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CMT-dos > Acid-Base Disorders > Flashcards

Acid-Base Disorders Flashcards

1
Q

pH

A

Quantitative measurement of the acidity or basicity of a solution
Concentration of hydrogen ions in solution

Normal arterial blood pH is approximately 7.40…Why this number?

The normal range is tightly regulated to stay between 7.35 and 7.45

Acidemia: more hydrogen ions (H+) in the blood = pH < 7.35
Alkalemia: more hydroxide ions (OH–) in the blood = pH > 7.45

Logarithmicscalefrom 1 to 14
1 = maximally acidic, 14 = maximally basic
7 = neutral point: equal concentrations of H+and OH–

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2
Q

Acids

strong and weak

A

Compounds that can donate protons (H+)or accept electrons
H+are released when acids dissociate in solution → ↓ pH

Strong acids:
Fully ionize in water
More H+released into water → greater effect on pH
Example:hydrochloric acid (HCl)

Weak acids:
Partially ionize in water
Less H+released into water → relatively less effect on pH
Example: carbonic acid (H2CO3)

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3
Q

Acids classified by volatility

A

Volatile acids:
Can change phase into a gas → removable through thelungs
Primary example: CO2
Produced through aerobic metabolism

Nonvolatile (fixed) acids:
Cannot change phase into a gas → not removable through thelungs
Removed by thekidneys
Produced through anaerobic metabolism and the GI tract
Examples: lactic acid,uric acid,sulfuric acid,phosphoric acid

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4
Q

Bases
Classified by

A

Compoundsthat can accept protons (H+) or donate electrons
Hydroxide ions (OH–) are released when bases dissociate into solution:
OH–combine with free H+to form H2O
Net result is less [H+] → ↑ pH (becomes more basic)

Classified by strength:
Strong bases:
Fully ionize in water
More OH–released into water → greater effect on pH
Example:sodiumhydroxide (NaOH)

Weak bases:
Partially ionize in water
Less OH–released into water → relatively less effect on pH
Examples:bicarbonate (HCO3), ammonia (NH3)

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5
Q

Buffers

A

Substances that consume or releases hydrogen ions (H+) to stabilize the pH

Categorized asbicarbonate and nonbicarbonate buffers:

Bicarbonate (HCO3):
Most physiologically important buffer
HCO3–+ H+⇆ H2CO3⇆ CO2+ H2O

Nonbicarbonate buffers:
Less physiologically important
Examples:proteins (albumin, hemoglobin), phosphates

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6
Q

Acid-Base Homeostasis
Henderson-hasselbach equation

A

Thus acid-base balance is maintained by:
Chemical buffering
Pulmonary activity (CO2)
Renal activity (HCO3)

The relationship between pH, acids, and bases is described by the Henderson-Hasselbalch equation.

We can simplify it (not for calculations) for understanding the concepts of acid-base balance
pH = 𝐻𝐶𝑂3/𝑝𝐶𝑂2

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7
Q

Oxygen-Hemoglobin Dissociation Curve

A

Oxygen delivery to tissues
Oxygen-Hemoglobin Dissociation Curve
Relates the ability of hemoglobin to deliver oxygen to tissues
Graph depicting the relationship of the partial pressure of oxygen to the saturation of hemoglobin

Left shift (alkalotic):
Decreased partial pressure of oxygen, so the amount of oxygen needed to saturate hemoglobin 50% is lessened and that there is an increased affinity of hemoglobin for oxygen

Right shift (acidotic):
Increased partial pressure of oxygen, so the amount of oxygen needed to saturate hemoglobin 50% is increased and there is a decreased affinity of hemoglobin for oxygen

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8
Q

Arterial Blood Gas (ABG) Test

A

An ABG test is ordered to assess for acid-base disorders
Includes:
Oxygen content (O2CT) – amount of oxygen in the blood
pH
Partial pressure of carbon dioxide (PaCO2)
Partial pressure of oxygen (PaO2)
Bicarbonate (HCO3) – calculated value
Oxygen saturation (O2Sat) – measures how much Hgb in the blood is carrying oxygen

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9
Q

Venous Blood Gas (VBG)

A

A VBG can also provide useful information for acid-base disorders since the arteriovenous differences in pH and PCO2 are small

Venous blood compared to arterial blood
pH is 0.03-0.04 lower
PCO2 is 7-8 mm Hg higher
Calculated HCO3 is 2 mEq/L higher

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10
Q

Acid-Base Disorders

general

A

Two types of acid-base disorders:
Acidosis
Alkalosis
Further categorized by the type of primary disorder:
Metabolic
Respiratory

A respiratory or metabolic disorder/disturbance is often accompanied by a compensatory response → simple acid-base disorder
Compensatory response does not fully correct the problem
2 or 3 simultaneous disorders can be present → mixed acid-base disorder

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11
Q

Maintaining Acid-Base Balance

A

The body’s goal is to maintaining homeostasis
The body maintains a slightly alkaline pH in the range of 7.35 to 7.45
Slightly alkaline pH is ideal for biological processes

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12
Q

acid-base compensation

The buffering system

A

If an acid-base imbalance occurs, compensation mechanisms are activated:
The buffering system
Chemical buffers present in tissues that respond in seconds
Can handle minor change in the acid-base balance

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13
Q

acid-base compensation

Respiratory system

A

The respiratory system
Retention or elimination of CO2 within minutes
Can handle mild to moderate acid-base shifts

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14
Q

acid base compensation

the renal system

A

The renal system
Regulates bicarbonate (HCO3) and excreting fixed acids
Activated in hours, but works for 3-5 days

(The kidneys are the ultimate acid-ase regulator)

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15
Q

Cellular Respiration

A

Carbon dioxide is a byproduct of cellular respiration
CO2 + H2O ↔ H2CO3 (carbonic acid – weak acid) ↔ HCO3 (bicarbonate – weak base) + H
Requires the enzyme carbonic anhydrase
Found in RBCs, renal tubules, gastric mucosa, and pancreatic cells
This reaction serves as one of many buffer systems in the body

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16
Q

Acid Handling in lungs and kidneys

A

Lungsandkidneyswork to eliminate acid load
Ensures the buffering capability of the blood is not overwhelmed in maintaining a normal pH)

In the lungs:
The primary acid load produced by the body is in the form of CO2(a volatile acid)
CO2is eliminated through the respiratory tract
↑ CO2→ ↑respiration

In the kidneys:
Prevent excretion ofbicarbonate
Freely filtered at the glomerulus
100% is reabsorbed (80% proximal tubule, 10% thick ascending limb, 6% distal convoluted tubule, and 4% collecting duct)
Produce newbicarbonatethrough the renal ammonia metabolism

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17
Q

Step-by-Step Analysis of Acid-Base Status

respiratory vs metabolic

A

Determine acidosis versus alkalosis within the physiological range by looking at the blood pH
Determine the primary disorder by looking at the plasma bicarbonate (HCO3) and PCO2

Is it respiratory?
Primary respiratory disturbances will have a change in the pCO2
Elevated pCO2 → more acidic
Decreased pCO2 → more alkaline

Is it metabolic?
Primary metabolic disturbances will have a change in the HCO3
Elevated HCO3 → more alkaline
Decreased HCO3 → more acidic

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18
Q

Determine the degree of compensation

A

Compensation with either system will be reflected oppositely
Example:
Respiratory acidosis: CO2 should be elevated and if there is compensation metabolically, the HCO3 should be elevated as well

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19
Q

Winters formula

A

Winters formula is used to calculate respiratory compensation

This calculation provides the expected pCO2
pH level in the physiological range but the pCO2 and/or HCO3 are not within normal limits → likely a mixed disorder; compensation may not occur → clinical information is paramount

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20
Q
A
21
Q

anion gap

general

A

Calculated for primary metabolic disturbances
Measurement of the difference-orgap-between the negatively charged (chloride and bicarbonate) and positively charged (sodium and potassium * )
electrolytes
Helps to diagnose the cause of a metabolic acidosis
Anion gap increases with the loss of bicarbonate
The concentration of potassium in the blood is usually much lower compared to sodium, chloride, and bicarbonate; it iscommon practice to not use potassium when calculating the anion gap, as it usually has little effect

High anion gap = acidosis
Low anion gap = alkalosis

22
Q
A

CO2 should go opposite direction of pH for RESPIRATORY problems

23
Q
A

Respiratory problem
Acidosis

24
Q
A

Acidosis
Metabolic problem

25
Q

Metabolic acidosis

A

The process that results in the gain of hydrogen ions (H+) or the loss of HCO3

Net gain of hydrogen ions:
↑ acid production
lactic acidosis, ketoacidosis, toxic alcohols (methanol, ethylene glycol), medications (ASA overdose, chronic acetaminophen usage)
Impaired excretion
Renal tubular acidosis, renal failure

Loss of HCO3
Diarrhea (direct loss in stool), renal tubular acidosis (loss in urine), carbonic anhydrase inhibitors (stops reabsorption in the proximal tubule, so loss in urine)

26
Q

Metabolic acidosis

Primary (uncompensated) metabolicacidosis,arterial blood gas will show

A

pH ↓
HCO3 ↓
Partial pressure of arterial CO2(PCO2) ↓

Think: “So theacidosisisNOTdue to ↑ CO2; it must be due to ↓ serum HCO3”
Confirm by looking at HCO3 → will be low (< 22 mEq/L)

Compensation:
In primarymetabolicacid-base disorders, thelungsmay try to compensate in an attempt to normalize thepH
Lungs respond to metabolicacidosis by↑ventilation (hyperventilation)

27
Q

Metabolic acidosis

Clin Man

A

Symptoms may include:

  • Kussmaul respirations (rapid, deep, labored breathing)
  • Diarrhea- increased loss of bicarb
  • Ketoacidosis:
    Polyuria
    Polydipsia
    Epigastricpain
    Vomiting
  • Renal failure
    Dehydration
    Fluid overload
    Pruritis
    Oliguria

Methanol poisoning: visual symptoms (photophobia, blindness)

  • Salicylate overdose:
    Tinnitus
    Blurred vision
    Vertigo
28
Q

Metabolic acidosis

Tx

A

Directed at correcting the underlying etiology
Example: For ketoacidosis, giveinsulin and correct fluid and electrolyte abnormalities

Consider giving HCO3if:
Acidosisis severe (pH < 7.1)
The patient has severe kidney injury

29
Q

Respiratory alkalosis

A

The process that results in a decreased level of carbon dioxide (CO2) within the blood

30
Q

Respiratory alkalosis

causes

A

Anxiety/hyperventilation

Etiology:
Physiologic
Pregnancy
High altitude
Medications
Aspirin overdose
Nicotine overdose
Hypoxia-induced
PE
Pulmonary edema

Intracranial process
Stroke
TBI
Encephalitis
Psychologic
Anxiety
Psychosis

31
Q

Respiratory alkalosis

Primary (uncompensated) respiratory alkalosis – arterial blood gas will show

Compensation patho

A

pH ↑
PCO2↓
Compensation:
In primary respiratory acid–base disorders, the kidney may try to compensate in an attempt to normalize thepH
Kidneys respond torespiratory alkalosis by decreasing serum HCO3–through:
↓Secretion of H+
Urinary excretion of HCO3(normallybicarbonateis 100% absorbed)

32
Q

Respiratory alkalosis

clin man

A

Tachypnea
Dyspnea
Dizziness/light-headedness
Paresthesias (perioral, hands/feet) due to decreasedionized calcium
Psychologic symptoms:
Anxiety
Fear
Impending doom

33
Q

Respiratory alkalosis

A
34
Q

Respiratory alkalosis

Tx

A

Assess and address the ABCs (airway, breathing, andcirculation) if patient is in acute distress
Attempt to correct the underlying abnormality
Small dose of short-acting benzodiazepine to help with psychologic symptoms

35
Q

Respiratory acidosis

A

The process that results in an accumulation of carbon dioxide (CO2) due to abnormalgas exchange in thelungs

36
Q

Respiratory acidosis

causes

A
  • Decreased respiratory rate
    OSA, medications: opiates, benzodiazepines
  • Decreased tidal volume
    Cervical spine injuries above C3, muscular dystrophy, kyphoscoliosis, obesity
  • Severe ↓ lung diffusion capacity
    Emphysema, interstitial lung diseases, pulmonary fibrosis
  • Severe ventilation–perfusion mismatch
    Asthma, COPD, cystic fibrosis, interstitial lung diseases, pulmonary hypertension
37
Q

Primary (uncompensated) respiratory acidosis, thearterial blood gas will show:

A

pH ↓
PCO2(partial pressure of carbon dioxide) ↑ (hypercapnia)
Compensation:
In primary respiratory acid–base disorders, the kidney may try to compensate in an attempt to normalize thepH
Kidneysrespond to respiratory acidosis by increasing serum HCO3 through ↑secretion of H+

38
Q

Respiratory acidosis

clin man

A

Presentation ofhypercapnia:
Neurologic:
Anxiety/paranoia
Headaches
Somnolence
Delirium
Coma

Pulmonary:
Dyspnea

39
Q

Respiratory acidosis

Tx

A

Assess the ABCs:
Ensure that theairwayis secure
Administer supplemental O2
Ventilatory support as needed

Treat the underlying etiology
Examples:
COPD exacerbation:bronchodilatorsandcorticosteroids
Pneumoniain neuromuscular disorders: antibiotics
Avoid respiratory sedatives

40
Q

Metabolic alkalosis

A

Most common acid-base disturbance in hospitalizedpatients (ICU patients)
Process that results in the loss of hydrogen ions (H+) or the gain of HCO3

41
Q

Metabolic alkalosis

causes

A
  • Upper GI losses of hydrogen ions:
    Vomiting and/or nasogastric suctioning
  • ↑ Renal losses ofhydrogen ions:
    Mineralocorticoid excess:
    Primaryhyperaldosteronism
    Cushing’s syndrome
    Loop orthiazide diuretics
    ↑ distal tubular delivery of Na+→ ↑ distalsecretion of H+and K+
  • ↑ HCO3intake:
    Ingestion of non-absorbable antacids (calcium carbonate) or sodium bicarbonate pills
  • Contractionalkalosis:
    Decreased extracellular volume + stable HCO3= ↑ HCO3concentration
42
Q

Metabolic alkalosis

Primary (uncompensated) metabolicalkalosis,arterial blood gas will show

Compensation

A

pH ↑
Partial pressure of CO2(PCO2) ↑
HCO3 ↑
Think: “So thealkalosisisNOTdue to ↓ CO2; it must be due to ↑ serum HCO3”
Confirm by looking at HCO3→ will be high (> 28 mEq/L)
Compensation:
In primarymetabolicacid-base disorders, thelungs may try to compensate in an attempt to normalize thepH
Lungs respond to metabolicalkalosis by↓ventilation

43
Q

Metabolic alkalosis

chloride responsive causes

A

If urine chloride < 10 mEq/L

Etiologies:
Vomiting
Nasogastric suctioning
Diuretics
Volume depletion
Laxative abuse

chloride unresponsive ABCD
If urine chloride >20 mEq/L
Etiologies:
Aldosteronism (primary) – Conn syndrome
Bartter’s syndrome
Cushing’s syndrome
Depletion of magnesium

44
Q

Metabolic alkalosis

Clin man
Ca signs

A

Symptoms may include:
Vomiting
BP abnormalities:
Hypertension (primary mineralocorticoid excess)
Hypotension (↓effective circulating volume)
Hypokalemia

Hypocalcemia:
Tetany
Chvostek sign: contraction offacial muscles when thefacial nerve is tapped
Trousseau sign:carpopedal spasm with inflation of the BP cuff
Changes in mental status/seizures

Alkalosis promotes the binding of calcium to albumin and can reduce the

45
Q

Metabolic alkalosis

Tx

A

Directed at correcting the underlying etiology

Attempt to improve renal HCO3-excretion to resolvealkalosis:
Inpatients withoutedema (truevolume depletion): volume repletion withisotonicsaline

Inpatientswith ↓effective circulating volume (CHF, cirrhosis, renal artery stenosis):
Potassium chloride
K+-sparingdiuretics
Avoidisotonic saline as it will worsen symptoms without improvingalkalosis

46
Q
A
47
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48
Q
A

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