10.1 Cardiovascular and Respiratory Chronic Conditions

Cardiovascular and Respiratory Chronic Conditions

Chronic cardiovascular and respiratory diseases represent the leading causes of morbidity, functional impairment, hospitalization, and mortality among residents in long-term care, assisted living, and post-acute rehabilitation facilities. As the biological body ages, progressive structural and physiological alterations diminish cardiopulmonary reserve capacity, impair homeostatic compensatory reflexes, and increase vulnerability to systemic decompensation. For the Certified Nursing Assistant (CNA), understanding the pathophysiological mechanisms of these chronic illnesses is critical. Because nursing assistants provide direct, continuous personal care during activities of daily living (ADLs), they are uniquely positioned to detect early, subtle deviations in cardiopulmonary status before an acute, life-threatening crisis occurs.

Under the standards established by the Wyoming State Board of Nursing (WSBN) and federal Omnibus Budget Reconciliation Act (OBRA) regulations, CNAs function as vital clinical observers and reporters. They do not diagnose or prescribe, but they must master the clinical terminology, identify classic and atypical symptoms, enforce individualized care plans, maintain medical equipment within their defined scope of practice, and act decisively when clinical emergencies arise.

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Age-Related Cardiovascular and Respiratory Changes

Biological aging induces structural, cellular, and functional changes across the cardiovascular and respiratory systems. These physiological shifts reduce the resident's ability to adapt to physical exertion, infection, fluid overload, emotional stress, or sudden postural changes.

Cardiopulmonary Aging Summary:
=========================================================================
Cardiovascular System:    - Arteriosclerosis (loss of arterial elasticity)
                          - Myocardial hypertrophy and valve calcification
                          - Decreased cardiac output (resting & stress)
                          - Reduced baroreceptor sensitivity (orthostatic risk)
                          - Loss of intrinsic pacemaker cells in SA node
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Respiratory System:       - Calcification of costal cartilage (stiff chest wall)
                          - Loss of pulmonary elastic recoil and sarcopenia
                          - Alveolar enlargement & coalescence (less surface area)
                          - Decreased ciliary clearance & blunted cough reflex
                          - Increased susceptibility to aspiration & pneumonia
=========================================================================

Cardiovascular Alterations with Aging

1. Arteriosclerosis and Vascular Resistance: Collagen cross-linking and loss of elastin within the tunica media cause arteries to become stiff, rigid, and less compliant (arteriosclerosis). This increases systemic vascular resistance, leading to an age-associated rise in systolic blood pressure and increased cardiac workload.
2. Myocardial and Valvular Changes: The left ventricular wall frequently thickens (hypertrophy) to overcome increased arterial resistance. Cardiac valves—particularly the mitral and aortic valves—undergo progressive fibrous thickening and calcification, leading to valvular stenosis or regurgitant murmurs.
3. Decreased Cardiac Output and Pacemaker Decline: Resting stroke volume and maximum cardiac output decline with age. Within the cardiac conduction system, fibrous tissue and fat deposits replace up to 90% of the intrinsic pacemaker cells in the sinoatrial (SA) node by age 75, contributing to resting bradycardia, sinus pauses, and atrial dysrhythmias (especially atrial fibrillation).
4. Impaired Baroreceptor Reflex: Carotid and aortic arch baroreceptors become blunted and sluggish in responding to postural shifts. When an elderly resident moves rapidly from a supine to a standing position, compensatory vasoconstriction is delayed, causing orthostatic hypotension (a drop of ≥20 mmHg systolic or ≥10 mmHg diastolic), resulting in cerebral hypoperfusion, lightheadedness, syncope, and dangerous falls.

Respiratory Alterations with Aging

1. Loss of Chest Wall Compliance and Skeletal Sarcopenia: Calcification of costal cartilages and age-related thoracic kyphosis (curvature of the spine) make the thoracic cage rigid and difficult to expand. Concurrently, sarcopenia (loss of skeletal muscle mass and strength) weakens the diaphragm and intercostal muscles, increasing the physical work required to breathe.
2. Alveolar Alterations and Reduced Gas Exchange: Alveoli lose their elastic recoil and their septal walls progressively break down, coalescing into larger, less efficient air sacs. This reduction in functional capillary-alveolar surface area impairs the diffusion of oxygen into the blood and carbon dioxide out of the blood, resulting in lower resting baseline arterial oxygen levels (PaO2).
3. Diminished Defense Mechanisms: The respiratory mucosa atrophies, goblet cells produce thicker mucus, and the number and motility of protective respiratory cilia decline drastically. Paired with a blunted cough and gag reflex, elderly residents possess a compromised mucociliary escalator, making it difficult to clear aspirated debris, bacteria, or secretions from the tracheobronchial tree. This creates an ideal environment for acute bacterial, viral, and aspiration pneumonia.

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Coronary Artery Disease and Angina Pectoris

Coronary Artery Disease (CAD) is a progressive, chronic condition characterized by the accumulation of fibrofatty atherosclerotic plaques within the lumens of the coronary arteries that supply oxygenated blood to the myocardium (heart muscle). Over decades, the progressive narrowing (stenosis) of these vessels impedes myocardial perfusion.

Pathophysiological Progression: CAD -> Ischemia -> Angina -> Infarction
+-----------------------+     +------------------------+     +-----------------------+
| Atherosclerosis       | --> | Myocardial Ischemia    | --> | Angina Pectoris       |
| (Plaque accumulation) |     | (Oxygen demand exceeds |     | (Chest pain/pressure, |
|                       |     |  coronary supply)      |     |  temporary, no death) |
+-----------------------+     +------------------------+     +-----------------------+
                                           | (Prolonged complete occlusion)
                                           v
                              +------------------------+
                              | Myocardial Infarction  |
                              | (Tissue necrosis and   |
                              |  cellular death / MI)  |
                              +------------------------+

Angina Pectoris (Myocardial Ischemia)

When coronary blood flow is restricted but not completely blocked, transient myocardial ischemia occurs whenever myocardial oxygen demand exceeds the available arterial supply. The sensory nerve endings of the heart are stimulated by lactic acid accumulation, triggering the clinical symptom complex known as angina pectoris.

• Clinical Triggers: Physical exertion (ambulating, climbing stairs, lifting), emotional stress, acute anxiety, exposure to cold outdoor air, or heavy meal consumption (which diverts blood to the mesenteric circulation).
• Manifestations: Sensation of crushing tightness, squeezing, heaviness, suffocating pressure, or burning centered in the substernal chest. The discomfort frequently radiates to the left shoulder, down the inner aspect of the left arm, into the neck, lower jaw, throat, epigastrium, or interscapular region of the back. Stable angina typically lasts 3 to 5 minutes and subsides promptly when the trigger resolves or the resident rests.
• Medical Management: Angina is relieved by rest and the administration of sublingual nitroglycerin (a potent nitrate vasodilator that relaxes coronary and systemic veins, reducing preload and myocardial oxygen consumption).

[!IMPORTANT]

CNA Protocol for Acute Angina Episodes

1. Immediate Cessation of Activity: Stop all resident exertion immediately. Have the resident sit down or recline in a comfortable, upright Fowler's or semi-Fowler's position to reduce venous return to the heart and ease respiratory effort.
2. Never Leave the Bedside: Never abandon the resident to look for help. Stay with the resident to provide calm emotional reassurance, reduce sympathetic nervous system panic, and monitor consciousness.
3. Activate Emergency Call System: Use the resident call pendant or emergency wall light to summon the charge nurse immediately.
4. Scope of Practice Restriction: CNAs may NEVER administer nitroglycerin tablets, sprays, or patches. Nitroglycerin is a prescription cardiac medication that can induce profound, life-threatening hypotension and syncope. The licensed nurse must assess vital signs (specifically blood pressure) prior to administering each dose.
5. Vital Signs: Obtain a baseline blood pressure, radial pulse rate, and respiratory rate while awaiting the nurse, provided doing so does not delay calling the nurse.

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Myocardial Infarction (Heart Attack)

A Myocardial Infarction (MI) occurs when an atherosclerotic plaque inside a coronary artery ruptures, triggering immediate platelet aggregation and the formation of an occlusive thrombus (blood clot). This completely blocks downstream arterial perfusion, causing prolonged, irreversible myocardial tissue necrosis (cellular death).

Classic Presentation vs. Atypical Presentations

While public perception associates heart attacks with sudden, catastrophic collapse and clutching of the chest, clinical reality in healthcare facilities is markedly different, particularly among geriatric residents, females, and individuals with diabetes mellitus.

[!CAUTION]

Emergency Protocol for Suspected Myocardial Infarction

• Call for Immediate Emergency Assistance: Activate the facility emergency response team or call 911 immediately upon suspecting an acute coronary syndrome.
• Maintain Absolute Rest: Keep the resident seated in high Fowler's position. Do NOT allow the resident to walk, stand, or perform any physical activity, as even minimal skeletal muscle exertion increases myocardial oxygen demand and accelerates heart muscle necrosis.
• Loosen Constrictive Clothing: Loosen neck collars, belts, or tight garments to facilitate uninhibited venous return and thoracic expansion.
• Emergency Readiness: Maintain continuous airway monitoring. If the resident becomes unresponsive, pulseless, and breathless, immediately initiate CPR and summon an Automated External Defibrillator (AED).

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Congestive Heart Failure (CHF)

Congestive Heart Failure (CHF) is a chronic, progressive syndrome in which the cardiac muscle weakens, dilates, or stiffens, rendering the ventricles incapable of pumping an adequate volume of oxygenated blood to satisfy the metabolic and nutritional demands of peripheral tissues (forward failure), or capable of doing so only at the expense of elevated intracardiac filling pressures that cause fluid backflow and venous congestion (backward failure).

Heart Failure Hemodynamic Pathways:
=========================================================================
LEFT-SIDED HEART FAILURE:    Left Ventricle Fails
                             -> Blood backs up: Left Atrium -> Pulmonary Veins
                             -> Pulmonary Capillary Engorgement
                             -> Fluid forced into Alveoli (Pulmonary Edema)
                             -> Dyspnea, Orthopnea, Crackles, Pink Frothy Sputum
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RIGHT-SIDED HEART FAILURE:   Right Ventricle Fails
                             -> Blood backs up: Right Atrium -> Vena Cavae
                             -> Systemic Venous Congestion
                             -> Fluid forced into Peripheral Interstitial Space
                             -> Dependent Peripheral Edema, JVD, Ascites
=========================================================================

Left-Sided Heart Failure (Pulmonary Congestion)

The left ventricle fails to pump blood forward into the aorta. Blood pools in the left ventricle, backs up into the left atrium, and engorges the pulmonary veins and capillaries. The resulting hydrostatic pressure forces fluid out of the capillary lumen and into the pulmonary interstitium and alveoli.

• Dyspnea and Tachypnea: Severe shortness of breath, beginning on exertion and progressing to dyspnea at rest.
• Orthopnea: Inability to breathe comfortably while lying flat. In the supine position, venous blood from the lower extremities redistributes to the central thoracic circulation, overwhelming the failing left ventricle and drowning the alveoli in fluid. Residents require two, three, or four pillows to elevate their head and torso, or must sleep sitting upright in a recliner chair.
• Paroxysmal Nocturnal Dyspnea (PND): Sudden awakening 1 to 2 hours after falling asleep with severe, suffocating dyspnea, panic, and wheezing, relieved only by sitting upright on the side of the bed.
• Pulmonary Edema: When fluid inundates the alveoli, the resident develops audible bubbling lung sounds (rales or crackles), severe air hunger, cyanosis, and the production of pink, frothy sputum (fluid tinged with extravasated red blood cells). This is an acute medical emergency.

Right-Sided Heart Failure (Systemic Venous Congestion)

The right ventricle fails to pump blood into the pulmonary artery for oxygenation. Venous blood backs up into the right atrium, the superior and inferior vena cavae, and the peripheral venous circulation.

• Dependent Peripheral Edema: Fluid extravasates into subcutaneous tissues due to high venous pressures. In ambulatory or wheelchair-bound residents, edema accumulates in the lowest dependent areas—the feet, ankles, and pretibial shins. In bedbound residents, dependent edema settles over the sacrum, buttocks, and posterior thighs.
• Pitting Edema: When finger pressure is applied to the swollen tissue over a bony prominence for 5 seconds, a visible indentation (pit) remains after the finger is released.
• Jugular Vein Distention (JVD): Engorgement and bulging of the external jugular veins in the neck when the resident is sitting at a 45-degree angle.
• Ascites and Hepatomegaly: Fluid accumulation inside the peritoneal cavity (ascites), causing abdominal distention, taut shiny skin, and early satiety. Venous congestion of the liver causes hepatic enlargement and tenderness.
• Rapid Fluid Weight Gain: The most reliable and sensitive early indicator of worsening fluid retention in right-sided failure.

Comprehensive CNA Care Protocol for Congestive Heart Failure

Caring for a resident with chronic CHF requires vigilant observation, fluid monitoring, and physical comfort measures:

1. Daily Weight Monitoring:

   [!IMPORTANT] Daily weight is the gold standard for tracking fluid retention in CHF. A sudden gain reflects water retention, not body fat (1 liter of retained fluid equals approximately 2.2 pounds or 1 kilogram).

   • Standardization Rules: Weigh the resident every morning before breakfast, after their first morning void, wearing the same type and weight of clothing, and using the exact same calibrated scale (standing, chair, or bed scale).
   • Critical Reporting Threshold: Immediately report to the charge nurse any weight gain of ≥2 to 3 pounds in 24 hours or ≥5 pounds in a single 7-day week.
2. Strict Fluid Restriction and Intake & Output (I&O):
   • Many CHF residents are placed on physician-ordered fluid limits (e.g., 1,500 mL or 2,000 mL per 24 hours) to prevent hypervolemia. The CNA must record every milliliter of oral fluid consumed on their shift.
   • Ice Chip Rule: Ice chips melt to approximately half their volume in liquid (e.g., a 100 mL cup filled with ice chips equals 50 mL of liquid intake).
   • Distribute fluid allowances evenly across shifts and avoid leaving full water pitchers at the bedside if fluids are restricted.
3. Low-Sodium (Low-Salt) Nutrition Support:
   • Excess dietary sodium pulls water into the intravascular space, precipitating acute congestive crises. Verify meal trays against the dietary order (e.g., "2g Sodium Diet"). Remove table salt shakers from the meal tray. Remind residents to avoid high-sodium snacks (potato chips, canned soups, cured meats, pretzels).
4. Positioning and Lower Extremity Elevation:
   • To alleviate dependent edema while seated in a chair, elevate the resident's legs on a padded footstool or recliner footrest, ensuring heels are float-protected.
   • In bed, elevate legs on pillows to facilitate venous return, ensuring knees are not bent sharply (which obstructs popliteal venous flow).
   • Maintain the head of the bed in a semi-Fowler's (30–45°) or high Fowler's (60–90°) position to ease respiratory mechanics.
5. Anti-Embolic Stockings (TED Hose):
   • Apply prescribed graduated compression stockings in the morning before the resident rises from bed (before dependent gravity causes leg swelling). Inspect the skin over the heels and toes every shift for redness, constriction, or arterial compromise.

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Hypertension: The "Silent Killer"

Hypertension (HTN) is the chronic, sustained elevation of systemic arterial blood pressure. Clinical guidelines define hypertension as a resting systolic blood pressure ≥130 mmHg or a resting diastolic blood pressure ≥80 mmHg.

• The "Silent Killer": Hypertension rarely produces recognizable symptoms in its early to moderate stages. For years or decades, asymptomatic elevated pressures batter arterial walls, causing accelerated atherosclerosis and target-organ damage across the heart (hypertrophy, heart failure, MI), brain (stroke, vascular dementia), kidneys (nephrosclerosis, chronic kidney failure), and eyes (retinopathy).
• Hypertensive Crisis / Urgency Signs: If blood pressure rises abruptly to dangerous levels (e.g., systolic >180 mmHg or diastolic >120 mmHg), the resident may manifest acute symptoms requiring emergency nurse intervention: severe throbbing occipital headache, blurred or double vision, dizziness, tinnitus, epistaxis (nosebleeds), nausea, or acute chest discomfort.
• CNA Responsibilities: Measure blood pressure accurately using the correct cuff size (a cuff bladder that is too small falsely elevates blood pressure readings; a cuff that is too large falsely depresses readings). Support low-sodium diets, promote physical mobility within physician limits, and monitor for orthostatic dizziness when residents rise from beds or chairs, as antihypertensive medications frequently cause postural hypotension.

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Chronic Obstructive Pulmonary Disease (COPD)

Chronic Obstructive Pulmonary Disease (COPD) is a progressive, incurable respiratory disorder characterized by chronic airflow limitation that is not fully reversible. The condition represents a spectrum involving two primary overlapping disease processes:

COPD Dual Pathology Spectrum:
=========================================================================
CHRONIC BRONCHITIS ("Blue Bloater"):  - Chronic inflammation of bronchi/bronchioles
                                      - Goblet cell hyperplasia & excess mucus
                                      - Productive cough >= 3 months for 2 years
                                      - Cyanosis, peripheral edema, rhonchi
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EMPHYSEMA ("Pink Puffer"):            - Destruction of alveolar walls & capillaries
                                      - Loss of pulmonary elasticity & air trapping
                                      - Hyperinflation & Barrel Chest (1:1 AP)
                                      - Severe dyspnea, pursed-lip breathing
=========================================================================

Clinical Manifestations of COPD

1. Chronic Cough and Sputum: A persistent, productive cough producing tenacious mucus, typically worse in the morning.
2. Exertional Dyspnea Progressing to Resting Dyspnea: Progressive shortness of breath that initially limits physical ambulation and eventually makes simple ADLs (eating, bathing, dressing) exhausting.
3. Barrel Chest: In emphysema, chronic air trapping and alveolar hyperinflation permanently expand the thoracic rib cage, altering the normal anteroposterior-to-transverse thoracic ratio from 1:2 to 1:1 (a rounded, barrel-shaped chest).
4. Digital Clubbing: Painless, bulbous enlargement of the distal fingertips with loss of the normal angle between the nail bed and cuticle, resulting from chronic long-term tissue hypoxia.

Clinical Interventions for Dyspneic Residents

• Tripod Positioning: When experiencing acute dyspnea, residents with COPD instinctively lean forward, resting their elbows or hands on their knees or on a padded overbed table. This tripod position stabilizes the shoulder girdle, relieves pressure from abdominal organs against the inferior surface of the diaphragm, and maximizes the mechanical efficiency of the accessory respiratory muscles (scalene and sternocleidomastoid muscles).
• Pursed-Lip Breathing: A specialized breathing technique that prevents premature small airway collapse during exhalation:
  1. The resident inhales slowly and deeply through the nose for a count of 2.
  2. The resident puckers or purses their lips as if whistling or preparing to blow out a birthday candle.
  3. The resident exhales slowly and gently through pursed lips for a count of 4 (twice as long as inhalation).
  4. Mechanism: Pursed-lip breathing generates positive backpressure throughout the bronchial tree during expiration, splinting open collapsing bronchioles and allowing trapped carbon dioxide to escape.

The Hypoxic Drive and Oxygen Warning in COPD

In healthy individuals, the primary physiological trigger to breathe is an elevated level of carbon dioxide in arterial blood (hypercapnic drive), detected by central chemoreceptors in the medulla oblongata.

[!WARNING]

The Hypoxic Drive Warning

• In residents with advanced, end-stage COPD, arterial carbon dioxide levels remain chronically elevated for years. Over time, central chemoreceptors become desensitized and adapt to high CO2 levels, relinquishing control of ventilation.
• The body's secondary respiratory control system—peripheral chemoreceptors located in the aortic arch and carotid bodies—takes over, stimulating respiration in response to low arterial oxygen levels (hypoxic drive).
• The Clinical Hazard: If a high concentration of supplemental oxygen (e.g., >2 to 3 liters per minute via nasal cannula) is administered to a resident whose ventilation depends on hypoxic drive, the peripheral chemoreceptors sense abundant oxygen and "turn off" the neurological drive to breathe.
• Consequence: The resident develops hypoventilation, acute carbon dioxide retention (carbon dioxide narcosis), progressive somnolence, lethargy, respiratory depression, coma, and respiratory arrest.
• Standard of Care: Low-flow oxygen (typically 1 to 2 L/min, rarely exceeding 3 L/min unless explicitly ordered and monitored in subacute units) is the standard for chronic COPD residents.

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Pneumonia: Types and Geriatric Nuances

Pneumonia is an acute inflammation and infection of the lung parenchyma (alveoli and bronchioles), leading to alveolar consolidation where air spaces become filled with exudative inflammatory fluid, white blood cells, and cellular debris.

Etiology and Types

• Bacterial Pneumonia: Typically caused by Streptococcus pneumoniae. Tends to present abruptly with high fever, rigors (shaking chills), tachypnea, and productive cough with rust-colored or yellowish-green purulent sputum.
• Viral Pneumonia: Caused by influenza, respiratory syncytial virus (RSV), or SARS-CoV-2. Presents with generalized malaise, headache, dry nonproductive cough, and fever.
• Aspiration Pneumonia: Occurs when foreign materials (food, liquids, saliva, vomitus, or regurgitated gastric contents) are inhaled into the lower tracheobronchial tree. Acidic gastric contents cause severe chemical pneumonitis, followed by secondary anaerobic bacterial infection. Extremely prevalent in residents with dysphagia, post-stroke hemiparesis, Parkinson's disease, and late-stage dementia.

Atypical Presentation in Frail Elderly Residents

Because of immunosenescence (age-related immune system deterioration), frail geriatric nursing home residents frequently do NOT mount a high fever or produce a robust productive cough when suffering from severe pneumonia.

Atypical Geriatric Pneumonia Warning Signs:
+-------------------------------------------------------------------------+
| 1. Sudden onset of acute confusion or delirium (cardinal sign).         |
| 2. Increased tachypnea (respirations > 24 to 28 bpm) and subtle hypoxia. |
| 3. New-onset lethargy, profound weakness, or falling out of bed.        |
| 4. Total loss of appetite (anorexia) or refusal to drink liquids.       |
| 5. Subtle drop in baseline functional independence during ADLs.         |
+-------------------------------------------------------------------------+

CNA Aspiration Prevention Standards

1. 90-Degree Upright Seating: Maintain the resident in a full upright high Fowler's (90-degree) position during all meals, snacks, and oral medication administration.
2. Post-Meal Positioning: Keep the resident seated upright for at least 30 to 60 minutes after eating to prevent postprandial gastroesophageal reflux and micro-aspiration.
3. Dietary Consistency Adherence: Strictly adhere to speech-language pathologist orders regarding texture-modified diets (pureed, mechanical soft) and thickened liquids (nectar-thick, honey-thick, or pudding-thick). Never offer unthickened water or thin juices to a resident prescribed thickened liquids.
4. Oral Hygiene: Provide meticulous oral hygiene before meals to reduce the oral bacterial burden and after meals to clear food pocketed inside the cheeks (buccal pocketing).

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Tuberculosis and Airborne Isolation Precautions

Tuberculosis (TB) is an infectious, chronic granulomatous disease caused by the acid-fast bacillus Mycobacterium tuberculosis. While TB most commonly attacks the pulmonary parenchyma, it can disseminate to the kidneys, spine (Pott's disease), brain, and lymph nodes.

Transmission Dynamics

TB is transmitted exclusively via the airborne route. When an individual with active, untreated pulmonary TB coughs, sneezes, speaks, laughs, or sings, minute droplet nuclei (1 to 5 microns in diameter) are expelled into the ambient atmosphere. Due to their minuscule size, these droplet nuclei remain suspended in room air currents for hours and can be inhaled directly into the alveoli of a susceptible host.

Clinical Manifestations of Active Tuberculosis

• Chronic, persistent productive cough lasting longer than 3 weeks
• Hemoptysis (coughing up blood or blood-streaked sputum)
• Profuse, drenching night sweats that soak bed linens
• Low-grade afternoon fever and recurrent chills
• Unexplained anorexia and progressive, severe weight loss ("consumption")
• Pleuritic chest pain and chronic, debilitating fatigue

Infection Control Protocols for the CNA

1. Airborne Infection Isolation Room (AIIR): Active TB residents must be placed in a specialized negative-pressure room. Negative pressure ensures that when the room door is opened, air flows inward from the corridor into the room rather than outward into public hallways. Air must be exhausted directly outdoors or passed through high-efficiency particulate air (HEPA) filters, with a minimum of 6 to 12 air exchanges per hour.
2. Continuous Door Closure: The isolation room door must remain firmly closed at all times.
3. Personal Protective Equipment (PPE):
   • Before crossing the threshold into the room, the CNA must don an OSHA-mandated, NIOSH-certified, fit-tested N95 particulate respirator mask (or a Powered Air-Purifying Respirator / PAPR). Standard surgical paper masks do not filter airborne droplet nuclei and are strictly inadequate for healthcare staff.
   • Perform a seal check (positive and negative pressure check) every time the N95 respirator is donned.
   • Remove the respirator only after exiting the room and closing the isolation door.
4. Resident Transport Restrictions: Residents in airborne isolation should leave the room only for essential medical diagnostics. During transport, the resident must wear a standard surgical mask to capture respiratory droplets at the source (the resident does not wear an N95).

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Oxygen Therapy: Scope of Practice and Safety Rules

Supplemental oxygen is a medical gas classified and regulated as a prescription drug. Under Wyoming State Board of Nursing regulations and federal healthcare standards, the administration of oxygen requires a licensed healthcare practitioner's order that specifies the delivery device, flow rate, and target saturation parameters.

CNA Scope of Practice Boundary: Oxygen Therapy
+-------------------------------------------------------------------------+
| CNAs MAY:                                                               |
|  [x] Check tubing for kinks, loops, twisting, or disconnects.           |
|  [x] Verify nasal prongs are curving downward into the nostrils.         |
|  [x] Inspect skin behind ears, across cheeks, and under nares.          |
|  [x] Apply water-soluble lubricant to dry nares.                        |
|  [x] Ensure humidifier bottle is bubbling sterile water properly.       |
|  [x] Enforce oxygen fire safety rules (signs, cotton blankets, no flame).|
+-------------------------------------------------------------------------+
| CNAs MAY NEVER:                                                         |
|  [!] Initiate oxygen therapy on a resident.                             |
|  [!] Adjust, titrate, or change the flow rate (liters per minute / Lpm).|
|  [!] Turn oxygen regulators or wall flow meters on or off.              |
|  [!] Apply petroleum-based lubricants (Vaseline) to nose or face.       |
+-------------------------------------------------------------------------+

Clinical Management of Oxygen Delivery Devices

• Nasal Cannula: The most common low-flow device, delivering 1 to 6 L/min (approximate FiO2 of 24% to 44%).
  • Prong Alignment: Verify that the curved prongs of the nasal cannula point curving downward into the nostrils, following the natural anatomical curvature of the nasal passages. Never insert prongs pointing upward toward the nasal bridge.
  • Tubing Security: Route tubing over both ears and adjust the sliding cinch comfortably beneath the chin. Ensure tubing is not cinched tightly, causing skin necrosis.
• Tubing Maintenance: Check the entire length of tubing periodically to ensure it is free of kinks, is not trapped under bed wheels or chair casters, and is not a tripping hazard on the floor.
• Humidification: When oxygen flow rates exceed 3 to 4 L/min, high-flow dry gas desiccates the nasal mucosa. A humidifier bottle containing sterile water is attached to the flow meter. The CNA must verify that bubbles are continuously forming in the water; lack of bubbling indicates an empty bottle, a loose seal, or an obstructed supply.
• Nasal Dryness and Mucosal Care:

  [!IMPORTANT] To treat dry, irritated nares in an oxygen-dependent resident, apply ONLY water-soluble lubricants (such as K-Y Jelly or water-based saline gel). NEVER apply petroleum jelly (Vaseline), mineral oil, or oil-based lotions. In an oxygen-enriched environment, petroleum is highly combustible. Furthermore, inhaling microscopic oil droplets into the lungs can cause exogenous lipoid pneumonia.

• Skin Breakdown Checks: Regularly inspect high-pressure areas for pressure injuries: the tops of both ears (where tubing rests), the cheekbones, the edges of the nares, and the back of the neck. Apply foam ear protectors if ordered.

Oxygen Fire Prevention Standards

Oxygen does not burn by itself, but it is a powerful accelerant of combustion—materials ignite at much lower temperatures and burn with extreme violence in an oxygen-rich atmosphere.

• Signage: Post conspicuous "OXYGEN IN USE — NO SMOKING" warning signs on the outside of the resident's door and directly above the head of the bed.
• Flames and Smoking Ban: Strictly prohibit smoking, matches, lighters, electronic cigarettes, candles, or open flames within a minimum radius of 50 feet of oxygen equipment.
• Static Electricity Control: Prohibit wool blankets, nylon garments, and synthetic fabrics that generate static sparks. Use only 100% cotton blankets and linens.
• Electrical Safety: Ensure all electrical equipment in the room is three-pronged, grounded, and inspected. Do not use electrical equipment prone to sparking (electric razors, hair dryers, motorized toys, heating pads) while oxygen is flowing.
• Cylinder Safety: Store compressed gas cylinders in upright positions secured in approved metal stands or wall brackets. Never leave an oxygen tank standing unsupported or lying loose on a bed or floor.