ACLS 冠狀動脈灌注壓 Coronary perfusion pressure (CPP)

2024-01-24 08:37AM
參考資料 Coronary Perfusion Pressure- Samuel J. Heward; Jason Widrich. Last Update: March 16, 2023.
2024-01-24 08:37AM
參考資料 冠狀動脈灌注壓- Samuel J. Heward; 賈森·維德里奇。最後更新：2023 年 3 月 16 日。

筆記
1. 冠狀動脈血流. 在左心室舒張期開始進入. 左心室舒張期末壓(舒張期壓力最小的時候)會影響 CPP. 主動脈舒張期壓力. 減去左心室舒張期末壓. 這之間壓力差即為 CPP
2. 冠狀動脈左右各一條. 右側冠狀動脈供應右心室心肌灌流.
右冠狀動脈有一主分支-後室間支（Ramus interventricularis posterior (RIVP)）。右室、右房、左室部分、後壁、竇房結、房室結正常情況下由右冠狀動脈提供血液(參考資料.台中榮總嘉義分院-冠狀動脈疾病)
3. 主動脈舒張壓雖然會影響冠狀動脈灌注壓. 但冠狀動脈血流還受到血管阻力影響. 心臟可透過調整阻力. 來增加或減少冠狀動脈血流量. 
 



(下面中文部分. 使用google自動翻譯)
定義/簡介
冠狀動脈灌注壓 (CPP) 是負責冠狀動脈以及心肌灌注的壓力梯度；這確保了心肌的氧氣輸送。維持 CPP 至關重要，因為在靜止條件下，心肌吸氧率是所有器官中最高的，約 70% 至 80%；因此，透過增加冠狀動脈灌注壓或誘導冠狀血管舒張來增加冠狀動脈流量是增加心肌氧供應的主要手段。[1] [2]如果冠狀動脈灌注不足，就會導致心肌缺血，進而導致梗死，在美國每年的發生率約為79萬例。[1] [2]

本文旨在：
1) 定義 CPP 並描述其產生的壓力
2) 解釋 CPP 如何促進冠狀動脈血流
3) 解釋 CPP 在心臟病中如何改變
4) 降低 CPP 的作用2 型心肌梗塞
5) 心血管疾病中CPP 的治療修改

左心室的 CPP 是由主動脈舒張壓和左心室舒張末壓 (LVEDP) 之間的壓力梯度建立的[3]：

冠狀動脈灌注壓 ( CPP) = 主動脈舒張壓– 左心室舒張末期壓力(LVEDP)

CPP 是基於舒張壓，因為左心室心肌在舒張期而不是收縮期得到灌注。右冠狀動脈和左冠狀動脈皆起源於主動脈根部的冠狀竇，然後分為右冠狀動脈、左迴旋支和前降支[4]；因此，驅動冠狀動脈血流的壓力來自主動脈根部。這些動脈沿著心外膜表面延伸，然後分支穿過心肌，形成心內膜下叢以灌注心肌。由於這些血管穿過心肌，收縮期心肌收縮會壓迫動脈分支並阻止灌注。因此，冠狀動脈灌注發生在舒張期而不是收縮期。從主動脈舒張壓減去 LVEDP，因為冠狀動脈血流是從心外膜流向心內膜區域。

雖然驅動體循環需要左心室高壓力，但右心室產生較低壓力來灌注肺循環。因此，右心室壓力遠低於左心室施加的壓力。右心室灌注主要發生在收縮期，因為主動脈收縮壓超過右心室收縮壓。[5]當主動脈舒張壓以較小的差值超過右心室舒張末壓時，舒張期右心室的灌注也較小。[3] [4] [5]

冠狀動脈灌注壓和冠狀動脈血流量
值得注意的是，CPP 並不是冠狀動脈血流量的唯一決定因素。雖然 CPP 提供驅動冠狀動脈灌注的壓力，但冠狀動脈自動調節描述了允許冠狀動脈血流量在 60 至 180mmHg 之間的 CPP 範圍內匹配心肌需求的過程。[6]冠狀動脈收縮和血管舒張負責自我調節；當 CPP 降低時，血管舒張將改善流量，而當 CPP 升高時則相反。[1]這些組合過程可以用歐姆定律來解釋[6] [1]：

流量 = 血管內的壓力差/阻力

因此，CPP 代表冠狀動脈血管內的壓力梯度，而阻力是透過自動調節來介導的，以傳遞所需的流量。[7]多種因素導致自動調節中發生的冠狀血管收縮和血管舒張。這些可分為神經激素、內分泌、代謝和內皮源性（表 1）。CPP 和冠狀動脈自動調節的組合對於確保充足的心肌供氧至關重要，因為在靜止條件下，心臟吸氧量是所有器官中最高的，約為 70% 至 80%。[2]臨床上，全身缺氧、冠狀動脈灌注減少可造成心肌缺血；在這種情況下，透過增加 CPP 和誘導冠狀血管舒張來增加冠狀動脈血流量是增加心肌氧氣輸送的主要方法。最後，值得一提的是，由於左心室灌注發生在舒張期，心搏過速會減少舒張期所用時間的相對比例，進而減少心肌灌注。[8]心血管疾病中 CPP 的改變和自動調節將在 2 型心肌梗塞（CPP 降低導致的梗塞）之前討論。[7] [2] [8]

表 1. 冠狀動脈自動調節受到神經激素、內分泌、代謝和內皮衍生系統的控制，這些系統會誘導冠狀動脈血管收縮或血管舒張。
轉至：心血管疾病中冠狀動脈灌注壓的
臨床意義常見心臟疾病（包括心臟衰竭和冠狀動脈疾病）中 CPP 會降低；患有這些病症的患者更容易發生心肌缺血。

左心室射血受損定義為收縮性心臟衰竭；這會增加 LVEDP，從而減少 CPP 和左心室灌注。[9] LVEDP 在舒張性心臟衰竭時也會增加。[10]交感神經驅動的代償性增加最初會增加心肌收縮力和血壓，從而增加主動脈舒張壓以維持全身和冠狀動脈血流。[11]然而，收縮壓的升高也會增加心臟後負荷並促進心臟重塑。因此，在 LVEDP 升高的背景下，由於心肌肥厚和後負荷增加，心肌需氧量增加；心肌很容易缺血。[9] [10] [11]

導致冠狀動脈管腔狹窄的動脈粥狀硬化斑塊是冠狀動脈疾病的特徵。斑塊阻礙冠狀動脈循環的血流，需要斑塊遠端的代償性冠狀血管舒張以維持冠狀動脈血流和心肌氧輸送。隨著狹窄的進展，冠狀動脈流量變得依賴 CPP。當 CPP 因自動調節失敗而無法維持冠狀動脈灌注時，就會發生心肌缺血。[7] [12]冠狀動脈灌注減少導致的心肌梗塞將是下面討論的主題。[7] [12]

2 型心肌梗塞的冠狀動脈灌注壓

1 型心肌梗塞意味著冠狀動脈粥狀硬化斑塊破裂，隨後血栓形成和動脈腔狹窄。[13] 2型心肌梗塞的發生獨立於冠狀動脈粥狀硬化斑塊破裂，而非由心肌氧供需失衡所引起。心肌氧氣輸送減少可能是由低血壓伴隨 CPP 減少、全身缺氧或貧血引起的。心肌需氧量增加可能是因為後負荷增加或快速心律不整所致。2型心肌梗塞可能是多因素造成的；例如，快速心律不整可能會增加需氧量並減少每搏輸出量，導致低血壓和 CPP 降低。根據上述生理原理，患有心臟病（包括冠狀動脈疾病和心肌肥厚）的患者對CPP有依賴性，因此對降低CPP和減少心肌氧氣輸送的耐受性較差。[13]

1 型和 2 型心肌梗塞與相似的死亡率相關[14]。然而，儘管近幾十年來 1 型心肌梗塞的規範化治療已改善了預後，但由於缺乏公認的定義和治療，2 型心肌梗塞的治療仍存在困難。緊急治療包括恢復血壓，從而重建 CPP。本文將討論透過藥物和機械療法對 CPP 進行治療修改，下文將討論。[14]

冠狀動脈灌注壓的治療性改變

改變 CPP 的治療方法的兩個例子是三硝酸甘油和主動脈內球囊泵 (IABP)。三硝酸甘油 三

硝酸甘油是一種用於急性治療1 型心肌梗塞的藥物。研究表明，低劑量三硝酸甘油酯給藥可降低 LVEDP，但不會降低主動脈舒張壓，從而增加 CPP。[15]三硝酸甘油酯的主要作用是擴張中心靜脈，降低心臟前負荷；根據弗蘭克-斯塔林定律，這會減少每搏輸出量，因此心肌需氧量會減少。[16] [15]主動脈內球囊反搏

IABP 是急性衰竭心臟中最常使用的機械支持形式。[17]它經皮放置，位於主動脈弓遠端的降主動脈。充氣發生在舒張期，這會增加主動脈舒張壓，從而增加 CPP 並增加心肌氧氣輸送。LVEDP 和心臟後負荷降低，進而降低心肌需氧量。因此，IABP 可同時增加心肌供氧量並減少需氧量。[17]

Pearls
由於冠狀動脈解剖結構的排列，左心室心肌灌注發生在舒張期而非收縮期。
冠狀動脈灌注壓是心肌供氧的重要決定因素；局部因素在一定範圍的冠狀動脈灌注壓下調節冠狀動脈血流。
如果循環休克患者冠狀動脈灌注壓急劇降低，則可能發生第2型心肌梗塞；這與眾所周知的 1 型心肌梗塞的病因不同。




護理、聯合健康和跨專業團隊幹預

冠狀動脈灌注壓和跨專業團隊監測

血壓是醫院和社區醫療機構中的常見測量方法。需要足夠的血壓來推動血液流向器官。冠狀動脈灌注壓（CPP）是用來測量冠狀動脈流量的術語。[1]本節將介紹CPP及其對心肌梗塞、心肺復甦術（CPR）及低血壓的影響。[1]

冠狀動脈灌注壓

血壓是冠狀動脈血流量的重要決定因素。有趣的是，雖然非心臟器官在收縮期（心臟收縮）和舒張期（心臟舒張）期間得到灌注，但心臟收縮期間產生的高壓會阻礙冠狀動脈血流。[1]因此，冠狀動脈血流發生在心臟舒張期間，而舒張壓是CPP的主要決定因素。血壓過高和過低都會對醫院和社區環境中的患者造成危險。[1]

心肌梗塞

因心臟血液供應不足而導致的心肌梗塞是美國常見的死亡原因，每年有79萬例。治療的進步和護理的改善改善了心肌梗塞後的長期存活率。[18]跨專業團隊成員（包括護理人員和物理治療師）的參與對於確保心肌梗塞後患者的最佳治療效果至關重要。對這些患者進行有創或頻繁的非侵入性血壓監測，以確保血壓得到最佳管理，因為低血壓和高血壓都可能對心臟病患者有害，並且應上報給治療醫生，因為任何一種都可能對患者的治療結果有害。低血壓會降低 CPP 並加重心肌缺血，而高血壓會增加心肌需氧量，因為心臟收縮會產生更大的泵血力。[18]

許多患者在心肌梗塞後會採用三硝酸甘油舌下噴劑或靜脈注射進行治療。高劑量時，三硝酸甘油輸注可降低血壓。[19]雖然收縮壓的降低對於減少心臟需氧量是有利的，但舒張壓的過度降低會降低CPP並加劇心肌缺血。因此，臨床團隊應在治療開始時確定血壓目標，並相應調整輸注量。[19]

心肺復甦

心驟停是指由於一系列潛在的根本原因導致心輸出量停止的狀態。對於心臟驟停的患者，需要進行心肺復甦，暫時取代肺部的氧合功能和心臟的泵血功能，同時進行治療，恢復患者的自主循環。在 CPR 期間維持 CPP 很重要，因為由於缺乏心輸出量，這些患者無法維持冠狀動脈或腦灌注。人類研究表明，較高的 CPP 與較高的患者存活率有關。[20] [21]胸外按壓是有效心肺復甦術的關鍵組成部分。它們的使用暫時代替心臟的泵血功能來產生 CPP。心肺復甦術方案中使用腎上腺素；其作用是使舒張壓升高，進而提高CPP。[21]這些因素說明了跨專業團隊依協議實施高品質心肺復甦術的重要性。[20] [21] [3 級]

低血壓

低血壓是醫院住院病患常見的臨床表現，由多種原因引起。當血壓無法確保器官灌注時，低血壓和循環性休克最常見是由於血液容量不足（循環血容量低）和敗血症（對感染的免疫反應異常）引起的。當低血壓達到無法維持 CPP 的程度時，就會發生心肌梗塞。這種類型的心肌梗塞是由低血壓引起的，而不是冠狀動脈中存在血栓。患有這種類型的心肌梗塞的患者與冠狀動脈血栓引起的心肌梗塞的患者俱有相似的死亡率。[22]現有治療大出血的方案，而拯救敗血症運動提出了一系列建議，以提高對敗血症的認識和管理，以預防併發症，包括 2 型心肌梗塞[23]。敗血症患者使用靜脈輸液，大出血患者使用血液製品進行積極復甦是維持目標血壓和預防低血壓後果（包括心肌梗塞）的建議策略。透過觀察生命徵象和升級進行早期發現對於確保最佳的患者治療效果至關重要。[22] [23]
轉至：
護理、聯合健康和跨專業團隊監測

頻繁觀察生命徵象對於識別患者病情的變化至關重要，這可能需要改變臨床管理。上述例子強調了這種監測的重要性以及這些條件背後的生理學。

Definition/Introduction
Coronary perfusion pressure (CPP) is the pressure gradient responsible for coronary and, thus, myocardial perfusion; this ensures myocardial oxygen delivery. Maintaining CPP is vital because rates of myocardial oxygen extraction are the highest of any organ at approximately 70 to 80% under resting conditions; augmentation of coronary flow by either increasing coronary perfusion pressure or inducing coronary vasodilation is, therefore, the predominant means for increasing myocardial oxygen supply.[1][2] If coronary perfusion is inadequate myocardial ischemia and ensuing infarction result, the incidence of which is approximately 790,000 per year in the United States.[1][2]

This article aims to:1) Define CPP and describe from which pressures it is derived
2) Explain how CPP contributes to coronary blood flow
3) Explain how CPP becomes altered in cardiac disease
4) The role of reduced CPP in type 2 myocardial infarction
5) Therapeutic modification of CPP in cardiovascular disease

CPP in the left ventricle is established by the pressure gradient between the aortic diastolic blood pressure and the left ventricular end-diastolic pressure (LVEDP) [3]:

Coronary Perfusion Pressure (CPP) = Aortic Diastolic Pressure – Left Ventricular end-diastolic Pressure (LVEDP)

CPP is based on diastolic pressures because the left ventricular myocardium gets perfused during diastole rather than systole. The right and left coronary arteries both originate from the coronary sinuses at the aortic root prior to division into the right coronary and left circumflex and anterior descending arteries [4]; therefore, the pressure which drives coronary flow derives from the aortic root. These arteries extend along the epicardial surface before branching through the myocardium to form subendocardial plexuses to perfuse the myocardium. Because these vessels traverse the myocardium, myocardial contraction during systole compresses arterial branches and prevents perfusion. Therefore, coronary perfusion occurs during diastole rather than systole. LVEDP is subtracted from aortic diastolic pressure because coronary blood flow occurs from epicardial to endocardial regions.

While high left ventricular pressures are required to drive systemic circulation, the right ventricle generates lower pressures to perfuse the pulmonary circulation. Therefore, the right ventricular pressures are far lower than the pressures exerted by the left ventricle. Right ventricular perfusion occurs predominantly in systole because systolic aortic pressure exceeds systolic right ventricular pressure.[5] The right ventricle is also perfused to a lesser degree in diastole when aortic diastolic pressure exceeds right ventricular end-diastolic pressure by a smaller differential.[3][4][5]
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Issues of Concern

Coronary Perfusion Pressure and Coronary Blood Flow

It is important to note that CPP is not the only determinant of coronary blood flow. While CPP provides the pressure which drives coronary perfusion, coronary autoregulation describes the process which allows coronary blood flow to match myocardial demand over a range of CPP between 60 to 180mmHg.[6] Coronary vasoconstriction and vasodilation are responsible for autoregulation; when CPP is reduced, vasodilation will improve flow, and the opposite is true when CPP becomes elevated.[1] These combined processes can be explained by Ohm’s Law[6][1]:

Flow = Difference in pressure across a vessel/resistance

Therefore, CPP represents the pressure gradient across the coronary vasculature, while resistance is mediated by autoregulation to deliver the required flow rates.[7] Multiple factors are responsible for the coronary vasoconstriction and vasodilation that occurs in autoregulation. These can categorize into neurohormonal, endocrine, metabolic, and endothelial-derived (Table 1). The combination of CPP and coronary autoregulation are crucial in ensuring adequate myocardial oxygen delivery because cardiac oxygen extraction is the highest of any organ at approximately 70 to 80% under resting conditions.[2] Clinically, systemic hypoxia and decreased coronary perfusion can cause myocardial ischemia; increasing coronary blood flow by increasing CPP and inducing coronary vasodilation are the predominant means by which myocardial oxygen delivery can increase in such circumstances. Finally, it bears mentioning that because left ventricular perfusion occurs in diastole, tachycardia decreases the relative proportion of time spent in diastole and therefore reduces myocardial perfusion.[8] Alterations in CPP and autoregulation in cardiovascular disease will be discussed before type 2 myocardial infarction, infarction resulting from decreased CPP.[7][2][8]

Table 1. Coronary autoregulation is under the control of neurohormonal, endocrine, metabolic, and endothelial-derived systems, which induce either coronary vasoconstriction or vasodilation.
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Clinical Significance

Coronary Perfusion Pressure in Cardiovascular Disease

CPP becomes reduced in common cardiac conditions, including heart failure and coronary artery disease; patients with these conditions are more prone to myocardial ischemia.

The impaired ejection of blood from the left ventricle defines systolic heart failure; this increases LVEDP, and thus CPP and left ventricular perfusion are reduced.[9] LVEDP also increases in diastolic heart failure.[10] Compensatory increases in sympathetic drive initially increase myocardial contractility and blood pressure, which increases aortic diastolic pressure to maintain systemic and coronary blood flow.[11] However, increases in systolic blood pressure also increase cardiac afterload and promote cardiac remodeling. Therefore, myocardial oxygen demand increases due to hypertrophy of the myocardium and increased afterload on a background of raised LVEDP; the myocardium will be vulnerable to ischemia.[9][10][11]

Atherosclerotic plaques causing stenosis of coronary vessel lumens characterize coronary artery disease. Plaques impede flow through coronary circulation, necessitating compensatory coronary vasodilation distal to the plaque to maintain coronary flow and myocardial oxygen delivery. As stenosis progresses, the coronary flow becomes dependent on CPP. Myocardial ischemia occurs when CPP is unable to sustain coronary perfusion as autoregulation fails.[7][12] Myocardial infarction resulting from reduced coronary perfusion will be a topic of discussion below.[7][12]

Coronary Perfusion Pressure in Type 2 Myocardial Infarction

Type 1 myocardial infarction implies the rupture of a coronary atherosclerotic plaque with subsequent thrombus formation and stenosis of the arterial lumen.[13] Type 2 myocardial infarction occurs independently from coronary atherosclerotic plaque rupture instead of resulting from an imbalance in myocardial oxygen supply and demand. Decreased myocardial oxygen delivery may be caused by hypotension with reduced CPP, systemic hypoxia, or anemia. Increased myocardial oxygen demand may result from increased afterload or tachyarrhythmia. Type 2 myocardial infarction may be multifactorial; for example, tachyarrhythmia may increase oxygen demand and reduce stroke volume with subsequent hypotension and reduced CPP. According to the physiologic principles discussed above, patients with pre-existing cardiac disease, including coronary artery disease and myocardial hypertrophy, are reliant on CPP, so are less tolerant of reduced CPP and decreased myocardial oxygen delivery.[13]

Type 1 and 2 myocardial infarctions are associated with similar mortality rates [14]. However, while protocolized management of type 1 myocardial infarction has improved outcomes in recent decades, difficulties exist regarding the management of type 2 myocardial due to a lack of accepted definitions and treatment. Acute management involves the restoration of blood pressure and, thus re-establishment of CPP. This article will discuss the therapeutic modification of CPP by pharmacological and mechanical therapies will be discussed below.[14]

Therapeutic Modification of Coronary Perfusion Pressure

Two examples of therapies that modify CPP are glyceryl trinitrate and the intra-aortic balloon pump (IABP).Glyceryl Trinitrate

Glyceryl trinitrate is an agent used in the acute management of type 1 myocardial infarction. Studies have shown that low-dose glyceryl trinitrate administration reduces LVEDP without reducing aortic diastolic pressure, thus increasing CPP.[15] The predominant action of Glyceryl trinitrate is central venous dilatation, which reduces cardiac preload; this reduces stroke volume according to the Frank-Starling law, and therefore, myocardial oxygen demand decreases.[16][15]Intra-Aortic Balloon Pump

The IABP is the most commonly used form of mechanical support in the acutely failing heart.[17] It is placed percutaneously and sits in the descending aorta distal to the aortic arch. Inflation occurs during diastole, which increases aortic diastolic blood pressure to increase CPP and augment myocardial oxygen delivery. LVEDP and cardiac afterload are reduced, which decreases myocardial oxygen demand. IABPs, therefore, simultaneously increase myocardial oxygen supply and decreased oxygen demand.[17]

Pearls
Left ventricular myocardial perfusion occurs in diastole rather than systole due to the arrangement of the coronary anatomy.
Coronary perfusion pressure is a significant determinant of myocardial oxygen supply; local factors regulate coronary flow across a range of coronary perfusion pressures.
If coronary perfusion pressure becomes acutely reduced in patients with circulatory shock, type 2 myocardial infarction may occur; this has a different etiology from the widely known type 1 myocardial infarction.




Nursing, Allied Health, and Interprofessional Team Interventions

Coronary Perfusion Pressure and Interprofessional Team Monitoring

Blood pressure is a common measurement in both hospital and community healthcare settings. Adequate blood pressure is required to drive blood flow to organs. Coronary perfusion pressure (CPP) is the term used to measure the flow through coronary arteries.[1] This section will introduce CPP and its effect on myocardial infarction, cardiopulmonary resuscitation (CPR), and hypotension.[1]

Coronary Perfusion Pressure

Blood pressure is a vital determinant of coronary blood flow. Interestingly, while the non-cardiac organs get perfused during systole (cardiac contraction) and diastole (cardiac relaxation), the high pressures generated in the heart during contraction impede coronary blood flow.[1] Therefore, coronary blood flow occurs during cardiac relaxation, and diastolic blood pressure is a major determinant of CPP. Both excessively high and low blood pressure can be hazardous to patients in hospital and community settings.[1]

Myocardial Infarction

Myocardial infarction due to inadequate blood supply to the heart is a common cause of mortality in the United States, with 790000 cases per year. Therapeutic advances and improvements in care have led to improvements in long-term survival post-myocardial infarction.[18] The involvement of interprofessional team members, including nursing staff and physical therapists, is crucial in ensuring optimal patient outcomes post-myocardial infarction. Invasive or frequent non-invasive blood pressure monitoring is undertaken in these patients to ensure blood pressure is optimally managed, as both hypotension and hypertension can be harmful in cardiac patients and should be escalated to the treating physician as either can be detrimental to patient outcomes. Hypotension reduces CPP and can worsen myocardial ischemia, while hypertension will increase myocardial oxygen demand because cardiac contraction will have a greater force against which to pump.[18]

Many patients will be treated with glyceryl trinitrate sublingual spray or intravenous infusion after myocardial infarction. At high doses, glyceryl trinitrate infusions decrease blood pressure.[19] Although a decrease in systolic blood pressure is desirable to reduce cardiac oxygen requirement, excessive decreases in diastolic blood pressure decrease CPP and worsen myocardial ischemia. Targets for blood pressure should, therefore, be established by the clinical team on commencement of therapy, and infusions titrated accordingly.[19]

Cardio-Pulmonary Resuscitation

Cardiac arrest describes a state where cardiac output ceases due to an array of potential underlying causes. CPR is necessary for patients who have had cardiac arrest to temporarily replace the oxygenation function of the lungs and the pumping function of the heart while rendering treatment to return the patient’s spontaneous circulation. It is important to maintain CPP during CPR because, due to the absence of cardiac output, these patients are unable to maintain coronary or cerebral perfusion. Studies in humans have shown that greater CPP is associated with higher rates of patient survival.[20][21] Chest compressions are a key component of effective CPR. Their use temporarily replaces the pumping function of the heart to generate CPP. Adrenaline is used in CPR protocols; its action is to increase diastolic blood pressure to increase CPP.[21] These factors illustrate the importance of protocolized, high-quality CPR delivery by the interprofessional team.[20][21] [Level 3]

Hypotension

Hypotension is a common clinical finding in hospital inpatients and arises from a wide array of causes. Hypotension and circulatory shock, when blood pressure is unable to ensure organ perfusion, most commonly result from hypovolemia (low circulating blood volume) and sepsis (abnormal immune response to infection). When hypotension occurs to the extent that CPP is not maintained, a myocardial infarction occurs. This type of myocardial infarction results from low blood pressure rather than the presence of a thrombus in the coronary arteries. Patients who suffer from this type of myocardial infarction have a similar mortality rate compared to patients with myocardial infarction resulting from a coronary artery thrombus.[22] Protocols exist for the management of major hemorrhage while the Surviving Sepsis Campaign has produced a range of recommendations to improve recognition and management of sepsis to prevent complications, including type 2 myocardial infarction [23]. Aggressive resuscitation with intravenous fluids in sepsis and blood products in major hemorrhage is the recommended strategy to maintain target blood pressure and prevent consequences of hypotension, including myocardial infarction. Early detection through observation of vital signs and escalation is crucial in ensuring optimal patient outcomes.[22][23]
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Nursing, Allied Health, and Interprofessional Team Monitoring

Frequent observation of vital signs is crucial to identify changes in the patient's condition, which may require changes in clinical management. The above examples highlight the importance of this monitoring and the physiology which underlies these conditions.