Acid base balance (incomplete)

week 3

H+

• vital to life

• expressed as pH

• circulate in 2 forms

  • volatile hydrogen of carbonic acid

  • nonvolatile form of hydrogen and organic acid

What are produced as end products of metabolism?

acids

Acids contain

hydrogen ions

Acids

• hydrogen ion donors- they give up H+ to neutralize or decrease the strength of an acid or to form a weaker base

• Lungs excrete 13,000-30,000 mEq of volatile hydrogen per day in the form of carbonic acid (H2CO3) as CO2

• The kidneys excrete 50 mEq of nonvolatile acids per day

More H+ correlate with lower pH

strength of an acid is determined by

the number of hydrogen ions it contains

number of hydrogen ions in body fluid determines ts

acidity, alkalinity, or neutrality

Bases

• contain no hydrogen ions (H+)

• hydrogen ion (H+) acceptors

• accept hydrogen ions (H+) from acids to neutralize or decrease the strength of a base or to form a weaker acid

pH 6.9 suggest

individual is close to death

slide 6-7

Buffer

weak acid/base that can combine with strong acids/bases to minimize changes in pH

Major buffer systems: intracellular

• potassium-hydrogen ion exchange

• increase H+ → H+ moves into cells & K+ moves out

• decrease H+ → H+ moves out of cells & K+ moves in

Major buffer systems: extracellular

• Protein buffers:

  • Hgb (80%)

  • Albumin & plasma globulins (20%)

• Bicarbonate buffer: carbonic acid + bicarbonate

• Phosphate buffer: HPO4-2 + H+  H2PO4-

• Bone buffer: 2H+ + CO32-  CO2 + H2O

Buffers as regulatory systems for H+ concentration in blood

• fastest acting regulatory system

• immediate protection against changes in H+ concentration in ECF

• function to keep pH within narrow limits of stability when too much acid/base is released

• react immediately with acids or bases to minimize changes in pH

• absorb or release H+ as needed

• serve as a transport mechanism that carries excess hydrogen ions (H+) to the lungs

• once primary buffer systems react, they are consumed, leaving the body less able to withstand further stress until they are replaced

What role does K+ play in major intracellular buffer?

• K+ plays an exchange role in acid-base balance

• K+ level changes to compensate for hydrogen ion level changes

• In acidosis:

  • Body protects itself from acid state by moving hydrogen ions (H+) into the cell  potassium (K)  moves out to make room for hydrogen ions (H+) & the potassium (K) level goes up

• In alkalosis:

  • Cells release hydrogen ions (H+) into the blood in an attempt to increase the acidity of the blood and combat alkalinity  potassium (K) moves into the cells and the potassium (K) level goes down

In DKA (diabetic ketoacidosis), you need to keep an eye on their potassium because

• the blood test may show normal/high potassium levels despite potassium being low

• insulin is the primary treatment for DKA but it causes both glucose and potassium to leave blood and enter cells→ rapid drop in potassium levels when it is already low can cause the heart to stop

Major buffer systems in extracellular fluid

if we have an acidic pH, what happens to serum chloride?

serum chloride decreases

• serum bicarb decreases less base= acidic

• pH decreases

• HCO3 out; CI in

if we have an alkaloid pH, what happens to serum chloride?

serum chloride increases

• serum bicarb increases more base= alkalotic

• pH increases

• HCO3 in; CI out

• HCO3= bicarbonate

14-17

Second defense that interacts with the buffer system to maintain acid-base balance

lungs

In acidosis

• pH goes down & respiratory rate/depth go up in an attempt to blow off acids

• carbonic acid (created by neutralizing action of bicarbonate) can be carried to the lungs where it is reduced to carbon dioxide (CO2) + water and exhaled, thus hydrogen ions (H+) are inactivated & excreted

In alkalosis

pH goes up & respiratory rate and depth go down

Carbon dioxide (CO2) is retained & carbonic acid builds to neutralize and decrease the strength of excess bicarbonate

how long does it take to correct deficit/excess H+ in lungs

in ½ minute you can correct a deficit or excess

lungs is faster than kidneys at correcting acid base

Lungs

• action of lungs is reversible in controlling an excess or deficit

• can hold H+ until deficit is corrected or can inactivate hydrogen ions, changing them to water molecules to be exhaled as carbon dioxide (CO2), thus correcting excess

Lungs are only capable of inactivating H+ carried by

carbonic acid

• Kidneys excrete other excess hydrogen ions

Anion Gap is equal to

• [Na+] - ([HCO3-]+[Cl-])

• concentration of unmeasured anions (other than Bicarb & CI)

• phosphates, sulfates, ketone bodies, lactic acid & proteins

everything before slide 33

What happens in diabetic ketoacidosis (DKA)?

• Insulin is given to speed up movement of serum glucose into cell→ decreasing concurrent ketosis

• When glucose is being properly metabolized, body stop converting fats to glucose

What do you need to monitor for in DKA

• monitor for circulatory collapse due to polyuria which may result from hyperglycemic state, as polyuria or diuresis may lead to extraceullar volume deficit

What happens in renal failure?

• dialysis may be used to remove protein & waste products, thereby lessening the acidosis state

• diet low in protein & high in calories will lessen the amount of protein waste products due to protein catabolism; this in turn, will lessen the acidosis

Metabolic acidosis treatment

Definition of Metabolic acidosis

Cause of metabolic acidosis

How does body compensate for metabolic acidosis?

What will the pH look like if metabolic acidosis is compensated?

pH will be low normal; less than

why does the graph show that the metabolic acidosis has been compensated?

the ratio has been restored to 20:1

which part of the body compensate when there’s an issue with the metabolic system?

respiratory system compensate for problem in metabolic system

Metabolic alkalosis

• deficit of carbonic acid (H₂CO₃) & decrease in hydrogen ion concentration

• Results from the accumulation of base or from a loss of acid without a comparable loss of base in body fluids

• we either took on too much base or lost too much acid

Metabolic alkalosis causes

• malfunction of metabolism leading to an increased amount of basic solution in the blood and a decrease in available acids in the blood

• ingestion of excess sodium bicarbonate (causes an increase in the amount of base in the blood)

• excessive vomiting (leads to excessive loss of acids)

• GI suctioning

• Diuretics

• hyperaldosteronism

• massive transfusion of whole blood

How does GI functioning contribute to metabolic alkalosis?

it leads to an excessive loss of acids from the suctioning

How does diuretics contribute to metabolic alkalosis?

loss of hydrogen ions and potassium causes a compensatory increase in the bicarbonate in the blood

How does hyperaldosteronism contribute to metabolic alkalosis?

increased renal tubular reabsorption of sodium occurs with the resultant loss of hydrogen ions

How does massive transfusion of whole blood contribute to metabolic alkalosis?

citrate anticoagulant used for storage of blood in metabolized to bicarbonate

• could cause hypocalcemia so blood centers would also give calcium

Metabolic alkalosis etiologies

• excess gain of bicarbonate

• increased bicarb retention

  • loss of chloride

• excessive loss of H+

• volume contraction

  • loss of body fluids

  • diuretic therapy

• abrupt correction of respiratory acidosis by mechanical ventilation

excessive loss of H+ occur through

• NG suctioning (most common reason)

• vomiting

• bulimia

• potassium deficit

  • prolonged diuretic therapy (lassie & thiazides)

  • hyperaldosteronism

excess gain of bicarbonate can occur through

• administration or ingestion of HCO3

• administration of solutions containing lactate

• administration of citrate containing blood transfusions

• NaHCO3 during CPR

Metabolic alkalosis assessment

• respiratory rate & depth go down to conserve carbon dioxide (CO2)

• nausea, vomiting, diarrhea

• numbness & tingling in the extremities

• restlessness and twitching in the extremities

• hypokalemia

• hypocalcemia

• sinus tachycardia

• dysrhythmias

Metabolic alkalosis neural manifestations

• confusion

• hyperactive DTRs

• tetany

• convulsions

• paresthesias in fingers & toes

• circumoral paresthesias

• carpopedal spasm

Metabolic alkalosis cardiovascular manifestations

• hypotension

• dysrhythmias

Metabolic alkalosis GI manifestations

nausea and vomiting

How do you compensate for metabolic alkalosis?

• decrease in RR & depth

• increase in urine pH

slide 44-45

Metabolic alkalosis definition

fixed acid deficit

cause of Metabolic Alkalosis

• base accumulation

• loss of acid

Metabolic Alkalosis compensation

• respiratory retention of H₂CO₃ (CO₂ + H₂O)

47 chart

Respiratory acidosis

• total concentration of buffer base is lower than normal with a relative increasing hydrogen ion (H+) concentration

• more hydrogen ions circulating in the blood than can be absorbed by the buffer system

Causes of respiratory acidosis

• due to primary defects in the function of the lungs or by changes in normal respiratory patterns due to secondary problems

• remember that any condition that causes an obstruction of the airway or depresses respiratory status can cause respiratory acidosis

• hypoventilation

• infection

• medication

• pneumonia

• Atelectasis

• brain trauma

• emphysema

• asthma

• bronchitis

• pulmonary edema

• bronchiectasis

Respiratory acidosis causes: hypoventilation

carbon dioxide is retained and hydrogen ions increase leading to the acid state; carbonic acid is refined and the pH goes down

Respiratory acidosis causes: infection

caused by inflammation and bacterial agents aeration decreases due to the obstruction of airways

Respiratory acidosis causes: medications

sedatives, narcotics, and anesthetics depress the respiratory center leading to hypoventilation; an increase in hydrogen ions occurs leading to carbon dioxide narcosis

Respiratory acidosis causes: pneumonia

caused by infection, irritants, and immobility; obstruction of airway passages leads to inadequate oxygenation due to fluid accumulation

Respiratory acidosis causes: Atelectasis

excessive mucus collection with the collapse of alveolar sacs caused by mucus plugs, infectious drainage, or anesthetic medications, results in decreased respiration

Respiratory acidosis causes: brain trauma

excessive pressure on the respiratory center or medulla oblongata depresses respiration

Respiratory acidosis causes: emphysema

loss of elasticity of alveoli sacs restrict air flow in and out, primarily out, leading to an increased carbon dioxide (co2) level

Respiratory acidosis causes: asthma

spasms due to allergens, irritants, or emotions cause the smooth muscles of the bronchioles to constrict

Respiratory acidosis causes: bronchitis

inflammation causes airway obstruction

Respiratory acidosis causes: pulmonary edema

extracellular accumulation of fluid in acute congestive heart failure (CHF) causes disturbances in alveolar diffusion and perfusion

Bronchiectasis

• bronchi become dilated due to inflammation; destructive changes and weakness in the walls of the bronchi occur

Respiratory acidosis etiologies

Acute***

• lung disease

  • acute pulmonary edema

  • aspiration

  • atelectasis

  • pneumothorax

  • severe pneumonia

• depression of respiratory center

  • sedative or narcotic overdose

  • head injury

Chronic Lung disease

• chronic bronchitis

• asthma

• cystic fibrosis

• emphysema

• COPD

Chest wall & respiratory muscles

• obesity

• post op pain

• high abdominal or thoracic incisions

• abdominal distention from ascites or bowel obstruction

Respiratory acidosis assessment

• respiratory rate & depth will increase

• headache, mental status changes, confusion

• drowsiness, restlessness

• visual disturbances

• diaphoresis

• cyanosis as the hypoxia becomes more acute

• hyperkalemia

• rapid and irregular pulse leading to dysrhythmias and vernacular fibrillation

Respiratory acidosis manifestations

Neural

• dilation of cereal vessels & depression of neural function

• feeling of fullness in head

• headache, weakness

• behavior changes- confusion, depression, paranoia, hallucinations

• tremors, paralysis, depressed DTRs

• stupor & coma

Skin

• warm & flushed

Cardiac

• tachycardia

Respiratory

• dyspnea and cyanosis

Compensation

• acid urine

Interventions for respiratory acidosis

• maintain patent airway

• improve ventilation and aeration based on the clinical manifestations

• monitor for signs of respiratory distress

• administer oxygen as prescribed

• place client in semi-fowler’s position unless contraindicated

• encourage & assist client to turn, cough & deep breathe

• prepare to administer chest physiotherapy & postural drainage as prescribed

• encourage hydration to thin secretions unless excess fluid intake is contraindicated

• suction client as necessary

Respiratory acidosis interventions 4 parts

1. reduce

• reduce restlessness by improving ventilation other than by the administration of sedatives and narcotics

2. monitor

monitor electrolyte values

3. avoid

avoid use of tranquilizers, narcotics & hypnotics because they further depress respiration

4. administer

administer antibiotics for infection as prescribed

Respiratory acidosis treatment

• encourage TCDB every 2 hrs

• chest PT

• suctioning

• semi-fowler’s or orthopedic position

• encourage fluids

• supplemental O2 to treat hypoxemia (use with caution in COPD d/t loss of hypoxemic stimulus)

• monitor VS, ABGs, serum K+ levels

• bronchodilators

• antibiotics for pneumonia

• administer sedatives with caution

• be prepared for intubation & mechanical ventilation

Respiratory acidosis definition

carbonic acid excess

cause of Respiratory acidosis

altered alveolar ventilation leading to retention of carbon dioxide

Respiratory acidosis compensation

• renal retention of HCO3-

• acidic urine excreted

slide 59 chart

Respiratory alkalosis

• deficit of carbonic acid (H₂CO₃) & decease in hydrogen ion concentration

• Results from accumulation of base or from loss of acid without a comparable loss of base in the body fluids

causes for respiratory alkalosis

• due to conditions that cause over-stimulation of respiratory system

• hyperventilation

  • rapid respiration causes blowing off of carbon dioxide→ leads to decrease in carbonic acid

• hysteria

  • often neurogenic in nature and related to psychoneurosis; however, this condition leads to vigorous breathing & excessive exhaling of carbon dioxide

• over-ventilation by mechanical ventilators

  • administration of oxygen and the depletion of carbon dioxide can occur from mechanical ventilation; client may be hyperventilated by mechanical ventilation

• conditions that increase metabolism such as fever

• pain/brain trauma

  • causes overstimulation of the respiratory center in the brain stem with resultant carbonic acid deficit

• salicylates

• hypoxia

Respiratory alkalosis causes: hypoxia

• causes respiratory stimulation with resultant carbonic acid deficit

Respiratory alkalosis causes: salicylates

• stimulate the respiratory center causing hyperventilation

Respiratory alkalosis etiologies

• excessive ventilation

  • extreme anxiety (most common)

  • hypoxemia

  • stimulation of respiratory center

    • high fever

    • early salicylate (aspirin) poisoning

    • encephalitis

    • CNS lesions affecting respiratory center

    • increase blood ammonia

• excessive mechanical ventilation (may deliberate to decreased cerebral edema)

• pregnancy (increase sensitivity to CO2)

• hyperventilation during L & D

Taking a bottle of aspirin initially start off as respiratory acidosis but it eventually develops into

metabolic acidosis

Respiratory alkalosis assessment

• initially hyperventilation & respiratory stimulation will cause rapid respiration (tachypnea); To compensate, RR & depth decreases

• headache, mental status changes

• vertigo= dizziness

• lightheadedness

• paresthesias as tingling of the fingers and toes

• hypokalemia

• hypocalcemia

• tetany

• convulsions

Respiratory alkalosis manifestations

cerebral vasoconstriction

• lightheadedness, syncope

• inability to concentrate

• blurred vision, vertigo

• loss of consciousness

neuromuscular irritability

• paresthesias

• tinnitus

• carpopedal spasms (Trousseau’s sign)

• spasms (Cvostek’s)

• tetany, twitching

• hyperactive DTRs

• seizures, convulsions, coma

cardiovascular

• cardiac dysrhythmias

hyperventilation

• rapid deep respirations

• dry mouth

GI function

• N & V, epigastric pain

Respiratory alkalosis interventions

• maintain patent airway

• provide emotional support and reassurance to the client

• encourage appropriate breathing patterns

• assist with breathing techniques and apply breathing aids as prescribed

• voluntary holding of breath

• rebreathe exhaled carbon dioxide (co2)

• rebreathing mask as prescribed

• carbon dioxide breaths as prescribed

• provide cautious care with ventilator clients so that the client is not forced to take breaths too deeply or rapidly

• monitor electrolyte values

• administer medications as ordered

• prepare to administer calcium gluconate for tetany as prescribed

Respiratory alkalosis treatment

• monitor VS

• encourage breathing slowly and less deeply

• breath into paper bag

• use rebreather mask

• administer sedatives

• correct underlying cause

• monitor ABGs

• adjust mechanical ventilator settings

• monitor K+ levels

• provide emotional support

Respiratory alkalosis definition

carbonic acid (H₂CO₃) deficit

Respiratory alkalosis cause

hyperventilation leading to excessive elimination of carbon dioxide (CO2)

Respiratory alkalosis compensation

renal excretion of HCO3-

slide 69 chart

70

stick needle in compromised artery because

if you stick it in good artery, you may cause blood to spill out and possibly hinder normal flow

performing Allen’s test

1. ask client to make tight fist

2. apply direct pressure over client’s ulnar & radial arteries

3. while pressure is applied, ask client to open their hand

4. remove pressure from ulnar artery & assess color of extremity distal to pressure point

pH 7.0 and 6.9 indicate patient

is approaching death

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