Applied cardiopulmonary pathophysiology : ACP最新文献

The presence of ventricular ectopic activity in the post-myocardial infarction patient, especially associated with left ventricular dysfunction, has been associated with a high incidence of sudden cardiac death. To test the PVC hypothesis, that PVC suppression in asymptomatic patients with ventricular arrhythmias post-myocardial infarction might reduce sudden death rate, the cardiac arrhythmia suppression trial (CAST) was performed. In patients treated with encainide or flecainide, total mortality at 10 months was 7.7% compared to only 3% overall mortality on placebo. The increase in mortality and sudden cardiac death with these two drugs raised the question of whether PVC suppression in this group of patients should be attempted. In addition, the extrapolation of the results of this study to other patient groups has resulted in a change of our antiarrhythmic prescription habits. Criticism of the CAST study has included a low placebo mortality, which may have been secondary to entry of low-risk groups of patients, deaths in the open label titration groups not being included, and recent advances in thrombolysis and revascularization. In addition, this low placebo mortality may have been explained by the concept that drug-responsive arrhythmias may have more benign prognosis. The above results suggest that, except for the use of beta blockers, benefits of other anti-arrhythmic drug treatment in the post-infarction patient with asymptomatic benign and potentially lethal ventricular arrhythmias is questionable. Flecainide and encainide should be avoided in this group of patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Under normal circumstances, O 2 transport (TO 2 = cardiac output x arterial O 2 content) is regulated to provide sufficient O 2 to meet the demands of oxidative phosphorylation, quantified as the O 2 consumption (VO 2). When metabolic demands increase, TO 2 is augmented and in addition, the fractional extraction of the delivered O 2 by the tissues, the O 2ER, also increases, to levels as high as 0.80 at maximum VO 2. If TO 2 is decreased, at least in the experimental animal, VO 2 can be maintained initially by an increase in O 2ER, but eventually this mechanism is exhausted, VO 2 begins to fall, and the body invokes anaerobic means of energy generation to maintain cell integrity. In normal man, this critical level of TO 2 (TO 2crit) has not been determined, but in experimental animals it has been found once the O 2ER exceeds 0.50. Patients with sepsis and the adult respiratory distress syndrome have a very high mortality and usually die as a result of multiple organ failure. They have in addition, an apparent abnormality in their ability to extract and utilize the delivered O 2. Despite a TO 2 which is often higher than normal, patients with sepsis commonly have a lactic acidosis and when TO 2 is reduced, both groups of patients are usually unable to increase their O 2ER above the normal resting value of 0.33.(ABSTRACT TRUNCATED AT 250 WORDS)

In 15 patients with asthma attack, evidence of the uneven distribution of air flow during controlled ventilation was obtained by detection of ventilatory asynchronism expressed by the incurvated profile of tracheal pressure waves associated with the repetitive interruptions of air flow. It was observed that low values of PEEP (mean: 5 +/- 2.5 cm H 2O) induced an increase in transbronchial pressure able to overcome ventilatory asynchronism. In these conditions, an appropriate ventilation-perfusion ratio was restored and improved gas exchanges as indicated by the mean increase of arterial PO 2 from 66.3 mmHg (+/- 2.57) to 96.89 mmHg (+/- 4.41) (p = 0.0005) associated with a mean decrease in arterial PCO 2 from 53.66 mmHg (+/- 2.71) to 42.07 mmHg (+/- 1.64) (p = 0.0005). Simultaneously hemoglobin oxygen saturation rose from 82.31% (+/- 1.97%) to 95.74% (+/- 0.5%). In our patients, such values of PEEP were not high enough to influence the pulmonary arterial circulation. The means of the pulmonary arterial pressures obtained before (syst.: 32.3; diast.: 15.1; mean: 22.00 mmHg) were quite the same (p greater than 0.2) as with PEEP (syst.: 32.00; diast.: 14.00; mean: 21.1 mmHg). The mean of the wedge pressure was found to be 8.3 (+/- 74 mmHg) prior to and 8.4 (+/- 0.68 mmHg) after PEEP (p greater than 0.3). Mean cardiac output rose slightly from 5.27 l/min (+/- 0.24) to 5.77 l/min (+/- 0.38) during PEEP (p = 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Reversal of cardiac arrest is contingent on rapid and effective restoration of myocardial blood flow. Thirty years have elapsed since closed-chest cardiopulmonary resuscitation (CPR) was introduced in clinical practice. Because of its technical simplicity and noninvasiveness, CPR was rapidly implemented and almost universally utilized for cardiac resuscitation. However, there is increasing concern about its value for cardiac resuscitation since the limited hemodynamic efficacy of precordial compression accounts for a disappointingly low success rate. More invasive interventions by which blood flow is restored such as open-chest cardiac massage or extracorporeal circulation are consistently more effective than conventional CPR. Experimentally, both methods restore systemic and myocardial perfusion to viable levels and thereby increase the likelihood of restoring spontaneous circulation even after prolonged cardiac arrest or failure of conventional CPR.

ARDS is still characterized by an exceedingly high mortality rate. Methods are then needed to detect ARDS at the earliest clinical stage. Over the last decade, radioisotopic techniques have developed, aimed at demonstrating an abnormal neutrophil sequestration in the lung or detecting functional alterations of the pulmonary alveolar-capillary barrier, which likely precede the onset of respiratory distress. Preliminary application of these techniques in patients with ARDS yielded conflicting results in terms of sensitivity and specificity. On the contrary, lung vascular abnormalities have been consistently observed in patients with ARDS studied by perfusion lung scanning. They consist of focal, non segmental perfusion defects, mostly peripheral and dorsal, with redistribution of blood flow to non-dependent lung regions. This scintigraphic pattern may be considered typical of ARDS since it is not observed in other acute lung disorders. Perfusion abnormalities on lung scans are detectable from the very early stage of ARDS and correlate with the severity of the syndrome as reflected by gas exchange, central hemodynamics, and chest radiography. Perfusion lung scanning may then be used in the early detection and evaluation of vascular injury in ARDS.

This paper reviews a continuous integrated computer based approach to monitoring oxygen supply (DO 2) and consumption (VO 2) relationships. A description of the technologic methodology and potential advantages over intermittent thermodilution monitoring are discussed. Lastly, the preliminary results of investigations in two populations (abdominal aortic surgery and adult respiratory distress syndrome) are presented.

Measurement of the alveolo-capillary transfer of radiolabelled solutes provides information about the integrity of the alveolo-capillary barrier. The transfer of 99mTc-diethylen triamine penta-acetate ( 99mTc-DTPA) can be easily measured after tracer delivery in aerosol form and external monitoring of radiation over the lung. Although the technique has been used extensively for more than ten years, the basic mechanisms for pulmonary clearance of 99mTc-DTPA remain incompletely understood. Experimental evidence that the rate of clearance partly reflects the functional integrity of the pulmonary surfactant system is reviewed together with clinical studies with possible relation to surfactant function.

Fiberoptic bronchoscopy has revolutionized the practice of modern pulmonary medicine. It is estimated that as many as 98% of all bronchoscopies are currently performed using the flexible instrument, and most bronchoscopists have never been trained in the technique of rigid bronchoscopy.

Although antiarrhythmic drugs are commonly used in patients with supraventricular tachycardia, their use is limited due to inefficacy, side effects and patient compliance problems. Nonpharmacologic therapies used in the treatment of supraventricular tachycardia include: antitachycardia pacing, DC and radiofrequency catheter ablation and surgical therapy. Although certain pacing techniques can prevent the initiation of tachycardia, antitachycardia pacing is primarily used to terminate the supraventricular tachycardia once it has occurred. In patients with primary atrial tachycardias that are refractory to treatment, DC or radiofrequency catheter ablation can be used to modify or completely ablate the AV junction with resultant complete heart block. With DC AV junction ablation, 65% of patients will have resultant third degree AV block and 20% of patients will have modification of AV condition. Results with radiofrequency ablation have shown efficacy rates ranging from 56-9470 and can be used without the need for general anesthesia. Both forms of catheter ablation can be used to selectively alter the retrograde limb of an AV node reentrant circuit. Catheter ablation has been successful in ablating accessory pathways. DC catheter ablation has been predominantly used in posterior paraseptal pathways. More recently, radiofrequency catheter ablation of the ventricular insertion site of accessory pathways has demonstrated usefulness in selective laboratories. Surgical therapy for supraventricular tachycardia has been used for excision and/or ablation of an atrial ectopic focus, surgical ablation of the AV node in patients with refractory atrial tachyarrhythmias and microsurgery of the AV node in patients with AV node reentrant tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)