MOD 2 Study Guide (plus Qz Questions)

Direct effects of positive pressure

tachycardia, decreases preload, decreases venous return to the right ventricle, decrease venous blood flow from peripheral, increases inter-thoracic pressure, decreases cardiac output

Cricothyroid complications

pneumothorax (placed to laterally, into the lung), esophageal injury (needle went to deep), catheter dislodges (movement or not secured), air flowing into neck/upper chest cause emphysema (air leaking anywhere or ventilation escaping/bad seal), bleeding from vessels

How to determine cuff is inflated

pilot tube is inflated

Cric Delayed complications

tracheal stenosis (scaring), cartilage damage (not placing correct position plus aggressive intervention), possible infection (24-48 hrs later)

What oxygen devices does not affect cardiac output

nasal cannula, Venturi mask, face mask, NRB

What oxygen devices affects cardiac output

Bag mask, CPAP, Ventilator, Manual oxygen trigger

Rales or crackles are found in which anatomical area?

smaller airway

Softer, medium pitched breath sounds heard over the mainstem bronchi are known as

bronchovesicular

Which of the following is the condition presenting with hypertrophy (the increase in the size of cells) of the right ventricle resulting from disorders of the lung?

cor pulmonale

During inspiration which anatomical structure causes turbulance that facilitates entrapment and removal of inhaled foreign particles

turbinates

Define turbinates

the superior, middle, and inferior structures on the walls of the nasal cavity that help condition incoming air

Define uvula

located in the nasopharynx at the back of the palates, along with the tonsils or adenoids

Define epiglottis

a leaf-shaped cartilage in the hypopharynx that prevents food from entering the respiratory tract during swallowing and serves as a key landmark for endotracheal intubation

Define larynx

the complex midline neck structure that joins the pharynx with the trachea and contains the glottic opening, vocal cords, thyroid and cricoid cartilages, and arytenoid cartilage

Define vallecula

a fold formed by the base of the tongue and the epiglottis, located in the hypopharynx

Define carina

a ridge of cartilage at the base of the trachea that splits into the left and right main bronchi

Define bronchi

the large air passages that branch from the trachea into the right and left primary ones, leading to the lungs.

Define bronchioles

branches of the bronchi extending throughout the lungs.

Define cilia

bronchus in the lungs are lined with these hair-like projections that move microbes and debris up and out of the airways

Define alveoli

clusters of air sacs at the ends of alveolar ducts, surrounded by pulmonary capillaries where gas exchange occurs.

Define phrenic nerve

arising from cervical nerves 3, 4, and 5, innervates the diaphragm

Define apnea

Absence of breathing.

Define eupnea

Normal rate and pattern of breathing.

Define dyspnea

An abnormality of breathing rate, pattern, or effort.

Define aortic arch

top, curved segment of the aorta that distributes oxygen-rich blood from the heart to the head, neck, and arms

Define hypoxia

condition where there is an insufficient supply of oxygen at the tissue and cellular level to maintain normal body functions

Define hypoxemia

condition characterized by low oxygen tension or concentration in arterial blood

Define medulla

the lowest part of the brainstem that connects the higher levels of the brain to the spinal cord; controls involuntary, life-sustaining autonomic functions that you do not have to think about

Define arytenoid foids

forms a pyramid-shaped posterior attachment for the vocal cords and is an important landmark for endotracheal intubation.

Define cricoid cartilage

lies beneath the thyroid cartilage and forms the inferior border of the larynx; it is often considered the first tracheal ring and, unlike other laryngeal cartilages, forms a complete ring; in children, it is the narrowest part of the laryngeal airway.

Define thyroid cartilage

the main, shield‑shaped laryngeal cartilage; larger in men, it forms the anterior neck prominence called the Adam’s apple and houses the glottic opening directly behind this prominence.

Define cricothyroid membrane

connects the inferior border of the thyroid cartilage to the superior aspect of the cricoid cartilage. It is an important landmark and the site for surgical airway techniques

Describe the differences between the visceral pleura, parietal pleura, and pleural space

The visceral pleura is the thin, smooth membrane that directly covers and envelops the lungs themselves - it has no nerve fibers, so it does not transmit pain sensations/ The parietal pleura is the membrane that lines the interior of the thoracic (chest) cavity - does contain nerve fibers and can generate significant pain when inflamed/ The pleural space is the potential space between the visceral and parietal pleura - normally contains a small amount of pleural fluid that lubricates the two layers, allowing the lungs to move smoothly against the thoracic wall during breathing (if air enters this space freely, the lung can collapse, producing a pneumothorax)

What are the respiratory complications that can occur in visceral pleura

Injury to lung tissue (including barotrauma from mechanical ventilation) can rupture alveoli and allow air to leak into the pleural space, producing pneumothorax with associated alveolar collapse (atelectasis). As more alveoli collapse, a ventilation/perfusion mismatch develops, causing hypoxemia and hypercarbia (acidosis) and potentially life‑endangering respiratory compromise.

What are the respiratory complications that can occur in parietal pleura

Pulmonary injuries affecting the tissues that support the lung and allow contact with the interior thoracic cavity can lead to simple pneumothorax, open pneumothorax, tension pneumothorax, hemothorax, and pulmonary contusion, all of which impair ventilation and gas exchange and can result in hypoxemia and systemic hypoxia.

What are the respiratory complications that can occur in pleural space

Air entering the pleural space causes simple or tension pneumothorax. Progressive air accumulation collapses the lung, produces atelectasis and ventilation/perfusion mismatch, and leads to hypoxemia, hypercarbia, and systemic hypoxia. In tension pneumothorax, rising intrapleural pressure also compresses the mediastinum and uninjured lung, severely compromising breathing.

What are the structural differences between the right and left main bronchus?

The right mainstem bronchus is almost a straight continuation of the trachea, while the left mainstem bronchus angles more acutely to the left; Because the right side is straighter, aspirated material and endotracheal tubes that are advanced too far tend to pass into the right mainstem bronchus, so aspiration pneumonia and unintended one‑lung ventilation occur more commonly on the right

What does a chemoreceptor do in relation to the respiratory system?

specialized sensors that help regulate breathing automatically; (1) central chemoreceptors in the medulla and peripheral chemoreceptors in the carotid bodies and the arch of the aorta monitor blood chemistry - Decreased PaO₂ (oxygen)/ Increased PaCO₂ (carbon dioxide)/ Decreased pH (more acidic); (2) The primary driver is CO₂ - changes in arterial PCO₂ alter the pH of the cerebrospinal fluid - Increased PCO₂ → decreased CSF pH → central chemoreceptors stimulate the respiratory center → respiration increases to blow off CO₂ / Decreased PCO₂ → increased CSF pH → chemoreceptor stimulation falls → respiration slows. (3) Peripheral chemoreceptors also signal the brainstem to increase respiration when arterial PCO₂ rises. In this way, chemoreceptors continually adjust respiratory rate and depth to maintain normal gas levels and acid–base balance.

What is the responsibility of a baroreceptor?

pressure sensor that helps the body maintain stable blood pressure and blood volume through a rapid negative feedback loop

Define minute volume

The amount of gas moved in and out of the respiratory tract in 1 minute; calculated as tidal volume × respiratory rate.

Define tidal volume

The average volume of gas inhaled or exhaled in one respiratory cycle.

Define dead air space/residual air space

the portion of the tidal volume that does not take part in gas exchange and remains in the air passageways/ the air that remains in the lungs at all times and helps maintain alveolar patency

During inhalation, the intercostal muscles and diaphragm physically are

diaphragm contracts and flattens, moving downward/ the intercostal muscles contract, pulling the ribs up and outward and increasing the anteroposterior and lateral diameters of the chest/ Together, this increases thoracic cavity volume and lowers intrathoracic pressure below atmospheric pressure, so air is drawn into the lungs.

During exhalation, the intercostal muscles and diaphragm physically are

diaphragm relaxes and moves upward into the thoracic cavity/ the intercostal muscles relax so the ribs return to their normal position and move closer together/ This decreases thoracic cavity volume and raises intrathoracic pressure above atmospheric pressure, so air is pushed out of the lungs. In normal resting breathing, exhalation is largely a passive process of muscle relaxation and elastic recoil.

Define the term pulsus paradoxus and how does that relate to the respiratory system?

abnormally large drop in systolic blood pressure during inspiration (normally, systolic pressure falls slightly (less than 10 mmHg) when a person inhales); this fall in systolic pressure during inspiration exceeds 10 mmHg/ the change occurs with the normal respiratory cycle—specifically during inhalation—due to altered intrathoracic pressures. [Conditions that increase intrathoracic pressure or impair cardiopulmonary function (such as COPD, asthma, or pericardial tamponade) can exaggerate this inspiratory drop in systolic pressure]; it is a cardiovascular sign that reflects abnormal interaction between breathing mechanics, intrathoracic pressure changes, and cardiac output.

Know the indications, contraindications, liters of oxygen required, and procedure for using Nasal cannula

Indicated for low‑to‑moderate oxygen requirements and for long‑term oxygen therapy; is used when the patient needs supplemental oxygen but does not require a mask or positive‑pressure ventilation. Contraindicated for complete nasal obstruction, severe facial or skull base trauma, severe nasal deformities or active nosebleeds (epistaxis), Untreated pneumothorax, Immediate need for intubation or severe hemodynamic instability, or Recent nasal or sinus surgery. 2-6L/min up to 40% oxygen, Flow rates above 6 L/min dry and damage the nasal mucosa and are generally avoided for comfort. Steps to use - *Place the nasal cannula catheter at the nares *Set the oxygen flow (typically up to 6 L/min for standard use) *Cannula is generally well tolerated for ongoing low‑to‑moderate oxygen supplementation *In advanced airway management, a high‑flow cannula may be placed under a mask during preoxygenation or left in place during intubation attempts to provide passive oxygenation, as long as the airway is open.

Know the indications, contraindications, liters of oxygen required, and procedure for using NRB

indicated for patients with high oxygen requirements, used it for initial management when the highest possible inspired oxygen concentration. Contraindicated for Apnea or Inadequate Tidal Volume, High Risk of Aspiration or Inability to Protect the Airway, Severe Facial Trauma or Burns, Poor Patient Tolerance or Agitation, and Home or Long-Term Therapy Settings. Set at 15 L/min providing 80%-100% O2. Steps to use - *Select a nonrebreather mask with one‑way side ports and an attached reservoir bag *Connect to oxygen and set flow to 15 L/min *Ensure the reservoir bag is inflated and the mask is fit tightly to the face to minimize room air entrainment *Continuously reassess the patient to confirm that the NRB and flow rate are adequate; if hypoxemia persists, consider positive‑pressure ventilation (e.g., CPAP/BiPAP or BVM with PEEP).

Know the indications, contraindications, liters of oxygen required, and procedure for using BVM

indicated for patients who are not breathing or not breathing adequately and require assisted ventilation/ serve as a bridge to more invasive airway techniques. Contraindicated for Complete Upper Airway Obstruction, Severe Facial Trauma, and Active Vomiting or Regurgitation. 10-15 L/min, 90/95-100% O2. Steps to use - *Use an appropriately sized BVM and mask (pediatric or adult, depending on patient) *Attach the BVM to 10–15 L/min oxygen and ensure the reservoir is in place *Position the patient’s airway (head‑tilt/chin‑lift or jaw‑thrust as appropriate) *Place the mask over nose and mouth, avoiding pressure on the eyes, and obtain a tight seal (ideally with a two‑rescuer technique - one holds the mask and airway, one squeezes the bag) *Deliver gentle ventilations, using the lowest pressure needed to see chest rise, and allow adequate time for exhalation to avoid barotrauma and gastric distention *Continuously assess chest rise, lung sounds, and clinical improvement; use waveform capnography to confirm effective mask seal and ventilation.

Know the indications, contraindications, liters of oxygen required, and procedure for using Venturi mask

indicated for when a patient needs precise, controlled oxygen concentrations rather than very high FiO₂. It is particularly useful for COPD patients who benefit from careful control of inspired oxygen concentration. Contraindicated for Facial Trauma or Burns, Severe Hypoxemia, Mask Intolerance or Claustrophobia, and Airway Obstruction. Masks can deliver 24%, 28%, 35%, and 40% oxygen, liter flow depends on the desired oxygen concentration. Steps to use - *Select a Venturi mask and the appropriate dial setting or interchangeable cap for the desired FiO₂ (24, 28, 35, or 40%) *Connect the mask to oxygen and set the flow rate according to the selected concentration (per device instructions) *The system uses a jet orifice and Venturi effect to entrain room air and deliver a precise oxygen mixture regardless of the patient’s rate and depth of breathing *Apply the mask to the patient’s face and reassess frequently to ensure the delivery method and flow rate remain adequate for the patient’s condition.

Know the indications for use and how to measure an oropharyngeal BLS airway

indicated for patients with no gag reflex (profoundly unconscious), Helps manage unconscious patients who are breathing spontaneously or need mechanical ventilation, Holds the base of the tongue away from the posterior oropharynx, preventing tongue obstruction of the glottis, and Facilitates suctioning and can act as a bite block and protect an endotracheal tube. Contraindicated for conscious or semiconscious patients who have a gag reflex. Measured by - [OPAs come in sizes #0 (neonate) to #6 (large adult)], Place the flange beside the patient’s cheek, parallel to the front of the teeth, A properly sized OPA extends from the patient’s mouth to the angle of the jaw (Too long - can press the epiglottis against the laryngeal entrance and obstruct the airway/ Too short - will not adequately hold the tongue forward)

Know the indications for use and how to measure an nasopharyngeal BLS airway

indicated for obtunded or unconscious patients (reduced mental acuity) who may or may not have a gag reflex, Appropriate when you need to bypass the tongue and maintain a patent airway, including when - The patient has a gag reflex (where an OPA would be contraindicated) or There is injury to the oral cavity or clenched teeth. Measured by choose a tube slightly smaller than the patient’s nostril, equal to or slightly longer than the distance from the patient’s nose to the earlobe (Too small/short → may not extend past the tongue, fails to maintain airway/ Too long → may pass into the esophagus, causing hypoventilation and gastric distention with positive pressure) *to measure in children, Use the outside diameter of the child’s little finger and avoid using in infants all together.

What is the difference in the patient presentation that indicates the use of oropharyngeal vs nasopharyngeal?

Unconscious, no gag reflex → OPA/ Has gag reflex or oral/facial trauma/clenched teeth → NPA (unless contraindicated by skull/midface fracture)

Know the indications, contraindications, and procedure for using Combitube:

indicated for patients >4 feet tall, used when you need a blindly inserted airway that can ventilate whether it lands in the esophagus (most common) or trachea, Appropriate when conventional endotracheal intubation is difficult or delayed, and you need rapid airway control and ventilation. Contraindicated for patients with an intact gag reflex, risk of trauma, including esophageal perforation, and tissue ischemia from high cuff volumes. Procedure includes insert blindly through the mouth into the posterior oropharynx and gently advance, recognize that the tube may enter either the esophagus or trachea, but esophageal placement is most common, Lumen/Port #1 (long, blue, proximal port) – designed to ventilate when the tube is in the esophagus and Lumen/Port #2 (short, clear, distal port) – ventilates if the tube is in the trachea. It has two cuffs - a large (~80/100 mL) distal cuff and a smaller (~15/25 mL) proximal pharyngeal cuff. After insertion, ventilate first through the longer, blue port (#1) - If you get chest rise and breath sounds, the tube is in the esophagus; continue ventilating via port #1 with cuffs inflated. If ventilation via port #1 is unsuccessful, switch and ventilate through the short clear port (#2), indicating tracheal placement. Use clinical assessment (chest rise, auscultation) and standard confirmation techniques to verify effective ventilation, and secure the tube.

Know the indications, contraindications, and procedure for using IGel

indicated for facilitating oxygenation and ventilation without entering the glottis; used as a primary or secondary airway device instead of endotracheal intubation, comes in adult and multiple pediatric sizes. Contraindicated for gag reflex, Conscious or responsive patients, Known or suspected upper airway obstructions, Trismus or limited mouth opening, Caustic substance ingestions, Extensive or major trauma, Known esophageal disease, and Laryngectomy patients with an open stoma. Procedure includes insertation blindly, positioned above the vocal cords to form a seal, a passageway for a gastric tube, allowing stomach decompression once placed, and then ventilation is provided via a bag‑valve device or ventilator.

Know the indications, contraindications, and procedure for using King LTD

a single‑lumen retroglottic extraglottic airway used when you need a blind airway device, It is supplied in three adult sizes based on height and two pediatric sizes. Contraindicated for Responsive patients who have an intact gag reflex, Patients under 4 feet tall, Known or suspected caustic substance ingestion (risk of esophageal perforation), Known esophageal disease, and Present airway obstruction. Procedure includes inserting blindly into the airway so that its large pharyngeal and smaller esophageal balloons sit in the hypopharynx and esophagus, Inflate both balloons via the single inflation port with one syringe, Ventilate through the proximal lumen; the device can generate significant airway pressures and provides substantial aspiration reduction and stabilization at the base of the tongue.

Know the indications, contraindications, and procedure for using LMA

a supraglottic extraglottic airway and commonly used in the OR. Contraindicated for Restricted mouth opening, Complete upper airway obstruction, Conscious patients, Full stomach or non-fasted status, Gastrointestinal conditions, Pregnancy, and Morbid obesity. Procedure includes selecting the size, testing the cuff, lubricating, position the patient in sniffing posistion, open mouth, advance along palate until resistance against the upper esophageal sphincter over the laryngeal opening, inflate cuff, verify placement, and secure tube.

Describe the patient presentation requiring the use of humidified oxygen

Toxic inhalation exposure, Facial/oral/throat burns or particulate matter - hoarseness/ “brassy” cough/ stridor suggesting laryngeal edema and an irritable airway, wheezing (bronchospasm) or crackles/rales (pulmonary edema), Signs of hypoxia with possible irritation

Describe the purpose of interpreting EtCO2

used to assess patient’s status - metabolism, circulation, and ventilation; EtCO2 reflects how much CO2 is produced by cells (metabolism), transported to the lungs (cardiac output and perfusion), and eliminated by ventilation. Changes in EtCO2 help you recognize problems such as shock, decreased cardiac output, or hypoventilation/hyperventilation/ Detecting exhaled CO2 after intubation confirms that the endotracheal tube is in the trachea and that the patient is being ventilated, especially when using continuous waveform capnography/ Continuous capnography lets you monitor tube location during transport, evaluate the effectiveness of resuscitation and adequacy of ventilation, guide CO2 levels in suspected raised ICP, and even help predict outcomes in cardiac arrest and trauma.

Describe the purpose of interpreting pulse oximetry

used to assess and continuously monitor how well oxygen is being delivered to a patient’s tissues; hemoglobin oxygen saturation (SpO₂) - provides a rapid, noninvasive, and generally accurate estimate of arterial oxygen saturation in peripheral tissues, often detecting oxygenation problems earlier than changes in blood pressure, pulse, or respiratory rate/ Establish a baseline and guide therapy - use SpO₂ to determine the patient’s initial oxygenation status, decide whether supplemental oxygen is needed, and then adjust oxygen flow to restore normoxia while avoiding hyperoxia and oxygen toxicity/ Monitor response to interventions - Continuous readings allow you to see whether oxygen therapy, ventilation, or other treatments are improving or worsening oxygen delivery/ Pulse oximetry is called the “fifth vital sign” and is an important but it must be interpreted alongside the full clinical assessments, not alone.

Describe the purpose of interpreting capnography

used to evaluate ventilation, circulation, and metabolism in real time by measuring exhaled CO₂ and displaying it as a waveform (capnogram); Confirm and monitor advanced airway placement - Continuous quantitative waveform capnography is the standard of care to verify that an endotracheal or extraglottic airway is in the trachea and to detect accidental displacement, including during cardiac arrest/ Assess ventilation and troubleshoot problems - The EtCO₂ value and waveform shape help identify hypoventilation/hyperventilation, bronchospasm (e.g., “shark‑fin” pattern in asthma/COPD), pulmonary embolus, and mechanical ventilation issues, and can give a rough estimate of tidal volume during manual ventilation/ Monitor patient status and response to treatment - trends in EtCO₂ correlate with cardiac output and effectiveness of CPR, can help identify sepsis (low EtCO₂), and guide CO₂ levels in head trauma and stroke.

How would you know if you are ventilating a patient with a BVM properly?

visible chest rise, auscultation of lung sounds, clinical improvement, device and seal checks, and waveform capnography

What is the curved ET blade designed to do, and what is the landmark for insertion?

used to sweep the tongue aside - Its large flange lets you move the tongue from the right side of the mouth to the left, clearing the line of sight/ Lift the epiglottis indirectly - The blade is advanced until its tip fits into the vallecula, where it presses on the hyoepiglottic ligament. This pressure lifts the epiglottis and exposes the glottic opening for tube placement. The Landmark for insertion is the vallecula (the space just above the tip of the epiglottis, between the base of the tongue and the epiglottis), the curved blade tip is positioned in this vallecula before lifting to visualize the vocal cords.

Identify the complications of the lack of an airtight seal on a BVM mask

Inadequate volume delivery - A poor mask seal is specifically noted as a cause of inadequate volume delivery. Much of the air you squeeze into the bag escapes around the mask instead of entering the lungs, so the patient is not ventilated effectively/ Failure to deliver high‑concentration oxygen/PEEP - The BVM can deliver 90–95% oxygen and passive PEEP only when there is a tight mask seal and a patent airway. With a leaky seal, the patient receives less oxygen and any intended PEEP effect is lost/ Misleading assessment of ventilation - With a poor seal, you may see little or no chest rise, abnormal bag compliance, and an absent or abnormal capnography waveform, all indicating ineffective mask ventilation.

What airway intervention is a definitive airway in the field?

endotracheal intubation; Bypasses the entire upper airway by placing a tube directly into the trachea, Provides the most effective method of controlling a patient’s airway, in both adults and children, and Is used when the patient has no gag reflex and cannot protect the airway, or when basic and extraglottic airways are insufficient.

Compare and contrast the types of patient presentations that determine whether to use a nasal cannula or NRB device

Nasal cannula (low to moderate O₂ needs, stable presentation) - delivers up to about 40% O₂ at 6 L/min, Indicated for low‑to‑moderate oxygen requirements and long‑term oxygen therapy. Typical presentation - Mild dyspnea or mild hypoxemia, Stable respiratory rate and effort, Able to tolerate a simple device at the nares, Patients “generally tolerate the nasal cannula well,” so it’s used when you only need to supplement oxygen rather than give very high concentrations. Nonrebreather mask – high O₂ needs, more compromised presentation, Provides the highest oxygen concentration of the standard devices, about 80% O₂ at 15 L/min with a tight fit, Indicated for patients with high oxygen requirements; commonly used for initial management of significantly ill or injured patients. Typical presentation - Moderate to severe hypoxemia, Increased work of breathing or significant distress, Need for rapid, high‑concentration oxygen delivery, Any patient who “requires a nonrebreather should be closely monitored for refractory hypoxemia” that might require escalation to positive‑pressure ventilation.

What is the mathematical formula to calculate the proper endotracheal tube size for a child?

ET Size = (Age in years + 16)/ 4

When using a stylet to insert an endotracheal tube, what is the landmark that tells you to stop insertion?

tube is advanced until the "vocal cord" marking on the ETT is at the level of the vocal cords, or until the distal cuff just disappears beyond the vocal cords.

Identify two complications of a lack of an airtight mask seal when ventilating with a bag-valve-mask (BVM)

Inadequate volume delivery and Failure to deliver high‑concentration oxygen/effective PEEP

What is the minimum safe residual pressure (psi) for an oxygen tank?

200 psi

What is the minimum safe maximum pressure (psi) for an oxygen tank?

2,000-2,400 psi

What anatomical structure measures carbon dioxide levels?

chemoreceptors, located in the medulla oblongata

Oxygen and blood pressure are measured by what structures?

chemoreceptors (caradid/aortic bodies) and baroreceptors (pressoreceptors, carotid sinuses and aortic arch)

What do SpO2 and PO2 indicate?

SpO₂ (peripheral oxygen saturation) Measured noninvasively by pulse oximetry/ Indicates the percentage of hemoglobin that is bound to oxygen in peripheral blood/ Reflects how well oxygen is being delivered to tissues via hemoglobin. Normal at sea level is roughly 96–99%, with lower ranges indicating mild, moderate, or severe hypoxemia. PO₂ (often written PaO₂ – partial pressure of oxygen) Measured from arterial blood gases/ Indicates the partial pressure of oxygen dissolved in plasma, usually in torr or mmHg/ Drives oxygen loading onto hemoglobin - as PaO₂ increases, hemoglobin’s affinity for oxygen and saturation increase (shown by the oxyhemoglobin dissociation curve)

Compare and contrast the differences between PEEP and CPAP

CPAP (Continuous Positive Airway Pressure) is a positive airway pressure (PAP) mode delivered via a tight‑fitting face mask to a spontaneously breathing patient, Maintains a steady level of pressure during both inhalation and exhalation/ Main uses include Keeps pharyngeal/upper airway structures from collapsing (e.g., sleep apnea), Prehospital use in respiratory distress (asthma, COPD, pulmonary edema/CHF, pneumonia) to improve oxygenation and avoid intubation, Forces fluid out of alveoli in acute CHF and recruits atelectatic lung areas; PEEP (Positive End‑Expiratory Pressure) is an adjunct to ventilatory devices (bag‑valve mask, extraglottic airways, endotracheal tubes), Added via a valve between the ventilatory device and mask/airway, Provides pressure only at the end of expiration, not throughout the whole cycle/ Main uses include Prevents alveolar collapse when normal physiologic back‑pressure (like vocal cords) is bypassed by intubation, Used in premature newborns with low surfactant, and adults with ARDS, pulmonary edema, drowning, COPD, and Improves oxygenation by recruiting and maintaining alveoli that would close due to atelectasis. *PEEP = end‑expiration only; CPAP = entire respiratory cycle - PEEP = ventilated/intubated patients; CPAP = awake, spontaneously breathing patients via mask. Both create back‑pressure to keep alveoli open and improve oxygenation, but excessive pressures in either can cause barotrauma and decreased cardiac output, so both must be titrated carefully.

How does hyperventilating a patient cause hypocarbia?

Hyperventilating a patient means breathing for them too fast or too deeply, which increases minute ventilation (the total volume of air moved in and out per minute)/ Hyperventilation lowers CO₂ levels - “Hyperventilation lowers CO₂ levels and can be the result of an increased respiratory rate or deeper respiration, both of which increase the minute volume"/ Mechanism - Carbon dioxide (CO₂) is continuously produced by metabolism. Under normal ventilation, CO₂ produced = CO₂ eliminated at the alveoli/ When you hyperventilate - Each breath brings in more fresh air and washes CO₂ out of the alveoli more quickly/ Alveolar CO₂ falls, so less CO₂ remains dissolved in arterial blood/ This excessive CO₂ elimination leads to hypocapnia/hypocarbia (low PaCO₂), which can cause respiratory alkalosis (as described under respiratory alkalosis

Define the difference between hypoxia and hypoxemia? What differences in s/s pressure do you see in the patients?

*Hypoxemia = low oxygen in blood (low saturation/PaO₂) and Hypoxia = low oxygen at the tissues (can be due to hypoxemia, low hemoglobin, or poor circulation). Hypoxemia is Low oxygen level in arterial blood/ Reflected by low SpO₂ on pulse oximetry (or low PaO₂ on blood gas)/ hypoxemic patients are those with low saturation - SpO₂ below about 95% suggests hypoxemia, with severity increasing as SpO₂ falls (mild, moderate, severe hypoxemia). Hypoxia is Inadequate oxygen delivery to tissues/cells/ Can be caused by hypoxemia, but may also occur even when SpO₂ is normal, for example

What are the signs/symptoms of inadequate respirations?

Altered mental status – confusion, apprehension, agitation/ Shortness of breath while speaking – unable to speak full sentences/ Retractions – supraclavicular, suprasternal, intercostal (skin pulling in between ribs/above sternum)/ Asymmetric chest wall movement – one side moving less or differently/ Accessory muscle use – neck, intercostal, or abdominal muscles visibly working to breathe/ Cyanosis – bluish discoloration of lips, tongue, or extremities/ Audible sounds – wheezing, stridor, grunting/ Abnormally rapid, slow, or shallow breathing relative to age norms/ Nasal flaring – especially in infants and children.

Describe the term pulsus paradoxus. In what types of patients will you see this?

Pulsus paradoxus is an exaggerated drop in systolic blood pressure during inspiration, a drop of greater than 10 mmHg in the systolic blood pressure during the inspiratory phase of respiration; detect it by noting a difference of more than 10 mmHg between the pressure where Korotkoff sounds are heard only in expiration and the pressure where they are heard in both inspiration and expiration; Patients and conditions where you see this include COPD (especially emphysema), Asthma, Pericardial tamponade (classic association), Pericardial effusions, and Hypovolemia

What is the pathophysiology of a pulmonary embolus? What types of patients might experience a PE? What are the signs/symptoms of a pulmonary embolus?

a blood clot or other particle that lodges in a pulmonary artery, blocking blood flow through that vessel, Most emboli arise from deep venous thrombosis in the lower extremities (thigh/calf), When the clot travels to the lungs and occludes a pulmonary artery - The affected lung segment is still ventilated but no longer perfused, creating a ventilation–perfusion mismatch (perfusion disorder), The right heart must pump against increased resistance, raising pulmonary capillary pressure and potentially leading to right‑heart failure and cardiovascular collapse in massive PE, Overall pulmonary blood flow falls, causing hypoxemia. Patients at risk for PE include Deep venous thrombosis (prolonged immobility (bedridden, long travel), recent major surgery, fractures of pelvis/hip/leg), Atrial fibrillation, malignancy, obesity, paralysis, trauma to leg vessels, venous catheters, Pregnancy with venous pooling [use of estrogen/progestin hormones (especially smokers)], Sources of emboli - mainly blood clots, but also fat (after fractures), air (central line placement), amniotic fluid, tumor cells, and foreign bodies. Signs and symptoms of PE include Sudden onset of severe, unexplained dyspnea/ Pleuritic chest pain (sharp, worse with breathing)/ Cough, usually non‑productive, occasionally with hemoptysis/ Labored breathing, tachypnea, tachycardia/ Often normal or minimal lung sounds; sometimes rare crackles, wheezing, or a pleural friction rub/ Signs of right‑heart failure in massive PE

Describe the type of lung sounds you would hear in a spontaneous pneumothorax

side‑to‑side inequality of breath sounds (decreased or absent breath sounds over the affected side)

Describe the type of lung sounds you would hear in a tension pneumothorax

breath sounds become very faint and then absent on affected side (Percussion - Hyperresonant on the affected side; contralateral side becomes somewhat dull with progressively fainter breath sounds as tension worsens)

Describe the type of lung sounds you would hear in a asthma

Wheezing – a whistling sound due to narrowing of the airways by edema, bronchoconstriction, or foreign material

Describe the type of lung sounds you would hear in a anaphylaxis

wheezing from airway narrowing; in severe upper‑airway involvement, stridor could be heard

Describe the type of lung sounds you would hear in a croup

Stridor – a harsh, high‑pitched sound heard on inspiration, characteristic of an upper airway obstruction

Describe the type of lung sounds you would hear in a cardiac tamponade

muffled heart sounds (pericardial tamponade); lung sounds themselves are typically not the primary abnormality.

What are columnar lung sounds?

regular breath sounds/not a breath sound

Describe the pathophysiology of chronic bronchitis. Identify the signs/symptoms and treatment

Pathophysiology - Chronic overproduction of mucus narrows bronchial passages and lowers alveolar ventilation. Gas exchange decreases, causing hypoxia and hypercarbia. Elevated PaCO₂ → irritability, somnolence, headaches, personality changes, pulmonary vasoconstriction → pulmonary hypertension and cor pulmonale/ Signs/symptoms - Heavy smoking history; frequent respiratory infections; productive cough for ≥3 months/year for ≥2 years; daily sputum; overweight, cyanotic “blue bloater”; rhonchi from mucus plugs; signs of right‑heart failure (JVD, ankle edema, hepatic congestion)/ Treatment (field) - Goals are to relieve hypoxia and reverse bronchoconstriction. Give supplemental oxygen (guided by pulse oximetry), bronchodilators, monitor closely for respiratory depression, and be ready to assist ventilations.

Describe the pathophysiology of emphysema. Identify the signs/symptoms and treatment

Pathophysiology - Loss of elasticity and enlargement of alveoli (“stiffening”), requiring higher pressures for gas exchange and leading to air trapping and barrel chest. Often coexists with chronic bronchitis; together they form COPD/ Signs/symptoms - Smoking history; barrel chest, prolonged expiratory phase, rapid resting RR; thin (calories spent on breathing), pink from polycythemia “pink puffer”; hypertrophied accessory muscles; diminished breath sounds, possible wheezes/rhonchi; clubbing; possible right‑heart failure (JVD, edema)/ Treatment (field) - Same goals as chronic bronchitis—relieve hypoxia and bronchoconstriction. High‑concentration oxygen (titrated with SpO₂ and capnography), nebulized β₂‑agonists (e.g., albuterol), anticholinergics, corticosteroids; consider CPAP/BiPAP/PEEP if present; monitor closely.

Describe the pathophysiology of cystic fibrosis. Identify the signs/symptoms and treatment

Pathophysiology - Genetic exocrine disease causing chronic, copious mucus overproduction, inflammation and hyperinflation of small airways and alveoli, chronic infections, and erosion of pulmonary blood vessels. Also causes GI, pancreatic, and glucose‑intolerance problems. Leads to progressive lung damage, pulmonary hypertension, and cor pulmonale; considered terminal, with few patients living beyond ~40/ Signs/symptoms - Chronic cough with heavy mucus; recurrent infections; hemoptysis; risk of pneumothorax and severe pulmonary hemorrhage; signs of right‑heart strain/ Treatment (field) - No specific prehospital curative treatment. Supportive care

Describe the pathophysiology of myasthenia gravis. Identify the signs/symptoms and treatment

Pathophysiology - Autoantibody attack (The immune system produces abnormal IgG autoantibodies that target components of the postsynaptic neuromuscular junction), Receptor destruction (In most cases, these antibodies target nicotinic acetylcholine receptors (AChR). Other targets include muscle-specific kinase (MuSK) or LRP4), Blocked signaling (Antibodies block, alter, or destroy the acetylcholine receptors, preventing the neurotransmitter acetylcholine from binding effectively), Impaired contraction (complement activation leads to the destruction of the postsynaptic membrane architecture, reducing muscle fiber response and causing rapid muscle fatigue with repeated use)/ Signs and Symptoms - Ocular weakness (Drooping eyelids (ptosis) and double vision (diplopia) are often the first signs), Bulbar weakness (difficulty speaking (slurred or nasal speech), chewing, and swallowing (dysphagia), which can cause choking or nasal regurgitation of liquids), Facial and expression changes (trouble smiling or raising eyebrows due to quick muscle tiring), Limb and neck weakness (Weakness in the arms, hands, legs, and neck, making it hard to hold up the head or walk steadily), Fluctuating fatigue (Weakness worsens with physical activity and improves after a period of rest, often being mild in the morning and severe by the end of the day), Myasthenic crisis (A life-threatening emergency involving severe respiratory muscle weakness that impairs breathing)/ Treatment - Cholinesterase inhibitors (Medications like pyridostigmine slow down the breakdown of acetylcholine, keeping it in the neuromuscular junction longer to improve muscle strength), Immunosuppressants (Corticosteroids (such as prednisone) and non-steroid agents (such as azathioprine) reduce the immune system's production of harmful antibodies), Rapid immunotherapies (plasmapheresis (plasma exchange) or intravenous immunoglobulin (IVIG) physically remove or neutralize abnormal antibodies during severe flare-ups or crises), Thymectomy (Surgical removal of the thymus gland helps rebalance the immune system and can reduce symptoms or induce remission, especially if a thymoma (tumor) is present)

Describe the differences between left and right heart failure and how the respiratory system is affected by these conditions

Left heart failure Pathophysiology - *Left ventricular failure → direct lung involvement with pulmonary edema - crackles, labored breathing, hypoxia/ Right ventricular failure → systemic venous congestion, but often secondary to lung disease/pulmonary hypertension; respiratory symptoms may come from the underlying lung pathology or coexisting left‑sided failure, not from right failure alone* The left ventricle fails as an effective forward pump, It cannot eject all the blood delivered from the right heart via the lungs, Left atrial pressure rises, then pressure is transmitted to pulmonary veins and capillaries, When pulmonary capillary pressure becomes too high, plasma is forced into the alveoli, producing pulmonary edema, Progressive fluid accumulation in the alveoli decreases lung oxygenation capacity and can lead to death from hypoxia. Respiratory effects / signs - Dyspnea (shortness of breath), Noisy, labored breathing, Rales (crackles) at the bases from alveolar fluid, Coughing with blood‑tinged sputum, Tachypnea [adventitious lung sounds (crackles, rhonchi with more severe edema, sometimes wheezes as bronchioles constrict to limit fluid entry], End‑stage: respiratory failure. Right heart failure Pathophysiology - The right ventricle fails as an effective forward pump, so blood backs up into the systemic venous circulation → venous congestion, Commonly caused by left ventricular failure, but also by systemic hypertension, pulmonary hypertension, cor pulmonale from COPD, and pulmonary embolism (acute form of pulmonary hypertension), Chronic high pressures in pulmonary arteries from lung disease lead to right ventricular and right atrial enlargement, and eventually right heart failure. Respiratory effects / signs (indirect) - tachycardia, Neck veins engorged and pulsating (JVD), Peripheral edema (legs, body), abdominal distention/ascites, engorged liver and spleen, Right failure itself does not directly flood the alveoli like left failure; however, it frequently occurs because of chronic lung disease and pulmonary hypertension, and CHF overall can progress to pulmonary edema and respiratory failure

Describe the pathophysiology of CHF. Identify the signs/symptoms and treatment

Pathophysiology - CHF is a clinical syndrome where the heart’s mechanical performance is compromised so cardiac output cannot meet body needs, Commonly divided into left and right ventricular failure [Left ventricular failure - Left ventricle fails as a forward pump → pressure backs up into left atrium → pulmonary veins/capillaries → pulmonary capillary pressure rises → plasma forced into alveoli → pulmonary edema → hypoxia and respiratory failure/ Right ventricular failure - Leads to systemic venous congestion and peripheral edema (described generally as cor pulmonale in lung disease patients elsewhere)]/ Reduced stroke volume leads to fluid overload in tissues (pulmonary, peripheral, sacral, ascites). Signs and symptoms - Pulmonary edema, Tachypnea, labored/noisy breathing, Crackles at lung bases; rhonchi when fluid reaches larger airways; wheezes (“cardiac asthma”) as bronchioles constrict to protect lungs, Cough with clear or pink‑tinged frothy sputum, Progressive or acute shortness of breath, especially paroxysmal nocturnal dyspnea (PND); pillow orthopnea (needing multiple pillows to sleep), Fluid overload/poor perfusion, Peripheral edema (ankles to mid‑calf/knees), possible sacral edema; pitting 0–4+, Mottling, pallor, diaphoresis, cyanosis, Jugular venous distention; abnormal/alternating pulses (pulsus alternans, pulsus paradoxus), Cardiac history (Prior MI, cardiomegaly, hypertension, valvular disease, arrhythmias), Mild chest pain or generalized weakness from ischemia or MI, Decompensation (Blood pressure often elevated but can drop quickly in decompensation, Altered or decreased level of consciousness indicates impending respiratory failure). Treatment - Do not have the patient lie flat, Seat upright with feet dangling to promote venous pooling and decrease preload; avoid exertion (no standing/walking), Check ABCs and treat life threats, for severe pulmonary edema or respiratory failure - assist breathing with 100% oxygen via BVM, prepare for intubation if indicated, CPAP/BiPAP can be very beneficial for acute CHF to improve oxygenation and push fluid out of alveoli, review current medications and check compliance, Monitor blood pressure, heart rate, rhythm, oxygen saturation, and look for rapid changes, Ongoing assessment/Reassess/Document edema pattern, respiratory findings, and progression of dyspnea

Describe the pathophysiology of pulmonary hypertension. Identify the signs/symptoms and treatment

Pathophysiology - Pulmonary hypertension is elevated pulmonary artery pressure (often from chronic lung disease or PE) that leads to right‑heart strain and failure. Clinically you see signs of right‑sided congestion (JVD, edema, hepatosplenomegaly, ascites), plus dyspnea and hypoxia when associated with PE or CHF. Field management focuses on oxygenation, support of ventilation and circulation, and rapid transport for definitive care, guided by the underlying cause Pulmonary hypertension is described as increased pressure in the pulmonary arteries, In chronic lung disease (especially COPD), ventilation–perfusion problems and hypoxia lead to pulmonary vasoconstriction, raising pressures in the pulmonary arterial tree, Over time, this chronic high pulmonary arterial pressure (Makes the right ventricle pump against increased resistance), Causes right ventricular enlargement and right atrial enlargement, If untreated, progresses to right heart failure (cor pulmonale), Pulmonary embolism is described as essentially an acute form of pulmonary hypertension

Describe the pathophysiology of cor pulmonale. Identify the signs/symptoms and treatment

Pathophysiology - heart failure due to pulmonary disease, chronic lung disease (most commonly COPD) causes pulmonary hypertension—increased pressure in the pulmonary arteries, Over time, that high pressure forces the right ventricle to pump against increased resistance, leading to - Right ventricular enlargement, Right atrial enlargement, Eventual right ventricular failure (right heart failure) with systemic venous congestion, So cor pulmonale is essentially right‑sided heart failure secondary to chronic pulmonary disease–induced pulmonary hypertension. Signs and symptoms - Tachycardia, Neck veins engorged and pulsating (JVD), Edema of body and lower extremities, Engorged liver and spleen, Abdominal distention/ascites, Pulmonary edema can coexist if overall CHF is present, with tachypnea, crackles, rhonchi, and wheezes. Treatment - care follows CHF/right‑heart failure principles - Do not lay the patient flat, Seat upright with feet dangling to promote venous pooling and decrease preload, Assess ABCs; treat life threats, If pulmonary edema or respiratory failure is present

Describe the pathophysiology of pneumonia. Identify the signs/symptoms and treatment

Pathophysiology - an infection of the lungs caused by bacterial, viral, fungal, or other agents, It is especially common and deadly in the very young, elderly, and immunocompromised (HIV, cancer, immunosuppressive therapy), Normally, mucus and ciliary action protect the respiratory tract - here there is defect in mucus production, ciliary function, or both, allowing pathogens to invade, infection begins in one lung region and can spread to nearby alveoli, sometimes involving an entire lobe or both lungs (bronchopneumonia, lobar, or interstitial patterns), As disease progresses, fluid and inflammatory cells collect in alveoli and alveolar collapse can occur, described as primarily a ventilation disorder - infected, fluid‑filled, or collapsed alveoli ventilate poorly, impairing gas exchange, Infection can extend into the bloodstream, potentially causing septic shock. Signs and symptoms - Typical community‑acquired bacterial pneumonia = Acute onset of Chills (often described as “bed shaking”), High‑grade fever (but fever can be absent, especially in geriatrics), Dyspnea, Pleuritic chest pain (worse with deep inspiration), Productive cough with phlegm (yellow–brown, possibly blood‑streaked), Patients generally appear ill, with generalized weakness and malaise, If lower lobes are involved, chief complaint can be upper abdominal pain. Physical exam includes finding Fever, tachypnea, tachycardia, and possible respiratory distress, auscultation

What classification of medication does the patient receive if they use their MDI? What is the therapeutic purpose of this medication? What symptoms would a patient present that indicate they should use their MDI inhaler? What side effects might the paramedic see after usage?

used mainly to deliver inhaled beta‑agonist bronchodilators (e.g., albuterol, metaproterenol, levalbuterol) for asthma and COPD. therapeutic purpose - Inhaled beta‑agonist bronchodilator (delivered by MDI or nebulizer), correct hypoxia (by improving airflow and ventilation), Reverse bronchospasm (relax bronchial smooth muscle, open narrowed airways), Help decrease inflammation as part of overall asthma/COPD management (often combined with steroids per medical direction). Symptoms are for Patients with asthma or COPD who - Have bronchospasm with wheezing, dyspnea, and difficulty speaking in full sentences, Are experiencing an acute asthma attack or COPD exacerbation with increased work of breathing (For severe acute emergencies, the text recommends a nebulizer rather than MDI because it delivers more medication). Side effects - Oral thrush, hoarseness, sore throat, tremors, heart palpatations, muscle cramps, headaches, renal insufficiency, bone thinning, vision changes

What can the paramedic do to improve alignment of an infant's airway when they are lying supine?

because trachea is softer and more flexible, hyperextension of the neck can collapse the trachea - To optimize airway alignment while avoiding collapse - Avoid hyperextension of the neck. Open the airway gently/ For trauma patients less than 3 years old, when supine, place support under the upper torso or shoulders (not under the head). This helps bring the airway into a neutral/sniffing alignment without over‑flexing or extending the neck/ Keep the nares clear in infants under 6 months (they are obligate nose breathers).

What is the anatomical difference between an infant's and an adult's airway?

Narrower airways at all levels → more easily blocked by secretions/obstructions, Obligate nose breathers (infants) - blocked nose can cause significant distress because they don’t automatically switch to mouth breathing, Proportionally larger tongue in infants/children → more easily occludes the airway when unconscious, Softer, more flexible trachea → can collapse if the neck/head is hyperextended, Higher larynx (around C3–C4) that extends into the pharynx, Cricoid ring is the narrowest part of the pediatric airway (below the cords), whereas in adults the vocal cords level is functionally narrowest, Omega‑shaped, floppier epiglottis in infants, extending at a 45° angle into the airway, more funnel‑shaped, with smaller, more flexible structures than the cylindrical adult airway

How does the body compensate for a diminished tidal volume?

increasing the respiratory rate

What anatomical structure constricts during an asthma attack?

bronchioles