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Biomedical subjects

D L Carden

Publications and source records attributed to D L Carden.

46 records · Page 3Linked to original sources
PubMed1985

Immediate emergency department external cardiac pacing for prehospital bradyasystolic arrest.

Approximately 25% of patients in prehospital cardiac arrest present in bradyasystolic rhythms, and their long-term prognosis is very poor. Our study was undertaken to determine the utility of immediate emergency department (ED) external cardiac pacing in this situation. Twenty patients presenting with bradyasystolic prehospital cardiac arrest were entered in the study. All received the usual advanced cardiac life support therapy, but also were externally paced immediately using an automated external defibrillator and pacemaker (AEDP). Only two of 20 patients showed evidence of electrical capture, and none developed pulses with pacing. Four of the 20 patients developed a sinus rhythm and blood pressure during resuscitation. Three survived to leave the ED, but none survived to leave the hospital. An increase in the rate of bradycardia and pulseless idioventricular rhythms that was independent of electrical capture or pharmacologic therapy was noted occasionally. Although survival was not enhanced using the AEDP, the device was reliable, easy to use, and free of complications. External cardiac pacing warrants further investigation in the prehospital setting.

Adult↗
PubMed1985

Comparison of central venous and arterial pH and PCO2 during open-chest CPR in the canine model.

Arterial blood gases are difficult to obtain during cardiopulmonary resuscitation (CPR) in human beings, and the possibility of venous sampling is raised frequently. The reliability of central venous gases as a substitute for arterial blood gases in assessing acid base status, however, has not been investigated adequately under conditions of CPR. Therefore, femoral arterial and central venous catheters were placed in 24 mongrel dogs, and ventricular fibrillation was electrically induced. After varying predetermined downtimes from five to 60 minutes, open-chest CPR was begun, and arterial and central venous blood gases were simultaneously drawn every five minutes during a 30-minute period. Arterial pH (pHa) was consistently higher than central venous pH (pHcv) by an average of .048 units. A significant correlation existed between the pHa and pHcv at all times during CPR, with an overall r = .9771 (P less than .0001). The difference between central venous PCO2 (PcvCO2) and arterial PCO2 (PaCO2) was 5.17 mm Hg prior to cardiac arrest, but it increased 300% to a mean of 15.51 mm Hg during CPR. Correction of pHcv using conventional methods to account for this respiratory component decreased the correlation between pHa and pHcv to r = .6905. The ability of pHcv to substitute for pHa was assessed, and showed a sensitivity of 100% when pHa of 7.2 was used as a criterion for treatment. In this model, pHcv is a sensitive indicator of pHa and it may be used to guide bicarbonate therapy. The increased PcvCO2 during CPR probably results from the marked tissue lactic acid production and subsequent shift of the bicarbonate buffer into free carbon dioxide.

Analysis of Variance↗
PubMed1985

Ionized calcium during CPR in the canine model.

The purpose of our study was to determine ionized calcium levels during cardiopulmonary resuscitation (CPR). Following placement of ascending aortic catheters in 15 adult mongrel dogs, ventricular fibrillation was induced electrically. After five minutes without therapy, mechanical external CPR was instituted. Animals received either standard CPR (S-CPR, n = 8) or simultaneous compression and ventilation CPR (SCV-CPR, n = 7) for 30 minutes. Ionized calcium levels were obtained prior to fibrillation and every five minutes during CPR. Mean ionized calcium levels during CPR (1.27 +/- 0.06 mmol/L) did not differ significantly from prearrest levels (1.27 +/- 0.07 mmol/L) at any point during CPR. This was true when the dogs were analyzed together (P = 0.1293) and when the animals receiving S-CPR (P = 0.4465) and SCV-CPR (P = 0.5470) were analyzed by groups. Defibrillation was attempted in all animals and resulted in electromechanical dissociation in three. None of these dogs was hypocalcemic either prior to arrest or during CPR, and none developed an effective rhythm with the administration of calcium. Furthermore, three of the four animals receiving calcium developed markedly elevated ionized calcium levels. Hypocalcemia apparently does not occur during CPR. The beneficial effect of calcium in reported cases cannot be explained routinely by correction of hypocalcemia. Further studies are needed to define the role of calcium administration, if any, in CPR.

Animals↗
PubMed1984

High-dose corticosteroids in the treatment of pulseless idioventricular rhythm.

Pulseless idioventricular rhythm (PIVR) is a slow electrical rhythm of ventricular origin without mechanical activity, and it is associated with a mortality rate that approaches 100%. In 1976 high-dose corticosteroids were advocated as beneficial in the treatment of PIVR. A critical review of the early literature suggests that the favorable outcome may have been attributable to variables other than treatment with high-dose steroids. Recent prospective clinical trials have not confirmed the salutory effect of steroids in this dysrhythmia.

Adrenal Cortex Hormones↗
PubMed1983

Pneumonia and lung abscess.

The epidemiologic, microbiologic, radiographic, and clinical presentations of pneumonias caused by the most common pathogens are discussed in detail, and current recommendations for hospitalization are reviewed. Also considered are the clinical characteristics, diagnosis, and treatment of primary and secondary lung abscess.

Diagnosis, Differential↗
PubMed1983

Atelectasis.

The pathogenesis, clinical presentation, radiographic signs, and treatment of atelectasis are reviewed.

Bronchography↗
PubMedDate not supplied

Hyperkalemia during human cardiopulmonary resuscitation: incidence and ramifications.

Although hypokalemia has been reported after cardiac arrest and successful resuscitation, experimental data indicate that potassium is released from cells during ischemia. The purpose of this investigation was to study serum potassium concentration ([K+]) during closed chest cardiopulmonary resuscitation (CC-CPR) in humans. Twenty-two patients presenting to the emergency department (ED) in cardiopulmonary arrest had simultaneous measurement of central venous and arterial [K+] and blood gases during CC-CPR utilizing current advanced cardiac life support protocols and a pneumatic chest compressor and ventilator. Mean arterial and central venous [K+] were 5.0 +/- 1.3 and 5.6 +/- 2.9 mEq/L, respectively, (p greater than .05) with 7 patients having [K+] of greater than 6 mEq/L. Significant hyperkalemia does occur in some patients during cardiac arrest and CC-CPR. Because poor tissue perfusion during CC-CPR impairs exchange between the interstitial and intravascular compartments, increases in interstitial [K+] would be expected to be even greater. Interstitial hyperkalemia may play a role in the genesis of wide complex electromechanical dissociation (EMD) seen after prolonged cardiac arrest. Since calcium has long been known to be beneficial in the treatment of hyperkalemia-induced dysrhythmias, the success of calcium chloride in treating wide complex EMD may be on the basis of this phenomenon.

Aged↗
PubMedDate not supplied

Mechanisms of postischemic vascular dysfunction in skeletal muscle: implications for therapeutic intervention.

In 1981, it was first proposed that xanthine oxidase-derived reactive oxygen metabolites contribute to the microvascular and parenchymal cell damage which occurs when ischemic tissues are reperfused. Figure 1 summarizes a scheme that has been proposed to explain the interaction of xanthine oxidase-derived oxidants, neutrophil infiltration, and the microvascular dysfunction which occurs in postischemic tissue. According to this proposal, xanthine oxidase-derived oxidants, produced at the time of reperfusion, initiate the formation and release of proinflammatory agents, which subsequently attract and activate neutrophils. The activated granulocytes adhere to vascular endothelium, extravasate, and release cytotoxic oxidants and/or non-oxidative toxins (e.g. proteases) which contribute to tissue destruction. The objective of this review is to summarize the supportive evidence for this scheme in postischemic skeletal muscle and to identify the components of the mechanism that may be amenable to pharmacologic intervention.

Animals↗