Acid Base Disorders Flashcards

1
Q

acidemia

A

Acidemia is a decreased blood pH (normal is 7.36-7.44)

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2
Q

Acidosis

A

Acidosis is a clinical process in the body that decreases blood pH

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3
Q

Alkalemia

A

Alkalemia is an increased blood pH (normal is 7.36-7.44)

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4
Q

Alkalosis

A

Alkalosis a clinical process in the body that increases blood pH

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5
Q

Hyperkapnia and hypokapnia

A

Refers to increased or decreased pCO2in the blood

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6
Q

Ventilation

A

Process by which inhaled air (including O2) reaches the alveoli of the lungs where gas exchange occurs and exhaled air (including CO2) leaves the lungs

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7
Q

Minute Ventilation

A

Rate by which air reaches the alveoli.
Measured in Liters/minutes
Equal to Respiratory Rate (breaths per minute) x Tidal Volume (amount of air taken during one breath)

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8
Q

Hyperventilation vs. hypoventilation

A

Refers to increased or decreased minute ventilation rate respectively

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9
Q

Ventilation and pCO2

A

Hyperventilation leads to hypokapnia

Hypoventilation leads to hyperkapnia

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10
Q

Anion Gap is normally less than

A

10

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11
Q

Causes of Acid-Base Disorgers High Anion Gap Metabolic Acidosis

A
Mnemonics is MUDPILES
Methanol
Uremia (End Stage Renal Disease)
Diabetic ketoacidosis
Paraldehyde
Infection, Iron, Isoniazide
Lactic acidosis
Ethylene glycol (antifreeze), alcohol
Salicylates, starvation ketoacidosis
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12
Q

Uremic acidosis

A

Occurs when renal function is severely decreased (Creatinine clearance is less than 25ml/min)
Due to
decreased excretion of acids
decreased excretion of H+
Decreased reabsorption/synthesis of HCO3
Accumulation of organic and inorganic anions
Phosphates
Sulfates

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13
Q

Lactic Acidosis causes

A

anaerobic metabolism in the tissues from
Hypoxemia
Circulatory failure (hypotension, sepsis)
Peripheral vessels blockage
Anemia
Liver failure due to decreased clearance
Thiaminedeficiency
Hypophosphatemia
Sepsis (due to decreased perfusion of the tissues, impaired gluconeogenesis and poor clearance)
Seizures (due to release of lactate from muscles)
Short-lived

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14
Q

Lactic acidosis meds

A

Metformin
Some HIV meds
Isoniazide (toxic levels)

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15
Q

lactic acidosis diagnosed by

A

measuring arterial or venous level

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16
Q

Respiratory acidosis and alkalosis

A

are clinical processes that occur due to increase or decrease in ventilation and usually associated with pulmonary diseases

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17
Q

Metabolic acidosis and alkalosis

A

are clinical processes that are not due to ventilation problems

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18
Q

Henderson-hasselbach equation

A

pH = 6.1 + log HCO3-/0.03 x pCO2

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19
Q

Respiratory Acidosis

A

Hypoventilation > hyperkapnia > acidosis

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20
Q

Respiratory Alkalosis

A

Hyperventilation > hypokapnia >

alkalosis

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21
Q

Metabolic acidosis

A

Over-production or accumulation of acid
Loss of base (HCO3-)
Under-excretion of acid
All of the above will decrease HCO3and will decrease pH

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22
Q

Metabolic Alkalosis

A

Loss of acid
Under-excretion of base
Leads to increased HCO3and increased pH

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23
Q

Primary acid-base disorder

A

results from a pathological process

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24
Q

Secondary acid-based “disorder”

A

is a normal physiological compensation in response to a primary acid-base disorder

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25
Q

buffering

A

within minutes

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26
Q

Respiratory compensation (in metabolic disorders)

A

within hours

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27
Q

Metabolic compensation by kidneys

A

within 2-3 days

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28
Q

acute vs chronic acid-base disorders

A

Acute acid-base disorders results from the conditions that develop within hours of presentation
Chronic acid-base disorders are at least several days old
These terms are usually reserved to respiratory acid-base disorders

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29
Q

Acute respiratory disorders are compensated or not

A

uncompensated (resulting in acidemia or alkalemia).

30
Q

Chronic respiratory disorders are compensated or not?

A

fully compensated (pH is close to normal) and developed more than 2-3 days before presentation,

31
Q

Sub-acute resp disorders are compensated or not?

A

partially compensated (within 2 days frame)

32
Q

metabolic disorders are compensated or not?

A

could be fully or partially compensated depending on the degree of the acidosis/alkalosis and on a lung function

33
Q

mixed disorders

A

include combination of several acid-base disorders. They are very common
Metabolic acidosis and metabolic alkalosis
Respiratory acidosis and metabolic acidosis
Chronic respiratory acidosis and metabolic alkalosis
Etc.

34
Q

Causes of resp acidosis

A

Decreased RR

Decreased TV

35
Q

Causes of metabolic acidosis

A
High AG
       Mudpiles
Normal AG
       Renal Loss (RTA)
       Extra-renal loss (diarrhea)
36
Q

From Hypoventilation

A
From decreased RR
Decreased respiratory drive
Drugs
Coma
Stroke
From decreased Tidal Volume
Neuro-muscular disorders
Severe kyphoscoliosis
Airways obstruction
COPD
Obstructive sleep apnea/Obesity
37
Q

Anion Gap

A

A.G.=Na+–HCO3–Cl-
Calculated from metabolic profile/electrolytes blood test
Represents unmeasured anions in the plasma
Anionic proteins (albumin)
Phosphate
Sulfate
Organic anions

38
Q

Diabetic Ketoacidosis

A

Insulin deficiency >increased lypolysis increased fatty acid delivery to liver >production of ketones >acidosis
Associated with hyperglycemia
More often in Type I Diabetes Mellitus, but may happen in Type II as well
Usually part of the presentation of a new onset of type I DM
May be precipitated by patient’s non-compliance with insulin, infection, pancreatitis

39
Q

Alcoholic Ketoacidosis

A

Large ethanol intake leads to altered hormonal and enzymatic activities leading to increase in ketones production
No hyperglycemia
High osmolal gap

40
Q

Osmolal Gap

A

Alcoholic Ketoacidosis
OG (normal is less than 10)
Difference between measured serum Osmolality and calculated serum osmolality
Calculated Osmolality = 2 (Na+) + (Glucose/18) + BUN/2.8
OG should be equal to Ethanol level/4.6
If OG more than that, look for other alcohols

41
Q

Ethylene Glycol poisoning

A
Found in antifreeze and in industrial solvents
Metabolites are highly toxic
Increased OG
Calcium Oxalate crystals in urine
Acute Renal Failure is common
42
Q

Methanol poisoning

A

Found in wood alcohol and windshield fluid
Causes blindness and acute renal failure
Increased OG

43
Q

Salicylates poisoining

A

Usually a result of accidental or intentional overdose

May cause metabolic acidosis and/or respiratory alkalosis

Symptoms
Hemorrhage
Fever
nausea and vomiting,
Diaphoresis
Tinnitus
Pulmonary edema
44
Q

Causes of normal ag metabolic acidosis

A

Diarrhea or Ileal drainage with stoma/bypasses

Decrease reabsorption of HCO3 by renal tubules (therefore increased loss)

increase in anion intakes

large amount of nacl (expansion acidosis)

45
Q

Diarrhea or Ileal drainage with stoma/bypasses

A

Due to loss of HCO3

Except for Chloride wasting diarrhea with villous adenoma

46
Q

Decrease reabsorption of HCO3 by renal tubules (therefore increased loss)

A

Renal Tubular Acidosis

Due to diuretics ( carbonic anhydrase inhibitors [CAI])

47
Q

Increase in anion intakes

A

Parenteral nutrition

48
Q

Large amount of NaCl (expansion acidosis)

A

Due to dilution of the bicarbonate and to decreased renal bicarbonate reabsorption as a result of volume expansion

49
Q

renal tubular acidosis

A

3 types
RTA Type I
RTA Type II
RTA Type IV

50
Q

RTA type I

A

Decreased hydrogen ions excretion in the collecting ducts leading to alkaline urine and acidic serum
Increased calcium excretion and decreased citric acid concentration leading to kidney stone formation
Increased potassium loss leading to hypokalemia

51
Q

RTA type II

A

Defect in bicarbonate reabsorption in proximal tubules, so more bicarbonate is excreted, lowering serum bicarbonate and leading to acidemia and elevation in urine bicarbonate concentration.
Increased Ca in the urine, but rarely leading to kidney stones due to normal citric acid concentration.
Because distal tubules work OK, ability to acidify urine in response to acidemia is intact, so urine pH is low.
High K loss also will lead to hypokalemia

52
Q

RTA type IV

A

Occur in patient with moderate chronic renal failure
Due to insufficient aldosteroneproduction (hypo-reninemic) and/or aldosteronetubular resistance (due to renal failure)
Insufficient K excretion leads to hyperkalemia

53
Q

RTA type I

Urine PH
Serum K
Kidney stones

A

> 5.5
low
yes

54
Q

RTA type II

Urine PH
Serum K
Kidney stones

A
55
Q

RTA type IV

Urine PH
Serum K
Kidney stones

A
56
Q

Urinary Anion Gap

A

To differentiate between renal and extrarenal HCO3loss (RTA vs. diarrhea)
Urine (Na++ K+) -Cl-
Negative in extrarenal loss
Due to high level of unmeasured NH4+
Excretion of NH4+ by healthy kidneys is a compensatory mechanism for acidosis
Positive or non-existent in renal loss
Due to low level of NH4+ and increased level of HCO3

57
Q

Respiratory Alkalosis list of causes

A
Usually acute
Pain
Anxiety
Salicylates overdose
Fever
Sepsis
Hypoxia from some pulmonary disorders
CHF
Pneumonia
PE
Mild asthma
Mechanical ventilation
58
Q

Metabolic alkalosis causes

A

Vomiting/NG suction
Due to lose of hydrochloric acid
Contraction alkalosis due to increased HCO3-reabsorption
Dehydration
Diuresis (with diuretics other than CAI)
Hypokalemia
Due to resulting increased mineralocorticoid secretion
Recent correction of chronic respiratory acidosis
Due to recent metabolic compensation.

59
Q

Metabolic acidosis clinical manifestation

A
Kussmal respiration (sign of respiratory compensation)
Nausea/vomiting
Cardiac effects
Arrhythmia
Hypotension
Neurological effects
Confusion
Lethargy
Coma
Symptoms of underlying disease
60
Q

Respiratory Acidosis Clinical manifestation

A
Ineffective respiration/respiratory distress
Cardiac effects
Arrhythmia
Hypotension
Neurological effects
Confusion
Lethargy
Coma (hypercapnic), CO2narcosis
Symptoms of underlying disease
61
Q

Metabolic alkalosis clinical manifestation

A
Decreased respiration (compensatory). This may lead to ineffective respiration and hypoxia
Neurological
Parasthesia
Carpopedal spasm due to secondary hypocalcemia
Confusion
Seizures
Dizziness
Coma
Weakness
62
Q

Respiratory alkalosis clinical manifestations

A
Hyperventilation
Neurological
Parasthesia
Dizziness
Symptoms of underlying disease
63
Q

Basic rules for interpreting ABG

A

Determine the predominate process by assessing blood pH
Differentiate between primary and secondary (compensatory) acid-base disturbances
Remember: BODY NEVER OVER-COMPENSATES
Determine if simple or mixed acid-base disorder presents
When math is about to fail you, pay attention at the clinical picture
Remember, you have a patient, not just the numbers.

64
Q

Main ABG numbers

A

ph7.4
pco2 40
hco3 24

65
Q

Step 1 for ABG

A

Look at pH: acidemia (7.4).

66
Q

step 2 for abg

A

Look at HCO3-to determine if primary process is metabolic or respiratory

If HCO3 follows pH, process is metabolic. If goes in the opposite direction, process is respiratory.

67
Q

Step 3 for abg

A

Determine if process is compensated (chronic), uncompensated (acute), or partially compensated (somewhere in between)

With metabolic disturbances, it’s easy. Look back at pH. If it’s normal, the process is compensated. If it’s abnormal, it’s uncompensated.

68
Q

step 4 for abg

A

Calculate anion gap to classify the metabolic acidosis or to determine if there is a mixed disorder with other types of acid-base disturbances

69
Q

step 5 for abg

A

If anion gap is present, Calculate delta-delta gap to find mixed disorders

D AG = (AG –10)/(24-HCO3)
If D AG is 1-1.6, pure high AG metabolic acidosis
If D AG is less than 1.0, concomitant non-AG acidosis
If D AG is more than 1.6, concomitant metabolic alkalosis is present

70
Q

step 6 for abg

A

If metabolic disorder, look at pCO2 to determine if additional respiratory process exist.

If changed in the opposite direction from HCO3, additional respiratory acid-base disorder of the same polarity as metabolic one exists.

71
Q

step 7 for abg

A

Refer back to clinical picture and see if your calculations make any clinical sense