Vasoplegia, or vasoplegic syndrome (VS), presents a well-recognized challenge in the perioperative environment. The literature generally describes vasoplegia, a form of vasodilatory shock, as low systemic vascular resistance (SVR) that manifests as severe hypotension in the presence of normal or supranormal cardiac output.1 There is no universal consensus, however, on a clinical definition.2 Typically, the definition includes (1) severe hypotension (Mean Arterial Pressure [MAP] < 50 mm Hg); (2) low SVR (SVR < 800 dyn*sec/cm5; SVRI < 1600 dyn*sec/cm5 *m2); (3) normal or high cardiac output (cardiac index [CI] > 2.2 L/min/ m2); and (4) the absence of an appropriate response to volume expansion and catecholamine therapy.2–5
Vasoplegia pathophysiology presents a complex phenomenon; fundamentally, however, vasoplegia manifests as a loss of vascular smooth muscle contraction.6,7 Perturbation of several intrinsic processes may contribute to the development of vasoplegia: nitric oxide, prostanoids, endothelin-1, hydrogen sulfide, and reactive oxygen species production.1 Typically, the influx of calcium into the cytoplasm through voltage-gated channels triggers the downstream effect of vasoconstriction. Dysregulation in this process, such as channel deactivation or prolonged activation, potentially contributes to the vasodilation seen in vasoplegia.6
Vasoplegia occurs in all shock states; it particularly appears in cardiogenic, hemorrhagic, septic, and anaphylactic shock. Vasoplegia also develops more generally during ischemia-reperfusion, such as in cardiac arrest or multiple trauma.8 It is a common complication of major cardiovascular surgery: vasoplegia affects 5% to 45% of all cardiopulmonary bypass procedures.6,9–11
The literature recognizes many risk factors associated with significantly increased incidence of vasoplegia. Blood transfusion, cardiopulmonary bypass, and organ transplantation raise a patient’s risk for vasoplegia, as do trauma, burns, and sepsis.2 Patients who use a cardiac ventricular assist device also appear prone to vasoplegia.2 Finally, numerous medications show an association with the syndrome, including amiodarone, protamine, heparin, aprotinin, metformin, and angiotensin-converting enzyme (ACE) inhibitors. 2 Many large cohort and case-control studies suggest that preoperative usage of ACE inhibitors can lead to peri- and postoperative vasoplegia.2,12–15
Generally, clinicians recognize vasoplegia by a persistent inability to maintain appropriate blood pressure without high-dose vasopressor drugs.6 Specifically, if a patient’s diastolic blood pressure drops, clinicians can assess the vasopressor dosage they need to administer to maintain appropriate MAP.8,16 A high-dose vasopressor often indicates vasoplegia, especially if the patient exhibits normal cardiac function.8 In addition, clinicians should identify the presence of hypotension, low SVR, and normal or high cardiac output, based on the definition above.6
Proper management of vasoplegia requires early recognition of the condition.6 Initially, treatment comprises volume replacement and the administration of traditional vasoconstrictors, such as phenylephrine.2 If unsuccessful, clinical recommendations are to restore hemodynamic parameters using catecholamine therapy.2 Clinicians, however, need to consider either the addition of or a switch to a non-catecholamine agent, if high-dose catecholamine therapy results in negative side effects or if the patient does not respond appropriately to the therapy.6,8 Recommendations suggest that clinicians use vasopressin as a first-line non-catecholamine agent, often together with catecholamines. If still unsuccessful, the literature recommends clinicians consider methylene blue, hydroxocobalamin, and angiotensin II.1
Vasoplegia resolves shortly after therapeutic intervention for most patients. Sometimes, however, severe hypotension lasts for a prolonged period of time. These cases are associated with increased morbidity and mortality.7 Norepinephrine- and catecholamine-resistant vasoplegia also exhibit poor prognoses.11 Catecholamine-resistant vasoplegia that lasts for more than 36 to 48 hours, in particular, has a mortality rate up to 25%.9 Furthermore, the literature also associates vasoplegia with the following: longer hospital and ICU stays, prolonged mechanical ventilation, and more sternal infections.18
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