Keeping American Heart Association ACLS standards and guidelines current.
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Biomedical subjects
Publications and source records attributed to R E Kerber.
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To determine the risk and time to cerebrovascular complications with idiopathic hypertrophic subaortic stenosis, we studied 119 patients (66 men and 53 women) with evidence of this disease based on strict echocardiographic criteria and followed them up for a mean +/- SEM of 6.5 +/- 0.6 years. Cerebral ischemic events occurred in 26 patients (22%), and in five patients stroke was the initial presenting event. Men had cardiac symptoms at a younger age than women, but there was no significant difference in age at the time of stroke. Cardioembolic cerebrovascular events were associated with atrial fibrillation and left atrial enlargement, whereas atheroembolic events were associated with hypertension. An increased risk of stroke was associated with female sex, mitral anulus calcification, hypertension, and atrioventricular conduction delay. Unlike most previous series, this study shows that patients with idiopathic hypertrophic subaortic stenosis may present with stroke.
Echocardiographic techniques to visualize normal and atherosclerotic coronary arteries include transthoracic, transesophageal, epicardial (intraoperative), and intravascular approaches. All are capable of visualizing portions of the coronary arteries, especially proximal, and demonstrating atherosclerotic lesions. However, none of these methods are able, at present, to completely examine the coronary tree, and therefore none are ready to be used as a standard clinical technique for the diagnosis and management of coronary artery disease. Technological advances will enhance the future clinical value and applicability of these techniques.
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"Pharmacologic" stress testing with inotropic stimulation is useful in the detection of coronary artery disease when ventricular dysfunction is provoked. However, abnormal diastolic filling may be masked or mimicked because of the influence of aging, heart rate, and loading conditions. We evaluated age effects on left ventricular filling at rest in young (n = 5) and old (n = 6) purebred beagles that were free of occlusive coronary disease and left ventricular hypertrophy, and we also evaluated age-related differences in left ventricular filling velocities in response to dobutamine and phenylephrine. Pulsed Doppler echocardiography of left ventricular filling velocities was performed at baseline and then after the administration of dobutamine (10 to 20 micrograms/kg/min) infusion. Repeat baseline recordings were obtained and then phenylephrine was administered intravenously in doses of 5 to 25 micrograms/kg/min until systolic arterial pressure increased by at least 30 mm Hg above baseline. At baseline, Doppler echocardiography revealed that there were no significant differences in the early (E) velocity or velocity time interval (VTI), and atrial (A) velocity or the A/E velocity ratio between the young and old groups. However, the A VTI and the A/(A + E) VTI ratio were significantly increased in the old group. With dobutamine administration, the E velocity did not significantly increase from baseline in either group. The E VTI, A velocity and A VTI increased significantly in both groups, but the increases were not different between groups. With phenylephrine infusion there was a significant decrease in the E VTI in the old group but neither the A/E velocity or the A/(A + E) VTI ratio significantly changed from baseline.(ABSTRACT TRUNCATED AT 250 WORDS)
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Determination of magnetic resonance (MR) relaxation times (T1 and T2) and ultrasound backscatter are potential methods of noninvasive myocardial tissue characterization. The authors postulated that infarct-related collagen deposition in a canine chronic myocardial infarction model would alter T1 and T2 relaxation times. Further, we sought to compare the changes in T1 and T2 with backscatter measurements. Eight animals were studied 4 to 6 weeks after occlusion of the left anterior descending coronary artery; standard echocardiography showed each to have left ventricular wall motion abnormalities. Time-averaged backscatter and cyclic backscatter variation (at 5 MHz) were measured in the open-chest animal with corresponding normal and infarcted areas undergoing in vitro T1 and T2 measurements (at 20 MHz) and water and hydroxyproline concentration analysis. Significant increases in T2, time-averaged ultrasound backscatter, and hydroxyproline concentration were found in the infarcted myocardium compared with normal muscle. Cyclic variation in backscatter and water content were not significantly different between the two groups. Although backscatter, T2, and tissue collagen content increased in the infarcted myocardium, a significant relationship was not found among these variables.
Dual pathway sequential DC shocks reduce energy requirements for internal defibrillation. Our purpose was to determine if dual pathway shocks similarly reduce energy requirements or improve shock success in transthoracic (external) defibrillation. We studied 39 closed-chest anesthetized mongrel dogs. The dual pathways used were left chest to right chest and left chest to posterior. In eight dogs we also assessed dual shock pathways oriented orthogonally, left lower chest to right upper chest and left upper chest to right lower chest. Four different dual pathway groups were studied: group 1: simultaneous shocks, sinusoidal waveform; group 2: sequential shocks, sinusoidal waveform, 100-msec shock separation, orthogonal shock pathways; group 3: sequential shocks, sinusoidal waveform, 100 msec shock separation; and group 4: sequential shocks, rectangular waveform (sequential shocks: 2 pulses, 2.5 msec each, 0.1-msec separation; single shock: 1 pulse, 5 msec). Shocks were given at 50 (J) joules, 100 J and 150 J and curves of energy versus success compared for dual pathway shocks versus single shocks. We found that the highest mean success rates (96 +/- SD 9%) were achieved by simultaneous sinusoidal waveform dual pathway shocks at 100 J; this was identical to results achieved by the single pathway sinusoidal waveform comparison shocks at 100 J. Sequential dual pathway sinusoidal shocks separated by 100 msec achieved a mean success rate of 79 +/- 31% at 150 J; the comparison single pathway mean success rate was similar: 81 +/- 22% at 150 J. Thus, dual pathway sequential or simultaneous transthoracic shocks did not demonstrate clear superiority over single pathway shocks.
Two-dimensional echocardiography is an excellent technique for detecting left ventricular thrombi, however, acute clot is sometimes difficult to differentiate from adjacent myocardium and intracavitary signals. We hypothesized that quantitative assessment of the acoustic properties of acute left ventricular thrombi using a quantitative backscatter imaging system would permit the differentiation of thrombus from adjacent myocardium and intracavitary echoes. Acute, experimental left ventricular thrombi in seven dogs were evaluated with a quantitative backscatter imaging system that allowed the measurement of relative integrated backscatter and cyclic (i.e., diastolic minus systolic) variation in integrated backscatter. Coronary ligation abolished the cyclic variation in relative backscatter that occurred in normal myocardium. The end-diastolic relative backscatter in the thrombus (16.9 +/- 1.3 dB) was significantly higher than in apical myocardium (13.2 +/- 0.6 dB, p less than 0.05). There was no significant difference in the cyclic variation in relative backscatter among thrombus, ischemic myocardium, or intracavitary blood. Thus, the quantitative assessment of the acoustic properties of left ventricular thrombi can be useful in their detection and in the differentiation from myocardium and intracavitary signals.
Because the cause and natural history of amaurosis fugax and ocular infarction are unknown in most younger patients, we reviewed the records of 83 patients who had become symptomatic before the age of 45. Cerebral transient ischemic attacks had occurred in 9 of these patients but no case of stroke was found. A striking feature of these patients was that 41% had headache or orbital pain accompanying their amaurotic spells and an additional 25.3% had severe headaches independent of the visual loss. Results of laboratory studies were rarely abnormal and echocardiography disclosed that only 1 patient had previously unknown heart disease. Mitral valve prolapse was detected in 6.5%, a figure similar to that expected for the general population. Of the original 83 patients, 42 were reexamined after a mean period of 5.8 years. None of the patients in this group had had a stroke, and the clinical status at follow-up was not found to correlate with the duration of the visual loss (amaurosis fugax versus ocular infarction), frequency (single versus recurrent episodes), sex, presence of headache or heart disease, cigarette smoking, use of oral contraceptives, or abnormal findings on echocardiograms or laboratory studies. We conclude that amaurosis fugax and ocular infarction occurring in the younger patient are probably associated with a more benign clinical course than that seen in older persons and that migraine is a likely cause for the episodes of visual loss in a majority of this group. Because of this, we believe that a conservative approach to the evaluation of such patients seems warranted.
We have used a high frequency epicardial echocardiographic technique to visualize and measure coronary artery lumens and walls in patients undergoing cardiac surgery. A 12 MHz probe (Surgiscan, Biosound Corp.) is sterilized and placed on the exposed epicardial coronary arteries. Transverse cross-sectional views are obtained from the arteries on the anterior surface of the heart: the right coronary artery to the cardiac margin and the left anterior descending coronary artery to the cardiac apex. Numerous echocardiographic-angiographic-pathological correlations have been obtained from this work. We have validated the echocardiographic lumen and wall measurements by comparing the echo measurements to histological material from pressure-distended coronary arterial segments (from animals and fresh human autopsy specimens). We have shown by comparison with angiography that coronary arteries which appear normal or only minimally diseased by angiograms are often diffusely and severely atherosclerotic. We have also evaluated the shape of atherosclerotic lesions and demonstrated a wide range of lumen shapes (oval, circular, complex) and location within the residual coronary lumen (eccentric vs. concentric). Highly eccentric lesions are characterized by relative preservation of portions of the arterial wall, and this may preserve vasoreactivity of the atherosclerotic vessel. We have also demonstrated remodeling of atherosclerotic lesions: enlargement of the total arterial area (wall plus lumen) as a compensatory mechanism to preserve the arterial lumen in the face of encroaching atherosclerosis. High frequency epicardial echocardiography offers an accurate, real-time, in-vivo method for the anatomic and functional evaluation of coronary atherosclerosis. This dynamic, in-vivo technique supports and extends information previously obtainable only from pathologic studies.(ABSTRACT TRUNCATED AT 250 WORDS)
The hemodynamic response to sequences of ventricular fibrillation and defibrillation includes an adrenergic component that is important for the maintenance of blood pressure after successful defibrillation. Because calcium channel blocking drugs have antiadrenergic effects, we hypothesized that they might blunt the adrenergic response to defibrillation. Ventricular fibrillation was induced in 35 closed-chest dogs. Each received 4 to 7 direct current transthoracic shocks at three energy levels to determine defibrillation energy requirements. Heart rate and blood pressure were recorded. Energy sequences were repeated after 45 minutes of no intervention (control, n = 5) or after 45-minute infusions of diltiazem (0.1 mg/kg/min, n = 10), verapamil (0.1 mg/kg bolus plus 0.01 mg/kg/min, n = 10), or nifedipine (40 micrograms/min for 3 minutes plus 2 to 20 micrograms/min adjusted to maintain a 10 mm Hg drop in mean arterial pressure, n = 10). Our results show that the normal post-shock rise in mean arterial pressure was blunted by the calcium channel blockers diltiazem (systolic arterial pressure at 15 and 60 seconds post-shock, pre-drug versus post-drug: 102 +/- 9 versus 64 +/- 9 mm Hg and 113 +/- 10 versus 87 +/- 6 mm Hg; p less than 0.05) and verapamil (108 +/- 9 versus 78 +/- 12 mm Hg and 113 +/- 7 versus 90 +/- 10 mm Hg, p less than 0.05). There were no differences in blood pressure responses after nifedipine treatment or no drug. Heart rate responses were not altered by diltiazem or verapamil; after nifedipine administration, post-shock heart rates were slower.(ABSTRACT TRUNCATED AT 250 WORDS)
Hand-agitated diatrizoate meglumine/diatrizoate sodium (MD-76) was injected above the aortic valve in seven dogs during two-dimensional echocardiographic imaging to determine the ability of contrast appearance variables (i.e., peak background-subtracted gray level intensity, time to peak contrast appearance and maximal slope of the contrast appearance curve) to predict myocardial blood flow. Regional perfusion was altered by a critical coronary stenosis (around the left anterior descending coronary artery) or by administering intracoronary adenosine (into the left circumflex coronary artery), or both. Changes in regional blood flow between control and interventions were compared with the changes in the contrast appearance variables. In addition, the ability of intracyclic variability of gray level intensity to predict myocardial perfusion was assessed. In the determination of absolute myocardial perfusion, background-subtracted peak gray level intensity and the maximal slope of the appearance curve demonstrated a fair correlation (r = 0.67 and 0.51, respectively, p less than 0.0001). However, time to peak contrast appearance did not correlate (r = 0.14, p = 0.31). Intracyclic variability of gray level intensity at control (before contrast injection) and after contrast injection also did not correlate with perfusion (r = 0.18 and 0.06, respectively). In the evaluation of relative changes in myocardial blood flow, the percent change in the maximal slope of the appearance curve correlated with the percent change in blood flow (r = 0.77, p less than 0.0001). Seven of the eight regions with greater than 3.5-fold increase in blood flow were identified by an increase in maximal slope of greater than 50%.(ABSTRACT TRUNCATED AT 250 WORDS)
To test the hypothesis that tissue hyperemia and edema in the current pathway cause a decrease in transthoracic impedance (TTI) following direct current (DC) shock, the thoracic-skin and skeletal blood flow and blood volume were measured in anesthetized dogs after three 100-J shocks. TTI declined 11% (P less than 0.01) after DC shocks. Blood flow increased 10-fold in skeletal muscle from 0.9 +/- 0.2 to 11.3 +/- 2.6 (SE) ml.100 g-1.min-1 (P less than 0.05). Blood flow did not change outside the current pathway. Blood volume increased in skin in the current pathway from 7.6 +/- 1.5 ml/100 g preshock to 17.5 +/- 2.0 ml/100 g (P less than 0.01) at 60 min after shock; skeletal muscle blood volume did not change. We also determined postshock tissue weight before and after 72 h of drying at 70 degrees C. The percentage decline from wet weight after drying was 68.4 +/- 3.4% in the current pathway vs. 64 +/- 3.8% outside the pathway (P less than 0.05), indicating the tissue in the current pathway was more edematous. Finally, hindlimb edema was induced by deliberate overperfusion. As hindlimb circumference (edema) increased, impedance declined. We conclude that increases in tissue blood flow or tissue blood volume or tissue edema contribute to the decline in transthoracic impedance after DC shock.
Successful cardioversion is dependent on the delivery of sufficient current. Current is determined by energy and transthoracic impedance (TTI). Our purpose was to assess factors affecting TTI in humans. Twenty-eight patients undergoing elective cardioversion were monitored up to 48 hours after shock delivery. We also studied 10 normal subjects, who did not receive shocks, for comparison. TTI declined 8% in the first hour in patients who received shocks, but also 6% in the normal subjects who wore the same pads for 1 hour but received no shocks. Twenty-four hours later, TTI returned to baseline in the nonshocked subjects but remained reduced (93% of control, p less than 0.05) in the shocked patients. There was a correlation between the total energy delivered and the decline in TTI (r = 0.69). TTI was 9% lower at end-expiration than at end-inspiration (55 +/- 3 vs 50 +/- 3 ohms, mean +/- standard error of the mean, p less than 0.01, paired t test). In the normal subjects, when a nonsalt-containing coupling agent (ultrasound coupling gel) was compared with a salt-containing gel (Redux paste), TTI was 20% higher (65 +/- 5 vs 54 +/- 4 ohms, p less than 0.01) with the nonsalt-containing gel. When no coupling agent was used, TTI was markedly higher, 160 +/- 18 ohms (p less than 0.01 vs control). After 1 hour, TTI decreased 6% in the normal subjects when salt-containing gel was used, but did not change when a nonsalt gel was used.(ABSTRACT TRUNCATED AT 250 WORDS)
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Contrast agents were injected via the intracoronary route in eight dogs during two-dimensional echocardiographic imaging to determine the influence of microbubble size and concentration, injection rate, and coronary vasodilation on risk area and peak gray level measurement. At an injection rate at 13 cc/sec, the average background-subtracted peak gray level intensity of hand-agitated diatrizoate meglumine/diatrizoate sodium was significantly (p less than 0.01) higher than that of hand-agitated diatrizoate meglumine/diatrizoate sodium + 0.9% saline, sonicated diatrizoate meglumine/diatrizoate sodium, and sonicated 70% sorbitol. These differences were abolished by the use of 38 cc/sec injection rates and intracoronary injection of adenosine. Perfusion area determinations as assessed by planimetry were unaffected by the contrast agent used, the injection rate, or by intracoronary administration of adenosine. We conclude that risk area measurement by the ultrasound contrast technique is not affected by varying contrast agents, injection rates, or vasodilation. However, peak gray level intensity is variable among contrast agents and may result in variability of time-activity curve analysis.