口服血压增强剂用于静脉静脉压缩剂断奶
John C Robinson1, Mariam ElSaban2, Nathan J Smischney3
1Department of Pharmacy, Mayo Clinic, Phoenix, AZ 85054, United States.
World journal of clinical cases
|December 27, 2024
概括
口服的血管活性剂有助于让患者不再使用用于低血压的静脉压缩剂. 本综述涵盖了它们的药理学,用途和在重症监护机构中的安全性.
科学领域:
- 关键护理医学 关键护理医学
- 药理学 药理学是指药理学的学科.
- 重症监护室的重症监护室的重症监护室.
背景情况:
- 静脉注射 (IV) 血管压缩剂对于管理低血压和休克至关重要.
- 使用口服血管活性剂将患者从静脉压缩剂中解脱是常见的,但缺乏确的证据.
- 米多德林经常被研究,但有局限性和潜在的不良影响.
研究的目的:
- 为重症监护室 (ICU) 设置提供口服血管活性剂的全面审查.
- 讨论这些药物的药理学,临床应用,剂量和安全性.
- 探索具有不同作用机制的新兴替代口服血管活性剂.
主要方法:
- 对口服血管活性剂的药理学和临床研究的文献综述.
- 对midodrine和其他口服血管活性药物的现有数据的分析.
- 综合有关ICU患者疗效,安全性和剂量策略的信息.
主要成果:
- 存在相互矛盾的证据,关于口服药物对IV血管压缩剂断奶的好处.
- 米多德林的副作用可能会限制其在特定患者群体中的使用.
- 一些患者需要持续的静脉压缩剂支持,因为他们对中素的折射性.
结论:
- 口服血管活性剂越来越多地被认为有助于从IV血管压缩剂释放.
- 在选择口服药物时,应考虑其药理学,疗效和安全性.
- 对耐火性低血压的替代口服血管活性剂的进一步研究是有必要的.
相关概念视频
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
299
The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
299
Antihypertensive Drugs: Vasodilators
426
Vasodilators, primarily affecting the smooth muscles within arterial and venous walls, are commonly used for hypertension treatment. Medications such as minoxidil and hydralazine primarily target arteries and arterioles, while sodium nitroprusside acts on arterioles and venules. Minoxidil, functioning as a prodrug, is metabolized by hepatic sulfotransferase into its active form, minoxidil sulfate, after oral administration. This metabolite binds to the sulfonylurea receptor (SUR) component of...
426
Heart Failure Drugs: β-Blockers
257
β-adrenergic antagonists, commonly known as β-blockers, block the effects of sympathetic neurotransmitters such as noradrenaline (NA) and adrenaline (ADR). They have several beneficial effects in heart failure treatment. They reduce heart rate, the force of contraction, and cardiac muscle relaxation. They also slow the atrial-ventricular conduction rate and raise the threshold for arrhythmias. The concentration of β-blockers determines their effects on bronchodilation,...
257
Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors
373
Angiotensin-converting enzyme (ACE), a vital component of the renin-angiotensin-aldosterone system, is abundant in lung endothelial cells. ACE converts the inactive decapeptide, angiotensin I, into the active octapeptide, angiotensin II. This potent vasoconstrictor narrows blood vessels, increasing resistance to blood flow and elevating blood pressure. Angiotensin II also stimulates aldosterone production, encouraging kidney cells to reabsorb more sodium and water from urine, thereby increasing...
373
Adrenergic Agonists: Therapeutic Uses
673
Adrenergic agonists have diverse therapeutic uses across various medical conditions and emergencies.
Emergency and Intensive Care Unit (ICU) applications: Pressor agents increase blood pressure, heart rate, and contractility in shock and organ failure situations. Dopamine can induce vasodilation and stimulate adrenoceptors. Endogenous catecholamines are effective in treating cardiogenic shock. α2-agonists like clonidine can reverse anesthesia-induced hypertension.
Allergies and...
Emergency and Intensive Care Unit (ICU) applications: Pressor agents increase blood pressure, heart rate, and contractility in shock and organ failure situations. Dopamine can induce vasodilation and stimulate adrenoceptors. Endogenous catecholamines are effective in treating cardiogenic shock. α2-agonists like clonidine can reverse anesthesia-induced hypertension.
Allergies and...
673
Antihypertensive Drugs: Angiotensin II Receptor Blockers
528
In the renin-angiotensin-aldosterone system, a hormone called angiotensin II plays a crucial role. It binds to the AT1 receptors in vascular smooth muscles coupled with Gq proteins. The activation of these receptors activates an enzyme called phospholipase C, which releases two molecules: inositol trisphosphate and diacylglycerol. These molecules cause a chain reaction that leads to the phosphorylation of myosin light chains and promotes interaction between actin and myosin, leading to smooth...
528


