Cardiac asthma presenting as status asthmaticus: deleterious effect of epinephrine therapy.

Epinephrine is a potent bronchodilator currently used to treat severe asthma, although there is no proven advantage of this drug over beta 2 adrenergic agonists. By contrast, as demonstrated here, the use of such a potent vasoconstrictor can worsen hemodynamic status when left ventricular dysfunction is associated with asthma or is the cause for dyspnea. We describe the case of a 60-year-old man with an history of chronic asthmatic bronchitis admitted for status asthmaticus. Bronchodilator therapy, including high dosages of intravenous epinephrine, failed to improve the patient and he was intubated and mechanically ventilated. Several hours later, a right heart catheterization revealed severe unexpected left heart dysfunction with a capillary wedge pressure of 45 mmHg and a cardiac index of 1.7 l/min/m2. Epinephrine was gradually stopped which resulted in a decrease in mean arterial blood pressure and an improvement of hemodynamic status. He was discharged on home mechanical ventilation. In this patient, ischemic left heart failure was revealed by a clinical picture mimicking status asthmaticus. Epinephrine, given as bronchodilator therapy on an empiric basis precipitated the patient into cardiogenic shock. Therefore this drug should not be recommended in face of the possibility of cardiac asthma or associated cardiac dysfunction.

Nebulized morphine for paroxysmal cough and dyspnea in a nursing home resident with metastatic cancer.

Nursing homes continue to be challenged with the task of caring for patients in various stages of disease. Historically, the death of a long-term care patient in this setting is not unusual; however, researchers and clinicians are focusing increasingly on the quality of life at the end of life, regardless of location. The long-term care facility is an ideal setting in which to begin to effectively address these issues, especially as individual patients in need present for care. Although the care of many of our geriatric patients meets the definition of palliative care, no where is the need greater, and more obvious, than in the patient presenting with terminal illness. Aggressive treatment of distressing symptomatology contributes to overall quality of life, and returns to the patient some of the freedom and autonomy usurped by the disease process. It is particularly rewarding for the interdisciplinary team to be successful in controlling symptoms in the patient with limited life expectancy, thus allowing the patient to complete unfinished tasks and enjoy quality time with family and friends. Often the "triumphs" in the nursing home are few and fleeting; abolishing pain, distress, and suffering is both personally and professionally satisfying for everyone involved. We presented a review of the available literature on a technique in palliative medicine which is still evolving. Additional, we presented its practical use in a frail, elderly nursing home resident admitted with end-stage metastatic breast carcinoma. The geriatric adage of "start low, and go slow" was effectively borne out in the management of this resident's most difficult symptoms, shortness of breath and paroxysmal cough leading to symptomatic atrial fibrillation. The key to the management of the frail elderly patient goes beyond " start low and go slow" to "aggressively titrate as needed but no further" in order to meet the needs of the individual patient and avoids unwanted side effects.

[Experience in using nitroglycerin in the acute period of myocardial infarct]. / Opyt primeneniia nitroglitserina v ostrom periode infarkta miokarda.

To treat the left ventricular insufficiency, complicating myocardial infarction, and to limit the area of the ischemic damage of myocardium the authors used nitroglycerin solution. It is established that the nitroglycerin injection stops effectively the acute left ventricular insufficiency in myocardial infarction. Results of investigations show the decrease of the ischemic zone of the damaged myocardium in the acute period of infarction under the influence of nitroglycerin. It is concluded that intravenous drop administration of nitroglycerin is rational, under thorough control of the arterial pressure, the central venous pressure and intracardiac haemodynamics.

[Effect of drugs on the permeability of the histohematic barriers in a complicated course of myocardial infarct]. / Medikamentoznoe vozdeistvie na pronitsaemost' gistogematicheskikh bar'erov pri oslozhnennom techenii infarkta miokarda.

The investigations have shown the pathogenetic role of enhanced capillary permeability on the development of myocardial infarction and its complications. To a definite degree the above disorders are conditioned by the activation of the kallikrein-kinin system. This made us try contrykal with heparin in the comprehensive system of treatment of these patients. A clear-cut clinical and laboratory effect has been obtained which justifies recommending the use of protease inhibitors in complicated myocardial infarction.

[Therapeutic use of nitroglycerin in pulmonary edema and cardiac asthma in myocardial infarct patients]. / Lechebnoe primenenie nitroglitserina pri oteke legkikh i serdechnoi astme u bol'nykh infarktom miokarda.

The effect of sublingual medication with nitroglycerin taken in a dose of 0.5-1 mg was studied in 101 patients with myocardial infarction (77 had pulmonary edema and 34 had cardiac asthma). In patients with edema of the lungs nitroglycerin reduced dyspnoea, in some cases of cardiac asthma it arrested the attack. It was found that nitroglycerin reduced central venous pressure, the diastolic-systolic index of the pulmonary rheogram, the systolic, diastolic and mean pressure in the pulmonary artery, and arterial pressure in the greater circulation. With the intake of the drug, cardiac output decreased almost significantly, whereas the peripheral pressure did not change. It is concluded that the use of nitroglycerin in a dose of 0.5 mg in the treatment of cardiac asthma and pulmonary edema in patients with acute myocardial infraction is advisable.

Application of a combination of sublingually administered vasodilating drugs for rapid action on pulmonary hypertension in patients with cardiac asthma and with pulmonary oedema.

Eight patients with pulmonary oedema and 6 patients with cardiac asthma (primary disease: in 7 patients acute myocardial infarction, in 6--hypertension, in 1--mitral defect) were given sublingually a combination of 0.5 mg nitroglycerin, 10 mg Isodinit (isosorbid dinitrate) and 4 mg Sidnofarm (molsidomine) in powder form. This resulted in a rapid, pronounced and protracted reduction of dyspnoea, pulmonary congestion, respiration rate, and heart rate in the course of a four-hour observation rate, in more than 80% of cases. In patients with high blood pressure it dropped by 27% vs. the initial level; in patients with hypotension the change was only minimal. Pulmonary diastolic pressure began to drop from the 3rd minute after administration of the agents and the maximal decrease was attained after 30 min (34% of the initial value); even 4 hours after administration the values were below the initial level. The mentioned drug combination appears to be valuable especially in the first stage of treatment of cardiac asthma and pulmonary oedema.

Asthma, beta-agonists, and development of congestive heart failure: results of the ABCHF study.

BACKGROUND: Previous studies demonstrated an association between asthma and idiopathic dilated cardiomyopathy (IDCM), raising concerns regarding chronic beta-agonist inhaler use. The purpose of this investigation was to replicate that association. METHODS AND RESULTS: We identified 67 patients with IDCM and 130 controls with predominately ischemic cardiomyopathy. Patients were administered a structured, detailed phone survey by blinded interviewers, and had chart abstractions performed. We had 80% power to detect an odds ratio (OR) > or = 2.6 for the relation of asthma and IDCM. A history of asthma was present in 19.4% v 12.3% for cases and controls respectively, OR, 1.72, (95% confidence interval [CI], 0.72, 4.09), P = .18. The duration of asthma was higher in cases: 32.3 (19.7) years v 13.8 (15.0) years (P = 0.007). With adjustment for confounders, multivariate analyses revealed no significant relations between asthma or beta-agonist use and the later development of IDCM. CONCLUSIONS: It is unlikely that previously occurring asthma or beta-agonist use has a strong relationship to the development of IDCM; however, IDCM and atopic diseases may cluster in families, warranting further work into the genetic relations between atopy and IDCM.