Invited commentary: surgical residency training.
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Biomedical subjects
Publications and source records attributed to A Harken.
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To evaluate regional differences in thickness and systolic function of human myocardium perfused by angiographically normal coronary arteries in valvular and ischemic heart disease, we performed intraoperative epicardial M-mode mapping of ventriculographically normal wall regions (perfused by normal coronary arteries) in 22 subjects undergoing either coronary bypass surgery for stenoses in other vessels (n = 15) or mitral (n = 5) and/or aortic valve replacement (n = 4). In patients in whom both anterior and inferior walls were ventriculographically normal and normally perfused (n = 6), comparison of the two walls showed the anterior wall to be thicker at both end diastole and end systole, but there was no difference in the percentage of systolic thickening. Analysis of myocardium along the long axis revealed apical sites to be thinner than basal sites at both end diastole and end systole. Percentage of systolic thickening was also increased at apical sites. In patients in whom only the anterior wall was normal, a similar decrease in anterior wall thickness was noted at the apex. Thus systematic regional heterogeneity along both the left ventricular major and minor axes is found in the chronically diseased human heart as it is in the normal heart. Assessment of myocardial structure and function and of the effects of therapeutic interventions must take this heterogeneity into account.
Despite evidence for calcium-induced damage in the postischemic myocardium, calcium remains a frequently used inotropic agent following cardiopulmonary bypass surgery with cardioplegic arrest. The purpose of this study was (1) to challenge the postischemic myocardium with incremental doses of ionized calcium, and (2) to relate postischemic calcium reperfusion concentration to final recovery of left ventricular contractile function. Rabbit hearts (N = 38) were perfused and equipped with a ventricular balloon to monitor developed pressure (DP) +/- dp/dt, and left ventricular end diastolic pressure (LVEDP). Hearts underwent 40 min of global ischemia. Hearts were then assigned to one of four groups to receive a variable calcium concentration (0.6, 1.2, 2.5, 5.0 mM) for the initial 5 min of reperfusion followed by 55 min of reperfusion (Ca+2 = 1.25 mM). No differences were found between groups for final recovery of DP +/- dp/dt, or final LVEDP. It was concluded that: (1) within the physiologic range, variable calcium infusions during the first 5 min of postischemic reperfusion do not impair final recovery of LV contractile function, (2) irreversible partial recovery of left ventricular function appears due to mechanisms other than mitochondrial or myofibrillar calcium loading during reperfusion, and (3) infused calcium is a safe inotropic agent even in the postischemic myocardium.
Mapping-guided endocardial resection has proved to be an effective therapy for recurrent sustained ventricular tachycardia. However, some patients cannot be mapped during ventricular tachycardia, so that guidance from findings during normal sinus rhythm would be highly desirable. We examined the frequency, timing, and duration of several abnormal types of electrograms recorded endocardially during sinus rhythm and related these findings to activation mapping during sustained ventricular tachycardia. Thirteen patients with extensive myocardial infarction complicated by recurrent sustained ventricular tachycardia were studied intraoperatively during sinus rhythm and induced ventricular tachycardia with a standardized mapping scheme involving the entire endocardial surface. Fractionated electrograms (multicomponent with amplitude less than 1 mV and duration greater than 50 msec) were recorded in all patients. This type of electrogram could be recorded at up to 36% of mapped sites. Split electrograms (two components separated by isoelectric period) were also frequently seen but involved only a mean of 5.8% of mapped sites. Late electrograms (inscribed entirely after the QRS complex) were only recorded in four of 13 patients at a mean of 5% of mapped sites. The location of these electrograms was related to an arbitrary 8 cm2 zone around the earliest site of endocardial activation recorded during ventricular tachycardia. The longest fractionated electrogram was closely related to nine of 22 morphologies of induced ventricular tachycardia, split electrograms were related to seven of 16 morphologies, and late electrograms to two of four morphologies. We have concluded that extremely abnormal electrograms recorded endocardially during sinus rhythm are widespread in patients with extensive myocardial infarction complicated by ventricular tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)
UNLABELLED: The onset of global myocardial ischemia was related to mechanical function (intraventricular pressure), cellular redox state (NADH fluorophotography), and high energy profile (phosphorous-31 nuclear magnetic resonance). Ten rabbit hearts were excised and perfused on a modified Langendorff apparatus (37 degrees C; pO2 480 Torr). Developed pressure and positive and negative dp/dt were determined at control, 1-10, 15, 30, 45, and 60 sec of acute global ischemia. NADH fluorophotographs were taken at control, 1-10, 15, 20, 30, 60 sec, and 5, 10, and 30 min. P-31 NMR spectra in 14 guinea pig hearts under identical conditions were obtained at control, 1, 5, 10, 20, 40, and 60 min of acute global ischemia. LV contractility diminished within 1 sec (P less than 0.01) of ischemia and dropped to less than 35% of control by 1 min. Reduction of mitochondria was detected by epicardial NADH fluorophotography at 2 sec of ischemia. Cellular pH diminished 0.3 pH units by 5 min. Adenosine triphosphate (ATP) concentration remained at control levels while phosphocreatine (PCr) dropped to 63 +/- 8.5% of control by 1 min of ischemia. CONCLUSIONS: After the onset of global ischemia (1) mitochondrial electron transport ceases by 2 sec; (2) acidosis develops immediately; (3) LV contractility diminishes by 1 sec; (4) ATP concentration appears to be buffered by PCr, and is dissociated from myocardial function.
The influence of mixed venous oxygen tension (PVO2) on blood flow to the atelectatic left lung was studied at normal and reduced cardiac outputs (CO) using extracorporeal veno-venous bypass in six pentobarbital anesthetized, mechanically ventilated dogs. Aortic and left pulmonary artery flows; airway, left atrial, central venous, pulmonary, and systemic arterial pressures; hemoglobin, arterial, and mixed venous blood gases were measured. The blood flow reduction observed in atelectasis was altered by the PVO2. Approximately 50% of blood flow was diverted away from atelectatic lung when PVO2 was low (24 +/- 2 mmHg) or normal (46 +/- 2 mmHg) (mean left lung blood flow [QL%] was 23.2 +/- 4.6% with low PVO2 and 19.0 +/- 3.4%, with normal PVO2). When PVO2 was increased to greater than 100 mmHg, diversion of blood flow away from atelectatic lung did not occur and QL% was nearly the flow expected for normoxic ventilated left lung (mean QL% = 40.4 +/- 5.9%). Shunt (QS/QT%) was significantly greater when PVO2 was high than when it was normal or low (mean QS/QT% = 51.7 +/- 5.6%, 31.0 +/- 3.1%, 26.0 +/- 3.4% with high, normal, and low PVO2, respectively). Mean PaO2 was significantly greater when PVO2 was high than when PVO2 was normal or low, despite the increase in QL% and QS/QT% (PaO2 = 327 +/- 25 mmHg, 220 +/- 32 mmHg, 115 +/- 21 mmHg with high, normal, and low PVO2, respectively). A 40% reduction in cardiac output significantly decreased transmural pulmonary artery pressure but did not affect PaO2, QS/QT%, or QL%.(ABSTRACT TRUNCATED AT 250 WORDS)
A technique for epicardial mapping of segmental myocardial function at multiple sites over both right and left ventricles was developed using a high-resolution, 7.5-MHz, short-focus, miniaturized, M-mode echocardiographic transducer worn on the fingertip. Myocardial function was determined from the extent and time course of systolic thickening and diastolic thinning at each site mapped. The technique was characterized in an open-chest canine model of myocardial ischemia. Ischemia was induced by transient or permanent coronary occlusion in 17 dogs. Acute occlusions produced reduced segmental thickening within 10-15 seconds and, often, overt systolic thinning of ischemic myocardium. Rhodamine fluorescence perfusion maps were compared with echocardiographic maps in nine dogs. Segmental thickening was reduced in perfused segments adjacent to, but not involved by, ischemia, as well as ischemic segments. Reproducibility appeared satisfactory for quantitative analysis of grouped data on multiple segments, and qualitative analysis in individual segments. Initial human studies performed during coronary bypass surgery in 11 subjects showed echocardiographic abnormalities in the six patients with ventriculographic abnormalities and in four with normal ventriculograms. Transmural infarctions were akinetic, showing no change in thickness throughout the cardiac cycle. Hypokinetic segments distal to high-grade coronary stenosis were common, although most segments distal to stenosis contracted normally. Reversal of segmental contraction abnormalities by coronary bypass grafting was shown in three subjects, while worsening of function was seen in previously abnormal segments in two and in a previously normal segment in one subject. Epicardial echocardiographic mapping is a practical method for intraoperative assessment of myocardial function during coronary surgery in man that may enhance our understanding of the pathophysiology of coronary disease and the effects of coronary surgery.
We investigated coronary-artery spasm in six patents who had had unexpected hemodynamic collapse within two hours after cardiopulmonary bypass for myocardial revascularization. All six had profound hypotension and recurrent ST-segment elevation in electrocardiographic Leads II, III, and aVF. All had either normal or noncritical luminal irregularities of dominant right coronary arteries and more than 75 per cent occlusions in the left coronary circulation. Right-coronary-artery spasm, which was reversed after intracoronary nitroglycerin, was demonstrated angiographically in one patient; a patent right coronary artery was found at autopsy in another patient. Three patients died despite large intravenous doses of nitroglycerin. Two patients who had been unresponsive to intravenous nitroglycerin recovered after direct infusion of nitroglycerin into the right coronary artery. Coronary-artery spasm immediately after myocardial revascularization may cause circulatory collapse and death; although the spasm may be refractory to usual therapy, it may respond to intracoronary nitroglycerin.
During a five-year period, 178 patients had the intraaortic balloon pump (IABP) inserted for circulatory support. The IABP was used most frequently as an adjunct for weaning patients from cardiopulmonary bypass. Seventy-seven of 103 patients (75%) were successfully weaned from cardiopulmonary bypass with the IABP, and 36 of them (35%) ultimately survived hospitalization. Other indications for the IABP included circulatory support before cardiac operation (16 patients), operative prophylaxis in high-rish patients (13), and postoperative hemodynamic support (23). Additionally, the IABP was placed in 23 patients who did not undergo cardiac operation. The incidence of IABP-related complications was significantly less when the IABP was inserted through the ascending aorta (4%) intraoperatively compared with the femoral or iliac artery (25%) (p less than 0.05). This was due primarily to vascular complications and groin wound infections that occurred with the femoral or iliac artery approach. IABP-related spinal cord paralysis developed in 3 patients (1.7%). We conclude that the IABP is an effective support device for treating patients with left ventricular failure particularly when weaning them from cardiopulmonary bypass. However, the risk of complications, including paraplegia, must be carefully weighed when use of the IABP is considered, especially in situations in which its efficacy is less clear.
Effects of intermittent (IPPB) and positive eng-expiratory pressure (PEEP) ventilation on accumulation of pulmonary edema were compared, in dogs, after infusion of oleic acid. Pulmonary extravascular water was approximated as lung thermal volume (LTV), a double indicator method based on differential transit time for simultaneously injected right-to-left conductivity and thermal pulses. LTV was found to be decreased in animals treated with PEEP. The possibility that observed LTV changes reflect only the effect of PEEP on flow distribution, not lung water, was examined by alternating PEEP and IPPB; short-term changes in LTV did not occur. Mean values of other factors influencing pulmonary water transfer, e.g., pulmonary capillary wedge pressure, serum protein, arterial blood gasses, were not significantly different with or without PEEP. It was concluded that, for the oleic acid lesion, PEEP effects a small reduction in the rate of accumulation of pulmonary edema.
Ten mongrel dogs were placed on 5 and 10 cm. H20 of CPPV. Cardiac output, pulmonary vascular resistance and pleural pressures were measured. At 5 cm. H20/CPPV there was no significant change in cardiac output or pulmonary vascular resistance. At 10 cm. H20 CPPV cardiac output significantly decreased and pulmonary vascular resistance increased. The physiologic basis for these changes is discussed and related to the clinical situation.
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