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Clinical Definitions and Diagnostic Aids

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1 Clinical Definitions and Diagnostic Aids
Respiratory acidosis = PaCO2 > 45 mmHg Respiratory alkalosis = PaCO2 < 35 mmHg Metabolic acidosis = HCO3- < 22 mmHg or Base Deficit of < -2 Metabolic alkalosis = HCO3- > 28 mmHg or Base Excess of > +2

2 Case #4 22 year old diabetic found unresponsive
P = 102, BP = 110/80, f = 20, T = 36.2 C ABG PaO2 = 90, PaCO2 = 36, pH = 7.12, HCO3- = 8, BD = -20

3 Metabolic Acidosis Definition: low HCO3- <22 mEq/L or BD < -2
Cause: retained fixed acids (or HCO3- loss) Treatment: Correct cause! Give NaHCO3 if necessary to correct pH to > 7.20

4 Anion Gap In Metabolic Acidosis
[Na+] - ([Cl-] + [HCO3-]) = 8-16 mmol/L If > 18, there are unmeasured anions, such as: lactate ketones salicylate ethanol ethylene glycol (anti-freeze) Anion gap is another common diagnostic calculation. It is used to help differentiate between causes of metabolic acidosis. It should be emphasized that ECF is an electro-neutral solution in which the total number of anions and cations must be equal, such that there is no actual anion gap in plasma! The calculation assesses the difference between unmeasured cations (other than Na+) and unmeasured anions (other than Cl- and HCO3 -). In most cases of metabolic acidosis, the addition of a fixed acid results in lowering of HCO3 through buffering and thus an increased anion gap, according to the calculation shown. In effect the “anion gap” is occupied by the conjugate base anion of the fixed acid (e.g. lactate). In most cases of metabolic acidosis anion gap is increased. If the cause of the metabolic acidosis results in a rise in Cl- (for example diarrhea in which selective HCO3 loss occurs in exchange for Cl), then metabolic acidosis results which is “hyperchloremic” and the anion gap is found to be normal.

5 Compensation: Opposing Metabolic And Respiratory Effects Aimed At Returning pH Towards Its Normal Value Primary Metabolic Acidosis Acute or chronic Decreased HCO3- Response? For every 1 mEq decrease in HCO3- PaCO2 is expected to decrease mmHg Secondary respiratory alkalosis

6 So what does this mean? Lactic Acid + HCO3 ↔ lactate- + H2O + CO2
So increasing Lactic acid leads to lactate replacing HCO3 If anion gap is unchanged in metabolic acidosis suggest other reason for acidosis (eg diarrhoea – loss of HCO3 but gain in Cl-

7 Diagram source unknown

8 Case #2 36 year old heroin addict found unresponsive with needle in arm P = 102, BP = 110/80, f = 5, T = 35.2 C ABG: PaO2 = 70, PaCO2 = 80, pH = 7.00, HCO3- = 23

9 Ventilatory Acidosis Definition – PaCO2 > 45 mm Hg
Ventilatory insufficiency or failure Cause: Hypoventilation Low VA (i.e., low VE and/or high VD) Treatment: Increase VE, lower VD/Vt Eliminate CNS depression of ventilation

10 Compensation: Opposing Metabolic And Respiratory Effects Aimed At Returning pH Towards Its Normal Value Primary Respiratory Acidosis Increased PaCO2 Chronic (> 3-5 days) Response? For every 1 mm Hg increase in PaCO2 HCO3- is expected to increase 0.4 mEq Secondary metabolic alkalosis

11 Case #5 6 week old infant is lethargic with history of vomiting increasing for 1 week P = 122, BP = 85/60, f = 24, T = 37.2 C ABG PaO2 = 90, PaCO2 = 44, pH = 7.62, HCO3- = 36, BE = +12

12 Metabolic Alkalosis Definition: high HCO3- >28 mEq/L or BE > +2
Cause: fixed acids loss Treatment: Correct cause! Prevent HCO3- retention (correct pH to <7.50) (How?) Give acetazolamide(CA inhibitor) or H+ in extremes

13 Compensation: Opposing Metabolic And Respiratory Effects Aimed At Returning pH Towards Its Normal Value Primary Metabolic Alkalosis Acute or chronic Increased HCO3- Response? For every 1 mEq increase in HCO3- PaCO2 is expected to increase mmHg Secondary respiratory acidosis

14

15 Comments On Compensation…
Recall HH – compensation aims to normalize pH by restoring [HCO3]:PCO2 ratio towards normal. The “Primary” disturbance is the one that is consistent with the pH

16 Case #3 16 year old with closed head injury after a fall from 15 feet
P = 132, BP = 115/90, f = 32, T = 37.2 C ABG: PaO2 = 110, PaCO2 = 26, pH = 7.52, HCO3- = 22, BD = 1

17 Ventilatory Alkalosis
Definition – PaCO2 < 35 mm Hg Hyperventilation Cause: High VA (i.e., high VE = f x Vt) Treatment: (usually none!) Decrease VA Sedation

18 Compensation: Opposing Metabolic And Respiratory Effects Aimed At Returning pH Towards Its Normal Value Primary Ventilatory Alkalosis Decreased PaCO2 Chronic (> 3-5 days) Response? For every 1 mm Hg decrease in PaCO2 HCO3- is expected to decrease 2-5 mEq Secondary metabolic acidosis

19

20 Normally blood has a PCO2 of 40 mm Hg which gives us a blood pH of 7
Normally blood has a PCO2 of 40 mm Hg which gives us a blood pH of 7.4, and a HCO3 - concentration of 24 mM. So PCO2, H+ and HCO3 are all dependent variables – i.e. changing 1 changes the others. The Davenport diagram can be used to quickly ascertain if alkalosis is respiratory or metabolic in origin – and is a graphical representation of the above chemical equilibrium. The x-axis represents the pH, the y-axis the HCO3 - concentration, and the back vertical lines are PCO2 isopleths (20, 40 and 60 mm Hg PCO2). A PCO2 of 40 mm Hg with a pH of 7.4 gives a HCO3 - concentration of 24 mM – this is normal for blood values. The red diagonal arrow is called the buffer line and represents what happens to HCO3 - and pH if the PCO2 is changed, e.g. if PCO2 rises to 60 mm Hg, then moving the black dot up the buffer line (to the left) until we reach PCO2 of 60 mm Hg, would give us a pH of 7.25 and a HCO3 of just below 30 mM. This would represent the effects of hypoventilation; as PCO2 increases the reaction (H2O + CO2 reaction) is driven to the right to form more H+ (a drop in pH) and more HCO3 -. On the other hand if the PCO2 falls to 20 mm Hg, then following the buffer line to the right, we see that pH increases and the HCO3 - falls (pH now 7.55 and HCO3 - ~ 20 mM). Remember that the Davenport diagram is just a graphical representation of the CO2 + H2O ↔ H+ + HCO3 equilibrium reaction. On the other hand if a patient has the following parameters pH 7.2, HCO3 - 15 mM and PCO2 40 mm Hg, we can immediately see that the patient has acidosis (pH 7.2!), but with a PCO2 of 40 mm Hg (normal) this is not primarily caused by a respiratory process. Therefore this patient would have metabolic acidosis. You can see that with metabolic acidosis HCO3 - concentrations fall as pH becomes more acidic, whereas with respiratory acidosis HCO3 - levels rise with increasing acidity. Davenport diagram showing the relationships among HCO3-, pH, and PCO2. A shows the normal buffer line BAC

21 pH 7.2, HCO3- 15 mM and PCO2 40 mm Hg ? metabolic acidosis

22 Davenport diagram showing the relationships among HCO
3, pH, and PCO2. . B shows the changes/compensation occurring in respiratory and metabolic acidosis and alkalosis

23 Overview of Potassium Homeostasis
1) Internal potassium homeostasis. Cells exist in a steady state where potassium uptake via the Na/K-ATPase is balanced by potassium leak through ion channels. Regulation of exchange between intra- and extracellular fluid is known as internal potassium homeostasis. Factors which affect internal potassium balance are important in the regulation of plasma [potassium]. Skeletal muscle cells are the major single pool of potassium in the body and are the most important cells in relation to internal potassium homeostasis. 2)External potassium homeostasis. The typical Western diet contains around 80mEq of potassium per day. Maintenance of potassium homeostasis requires that the rate of potassium excretion matches daily intake. This is known as external potassium homeostasis. Fine regulation of renal potassium output is the major control mechanism ensuring external balance. Losses from the GI tract in feces are generally about 10% of dietary intake, though this can become a large source of potassium loss in diarrhea.

24 Factors Affecting Internal K+ Exchanges
K+ ingestion insulin liver, skeletal muscle Exercise epinephrine skeletal muscle (beta2 receptors) K+ cell aldosterone (skeletal muscle) High plasma [K+] Insulin/glucose infusions are used clinically to control hyperkalemia. The final common pathway for increased cellular potassium uptake with insulin, aldosterone and epinephrine is increased Na/K-ATPase activity. Hormonal regulation of internal potassium exchange is an important aspect of potassium balance. Insulin, even at basal levels, affects potassium uptake by liver and skeletal muscle cells. At high concentrations, following a meal, insulin accelerates potassium uptake. Considering that we may eat our entire extracellular potassium content in a single meal, it is vital that ingested potassium be quickly sequestered intracellularly to prevent hyperkalemia. Insulin is very important to physiological potassium balance. Insulin/glucose infusions are used clinically to control hyperkalemia. Aldosterone is secreted in direct response to a rise in plasma potassium. Aldosterone produces a modest increase in uptake of potassium by skeletal muscle. Its more important action is increased renal potassium excretion. Epinephrine and other beta receptor agonists stimulate potassium uptake in skeletal muscle. Its effects are additive with those of aldosterone and insulin. There is increased epinephrine secretion after a potassium rich meal. Epinephrine is also important during exercise. Dynamic exercise is associated with release of potassium from working muscle cells, which is an important aspect of the locally controlled increase in blood flow to working muscle. During intense work, enough potassium may be released to produce potentially dangerous levels of plasma potassium. Trained altheletes have adaptive changes that increase the rate of potassium re-uptake. The high levels of epinephrine associated with exercise are important for stimulating potassium re-uptake. The final common pathway for increased cellular potassium uptake with insulin, aldosterone and epinephrine is increased Na/K-ATPase activity.

25 Alkalosis: Acidosis: Acid/Base Balance (hyperkalemia) (hypokalemia)
• As hydrogen ions move into and out of the cells in the body, there is a corresponding movement of potassium in the opposite direction by ion transport proteins that link hydrogen ion movement to potassium ion movement. This movement helps maintain electrical balance inside the cells. Alkalosis: Acidosis: H+ K+o (hypokalemia) K+ H+ K+o H+ (hyperkalemia)

26 A K+ Load Must Be Quickly Removed To Protect Plasma [K+]
100 K+ moved into cells % response 50 Renal K+ excretion potassium normally enters the ECF via the GI tract, but may also be released from the ICF for example during exercise, acidemia, tissue damage and treatment with betaadrenergic receptor antagonists. The renal response to hyperkalemia is slow, taking minutes to hours to produce. Maintenance of optimal serum potassium therefore requires a control system to temporarily sequester potassium inside cells. These hormonal responses, described above, occur in a few minutes. Time courses for the renal and extrarenal control systems are shown in the slide. 6 12 Hours K+ load

27 Renal K+ Handling Involves Filtration, Reabsorption And Secretion
PCT (FE=30%), TALH (FE=10%) Secretion: DCT & CCD (FE = 10 to 150%)  In states of low dietary potassium intake The rate of renal potassium excretion varies over a wide range according to changes in dietary intake. The rate of renal potassium excretion varies over a wide range according to changes in dietary intake. In states of low dietary potassium intake, renal tubular reabsorption is stimulated and almost all filtered potassium is reabsorbed. More commonly the kidney must deal with the problem of dietary potassium excess. The renal system has a large capacity to increase potassium excretion, with fractional excretion reaching maximally %, compared to a typical value of 10-20% of the filtered load. At all rates of excretion the majority of filtered potassium is first reabsorbed. About 70% of the filtered potassium load is reabsorbed in the proximal tubule and a further 20% is usually reabsorbed in the thick ascending limb of Henle’s loop. In contrast to sodium, potassium is able to enter the urine via secretion. This occurs in the late distal tubule and cortical collecting duct. When potassium excretion is increased, it is potassium secretion that increases. When potassium excretion is reduced, secretion is inhibited and net potassium reabsorption occurs in the collecting duct.  dietary potassium excess FE K+ = 10 – 150+%

28 K+ Excretion Is Determined By K+ Secretion In The Collecting Duct
aldosterone + 3Na+ Lumen Blood K+ Principal cell

29 Case #6 63 year old with history of COPD due to tobacco abuse
P = 92, BP = 135/90, f = 26, T = 37.0 C ABG PaO2 = 65, PaCO2 = 55, pH = 7.34, HCO3- = 31, BE = +9 Acid-base status? Primary disorder? Secondary disorder? Compensation?

30 Case #7 39 year old with history of chronic renal insufficiency due to hypertension P = 82, BP = 148/95, f = 20, T = 36.1 C ABG PaO2 = 88, PaCO2 = 30, pH = 7.33, HCO3- = 14, BD = -11 Acid-base status? Primary disorder? Secondary disorder? Compensation?

31 Mixed Acid-Base Disorders
Most common acid-base disorders Multiple disorders Usually one acidosis and one alkalosis pH usually partially or completely corrected

32 Case #1 Review 26 YO male involve in MVC
Hypotensive and tachycardia at crash scene Altered mental status and multiple severe injuries pH = 7.38; PaCO2 = 30 mm Hg; HCO3- = 18 mEq/L, BD = -8 mEq/L Acid-base status? Primary disorder? Secondary disorder? Compensation?

33 Key Points Acid-base disorders are common and important clinical concerns Accurate diagnosis is essential to proper treatment Primary disorders are complicated by secondary disorders occurring at a different time course


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