Advanced EMT Notes: Respiratory Distress, Anatomy, and Pathophysiology

Introduction to Respiratory Emergencies and Pathophysiology

General Progression of Respiratory Distress: * Patients in respiratory distress can rapidly deteriorate into respiratory failure and respiratory arrest. * Regardless of the underlying cause, death follows quickly without intervention to restore ventilation and oxygenation.
Mechanisms of Oxygen Deficit: * Delivery of oxygen to tissues can be interfered with by various respiratory system problems. * Two primary factors exacerbate oxygen deficits by increasing demand: 1. Stress Response: The terror associated with the sensation of being unable to breathe triggers a stress response, increasing cellular oxygen demand. 2. Physical Effort: Increased use of respiratory muscles (work of breathing) creates a higher need for oxygen in a setting where supply is already compromised. * Inadequate oxygen leads to inefficient energy production and respiratory acidosis. * Homeostasis is overwhelmed by the combination of the uncorrected primary problem, physical exhaustion, and systemic acidosis.
Advanced EMT Role and Management Goals: * Quickly recognize breathing difficulty and intervene to ensure an open airway, adequate ventilation, and circulation of oxygenated blood. * Specific treatment may address the underlying cause, or the focus may remain on supportive care (airway, ventilation, oxygenation) during rapid transport to definitive care. * Transport should ideally be to the facility where the patient is normally admitted, facilitated by modern electronic charting and inter-facility data access. * Clinical competence requires understanding anatomy, physiology, and pharmacology, including when $IV$ fluids are beneficial versus harmful.

Anatomy and Physiology Review

The Pathway of Oxygen: * Life depends on atmospheric oxygen reaching individual cells via the blood. * The process relies on structured coordination between the respiratory and circulatory systems.
System Components and Functions: * Nasal Cavity: Cleanses, warms, and humidifies inhaled air. * Pharynx and Larynx: Carries air to the trachea and produces sound. * Trachea: Transports air to and from the lungs; composed of sturdy cartilage rings to prevent collapse. * Bronchial Tubes: Air passageways inside the lungs; also composed of cartilage rings. * Lungs: Site of gas exchange between air and blood. * Alveoli: Microscopic air sacs where gas exchange occurs.
Requirements for Effective Respiration: * Adequate atmospheric oxygen. * Patent upper and lower airways. * Close contact between alveoli and the capillary network. * Sufficient hemoglobin in red blood cells to transport oxygen. * Proper body temperature and acid-base balance to facilitate external respiration (lung-to-blood exchange) and internal respiration (blood-to-cell exchange).
Ventilation and Perfusion Coordination: * Right Side of Heart: Receives deoxygenated blood high in $CO_2$ and pumps it through the pulmonary artery to the lungs. * Left Side of Heart: Receives oxygenated blood low in $CO_2$ and pumps it through the arterial/capillary system to the cells. * Interference with any part of this system leads to hypoxia, cell dysfunction, and death.

Cellular Metabolism and the Lung Environment

Aerobic Metabolism: * Efficient energy production occurring in the presence of oxygen ( $O_2$ ). * $O_2$ binds to hydrogen ions ( $H^+$ ) produced during metabolism. * Byproducts are water ( $H_2O$ ) and carbon dioxide ( $CO_2$ ), which are easily eliminated.
Anaerobic Metabolism: * Occurs when oxygen is absent; energy production is severely limited. * $H^+$ accumulates as lactic acid, decreasing systemic $pH$ and causing acidosis. * This is a short-term compensatory mechanism that results in death if oxygenation is not restored.
Structure and Function of the Lungs: * Lungs consist of millions of alveoli. * The trachea divides at the carina into the right and left mainstem bronchi, entering lungs at the hilum. * Bronchi divide into smaller branches serving two lobes in the left lung and three lobes in the right lung. * Bronchioles: Microscopic branches with smooth muscle instead of cartilage; diameter changes based on ventilation needs. * Beta2 Receptors: Located on bronchiole smooth muscle; respond to epinephrine or sympathomimetic drugs to cause bronchodilation.
The Respiratory Membrane: * Mucociliary Clearance: Mucus-secreting cells trap contaminants, and cilia (hairlike projections) sweep them upward. Nicotine paralyzes these cilia. * Diffusion Barrier: Distal bronchioles and alveoli are a single cell-layer thick. The respiratory membrane consists of the alveolar and capillary walls. * Diffusion only occurs over short distances; it is hindered by extracellular fluid accumulation between walls or fluid/pus (edema or pneumonia) within the alveoli.

Principles of Ventilation

Chemical Stimuli: * Primary stimulus: Increased levels of carbon dioxide ( $CO_2$ ) in the blood and cerebrospinal fluid ( $CSF$ ). * Secondary stimulus: Decreased levels of oxygen ( $O_2$ ).
Inspiration (Active Process): * Chemical changes stimulate the medulla (inspiratory center) of the brainstem. * Nervous impulses cause the diaphragm to flatten and intercostal muscles to lift the ribs upward/outward. * Increased thoracic volume creates a vacuum (negative pressure) in the pleural space, lowering intrapulmonary pressure below atmospheric pressure. * Air moves from higher (atmosphere) to lower (lungs) pressure.
Lung Volumes and Dead Space: * Tidal Volume: Average air per breath is $5-7\,mL/kg$ (approx. $500\,mL$ in adults). * Anatomical Dead Space: Approximately $150\,mL$ of air remains in the conduction pathways (trachea, bronchi) and is unavailable for gas exchange. * Alveolar Ventilation: The actual amount of air reaching alveoli (approx. $350\,mL$ in the average adult). * Clinical Pearl: Shallow breathing decreases tidal volume, significantly reducing alveolar ventilation because dead space volume is constant.
Expiration (Passive Process): * Stimulated by the Hering-Breuer reflex: stretch receptors in the lungs signal the brain to inhibit inspiration. * Muscles relax, thoracic volume decreases, and intrapulmonary pressure exceeds atmospheric pressure, forcing air out.

Patient Assessment Strategies

General Assessment: * Dyspnea: Mild shortness of breath to severe inability to speak. * Signs of Distress: Tripod position, wheezing, coughing, accessory muscle use. * Signs of Failure/Arrest: Cyanosis, altered mental status ( $AMS$ ), weak respiratory effort, or apnea.
Classification of Respiratory Status (Table 20-1): * Normal Breathing: Rate $12-20\,\text{per minute}$ ; adequate tidal volume; clear breath sounds; no intervention needed if $SpO_2 \ge 95\%$ . * Respiratory Distress: Rates slightly abnormal; tidal volume variable; may have stridor, wheezing, rhonchi, or crackles; anxious appearance; supplemental $O_2$ to target $95\%\,SpO_2$ . * Respiratory Failure: Rate $\le 8$ or $\ge 30$ ; inadequate tidal volume; diminished breath sounds; fatigue, cyanosis, and confusion; intervention requires CPAP, $BVM$ , or $FROPVD$ . * Respiratory Arrest: Agonal or absent respirations; minimal to absent air movement; cyanotic and unresponsive; necessitates ventilation with $BVM$ , $FROPVD$ , or $ATV$ .
Specific Clinical Indicators: * Irregular Respirations: Often indicate a neurological problem. * Hypoxia Indicators: Tachycardia (adults), Bradycardia (pediatrics), No heart rate change (geriatrics). * Positioning: Sitting upright or leaning forward (tripod) provides maximum comfort.

Advanced EMT Interventions

Scene Size-Up and Primary Assessment: * Hypoxic patients may behave irrationally due to cerebral dysfunction. * If a patient is unresponsive with no pulse (check for $10\,\text{seconds}$ ), start chest compressions and apply an $AED$ . * Assess ease of speech: Can the patient speak in full sentences or only fragmented words? * Priority: Dyspnea is always a high-priority transport condition.
Secondary Assessment and History: * Auscultate breath sounds and monitor vitals (oximetry, capnometry, cardiac monitoring). * Check for peripheral edema (indicative of heart failure). * Assess for medications as clues to chronic illness.
Medications Categorization (Table 20-2): * Antibiotics: e.g., Amoxicillin, Azithromycin ( $Zithromax$ ), Ciprofloxacin ( $Cipro$ ); treat bacterial infections like pneumonia. * Corticosteroids: e.g., Prednisone, Fluticasone ( $Flovent$ ); reduce inflammation in asthma and $COPD$ . * Mast Cell Stabilizers/Leukotriene Inhibitors: e.g., Cromolyn ( $Intal$ ), Montelukast ( $Singulair$ ); inhibit inflammatory mediators. * Short-acting Beta2 Agonists: e.g., Albuterol ( $Proventil$ ), Levalbuterol ( $Xopenex$ ); fast-acting bronchodilation. * Long-acting Beta2 Agonists: e.g., Salmeterol ( $Serevent$ ), Formoterol; slower acting, longer duration. * Anticholinergics: e.g., Ipratropium ( $Atrovent$ ), Tiotropium ( $Spiriva$ ); inhibit bronchoconstriction. * Xanthines: e.g., Theophylline; stimulates respiratory drive but carries risk of cardiac dysrhythmia. * Antitussives: Codeine, Dextromethorphan; suppress dry coughs. * Expectorants/Mucolytics: Guaifenesin, Acetylcysteine; thin mucus. * Pancreatic Enzymes: e.g., Pancrelipase ( $Pancrease$ ); used in Cystic Fibrosis to aid digestion.
Treatment Modalities: * CPAP: Indicated for pulmonary edema to improve gas exchange. * Nitroglycerin: Consider if pulmonary edema is caused by heart failure (per protocol). * Epinephrine: Indicated for anaphylactic respiratory distress. * Target SpO2: Standard patients $\ge 95\%$ . $COPD$ patients reach a target of $88-92\%$ .

Specific Respiratory Disorders

Chronic Obstructive Pulmonary Disease (COPD): * Third leading cause of death in the United States. * Includes Emphysema and Chronic Bronchitis; most patients have elements of both. * Causes: Smoking ( $85-90\%$ of cases), secondhand smoke, occupational hazards, or rare genetic protein deficiency ( $2-3\%$ of cases). * Pathophysiology: Progressive destruction of lung tissue, decreased airway diameter, loss of elasticity, inflammation/mucus obstruction, and decreased alveolar surface area for exchange.