Augmentation of Venous Return by Adrenergic Agonists during Spinal Anesthesia

Butterworth, John F.; Piccione, William; Berrizbeitia, Luis D.; Dance, Garland; Shemin, Richard J.; Cohn, Lawrence H.

doi:10.1213/00000539-198606000-00009

Cited by 38 publications

(6 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The increase in CI and reduction in TPR with ephedrine treatment in dogs is consistent with other studies (Grandy et al 1989;Wagner et al 1993;Lee et al 2002). Although the increase in CO has also been shown to be due to increased venous return caused by selective venoconstriction (Butterworth et al 1986;Lawson & Meyer 1996), the effect on cardiac b 1 -receptors is the primary mechanism (Lawson & Meyer 1996;Stoelting 1999;Hoffman 2001). We did not measure central venous pressure in these dogs and thus have no estimation of alterations in venous return.…”

Section: Discussionsupporting

confidence: 88%

“…This is explained by persistent occupation of both the adrenergic receptors by the first dose of ephedrine or depletion of norepinephrine stores (Stoelting 1999). It is also possible that a better response may have been obtained if a higher dose of ephedrine was used in the repeated bolus (Butterworth et al 1986). Alternatively, an infusion of ephedrine could be considered as has been used in humans (Gajraj et al 1993;Critchley et al 1995;Chan et al 1997).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Use of ephedrine and dopamine in dogs for the management of hypotension in routine clinical cases under isoflurane anesthesia

Chen

Sinclair

Dyson

2007

Veterinary Anaesthesia and Analgesia

View full text Add to dashboard Cite

Section: Discussionsupporting

confidence: 88%

Section: Discussionmentioning

confidence: 99%

Use of ephedrine and dopamine in dogs for the management of hypotension in routine clinical cases under isoflurane anesthesia

Chen

Sinclair

Dyson

2007

Veterinary Anaesthesia and Analgesia

View full text Add to dashboard Cite

“…Ephedrine is a predominantly indirectly acting α‐ and β‐adrenoceptor agonist commonly used in the treatment and prevention of spinal‐induced hypotension, which has been shown to be effective for these purposes [21, 22]. It has been reported to precipitate coronary artery vasospasm resulting in myocardial ischaemia when ingested for relief of sinus congestion and when used as a recreational drug [4, 5].…”

Section: Discussionmentioning

confidence: 99%

Myocardial infarction associated with the administration of intravenous ephedrine and metaraminol for spinal‐induced hypotension

Khavandi¹,

Gatward²,

Whitaker³

et al. 2009

Anaesthesia

View full text Add to dashboard Cite

SummaryA 31-year-old female with no risk factors for cardiac disease suffered a peri-operative myocardial infarction during an elective gynaecological procedure under spinal anaesthesia. The timing and nature of cardiac symptoms suggest that the myocardial infarction was caused by coronary artery vasospasm secondary to ephedrine and ⁄ or metaraminol, which were administered to treat spinalinduced hypotension. We review the recent literature and case reports on myocardial infarction attributed to sympathomimetic drugs, and recommend the use of sublingual or intravenous nitrates when signs or symptoms of coronary arterial vasospasm become evident during their use. Spinal anaesthesia is associated with cardiovascular complications, most notably hypotension and bradycardia [1], which often necessitate the use of sympathomimetic drugs such as ephedrine and metaraminol. These agents can cause coronary artery vasospasm, which is thought to be due to their action on alpha-adrenergic receptors on large epicardial arteries [2]. There have been several case reports of myocardial injury as a result of such vasospasm [3][4][5][6]. We describe a case of myocardial infarction in a fit, healthy woman, the signs and symptoms of which were closely temporally related to the administration of ephedrine and metaraminol for spinal-induced hypotension. Case reportA 31-year-old female with a history of stress incontinence was scheduled for an elective tension-free vaginal tape (TVT) procedure under spinal anaesthesia. She had previously received epidural analgesia, with no complications, for two normal vaginal deliveries. She had no history of cardiovascular disease and no risk factors. There was no history of illicit drug use. She was fit and healthy and regularly cycled 20 miles.Prior to insertion of the spinal anaesthetic, she was given 1 l of Hartmann's solution intravenously. She was very anxious about the procedure and so was given intravenous midazolam 2 mg in 1-mg increments. Blood pressure was recorded as 120 ⁄ 72 mmHg and heart rate 74 beats.min )1 . Spinal anaesthesia was induced with 2.7 ml hyperbaric bupivacaine 0.5%. Ten minutes after induction of anaesthesia, her blood pressure fell to 105 ⁄ 65 mmHg and her heart rate to 60 beats.min. She complained of feeling faint and became pale. She was treated with intravenous ephedrine 5 mg, followed by intravenous metaraminol 1 mg. Her blood pressure rose to 180 ⁄ 120 mmHg and she developed a sinus tachycardia of 120 beats.min )1 with frequent ventricular ectopic beats. This was associated with chest tightness and anxiety. She was given a further 2 mg intravenous midazolam in 1-mg increments. After 5 min, her chest discomfort had resolved and the procedure was completed without further complication or significant blood loss. She was transferred to the recovery room.

show abstract

“…These compensatory mechanisms are generally more effective in younger patients. 1 The hemodynamic consequences of SA also result in a sympathetic block of the venous reservoir 2 which then leads to pooling of blood in the capacitance vessels in the lowermost regions. 3 When the level of the sensory block is higher than or equal to T6, this pooling in the hepatosplanchnic region can affect up to 20% of the circulating blood volume and this volume can be mobilized by the use of vasopressors.…”

Section: Effect Of Sa On the Resistive And Capacitive Vascular Systemsmentioning

confidence: 99%

<p>Control of Spinal Anesthesia-Induced Hypotension in Adults</p>

Ferré

Martin

Bosch

et al. 2020

LRA

View full text Add to dashboard Cite

Spinal anesthesia-induced hypotension (SAIH) occurs frequently, particularly in the elderly and in patients undergoing caesarean section. SAIH is caused by arterial and venous vasodilatation resulting from the sympathetic block along with a paradoxical activation of cardioinhibitory receptors. Bradycardia after spinal anesthesia (SA) must always be treated as a warning sign of an important hemodynamic compromise. Fluid preloading (before initiation of the SA) with colloids such as hydroxyethyl starch (HES) effectively reduces the incidence and severity of arterial hypotension, whereas crystalloid preloading is not indicated. Co-loading with crystalloid or colloid is as equally effective to HES preloading, provided that the speed of administration is adequate (ie, bolus over 5 to 10 minutes). Ephedrine has traditionally been considered the vasoconstrictor of choice, especially for use during SAIH associated with bradycardia. Phenylephrine, a α 1 adrenergic receptor agonist, is increasingly used to treat SAIH and its prophylactic administration (ie, immediately after intrathecal injection of local anesthetics) has been shown to decrease the incidence of arterial hypotension. The role of norepinephrine as a possible alternative to phenylephrine seems promising. Other drugs, such as serotonin receptor antagonists (ondansetron), have been shown to limit the blood pressure drop after SA by inhibiting the Bezold-Jarisch reflex (BJR), but further studies are needed before their widespread use can be recommended.

show abstract

Augmentation of Venous Return by Adrenergic Agonists during Spinal Anesthesia

Cited by 38 publications

References 0 publications

Use of ephedrine and dopamine in dogs for the management of hypotension in routine clinical cases under isoflurane anesthesia

Use of ephedrine and dopamine in dogs for the management of hypotension in routine clinical cases under isoflurane anesthesia

Myocardial infarction associated with the administration of intravenous ephedrine and metaraminol for spinal‐induced hypotension

<p>Control of Spinal Anesthesia-Induced Hypotension in Adults</p>

Contact Info

Product

Resources

About