2012年11月11日 星期日


Base Excess 的臨床意義

ABG (Arterial Blood Gas)



pH is a measurement of the acidity of the blood, reflecting the number of hydrogen ions present. 
Lower numbers mean more acidity; higher number mean more alkalinity.
pH is Elevated (more alkaline, higher pH) with:

·        Hyperventilation
·        Anxiety, pain
·        Anemia
·        Shock
·        Some degrees of Pulmonary disease
·        Some degrees of Congestive heart failure
·        Myocardial infarction
·        Hypokalemia (decreased potassium)
·        Gastric suctioning or vomiting
·        Antacid administration
·        Aspirin intoxication
·        Lasix
·        Steroid


pH is Decreased (more acid, lower pH) with:
  • Strenuous physical exercise
  • Obesity
  • Starvation
  • Diarrhea
  • Ventilatory failure
  • More severe degrees of Pulmonary Disease
  • More severe degrees of Congestive Heart Failure
  • Pulmonary edema
  • Cardiac arrest
  • Renal failure
  • Lactic acidosis
  • Ketoacidosis in diabetes

pCO2 (Partial Pressure of Carbon Dioxide) reflects the the amount of carbon dioxide gas dissolved in the blood. 
Indirectly, the pCO2 reflects the exchange of this gas through the lungs to the outside air. Two factors each have a significant impact on the pCO2. The first is how rapidly and deeply the individual is breathing:
  • Someone who is hyperventilating will "blow off" more CO2, leading to lower pCO2 levels
  • Someone who is holding their breath will retain CO2, leading to increased pCO2 levels
The second is the lungs capacity for freely exchanging CO2 across the alveolar membrane:
  • With pulmonary edema, there is an extra layer of fluid in the alveoli that interferes with the lungs' ability to get rid of CO2. This leads to a rise in pCO2.
  • With an acute asthmatic attack, even though the alveoli are functioning normally, there may be enough upper and middle airway obstruction to block alveolar ventilation, leading to CO2 retention.
Increased pCO2 is caused by:
  • Pulmonary edema
  • Obstructive lung disease
Decreased pCO2 is caused by:
  • Hyperventilation
  • Hypoxia
  • Anxiety
  • Pregnancy
  • Pulmonary Embolism (This leads to hyperventilation, a more important consideration than the embolized/infarcted areas of the lung that do not function properly. In cases of massive pulmonary embolism, the infarcted or non-functioning areas of the lung assume greater significance and the pCO2 may increase.)

PO2 (Partial Pressure of Oxygen) reflects the amount of oxygen gas dissolved in the blood. It primarily measures the effectiveness of the lungs in pulling oxygen into the blood stream from the atmosphere.
Elevated pO2 levels are associated with:
  • Increased oxygen levels in the inhaled air
  • Polycythemia
Decreased PO2 levels are associated with:
  • Decreased oxygen levels in the inhaled air
  • Anemia
  • Heart decompensation
  • Chronic obstructive pulmonary disease
  • Restrictive pulmonary disease
  • Hypoventilation

CO2 Content is a measurement of all the CO2 in the blood. 
Most of this is in the form of bicarbonate (HCO3), controlled by the kidney. A small amount (5%) of the CO2 is dissolved in the blood, and in the form of soluble carbonic acid (H2CO3).
For this reason, changes in CO2 content generally reflect such metabolic issues as renal function and unusual losses (diarrhea). Respiratory disease can ultimately effect CO2 content, but only slightly and only if prolonged.
Elevated CO2 levels are seen in:
  • Severe vomiting
  • Use of mercurial diuretics
  • COPD
  • Aldosteronism
Decreased CO2 levels are seen in:
  • Renal failure or dysfunction
  • Severe diarrhea
  • Starvation
  • Diabetic Acidosis
  • Chlorthiazide diuretic use

Base Excess or Base Deficit
Whenever there is an accumulation of metabolically-produced acids, the body attempts to neutralize those acids to maintain a constant acid-base balance. 
This neutralizing is achieved by using up various "buffering" compounds in the blood stream, to bind the acids, disallowing them from contributing to more acidity.
About half of these buffering compounds come from HCO3, and the other half from plasma and red blood cell proteins and phosphates.
The words "base deficit" and "base excess" are equivalent and are generally used interchangeably. The only difference is that base deficit is expressed as a positive number and base excess is expressed as a negative number.
A "Base Deficit" of 10 means that 10 mEqu/L of buffer has been used up to neutralize metabolic acids (like lactic acid). Another way to say the same thing would be the "Base Excess is minus 10."
More Negative Values of Base Excess may Indicate:
  • Lactic Acidosis
  • Ketoacidosis
  • Ingestion of acids
  • Cardiopulmonary collapse
  • Shock
More Positive Values of Base Excess may Indicate:
  • Loss of buffer base
  • Hemorrhage
  • Diarrhea
  • Ingestion of alkali


    Source from: http://en.wikipedia.org/wiki/Base_excess

    Comparison of the base excess with the reference range assists in determining whether an acid/base disturbance is caused by a respiratory, metabolic, or mixed metabolic/respiratory problem. While carbon dioxide defines the respiratory component of acid-base balance, base excess defines the metabolic component. Accordingly, measurement of base excess is defined under a standardized pressure of carbon dioxide, by titrating back to a standardized blood pH of 7.40.
    The predominant base contributing to base excess is bicarbonate. Thus, a deviation of serum bicarbonate from the reference range is ordinarily mirrored by a deviation in base excess. However, base excess is a more comprehensive measurement, encompassing all metabolic contributions.

    Definition

    Base excess is defined as the amount of strong acid that must be added to each liter of fully oxygenated blood to return the pH to 7.40 at a temperature of 37°C and a pCO2 of 40 mmHg (5.3 kPa).[2] A base deficit (i.e., a negative base excess) can be correspondingly defined in terms of the amount of strong base that must be added.
    A further distinction can be made between actual and standard base excess: actual base excess is that present in the blood, while standard base excess is the value when thehemoglobin is at 5 g/dl. The latter gives a better view of the base excess of the entire extracellular fluid.[3]
    The term and concept of base excess were first introduced by Poul Astrup and Ole Siggaard-Andersen in 1958.

    Estimation

    Base excess can be estimated from the serum bicarbonate concentration ([HCO3-]) and pH by the equation:[4]
     Base~excess = 0.93 \times \left ( \left [ HCO_3^- \right ] - 24.4 + 14.8 \times \left ( pH - 7.4 \right ) \right )
    with units of mEq/L. The same can be alternatively expressed as
     Base~excess = 0.93 \times [HCO_3^-] + 13.77 \times pH - 124.58


Oxygen Saturation (SO2) measures the percent of hemoglobin which is fully combined with oxygen. 
While this measurement can be obtained from an arterial or venous blood sample, it's major attractive feature is that it can be obtained non-invasively and continuously through the use of a "pulseoximeter."
Normally, oxygen saturation on room air is in excess of 95%. With deep or rapid breathing, this can be increased to 98-99%. While breathing oxygen-enriched air (40% - 100%), the oxygen saturation can be pushed to 100%.
Oxygen Saturation will fall if:
  • Inspired oxygen levels are diminished, such as at increased altitudes.
  • Upper or middle airway obstruction exists (such as during an acute asthmatic attack)
  • Significant alveolar lung disease exists, interfering with the free flow of oxygen across the alveolar membrane.
Oxygen Saturation will rise if:
  • Deep or rapid breathing occurs
  • Inspired oxygen levels are increased, such as breathing from a 100% oxygen source



Protocolized versus non-protocolized weaning for reducing the duration of mechanical ventilation in critically ill adult patients (Review)

The Cochrane Library 2011, Issue 7
Blackwood B, Alderdice F, Burns KEA, Cardwell CR, Lavery G, O’Halloran P

Grand round reporter:林美妙
Date101.12.5

Background
Reducingweaning time is desirable inminimizing potential complications frommechanical ventilation. Standardizedweaning protocols are purported to reduce time spent onmechanical ventilation.However, evidence supporting their use in clinical practice is inconsistent.

Objectives
To assess the effects of protocolized weaning from mechanical ventilation on the total duration of mechanical ventilation for critically ill adults; ascertain differences between protocolized and non-protocolized weaning in terms of mortality, adverse events, quality of life, weaning duration, intensive care unit (ICU) and hospital length of stay (LOS); and explore variation in outcomes by type of ICU, type of protocol and approach to delivering the protocol.

Search methods
We searched the Cochrane Central Register of Controlled Trials (The Cochrane Library Issue 1, 2010), MEDLINE (1950 to 2010),EMBASE (1988 to 2010), CINAHL (1937 to 2010), LILACS (1982 to 2010), ISI Web of Science and ISI Conference Proceedings (1970 to 2010), Cambridge Scientific Abstracts (inception to 2010) and reference lists of articles.We did not apply language restrictions.

Selection criteria
We included randomized and quasi-randomized controlled trials of protocolized weaning versus non-protocolized weaning from mechanical ventilation in critically ill adults.

Data collection and analysis
Three authors independently assessed trial quality and extracted data. A priori subgroup and sensitivity analyses were performed. We contacted study authors for additional information.

Main results
Eleven trials that included 1971 patients met the inclusion criteria. The total duration of mechanical ventilation geometric mean in the protocolized weaning group was on average reduced by 25% compared with the usual care group (N = 10 trials, 95% CI 9% to 39%, P = 0.006); weaning duration was reduced by 78% (N = 6 trials, 95% CI 31% to 93%, P = 0.009); and ICU LOS by 10% (N = 8 trials, 95% CI 2% to 19%, P = 0.02). There was significant heterogeneity among studies for total duration of mechanical ventilation (I2 = 76%, P < 0.01) and weaning duration (I2 = 97%, P < 0.01), which could not be explained by subgroup analyses based on type of unit or type of approach.

Authors’ conclusions
There is some evidence of a reduction in the duration of mechanical ventilation, weaning duration and ICU LOS with use of standardized protocols, but there is significant heterogeneity among studies and an insufficient number of studies to investigate the source of this heterogeneity. Although some study authors suggest that organizational context may influence outcomes, these factors were not considered in all included studies and therefore could not be evaluated.

2012年10月29日 星期一

痛風與飲食 文自:http://ccnia.tnua.edu.tw/~ljk/health2/pulin.htm


痛風病人該如何吃,最近有新發現。在2004年《新英格蘭醫學》期刊中,哈佛醫學院麻省總醫院Hyon Choi 醫生指出,僅肉類、海鮮類食物,才會增加痛風機率,高普林蔬菜不會影響尿酸。
報導╱王雪玲、劉詩翎 攝影╱楊明龍、高大鈞
書田診所家庭醫學科主任何一成表示,過去痛風飲食多半建議採低普林飲食,對高普林食物要嚴格禁止,低普林食物似乎就可放心大吃。應更深入去區分,如高普林食物中,植物性高普林食物較好,低普林食物中澱粉類不要吃太多,以免尿酸不易排出。
飲食注意
尿酸是普林經過肝臟代謝後的產物。而體內普林的來源,除從含核蛋白的食物中取得外,也可由身體自行合成及身體組織分解。
所以談到痛風飲食就會談到食物含普林的多寡,但中華民國營養師公會理事長金惠民指出,痛風飲食不等於完全採低普林飲食,高普林的食物吃進肚子內是否會轉成尿酸目前缺乏臨床證據,只是在痛風發作急性期時,儘量避免高普林食物即可。
採取均衡飲食
何一成主任表示,根據研究,嚴格採低普林飲食控制只能讓血中的尿酸降低1mg/dl(毫克╱每百毫升),痛風病人不必太計較所吃食物普林多寡;但不代表可大吃特吃,因完全不節制,過量食用高普林食物,血中尿酸會上升4mg/dl,最好飲食健議,其實與一般人一樣採均衡飲食即可。
高普林挑著吃食物每百公克食物含150毫克到1000毫克普林,就屬於高普林食物。主要包括酵母粉、黃豆、蘆筍、紫菜、香菇等,還有內臟類食物如豬肝、豬小腸等,另外魚類中的沙丁魚及蝦貝類都屬於高普林食物。
注意
1.高普林食物應再區分是動物性或植物性,動物性如內臟及海鮮類要少吃,而植物性的高普林食物如豆類、香菇、紫菜等仍可適量攝取。衛生署就建議,黃豆及相關製品如豆腐、豆干、豆漿、豆芽等,雖含高量的普林,但因普林的種類與肉類不同,只要急性痛風發作期避免即可,平常還是可以攝取。
2.普林會溶在湯中,所以痛風的人要避免喝肉湯、肉汁及雞精等。
低普林要選擇
食物 低普林的食物是指每百公克含普林僅0到25毫克的食物,如蔬菜類的菠菜、空心菜、芥菜等及各類的水果、奶類;五穀根莖類的馬鈴薯、糯米、麵線等與各種植物油。
注意
1.低普林的飲食對痛風病人不但降低血中尿酸的成效有限外,不少澱粉類的低普林食物,吃太多容易使血糖及脂肪上升,會使身體排除尿酸的能力降低,所以採低普林飲食也要注意,不能毫無限制的攝取澱粉類的食物。
2.油脂類的食物雖然含的普林不高,但油脂會阻擋尿酸的排除,痛風的人也不宜吃太油,可選擇不飽和脂肪酸的油脂如橄欖油、大豆油及葵花油。
3.奶類或蛋類不但是低普林食物,還有助於降低尿酸,若在急性痛風期,無法吃動物性的蛋白質,可改吃奶類或蛋類,來補充蛋白質。另外,痛風的人可多吃葉菜類的蔬菜及水果,因為蔬果多半是鹼性食物,會使身體排出的尿液偏向鹼性,有助於尿酸溶解在尿液中排除到體外。
了解成因 尿酸鹽沈積
痛風是因體內尿酸生成過多或尿酸排泄受阻,導致過多的尿酸鹽沈積在血液及關節處,引起關節腫痛。最易侵襲的部位以足部大腳趾關節最常見,其次是踝關節、足背、膝關節,甚至全身各處關節。
高尿酸血症
罹患痛風的機率會隨著血液中尿酸濃度的增加而上升。男性每100毫升血液中尿酸值7毫克以上,女性6毫克以上,稱為高尿酸血症;有高尿酸血症,但尿酸鹽未累積在關結處,未引發關節腫痛,不算痛風。高尿酸血症只是痛風高危險因子。
避免喝啤酒
喝酒會加速新陳代謝,使肝臟分解尿酸,且酒精代謝後的產物也會抑制腎臟排除尿酸,所以痛風的人要儘量避免喝酒。若要喝酒,同樣的酒精濃度,蒸餾酒會比啤酒好。
喝茶不過量
喝茶可以利尿,使不少人認為喝茶可預防痛風。何一成主任指出,喝茶利尿,但不代表可降低尿酸,且茶葉屬於發芽類也屬於高普林,加上喝茶會促進新陳代謝,也會促使肝臟分解普林,建議每天喝茶不要超過500cc。
多補充水份
建議痛風的人一天要喝3000cc的水以利尿酸排出。且注意補充水份及糖份,如劇烈運動前先喝200cc水,每運動30分鐘再補充200cc水及糖份,缺水會使血液濃縮,尿酸易沈澱在關節等組織中。糖份可避免身體組織分解出普林。
生活配合 必須適當減肥
肥胖會使腎臟排除尿酸的能力降低,所以體重過重的人,可適當減肥,使腎臟容易代謝尿酸,有助於減少痛風的發作。不過減肥的速度不能過快,每周減重0.5公斤。若因減肥斷食或是本身有疾病,導致胃口不佳,要注意補充含糖的食物如蜂蜜、果汁等,以免身體將肝醣代謝完後,就會分解身體本身組織,代謝普林,也會使尿酸升高,引發痛風。
痛風的人若要以劇烈運動來減肥,每次運動時間最好限1小時。劇烈運動時,除會流汗使水份喪失外,肝醣也會來不及分解,使身體組織分解出普林。

2012年10月28日 星期日


梁靜茹 - 不必在乎我是誰


作詞:李宗盛
作曲:李宗盛
編曲:Terence Teo
原唱:林憶蓮

我覺得有點累 我想我缺少安慰
我的生活如此乏味 生命象花一樣枯萎
我整夜不能睡 可能是因為煙和咖啡
如果是因為沒有人陪 我願意敞開心扉

幾次真的想讓自己醉
讓自己遠離那許多恩怨是非
讓隱藏已久的渴望 隨風飛
喔 忘了我是誰
女人 若沒人愛 多可悲
就算是有人聽我的歌會流淚
我還是真的期待 有人追
何必在乎我是誰

我想你說得對 寂寞使人憔悴
是寂寞使人心碎 戀愛中的
人才美
我想我做得對 我想我不會後悔
不管春風怎樣吹 讓我先好好愛一回


梁靜茹 - 夢醒時分



你說你愛了不該愛的人 你的心中滿是傷痕

你說你犯了不該犯的錯 心中滿是悔恨

你說你嚐盡了生活的苦 找不到可以相信的人

你說你感到萬分沮喪 甚至開始懷疑人生

早知道傷心總是難免的 你又何苦一往情深

因為愛情總是難捨難分 何必在意那一點點溫存

要知道傷心總是難免的 在每一個夢醒時分

有些事情你現在不必問 有些人你永遠不必等




梁靜茹 - 問




誰讓你心動 誰讓你心痛 誰會讓你偶爾想要擁她在懷中 誰又在乎你的夢 誰說你的心思她會懂 誰為你感動 如果女人 總是等到夜深 無悔付出青春 她就會對你真 是否女人 永遠不要多問 她最好永遠天真 為她所愛的人 誰讓你心動 誰讓你心痛 誰會讓你偶爾想要擁她在懷中 誰又在乎你的夢 誰說你的心思她會懂 誰為你感動 只是女人 容易一往情深 總是為情所困 終於越陷越深 可是女人 愛是她的靈魂 她可以奉獻一生 為她所愛的人 如果女人 總是等到夜深 無悔付出青春 她就會對你真 只是女人 容易一往情深 總是為情所困 終於越陷越深 可是女人 愛是她的靈魂 她可以奉獻一生 為她所愛的人

痛風及高尿酸血症的處置 - 成醫藥誌

http://140.116.253.135/NewHomePage/manager/form/periodical/file/%E7%97%9B%E9%A2%A8%E5%8F%8A%E9%AB%98%E5%B0%BF%E9%85%B8%E8%A1%80%E7%97%87%E7%9A%84%E8%99%95%E7%BD%AE.pdf