Acid-Base Disorders Flashcards
how is acid base controlled within the body normally
labs you would get
buffer systems
1. bicarbonate productionand recycling: from the kidneys
- the principle buffering system of the extracellular fluid (the serum)
- transcellular H+ and K+ exchange (H+ in and K+ out)
- Protein: can act as an acid or a base
- bone: excess H+ can be exchanged for K+ or Na+
lungs
- remove and or retain CO2 via ventilation
Kidneys
- excrete H+ and reabsorb HCO3- OR
- excrete HCO3- and reabsorb H+
depending on what you need
COs controlled by lungs: increased respiration will decrease PCO2 & decreased respiration will increased PCO2
HCO3- is controlled by the kidneys
normal pH: 7.35-7.45
CO2 + H20 = H+ + HCO3-
Labs for understanding acid/base disorders
BMP and ABG
BMP: a venous draw
- CO2 is an indirect measurement of HCO3- (base)
- CO2 high: alkalosis
- CO2 low: acidosis
- electrolytes on the BMP help to calculate the anion gap (comes measured
ABG: arterial blood gas
- pH : > 7.45 will be alkalosis
- < 7.35 will be acidic
PCO2: partial pressure of CO2 in the blood: a measure of ventilation
normal is 35-45
- slower breathing: more CO2 kept in –> forms an acid = acidosis
- faster breathing: more CO2 blown off = alkalosis
HCO3- : bicarb measure
normal 21-28
low bicarb: acidosis
high bicarb: alkalosis
ROME RULE for determining acid base disorder origins
ROME
R= respiratory is O= opposite
HIGH pH = PCO2 LOW = respiratory alkalosis
LOW pH = PCO2 HIGH = respiratory acidosis
M= metabolic is E = equal
HIGH pH = HIGH HCO3- = metabolic alkalosis
LOW pH = LOW HCO3- = metabolic acidosis
Metabolic Acidosis
- two ways it can occur
- two types
how the gap is calculated
- due to an increase in H+ in serum
- due to a decrease in HCO3- in serum
two types
1. increased anion gap
2. normal anion gap
Gap Calculation
- gap = ability to detect the increase in plasma anions (those - and other than HCO3- & Cl-)
- normal gap = 4-12
- > 12 = increased
calculation: (Na+) - (HCO3- + Cl-)
corrected gap = accounts for the amount of Cl- bound to albumin
corrected = measure gap + (2.5 x {4 - serum albumin})
Reasons for an increased anion gap metabolic acidosis
Think of things which will increase the anion concentration within the blood – with the addition of OTHER anions (not just decreasing the level of HCO3- or Cl- and compensating with the ther (HCO3- or Cl-)
the addion of other H+ acids within the body (the ones below) result in an increase use of HCO3- to bind to these acids –> therefore increasing the anion gap (increased amounts of other anions within the blood)
increased anion gap = > 12 meq/L
MUDPILES (GOLDMARK)
M: methanol (toxic alcohol)
U: uremia (from CKD late stages)
D: DKA (conversion of fat to energy results in acids)
P: Paraldehyde (drug)
I: isoniazid, iron (TB med, iron supplements)
L: lactic acidosis (2 kinds) ( non O2 energy)
E: eythlene glycol (from antifreeze)
S: salicylates (NSAIDS overdose)
what happens during a lactic acid metabolic acidosis
lactic acid: increased anion gap metabolic acidosis
L-lactatic acid is most common
-Two types: A & B
A = hypoxic: more common : the result of tissue hypoxia which results in the cells using anaerobic resipiration adn releasing this as a result
B = from a reduced ability of the mitchondria to use oxygen properly due to toxins (metformin) or other meatbolic issues of the body
D-lactic acid: less common
- a carbohydrate malabsorbtion: fermented bacteria within short gut syndrome
- a resulting metabolic acidodis occurs after meals –> leading to ataixa, AMS, slurred speech because of the acidotic state
Ketoacidosis
three types
Ketoacidosis: a type of metablic acidosis with an evelated anion gap
an insulin deficiency + glucagon excess = body using its own fatty acids stores to make energy
the byproduct of this is acids : acetoacetate & beta-hydroxybutyrate
- diabetic ketoacidosis
- hyperglycemia + metabolic acidosis of anion gap due to lack of insulin = ketone production (ACIDS) (treat with giving insulin) - Fasting Ketoacidosis
- hepatic production of ketones due to LOW insulin from a fating state - Alcoholic Ketoacidosis
- alcohol metabolism –> decreases gluconeogenesis –> produces ketones (treat by giving glucose)
Toxin Causing Metabolic Acidosis
Uremic Acidosis
Toxins: increase endogenous secretion of acids which therefore increase the anion gap
Uremic Acidosis
- when the GFR falls below 15-30 the kidneys can no longer produce ammonia (NH4) – accumulaion of anions left with NH3 and H+ – increases the gap
what are the 3 reasons for a normal anion gap metabolic acidosis
- GI loss of HCO3- (diarrhea)
- Renal Tubular Acidosis (RTA)
- Dilutional Acidosis: a rapid volume explansion with normal saline without any bicarb (too much Na+)
(GRD)
What is Renal Tubular Acidosis and how does it cause a metabolic acidosis
- hyperchloremic acidosis = normal anion gap = normal GFR (no diarrhea) = RTA
whats happening: body cant excrete H+ as ammonium, or it cant filter HCO3- back
Subtypes
- ditasl RTA: cant excrete H+ (hypokalemic)
- proximal RTA: excrete too much HCO3- (normal or hypokalemia)
- hyporeninemic hypoaldosteronemic RTA: inhibited ability of ammonia creation due to hypoaldosteronism (with HYPERkalemia)
Metabolic Acidosis
Signs and Symptoms
Diagnosis
Treatment
Symptoms
- signs of the underlying cause
- abdominal pain, N/V
- weakness lethargy confusion & coma
- hyperventilation (compensatory mechanism)
- in severe: kussmaul breathing: deep regular breathing
Diagnosis
BMP
- shows anion gap (elevated or normal)
- +/- hyperkalemia
- decreased CO2 (because acidosis or compensating and trying to blow off CO2)
ABG
- pH: low
- HCO3-: low
- PCO2: low (compensating by getting rid of the CO2)
Treatment
elevated gap
- treat underlying cause
- sodium bicarb used if severe acidosis pH < 7.1-7.2
normal gap
- treat the cause
- if cause is RTA: give oral NaHCO3 or KHCO3 (bicarb) & manage potassium (supplement in type I and II but restrict in type III)
Metabolic Alkalosis
what is it
two subtypes
due to
1. a decrease in the level of H+
2. an increase in the level of HCO3-
the PCO2 : rarely exceeds 55 mmhg (if its more than this, consider a respiratory issue)
Types
1. chloride responsive
2. chloride unresponsive
Chloride Responsive Metabolic Alkalosis
Causes
a loss of extracellular chloride and extracellular volume
Causes
- renal alkalosis : diueretics, PCN/phosphate, post hypercapnia
- GI alkalosis: vomiting/NG tube, transfusion, antacids
lost Cl- = think saline responsive
Chloride Unresponsive Metabolic Alkalosis
Causes
wont respond to saline
Causes
- surpluse of mineralcorticoids: these stimulate sodium reabsorbtion & foster secretion of hydrogen and potassium
- Bartter and GItelman syndrome: metabolic alkalosis + hypokalemia + normotension
- increased alkali ingetsion & poor renal function (cant compensate)
Metabolic Alkalosis
symptoms
Diagnosis
Treatment
Symptoms
- no key signs
- weakness, poor reflexs if hypokalemia
- hypopnea if severe (holding onto CO2)
Diagnosis
ABG
- pH: high
- HCO3- : high
- CO2: high (compensatory increase)
BMP
- increased CO2
- hypokalemia, hypochloremia
Urine Chloride: will differentiate between responsive and not
- responsive: Urine Cl : < 20 ml
- unresponsie Urine Cl: > 20 (normal)
Treatment
chloride responsive :
- give saline to volume expand
- cholride from the saline will reduce bicarb + increase exchange of Cl for bicarb
- if hypokalemia: give KCl
Chloride unresponsive :
- treat underlying cause
- corect the K+
