John M. Field

Part 1: Executive Summary 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care

The goal of therapy for bradycardia or tachycardia is to rapidly identify and treat patients who are hemodynamically unstable or symptomatic due to the arrhythmia. Drugs or, when appropriate, pacing may be used to control unstable or symptomatic bradycardia. Cardioversion or drugs or both may be used to control unstable or symptomatic tachycardia. ACLS providers should closely monitor stable patients pending expert consultation and should be prepared to aggressively treat those with evidence of decompensation.

Part 1: Executive Summary

Mary Fran Hazinski, Co-Chair*; Jerry P. Nolan, Co-Chair*; John E. Billi; Bernd W. Böttiger; Leo Bossaert; Allan R. de Caen; Charles D. Deakin; Saul Drajer; Brian Eigel; Robert W. Hickey; Ian Jacobs; Monica E. Kleinman; Walter Kloeck; Rudolph W. Koster; Swee Han Lim; Mary E. Mancini; William H. Montgomery; Peter T. Morley; Laurie J. Morrison; Vinay M. Nadkarni; Robert E. O’Connor; Kazuo Okada; Jeffrey M. Perlman; Michael R. Sayre; Michael Shuster; Jasmeet Soar; Kjetil Sunde; Andrew H. Travers; Jonathan Wyllie; David Zideman

Implementation and Integration of Prehospital ECGs Into Systems of Care for Acute Coronary Syndrome A Scientific Statement From the American Heart Association Interdisciplinary Council on Quality of Care and Outcomes Research, Emergency Cardiovascular Care Committee, Council on Cardiovascular Nursing, and Council on Clinical Cardiology

Clinical case: A 58-year-old woman called 9-1-1 with acute onset of chest pain that had persisted for 30 minutes. She had a history of hypertension, hyperlipidemia, and type 2 diabetes mellitus but no previous history of myocardial infarction or heart failure. Her medications included aspirin, atorvastatin, lisinopril, and metoprolol. Paramedics were dispatched, and a prehospital ECG demonstrated 3- to 4-mm ST-segment elevation in leads I, aVL, and V2 through V6 (Figure 1). Her examination revealed a regular pulse of 90 bpm, a blood pressure of 100/60 mm Hg, clear lungs, and normal heart sounds with no murmurs. Paramedics interpreted the prehospital ECG and activated the catheterization laboratory en route to the hospital. On hospital arrival, the patient was transported directly to the catheterization laboratory. Coronary angiography demonstrated an occluded proximal left anterior descending artery, which was successfully treated with balloon angioplasty and a stent. The pertinent time intervals were as follows: paramedic dispatch to balloon time, 56 minutes; paramedic arrival at the scene to balloon time, 46 minutes; hospital door to balloon time, 23 minutes. Her biomarkers revealed a peak troponin T of 2.42 ng/mL and a peak creatine kinase muscle-brain isoenzyme of 26.8 ng/mL. An echocardiogram demonstrated normal left ventricular ejection fraction of 55%, with mild anterior hypokinesis, and the patient was discharged on hospital day 3. Figure 1. Prehospital ECG. American Heart Association national guidelines,1–3 as well as other consensus and scientific statements,4–11 recommend that emergency medical services (EMS) acquire and use prehospital ECGs to evaluate patients with suspected acute coronary syndrome. Despite these recommendations, prehospital ECGs are used in fewer than 10% of patients with ST-segment–elevation myocardial infarction (STEMI),12,13 and this rate has not substantially changed since the mid-1990s. Furthermore, even when a prehospital ECG is acquired, the information is often not …

Cardiac catheterization in morbidly obese patients

The safety and findings of cardiac catheterization and coronary angiography in morbidly obese patients with suspected coronary heart disease (CHD) have not been fully examined in the modern era. From a database of 4,978 patients undergoing diagnostic cardiac catheterization, we identified 110 with morbid obesity (body mass ≥ 145 kg and body mass index ≥ 40 kg/m2). Relative to all the other patients in this database, morbidly obese patients had a lower prevalence of CHD (45% vs. 72%; P < 0.05), reflecting a higher prevalence of false positive noninvasive tests. Overall, noninvasive tests were only 75% sensitive and 39% specific for CHD in this group. Use of radial access (66%) and femoral closure devices (24%) was much more frequent in the morbidly obese cohort. Complications were no more frequent in the morbidly obese group, with major (0 vs. 0.9%) and minor (4.7% vs. 3.5%) adverse outcomes being similar to the rest of the database. We conclude that cardiac catheterization using the radial artery or a femoral closure device is a safe and effective method of evaluating CHD in morbidly obese patients. In contrast, noninvasive testing is frequently not definitive and may be misleading. Cathet Cardiovasc Intervent 2002;56:174–177.

Effects of morphine sulfate on human coronary blood flow.

Because morphine causes coronary vasoconstriction in conscious dogs, human coronary blood flow was measured with the thermodilution technique before and after administration of morphine sulfate, 0.2 mg/kg body weight (maximum 15 mg) intravenously, in 10 patients to determine if the canine experience is clinically applicable. Coronary blood flow increased from a baseline value of 104.4 +/- 13.4 (mean +/- standard error of the mean) to 113.0 +/- 17.4 ml/min (difference not significant) 15 minutes after the administration of morphine. Baseline coronary vascular resistance was 1.14 +/- 0.19 mm Hg/ml/min; 15 minutes after morphine administration the resistance value was 1.02 +/- 0.17 (P less than 0.025). There was no significant change between baseline values and values 15 minutes after morphine administration in systemic mean arterial pressure (98.2 +/- 5.3 to 92.8 +/- 4.7 mm Hg); heart rate (69.5 +/- 3.5 to 72.6 +/- 3.4 beats/min), left ventricular ejection time (0.345 +/- 0.009 to 0.342 +/- 0.007 second) or tension-time index (2,324 +/- 128 to 2,291 +/- 149 mm Hg/sec per min). The slight coronary vasodilation noted after morphine administration in this study is in marked contrast to the significant coronary vasoconstriction demonstrated in the unanesthetized dog.

Oral terbutaline sulfate--amelioration of exercise-induced bronchospasm.

Bronchospasm can be induced in asthmatics when exercised according to a multistage branching treadmill protocol that allows them to achieve 80 per cent of their age-predicted maximal heart rate. This present study was undertaken to investigate the effect of oral terbutaline sulfate in ameliorating exercise-induced bronchospasm. Ten asthmatics were exercised, and FEV1.0 and MMEFR were assessed while standing, using a Jones Pulmonar II waterless spirometer at 5, 15, and 30 minutes after exercise. Three hours before exercise, the subjects received no medication, oral placebo, or 5 mg terbutaline sulfate orally. At all time intervals after exercise, the pulmonary function of the group pretreated with oral terbutaline was superior when compared to the no-medication group (P less than 0.01) and to the placebo-treated group (P less than 0.05). Oral terbutaline appeared to normalize the exercise tolerance of the asthmatics and restore physiologic pulmonary airway conductance by the parameters of FEV1.0 and MMEFR.

The pharmacologic effect of aerosolized terbutaline sulfate in exercise-induced bronchospasm.

Bronchospasm can be induced in asthmatics when exercised according to a multistage branching treadmill protocol that allows them to achieve 80 per cent of maximal age-predicted heart rate. This degree of exercise is usually achievable and allows inducible bronchospasm to occur. This present study was undertaken to investigate the effect of terbutaline sulfate aerosol in exercise-induced broncho-spasm. Asthmatics were exercised to 80 per cent of their maximal heart rate, and FEV1.0 and MMEFR were assessed while standing using a Jones Pulmonar II waterless spirometer at 5, 15, and 30 minutes after exercise. After a standard rest period defined by a return to baseline of FEV1.0, MMEFR, and heart rate for 30 minutes, the subjects were administered either 0.50 mg aerosolized terbutaline sulfate or placebo and then exercised again. The pulmonary function parameters were again recorded after this exercise. Preterbutaline and postplacebo exercise resulted in a significant reduction in FEV1.0 and MMEFR, while after treatment with terbutaline not only did bronchospasm not occur but bronchodilation occurred (P less than 0.01). Inhaled terbutaline appeared to normalize the exercise tolerance of the asthmatics and restore physiologic pulmonary airway conductance according to the parameters of FEV1.0 and MMEFR.

Clinical features of left main equivalent coronary disease

Abstract The clinical presentation and hemodynamic, ventriculographic and coronary arterial findings of 70 patients with left main equivalent coronary artery disease (70 percent or greater reduction in luminal diameter of the left anterior descending and left circumflex vessels prior to any major branches) were compared with those of 75 patients with 60 percent or greater reduction in luminal diameter of the left main coronary artery. The group with left main equivalent disease did not differ significantly from the group with left main stenosis in any clinical descriptors including New York Heart Association functional class, age, sex distribution, type of presenting symptom or history of congestive heart failure or myocardial infarction. Similarly, the two groups did not differ in ejection fraction, cardiac index, left ventricular end-diastolic pressure, left ventricular end-diastolic volume index, extent of left ventricular contraction abnormality or prevalence of associated significant right coronary arterial obstruction. Of the 70 patients with left main equivalent disease, 31 were deemed to be in operable condition but did not undergo coronary bypass surgery for 1 or more months (mean 4.2 months, range 1 to 12). With the exception of four patients who underwent early operation because of unremitting symptoms, the groups undergoing early and delayed operation did not differ in symptomatic state. In the interim between cardiac catheterization and delayed operation, no patient died and one patient (3 percent) had an acute myocardial infarction. These low morbidity and mortality rates differ strikingly from those of patients with left main stenosis reported in the randomized Veterans Administration study, although the patients in the two studies manifested comparable severity of symptoms, extent of left ventricular contraction abnormality and associated right coronary disease. The results suggest that left main equivalent disease, as defined by obstruction of the left anterior descending and circumflex coronary arteries, does not carry the same short-term prognosis as left main coronary artery disease, but probably behaves more like ordinary two or, if the right coronary artery is also obstructed, three vessel coronary artery disease. In this sense, the term left main equivalent disease is a misnomer causing an unnecessary sense of urgency and alarm.

Measurement of plasma prostaglandins during exercise-induced bronchospasm

Bronchospasm following exercise is a phenomenon which occurs in most patients with reversible airway disease. The pathophysiologic mechanism leading to this bronchoconstriction with exercise has not yet been defined. Recently, prostaglandins have been implicated in the etiology of asthma. The purpose of this investigation was to determine changes in plasma prostaglandins occurring during exercise-induced asthma. Eight ambulant asthmatics were chosen for baseline pulmonary spirometry and peripheral venous blood prostaglandin E and F levels. The asthmatics were then exercised to 80% of their age-predicted maximal heart rate via a multistage branching treadmill protocol. At 5, 15, and 30 min following exercise, pulmonary spirometry was again performed and peripheral venous blood collected at the indicated times. Clinical bronchospasm as characterized by audible wheezing and greater than 15% decrease in FEV1 and MMEFR was obtained in all of the asthmatics. Peripheral PGE and PGF2alpha determinations following this exercise protocol were not altered significantly: (PGE: 0 min, 238; 5 min, 185; 15 min, 248; 30 min, 256 pg/ml); (PGF2alpha: 0 min, 50; 5 min, 24; 15 min, 25; 30 min, 17 pg/ml) (p less than 0.1). In summary, no significant change in peripheral blood prostaglandin E and F2alpha levels as determined by radioimmunoassay was noted at the time of exercise-induced bronchospasm.

Peripheral plasma determinations of prostaglandin E in asthmatics

Prostaglandins, unsaturated fatty acid derivatives with diversified pharmacologic activity, have recently been implicated in the pathophysiology of reversible airway disease. This study attempted to elucidate baseline prostaglandin E (PGE) plasma levels in asthmatics and the change in these levels after stimulation by a beta-adrenergic agent. Fourteen stable, ambulant patients with reversible airway disease and 28 nonatopic control subjects were studied. All had baseline PGE levels performed. The asthmatics were asked to abstain from all medication for 10 hr prior to evaluation. After baseline evaluation consisting of plasma PGE determination, pulmonary function test, blood pressure, and heart rate, 375 mug of aerosolized terbutaline sulfate was administered to 8 of the asthmatics plus 4 of the nonatopic control subjects; the above measurements were repeated at 15, 30, and 60 min after administration. There was a statistically significant difference in baseline plasma PGE levels between the asthmatics (PGE = 432 +/- 81) and the nonatopic control subjects (PGE = 89 +/- 9) (p less than 0.002). Following terbutaline administration, there was no significant change observed in PGE levels in asthmatic or in control individuals (asthmatics: 0 min, 570, 15 min, 513, 30 min, 514, 60 min, 608; normal subjects: 0 min, 138, 15 min, 137, 30 min, 143, 60 min, 214). In summary, we observed a significant difference in baseline PGE levels between asthmatic and nonatopic control persons. No change, however, was noted in PGE levels after beta-adrenergic receptor stimulation. This observation is consistent with the current hypothesis that beta-adrenergic agents act independently of prostaglandins to increase adenyl cyclase and modify bronchiole smooth muscle tone.