The impact of catecholamines on skeletal muscle following massive burns: Friend or foe?

Profound skeletal muscle wasting in the setting of total body hypermetabolism is a defining characteristic of massive burns, compromising the patient's recovery and necessitating a protracted period of rehabilitation. In recent years, the prolonged use of the non-selective beta-blocker, propranolol, has gained prominence as an effective tool to assist with suppressing epinephrine-dependent burn-induced hypermetabolism and by extension, blunting muscle catabolism. However, synthetic ß-adrenergic agonists, such as clenbuterol, are widely associated with the promotion of muscle growth in both animals and humans. Moreover, experimental adrenodemedullation is known to result in muscle catabolism. Therefore, the blunting of muscle ß-adrenergic signaling via the use of propranolol would be expected to negatively impair muscle protein homeostasis. This review explores these paradoxical observations and identifies the manner by which propranolol is thought to exert its anti-catabolic effects in burn patients. Moreover, we identify potential avenues by which the use of beta-blocker therapy in the treatment of massive burns could potentially be further refined to promote the recovery of muscle mass in these critically ill patients while continuing to ameliorate total body hypermetabolism.

Angiotensin II and Vasopressin for Vasodilatory Shock: A Critical Appraisal of Catecholamine-Sparing Strategies.

Vasodilatory shock is a serious medical condition that increases the morbidity and mortality of perioperative and critically ill patients. Norepinephrine is an established first-line therapy for this condition, but at high doses, it may lead to diminishing returns. Oftentimes, secondary noncatecholamine agents are required in those whose hypotension persists. Angiotensin II and vasopressin are both noncatecholamine agents available for the treatment of hypotension in vasodilatory shock. They have distinct modes of action and unique pharmacologic properties when compared to norepinephrine. Angiotensin II and vasopressin have shown promise in certain subsets of the population, such as those with acute kidney injury, high Acute Physiology and Chronic Health Evaluation II scores, or those receiving cardiac surgery. Any benefit from these drugs must be weighed against the risks, as overall mortality has not been shown to decrease mortality in the general population. The aims of this narrative review are to provide insight into the historical use of noncatecholamine vasopressors and to compare and contrast their unique modes of action, physiologic rationale for administration, efficacy, and safety profiles.

Association between high dose catecholamine support and liver dysfunction following cardiac surgery.

BACKGROUND: Cardiac surgery using cardiopulmonary bypass is a well-established procedure. However, up to 20% to 30% of patients require high dose vasopressor or inotropic support following surgery, enhancing the risk of organ dysfunction and impacting mortality. Nonalcoholic fatty liver disease (NAFLD) is a frequent finding in these patients and may be involved in the pathophysiology of vasoplegia and cardiac failure. METHODS: Retrospective analysis of 463 patients undergoing elective cardiac surgery in 2014 at our institution. NAFLD was defined using the NAFLD fibrosis score and the vasoactive-inotropy score was used to determine postoperative vasopressor and inotropic dependency. RESULTS: Patients with NAFLD more often presented with high vasopressor or inotropic support compared to patients without NAFLD, resulting in significant differences after 6 hours (n = 20 [27.0%] of 74 patients), 12 hours (n = 20 [27.0%] of 74 patients), and on the first postoperative day (n = 12 [16.4%] of 73 patients) of intensive care unit (ICU) treatment. Multivariate analysis revealed time of catecholamine application (P = .001), preoperative left ventricular ejection fraction (P = .001), type of surgery (P = .001), model of endstage liver disease on hospital admission (P = .002), pre-existing pulmonary hypertension (P = .004) and NAFLD-time interaction (P = .05) as independent predictors of high vasopressor and inotropic support. Patients with NAFLD had higher degrees of extrahepatic organ dysfunction, were more dependent on hemodialysis, spent more days in the ICU and within the hospital. Patients with NAFLD and high catecholamine support had the highest mortality rates among the study population. CONCLUSIONS: NAFLD is a common finding in elective cardiac surgery patients. Anesthesiologists and intensivists should be sensitive for the specific risk profile of this population.

ST-Segment Elevation Myocardial Infarction Related to Potential Spontaneous Coronary Thrombosis in Pheochromocytoma Crisis.

Pheochromocytoma crisis is a rare and possibly fatal emergency. Hypersecreted catecholamines may result in myocardial injury via its direct toxic effect on cardiomyocytes or mediating vasoconstriction which will reduce coronary blood flow in this special setting. Interestingly, several case studies have reported the occurrence of ST-segment elevation myocardial infarction in patients with pheochromocytoma crisis. However, no one found the angiographic evidence of occlusive thrombus in the infarct-related coronary artery. Additionally, pheochromocytoma can induce hypercoagulability and promote thrombosis, but spontaneous coronary thrombosis has never been reported in this condition. Here, we report an unusual case of pheochromocytoma crisis presenting with STEMI due to spontaneous coronary thrombosis.

Recurrent Catecholamine-Induced Cardiomyopathy and Hypertensive Emergencies: A presentation of Pheochromocytoma and Related Concerns.

Catecholamine-induced cardiomyopathy (CIC) and pheochromocytoma are both rare entities, and their exact incidence and prevalence are unknown. Pheochromocytoma has been implicated as one of the causes of CIC or Takotsubo syndrome (TTS) by means of case reports and retrospective reviews. However, the evaluation of any patient with TTS and pheochromocytoma is often faced with multiple challenges due to its rarity and atypical presentations, which subsequently leads to delay in diagnosis. Here, we present a case of a 51-year old female who had three distinct episodes of TTS and now presented in a hypertensive emergency with angina, palpitations, headache, nausea, and vomiting. She was treated for non-ST elevation myocardial infarction (NSTEMI) but coronary angiogram revealed patent coronary arteries. Due to the paroxysmal nature of her hypertensive emergencies and variable blood pressure response, pheochromocytoma was suspected. On further evaluation, she was found to have elevated metanephrines and a 6.3 cm left adrenal mass on CT scan. This case emphasizes the importance of considering or identifying pheochromocytoma as an underlying primary etiology for recurrent episodes of TTS and related concerns such as choice of anti-hypertensive agents.

Clinical features, complications, and outcomes of exogenous and endogenous catecholamine-triggered Takotsubo syndrome: A systematic review and meta-analysis of 156 published cases.

Innumerable physical stress factors including externally administered catecholamines, and pheochromocytomas and paragangliomas (PPGLs) have been reported to trigger Takotsubo syndrome (TS). A systematic search of PubMed/MEDLINE identified 156 patients with catecholamine-induced TS up to December 2017. Data were compared within the catecholamine-induced TS cohort, but some comparisons were also done to a previously published large all-TS cohort (n = 1750). The mean age was 46.4 ± 16.4 years (72.3% women). The clinical presentation was dramatic with high complication rates in (68.2%, n = 103; multiple complications 34.6%, n = 54). The most common TS ballooning pattern was apical or mid-apical (45.2%, n = 69), followed by basal pattern (28.8%, n = 45), global pattern (16.0%, n = 25), mid-ventricular (8.3%, n = 13), focal (0.6%, n = 1), and unidentified pattern (1.9%, n = 3). There was an increase in the prevalence of apical sparing ballooning pattern compared to all-TS population (37.7% vs 18.3%, P < .00001). Higher complication rates were observed in TS with global ballooning pattern compared to apical ballooning pattern (23/25, 92% vs 38/65, 58.5%; P = .0022). Higher complication rates were observed in patients with age < 50 years than patients >50 years (73/92, 79.3% vs 29/56, 51.8%, P = 0.0009). Recurrence occurred exclusively in patients with PPGL-induced TS (18/107 patients, 16.8%). PPGL-induced TS was characterized by more global ballooning's pattern (22/104, 21.2% vs 3/49, 6.1%, P = 0.02), and lower left ventricular ejection fraction (25.54 ± 11.3 vs 31.82 ± 9.93, P = 0.0072) compared to exogenous catecholamine-induced TS. In conclusion, catecholamine-induced TS was characterized by a dramatic clinical presentation with extensive left ventricular dysfunction, and high complication rate.

A case of catecholamine-induced cardiomyopathy treated with extracorporeal membrane oxygenation.

A 55-year-old female patient was presented with severe dyspnea due to sudden onset of heart failure (ejection fraction (EF) <10%). Echocardiogram showed a takotsubo pattern with an akinetic apical segment. Coronary angiography did not reveal any obstructive disease. She became hypotensive which was refractory to conventional pressor agents. Catecholamine-induced cardiomyopathy was suspected after the CT scan of the abdomen showed a 4 cm necrotic right adrenal mass consistent with pheochromocytoma (PHEO). Venous arterial extracorporeal membrane oxygenation and α blockers were initiated. There was a rapid improvement in cardiac function with EF normalising in 1 week. Subsequently, ß-blockers were added and right adrenalectomy was done 3 weeks after the admission. She did extremely well after surgery with her blood pressure normalising without the need for antihypertensive therapy. Genetic evaluation revealed no pathogenic mutations implicated in the development of PHEO.

Treatments targeting inotropy.

Acute heart failure (HF) and in particular, cardiogenic shock are associated with high morbidity and mortality. A therapeutic dilemma is that the use of positive inotropic agents, such as catecholamines or phosphodiesterase-inhibitors, is associated with increased mortality. Newer drugs, such as levosimendan or omecamtiv mecarbil, target sarcomeres to improve systolic function putatively without elevating intracellular Ca2+. Although meta-analyses of smaller trials suggested that levosimendan is associated with a better outcome than dobutamine, larger comparative trials failed to confirm this observation. For omecamtiv mecarbil, Phase II clinical trials suggest a favourable haemodynamic profile in patients with acute and chronic HF, and a Phase III morbidity/mortality trial in patients with chronic HF has recently begun. Here, we review the pathophysiological basis of systolic dysfunction in patients with HF and the mechanisms through which different inotropic agents improve cardiac function. Since adenosine triphosphate and reactive oxygen species production in mitochondria are intimately linked to the processes of excitation-contraction coupling, we also discuss the impact of inotropic agents on mitochondrial bioenergetics and redox regulation. Therefore, this position paper should help identify novel targets for treatments that could not only safely improve systolic and diastolic function acutely, but potentially also myocardial structure and function over a longer-term.

The apelinergic system as an alternative to catecholamines in low-output septic shock.

Catecholamines, in concert with fluid resuscitation, have long been recommended in the management of septic shock. However, not all patients respond positively and controversy surrounding the efficacy-to-safety profile of catecholamines has emerged, trending toward decatecholaminization. Contextually, it is time to re-examine the "maintaining blood pressure" paradigm by identifying safer and life-saving alternatives. We put in perspective the emerging and growing knowledge on a promising alternative avenue: the apelinergic system. This target exhibits invaluable pleiotropic properties, including inodilator activity, cardio-renal protection, and control of fluid homeostasis. Taken together, its effects are expected to be greatly beneficial for patients in septic shock.

[Catecholamine-induced myocarditis in pheochromocytoma]. / Miocardite indotta da catecolamine in feocromocitoma.

Pheochromocytoma is a rare tumor, usually benign, potentially lethal in case of crisis with acute release of catecholamines. The heart is a target and the clinical presentation can mimic various cardiac conditions, thus rendering diagnosis elusive. Cardiac magnetic resonance is a valuable non-invasive diagnostic tool for the evaluation of cardiomyopathies; it allows the identification of catecholamine-induced myocarditis pattern and, in some cases, it can detect the primary tumor. The definitive treatment of pheochromocytoma is surgical, while the acute crisis may require mechanical support to circulation. We here report a case of pheochromocytoma in a 25-year-old man complicated by catecholamine-induced myocarditis and heart failure.

Catecholamine-Induced Chest Pain Mimicking Infarction Due to an MIBG-Negative and DOPA-Positive Succinate Dehydrogenase Syndrome Subunit B-Related Pheochromocytoma.

This 16-year-old boy presented with acute retrosternal pain possibly representing acute myocardial infarction. Cardiac enzymes were within reference ranges. There were marked increases in metanephrine to 3299 µg/24 h (reference, <400 µg/24 h), normetanephrine to 1309 µg/24 h (reference, 0-390 µg/24 h), and chromogranin A to 1605 ng/mL (reference, 0-150 µg/24 h). An incidental left adrenal mass was found during CTPA performed to exclude pulmonary embolism. I-MIBG scintigraphy was negative, and genetic screening detected SDHB (succinate dehydrogenase syndrome subunit B) gene mutation. Based on the gene mutation, F-DOPA PET/CT was performed, confirming a left-sided pheochromocytoma.

Endothelial Dysfunction in Resuscitated Cardiac Arrest (ENDO-RCA): safety and efficacy of low-dose prostacyclin administration and blood pressure target in addition to standard therapy, as compared to standard therapy alone, in post-cardiac arrest syndrome patients: study protocol for a randomized controlled trial.

BACKGROUND: Morbidity and mortality following initial survival of cardiac arrest remain high despite great efforts to improve resuscitation techniques and post-resuscitation care, in part due to the ischemia-reperfusion injury secondary to the restoration of the blood circulation. Patients resuscitated from cardiac arrest display evidence of endothelial injury and coagulopathy (hypocoagulability, hyperfibrinolysis), which in associated with poor outcome. Recent randomized controlled trials have revealed that treatment with infusion of prostacyclin reduces endothelial damage after major surgery and AMI. Thus, a study is pertinent to investigate if prostacyclin infusion as a therapeutic intervention reduces endothelial damage without compromising, or even improving, the hemostatic competence in resuscitated cardiac arrest patients. Post-cardiac arrest patients frequently have a need for vasopressor therapy (catecholamines) to achieve the guideline-supported blood pressure goals. To evaluate a possible catecholamine interaction with the primary endpoints of this study, included patients will be randomized into two different blood pressure goals within guideline-recommended targets. METHODS/DESIGN: A randomized, placebo-controlled, double-blind investigator-initiated pilot trial in 40 out-of-hospital-cardiac-arrest (OHCA) patients will be conducted. Patients will be randomly assigned to either the active treatment group (48 hours of active study drug (iloprost, 1 ng/kg/min) or to the control group [placebo (saline) infusion]. Target mean blood pressure levels will be allocated 1:1 to 65 mmHg or approximately 75 mmHg, which gives four different permutations, namely: (i) iloprost/65 mHg, (ii) iloprost/75 mmHg, (iii) placebo/65 mmHg, and (iv) placebo/75 mmHg. All randomized patients will be treated in accordance with state-of-the art therapy including targeted temperature management. The primary endpoint of this study is change in biomarkers indicative of endothelial activation and damage, [soluble thrombomodulin (sTM), sE-selectin, syndecan-1, soluble vascular endothelial growth factor (sVEGF), nucleosomes] and sympathoadrenal over activation (epinephrine/norepinephrine) from baseline to 48 hours post-randomization. The secondary endpoints of this trial will include: (1) the hemostatic profile [change in functional hemostatic blood test (thrombelastography (TEG) and whole blood platelet aggregometry (multiplate)) blood cell and endothelial cell-derived microparticles]; (2) feasibility of blood pressure target intervention (target 90 %); (3) interaction of primary endpoints and blood pressure target; (4) levels of neuron-specific enolase at 48 hours post-inclusion according to blood pressure targets. DISCUSSION: The ENDO-RCA study is a pilot study trial that investigates safety and efficacy of low-dose infusion of prostacyclin administration as compared to standard therapy in post-cardiac arrest syndrome patients. TRIAL REGISTRATION: Trial registration at ClinicalTrials.gov (identifier NCT02685618 ) on 18 February 2016.

Lesson of the month 2: Catecholamine-induced cardiomyopathy - pitfalls in diagnosis and medical management.

Cardiomyopathy as the initial presentation of phaeochromocytoma (PCA) is uncommon. Diagnostic work-up and perioperative management may be challenging within this context. We report three cases of PCA presenting with cardiomyopathy to illustrate the pitfalls in diagnosis and management. None of the patients had typical adrenergic symptoms and all three were established on beta-blockers prior to diagnosis. Their fractionated plasma catecholamine levels were elevated and the diagnosis of PCA was confirmed with various imaging modalities and post adrenalectomy. Interpretation of fractionated catecholamine levels in the context of established cardiomyopathy is difficult as cardiac failure of any aetiology generates an adrenergic response. Hence screening all patients with idiopathic cardiomyopathy is likely to generate a high false-positive rate. However, a high index of suspicion should prompt further diagnostic work-up in patients with idiopathic cardiomyopathy for occult PCAs. Peer-reviewed guidelines are required to guide the investigation and management of suspected catecholamine-induced cardiomyopathy.

Functional brown adipose tissue limits cardiomyocyte injury and adverse remodeling in catecholamine-induced cardiomyopathy.

Brown adipose tissue (BAT) has well recognized thermogenic properties mediated by uncoupling protein 1 (UCP1); more recently, BAT has been demonstrated to modulate cardiovascular risk factors. To investigate whether BAT also affects myocardial injury and remodeling, UCP1-deficient (UCP1(-/-)) mice, which have dysfunctional BAT, were subjected to catecholamine-induced cardiomyopathy. At baseline, there were no differences in echocardiographic parameters, plasma cardiac troponin I (cTnI) or myocardial fibrosis between wild-type (WT) and UCP1(-/-) mice. Isoproterenol infusion increased cTnI and myocardial fibrosis and induced left ventricular (LV) hypertrophy in both WT and UCP1(-/-) mice. UCP1(-/-) mice also demonstrated exaggerated myocardial injury, fibrosis, and adverse remodeling, as well as decreased survival. Transplantation of WT BAT to UCP1(-/-) mice prevented the isoproterenol-induced cTnI increase and improved survival, whereas UCP1(-/-) BAT transplanted to either UCP1(-/-) or WT mice had no effect on cTnI release. After 3 days of isoproterenol treatment, phosphorylated AKT and ERK were lower in the LV's of UCP1(-/-) mice than in those of WT mice. Activation of BAT was also noted in a model of chronic ischemic cardiomyopathy, and was correlated to LV dysfunction. Deficiency in UCP1, and accompanying BAT dysfunction, increases cardiomyocyte injury and adverse LV remodeling, and decreases survival in a mouse model of catecholamine-induced cardiomyopathy. Myocardial injury and decreased survival are rescued by transplantation of functional BAT to UCP1(-/-) mice, suggesting a systemic cardioprotective role of functional BAT. BAT is also activated in chronic ischemic cardiomyopathy.

Oclusión intestinal en una paciente portadora de un Feocromocitoma no diagnosticado. Manejo anestésico / Intestinal occlusion in a patient with an undiagnosed pheochromocytoma. Anesthetic management

El feocromocitoma es un tumor productor de catecolaminas que procede de las células cromafines del sistema nervioso simpático que puede causar hipertensión severa entre otros trastornos sistémicos. Pueden ser esporádicos o encontrarse asociados a varias enfermedades genéticas: neoplasia endocrina múltiple tipo 2, enfermedad de von Hippel-Lindau, neurofibromatosis de tipo 1 y paraganglioma familiar. Cuando un paciente en el que se sospecha la presencia de un feocromocitoma se presenta con una ugencia quirúrgica representa un gran desafío para el anestesiólogo, ya que en esta situación la mortalidad aumenta notablemente. Presentamos el caso de una paciente que resultó ser portadora de un feocromocitoma, integrando un síndrome MEN 2b con masas suprarrenales bilaterales que se presentó en la urgencia con una oclusión intestinal con una crisis hipertensiva severa con edema agudo de pulmón.

Pheochromocytoma is a tumor catecholamine-producing derived from chromaffin cells of the sympathetic nervous system that can cause severe hypertension among other systemic disorders. They may be sporadic or be associated with several genetic diseases: multiple endocrine neoplasia type 2, von Hippel-Lindau, neurofibromatosis type 1 and familial paraganglioma disease. When a patient who is suspected the presence of a pheochromocytoma presents with a surgical urgency represents a great challenge for the anesthesiologist, since in this situation the mortality increases significantly. We report the case of a patient who was found to be carrying a pheochromocytoma, integrating a MEN 2b syndrome with bilateral adrenal masses showed the urgency with bowel obstruction with severe hypertensive crisis with acute pulmonary edema.

Feocromocitoma é um tumor produtor de catecolamina derivada de células cromafins do sistema nervoso simpático que pode causar hipertensão grave entre outros distúrbios sistémicos. Eles podem ser esporádica ou estar associada a várias doenças genéticas: neoplasia endócrina múltipla tipo 2, von Hippel-Lindau, a neurofibromatose tipo 1 e doença paraganglioma familiar. Quando um paciente no qual a presença de um feocromocitoma suspeito apresenta-se com um ugencia cirúrgica representa um grande desafio para o anestesiologista, uma vez que nesta situação os mortalidade aumenta significativamente. Relatamos o caso de um paciente que foi encontrado carregando um feocromocitoma, integrando MEN 2b síndrome com massas adrenais bilaterais mostrou a urgência com obstrução intestinal com crise hipertensiva grave com edema pulmonar agudo.

A single pathophysiological pathway in Takotsubo cardiomyopathy: Catecholaminergic stress.

BACKGROUND: Takotsubo cardiomyopathy (TTC) continues to be under-diagnosed, due to its varying presentation, with potentially serious consequences if treatment is delayed. AIMS: To demonstrate the consistent involvement of catecholaminergic stress in TTC, regardless of the trigger. METHODS: Between 01 July 2009 and 31 August 2013, patients managed in our centre for thoracic pain syndrome, with or without troponin release, were followed up prospectively. TTC was diagnosed from the apical ballooning seen on left ventricular imaging (angiography or transthoracic echocardiography) in the absence of a significant coronary artery lesion. Triggers (emotional trauma, surgical stress and ß2-mimetic intoxication) were recorded; catecholamine-secreting tumours were screened for with a urinary methoxylate-derivative assay. RESULTS: TTC was diagnosed in 40 out of 2754 (1.5%) patients with thoracic pain syndrome, with or without troponin release. Triggers were emotional trauma (n=29, 72.5%), surgical stress (n=5, 12.5%), adrenergic intoxication (n=3, 7.5%) and catecholaminergic tumour (n=3, 7.5%). Mean left ventricular ejection fraction at admission was 38.0 ± 15.7%. Eight (20%) patients initially showed cardiogenic shock. In-hospital mortality was 7.5%, with no deaths from cardiogenic causes. Thirty-five (94.6%) of the survivors had recovered a normal left ventricular ejection fraction (> 55%) by discharge. CONCLUSION: Whatever the trigger, the common denominator in TTC is catecholaminergic stress. Classically suggested after emotional trauma, TTC may also be induced by surgical stress or endogenous or iatrogenic ß2-mimetic intoxication. The various contexts all have a similarly excellent cardiovascular prognosis if treated early.

[Anesthetic management for laparoscopic pheochromocytoma resection in a patient with cardiac dysfunction under dynamic monitoring].

A 51-year-old women with cardiac dysfunction due to catecholamine-induced cardiomyopathy underwent laparoscopic adrenalectomy for pheochromocytoma. Her preoperative cardiac status was New York Heart Association (NYHA) class IIand left ventricular ejection fraction (LVEF) was 45%. In her anesthetic management, we used FloTrac® system and monitored arterial pressure-based cardiac output (APCO) and stroke volume variation (SVV) continuously as the indicator of intraoperative hemodynamics. Although her hemodynamics fluctuated highly during manipulation of the tumor and after ligation of adrenal vein intraoperatively, we could manage them rapidly by adjusting administration of vasodilator or pressor agents and appropriate volume expansion under monitoring APCO and SVV. The operation was completed successfully and postoperative course was almost uneventful. As laparoscopic pheochromocytoma resection is accomplished in a brief period with less surgical invasion compared with laparotomy, it may be possible to manage hemodynamics of the patient with cardiac dysfunction properly under dynamic monitoring using FloTrac® system.

Intravenous arginine vasopressin infusion in refractory vasodilatory shock: a clinical study.

OBJECTIVE: To assess the efficacy of arginine vasopressin (AVP) as a rescue therapy in children with catecholamine refractory vasodilatory shock and its effect on various hemodynamic, clinical, and laboratory variables. METHODS: This prospective hospital based study was conducted from January 2008 through July 2008 at a tertiary pediatric cardiac critical care unit. Twelve post cardiac surgery patients with advanced vasodilatory shock requiring intravenous vasopressin infusion longer than 60 min were included and continuous vasopressin infusion was given. The primary outcome measures were restoration of Mean arterial blood pressure (MAP) after starting AVP infusion and decrease in other concurrent catecholamines requirement. The secondary outcome measures were survival to hospital discharge, adverse effects, and laboratory variables. RESULTS: Vasopressin was infused in the dose range of 0.0005 to 0.003 units/kg/min for a mean duration of 55.6 h. MAP improved from 41.08 ± 6.15 mmHg at baseline to 48.92 ± 10.05 mmHg after 1 h (P < 0.05), to 57.01 ± 8.30 mmHg after 4 h of AVP infusion (P < 0.001), and to 62.33 ± 8.55 mmHg after 12 h (P < 0.001), which further increased to 71.75 ± 9.55 mmHg after 24 h (P < 0.001). Inotrope score and requirement of other concurrent inotropes declined significantly in all patients after starting AVP infusion (P < 0.001). Lactate levels also declined significantly (P < 0.0001). No significant adverse effect due to end organ ischemia was observed. Only one patient expired while on vasopressin infusion due to refractory hypotension. CONCLUSIONS: Concurrent addition of vasopressin at an appropriate stage help improving MAP significantly with decreased dependence on high dose catecholamines without any significant adverse effects.