Acid-Base Disorders Flashcards

(48 cards)

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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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
Metabolic acidosis
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)
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# Metabolic acidosis Primary (uncompensated) metabolic acidosis, arterial blood gas will show
pH ↓ HCO3 ↓ Partial pressure of arterial CO2 (PCO2) ↓ **Think: “So the acidosis is NOT due to ↑ CO2; it must be due to ↓ serum HCO3”** Confirm by looking at HCO3 → will be low (< 22 mEq/L) Compensation: In primary **metabolic** acid-base disorders, the **lungs may try to compensate** in an attempt to normalize the pH Lungs respond to metabolic **acidosis by ↑ ventilation (hyperventilation)**
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# Metabolic acidosis Clin Man
Symptoms may include: * **Kussmaul respirations (rapid, deep, labored breathing)** * Diarrhea- increased loss of bicarb * Ketoacidosis: Polyuria Polydipsia Epigastric pain Vomiting * Renal failure Dehydration Fluid overload Pruritis Oliguria Methanol poisoning: visual symptoms (photophobia, blindness) * Salicylate overdose:  Tinnitus Blurred vision Vertigo
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# Metabolic acidosis Tx
Directed at correcting the underlying etiology Example: For ketoacidosis, give insulin and correct fluid and electrolyte abnormalities **Consider giving HCO3 if: Acidosis is severe (pH < 7.1) The patient has severe kidney injury**
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Respiratory alkalosis
The process that results in a decreased level of carbon dioxide (CO2) within the blood
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# Respiratory alkalosis causes
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
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# Respiratory alkalosis Primary (uncompensated) respiratory alkalosis – arterial blood gas will show Compensation patho
pH ↑ PCO2 ↓ Compensation: In primary **respiratory** acid–base disorders, the **kidney may try to compensate** in an attempt to normalize the pH Kidneys respond to respiratory alkalosis by decreasing serum HCO3– through: ↓ Secretion of H+ Urinary excretion of HCO3 (normally bicarbonate is 100% absorbed)
32
# Respiratory alkalosis clin man
Tachypnea Dyspnea Dizziness/light-headedness Paresthesias (perioral, hands/feet) due to decreased ionized calcium Psychologic symptoms: Anxiety Fear Impending doom
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# Respiratory alkalosis
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# Respiratory alkalosis Tx
Assess and address the ABCs (airway, breathing, and circulation) if patient is in acute distress Attempt to correct the underlying abnormality Small dose of short-acting benzodiazepine to help with psychologic symptoms
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Respiratory acidosis
The process that results in an accumulation of carbon dioxide (CO2) due to abnormal gas exchange in the lungs
36
# Respiratory acidosis causes
* 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
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Primary (uncompensated) respiratory acidosis, the arterial blood gas will show:
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 the pH Kidneys respond to respiratory acidosis by increasing serum HCO3 through ↑ secretion of H+
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# Respiratory acidosis clin man
Presentation of hypercapnia: Neurologic: Anxiety/paranoia Headaches Somnolence Delirium Coma Pulmonary:  Dyspnea
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# Respiratory acidosis Tx
Assess the ABCs: Ensure that the airway is secure Administer supplemental O2 Ventilatory support as needed Treat the underlying etiology Examples: COPD exacerbation: bronchodilators and corticosteroids Pneumonia in neuromuscular disorders: antibiotics Avoid respiratory sedatives
40
Metabolic alkalosis
Most common acid-base disturbance in hospitalized patients (ICU patients) Process that results in the loss of hydrogen ions (H+) or the gain of HCO3
41
# Metabolic alkalosis causes
* **Upper GI losses of hydrogen ions: Vomiting and/or nasogastric suctioning** * **↑ Renal losses of hydrogen ions:** Mineralocorticoid excess: Primary hyperaldosteronism Cushing's syndrome **Loop or thiazide diuretics** ↑ distal tubular delivery of Na+ → ↑ distal secretion of H+ and K+ * **↑ HCO3 intake:** Ingestion of non-absorbable antacids (calcium carbonate) or sodium bicarbonate pills * **Contraction alkalosis:** Decreased extracellular volume + stable HCO3 = ↑ HCO3 concentration
42
# Metabolic alkalosis Primary (uncompensated) metabolic alkalosis, arterial blood gas will show Compensation
pH ↑  Partial pressure of CO2 (PCO2) ↑  HCO3 ↑ **Think: “So the alkalosis is NOT due to ↓ CO2; it must be due to ↑ serum HCO3” Confirm by looking at HCO3→ will be high (> 28 mEq/L)** Compensation: In primary **metabolic** acid-base disorders, the **lungs may try to compensate** in an attempt to normalize the pH Lungs respond to metabolic **alkalosis by ↓ ventilation**
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# Metabolic alkalosis chloride responsive causes
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
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# Metabolic alkalosis Clin man Ca signs
Symptoms may include: Vomiting BP abnormalities: Hypertension (primary mineralocorticoid excess) Hypotension (↓ effective circulating volume) Hypokalemia Hypocalcemia: Tetany Chvostek sign: contraction of facial muscles when the facial 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
# Metabolic alkalosis Tx
Directed at correcting the underlying etiology Attempt to improve renal HCO3- excretion to resolve alkalosis: In patients without edema (true volume depletion): **volume repletion with isotonic saline** In patients with ↓ effective circulating volume (CHF, cirrhosis, renal artery stenosis): Potassium chloride K+-sparing diuretics Avoid isotonic saline as it will worsen symptoms without improving alkalosis
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