Chapter 20: Respiratory Disorders Notes

Introduction to Respiratory Distress, Failure, and Arrest

• Respiratory Distress Characteristics:

  • Respiratory distress is a condition that can rapidly deteriorate into respiratory failure and respiratory arrest.

  • Death follows quickly unless measures are taken to restore ventilation and oxygenation.

  • The condition can interfere with the delivery of oxygen to the tissues.

  • It is exacerbated by the body's stress response, which increases the demand for oxygen, and the increased use of respiratory muscles creates an even higher need for cellular oxygen in the face of the decreased supply.

• Metabolic and Physiological Impact:

  • Cellular metabolism occurring with inadequate oxygen leads to inefficient energy production and the development of respiratory acidosis.

  • A combination of an uncorrected underlying problem, exhaustion, and acidosis can overwhelm the body's attempts to compensate and restore homeostasis.

• EMS Priorities:

  • Quickly recognize difficulty breathing and intervene immediately.

  • Ensure an open airway, adequate ventilation, and circulation.

  • A thorough understanding of the anatomy, physiology, and pathophysiology of the respiratory system is essential to providing the best care.

Anatomy and Physiology Review: The Need for Oxygen

Cellular Energy Production, and thus life itself, depends on oxygen from the atmosphere reaching each individual cell.

- Requirements for Cellular Energy Production:

For oxygen to reach the microscopic alveoli of the lungs, where gases are exchanged with the circulatory system, there must be an…

• Adequate amount of oxygen in the atmosphere.

• The entire airway (upper & lower) must be open to allow air to reach the alveoli.

• Each alveolus must be in close contact with a network of capillaries.

so that oxygen and carbon dioxide can be exchanged between the lungs and the blood.

The red blood cells (RBC) must contain an…

• Adequate amount of hemoglobin to carry oxygen to the cells.

- The body’s temperature, acid–base balance, and other factors must be in the proper ranges for hemoglobin to accept oxygen from the lungs (external respiration) and release it to the cells (internal respiration).

• A cardiovascular system that is working effectively.

- The right side of the heart must be able to receive deoxygenated blood that is high in carbon dioxide and pump it through the pulmonary artery and into the lungs.

- The left side of the heart must be able to receive oxygenated blood that is low in carbon dioxide and pump it through the arterial and capillary systems to the cellular level.

Anything that interferes with these requirements can lead to hypoxia, cell dysfunction, and cell death.

Cells must produce energy to carry out their functions.

• Types of Metabolism:

  • Aerobic Metabolism: Energy production in the presence of oxygen is efficient and results in byproducts that are easily eliminated by the body.

  • Anaerobic Metabolism: Energy production is severely limited. Hydrogen ions ($H^+$) accumulate as lactic acid, decreasing pH and causing acidosis.

- Anaerobic Metabolism is a short-term compensatory mechanism when the body’s need for oxygen is greater than its supply. Unless oxygenation is restored, death will occur.

The accumulation of lactic acid decreases the body’s pH, leading to acidosis.

Anatomy and Physiology Review: Respiratory System Structure and Function

The lungs are spongy tissues with millions of microscopic air sacs, called alveoli, which allow the exchange of gases between the internal environment of the body and the atmosphere.

Structure and Function of the Lungs:

• Passageway of Air:

  1. Mouth and nose

  2. Pharynx

  3. Larynx

  4. Trachea

  5. Right and left mainstem bronchi

  6. Right and left lung (Left lung= 2 lobes, Right lung= 3 lobes).

  7. Bronchioles

  8. Alveolus

The trachea and bronchi are composed of sturdy cartilage rings that keep them from collapsing.

• Bronchioles and Smooth Muscle:

  • Bronchioles contain smooth muscle that allows the diameter to change in response to the amount of alveolar ventilation requirements.

  • This smooth muscle cells have sympathetic $\text{beta}_2$ receptors that respond to epinephrine, as well as to drugs with $\text{beta}_2$ properties.

  - The effect of $\text{beta}_2$ receptor stimulation is smooth muscle relaxation, which increases bronchodilation (an increase of the diameter of the bronchioles).

  • The lining of the respiratory tract contains cells that secrete mucus, which traps contaminants that enter the respiratory system along with air.

  • Microscopic, hair-like cellular projections called cilia, sweep the mucus upward, along with trapped contaminant particles, so they can be expelled.

- The cilia are paralyzed by the nicotine in tobacco smoke, which impairs the ability to clear the lungs of toxins.

The Respiratory Membrane:

• The walls of the distal (terminal) bronchioles and alveoli are a single cell-layer thick.

• A network of capillaries is also single cell-layer thick.

• A network of capillaries surrounds each alveolus.

• The alveoli and capillaries are in close contact with each other, separated by a small amount of extracellular fluid.

• The alveolar and capillary walls together are called the respiratory membrane.

- Because oxygen and carbon dioxide can diffuse only short distances, this respiratory membrane must remain thin.

• The alveoli and capillaries together form the respiratory membrane, separated by extracellular fluid.

- The distance between the red blood cells in the capillaries and the air within the alveoli is increased if extracellular fluid accumulates between the capillary and alveolar walls, or if there is fluid or pus within the alveoli.

• The direction of diffusion of gases depends on the concentrations (partial pressures) on each side of the cell membrane.

- Gases diffuse from where they are higher in concentration to where they are lower in concentration.

Physiology of Ventilation

Stimulus for Breathing:

• Chemically, ventilation is stimulated primarily by an increased level of carbon dioxide in the blood and in cerebrospinal fluid.

• A secondary stimulus is a decreased level of oxygen. Those chemical changes stimulate the inspiratory center of the brain, located in the medulla of the brainstem.

• The inspiratory center sends nervous impulses to the diaphragm and intercostal muscles, causing them to contract.

Mechanics of Inspiration:

• Muscular contraction increases the volume of the thoracic cavity.

- Muscular contraction flattens and lowers the diaphragm and lifts the ribs upward and outward, increasing the volume of the thoracic cavity.

The increase in thoracic volume creates a vacuum in the potential space between the parietal and visceral pleura, causing the lungs to expand. There is an inverse relationship between the volume of a gas and its pressure. The increased intrapulmonary (within the lung) volume results in intrapulmonary pressure that is lower than atmospheric pressure.

• Based on the inverse relationship between the volume of a gas and its pressure, air moves from areas of higher pressure (environment) to areas of lower pressure (lungs).

The Diaphragm and Intercostal Muscles Contract, Increasing the Volume of the Thoracic Cavity,
Which Lowers Intrathoracic (and Intrapulmonary) Pressure and Thus Allows Inspiration.

• Mechanics of Expiration:

  • Expiration is stimulated by the Hering–Breuer reflex.

- The Hering-Breuer reflex is a protective respiratory mechanism that prevents the lungs from over-inflating.

- When lung volume exceeds normal levels, stretch receptors activate the Vagus nerve to inhibit the brain's inspiratory center, immediately stopping inhalation and triggering exhalation

• When stretch receptors in the lungs are activated, nervous signals stimulate the expiratory center and inhibit the inspiratory center in the brainstem.

• The diaphragm and intercostal muscles relax, reducing thoracic volume.

• This creates a higher intrapulmonary pressure compared to the environment, causing air to flow out of the lungs.

- The Diaphragm and Intercostal Muscles Relax, Which Reduces the Volume of the Thoracic
Cavity and Increases Intrathoracic (and Intrapulmonary) Pressure, Allowing Expiration.

When more carbon dioxide is produced and more oxygen is required, the respiratory rate is faster and the depth is increased.

Anything that decreases tidal volume decreases alveolar ventilation.

Shallow breathing means that the amount of oxygen delivered to the cells is decreased.

Increased respiratory rate and depth reflect increased carbon dioxide and insufficient oxygen to meet cellular demand.

• Lung Volumes:

  • Tidal Volume: The amount of air that moves in and out of the lungs. The average for an adult is $5–7\,mL/kg$ (approximately $500\,mL$).

  • Anatomical Dead Space Air: Approximately $150\,mL$ of air remains in the airway and is unavailable for gas exchange.

The amount of air available for alveolar ventilation is 350 mL.

The volume of anatomical dead space does not change.

For Example: If tidal volume decreases to 300 mL, 150 mL remains in the dead space, and alveolar ventilation is decreased to 150 mL.

General Assessment and Management of Respiratory Emergencies

• Degrees of Respiratory Problems:

  • Mild Dyspnea: Characterized by being short of breath.

  • Severe Dyspnea (Respiratory Distress): Patient is barely able to speak, may be in a tripod position, wheezing, coughing, and using accessory muscles.

  • Hypoxia and Exhaustion: Characterized by cyanosis, altered mental status, and weak respiratory effort. This leads directly to respiratory failure.

  • Respiratory Arrest: Characterized by ineffective respiratory effort or apnea (total cessation of breathing).

• Comparison of Findings:

  • Normal Breathing: Eupnea

    • Rate: $12–20\,per\,minute$.

    • Tidal Volume: Free movement of air, adequate depth.

    • Breath Sounds: No abnormal sounds; present and equal.

    • Work of Breathing: Normal.

    • Appearance: Good skin color.

    • Interventions: None if $S p O_2 \ge 95 \%$

  • Respiratory Distress:

    • Rate: May be normal, but likely slightly outside normal range.

    • Tidal Volume: May be increased or decreased.

    • Breath Sounds: May have stridor, wheezing, rhonchi, or crackles (rales); sounds may be diminished or unequal.

    • Work of Breathing: Slightly to moderately increased.

    • Appearance: Anxious.

    • Interventions: Administer supplemental oxygen, as needed, to maintain target $S p O_2$ of $95 \%$

Signs of Respiratory Distress:

• Respiratory Failure:

  • Rate: $8$ or less, or $30$ or greater.

  • Tidal Volume: Inadequate.

  • Breath Sounds: May have stridor, wheezing, rhonchi, or crackles (rales); sounds may be diminished, reflecting inadequate air movement.

  • Work of Breathing: Increased, but patient may show signs of fatigue.

  • Appearance: Anxious, becoming cyanotic, decreasing responsiveness, confused.

  • Interventions: Assist ventilations with CPAP, BVM, or FROPVD; administer supplemental oxygen.

• Respiratory Arrest:

  • Rate: Agonal or absent.

  • Tidal Volume: Minimal to absent.

  • Breath Sounds: Absent.

  • Work of Breathing: Minimal to absent.

  • Appearance: Decreased responsiveness, cyanotic.

  • Interventions: Provide ventilations with BVM, FROPVD, or ATV; supplemental oxygen.

FROPVD = Flow-Restricted, Oxygen-Powered Ventilation Device (FROPVD)

ATV = Automatic Transport Ventilator (ATV)

All patients with inadequate ventilations require assistance by bag-valve-mask device with supplemental oxygen.

• Maintaining patient’s airway, breathing, oxygenation, and circulation are critical.

• Attempt to reverse underlying cause.

• The patient’s history is often the key to determining the underlying cause of the problem. If you are unable to obtain a medical history from the patient or bystanders, check for medications.

• Oxygenation Targets:

  • General target: Maintain $S p O_2$ of $95 \%$.

  • Patients with COPD: Target $S p O_2$ is $88 \%-92 \%$.

Clinical Reasoning and Treatment Protocol

Scene Size-Up:

• Scene Safety/PPE.

- Occasionally, a respiratory emergency may not be obvious. Hypoxic patients can behave irrationally because of cerebral dysfunction. Always consider that there may be a medical or traumatic cause for the patient’s behavior.

• Form general impression.

- SEE: You may see exaggerated chest and abdominal movement and use of accessory muscles, indicating labored breathing.

- SEE: You may see cyanosis, especially of the lips, ears, and nail beds.

- PT APPEARANCE: The patient may appear drowsy or confused.

- HEAR: You may hear wheezing, coughing, crackles (rales), or stridor.

• Establish level of responsiveness.

• Check patient position. (Tripod Position?)

• Listen to ease of speaking.

- As you introduce yourself and ask about the patient’s problem, can he speak an entire sentence without taking a breath? Or must he take a breath after two or three words?

Primary Assessment:

• Ensure an open airway

- As Needed: Use manual positioning, suction, and basic airway adjuncts.

• Assess breathing adequacy

- If inadequate: Assist with BVM and supplemental oxygen.

• Assess pulse: Tachycardia is often an indication of hypoxia.

• Determine transport priority: Distress can progress quickly to failure & arrest, so consider patients with this complaint a high priority.

- Effective prehospital treatment can improve condition.

- Request paramedic assistance as needed.

Pediatric Care: Pediatric patients often exhibit bradycardia, rather than tachycardia, in response to hypoxia.

Geriatric Care: Elderly patients may not exhibit an increase in heart rate in response to hypoxia

Secondary Assessment:

• Focus on physical assessment details that are MOST relevant:

- Auscultation

- Vital signs

- Pulse oximetry

- Capnometry

- Cardiac monitoring

• Medical history check; particularly for conditions & medications indicating respiratory illness.

• Treatments:

  • Airway management: Patients who are unresponsive and without a gag reflex may require the use of intubation, a dual lumen, or a supraglottic airway device.

  • Continuous positive airway pressure (CPAP) may be indicated to provide ventilatory support for patients with pulmonary edema.

  • IV fluids, Nitroglycerin, or Epinephrine depending on the cause

- IV fluids are important in patients with asthma and pneumonia.

- Bronchodilators can assist patients with asthma or COPD.

- If protocols allows, patients with pulmonary edema from heart failure can benefit from nitroglycerin.

- If the underlying cause of dyspnea is a severe allergic reaction (anaphylaxis), epinephrine may be indicated.

Reassessment:

Always anticipate the potential for deterioration in patients with respiratory emergencies.

Ongoing respiratory distress, hypercapnia, acidosis, and hypoxia can lead to exhaustion.

Patients with respiratory distress can progress quickly to respiratory failure and arrest.

• Frequently reassess the patient’s mental status.

- A change in mental status is a sign of hypoxia.

• Ensure that the patient can maintain an open airway.

- Be ready to use suction, positioning, and basic airway adjuncts as needed.

• Monitor the effectiveness of ventilations

- Assisting with a bag-valve-mask device or implementing CPAP as indicated.

- Auscultate the breath sounds for changes and communicate with the patient to determine whether treatment has relieved his symptoms.

Recheck the vital signs and SpO2.

- If cardiac monitoring and capnometry have been implemented, reassess their results frequently as well.

• Be prepared to change treatment, if needed, based on the results of reassessment.

Clinical-Reasoning Process

Understanding the pathophysiology of various causes of difficulty breathing will help you know what questions to ask as you begin to develop and test hypotheses about the underlying cause of a respiratory emergency.

A history of emphysema, for example, tells you not only that the patient has a chronic respiratory disease but also that he is at risk of heart failure, cardiac dysrhythmia, and complications related to long-term corticosteroid use.

On the other hand, sudden respiratory distress in a patient with no history of respiratory disease should lead you to think of acute emergencies, such as pulmonary embolism or spontaneous pneumothorax.

Respiratory Pharmacology (Table 20-2)

• Antibiotics: Amoxicillin, Azithromycin (Zithromax), Ciprofloxin (Cipro), Erythromycin (used for pneumonia, bronchitis).

• Anti-inflammatories (Steroids): Prednisone, Fluticasone (Flovent), Triamcinolone (Azmacort), Beclomethasone (Beclovent).

• Anti-inflammatories (Mast Cell Stabilizers): Cromolyn (Intal).

• Anti-inflammatories (Leukotriene Inhibitors): Montelukast (Singulair).

• Bronchodilators (Short-acting $\text{beta}_2$ agonists): Albuterol (Proventil), Levalbuterol (Xopenex) – cause fast-acting smooth muscle relaxation.

• Bronchodilators (Long-acting $\text{beta}_2$ agonists): Terbutaline (Brethine), Salmeterol (Serevent), Formoterol – slower acting, longer duration.

• Bronchodilators (Anticholinergics): Ipratropium (Atrovent), Tiotropium (Spiriva) – inhibit cholinergic bronchoconstriction.

• Bronchodilators (Xanthines): Theophylline – stimulates respiratory drive, linked to cardiac dysrhythmias.

• Cough Suppressants (Antitussives): Codeine, Hydrocodone, Dextromethorphan – suppress dry cough via CNS.

• Expectorants/Mucolytics: Guaifenesin (expectorant), Acetylcysteine (mucolytic) – thin mucus.

• Pancreatic Enzymes: Pancrelipase (Pancrease) – used in Cystic Fibrosis to support digestion.

Chronic Obstructive Pulmonary Disease (COPD)

• General Overview:

  • Includes both emphysema and chronic bronchitis.

  • The third leading cause of death in the United States.

  • Typically caused by cigarette smoking and occurs in middle age.

  • Smoking causes 85-90% of COPD deaths.

  • Most other cases can be attributed to secondhand smoke exposure, occupational exposure, and air pollution.

  • Rarely (2 to 3% of cases), emphysema is caused by a genetic disorder in which there is a deficiency of a lung-protective protein.

  • COPD Difficulty breathing is caused by progressive destruction of lung tissue with one or more of the following: decreased diameter of the small airways, loss of elasticity of the airways, obstruction because of inflammation and increased mucus production, and decreased alveolar surface area for gas exchange.

Pathophysiology and Complications:

• Right ventricle must work harder to circulate blood through the lungs due to increased resistance to blood flow from damaged capillary beds.

• Increased resistance leads to the right ventricle working harder, resulting in right-sided heart failure and pulmonary artery hypertension.

• Right-sided heart failure results in edema, particularly of the lower extremities and within the abdomen.

• Right-sided heart failure caused by pulmonary disease is called cor pulmonale.

Cor pulmonale: is right-sided heart failure that occurs because of increased resistance in the pulmonary vasculature.

• Chronic hypoxia leads to clubbing of the fingers and a hypoxic drive.

Chronic Bronchitis: is characterized by a cough that produces sputum for a total of three months during two consecutive years.

• Patients have an increased size of mucus-producing cells in bronchi.

- This results in Persistent "smoker’s cough."

• Destruction of the cilia that line the airway makes it more difficult to rid the airway of the mucus, which allows bacteria to become trapped in the lungs. The patient is stable for periods of time but has episodes of decompensation called acute exacerbation, often caused by infection.

• Patients with chronic bronchitis are typically over 50 years old.

• As the disease progresses, the patient may take on the classic appearance referred to as a blue bloater. Patients with chronic bronchitis become cyanotic during exacerbations and are prone to right-sided heart failure, which leads to peripheral edema.

• During acute exacerbations, the patient’s cough may be more frequent and more productive, there may be a change in the character of sputum, and wheezing may occur as a result of bronchoconstriction.

• Patients with chronic bronchitis are prone to hypercapnia, which can lead to confusion, drowsiness, and headache.

Emphysema:

• Patients with emphysema have extensive destruction of the walls of the alveoli, resulting in reduced surface area for gas exchange.

• Because of chronic hypoxia, the body compensates by increasing production of red blood cells to carry oxygen. The increased red blood cell level allows the patient to have good skin color, despite being short of breath.

- The classic presentation of a patient with emphysema is thus called the pink puffer.

• Patients with emphysema also are prone to acute exacerbations, which may be triggered by exposure to smoke, cold air, or other irritants.

• The level of respiratory distress increases, and narrowed airways result in wheezing.

• Patients with emphysema tend to be thin, with well-developed accessory muscles of respiration.

• Air trapped within the damaged alveoli leads to a barrel-chested appearance.

• The tendency of the damaged alveoli to collapse causes patients to compensate by breathing through pursed lips.

• This provides increased resistance to expiration and keeps pressure in the lungs higher. This reflex results in conditions similar to positive end-expiratory pressure (PEEP) ventilation used in automatic ventilator settings.

COPD Management:
– Improve ventilation and oxygenation
– CPAP or BVM is indicated
– Supplemental oxygen to maintain SpO2 88–93%
– Humidified oxygen
– Sympathetic beta2 agonist (albuterol) per protocol
– Sympatholytic (ipratropium) per protocol
– IV fluids if indicated

Asthma

• Pathophysiology: Chronic inflammation of bronchioles and bronchoconstriction during attacks.

• Triggers: Cigarette smoke, pet dander, pollutants, exercise, respiratory infections.

• Milder Attack Signs: Nonproductive cough, expiratory wheezing, chest tightness, tachycardia (< 150\,bpm), S p O_2 > 95 \% \text{ before oxygen}.

• Severe Attack Signs: Inability to speak, exhaustion, confusion, cyanosis, diminished/absent breath sounds, tachycardia or bradycardia, respiration > 30\,per\,minute, S p O_2 < 90 \% \text{ with oxygen}.

• Status Asthmaticus: A severe, life-threatening attack that does not respond to bronchodilators; approaching respiratory failure.

• Treatment: Assess responsiveness and airway. Immediate life threats (cyanosis, exhaustion) require ventilation assistance and transport. Consult for subcutaneous or intramuscular epinephrine in status asthmaticus.

Pulmonary Embolism (PE)

• Mechanism: Obstruction of blood flow by an embolus (clot) in the pulmonary arterial system.

• Consequence: Ventilation-perfusion (V/Q) mismatch; hypoxia occurs because blood cannot reach alveoli for re-oxygenation.

• Risk Factors: Deep vein thrombosis (DVT), recent surgery, cancer, immobilization, estrogen use, pregnancy.

• Signs and Symptoms: Unexplained dyspnea, tachycardia, hypotension, pleuritic chest pain, hemoptysis, swelling of one leg (calf), and a feeling of dread.

• Prehospital Care: Titrate oxygen, IV fluids, and notify destination; be prepared for cardiac arrest.

Pulmonary Edema

• Definition: Increase in interstitial fluid increasing gas diffusion distance between alveoli and capillaries.

• Cardiogenic Pulmonary Edema:

  • Caused by left-sided heart failure.

  • Signs: Orthopnea (needs to sit up to breathe), paroxysmal nocturnal dyspnea (PND), pink frothy sputum, and JVD.

  • Management: CPAP and sublingual Nitroglycerin.

• Noncardiogenic Pulmonary Edema / ARDS:

  • Caused by Acute Respiratory Distress Syndrome (ARDS) or delayed toxin-induced lung injury.

  • ARDS carries a high mortality rate; treatment focus rests on ventilation and oxygenation.

Pneumothorax

• Spontaneous (Simple) Pneumothorax:

  • Air accumulates in the pleural cavity without trauma, caused by a ruptured bleb.

  • Signs: Mild to severe dyspnea, decreased lung sounds on the affected side.

• Tension Pneumothorax:

  • Large defect in the lung; air continues to accumulate and cannot escape.

  • Comprises the mediastinum and collapses the opposite lung.

  • Signs: Severe dyspnea, cyanosis, distended neck veins (JVD), hypotension, and tracheal deviation (late sign).

  • Management: Needle thoracostomy by ALS to decompress the chest.

Infectious Respiratory Diseases

• Pneumonia:

  • Inflammation of lungs; can be community-acquired or nosocomial (hospital-acquired).

  • Symptoms: Fever, shaking chills, yellow or rust-colored productive cough, localized crackles/rhonchi.

• Acute Bronchitis:

  • Viral or bacterial inflammation with increased mucus producing rhonchi and yellow/green sputum.

• Viral Diseases: Influenza, SARS, and HPS are serious. Influenza presents with malaise, fever, muscle pain, and cough.

Lung Cancer and Cystic Fibrosis

• Lung Cancer:

  • Types: Small cell and non-small-cell.

  • Stages: Range from $0$ (localized) to $5$ (extensive metastasis).

  • Complications: Respiratory depression from narcotics, pathological fractures from bone metastasis, and behavioral changes from brain metastasis.

• Cystic Fibrosis:

  • Rare genetic disease of secretory glands causing extremely viscous mucus.

  • Leads to obstructed airways and life-threatening infections.

  • Management: Humidified oxygen, IV fluids, and bronchodilators for wheezing.