Small changes in diameter increases difficulty of breathing

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

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

Keeps smooth muscle areas open

Pneumotaxic center - controls breathing rate and pattern

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

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

Tissue lining the lungs and rib cage

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

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

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

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

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

Interstitial fluid pressures

Factors that relax smooth muscles in bronchi and bronchioles

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

Contraction of bronchiolar smooth muscle and bronchoconstriction

When V/Q mismatched there will be differences between

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

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

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

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

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

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

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

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

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

Contraction of bronchiolar smooth muscle and bronchoconstriction

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

Brain stem center controls Inspiration

This molecule crosses BBB to combine with H2O to create bicarbonate

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

Alveolar Pressure

Chest wall compliance is decreased

Groups of Medulla

Tissue lining the rib cage

Conducting Airways

Pulls rib cage down and in during exhalation

Balance between alveolar ventilation and alveolar blood flow

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

Conducting zones = 30% of total lung capacity

Intrathoracic

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.

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

Tissue lining the lungs

PaO2 will be normal if

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

Brain stem center controls exhalation

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.

Decreased Compliance Curve

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

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

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

Airways are obstructed

Increased Resistance Curve

Tidal volume + Inspiratory reserve volume

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

Volume of inspired and expired air with each breath

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

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

Tidal volume x respiratory rate

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

Anatomic dead space + alveoli without blood flow

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

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)

Excess fluid in pleural space

Normal SpO2 range

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

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)

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

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

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

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

Extra-Thoracic

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

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

Contraction of bronchiolar smooth muscle and bronchoconstriction

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

Fills the space between the visceral and parietal pleura

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

Anatomy of Pulmonary Circulation

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

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

SvO2 normal range

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

Reduces the surface tension and disrupts the water molecules

Continuous blood blow (capillary pressure > alveolar pressure)

Causes CO2 trapping

Pressure in pulmonary capillaries

Difference between pleural and alveolar pressures

During exercise (increased CO) all areas of lungs get

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

Lung compliance is decreased with

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

No blood flow (capillary pressure < alveolar pressure)

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

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

Respiratory Zone

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

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