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      Push-dose pressors for immediate blood pressure control

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      Clinical and Experimental Emergency Medicine
      The Korean Society of Emergency Medicine

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          Abstract

          INTRODUCTION When a patient’s blood pressure drops to critical levels, dysrhythmia and cardiac arrest ensue. While this level is patient dependent, Brunauer et al. [1] have identified a mean arterial pressure of 45 mmHg to be a critically low blood pressure associated with hemodynamic collapse. When a patient is moving towards this blood pressure, whether due to their disease state or iatrogenic factors, we must act immediately. Fluids, even when infused under pressure, take time to exert a significant effect. Vasopressor infusions require mixing, pump set-up, and available nursing staff. For decades in the operating room, bolus administration of intravenous vasopressors and inotropes have been used by anesthesiologists to temporize blood pressure. However, this technique has not penetrated into standard emergency medicine or intensive care practice. These ‘push-dose pressors’ are the perfect solution to short-lived hypotension, e.g., post intubation or during procedural sedation. They also can act as a bridge to infusion vasopressors, while the latter are being mixed or while a central line is being placed [2]. The standard push-dose pressors in the anesthesia armamentarium are phenylephrine and ephedrine. While phenylephrine is a useful drug for the emergency department because of its short half-life and easy dosing, ephedrine may not be ideal. Ephedrine has a long half-life and when misdosed, has been associated with cardiac complications. Instead, epinephrine may be the ideal second push-dose pressor for the emergency department and intensive care unit. Phenylephrine is a pure vasoconstrictor, so its use makes sense in tachycardic patients, because it will not increase the heart rate and may even decrease it by reflex parasympathetic response. Epinephrine is an inopressor; in addition to vasoconstriction, it will increase heart rate and inotropy. SAFETY Both drugs are safe to use in peripheral lines. Phenylephrine is approved for use intramuscularly or subcutaneously, so obviously extravasation from an intravenous line should not be concerning. The epinephrine concentration we use for push-dosing is the same as that contained in lidocaine with epinephrine (1:100,000). So, unless your intravenous line is located in those rare areas where local anesthetics with epinephrine may be a problem (i.e., tip of nose, penis, toes), there are no extravasation worries. PHENYLEPHRINE DOSING AND USE As mentioned above, phenylephrine is a pure alpha agent, so there is no intrinsic inotropy, but the increase in heart perfusion from normalizing the mean arterial pressure can improve cardiac output. The onset of effects is seen in <1 minute and while the duration of a single dose may last 20 minutes, in almost all cases the effects are gone within five minutes. Mixing instructions: Take a 3 mL syringe and draw up 1 mL of phenylephrine from the vial of phenylephrine 10 mg/mL. Inject this into a 100 mL bag of normal saline. Now you have 100 mL of phenylephrine with a concentration of 100 mcg/mL. Draw up some into a syringe; each milliliter in the syringe is 100 mcg. Label the syringe. Dose: 0.5–2 mL (50–200 mcg) every 1–5 minutes. Phenylephrine is also available commercially in premixed syringes. This may represent the only reason to use push-dose phenylephrine in preference to epinephrine. EPINEPHRINE DOSING AND USE Epinephrine has alpha 1 and 2 and beta 1 and 2 effects, so it is an inopressor. The onset of effects are seen in <1 minute and while the duration of a single dose may last 10 minutes, in almost all cases the effects are gone within five minutes. Mixing instructions: Take a 10 mL syringe filled with 9 mL of normal saline. If premade saline syringes are available, eject 1 mL of saline from the 10 mL saline syringe. Into this syringe, draw up 1 mL of epinephrine from the cardiac epinephrine amp (cardiac amp contains 10 mL of epinephrine concentration 100 mcg/mL or 1:10,000). Shake well. Now you have 10 mL of epinephrine 10 mcg/mL (1:100,000). Label the syringe. Dose: 0.5–2 mL (5–20 mcg) every 1–5 minutes. When faced with a crashing patient with hypotension, some may choose to avoid mixing and simply administer a full amp (1 mg) of cardiac epinephrine. Choosing this strategy can result in malignant hypertension, dysrhythmia, and cardiac arrest [3]. Do not give cardiac arrest doses (1 mg) to patients with a pulse. If due to expediency, mixing must be avoided, give 0.5 mL of the cardiac epinephrine. This amount is easily seen on the gradations of a cardiac epinephrine syringe. While the delivered dose (50 mcg) is still higher than ideal, it is far safer than administration of the entire amp. Given the time of mixing push-dose concentrations is less than 10 seconds, the far safer course is to simply avoid pushing any epinephrine directly from a cardiac amp. CONCLUSION Push-dose pressors have been used for decades in the operating room. The translation of this technique to the emergency department or intensive care unit is logical and useful. If only one push-dose pressor is to be used, epinephrine should be the choice. While literature to support the use of push-dose pressors outside of the operating room is only now emerging, its use in temporizing critically low blood pressures can be life-saving.

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          Epinephrine in anaphylaxis: higher risk of cardiovascular complications and overdose after administration of intravenous bolus epinephrine compared with intramuscular epinephrine.

          Epinephrine is the drug of choice for the management of anaphylaxis, and fatal anaphylaxis is associated with delayed epinephrine administration. Data on adverse cardiovascular (CV) complications and epinephrine overdose are limited.
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            The arterial blood pressure associated with terminal cardiovascular collapse in critically ill patients: a retrospective cohort study

            Introduction Liberal and overaggressive use of vasopressors during the initial period of shock resuscitation may compromise organ perfusion and worsen outcome. When transiently applying the concept of permissive hypotension, it would be helpful to know at which arterial blood pressure terminal cardiovascular collapse occurs. Methods In this retrospective cohort study, we aimed to identify the arterial blood pressure associated with terminal cardiovascular collapse in 140 patients who died in the intensive care unit while being invasively monitored. Demographic data, co-morbid conditions and clinical data at admission and during the 24 hours before and at the time of terminal cardiovascular collapse were collected. The systolic, mean and diastolic arterial blood pressures immediately before terminal cardiovascular collapse were documented. Terminal cardiovascular collapse was defined as an abrupt ( 50% compared to preceding values) followed by cardiac arrest. Results The mean ± standard deviation (SD) values of the systolic, mean and diastolic arterial blood pressures associated with terminal cardiovascular collapse were 47 ± 12 mmHg, 35 ± 11 mmHg and 29 ± 9 mmHg, respectively. Patients with congestive heart failure (39 ± 13 mmHg versus 34 ± 10 mmHg; P = 0.04), left main stem stenosis (39 ± 11 mmHg versus 34 ± 11 mmHg; P = 0.03) or acute right heart failure (39 ± 13 mmHg versus 34 ± 10 mmHg; P = 0.03) had higher arterial blood pressures than patients without these risk factors. Patients with severe valvular aortic stenosis had the highest arterial blood pressures associated with terminal cardiovascular collapse (systolic, 60 ± 20 mmHg; mean, 46 ± 12 mmHg; diastolic, 36 ± 10 mmHg), but this difference was not significant. Patients with sepsis and patients exposed to sedatives or opioids during the terminal phase exhibited lower arterial blood pressures than patients without sepsis or administration of such drugs. Conclusions The arterial blood pressure associated with terminal cardiovascular collapse in critically ill patients was very low and varied with individual co-morbid conditions (for example, congestive heart failure, left main stem stenosis, severe valvular aortic stenosis, acute right heart failure), drug exposure (for example, sedatives or opioids) and the type of acute illness (for example, sepsis). Electronic supplementary material The online version of this article (doi:10.1186/s13054-014-0719-2) contains supplementary material, which is available to authorized users.
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              Upstairs care downstairs: delayed sequence intubation (DSI) [Internet]

              S Weingart (2010)
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                Author and article information

                Journal
                Clin Exp Emerg Med
                Clin Exp Emerg Med
                CEEM
                Clinical and Experimental Emergency Medicine
                The Korean Society of Emergency Medicine
                2383-4625
                June 2015
                30 June 2015
                : 2
                : 2
                : 131-132
                Affiliations
                Critical Care Corner Section Editor
                Author notes
                Correspondence to: Scott Weingart  Stony Brook Medicine, 101 Nicolls Rd, Stony Brook, NY 11794, USA  E-mail: scott.weingart@ 123456stonybrookmedicine.edu
                Article
                ceem-15-010
                10.15441/ceem.15.010
                5052865
                27752585
                583f4459-0371-42ca-b1e4-a8fdad3fcf2e
                © 2015 The Korean Society of Emergency Medicine

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 17 February 2015
                : 1 March 2015
                : 1 March 2015
                Categories
                Critical Care Corner

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