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2006, Surgical Clinics of North America
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19 pages
1 file
Cardiovascular failure is a frequent event in critically ill patients. It can be defined as hypotension despite adequate fluid resuscitation or the need for vasopressors to maintain a normotensive state. Although a useful tool in categorizing organ failure, this definition fails to capture the physiologic state as it relates to organ perfusion and oxygen delivery at the tissue level. When viewed from this perspective, it is important to understand that cardiovascular failure is related to the shock state in so far as the latter is an inevitable consequence of the former without prompt and aggressive intervention. A second important concept in understanding the failing heart is that the heart and blood vessels function as a single unit. Therapy directed at one component of the system invariably affects the other. This becomes critical when the intervention has significant untoward effects, such as the consequences of increasing blood pressure using a vasoconstricting agent and the associated increase in myocardial oxygen demand. For this reason, therapeutic measures should be directed at reversing the state of physiologic failure to achieve clinically significant end points. These are restoration of adequate oxygen delivery with the reversal of the clinical signs of cardiovascular failure (use of vasoactive-cardiotonic agents or aortic counterpulsation for acute ischemic pump failure); and treatment of the underlying cause (antibiotics for sepsis, revascularization of the ischemic myocardium).
European Heart Journal: Acute Cardiovascular Care, 2013
To examine the use of the treatments for acute heart failure (AHF) recommended by ESC guidelines in different clinical presentations and blood pressure groups. Methods: The use of intravenous diuretics, nitrates, opioids, inotropes, and vasopressors as well as non-invasive ventilation (NIV) was analysed in 620 patients hospitalized due to AHF. The relation between AHF therapies and clinical presentation, especially systolic blood pressure (SBP) on admission, was also assessed. Results: Overall, 76% of patients received i.v. furosemide, 42% nitrates, 29% opioids, 5% inotropes and 7% vasopressors, and 24% of patients were treated with NIV. Furosemide was the most common treatment in all clinical classes and irrespective of SBP on admission. Nitrates were given most often in pulmonary oedema and hypertensive AHF. Overall, only SBP differed significantly between patients with and without the studied treatments. SBP was higher in patients treated with nitrates than in those who were not (156 vs. 141 mmHg, p<0.001). Still, only one-third of patients presenting acute decompensated heart failure and SBP over 120 mmHg were given nitrates. Inotropes and vasopressors were given most frequently in cardiogenic shock and pulmonary oedema, and their use was inversely related to initial SBP (p<0.001). NIV was used only in half of the cardiogenic shock and pulmonary oedema patients. Conclusions: The management of AHF differs between ESC clinical classes and the use of i.v. vasoactive therapies is related to the initial SBP. However, there seems to be room for improvement in administration of vasodilators and NIV.
Revista Española de Cardiología (English Edition), 2015
Acute heart failure is globally one of most frequent reasons for hospitalization and still represents a challenge for the choice of the best treatment to improve patient outcome. According to current international guidelines, as soon as patients with acute heart failure arrive at the emergency department, the common therapeutic approach aims to improve their signs and symptoms, correct volume overload, and ameliorate cardiac hemodynamics by increasing vital organ perfusion. Recommended treatment for the early management of acute heart failure is characterized by the use of intravenous diuretics, oxygen, and vasodilators. Although these measures ameliorate the patient's symptoms, they do not favorably impact on short-and long-term mortality. Consequently, there is a pressing need for novel agents in acute heart failure treatment with the result that research in this field is increasing worldwide.
Artificial Organs, 1996
For the evaluation of the hemodynamic interaction between the natural heart and an assist device, a reversible pharmacological model based on the channel blocker Verapamil under hyperkalemia, was developed for deterioration of left ventricular function. Four calves weighing 70-90 kg underwent standard implantation for left at rioaortal assist (BioMedicus, BP-80), pump anesthesia (oxygenhsoflurane [ 1 %]; 8 mg/kg of BW/h ketamine). and of ventricular demand pacing at 120 bpm. Left atrial pressure (LAP), ventricular pressure (LVP), aortic pressure (AoP), pulmonary arterial (Qpulm) pressures, and graft flow (Qgraft) were monitored. The hemodynamic effects of anesthetic overdose (2% Isoflurane) were compared with those of Verapamil (Isoptin: 0.2 mg/kg BWlh 5 mmol/kg of BW/h of KCI ) medication. Both reg-__ ___ ~~
This article is a short review of vasoactive drugs which are in use in today's clinical practice. In the past century, development of vasoactive drugs went through several phases. All of these drugs are today divided into several groups, depending on their place of action, pharmacological pathways and/or effects on target organ or organ system. Hence, many different agents are today in clinical practice, we have shown comparison between them. These agents provide new directions in the treatment of cardiovascular compromise, suggesting that the primary goal of therapy is to enhance tissue perfusion by both producing a vasodilatory effect of the circulation and reversing hemodynamic failure using inotropic agents, with increased attention to minimize their inherent risks and side effects.
Intensive Care Medicine
Purpose: Acute heart failure (AHF) causes high burden of mortality, morbidity, and repeated hospitalizations worldwide. This guidance paper describes the tailored treatment approaches of different clinical scenarios of AHF and CS, focusing on the needs of professionals working in intensive care settings. Results: Tissue congestion and hypoperfusion are the two leading mechanisms of end-organ injury and dysfunction, which are associated with worse outcome in AHF. Diagnosis of AHF is based on clinical assessment, measurement of natriuretic peptides, and imaging modalities. Simultaneously, emphasis should be given in rapidly identifying the underlying trigger of AHF and assessing severity of AHF, as well as in recognizing end-organ injuries. Early initiation of effective treatment is associated with superior outcomes. Oxygen, diuretics, and vasodilators are the key therapies for the initial treatment of AHF. In case of respiratory distress, non-invasive ventilation with pressure support should be promptly started. In patients with severe forms of AHF with cardiogenic shock (CS), inotropes are recommended to achieve hemodynamic stability and restore tissue perfusion. In refractory CS, when hemodynamic stabilization is not achieved, the use of mechanical support with assist devices should be considered early, before the development of irreversible end-organ injuries. Conclusion: A multidisciplinary approach along the entire patient journey from pre-hospital care to hospital discharge is needed to ensure early recognition, risk stratification, and the benefit of available therapies. Medical management should be planned according to the underlying mechanisms of various clinical scenarios of AHF.
European Journal of Pharmacology, 2011
As a critical component of post-resuscitation care, prompt optimization of hemodynamic status by means of targeted interventions is vital in order to maximize the likelihood of good outcome. Vasoactive agents play an essential role in the supportive care of post cardiac arrest patients. The administration of these agents is associated with serious side-effects and therefore they should be used in the minimal dose necessary to achieve low-normal mean arterial pressure and adequate systematic perfusion. Careful and frequent serial evaluation of the patient is important primarily to assess volume status and adequacy of circulatory support. Continuous monitoring of blood pressure and laboratory parameters is essential both to accurately titrate therapy and because inotropes and vasopressors have the potential to induce life-threatening side-effects. The clinical efficacy of inotropes and vasopressors has been largely investigated through examination of their impact on hemodynamic end points, and clinical practice has been driven in part by expert opinion, extrapolation from animal studies, and physician preference. Clearly these agents should all be considered as supportive measures to stabilize the patient prior to some form of definitive therapy.
Critical Care, 2003
Introduction Cardiac surgery with cardiopulmonary bypass (CPB) is a recognized trigger of systemic inflammatory response, usually related to postoperative acute lung injury (ALI). As an attempt to dampen inflammatory response, steroids have been perioperatively administered to patients. Macrophage migration inhibitory factor (MIF), a regulator of the endotoxin receptor, is implicated in the pathogenesis of ALI. We have previously detected peak circulating levels of MIF, 6 hours post CPB. Experimental data have shown that steroids may induce MIF secretion by mononuclear cells. This study aims to correlate levels of MIF assayed 6 hours post CPB to the intensity of postoperative pulmonary dysfunction, analysing the impact of perioperative steroid administration.
Research Reports in Clinical Cardiology, 2014
Acute heart failure (AHF) represents a major burden in developed countries. However, pharmacological approaches have remained almost the same for 30 years and are still based on consensus rather than evidence, given that no medical therapy has been shown to positively affect clinical outcomes. Current pharmacological approaches are still based on decongestion by using diuretics in almost all patients, plus either vasodilators or inotropic agents to improve hemodynamics according to perfusion status. The role of loop diuretics (furosemide) and nitrates (nitroglycerin and nitroprusside) is well established, but new agents such as vasopressin and adenosine antagonists, as well as nesiritide, have failed to show any additional value. In the presence of hypoperfusion, the use of inotropics must be considered despite the lack of benefit in terms of survival, and the use of phosphodiesterase inhibitors and levosimendan has not shown any significant advantages over catecholamines (dobutamine). AHF involves a wide spectrum of patients and syndromes, and this probably accounts for the failure of trials set up to evaluate new therapeutic approaches for improving outcomes: therapies need to be tailored to specific patients. At this time, serelaxin represents a promising new agent which has a multifaceted effect, including organ protection, and has shown encouraging results when tailored for a well defined population. In addition, the role of ularitide, a synthetic form of the natriuretic peptide urodilatin, and the new cardiac myosin activators, as a new class of inotropic agents, will be established in the near future by ongoing trials. Therefore, AHF continues to be an unsolved problem and, in light of the lessons learned, new pharmacological approaches should be tailored to well defined AHF populations, incorporating concepts such as "the sooner the better", "improve and stabilize", and "prevent organ damage", in order to be able to improve clinical outcomes, including both mortality and readmission rates.
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