Acid Base Balance Alterations

Acids

hydrogen ion donors, strength depends on how many H+ ions are released

circulate in 2 forms → volatile acids or nonvolatile fixed acids

accumulation can lead to acidosis, type depends on whether the acid is volatile (respiratory) or nonvolatile (metabolic)

Volatile Acids

formed from CO2 and eliminated via the lungs

ex: carbonic acid

Nonvolatile Fixed Acids

formed from metabolism of proteins and fats and are excreted by the kidneys

ex: lactic acid and ketoacids

Bases

hydrogen ion acceptors

main physiological one is bicarbonate (HCO3-) which buffers excess H+ and helps maintain blood pH

bicarbonate is regulated by the kidneys and plays a key role in acid-base compensation

Buffers

weak acids/bases that neutralize strong acids/bases to minimize pH changes

keep pH in the normal range (7.35-7.45)

act quickly but can be overwhelmed with excess acids or bases

major systems → intracellular and extracellular (protein and bicarbonate)

Blood pH Ratio

normal arterial pH → 7.35-7.45 maintained by 20:1 ratio of bicarbonate to carbonic acid

lower ratio → blood is acidic with a lower pH

higher ratio → blood is alkaline with a higher pH

Bicarbonate Range

22-26

Intracellular Buffer

when H+ increases in blood (acidosis) → H+ moves into cells and K+ moves out to increase serum potassium

when H+ decreases in blood (alkalosis) → H+ moves out of cells and K+ moves in to lower serum potassium

Protein Buffer System

proteins are amphoteric and can act as either an acid or base

ex: hemoglobin and albumin (most common) and globulins

Carbonic Acid Bicarb Buffer System

H⁺ + HCO₃⁻ ⇌ H₂CO₃ ⇌ CO₂ + H₂O

major plasma buffer that neutralizes excess H+ by binding it to bicarb

if H+ increases → HCO3 binds to H+ and forms H2CO3 thats broken down to CO2 and exhaled

if H+ decreases → H2CO3 dissociates to release H+ and stabilize pH

too much H+ or loss of HCO3- exceeds buffer capacity and free H+ accumulates and pH drops more

CO2 Transport

CO2 diffuses into RBCs and reacts with H2O to form H2CO3 (via carbonic anhydrase)

H2CO3 dissociates into H+ and HCO3-

H+ binds hemoglobin to prevent large pH change until overwhelmed

HCO3- exits the RBC and CL- enters (chloride shift)

if ↑ CO₂ → ↑ H⁺ → ↓ pH

if ↓ CO₂ → ↓ H⁺ → ↑ pH

Lung Compensation

happens within seconds

this is true when the cause is metabolic and buffer systems in blood are overwhelmed → when the cause of the pH imbalance is not due to the respiratory balance

Acidosis Lung Compensation

respiratory rate and depth go up in an attempt to blow off acids

carbonic acid can be carried to the lungs where it is reduced to CO2 and water and then exhaled

Alkalosis Lung Compensation

respiratory rate and depth go down

CO2 is retained and carbonic acid builds to neutralize and decrease the strength of excess bicarbonate

Kidney Compensation

the main way the body compensates for pH imbalances caused by the respiratory system when buffer systems are no longer effective

kidneys can also correct metabolic imbalances, but their ability is limited if the kidneys themselves are the issue

slower than lungs, takes hours and up to 2-3 days to fully correct pH

Acidosis Kidney Compensation

kidneys secrete more H+ into the tubules

reabsorb more bicarb

Alkalosis Kidney Compensation

kidneys secrete less H+

excrete more bicarb

Respiratory Acid Alkalosis

caused by abnormal CO2 levels due to changes in ventilation

key indicator → PaCO2

acidosis → increased CO2

alkalosis → decreased CO2

Metabolic Acid Alklalosis

caused by all other non respiratory factors

key indicator → HCO3-

acidosis → low bicarb

alkalosis → high bicarb

pH Compensation

the bodys attempt to correct pH by using the opposite system

if the cause is respiratory = kidneys respond

if the cause is metabolic = lungs primarily respond

Metabolic Acidosis

total bicarb conc is low

relative excess of hydrogen ions caused by accumulation of nonvolatile acids that exceed available bicarb

compensation → body responds by increasing respiratory rate and depth to eliminate CO2 and raise pH

Metabolic Acidosis Causes

diabetic ketoacidosis → increased fat metabolism that causes a buildup of ketones

renal failure → low H+ excretion and bicarb reabsorption and decreased ammonium excretion

hypoxia → anaerobic metabolism increases lactic acid

aspirin overdose → high H+ conc from excess acetylsalicylic acid

severe diarrhea → loss of alkaline intestinal/pancreatic secretions that lowers base

excess fat catabolism → increased ketones and acid buildup

high fat diet → high fat metabolism that increases ketone production

Anion Gap

formula → AG = [Na⁺] – ([Cl⁻] + [HCO₃⁻]), normal range is 8-16

measures the balance between positive and negative ions in blood

Na+ is main positive and Cl- and HCO3- are main negative ions

other measured negative ions include lactate, phosphate, and sulfate

used to help find the cause of metabolic acidosis

High Anion Gap Acidosis

extra acids (lactic acid), HCO3- decreases and Cl- stays the same

Normal Anion Gap Acidosis

HCO3- is lost and Cl- increases to keep the balance (electroneutrality)

Metabolic Acidosis High Anion Gap Causes

lactic acidosis (shock or heart failure)

diabetic ketoacidosis

aspiring (salicylate) poisoning

renal failure (low acid excretion)

Metabolic Acidosis Normal Anion Gap Causes

bicarb loss → diarrhea, intestinal suction, and carbonic anhydrase inhibitors

hormonal cause → hypoaldosteronism (low bicarb retention)

chloride gain → excess Cl- reabsorption by kidneys and large volumes of NaCl infusion

Metabolic Acidosis Symptoms

neural → weakness, lethargy, general malaise, twitching, confusion, stupor, and coma

cardiac → peripheral vasodilation (warm flushed skin), low heart rate, risk of dysrhythmias due to electrolyte shifts

GI → anorexia, nausea, vomiting, and abdominal pain

skeletal → bone disease

endocrine → fruity breath (diabetic ketoacidosis)

respiratory comp → kussmaul resp and increased RR and depth

electrolyte shifts comp → hyperkalemia and hypercalcemia (ionized Ca) and cells taking up more H+ and releasing more K+ into blood

renal comp → more ammonium in urine

Metabolic Acidosis Interventions

identify and treat the underlying cause

monitor vital signs and respiratory status

ensure patients airway

assess LOC and for signs of CNS depression

monitor electrolytes, especially potassium

maintain strict I&O, assist with fluid/electrolyte replacement

implement seizure precautions

administer prescribed IV fluids

monitor potassium closely for values dropping as acidosis is corrected

Lactic Acidosis Acidosis Interventions

administer oxygen to improve tissue perfusion and reduce anaerobic metabolism

Diabetic Ketoacidosis Acidosis Interventions

give insulin to move glucose into cells and reduce fat metabolism and ketone production

Renal Failure Acidosis Interventions

dialysis to remove waste products contributing to acidosis

low protein and high calorie diet to reduce protein catabolism and acid load

Metabolic Acidosis Respiratory Comp

primary compensation and faster

hyperventilation increases the CO2 loss

lower CO2 → respiratory alkalosis

ex: kussmaul respirations

starts within mins to hours

Metabolic Acidosis Renal Comp

secondary compensation and slower

increased H+ excretion and bicarb reabsorption and generation

takes hours to days

Metabolic Acidosis if Cause is Renal Failure

kidneys cant excrete H+ or regenerate bicarb

respiratory compensation is the only effective mechanism

acidosis may persist unless treated with dialysis, bicarb, and a low protein high calorie diet

Metabolic Alkalosis

deficit of carbonic acid (H2CO3) and lower hydrogen ion conc

caused by accumulation of base or loss of nonvolatile acids without equivalent base loss

compensation → hypoventilation with higher CO2 retention and high carbonic acid to help restore pH

Metabolic Alkalosis Causes

excessive intake of sodium bicarb (alka-seltzer)

GI acid loss → vomiting and NG suction

diuretics (especially loop and thiazide)

hyperaldosteronism → aldosterone leads to high H+ secretion and causes hypokalemia = triggers K+/H+ shift (H+ enters cells and worsens alkalosis)

aldosterone also causes higher K+ secretion further making the hypokalemia worse → massive blood transfusion where citrate is metabolized to bicarb

Metabolic Alkalosis Symptoms

neural → confusion, hyperactive DTRs, tetany, convulsions, paresthesias, circumoral paresthesias, carpopedal spasm, and restlessness

cardiac → hypotension and dysrhythmias

GI → nausea and vomiting

respiratory comp → low RR and depth

renal comp → high urine pH

electrolyte imbalance comp → hypokalemia and hypocalcemia (less ionized Ca)

Metabolic Alkalosis Treatment

correct the underlying cause of the imbalance

administer IV (normal saline) and electrolyte replacements (K+/Cl-)

provide adequate chloride to promote NaCl reabsorption and HCO3- excretion

monitor cardiac rhythm for signs of hypokalemia

educate on risks of excess sodium bicarb use and important of KCl supplementation with loop/thiazide diuretics

Metabolic Alkalosis Respiratory Comp

primary compensation thats faster

hypoventilation slows CO2 loss

higher CO2 → respiratory acidosis

helps raise carbonic acid and lower the pH

begins within minutes to hours

Metabolic Alkalosis Renal Comp

secondary compensation and is slower

if respiratory compensation is inadequate the kidneys may lower bicarb reabsorption and increase H+ retention

takes hours to days

Metabolic Alkalosis if Kidneys are the Cause Comp

ex: diuretics and hyperaldosteronism issues

renal compensation is impaired

respiratory compensation becomes the main and limited mechanism

alkalosis may persist until the underlying cause is corrected

Respiratory Acidosis

excess carbonic acid due to CO2 retention

caused by hypoventilation → inadequate rate/depth of breath that increases CO2 conc

compensation → slow renal where kidneys retain bicarb and acidic urine is excreted, begins hours to days

Respiratory Acidosis Causes

CNS depression that decreases respiratory drive → brain trauma affecting medulla oblongata and meds like narcotics, sedatives, and anesthetics

lungs that decrease gas exchange/airflow → pneumonia, atelectasis (lung collapse), emphysema, asthma, bronchitis, pulmonary edema, and bronchiectasis

even breath holding long enough can cause pH to drop

Respiratory Acidosis Symptoms

neural → dilation of cerebral vessels and depression of neural function, drowsiness, feeling of fullness in head, headache, weakness, behavior changes (confusion, depression, paranoia, hallucinations), tremors, paralysis, depressed DTRs, and stupor and coma

skin → warm and flushed

cardiac → tachycardia

respiratory → dyspnea (likely the cause) and cyanosis

Respiratory Acidosis Interventions

maintain patient airway

improve ventilation and aeration based on clinical manifestations

monitor for signs of respiratory distress

monitor lab values

administer oxygen

place client in semi-fowlers position unless contraindicated

encourage and assist client to turn, cough, and deep breathe

prepare to administer chest physiotherapy and postural drainage

encourage hydration to thin secretions unless excess fluid intake is contraindicated

suction client and give antibiotics as necessary

Respiratory Alkalosis

carbonic acid (H2CO3) deficit due to excess CO2 loss

compensation → renal and slow with high renal excretion of bicarb that begins within hours to days

Respiratory Alkalosis Causes

hyperventilation → CO2 elimination exceeds production that increases pH

hysteria or anxiety → emotional distress triggers rapid breathing

mechanical over ventilation → ventilator settings deliver breaths that are too fast or deep causing excess CO2 loss

pain or brain trauma → stimulates the respiratory center in the brain

hypoxia → low oxygen levels stimulate increased respiratory rate

Respiratory Alkalosis Symptoms

headache, mental status changes (confused or irritable), vertigo, lightheadedness, paresthesias (tingling in fingers and toes)

electrolyte imbalances → hypokalemia and hypocalcemia = high pH increases calcium binding to albumin

carpopedal spasms (trousseaus sign), facial twitching (chvosteks sign), and tetany and convulsions

Respiratory Alkalosis Interventions

provide emotional support and reassurance

encourage controlled breathing patterns

assist with breathing techniques or aids

use rebreathing strategies (paper bag, mask, or CO2)

support voluntary breath holding if appropriate

monitor and adjust mechanical ventilation settings

monitor electrolytes (especially calcium and potassium)

administer meds

be prepared to give calcium gluconate for tetany if ordered

Primary Imbalance

the initial cause of the acid base disturbance

can be respiratory or metabolic in origin

usually related to an acute condition

Compensated Imbalance

the bodys attempts to restore pH by creating a secondary imbalance

respiratory imbalances → compensated by renal system

metabolic imbalances → compensated by respiratory system

Combined Imbalances

both respiratory and metabolic disturbances occur at the same time

can involves → both acidosis, both alkalosis, or one acidosis + one alkalosis

No Compensation

pH is abnormal

only one (CO2 or HCO3-) are abnormal

if its CO2 thats abnormal its respiratory

if its bicarb that abnormal its metabolic

Partial Compensation

pH is abnormal

both CO2 and bicarb are abnormal

Full Compensation

pH is normal

both CO2 and bicarb are abnormal

pH and CO2 in Opposite Directions

respiratory issue

pH and Bicarb in Same Direction

metabolic issue