Summary GNUR 293 Exam 2 study guide, complete A+ guide, updated 2025.

Exam 2 study guide
Acid-Base Imbalances
1) Be able to interpret ABG values. Also, be able to know the anticipated values for each acid-base
imbalance.
ABG Arterial Blood Gas




PaO2 80-100mm Hg
SaO2 (Oxygen saturation) > 95%
2) Describe the systems that maintain acid-base homeostasis.
1carbonic acid: 20 base bicarbonate
Buffer systems:
 Phosphate  phosphate binds to hydrogen and excretes through urine (happens when
bloods has too much hydrogen aka acidic)
 Protein Subsystems
o Hemoglobin Only RBC, release hydrogen when needed (happens when blood
is alkaline does not have enough hydrogen)
o Amino acid all proteins very flexible can release or bind to hydrogen when
needed (blood basic release H ions) (blood acidic bind to H ions to become more
basic)
o Plasma Protein  Protein in the blood (albumin) Can release the hydrogen ion
 Binds to calcium = reducing calcium levels
 causes hypocalcemia
 Hydrogen/Potassium Exchange
o Acidic Blood -> Potassium comes in when H+ is kicked out of blood, to maintain
charge (Hyperkalemia)
o Alkaline Blood -> Potassium leaves the place H+ coming in to maintain charge
(Hypokalemia)
 Carbonic acid- bicarbonate 




o Blood Acidotic State: (From pic above goes right to left)
 Hydrogen levels increase
 Bicarbonate (HCO3) combine w H+, Carbonic acid breaks down =
breath out CO2 (Goal to reduce H+)
o Blood Alkalotic state: (From pic above goes left to right)
 Hydrogen levels decrease
 Break down H2CO3 to gain H+ (Goal to increase H+)
 Respiratory system

, o Increase respiratory rate, decrease CO2 (Exhale more) = Acid decreases
o Decrease respiratory rate, increase CO2 ( Do not release much)= acid increase
 Renal System
o Main goal-> Eliminate H+ and Reabsorb HCO3
o Blood acidotic (increase H+) - increase elimination of H+, increase reabsorptions
of HCO3
o Blood alkalotic (decrease H+)- decrease elimination of H+, decrease reabsorption
of HCO3
3) Identify patients who are at risk for each acid-base imbalance. Be able to explain the
pathophysiology for each. Identify potential acid-base imbalances given clinical manifestations
and a clinical scenario.
 Respiratory Acidosis carbonic acid excess
o At Risk-> Cannot catch my breath (bronchitis, pulmonary edema, emphysema,
pneumonia)
 Hypoventilation
 Respiratory depression
 Inadequate chest expansion
 Airway Obstruction
 Impaired alveolar-capillary exchange
o Pathophysiology->
 Not breathing out CO2 = too much CO2 remaining in system leads to
excess H+ ions
o Acid Base Imbalance->
 pH< 7.35
 PaCO2 > 45mm Hg
 Respiratory Alkalosis carbonic acid deficit
o At Risk-> Breathing too fast
 Hyperventilation
 Hysteria/anxiety, pain, fever, alcohol withdrawing
 Stimulates brainstem: acetylsalicylic overdose, meningitis, head injury,
sepsis, hypoxemia
o Pathophysiology->
 Breathing too much CO2 = H+ unable to be created causing alkalosis
o Acid Base Imbalance->
 pH > 7.45
 PaCO2 < 35 mm Hg
 Metabolic Acidosis bicarbonate deficit
o At Risk-> Unable to excrete H+, or unable to reabsorb HCO3
 Ketoacidosis
 Latic acid accumulation
 Sever prolonged diarrhea (loss base = acid problem)
 Kidney disease
 Malnutrition
 Excessive acetylsalicylic acid (aka aspirin)
o Pathophysiology->
 Not reabsorbing HCO3 = can’t excrete CO2 through respiration after its
breakdown
 Want them to breath more increase respiratory rate
o Acid Base Imbalance->
 pH < 7.35

,  HCO3
 Metabolic Alkalosis  bicarbonate excess
o At Risk-> excreting too much H+ and reabsorbing too much HCO3
 Prolonged committing or gastric suction
 Prolonged diuretic therapy
 Massive blood transfusion
 Hyperaldosteronism- excretes K+, hypokalemia
 Kicks out H+, K+ (potassium) goes in
 Antacid abuse
o Pathophysiology->
 Too much carbonate being made CO2 is being released, causing
reduction H+ = making blood basic
o Acid Base Imbalance->
 pH > 7.45
 HCO3
4) Discuss the compensatory mechanisms, common signs and symptoms, and interventions for each
acid-base imbalance.
 Respiratory Acidosis carbonic acid excess
o Compensation
 Kidneys reabsorb HCO3 and excrete H+
o Signs/Symptoms
 Low blood pressure, warm flushed skin
 Hyperkalemia, Dysrhythmia
 Hypoventilation w hypoxia
 Headache, drowsy, blurred vision, disoriented, coma
o Interventions
 Assess and monitor respiratory status
 Monitor ABG, ECG, electrolyte (K-potassium)
 High Fowler’s position
 Oxygen therapy
 Pursed lip breathing (increasing CO2)
 Pulmonary hygiene
o Treatment
 Bronchodilators (help open airway)
 Antibiotics
 Mucolytics
 Steroids
 Binders
 Respiratory Alkalosis carbonic acid deficit
o Compensation
 Rarely occurs
o Signs/Symptoms
 Lightheaded, lethargic, confused
 Nausea, vomiting
 Hypokalemia
 Hypocalcemia, tetany, numbness, tingling of extremities, seizures
 Dysrhythmias
o Interventions
 Assess and monitor respiratory status
 Monitor ABG, ECG, electrolytes (K-potassium, Ca- calcium)

,  Provide calm environment, breath slow, relaxation techniques,
REBREATH CO2 (paper bag)
 Protect from injury
o Treatment
 Treat the cause of hypoxemia
 Sedatives
 Anti-anxiety medications
 Metabolic Acidosis bicarbonate deficit
o Compensation
 Release more CO2 through respiration, decrease plasma CO2
 Kussmaul respiration-> deep & rapid (involuntary)
 Kidney reabsorbs HCO3 and excrete H+
o Signs/Symptoms
 Hyperkalemia, dysrhythmia
 Abdominal pain, diarrhea
 Low blood pressure, cold clammy skin
 Kussmaul breathing- deep rapid respirations
o Interventions
 Monitor VS & respiratory status, ABG, ECG, K+
 Assess level of consciousness + input & output
 Diabetic ketoacidosis
o Treatment
 Treat cause
 Metabolic Alkalosis  base bicarbonate excess
o Compensation
 Reduce respiratory rate. Increase plasma CO2
 Kidney->
 Decrease excretion H+
 Decrease reabsorption of HCO3
 Excrete HCO3
o Signs/Symptoms
 Hypokalemia, hypocalcemia
 Dysrhythmia
 Hypoventilation
 Drowsy, dizzy, & confused
o Interventions
 Monitor VS & respiratory status, ABG ECG, K+, Ca+
 Assess level of consciousness, input & output
 Protect from injury, teach use of antacids, teach signs of hypokalemia
o Treatment
 Treat underlying problem
 CI (chloride) administration to enhance renal absorption of Na+ &
excretion OF HCO3
5) Discuss the electrolytes imbalance associated with acid-base imbalance. Understand the
pathophysiology.
 Respiratory Acidosis carbonic acid excess
o Hyperkalemia:
 Hydrogen-Potassium exchange buffer:
 Acidic Blood