Metabolic Acid-Base Disorders

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TRANSCRIBED BY: Katherine J. Villareal & Renchi Limjoco COPYREAD BY: DDHV

ACID-BASE BALANCE

Maintenance of the hydrogen ion concentration of the body fluids by 3 control systems:

1. Body buffers 2. Lungs – in charge of the pCO2 3. Kidneys – in charge of the HCO3

Chief Buffers in the Blood (to maintain acid-base status):

1. Bicarbonate/Carbonic acid system 2. Plasma proteins 3. Hemoglobin inside RBC

Intracellular buffers:

1. Phosphate 2. Protein

HENDERSON-HASSELBACH EQUATION

H+ = 24 x pCO2 HCO3

-

pH = pK + log HCO3-

H2CO3

= 6.1 + log 24 1.2

= 7.4

pH is the negative logarithm of hydrogen ion concentration

“puissance hydrogen” coined by Hasselbach

Water at 25° contains 1/10,000,000 or 10-7 moles/L of hydrogen ions thus pH = 7

H2CO3 is calculated by multiplying pCO2 by 0.03

Body tries to maintain the HCO3-ratio at 20:1

H2CO3

Normal body pH = 7.38-7.42 (just remember 7.35-7.45)

In extreme cases, pH ranges from 6.8 to 7.7

RENAL REGULATION OF BICARBONATE LEVELS

A. Reabsorption of filtered bicarbonate - HCO3 is a small molecule that is readily filtered. - Primarily absorbed in the proximal tubule (absorbs

>50% of filtered HCO3) - Proximal renal tubular acidosis damage in the

proximal tubules so it will not be able to reabsorb the HCO3, leading to acidosis

B. Addition of “new” bicarbonate - Via secretion of H

+ into the lumen to form carbonic

acid - Mainly in the distal tubule

- Distal renal tubular acidosis results when the distal tubule fails to excrete enough H+ (so your blood has more H+) acidosis

- Average daily acid excretion is 1 meq/kg = 70 meq/day in the form of: 1. Ammonium ion = 50 meq/day

- Most common way - Ammonia is manufactured in the tubules

and is secreted into the lumen - Hydrogen ion attaches ammonium

2. Titratable acid = 20 meq/day - Sulfuric, phosphoric acid

3. Hydrogen ion itself = 0.01 meq/day

Acidosis/Alkalosis – refers to a process which cause acid or alkali to accumulate

Acidemia/Alkalemia – refers to the actual fall or rise in blood pH

Effect of pCO2 and H+ changes on pH:

For every sudden change of 10 mmHg in pCO2 or 10 meq/L of H+, an opposite change occurs about 0.10 in pH Example:

pCO2 pH H+

40 7.40 40

30 7.50 30

50 7.30 50

APPROACH TO PATIENTS WITH ACID-BASE DISORDERS

STEPS: 1. Careful history

- Even before you request for ABG, you should already know what to expect!

- So you can also assess if the results you got are correct, because if it is incompatible with your clinical assessment of the patient, then it may be a lab error

2. Thorough physical examination 3. Analyze blood gas result (pH, pCO2, HCO3

-) to check for

lab errors - Through the acid-base map

4. Determine primary acid-base disorder (i.e. what explains the pH change) - Look at the pH, pCO2, and HCO3

- - General principle: the body does not

overcompensate! 5. Compute for the anion gap

- To find out if there is hidden metabolic acidosis because sometimes it’s not obvious from the pH, pCO2, and HCO3

-

6. Check for mixed disorders. The 4 that can coexist: - One (1) respiratory (either acidosis or alkalosis) with

three (3) metabolic problems namely (a) metabolic

LEGEND: Normal text : lecture and recording

Clinical application: If you have a patient who is not urinating (anuric), end-stage, GFR 0, he would retain 70 meq/day of acid. That’s why patients with renal failure are expected to be acidotic.

Clinical application: Patients with anemia (low hemoglobin, low plasma protein, muscle mass) are at risk of wide swings in pH during illness/injury because of lack of buffers.

METABOLIC ACID-BASE DISORDERS Dr. Albert Chua 02.22.11

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alkalosis, and 2 types of metabolic acidosis: (b) high anion gap and (c) hyperchloremic-normal-anion gap acidosis.

- If you simply look at the pH, pCO2, and HCO3-,

without making any computations, you will only get the primary acid-base problem.

STEP 1 & 2: HISTORY AND PHYSICAL EXAMINATION

Common Settings of Mixed Acid-Base Disorders:

Respiratory Acidosis Respiratory Alkalosis

Metabolic Acidosis

a. Cardiopulmonary arrest

b. Severe pulmonary edema

c. Poisoning

a. Salicylate intoxication b. Sepsis c. Severe liver disease

Metabolic Alkalosis

a. COPD with vomiting or diuretics

a. Critically ill patients b. Severe liver disease

with vomiting

In addition to the 4 combinations presented in the table, Metabolic Acidosis + Metabolic Alkalosis may also occur in the following scenarios: a. renal failure with vomiting b. alcoholic ketoacidosis with vomiting Examples: (refer to the table above) Severe pulmonary edema - difficulty of breathing so there is respiratory acidosis

because CO2 is retained - cardiac function is affected so there is poor perfusion

hence metabolic acidosis Sepsis - expect metabolic acidosis because of the lactic acidosis

that arise from sepsis - sepsis affects the brain making the patient breathe

faster, so expect respiratory alkalosis Renal failure with vomiting - expect metabolic acidosis because of renal failure - vomiting (may be severe) is present so also expect

metabolic alkalosis

STEP 3: FOUR WAYS TO CHECK FOR LAB ERRORS

A. pH, HCO3, pCO2 values must be compatible with Henderson-Hasselbach equation or Acid-Base Map

Example: pH = 7.2; HCO3- = 19; pCO2 = 25

*The above blood gas result cannot be correct based on the acid-base map because if you try the plot the 3 given values, they do not intersect on one point. *Based on the Henderson-Hasselbach equation, the lab result is also not correct. H

+ = 24 x pCO2 = 24 x 25 = 32

HCO3- 19

Expected pH will be = ∆H x 0.1 + 7.4 10 = (40-32) x 0.1 + 7.4 = 7.48 10 B. Check venous CO2 content

- The arterial HCO3 level is usually 1-2 meqs/L less than venous CO2 content. The difference values should not be very far.

C. Potassium levels - Most of the time:

a. ACIDOSIS leads to HYPERkalemia b. ALKALOSIS leads to HYPOkalemia

- This is due to shifting of H+ and K+. If there is too much H+ in the blood, H+ will go into the cell. Since a positive ion went in, a positive ion has to get out, so K+ gets out of the cell to enter the blood. So K+ in the blood is high (i.e HYPERkalemia) but your total K

+ is

really unchanged, it just moved. If acidosis is corrected, the K+ will be normal again.

A change in pH of 0.1 is associated with an opposite change of 0.5 meqs/L in plasma potassium. Example: if pH decreased from 7.3 to 7.2, you expect the K

+ to increase, for example from 3.5 to 4.

D. Plasma chloride relative to plasma sodium and HCO3

- levels - Your sodium and chloride change usually due to the

degree of hydration or water balance. (Remember: serum Na

+ is to assess for water balance!)

- Disproportionate change of chloride to sodium levels indicate acid-base disorders aside from the effect of hydration

- Na+ and Cl- go in the same direction proportionately if there is no acid-base problem (eg. Na+ dropped 10% because you gave additional 10% water, then Cl- will also drop 10%)

Clinical application: Patient is in the ER, with a pH of 7.2 (acidotic), K+ is 3 (also low, recall that normal K is 3.5-4.5). This means that even before the patient became acidotic, his K+ level was already low, lower than his current K+ of 3. If the patient’s normal pH was 7.4 and it went down to 7.2, then there was a 1 meq change in plasma K+, meaning his initial K+ was only 2. What to do: If you treat the pH first (by giving HCO3-), the patient’s potassium will go back to its normal value, and then the patient may have an arrest because you induced him to further hypokalemia. Potassium is very much depleted, so in this case give K

+ first before you treat the pH.

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- Chloride and HCO3- tend to move in opposite

direction: a. Metabolic alkalosis (↑HCO3) chloride levels b. Metabolic acidosis (↓HCO3) or normal

chloride levels; it does not go down because the body also wants to maintain the amount of negatively charged particles (HCO3

- or Cl

-).

Summary: Acidosis: ↓pH; ↓HCO3 or ↑pCO2; ↑K+; if metabolic: ↑Cl- or N Alkalosis: ↑pH; ↑HCO3 or ↓pCO2; ↓K+; if metabolic: ↓Cl-

STEP 4: DETERMINE PRIMARY ACID-BASE DISORDER

SIMPLIFIED ACID-BASE CATEGORIES AS DEFINED BY THE pCO2 AND BICARBONATE LEVELS:

pCO2

mmHg (mean = 40)

Bicarbonate meq/L (mean = 24)

<22 22-26 >26

>45 Combined metabolic and respiratory acidosis

Respiratory acidosis

Metabolic alkalosis and respiratory acidosis

35-45 Metabolic acidosis

Normal Metabolic alkalosis

<35 Metabolic acidosis and respiratory alkalosis

Respiratory alkalosis

Combined metabolic and respiratory alkalosis

EXPECTED COMPENSATION FOR PRIMARY ACID-BASE DISORDERS:

*Need to memorize compensation for metabolic acidosis! *Compensation always goes to the same direction as the original problem.

STEP 5: COMPUTE FOR THE ANION GAP

ANION GAP = Na+ - (Cl- + HCO3-)

Normal value = 10 ± 4 mEq/L

Anion Gap reflects the concentration of those anions that actually are present in serum but are routinely not measured, like: a. negatively charged plasma proteins (mainly albumin) b. phosphates c. sulfates d. organic acids

*So if you have low albumin, you expect the anion gap to be low. Major Causes of a Decreased Anion Gap (nice to know according

to sir) 1. Increased Unmeasured Cations

a. Increased serum cationic proteins: Polyclonal gammopathy, Multiple myeloma

b. Lithium intoxication c. Polymixin B administration

2. Decreased Unmeasured Anions a. Hypoalbuminemia b. Overhydration c. Hyperchloremic acidosis

3. Error in measurements of Na+, Cl

-, or HCO3

- concentration

a. Underestimation of serum sodium concentration (may be seen in patients with increased serum viscosity)

b. Overestimation in serum chloride concentration (may be seen in patients with bromism, a disease caused by chronic exposure to bromine)

c. Overestimation in serum bicarbonate concentration Etiology of METABOLIC ACIDOSIS Normochloremic High Anion Gap 1. Ketoacidosis (ketone bodies are acids)

a. Diabetic b. Ethanol intoxication c. Starvation

2. Poisonings a. Salicylates b. Ethylene glycol c. Methanol d. Paraldehyde

3. Uremia 4. Lactic Acidosis – very common (types below are only nice to

know) a. Type A – most common type. Usually due to:

o Poor tissue perfusion o Shock (cardiogenic, hemorrhagic, septic) o Acute hypoxemia o Carbon monoxide poisoning

b. Type B – no drop in BP. Usually due to: o Various common disorders such as Diabetes

Mellitus, Renal failure, Liver disease, Infection, Leukemia, Pancreatitis, Anemia, Poliomyelitis

o Ingestion or administration of drug or toxic substances: Phenformin, Metformin, Salicylates, Ethanol, Methanol, Sorbitol, Xylitol, Dithiazinine, Cyanide, Streptozotocin, Isoniazid, Nitroprusside

o Hereditary forms: Glucose-6-phosphate deficiency, Fructose 1,6-diphosphatase deficiency

o D-Lactic acidosis in short bowel syndrome *Renal failure can be seen in normochloremic high anion gap acidosis and hyperchloremic acidosis

Disorder Response pH Compensation Limits

Met. Acidosis

HCO3

- pCO2 pCO2 = 1.5 x

HCO3- + 8 + 2

or ∆pCO2 = 1-1.5 x ∆HCO3

-

10 mmHg

Met. Alkalosis

HCO3

-

pCO2 ∆pCO2 = 0.5-1 x ∆HCO3

- 60-70 mmHg

Resp. Acidosis

pCO2 HCO3- Acute: ∆HCO3

- =

0.1 x ∆pCO2

Chronic: ∆HCO3-

= 0.2 x ∆pCO2

32 meq/L 45 meq/L

Resp. Alkalosis

pCO2 HCO3- Acute: ∆HCO3

- = 0.2 x ∆pCO2

Chronic: ∆HCO3-

= 0.5 x ∆pCO2

18-20 meq/L 12-15 meq/L

Clinical application: If you see a patient whose sodium is elevated, but whose chloride is down, what does that mean? Why is the sodium and chloride disproportionate? That’s a clue that you need to check for the acid-base, because there is a problem in the bicarbonate level.

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Etiology of HYPERCHLOREMIC METABOLIC ACIDOSIS (normal anion gap) 1. Hypokalemic Variants

a. Gastrointestinal Causes o Diarrhea is the most common GI cause (where

the patient loses HCO3- but kidney retains Cl

-)

o Small bowel, biliary, or pancreatic fistula o Ureterosigmoidostomy o Cholestyramine chloride ingestion o Administration of ammonium chloride, calcium

chloride, arginine chloride, etc b. Renal Causes

o Carbonic anhydrase inhibitors o Posthypocapnic metabolic acidosis (low HCO3) o Renal tubular acidosis (proximal or distal) is the

most common renal cause (where the patient is acidotic, but urine is alkaline)

2. Hyperkalemic Variants (don’t need to memorize) a. Decreased Mineralocorticoid Secretion

o Addison’s Disease o Hypoaldosteronism o Some adrenogenital syndromes o Hyporeninemic hypoaldosteronism

b. Decreased Mineralocorticoid Action o Renal diseases (eg. interstitial nephritis,

hydronephrosis, early renal failure, etc) o Acute and chronic renal failure

c. Hyperkalemia coupled with ECF Volume Expansion (high K+ inhibit renal NH3 synthesis)

STEP 6: CHECK FOR MIXED DISORDERS

Clues to suspect presence of mixed disorders: 1. A normal pH usually signifies a mixed disorder with the

exception of Chronic Respiratory Alkalosis (because the kidneys may have compensated already)

2. If pCO2 and HCO3-deviate in opposite directions, a mixed

disorder is present 3. A pH change in the opposite direction to that predicted

from the primary disorder signifies a mixed disorder 4. Compute for the predicted compensation and compare

with the actual values.

- Recall compensation for metabolic acidosis. If your computed pCO2 compensation exceeds the actual pCO2 result (from the lab ABG), the patient may have a concomitant respiratory alkalosis (since there is no such thing as overcompensation). If, however, your computed pCO2 compensation is less than the actual pCO2 result, the patient has a concomitant respiratory acidosis.

5. ∆AG = ∆HCO3- (Note: means change)

a. AG = HCO3- (normal compensation)

- Example: 1 meq of acid is titrated (goes down) by 1 meq of HCO3

- - Recall that the normal Anion Gap is 10+4 hence

the upper limit of AG is only 14.

AG is computed as Anion Gap [from the formula Na+ - (Cl- + HCO3

-)] minus a constant 14 [since this is the known upper limit of AG]. Eg. If you computed for AG and you get

20, then AG (20 minus 14) is 6. On the other hand, ∆HCO3

- is 24 [the known

mean normal value of HCO3- ] minus the

given HCO3- [from the lab ABG results]. Eg.

knowing that the normal mean bicarbonate is 24 and if hypothetically there is no other

acid-base problem (i.e. compensation is ∆AG = ∆HCO3

-), you can expect the bicarbonate to change by 6 also (so you expect your ∆HCO3

- ABG result to be 18 from 24 minus 6). If this does not happen, then there may be a mixed problem.

b. If AG >HCO3-

- Think of combined high AG metabolic acidosis and metabolic alkalosis (because something is preventing HCO3

- to drop its amount)

c. If AG <HCO3-

- Think of combined high AG and hyperchloremic metabolic acidosis (because this pushes the HCO3

- down) Urine Anion Gap = (Na + K) – Cl - Normal value = 0 to -50 - Reflects urine NH4 excretion - Positive value seen with distal renal tubular acidosis to

differentiate it from diarrhea

DIAGNOSTIC AND THERAPEUTIC CLASSIFICATION OF METABOLIC ALKALOSIS

Chloride Responsive (Urine Cl < 10 meq/L)

Chloride Resistant (Urine Cl > 20 meq/L)

a. Gastric fluid loss b. Postdiuretic therapy c. Posthypercapnia d. Congenital chloride

diarrhea

a. Primary aldosteronism b. Primary reninism c. Hyperglucocorticoidism d. Hypercalcemia e. Deoxycorticosterone (DOC)

excess syndrome f. Liddle’s syndrome g. Licorice h. Carbenoxolone i. Chloruretic agents j. Bartter’s syndrome k. Potassium depletion

*Chloride responsive – the metabolic alkalosis will be corrected if you give sodium chloride.

TREATMENT FOR METABOLIC ACIDOSIS

Most important in the treatment of acid-base disorders: look for the cause

Emergency treatment: give bicarbonate. You should know how much bicarbonate to give.

Bicarbonate deficit = body weight x 50% x (desired – actual HCO3

-)

*Why 50%? Because water comprises 50% of your body weight and HCO3

- only distributes in the water compartment.

Desired HCO3- is usually 24 which is the mean normal

HCO3-

Correct only half of the deficit (because this is only an estimation and if you overcorrect, you may be introducing another problem), then re-evaluate

Each 50 ml ampule of 7.5% NaHCO3- contains 44.6 meqs

of HCO3-

Preferable to give the NaHCO3- by infusion (push slowly

because it is painful/burning to the blood vessel) as an isotonic solution. Example: incorporating 2 ampules NaHCO3

- into 1 liter of D5W or D5 0.3 NaCl

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HAZARDS OF NaHCO3- THERAPY IN LACTIC ACIDOSIS

1. Hypernatremia – NaHCO3- contains a lot of sodium

2. Volume overload – because sodium will attract water in the interstitial space into the intravascular space (if patient has a weak heart, may have pulmonary congestion)

3. Enhanced lactic acid production 4. Metabolic alkalosis 5. Decreased tissue oxygen delivery – Note that acidosis

compensation is to dilate in the periphery because the body is trying to improve tissue perfusion. If you correct the acidosis with NaHCO3

-, you will push the patient to

alkalosis thus the vessels constrict hence decreased oxygen delivery.

6. Depression of myocardial contractility **Give only in severe acidosis pH < 7.2 (for life-saving) because pH = 7.2 can affect cardiac function (patient may go into arrhythmia, failure).

GENERAL PRINCIPLES IN IV FLUID/ELECTROLYTE AND ACID-BASE MANAGEMENT

1. Do not completely rely on laboratory results - Repeat labs if not compatible with clinical scenario

or clinical manifestation of the patient 2. Correct only half of the computed deficit 3. Correct volume status as priority

- Example: The patient is in shock and metabolic acidosis developed. The treatment is to restore BP because if you restore BP, the acidosis will also be corrected without you doing anything else.

4. Rate of correction is proportional to rate of development of the disorder - If the patient is chronically acidotic, don’t give too

much HCO3- because the patient has already

adjusted to the disorder. Give oral HCO3-, not IV. But

if it is acute, then treat acutely or aggressively. 5. Re-evaluate frequently

- Do blood gas every hour or every 2 hours if necessary

CASES

CASE 1

25 year old male, came to the ER with history of frequent LBM, vomiting, and fever of 4 days duration. Patient is drowsy, non-ambulatory BP = 80/50, HR = 120/min, RR = 36/min, T = 39 C, Wt = 50 kg STEP 1 and 2. Given the history and PE, what derangements will you expect to see when you request for ABG? o Metabolic alkalosis from vomiting o Metabolic acidosis from the diarrhea/LBM (or also

possible from renal failure as you will see from patient’s crea level)

o Respiratory alkalosis because the fever may be a sign of sepsis

Na = 158 meq/L (high), K = 3 (low), Cl = 120 (high) Creatinine = 2 mg% (renal failure present), pH = 7.3, pCO2 = 21, HCO3 = 12 STEP 3. Check in the acid-base map for lab error:

STEP 4. What is the primary acid-base disorder given the ABG? Metabolic Acidosis STEP 5. AG = 158 – (120 + 12) = 26 hence High AG Metabolic Acidosis. Recall that normal AG is 10 ± 4 mEq/L Most probably not from diarrhea because diarrhea will give a normal anion gap metabolic acidosis Cause is probably sepsis or renal failure STEP 6. Check for mixed disorder. a. Expected/calculated pCO2 = 1.5 (12) + 8 = 26 (but the

ABG pCO2 result was only 21) hence the patient may likely have a concomitant Respiratory Alkalosis. Recall that if calculated pCO2 exceeds the ABG pCO2 result, there is a concomitant Respiratory Alkalosis.

b. Compute: ∆AG = 26 (computed AG from Step 5) – 14 (upper

limit of AG) = 12 ∆HCO3 = 24 (normal mean HCO3) – 12 (lab ABG

result) = 12

Since AG = HCO3-, there is no concomitant

Metabolic Alkalosis (contrary to what we initially expected from our history and PE on Step 1 & 2)

FINAL DIAGNOSIS: High AG Metabolic Acidosis with concomitant Respiratory Alkalosis

CASE 2 65 year old male with history of coronary artery disease, admitted for difficulty of breathing and decreasing urine output. BP = 140/80, PR = 110, RR = 30, Wt = 65 kg Bilateral crackles, Grade 2 bipedal edema Serum Na = 125 meq/L (low), Serum K = 6 (high), Chloride = 90 (low), Creatinine = 2 mg/dl (renal failure) pH = 7.23, pCO2 = 50, HCO3

- = 18 CHF, Acute Renal Failure STEP 1 and 2. Given the history and PE, what derangements will you expect to see when you request for ABG? o Respiratory acidosis from difficulty of breathing

Clinical application: 60 kg patient, actual HCO3

- is 15.

Bicarbonate deficit = 60 x 50% x (24-15) = 30 x 9 = 270 meq of HCO3

- Give only half (~130 meq) preferably by infusion.

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o Metabolic acidosis from renal failure (patient has decreased urine output) or from patient’s heart failure (history of CHF)

STEP 3. Check Acid-Base map: no lab error STEP 4. What is the primary acid-base disorder given the ABG? Metabolic Acidosis STEP 5. Anion Gap = 125 – (90 + 18) = 17 hence High AG Metabolic Acidosis STEP 6. Check for mixed disorder. Since pCO2 and HCO3

- went in opposite directions, this case is likely a mixed problem. a. Expected/calculated pCO2 = 1.5 (18) + 8 = 35 (but the

ABG pCO2 result was 50) hence the patient may likely have a concomitant Respiratory Acidosis. Recall that is the computed pCO2 compensation is less than the actual pCO2 result, the patient has a concomitant respiratory acidosis.

b. Compute: ∆AG = 17 – 14 = 3 ∆HCO3 = 24 – 18 = 6

Since AG <HCO3-, this case is a combined High AG

metabolic acidosis and Hyperchloremic metabolic acidosis probably due to renal failure

----------------------------------------------------------------------------------

Orderly disordered SHAWT AWT:

Sa pag-gawa ng trans; Salamat kay Kat Villareal sa pag transcribe ng audio and pag organize! Wuhoo!

Hello sa frating gutom! OH! And iniinvite ko pala ang class sa December, may coming out party kaming i-oorganize para sa isang kaibigan! Abangan!// hahahaha!!

Lastly, Gusto ko lang mag share ng Starbucks funny quote of the month:

“Tinanong sa nanay ko, kung bakit isa daw sa’amin, malaki ang ulo,

Sabi ng nanay ko, wala, ganun lang talaga.” “Hindi naman ako in denial”

–Rey Lim, 2011 For food for thought: http://zeitgeistmovie.com/

Isang malaking YAHOO!!! Hehe. Hindi na kami nagsama ng book part kasi sabi naman ni sir, we just have to understand, so probably magbibigay sya ng cases. Sana makatulong ‘tong trans na to, sana naintindihan nyo. Hehe. Onting bati lang: Hello sa BEST GROUP 10!!! Jewelle, Maro, JM, Dash, Keilah, Eeebee, Maria, Kat Virtusio, Joni, Shar, Keith, Zambeeey! Alam ko madami na sa atin ang super panic dahil ilang araw nalang ang natitira, pero kaya natin to!!! I BELIEVE. Hello din sa original Super Cool and Non-nerdy Ortigas Study Club (SCNN OSC) of the UERMMMCI College of Medicine: Miko Ramoso, Kat Virtusio, May Tiu, at Karen Sta. Ana (you’ll be reading this next year hehe ) and friends: Carlo Tanada and Marth Tarroza. At Hello na din sa PUSOY DOS/Counterstrike/L4D friends: the above mentioned plus

Co-Neil Relato (ADIK KA!!!), Al Omar “Gold Standard” Salting, Reynaldo Lim (hindi na ko hihirit dahil inunahan na ko ni Renchi haha), Mikki Lugti, Renchi Limjoco, at Jamie Manzana. DEAL NA! -Kat J

“When I woke up this morning, I asked myself: what are some secrets of success in life? I found the answer right in my room! Fan said: be cool. Roof said: aim high. Window said: see the world. Clock said: every minute is precious. Mirror said: reflect before you act. Door said: push hard for your goals. And don’t forget, the floor said: kneel down and pray.” Hindi nako makapag-shout-out dahil pine-pressure ako ni Kat J. mag-upload haha. Peace Kat! I’m texting you right now as I type. Thank you Kat and Renchi! I hope this trans helps us, 2012. Intindihan lang natin ang basic principles ng Acid-Base, tas madali na mag-analyze ng cases. God bless us all! – Daph, M.D. (Magiging Doctor)

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Metabolic Acid-Base Disorders