Patho Respiratory

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Conducting Airways

Nose, Pharynx, Larynx, Trachea, Bronchi, Bronchioles

Extra-Thoracic

Nose, Pharynx, Larynx

Intrathoracic

Trachea, Bronchi, Bronchioles

Respiratory Zone

Terminal Bronchi, Alveoli, Aveolar Capillaries

Keeps smooth muscle areas open

Transpulmonary Pressures

Factors that relax smooth muscles in bronchi and bronchioles

Sympathetic (Beta-2 and Epi)

Contraction of bronchiolar smooth muscle and bronchoconstriction

Parasympathetic from vagas nerve releasing acetylcholine

Contraction of bronchiolar smooth muscle and bronchoconstriction

Release of leukotrines and histamine from lung cells and endothelium

Contraction of bronchiolar smooth muscle and bronchoconstriction

Histamine released from mast cells

Small changes in diameter increases difficulty of breathing

Airway Resistance

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

Pleural Pressure

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

Alveolar Pressure

Chest expansion (-1) air moves in. Chest recoil (+1) air moves out.

Difference between pleural and alveolar pressures

Transpulmonary Pressure

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

Transpulmonary Pressure

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)

Pneumothorax

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

Pneumothorax

Increased Resistance Curve

Asthma and COPD

Decreased Compliance Curve

PNE and Pulmonary Edema

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

Pores of Kohn and Canal of Lambert

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

Surfactant

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

Diaphram

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

External intercostals

Pulls rib cage down and in during exhalation

Internal intercostals and abdominal recti

Tissue lining the lungs and rib cage

Pleura

Tissue lining the lungs

Visceral Pleura

Tissue lining the rib cage

Parietal Pleura

Fills the space between the visceral and parietal pleura

Pleural fluid

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

Lung compliance

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

Surface tension elastic force

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

Contractile force

Reduces the surface tension and disrupts the water molecules

Surfactant

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

Rigidity of mature rib cage

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

Cartilaginous ribs of children

Lung compliance is decreased with

Pulmonary edema or infection

Chest wall compliance is decreased

Scoliosis and obesity

Airways are obstructed

Bronchospasm or mucous plugging

Volume of inspired and expired air with each breath

Tidal volume

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

Inspiratory reserve volume

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

Expiratory reserve volume

Tidal volume + Inspiratory reserve volume

Inspiratory capacity

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

Functional residual capacity

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

Vital capacity

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

Total lung capacity

Tidal volume x respiratory rate

Minute ventilation

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

Alveolar ventilation

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

Dead space

Anatomic dead space + alveoli without blood flow

Physiologic dead space

Conducting zones = 30% of total lung capacity

Anatomic dead space

Causes CO2 trapping

Dead spaces

Anatomy of Pulmonary Circulation

RV—>Pulmonary Artery—>Pulmonary Capillary Bed—>Pulmonary Vein—>LA

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

Bronchial vessels

Balance between alveolar ventilation and alveolar blood flow

V/Q matching

When V/Q mismatched there will be differences between

Alveolar O2 and PaO2, ETCO2 and PaCO2

PaO2 will be normal if

Patient has lung disease and intact V/Q because body has shunted blood to alveoli that are perfused

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

Physiologic shunting

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.

Physiologic dead space

No blood flow (capillary pressure < alveolar pressure)

Zone I

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

Zone II

Continuous blood blow (capillary pressure > alveolar pressure)

Zone III

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

Zone I

During exercise (increased CO) all areas of lungs get

Zone III

Pressure in pulmonary capillaries

Low, 7mmHg

Interstitial fluid pressures

Negative, -5 to -8 mmHg

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

Mean filtration pressure

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

Pulmonary edema

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

Causes of pulmonary edema

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

Pleural fluid

Excess fluid in pleural space

Pleural effusion

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

Causes of Pleural Effusion

Normal SpO2 range

97-100%

SvO2 normal range

75%

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

CO2 Transport

Groups of Medulla

Dorsal and Ventral

Brain stem center controls Inspiration

Dorsal

Brain stem center controls exhalation

Ventral

Pneumotaxic center - controls breathing rate and pattern

Pons

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

Dorsal respiratory neurons

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

Ventral respiratory neurons

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

Central Chemoreceptors

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

COPD

This molecule crosses BBB to combine with H2O to create bicarbonate

CO2

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

Peripheral chemoreceptors

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

Irritation receptors

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

Stretch receptors

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

Pulmonary C-Receptors (J receptors)

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 embolism

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

PAH

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

Pulmonary Artery Hypertension

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

Obstructive Lung Disease

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

Asthma

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

Early Asthma Response

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

Late Response Asthma

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

Asthma

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

COPD

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.

Chronic Bronchitis

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

Emphysema

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

Chronic Bronchitis

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)

Emphysema

100

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

Croup

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