Biomedical subjects
Publications and source records attributed to J M Criley.
Placement of flow-directed Swan-Ganz catheters without fluoroscopic guidance occasionally results in placement in positions other than the pulmonary artery. In the case presented, the inadvertent placement of such a catheter into the left pericardiophrenic vein was probably facilitated by distortion of the right heart and systemic venous anatomy.
Two patients were discovered to have pulsatile saccular lesions at the base of the left ventricle and mitral regurgitation following blunt trauma to the chest. These aneurysms resembled annular subvalvular aneurysms which have previously been reported as congenital defects in African blacks and as acquired lesions following endocarditis or mitral valve replacement. The first patient had two aneurysms, while the second had an aneurysm in continuity with a traumatic ventricular septal defect. These aneurysms were detected by echocardiography and magnetic resonance imaging and should be sought in patients who develop valvar regurgitation following chest trauma.
A 28-year-old woman with pulmonary atresia underwent a modified Fontan procedure that utilized a valved aortic homograft; she developed stenosis of the distal anastomosis between the homograft and the pulmonary artery. Because of the increased risk of reoperation, balloon angioplasty of this stenotic lesion was performed successfully. In the subsequent 11 months she has remained asymptomatic. Balloon angioplasty was a successful alternative to reoperation in this patient.
Measurement of cardiac output (CO) requires right-sided cardiac catheterization. However, to save time and reduce costs, only left-sided cardiac catheterization is usually performed in most patients with suspected coronary artery disease. Thus, CO is not measured. To determine if CO can be measured from the left side of the heart, 24 patients undergoing cardiac catheterization had near-simultaneous determination of CO after indocyanine green dye was injected into the pulmonary artery and left ventricular (LV) cavity. There was close agreement between pulmonary artery and LV derived cardiac outputs (Pulmonary artery = 0.93 LV + 0.12). The pulmonary artery derived CO was 5.7 +/- 2.0 liters/min and the LV derived CO was 6.1 +/- 2.2 liter/min. Also, there was a close relation between pulmonary artery derived stroke volume (82 +/- 33 ml) and LV derived stroke volume (86 +/- 36 ml). Thus, CO can be accurately measured after injection of indocyanine green dye into the LV cavity.
To define alterations in myocardial mitochondrial function due to hypoperfusion, oxidative phosphorylation was simultaneously studied in 17 control (stable perfusion pressure) rat hearts and 17 hypoperfused isolated rat hearts. Hypoperfusion for 30 minutes was achieved by a reduction in coronary perfusion pressure from 77.8 +/- 1.2 mm Hg (mean +/- SEM) to 20.2 +/- 1.8 mm Hg in the experimental group (control perfusion pressure after 30 minutes 75.6 +/- 1.2). Hypoperfusion caused a reduction in left ventricular developed pressure to 20.5 +/- 1.5 mm Hg (versus control 74.8 +/- 3.3, p less than 0.0001), a reduction of coronary flow rate to 4.9 +/- 0.3 ml/min (versus control 19.4 +/- 1.2, p less than 0.0001), and a drop in myocardial oxygen consumption to 0.06 +/- 0.005 ml O2/min (versus control 0.17 +/- 0.01, p less than 0.0001). Myocardial lactate production was increased by hypoperfusion (3.0 +/- 0.6 mumol/min) compared with controls (0.7 +/- 0.5, p less than 0.02), but myocardial creatine kinase release was similar in the hypoperfused and control groups. Hypoperfusion was associated with an augmentation of state 3 mitochondrial respiration with glutamate and malate as respiratory substrates (448.8 +/- 14.0 ng atoms O/min/mg mitochondrial protein versus controls 290.7 +/- 13.4, p less than 0.001). When rates were normalized for mitochondrial malate dehydrogenase (MDHm), state 3 respiration was still increased in hypoperfused hearts (24.1 +/- 2.1 ng atoms O/min/IU MDHm) compared with controls (15.5 +/- 1.6, p less than 0.02). The rates of dinitrophenol-uncoupled electron transport were similar to the rates of state 3 respiration in both the hypoperfused and control groups.(ABSTRACT TRUNCATED AT 250 WORDS)
A new automated edge detection program has been developed to estimate left ventricular mass from single photon emission computed tomographic (SPECT) 201Tl images and 14 dogs were studied. Six of the 14 dogs underwent imaging before and 5 hr after coronary artery occlusion with a closed-chest technique. True left ventricular mass was determined at time of killing within 1 hr of the last 201Tl study. Left ventricular mass determined by tomography correlated well with autopsy left ventricular mass (r = 0.94; p less than 0.001, s.e.e. = 5.9 g) over a range of 62-156 g. The intraobserver variation between repeated measurements of the same SPECT study yielded an r = 0.99; p less than 0.0001; s.e.e. = 2.3 g. The reproducibility of the mass determination was assessed in four animals with two studies performed 10-14 days apart. The estimate of left ventricular mass from the two studies were highly correlated (r = 0.98; p less than 0.001) with a mean absolute difference of 4 g (3.3%). In the six dogs with a control and postinfarct study the mean total left ventricular mass by 201Tl tomography varied by less than 3.8% (r = 0.89; p less than 0.001). In conclusion, tomographic imaging with 201Tl can define left ventricular mass accurately and reproducibly in the dog model. The ability of this 201Tl tomographic left ventricular mass program to measure both normal and infarcted tissue accurately suggests the possibility of documenting interventions designed to alter left ventricular mass and of sizing acute infarcts and assessing interventions that may alter acute infarct size.
There has been a longstanding controversy about the significance of intracavitary pressure gradients in hypertrophic cardiomyopathy (HCM). It has been generally assumed that the gradient is the result of an 'obstruction' that impedes left ventricular outflow and which can be relieved by operative intervention. In the first decade after the discovery of HCM (1957-66), the site of 'obstruction' was thought to be a muscular sphincter or contraction ring in the submitral region of the left ventricle, and operations designed to emulate pyloromyectomy (for hypertrophic pyloric stenosis) were developed. Following a challenge to the existence of the 'contraction ring' and an alternative non-obstructive explanation of the pressure gradient, the site of 'obstruction' was translocated to a point of apposition between the anterior mitral leaflet and the interventricular septum, a result of systolic anterior motion (SAM) of the mitral valve. Despite the translocation of the site and mechanism of 'obstruction', the operation for 'relief of obstruction' has not changed significantly. The newer site of 'obstruction' has been challenged on the grounds that the ventricle is not demonstrably impeded in its emptying; when a gradient is provoked, the ventricle empties more rapidly and more completely than it does without a gradient. In addition to a non-obstructive explanation of the gradient, other phenomena thought to be indicative of 'obstruction' can be explained by rapid and complete emptying of the ventricle (cavitary obliteration). Since the morbidity and mortality of symptomatic HCM patients without pressure gradients may exceed that of patients with pressure gradients, it is suggested that 'obstruction' may be unimportant in the pathophysiology of HCM and attention should be focused on abnormal diastolic function and life threatening arrhythmias.
Fourteen patients with hypertrophic cardiomyopathy, 40 with aortic stenosis, and 4 with discrete subaortic stenosis had phonocardiograms during left heart catheterization that showed changes in the magnitude of the murmur in response to increases in the postextrasystolic gradient. All patients showed increases in the gradient of the left ventricular outflow tract during the postextrasystolic beat. Of the 44 patients with aortic stenosis and discrete subaortic stenosis, 42 (95%) had increases in murmur magnitude, in contrast to 9 (64%) of 14 patients with hypertrophic cardiomyopathy. Only 2 of 7 patients with hypertrophic cardiomyopathy and resting gradients of more than 25 mm Hg had murmur increases. Our study shows that the systolic murmur in hypertrophic cardiomyopathy, unlike the outflow tract murmur in aortic stenosis or discrete subaortic stenosis, does not track consistently with the magnitude of the outflow tract gradient.
Blood flow during closed-chest CPR may result from variations in intrathoracic pressure rather than selective compression of the cardiac ventricles. During chest compression, the thoracic and abdominal cavities are subjected to positive pressure fluctuations. It has been suggested that compression of the abdomen may improve left heart outflow during CPR by limiting diaphragmatic movement or improving venous return. Abdominal compression has been performed experimentally with pneumatic abdominal binders and with the abdominal compartment of the conventional military antishock trouser (MAST) garment. The MAST garment might also improve cardiac output with CPR through an "autotransfusion" effect. In animal studies, MAST-augmented CPR has improved systolic pressures; it has not been shown to improve vital organ perfusion. In the only available clinical study, CPR with the MAST did not improve survival from prehospital cardiac arrest when compared with conventional CPR alone. If inflation of the MAST does produce blood displacement from the peripheral to the central venous circulation, such an effect may be detrimental in that the arteriovenous pressure gradients necessary for vital organ flow may be adversely affected. Inflation of the MAST during CPR may also adversely effect artificial ventilation. Selective abdominal binding also increases systolic pressures during CPR but does not improve subdiaphragmatic venous return. Although abdominal binding may increase common carotid flow, it has not been shown to improve cerebral or myocardial perfusion when compared with conventional CPR alone. These CPR adjunct techniques have not been shown to improve outcome from cardiac arrest and should remain experimental until further well-designed studies addressing regional vital organ flow and outcome of resuscitation are performed.
The ability of cardiopulmonary resuscitation (CPR) to provide adequate vital organ blood flow during prolonged resuscitation has long been questioned, as has the mechanism of blood flow during CPR. Because coughing during cardiac arrest has been shown to produce adequate anterograde flow to maintain consciousness in man without compressing the heart, cough CPR has been used as a model of a pure "thoracic pump" mechanism on which to base modifications of CPR. In the thoracic pump mechanism, the left heart is a passive conduit for blood expressed from the pulmonary vasculature to the aorta, and there is selective flow to the brachiocephalic vascular bed because of its low pressure veins, which are protected by closure of thoracic inlet venous valves. Right heart flow from systemic veins to the lungs occurs between applications of pressure. Four alternative modalities exploiting the thoracic pump concept were studied in dogs during ventricular fibrillation with angiographic and pressure recordings: cough CPR, simultaneous chest compression and lung inflation, abdominal compression with lung inflation, and inflation of a vest and binder. The latter technique was associated with successful defibrillation and recovery after more than 30 min of circulatory support during ventricular fibrillation. Preliminary studies in a primate preparation indicate that this technique might be useful for prolonged circulatory support in man when defibrillation is not initially available or successful.
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Parasympathetic tone may be high during ventricular asystole because of reflex vagal stimulation from a number of sources. Eight patients in cardiac arrest were treated with cardiopulmonary resuscitation. All eight patients had ventricular asystole as the initial rhythm or as the result of defibrillation. Six patients failed to respond to 5 cc to 20 cc of 1:10,000 epinephrine intravenously (IV). In all eight cases a regular rhythm (sinus in seven, idioventricular in one) appeared within 30 seconds of administration of the last dose of atropine (1 mg to 2 mg IV). Five patients (62.5%) lived 12 hours, three (37.5%) were discharged from the hospital. These results suggest that atropine may be of value in the treatment of ventricular asystole.
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Changes in ejection fraction (EF) and segmental wall motion (SWM) have been shown to be sensitive indicators of left ventricular (LV) function. This information is only obtainable by contrast angiography or gated blood pool scans. Gated studies assume a fixed geometry for the LV for EF determinations, are lengthy and limited primarily to the LAO projection. We correlated contrast and Tc-99m pertechnetate angiograms by singl pass radioisotope angiography (immediately preceding the contrast study) in 12 patients. EF was calculated from the LV time/activity curve and values ranged from .21 to .72. Angiographic correlation yielded r = 0.97. Regional LV wall motion was evaluated by dividing a summated cardiac cycle into 16 frames and dynamically and sequentially displaying these frames. Regional wall motion evaluation of four LV quadrants correlated well with angiography (r = 0.97). For quantitation these images were divided into four anterior and four inferior segments and the areas of respective segments were compared and expressed as a shortening fraction. SWM compared favorably with angiographic determinations (r ranged from 0.70 to 0.99). Thus, single pass radioisotopic determinations of EF and SWM in the RAO projection correlated well with the angiographic values and provide essential quantitative information of LV function otherwise unobtainable at the bedside.
Transvenous right ventricular pacemaker catheters were implanted in 18 mongrel dogs for periods of 2 to 18 months (average 4.9 months). Heart block was produced in 15 of these dogs by injection of 37 per cent formaldehyde into the interatrial septum. In the other three dogs which served as controls, no heart block was produced and no electrical stimulation was applied to the implanted catheters. After the animals had been put to death, gross and microscopic examination of the hearts revealed four categories of morphological changes: (1) connective tissue sheath formation around the catheters, (2) endocardial papillary thickening, (3) interatrial septal changes, and (4) myocardial damage. Changes 1, 2, and 4 occurred in one or more intracardiac locations in all 18 dogs. Change 3 occurred only in the 15 dogs in which heart block was produced. The most striking histologic findings were areas of cartilagenous metaplasia in endocardium an underlying myocardium and areas of marked cellular proliferation of the endocardial cells both in the endothelium and underlying stroma. Chronic implantation of transvenous intracardiac pacemaker catheters in dogs consistently produces morphologic changes which may interfere with cardiac and pacemaker function and may hinder attempts to remove nonfunctional or unneeded catheter electrodes. The changes observed appear to be related to the presence of foreign material per se and not external electrical stimulation of the heart.
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