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PT2B2 > Lecture 51-52 - Acid Base Disorders > Flashcards

Lecture 51-52 - Acid Base Disorders Flashcards

1
Q

what are the “rules” of a “simple” acid base disorder?

A

pH is not brought back to normal by compensation

Bicarb and PCO2 move together

Compensations resolves as primary resolves

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2
Q

metabolic acidosis – characterize the scenarios (what are the values of pH, HCO3 and PCO2)

A

pH low

Decreased HCO3- (Increased H+, decreased pH)

Compensatory Drop in PaCO2 (hyperventilation; secondary respiratory alkalosis)

If simple – then it’s in the predicted range (on the acid base map)

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3
Q

physiological effects of a metabolic acidosis

A
  • Hb-O2 Dissociation shifts Right and increased O2 to tissues
  • Depressed CNS
  • Arrhythmias
  • Decreased Cardiac Contractility
  • Hyperkalemia
  • Decreased pulmonary blood flow
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4
Q

3 classes of adaptation to an acid base disorder; time frame for each

A

Compensation: buffer (immediately)

Compensation: Respiratory/Metabolic response (eg hyperventilate to expel more PCO2, compensating for a metabolic acidosis) (minutes)

Elimination: secretion through the kidney (days)

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5
Q

what three mechanisms are to eliminate extra H+ via the kidney in metabolic acidosis

when does this occur?

A

3-4 days after onset of metabolic acidosis, increased renal excretion of H+ will take place:

1) PCT: H+ secretion, Bicarb reclamation
2) Titratable acids (Phosphates and sulfates)
3) CD: Buffering with NH3 —> NH4+

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6
Q

what is your differential for a high anion gap metabolic acidosis?

A

MUDPILES

Methanol -- Formaldehyde 
Uremia -- creatinine 
DKA  -- ketones 
Propylene Glycol -- increased Osm Gap/Lactate 
Iron Tablets; Isoniazid  - Check Meds 
Lactic acidosis -- Lactate 
Ethylene glycol -- metabolized to Oxalate/Increased Osm Gap; 
Salicylates  -- Level
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7
Q

what is your differential for a normal (hyperchloremic) anion gap metabolic acidosis?

A

HEARD-CCU
Hyperalimentation – eating too much protein/acid
Expansion
Acetazolamide – (CA inhibiton, blocks H+ excretion)
RTA
Diarrhea

Cholestyramine – exchange resisn bind chol and release H+

Carbonic Anhydrase Inhibition

Uteros Igmoidostomy –

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8
Q

if there is a normal anion gap metabolic acidosis, but the urine is alkaline (ph > 5.5) what should you add to your differential?

A

Distal Tubule RTA (TYPE 1)

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9
Q

Renal tubular acidosis Type 1 -

What is the defect? 
Urine ph? 
what is the plasma K?
what is the plasma bicarb?
Complication? 
Causes?
A

defect in H+ secretion of alpha IC cells of the Collecting Tubule (distal); no new HCO3 is generated; metabolic acidosis

urine ph > 5.5

Low plasma K - not secreting H+, therefore not reabsorbing K+ via IC

Plasma bicarb (<15) - Not secreting H+, therefore not generating new HCO3

Complication: Calcium kidney stones

Causes: Autoimmune (Sjogrens, RA), AmphoB, Hypercalciuria

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10
Q

Renal tubular acidosis Type 2 -

What is the defect? 
Urine ph? 
what is the plasma K?
what is the plasma bicarb?
Complication? 
Causes?
A

Defect in PCT reabsorption of HCO3; increased HCO3 excretion; metabolic acidosis

pH < 5.5

Plasma K: Low – wasting of substances that would have otherwise been resorbed in the PCT

Plasma bicarb: > 15

Complication: Rickets

Causes: Fanconi syndrome (generalized PCT dysfunction), Carbonic anhydrase inhibition

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11
Q

RTA type 4 –

what is the defect?
Urine ph?
what is the plasma K?
what is the plasma bicarb?

A

Defect: hypoaldosteronism; (therefore decreased H+ secretion and decreased NH4+ secretion)

Urine Ph < 5.5

Plasma K: Hyperkalemia; because not upregulating ENAC and ROMK channels wth aldo; more K retention

Bicarb: > 15

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12
Q

What is the only acid base disorder that is “maintained” even when the principle issue is resolved ?

A

Metabolic alkalosis

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13
Q

Metabolic alkalosis – describe the situation

A

Primary Problem: Increase of HCO3

PH - increased

Respiratory Compensatory Response: Increased PaCO2 (acidic, eg hypoventilation)

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14
Q

Effects of metabolic alkalosis:

A 
○ Shifts HB-O2 dissociation to the left -- -decreased O2 delivery to the tissues 
		○ Decreased cerebral blood flow
		○ Arrhythmias 
		○ Tetany 
		○ Seizures
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15
Q

potential causes of metabolic alkalosis ?

A

Loss of H+

Extra Renal –
GI: Bicarbonate ingestion, Vomiting (most commonly)
H+ Trancellular shift – Hypokalemia

Renal:
Diuretics

Gain Bicarb
An actual bicarb injection
Citrate infusions (with blood) – converts to bicarb

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16
Q

difference between transient and maintained metabolic alkalosis?

A

Transient –metabolic alkalosis resolves after the increased bicarbonate loading has stopped
Extra Bicarb is lost by the kidney (bicarbinaturia)
Bicarb reclamation is not increased;
H+ secretion is not increased

Maintained: Alkalosis persists even after the increased bicarb has resolved
Increased H+ secretion
Which is manifested by a paradoxical Aciduria

17
Q

three scenarios that can lead to maintained metabolic alkalosis

what will be the clue for maintained metabolic alkalosis?

which is the common scenario

A

Clue: paradoxical aciduria in setting of alkalosis

Three scenarios:
Volume Depletion
CL Depletion – most commonly
K Depletion

18
Q

How does Volume Depletion lead to a maintained metabolic alkalosis?

how do you treat this?

A

Volume Deplete –> increased Na reabsorption
Na initially absorbed with Cl
When CL runs out Na is absorbed with organic acids
When Organic acids run out, Na is exchanged for H+
Increased H+ excretion = paradoxical aciduria and maintenance of alkalosis

Treat: saline

19
Q

How does Chloride depletion lead to a maintained metabolic alkalosis?

how can you treat this ?

A

Beta IC cells function: Dump HCO3- in exchange for Cl -
When the body is Chloride deplete, the function of the alpha IC cell takes over

Alpha IC function: secrete H+, resulting in HCO3- reabsorption

Treat: Saline

20
Q

How does K depletion lead to maintained metabolic alkalosis?

How do you treat this?

A

Really really low K – the renal tubular cells will resorb as much K as possible into the blood, but this is in exchange for H+
Results in an intracellular acidosis
Cells dump H+ into the urine

CANNOT TREAT WITH SALIDE

21
Q

describe the clinical algorithm for a maintained metabolic alkalosis ?

A

Check Urine Chloride -
§ If low – treat with saline
§ If normal — check urine potassium

Urine Potassium
§ If low – suggest K loss from somewhere else (GI)
§ If high — suggest K loss from kidney (possible +/- hyperaldo)

□ Treat: K+ & Anion

22
Q

In regards to respiratory disorders, what is different about the compensatory adaptations?

In light of this difference, what is always important to consider when evaluating the acid/base graphs for predicted ranges of values?

A

No respiratory compensation (bc there is something wrong with the lungs)

There is only: extraceullar buffering, intracellular buffering, and renal secretion changes (but the latter takes days to reach maximally)

acute vs chronic respiratory acidosis/alkalosis

23
Q

Describe the profile of respiratory acidosis

A

Increased PaCO2 (due to poor gas exchange)
Decreased PH
Increased bicarb – Compensatory
This is simple secondary increase in bicarb if withn the appropriate confidence bands (acute, chronic, or btw)

Increased H+ occurs days later (kidey dumps H+ and reclaims HCO3)

24
Q

Causes of respiratory acidosis

A

§ CNS Depression – Narcotics
§ Respiratory Muscle Dysfunctions – myopathies
§ Airway obstruction –
§ Poor Gas exchange – pulmonary edema
Impaired lung motions – Pneumothroax, hemothorax, flail chest

25
Q

Describe the profile of respiratory alkalosis

A 
Decreased PaCO2 
Increased PH 
Decreased HCO3 -- compensatory 
	Simple -- if within the confidence bands 
		Acute, chronic or in btw

§ Decreased renal H+ secretion (increase H+ resorbtion)

26
Q

Causes of respiratory alkalosis

A 
Hypoxemia 
Lung disease
Sepsis -- some patients hyperventilate 
Salicylates
CNS stimulants
27
Q

what clues might lead you to a dx of a mixed acid base disturbance?

A

□ Take H&P
□ Compensation back to normal PH
□ Compensation maps outside the confidence bands
□ Presumed compensatory responses do not resolve

28
Q

what should be the first step for any patient with presumed acid base disturbance?

A

CALCULATE THE ANION GAP

if high, then at least one of the acid base disturbances is a anion gap metabolic acidosis (MUDPILES)

29
Q

what is Winter’s formula and how is it used?

A

PaCO2 = [1.5 x HCO3] + 8

only used in metabolic acidosis to determine if there is appropriate respiratory compensation

PT2B2 (25 decks)

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