BADR

B-icarb loss (GI/renal)

A-cid loads (amino acids)

D-ilution by non-bicarb solutions

R-enal deficits (impairment of H+ or NH4 secretions, hyperchloremia, bicarb loss

LUK

L-actic acidosis

U-remia

K-etoacidosis (diabetic, alcohol, starvation)

1. Intraventricular hemorrhage

2. Hypernatremia

3. Hyperosmolarity

4. Left shift of oxyhemoglobin curve

5. Rebound alkalosis

1. pH 7.2 or lower

2. Resp. acidosis has been corrected.

3. Volume status corrected.

mEq HCO₃ = (kg x BE x 0.2)

Give 1/2 calculated dose, then retest ABG

1. CNS depression

2. Neuropathies

3. Sleep disorders

4. Airway obstruction

5. Increased dead space

6. Pulmonary embolus

7. Aspiration

8. Myopathies

9. Chest wall abnormalities

10. Obesity

11. Ventilator malfunction

12. Parenchymal lung dz

13. PNA

14. Interstitial lung dz

1. Large carb loads

2. Intense shivering

3. Thyroid storm

4. TPN

5. MH

6. Prolonged SZ

7. Burns

8. Fever

1. Primary increase in plasma HCO₃

2. Excess retention of bicarb or loss of H^{+ (diuretics - H+ secretion, increased aldosterone - H+ secretion, vomiting or gastric suction, severe hypokalemia and severe hypercalcemia)}

3. Chronic steroid therapy (RA)

1. Primary decrease in HCO₃

2. Consumption of bicarb by a strong nonvolatile acid (gap)

3. Renal/GI wasting of bicarb (diarrhea)

4. Rapid dilution of ECF by a non-bicarb solution (no gap)

SEMP

S-alicylates (NSAIDs)

E-thylene glycol (antifreeze)

M-ethanol (paint thinner)

P-araldehyde (anticonvulsant)

1. Left shift of the oxyhemoglobin curve

2. Tissue hypoxia

3. Hypokalemia

4. Decreased ionized calcium

5. Circulatory depression

6. Coronary vasospasm

7. Neuromuscular irritability

8. Decreased cerebral blood flow

9. Increased SVR

10. Bronchoconstriction

11. Decreased PVR

12. Increased neuronal activity

9. 

1. Prolonged opioid action due to increased protein binding
2. Cerebral ischemia due to decreased blood flow
3. Atria + ventricular dysrhythmia especially with hypokalemia
4. Prolongation of NMB

Base deficit signals

1. Hypoxia
2. Hypoperfusion
3. Inability to utilize O
4. Severity of shock
5. O2 to tissues
6. Adequacy of fluid resuscitation

-2 to 2

-2 to -5.5 (mild)

-6 to -14 (moderate)

<-14 (severe)

< -14 or doesn't correct in 24 hours is a strong indicator of MODS and mortality

1. Atelectasis
2. PNA
3. PE
4. Pleural effusion
5. Hemo/Pneumothorax
6. High altitude with low FiO₂

1. CNS depression
2. High spinal cord lesion
3. Phrenic nerve lesion
4. Neuromuscular disorders
5. Severe kyphoscoliosis
6. COPD
7. Advanced type 1 hypoxia, untreated

1. Myocardial + smooth muscle depression
2. Reduced cardiac cotnractility
3. Reduced SVR
4. Increased PVR
5. Severe tissue hypoxia
6. Less responsive to pressors/catecholamines
7. Decreased threshold for v-fib
8. Progressive hyperkalemia -> cells give up Ca++
9. CNS depression (from CO2 narcosis)
10. Decreased neuronal activity

1. Potentiation of depressant effects of anesthesia to CNS and circulation
2. Decreased airway reflexes
3. Changes the fraction of drugs to non-ionized form
4. Resp. acidosis augments NMBs

1. Hypothermia
2. Hypocarbia
3. Alkalosis
4. Decreased 2-3 DPG

Oxygen affinity increases. Oxygen picks up easier in the lungs, but is harder to release at the tissues.

1. Hyperthermia
2. Hypercarbia
3. Acidosis
4. Increased 2-3 DPG

Oxygen affinity decreases. Easier to unload oxygen at the cells, but more difficult to pick up at the lungs.

1. RR >35
2. VC <15cc/kg adult  <10cc/kg child
3. Negative insp. force <20
4. PaO2 <70mmHg on FiO2 40%
5. A-aO2 gradient >350 mmHg on FiO2 100%
6. PaCO2 >55
7. Vd/Vt >0.6

True/False

The chemical acid-base buffers fixes the problem by soaking up the acid or bicarb.

False

The chemical acid-base buffers do NOT fix the problem, they just soak up the acid or bicarb while waiting for something better.

Renal buffering is measurable within 12 - 24 hours, and it reaches maximum buffering in

5 days.

1. Hemoglobin: Hgb/Hb
2. Proteins: PrH/Pr
3. Bone is a buffer: Soaks up H+ and gives up Ca++. Anyone with chronic acidosis will have brittle bones.

Protein and bones buffer within 2-4 hours.

Phosphates: H₂PO₄/HPO₄

Ammonia: NH₃/NH₄

Urine creates more acids or more CO₂

True/False

Plasma bicarb is immediate, but it cannot fully compensate for respiratory acidosis.

True/False

Changes in PaO₂ stimulates baroreceptors in the brain (medulla) and carotid bodies.

False

Changes in PaO₂ stimulates chemoreceptors in the brain (medulla) and carotid bodies.

True/False

Renal compensation is considered the most powerful and the slowest.

What is a normal A-aDO2_?

Changes in SvO₂ (COAL)

1. C-ardiac output -> is O2 circulating?
2. O-xygen consumption -> tissues using O2?
3. A-rterial O2 content -> do we have enough Hgb?
4. L-oading of Hgb (SaO2) - Hgb loaded with O2?

[(CaO2-CvO2)/CaO2] = 25%

We only use 25% of the oxygen circulating in our body.

This gives us an oxygen reserve.

ABG sample alone - 15 minutes

ABG sample in slush - 60 minutes

Wait 5 minutes for healthy lungs

Wait 30 minutes for diseased lungs.

Kg x 10^3/4

70 kg = 242 ml/min

kg x 8^3/4

70 kg = 194 ml/min

True/False

We must calculate the A-a gradient because we cannot estimate how much oxygen is in the alveoli with end-tidal oxygen concentrations.

Estimates a shunt.

Normal dead space = 1 ml/kg

GETA doubles dead space.

True/False

Dead space is zone 2 and decreases while under anesthesia.

False

Dead space is zone 1 and increases while under anesthesia.

True/False

Dead space changes ETCO₂ and arterial content, not SpO₂.

True/False

If we have hypoventilation, we will have an increased ETCO₂ because of a buildup of CO₂.

False

If we have hypoventilation, we will have a decreased ETCO₂, and that is because most of the exhaled breath is dead space (diluted) even though arterial CO₂ is rising.

DLO₂ = Oxygen diffusing capacity.

21ml/min/mmHg diffusion gradient

Fluid in the lungs changes diffusion of oxygen. We don't measure diffusion with oxygen, we measure it with carbon monoxide.