Acid/Base Imbalances Flashcards
1
Q
3 ways to regulate acid-base balance:
A
- Buffer system (react immediately)
- Respiratory system (responds in minutes and reaches max effectiveness in hours)
- Renal system (response 2-3 days but can maintain balance indefinitely)
2
Q
buffer system
A
- Fastest acting system and primary regulator of acid-base balance
- Act chemically to change strong acids into weaker acids or to bind acids and neutralize their effect
- All body fluids contain buffers
- Major buffer system is carbonic-acid bicarbonate
- Other buffers include phosphate, protein, and hemoglobin
- Cell can act as a buffer by shifting of H+ in and out
- Minimize effects of acids on blood pH until they can be excreted by body
- Combining strong acid with a base prevents acid from causing large decrease in pH
- Carbonic acid (H2CO3) broken down to H20 and CO2 (excreted by lungs)
3
Q
respiratory system
A
- Lungs help maintain normal pH by excreting CO2 and water, which are byproducts of cellular metabolism
- When released in circulation, CO2 enters RBCs and combines with H20 to form H2CO3 (carbonic acid)
- Carbonic acid dissociates into H+ and bicarb (HCO3-)
- Free H+ is buffered by hemoglobin molecules and bicarb diffuses into plasma
- In pulmonary capillaries, process is reversed → CO2 is formed and excreted by the lungs
- CO2 + H20 ⇋ H2CO3 ⇋ H+ HCO3-
- If a respiratory problem is the cause of an acid-base imbalance (respiratory failure), it loses its ability to correct a pH alteration
CO2 or H+ levels increase
- Increase respiratory rate (“blow off” excess CO2)
- Remove more CO2 or acid from the body
CO2 or H+ levels decrease
- Decrease respiratory rate (retain CO2)
- Retain more CO2 and increase acid levels in the body
4
Q
renal system
A
- Can take up to 24 hours to start working
- Under normal conditions, kidneys reabsorb and conserve bicarbonate they filter
- Kidneys can generate additional bicarb and eliminate excess H+
- Kidneys regulate acid-base balance by:
- Secretion of small amounts of free H+ into the renal tubule
- Combination of H+ with ammonia (NH3) to form ammonium (NH4)
- Excretion of weak acids
- Kidneys normally excrete acidic urine (average pH=6)
- pH of urine can decrease to 4 and increase to 8
- If renal system is the cause of an acid-base imbalance (renal failure), it loses its ability to correct a pH alteration
5
Q
The three renal mechanisms of acid elimination are
A
1) secretion of small amounts of free hydrogen into the renal tubule
2) combination of H+ with ammonia (NH3) to form ammonium (NH4−), and
3) excretion of weak acids
6
Q
respiratory acidosis
A
- caused by hypoventilation
- Results from a buildup of CO2
- Respiratory acidosis - decrease in the body fluid pH due to an excess of CO2 (>45 mm Hg)
- CO2 excess happens when ventilation decreases (hypoventilation) → leads to the accumulation of CO2 because it is not being exhaled → this interferes with the carbonic acid-bicarbonate buffer system → lowers the pH of blood
- Carbonic acid accumulates in blood → academia
- If CO2 is not eliminated from blood, acidosis results
- Compensation: kidneys conserve bicarb and secrete H+ into urine
7
Q
common causes of respiratory acidosis
A
- Chronic obstructive pulmonary disorder (COPD)
- Barbiturate or sedative overdose
- Chest wall abnormality (obesity)
- Severe pneumonia
- Atelectasis
- Respiratory muscle weakness (Guillain-Barre syndrome)
- Mechanical hypoventilation
8
Q
clinical manifestations of respiratory acidosis
A
- drowsiness, disorientation, dizziness, headache, coma
- decreased BP, V fib, warm flushed skin
- seizures
9
Q
nursing management of respiratory acidosis
A
- Use semi-fowler’s position to facilitate ventilation
- Suction as needed to remove excessive mucus
- Assess patency of airway – respiratory rate, breath sounds
- Assess tachycardia secondary to hypoxia
- Teach patient to use an incentive spirometer
- Encourage patient to turn, cough and deep breath
- Encourage ambulation
- Administration of medications (e.g., Narcan)
10
Q
respiratory alkalosis
A
- occurs with hyperventilation
- Caused by a loss of CO2 through the lungs due to hyperventilation
- Primary cause is hypoxemia from acute pulmonary disorders (eg, pneumonia, pulmonary embolus) (lungs try to quickly compensate and end up hyperventilating)
- Decreased arterial CO2 levels lead to a decrease in carbonic acid concentration in the blood and an increase in pH
- Compensated respiratory alkalosis uncommon unless patient is on ventilator or has CNS condition
- Compensation: decreased levels of bicarb
11
Q
common causes of respiratory alkalosis
A
- Hypoxia (not getting enough oxygen)
- Pulmonary emboli (clot in lungs that blocks blood flow)
- Anxiety, fear
- Pain
- Exercise
- Fever
- Stimulated respiratory center caused by septicemia, encephalitis, brain injury, salicylate poisoning
- Mechanical hyperventilation
12
Q
clinical manifestations of respiratory alkalosis
A
- lethargy, lightheadedness, confusion
- tachycardia, dysrhythmias (related to hypokalemia)
- nausea, vomiting, epigastric pain
- tetany, numbness, tingling of extremities, hyperreflexia, seizures
13
Q
nursing management of respiratory alkalosis
A
- Identify and correct precipitating cause
- Try to relax or calm down the patient by providing relaxation techniques
- Rebreathing CO2 from a closed system (e.g., paper bag)
- If the patient is having pain, treat it with analgesics
- If the patient is experiencing a fever, treat it
14
Q
metabolic acidosis
A
- Low levels of bicarb
- (base bicarbonate deficit) occurs when an acid other than carbonic acid accumulates in the body OR when bicarbonate is lost from body fluids.
- Both cases = bicarbonate deficit
- Addition of H+ to the ECF (from acids other than CO2) or loss of bicarbonate ions
- Can results from an addition of lactic acid, uric acid, or ketones to the blood
- Compensation: increase CO2 expiration by lungs (breath faster)
- Develop Kussmaul’s respirations (deep, rapid breathing, controlled)
- Kidneys also attempt to excrete additional acid
15
Q
anion gap
A
- help determine the source of acidosis
- Normal anion gap is 8-16 mmol/L
- Anion gap increases (high number; greater than 16) in metabolic acidosis associated with acid gain
- Normal anion gap (8-16) from metabolic acidosis associated with bicarbonate loss
