Donna L Carden

An evaluation of cocaine-induced chest pain

STUDY OBJECTIVE To determine if enzymatic evidence of acute myocardial injury is present in patients complaining of chest pain after cocaine use when the ECG is normal or nondiagnostic. DESIGN Serial ECG and creatinine kinase (CK) and CK isoenzymes (CK-ISO) determinations were performed at time of emergency department presentation and every six hours over 12 hours on individuals complaining of chest pain within six hours of last cocaine use. SETTING ED of an urban tertiary care center. TYPE OF PARTICIPANTS Forty-two individuals with a mean age of 28.5 years. INTERVENTIONS Patients with positive CK-ISOs were admitted immediately to formally rule out myocardial infarction. Patients developing ECG changes during observation period also were admitted even if CK-ISOs were normal. Patients with unchanged ECGs and normal CK-ISOs were discharged after 12 hours of observation. RESULTS Eight patients (19%) had elevated CK and CK-ISO values at presentation. Two of these patients had elevated values on three sequential determinations and were believed to have sustained acute myocardial infarction. Six patients had elevated CK and CK-ISOs at presentation only. ECGs remained normal or nondiagnostic in all patients. CONCLUSIONS Enzymatic evidence of acute myocardial injury may occur in patients who develop chest pain after cocaine use and have normal or nondiagnostic ECGs. This injury may reflect acute infarction or transient ischemia. Single or serial normal or nondiagnostic ECGs do not rule out ischemia or injury in this group of patients.

Aortic and right atrial pressures during standard and simultaneous compression and ventilation cpr in human beings

Coronary perfusion pressure, as reflected by the diastolic aortic to right atrial (Ao-RA) pressure gradient, has been shown to correlate well with coronary blood flow during standard external CPR (SE-CPR) and is an important determinant of successful cardiac resuscitation. Few studies have documented such Ao-RA gradients in human beings, however. Twenty patients sustaining out-of-hospital cardiopulmonary arrests and basic cardiac life support were instrumented with thoracic aortic and right atrial catheters on arrival in the emergency department. The mean time from arrival in the ED to catheter placement was 16.5 +/- 6.0 minutes. With SE-CPR, peak systolic aortic and right atrial pressures were 73.7 +/- 20.2 mm Hg and 69.6 +/- 18.3 mm Hg, respectively. End diastolic aortic and right atrial pressures were 27.9 +/- 7.3 mm Hg and 20.3 +/- 7.2 mm Hg, respectively, with an end diastolic gradient of 7.9 +/- 9.1 mm Hg. Three patients had systolic Ao-RA gradients of more than 25 mm Hg, which is consistent with some cardiac compression as a mechanism of flow. Five patients also had one-minute trials of simultaneous compression and ventilation CPR (SCV-CPR). Ao-RA end diastolic gradients decreased in four of the five during SCV-CPR. No patient in this study was resuscitated successfully. We conclude that ED SE-CPR provides little coronary perfusion for victims of prehospital cardiac arrest. Although SCV-CPR has been shown to improve carotid blood flow in human beings, it appears to have an adverse effect on the already minimal myocardial perfusion provided by SE-CPR.

Cardiopulmonary bypass vs CPR as treatment for prolonged canine cardiopulmonary arrest

Although in vitro studies have demonstrated functional recovery of neurons after prolonged ischemia, in vivo experience with patients resuscitated from cardiopulmonary arrest demonstrates much less cerebral resistance to global ischemia. The purpose of our investigation was to compare the effectiveness of femoro-femoral veno-arterial cardiopulmonary bypass (CPB) to standard cardiopulmonary resuscitation in the treatment of prolonged cardiopulmonary arrest. Ten mongrel dogs were electrically fibrillated and left in cardiopulmonary arrest without any therapy for 12 minutes. Subsequently, either CPB (n = 5) or CPR (n = 5) was initiated and resuscitation attempted according to a standardized protocol that included administration of the calcium channel blocker lidoflazine in an effort to optimize cerebral and myocardial recovery. If there was return of spontaneous circulation, the animal was managed in an intensive care setting with invasive hemodynamic monitoring and ventilatory support for up to nine hours. Neurologic function was graded using a standardized neurologic deficit scoring (NDS) system at 12 hours after insult and daily for one week or until death. Prearrest hemodynamic and metabolic parameters were comparable in both groups (P greater than .05). All CPB animals were resuscitated successfully and alive at 24 hours after insult as opposed to none in the CPR group (P less than .005). In addition, three of the CPB animals were neurologically normal at final grading with NDS scores of zero. The other two CPB animals had persistent severe neurologic impairment and a mean NDS score of 51%. Thus CPB is more effective than CPR in the treatment of prolonged cardiopulmonary arrest. The improved outcome probably results primarily from improvement in blood flow with CPB.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

Selective venous hypercarbia during human CPR: Implications regarding blood flow

Thirty-five patients presenting to the emergency department in cardiopulmonary arrest had simultaneous measurement of central venous (cv) and arterial (a) blood gases during CPR with a pneumatic chest compressor and ventilator. The mean cv, arterial pH, and PCO2 values were markedly different (P less than .001). The mean pH gradient (pHa - pHcv) was .31 +/- .10 units and the mean PCO2 gradient (PcvCO2 - PaCO2) was 60.5 +/- 23.6 torr. This selective venous hypercarbia is probably due to a cardiac output that is inadequate to eliminate the CO2 produced from both residual aerobic metabolism and the buffering of anaerobically produced lactic acid. Central venous blood gases are probably a better reflection of actual tissue environment during prolonged cardiac arrest than are arterial blood gases.

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.

Lactic acidosis during closed-chest CPR in dogs

Survival after out-of-hospital cardiac arrest is intimately related to the time from cardiovascular collapse to the initiation of CPR, or downtime. Furthermore, the reperfusion technique that optimizes coronary and cerebral blood flow after cardiac arrest may also be dependent on downtime. Peak blood lactate levels have been shown to be unchanged throughout resuscitation and predictive of downtime in dogs subjected to cardiopulmonary arrest and open cardiac massage. The purpose of this study was to determine the course of arterial lactate levels in dogs subjected to a fibrillatory cardiopulmonary arrest and conventional closed-chest CPR (CCPR). Fourteen dogs were subjected to five minutes of cardiopulmonary arrest and 30 minutes of CCPR. Resuscitation was performed according to a standardized protocol. Arterial lactic acid samples were collected at timed intervals throughout the experiment. Mean arterial lactic acid levels increased significantly with each sampling interval during 30 minutes of CCPR (overall P less than .05). In nine dogs successfully resuscitated, there were no significant differences in mean arterial lactic acid levels after the return of spontaneous circulation (ROSC). Open-chest resuscitation after five minutes of ventricular fibrillation in dogs results in peak lactic acid levels that do not change significantly once internal cardiac massage is initiated. In contrast, CCPR in similarly arrested dogs does not appear to provide adequate tissue oxygenation and/or perfusion to prevent continuous lactic acid accumulation.

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.

Vital signs including pulsus paradoxus in the assessment of acute bronchial asthma

One hundred nine episodes of acute bronchial asthma were studied both before and after treatment in the emergency department, comparing the pulse rate, respiratory rate, and pulsus paradoxus to the one second forced expiratory volume (FEV 1 ). The purpose of this study was to assess the reliability of these clinical parameters in predicting the degree of airway obstruction in acute bronchial asthma. Pulse, respiratory rate, and pulsus paradoxus showed poor correlation to FEV 1 (or % predicted value) both pre- and post-treatment. Further, of all patients presenting with a pre-treatment FEV 1 less than or equal to 1.0 liter, 36% had a normal pulse (⩽ 100/min), 17% had a respiratory rate less than or equal to 20/min, and 33% had no pulsus paradoxus. Following therapy, 44% of those patients with persistent severe airway obstruction (FEV 1 ⩽ 1.6 L) had a normal pulse, 38% had a respiratory rate less than or equal to 20/min, and 71% had no pulsus paradoxus. Pulse rate, respiratory rate, and degree of pulsus paradoxus are unreliable indices of the degree of airway obstruction in the assessment of acute bronchial asthma, and abnormalities of these clinical parameters tend to disappear with minimal improvement in airway obstruction. Thus pulse rate, respiratory rate, and pulsus paradoxus cannot be substituted for pulmonary function measurements in assessing acute bronchial asthma.

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.