Abnormal Ventilation and Major Respiratory Emergencies

Hypoventilation and Hyperventilation Disorders

Overview

Hyperventilation and hypoventilation can occur as signs of many different medical emergencies. Their causes can range from relatively mild conditions, such as anxiety, to serious and potentially life-threatening problems, including pulmonary embolism or respiratory failure.

Because abnormal ventilation may indicate significant underlying illness, EMS providers must recognize the pattern of breathing, identify possible causes, and provide appropriate treatment based on the patient’s overall condition.

Key Topics

This section focuses on several important respiratory concepts, including:

Anatomy of the Respiratory System

The respiratory system contains structures that allow air to travel from the outside environment into the lungs, where oxygen and carbon dioxide can be exchanged.

The airway is generally divided into the upper airway and lower airway.

Upper Airway Structures

Nasal Cavity

The nasal cavity is one of the uppermost portions of the respiratory tract and serves as an important passage for inhaled and exhaled air.

Important anatomical features include:

Oral Cavity

The oral cavity, or mouth, provides another pathway for airflow into the respiratory tract.

Its major structures include:

The mouth can serve as an important alternative airway passage, particularly when airflow through the nose is limited or when airway management procedures are required.

Pharynx

The pharynx is a muscular passage extending from the area behind the nasal and oral cavities toward the esophagus and larynx.

It serves as a shared pathway for air and swallowed substances and allows air to move between the upper airway and the lower respiratory tract.

The pharynx is divided into three primary regions.

Nasopharynx

The nasopharynx is the highest portion of the pharynx.

Oropharynx

The oropharynx is located behind the oral cavity.

Laryngopharynx

The laryngopharynx is especially important in airway assessment and management.

Larynx

The larynx is a complex structure that connects the pharynx with the trachea.

It is located near the midline of the neck, below the hyoid bone and anterior to the esophagus.

The larynx plays several important roles, including:

Major structures of the larynx include:

Understanding these structures is particularly important during airway assessment, ventilation, and advanced airway procedures.

Anatomy of the Lower Respiratory Tract

The lower airway begins below the larynx and includes the structures that conduct air into the lungs, where gas exchange eventually occurs.

Trachea

The trachea is the first major structure of the lower respiratory tract.

Carina

The carina is the point where the trachea divides into the right and left mainstem bronchi.

Right Mainstem Bronchus

Left Mainstem Bronchus

Alveoli

The alveoli are microscopic air sacs located at the terminal ends of the bronchioles.

Lung Lobes

The lungs are divided into sections called lobes, and the number of lobes differs between the right and left lungs.

Right Lung

The right lung is divided into three lobes:

Left Lung

The left lung contains two lobes:

The left lung is slightly smaller than the right because it shares space within the chest with the heart.

Pleura

The pleura are thin layers of membranous connective tissue that surround the lungs and line the inside of the thoracic cavity.

There are two primary pleural layers.

Visceral Pleura

The visceral pleura directly covers the outer surface of the lungs.

Parietal Pleura

The parietal pleura lines the inner surface of the thoracic cavity.

Pleural Space

The small potential space between the visceral and parietal pleura is known as the pleural space.

Respiration and Ventilation

Although the terms respiration and ventilation are sometimes used interchangeably, they describe different processes.

Respiration

Respiration refers to the exchange of gases between a living organism and its environment.

In the lungs, pulmonary respiration occurs when oxygen and carbon dioxide move between the alveoli and the blood within the pulmonary capillaries.

Ventilation

Ventilation is the mechanical movement of air into and out of the lungs.

Normal ventilation consists of two phases:

The movement of air depends largely on changes in pressure within the thoracic cavity.

The Normal Respiratory Cycle

Normal breathing occurs through a coordinated sequence of pressure changes, respiratory muscle activity, and lung expansion.

1. Resting Position

At the end of a normal exhalation, pressure inside the lungs is approximately equal to atmospheric pressure, so there is no significant movement of air.

2. Respiratory Stimulation

Respiratory centers in the brainstem send signals through the phrenic nerve to stimulate the diaphragm.

3. Diaphragm Contraction

The diaphragm contracts and moves downward.

This increases the volume of the thoracic cavity and decreases intrathoracic pressure.

4. Air Enters the Lungs

When pressure inside the thorax falls below atmospheric pressure, air is drawn through the airway and into the lungs.

This pressure difference allows inhalation to occur.

5. Lung Expansion

The visceral and parietal pleura normally remain closely opposed to each other.

As the chest wall expands, the lungs follow the movement of the thoracic cavity and expand with it.

6. Alveolar Inflation

Air entering the lungs travels through the conducting airways until it reaches the alveoli, causing them to expand.

7. Gas Exchange

As the alveoli expand, their thin walls remain closely associated with the surrounding pulmonary capillaries.

Oxygen and carbon dioxide diffuse across the alveolar-capillary membrane according to their partial-pressure gradients.

8. End of Inspiration

As the lungs fill, pressure inside the alveoli eventually becomes equal to atmospheric pressure again.

At this point, airflow into the lungs stops.

9. Limiting Excessive Inflation

Stretch receptors within the lungs can send signals through the vagus nerve that help inhibit further inspiration when the lungs become sufficiently expanded.

This protective response contributes to preventing excessive lung inflation.

10. Beginning of Exhalation

At the end of inspiration, the diaphragm and other inspiratory muscles relax.

The thoracic cavity becomes smaller, causing pressure within the lungs to rise above atmospheric pressure.

11. Air Leaves the Lungs

The natural elastic recoil of the lungs pushes air outward through the airways.

This process is known as exhalation or expiration.

Exhalation continues until pressures inside and outside the lungs equalize again.

Minute Ventilation

One useful way to understand hyperventilation and hypoventilation is by examining minute ventilation, which represents the total amount of air moved into or out of the respiratory system during one minute.

Minute ventilation is calculated as:

Minute Ventilation = Tidal Volume × Respiratory Rate

Where:

Changes in either respiratory rate or tidal volume can significantly alter overall ventilation.

Hyperventilation

Hyperventilation occurs when ventilation exceeds the body’s metabolic need for carbon dioxide removal.

It may involve an increased respiratory rate, increased depth of breathing, or both.

The general sequence is:

Increased alveolar ventilation → Increased carbon dioxide elimination → Decreased blood carbon dioxide levels → Respiratory alkalosis

When excessive carbon dioxide is removed from the bloodstream, the blood becomes more alkaline.

An increased metabolic rate can also stimulate increased ventilation because the body may produce greater amounts of carbon dioxide and require additional oxygen.

Hyperventilation Syndrome

Hyperventilation syndrome refers to excessive ventilation that is often associated with anxiety, fear, emotional distress, or panic when no primary pulmonary abnormality adequately explains the symptoms.

The respiratory centers in the brain may become stimulated, causing the patient to breathe faster or deeper than necessary.

Patients may complain of:

However, providers should not automatically assume that rapid breathing is caused by anxiety. Serious medical conditions must be considered and excluded whenever appropriate.

Causes of Hyperventilation

Hyperventilation can develop from many different conditions.

Emotional Causes

Possible emotional triggers include:

Metabolic Conditions

Certain metabolic disorders can stimulate increased ventilation, particularly when the body attempts to compensate for abnormal acid-base conditions.

Examples may include:

Medical Conditions

Medical causes may include:

Environmental Causes

Environmental conditions that may increase ventilation include:

Fever and Increased Metabolism

Fever and hyperthyroidism can increase the body’s metabolic rate.

As cellular metabolism rises, oxygen demand and carbon dioxide production may also increase. The respiratory system may respond by increasing ventilation.

Liver Failure and Hyperventilation

Severe liver dysfunction can lead to accumulation of substances such as ammonia and other metabolic abnormalities.

These changes may stimulate the respiratory centers and contribute to hyperventilation.

When excessive carbon dioxide is eliminated because of increased ventilation, the patient may develop respiratory alkalosis rather than metabolic alkalosis.

Effects of High Altitude on Ventilation

At higher elevations, atmospheric pressure decreases. As a result, the partial pressure of oxygen is lower and less oxygen is available to move into the bloodstream with each breath.

The body initially compensates by increasing ventilation, which may include a faster or deeper breathing pattern.

Over time, additional physiologic adaptations can occur, including increased production of red blood cells to improve oxygen-carrying capacity.

Symptoms caused by altitude exposure may improve through:

Hypoventilation

Hypoventilation occurs when ventilation is inadequate to remove the amount of carbon dioxide being produced by the body.

Although a slow respiratory rate can cause hypoventilation, respiratory rate alone does not determine whether ventilation is adequate. A patient can also hypoventilate with a normal respiratory rate if breaths are too shallow or ineffective.

The general process is:

Decreased alveolar ventilation → Increased carbon dioxide retention → Rising PaCO₂ or ETCO₂ → Respiratory acidosis

As carbon dioxide accumulates in the bloodstream, blood becomes increasingly acidic.

Common Causes of Hypoventilation

Hypoventilation may result from problems involving the brain, airway, chest wall, or lungs.

Possible causes include:

Respiratory Acidosis

Hypoventilation can lead to respiratory acidosis when the lungs are unable to remove carbon dioxide at the same rate that it is being produced through cellular metabolism.

As carbon dioxide accumulates:

Respiratory acidosis therefore commonly involves:

Elevated carbon dioxide + decreased blood pH

The severity of the condition depends on how rapidly carbon dioxide accumulates, the underlying cause, and the body’s ability to compensate.

Recognizing Abnormal Ventilation

Evaluation should include respiratory rate, depth, effort, mental status, oxygenation, capnography when available, and the overall clinical presentation.

Normal Adult Values

Typical values for a resting adult include:

These ranges should be interpreted together with the patient’s condition rather than used alone.

Findings Consistent With Hyperventilation

Hyperventilation commonly produces excessive carbon dioxide elimination.

Typical findings may include:

Respiratory Alkalosis

Excessive carbon dioxide loss decreases carbonic acid in the bloodstream.

As a result:

Findings Consistent With Hypoventilation

Hypoventilation results from inadequate alveolar ventilation rather than simply a respiratory rate below a specific number.

Possible findings include:

Respiratory Acidosis

When ventilation is inadequate, carbon dioxide accumulates.

As a result:

Symptoms Associated With Hyperventilation

Patients who are hyperventilating may experience:

Because serious conditions can also cause rapid breathing, hyperventilation should not automatically be assumed to be anxiety-related.

Symptoms Associated With Hypoventilation

Patients with inadequate ventilation may develop:

Progressive hypoventilation may eventually result in respiratory failure or respiratory arrest.

Assessment and Management of Abnormal Ventilation

Primary Assessment

Begin with the ABCs: airway, breathing, and circulation.

Airway

Determine whether the airway is open and clear.

Listen for signs of obstruction such as:

If airway positioning is required:

Suction the airway when secretions, blood, or vomitus are interfering with airflow.

Breathing

Determine whether the patient’s breathing is adequate.

Assess:

Patients with inadequate respiratory drive or ineffective ventilation may require assisted ventilation.

Ventilatory Support

Depending on the patient’s condition, treatment may include:

Oxygen and ventilatory support should be adjusted to maintain adequate oxygenation and ventilation according to the patient’s condition and local protocol.

Capnography can help guide ventilation, with an ETCO₂ near the normal physiologic range often used as one component of reassessment.

Airway Adjuncts

Patients who require assisted ventilation or have a decreased level of consciousness may benefit from an airway adjunct when appropriate.

Options include:

The device selected depends on the patient’s level of consciousness, gag reflex, and potential contraindications.

Advanced Airway Management

At the paramedic or advanced-provider level, endotracheal intubation or another advanced airway may be considered when:

Additional Treatment Considerations

Supplemental oxygen should never be intentionally withheld from a genuinely hypoxemic patient who needs it.

Hyperventilation and Paper Bags

Patients who are hyperventilating should not be instructed to breathe into a paper bag.

Although rebreathing exhaled air can increase carbon dioxide levels, it can also reduce available oxygen and worsen an unrecognized medical problem.

Rapid breathing can occur with serious illnesses such as:

For this reason, treatment should focus on identifying the cause, reassuring the patient when appropriate, and correcting any underlying medical problem.

Transport for medical evaluation should be encouraged when symptoms are significant, persistent, unexplained, or associated with concerning findings.

Secondary Assessment

After immediate threats to the airway, breathing, and circulation have been addressed, perform a more detailed assessment.

Patient History

Obtain history from the patient whenever possible.

If the patient cannot provide reliable information, obtain additional details from:

Important information may include:

Physical Examination

Respiratory patients require repeated evaluation of the airway, breathing, and circulation.

The physical examination should include inspection, auscultation, and palpation.

Inspection

Observe the patient for:

Tripod Position

A patient in the tripod position typically sits or leans forward while supporting the upper body with the hands or elbows.

This position may help recruit accessory muscles and can indicate significant respiratory distress.

Orthopnea

Orthopnea refers to difficulty breathing while lying flat.

Patients may report that their breathing improves when they sit or stand upright.

Auscultation

Listen carefully for movement of air.

Begin by assessing airflow at the mouth and nose, then auscultate the chest systematically and compare both sides.

Important areas include:

Listen for abnormalities such as:

Any abnormal finding should be interpreted together with the patient’s history and overall respiratory presentation.

Palpation

Palpate the chest to assess:

Abnormal findings may suggest trauma, pneumothorax, rib injury, or another condition contributing to inadequate ventilation.

Pulmonary Edema: Recognition, Causes, and Management

Overview

Pulmonary edema is the abnormal accumulation of fluid within the lung tissue and alveolar spaces.

This occurs when fluid moves out of the pulmonary blood vessels and into the surrounding lung tissue or alveoli. As fluid builds up, the distance between inhaled oxygen and the pulmonary capillaries increases, making gas exchange more difficult.

Pulmonary edema is commonly associated with congestive heart failure (CHF), although several noncardiac conditions can also produce it.

Pathophysiology

Pulmonary edema can generally be divided into two major categories:

Cardiogenic Pulmonary Edema

Cardiogenic pulmonary edema commonly develops when the heart cannot pump blood effectively.

Possible causes include:

Coronary artery disease is one of the most common underlying causes of heart failure.

When ventricular pumping ability declines, cardiac output may decrease. Blood remaining within the ventricle increases filling pressure, which can eventually cause blood to back up into either the pulmonary or systemic circulation.

Left-Sided Heart Failure

When the left ventricle fails to pump blood forward effectively:

Left-sided heart failure therefore commonly produces significant respiratory symptoms.

Right-Sided Heart Failure

When the right ventricle cannot pump blood effectively into the pulmonary circulation:

Common findings may include:

Right-sided and left-sided heart failure can occur together.

Compensation in Chronic Heart Failure

Patients with chronic CHF may develop several compensatory mechanisms that temporarily help maintain circulation despite reduced cardiac function.

The body may attempt to improve cardiac output by altering:

Although these mechanisms may initially support blood pressure and perfusion, they can eventually increase the workload of the heart and contribute to worsening heart failure and fluid retention.

Noncardiogenic Pulmonary Edema

Noncardiogenic pulmonary edema occurs when the alveolar-capillary membrane becomes damaged or unusually permeable.

Fluid can then leak into the lung tissue even when heart failure is not the primary problem.

Possible causes include:

Damage to the alveoli and pulmonary capillaries can produce severe hypoxemia because fluid interferes with normal oxygen diffusion.

Recognizing Pulmonary Edema

The clinical presentation may vary depending on the cause and severity.

General Signs and Symptoms

Possible findings include:

Some patients may report that symptoms worsened following travel, exertion, medication changes, infection, or other recent events.

Orthopnea

Orthopnea is shortness of breath that becomes worse when the patient lies flat.

Patients may prefer to sit upright or sleep with several pillows because an elevated upper body often improves breathing.

Lung Sounds

Pulmonary edema commonly produces abnormal breath sounds.

Crackles

Crackles often begin in the lower lung fields and may progress upward as fluid accumulation becomes more severe.

Crackles may indicate that fluid has moved from the pulmonary circulation into the interstitial tissues or alveoli.

As this occurs:

Wheezing

Some patients with heart failure may also develop wheezing.

This presentation is sometimes referred to as cardiac asthma, although it is caused by heart failure and pulmonary congestion rather than primary asthma.

Signs of Right-Sided Heart Failure

Findings associated with systemic venous congestion may include:

Cardiogenic Shock

Severe heart failure, pulmonary edema, or myocardial infarction may result in cardiogenic shock when the heart can no longer provide adequate cardiac output to support tissue perfusion.

Possible findings include:

Acute Pulmonary Congestion

Patients with significant pulmonary congestion may demonstrate:

Pink or blood-tinged frothy sputum can occur in severe pulmonary edema and should be considered a concerning finding.

Prehospital Treatment

The major goals of prehospital management are to:

Calm reassurance can also help reduce anxiety and unnecessary sympathetic stress.

Initial EMS Management

Management should be based on the patient’s presentation and local protocols.

Important steps may include:

Oxygen Therapy

Supplemental oxygen should be administered when the patient is hypoxemic or demonstrates inadequate oxygenation.

Oxygen should generally be titrated to the patient’s clinical condition and local protocol rather than administered automatically at maximum concentration to every patient.

Positive-Pressure Ventilation

For alert patients with moderate to severe respiratory distress, noninvasive positive-pressure ventilation may provide significant benefit.

Options may include:

These therapies may help by:

Blood pressure should be monitored closely because positive-pressure ventilation can reduce preload and may worsen hypotension in some patients.

Blood Pressure Considerations

Many protocols consider positive-pressure ventilation and vasodilator therapy when systolic blood pressure is adequate.

Patients with pulmonary edema who are significantly hypotensive may require a different treatment approach because aggressive reduction in preload or blood pressure can worsen perfusion.

Treatment should therefore be guided by blood pressure, overall perfusion, and local medical direction.

Suspected Acute Coronary Syndrome

When pulmonary edema appears related to myocardial ischemia or acute coronary syndrome, EMS providers should evaluate and manage the patient according to applicable ACS protocols.

This may include:

In-Hospital Evaluation

Hospital assessment may include:

Blood Gas Testing

Arterial or venous blood gas measurements can provide information about:

Brain Natriuretic Peptide

BNP or related natriuretic peptide testing may support the diagnosis of heart failure when the cause of the patient’s respiratory symptoms is uncertain.

Results must be interpreted together with the patient’s history, examination, and other diagnostic findings.

Hemodynamic Monitoring

In critically ill patients, invasive monitoring may sometimes be used to evaluate pressures within the cardiovascular system.

This information can help determine:

Fluid Removal Therapy

Patients with significant fluid overload may receive diuretics or other fluid-removal treatments.

In selected patients, ultrafiltration or aquapheresis may be used to remove excess fluid when conventional treatment is inadequate or inappropriate.

Advanced Cardiac Support

Patients with severe heart failure or cardiogenic shock may require mechanical circulatory support.

Depending on the clinical situation, options may include:

Some patients with severe chronic heart failure and markedly reduced ejection fraction may also be considered for implanted cardiac devices depending on their underlying condition and expected prognosis.

Important Medication Consideration

Older treatment approaches sometimes included routine morphine administration for acute pulmonary edema or CHF.

Morphine is no longer routinely recommended solely for pulmonary edema because it may cause respiratory depression, hypotension, and other adverse effects. Its use should be limited to specific indications and local protocols rather than considered a standard treatment for acute CHF.

Pulmonary Embolism: Development, Effects, and Clinical Significance

Overview

An acute pulmonary embolism (PE) is a potentially life-threatening emergency that occurs when a blood clot or other embolic material travels into the pulmonary circulation and blocks blood flow through one or more pulmonary arteries.

Pulmonary embolism can range from a small obstruction with subtle symptoms to a massive event resulting in severe shock or sudden cardiac arrest.

Because the presentation is not always obvious, EMS providers should maintain a high level of suspicion when a patient’s history, risk factors, and symptoms suggest the possibility of PE.

Prehospital management primarily focuses on supporting:

Treatment should remain within the provider’s scope of practice and follow local protocols.

How Pulmonary Embolism Develops

Deep Vein Thrombosis

A deep vein thrombosis (DVT) occurs when a blood clot forms within a deep vein.

DVTs most commonly develop in the lower extremities, although they can occur in other parts of the body.

A clot may remain attached to the vessel wall or a portion may break free and begin traveling through the bloodstream.

Formation of an Embolus

When part or all of a clot separates from its original location and travels through the circulation, it becomes an embolus.

A clot originating in the lower extremity generally follows this pathway:

  1. The embolus travels through the veins of the leg.
  2. It enters the inferior vena cava (IVC).
  3. It reaches the right atrium.
  4. It moves through the right ventricle.
  5. It is pumped into the pulmonary artery.
  6. It continues through the pulmonary circulation until it becomes lodged in a vessel that is too small for it to pass through.

Once trapped, the embolus partially or completely blocks blood flow to a portion of the lungs.

Pathophysiology of Pulmonary Embolism

The severity of PE depends largely on:

Small Pulmonary Emboli

A small clot may block a relatively small peripheral pulmonary artery.

The patient may experience mild or nonspecific symptoms, and some small emboli may initially be difficult to recognize.

Multiple small emboli can also occur at the same time and obstruct several pulmonary vessels.

Large Pulmonary Emboli

A larger clot may obstruct one of the major pulmonary arteries, significantly reducing blood flow through the lungs.

This can rapidly cause:

Saddle Pulmonary Embolism

A saddle embolus is a large clot positioned near the point where the main pulmonary artery divides into the right and left pulmonary arteries.

A large saddle embolus can interfere with blood flow to both sides of the pulmonary circulation and may produce sudden cardiovascular collapse.

However, the term “saddle embolus” describes the clot’s location and does not by itself determine the patient’s exact clinical severity.

Respiratory Effects

When a pulmonary artery is blocked, blood can no longer adequately reach the alveoli supplied by that vessel.

The affected region of the lung may continue to receive air but receives little or no blood flow.

This creates a ventilation-perfusion mismatch.

Increased Dead Space

A ventilated area of lung that receives inadequate blood flow contributes to physiologic dead space.

In this situation:

As a result, the patient may develop:

Patients often increase their respiratory rate in an attempt to compensate.

Pulmonary Infarction

If blood flow remains significantly reduced for a prolonged period, a portion of lung tissue may become injured or infarcted.

A pulmonary infarction can contribute to:

Cardiovascular Effects

A large PE can produce major changes in the cardiovascular system.

When a clot significantly obstructs pulmonary blood flow, resistance within the pulmonary circulation rises suddenly.

The right ventricle must then pump against much greater resistance.

Obstructive Shock

A massive pulmonary embolism can cause obstructive shock.

The physical obstruction prevents normal forward movement of blood through the pulmonary circulation.

This results in:

Right Ventricular Strain and Failure

The right ventricle is not designed to pump against sudden, severe increases in pulmonary vascular resistance.

As pressure increases, the right ventricle may dilate and begin to fail.

Possible findings associated with significant right ventricular strain include:

Peripheral edema and abdominal fluid accumulation are more commonly associated with longer-standing right-sided heart failure and may not develop during a sudden acute PE.

Interventricular Septal Shift

As the right ventricle becomes severely enlarged, it can push the interventricular septum toward the left ventricle.

This reduces the amount of space available for the left ventricle to fill.

Reduced left ventricular filling leads to:

If the obstruction is severe and circulation cannot be maintained, the patient may progress to cardiovascular collapse and cardiac arrest.

Recognizing and Managing Suspected Pulmonary Embolism

Clinical Recognition

Pulmonary embolism can present in many different ways, which makes it difficult to confirm in the prehospital setting.

Patients may complain of:

Physical examination may reveal:

Relevant Medical History

A thorough history may reveal previous or current risk factors for venous thromboembolism.

Important findings may include:

A classic presentation may involve a patient with known risk factors who suddenly develops shortness of breath and pleuritic chest pain.

Additional findings may include hemoptysis or signs of obstructive shock.

However, patients do not always present with this full pattern. Some may have only mild or nonspecific symptoms, and EMS providers often cannot determine the exact cause of the patient’s condition in the field.

Stable and Unstable Pulmonary Embolism

Determining whether the patient has significant hemodynamic compromise is important because it helps identify severity.

Hemodynamically Stable Patient

A patient with a suspected PE may be considered relatively stable when:

Smaller emboli are more likely to present this way, although clinically significant PE can still be present.

Even patients who appear stable should be transported for further evaluation because a PE cannot be ruled out based on field assessment alone.

Hemodynamically Unstable Patient

An unstable patient demonstrates evidence of significant circulatory compromise.

Possible findings include:

For example, a patient whose blood pressure falls from 140/90 mmHg to 98/40 mmHg has experienced a significant reduction in perfusion and should be considered concerning for major hemodynamic compromise.

Hospital Evaluation

Any patient with findings suspicious for PE should be transported to a facility capable of diagnostic testing.

Hospital evaluation may include:

CT pulmonary angiography is commonly used to evaluate the pulmonary arteries for emboli in patients who are appropriate candidates for contrast-enhanced imaging.

Prehospital Treatment and Management

Management should begin with assessment and stabilization of the airway, breathing, and circulation.

Airway

Ensure that the airway remains open and protected.

Provide airway positioning, suctioning, or airway adjuncts if necessary.

Breathing

Assess:

Supplemental oxygen should be administered when the patient is hypoxemic or according to local protocol.

Patients with inadequate ventilation may require assisted ventilation using a bag-valve mask.

Circulation

Evaluate:

Treat shock supportively and reassess frequently.

Transport Priority

Rapid transport is appropriate when the patient demonstrates serious findings such as:

The receiving hospital should be capable of providing advanced diagnostic and definitive treatment whenever possible.

Chest Pain and Aspirin Considerations

Because chest pain from pulmonary embolism can resemble acute coronary syndrome, myocardial ischemia should remain part of the differential diagnosis.

Aspirin may be appropriate when the patient has symptoms consistent with suspected acute coronary syndrome and no contraindications, according to local protocol.

Aspirin is not a specific treatment for pulmonary embolism, so it should not be administered solely because PE is suspected.

ALS Involvement

Advanced Life Support should be considered when available, particularly for patients with:

However, transport should not be unnecessarily delayed while waiting for ALS when definitive care is available at the hospital.

An ALS intercept may be appropriate when it can occur without significantly delaying transport.

Definitive Hospital Treatment

Definitive treatment for PE occurs in the hospital and depends on the patient’s stability, clot burden, and overall risk.

Treatment may include:

The specific treatment plan depends on the patient’s severity, bleeding risk, underlying conditions, and available hospital resources.

Pneumonia: Causes, Development, Recognition, and Diagnosis
Understanding Pneumonia

Pneumonia is an infection of the lower respiratory tract that commonly affects the bronchi, bronchioles, and alveoli.

The infection may be caused by:

Regardless of the organism responsible, pneumonia commonly produces inflammation and irritation within the lower airways. As the infection progresses, swelling, mucus, and fluid accumulation may interfere with normal ventilation and gas exchange.

Pneumonia Statistics

According to the American Thoracic Society and related sources:

How Pneumonia Affects the Respiratory System

Pneumonia primarily develops within the lower airway and lung tissue.

The process generally occurs as follows:

  1. Bacteria, viruses, fungi, or other infectious organisms enter the respiratory tract.
  2. The organisms travel deeper into the lungs and may reach the alveoli.
  3. The immune system recognizes the microorganisms as foreign and begins an inflammatory response.
  4. Inflammation causes swelling, airway irritation, mucus production, and fluid accumulation.
  5. Fluid and inflammatory material may collect within the alveoli.
  6. Normal airflow and gas exchange become less efficient.
  7. Oxygenation may decrease as more lung tissue becomes involved.

The degree of respiratory impairment depends on the severity and location of the infection, the patient’s overall health, and the amount of lung tissue affected.

Common Causes of Pneumonia

Pneumonia is generally associated with three major categories of infection.

Classification by Source of Infection

Community-Acquired Pneumonia

Community-acquired pneumonia (CAP) develops outside hospitals or other healthcare facilities.

Transmission or exposure may occur through:

Environmental factors that may increase respiratory risk include:

Risk Factors for Community-Acquired Pneumonia

Certain medical conditions and patient characteristics may increase the likelihood of pneumonia, including:

Hospital-Associated Pneumonia

Ventilator-associated pneumonia (VAP) is a form of pneumonia associated with invasive mechanical ventilation.

Risk Factors for Hospital- and Ventilator-Associated Pneumonia

Factors that may increase the likelihood of HAP or VAP include:

Recognizing Pneumonia

The signs and symptoms of pneumonia vary depending on the patient, infectious organism, severity of disease, and amount of lung involvement.

Common Signs and Symptoms

Patients may experience:

Respiratory examination may reveal:

Pneumonia in Older Adults

Older adults may not always demonstrate the classic signs of infection.

Instead of developing a high fever, some geriatric patients may have:

A sudden change in mental status in an older adult may sometimes be an important early sign of infection.

Pneumonia in Pediatric Patients

Children with pneumonia may demonstrate additional respiratory findings, including:

Infants and younger children can deteriorate rapidly, so changes in respiratory effort, color, mental status, and oxygenation require careful attention.

Potential Complications

Severe pneumonia can lead to significant and potentially life-threatening complications.

These may include:

As infection and inflammation worsen, oxygenation may become increasingly impaired and the patient may require advanced respiratory support.

Diagnosing Pneumonia

Confirming pneumonia generally requires a combination of patient history, physical assessment, laboratory testing, and diagnostic imaging.

Physical Assessment

Evaluation commonly includes:

Medical History

Important history may include:

Laboratory Testing
Hospital evaluation may include:

Pneumonia Care and Management

Prehospital Care

Hospital Management