Acid-Base Imbalances Risk Factors/Causes Pathophysiology Signs and Symptoms Managements

COPD – primary risk factor COPD H – Headache Maintain patent airway.

• ARDS ↓ H – Hypercapnea Give medications as prescribed
• Asthma ↓ Pulmonary surface area for gas exchange W – Warm, flushed skin (antibiotics or bronchodilators).
• Chronic bronchitis ↓ T – Tachycardia Administer oxygen at 1-2 lpm as
• Emphysema ↑ Dead space B – Blurring of vision ordered.
• Pulmonary edema ↓ I – Irritability Perform tracheal suctioning, postural
Hypoventilation D – Decreased LOC drainage, and DBCE.
↓ Administer oral and IVF as ordered.
↑ CO2 retention Late Signs Teach patient how to perform pursed-
Respiratory Acidosis ↓ ↓ ↓ D – Disorientation lip breathing.
↓ pH Hypercapnea CO2 readily crosses ↓ pH, ↑ H+ ions C – Confusion
↑ H+ ↓ the blood brain ↓ C – Coma
↑ CO2 ↑ RR, ↑ PR, and barrier H+ move to ICF
respiratory depth ↓ from ECF S. electrolyte imbalance
Cerebral ↓ H - Hyperkalemia
vasodilation K+ ions move to
↓ ECF from ICF
Headache, blurring ↓
of vision, altered or Hyperkalemia
↓ LOC, tachycardia
Anxiety or panic attacks Anxiety/Panic T – Tachycardia Treat the underlying cause; removing
↓ A – Anxiety causative agent such as phobia.
Hyperventilation R – Restlessness For anxiety, provide anxiolytics and
↓ ↓ ↓ L – Lightheadedness sedatives as ordered.
Respiratory Alkalosis ↓ CO2 ↑ pH ↓ H+ P – Paresthesia Advise patients to breathe into brown
↑ pH ↓ ↓ ↓ D – Decreased LOC paper bag with cupped hands.
↓ H+ Cerebral ↑ Binding of CHON H+ move from ICF I – Increased DTRs Allay the anxiety. Recommend activities
↓CO2 vasoconstriction to Ca2+ to ECF P – (+) Chvostek’s & (+) Trousseau that promote relaxation such as deep-
↓ ↓ ↓ T – Tetany breathing exercises.
Lightheadedness Hypocalcemia K+ move to ICF C – Convulsions Provide undisturbed rest periods.
↓ ↓ S – Seizures Stay with the patient during periods of
↓ Cell wall integrity Hypokalemia extreme stress & anxiety.
↑ Cell wall Offer reassurance and maintain a calm
permeability & quiet environment.
↓ Institute safety and seizure
↑ Cell excitability precautions.
↑ NMI
Metabolic Acidosis Acute renal failure Acute renal failure K – Kussmaul’s respiration NaHCO3 per IV.
↓ pH ↓ H – Headache - It is an alkalinizing solution used to
↑ H+ Kidneys do not excrete excess acids H – Hyperkalemia signs: reduce the effects of acidosis on
↓ HCO3- ↓ ↓ • Muscle weakness cardiac function.
↓ pH ↑ H+ • Oliguria - Flush with NSS.
↓ ↓ • Respiratory distress Dialysis for renal failure.
↓ Binding of CHON to Ca2+ H+ move to ICF from ECF • Dominant cardiac contractility Institute safety precautions.
↓ ↓ • Hyperreflexia Keep the clocks, calendars, and familiar
Hypercalcemia Hyperkalemia objects at bedside. Orient patient to
 ↓ HCO3- time, place, and circumstances as
↓ ECG Changes needed. Allow S/O to remain with the
↑CO2 in the blood T – Tall T wave client as much as possible.
↓ ↓ P – Prolonged PR interval
Cerebral vasodilation Lungs compensate W – Wide QRS complex
↓ ↓ P – Prolonged ST segment
Headache ↑ RR, ↑ Respiratory depth
(Kussmaul’s respiration)
Metabolic Alkalosis Excessive loss of acid Vomiting/Lavage/Diuresis D – Disorientation Administer oxygen as ordered.
↑ pH Prolonged gastric suctioning and ↓ C – Confusion Seizure precautions.
↓ H+ lavage Loss of H+ and Cl- T – Tremors Maintain patent IV.
↑ HCO3- Frequent vomiting ↓ ↓ ↓ P – Paresthesia Administer diluted K solutions with an
↑ pH ↑ HCO3- ↓ H ions D – Decreased LOC infusion pump.
Other causes ↓ ↓ N/V – Nausea/vomiting Monitor I&O.
Thiazides Alkalosis H ions move from Infuse ammonium chloride no faster
Compensatory
Furosemide ↓ ICF to ECF Complication (Late Sign) than 1L over 4 hours.
Mechanism:
Diuretics that deplete K+ stores, ↑ Binding of Ca2+ ↓ T – Tetany Administer Diamox (Carbonic
↓ pH hydrogen, and chloride ion loss from C - Convulsion Anhydrase Inhibitor) as ordered.
and CHON K moves from ECF
↓HCO3- kidneys - This increases renal excretion of
↓ to ICF
↑CO2 HCO3-.
Hypocalcemia ↓
Hypokalemia

Compensatory:
The kidneys retain
H ions and removes
HCO3-.