Why Does Potassium Increase In Metabolic Acidosis?

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Anion gap usmle - anion gap metabolic acidosis normal anion gap metabolic acidosis

5.4 Metabolic Acidosis - Metabolic Effects

5.4 Metabolic Acidosis - Metabolic Effects A metabolic acidosis can cause significant physiological effects, particularly affecting the respiratory and cardiovascular systems. Hyperventilation ( Kussmaul respirations ) - this is the compensatory response Shift of oxyhaemoglobin dissociation curve (ODC) to the right Decreased 2,3 DPG levels in red cells (shifting the ODC back to the left) Sympathetic overactivity (incl tachycardia, vasoconstriction,decreased arrhythmia threshold) Resistance to the effects of catecholamines Increased bone resorption (chronic acidosis only) Shift of K+ out of cells causing hyperkalaemia 5.4.2 Some Effects have Opposing Actions. The cardiac stimulatory effects of sympathetic activity and release of catecholamines usually counteract the direct myocardial depression while plasma pH remains above 7.2. At systemic pH values less than this, the direct depression of contractility usually predominates. The direct vasodilatation is offset by the indirect sympathetically mediated vasoconstriction and cardiac stimulation during a mild acidosis. The venoconstriction shifts blood centrally and this causes pulmonary congestion. Pulmonary artery pressure usually ri Continue reading >>

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  1. NeuroGeneration

    tl;dr: I have high FBG (100-115) and postprandial for high sugar experiments (can get as high as 143), regardless of diet (it all started with keto, after which I progressed to VLC, paleo and now, 300+ g/day of mostly "clean" carbs), training or not training for 2 weeks, little sleep or a lot of sleep, etc. I am very lean, muscular and active, all of my blood markers are great (hba1c is borderline at 5.6), have no familial history, am not a high-risk ethnic group, and eat very "clean". Theories include potentially being unintentionally hypocaloric, physiological insulin resistance (but its been weeks), disruptive sleep, overtraining (though I believe I disproved this by taking 2 weeks off with the same #s), or something else altogether. Seeing endocrinologist who does not believe it is diabetes, but agrees it's odd. We're running labs next week. Until then, lab results are included in post below. ANY IDEA WHAT COULD BE GOING ON???
    Hi Guys,
    I've been searching for some answers on this issue for a while, and beyond picking up clues, haven't come to any solid answers. Any help is appreciated.
    My issue is high fasting blood glucose (100 - 115) and relatively high post prandial (as high as 143, typically below 140). Now, before you jump to the conclusion of diabetes (which even my new endocrinologist, who's beginning to run tests doesn't think it is), please read on.
    Throughout my life, I've had a high protein, high carb, low-fat (20-25%) diet, up until about 2.5 years ago. I read a Maffetone book and switched to low-carb, whole foods.
    At first I think I went too far, because I was beginning to show signs of depression. I upped the carbs by a bit (1/2 box of Kashi GoLean Crunch each night!) and I felt better. About 15 months ago, I experimented with keto for 6 months. I fell into chronic depression. My friend reminded me, "don't you remember being depressed the first time?", but I was determined. I suspect a lot of the depression was due to terrible sleep, which was constantly interrupted by very low-carb cortisol / catecholamine spikes. I switched to low-carb paleo. Better, but not enough.
    I bought a glucometer during my keto period to check if I was in ketosis. I was consistently above .7. One day I decided to check my FBG and saw that it was 110. This concerned me, but I then read about physiological insulin resistance (more on this below for those unfamiliar). I also seemed to have reactive hypoglycemia, because after experimenting with a few carbs, post prandial would sometimes drop into the 90's.
    While in paleo, consuming 100-150 g/day of carbs, I pulled out the glucometer again, to find that my FBG was still the same (100 - 115). This concerned me. I decided that since I had done well throughout my life with high carb/protein, low fat, I would go back to it. This was about 4 weeks ago. My FBG is still the same, I feel tired when I wake up (I still move a lot in my sleep, but I'm not nearly as conscious when I wake up as I was during low-carb/keto; definitely more restorative than keto). My post-prandial can slightly exceed 140.
    I'm a very active weight lifter and HIIT trainer. My stats below will tell you more about that – but the point is, I'm very much physically healthy, with plenty of muscle that's being depleted daily, theoretically thirsty to swallow up carbs. Also, I find it odd how my fasting & postprandial numbers are the same, regardless of how few or many carbs I ingest, the timing of my meals, whether I go a couple weeks without exercise or I train intensely for days...
    Here's what I already know / have learned:
    Low carb can cause "physiological insulin resistance." This is well-known and accepted among low-carbers. They treat it as low/no long-term risk, though I don't think anyone has proven that to be the case. I'd prefer to have my blood glucose below 90.
    I'm aware of the dawn phenomenon, but that doesn't seem to be the case for me, since I see high numbers at other times, too.
    I once suspected overtraining, but have ruled that out after going two weeks without training, with no changes to my numbers.
    I may currently be calorically restricted. Could this be an explanation? With keto & paleo I was probably eating about 3,000 cals/day. I've come to learn that my basal rate is 1,900, my training uses 600 - 1000, and I walk 5+ miles /day, so my lifestyle probably burns another 1,000. In other words, I should probably be consuming closer to 4,000 calories. The issue right now is that I do not have the appetite to consume 4,000 calories of whole foods, so this week I decided to add in some gluten-free granola & fruits to up my numbers to be closer to my daily expenditure (at least for now, while trying to figure this out).
    I've included some notable quotes related to low carb / high blood glucose at the bottom of this post. Please at least read the quotes before you comment.
    Stats (taken during paleo / moderate carb phase 5 months ago; may have been hypocaloric. I will have new stats in just over a week):
    Male, 29, 9% bf, 5'10 178lbs
    HbA1c = 5.6
    TSH: 1.82
    Free T3: 3.4
    Free T4: 1.2
    Test: 475
    Free Test: 66

    Note: Libido is moderate to low with occasional spikes
    ALT / SGPT, ALP, Billirubin, Albumin, Tot Prot, Globulin, A/G Ratio all good.
    AST / SGOT slightly high (44); could be from alcohol 2 days prior or exercise 1 day prior.
    Kidney health, bone health, blood health, vitamins & minerals all optimal levels.
    hs-CRP: .02
    LDL: 150
    HDL: 90
    Triglycerides: 76
    I'm not gaining weight / fat, other than a small amount from upping my cals and not training much over the past 2 weeks (maybe 1% increase in bf%; I've had 7-10% bf since I was a child, regardless of diet and activity levels).
    My resting heart rate averaged 56 this week.
    My HRV info for this week:

    AVNN: 1104
    SDNN: 94.7
    rMSSD: 67.5
    pNN50: 31.53
    LF: .301
    HF: .116

    Exercise 5-6 days/wk.
    HIIT 2 days
    weights 4 days
    Most workouts are 45 - 70 minutes
    I throw in some 5-6 mile cardio about 1x/wk
    I meditate daily and do not feel much anxiety / stress. Nearly all of my stress would be physiological.
    Diet & Sleep:

    2.5 years ago: Low-carb diet (not strict, but I'd estimate 150-200 g/day)
    1 year ago: I followed keto for 6 months; began blood glucose / ketone readings, noticed high levels of FBG. Believed it to be gluconeogenesis via physiological insulin resistance
    6 months ago: I switched to VLC / low carb (100-150g/day). Issue remained.
    1.5 months ago: I stopped experimenting with 2x weekly 16-18 hour fasts, after about 9 months
    1 month ago: I progressively added more carbs in.
    Poor sleep for past 18+ months. I fall asleep immediately, but toss and turn a lot (video). I get about 3 periods of 40-50 mins of no movement per night.
    When I'm low-carb, I consciously wake up, energized. When I'm higher carb, I wake up, though barely consciously. I fall back asleep more easily too, with carbs. I presume it's cortisol spurring gluconeogenesis?
    I considered overtraining. I took nearly 2 weeks off with no changes, and have therefor ruled this out.
    I considered low-carb, so I upped my carbs into the hundreds of grams (300-400 /day).

    Note, my mood is much improved after adding carbs back in, but blood glucose issues remain.
    I considered hypocaloric diet. Low carb paleo made me less hungry. Or, rather, not feeling the sensation of hunger as often (no more cravings for food). Over the past 2 weeks I've experimented and have found that I can eat more food than I thought, without feeling full. Being hypocaloric is a theory, leading to blood sugar regulation issues, but I haven't come across many papers on this.
    Poor sleep contributing to poor cortisol / blood sugar control, sparking a negative feedback loop?
    Stimulants. I removed them (coffee, tea) completely for a week with no effect.
    The fact that my numbers don't shift no matter what I do to my diet (add calories, remove calories, add carbs, add sugar, reduce training), my postrprandial never goes beyond 143 even when I have a "test" dessert fest and I never go below 80, I have no familial history, all other blood markers are great, I'm very fit, and these issues persist regardless of carb intake, makes me believe that it's not t1 or t2 diabetes.
    Maybe I'm still not getting enough calories and need to continue to up them? This will be hard with "clean" calories; I think it would require cereals or sugary foods for me to go any higher with my intake at this point.
    Some people on low carb forums state that it takes them 3+ weeks for their FBG to normalize after adding carbs back in (much longer than the 3 days for an OGTT that some quote). Maybe I take a little longer and should give it another week or two?
    Maybe I need to change my final meal timing / size / macronutrient composition, to prevent gluconeogenesis during my sleeping "fast"? Though, I have tried lots of honey (3 tbsp) / cottage cheese (2-3 servings) / nuts (small handful) just before bed with no effect.
    Maybe I'm totally off and it's something else altogether?
    "...asked about his gradual yet progressively rising fasting blood glucose (FBG) level over a 10 year period of paleolithic LC eating. Always eating less than 30g carbohydrate per day. Initially on LC his blood glucose was 83mg/dl but it has crept up, year by year, until now his FBG is up to 115mg/dl. Post prandial values are normal. He wanted to know if he was developing diabetes." http://high-fat-nutr...istance.html[1]
    "Still, a complaint that one sees a lot from people who have been doing glycogen-depleting exercise and intermittent fasting for a while is that their fasting blood glucose levels go up. This is particularly true for obese folks (after they lose body fat), as obesity tends to be associated with low GH levels, although it is not restricted to the obese. In fact, many people decide to stop what they were doing because they think that they are becoming insulin resistant and on their way to developing type 2 diabetes. And, surely enough, when they stop, their blood glucose levels go down." http://healthcorrela...ing.html?m=1[2]
    "Now I had something to tell my dad and others who'd been faithfully doing LC and became horrified, then scared, at fasting blood glucose measurements (which is primarily how the health community screens people for diabetes). I really didn't concern myself with it again—for all these last almost 7 years. OK, so long as post-prandial is fine (caveat: AFTER AN LC MEAL!), nothing to worry about; and combined with good HbA1c, and the fact that so far as we know, this condition will reverse in normal people after a few days of carbage, then just relax.
    ...That was until earlier this year when one of my collaborators, "Duck Dodgers," clued me into something. What if there are no populations on earth that we know of where you can observe the long-term effects of "physiological insulin resistance?""
    ..."then you would expect them to feature "physiological" insulin resistance—just like the thousands of LCers in various forums, my blog comments, and in my dad—right?" http://freetheanimal...hydrate.html[3]

  2. StevesPetRat

    Try thiamine.
    If you require more details, ask.

  3. xEva

    NeuroGeneration, I did the read your whole post, only skimmed it, but this is very common in people who were recently in ketosis due to fasting or a ketogenic diet. It's good that you monitor your BG, that's the best thing to quickly learn what works for you (and how a lot of popular books about diets a wrong or at least incomplete).
    First, it takes 2-3 weeks to adjust to living mostly on glucose (just as it takes a while to adapt to a ketosis). Second, paradoxically, increasing carbs --even simple carbs!-- at the last meal of the day, while at the same time eschewing fats, will get your BG in the normal range quickly. Also B5 and some other vitamins/supplements help, but not as fast as switching to higher carbs and low to no fats. You need to do this only for a while, a week or two, while you adjust. That was my experience.
    This has to do with an ancient adaptation to "ketosis of starvation", when glucose is deliberately ignored by the skeletal muscles as 'protein-sparing' strategy. High levels of fatty acids stimulate this adaptative response (and fatty acids remain high after ketosis due to simple metabolic enertia, that's why eschewing fats for a while helps).
    Also, you need to consider what diet is best for you long-term. You can be on any type of a diet if it is severely calory-restricted. But if your intake of calories is more or less normal, you have to choose either keto or carb. Remaining in this in-between land is no good, as it keeps your glucose levels chronically high and can lead to real insulin resistance.
    Edited by xEva, 13 February 2015 - 06:41 PM.

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What is BLOOD PLASMA? What does BLOOD PLASMA mean? BLOOD PLASMA meaning, definition & explanation. Blood plasma is the pale straw (yellow) coloured liquid component of blood that normally holds the blood cells in whole blood in suspension; this makes plasma the extracellular matrix of blood cells. It makes up about 55% of the body's total blood volume. It is the intravascular fluid part of extracellular fluid (all body fluid outside of cells). It is mostly water (up to 95% by volume), and contains dissolved proteins (6–8%) (i.e.—serum albumins, globulins, and fibrinogen), glucose, clotting factors, electrolytes (Na+, Ca2+, Mg2+, HCO3-, Cl-, etc.), hormones, and carbon dioxide (plasma being the main medium for excretory product transportation). Plasma also serves as the protein reserve of the human body. It plays a vital role in an intravascular osmotic effect that keeps electrolytes in balanced form and protects the body from infection and other blood disorders. Blood plasma is prepared by spinning a tube of fresh blood containing an anticoagulant in a centrifuge until the blood cells fall to the bottom of the tube. The blood plasma is then poured or drawn off. Blood plasma has a density of approximately 1025 kg/m3, or 1.025 g/ml. Blood serum is blood plasma without clotting factors; in other words, "pure" blood. Plasmapheresis is a medical therapy that involves blood plasma extraction, treatment, and reintegration. It is on the WHO Model List of Essential Medicines, the most important medications needed in a basic health system.

The Plasma Potassium Concentration In Metabolic Acidosis: A Re-evaluation

Volume 11, Issue 3 , March 1988, Pages 220-224 The Plasma Potassium Concentration in Metabolic Acidosis: A Re-evaluation Get rights and content The purpose of these investigations was to describe the mechanisms responsible for the change in the plasma [K] during the development and maintenance of hyperchloremic metabolic acidosis. Acute metabolic acidosis produced by HCl infusion resulted in a prompt rise in the plasma [K], whereas no change was observed during acute respiratory acidosis in the dog. After 3 to 5 days of acidosis due to NH4Cl feeding, dogs became hypokalemic; this fall in the plasma [K] was due largely to increased urine K excretion. Despite hypokalemia, aldosterone levels were not low, and the calculated transtubular [K] gradient was relatively high, suggesting renal aldosterone action. Thus, rather than anticipating hyperkalemia in patients with chronic metabolic acidosis due to a HCl load, the finding of hyperkalemia should suggest that the rate of urinary K excretion is lower than expected (ie, there are low aldosterone levels or failure of the kidney to respond to this hormone). Continue reading >>

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  1. LH8540

    Hi all,
    Has anyone found after losing weight with 5:2 fasting that their metabolism is significantly lower than before? The New York Times just wrote a story where many scientists have confirmed that people who lose weight will have slower metabolisms than before: http://mobile.nytimes.com/2016/05/02/health/biggest-loser-weight-loss.html
    I do not want to lose weight from 5:2 only to find that my metabolism is slower than before and won’t be able to keep the weight off unless trying harder than I would have had to before doing 5:2.
    This article talks specifically about 5:2, and a researcher warns that 5:2 fast may slow your metabolism (4th paragraph from the bottom):
    Please share your experiences if you have found your metabolism is slower.


    Take the test in BMI calculator, put your data and weight 300lb note the BMR, let’s that you lost weight 100lb and now with 200lb, see the BMR decreased.
    A person’s metabolism decreases as it weighs less. spends up more energy to move a heavy body,.
    As we have to correct thinning calculate the BMI calculator.

  3. K- Lo

    Anaide, yes, BMR decreases as weight decreases. What the article points out is that the Biggest Losers have BMR significantly lower that the average person at the same weight. And that is why they regain the weight. Not bad habits, not sloth, not anything that people can’t point fingers at. Through no fault of their own, they regain the weight because their metabolisms have slowed to a trickle, so to speak.

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What is BASAL METABOLIC RATE? What does BASAL METABOLIC RATE mean? BASAL METABOLIC RATE meaning - BASAL METABOLIC RATE definition - BASAL METABOLIC RATE explanation. Source: Wikipedia.org article, adapted under https://creativecommons.org/licenses/... license. Basal metabolic rate (BMR) is the minimal rate of energy expenditure per unit time by endothermic animals at rest. It is reported in energy units per unit time ranging from watt (joule/second) to ml O2/min or joule per hour per kg body mass J/(hkg)). Proper measurement requires a strict set of criteria be met. These criteria include being in a physically and psychologically undisturbed state, in a thermally neutral environment, while in the post-absorptive state (i.e., not actively digesting food). In bradymetabolic animals, such as fish and reptiles, the equivalent term standard metabolic rate (SMR) is used. It follows the same criteria as BMR, but requires the documentation of the temperature at which the metabolic rate was measured. This makes BMR a variant of standard metabolic rate measurement that excludes the temperature data, a practice that has led to problems in defining "standard" rates of metabolism for many mammals. Metabolism comprises the processes that the body needs to function. Basal metabolic rate is the amount of energy expressed in calories that a person needs to keep the body functioning at rest. Some of those processes are breathing, blood circulation, controlling body temperature, cell growth, brain and nerve function, and contraction of muscles. Basal metabolic rate (BMR) affects the rate that a person burns calories and ultimately whether that individual maintains, gains, or loses weight. The basal metabolic rate accounts for about 60 to 75% of the daily calorie expenditure by individuals. It is influenced by several factors. BMR typically declines by 12% per decade after age 20, mostly due to loss of fat-free mass, although the variability between individuals is high. The body's generation of heat is known as thermogenesis and it can be measured to determine the amount of energy expended. BMR generally decreases with age and with the decrease in lean body mass (as may happen with aging). Increasing muscle mass has the effect of increasing BMR. Aerobic (resistance) fitness level, a product of cardiovascular exercise, while previously thought to have effect on BMR, has been shown in the 1990s not to correlate with BMR when adjusted for fat-free body mass. But anaerobic exercise does increase resting energy consumption (see "aerobic vs. anaerobic exercise"). Illness, previously consumed food and beverages, environmental temperature, and stress levels can affect one's overall energy expenditure as well as one's BMR. BMR is measured under very restrictive circumstances when a person is awake. An accurate BMR measurement requires that the person's sympathetic nervous system not be stimulated, a condition which requires complete rest. A more common measurement, which uses less strict criteria, is resting metabolic rate (RMR).

Hypokalaemia And Metabolic Acidosis

Home | Education | Hypokalaemia and Metabolic Acidosis 35 year old Aboriginal female presents with a 2/52 Hx of weakness, thirst and nausea. Presents to ED unable to lift her hands. Admitted 3/12 ago with something similar but doesnt know what it was and her medical notes are not immediately available. No other past medical history of note. Examination reveals a quiet, dehydrated lady with generalised non-lateralising weakness in all 4 limbs. Bedside venous blood gas results included: Sinus rhythm with sinus arrhythmia at a rate of 72 bpm. U waves noted most prominently in leads V1-V3 Sinus arrhythmia [sinus rhythm with slight variation (>0.16 seconds) in the sinus cycles] Normal anion gap metabolic acidosis. The 2 most common causes in ED Other causes are many and varied. There are several mnemonics out there the most recent edition of Rosen suggests: F-USED CARS Basically (and rather obviously), a metabolic acidosis is caused by either excess acid or a loss of alkali. Excess acid may be produced by the body itself or may be exogenous. Calculating the anion gap is used in the context of having made a diagnosis of a metabolic acidosis to help determine possible causes. Its an arti Continue reading >>

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  1. silver lady

    As the above asks.
    Replies greatly appreciated XO XO R.

  2. silver lady

    any one???

  3. silver lady


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