gauche) et régionale (index de raccourcissement segmentaire) ainsi que de la vélocité du débit coronarien diastolique. L’hémodynamique systémique et coronaire et la perfusion régionale ont été mesurées à l’état de conscience et pendant l’anesthésie avec des concentrations hypotensives équivalentes de desflurane, d’isoflurane et d’halothane. Les trois agents (P < 0,05) ont augmenté la fréquence cardiaque et diminué la tension artérielle moyenne et le dP/dtmax ventriculaire gauche. La perfusion myocardique est demeurée inchangée aux régions subendocardique, midendocardique et subépicardique pendant l’administration de desflurane. On n’observe pas de redistribution du débit intramyocardique (rapport endo./épi.) pendant l’anesthésie au desflurane. Bien que la perfusion régionale soit réduite (P < 0,05) de façon proportionnelle pour les concentrations élevées d’isoflurane et d’halothane, la redistribution de débit sanguin myocardique n’est pas observée pendant l’anesthésie avec ces agents. Alors que les trois agents volatils diminuent le débit sanguin au cortex rénal, seul le desflurane en diminue la résistance vasculaire. Le débit sanguin hépatique diminue sous halothane mais non sous isoflurane et desflurane. Une diminution simultanée des résistances hépatiques survient pendant l’administration de desflurane et d’isoflurane. Des baisses de débit sanguin à l’intestin et aux muscles squelettiques proportionnelles à la concentration sont observées pendant l’anesthésie à l’halothane et l’isoflurane mais ne surviennent pas sous desflurane. Ces résultats suggèrent le maintien par le desflurane des débits sanguins myocardique, hépatique, intestinal et musculaire alors que l’halothane et l’isoflurane diminuent la perfusion tissulaire régionale de ces lits vasculaires à différents degrés pendant l’hypotension systémique chez le chien.

A novel alpha2-adrenoceptor antagonist attenuates the early, but preserves the late cardiovascular effects of intravenous dexmedetomidine in conscious dogs☆

OBJECTIVES To test the hypothesis that L-659,066, a peripherally acting alpha 2-adrenoceptor agonist, will abolish the early pressor response but preserve the late depressor action of intravenous dexmedetomidine in conscious, unsedated dogs. DESIGN A prospective investigation. SETTING A laboratory research. PARTICIPANTS Nine chronically instrumented dogs. INTERVENTIONS Dogs received dexmedetomidine, 5 micrograms/kg intravenously, in the presence or absence of L-659,066, 0.1, 0.2, or 0.4 mg/kg intravenously, pretreatment in a random fashion determined with a Latin square design on different experimental days. MEASUREMENTS AND MAIN RESULTS Systemic and coronary hemodynamics were assessed under control conditions, 30 minutes after administration of L-659,066 and 5 and 60 minutes after intravenous administration of dexmedetomidine. Dexmedetomidine alone acutely increased mean arterial pressure (106 +/- 3 to 175 +/- 4 mmHg; p < 0.05), left ventricular (LV) systolic and end-diastolic pressures, systemic vascular resistance (3,400 +/- 350 to 13,360 +/- 2,290 dyne.s.cm-5; p < 0.05), and coronary vascular resistance (2.69 +/- 0.19 to 4.18 +/- 0.43 mmHg.Hz-1.10(-2); p < 0.05) and decreased LV +dP/dtmax and cardiac output (2.6 +/- 0.3 to 1.3 +/- 0.2 L/min; p < 0.05). Dexmedetomidine alone decreased heart rate, mean arterial pressure, and LV systolic pressure and caused sustained reductions in +dP/dtmax and cardiac output up to 60 minutes after administration. L-659,066 alone increased heart rate, +dP/dtmax, cardiac output, and coronary blood flow velocity and decreased systemic vascular resistance. Mean arterial and LV pressures and coronary vascular resistance were unchanged. Pretreatment with L-659,066 abolished the acute dexmedetomidine-induced increases in mean arterial pressure, LV pressures, systemic and coronary vascular resistance and decreases in +dP/dtmax and cardiac output. In contrast, reductions in mean arterial pressure and LV systolic pressure observed 60 minutes after administration of dexmedetomidine were preserved in dogs receiving L-659,066. Cardiac performance, systemic vascular resistance, and coronary hemodynamics were also maintained to a greater degree 60 minutes after dexmedetomidine administration in the presence of L-659,066. CONCLUSION L-659,066 prevents the immediate pressor effects of 5 micrograms/kg of intravenous dexmedetomidine but preserves the majority of the late beneficial cardiovascular effects of this selective alpha 2-adrenoceptor agonist in conscious dogs.

α-Adrenergic control of blood flow during exercise: effect of sex and menstrual phase

Sex differences exist in autonomic control of the cardiovascular system. This study was designed to directly test sex or female menstrual phase-related differences in α-adrenergic control of blood flow during exercise. We hypothesized that women would exhibit reduced α-adrenergic vasoconstriction compared with men during exercise; in addition, women would constrict less during the early luteal than the early follicular phase of the female menses. Young men (n = 10) were studied once and women (n = 9) studied twice, once during the early follicular phase and once during the early luteal phase of female menses. We measured forearm blood flow (FBF; Doppler ultrasound of the brachial artery) during rest and steady-state dynamic exercise (15 and 30% of maximal voluntary contraction, 20 contractions/min). A brachial artery catheter was inserted for the local administration of α-adrenergic agonists [phenylephrine (PE; α(1)) or clonidine (CL; α(2))]. Blood flow responses to exercise [forearm vascular conductance (FVC)] were similar between all groups. At rest, infusion of PE or CL decreased FVC in all groups (40-60% reduction). Vasoconstriction to PE was abolished in all groups at 15 and 30% exercise intensity. Vasoconstriction to CL was reduced at 15% and abolished at 30% intensity in all groups; women had less CL-induced constriction during the early luteal than early follicular phase (P < 0.017, 15% intensity). These results indicate that vasodilator responses to forearm exercise are comparable between men and women and are achieved through similar paths of α-adrenergic vascular control at moderate intensities; this control may differ at low intensities specific to the female menstrual phase.