David S. Sheps

Clinical, electrophysiologic and hemodynamic profile of patients resuscitated from prehospital cardiac arrest.

Abstract Of 352 prehospital cardiac arrest patients studied during a three year period, the initial mechanism recorded by rescue personnel was ventricular fibrillation in 220 (62 per cent), ventricular tachycardia in 24 (7 per cent) and bradyarrhythmias or asystole in 108 (31 per cent). Early survival was best in the group with ventricular tachycardia (16 of 24 patients resuscitated and survived hospitalization—67 per cent); the prognosis was worst in the group with bradyarrhythmias asystole (nine of 108 admitted to the hospital alive—none survived hospitalization); and 51 of 220 patients with ventricular fibrillation (23 per cent) were resuscitated and survived subsequent hospitalization, a significantly better outcome than previously reported for ventricular fibrillation. Central nervous system damage accounted directly or indirectly for 28 of 48 in-hospital deaths (59 per cent), and hemodynamic abnormalities for 31 per cent. Only five in-hospital deaths (10 per cent) were primary arrhythmic. The majority of survivors had evidence of left ventricular hemodynamic abnormalities (mean left ventricular end-diastolic pressure=17.80 ± 8.99 mm Hg; mean cardiac index=2.62 ± 0.72 liters/min/m 2 ; mean ejection fraction=38.58 ± 17.55 per cent), but approximately one third of the surviving patients had normal left ventricular function. Early in-hospital electrophysiologic data demonstrated persistent, drug-resistant complex ventricular arrhythmias during the first 72 hours; but intracardiac electrophysiologic studies elicited specific patterns only in patients with ventricular tachycardia, whose arrhythmias were reproducible in five of six patients studied. The risk of recurrent ventricular fibrillation in the first 72 hours was predicted better by coexistent conducting system abnormalities, than by the persistent ventricular arrhythmia alone. We conclude that the electrical mechanism of prehospital cardiac arrest provides early prognostic information, that early survival rates are improving and that one third of the discharged survivors have normal indices of left ventricular function. The presence of conducting system abnormalities identifies a subgroup at high risk for in-hospital recurrent ventricular fibrillation.

Antiarrhythmic drug therapy in survivors of prehospital cardiac arrest: comparison of effects on chronic ventricular arrhythmias and recurrent cardiac arrest.

We studied the long-term effects of membrane-active antiarrhythmic agents on chronic ventricular arrhythmias in patients who have survived prehospital cardiac arrest. Among 16 patients treated with a dose-adjusted, plasma level-monitored antiarrhythmic regimen, eight have survived for longer than 12 months eight have had recurrent cardiac arrests (RCAs). Monthly Holter monitor tapes (HIM) recorded during the 4 months before the eight RCAs were compared with monthly HM tapes matched for time of entry duration of follow-up in the eight patients who did not have RCAs. Transient or persistent complex ventricular ectopic depolarizations (VEDs) have been recorded on 47 of the 63 monthly HM tapes (75%). The difference between VEDs in the RCA patients (mean 153 VEDs/hr, median 19 VEDs/hr) VEDs in the patients who have not had RCA (mean 122 VEDs/hr, median 8 VEDs/hr) was not significant (p ≥ 0.2); nor was there a predictable relationship between therapeutic plasma levels of antiarrhythmic agents the frequency complexity of chronic asymptomatic VEDs (therapeutic levels mean 104 VEDs/hr, median 6 VEDs/hr; subtherapeutic levels – mean 184 VEDs/hr, median 21 VEDs/hr). Differences were not significant (p ≥ 0.1). In contrast, all eight RCA patients had unstable plasma levels (21 of 31 determinations subtherapeutic) while six of the eight patients who have not had RCA had consistently therapeutic levels (p ≤ 0.01). Thus, adequate plasma levels of antiarrhythmic agents may protect against RCA, despite failure to suppress VEDs predictably. The apparent dissociation between predictable suppression of chronic VEDs protection against RCA suggests that clinical effectiveness of these agents may not be best measured by their effect on chronic VEDs.

Decreased frequency of exercise-induced ventricular ectopic activity in the second of two consecutive treadmill tests.

Two exercise tests were performed with an intervening rest period of 45 minutes in a group of 13 subjects with previously identified exercise-induced ventricular arrhythmias and no resting arrhythmias. Both normal subjects and patients with heart disease were included in the group. The level of stress was equal in both tests as judged by similar rate-pressure products at peak exercise. There was a significant decrease (P < 0.05) in the number of VPCs induced by exercise during and after the second test. When the number of VPCs on test I and test II in the same patients were compared, a regression line fitted the data well (r = 0.92). Analysis of the recovery periods revealed significant (P < 0.01) decreases in systolic blood pressure at one and three minutes post exercise, comparing the second to the first test. The underlying mechanism may be decreased myocardial oxygen demand during the second test as the lowered rate-pressure products during recovery (P < 0.01) reflect. The results of this study indicate that tests of effectiveness of an antiarrhythmic drug should not be based solely on a decrease in the amount or severity of ventricular irritability between two successive exercise tests, one immediately before and the other following administration of the drug.

Exercise-induced increase in diastolic pressure: Indicator of severe coronary artery disease

The diastolic blood pressure response to treadmill exercise testing was analyzed in 281 patients. Diastolic blood pressure was measured at rest, during each stage of exercise, immediately on recovery, and 1, 3 and 5 minutes into the recovery period. No change or a decrease in diastolic blood pressure was considered a normal response. An increase in diastolic blood pressure of more than 15 mm Hg on at least two determinations, comparing values at rest with those on exercise, was considered an abnormal response. Only patients showing a normal increase in systolic blood pressure during exercise were included. Two hundred and nine patients had a normal and 72 patients an abnormal diastolic blood pressure response. In a subgroup of 41 patients who underwent coronary arteriography, 50 percent of patients with a normal diastolic pressure response had normal coronary arteries, compared with 17 percent of those with an abnormal response (P < 0.03). Only 11 percent of patients with a normal diastolic pressure response had triple vessel or left main coronary artery disease, compared with 44 percent of patients with an abnormal response (P < 0.03). Blood pressure at rest (13284mm Hg) and peak heart rate (mean 155 beats/min) were similar in each group. There was no significant difference between exercise-induced ischemic S-T segment changes in the two groups (13 percent for patients with a normal diastolic pressure response versus 15 percent for those with an abnormal diastolic pressure response). In conclusion, an abnormal diastolic pressure response to treadmill testing may be a good indicator of coronary artery disease even in the absence of S-T segment changes.

A Search for Modulation in Intermittent Ventricular Parasystole

As recently described by Moe et al., parasystolic modulation implies that the ectopic cycle length of a parasystolic focus can be increased or decreased by electrical influences transmitted across the zone of protection. A search for this phenomenon was made in nine patients with intermittent ventricular parasystole resulting from protection only during specific portions of the cycle. All nine patients had a period of relatively early protection affecting the initial 55–67% of the cycle preceding a period of resetting during which the parasystolic focus was discharged and fully recycled. In addition, two patients had a period of relatively late parasystolic protection. Pseudo‐resetting (apparent resetting in the surface leads without interruption of activity within the parasystolic focus itself), seen throughout the entire period of late protection in these two patients, and during the relatively refractory period in one patient, was identified because the R waves causing apparent resetting were encompassed by parasystolic‐to‐parasystolic intervals equalling twice the ectopic cycle length. Our findings indicate that parasystolic modulation did not occur in the type of intermittent ventricular parasystole included in this study. That is, the parasystolic focus was either not affected (not modulated) during specific (early or late) portions of the cycle, or normally reset (discharged and fully recycled, but neither depressed, nor enhanced) in other portions of (he cycle. This study does not exclude the occurrence of modulation in other types of parasystole, nor in some automatic nonparasystolic rhythms.

Resting peripheral blood lactate elevation in survivors of prehospital cardiac arrest: Correlation with hemodynamic, electrophysiologic and oxyhemoglobin dissociation indexes☆

Thirteen patients who were survivors of sudden unexpected cardiac arrest in the community were followed up for up to 3 years. All showed an anomalous relation between erythrocyte levels of oxygen dissociation (P50) and 2,3-diphosphoglyceric acid (2,3-DPG). This could not be explained by hemoglobinopathy, carbon monoxide or methemoglobinemias. Because lactate accumulation in red blood cells may alter oxygen dissociation, whole blood and red blood cell lactate levels were measured. An average of 4.4 measurements per patient were obtained over a mean time of 5.6 months of the post-hospital phase of the follow-up period, which had a total mean duration of 22 months. The patients did not have overt congestive heart failure and were not acidotic (mean venous pH = 7.35). Lactate levels were elevated (mean = 15.1 mg/100 ml ± 0.8 mg/100 [standard error of the mean], compared with normal values of 7.6 mg/100 ml ± 1.4 mg/100 ml; P < 0.01). When lactate was plotted against red blood cell 2,3-diphosphoglycerate, a positive curvilinear relation was found (r2 = 0.12, P < 0.05). The production of lactate in chronic ischemia may increase red blood cell 2,3-diphosphoglycerate through glycolysis. The expected effect on oxygen dissociation of this increase in 2,3-diphosphoglycerate is offset by a counterbalancing leftward shift of the oxyhemoglobin dissociation curve by an increase in red blood cell lactic acid. When lactate was compared with left ventricular ejection fraction, there was a significant negative correlation (r = 0.86, P < 0.01). Serial 24 hour ambulatory electrocardiograms (mean 4 per patient) were analyzed for changes in quantity and severity of ventricular arrhythmia at the time of lactate determinations. Six patients had lactate level variation of more than 30 percent, and five of these six patients had an increase in quantity and severity of ventricular ectopic activity when their lactate levels were in the higher range. We conclude that elevated resting lactate levels correlate with impaired ventricular function, and fluctuations in a given patient may identify changes in clinical and electrophysiologic status.

Prehospital Cardiac Arrest: Early and Long-Term Clinical and Electrophysiologic Characteristics

Unexpected cardiac arrest in an out-of-hospital environment is a worldwide problem of enormous magnitude. Estimates for the United States alone suggest that 300,000 to 600,000 sudden deaths occur each year, with the broad range of estimates reflecting various definitions of “sudden death” (1). Until recently, studies of the nature and characteristics of sudden death victims remained entirely in the realm of epidemiologists and pathologists, since prehospital cardiac arrest was virtually 100% fatal. The clinical characteristics of patients dying suddenly and unexpectedly in the community were derived retrospectively from pathologic data, and the electrophysiologic characteristics were speculated upon from other clinical settings. The development of community-based emergency medical systems during the past decade, however, has led to the survival of a significant percentage of prehospital cardiac arrest victims; and, at the same time, has provided clinical investigators with the ability to study the clinical and electrophysiologic characteristics of individuals who have survived an unexpected, out-of-hospital cardiac arrest (2–4). Moreover, since survivors of prehospital cardiac arrest are at high risk for a recurrent cardiac arrest (approximately 30%) in the first year after the initial event (3, 4), it is also possible to study the characteristics of patients at risk for a future event.

Depression of intramyocardial oxyhemoglobin dissociation by angiographic contrast media

The effect of the addition of radiographic contrast material (Renografin) to blood on the oxyhemoglobin dissociation curve and P50 was measured by a metabolic deoxygenation technique in a strongly buffered red cell suspension. With incubation time constant, increasing doses produced progressive decreases in P50. With incubation time varied at a constant dose, a decrease in P50 was seen after only one minute. In addition, in vivo studies were performed on 11 patients undergoing cardiac catheterization. Simultaneous proximal coronary sinus and aortic samples were drawn as controls, and then at one minute and five minutes after injection of the left coronary artery. In eight patients studies were performed after, and in three prior to left ventriculography. At one minute after left coronary injection there was a significant decrease of coronary sinus as compared to aortic P50 (p less than .10) (only when left ventriculography was performed prior to coronary arteriography). The magnitude of these effects in vivo is unknown, but they would be expected to be more severe in areas distal to a critical coronary lesion due to stasis of blood flow and ischemic metabolic changes.

Pseudohypertension Due to Diffuse Vascular Calcification in Chronic Renal Failure

Excerpt Metastatic soft-tissue calcification is a well-known complication of chronic renal failure. We describe pseudohypertension (that is, cuff systolic blood pressure higher than 300 mm Hg witho...

Effect of a Physical Conditioning Program upon Left Ventricular Ejection Fractions Determined Serially by a Noninvasive Technique

6 clinically normal subjects underwent a 3-month physical conditioning program with the ejection fractions determined before and after physical conditioning using a scintillation probe. All subjects achieved a conditioning effect as evidenced by increased treadmill test duration after conditioning (mean duration before conditioning: 658 vs. 715 sec after conditioning; p less than 0.02). All 6 subjects increased resting ejection fractions after conditioning (mean ejection fraction before conditioning: 54.5 +/- 5.4%; mean ejection fraction after conditioning: 67.0 +/- 9.0%; p less than 0.01). Thus, an aerobic physical conditioning program appears to increase resting ejection fractions in normal subjects.