Increase In Myocardial Oxygen Consumption Research Articles

Contribution of local metabolic control to coronary pressure-flow autoregulation

The coronary circulation has an innate ability to maintain constant blood flow over a wide range of perfusion pressures. This study interrogated the local metabolic hypothesis, which proposes that myocardial oxygen tension, indexed by coronary venous PO 2 (CvPO 2 ), determines the degree of coronary pressure-flow autoregulation by increasing the production of vasodilator metabolites as coronary perfusion pressure (CPP) is reduced. We tested this hypothesis by examining the extent to which dobutamine-induced increases in myocardial oxygen consumption (MVO 2 ) under both normoxic and hypoxemic conditions, influences coronary autoregulatory capability. Experiments were performed on open-chest anesthetized swine during 20 mmHg stepwise changes in coronary perfusion pressure (CPP) from 140 to 40 mmHg, via servo-controlled roller pump. Measurements were made in 3 conditions: a) normoxia (n = 7); b) normoxia with dobutamine (10 μg/kg/min, iv; n = 7); and c) hypoxemia (PaO 2 36-38 mmHg) plus dobutamine (n = 5). Under control-normoxic conditions, CvPO 2 decreased from 38 ± 2 to 22 ± 1 mmHg and coronary blood flow fell from 0.93 ± 0.15 to 0.32 ± 0.03 ml/min/g as CPP was reduced from 140 to 40 mmHg. Administration of dobutamine significantly increased heart rate (~60%; P < 0.001), but the combination of hypoxemia plus dobutamine did not further influence heart rate. Further, dobutamine with and without hypoxemia significantly increased MVO 2 (P < 0.001); however, CvPO 2 was reduced (P < 0.001) only in the presence of hypoxemia. Calculation of closed-loop autoregulatory gain (Gc) over a CPP range of 120 to 60 mmHg (value of 1 represents perfect autoregulation) was unaffected by dobutamine alone but tended to increase when dobutamine infusion was combined with reductions in PaO 2 ≤ 40 mmHg (P = 0.069). Additional analysis of the autoregulatory slope within this same CPP range revealed no differences between groups. However, there was a significant inverse association between Gc and CvPO 2 , measured at CPP of 100 mmHg, in the absence and presence of dobutamine-induced increases in MVO 2 ± hypoxemic conditions (P < 0.001, r = -0.722). The relationship of coronary resistance (CPP range of 120 to 60 mmHg) relative to respective CvPO 2 revealed that decreases in CvPO 2 were not associated with changes in coronary resistance until CvPO 2 fell below a relative threshold of ~ 25 mmHg (r = 0.88). These findings support the interpretation that the sensitivity of coronary autoregulatory behavior is directly coupled with the activation of local metabolic vasodilator pathways below a critical level of myocardial oxygenation. This work was supported by National Institutes of Health grant R01 HL158723. This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Oxygen-sensing pathways below autoregulatory threshold act to sustain myocardial oxygen delivery during reductions in perfusion pressure.

The coronary circulation has an innate ability to maintain constant blood flow over a wide range of perfusion pressures. However, the mechanisms responsible for coronary autoregulation remain a fundamental and highly contested question. This study interrogated the local metabolic hypothesis of autoregulation by testing the hypothesis that hypoxemia-induced exaggeration of the metabolic error signal improves the autoregulatory response. Experiments were performed on open-chest anesthetized swine during stepwise changes in coronary perfusion pressure (CPP) from 140 to 40mmHg under normoxic (n = 15) and hypoxemic (n = 8) conditions, in the absence and presence of dobutamine-induced increases in myocardial oxygen consumption (MVO2) (n = 5-7). Hypoxemia (PaO2 < 40mmHg) decreased coronary venous PO2 (CvPO2) ~ 30% (P < 0.001) and increased coronary blood flow ~ 100% (P < 0.001), sufficient to maintain myocardial oxygen delivery (P = 0.14) over a wide range of CPPs. Autoregulatory responsiveness during hypoxemia-induced reductions in CvPO2 were associated with increases of autoregulatory gain (Gc; P = 0.033) but not slope (P = 0.585) over a CPP range of 120 to 60mmHg. Preservation of autoregulatory Gc (P = 0.069) and slope (P = 0.264) was observed during dobutamine administration ± hypoxemia. Reductions in coronary resistance in response to decreases in CPP predominantly occurred below CvPO2 values of ~ 25mmHg, irrespective of underlying vasomotor reserve. These findings support the presence of an autoregulatory threshold under which oxygen-sensing pathway(s) act to preserve sufficient myocardial oxygen delivery as CPP is reduced during increases in MVO2 and/or reductions in arterial oxygen content.

Impaired insulin-stimulated myocardial glucose metabolic rate is associated with reduced estimated myocardial energetic efficiency in subjects with different degrees of glucose tolerance

BackgroundAlterations in myocardial mechano-energetic efficiency (MEEi), which represents the capability of the left ventricles to convert the chemical energy obtained by oxidative metabolism into mechanical work, have been associated with cardiovascular disease. Although whole-body insulin resistance has been related to impaired myocardial MEEi, it is unknown the relationship between cardiac insulin resistance and MEEi. Aim of this study was to evaluate the relationship between insulin-stimulated myocardial glucose metabolic rate (MrGlu) and myocardial MEEi in subjects having different degrees of glucose tolerance.MethodsWe evaluated insulin-stimulated myocardial MrGlu using cardiac dynamic positron emission tomography (PET) with 18F-Fluorodeoxyglucose (18F-FDG) combined with euglycemic-hyperinsulinemic clamp, and myocardial MEEi in 57 individuals without history of coronary heart disease having different degrees of glucose tolerance. The subjects were stratified into tertiles according to their myocardial MrGlu values.ResultsAfter adjusting for age, gender and BMI, subjects in I tertile showed a decrease in myocardial MEEi (0.31 ± 0.05 vs 0.42 ± 0.14 ml/s*g, P = 0.02), and an increase in myocardial oxygen consumption (MVO2) (10,153 ± 1375 vs 7816 ± 1229 mmHg*bpm, P < 0.0001) as compared with subjects in III tertile. Univariate correlations showed that insulin-stimulated myocardial MrGlu was positively correlated with MEEi and whole-body glucose disposal, and negatively correlated with waist circumference, fasting plasma glucose, HbA1c and MVO2. In a multivariate regression analysis running a model including several CV risk factors, the only variable that remained significantly associated with MEEi was myocardial MrGlu (β 0.346; P = 0.01).ConclusionsThese data suggest that an impairment in insulin-stimulated myocardial glucose metabolism is an independent contributor of depressed myocardial MEEi in subjects without history of CHD.

Perioperative Myocardial Injury/Infarction After Non-cardiac Surgery in Elderly Patients.

At present, we have entered an aging society. Many diseases suffered by the elderly, such as malignant tumors, cardiovascular diseases, fractures, surgical emergencies and so on, need surgical intervention. With the improvement of Geriatrics, surgical minimally invasive technology and anesthesia level, more and more elderly patients can safely undergo surgery. Elderly surgical patients are often complicated with a variety of chronic diseases, and the risk of postoperative myocardial injury/infarction (PMI) is high. PMI is considered to be the increase of cardiac troponin caused by perioperative ischemia, which mostly occurs during operation or within 30 days after operation, which can increase the risk of short-term and long-term death. Therefore, it is suggested to screen troponin in elderly patients during perioperative period, timely identify patients with postoperative myocardial injury and give appropriate treatment, so as to improve the prognosis. The pathophysiological mechanism of PMI is mainly due to the increase of myocardial oxygen consumption and / the decrease of myocardial oxygen supply. Preoperative and postoperative risk factors of myocardial injury can be induced by mismatch of preoperative and postoperative oxygen supply. The treatment strategy should first control the risk factors and use the drugs recommended in the guidelines for treatment. Application of cardiovascular drugs, such as antiplatelet β- Receptor blockers, statins and angiotensin converting enzyme inhibitors can effectively improve postoperative myocardial ischemia. However, the risk of perioperative bleeding should be fully considered before using antiplatelet and anticoagulant drugs. This review is intended to describe the epidemiology, diagnosis, pathophysiology, risk factors, prognosis and treatment of postoperative myocardial infarction /injury.

Modalities of Left Ventricle Decompression during VA-ECMO Therapy.

Veno-arterial extracorporeal membrane oxygenation (VA-ECMO) is used to sustain circulatory and respiratory support in patients with severe cardiogenic shock or refractory cardiac arrest. Although VA-ECMO allows adequate perfusion of end-organs, it may have detrimental effects on myocardial recovery. Hemodynamic consequences on the left ventricle, such as the increase of afterload, end-diastolic pressure and volume, can lead to left ventricular (LV) distention, increase of myocardial oxygen consumption and delayed LV function recovery. LV distention occurs in almost 50% of patients supported with VA-ECMO and is associated with an increase in morbidity and mortality. Thus, recognizing, preventing and treating LV distention is key in the management of these patients. In this review, we aim to discuss the pathophysiology of LV distention and to describe the strategies to unload the LV in patients supported with VA-ECMO.

The inodilator levosimendan: 20 years of experience in various settings of cardiac care

Levosimendan emerged in the 1990s as a first-in-class inotrope and vasodilator that enhances cardiac contractility by sensitizing the contractile response to cardiac troponin C and causes vasodilatation by opening potassium-dependent ATP channels on vascular smooth muscle cells. Since its clinical debut in 2000, it has established itself as a valuable resource in the management of acute decompensated heart failure and is one of very few successful medical innovations of its kind in that field in recent decades. Its pharmacology is notable for delivering inotropy without an increase in myocardial oxygen consumption and for an array of secondary (‘pleiotropic’) effects that include an anti-ischemic effect, pre-conditioning and post-conditioning and cardioprotective effects and anti-oxidative effects. Proceeding from those properties it has been proposed that in addition to its use in various scenarios of low cardiac output levosimendan may be beneficial in other conditions associated with acutely decompensated heart failure, including right ventricular failure, subarachnoid hemorrhage, and cardiogenic shock with multi-organ dysfunction. The potential of levosimendan for kidney protection in situations of the cardio-renal syndrome has been identified. Additional lines of investigation include the use of levosimendan for perioperative hemodynamic support, its administration as repeated intermittent infusions to sustain patients with advanced heart failure and its application in a range of critical care settings. Levosimendan has also provided a template and a starting point for the development of a new generation of cardio-active drugs and is currently being evaluated in advanced clinical trials for the management of pulmonary hypertension in patients with heart failure with preserved ejection fraction.

The many faces of myocardial ischaemia and angina

Obstructive disease of the epicardial coronary arteries is the main cause of angina. However, a number of patients with anginal symptoms have normal coronaries or non-obstructive coronary artery disease (CAD) despite electrocardiographic evidence of ischaemia during stress testing. In addition to limited microvascular vasodilator capacity, the coronary microcirculation of these patients is particularly sensitive to vasoconstrictor stimuli, in a condition known as microvascular angina. This review briefly summarizes the determinants and control of coronary blood flow (CBF) and myocardial perfusion. It subsequently analyses the mechanisms responsible for transient myocardial ischaemia: obstructive CAD, coronary spasm and coronary microvascular dysfunction in the absence of epicardial coronary lesions, and variable combinations of structural anomalies, impaired endothelium-dependent and/or -independent vasodilation, and enhanced perception of pain. Lastly, we exemplify mechanism of angina during tachycardia. Distal to a coronary stenosis, coronary dilator reserve is already recruited and can be nearly exhausted at rest distal to a severe stenosis. Increased heart rate reduces the duration of diastole and thus CBF when metabolic vasodilation is no longer able to increase CBF. The increase in myocardial oxygen consumption and resulting metabolic vasodilation in adjacent myocardium without stenotic coronary arteries further acts to divert blood flow away from the post-stenotic coronary vascular bed through collaterals.

The blood pressure and heart rate during sauna bath correspond to cardiac responses during submaximal dynamic exercise

ObjectivesIn the present study, the reaction of blood pressure and heart rate are examined during and after a single acute sauna application. DesignIn 19 healthy adult volunteers (7 women, aged 46.4±10.2 years, BMI 24.4±2 kg /m2), blood pressure (BP) and heart rate (HR) were measured during a 25-minute sauna session (93°C, 13 % humidity) and during a subsequent 30-minute rest period. The parameters obtained were compared with the BP and HR responses during submaximal dynamic exercise testing. ResultsThe heat exposure resulted in a significant (p<0.01) and progressive increase in systolic and diastolic BP. After the sauna bath, BP decreased and showed significantly (p<0.001) lower values compared to baseline. HR also increased continuously during heat application (p<0.001), resulting in a significant increase (p<0.001) in systolic BP x HR as a measure of myocardial oxygen consumption. After the end of the sauna session, both the BP and the HR decreased steadily (p<0.001).When comparing BP and HR during the sauna session with the reaction during a dynamic exercise test, sauna bathing was equivalent to an exercise load of about 60-100 watts. ConclusionsContrary to popular belief, acute sauna use does not lead to a reduction, but to an increase in BP and HR with a consequent increase in myocardial oxygen consumption. The cardiac load during the sauna use corresponds to a moderate physical load of 60-100 watts.

Cardiovascular effects and risks of recreational alpine skiing in the elderly

ObjectivesAlpine skiing is one of the most popular recreational winter sports and attracts millions of tourists every year alone in the Alpine region. Several studies highlight the positive effects of alpine skiing as aerobic physical training and isometric muscle activity that is able to increase exercise capacity and reduce cardiovascular risk factors. However, a certain cardiovascular risk mainly related to an abrupt increase of myocardial oxygen consumption during skiing especially in otherwise sedentary subjects and effects of hypoxia in untrained patients have to be acknowledged. DesignIn this article, we provide an up-to-date evaluation of risks and benefits of alpine skiing in relation of cardiovascular disease and elderly persons. MethodsNarrative Review. ResultsIn the first section, the current recommendations of physical activity and effects of alpine skiing – with particular attention to the elderly population – are described. In the second section, the present knowledge regarding cardiovascular risk and alpine skiing is summarized and possible pathophysiological mechanisms are highlighted. Finally, a summary regarding actual clinical recommendations is provided. ConclusionsAlpine skiing may safely be recommended also to the elderly if certain precautions are applied, as the benefits outbalance the potential risks in most subjects.

Vasopressors and inotropes: use in paediatrics

The cardiovascular system is a dynamic system, which is required to ensure adequate delivery of oxygen, nutrients, and hormones to the tissues that are necessary for cell metabolism. It also synthesises and modifies the vasoactive components that regulate vascular tone and myocardial function. These vasoactive components have demonstrated their beneficial effects in the management of paediatric patients in a critical condition with heart failure and shock. However, their use and abuse brings harmful effects, increases mortality, and is associated with arrhythmias. An increase in myocardial oxygen consumption favours the presence of ischaemia, therefore it is necessary to know the mechanism of action and indications of these drugs to minimise their harmful effects. The purpose of this review is to describe the pharmacology and clinical applications of inotropic and vasopressor agents in the paediatric patient in acritical condition.

Is Two Better Than One? Anticipation of a Favorable Hemodynamic Profile by Combining the Hypnotic Drugs for Induction of Anesthesia.

Is Two Better Than One? Anticipation of a Favorable Hemodynamic Profile by Combining the Hypnotic Drugs for Induction of Anesthesia.

Toward safe inotropic therapy.

The use of currently available positive inotropic agents is associated with an unfavorable clinical outcome. The disappointment with positive inotropic therapy is to some extent foreseeable as currently available inotropic agents may precipitate ventricular arrhythmias due to a diastolic rise in intracellular [Ca], trigger/worsen myocardial ischemia due to an increased oxygen demand, and foster fuel deprivation from an energy starved heart. Safe use of presently available inotropic agents and development of novel inotropic agents must ensure that they are not associated with a diastolic rise in intracellular [Ca], an increase in myocardial oxygen consumption, and energy expenditure. Agents that improve left ventricular systolic performance through prolongation of left ventricular ejection time and not through increased myocardial contractility, that is, myosin activators, may be associated with a favorable outcome as they do not affect diastolic intracellular [Ca], myocardial oxygen demand, and presumably fuel expenditure.

Hypertension, Autonomic Storm, Increased Counter Regulatory Hormones and Suppressed Insulin in Acute Myocarditis in Scorpion Envenoming Syndrome

Death due to scorpion envenoming syndrome is a common event in many of the tropical and non-tropical counties. Initial transient hypertension is commonly observed in scorpion sting victims. Scorpion envenoming causes autonomic storm resulting in initial transient hypertension followed by hypotension, cold clammy skin, hypothermia, cardiovascular disturbances, acute myocarditis, sarcolemmal defects, pulmonary oedema, acute pancreatitis, disseminated intravascular coagulation (DIC), Adult respiratory distress syndrome (ARDS), and many other clinical manifestations. All these manifestations could be due to sudden increase in catecholamines, angiotensin II, glucagon, Cortisol and either due to suppressed insulin secretion or insulin resistance and death. The sudden increase of metabolic A in counter-regulatory hormones along with either suppressed insulin secretion/or insulin resistance results in glycogenolysis in liver, cardiac and skeletal muscles causing hyperglycemia and a sudden increase in free fatty acid levels. Free Fatty Acids increase the susceptibility of the ventricles to the disorganized electrical behavior, inhibit cardiac sarcolemmal Na+-K+ ATPase activity, increase the tendency to intravascular thrombus, increase myocardial oxygen consumption, interfere with tropomyosin-troponin activation of Actin-Myosin coupling, show detergent effects on cell membranes and they could alter the stabilization of lysosomal membranes and probably become toxic to the myocardium. Based on our animal experiments in which insulin administration reversed the metabolic and ECG changes induced by scorpion envenoming and treating the poisonous scorpion sting victims with insulin, we consider that insulin has a primary metabolic role in preventing, counter-acting and reversing all the deleterious effects of FFA by inhibiting the catecholamine induced by lipolysis, and increasing intra-cellular K+, facilitating glucose transport to the myocardium and glucose metabolism through different pathways. Administration of insulin-glucose infusion to scorpion sting victims appears to be the physiological basis for the control of the metabolic response when that has become a determinant to survival. Treatment using continuous infusion of regular crystalline insulin should be given at the rate of 0.3 U/g glucose and glucose at the rate of 0.1 g/kg body weight/hour, for 48 - 72 hours, with supplementation of potassium as needed and maintenance of fluid, electrolytes and acid-base balance.

Cardiac resynchronization therapy and AV optimization increase myocardial oxygen consumption, but increase cardiac function more than proportionally

BackgroundThe mechanoenergetic effects of atrioventricular delay optimization during biventricular pacing (“cardiac resynchronization therapy”, CRT) are unknown. MethodsEleven patients with heart failure and left bundle branch block (LBBB) underwent invasive measurements of left ventricular (LV) developed pressure, aortic flow velocity-time-integral (VTI) and myocardial oxygen consumption (MVO2) at 4 pacing states: biventricular pacing (with VV 0ms) at AVD 40ms (AV-40), AVD 120ms (AV-120, a common nominal AV delay), at their pre-identified individualised haemodynamic optimum (AV-Opt); and intrinsic conduction (LBBB). ResultsAV-120, relative to LBBB, increased LV developed pressure by a mean of 11(SEM 2)%, p=0.001, and aortic VTI by 11(SEM 3)%, p=0.002, but also increased MVO2 by 11(SEM 5)%, p=0.04.AV-Opt further increased LV developed pressure by a mean of 2(SEM 1)%, p=0.035 and aortic VTI by 4(SEM 1)%, p=0.017. MVO2 trended further up by 7(SEM 5)%, p=0.22.Mechanoenergetics at AV-40 were no different from LBBB.The 4 states lay on a straight line for Δexternal work (ΔLV developed pressure×Δaortic VTI) against ΔMVO2, with slope 1.80, significantly >1 (p=0.02). ConclusionsBiventricular pacing and atrioventricular delay optimization increased external cardiac work done but also myocardial oxygen consumption. Nevertheless, the increase in cardiac work was ~80% greater than the increase in oxygen consumption, signifying an improvement in cardiac mechanoenergetics. Finally, the incremental effect of optimization on external work was approximately one-third beyond that of nominal AV pacing, along the same favourable efficiency trajectory, suggesting that AV delay dominates the biventricular pacing effect — which may therefore not be mainly “resynchronization”.

Myocardial Perfusion Imaging Study of CO2-Induced Panic Attack

Chest pain is often seen alongside with panic attacks. Moreover, panic disorder has been suggested as a risk factor for cardiovascular disease and even a trigger for acute coronary syndrome. Patients with coronary artery disease may have myocardial ischemia in response to mental stress, in which panic attack is a strong component, by an increase in coronary vasomotor tone or sympathetic hyperactivity setting off an increase in myocardial oxygen consumption. Indeed, coronary artery spasm was presumed to be present in cases of cardiac ischemia linked to panic disorder. These findings correlating panic disorder with coronary artery disease lead us to raise questions about the favorable prognosis of chest pain in panic attack. To investigate whether myocardial ischemia is the genesis of chest pain in panic attacks, we developed a myocardial perfusion study through research by myocardial scintigraphy in patients with panic attacks induced in the laboratory by inhalation of 35% carbon dioxide. In conclusion, from the data obtained, some hypotheses are discussed from the viewpoint of endothelial dysfunction and microvascular disease present in mental stress response.

A Case of Acute Heart Failure With Intravenous Acetazolamide Administration for Evaluation of Cerebrovascular Reactivity

A man in his seventies presented with a history of cerebral infarction with occlusion of the left middle cerebral artery, diabetes mellitus, renal dysfunction, as well as prior myocardial infarction and arteriosclerosis obliterans. About 45 min after intravenous administration of 1,000 mg of acetazolamide for acetazolamide-augmented cerebrovascular single-photon emission computed tomography, he experienced dyspnea and tightness in his chest which worsened. Hypertension, regular tachycardia, and wheezing and rales were noted. Symptoms and vital signs did not improve despite many life-saving treatments. In patients with severe coronary artery disease with low ischemic threshold, as in the present case, acetazolamide might reduce peripheral vascular resistance, increase the cardiac output ratio, increase myocardial oxygen consumption by increasing cardiac output, and induce myocardial ischemia with elevation of double product. Although the frequency of acute heart failure due to myocardial ischemia after an acetazolamide challenge may be low, its occurrence in patients with severe arteriosclerotic disease should be routinely considered. J Med Cases. 2013;4(7):495-498 doi: http://dx.doi.org/10.4021/jmc1315w

Cardiac resynchronization therapy (CRT): Clinical trials, guidelines, and target populations

Over the last 10 years, several large, well-designed clinical trials have firmly established the role of cardiac resynchronization therapy (CRT) as a recommended treatment strategy for moderate-to-severe heart failure (HF). A review of the relevant results from the MUSTIC, MIRACLE, CONAK-CD, and MIRACLE ICD trials reveals that in patients with New York Heart Association (NYHA) class III-IV HF, CRT produces consistent improvements in quality of life, functional status, and exercise capacity while also providing strong evidence for reverse remodeling and diminished functional mitral regurgitation, resulting in reductions in both HF hospitalizations and all-cause morbidity and mortality. In patients with earlier NYHA class I-II HF, the benefit of CRT has been more controversial. The principal ongoing challenges addressed in this article include the substantial 30% of patients who receive a CRT device but fail to respond, the wide variations in how to define "response" vs "nonresponse," and how to identify patients who will benefit from CRT, especially narrow QRS (<120 ms), those with right bundle branch block, and those with mild-to-moderate (NYHA class I-II) HF. An important result of this uncertainty is the lack of a good sense of the optimal rate of CRT implantation, making consideration of the data reviewed in this article crucial for identifying important gaps of knowledge and mechanisms of action that need to be studied in the near future.

Hypothermia in cardiogenic shock

Cardiogenic shock is a state of inadequate systemic tissue perfusion, despite adequate left ventricular filling pressure. It is caused by extensive myocardial damage and appears to be aggravated by a systemic inflammatory response [1-4]. The result is hypotension with metabolic acidosis and often a fatal outcome. The condition affects approximately 5% of the patients with myocardial infarction, and carries a dismal prognosis if it prevails after reperfusion. Therapeutic hypothermia has several properties of potential benefit in cardiogenic shock: Experiments with isolated myofibrils, papillary muscles and cross-circulated hearts have demonstrated that mild hypothermia increases myocardial contractility [5-7]. In the in vivo heart, mild hypothermia has been found to increase stroke volume and cardiac output [6,8]. The increase in contractility is considered to be mediated by an increased myofilament sensitivity to existing Ca2+, without a corresponding increase in myocardial oxygen consumption [9]. Moreover, hypothermia reduces the metabolic rate with 5 to 7%/°C [10,11], thereby reducing the demand on the circulation from the peripheral tissues. In an experimental setting, it also has the ability to reduce infarct size if applied prior to reperfusion [12,13]. In dog-based and porcine-based models of cardiogenic shock secondary to ischemia, therapeutic hypothermia has improved hemodynamic and metabolic parameters, and reduced mortality [14,15]. No randomized controlled trials of therapeutic hypothermia in cardiogenic shock in humans exist, but case series indicate that the effects observed in animal experiments can be reproduced [16-19]. In conclusion, therapeutic hypothermia is a promising treatment option for patients in cardiogenic shock that warrants further investigation.

A12 Ischemic Heart Disease and Weaning from Mechanical Ventilation, how efficient Esmolol can be when Extubation is unsuccessful?

Background and Goal of Study: Patients with ischemic heart disease are known to tolerate hemodynamic stress poorly. As a consequence of their coronary artery disease, ischemic episodes may develop during, or shortly after tracheal tube removal. We describe a case with coronary artery disease that developed repeated episodes of pulmonary oedema each time extubation was attempted. We describe a case of patient with ischemic heart disease and the difficulties in weaning and extubation. Methods: A 70 year old male was submitted urgently because of an abdominal aneurysm. The patient was hemodynamically stable throughout the intervention that lasted 4 hours and on ICU admission, (Heart rate 100/min, and blood pressure 130/65mmHg). Despite trying twice the patient did not achieve successful extubation, in both instances, after extubation, he presented with a rapid shallow breathing and low arterial oxygen saturation. On auscultation, he presented crepitations in middle zones of both lung fields and the chest X-ray was indicative for pulmonary oedema. A trans-thoracic echo that was performed showed normal systolic ventricular function and diastolic dysfunction with abnormal relaxation, patient was therefore given initially esmolol 500 μg/kg/min (iv.) followed by an infusion of 50 μg/kg/min. Sedation was gradually decreased and infusion rate of esmolol was increased. Patient was extubated successfully under 100 μg/kg/min and was discharged from the ICU two days later. Results: Extubation stress in patients with coronary artery disease cause excessive increases in myocardial oxygen consumption thereby altering the supply/demand ratio. Our patient was experiencing ischemic left ventricular dysfunction during weaning, secondary to catecholamine release due to upper airway stimulation by the tracheal tube. This was manifested as hypertension, tachycardia and episodes of pulmonary oedema, which were rapidly resolved with sedation. Conclusions: Using esmolol, a short/acting beta/blocker, allowed successful extubation of patient who developed repeated episodes of pulmonary oedema each time extubation was attempted.

Use of beta-blockers for the treatment of cardiac arrest due to ventricular fibrillation/pulseless ventricular tachycardia: A systematic review

IntroductionAdvanced Life Support guidelines recommend the use of epinephrine during Cardiopulmonary Resuscitation (CPR), as to increase coronary blood flow and perfusion pressure through its alpha-adrenergic peripheral vasoconstriction, allowing minimal rises in coronary perfusion pressure to make defibrillation possible. Contrasting to these alpha-adrenergic effects, epinephrine's beta-stimulation may have deleterious effects through an increase in myocardial oxygen consumption and a reduction of subendocardial perfusion, leading to postresuscitation cardiac dysfunction. ObjectiveThe present paper consists of a systematic review of the literature regarding the use of beta-blockade in cardiac arrest due to ventricular fibrillation (VF) and pulseless ventricular tachycardia (VT). MethodsStudies were identified through MEDLINE electronic databases research and were included those regarding the use of beta-blockade during CPR. ResultsBeta-blockade has been extensively studied in animal models of CPR. These studies not only suggest that beta-blockade could reduce myocardial oxygen requirements and the number of shocks necessary for defibrillation, but also improve postresuscitation myocardial function, diminish arrhythmia recurrences and prolong survival. A few case reports described successful beta-blockade use in patients, along with two prospective human studies, suggesting that it could be safe and effectively used during cardiac arrest in humans. ConclusionEven though the existing literature points toward a beneficial effect of beta-blockade in patients presenting with cardiac arrest due to VF/pulseless VT, high quality human trials are still lacking to answer this question definitely.