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Therapeutics 1 > Acid-Base > Flashcards

Acid-Base Flashcards

1
Q

Metabolic disorders involve changes in _____, while respiratory disorders involve changes in _____.

A

HCO3-, pCO2

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2
Q

normal pCO2 level (ABG)

A

35-45 mmHg, “remember 40”

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3
Q

normal HCO3- level (ABG)

A

22-26 mEq/L “remember 24”

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4
Q

normal pO2 and O2 sat

A

95-100 mmHg, >95%

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5
Q

cardiovascular effects of acidosis

A

(1) decreased cardiac output
(2) diminished contractility
(3) increased pulmonary vascular resistance
(4) arrhythmias

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6
Q

metabolic effects of acidosis

A

(1) insulin resistance
(2) hyperkalemia
(3) inhibition of anaerobic glycolysis (generates lactic acid)

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7
Q

CNS effects of acidosis

A

(1) coma

(2) altered mental status

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8
Q

other effects of acidosis

A

(1) decreased respiratory muscle strength
(2) dyspnea
(3) hyperventilation (respiratory compensation)

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9
Q

cardiovascular effects of alkalosis

A

(1) decreased coronary blood flow
(2) arteriolar constriction
(3) decreased anginal threshold
(4) arrhythmias

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10
Q

metabolic effects of alkalosis

A

(1) decreased potassium, calcium, and magnesium

(2) stimulation of anaerobic glycolysis

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11
Q

CNS effects of alkalosis

A

(1) reduced cerebral blood flow

(2) seizures

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12
Q

other effects of alkalosis

A

(1) decreased respiration (to conserve pCO2 and lower pH)

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13
Q

What are three ways acids are formed in the body?

A

(1) aerobic glycolysis (generates CO2)
(2) diet (0.1 mEq/kg/day consumed)
(3) nonvolatile acid production (lactic and pyruvic acid, TG oxidation to ketone bodies, AA metabolism)

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14
Q

three standard physiological pH regulation mechanisms

A

(1) buffering
(2) renal regulation
(3) ventilation

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15
Q

What three buffers are present in the body?

A

bicarbonate/carbonic acid, phosphate, and proteins

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16
Q

The bicarbonate buffer has ______ onset and ______ buffering capacity.

A

rapid, intermediate

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17
Q

The phosphate buffer has ______ onset and ______ buffering capacity.

A

intermediate, intermediate

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18
Q

Which buffering system has a rapid onset but a limited capacity?

A

proteins

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19
Q

Describe how the body uses the bicarbonate/carbonic acid buffering system.

A

varying the amount of HCO3- (kidneys) and CO2 (lungs) present in the blood, used as first line of pH defense because it is present in the largest amount and is the most readily available

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20
Q

Which two proteins are primarily involved in buffering?

A

albumin, hemoglobin

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21
Q

Where is a majority of filtered bicarbonate reabsorbed?

A

proximal convoluted tubule

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22
Q

Describe the mechanism for bicarbonate reabsorption in the PCT.

A

As filtered bicarbonate passes through the tubule, it combines with excreted H+ to form carbonic acid. Carbonic anhydrase forms CO2 and HCO3- from this, both of which pass readily through the membranes of cells lining the tubule. Once inside the cell, they are converted back into carbonic acid. After dissociation, bicarbonate passes through channels in the basilar membrane (with sodium) back into the blood, while the H+ is excreted back into the tubule.

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23
Q

How do carbonic anhydrase inhibitors cause acidosis?

A

Anything that limits H+ secretion will limit bicarbonate reabsorption. CA inhibitors prevent the entry of CO2 and H2O back into tubular cells because they are no longer being made from carbonic acid. HCO3- is no longer salvaged by H+, and corresponding acidosis occurs.

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24
Q

By which two mechanisms is new bicarbonate generated? Of these two mechanisms, which has a greater capacity to generate bicarbonate?

A

ammonium excretion and titratable acidity, ammonium excretion to a greater extent due to increased availability of ammonia compared to phosphate

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25
Q

What role does the DCT play in H+ levels?

A

active H+ secretion into the tubular lumen

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26
Q

Which pH regulatory mechanism has both a rapid onset and a large capacity?

A

ventilation

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27
Q

What effect does an increase in pCO2 have on ventilation?

A

Chemoreceptors (peripheral and central) that detect an increase in pCO2 increase the rate and depth of ventilation, excreting more CO2 and increasing pH.

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28
Q

How could liver dysfunction create an acid-base imbalance?

A

When the liver cannot properly synthesize urea from bicarbonate and ammonium, they will both increase in concentration. The more acidic ammonium can be excreted in the urine, but bicarbonate is retained, so alkalosis occurs.

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29
Q

When a single acid-base disorder is present, how do the trends of HCO3- and pCO2 levels compare?

A

Their levels will follow each other unless a mixed acid-base disorder is present. This can be understood with the Henderson-Hasselbalch equation: pH=pKa + log(HCO3-/pCO2). The structure of this equation explains why the trends match. For example, metabolic alkalosis involves an increase in HCO3- levels. To keep pH constant, by this equation, pCO2 must also increase.

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30
Q

This acid-base disorder is characterized by a low pH, low serum HCO3- and a decrease in pCO2.

A

metabolic acidosis (if it were respiratory, pCO2 would be high and HCO3- would follow as compensation)

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31
Q

After it is determined a patient has metabolic acidosis, what is the very next step in determining the pathophysiology and treatment?

A

calculating the anion gap [Na - (Cl + HCO3)]

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32
Q

In metabolic acidosis, how much should pCO2 decrease in response to decreased HCO3-?

A

pCO2 should fall by about 1 to 1.5x the amount that serum HCO3- falls.

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33
Q

In metabolic alkalosis, how much should pCO2 increase to compensate for a given increase in HCO3-?

A

pCO2 should increase by 0.4 to 0.6 times the increase in serum HCO3-.

34
Q

How should the trend in plasma HCO3- compare to the increase in pCO2 in both acute and chronic respiratory acidosis?

A

acute: HCO3- increase=0.1 pCO2 increase
chronic: HCO3- increase=0.4 pCO2 increase

35
Q

How should the trend in plasma HCO3- compare to the decrease in pCO2 in both acute and chronic respiratory alkalosis?

A

acute: HCO3- decrease=0.1-0.3 pCO2 decrease
chronic: HCO3- decrease=0.2-0.5 pCO2 decrease

36
Q

Name two ways that bicarbonate losses could be related to a GI issue.

A

(1) diarrhea-HCO3- moving too fast to be absorbed in GI tract
(2) pancreatic fistulas/biliary drainage-loss of fluid rich in HCO3-

Both of these involve loss of GI fluid, which is heavily alkalinized by bicarb to neutralize the acidic contents of the stomach as they pass into the intestines.

37
Q

Name six possible causes of non-anion gap acidosis.

A

(1) GI loss of bicarb
(2) T2RTA (failure of PCT to absorb bicarb)
(3) T1RTA (failure of DCT to pump H+ into tubular lumen)
(4) T4RTA (hypoaldosteronism reduces H+ secretion, corresponding hyperkalemia also leads to acidosis)
(5) exogenous acid or chloride administration via TPN, HCl, ammonium chloride
(6) chronic renal failure (less H+ secretion, less ammonia production)

38
Q

What are some causes of T2RTA?

A

heavy metal toxicity, carbonic anhydrase inhibitor therapy, topiramate

39
Q

Outline the pathophysiologic progression of T2RTA, from initial bicarb loss to hypokalemia.

A

When the reabsorptive threshold for bicarb is lowered and more bicarb is lost in the urine, sodium and water follow. This extra fluid loss stimulates aldosterone release to maintain perfusion to the kidneys. While aldosterone may salvage some volume from the urine, it does so at the cost of potassium secretion. Hypokalemia results. Additionally, to distinguish this from T1RTA, these patients can still acidify their urine.

40
Q

Primary tubule defects, amphotericin B, SLE, myeloma, and lithium are all potential causes of:

A

T1RTA

41
Q

What effect does T1RTA have on the pH of urine?

A

Patients with T1RTA cannot maximally acidify their urine, as they cannot excrete H+ into the tubular lumen in the DCT.

42
Q

Hypoaldosteronism and hyperkalemia are characteristic of which type of RTA?

A

T4RTA. Hypoaldosteronism causes less H+ secretion. Also, less aldosterone leads to increased K+ retention, which can cause further H+ retention.

43
Q

What does the MUDPILES acronym describe?

A 
possible cause of anion gap acidosis 
Methanol intoxication
Uremia
Diabetic ketoacidosis
Poison/Paraldehyde/propylene glycol
Intoxication/Infection
Lactic Acidosis
Ethylene glycol
Sepsis/Salicylates
44
Q

What is a normal anion gap?

A

3-11 mEq/L

45
Q

Once it is determined a patient has an elevated anion gap, what should be your next step?

A

calculating the delta gap (difference between normal anion gap and patient’s anion gap)

46
Q

Why is the ability to convert pyruvate to lactic acid so crucial?

A

It allows continued regeneration of NAD+ (and, thus, energy production) in hypoxic conditions. Particularly important for exercising muscle and RBCs.

47
Q

How is lactic acid normally cleared from the body?

A

conversion to pyruvate by the liver, disposed of by kidney/muscle/CNS

48
Q

Which buffering system in the body normally accounts for transient increases in lactic acid?

A

bicarb

49
Q

Name some drugs that can cause lactic acidosis.

A

NRTIs, metformin, isoniazid, linezolid, ethanol, propylene glycol, propofol

50
Q

How does shock contribute to the development of lactic acidosis?

A

Poor organ perfusion, specifically of the liver, which plays a significant role in clearance of lactic acid.

51
Q

Of the listed causes of lactic acidosis, which is self-limiting and will resolve as the temporary underlying condition subsides?

A

seizures, as the patient stops seizing, the transient increase in anaerobic activity will allow lactic acid levels to return to normal

52
Q

Failure of which to organs crucial to lactate removal will cause its buildup in the blood?

A

liver and kidneys

53
Q

Malnutrition and rhabdomyolysis are two causes of which acid base disorder?

A

lactic acidosis (a type of anion gap acidosis)

54
Q

Describe how salicylate toxicity could lead to anion gap acidosis.

A

Accumulation of an organic acid like salicylic acid will both acidify the blood and cause an anion gap (replacement of Cl- with some other anion).

55
Q

What are some symptoms of lactic acidosis?

A

(1) kussmaul respirations (deep and fast, trying to get rid of CO2)
(2) peripheral vasodilation (flushing and tachycardia result)
(3) hyperkalemia
(4) lethargy or coma
(5) N/V
(6) bone demineralization (in attempt to activate phosphate buffer system)

56
Q

Under what condition is acute treatment with bicarbonate appropriate?

A

(1) severe acidosis, pH < 7.1-7.15
(2) hyperkalemia (bicarb pushes K+ back into cells)
(3) cardiac arrest after defibrillation, ventilation, and medications have failed

57
Q

Describe how bicarb is dosed.

A

The dose of bicarb, in mEq, is calculated by:

[0.5 L/kg * IBW] x (desired 12 mEq - measured)

Once this dose is calculated, 1/2-1/3 of this amount is given.

58
Q

Why is bicarbonate dosed so conservatively?

A

If too much bicarb is given, you can overcorrect and quickly make the patient alkalotic and hypokalemic. Overalkalinization reduces cerebral blood flow and shifts the Hgb saturation curve to the left, impairing tissue oxygenation. Because it is formulated with a sodium counterion, bicarb therapy risks hypernatremia/hyperosmolarity. Lastly, bicarb is converted to CO2 in the blood, which can enter the CNS and acidify the CSF.

59
Q

What is tromethamine used for, and how does it work?

A

steals a proton from carbonic acid to form an HCO3 molecule, used for acidosis

60
Q

What are the physiologic characteristics of metabolic alkalosis?

A

high pH, high HCO3-, compensatory high pCO2 (by hypoventilation)

61
Q

Name 4 causes of metabolic alkalosis.

A

(1) loss of acid from GI tract
(2) administration of HCO3-
(3) contraction alkalosis (loss of Cl- rich, HCO3- poor fluid)
(4) renal impairment of HCO3- absorption

62
Q

What effect does volume/chloride depletion have on the pH of blood?

A

When arterial blood volume decreases, the kidney’s ability to excrete HCO3- decreases as well due to decreased pressure driving filtration. In addition, the ability to reabsorb bicarb increases as aldosterone released during volume depletion stimulates sodium and water retention (bicarb follows sodium).

63
Q

What is the most common cause of saline-responsive alkalosis?

A

excessive diuresis

64
Q

After diuresis, what are two more causes of metabolic alkalosis?

A

(1) excessive NG suctioning or vomiting (chloride loss)

(2) exogenous HCO3 administration in TPN or from bicarb therapy

65
Q

Why does hypochloremia have the potential to make someone alkalotic?

A

Normally, chloride is the anion reabsorbed with sodium. Without sufficient chloride to match sodium reabsorption, extra bicarb with be reabsorbed.

66
Q

How does excessive diuresis lead to alkalosis?

A

Diuresis causes volume depletion if done in excess. Volume depleted patients have an increased ability to reabsorb bicarb with stimulation of the RAAS system. Also, increased aldosterone stimulates increased H+ excretion, which is associated with bicarb reabsorption in the PCT and bicarb generation in the DCT, both of which contribute to alkalosis.

67
Q

Once a patient has developed alkalosis, how is it maintained? (3 ways)

In other words, how do some of the body’s natural responses to reduced GFR, hypokalemia, and hypochloremia accentuate existing alkalosis?

A

(1) reduced GFR increases sodium reabsorption, causing H+ secretion and corresponding increases in bicarb levels
(2) effects of hypokalemia: with less K+ around, more H+ is secreted
(3) enhanced HCO3 reabsorption due to hypochloremia

68
Q

What is the key difference between saline-responsive and saline-resistant alkalosis?

A

With saline-resistant alkalosis, there is no chloride depletion.

69
Q

What are 3 causes of saline-resistant alkalosis?

A

(1) hypokalemia–increased H+ excretion
(2) impaired NaCl reabsorption–renal tubular chloride wasting or Bartter’s syndrome
(3) increased mineralocorticoid activity–directly stimulates collecting duct H+ secretion, also causes hypokalemia and its associated alkalosis

70
Q

What are the symptoms of saline-resistant alkalosis?

A

(1) muscle cramps–hypokalemia
(2) postural dizziness
(3) cellular hypoxia–Hgb left shift
(4) myocardial suppression/CV collapse

71
Q

What are the two most common treatment methods for saline-responsive alkalosis?

A

(1) NS infusion–good for volume and chloride replacement

(2) carbonic anhydrase inhibitors–decrease HCO3- reabsorption

72
Q

How should saline-resistant alkalosis be treated?

A

(1) correction of hypokalemia with potassium sparing diuretic or KCl supplementation
(2) decrease or cease use of drugs with mineralocorticoid activity
(3) spironolactone–mineralocorticoid receptor antagonist

73
Q

This acid-base disorder is characterized by low pH, high HCO3-, and high pCO2.

A

respiratory acidosis

74
Q

What are some common causes of respiratory acidosis?

A

Anything that slows breathing will cause an increase in pCO2 and corresponding acidosis. These can include asthma, airway obstruction, COPD, reduced stimulation from CNS, HF, lung failure, neuromuscular defects that affect diaphragm, and improper ventilator use.

75
Q

How is respiratory acidosis treated?

A

The overall goal is to correct the underlying cause. For maintenance, patients can be put on a ventilator and given supplemental oxygen. No matter your treatment, you want to prevent rapid correction to avoid alkalosis.

76
Q

Which acid-base disorder is characterized by high pH, low pCO2, and low HCO3-?

A

respiratory alkalosis

77
Q

Describe the pathophysiology of respiratory alkalosis.

A

Anything that increases the breathing rate will lower pCO2 levels and make the blood more alkalotic. Anxiety, pain, injury, and trauma will all stimulate the respiratory drive. In the periphery, hypoxia, hypotension, high altitude, and HF can also stimulate the respiratory drive. Also listed are salicylate toxicity, ventilation misuse, and pulmonary edema/embolism.

78
Q

What are the symptoms of respiratory acidosis?

A

confusion, seizures, headache, tachycardia, hypotension, dyspnea, SOB

79
Q

What are the symptoms of respiratory alkalosis?

A

confusion, seizures, lightheadedness, reduced cerebral blood flow, cramps, N/V

80
Q

How is respiratory alkalosis treated?

A

You need to slow the respiratory drive however you can. Ventilation is often used, but sedation and paralysis can be used in extreme situations.

Therapeutics 1 (24 decks)

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