Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In vivo anaphylaxis is associated with respiratory distress and cardiovascular failure. The present investigation was designed to further characterize respiratory and cardiac anaphylactic events. In guinea pigs, sensitization was produced by subcutaneous application of ovalbumin together with Freund's adjuvant. Fourteen days after sensitization, the effects of an intravenous infusion of ovalbumin were tested in the anesthetized artificially ventilated guinea pigs. The renewed application of the antigen induced an initial increase of left ventricular pressure which was followed by a rapid decrease 5 min after antigenic challenge. Enddiastolic left ventricular pressure increased within 3 min, thus indicating left ventricular pump failure. In the same time range, ECG recordings uniformly showed signs of acute myocardial ischemia. In addition, heart rate steadily decreased. All animals died within 15 min. Simultaneously with cardiac anaphylactic malfunction, severe arterial hypoxia and carbon dioxide retention occurred, revealing respiratory distress. Histamine is known as a potent bronchoconstrictor via histamine H1-receptor stimulation. Administration of H1-receptor antagonists to improve respiration may therefore provide further information on the contribution of pulmonary malfunction to anaphylactic cardiovascular shock. Therefore, additional experiments were performed with sensitized guinea pigs pretreated with the histamine H1-receptor blocker mepyramine. In these experiments the antigenic challenge induced a dissociation of cardiac and respiratory manifestation of anaphylaxis. Despite inhibition of hypoxia and carbon dioxide retention, left ventricular pump failure and occurrence of myocardial ischemia were delayed but not suppressed. It is concluded that histamine is an important mediator of anaphylactic respiratory distress. However, vasoactive anaphylactic mediators other than histamine are primarily involved in anaphylactic cardiac malfunction occurring during the later phase of systemic anaphylaxis.
 ...
PMID:Effects of histamine H1-receptor blockade on respiratory and cardiac manifestation of systemic anaphylaxis. 168 6

Acute postoperative hypertension (APH) has been documented in the PACU. Over half of the patients who exhibit APH have pre-existing primary hypertension. Sustained blood pressure (BP) elevation increases the risk of myocardial ischemia, infarction, surgical site bleeding, or cerebral hemorrhage in these patients. Following surgery and anesthesia, increased sympathetic stimulation caused by a high level of circulating catecholamines can lead to APH. Some direct perioperative stimulants include pain, anxiety, hypoxia, hypercapnia, hypothermia, shivering, volume overload, and bladder distension. Nursing interventions are directed toward identifying and relieving the cause of APH. Antihypertensive drug therapy with vasodilators or adrenergic inhibitors is used if initial nursing interventions are not effective. Vasodilators frequently used are hydralazine, sodium nitroprusside, and nitroglycerin. Nicardipine has recently been introduced as an intravenous calcium channel blocker. Vasodilators are effective in BP reduction but may cause reflex tachycardia when used alone. Adrenergic inhibitors, such as esmolol and labetalol, block alpha and/or beta receptors to decrease heart rate and BP. Labetalol's effectiveness, relative freedom from side effects, and ease of administration have made it a useful drug in the treatment of APH.
 ...
PMID:Acute postoperative hypertension in the hypertensive patient. 173 70

We prospectively evaluated 20 patient admissions for severe exacerbation of childhood asthma at The Children's Hospital, Boston, to detect evidence of cardiotoxicity. Evidence of cardiotoxicity was found in all six patient admissions for which isoproterenol infusion was utilized. This included marked elevation of serum creatine phosphokinase isoenzyme (CPK-MB) levels and electrocardiogram abnormalities consistent with transient myocardial ischemia. Peak serum CPK-MB levels were significantly lower and electrocardiogram abnormalities were significantly less frequent during 14 patient admissions for which isoproterenol infusion was not utilized. Risk factors associated with cardiotoxicity included tachycardia, hypercapnia, acidosis, and intravenous isoproterenol therapy. We conclude that cardiotoxicity is not infrequent during therapy for severe exacerbations of childhood asthma. Electrocardiograms and measurement of serum CPK-MB levels are sensitive, useful, and readily obtained indicators of cardiotoxicity. Abnormalities of these studies may detect cardiotoxicity prior to the occurrence of more blatant or catastrophic manifestations of cardiotoxicity. We therefore recommend serial monitoring of serum CPK-MB levels and electrocardiograms for all children requiring an admission to the intensive care unit for management of severe asthmatic exacerbation.
 ...
PMID:Cardiotoxicity during treatment of severe childhood asthma. 164 Dec 99

Lactate extraction (defined as arteriovenous lactate concentration difference divided by arterial concentration and expressed as a percent) is often reported as the indicator of anaerobic cardiac metabolism in studies dealing with myocardial ischemia. However, lactate extraction ignores the effect of regional blood flow and, therefore, fails to consider the total mass of lactate consumed or produced (lactate flux). This study examined the relationship between lactate flux and calculated lactate extraction. Fourteen anesthetized dogs were instrumented to allow sampling of blood from the left anterior descending coronary artery (LADa) and vein (LADv) and a circumflex coronary vein (CFXv), as well as measurement of regional myocardial blood flow (RMBF) using microspheres, and measurement of systemic hemodynamic variables. Complete data sets (before LADa occlusion, after 15 minutes of LAD occlusion, and after 1 hour of reperfusion) were obtained in nine dogs. Only minor systemic hemodynamic changes occurred during LADa occlusion when compared with "before" and "after" values. Likewise, LADa occlusion produced only minor alterations in blood gas tensions, pH, concentrations of glucose, lactate, and RMBF in samples from the CFX perfusion zone. In contrast, LAD occlusion decreased RMBF in the LADa perfusion zone and produced significant hypercarbia and acidemia, as well as an increased LADv lactate concentration. In the LAD zone, lactate extraction decreased significantly from 15.9% +/- 7.0% before LAD occlusion to -77.4% +/- 21.8% during LAD occlusion (P less than 0.05). However, lactate flux (arteriovenous concentration difference x RMBF) in the LAD zone before and during LAD occlusion was not statistically significantly different (1.3 +/- 0.8 mg/min/100 g and -1.5 +/- 0.8 mg/min/100 g, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Lactate extraction fails to accurately reflect regional lactate production in ischemic myocardium. 252 Jun 57

The histories and the results of the postmortem examinations of 507 patients with chronic pulmonary heart disease were studied. In 62.6% of them left ventricular hypertrophy was found. As probable causes for this left ventricular hypertrophy are suggested: arterial hypertension, ischemic heart disease, hypoxemia, hypercapnia, heart failure, diabetes mellitus. The weight measurement correlations between the left and the right heart ventricles were studied in: "normal hearts", hearts with right ventricular, hypertrophy only, hypertrophy of both ventricles, left ventricular hypertrophy only. A correlation between the mass increase and the wall thickness of the ventricles was established. In the patients with chronic pulmonary heart disease and hypertrophy of both ventricles the mass and the wall thickness of the ventricles increase simultaneously. The possible pathogenetic mechanisms of the left ventricular involvement in patients with chronic pulmonary heart disease are discussed.
 ...
PMID:[Left heart ventricle in chronic cor pulmonale patients. Etiological, pathomorphological and organ weight measurement studies]. 296 38

Three harbor seals Phoca vitulina richardsi and five spotted seals Phoca vitulina largha were used in studies of acute episodes of local myocardial ischemia in open-chest, anesthetized animals and of coronary blood flow and regional function as indicated by left ventricular segment dimensions during experimentally simulated dives of conscious, instrumented animals. We observed that seal myocardium, in which there are few coronary anastomoses, responded to brief local occlusion with prompt local dysfunction and systolic bulging; coronary flow in the nondiving seal oscillated irregularly and declined with spontaneous apnea and related falling heart rate; flow continued to oscillate but was much reduced during dives, frequently ceasing entirely for periods as long as 45 s; ventricular segment dimension shortening was reduced intermittently during dives; and elevated heart rate induced during dives by cardiac pacing or by administration of atropine diminished or eliminated the reductions in coronary blood flow. Responses of seal heart reflect the reduction in cardiac metabolic demand during diving and the seal's myocardial adaptation for enhanced anaerobic glycolysis. The seal heart can maintain mechanical function during dives with minimal coronary perfusion, despite the progressive and ultimately profound hypoxia, hypercapnia, and acidosis. Reduced cardiac metabolism, copious glycolytic reserves, and metabolite washout by intermittent brief bursts of coronary blood flow are apparently sufficient to support continued cardiac function, even though the seal heart has little tolerance for acute localized ischemia.
 ...
PMID:Coronary blood flow and myocardial segment dimensions during simulated dives in seals. 407 82

The haemodynamic effects of non-steroidal anti-inflammatory (NSAI) drugs can be attributed either to their common property of inhibiting the formation of prostaglandins (PG) in the cardiovascular system, or to direct actions on the tone and sensitivity of the resistance vessels in various regions. Indomethacin (IND) is the most frequently studied NSAI drug, in animals and in man. Its cardiovascular effects differ somewhat from those of other NSAI, due to the fact that, besides inhibiting PG formation, IND acts as a direct vasoconstrictor. The stimulatory effect of IND in vascular smooth muscle results in an increased systemic vascular resistance which, although partially compensated by a decreased cardiac output, gives rise to a moderate increase in systemic blood pressure. The vasoconstrictor effect of IND is of particular interest in patients with ischemic heart disease, since it lowers their already decreased coronary flow, and may thereby accentuate the risk of myocardial infarction. Administration of IND also leads to a decreased blood flow in the splanchnic region, the kidneys, and the brain. The cerebral blood flow is lowered by 25-35%; in addition, IND almost entirely erases the hyperemic flow response to hypercapnia. Of other NSAI drugs, at least aspirin and naproxen are completely devoid of such actions on the cerebral circulation. A common vascular effect of all NSAI drugs is a diminution of reactive hyperemia, the local hyperemia that develops in a tissue subjected to a short period of arterial occlusion. Part of this hyperemic response is dependent on an intact vascular PG formation and consequently it is inhibited when PG formation is blocked. In contrast, NSAI drugs do not affect the functional increase in the blood flow in working skeletal muscle.
 ...
PMID:Central and peripheral haemodynamic effects of non-steroidal anti-inflammatory drugs in man. 659 1

During the global myocardial ischemia of cardiac arrest and during regional myocardial ischemia due to local impairment of coronary blood flow, intramyocardial carbon dioxide tensions (Pmco2) of ischemic myocardium increase to levels exceeding 400 Torr. The mechanism of such myocardial hypercarbic acidosis is as yet incompletely understood, specifically whether these increases in Pmco2 are due to increased oxidative metabolism, decreased CO2 removal, or buffering of metabolic acids. We therefore measured Pmco2 and the total CO2 content of rat hearts harvested before, during, and after resuscitation from cardiac arrest. Pmco2 significantly increased from an average of 63 to 209 Torr during a 4-min interval of untreated ventricular fibrillation. This was associated with concurrent decreases in intracellular pH from an average of 7.03 to 6.02 units. The total CO2 content of the myocardium simultaneously decreased from 17.0 to 16.5 mmol/kg. Accordingly, increases in Pmco2 and [H+] were observed in the absence of increases in the total CO2 content and therefore the calculated myocardial bicarbonate. These observations in the rat model implicate buffering of metabolic acids by bicarbonate rather than increases in CO2 production or decreases in CO2 removal as the predominant mechanism accounting for myocardial hypercarbia.
 ...
PMID:Mechanisms of myocardial hypercarbic acidosis during cardiac arrest. 761 73

Patients in the ICU who require intubation and mechanical ventilation benefit from adequate sedation and analgesia. Traditionally, this has been achieved using benzodiazepines and opioids. Alternatively, propofol is being administered for sedation of patients in the ICU with increasing frequency. Propofol has a number of properties that make it a potentially superior choice for sedation of intubated ICU patients. The rapid onset and offset of sedation with propofol, even after prolonged administration, allow for greater control over the level of sedation and more rapid weaning from mechanical ventilation. In addition, long-term administration of propofol does not appear to be associated with the development of tolerance, addiction, or withdrawal following discontinuation. Propofol suppresses cellular oxygen consumption and carbon dioxide production without increasing anaerobic metabolism. This may be beneficial in patients with severe hypoxemia, hypercarbia, or myocardial ischemia. Finally, the use of propofol may reduce or eliminate the need for other medications in these patients such as muscle relaxants, antihypertensives, lipid nutritional supplements, and analgesics, thereby simplifying their medication regimens and reducing the overall cost of their care while in the ICU. Propofol can be administered to critically ill patients for sedation with a high degree of safety and efficacy. Propofol causes systemic vasodilatation which may result in unwanted hypotension, especially in patients who are already hemodynamically compromised. Propofol also causes ventilatory depression, so its use should be restricted in the ICU to patients whose airway is protected by an endotracheal tube and whose ventilation is closely monitored. Finally, continuous administration of propofol may cause clinically significant hypertriglyceridemia in patients with disordered triglyceride metabolism, or in patients receiving excessive doses of propofol or parenteral lipid supplements. Although propofol is more expensive than equipotent doses of other sedative agents, the additional cost of using propofol for sedation of critically ill patients in the ICU may be more than offset by the savings accrued from faster times to extubation, shorter ICU stays, and the use of fewer medications to manage these patients. Further research needs to be done to determine the potential clinical and cost benefits of using propofol for sedation of patients in the ICU.
 ...
PMID:Propofol: a new drug for sedation in the intensive care unit. 763 54

This randomized double-blind study compared the hemodynamic and metabolic effects of pancuronium and vecuronium during treatment of shivering after cardiac surgery with hypothermic cardiopulmonary bypass. Thirty sedated and pain-free patients who shivered after cardiac surgery were treated with pancuronium (n = 15) or vecuronium (n = 15) 0.08 mg/kg. Baseline values of heart rate (HR), mean arterial pressure, arterial and venous blood gases, total body oxygen consumption indexed to body surface area (VO2-I), and pressure work index (PWI, an estimate of myocardial oxygen consumption) were measured on arrival in the intensive care unit, at onset of shivering, and repeatedly for 2 h after treatment. Continuous ST segment analysis of leads II and V5 were used for detection of myocardial ischemia. Treatment of shivering with pancuronium decreased VO2-I by 32% (P = 0.0001). This was accompanied by a 14% increase in HR (P = 0.001) and a 10% increase in PWI (P = 0.03). Vecuronium decreased VO2-I by 36% (P = 0.003) with a 4% decrease in HR (P = 0.04) and a 6% decrease in PWI (P = 0.06). Myocardial ischemia (n = 3) and ventricular arrhythmias (n = 3) occurred in five patients treated with pancuronium. Only one patient treated with vecuronium had ventricular arrhythmia (P = 0.08). Seven patients treated with pancuronium and eight treated with vecuronium were taking beta-adrenergic blockers preoperatively which was associated with lower HR (96 +/- 16 vs 109 +/- 15 bpm; P = 0.025) and lower PWI (8.8 +/- 1.2 vs 10.7 +/- 1.92 mL.min-1 x 100 g-1; P = 0.003) at onset of shivering. However, beta-adrenergic blockers did not attenuate the relative HR increase induced by pancuronium. No relationship was found between hypercapnia and tachycardia or hypertension. These results suggest that, when compared to pancuronium for treatment of postoperative shivering, vecuronium may be advantageous because it does not increase myocardial work. The disproportionate relationship between VO2-I and PWI after treatment with muscle relaxants indicates that increased VO2-I does not contribute significantly to the hemodynamic disturbances associated with shivering. These disturbances are more likely the results of increased adrenergic activity related to pain and recovery from anesthesia. Shivering and its associated hemodynamic disturbances appear to be concomitant but independent signs of awakening.
 ...
PMID:Pancuronium or vecuronium for treatment of shivering after cardiac surgery. 791 90


1 2 3 Next >>