ACID BASE LECTURE

Acid-Base Balance Fundamentals & Physiological Mechanisms

• Acid-base balance is regulated by the movement and shift of hydrogen ions ($H^+$) into and out of cells throughout the body.

• Chemical and buffer systems consist of electrolytes and plasma proteins (specifically albumin) that shift across cell membranes to maintain physiological equilibrium.

• Normal systemic balance maintains blood pH within a tight physiological range; a blood pH below $7.35$ is categorized as acidosis, whereas elevated pH indicates alkalosis.

• The respiratory system acts as the body's rapid second line of defense to compensate for pH shifts by altering the rate and depth of ventilation to adjust arterial carbon dioxide ($CO_2$) levels.

Respiratory Acidosis

• Pathophysiology:

  • Occurs when hypoventilation or respiratory depression impairs carbon dioxide clearance, causing acidic $CO_2$ to accumulate in the bloodstream.

• Laboratory & Diagnostic Values:

  • pH Level: $\text{pH} < 7.35$

  • Normal $CO_2$ Range: $35\text{ to }40$

  • Acidotic $CO_2$ Threshold: $CO_2 > 55$

• Physiological Compensation:

  • The renal system (kidneys) compensates by reabsorbing bicarbonate ($HCO_3^-$) and excreting metabolic acids in urine over hours to days.

• Etiologies & Risk Factors:

  • Central Nervous System & Respiratory Depression: Opioid overdose, sedatives, and central nervous system depressants.

  • Severe Lung Infections: Pneumonia (impairs alveolar oxygen exchange and causes fluid buildup).

  • Pulmonary Embolism (PE):

  • Chronic PE: Slow clot formation over time leads to a progressive decrease in respiratory function and rate.

  • Acute PE: Sudden pulmonary arterial occlusion causing immediate gas exchange failure.

  • Chronic & Acute Airway Diseases: Chronic Obstructive Pulmonary Disease (COPD) and acute pulmonary edema.

• Assessment Findings & Clinical Manifestations:

  • Neurological: Progressive headaches caused by $CO_2$-induced cerebral vasodilation.

  • Cardiovascular:

  • Hypotension: Excess systemic acid functions as a direct vasodilator in the vascular bed, dropping systemic vascular resistance and blood pressure.

  • Cardiac Dysrhythmias: Systemic acidosis forces $H^+$ into cells, causing potassium ($K^+$) to shift out of cells into the bloodstream, producing hyperkalemia and EKG abnormalities.

  • Respiratory Auscultation: Auscultation of adventitious breath sounds, specifically crackles, indicating fluid accumulation in alveolar spaces.

• Nursing Interventions & Medical Management:

  • Oxygen Therapy:

  • Administer supplemental oxygen per standing facility orders (typically titrated to maintain $SpO_2$ between $88\text{\%}$ and $92\text{\%}$).

  • Special Caution: Avoid high-flow oxygen administration in COPD patients to preserve their hypoxic respiratory drive.

  • Pulmonary Hygiene & Airway Clearance:

  • Encourage deep breathing and coughing exercises.

  • Incentive Spirometry: Ensure the device is placed at the bedside table within immediate reach. Instruct the patient to perform incentive spirometry $1\text{ hour}$ while awake ($q1h$ while awake).

  • Pharmacotherapy:

  • Bronchodilators to open airways.

  • Antibiotics for underlying pulmonary infections (e.g., pneumonia).

  • Mucolytics and Exponents: Expectorants such as guaifenesin (Mucinex) to thin and mobilize tenacious pulmonary secretions.

  • Invasive Airway Management: Endotracheal intubation and mechanical ventilation serve as the final line of defense when non-invasive measures fail.

Respiratory Alkalosis

• Pathophysiology:

  • Occurs when hyperventilation causes excessive blowing off of acidic $CO_2$, leading to a deficit of arterial carbon dioxide.

• Laboratory & Diagnostic Values:

  • pH Level: $\text{pH} > 7.45$

  • $CO_2$ Level: $CO_2 < 35$

  • Respiratory Rate: $\text{Respiratory Rate} > 20\text{ breaths/min}$

• Physiological Compensation:

  • The renal system compensates by excreting excess bicarbonate ($HCO_3^-$) into the urine, which may present as increased urinary output.

• Etiologies & Risk Factors:

  • Febrile States: Fever causes hypermetabolism and elevated respiratory rates as the body attempts to offload heat.

  • Aspirin Toxicity (Salicylate Poisoning): Direct stimulation of the medullary respiratory center causes central hyperventilation.

  • Controlled Mechanical Ventilation: Incorrect ventilator settings (excessive tidal volume or respiratory rate) or a patient breathing spontaneously over the set ventilator rate.

  • Anxiety, Panic Attacks, & Hysteria: Severe mental health crises triggering rapid hyperventilation.

  • Pain Dynamics:

  • Acute Traumatic Pain: Sudden severe pain (e.g., a compound leg fracture) causes sympathetic activation and hyperventilation, leading to respiratory alkalosis.

  • Surgical/Abdominal Pain: Post-operative pain (e.g., post-sternotomy or abdominal incision) causes patients to suppress breathing, leading to hypoventilation and respiratory acidosis instead.

  • Neurological Impairment: Traumatic Brain Injury (TBI), cerebrovascular accidents (stroke), or localized brain lesions affecting respiratory centers.

  • Acute Asthma & Anaphylaxis: Sudden severe airway constriction and panic leading to hyperventilation and sensations of impending doom.

• Assessment Findings & Clinical Manifestations:

  • Neuromuscular & Electrolyte Shifts:

  • Hypokalemia and hypocalcemia resulting from cellular ion shifts.

  • Positive Chvostek's sign and Trousseau's sign secondary to low serum calcium.

  • Paresthesias: Tingling and numbness in extremities, circumoral region, and fingers.

  • Cardiovascular & Central Nervous System:

  • Tachycardia due to anxiety and sympathetic activation.

  • Dizziness, confusion, fatigue, syncope (passing out due to transient cerebral vasoconstriction and loss of $CO_2$).

• Nursing Interventions & Medical Management:

  • Oxygen Therapy: Administer oxygen to relieve tissue hypoxia and reduce panic drive.

  • Anxiolytic Administration: Administer PRN or scheduled benzodiazepines (e.g., lorazepam [Ativan], alprazolam [Xanax]) to calm anxiety and slow ventilation.

  • Rebreathing Techniques: Utilize the paper bag rebreathing method to force the re-inhalation of expired $CO_2$.

  • Mechanical Ventilator Adjustments: Decrease respiratory rate or tidal volume settings on the ventilator.

  • Electrolyte Replacement: Continuously monitor and replace serum calcium ($Ca^{2+}$) and potassium ($K^+$) as ordered.

  • Non-Pharmacological Calming Measures: Coach the patient in slow, controlled breathing techniques (in through the nose, out through the mouth).

Metabolic Acidosis

• Pathophysiology:

  • Characterized by an accumulation of metabolic acids or a direct excessive loss of bicarbonate ($HCO_3^-$) base from the body.

• Laboratory & Diagnostic Concepts:

  • pH Level: $\text{pH} < 7.35$

  • $HCO_3^-$ Level: Decreased serum bicarbonate.

  • Anion Gap: A calculated serum electrolyte parameter utilized by physicians to determine whether metabolic acidosis is caused by acid addition (e.g., ketoacids, lactic acid) or bicarbonate loss, guiding targeted treatment.

• Etiologies & Risk Factors:

  • Accumulation of Metabolic Acid:

  • Diabetic Ketoacidosis (DKA): Excessive breakdown of fats producing acidic ketone bodies.

  • Renal Failure / Insufficiency: Inability of impaired kidneys to excrete hydrogen ions or reabsorb bicarbonate.

  • High-Fat Diets & Severe Malnutrition/Anorexia: Fat breakdown for energy releases fatty acids and ketones into circulation.

  • Lactic Acidosis: Tissue hypoperfusion secondary to severe sepsis, shock, or rhabdomyolysis.

  • Aspirin Toxicity: Systemic ingestion of acidic acetylsalicylic acid.

  • Excessive Ingestion of Alcohol: Causes accumulation of toxic acidic metabolites.

  • Carbonic Anhydrase Inhibitor Medications: Pharmacological inhibition of renal bicarbonate reabsorption.

  • Loss of Bicarbonate Base ("Base Out the Butt"):

  • Severe Uncontrolled Diarrhea: Rapid clearance of alkaline secretions from the lower GI tract.

  • Surgical Ostomies & Ileostomies: Continuous drainage of highly alkaline fluid from lower GI openings.

  • GI Fistulas: Abnormal open connections leaking pancreatic and intestinal fluids.

• Physiological Compensation:

  • The respiratory system compensates by deep, rapid breathing (Kussmaul respirations) to blow off acidic $CO_2$ gas.

• Assessment Findings & Clinical Manifestations:

  • Respiratory: Deep, rapid hyperventilation.

  • Neurological: Central nervous system depression, lethargy, muscle weakness, severe confusion.

  • Cardiovascular: Hypotension caused by acid-induced peripheral vasodilation; hyperkalemia leading to fatal EKG dysrhythmias.

  • Gastrointestinal: Severe nausea and vomiting as the body attempts to purge gastric acid in compensation.

• Nursing Interventions & Medical Management:

  • Treatment of Underlying Cause: Administer antidiarrheals for lower GI loss.

  • Exogenous Base Replacement:

  • Administer Sodium Bicarbonate ($NaHCO_3$) via IV infusion, IV push in critical emergencies, or oral (PO) routes for chronic renal insufficiency.

  • Mandatory Safety Check: Continuously monitor serum sodium ($Na^+$) levels during sodium bicarbonate therapy to prevent hypernatremia.

  • DKA Management: Rapid rehydration with IV isotonic fluids, continuous IV regular insulin infusion, and strict blood glucose monitoring.

Metabolic Alkalosis

• Pathophysiology:

  • Occurs due to excessive loss of acid from the upper gastrointestinal tract or an accumulation/retention of bicarbonate base.

• Laboratory Values:

  • pH Level: $\text{pH} > 7.45$

  • $HCO_3^-$ Level: Elevated serum bicarbonate.

• Etiologies & Risk Factors:

  • Upper GI Acid Loss ("Acid Out the Mouth"):

  • Severe or persistent emesis (vomiting).

  • Continuous Nasogastric (NG) Tube Suctioning: Continuous removal of hydrochloric acid ($HCl$) from the stomach (e.g., for bowel obstructions).

  • Upper GI Tract Fistulas.

  • Endocrine / Hormonal Mechanisms:

  • Hyperaldosteronism & Cushing's Syndrome: Excessive aldosterone secretion causes renal retention of sodium ($Na^+$) and fluid alongside continuous excretion of potassium ($K^+$) and hydrogen ($H^+$) ions.

  • Pharmacological Mechanisms & Iatrogenic Causes:

  • Loop Diuretics & Thiazide Diuretics: Increase renal excretion of potassium ($K^+$) and hydrogen ($H^+$) ions in urine.

  • Ingestion of Excessive Antacids: Overuse of calcium carbonate or baking soda.

  • Excessive Anticoagulant Citrate: Citrate contained in massive blood transfusions or continuous renal replacement therapy breaks down metabolically into bicarbonate.

  • Over-administration of Sodium Bicarbonate: Excessive treatment for pre-existing acidosis.

• Physiological Compensation:

  • The respiratory system compensates by decreasing respiratory rate and depth (hypoventilation / respiratory depression) to retain acidic $CO_2$

• Assessment Findings & Clinical Manifestations:

  • Respiratory: Hypoventilation and respiratory depression.

  • Musculoskeletal & Neurological: Muscle tremors, hyperreflexia, tetany, and tingling secondary to hypocalcemia and hypokalemia.

  • Cardiovascular: EKG changes secondary to hypokalemia; severe hypotension resulting from rapid volume depleted states (dehydration from continuous vomiting or suctioning).

• Nursing Interventions & Medical Management:

  • Stop Acid Loss:

  • Administer prescribed antiemetic pharmacotherapy for vomiting (e.g., ondansetron [Zofran], promethazine [Phenergan], prochlorperazine [Compazine], or haloperidol [Haldol]).

  • Discontinue or reduce continuous NG tube suctioning per provider order.

  • Keep the patient strictly NPO (Nothing by Mouth) while actively vomiting.

  • Electrolyte & Fluid Replacement:

  • Discontinue loop or thiazide diuretics.

  • Administer IV fluid rehydration and replacement potassium ($K^+$) / calcium ($Ca^{2+}$) supplementation.

Legal Scope of Practice & Medication Administration Principles

• Strict Adherence to Provider Orders:

  • Nurses are legally bound to administer medications strictly according to the specific indication detailed in the written order.

  • Practice Boundary Example: If acetaminophen (Tylenol) is ordered PRN strictly for "fever / temperature elevation," a nurse CANNOT legally administer it for "pain." A separate or updated order specifically indicating pain must be obtained from the provider.

  • Practice Boundary Example: If diphenhydramine (Benadryl) is ordered PRN strictly for "itching / allergic response," a nurse CANNOT legally administer it as a sedative for "sleep / insomnia."

• Legal Safeguards:

  • Deviating from specified order indications exposes nursing staff to severe legal liability during cross-examinations in court proceedings.

  • When an unlisted indication is required, the nurse must communicate directly with the provider (e.g., via secure chat or telephone) to obtain a modified order prior to administration.

Arterial Blood Gas (ABG) Collection & Clinical Procedures

• Clinical Context:

  • In hospital critical care settings, Respiratory Therapists (RT) routinely perform arterial punctures bedside and analyze samples immediately on point-of-care machines, providing instant diagnostic receipts to providers.

• Outpatient & Home Health Manual Collection Procedure:

  • Primary Anatomical Site: Radial artery.

  • Pre-Puncture Mandatory Assessment: Perform Allen's Test prior to arterial puncture to verify collateral circulation through the ulnar artery.

  • Step-by-Step Collection Sequence:

  1. Perform and document a positive Allen's Test.

  2. Perform radial artery puncture using a specialized heparinized syringe.

  3. Gently roll the filled syringe between the palms to mix the heparin anticoagulant evenly and prevent micro-clot formation.

  4. Immediately submerge the heparinized arterial syringe in an ice bath slurry.

  5. Transport the iced specimen immediately to the laboratory.

  • Hemostasis & Direct Post-Puncture Pressure:

  • Apply direct manual pressure continuously over the arterial site for $5\text{ to }10\text{ minutes}$.

  • Prolonged Pressure Rule: If the patient is receiving anticoagulant therapy (blood thinners), apply direct manual pressure for significantly longer than $10\text{ minutes}$ and apply a tight pressure dressing.