Myocardial Perfusion Pressure Research Articles

Vasodilation and mechanism of action of propofol in porcine coronary artery.

A decrease in myocardial perfusion pressure may reduce myocardial blood flow. However, it may not significantly affect myocardial perfusion when in presence of a concurrent coronary artery vasodilation. However, the effects of propofol in coronary arteries are not well determined. In this study, the effects of propofol on porcine coronary artery responses to vasoactive agents that operate through voltage- and receptor-mediated calcium mechanisms were investigated. Hearts of adult pigs (n = 103) were obtained from a slaughter house, and the left anterior descending coronary arteries were dissected. The arteries were cut into vessel rings and prepared with and without the endothelium organ chambers filled with buffered salt solution. The effect of propofol (10(-7), 10(-6), 10(-5), and 10(-4) M) on vascular smooth muscle contraction caused by intracellular Ca(2+)-influx through voltage- and receptor-mediated mechanism also was studied at a cellular level. Propofol relaxed coronary rings that were contracted by KCl, norepinephrine (NE), serotonin (5-HT), or carbachol (CCh). The minimal concentrations of propofol that produced significant vasorelaxation ranged from 3.16 x 10(-7) M to 3.16 x 10(-6) M. Vasodilation was more pronounced in rings contracted by NE, 5-HT, and CCh than by KCl. Propofol (10(-5) M) attenuated coronary vasoconstriction in response to cumulative concentrations of KCl, NE, 5-HT, and acetylcholine. Maximal contractions produced by NE and 5-HT were inhibited to a greater degree than contractions produced by KCl. Propofol at concentrations of 10(-5) M and higher attenuated a contraction in response to CaCl2 in vascular rings depolarized by KCl, but concentrations of 10-M did not attenuate contractions. Vasoconstriction in response to calcium entry in the presence of NE (and nifedipine 10(-6) M) was attenuated by propofol at concentrations of 10(-6) M and higher. Caffeine-induced contraction, caused by intracellular calcium release, was attenuated only at 10(-4) M of propofol. Propofol possesses vasodilator effect and attenuates the effects of vasoconstrictor agents in porcine coronary artery. Further, an antagonism of calcium channels may be responsible for these effects of propofol.

Haemodynamic effects of enalaprilat and preload in acute severe heart failure complicating myocardial infarction.

In this study, the acute haemodynamic effects of angiotensin converting enzyme (ACE) inhibition with intravenous enalaprilat alone or in combination with preload restoration were determined in patients with severe heart failure complicating acute myocardial infarction. Ten patients with raised pulmonary arterial wedge pressure (PAWP > or = 18 mmHg) were first studied during constant conventional vasodilation with diuretic and inotropic medication, by monitoring central haemodynamics and arterial blood gases. The same variables were measured before enalaprilat infusion, after preload reduction with enalaprilat (1 mg.h-1, rate doubled every 30 min until PAWP decreased > or = 25% or up to total cumulative dose of 10 mg) and after preload restoration with fluid loading (4% albumin given 15 ml.min-1 to restore PAWP to baseline) during continuous low dose enalaprilat infusion. Enalaprilat alone (median dose 0.9 mg) reduced significantly the PAWP (from 25 to 17 mmHg; P = 0.004), the mean arterial pressure (from 87 to 83 mmHg; P = 0.008), the mean pulmonary arterial pressure and the right atrial pressure. The cardiac index, stroke volume index and systemic vascular resistance index remained unchanged. Preload restoration during continuous enalaprilat infusion (median dose of 4% albumin 230 ml, and enalaprilat 0.2 mg) did not further enhance left ventricular function; rather, there was a nearly significant decrease in myocardial perfusion pressure. Arterial oxygenation remained unchanged throughout the study. In conclusion, adding intravenous enalaprilat to conventional therapy makes it possible to relieve pulmonary congestion while maintaining the cardiac function and arterial oxygenation. Preload restoration during continuous ACE inhibition offers no further advantages, and may have adverse effects, since the myocardial perfusion pressure may fall.

Left-Ventricular Unloading by Transvalvular Axial Flow Pumping in Experimental Cardiogenic Shock and during Regional Myocardial Ischemia

The efficacy of the transfemoral left-ventricular assist device Hemopump (HP; 21 Fr outer diameter) was examined in experiments with adult sheep in two different models of cardiogenic shock (tachycardia shock; ischemia shock), and during ventricular fibrillation. During tachycardia (high frequency pacing-induced; n = 14), HP assist led to a significant increase in cardiac output (from 2.2 to 2.8 liters/min), mean aortic pressure (from 47.6 to 65.6 mmHg), and myocardial perfusion pressure (from 25.5 to 59.0 mmHg). Simultaneously, a normalization of body oxygen-uptake (from 1.4 to 2.5 ml/min.kg), a decrease in myocardial oxygen consumption (from 6.1 to 4.8 ml/min.100 g), and a normalization of myocardial lactate metabolism were observed during HP assist. During regional myocardial ischemia (PTCA balloon occlusion of the proximal LAD (3.5 min; n = 12), HP assist led to significant decrease in LV end-diastolic pressure (from 21.1 to 12.1 mmHg), and increase in diastolic aortic pressure (from 58 to 67 mmHg) resulting in significant increase in coronary perfusion pressure. In the early reperfusion period, myocardial release of both lactate and potassium was significantly lowered with HP assist. During ventricular fibrillation (induced by electrical stimulation; n = 9), HP flow rates decreased from 2.5 (after 10 min) to 2.1 liters/min (after 30 min). Mean aortic pressures simultaneously decreased from 64.0 to 54.6 mmHg. Perfusion conditions were sufficient for maintenance of aerobic myocardial metabolism, but were borderline for peripheral circulation. Our hemodynamic and metabolic data demonstrate beneficial effects of cardiac assist with the Hemopump 21 Fr in both tachycardia-induced severe cardiogenic shock and during acute regional myocardial ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Need for Active Left-Ventricular Decompression during Percutaneous Cardiopulmonary Support in Cardiac Arrest

During ventricular fibrillation, myocardial hemodynamic and metabolic effects of percutaneous cardiopulmonary support (PCPS) were analyzed in 11 adult sheep (body weight 77-112 kg). During supported fibrillation, an abrupt increase in left-ventricular pressures with alignment to aortic pressures was observed in 2 animals, which was probably due to spontaneous aortic regurgitation, and resulted in deterioration of coronary perfusion. In 9 animals, left-ventricular pressures rose from 22.9 +/- 4.9 to 31.2 +/- 7.9 mm Hg elevating left ventricular wall stress from 16,750 +/- 8,745 to 28,835 +/- 8,892 dyn/cm2 after 10 min of PCPS-supported fibrillation (mean flow rate 4.5 +/- 0.7 liters/min). Simultaneously, myocardial perfusion pressures decreased from an average of 32.4 +/- 11.7 to 22.3 +/- 9.4 mm Hg and myocardial lactate release was observed. Additional transapical LV venting using a 9-Fr catheter led to a decrease in both LV pressure (to 25.7 +/- 5.3 mm Hg) and wall stress (to 20,612 +/- 7,499 dyn/cm2). Left-ventricular decompression decreased myocardial oxygen consumption (from 5.3 +/- 1.4 to 4.8 +/- 0.9 ml/min.100 g), and reduced myocardial lactate release, which indicates myocardial protection. Protective effects were most pronounced using 12-Fr-, and 21-Fr-venting cannulas (with 21 Fr: decrease in myocardial oxygen consumption to 2.7 +/- 0.6 ml/min.100 g, and reversal of myocardial lactate release to lactate uptake during fibrillation). Conclusions. Hemodynamic and metabolic data clearly demonstrate the deleterious effects of PCPS to the unvented left ventricle during cardiac arrest. The results emphasize the need for active left-ventricular decompression during PCPS in ventricular fibrillation.

Optimizing Resuscitation Outcomes with Pharmacologic Therapy

Pharmacologic therapy plays a key role in the emergency resuscitation of patients with cardiac arrest. The Advanced Cardiac Life Support guidelines sanctioned by the American Heart Association provide flexible treatment protocols (algorithms) that serve as a valuable tool for clinicians. Vasoactive (vasopressive) therapy with epinephrine is of primary importance in all patients with nonperfusing rhythms (for example, ventricular fibrillation [VF], pulseless ventricular tachycardia [VT], electromechanical dissociation [EMD], and asystole) because it raises myocardial and cerebral perfusion pressures, thereby increasing the likelihood of successful resuscitation. Antiarrhythmic drugs play a secondary role to electrocardioversion in the treatment of VF and pulseless VT. Despite continued investigation and recent advances in our understanding of the role of drugs and other therapeutic interventions, the short-term and long-term prognoses of patients with cardiac arrest, especially out-of-hospital arrest, remain dismal. Clearly, much study into the prevention and treatment of sudden cardiac death is desperately needed.

Effects of graded doses of epinephrine on both noninvasive and invasive measures of myocardial perfusion and blood flow during cardiopulmonary resuscitation.

Epinephrine administered during cardiopulmonary resuscitation (CPR) is known to increase aortic diastolic and myocardial perfusion pressures, while enhancing myocardial blood flow. Optimal dosing of epinephrine during CPR is less certain. Interest in high-dose epinephrine use under such circumstances is increasing. The effect of different doses of epinephrine on simultaneously measured perfusion pressures, myocardial blood flow, cardiac output, and end-tidal CO2 (PCO2) (used as an indirect measure of cardiac output during CPR) is unknown. Prospective, sequential evaluation of no epinephrine, standard dose epinephrine, and high-dose epinephrine. An experimental resuscitation laboratory. Twelve domestic swine. Myocardial perfusion pressure, myocardial blood flow, cardiac output, and end-tidal PCO2 were studied after various doses of epinephrine were administered during prolonged CPR. After 3 mins of untreated ventricular fibrillation, each animal received 5 mins of CPR without epinephrine, 5 mins of CPR after standard dose epinephrine (0.02 mg/kg), and 5 mins of CPR after high-dose epinephrine (0.2 mg/kg). Cardiac output and regional myocardial blood flow values were measured with nonradioactive, colored microspheres. Myocardial perfusion pressure (aortic diastolic minus right atrial diastolic) was significantly (p < .05) increased over baseline with high-dose epinephrine (35 +/- 8 vs. 14 +/- 4 mm Hg), but not with standard dose epinephrine (20 +/- 5 vs. 14 +/- 4 mm Hg). Epinephrine's effect on myocardial blood flow was similar, increasing after the high dose (71 +/- 21 vs. 20 +/- 5 mL/min/100 g; p > .05), but not with the standard dose (23 +/- 6 vs. 20 +/- 5 mL/min/100 g). Cardiac output decreased significantly (p < .05) after high-dose epinephrine (7 +/- 1 vs. 13 +/- 1 mL/min/kg). Mean end-tidal PCO2 levels were lower after high-dose epinephrine (15 +/- 2 vs. 20 +/- 2 mm Hg; p < .05) but not after standard dose epinephrine (19 +/- 2 vs. 20 +/- 2 mm Hg). Standard dose epinephrine had minimal effect on myocardial perfusion pressure, myocardial blood flow, cardiac output, or end-tidal PCO2. High-dose epinephrine enhanced myocardial perfusion pressure and myocardial blood flow despite significantly decreasing cardiac output.

Protective effects of the Hemopump left ventricular assist device in experimental cardiogenic shock.

The efficacy of the new cable-driven rotating left ventricular assist device Hemopump in cardiogenic shock was examined in experiments with adult sheep (n = 14; body weight 50-71 kg). Shock was induced by high frequency ventricular pacing. Aortic, pulmonary, central venous and left ventricular pressures as well as electromagnetic measurements of coronary blood flow were recorded continuously; cardiac output was measured by thermodilution technique. Blood samples for determination of oxygen content, electrolytes and lactate were taken under control conditions, in shock, and during pump intervention at different levels of pump speed. Vascular resistance, total body and myocardial oxygen consumption as well as myocardial uptake and release of lactate were calculated. High frequency pacing led to a significant decrease in cardiac output (from 3.8 +/- 0.8 to 2.2 +/- 1.6 l/min), mean aortic pressure (89.1 +/- 14.4 to 47.6 +/- 7.2 mmHg), and total body oxygen consumption (2.6 +/- 0.3 to 1.4 +/- 0.7 ml/min per kg), as well as myocardial release of lactate (arterial coronary-venous difference of lactate: 0.27 +/- 0.26 to -0.32 +/- 0.72 mmol/l). Hemopump assist in this condition resulted in a significant increase in cardiac output (to 2.8 +/- 0.6 l/min), mean aortic pressure (to 65.6 +/- 13.9 mmHg), and myocardial perfusion pressure (from 25.5 +/- 11.0 to 59.0 +/- 14.7), and led to nearly normal total body oxygen consumption (2.5 +/- 0.7 ml/min per kg), a decrease in myocardial oxygen consumption (from 6.1 +/- 2.1 in shock, to 4.8 +/- 1.7 ml/min per 100 g), and to normal arterial coronary-venous difference of lactate (0.24 +/- 0.26 mmol/l).(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of bicarbonate on resuscitation from cardiac arrest

This study attempted to determine the effect of bicarbonate administration on resuscitation in a porcine model of prolonged cardiac arrest. After instrumentation, 26 swine were subjected to ventricular fibrillation for 15 minutes (16 animals) or 20 minutes (ten animals) with no resuscitative efforts. Resuscitation attempts with open-chest cardiac massage and epinephrine were used in all animals after the arrest period. The experimental group was given sodium bicarbonate (3 mEq/kg), and the control group received 3% saline (5 mL/kg) at the initiation of cardiac massage. Resuscitation success, hemodynamics, and arterial and mixed venous gases were compared in the bicarbonate and hypertonic saline-treated groups. There was no difference in resuscitation rates between bicarbonate and nonbicarbonate-treated swine. After 15 minutes of ventricular fibrillation, six of eight bicarbonate-treated swine were resuscitated successfully compared with five of eight hypertonic saline-treated animals. None of the five bicarbonate-treated or five hypertonic saline-treated swine that underwent 20 minutes of ventricular fibrillation were resuscitated. The arterial and mixed venous pH values were significantly different in the bicarbonate-treated animals from values in the control group. There was no difference in systolic or diastolic blood pressures or myocardial perfusion pressure between the bicarbonate and hypertonic saline-treated animals. Despite correlation of arterial and venous acidemia, the use of sodium bicarbonate did not improve resuscitation from prolonged cardiac arrest.

Echocardiographic assessment of mitral valve function during mechanical cardiopulmonary resuscitation in pigs

Using two-dimensional and M-mode echocardiography, mitral valve function was assessed during mechanical cardiopulmonary resuscitation (CPR). In 10 anesthetized pigs CPR began 1 min after induction of ventricular fibrillation; in all pigs three different compressive forces (200, 350, and 500 Newton [N]) were applied in randomized sequence for 3 min each, thus resulting in a reduction of anterior-posterior chest diameter by 15%, 20%, and 25%, respectively. Echocardiographic recordings of adequate technical quality were obtained from seven animals. During ventricular fibrillation, mitral valve leaflets showed fibrillatory movements without closure. During CPR systole with a compressive force of 200 N, the mitral valve closed in 114 of 700 CPR cycles (16%). This rate increased significantly (P less than 0.001) to 399 of 584 cycles (68%) with 350 N, and further to 470 of 494 cycles (95%) with 500 N. The higher mitral valve closure incidence was linked to statistically significant increases in systolic cerebral (+125%) and diastolic myocardial perfusion pressures (+136%) and cardiac output. We thus conclude that with low compressive force blood flow during mechanical CPR is due mainly to the chest pump mechanism, whereas the cardiac pump mechanism is effective with high compressive forces.

Production and Biologic Interactions of Prostacyclin and Platelet-Activating Factor in Acute Myocardial Ischemia in the Perfused Rabbit Heart

This study showed that the 1-O-hexadecyl form of platelet-activating factor (PAF) is released along with 6-keto-prostacyclin1 alpha (6-keto-PGF1 alpha) in the perfusates of ischemic-isolated rabbit heart. During the early phase of the reperfusion, the release of PAF and 6-keto-PGF1 alpha was particularly increased (PAF, from 5.4 +/- 1.2 to 19.7 +/- 2.0 ng/min; 6-keto-PGF1 alpha, from 2.3 +/- 0.1 to 27.4 +/- 1.8 ng/min) and this event was coupled with the characteristic mechanical alterations of myocardial performance and perfusion pressure (PP). These changes were effectively antagonized by pretreatment of the hearts with both prostacyclin (PGI2, 20 ng/ml) and the PGI2-releaser defibrotide (400 micrograms/ml). The protecting activity observed with PGI2 was paralleled by a reduction in the rate of PAF release during reperfusion (from 19.7 +/- 2.0 to 6.8 +/- 0.2 ng/min). In defibrotide-treated preparations, inhibition of PAF formation was associated with a pronounced stimulation of 6-keto-PGF1 alpha generation, which was particularly marked on reperfusion (from 27.4 +/- 1.8 to 197.5 +/- 8.2 ng/min). Indomethacin (1 microgram/ml) ablated the antiischemic effect of defibrotide but did not potentiate the rate of formation of PAF despite inhibition of 6-keto-PGF1 alpha biosynthesis. From these results, we conclude that in a model of severe myocardial ischemia, in which the major determinants of cardiac performance are under control, generation of PAF and PGI2 appears to play an important biologic role in determination of the severity of myocardial ischemic damage.

Cardiac and Hemodynamic Effects of Diltiazem During Exercise-Induced Myocardial Dysfunction in Dogs

The effects of diltiazem were tested in chronically instrumented dogs in a model of exercise-induced myocardial dysfunction. Since various bradycardiac agents have beneficial effects on myocardial function during ischemia, it was of interest to find out how a decrease in afterload, possibly combined with a decrease in myocardial oxygen demand, influences dysfunction. Therefore, diltiazem (1 mg/kg i.v.) was tested during critical stenosis of the circumflex branch of the left coronary artery, which led to exercise-induced myocardial dysfunction. At rest, diltiazem causes a reflex increase in heart rate. During exercise, a decrease in heart rate and hence in myocardial oxygen demand was neutralized by a decrease in arterial blood pressure and hence a lowered myocardial perfusion pressure. Therefore, systolic shortening in the ischemic area improved neither at rest nor during exercise after diltiazem.

Echocardiographic Assessment of Mitral Valve Function During Mechanical Cardiopulmonary Resuscitation in Pigs

Using two-dimensional and M-mode echocardiography, mitral valve function was assessed during mechanical cardiopulmonary resuscitation (CPR). In 10 anesthetized pigs CPR began 1 min after induction of ventricular fibrillation; in all pigs three different compressive forces (200, 350, and 500 Newton [N]) were applied in randomized sequence for 3 min each, thus resulting in a reduction of anterior-posterior chest diameter by 15%, 20%, and 25%, respectively. Echocardiographic recordings of adequate technical quality were obtained from seven animals. During ventricular fibrillation, mitral valve leaflets showed fibrillatory movements without closure. During CPR systole with a compressive force of 200 N, the mitral valve closed in 114 of 700 CPR cycles (16%). This rate increased significantly (P less than 0.001) to 399 of 584 cycles (68%) with 350 N, and further to 470 of 494 cycles (95%) with 500 N. The higher mitral valve closure incidence was linked to statistically significant increases in systolic cerebral (+125%) and diastolic myocardial perfusion pressures (+136%) and cardiac output. We thus conclude that with low compressive force blood flow during mechanical CPR is due mainly to the chest pump mechanism, whereas the cardiac pump mechanism is effective with high compressive forces.

Myocardial contractility, blood flow, and oxygen consumption in healthy dogs during anesthesia with isoflurane or enflurane

Left ventricular contractility (V max), myocardial blood flow (MBF), and oxygen consumption (O 2C) were determined together with systemic hemodynamic parameters in a total of 21 mongrel dogs. Baseline recordings were obtained under basal anesthetic conditions with a narcotic (piritramid, IV). In the control group (n = 7), recordings were obtained during a three-hour observation period with infusion of piritramid. In experimental groups measurements were repeated with equi-anesthetic concentrations of isoflurane (0.7 and 1.4 vol%; n = 8) and enflurane (1.1 and 2.2 vol%; n = 6). Dose-dependent reductions of arterial pressure, cardiac output (CO) and peripheral vascular resistance were observed with isoflurane and enflurane. CO at the higher anesthetic level was depressed significantly more with enflurane. This difference was obviously due to a more severe depression of myocardial contractility with enflurane; V max was decreased by 18% and 26% with enflurane, but only by 10% and 17% with isoflurane ( P < 0.01). MBF and the fraction of CO received by the heart were increased above their baseline values with both concentrations of isoflurane. In contrast, the fraction of CO remained constant with enflurane while MBF decreased. O 2C was reduced due to decreases of afterload and left ventricular contractility. The reduction was greater with enflurane than with isoflurane. All parameters remained unchanged in the control group. The results of this study indicate that the most striking difference in the actions of isoflurane and enflurane on cardiac parameters is on myocardial vascular resistance; MBF is increased with isoflurane, but is decreased with enflurane although myocardial perfusion pressure is reduced by almost identical amounts. The stronger depression of systemic hemodynamic parameters with enflurane is due to its more pronounced negative inotropic effects.

Blood pressure, cigarette smoking and heart attack in the WHO co-operative trial of clofibrate.

In the WHO sponsored trial of clofibrate and its follow-up, about 15,000 men were observed for a mean period of 13.2 years. As expected, incidence of heart attacks (HA) was directly related to serum cholesterol, blood pressure (BP) and cigarette smoking. The previously reported lower incidence of HA in men receiving clofibrate compared with controls was most noticeable in hypertensive heavy smokers (P less than 0.01). BP was slightly lower in smokers than non-smokers (P less than 0.01). The difference in BP was greater in the trial visit before HA. Smokers also had higher plasma fibrinogen levels (P less than 0.05). The combination of reduced diastolic BP, and therefore myocardial perfusion pressure, with an increased thrombogenic tendency, might explain the high incidence of HA in smokers. Clofibrate apparently reduced fibrinogen levels, which might account for its specially good effect in preventing HA in smokers. However, the ill effects of smoking are still evident at a lower level in the men taking clofibrate and the drug is no substitute for giving up the habit. Clofibrate is not recommended for widespread use, except in subjects with marked lipid and/or blood fibrinogen abnormalities after dietary measures have been tried.

Myocardial perfusion pressure: a predictor of 24-hour survival during prolonged cardiac arrest in dogs.

Myocardial perfusion pressure, defined as the aortic diastolic pressure minus the right atrial diastolic pressure, correlates with coronary blood flow during cardiopulmonary resuscitation (CPR) and predicts initial resuscitation success. Whether this hemodynamic parameter can predict 24-h survival is not known. We examined the relationship between myocardial perfusion pressure and 24-h survival in 60 dogs that underwent prolonged (20 min) ventricular fibrillation and CPR. Forty-two (70%) animals were initially resuscitated and 20 (33%) survived for 24 h. Myocardial perfusion pressure was significantly greater when measured at 5, 10, 15 and 20 min of ventricular fibrillation in the resuscitated animals than in the non-resuscitated animals (P less than 0.01). Likewise, the myocardial perfusion pressure was also greater in the animals that survived 24 h than in animals that were resuscitated, but died before 24 h (P less than 0.02). Myocardial perfusion pressure measured after 10 min of CPR was 11 +/- 2 mmHg in animals never resuscitated, 20 +/- 3 mmHg in those resuscitated that died before 24 h and 29 +/- 2 mmHg in those that survived 24 h (P less than 0.05). A myocardial perfusion pressure at 10 min of CPR of 20 mmHg or less is an excellent predictor of poor survival (negative predictive value = 96%). Myocardial perfusion pressure is a useful index of CPR effectiveness and therefore may be a useful guide in helping to optimize resuscitation efforts.

Beta 2-mediated changes in central haemodynamics, coronary circulation and myocardial metabolism in canine.

The combined effect of terbutaline on systemic and coronary circulation was investigated in dogs to clarify its influence on myocardial oxygen supply and lactate balance. The dogs were anaesthetized and the chest opened. Coronary sinus blood flow and cardiac output were monitored by thermodilution, aortic pressure was measured by tip-transducer and heart rate by RR-interval on ECG, coronary sinus blood were analyzed for lactate, oxygen and carbon dioxide. Terbutaline caused a substantial systemic vasodilation and an increased heart rate, the total external cardiac work increased to a minor degree. Terbutaline increased arterial lactate concentration. Coronary vascular resistance was reduced after terbutaline. Even if myocardial perfusion pressure was reduced and an increased external cardiac work was present, no signs of myocardial distress was observed in lactate metabolism or coronary sinus oxygen content. In fact a tendency to increased myocardial aerobic metabolism was observed, as myocardial lactate consumption increased after terbutaline. Terbutaline seems to be a coronary vasodilator in dogs. However, the demand for oxygen secondary to both an increase in cardiac work and aerobic metabolism can be hazardous to the potentially ischaemic myocardium.

Role of Coronary Collateral Vessels During Transient Coronary Occlusion During Angioplasty Assessed by Hemodynamic, Electrocardiographic and Metabolic Changes

The clinical role of collateral vessels was evaluated during transient coronary occlusion by percutaneous transluminal coronary angioplasty in 22 patients with (8) and without (14) collateral vessels. Coronary occlusion pressure, the ratio of mean coronary occlusion pressure to mean aortic pressure and myocardial perfusion pressure at 40 s of balloon inflation were significantly higher in patients with than in patients without collateral vessels. The changes in left ventricular systolic and end-diastolic pressure, maximal rate of rise of left ventricular pressure (peak dP/dt) and maximal rate of fall of left ventricular pressure (negative peak dP/dt) during balloon inflation were less in patients with than in patients without collateral vessels. Myocardial lactate was produced in patients without collateral vessels but not in those with such vessels. Marked ST segment elevation in the electrocardiogram occurred in patients without collateral vessels but either ST segment depression or mild ST segment elevation was observed in patients with collateral vessels. This study indicates that collateral vessels limit myocardial ischemia during coronary occlusion, probably as a result of increased myocardial perfusion pressure.

Selective perfusion of ischemic myocardium during coronary venous retroinjection: A study of the causative role of venoarterial and venoventricular pressure gradients

Coronary venous retroinjection is often associated with preferential distribution of flow to ischemic myocardium. The purpose of this study was to define the mechanism of such retrodistribution of flow. In 24 anesthetized open chest dogs, Monastral blue dye (10 ml) was injected by way of a balloon catheter in the distal great cardiac vein as a marker for retrograde flow distribution. The injection rate (0.6 to 2.4 ml/s) was adjusted such that systolic pressure in the anterior interventricular vein ranged between 60 and 85 mm Hg. In 11 dogs with no ischemia and normal myocardial perfusion pressure (96 +/- 8 mm Hg), no myocardial staining occurred despite retrograde filling of epicardial veins. One minute after occlusion of the left anterior descending coronary artery, dye injections caused selective staining of the cyanotic area in 15 of 18 episodes, sparing the normal myocardium within the zone of retroperfused veins. In five dogs, with the arterial pressure less than 55 mm Hg, retroinjection resulted in homogeneous staining of all the myocardium drained by the retroperfused veins. Selective staining of the ischemic myocardium caused by retroinjection was associated with the following pressure gradients: during systole from the anterior interventricular vein to the occluded coronary artery, 31 to 58 mm Hg, and during diastole from the retroperfused veins to the left ventricular chamber, 9 to 28 mm Hg. There was no diastolic venoarterial gradient in the ischemic myocardium. In normal myocardium, retroinjection did not reverse the arteriovenous pressure gradient. In conclusion, retrograde flow is primarily directed to myocardium with low anterograde perfusion pressure. Selective retrograde penetration of acutely ischemic myocardium can thus be achieved by a mechanism consistent with the development of venoarterial and venoventricular pressure gradients.

SIMULTANEOUS CHEST COMPRESSION AND VENTILATION DOES NOT ENHANCE CEREBRAL AND MYOCARDIAL PERFUSION IN AN INFANT MODEL OF CARDIOPULMONARY RESUSCITATION

We evaluated whether simultaneous compression ventilation CPR (SCV-CPR) with high airway pressure improved cerebral (CBF) and myocardial (MBF) blood flow compared to conventional CPR (CON-CPR) in an infant model of CPR. CPR was performed on pentobarbital anesthetized piglets (3.5 - 6 kg) with epinephrine infusion. CON-CPR was performed (n=8), at 100 compressions/min, 60% duty cycle, and a 1:5 breath to compression ratio and 25 mmHg peak airway pressure. SCV-CPR was performed (n=8) at 60 compressions/min, duty cycle 60%, with 60 mmHg peak airway pressure. Sternal displacement was 20% in each group. There was no significant difference between CPR groups as regards systolic, mean, diastolic aortic and right atrial pressures, intracranial, cerebral perfusion (CPP), or myocardial perfusion (MPP) pressures, CBF and MBF, (microspheres). There was a progressive decrease in aortic, CPP and MPP in both groups with time. CBF (ml.min−1 .100 gm−1) decreased from 15±3 at 5 min to 5±1 at 50 min of (CON-CPR) and from 13±2 to 5±2 of SCV-CPR. MBF decreased from 38+7 at 5 rain to 1±1 at 50 min and from 40±7 to 9±4 of SCV-CPR. This study demonstrates that SCV-CPR with peak airway pressures of 60 mmHg neither improves the perfusion pressure over those generated by CON-CPR nor prevents the decrease of CBF and MBF with prolonged CPR in this infant model. Supported by NS20020.

Comparison of epinephrine and phenylephrine for resuscitation and neurologic outcome of cardiac arrest in dogs

A study was done comparing resuscitability and 24-hour neurologic outcome in fibrillating dogs that were treated with either phenylephrine (a primary alpha agonist) or epinephrine. Ventricular fibrillation was induced electrically in 18 dogs. After three minutes, standard CPR was instituted using a mechanical resuscitator. Dogs were given phenylephrine or epinephrine at nine minutes and defibrillation was attempted at 12 minutes. Dogs underwent hemodynamic monitoring and pharmacologic support, if necessary, for an additional 90 minutes. At four, eight, 12, and 24 hours, a standard neurologic examination was performed and deficit scores were assigned by an observer blinded to the drug given. Fourteen of the 18 dogs were resuscitated. There were no statistically significant differences in the epinephrine- or phenylephrine-treated groups with regard to number of animals resuscitated, time and interventions required for resuscitation, initial cardiac rhythm post resuscitation, or occurrence of ventricular fibrillation during resuscitation. No differences were found in arterial, central venous, or myocardial perfusion pressures during CPR. Phenylephrine-treated dogs tended to have higher mean pressures in the critical care period (15 to 30 minutes), although this was not significant. Total neurologic deficit scores were 127.8 +/- 83.8 for the phenylephrine-treated group and 129.4 +/- 87.4 for the epinephrine group. No significant differences were found in the level of consciousness, cranial nerve function, motor skills, or general behavior scores. We conclude that there is no difference in neurologic or cardiovascular outcome when phenylephrine is compared to epinephrine in a canine model of cardiac arrest and cardiopulmonary resuscitation.