Vasopressin and ACLS

[MS Medic]

I know vasopressin is an anti-diuretic hormone secreted by the pituitary gland. I know that v1 and v2 receptors decrease diuresis and cause vasoconstriction increasing arterial pressure, the second mimicking alpha adrenergic properties, but to my knowledge it does not simulate beta1 receptors on the heart in any way. How is it considered an acceptable substitute for epi in a cardiac arrest.

[chbare]

It looks as though vasopressin may cause cerebral vessel dilation and theoretically increase cerebral perfusion. Regarding the beta 1 stimulation: we do not give epinephrine based on beta 1 effects. Epinephrine's primary theoretical action is vasoconstriction and shunting of blood volume. In fact, beta 1 effects may theoretically increase post arrest myocardial oxygen consumption and post arrest arrhythmias. Therefore, in theory, vasopressin's lack of beta effects creates a better profile.

Note my extensive use of the word theoretical. This is because studies are all over the place. However, in human patients, survival to discharge does not seem to change with either agent.

Take care,

chbare.

[mobey]

I am sure you meant to include it in the OP, but it should be re-established that Vasopressin (AdH, Pitressin) is a single use drug in cardiac arrest, replacing either the first OR second dose of epi.

[Jwade]

Vasopressin

Vasopressin is a nonadrenergic peripheral vasoconstrictor that also causes coronary and renal vasoconstriction.58,59 Despite 1 promising randomized study (LOE 2),60 additional lower-level studies (LOE 5),61–63 and multiple well-performed animal studies, 2 large randomized controlled human trials (LOE 1)64,65 failed to show an increase in rates of ROSC or survival when vasopressin (40 U, with the dose repeated in 1 study) was compared with epinephrine (1 mg, repeated) as the initial vasopressor for treatment of cardiac arrest. In the large multicenter trial involving 1186 out-of-hospital cardiac arrests with all rhythms (LOE 1),65 a post-hoc analysis of the subset of patients with asystole showed significant improvement in survival to hospital discharge but not neurologically intact survival when 40 U (repeated once if necessary) of vasopressin was used as the initial vasopressor compared with epinephrine (1 mg, repeated if necessary).

A meta-analysis of 5 randomized trials (LOE 1)66 showed no statistically significant differences between vasopressin and epinephrine for ROSC, 24-hour survival, or survival to hospital discharge. The subgroup analysis based on initial cardiac rhythm did not show any statistically significant difference in survival to hospital discharge (LOE 1).66

In a large in-hospital study of cardiac arrest, 200 patients were randomly assigned to receive either 1 mg of epinephrine (initial rhythm: 16% VF, 3% VT, 54% PEA, 27% asystole) or 40 U of vasopressin (initial rhythm: 20% VF, 3% VT, 41% PEA, 34% asystole). There was no difference in survival to 1 hour (epinephrine: 35%, vasopressin: 39%) or to hospital discharge (epinephrine: 14%, vasopressin: 12%) between groups or subgroups.64

A retrospective analysis documented the effects of epinephrine alone (231 patients) compared with a combination of vasopressin and epinephrine (37 patients) in out-of-hospital cardiac arrest with VF/VT, PEA, or asystole. There was no difference in survival or ROSC when VF or PEA was the presenting rhythm, but ROSC was increased in the epinephrine plus vasopressin group among patients presenting with asystole.67

Because vasopressin effects have not been shown to differ from those of epinephrine in cardiac arrest, one dose of vasopressin 40 U IV/IO may replace either the first or second dose of epinephrine in the treatment of pulseless arrest (Class Indeterminate).

60. Lindner KH, Dirks B, Strohmenger HU, Prengel AW, Lindner IM, Lurie KG. Randomised comparison of epinephrine and vasopressin in patients with out-of-hospital ventricular fibrillation. Lancet. 1997; 349: 535–537.[CrossRef][Medline] [Order article via Infotrieve]

61. Lindner KH, Prengel AW, Brinkmann A, Strohmenger HU, Lindner IM, Lurie KG. Vasopressin administration in refractory cardiac arrest. Ann Intern Med. 1996; 124: 1061–1064.[Abstract/Free Full Text]

62. Mann K, Berg RA, Nadkarni V. Beneficial effects of vasopressin in prolonged pediatric cardiac arrest: a case series. Resuscitation. 2002; 52: 149–156.[CrossRef][Medline] [Order article via Infotrieve]

63. Morris DC, Dereczyk BE, Grzybowski M, Martin GB, Rivers EP, Wortsman J, Amico JA. Vasopressin can increase coronary perfusion pressure during human cardiopulmonary resuscitation. Acad Emerg Med. 1997; 4: 878–883.[Medline] [Order article via Infotrieve]

64. Stiell IG, Hebert PC, Wells GA, Vandemheen KL, Tang AS, Higginson LA, Dreyer JF, Clement C, Battram E, Watpool I, Mason S, Klassen T, Weitzman BN. Vasopressin versus epinephrine for inhospital cardiac arrest: a randomised controlled trial. Lancet. 2001; 358: 105–109.[CrossRef][Medline] [Order article via Infotrieve]

65. Wenzel V, Krismer AC, Arntz HR, Sitter H, Stadlbauer KH, Lindner KH. A comparison of vasopressin and epinephrine for out-of-hospital cardiopulmonary resuscitation. N Engl J Med. 2004; 350: 105–113.[Abstract/Free Full Text]

66. Aung K, Htay T. Vasopressin for cardiac arrest: a systematic review and meta-analysis. Arch Intern Med. 2005; 165: 17–24.[Abstract/Free Full Text]

67. Guyette FX, Guimond GE, Hostler D, Callaway CW. Vasopressin administered with epinephrine is associated with a return of a pulse in out-of-hospital cardiac arrest. Resuscitation. 2004; 63: 277–282.[CrossRef][Medline] [Order article via Infotrieve]

Edited October 2, 2009 by Jwade

[MS Medic]

I apologize. I was referring to the replacement in the first or second round of meds. Could someone please link or list where you found this information. I would love to see all the right places I have not been looking in.

[AnthonyM83]

While on the topic, wondering how many systems out there use it in the field?

Sure seems to make things easier (used it during NREMT testing just so I could concentrate on other things).

But it seems that if it's only pushed once, you might not get a good gauge as to how well it helped the patient.

On my first arrest during clinicals, patient kept gaining a pulse every round of EPI, then losing it within minutes. Doc just ordered more and more epi until he "stablized". But it took a bit to catch the relationship between epi and regaining pulse (b/c of all the other drugs being pushed & the delay).

[MS Medic]

I just switched employers and went through class orientation the day after these posts. The timing was odd because we went into this during protocol review and the service demands we give vasopressin first because of the reasons chbare mentioned.