Making best use of every healthcare provider's knowledge and skills.

In "Organizing Primary Care for an Integrated System" Rosser and Kasperski propose changing the way family physicians practice to address deficiencies in the current primary-care delivery system in Canada. These deficiencies include a growing shortage of physicians, particularly in rural areas of Canada; the growing dependence of Canadians on acute hospital emergency units or "walk- in clinics" for primary care; fragmentation and unnecessary duplication in the delivery of primary-care services; lack of understanding on the part of the community and hospital sectors of the role of the family-practice physician; a fee-for-service funding model that does not reward prevention and health-promotion initiatives by physicians and makes high-problem visits the most lucrative; and lack of clarity with regard to what the public should expect from their physicians.

Comox Valley Nursing Centre: from collaboration to empowerment.

The Comox Valley Nursing Centre was initiated as a two year demonstration project by the Registered Nurses Association of British Columbia (RNABC) and funded by the Ministry of Health. The purpose of the project was to demonstrate innovative nursing practice in a primary health care context. Findings from the project were expected to inform provincial health care planning, nursing scope of practice, and health and nursing policy development. A free standing nursing center was planned and implemented through a collaborative effort by RNABC, nurses and community residents. An external team of researchers evaluated the project using a variety of methods, including participatory action research. During the project an innovative nursing practice, based on principles of collaboration, developed and has continued during the extended provincial and regional funding of the Centre. Drawing from the evaluation findings, case studies and using Henneman, Lee and Cohen's (1995) concept analysis of collaboration, this paper describes how the principles of collaboration were actualized or suppressed. The paper examines how collaboration impacted empowerment for nurses, clients and the community. Lessons learned about the reciprocal relationships between collaboration and empowerment, implications for nursing practice, and how the approach can contribute to a better understanding of the impact of collaborative practice approaches on health care delivery are discussed.

Primary health care in action.

In a 40-page report on the Comox Valley Nursing Centre Demonstration Project RNABC says the project showed what nurses can do when they are allowed to practice the full scope of their profession. Overall, the project was a success in making a contribution to understanding the principles of primary health care and community-based nursing practice.

When is it appropriate to intervene?

I work in a long-term setting where the residents all have written levels of intervention. Last week I came across a resident who was choking on a piece of food and unable to breathe. Even though I knew he had a DNR order as a component of his written level of intervention, I initiated action to rescue him. In thinking about this afterward, and discussing it with colleagues, we began to question whether I should have done this since it could be said that I was acting against his wishes. What is your opinion on this?

Intravenous magnesium sulphate and reperfused myocardium: preservation of function and reduction of infarct size.

The aim of the study was to examine the effects of intravenous magnesium sulphate (MS) administration on myocardial contractile function and infarct size after occlusion of the left circumflex artery of the heart for 60 minutes. Under sodium pentobarbital anaesthesia (30 mg/kg. intravenously) the hearts of mongrel dogs (n = 13) were instrumented to measure left ventricular pressure (LVP), regional contractile function of the territories perfused by the left circumflex and anterior descending coronary arteries (%SS), mean arterial pressure (MAP), and coronary blood flow velocity (CFV). Immediately upon release of the coronary occlusion, either intravenous magnesium sulphate (100 mg/kg) or a dextrose vehicle (D5W) was infused. Animals were killed, their hearts excised and cut in 1 cm slices from apex to base and incubated in triphenyl tetrazolium chloride (TTC) for 20 minutes to measure infarcted areas. In the control group (n = 7), myocardial contractile function was severely depressed during the occlusion and displayed the same pattern of dysfunction during 3 h of reperfusion. The %SS of the area perfused by the circumflex artery at the end of the reperfusion period was 0.02 +/- 3 (mean + SEM) P < 0.05 vs MS; P < 0.05 vs pre-occlusion) and percentage of necrosis of the area at risk was 17.42 +/- 6 (P < 0.05 vs MS). In the magnesium sulphate group (n = 6), %SS was depressed during the occlusion as in the control group, but was preserved during reperfusion time, 9.8 +/- 1.0 (P < 0.05 vs D5W; P < 0.05 vs pre-occlusion) and showed significantly less percentage of necrotic tissue, 4.53 +/- 1 (P < 0.05 vs D5W). These results suggest that intravenous magnesium sulphate preserves myocardial contractile function and reduces infarct size significantly following a period of complete coronary occlusion.

N-acetylcysteine diminishes injury induced by balloon angioplasty of the carotid artery in rabbits.

The effect of N-acetylcysteine (NAC) on preventing or ameliorating the injury associated with percutaneous transluminal angioplasty was investigated in rabbits. Carotid artery angioplasty (CA) was performed on 8 control (vehicle-treated) rabbits and 7 rabbits treated with NAC, 250 mg/kg, administered orally in Nutrical paste for 10 days prior to and 10 days following CA. Single blind histologic evaluation of the angioplasty sites demonstrated a significant reduction in the incidence in vessel: 1) inflammation; 2) endothelial damage; 3) thrombus formation; 4) elastic lamina damage in the NAC rabbits. The percentage of control versus NAC treated animals exhibiting damage in each category were: inflammation: 75% vs 14%; endothelial damage: 88% vs 57%; thrombus formation: 88% vs 43%; laminal damage: 63% vs 14%. The results suggest that NAC treatment may be a valuable therapeutic agent in effectively preventing or reducing angioplasty-induced vessel damage.

Parenteral magnesium sulphate restores regional contractile function in the post-ischaemic canine myocardium.

The effects of parenteral magnesium sulphate (MS) on the regional contractile response of stunned myocardium was examined in 45 pentobarbital anaesthetized dogs. The hearts were instrumented to measure left ventricular pressure (LVP), coronary flow velocity (CFV), mean arterial blood pressure (MAP), and regional contractile function (percent segment shortening, %S; and end-diastolic segment length, EDL). Stunning was produced by a 10 min occlusion of the first descending branch of the left circumflex coronary artery. Immediately upon release of the occlusion, either magnesium sulphate or a dextrose vehicle (D5W, n = 15) was infused. Magnesium sulphate was given intravenously (IV-MS, 100 mg/kg, n = 15) or intracoronarily (IC-MS, 1.5 mg/kg, n = 15). Coronary occlusion was consistently associated with significant decreases in coronary flow velocity and %S in all groups. Following IV-MS, heart rate (HR) and mean arterial blood pressure decreased significantly from preocclusion values, whereas end-diastolic segment length tended to increase and left ventricular pressure remained constant. IC-MS did not produce any changes in heart rate, mean arterial blood pressure, end- diastolic segment length or left ventricular pressure. At the end of the magnesium sulphate infusion (IV or IC), and for the next 60 min, %S returned to or above pre-occlusion values (P < 0.05 vs. D5W). Dyskinesia and hypokinesia were abolished in the magnesium sulphate groups, but were still present in the D5W group at the end of the 60 min period (P < 0.05 vs. pre-occlusion). We conclude that parenteral magnesium sulphate significantly improves regional contractile function in the stunned myocardium. Data from the IC-MS group would suggest a direct myocardial effect, independent of changes in preload, afterload, heart rate or flow.

On the use of parenteral magnesium salts in the treatment of acute ischaemic heart disease: a brief review.

With the advent of pharmacological, mechanical and surgical revascularization as firstline therapies in acute coronary artery disease syndromes, the search for adjunctive pharmacotherapy against reocclusion and reperfusion injury has intensified. In addition, safe pharmacotherapeutic intervention conferring survival advantage is required for those at high risk ineligible for recanalization or beta blockade. Of major importance, in this vein, is the intriguing association between parenteral magnesium and the amelioration of myocardial ischaemia and the eradication of lethal ischaemic ventricular arrhythmias reasserted in both animal and human studies. In addition, in more recent years, parenteral magnesium has been linked to the amelioration of reperfusion injury in animal experiments. In this paper we shall review the literature with respect to myocardial ischaemia, its pathophysiology and treatments. In doing so, we shall present data that strongly supports the logistic use of parenteral magnesium compounds as essential therapy in the treatment of acute ischaemic heart disease associated with necrosis, and a potential role in ablating reperfusion injury.

Pressure-flow characteristics of intramural and total coronary collateral networks.

The purpose of the present investigation was to determine the pressure-flow (PF) relationship of intramural collaterals and to determine whether their characteristics differ significantly from those of the total collateral network, defined as the epicardial plus intramural collateral network. Because a significant portion of the collateral flow is diverted away from the retrograde flow measurement, we embolized the coronary vessel on which the retrograde flow was measured with spheres of various sizes until the retrograde flow was maximized and retrograde flow diversion blocked. The PF relationship was obtained before and after the epicardial collaterals were cauterized to determine the characteristics of the total and intramural collateral network. PF data for the collateral circulations were obtained by changing the inflow pressure to all coronary vessels simultaneously and by measuring the retrograde flow while maintaining the retrograde outflow pressure at 0 mmHg. The PF characteristics of the total and intramural collateral circulations could be fitted by either a second-degree polynomial or linear equation. In both cases the pressure intercept crossed the origin of the axes. The average contribution of intramural collaterals to total retrograde flow was 58 +/- 5%. We conclude that the PF characteristics of intramural collaterals parallel those of the total collateral circulation.

Hemodynamics of heartworm infection.

To determine the hemodynamic responsiveness of dogs testing positive for heartworms (direct blood smear), we compared the response of control and heartworm-infected animals to stellate stimulation (SS). Using the anesthetized, open-chest model, twenty dogs (10 control and 10 heartworm-positive) were instrumented to measure left ventricular pressure (LVP), arterial pressure (AP), and coronary flow velocity (CFV) of the left circumflex coronary artery. CFV was converted to flow per gram tissue (CBFG) by weighing the perfusion area of the circumflex artery. The average wet weight of the worm mass infecting the dogs was 1.0 +/- 0.1 g, which represented an average of 5% of the right ventricular free wall weight. Overall heart size and right ventricular weights were greater in the heartworm-positive animals, as well as heart weight to body weight ratios. Prior to SS, LVP was the same for both groups. However, dP/dt and CBFG were 21% and 19% lower, respectively, in the heartworm-positive animals. Stellate stimulation sufficient to produce a 30-mmHg rise in AP led to 25%, 13%, and 40% increases in LVP, dP/dt, and CBFG, respectively, in the control animals. Increases of 22%, 10%, and 52% in the same parameters were observed in the heartworm-positive animals. Although control dP/dt and CBFG in the heartworm-positive animals were lower than in the heartworm-negative animals, heartworm infection at this level did not hinder myocardial responsiveness to SS.

Effects of a coronary alpha 1-constriction on transmural left ventricular flow and contractile function.

Modulation of myocardial contractile function and perfusion by alpha 1-adrenergic receptors were examined in anesthetized dogs during left stellate ganglion stimulation. In 11 dogs, stellate stimulation significantly increased heart rate, mean arterial pressure, left ventricular systolic pressure, maximal rate of left ventricular pressure generation, segmental shortening and rate of shortening in anterior and posterior ventricular regions, and myocardial oxygen extraction. Myocardial lactate extraction decreased. The selective alpha 1-adrenergic antagonist prazosin (0.5 mg) injected into the circumflex artery during stellate stimulation caused significant additional increases in maximal rate of left ventricular pressure generation by 19 +/- 5% and in rate of shortening in posterior subendocardium by 20 +/- 6%. No changes were observed in posterior subepicardial or anterior subendocardial segmental contractile function. Myocardial oxygen and lactate extractions returned to their control values following prazosin injection. Regional left ventricular perfusion was measured using tracer microspheres in five additional dogs. Stellate stimulation increased subepicardial and subendocardial perfusion by 30%. Prazosin increased both subepicardial and subendocardial perfusion by an additional 36%. Stellate stimulation increased norepinephrine concentration in the coronary sinus, but no further increase was noted after blockage of alpha 1-receptors by prazosin. Thus, during sympathetic stimulation, an alpha 1-vasoconstriction existed uniformly across the left ventricular wall. However, blockade of this vasoconstriction was associated with an increase in contractile function only in the deeper muscle layers.

Endurance training alters arterial baroreflex function in dogs.

The present study was designed to determine whether 12 wk of daily exercise alter autonomic neural control of the heart during baroreflex stimulation in healthy dogs. We studied 16 untrained and 12 endurance-trained anesthetized dogs which were instrumented to measure arterial blood pressure (AP), carotid sinus baroreceptor pressure (CBP), electrocardiogram (ECG), heart rate (HR), and R-R interval (RR). The arterial baroreflex was studied during hypertension caused by i.v. bolus infusion of phenylephrine, hypotension caused by i.v. bolus infusion of nitroprusside, and bilateral carotid occlusion (BCO) in which carotid sinus pressure was reduced to 41 +/- 2 mm Hg (mean +/- SEM). Arterial baroreflex sensitivity, which was assessed by determining the change in heart interval (i.e., change in RR) per unit change in systolic AP (delta RR/delta AP), was significantly lower during the hypertensive challenge in the trained dogs compared to the untrained dogs (2.2 +/- 0.3 vs 6.8 +/- 1.5 ms.mm Hg-1, respectively). Similarly, the delta RR/delta AP was substantially lower during the hypotensive challenge in trained dogs vs the untrained dogs (1.2 +/- 0.3 vs 1.8 +/- 0.4 ms.mm Hg-1, respectively). In addition, the HR response to the BCO was significantly less in trained dogs (22 +/- 2 bpm) vs untrained dogs (32 +/- 5 bpm). The open-loop gain (Go), which was used to quantitate the effectiveness of the carotid baroreflex to increase mean systemic AP during BCO, was similar in both untrained and trained dogs (2.9 +/- 0.6 and 2.4 +/- 0.5, respectively). These data indicate that, while endurance training significantly reduces the HR component of the arterial baroreflex, the arterial pressure response apparently is not altered.

Microvascular occlusions promote coronary collateral growth.

The objective of this study was to examine whether myocardial ischemia without alterations in pressure gradients between large epicardial coronary arteries was a sufficient stimulus to produce coronary collateral growth and development. To accomplish this aim, we partially embolized the circumflex coronary perfusion territory with 25-microns diameter microspheres to produce multiple microvascular occlusions, sufficient to abolish or greatly attenuate coronary vasodilator reserve. The embolization procedure was performed in two groups of dogs during aseptic surgery. After the dogs recovered for 1-3 wk (short-term embolization) or 6-8 wk (long-term embolization), indexes of vascular growth were compared with a group of control animals in which all operative procedures were performed, except embolization. Retrograde blood flow, an index of collateral blood flow and coronary vascular resistance, was determined in an isolated beating empty heart preparation during coronary vasodilation with adenosine. Circumflex retrograde blood flow from the left anterior descending artery was increased from 0.09 ml.min-1.g-1 (sham) to 0.21 and 0.17 ml.min-1.g-1 in the short-term and long-term groups, respectively (P less than 0.05). Collateral blood flow from the septal artery was also increased from 0.03 ml.min-1.g-1 (sham) to 0.08 ml.min-1.g-1 (P less than 0.05) in the short-term group. Collateral contribution from the right coronary artery was not significantly altered in either group of embolization animals. The contributions of epicardial and intramyocardial collaterals to the total retrograde flow were also determined and were found to be different among the three experimental groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Intramural coronary collateral flow in dogs.

The objective of this study was to determine whether intramural collaterals contribute significantly to total retrograde flow (index of collateral flow). The left circumflex, left anterior descending, right, and septal coronary arteries were separately cannulated, and blood flows through these vessels were monitored on an isolated, blood-perfused beating heart preparation. Epicardial collaterals between the borders of the circumflex and right coronary perfusion territories were cauterized, and retrograde flow from the circumflex coronary artery was determined before and after cauterization. This procedure unmasked the intramural collateral flow component to retrograde flow. By occluding and unoccluding the coronary flows from the right, septal, and left anterior descending coronary arteries during these measurements, we were able to determine their contribution to epicardial and intramural collateral flow. We found that, after cauterization, an average of 58 +/- 3.6% of the total retrograde flow remained. The septal and left anterior descending coronary arteries contributed almost equally to this retrograde flow. We concluded that, because the epicardial collaterals were cauterized, the source of retrograde flow was from intramural collaterals and constituted about one-half of the measured retrograde flow in dogs with a native collateral circulation.