黑色字體是原文獻(xiàn)

紅色字體是機(jī)翻

藍(lán)色字體是人肉翻，校對，講解，注釋等等?

Deranged Physiology? Required Reading? Endocrinology, Metabolism and Nutrition

精神錯亂的生理學(xué)必讀《內(nèi)分泌學(xué)、代謝與營養(yǎng)》

Physiological adaptation to prolonged starvation

對長期饑餓的生理適應(yīng)

This is a summary of the physiological responses to the total or near-total absence of nutrition.

這是對完全或接近完全缺乏營養(yǎng)的生理反應(yīng)的總結(jié)。

The metabolic response to starvation is characterised by a switch from carbohydrate metabolism to fat cmetabolism, in the context of a hypometabolic state, with minimised catabolism.

在低代謝狀態(tài)下，對饑餓的代謝反應(yīng)的特征是從碳水化合物代謝轉(zhuǎn)變?yōu)橹敬x，分解代謝最小化。

說人話：對于餓了?代謝反應(yīng)的特征是一個轉(zhuǎn)變，就是說 你餓了，你的代謝特征會有一個轉(zhuǎn)變，這個轉(zhuǎn)變系蝦米呢，是從碳水分解→脂肪分解，當(dāng)然 這個有一個大背景，就是說是在低代謝低分解?情況下（這不廢話嘛，人類低分解低代謝肯定要么是虛弱要么餓極了唄。。）

Initially, stores of carbohydrate precursors (eg. glycogen) are depleted.

最初，碳水化合物前體（如糖原）的儲存被耗盡。

Then, in the first 24-48 hours there is increased gluconeogenesis from amino acids and glycerol.

然后，在最初的24-48小時內(nèi)，氨基酸和甘油的糖異生增加。

Subsequently, ketogenesis takes over, and much of the body metabolic needs are met by ketone bodies and free fatty acids.

隨后，酮體生成占據(jù)了主導(dǎo)地位，酮體和游離脂肪酸滿足了大部分身體代謝需求。

This is the consequence of decreasing insulin levels, and relatively increased influence from catecholamines and cortisol.

這是胰島素水平下降以及兒茶酚胺和皮質(zhì)醇影響相對增加的結(jié)果。

說人話，上述轉(zhuǎn)變，就是因為3個要素，1胰島素降了 2兒茶酚胺增了3皮質(zhì)醇增了

Over prolonged starvation, protein catabolism begins, resulting in degradation of structurally important proteins, and organ system dysfunction.

長期饑餓后，蛋白質(zhì)分解代謝開始，導(dǎo)致結(jié)構(gòu)重要的蛋白質(zhì)降解，器官系統(tǒng)功能障礙。

這句話機(jī)翻有問題，實際上會導(dǎo)致?系，重要的蛋白會產(chǎn)生結(jié)構(gòu)上?講解

The physiological adaptation to starvation has been asked about in Question 27 from the second paper of 2013. Specifically, the college wanted to know about the metabolic changes of starvation and the stress response.

Composition and quantity of nutrients stored in the human body

George F Cahill is the guru of food deprivation physiology. His 1970 article "Starvation in Man" remains a masterpiece of scientific writing. Therein one may find a table entitled "Fuel Composition Of Normal Man" which I have uselessly interpreted into another weird cylinder diagram.

Whatever the value of that may be.

2013年第二篇論文的問題27中提出了對饑餓的生理適應(yīng)。具體來說，學(xué)院想了解饑餓的代謝變化和壓力反應(yīng)。

人體內(nèi)儲存的營養(yǎng)成分和數(shù)量

喬治·F·卡希爾是食物匱乏生理學(xué)的大師。他1970年的文章《人的饑餓》仍然是科學(xué)寫作的杰作。在那里可以找到一張題為“普通人的燃料成分”的表格，我把它無用地解釋成了另一張奇怪的氣缸圖。

不管它的價值是什么。

這一大堆沒啥干貨，就不人肉矯正了。。

Anyway, each of us has about 20-25g of circulating fuel (of which the majority is glucose), worth about 113 calories. If we take this Homo vulgaris to be a 20 year old specimen measuring 70kg and 170cm, we can calculate that at their basal metabolic rate of 1800kcal/day they go through one blood volume worth of calories every 90 minutes.

無論如何，我們每個人都有大約20-25克的循環(huán)燃料（其中大部分是葡萄糖），價值大約113卡路里。如果我們把這個普通人作為一個20歲的標(biāo)本，測量70公斤和170厘米，我們可以計算出，在他們1800kcal/天的基礎(chǔ)代謝率下，他們每90分鐘消耗一個血液體積的熱量。

一個血液體積是什么鬼？然而貌似只能這么翻譯?。。

The total metabolic fuel stores in a normal human body

正常人體內(nèi)儲存的總代謝燃料

正常人體內(nèi)儲存的總代謝燃料

Thus, the circulating nutrient volume is constantly being consumed and replenished.

因此，循環(huán)營養(yǎng)物質(zhì)的體積不斷被消耗和補(bǔ)充。

Then, we have a rapidly available glycogen storehouse, of which two thirds resides in the muscle. There is a total 900kcal of this stuff, and it is also constantly being consumed and replenished. It is replenished after meals (when insulin drives glucose into cells and promotes glyconeogenesis) and it is consumed between meals (when glucagon activated glycogenolysis, releasing glucose out of cells).

然后，我們有了一個快速可用的糖原庫，其中三分之二存在于肌肉中。這種物質(zhì)總共有900千卡，而且還在不斷地消耗和補(bǔ)充。它在餐后補(bǔ)充（當(dāng)胰島素將葡萄糖驅(qū)動到細(xì)胞中并促進(jìn)糖原生成時），并在餐間消耗（當(dāng)胰高血糖素激活糖原分解，將葡萄糖釋放出細(xì)胞時）。

糖原有兩種，肝糖原and肌糖原，肌糖原多一些大概占了三分之二。

胰島素能夠把血糖中?葡萄弄到細(xì)胞里，并且把它們變成肝糖原

胰高血糖素則是讓肝糖原分解，讓他們?細(xì)胞里跑到血糖

Glycogen is a poor means of storing energy. It is a starch-like branching molecule, has a low calorie density, only about 4 kcal per gram. Cahill reminds us that this density is actually measured in dried glycogen - in reality, 2g of water is stored together with each 1g of glycogen (in order to maintain intracellular isotonicity) and this dilutes its energy density even further.

糖原是儲存能量的不良手段。它是一種淀粉樣支化分子，熱量密度低，每克僅約4千卡。Cahill提醒我們，這種密度實際上是用干糖原來測量的——事實上，每1g糖原儲存2g水（以保持細(xì)胞內(nèi)的等滲性），這會進(jìn)一步稀釋其能量密度。

就是說 糖原儲能其實也就那么回事而已，木有脂肪儲能牛叉。糖原里面有結(jié)合水（我猜的應(yīng)該是結(jié)合水?。。） 這結(jié)合水是為了維持細(xì)胞滲透壓平衡，然后因為里面有水，所以糖原實際把水去掉后，儲能就更不咋樣了

Fat, on the other hand, is stored in blobs which are essentially free of water. It is a much more efficient energy storage system. And the vast majority of the fat in the body is available as a metabolic fuel, if push comes to shove. Those blobs are cushioning, they serve a purely cosmetic role and if you need to burn them to survive, so be it- they will not be missed. Not only that, but fat has a far higher energy density - something like 9.4 kcal per gram.

另一方面，脂肪儲存在基本上不含水的團(tuán)塊中。這是一個效率高得多的儲能系統(tǒng)。如果情況緊急，體內(nèi)絕大多數(shù)脂肪都可以作為代謝燃料。這些斑點是緩沖的，它們純粹起到美容的作用，如果你需要燒掉它們來生存，那就順其自然吧——它們不會被錯過。不僅如此，脂肪的能量密度也高得多——大約每克9.4千卡。

這些斑點系緩沖?特喵的神馬鬼。。應(yīng)該就是說脂肪是用來緩沖的物質(zhì)，如果你要美容那就燒掉他們

Protein does not come in a fuel storage form. It is structurally important; all of your protein has some function, and to burn it as fuel would be a gesture of desperation. An organism which is consuming its own protein is truly struggling. That said, if your organism is struggling it has some 6kg or so of protein to get through before it dies.

蛋白質(zhì)不是以燃料儲存的形式出現(xiàn)的，它在結(jié)構(gòu)上很重要；你所有的蛋白質(zhì)都有一些功能，把它當(dāng)作燃料燃燒是一種絕望的姿態(tài)。一個正在消耗自身蛋白質(zhì)的有機(jī)體真的在掙扎。也就是說，如果你的生物體正在掙扎，它在死亡前有大約6公斤左右的蛋白質(zhì)需要通過。

換言之 當(dāng)糖原 脂肪都燒完了，那么離gg，還有6kg蛋白可以燒。

Metabolic adaptation to a brief period of fasting

The main change from the normal pattern is the refusal of the myocardium and skeletal muscle to use glucose. Instead, they switch over exclusively to free fatty acid and ketone metabolism.

短暫禁食的代謝適應(yīng)

與正常模式相比，主要的變化是心肌和骨骼肌拒絕使用葡萄糖。相反，它們完全轉(zhuǎn)向游離脂肪酸和酮的代謝。

The glycogen reserves in humans never get completely depleted. There is at all times a hepatic reserve, waiting to mobilise and rescue the organism from some sort of horrible situation.

人類體內(nèi)的糖原儲備從未完全耗盡。在任何時候都有一個肝臟儲備，等待著將生物體從某種可怕的情況下動員起來并拯救出來。

The diagram below is again a paraphrase of Cahill; the mass of nutrients given in it is the amount consumed in a 24 hour period.

下圖再次是對卡希爾的轉(zhuǎn)述；其中所含營養(yǎng)物質(zhì)的質(zhì)量是24小時內(nèi)所消耗的量。

饑餓過程中大量營養(yǎng)物質(zhì)代謝的變化

macronutrient metabolic changes during starvation

饑餓過程中大量營養(yǎng)物質(zhì)代謝的變化

Furthermore, the Cori cycle plays a more important role. 36g of the daily glucose is converted into lactate, which shuttles back to the liver.

此外，科里循環(huán)發(fā)揮著更重要的作用。每天36克的葡萄糖被轉(zhuǎn)化為乳酸，乳酸被送回肝臟。

介個循環(huán)我我沒聽過。。而且。。變回乳酸意義何在？

The liver uses free fatty acids to power the process of gluconeogenesis.

肝臟利用游離脂肪酸為糖異生過程提供動力。

介個好理解 糖異生分為脂肪 and 氨基酸兩種

Thus, any lactate converted back to glucose is really free fatty acid energy converted to glucose. In essence, all these Cori-cycling anaerobic glycolysis tissues are running on free fatty acid energy, and glucose and lactate merely act as vessels which contain that energy.

因此，任何轉(zhuǎn)化回葡萄糖的乳酸鹽實際上都是轉(zhuǎn)化為葡萄糖的游離脂肪酸能量。本質(zhì)上，所有這些科里循環(huán)厭氧糖酵解組織都是依靠游離脂肪酸能量運(yùn)行的，而葡萄糖和乳酸只是作為含有這種能量的血管。

這局話半懂不懂，血管翻譯成容器更好吧。。

?

Hormones responsible for the metabolic adaptation to brief fasting

負(fù)責(zé)代謝適應(yīng)短暫禁食的激素

說人話就是，你短期絕食，代謝肯定要適應(yīng)這種變化對吧，那是什么激素讓代謝產(chǎn)生了這種適應(yīng)呢

Well, its all about increasing the rate of lipolysis, is it not. And the rate of lipolysis in fatty tissues is governed by the intracellular content of cAMP, which responds to both insulin and noradrenaline.

好吧，這一切都是為了提高脂解的速度，不是嗎。脂肪組織中的脂解速率由細(xì)胞內(nèi)cAMP的含量決定，cAMP對胰島素和去甲腎上腺素都有反應(yīng)。

說白了就系camp干的好事，介個camp能對胰島素et去甲腎腺素有反應(yīng)，camp系一種腺苷，環(huán)磷酸腺苷，這玩意也是一種信使。。這玩意系atp脫了2個磷脂縮合的。。主要作用就系營養(yǎng)心肌，換言之 這玩意越多，脂代謝越快

second messenger systems involved in activation of hormone-sensitive lipase

參與激素敏感脂肪酶激活的第二信使系統(tǒng)

激素-敏感 ？敏感性激素把？

The major hormonal player in this adaptation is insulin, or rather, its lack. With the absence of regular glucose peaks (given the lack of eating) insulin levels drop. Insulin is the primary inhibitor of lipolysis, because the tyrosine kinase activity of its intracellular domain activates a phosphodiesterase, which keeps intracellular cAMP levels low. As insulin levels drop, the background sympathetic activity becomes unopposed, and the hormone sensitive lipase begins to dismantle their triglyceride stores, releasing delicious fatty acids into the bloodstream.

這種適應(yīng)的主要荷爾蒙因素是胰島素，或者更確切地說，它的缺乏。由于缺乏正常的葡萄糖峰值（考慮到缺乏進(jìn)食），胰島素水平下降。胰島素是脂解的主要抑制劑，因為其細(xì)胞內(nèi)結(jié)構(gòu)域的酪氨酸激酶活性激活磷酸二酯酶，使細(xì)胞內(nèi)cAMP水平保持在較低水平。隨著胰島素水平的下降，背景交感神經(jīng)活性變得沒有對抗，激素敏感的脂肪酶開始分解其甘油三酯儲存，向血液中釋放美味的脂肪酸。

因為挨餓，自然血糖低，自然胰島素下降。胰島素高→脂肪消耗慢。胰島素高→脂肪解就快。camp低→脂肪酶就活躍了，甘油三酯就開始變成脂肪酸了。這些脂肪酸開始參與三羧酸循環(huán)

(Yes, there are three lipases in the pathway, because there are three fatty acid molecules attached to the glycerol. Only the first lipase is hormone-sensitive.)

（是的，該途徑中有三種脂肪酶，因為甘油上有三個脂肪酸分子。只有第一種脂肪酶對激素敏感。）

介個有中學(xué)化學(xué)or生物基礎(chǔ)的應(yīng)該偶知道吧。。甘油三酯三個鍵，第一個鍵和后面兩個鍵連接的官能團(tuán)并不一樣，很合理。。

So, noradrenaline increases the rate of lipolysis (by affecting the bored and lonely beta-3 receptor, which doesn't seem to have much of a function outside of lipolysis), and insulin decreases the rate of lipolysis. Which effect is dominant in ICU patients who are frequently marinading in infusions of both noradrenaline and insulin? Hard to say. The catecholamine excess associated with critical illness definitely causes lipolysis, even in absence of exogenous catecholamines.

因此，去甲腎上腺素增加了脂解速率（通過影響無聊而孤獨(dú)的β-3受體，它似乎在脂解之外沒有太多功能），而胰島素降低了脂解的速率。在經(jīng)常浸泡在去甲腎上腺素和胰島素輸注中的ICU患者中，哪種影響占主導(dǎo)地位？很難說。與危重癥相關(guān)的兒茶酚胺過量肯定會導(dǎo)致脂解，即使在沒有外源性兒茶酚胺的情況下也是如此。

換言之β-3受體只會影響脂肪解，木有其他功能的樣子。。去甲腎上腺素這玩意是收camp影響的，camp低了，導(dǎo)致去甲腎上腺素高了，然后就增加了脂肪解

兒茶酚胺高了→脂肪gg快，胰島素高了→脂肪gg慢，去甲腎上腺素高了→脂肪gg快

Proteolysis in fasting is not studied as well as lipolysis, but it is clear that an insulin deficit also activates proteolytic pathways (because the administration of small amounts of intravenous dextrose seems to inhibit proteolysis)

禁食時的蛋白水解和脂解沒有得到研究，但很明顯，胰島素缺乏也會激活蛋白水解途徑（因為靜脈注射少量葡萄糖似乎會抑制蛋白水解）

這其實很好理解，胰島素少了→蛋白分解快。葡萄糖多了→蛋白水解慢 很合理的說poi

Which brings up an interesting question. Nobody ever just lies there and starves quietly for their first few days in the ICU. What happens to these patients?

這就引出了一個有趣的問題。沒有人會躺在那里，在重癥監(jiān)護(hù)室的頭幾天安靜地挨餓。這些病人怎么了？

這個其實好解釋吧。。病人都快gg了。。體內(nèi)各種信號系統(tǒng) 通道系統(tǒng)都亂了唄。。

They still starve.

But, if 150g (600kcal) or so of simple carbohydrate is delivered every day (which is 3 litres of 5% dextrose, or around 600ml of Jevity), the proteolytic pathway is switched off. Lipolysis continues, but the exogenous glucose results in enough insulin release to abort the ketogenesis.

他們?nèi)匀话ゐI。

但是，如果每天輸送150克（600千卡）左右的簡單碳水化合物（即3升5%葡萄糖，或約600毫升Jevity），蛋白水解途徑就會被切斷。脂解仍在繼續(xù)，但外源性葡萄糖會導(dǎo)致足夠的胰島素釋放，從而中止生酮。

換言之，血糖對于蛋白水解 et 脂肪水解雖然都有抑制作用。然而一個是直接的，一個是間接的。前者直接影響，然而原理我我還沒研究。后者則是間接影響，通過血糖→胰島素→脂肪水解

In short, feeding your patient even a tiny amount of carbohydrate will prevent ketosis and protein catabolism.

Sneakily, one can achieve the same effect by administering insulin as a part of an insulin-dextrose infusion. At protocol rate (80ml/hr) one ends up giving only 1920ml of 5% dextrose in 24 hours, which is just short of 100g (or 400kCal); but the exogenous insulin switches off the ketogenesis and proteolysis anyway.

簡而言之，給患者喂食哪怕是少量的碳水化合物也可以防止酮癥和蛋白質(zhì)分解代謝。

偷偷地，通過將胰島素作為胰島素-葡萄糖輸注的一部分來給藥，可以達(dá)到同樣的效果。按照方案速率（80ml/小時），24小時內(nèi)只能產(chǎn)生1920ml的5%葡萄糖，這還差100克（或400千卡）；但外源性胰島素?zé)o論如何都會切斷生酮和蛋白水解。

這個很好理解啦，血糖 et 胰島素是線性正相關(guān)，那你往患者體內(nèi)注入哪個其實意思都差不多的說喵。。?

Weight loss due to fasting

Rate of weight loss with starvationWith total acaloric fasting, a certain healthy 41 yr old member of a cloistered religious community lost 0.9kg per day for the first few days of the fast, a rate which decreased to a stable 0.3kg/day towards the third week of fasting.

禁食減肥

禁食減肥率在完全非傳統(tǒng)禁食的情況下，一位41歲的健康的與世隔絕的宗教團(tuán)體成員在禁食的頭幾天每天減重0.9公斤，在禁食的第三周，這一比率降至穩(wěn)定的0.3公斤/天。

基本數(shù)據(jù)跟我差不多 ，一般前3天掉1-3kg，后面每天0.7 0.5 0.6之類浮動 約到后面越少

This rate seems consistent among various experimentally fasted subjects. Most seem to lose about 20% of their body weight during a 30 day fast.

這一比率在各種實驗禁食的受試者中似乎是一致的。大多數(shù)人似乎在30天的禁食中減掉了大約20%的體重。

沒試過30days+，不發(fā)言了。。

The total amount of weight lost in the course of a fasting experiment is not representative of the critical care population. Our patients are infrequently monastic ovolactovegetarians with a normal BMI. Additionally, in a critical care setting the metabochanges in the rate of urinary electrolyte loss during starvationlic demands are greatly increased. One can only estimate that the ICU patient loses weight at a much faster rate, especially if burns, trauma or sepsis are involved.

禁食實驗過程中體重減輕的總量不能代表重癥監(jiān)護(hù)人群。我們的患者很少是體重指數(shù)正常的素食主義者。此外，在重癥監(jiān)護(hù)環(huán)境中，饑餓需求期間尿電解質(zhì)損失率的代謝變化大大增加。人們只能估計重癥監(jiān)護(hù)室患者的體重減輕速度要快得多，尤其是在涉及燒傷、創(chuàng)傷或敗血癥的情況下。

這個肯定 畢竟患者的身體比起健康人肯定有問題，尤其創(chuàng)傷燒傷類，本身還需要額外蛋白修復(fù)以及各種能量供應(yīng)，這個說得通，傻子都懂。但是患者尿電解質(zhì)損失率增加這個暫時理解不了，按理說病人體內(nèi)基礎(chǔ)代謝會更低，理論上每日代謝產(chǎn)物也會低。。怎么電解質(zhì)流逝還多呢

Electrolyte changes during prolonged starvation

The 41 yr old monk lost 0.9kg per day for the first few days of the fast. This initial rapid weight loss is not totally due to the loss of dry nutrient mass. Think about it: the burning of 0.9kg of fat protein and carbohydrate in one day day would yield 3150 kcal in total, which is insane (given that a basal metabolic rate we agreed on is 1800 kcal/day).

The extra weight loss is actually due to diuresis and natriuresis. The urinary loss of the sodium cation is obligatory loss. As ketone anions are lost in the urine, they require a cation to accompany them; initially this is sodium, and later in the fast it is ammonium.

Potassium decreases initially, and remains stable at around 3.0 mmol/L. There is a constant rate of urinary potassium loss, which is thought to be the result of lean tissue dissolving. It seems to parallel the rate of proteolysis, and it seems related to lean body mass.

Magnesium remains surprisingly stable.

Calcium remains stable

Phosphate remains stable

Uric acid levels increase, perhaps as a product of protein catabolism; not only that but urate seems to compete with ketoacids for renal tubular transport sites.

長期饑餓期間電解質(zhì)的變化

這位41歲的僧人在齋戒的頭幾天每天減重0.9公斤。這種最初的快速減肥并不完全是由于干燥營養(yǎng)物質(zhì)的損失。想想看：一天內(nèi)燃燒0.9公斤的脂肪蛋白和碳水化合物總共會產(chǎn)生3150千卡的熱量，這太瘋狂了（考慮到我們商定的基礎(chǔ)代謝率是1800千卡/天）。

額外的體重減輕實際上是由于利尿和利尿。尿中鈉離子的損失是必然的損失。由于酮陰離子在尿液中丟失，它們需要一種陽離子伴隨；一開始是鈉，后來禁食是銨。

很合理，tongniao必然帶走一部分陽離子。而且3150大卡幾乎是正常人2天的基礎(chǔ)代謝量，算算就會發(fā)現(xiàn)不對勁

鉀最初減少，并在3.0mmol/L左右保持穩(wěn)定。尿鉀的流失率是恒定的，這被認(rèn)為是瘦組織溶解的結(jié)果。它似乎與蛋白水解的速率相似，而且似乎與瘦體重有關(guān)。

受組織什么鬼，，應(yīng)該是瘦肉肌把。。這個也合理，當(dāng)瘦肉開始水解后，體內(nèi)蛋白分解會有一個拐點，之后曲線開始走平。。這個有空回頭把另個文獻(xiàn)講解下屆時會有圖表格的說。。

鎂保持驚人的穩(wěn)定。

鈣保持穩(wěn)定

磷酸鹽保持穩(wěn)定

尿酸水平升高，可能是蛋白質(zhì)分解代謝的產(chǎn)物；不僅如此，尿酸鹽似乎與酮酸競爭腎小管轉(zhuǎn)運(yùn)位點。

盲猜這是因為腎小管轉(zhuǎn)運(yùn)位點，這尿酸鹽 et 酮酸 ，準(zhǔn)確說是尿酸根 and 酮酸根 ，使用的系同一種同向轉(zhuǎn)運(yùn)體？

Cardiovascular effects of prolonged starvation

Heart rate decreases, and healthy fasted volunteers may get as bradycardic as 35 BPM.

The heart rate increases again (slightly ) after the 4th week.

Blood pressure decreases, and in the 1982 study by Kerndt et al the subject terminated his fast because the postural hypotension was interfering with his monastic duties.

ECG changes occur: most commonly, a right axis deviation and a decrease in T wave and QRS amplitude. Extreme starvation and malnutrition (eg. in long term prisoners of war) also results in QT interval prolongation, T wave inversion and ST depression.

長期饑餓對心血管的影響

心率下降，健康禁食的志愿者可能會出現(xiàn)35 BPM的心動過緩。

心率在第4周后再次（輕微）增加。

血壓下降，在1982年Kerndt等人的研究中，受試者終止了禁食，因為體位性低血壓干擾了他的修道職責(zé)。

心電圖發(fā)生變化：最常見的是右軸偏移以及T波和QRS波振幅下降。極度饑餓和營養(yǎng)不良（如長期戰(zhàn)俘）也會導(dǎo)致QT間期延長、T波倒置和ST段壓低。

這些其實是能理解的，但是然而。。為啥木有rmr數(shù)值？我我個人感覺這玩意其實對rmr影響更大。。心率四周后開始增加，是線性增加的嘛？

血壓down能理解，合情合理 沒啥好說。

t波右偏，一般兩種，一種先天性的 一般都是女的雌激素少，或者紊亂。后天性的 一般是冠心病or心肌缺血。。估計這和心肌缺血有干吧。。

qts波振幅下降一般是有心臟因素，肺部因素，然后就是營養(yǎng)不良 or 皮膚干燥了。。講到這里懂的都懂了唄。。

QT間期延長也分獲得性and先天性。獲得性主要就是電解質(zhì)紊亂 比如血k低，或者藥物作用。。介個肯定系血k濃度造成得啦。。

T波倒置。。一樣。?？诜鹽即可。。沒啥好說的。。

ST段壓低一般意味著心肌缺血。。