前天教課時. 有學員問到肺動脈壓的問題. 高海拔肺水腫的情況. 肺動脈壓力大概是多少.
高海拔肺水腫的成因來自於肺動脈高壓. 加上肺的各部位小動脈收縮程度不同. 肺的各部位微血管床的壓力也不同.
(肺的血管收縮主要來自於肺泡的缺氧. 而非血中的氧氣含量降低)
(有些慢性肺病患者. 血氧飽和度較低, 但並不會因全身組織缺氧造成肺動脈高壓)
正常肺動脈壓力 < 25mmHg (收縮壓 < 25 mmHg. 舒張壓< 9 mmHg)
肺動脈壓力> 35-40 mmHg 可能造成肺水腫 (微血管壓力可能超過 20mmHg)
肺部各處的動脈收縮比例不同. 收縮比較嚴重的. 因為血流相對較少. 局部微血管壓力也會相對較低. 收縮沒那麼明顯. 管徑比較大的部位. 微血管壓力會比較高. 這部位比較容易發生血漿滲漏至肺泡. 當一部分的血管滲漏. 會造成整體的氧氣交換能力更下降. 引發惡性循環, 造成各處都出問題
缺氧-> 肺部小動脈收縮(各處不平均)--> 肺動脈阻力上升, 心臟為了打出足夠的血量, 右心室加強收所造成肺動脈壓力上升 ---> 微血管壓力上升==> 血漿滲漏至血管外(組織間隙/肺泡)--> 肺泡氣體交換能力下降--> 更嚴重的缺氧
另外. 肺動脈壓力 25mmHg 相當於 34 公分水柱高. 而主動脈壓力如果用 120 mmHg 計算. 相當於 163 公分水柱高. 肺動脈壓力與主動脈差異極大. 因此重力造成的靜水壓對於肺部的影響非常大. 當一個人站著的時候. 肺部頂端至肺部底端壓力差大約 25 公分水柱高. 站著或躺平的姿態. 對於肺部頂端到肺部底部的壓力差變化會高達 25/(25+34)= 42% (躺平時. 肺頂部與底部壓力差為 0)
下面內容來自 uptodate High-altitude pulmonary edema
病理生理學
HAPE 是由於低壓缺氧引發的肺血氣屏障破壞導致血漿和一些紅血球在肺氣囊中異常積聚。這種故障是由於對高海拔地區缺氧的多種適應不良反應而產生的，包括通氣反應差、交感神經緊張、肺血管收縮過度和不均勻（肺動脈高壓）、內皮一氧化氮生成不足、內皮素生成過多和肺泡收縮不足。最終結果是血管外液體在肺泡腔內出現斑狀積聚，從而損害氣體交換，在嚴重的情況下可能致命。
個體易感性的顯著差異、某些個體、家族群體和上述病理生理因素的較高復發率表明，遺傳學顯然在 HAPE 風險中發揮重要作用。然而，HAPE 遺傳學研究是相互矛盾的，明確的結論難以捉摸。與HAPE 相關的基因包括一氧化氮、腎素-血管緊張素-醛固酮、缺氧誘導因子(HIF)、熱休克蛋白(HSP 70)、肺表面活性蛋白A1 和A2、水通道蛋白-5 和BMPR2通路中的基因與肺動脈高壓相關的基因[ 2,4,5 ]。
平均肺動脈壓高（超過 35 至 40 mmHg）似乎是起始事件。然而，雖然肺動脈壓升高對於 HAPE 至關重要，但這本身還不夠。另一個重要因素是血管收縮不均。血管收縮相對較小的特定節段和亞節段毛細血管床不成比例地暴露於因平均肺動脈壓升高而引起的微血管壓力升高（>20 mmHg）。這種不均勻的血管收縮和局部過度灌注導致肺泡毛細血管屏障失效和斑狀肺水腫[ 6 ]。
隨著肺泡毛細血管屏障的破壞，高分子量蛋白質、細胞和液體滲漏到肺泡腔。最終，基底內皮和上皮細胞膜被破壞，導致肺泡出血。
HAPE 的一個顯著特徵是該過程可透過下降或僅吸氧而快速逆轉。肺血管阻力和肺動脈壓力立即下降，並在治療或下降到低海拔後幾天內恢復正常。
PATHOPHYSIOLOGY
HAPE is the abnormal accumulation of plasma and some red blood cells in the lung air sacs due to a breakdown in the pulmonary blood-gas barrier, triggered by hypobaric hypoxia. This breakdown develops from a number of maladaptive responses to the hypoxia encountered at higher altitudes, including poor ventilatory response, increased sympathetic tone, exaggerated and uneven pulmonary vasoconstriction (pulmonary hypertension), inadequate production of endothelial nitric oxide, overproduction of endothelin, and inadequate alveolar fluid clearance, many of which are genetically determined [2,3]. The end result is a patchy accumulation of extravascular fluid in the alveolar spaces that impairs gas exchange and can, in severe cases, prove fatal.
Genetics clearly play an important role in the risk of HAPE, as suggested by the marked variability in individual susceptibility, the higher rates of recurrence among some individuals, familial groupings, and the pathophysiologic factors mentioned above. However, HAPE genetic studies are conflicting, and clear conclusions are elusive. Genes associated with HAPE have included those in the pathways for nitric oxide, renin-angiotensin-aldosterone, hypoxia-inducible factor (HIF), heat shock protein (HSP 70), pulmonary surfactant proteins A1 and A2, aquaporin-5, and the BMPR2 gene that is associated with pulmonary arterial hypertension [2,4,5].
High mean pulmonary artery pressure, in excess of 35 to 40 mmHg, appears to be the initiating event. However, while elevated pulmonary artery pressure is essential for HAPE, this by itself is insufficient. The other essential factor is uneven vasoconstriction. Specific segmental and subsegmental capillary beds with relatively less vasoconstriction are disproportionately exposed to elevated microvascular pressures (>20 mmHg) that arise from the elevated mean pulmonary artery pressure. This uneven vasoconstriction and regional overperfusion result in failure of the alveolar-capillary barrier and patchy pulmonary edema [6].
As disruption of the alveolar-capillary barrier progresses, high molecular weight proteins, cells, and fluid leak into the alveolar space. Eventually, basement endothelial and epithelial cell membranes are disrupted, leading to alveolar hemorrhage.
A striking feature of HAPE is the rapid reversibility of this process with descent or simply the administration of oxygen. Pulmonary vascular resistance and pulmonary artery pressure drop immediately and return to normal within days after treatment or descent to low altitude.
(補充. 在醫院經常放置的中心靜脈導管 CVP. 通常測出的壓力是 < 15 公分水柱(大約 11 mmHg), 甚至有時候會是負壓
下面這段是另一篇文獻的內容
縮寫
病理生理學
HAPE 是由於低壓缺氧引發的肺血氣屏障破壞導致血漿和一些紅血球在肺氣囊中異常積聚。這種故障是由於對高海拔地區缺氧的多種適應不良反應而產生的，包括通氣反應差、交感神經緊張、肺血管收縮過度和不均勻（肺動脈高壓）、內皮一氧化氮生成不足、內皮素生成過多和肺泡收縮不足。最終結果是血管外液體在肺泡腔內出現斑狀積聚，從而損害氣體交換，在嚴重的情況下可能致命。
個體易感性的顯著差異、某些個體、家族群體和上述病理生理因素的較高復發率表明，遺傳學顯然在 HAPE 風險中發揮重要作用。然而，HAPE 遺傳學研究是相互矛盾的，明確的結論難以捉摸。與HAPE 相關的基因包括一氧化氮、腎素-血管緊張素-醛固酮、缺氧誘導因子(HIF)、熱休克蛋白(HSP 70)、肺表面活性蛋白A1 和A2、水通道蛋白-5 和BMPR2通路中的基因與肺動脈高壓相關的基因[ 2,4,5 ]。
平均肺動脈壓高（超過 35 至 40 mmHg）似乎是起始事件。然而，雖然肺動脈壓升高對於 HAPE 至關重要，但這本身還不夠。另一個重要因素是血管收縮不均。血管收縮相對較小的特定節段和亞節段毛細血管床不成比例地暴露於因平均肺動脈壓升高而引起的微血管壓力升高（>20 mmHg）。這種不均勻的血管收縮和局部過度灌注導致肺泡毛細血管屏障失效和斑狀肺水腫[ 6 ]。
隨著肺泡毛細血管屏障的破壞，高分子量蛋白質、細胞和液體滲漏到肺泡腔。最終，基底內皮和上皮細胞膜被破壞，導致肺泡出血。
HAPE 的一個顯著特徵是該過程可透過下降或僅吸氧而快速逆轉。肺血管阻力和肺動脈壓力立即下降，並在治療或下降到低海拔後幾天內恢復正常。
PATHOPHYSIOLOGY
HAPE is the abnormal accumulation of plasma and some red blood cells in the lung air sacs due to a breakdown in the pulmonary blood-gas barrier, triggered by hypobaric hypoxia. This breakdown develops from a number of maladaptive responses to the hypoxia encountered at higher altitudes, including poor ventilatory response, increased sympathetic tone, exaggerated and uneven pulmonary vasoconstriction (pulmonary hypertension), inadequate production of endothelial nitric oxide, overproduction of endothelin, and inadequate alveolar fluid clearance, many of which are genetically determined [2,3]. The end result is a patchy accumulation of extravascular fluid in the alveolar spaces that impairs gas exchange and can, in severe cases, prove fatal.
Genetics clearly play an important role in the risk of HAPE, as suggested by the marked variability in individual susceptibility, the higher rates of recurrence among some individuals, familial groupings, and the pathophysiologic factors mentioned above. However, HAPE genetic studies are conflicting, and clear conclusions are elusive. Genes associated with HAPE have included those in the pathways for nitric oxide, renin-angiotensin-aldosterone, hypoxia-inducible factor (HIF), heat shock protein (HSP 70), pulmonary surfactant proteins A1 and A2, aquaporin-5, and the BMPR2 gene that is associated with pulmonary arterial hypertension [2,4,5].
High mean pulmonary artery pressure, in excess of 35 to 40 mmHg, appears to be the initiating event. However, while elevated pulmonary artery pressure is essential for HAPE, this by itself is insufficient. The other essential factor is uneven vasoconstriction. Specific segmental and subsegmental capillary beds with relatively less vasoconstriction are disproportionately exposed to elevated microvascular pressures (>20 mmHg) that arise from the elevated mean pulmonary artery pressure. This uneven vasoconstriction and regional overperfusion result in failure of the alveolar-capillary barrier and patchy pulmonary edema [6].
As disruption of the alveolar-capillary barrier progresses, high molecular weight proteins, cells, and fluid leak into the alveolar space. Eventually, basement endothelial and epithelial cell membranes are disrupted, leading to alveolar hemorrhage.
A striking feature of HAPE is the rapid reversibility of this process with descent or simply the administration of oxygen. Pulmonary vascular resistance and pulmonary artery pressure drop immediately and return to normal within days after treatment or descent to low altitude.
(補充. 在醫院經常放置的中心靜脈導管 CVP. 通常測出的壓力是 < 15 公分水柱(大約 11 mmHg), 甚至有時候會是負壓
(以右心房壓力作為參考點. 參考點壓力定義為0, 當然實際壓力不是 0)
下面這段是另一篇文獻的內容
縮寫
Pulmonary artery pressure (Ppa) (pressure pulmonary artery)
left atrial pressure (Pla) (pressure left atrial)
整個肺循環中的壓力和流量是高度脈動的。儘管肺迴路中的壓力脈動減少，但血流的脈動性質在靜脈側仍然存在。肺動脈壓(P pa ) 通常在收縮期約 25 毫米汞柱，在舒張期約 9 毫米汞柱。相對於全身動脈壓，P pa較低，重力造成的靜水壓差異導致肺部頂部到底部的血管壓力有顯著差異。如果將肺動脈視為大約25厘米高的血柱，則從肺底部到頂部將會有25厘米H paO（或18毫米汞柱）P2 2 O壓力）。這種壓力差導致血流分佈不均勻，正如隨後在「肺灌注的區域分佈」部分中討論的那樣。
P pa是透過將心導管或末端帶有氣球的漂浮導管插入肺動脈來測量的。51球囊膨脹導致導管前進（「浮動」）（圖 6-1），直到其「楔入」並閉塞外周肺動脈。球囊充氣後，在導管尖端測得的壓力稱為肺楔壓(P pw )。52,53該程序有效地將導管內腔內的靜態流體延伸到血管床中，因此測量的壓力位於該延伸柱接下來與血液流動的血管相連接的位置。楔壓（通常為 5 至 10 mm Hg）是肺靜脈匯合點血管壓力的估計值，因此反映了左心房壓力(P la )。
肺靜脈匯合處遠端的壓力變化（例如由肺小靜脈收縮引起的壓力變化）可以改變Pla和 P pw之間的關係。此外，導管尖端在肺部的精確位置也會影響 P pw的測量（圖 6-2）。區域 1 是肺泡壓力(Palv) 大於 P pa的肺部區域，P pa 大於肺靜脈壓力(P pv )，因此通過肺泡血管的血流最少。區域 2 是 P pa大於 Palv 的地方，Palv 又大於 P pv，因此流量隨著肺部向下移動而線性增加。將導管放置在上肺（區域 1 或區域 2）會導致 P pw與Pla不同，因為較高的肺泡壓力會阻塞液柱。在這些條件下，P pw提供的肺血管流出壓測量值不正確。導管楔入區域 3（其中 P pa大於 P pv，P pv 又大於 Palv），可以更準確地反映 P la。54,55已經提出了各種演算法來驗證 P pw的測量結果。55
Pulmonary Wedge Pressure
Pulmonary Hemodynamics- Pulmonary Vascular Pressures
Pressure and flow are highly pulsatile throughout the pulmonary circulation. Although the pressure pulsatility decreases across the pulmonary circuit, the pulsatile nature of the flow persists on the venous side. Pulmonary artery pressure (Ppa) is normally approximately 25 mm Hg during systole and 9 mm Hg during diastole. Relative to systemic arterial pressure, Ppa is low, and hydrostatic pressure differences due to gravity result in a substantial difference in vascular pressure from the top to the bottom of the lung. If the pulmonary artery is considered to be a column of blood approximately 25 cm high, there will be a 25 cm H2O (or 18 mm Hg) Ppa increase from the bottom to the top of the lung (1 mm Hg pressure = 1.36 cm H2O pressure). This pressure difference results in a nonuniform distribution of blood flow, as discussed subsequently in the “Regional Distribution of Pulmonary Perfusion” section.
Ppa is measured by inserting a cardiac catheter or a balloon-tipped flotation catheter into the pulmonary artery.51 Inflating the balloon leads to advancement (“floating”) of the catheter (Fig. 6-1) until it “wedges” and occludes a peripheral pulmonary artery. With the balloon inflated the pressure measured in the tip of the catheter is called the pulmonary wedge pressure (Ppw).52,53 This procedure effectively extends the static fluid within the catheter lumen into the vascular bed, and the measured pressure is thus at the site where this extended column next joins a vessel in which blood is flowing. The wedge pressure (normally 5 to 10 mm Hg) is an estimate of the vascular pressure at the point of confluence of pulmonary veins and hence reflects left atrial pressure (Pla).
Changes in pressure distal to the confluence of the pulmonary veins, such as that induced by constriction of the pulmonary venules, can alter the relationship between Pla and Ppw. Also, the precise location of the catheter tip in the lung influences the measurement of Ppw (Fig. 6-2). Zone 1 is the region of the lung in which the alveolar pressure (Palv) is greater than Ppa, which is greater than the pulmonary venous pressure (Ppv), and therefore there is minimal blood flow through the alveolar vessels. Zone 2 is where Ppa is greater than Palv, which is greater than Ppv, and therefore flow increases linearly as one moves down the lung. Positioning the catheter in the upper lung (in zone 1 or 2) results in a Ppw different from Pla because higher alveolar pressures occlude the fluid column. Under these conditions, Ppw provides an incorrect measurement of pulmonary vascular outflow pressure. A catheter wedged in zone 3, where Ppa is greater than Ppv, which is greater than Palv, more accurately reflects the Pla.54,55 Various algorithms have been proposed to validate measurements of Ppw.55
Pulmonary Hemodynamics- Pulmonary Vascular Pressures
Pressure and flow are highly pulsatile throughout the pulmonary circulation. Although the pressure pulsatility decreases across the pulmonary circuit, the pulsatile nature of the flow persists on the venous side. Pulmonary artery pressure (Ppa) is normally approximately 25 mm Hg during systole and 9 mm Hg during diastole. Relative to systemic arterial pressure, Ppa is low, and hydrostatic pressure differences due to gravity result in a substantial difference in vascular pressure from the top to the bottom of the lung. If the pulmonary artery is considered to be a column of blood approximately 25 cm high, there will be a 25 cm H2O (or 18 mm Hg) Ppa increase from the bottom to the top of the lung (1 mm Hg pressure = 1.36 cm H2O pressure). This pressure difference results in a nonuniform distribution of blood flow, as discussed subsequently in the “Regional Distribution of Pulmonary Perfusion” section.
Ppa is measured by inserting a cardiac catheter or a balloon-tipped flotation catheter into the pulmonary artery.51 Inflating the balloon leads to advancement (“floating”) of the catheter (Fig. 6-1) until it “wedges” and occludes a peripheral pulmonary artery. With the balloon inflated the pressure measured in the tip of the catheter is called the pulmonary wedge pressure (Ppw).52,53 This procedure effectively extends the static fluid within the catheter lumen into the vascular bed, and the measured pressure is thus at the site where this extended column next joins a vessel in which blood is flowing. The wedge pressure (normally 5 to 10 mm Hg) is an estimate of the vascular pressure at the point of confluence of pulmonary veins and hence reflects left atrial pressure (Pla).
Changes in pressure distal to the confluence of the pulmonary veins, such as that induced by constriction of the pulmonary venules, can alter the relationship between Pla and Ppw. Also, the precise location of the catheter tip in the lung influences the measurement of Ppw (Fig. 6-2). Zone 1 is the region of the lung in which the alveolar pressure (Palv) is greater than Ppa, which is greater than the pulmonary venous pressure (Ppv), and therefore there is minimal blood flow through the alveolar vessels. Zone 2 is where Ppa is greater than Palv, which is greater than Ppv, and therefore flow increases linearly as one moves down the lung. Positioning the catheter in the upper lung (in zone 1 or 2) results in a Ppw different from Pla because higher alveolar pressures occlude the fluid column. Under these conditions, Ppw provides an incorrect measurement of pulmonary vascular outflow pressure. A catheter wedged in zone 3, where Ppa is greater than Ppv, which is greater than Palv, more accurately reflects the Pla.54,55 Various algorithms have been proposed to validate measurements of Ppw.55
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