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The society for angiography and cardiovascular interventions (SCAI) staging of cardiogenic shock. Adapted with permission from Baran et al. 35 Abbreviations: CPR, cardiopulmonary resuscitation; CVP, central venous pressure; ECMO, extra corporeal membrane oxygenation; JVP, jugular venous pulsations; LFTs, liver function test; MAP, mean arterial blood pressure; PA Sat, pulmonary artery saturation; PCWP, pulmonary capillary wedge pressure; PEA, pulseless electrical activity; SBP, systolic blood pressure.
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This is a focused review looking at the pharmacological support in cardiogenic shock. There are a plethora of data evaluating vasopressors and inotropes in septic shock, but the data are limited for cardiogenic shock. This review article describes in detail the pathophysiology of cardiogenic shock, the mechanism of action of different vasopressors...
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![Fig. 1 Mortality risk by SCAI stages [54]. *Unadjusted mortality risk...](publication/362541181/figure/fig1/AS:11431281079996048@1660968520549/Mortality-risk-by-SCAI-stages-54-Unadjusted-mortality-risk-by-SCAI-stage-at-ICU_Q320.jpg)
Cardiogenic shock (CS) remains a leading cause of morbidity and mortality among patients with cardiovascular disease. In the past, acute myocardial infarction was the leading cause of CS. However, in recent years, other etiologies, such as decompensated chronic heart failure, arrhythmia, valvular disease, and post-cardiotomy, each with distinct hem...
Citations
... 8 Cardiogenic shock defined as patients with blood pressure less than 90mmHg supported by clinical features. 9 Hypertension defined as patients on antihypertensive medication, previously diagnosed or recently diagnosed with two average measurement systolic blood pressure more than 130 mmHg and or diastolic blood pressure more than 80mmHg. 10 Diabetes mellitus diagnosed as patients on treatment or presented with clinical symptoms and two sample fasting blood sugar more than 126mg/dl or two sample RBS more than 200mg/dl with or without HBA1C more than 6.5%. ...
Background and Objectives: Studies evaluating gender differences and outcomes in heart failure with reduced ejection fraction are limited in Iraq. The aim of this study was to assess the clinical characteristics, risk factors, outcomes and severity of heart failure with reduced ejection fraction in both genders. Patients and Methods: This is a prospective cohort study of 117 patients aged more than 18 years who had been admitted to the Hawler Cardiac Center or medical ward with heart failure with reduced ejection fraction for the period from December 2021 till 30th of October 2022. The clinical characteristics, severity of left ventricular systolic dysfunction and the outcomes over three months were compared between women and men. Results: One hundred seventeen patients were included in the study, 61 (52.1%) patients were male and 56 (47.9%) were female with male to female ration (1.09:1), p-value (0.017). Women presented with higher incidence of moderate left ventricular systolic dysfunction 36(64.2%), obesity 43 (76.8%) p-value=0.017*, dyslipidemia 27 (48.2%) p-value=0.038, pulmonary hypertension 4 (7.1%), atrial fibrillation 15(26.8%) and high cardiac hospitalization 12 (21.4%), while men have high incidence severe left ventricular systolic dysfunction 33(54.1% ) p-value=0.046, smoking 42 (68.9%); p-value <0.001 and ST-segment elevation myocardial infarction 28 (45.9%) p-value <0.001. the p-values off all above findings are less than <0.05 respectively Conclusions: There are major differences in risk factors, clinical presentation and outcomes between both genders. The majority of women presented with moderate left ventricular systolic dysfunction and higher rate of cardiac hospitalization while men presented with severe left systolic dysfunction associated with high incidence of ST-elevation myocardial infarction.
... The other main category of therapy used to increase blood pressure is vasopressors. These are typically recommended when fluid resuscitation fails to meet MAP goals, in some cases of severe hypotension, and for hypotension due to causes other than hypovolemia [23,59,60]. The relationship between fluids and vasopressors is particularly important in AKI in the setting of vasomotor shock, as kidney function can only improve by way of vasopressors once intravascular volume has been restored [61]. ...
Acute kidney injury (AKI) is a complex and life-threatening condition with multifactorial etiologies, ranging from ischemic injury to nephrotoxic exposures. Management is founded on treating the underlying cause of AKI, but supportive care—via fluid management, vasopressor therapy, kidney replacement therapy (KRT), and more—is also crucial. Blood pressure targets are often higher in AKI, and these can be achieved with fluids and vasopressors, some of which may be more kidney-protective than others. Initiation of KRT is controversial, and studies have not consistently demonstrated any benefit to early start dialysis. There are no targeted pharmacotherapies for AKI itself, but some do exist for complications of AKI; additionally, medications become a key aspect of AKI management because changes in renal function and dialysis support can lead to issues with both toxicities and underdosing. This review will cover existing literature on these and other aspects of AKI treatment. Additionally, this review aims to identify gaps and challenges and to offer recommendations for future research and clinical practice.
... Hemodynamic disturbances (change in blood pressure and/or heart rate) are often present during cardiac surgery and can be caused by underlying medication, cardiovascular pathology and impact of the ongoing surgery itself. Cardiac anaesthetists, on the other hand, are skilled and proactive in management of hemodynamic deter-minants with powerful vasoactive and inotropic drugs when having the objective of maintaining perfusion pressure within the desired range [37][38][39]. ...
Objective monitoring of per-operative nociception remains an unanswered challenge. Anaesthetists still mostly rely on signs of activation of the sympathetic nervous system, e.g., an increase in heart rate and blood pressure. These signs can be often blurred in cardiac surgery because of medication influencing heart rate and blood pressure or by severe hemodynamic disturbances. Such conditions create the potential for incompletely checked nociception which can lead to unrecognised "under the surface" stress reaction. We decided to investigate whether patients undergoing cardiac surgery maintained at the same level of monitored depth of anaesthesia would express differences in plasmatic level of stress hormone cortisol when given a different dose of opioid sufentanil. Nineteen patients undergoing elective cardiac surgery were included in our prospective randomised trial. All patients were anaesthetised by a standardised protocol (using midazolam, propofol, sevoflurane, sufentanil and rocuronium) and were maintained within the same range of anaesthetic depth monitored by monitor Conox (qCON 30-50). Patients were randomised in two groups. Group LS (lower sufentanil), n = 9, recieved TCI (target controlled infusion) sufentanil in dose of 0.25 ng/mL, group HS (higher sufentanil), n = 10, in dose of 0.75 ng/mL. 15 minutes after sternotomy we took blood samples for analysis of plasmatic levels of cortisol. Group LS had significantly higher plasmatic cortisol levels, median 700 nm/L, than HS, median 328 nm/L (p = 0.006). We conclude that a lower dose of sufentanil was associated with higher plasmatic level of cortisol and thus more significant activation of hypothalamic-pituitary-adrenal axis stress response. We emphasise that activation of stress response can be underestimated during cardiac surgery. Our result supports the need for developing an objective monitoring method of per-operative nociception.
... Furthermore, CS may be associated with systemic compensatory vasoconstriction secondary to a low cardiac output [26]. Noradrenaline, a potent vasoconstrictor, infused during states of high vascular resistance may potentially induce an exaggerated increase in vascular constriction, leading to peripheral ischemia [10,36,37], especially at high doses [33,38]. In our analysis, the delivery of noradrenaline at conventional doses via a PVC was not associated with an increased risk of side effects. ...
Background:
Vasopressors are frequently utilized for blood pressure stabilization in patients with cardiogenic shock (CS), although with a questionable benefit. Obtaining central venous access is time consuming and may be associated with serious complications. Hence, we thought to evaluate whether the administration of vasopressors through a peripheral venous catheter (PVC) is a safe and effective alternative for the management of patients with CS presenting to the intensive cardiovascular care unit (ICCU).
Methods:
A prospective single-center study was conducted to compare the safety and outcomes of vasopressors administered via a PVC vs. a central venous catheter (CVC) in patients presenting with CS over a 12-month period.
Results:
A total of 1100 patients were included; of them, 139 (12.6%) required a vasopressor treatment due to shock, with 108 (78%) treated via a PVC and 31 (22%) treated via a CVC according to the discretion of the treating physician. The duration of the vasopressor administration was shorter in the PVC group compared with the CVC group (2.5 days vs. 4.2 days, respectively, p < 0.05). Phlebitis and the extravasation of vasopressors occurred at similar rates in the PVC and CVC groups (5.7% vs. 3.3%, respectively, p = 0.33; 0.9% vs. 3.3%, respectively, p = 0.17). Nevertheless, the bleeding rate was higher in the CVC group compared with the PVC group (3% vs. 0%, p = 0.03).
Conclusions:
The administration of vasopressor infusions via PVC for the management of patients with CS is feasible and safe in patients with cardiogenic shock. Further studies are needed to establish this method of treatment.
... According to the 'Surviving Sepsis International Guidelines', norepinephrine is strongly recommended as the first-line drug for treating vasodilatory shock through its α 1 and β 1 adrenergic actions that help to improve BP and CO [49]. In recent times, norepinephrine has been regarded as the most common first-line vasopressor for small animals to treat vasodilatory hypotension in emergency and critical care medicine [50]. Norepinephrine is a sympathomimetic amine derived from tyrosine and is structurally similar to epinephrine, although it lacks a methyl group on its nitrogen atom. ...
... This chemical difference is attributed to its primary α 1 , α 2 , and β 1 adrenergic agonism. When compared to epinephrine, norepinephrine-associated peripheral vasoconstriction and venoconstriction in the venous beds (except the coronary vasculature) are more intense, while the β 1 activity is milder [20,50]. Increases in heart rate and myocardial contractility may be observed with β 1 agonism, but baroreceptor-reflex-mediated bradycardia is usually more common in response to α 1 -and α 2 -mediated vasoconstriction [20,43]. ...
... In vitro studies have suggested that arginine vasopressin may have higher vasoconstricting properties than norepinephrine, phenylephrine, and even angiotensin II. Exogenous or synthetic vasopressin is commonly recommended intravenously during cardiopulmonary resuscitation to aid in the return of spontaneous circulation or to treat vasodilatory and hemorrhagic shock [50,51,54]. Vasopressin is the most common second-choice vasopressor for cats and dogs in intensive care units for the treatment of vasodilatory shock [50]. ...
Isoflurane is a commonly used inhalation anesthetic in species undergoing veterinary care that induces hypotension, impacting organ perfusion, making it imperative to minimize its occurrence or identify effective strategies for treating it. This study evaluated and compared the hemodynamic effects of DOB, NEP, VAS, and HES in twelve isoflurane-anesthetized Beagle dogs. The order of the first three treatments was randomized. HES was administered last. Data were collected before treatments (baseline) and after 10 min of a sustained MAP of <45 mmHg induced by a high end-tidal isoflurane concentration (T0). Once treatment was initiated and the target MAP was achieved (65 to 80 mmHg) or the maximum dose reached, data were collected after 15 min of stabilization (T1) and 15 min after (T2). A 15 min washout period with a MAP of ≥65 mmHg was allowed between treatments. The intravenous dosage regimens started and were increased by 50% every five minutes until the target MAP or maximum dose was reached. The dosages were as follows: DOB, 5–15 μg/kg/min; NEP, 0.1–2 μg/kg/min; VAS, 0.5–5 mU/kg/min; and HET, 6% 1–20 mL/kg/min. DOB improved CO, DO2, and VO2, but reduced SVR. VAS elevated SVR, but decreased CO, DO2, and VO2. HES minimally changed BP and mildly augmented CO, DO2, and VO2. These treatments failed to reach the target MAP. NEP increased the arterial BP, CO, MPAP, and PAWP, but reduced HR. Norepinephrine infusion at 0.44 ± 0.19 μg/kg/min was the most efficient therapy for correcting isoflurane-induced hypotension.
... Furthermore, it reduces the risk of large vessel injury that can lead to bleeding whenever thrombolytics are being used (26). Norepinephrine (NE) is an alpha-adrenergic and beta-adrenergic drug that improves systemic pressure with a modest effect on inotropy and is also the vasopressor of choice in cardiogenic shock (24,27). Though no direct clinical data are available on the effects of this drug in patients with PE (7), NE is currently recommended as the first-line vasopressor for patients with PE, at a dose of 0.2-1.0 ...
Pulmonary embolism is a common and potentially fatal disease, with a significant burden on health and survival. Right ventricular dysfunction and hemodynamic instability are considered two key determinants of mortality in pulmonary embolism, which can reach up to 65% in severe cases. Therefore, timely diagnosis and management are of paramount importance to ensure the best quality of care. However, hemodynamic and respiratory support, both major constituents of management in pulmonary embolism, associated with cardiogenic shock or cardiac arrest, have been given little attention in recent years, in favor of other novel advances such as systemic thrombolysis or direct oral anticoagulants. Moreover, it has been implied that current recommendations regarding this supportive care lack enough robustness, further complicating the problem. In this review, we critically discuss and summarize the current literature concerning the hemodynamic and respiratory support in pulmonary embolism, including fluid therapy, diuretics, pharmacological support with vasopressors, inotropes and vasodilators, oxygen therapy and ventilation, and mechanical circulatory support with veno-arterial extracorporeal membrane oxygenation and right ventricular assist devices, while also providing some insights into contemporary research gaps.
... Despite being a staple of the pharmacologic therapy of cardiogenic shock, research studies on vasopressors and inotropes are quite few. 10 Patients with severe heart failure are the most difficult to treat of all patient groups who need inotropic treatment. In most circumstances, inotropes are only appropriate as a temporary treatment to keep patients stable until more permanent, frequently surgical, procedures may be planned. ...
Vasopressors and inotropes are often administered to critically ill patients in intensive care unit for the management and treatment of haemodynamic impairment, heart failure, septic and cardiogenic shock, trauma among certain other diseases. In patients with shock, vasopressors and inotropes are used to induce vasoconstriction or enhance cardiac contractility. Vasopressors induces vasoconstriction, which causes systemic vascular resistance, leading to increase in mean arterial pressure and elevates organ perfusion. While inotropes raise cardiac output, which helps maintain mean arterial pressure and body perfusion. Due to a decreased risk of side effects compared to other catecholamine vasopressors, norepinephrine is considered a first-line vasopressor titrated to attain an optimal arterial pressure. An inotrope such as dobutamine may be given to raise cardiac output to a sufficient level to fulfil tissue demand if tissue and organ perfusion still is not enough. Due to their strengthening effect on cardiac contractility, inotropes have been utilized in the care of patients with heart failure for decades, particularly for patients with systolic dysfunction, or heart failure with reduced ejection fraction. Along with their beneficial inotropic impact, they also have chronotropic and peripheral vascular effects. For patients with severely reduced cardiac output and peripheral organ hypoperfusion, they are most frequently employed in intensive care unit. Along with their benefits they are also associated with certain considerate side-effects. The purpose of this research is to review the available information about role of inotropes and vasopressors therapy in the intensive care unit.
... Milrinone is a phosphodiesterase 3 inhibitor, simulating the stimulation of β1 and β2 receptors [28]. The properties that make this agent stand out from other inotropic agents are its ability to increase ...
Cardiovascular diseases remain the leading cause of death globally, with acute myocardial infarction being one of the most frequent. One of the complications that can occur after a myocardial infarction is cardiogenic shock. At present, the evidence on the use of inotropic agents for the management of this complication is scarce, and only a few trials have evaluated the efficacy-adverse effects relationship of some agents. Milrinone and Dobutamine are some of the most frequently mentioned drugs that have been studied recently. However, there are still no data that affirm with certainty the supremacy of one over the other. The aim of this review is to synthesize evidence on basic and practical aspects of these agents, allowing us to conclude which might be more useful in current clinical practice, based on the emerging literature.
Cardiogenic shock (CS) is a complex and dreadful condition for which effective treatments remain unclear. The concerningly high mortality rate of CS emphasizes a need for developing effective therapies to reduce its mortality and reverse its detrimental course. This article aims to provide an updated and evidence-based review of the pathophysiology of CS and the related pharmacotherapeutics with a special focus on vasoactive and inotropic agents.
