cardiovascular-agents and Shock

To discuss the use of vasopressors and inotropes in cardiogenic shock.. The classic form or cardiogenic shock requires administration of inotropic and/or vasopressor agents to try to improve the impaired tissue perfusion. Among vasopressors various alpha-adrenergic agents, vasopressin derivatives and angiotensin can be used. The first-line therapy remains norepinephrine as it is associated with minimal adverse effects and appears to be associated by the best outcome in network meta-analyses. On the contrary, epinephrine is associated with an increased incidence of refractory shock and observational studies suggest an increased risk of death. Vasopressin may be an excellent alternative in tachycardiac patients or in the presence of pulmonary hypertension. Concerning inotropic agents, dobutamine is the first-line agent but levosimendan is an excellent alternative or additional agent in cases not responding to dobutamine. The impact on outcome of inotropic agents remains controversial.. Recent studies have refined the position of the various vasopressor and inotropic agents. Norepinephrine is recommended as first-line vasopressor agent by various guidelines. Among inotropic agents, selection between the agents should be individualized and based on the hemodynamic response.

Topics: Cardiotonic Agents; Cardiovascular Agents; Dobutamine; Humans; Shock; Shock, Cardiogenic; Vasoconstrictor Agents

We report the successful perioperative management of a patient with presumed mastocytosis undergoing pulmonary embolectomy. Postoperatively the patient went into vasodilatory shock, which was partly attributed to mast cell mediator release. H1- and H2-antagonists, steroids, and a single dose of methylene blue were given with improvement of hemodynamics. The patient was weaned off vasoactive substances and extubated by postoperative day 2. We discuss the perioperative management of patients with mastocytosis, briefly review the literature concerning anesthetic management for cardiac surgery in patients with this disorder, and discuss our patient's alternative but related diagnosis of idiopathic mast cell activation syndrome.

Topics: Cardiovascular Agents; Embolectomy; Hemodynamics; Histamine Antagonists; Humans; Male; Mastocytosis; Middle Aged; Pulmonary Embolism; Risk Factors; Shock; Steroids; Treatment Outcome

Intravenous lipid emulsion (ILE) and veno-arterial extracorporeal membrane oxygenation (VA-ECMO) are being used together or in close succession in the management of circulatory failure secondary to cardiotoxic drug poisoning. There have been reports of mechanical problems, including fat emulsion agglutination, clogging, increased blood clot formation and even cracking of parts of the machine, in patients concurrently receiving VA-ECMO and ILE as part of parenteral nutrition.. To ascertain the adverse effects associated with the combined use of ILE and ECMO in the poisoned patient.. PubMed and OVID (1966 to 9 June 2014) and EMBASE (1947 to 9 June 2014) were searched to identify publications relating to studies and/or case reports where ILE had been used at the same time when VA-ECMO was used - 7 were identified. In addition, the abstracts published between 2006 and 2013 inclusive of those from the North American Congress of Clinical Toxicology and the congresses of the European Association of Poisons Centres and Clinical Toxicologists were searched to identify additional cases and 2 were found. Finally all cases posted on lipidrescue.org were reviewed to determine if they related to the use of ILE with VA-ECMO and no new cases were identified. In vitro study. An in vitro study involving the continuous infusion of 20% ILE at 3 mL/h for 24 h demonstrated layering (separation of intact fat emulsion from blood) and agglutination (clumping resulting in little or no flow of fat emulsion through the circuit) in all circuits within 30 min of starting the fat emulsion infusion.. An observational study based in 42 centres that regularly used 'fat emulsion' during VA-ECMO treatment reported cracking of stopcocks (the valve which restricts flow in the VA-ECMO tubing) (n = 10, 23.8%); fat emulsion agglutination (n = 11, 26.2%); clogging and associated malfunction of the membrane oxygenator (n = 2, 4.8%); and increased blood clot formation in the circuits (n = 2, 4.8%). In a prospective observational study of 9 neonates on VA-ECMO receiving intravenous nutrition, layering and agglutination were seen in four sets of VA-ECMO tubing and blood clots were found in seven circuits. Nine case reports were identified where ILE was used with VA-ECMO for the management of circulatory failure/instability secondary to cardiotoxic drug poisoning. In two of these case reports, the authors specifically stated that ILE did not cause any mechanical complications with the VA-ECMO; the other seven reports made no comment as to whether there were any complications or not.. There is in vitro and clinical evidence that the combined use of ILE and extracorporeal membrane oxygenation may be associated with fat deposition in the VA-ECMO circuits and increased blood clot formation. Clinicians managing poisoned patients with both of these novel treatment modalities should be aware of these potential complications.

Topics: Adolescent; Adult; Cardiovascular Agents; Cardiovascular Diseases; Combined Modality Therapy; Equipment Design; Equipment Failure; Extracorporeal Membrane Oxygenation; Fat Emulsions, Intravenous; Female; Humans; Infant; Male; Middle Aged; Poisoning; Risk Factors; Shock; Treatment Outcome; Young Adult

Acute cardiogenic pulmonary edema and cardiogenic shock are two of the main forms of presentation of acute heart failure. Both entities are serious, with high mortality, and require early diagnosis and prompt and aggressive management. Acute pulmonary edema is due to the passage of fluid through the alveolarcapillary membrane and is usually the result of an acute cardiac episode. Correct evaluation and clinical identification of the process is essential in the management of acute pulmonary edema. The initial aim of treatment is to ensure hemodynamic stability and to correct hypoxemia. Other measures that can be used are vasodilators such as nitroglycerin, loop diuretics and, in specific instances, opioids. Cardiogenic shock is characterized by sustained hypoperfusion, pulmonary wedge pressure > 18 mmHg and a cardiac index < 2.2l/min/m(2). The process typically presents with hypotension (systolic blood pressure < 90 mmHg or a decrease in mean arterial pressure > 30 mmHg) and absent or reduced diuresis (< 0.5 ml/kg/h). The most common cause is left ventricular failure due to acute myocardial infarction. Treatment consists of general measures to reverse acidosis and hypoxemia, as well as the use of vasopressors and inotropic drugs. Early coronary revascularization has been demonstrated to improve survival in shock associated with ischaemic heart disease.

Topics: Acute Disease; Cardiovascular Agents; Combined Modality Therapy; Diagnosis, Differential; Diuresis; Heart Failure; Humans; Hypotension; Hypoxia; Myocardial Infarction; Myocardial Revascularization; Narcotics; Oxygen Inhalation Therapy; Pulmonary Edema; Respiration, Artificial; Sepsis; Shock; Shock, Cardiogenic; Sodium Potassium Chloride Symporter Inhibitors; Vasoconstrictor Agents; Vasodilator Agents; Ventricular Dysfunction, Left

Topics: Cardiotonic Agents; Cardiovascular Agents; Diagnosis, Differential; Fluid Therapy; Humans; Lactic Acid; Shock; Vasoconstrictor Agents; Vasodilator Agents

Circulatory failure recognition and treatment represents an important issue in critically ill infants and children. Early diagnosis and prompt institution of adequate treatment may be life-saving for pediatric patients with cardiocirculatory instability in the setting of intensive care. However, the hemodynamic status of the critically ill child is poorly reflected by baseline vital parameters or laboratory blood tests. A reliable tool for diagnosis and monitoring of evolution of both heart performance and vascular status is strictly needed. Advanced hemodynamic monitoring consists - among others - of measuring cardiac output, predicting fluid responsiveness and calculating systemic oxygen delivery. Identification and quantifying of pulmonary edema has also been recently appreciated in pediatric critical care. In the last decade, the number of vasoactive drugs has increased, together with a better understanding of clinical application of both different monitoring devices and treatment strategies.

Topics: Cardiovascular Agents; Child; Child, Preschool; Humans; Infant; Intensive Care Units, Pediatric; Shock

"Cardio-renal syndromes" (CRS) are disorders of the heart and kidneys whereby acute or chronic dysfunction in one organ may induce acute or chronic dysfunction of the other. The current definition has been expanded into five subtypes whose etymology reflects the primary and secondary pathology, the time-frame and simultaneous cardiac and renal co-dysfunction secondary to systemic disease: CRS type I: acute worsening of heart function (AHF-ACS) leading to kidney injury and/or dysfunction. CRS type II: chronic abnormalities in heart function (CHF-CHD) leading to kidney injury or dysfunction. CRS type III: acute worsening of kidney function (AKI) leading to heart injury and/or dysfunction. CRS type IV: chronic kidney disease (CKD) leading to heart injury, disease and/or dysfunction. CRS type V: systemic conditions leading to simultaneous injury and/or dysfunction of heart and kidney. These different subtypes may have a different pathophysiological mechanism and they may represent separate entities in terms of prevention and therapy.

Topics: Biomarkers; Cardio-Renal Syndrome; Cardiovascular Agents; Contrast Media; Diuretics; Gene-Environment Interaction; Heart; Humans; Kidney; Renal Blood Flow, Effective; Renin-Angiotensin System; Risk Factors; Shock; Terminology as Topic

Heart failure may lead to acute kidney injury and vice versa. Chronic kidney disease may affect the clinical outcome in terms of cardiovascular morbidity and mortality while chronic heart failure may cause CKD. All these disorders contribute to the composite definition of cardio-renal syndromes. Renal impairment in HF patients has been increasingly recognized as an independent risk factor for morbidity and mortality; however, the most important clinical trials in HF tend to exclude patients with significant renal dysfunction. The mechanisms whereby renal insufficiency worsens the outcome in HF are not known, and several pathways could contribute to the "vicious heart/kidney circle." Traditionally, renal impairment has been attributed to the renal hypoperfusion due to reduced cardiac output and decreased systemic pressure. The hypovolemia leads to sympathetic activity, increased renin-angiotensin-aldosterone pathways and arginine-vasopressin release. All these mechanisms cause fluid and sodium retention, peripheral vasoconstriction and an increased congestion as well as cardiac workload. Therapy addressed to improve renal dysfunction, reduce neurohormonal activation and ameliorate renal blood flow could lead to a reduction in mortality and hospitalization in patients with cardio-renal syndrome.

Topics: Biomarkers; Cardiac Output; Cardio-Renal Syndrome; Cardiovascular Agents; Disease Progression; Diuretics; Heart; Humans; Interdisciplinary Communication; Kidney; Kidney Function Tests; Medication Therapy Management; Patient Selection; Renal Blood Flow, Effective; Renin-Angiotensin System; Risk Factors; Shock; Water-Electrolyte Imbalance

Topics: Cardiovascular Agents; Humans; Shock

Shock is one of the most frequent situations encountered in the intensive care unit (ICU). Important new concepts have emerged for shock management in recent years. The concept of early goal-directed therapy has evolved from the basic management concepts for septic shock delivered in a structured fashion. Numerous cardiovascular techniques, methods, and strategies have been developed as novel alternatives to the use of the pulmonary artery catheter. Among these techniques, echocardiography, esophageal Doppler, and arterial pulse contour analysis show great promise. Prediction of responsiveness to fluid administration is a key component of the management of shock, as is assessing cardiovascular performance. The intensive care physician has several options to evaluate and treat shock. Further research should yield additional important advances.

Topics: Cardiovascular Agents; Echocardiography, Doppler; Fluid Therapy; Humans; Intensive Care Units; Monitoring, Physiologic; Shock; Shock, Septic

Successful management of neonatal shock is driven by the etiology and pathophysiology of the cardiovascular compromise. In the clinical practice, however, we only have a limited ability to recognize the etiology of the condition (hypovolemia, myocardial dysfunction or abnormal vasoregulation). Therefore, management is based on administration of fluid boluses and vasoactive medications according to personal preference rather than to the underlying pathophysiology. In addition, although management strategies aimed at improving systemic blood pressure may have been associated with a decrease in mortality in critically ill neonates, there are no prospective data on the effect of these management strategies on morbidity, especially on long-term neurodevelopmental outcome. This paper briefly reviews some of the more frequently encountered clinical presentations of neonatal shock and describes the developmentally regulated cardiovascular responses to the pathophysiology-driven management strategies used in these clinical presentations in the critically ill preterm and term neonate.

Topics: Cardiotonic Agents; Cardiovascular Agents; Humans; Hypotension; Infant, Newborn; Infant, Newborn, Diseases; Shock

The controversy surrounding the use of the pulmonary artery catheter, has stimulated research into alternative methods of haemodynamic monitoring. As yet, however, no new gold standard has emerged. In the future, interest in haemodynamic monitoring is likely to focus more on tissue perfusion and metabolism instead of central circulation. Important causes of shock in the ICU, apart from acute blood loss, are sepsis and acute heart failure. Septic shock results from vasodilatation and myocardial dysfunction. Early initiation of aggressive fluid resuscitation, if necessary accompanied by vasoactive and inotropic agents, improves survival. In addition, low dose corticosteroids have a positive impact on mortality. In the treatment of patients with acute heart failure, phosphodiesterase III-inhibitors are becoming part of standard therapy in addition to beta-adrenoceptor agonists, especially in patients who take beta-blockers.

Topics: 3',5'-Cyclic-AMP Phosphodiesterases; Adrenal Cortex Hormones; Adrenergic beta-Agonists; Cardiotonic Agents; Cardiovascular Agents; Cyclic Nucleotide Phosphodiesterases, Type 3; Fluid Therapy; Heart Arrest; Hemodynamics; Humans; Intensive Care Units; Monitoring, Physiologic; Perfusion; Phosphodiesterase Inhibitors; Shock; Shock, Septic

Distributive shock is defined as circulatory insufficiency induced by excessive dilatation of the peripheral vasculature or maldistribution of cardiac output. Septicemia, systemic inflammatory response syndrome, anaphylaxis, injuries to the central nervous system, and drug intoxication are causative factors of shock. Circulatory derangements induced by bacterial infection have been divided into hyperdynamic and hypodynamic shock. Administration of inotropic drugs, vasopressors, and/or vasodilators are primary treatments in this type of shock. Continuous infusion of norepinephrine to maintain blood pressure or administration of inoptropes such as dopamine or dobutamine are recommended to improve tissue perfusion. High-dose intravenous epinephrine is required to reestablish cardiac function, followed by continuous infusion of norepinephrine in severe anaphylactic shock. Vasoconstrictors such as norepinephrine, vasopressin, or amaminone are administered to maintain vascular tone in shock caused by nerve damage or drug overdose.

Topics: Anaphylaxis; Brain Injuries; Cardiovascular Agents; Dopamine; Epinephrine; Humans; Norepinephrine; Sepsis; Shock; Spinal Cord Injuries; Vascular Resistance

Shock continues to be a challenge for health care professionals because shock is not a single pathologic process but a complex series of interrelated events. After respiratory failure, shock is the second most common cause of death in children. The etiology of shock can be classified into three major categories: hypovolemic, cardiogenic, and distributive shock (septic shock). Despite the etiology of the shock state, if left untreated, the overwhelming response of the body to the inadequate perfusion is death. The key to successful management and treatment of shock is early recognition and rapid intervention.

Topics: Cardiovascular Agents; Critical Care; Humans; Nursing Assessment; Pediatric Nursing; Shock

In Part II of this review, recent aspects in shock therapy are discussed. Treatment of an animal in a state of shock is not an easy task, it is time-consuming and expensive. The basic aims of shock therapy are to remove the inciting cause (wherever possible), to increase the circulating blood volume in order to stimulate the cardiac output and tissue perfusion (by infusion of fluids and eventually vasoactive substances), and to reduce or correct the injurious effects of shock (oxygenation, corticosteroids, antibiotics, energy or substrates, vasoactive substances, diuretics, regulation of the acid-base balance, stimulation of RES, and treatment of DIC).

Topics: Adrenal Cortex Hormones; Animals; Anti-Bacterial Agents; Blood Transfusion; Cardiovascular Agents; Combined Modality Therapy; Disseminated Intravascular Coagulation; Diuretics; Fluid Therapy; Hemostasis; Mononuclear Phagocyte System; Oxygen Inhalation Therapy; Plasma Substitutes; Shock

Topics: Acidosis; Adrenal Cortex Hormones; Arteriovenous Anastomosis; Blood Coagulation Disorders; Blood Transfusion; Cardiovascular Agents; Child; Child, Preschool; Hemodynamics; Hormones; Humans; Hypoxia; Infant; Infant, Newborn; Microcirculation; Receptors, Adrenergic; Shock; Shock, Hemorrhagic; Shock, Septic

Effective use of cardiovascular drugs in the management of circulatory shock requires knowledge of the pathophysiologic changes occurring in the different types and stages of shock and an understanding of the specific hemodynamic actions of drugs used to correct shock. Objectives of therapy are to: (1) restore circulating blood volume, (2) ensure of increase perfusion of critical organs by selectively reducing arteriolar resistance, (3) augment cardiac output, and (4) increase perfusion pressure. If blood volume is not restored, drugs may be ineffective and can even induce deleterious effects. If reflex sympathetic discharge has induced generalized vasoconstriction, it is irrational to expect beneficial results from administration of exogenous vasconstrictor agents. Instead, selective vasodilatation of vascular beds in critical tissues (eg, myocardium, intestines, and kidneys) accompanied by increased perfusion pressure and cardiac output can prove useful. Large doses of adrenocorticosteroids are used commonly in the therapy of different shock conditions, based primary on empiric tests of efficacy. Although such steroids may not influence the course of shock by direct cardiovascular effects, beneficial actions may result from mechanisms such as protection of cell membrane integrity and stabilization of lysosomes.

Topics: Adrenal Cortex Hormones; Adrenergic alpha-Antagonists; Animals; Cardiovascular Agents; Dopamine; Epinephrine; Isoproterenol; Norepinephrine; Receptors, Adrenergic, alpha; Shock

Topics: Cardiovascular Agents; Humans; Shock; Vasoplegia; Vitamin K; Vitamins

Topics: Cardiovascular Agents; Fluid Therapy; Humans; Shock

Topics: Cardiovascular Agents; Fluid Therapy; Humans; Shock

Topics: Cardiovascular Agents; Fluid Therapy; Humans; Shock

Topics: Cardiovascular Agents; Fluid Therapy; Humans; Shock

Topics: Cardiopulmonary Resuscitation; Cardiovascular Agents; Congresses as Topic; Electric Countershock; Heart Arrest; Humans; Shock; Treatment Outcome; Wounds and Injuries

Topics: Cardiovascular Agents; Fluid Therapy; Humans; Plasma Substitutes; Shock; Sympathomimetics

Topics: Analgesics; Antidotes; Cardiovascular Agents; Drug Therapy; Emergencies; Humans; Hypnotics and Sedatives; Internal Medicine; Respiratory Tract Diseases; Shock

Topics: Cardiovascular Agents; Dopamine; Education, Nursing, Continuing; Humans; Nitroprusside; Norepinephrine; Programmed Instructions as Topic; Shock

Topics: Cardiovascular Agents; Humans; Nitroprusside; Shock; Sympathomimetics

Topics: Animals; Cardiovascular Agents; Dog Diseases; Dogs; Emergencies; Heart Arrest; Heart Diseases; Heart Failure; Resuscitation; Shock

Topics: Adrenergic Antagonists; Blood Transfusion; Cardiovascular Agents; Dihydroergotoxine; Ergot Alkaloids; Female; Humans; Pregnancy; Pregnancy Complications; Shock

Topics: Blood Transfusion; Cardiovascular Agents; Dihydroergotoxine; Ergot Alkaloids; Humans; Oxytocics; Plasma Substitutes; Shock

Topics: Burns; Cardiovascular Agents; Flavones; Muscle Relaxants, Central; Shock

Topics: Cardiovascular Agents; Ergot Alkaloids; Female; Obstetric Labor Complications; Oxytocics; Pregnancy; Shock

Topics: Cardiovascular Agents; Epistaxis; Hexamethonium; Hypertension; Muscle Relaxants, Central; Shock

Topics: Cardiovascular Agents; Ergot Alkaloids; Female; Humans; Hysterotomy; Injections, Intravenous; Oxytocics; Pregnancy; Shock; Uterus

Topics: Cardiovascular Agents; Hypertension; Muscle Relaxants, Central; Shock; Sympatholytics