Conducting Airways

Extra-Thoracic

Intrathoracic

Respiratory Zone

Keeps smooth muscle areas open

Factors that relax smooth muscles in bronchi and bronchioles

Contraction of bronchiolar smooth muscle and bronchoconstriction

Contraction of bronchiolar smooth muscle and bronchoconstriction

Contraction of bronchiolar smooth muscle and bronchoconstriction

Small changes in diameter increases difficulty of breathing

Increases suction pulling lungs with ribs (normally -5, when chest expands decreases to -7.5)

Measure pressure of respiratory tree when glottis is open = atmospheric pressure (0 cm H2O)

Alveolar Pressure

Difference between pleural and alveolar pressures

Elastic forces that cause lung collapse at end of exhalation are counteracted by PEEP, surfactant, and closed glottis

Breach of pleural spaces, air gets trapped, lung can’t expand because pleural space becomes equivalent to alveolar/atmospheric pressure (change from -4 to 0 mmHg)

Patient comes in to the clinic with dyspnea, tachycardia, deviated trachea, decreased breath sounds on affected side, hyperresonance to percussion.

Increased Resistance Curve

Decreased Compliance Curve

Channels between alveoli to allow communication. Implicated in alveolar diseases and ease of spread of pulmonary infections.

Coats inner alveoli and allows expansion during inhalation and prevents alveolar collapse on exhalation.

Contraction pulls lungs down during inhalation and relaxation/elastic recoil moves lungs up during exhalation

Raise and expand rib cage with help of sternocleidomastoid muscles on inhalation

Pulls rib cage down and in during exhalation

Tissue lining the lungs and rib cage

Tissue lining the lungs

Tissue lining the rib cage

Fills the space between the visceral and parietal pleura

Degree lungs expand per unit of change in transpulmonary pressure and determined by elastic forces in lung tissue, alveoli, lung interstitum, and pleural tension

Air-fluid interface creates a force that causes the alveoli to collapse inward

Alveoli are lined with small amounts of fluid - water molecules of alveolar fluid are attracted to water molecules in the air

Reduces the surface tension and disrupts the water molecules

There is greater muscular effort needed to expand the thorax and chest wall has limited recoil

The chest wall is less rigid and easier to expand but has strong recoil and more potential for collapse during exhalation

Lung compliance is decreased with

Chest wall compliance is decreased

Airways are obstructed

Volume of inspired and expired air with each breath

Maxium extra volume of air that can be inspired at the end of a normal volume

Maximum extra volume of air that can be expired at the end of a normal tidal volume

Tidal volume + Inspiratory reserve volume

Expiratory reserve volume + residual volume (amount of air that remains at the end of normal exhalation)

Inspiratory reserve volume + tidal volume + expiratory reserve volume (maximum volume that can be exhaled after maximum inhale)

Vital capacity + residual volume (maximum volume lung can be expanded)

Tidal volume x respiratory rate

The rate air reaches the gas-exchange areas of the lungs via diffusion

Space in respiratory system where no gas exchange occurs (alveoli without blood flow)

Anatomic dead space + alveoli without blood flow

Conducting zones = 30% of total lung capacity

Causes CO2 trapping

Anatomy of Pulmonary Circulation

From systemic circulation, provide oxygenated blood to trachea, bronchi, esophagus, visceral pleural and pulmonary arteries but doesn’t contribute to gas exchange

Balance between alveolar ventilation and alveolar blood flow

When V/Q mismatched there will be differences between

PaO2 will be normal if

V/Q is below normal = inadequate ventilation to oxygenate blood flowing through alveolar capillaries. Inability to shunt blood to alveoli that are perfused.

V/Q is above normal = alveoli are well ventilated but there are alveoli that are not well perfused. Something is blocking blood flow to these alveoli.

No blood flow (capillary pressure < alveolar pressure)

Intermittent blood flow (with peak pulmonary capillary pressure > alveolar pressure…diastolic capillary pressure < alveolar pressure)

Continuous blood blow (capillary pressure > alveolar pressure)

Blood flow occurs when PA pressures are too high (R HF or RVOT obstruction) or alveolar pressure too high (hyperinflation)

During exercise (increased CO) all areas of lungs get

Pressure in pulmonary capillaries

Interstitial fluid pressures

Net fluid movement from alveoli to interstitial space —> drains into lymphatics (keeps alveoli free of excess fluid)

Excess fluid in the alveoli impairing gas exchange and decreasing lung compliance

Increased left heart pressures, pulmonary over-circulation, increased pulmonary capillary permeability (inflammation)

Mucoid fluid in the pleural space that contributes to negative intrapleural pressure that prevents pulmonary edema

Excess fluid in pleural space

Blocked lymph drainage, LHF, Reduced Plasma Oncotic Pressure (causes increased fluid accumulation), Increased Permeability Membrane (inflammation)

Normal SpO2 range

SvO2 normal range

CO2 is bound to hemoglobin and transported (Carboxyhemoglobin), transport is bicarbonate, combines with blood protein (carbamino compounds), oxygen in alveoli displaces CO2 on Hbg promoting CO2 removal (Haldane effect) and ventilated out of the body

Groups of Medulla

Brain stem center controls Inspiration

Brain stem center controls exhalation

Pneumotaxic center - controls breathing rate and pattern

Vagal and glossopharyngeal nerves end in the medulla. Transmit signals from chemoreceptors and baroreceptors. Send signals to diaphram and intercostal muscles to controls rate of breathing and inspiration time

Inactive during normal breathing, fire during hypoventilation and signal inspiration, stimulate abdominal muscle contraction for forceful exhalation

Neurons in medulla, sense changes in pH of CSF, mechanism detects small changes in CO2 (1-2 mmHg), changes rate and depth and respirations

Chronic condition that can make central chemoreceptors less sensitive by increasing bicarbonate

This molecule crosses BBB to combine with H2O to create bicarbonate

Chemoreceptors in carotid and aortic bodies that sense changes in O2 concentration. Decreased PaO2 levels will increase respiratory rate.

Found in epithelium of conducting airways, sensitive to aerosols, gases, particles (induces cough) increases respiratory rate and can lead to Bronchospasm

When smooth muscle in bronchi, bronchioles, or lung parenchyma stretched —> signal medulla dorsal respiratory neurons to switch off Inspiration (Hering-Breuer Inflation Reflex)

Respond to increased pulmonary capillary pressures (eg LHF) —> initiate rapid, shallow breathing, causes laryngeal vasoconstriction and mucous secretion

Vasoconstriction to area of lung, decreased surfactant, high V/Q mismatch. Diagnosis - tachypnea, dyspnea, chest pain, hypoxia, pulmonary edema and atelectasis, pulmonary infarct and pulmonary HTN, decreased CO, elevated D-dimer (early test), CTA or MRA tests (confirm diagnosis), EKG changes with right strain, troponin level to help stratify risk of adverse outcomes. Treatment- fibrinolytics

Pulmonary artery pressure > 25 mmHg, associated with chronic hypoxia, LHF, valve disease causing dyspnea, chest pain,tachypnea, cough, JVD

Causes (idiopathic, genetic, connective tissue disease). Pathophysiology (vasoconstrictors overwhelm pulmonary vasodilators —> resistance of blood flow to lungs —> RV remodeling —> Cor Pulmonale (RHF)

Hallmarks: Worse on expiration —> prolonged expiratory phase and decreased FEV. Dyspnea. Wheezing (lower airways) and Stridor (upper airways)

Chronic inflammatory disease of bronchial mucosa causing hyperresponsiveness, bronchoconstriction, and obstruction

Antigen exposure —> cytokine response —> increased capillary permeability, mucosal edema and production, Bronchospasm

Inflammatory mediators —> Bronchospasm —> secretions —> obstruction—> air trapping —> hyperinflation —> V/Q mismatch —> hypoxemia —> CO2 retention —> acidosis —> respiratory failure

Treatment: Beta2 (albuterol), Anticholinergics, Steroids, and Antihistamines

Airflow obstruction that is not fully reversible and generally progressive. Generally, “acquired” but some genetic basis (alpha1-anti-trypsin deficiency)

Hypersecretion of mucus and chronic productive cough (3months/yr for 2+ yrs). Initially impacts large airways but ultimately affects all bronchial smooth muscle. Bronchial inflammation—> edema—> increased size and number of mucosal cells and goblet cells—> air trapping on expiration. V/Q mismatch—> hypoxemia—>mild cyanosis. Dyspnea on exertion. Chronic hypercarbia.

Enlargement of respiratory airways and destruction of alveolar zones. Breakdown of elastin —> loss of elastic recoil —> air trapping —> dyspnea —> hypoventilation —> hypercarbia. Structural changes (loss of alveolar cells) —> increased area for gas exchange + bullae and blebs —> V/Q mismatch —> hypoxemia. Systemic effects of chronic inflammation —> malnutrition and infection risk

Productive cough (classic sign), dyspnea (late in course), wheezing (intermittent), barrel chest (occasionally), prolonged exhalation (always), Cyanosis (common), chronic hypoventilation (common), Cor Pulmonale (common)

Productive cough (late in course), dyspnea (common), wheezing (minimal), barrel chest (classic sign), prolonged exhalation (always), Cyanosis (uncommon), chronic hypoventilation (late in course), Cor Pulmonale (late in course)

Caused from acute viral infection. Subglottic edema causes narrowing of airway and respiratory distress develops into barky cough and stridor