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PDAT3 > 1 - Acid Base Disorders > Flashcards

1 - Acid Base Disorders Flashcards

1
Q

Type of Disorder resulting from altercations in

CARBON DIOXIDE
CO2
(HCO3- = Base)

A

Resiratory Disorder

Lungs

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2
Q

Metabolic Base

states where…

A
  • *Excess Acid Produced**
  • –> buffering-associated decrease in HCO3-*

Kidneys are unable to retain HCO-3
or there is a GI Loss –> loss in plasma buffering capacity

  • *Renal Hydrogen Ion secretion is decreased**
  • -> decreased reabsorption of HCO3- = renal induced acidosis
  • Loss of Anions*
  • -> cause kidneys to generate/retain HCO3- to maintain neutrality
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3
Q

Alkalosis Vs Alkalemia

A

Alkalosis
abnormal process –> HIGHER Arterial pH

  • *Akalemia**
  • *Blood - Arterial pH**

>7.4

(>7.44)

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4
Q
  • *Arterial Blood Gas**
  • *NORMAL VALUES**

pH / PaCO2 / PaO2 / SaO2

Serum Chemistry Panel
HCO3-

A

7.4

40

24

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5
Q

Winter’s Formula

A
  • *PaCO2 = ( 1.5 x HCO3- ) + ( 8 +/- 2 )**
  • measured*

Used to determine PaCO after respiratory compensation
for Metabolic Acidosis

Respiratory comp occurs very quickly

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6
Q

MUD PILES

A

Major causes for
HIGH-ANION-GAP Metabolic Acidosis

Methanol, Uraemia, Diabetes,

Paraldehyde, Iron (and Isoniazid), Lactate,

Ethylene glycol, and Salicylate

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7
Q

Type of Disorder resulting from altercations in

**BICARBONATE = HCO-3
(PaCO2 = acid)**
A

METABOLIC Disorder

Kidneys

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8
Q

What if MEASURED PaCO2 DIFFERS from the PREDICTED value?
(Winter’s Formula)
Metabolic Acidosis –> Respiratory Compensation

If Actual PaCO < Winter’s prediction…

A

concurrent
resipiratory ALKAlosis

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9
Q

Compensation Chart

A
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10
Q

Delta Ratio > 1.6

►AG / ►​HCO3-

A

Change in HCO3 is less than expected from AG change

CONCURRENT METABOLIC ALKALOSIS

Actual HCO3 > Estimated HCO3
MORE BASIC than EXPECTED = Other Alkalosis occuring

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11
Q

Respiratory Acid

A

CO2 EXCRETION
via the Lungs

VCO2 = CO2 Production

VE = Minute Ventilation
(volume of gas inhaled / exhaled per munite)

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12
Q

Simple A-B Disorder

A

SINGLE Primary etiological acid/base disorder
MOST COMMON

—> Mixed acid base disorder
after first presentation

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13
Q

Decreased Respiratory Rate
Cause of Respiratory Acidosis

A

–> Reduced MINUTE Ventilation Ve

WONT BREATHE (respiratory center)
sedative OD
stroke / infection / sleep apnea
anything that depresses medullary control of RR(respiratory rate)

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14
Q

Excess Acid Production
Type of Metabolic Acidosis

A

Extra-Renal Acidosis​

Lactic Acidosis

Ketoacidosis

Ingestions/Infusions = MUDPILES
Toxic Alcohols =
Methanol /eth-glycol / dieth-glycol / prop-glycol
Salicylate Poisoning

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15
Q

Delta Ratio = 1

►AG / ►HCO3-

A

Nothing else going on,
aside from the Metabolic Disorder

(0.8 -1.6)

Change in AG is due to the change in HCO3

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16
Q

Respiratory Compensation
for Metabolic Alkalosis

A
  • Decreased Minute Ventilation*
  • -> INCREASE CO2 (more acidic)

Predicting That Value:
PaCO2 = (0.7 x HCO3‐measured) + 20 +/‐ 5

if Actual CO2 > Predicted CO2
conc. respiratory ACIDosis
since the actual ACID is GREATER than what we expect

if Actual < predicted = “ ALKAlosis

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17
Q

Metabolic Compensation
for Respiratory ALKAlosis

A

decreased retention / regeneration of renal HCO3

2 phase
Acute = decrease 10 mmHG PaCO : 2 mmol/L HCO3
Chronic = decrease 10 : 4
chronic is more efficient

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18
Q

Clinical Interpretation for
PRIMARY AB-Disorders

ph = 7.4

A

More likely than NOT
7.4 ph is MIXED** or **COMPENSATED
rarely 7.4, body will NOT overcompensate

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19
Q

Causes of
METABOLIC ALKALOSIS
increase in HCO3-

A

Hydrogen Ion Loss
absolute or relative from:
intracellular shift / GI loss / Renal loss

Excess admin/retention of HCO3

Volume of CONTRACTION
around a relatively stable amount of HCO3

20
Q

Excess Admin / Retention of HCO3
Cause of Metabolic Alkalosis

A

Sodium Bicarb
ALONG WITH
hypoVOLemia or reduced effective arterial BV or renal impairment

Massive Transfusion of citrated blood
ALONG WITH:
hypoVOLemia or reduced effective arterial BV or renal impairment

21
Q

Anion Gap

A

JUST A MEASUREMENT TOOL

AG = Na+ - (Cl- + HCO3)

~12

Anions - Cations

22
Q

COMPENSATION

Respiratory –helps–> Metabolic

A

when an AB disorder exists –> body atempts to return pH to normal

Metabolic Disturbance –> Lungs try to compensate

OCCURS QUICKLY
munites -> hours

only 1 phase

23
Q

Hydrogen Ion Loss
Cause of Metabolic Alkalosis

A

Intracellular Shift
hypoKALemia (most K is in cells)
extracellular K will get decreased to bring into cell

  • *GI Loss**
  • *Gastric secretions** = vomit / nasogastric suction

Renal Loss
loop or thiazide DIURETICS
lose water / Na / K (lose K, not potassium sparing)

24
Q

Diminished Renal Acid Secretion
Type of Metabolic Acidosis​

A

Renal Acidosis

Distal (TYPE 1) - RTA
Impaired H+ secretion in distal nephron –> progressive retention
normal Anion-gap metabolic acidosis

TYPE 4 = *hypoaldosteronism*
HYPERKalemia + HYPERChloremic metabolic acidosis

Chronic Renal Failure

25
Q

5 Step Approach

in determining which AB disorder a patient is having

A

Is there a Disorder in the contributors?
HCO3 = 24? // PaCO2 = 40?

Is there an -EMIA? if so ID it
excess acid / loss of base –> ACIDemia

Primary Metabolic or Respiratory?
if pH & PaCO2 are in OPPOSITE directions = RESPIRATORY
If in SAME direction = METABOLIC

If metabolic Disorder…. Acidosis
calculate AG –> delta ratio

Determine Compensation

26
Q

What if the MEASURED HCO3- DIFFERS from the PREDICTED value?

Metabolic Compensation
for Respiratory Acidosis

A

Actual > Predicted Value
( Acute (24hr>x<72) = 10:1 / Chronic = 10 : 3 )
concurrent metabolic ALKAlosis

Actual < Predicted Value
concurrent metabolic ACIDosis
OR
Not yet compensated (timing is key, >24 hours)

27
Q

Metabolic Compensation
for Respiratory Acidosis

A

INCREASED RETENTION
or
Regeneration of RENAL HCO3-

2 phase w/ metabolic compensation
Acute = increase of 10 mmHg PaCO2 to 1 mmol/L HCO3-
Chronic=10 : 3
chronic is MORE efficient

28
Q

Loss of Bicarbonate Base

Type of Metabolic Acidosis​

A
  • Extra-Renal Acidosis​*
  • Does NOT cause an ANION GAP*

Gastrointestinal
Severe Diarrhea, ureteral Diversion

Hyperchloremia
NaCl, CaCl2, etc
bodies attempts to maintain electrical neutrality

29
Q

Clinical Interpretation for
PRIMARY AB-Disorders

pH > 7.4

A

Respiratory ALKalosis
decrease in PaCO2
(acid)

Metabolic ALKalosis
Increase in HCO3-
(base)

30
Q

Causes of Respiratory ALKAlosis
decrease in PaCO2

A

Lungs are stimulated to
remove MORE CO2 than is produced metabolically in the tissues

CENTRAL
Anxiety / pain / fever / infection
injury / psychosis / hyperventilation syndrome / delerium

  • *PERIPHERAL**
  • *hypoxemic conditions** = high altitude / PE
  • *Induced** = iatragenic hyperventilation / intoxications
31
Q

Clinical Interpretation for
PRIMARY AB-Disorders

pH <7.4

A

Respiratory Acidosis
increase in PaCO2
(acid)

Metabolic Acidosis
decrease in HCO3-
(base)

32
Q

Renal Loss of Bicarbonate Base
Type of Metabolic Acidosis​

A

PROXIMAL = Type 2 - RTA
decrease in proximal HCO3- reabsorptive capacity
results in –> bicarb wasting –> fall in serum bicarb conc.

33
Q

Volume Contraction around a relatively stable # of HCO3-
Cause of Metabolic Alkolosis

A

LOSS of large volume of fluids
that has a HIGH CL-, but a low HCO3-
cause to be more BASIC / ALKALINE

HCO3- RISES
in this setting because there is contraction of EC Volume
around a constant quantity of extracellular HCO3
–> CL- simulatneously falls

34
Q

What if MEASURED PaCO2 DIFFERS from the PREDICTED value?
(Winter’s Formula)
Metabolic Acidosis –> Respiratory Compensation

If Actual PaCO > Winter’s prediction…

A

concurrent
resipiratory ACIDosis

35
Q

Causes of Respiratory Acidosis

A
  • reduced MINUTE VENTILATION*
  • *Ve** = (RR) x (VT)
  • Decreased Respiratory Rate* = WONT BREATHE
  • decreased VT* = tidal volume, CANT BREATHER
  • *Increased Deadspace**
  • *VD / VT**
36
Q

Respiratory Compensation

(for Metabolic Acidosis)

A
  • *INCREASED Minute Ventilation** (Ve)
  • -> to decrease CO2 (acid)

Winter’s Formula
used to determine PaCO2 AFTER compensation

37
Q

Decreased Vt (tidal volume)

Cause of Respiratory Acidosis

A

–> reduced Minute ventilation
Ve = RR x Vt

CAN’T BREATHE
(respiratory nerve/muscle fxn)
Diaphragmatic Paralysis
etc.

38
Q
  • *Metabolic Acidosis**
  • decreased HCO3-*
A

MOST COMMON
predominant, when INITIALLY presented

  • *Extra-Renal Acidosis**
  • *Excess Production of Acid
  • Loss of Bicarbonate Base***
  • *Renal Acidosis**
  • Diminished renal Acid secretion*
  • Renal LOSS of bicarbonate base*
39
Q

COMPENSATION

Metabolic –helps–> Respiratory

A

Respiratory Disturbance –> kidneys come to compensate

OCCURS SLOWLY
hours - day

2 Phases
Acute // Chronic
>24 but <72 hours // >72 hours

40
Q

What to do if it is a Metabolic Disorder?
5-Step Approach

A
  • *Calculate AG**
  • *Corrected AG** = Observed AG + 2.5 (4g/dL - obs albumin)

AG = Corrected AG - Normal AG (12)

HCO3- = Normal HCO (24) - measured HCO

Delta Ratio = AG / HCO

41
Q

Increased Deadspace

Cause of Respiratory Acidosis

A

Increased Vd / VT
caused by:

Anatomic Deadspace
short / shallow breathing = decreased Vt

  • *Alveolar Deadspace**
  • *parenchymal lung disease** = COPD / fibrosis
  • decreased perfusion* = severe PE / vascular disease
42
Q

What if the measured HCO3- differs from the predicted value?

Metabolic Compensation
for Respiratory ALKAlosis

A 
Acute = 10 : 2 decrease
Chronic = 10 : 4 decrease
  • *Actual > Predicted**
  • *NOT YET COMPENSATED** or conc. metabolic ALKAlosis

Actual < Predicted
conc metabolic Acidosis

43
Q

Delta Ratio < 0.8

►AG / ►​HCO3-

A

Change in HCO3 is MORE than the expected degree of AG change

CONCURRENT non-AG** **METABOLIC ACIDOSIS

44
Q

Acidosis vs Acidemia

A

Acidosis
abnormal process –> lower ARTERIAL ph if left unopposed

  • *Acidemia**
  • *BLOOD - Arterial pH**

<7.4
(<7.36)

45
Q

STEP 3

If

  • *pH** & PaCO2
  • *Same Vs Opposite Direction**

What type of Acid-Base Disorder?

A

pH & PaCO2 are in….

  • *SAME DIRECTION**
  • *Primary METABOLIC disorder**
  • OPPOSITE DIRECTION*
  • Primary RESPIRATORY disorder*

PDAT3 (23 decks)

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