Acid Base Disorders Flashcards

1
Q

acids produced by the body (+source) (4)

A
  1. sulfuric, phosphoric and uric acids - metabolism
  2. ketone bodies - fat oxidation
  3. lactic acid - anaerobic glucose metabolism
  4. carbonic acid - dissolved CO2
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2
Q

normal pH of body

A

7.38-7.42

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3
Q

mechanisms body uses to maintain alkaline pH

A
  1. buffer system of blood
  2. lungs regulate carbonic acid concentration
  3. kidneys regulate bicarb concentration
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4
Q

normal ratio bicarb/carbonic acid

A

20 parts bicarb to 1 part carbonic acid

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5
Q

carbonic acid

A

H2CO3

CO2 + H2O conversion by carbonic anhydrase in kidney

dissociates into H+ and bicarbonate ions

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6
Q

renal control of pH (H+)

A

H+ ions enter renal tubule in exchange for sodium ions

sodium enters plasma with HCO3

maintains concentration of sodium w/in body and removes acid

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7
Q

metabolic acidosis lab valvues

A

low pH

low bicarbonate

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8
Q

metabolic alkalosis

A

high pH

high bicarbonate

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9
Q

respiratory acidosis

A

low pH

high pCO2

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10
Q

respiratory alkalosis

A

high pH

low CO2

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11
Q

acidosis symptoms (CNS)

A

DEPRESSION of CNS

cardiac arrhythmia (hyperK)

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12
Q

alkalosis symptoms (CNS)

A

EXCITED CNS

altered mental status, spasm, contraction, seizures

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13
Q

acidosis symptoms (cardiac, vascular, pulmonary)

A

decreased CO, arrhythmias, increased risk of VFib

vasodilation/HoTN

vasoconstriction in lungs, hyperventilation (move blood thru faster and unload CO2)

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14
Q

alkalosis symptoms (cardiac, vascular, pulmonary)

A

increased contractility (then decrease) refractory ventricular arrhythmia

coronary vasospasm/constriction

vasodilation of pulmonary vasculature, hypoventilation (move blood thru slower)

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15
Q

acidosis symptoms (Neuro, endocrine)

A

confusion, coma

insulin resistance, inhibitor of ATP synthesis

hyperkalemia

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16
Q

alkalosis symptoms (Neuro, endocrine)

A

cerebral vasoconstriction – HA, lethargy, tetany, seizures

hypokalemia (all low electrolytes)

stimulation of anaerobic glycolysis/lactic acid production

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17
Q

acid base disturbance with normal ABG

A

compensatory acid base disorders often develop to counteract

however, the body NEVER overcorrects

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18
Q

2 things req. for diagnosing acid base problems

A

arterial blood gas
basic metabolic panel

clinical presentation often clues you in

management is focused on correcting UNDERLYING cause

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19
Q

pH values

normal, panic

A

normal: 7.35-7.45
panic: <7.3, >7.6

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20
Q

pCO2 values

normal, panic

A

norm: 35-45 mmHg

Panic: <20 or >70

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21
Q

HCO3 values

normal, panic

A

normal: 22-26
panic: <10, >40

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22
Q

venous blood gas

A

convert venous sample measurements to arterial if this is what is given

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23
Q

steps in approaching an acid base problem

A
  1. academia or alkemia?
  2. respiratory or metabolic?
  3. acute or chronic (if respiratory)?
  4. anion gap? (metabolic acidosis)
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24
Q

respiratory acidosis patho

A

increased pCO2

lungs fail to excrete carbon dioxide –> retention leads to rise in pCO2 in plasma

increased formation of carbonic acid and lowered pH

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25
compensatory mechanisms of respiratory acidosis
stimulate kidney to make more bicarb hold onto bicarb and excrete acid
26
respiratory acidosis lab values (clinical)
pH: low pCO2: high HCO3: elevated
27
causes of respiratory acidosis
sleep apnea stroke choking pneumonia CNS depressive meds (opioids) rib fracture/chest wall trauma
28
respiratory alkalosis
hyperventilation which lowers plasma carbonic acid
29
respiratory alkalosis compensatory
increasing renal excretion of bicarbonate
30
respiratory alkalosis labs
pH high pCO2 low HCO3 normal to low
31
causes of respiratory alkalosis
hypoxia (hyperventilation, high altitude) CNS problems (pregnancy, gram - sepsis) Pulmonary (PE)
32
increased amount of plasma bicarb
metabolic alkalosis often has concomitant K+ depletion and volume contraction
33
metabolic alkalosis compensatory mechanisms
decreased RR inefficient bc can't decrease RR enough to cure the issue
34
what induces metabolic alkalosis
diuretic therapy loss of gastric secretions (vomiting or nasogastric suction) large amounts of exogenous alkali
35
elevation in plasma bicarbonate concentration can result from
hydrogen loss hydrogen movement into cells alkali administration volume contraction
36
increased net bicarbonate reabsorption by kidney
volume and potassium depletion prevents excess bicarbonate from being excreted, worsening alkalosis
37
why does volume depletion cause increased renal bicarbonate?
kidney tries to hold onto Na+ to increase free water therefore, kidney reabsorbs sodium bicarbonate from tubule and water follows
38
potassium depletion increases metabolic alkalosis by:
1. hydrogen loss | 2. H+ movement into cells
39
hydrogen loss in metabolic alkalosis
potassium depletion causes distal pumps in kidney secrete H+ in exchange for K+
40
movement of hydrogen into cells worsens metabolic alkalosis by
H+ is moved into cells to move K+ out intracellular environment is acidotic, so H+ secretion by kidneys increases also raises plasma bicarb concentration, H+ is no longer in serum suffer
41
kidney compensation for K+ loss is ba bc
tries to correct volume contraction by absorbing sodium bicarbonate and excreting hydrogen worsens alkalosis req. simultaneous correction of K+ def.
42
etiologies of metabolic alkalosis (6)
1. GI acid loss 2. renal acid H+ loss 3. post-hypercapnia alkalosis 4. milk-alkali syndrome 5. administration of exogenous alkali 6. metabolic contraction alkalosis
43
metabolic alkalosis from GI acid loss
H+ in stomach is removed (vomiting or suctioning off) but no stimulation to stop producing bicarbonate therefore: net hydrogen loss and bicarbonate is still being produced/reabsorbed from kidney (decreased H w/o decreased HCO3)
44
metabolic alkalosis renal acid loss is caused by which hormone?
aldosterone
45
high levels of aldosterone cause
1. stimulation of H+ secretion in renal tubule 2. tubule lumen is more electronegative so Na+ reabsorption is not = to H+ loss distal K+ secretion is enhanced, resulting in concurrent hypokalemia
46
renal acid loss metabolic alkalosis
typically presents in pts on loop diuretic or TZD increase in H+ secretion and volume contraction = metabolic alkalosis
47
post hypercapnic metabolic alkalosis
COPD/acidosis pts hold onto bicarbonate to control mild respiratory acidosis the acidosis is rapidly fixed but kidney doesn't get stimulation to decrease Bicarb causing metabolic alkalosis
48
metabolic alkalosis due to milk alkali syndrome results when
1. increased alkaline load (oral calcium) 2. hypercalcemia-mediated constriction of afferent arteriole, induces renal AKI too much bicarb + increased base going in + kidney can't get rid of excess
49
metabolic alkalosis due to administration of exogenous alkali
giving large amounts of sodium bicarbonate or citrate 1. blood infusion (>8 units) 2. citrate rather than heparin to anticoagulant 3. extensive use of crack cocaine 4. FFP administration during plasmapheresis 5. correction alkalosis
50
metabolic contraction alkalosis
loos of relatively large volume of bicarbonate free fluid contraction of extracellular volume around constant quantity of extracellular bicarbonate
51
what causes metabolic contraction alkalosis
use of IV loop diuretics underlying electrolyte disorder coupled with high chloride loss
52
saline responsive metabolic alkalosis patients vitals
normotensive, volume contracted and hypokalemic
53
saline unresponsive patient vitals
normo or hypotensive fluid overloaded
54
causes of saline responsive metabolic alkalosis
renal causes (diuretic use, post-hypercapnia alkalosis) GI causes (vomiting/suctioning/diarrhea, exogenous alkali)
55
diuretic use and saline responsive metabolic alkalosis
high NaCl and H2O loss from meds cause contraction of vascular volume and relative concentration of HCO3 increases
56
treatment of saline responsive metabolic alkalosis
1. correction of volume depletion with normal saline | 2. correction of potassium depletion
57
correction of volume depletion in saline metabolic alkalosis
less bicarb and sodium reabsorbed, no longer volume contracted more bicarbonate secreted by kidney
58
correction of potassium depletion in saline metabolic alkalosis
K+ moves into cells, H+ moves out increased extracellular H+ buffers H+ leaving the cell causes pH to return to normal (stop kidney secretion of H+ and reabsorption of bicarb)
59
causes of in saline non responsive metabolic alkalosis
hyperaldosteroneism (kidney retains sodium and H+ is excreted) milk alkali syndrome
60
treatment of in saline unresponsive metabolic alkalosis
1. if pt is hypokalemic, KCl will correct both hypokalemia dn alkalosis 2. Acetazolamide (diamox) = inhibits renal sodium bicarb reabsorption and causes diuresis
61
mechanisms of metabolic acidosis
1. increased acid generation (ketoacidosis and lactic acidosis) 2. loss of bicarbonate (diarrhea) or bicarbonate precursors (ketoacidosis) 3. diminished renal excretion
62
amount of acid produced exceeds body's buffering capacity
metabolic acidosis fall in concentration of bicarbonate bc it is consumed in neutralization of excess acid
63
etiologies of metabolic acidosis
1. intestinal loss of bicarb 2. renal tubular acidosis 3. excessive acid production/diminshed excretion 4. lactic acidosis 5. poisons
64
metabolic acidosis due to intestinal loss of bicarb
too much acid precursor without bicarbonate excretion
65
metabolic acidosis due to RTA
genetic defect: kidney can't excrete adequate H+ or reabsorb adequate HCO3 three types (I, II, IV) hyperchloremic, metabolic acidosis w/o anion gap normal GFR, no diarrhea
66
uremia and metabolic acidosis
AKI or late stage CKD failing kidneys can't excretion acids from normal metabolism
67
ketosis and metabolic acidosis
metabolism of fat produces excess ketone bodies and decreases bicarbonate precursors found in DM, starvation, alcohol
68
lactic acid is normally produced?
by RBCs, skeletal muscles, skin, and brain metabolized by liver and kidney
69
when does accumulation of lactic acid occur?
``` tissue hypoxia (over production) hepatic failure (deficient removal) circulatory collapse ``` esp. seen in sepsis, bowel or extremity infarction, respiratory failure, seizures
70
main clinical feature of lactic acidosis?
hyperventilation this is due to the compensatory mechanisms this level exceeds 4-5 meq/L
71
poisons that can cause metabolic acidosis
``` carbon monoxide cyanide ethylene glycol methanol meds ```
72
meds that cause metabolic acidosis (5)
iron isoniazid metformin ibuprofen salicylates
73
carbon monoxide
odorless, colorless gas from exhaust, fire comes from improperly ventilated heater/appliances CO has a large affinity for HgB 250x that of oxygen -- therefore CO never unloads
74
10-20% carboxyhemoglobin
HA, dizziness, abd pain or nausea
75
30-40% carboxyhemoglobin
confusion, dyspnea, syncope
76
50-60% carboxyhemoglobin
HoTN, coma, seizures survivors may have permanent neurological deficits
77
treatment of CO poisoning
high flow oxygen HBO
78
Cyanide poisoning (patho, symptoms, tx)
cells fail to take up arterial oxygen HA, nausea, abdominal pain, dizziness, confusion, shock, seizures, death tx: cyanide antidote package
79
where is cyanide found?
``` industry labs apricot pits nitroprusside fires of burning plastics (firefighters) ```
80
methanol poising
wood alcohol organic solvent found in paint remover, industrial cleaners, and perfumes
81
when does methanol become harmful
metabolized to formaldehyde and then formic acid which accumulates metabolic acidosis and several adverse effects
82
methanol intoxication occurs byL
children ingesting poisons accidentally alcoholics substituting methanol for ethanol bootleg alcohol inhalation of methanol fumes by factory workers
83
effects of methanol
rapid retinal edema and permanent vision loss development of parkinsonism like movement disorder due to accumulation of formic acid in the putamen
84
methanol toxicity workup
anion gap metabolic acidosis osmolar gap methanol levels are detected, but not accurate if severe symptoms (vision loss) hemodialysis is indicated
85
ethylene glycol toxicity
found in antifreeze and radiator fluid, taste sweets occurs due to accidental ingestion, suicide attempts its appear drunk and develop severe anion gap acidosis, tachypnea, confusion, seizures and coma
86
ethylene glycol toxicity workup
serum calcium level and UA looking for calcium oxalate crystals profound anion gap acidosis and hypocalcemia
87
tx for methanol/ethylene glycol
ethanol - actual booze fomepizole (antizol or 4MP) - preferred slow conversion of methanol or ethylene glycol to toxic metabolites, therefore allowing them to be excreted hemodialysis is also one
88
anion gap
sorry out cause of metabolic acidosis represents unmeasured anions in serum sample Na - (HCO3 + Cl), normal value is 8-16
89
why is the anion gap useful?
bc irregardless of pH or HCO3 levels presence of increased anion gap always means there is underlying anion gap metabolic acidosis
90
decreased anion gap
low level of negative ion charge BAM Bromisim Albumin Multiple Myeloma
91
normal anion gap DURHAM
``` DURHAM Diarrhea Ureteral diversion Renal Tubular acidosis Hyperalimentation Addison's disease/Acetazolemide Miscellanous ```
92
increased anion gap
``` MUD PILES Methanol Uremia DKA/Drugs (metformin) Phosphate/paraldehyde Ischemia/Iron Lactate Ethylene Glycol Starvation ```