Healthy appearing patient with afib s/p ablation and returning for repeat ablation for recurrent afib. Anesthesia induced normally and patient VSS. 3 minutes after a request of a heparin bolus, patient dropped their SBP into the upper 40s, lower 50s. Patient recovered well after small bolus of epinephrine. ICE used to rule out pericardial effusion as well as confirm normal LVEF and RVEF.
What does an angiotensin receptor blocker (ARB) do?
Angiotensin II receptor blockers (ARBs) represent a newer class of effective and well tolerated antihypertensive agents 1. Several clinical studies have indicated the beneficial effects of ARBs in hypertensive patients such as reduction of left ventricular hypertrophy, decrease in ventricular arrhythmias, and improved diastolic function 1. Inhibitors of the renin-angiotensin system (RAS), either angiotensin converting enzyme (ACE) inhibitors or ARBs, mediate vasodilation and consequently decrease blood-pressure by different mechanisms 1. ARBs specifically inhibit angiotensin II from binding to its receptor, the Angiotensin-1 (AT 1) receptor on vascular smooth muscle cells. This blockade results in increased angiotensin II and normal bradykinin plasma levels. ARBs were developed to overcome several deficiencies of ACE inhibitors, which, by comparison, lead to decreased angiotensin II, but increased bradykinin levels. Hence, the key advantage of ARBs over ACE inhibitors is their lack of adverse effects related to bradykinin potentiation. ARBs have been shown to reduce morbidity and mortality associated with hypertension, and therefore, it is not surprising that an increasing number of patients scheduled for surgery are chronically treated with ARBs 2. However, RAS blockade increases the risk of severe hypotension during and after anesthetic induction. ACE-inhibitors are well known for inducing severe circulatory side effects during anesthesia, which led to the general recommendation to withhold the drug on the day of surgery 3.
Chronic AT 1 blockade also reduces the vasoconstrictor response to α 1 receptors activated by norepinephrine, which explains why ARB-induced hypotension can be so resistant to phenylephrine, ephedrine and norepinephrine 2, 8 Clinical studies have shown significant vasoconstrictor effects of vasopressin and increased cardiac filling during echocardiographic measurements 2.
Vasopressin or its synthetic analogues can restore the sympathetic response and may be useful pressors in cases of refractory hypotension during anaphylaxis 9 and septic shock 10 as well as in patients on RAS inhibitors, although norepinephrine has been reported to have a more favorable effect on splanchnic perfusion and oxygen delivery 11.
When conventional therapies such as: decreasing the anesthetic agent, volume expansion, phenylephrine, ephedrine, norepinephrine, and epinephrine are not effective, exogenous vasopressin may improve hypotension. To date, at least 5 clinical trials have demonstrated that patients on chronic ACEI/ARB undergoing general anesthesia, respond to exogenous vasopressin derivatives with an increase in blood pressure and fewer hypotensive episodes.6,7 Typically, a 0.5-1 unit bolus of AVP is administered to achieve a rise in mean arterial pressure.4 The subsequent recommended infusion dose is 0.03U/min for AVP and 1-2 mcg/kg/h for terlipressin. Caution should be used as V1 agonists have been associated with the following deleterious effects: reduction in cardiac output and systemic oxygen delivery, decreased platelet count, increased serum aminotransferases and bilirubin, hyponatremia, increased pulmonary vascular resistance, decrease in renal blood flow, increase in renal oxygen consumption, and splanchnic vasoconstriction.
Studies involving cardiac surgical patients suggest that MB treatment for patients with VS may reduce morbidity and mortality.5 It has also been suggested that the early use (preoperative use in patients at risk for VS) of MB in patients undergoing coronary artery bypass grafting may reduce the incidence of VS.5,9A bolus dose of 1-2mg/kg over 10-20 minutes followed by an infusion of 0.25mg/kg/hr for 48-72 hours is typically utilized in clinical practice and trials (with a maximum dose of 7 mg/kg).10 Side effects include cardiac arrhythmias (transient), coronary vasoconstriction, increased pulmonary vascular resistance, decreased cardiac output, and decreased renal and mesenteric blood flow.1 Both pulse and cerebral oximeter readings may not be reliable during MB administration due to wavelength interference.11,12 The use of MB is absolutely contraindicated in patients with severe renal impairment because it is primarily eliminated by the kidney.13 It may also cause methemoglobinemia and hemolysis.13 At high doses, neurotoxicity may occur secondary to the generation of oxygen free radicals. Neurologic dysfunction may be more severe in patients receiving serotoninergic agents such as: tramadol, ethanol, antidepressants, dopamine agonists and linezolid. Recommended doses for VS ranging from 1-3 mg/kg do not typically cause neurologic dysfunction.14 However, recent reports suggest that MB in doses even ≤ 1mg/kg in patients taking serotonin reuptake inhibitors (SSRIs) may lead to serotonin toxicity due to its monoamine oxidase (MAO) inhibitor property.15
VATs: Dilute liposomal bupivacaine (266 mg, 20 cc) mixed with 20 cc injectable saline. We use two syringes to save time (refill syringe between injections).
For planned thoracotomy, we add 60 cc injectable saline for wider injection.
The efficacy of this strategy requires attention to specific details, such as timing and technique of injection, dilution with saline, and injection of multiple interspaces (typically interspaces 3–10 when technically possible).
Inject EXPAREL slowly and deeply (generally 1-2 mL per injection) into soft tissues using a moving needle technique (ie, inject while withdrawing the needle)
Infiltrate above and below the fascia and into the subcutaneous tissue
Aspirate frequently to minimize the risk of intravascular injection
Use a 25-gauge or larger-bore needle to maintain the structural integrity of the liposomal particles
Inject frequently in small areas (1-1.5 cm apart) to ensure overlapping analgesic coverage
Patient safety is crucial for the delivery of effective, high-quality healthcare1 and is defined by the World Alliance for Patient Safety of WHO as ‘the reduction of risk of unnecessary harm associated with healthcare to an acceptable minimum’. The practice and delivery of healthcare is argued to be fundamentally and critically dependent on effective and efficient communication. Depending on physicians’ needs and responsibilities, handoff content will vary, requiring customization by individual physician groups; there is no “one size fits all” content.
0.2 mg/kg of methadone (based on ideal body weight, up to a maximal dose of 20 mg)250 mg of ketamine was added to the dextrose 5% in water bag (total volume 500 ml). 500 ml bags were connected to a pump that was programed to deliver an infusion of ketamine dosed at ideal body weight (or an equal volume of dextrose 5% in water) at a rate of 0.3 mg · kg−1 · h−1 from induction of anesthesia until surgical closure, at which time the infusion was decreased to 0.1 mg · kg−1 · h−1. The infusion was maintained at a rate of 0.1 mg · kg−1 · h−1 in the postanesthesia care unit (PACU) and for the next 48 postoperative hours. Dosing of ketamine was based on recommendations in the literature17,18 and from clinical experience at our institution.