Zeitschrift für Kardiologie
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Review
[Diagnosis, prevention and therapy of pulmonary complications in heart surgery interventions].
Pulmonary complications after cardiac surgery may be caused by preexisting disorders of the respiratory system, common risk factors (e.g., smoking), kind and duration of the surgical procedure, and the anesthesia performed. Preoperative lung function measurements do not allow a valid assessment of the frequency and severity of postoperative complications. However, the efficacy of the peroperative management with bronchodilating agents (beta 2-agonists, theophylline, corticosteroids) in patients with airflow limitation should be based on repeated lung-function testing. ⋯ Atelectasis and gas-exchange disturbances during anesthesia can be treated by ventilation with PEEP. An adequate and immediate management of postoperative pulmonary complications (atelectasis, respiratory failure, pneumonia) improves the outcome of patients after cardiac surgery. The role of perioperative physiotherapy for the reduction of pulmonary complications after cardiac surgery is not well established.
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Adverse effects of converting enzyme inhibitors are either substance-specific (neutropenia, proteinuria, skin rashes, taste disturbances) or due to the converting enzyme inhibition (hypotension, functional renal insufficiency, hyperkalemia, cough, angioedema). They are rare nowadays because of better knowledge of the pharmacokinetics and -dynamics of the converting enzyme inhibitors, resulting in lower dosage, and because of identifying patients at high risk. ⋯ Patients with collagen vascular disease, for example, systemic lupus erythematosus or scleroderma, should not be considered for long-term therapy with converting enzyme inhibitors because of the increased risk of neutropenia. Life-threatening angioedema may develop, mainly during the first few hours after drug administration.
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Despite numerous experimental and clinical investigations, the exact mechanisms involved in the development of cardiac pain are not completely understood. Sensory receptors for painful stimuli, presumably sympathetic sensory nerve endings, are located in the atria, the ventricles, and in the walls of the coronary arteries. These receptors fire at a background rate under normal hemodynamic conditions. ⋯ Still unknown is the role of the afferent vagal fibers in pain perception; however, a modulating influence on pain threshold and characteristics seems possible. Two main mechanisms may be responsible for cardiac pain during ischemic periods: a) chemical excitation of free sensory nerve endings by substances such as bradykinin, PGE2, adenosine, histamine, serotonin, or K+; b) abnormal motion of ischemic segments (dyskinesia, bulging) during systole and excitation of mechanical receptors by passive stretching, and probably a combination of a) and b): the release of chemical substances sensitizes mechanical receptors and lowers their threshold for nociceptive stimuli. These can be suppressed at various spinal or supraspinal levels.
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Cardiac nociceptive afferences are mainly transmitted by sympathetic nervous tracts. After passing the ganglion stellatum and neighbouring ganglia, the nerves enter the dorsal horn of the spinal cord at C8-Th9 (especially Th2-Th6). Here the nerve synapses for the first time, mainly to neurons which run up to the thalamus contralaterally by the tractus spinothalamicus. ⋯ Patients with silent myocardial ischemia have higher beta-endorphin levels compared to symptomatic patients at the same exercise level. This can be interpreted as expressing quantitative differences in a superior pain regulation system. Myocardial ischemia is experienced as angina pectoris pain when the peripheral nociceptive impulse rate is so pronounced that the prevailing inhibitory pain threshold can be overcome and when the pain pathways are intact.