Paramedic Exam

The chapters move from physiology to assessment tools, airway management, ventilation devices and respiratory emergencies, with pediatric and geriatric points throughout. Values follow current AHA guidelines, the National Model EMS Clinical Guidelines and the National EMS Education Standards; learn the principle and the commonly accepted dose.

This chapter reviews the structures you manage and the physiology that explains why patients become hypoxic or hypercapnic. Nearly every airway item on the exam can be solved by asking one question: is this a problem of oxygenation, ventilation, or both?

The upper airway runs from the nose and mouth to the glottis and warms, filters and humidifies air. Key landmarks for the paramedic are the nasopharynx, oropharynx, the tongue (the most common cause of airway obstruction in an unresponsive patient), the epiglottis, the vallecula (the space between the base of the tongue and the epiglottis, where a curved Macintosh blade tip sits), the arytenoid cartilages (the posterior landmarks of the glottic opening), the vocal cords, the thyroid cartilage (Adam's apple), the cricothyroid membrane and the cricoid cartilage, the only complete cartilaginous ring of the airway.

The cricothyroid membrane lies between the thyroid cartilage above and the cricoid cartilage below. It is the site for surgical and needle cricothyrotomy because it is superficial, relatively avascular and below the vocal cords.

The lower airway begins below the glottis: trachea, carina (at about the level of the angle of Louis, the fourth thoracic vertebra), right and left mainstem bronchi, bronchioles and alveoli. The right mainstem bronchus is shorter, wider and more vertical, so an endotracheal tube advanced too far usually enters the right side, producing absent or diminished left-sided breath sounds. Gas exchange occurs across the alveolar-capillary membrane, which is coated with surfactant to prevent alveolar collapse.

Children are not small adults, and the exam tests these differences directly.

Pediatric Versus Adult Airway Anatomy

The adult airway is roughly cylindrical, with the glottis as the narrowest point. The pediatric airway is traditionally taught as funnel shaped with the narrowest nondistensible point at the cricoid ring. This is why tube size, not just cord passage, matters, and why cuffed pediatric tubes are used with careful cuff pressure.

Memory Aid: Children have a "big head, big tongue, small reserve." Fix the position, open the mouth, and expect rapid desaturation.

Ventilation is the mechanical movement of air in and out of the lungs. Its lab marker is PaCO2, and its field marker is ETCO2. Oxygenation is loading oxygen onto hemoglobin, measured by SpO2 and PaO2. Respiration is gas exchange: external respiration at the alveoli and internal (cellular) respiration in the tissues.

A patient can be well oxygenated and poorly ventilated (an opioid overdose on a nonrebreather with an SpO2 of 97% and an ETCO2 of 68 mmHg), or ventilating well and poorly oxygenated (a pneumonia patient with an SpO2 of 84% and an ETCO2 of 32 mmHg). Supplemental oxygen fixes oxygenation. Only increased effective breaths fix ventilation.

Common Trap: A normal SpO2 on high-flow oxygen does not prove adequate ventilation. A slow, shallow breather can hold an acceptable SpO2 while CO2 climbs to dangerous levels. Capnography exposes the problem; pulse oximetry hides it.

Minute ventilation (mL/min) = tidal volume (mL) x respiratory rate (breaths/min).

Alveolar ventilation (mL/min) = (tidal volume - dead space) x respiratory rate. Anatomic dead space is about 150 mL in an adult (roughly 1 mL per pound of ideal body weight).

Worked example: An adult breathing 500 mL at 12 breaths/min has a minute ventilation of 6,000 mL (6 L/min) and alveolar ventilation of (500 - 150) x 12 = 4,200 mL/min. A second patient breathing 250 mL at 24 breaths/min has the same 6 L/min minute ventilation, but alveolar ventilation is only (250 - 150) x 24 = 2,400 mL/min. The fast, shallow breather is moving far less air to the alveoli. This is why rapid, shallow breathing is a sign of fatigue and impending failure, not adequate compensation.

Normal gas exchange requires both air (V) and blood (Q) in the same alveoli. Mismatch takes two extreme forms.

V/Q Mismatch Patterns

Exam Tip: A patient with hypoxia that does not improve with a nonrebreather suggests a shunt. The fix is positive end-expiratory pressure (CPAP or PEEP on the BVM or ventilator), which reopens fluid-filled or collapsed alveoli.

The curve is S shaped. On the flat upper part, PaO2 can fall from 100 to about 60 mmHg while SpO2 drops only from about 98% to 90%. Below an SpO2 of about 90% (PaO2 near 60), the curve becomes steep, and small further drops in PaO2 cause large drops in saturation. That is why 90% is a practical floor and why desaturation accelerates once it starts.

A right shift means hemoglobin releases oxygen more readily to the tissues. Causes: increased CO2, acidosis (low pH), increased temperature, and increased 2,3-DPG (as in chronic hypoxia). A left shift means hemoglobin holds oxygen more tightly. Causes: alkalosis, hypothermia, low CO2, carbon monoxide, fetal hemoglobin and decreased 2,3-DPG (as in stored blood).

Memory Aid: "Right shift, release." A hot, acidotic, exercising muscle needs oxygen, so the curve shifts right to unload it. Hyperventilating a patient (alkalosis, left shift) makes hemoglobin cling to oxygen, one more reason not to over-ventilate.

Central chemoreceptors in the medulla respond to CO2 (through hydrogen ion changes in the cerebrospinal fluid) and provide the primary drive to breathe. Peripheral chemoreceptors in the carotid and aortic bodies respond mainly to low PaO2 and also to acidosis. Some patients with chronic CO2 retention rely more heavily on the hypoxic signal, but the rise in PaCO2 that can follow high-flow oxygen in COPD is mostly due to worsened V/Q matching and the Haldane effect.

Common Trap: Never withhold oxygen from a hypoxic COPD patient. Titrate to an SpO2 of 88-92% in a known CO2 retainer and watch ETCO2 and mental status. Hypoxia kills faster than hypercapnia.

Ventilation (CO2 removal, ETCO2) and oxygenation (SpO2) are separate problems with separate fixes.

Alveolar ventilation falls sharply with fast, shallow breathing even when minute ventilation looks normal.

Shunt causes hypoxia that resists oxygen; PEEP or CPAP is the fix.

Below about 90% SpO2, the oxyhemoglobin curve is steep and desaturation accelerates.

Pediatric airways are higher, more anterior and funnel shaped; infants are obligate nose breathers and desaturate quickly.