Effects Of Respiratory Acidosis

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Respiratory acidosis #sign and symptoms of Respiratory acidosis Respiratory acidosis ABGs Analyse https://youtu.be/L5MWy1iHacI Plz share n subscribe my chanel is a condition that occurs when the lungs cant remove enough of the Suctioning https://youtu.be/hMJGkxvXTW0 carbon dioxide (CO2) produced by the body. Excess CO2 causes the pH of blood and other bodily fluids to decrease, making them too acidic. Normally, the body is able to balance the ions that control acidity. This balance is measured on a pH scale from 0 to 14. Acidosis occurs when the pH of the blood falls below 7.35 (normal blood pH is between 7.35 and 7.45).Rinku Chaudhary NSG officer AMU ALIGARH https://www.facebook.com/rinkutch/ Respiratory acidosis is typically caused by an underlying disease or condition. This is also called respiratory failure or ventilatory failure. Suctioning https://youtu.be/hMJGkxvXTW0 Normally, the lungs take in oxygen and exhale CO2. Oxygen passes from the lungs into the blood. CO2 passes from the blood into the lungs. However, sometimes the lungs cant remove enough CO2. This may be due to a decrease in respiratory rate or decrease in air movement due to an underlying condition such as: asth

Effects Of Respiratory Acidosis And Alkalosis On The Distribution Of Cyanide Into The Rat Brain

The aim of this study was to determine whether respiratory acidosis favors the cerebral distribution of cyanide, and conversely, if respiratory alkalosis limits its distribution. The pharmacokinetics of a nontoxic dose of cyanide were first studied in a group of 7 rats in order to determine the distribution phase. The pharmacokinetics were found to best fit a 3-compartment model with very rapid distribution (whole blood T1/2 = 21.6 3.3 s). Then the effects of the modulation of arterial pH on the distribution of a nontoxic dose of intravenously administered cyanide into the brains of rats were studied by means of the determination of the permeability-area product (PA). The modulation of arterial blood pH was performed by variation of arterial carbon dioxide tension (PaCO2) in 3 groups of 8 anesthetized mechanically ventilated rats. The mean arterial pH measured 20 min after the start of mechanical ventilation in the acidotic, physiologic, and alkalotic groups were 7.07 0.03, 7.41 0.01, and 7.58 0.01, respectively. The mean PAs in the acidotic, physiologic, and alkalotic groups, determined 30 s after the intravenous administration of cyanide, were 0.015 0.002, 0.011 0.001, and 0.008 Continue reading >>

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  1. taponte

    How to know if you are in ketosis.

    Well i am sure there is another post like this, because i read it before, but i dont remeber exactly what it said and I cant find it.
    The quesiton is just as the title says, how can i know if i am in ketosis or not?
    I have been reading and the people says that at the second day, or thirth day or X day they get in to ketosis, but how they know that?

  2. jumpingjupiter

    If you have never been in Ketosis buy some keto sticks. You can pick them up at most drug stores in the US and Canada. Ask the pharmisist if you can't find them on the shelf. Usually they will be with diabetic supplies. Lots of people will say not to waist your money but they are cheap and I get an instant gratification when I see the test strip turn color. Besides, it is always nice to see evidence that your effort is paying off.
    -odd metalic taste in your mouth and bad breath.
    -Odd smelling urine is another symptom.
    -You will pee like a race horse.
    - I also get cotton mouth (dry mouth and really foamy saliva). Not sure if anyone else gets this.

  3. Andypandy999

    Normally i pee like a race horse for 2 days after my carb up which means im back in ketosis, Breath smells like crap, my wee smells like meat, and i find i get really de-hydrated...

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Hello guys In this video discuss about the basic concept of acidosis and alkalosis and Discuss the topic of respiratory acidosis The cause Sign symptom and treatment Please subscribe my channel for more video And comment which video you want discuss in next videos. Thanks

Respiratory Acidosis, Hypercarbia

Respiratory acidosis is caused by relative hypoventilation. Major risk is associated hypoxemia. Clinical importance depends on context and severity, and rate of change. pH effect is important. Respiratory acidosis is an expected part of planned mechanical hypoventilation in ICU (permissive hypercapnia). Often combination of hypercapnia and hypoxia Most effects are neurologic, ranging from anxiety and confusion to stupor to coma. Management depends on the severity of hypoxemia, acidemia and patient's physiological reserve. Where possible reverse causes of altered mental state, particularly narcotics. If pCO2 > 80 mmHg, particularly if pH < 7.10, immediate mechanical ventilation Treat other medical or surgical emergencies, particularly intracranial. Do not miss the cause for hypoventilation, particularly in a drowsy or unconscious patient: Key diagnostic test is partial pressure of carbon dioxide (pCO2) from arterial blood gasses. Note that venous CO2 will often be only 5 mmHg greater than arterial. Arterial PCO2 reference range: 35 to 45 mmHg How do I know this is what the patient has? pH < 7.35, CO2 > 45 mmHg, Standard base excess (SBE )> 0 mmol/L, bicarbonate >24 mmol/L Acidemia Continue reading >>

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  1. LisaJA

    I'm 5 weeks in and for the past 2 weeks I've had truly repellent, revolting bad breath . My friends and family have rated it about a 7 or 8/10 . My teenager has to open the car windows , it's that bad ! It's ruining my social life - I wouldn't go to a party last weekend for fear of breathing on people :-( I've read up on it as much as I can find and checked - no, it's not down not drinking enough water. No, it's not down to eating too much protein. No, it's not down to oral health care - I brush, I floss, I mouthwash and tongue scrape .( And my mouth is actually loads fresher since removing sugar from my diet .) I read a reply somewhere to a similar question and the person enquired whether the post writer was in weeks 3-6 ..... so this leads me to ask, has anyone else had the bad breath ( possibly just between weeks 3-6 ) and then it gone away ? I really do want to stick to keto, I've lost over a stone already and have another 5 to go .... but this bad breath is a deal breaker ... Please tell me it gets better ........... please ....

  2. charlie_simms

    Strangely, I never got keto breath.

  3. pueve

    Me neither! At least I don't think that I've got kept breath! How do you know that you have it? What does it taste like?

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4.4 Respiratory Acidosis - Metabolic Effects

This can result in dyspnoea, disorientation, acute confusion, headache, mental obtundation or even focal neurologic signs. Patients with marked elevations of arterial pCO2 may be comatose but several factors contribute to this: Anaesthetic effects of very high arterial pCO2 (eg > 100mmHg) As a practical clinical example, the rise in intracranial pressure due to hypercapnia may be particularly marked in patients with intracranial pathology (eg tumours, head injury) as the usual compensatory mechanism of CSF translocation may be readily exhausted. Any associated hypoxaemia will contribute to an adverse outcome. The effects on the cardiovascular system are a balance between the direct and indirect effects. Typically, the patient is warm, flushed, sweaty, tachycardic and has a bouncing pulse. The clinical picture may be modified by effects of hypoxaemia, other illnesses and the patients medication. Arrhythmias may be present particularly if significant hypoxaemia is present or sympathomimetics have been used. Acutely the acidosis will cause a right shift of the oxygen dissociation curve. If the acidosis persists, a decrease in red cell 2,3 DPG occurs which shifts the curve back to the Continue reading >>

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  1. smorgan

    Originally Posted by ShottleBop
    Regarding the derivation of the 46:54 vs. 46:58 ratio for protein, please see these exerpts from the archives oover at Perfect Health Diet: "Ketogenic Diet". This reports the original ratio as 46/54 (which adds up to 100, and, to me, is more intuitive than 46/58): Maybe this "adding to 100" is where the discrepancy crept in. BTW, sources I read attributed the "original" formulation to someone else (the name I mentioned previously - Dr. Woodyatt).
    Adding to 100 has nothing to do with anything. The numbers just give the RELATIVE pro-keto or anti-keto effects of each macro-nutrient based on carbs being 1.0 "against". Fats are 90% pro and 10% against apparently adding up to the same magnitude as carbs. The two numbers for protein don't just relate to each other but to the other three numbers as well, so adding to 1 is irrelevant.
    Not a big difference in any case...

  2. jim55

    Sorry, just now came back. Yes the link worked fine!

  3. smorgan

    Here's another reference which mentions the 0.58 figure. Note that 100 years ago, these folks knew that the difference between glycolisis and ketosis is that the former is "mono-fuel" (glucose only need apply) where the latter is "multi-fuel" (the body is able to use both/either).
    Both Woodyatt and Wilder are mentioned so it doesn't seem like there was any discrepancy between them on the formula:

    A century ago, Woodyatt wrote: “antiketogenesis is an effect due to certain products which occur in the oxidation of glucose, an interaction between these products on the one hand and one or more of the acetone bodies on the other” (Woodyatt,
    1910). Shaffer (1921) calculated the number of “ketogenic” molecules versus molecules of glucose and concluded that the maximal ratio compatible with the oxidation of the “ketogenic” molecules becomes possible when their ratio is at least 1:1. Later, Woodyatt (1921) suggested the following equation for calculating KD composition:
    KR=(0.46 pg + 0.90 fg) : (1.0 cg + 0.58 pg + 0.1fg)
    Where KR is “ketogenic ratio,” g is grams, P is protein, F is fat, and C is CHO.
    Wilder and Winter (1922) defined the threshold of ketogenesis explaining it from the standpoint of condition where either ketone bodies or glucose can be oxidized. They arrived, together with Shaffer and Woodyatt, at the conclusion that KR for induction of
    ketogenesis should be 2:1 or higher.
    This is a very important point, not only methodologically, but also ideologically. The KR invariably indicates whether the CHO proportion is low enough for allowing the fat-mobilizing pathway and ketogenesis, or high enough for blocking it and supporting glycolysis instead. The latter option opens the energy “push” opportunity through CHO intake gateway with the consequences discussed above. On the other hand, ketogenesis introduces a fuel alternative to glucose, which can be crucial in metabolic pathologies. Last sentence: YEAH, LIKE T2 DIABETES!! What a PRICELESS, 100 year-old statement!
    (Emphasis mine)

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