Clase 37 Fisiología Respiratoria - Ventilación Pulmonar (IG:@doctor.paiva)

Name: Clase 37 Fisiología Respiratoria - Ventilación Pulmonar (IG:@doctor.paiva)
Uploaded: 2018-05-15T06:02:58.000Z
Duration: 1 h 20 min 37 s

Introduction to Pulmonary Physiology

Overview of the Class

The 37th class focuses on respiratory physiology, covering topics such as pulmonary ventilation, mechanics of breathing, surfactant function, surface tension, lung volumes and capacities, and alveolar ventilation.

Virtual Dissection of the Lungs

A virtual dissection is introduced where the head, skin, thorax, and heart are removed to reveal the lungs filled with alveoli responsible for gas exchange.

Alveoli facilitate gas exchange between oxygen and carbon dioxide; tissues continuously eliminate CO2 through veins leading to the right side of the heart.

Blood Flow in Pulmonary Circulation

Pathway of Oxygenated Blood

Deoxygenated blood travels from the right ventricle to the lungs via pulmonary arteries for oxygenation.

Once oxygenated in the lungs, blood returns to the left atrium and then to the left ventricle before being pumped into systemic circulation during ventricular contraction (systole).

Anatomy of the Respiratory System

Structure of Airways

The trachea divides into left and right main bronchi which further branch into segmental bronchi; first seven contain cartilage while subsequent bronchioles do not.

Terminal bronchioles lead to respiratory bronchioles and ultimately alveolar ducts and sacs where gas exchange occurs.

Mechanics of Breathing

Role of Smooth Muscle

Bronchioles consist mainly of smooth muscle allowing for bronchoconstriction or bronchodilation which is crucial for airflow regulation.

Definitions: Ventilation vs. Respiration

Ventilation refers to air movement between atmosphere and alveoli; respiration involves gas diffusion (O2 intake & CO2 expulsion).

Diaphragm's Function in Breathing

Importance in Respiration

The diaphragm is a key muscle innervated by the phrenic nerve; its contraction facilitates inhalation while relaxation aids exhalation.

Types of Breathing Movements

Two primary movements: diaphragmatic (quiet breathing at rest) involves vertical changes in thoracic cavity size; costal movement (forced breathing) involves rib elevation/depression affecting thoracic diameter.

Inspiration and Expiration Mechanics

Diaphragmatic Movement During Breathing

Respiratory Mechanics and Pressures

The Process of Inspiration

Inspiration is an active process involving the diaphragm, which moves upward due to positive pressure in the abdominal structures, facilitating air intake.

Key inspiratory muscles include external intercostals and scalene muscles, which elevate the thoracic cavity during forced breathing.

Expiratory muscles such as internal intercostals and rectus abdominis work to lower the thoracic cavity, contrasting with inspiratory actions.

Pulmonary Pressures During Breathing

Pleural pressure changes during inspiration (−75 cm H2O) and expiration (−5 cm H2O), indicating negative pressures that facilitate lung expansion.

Alveolar pressure also shifts from negative during inspiration (−1 cm H2O) to positive during expiration (+1 cm H2O), reflecting air movement in and out of the lungs.

Transpulmonary Pressure

The difference between alveolar pressure and pleural pressure is termed transpulmonary pressure, crucial for understanding lung mechanics and collapse tendencies.

Lung Compliance

Lung compliance refers to volume change per unit of pressure change; it reflects how easily lungs can expand under varying pressures.

Elastic forces within lung tissue are influenced by elastin and collagen fibers, contributing to overall lung elasticity.

Surface Tension Effects

Surface tension in alveoli arises from water molecules attempting to contract, creating a tendency for alveolar collapse.

Approximately one-third of collapsing forces are due to elastic properties (elastin/collagen), while two-thirds result from surface tension effects.

Role of Surfactant

Surfactant reduces surface tension in alveoli, preventing collapse by counteracting the attractive forces between water molecules on alveolar surfaces.

Understanding Pulmonary Surfactant and Lung Capacities

The Role of Surfactant in Alveoli

Surfactant is not produced by type II alveolar epithelial cells, which constitute 10% of the alveolar surface area. These cells do not secrete surfactant.

Surfactant consists of phospholipids, proteins, and ions, primarily phosphatidylcholine, which is crucial for reducing surface tension in the alveoli.

There is an inverse relationship between the radius of the alveolus and surface tension; as radius decreases, surface tension increases, leading to potential collapse.

Obstruction in pulmonary pathways increases surface tension within the alveoli, causing them to collapse due to increased pressure.

The formula for calculating this relationship indicates that lower radii result in higher pressures within the alveoli due to increased surface tension.

Clinical Implications of Alveolar Collapse

Conditions like atelectasis occur when obstructions (e.g., mucus plugs or foreign bodies) reduce alveolar radius and increase surface tension, leading to lung collapse.

Atelectasis is frequently observed in clinical settings due to its physiological basis related to airway obstruction and changes in alveolar dynamics.

Lung Volumes and Capacities

Basic Lung Volumes

Tidal volume (VT), approximately 500 ml, represents involuntary breathing during sleep without significant variation.

Inspiratory reserve volume (IRV), about 3000 ml, refers to maximum inhalation capacity beyond tidal volume.

Expiratory reserve volume (ERV), around 1100 ml, indicates maximum exhalation after a normal breath; residual volume remains at 1200 ml preventing total lung collapse.

Total Lung Capacity Calculations

Inspiratory capacity combines tidal volume (500 ml) with inspiratory reserve volume (3500 ml), totaling 4000 ml for normal inhalation capabilities.

Functional residual capacity sums expiratory reserve volume (1100 ml) with residual volume (1200 ml), equating to 2300 ml retained post-exhalation.

Vital capacity includes all volumes involved in voluntary breathing: IRV + VT + ERV = 4600 ml; total lung capacity adds vital capacity plus residual volume for a total of approximately 5800 ml.

Understanding Respiratory Volumes and Capacities

Key Concepts of Respiratory Volumes

The inspiratory reserve volume is highlighted, emphasizing the total capacity for inhalation, which includes tidal volume (the normal amount of air inhaled or exhaled) plus inspiratory reserve volume. The total lung capacity is approximately 5800 ml.

Variations in respiratory volumes can occur due to certain pathologies such as asthma and emphysema, affecting residual volume and inspiratory reserve volume.

The minute ventilation is introduced as the total amount of fresh air entering the lungs per minute, calculated by multiplying the tidal volume (approximately 500 ml) by the respiratory rate (12 breaths per minute), resulting in a typical value of 6000 ml/min.

Airway Functionality and Gas Exchange

All inhaled air travels through the airway structures to facilitate gas exchange; however, not all air contributes to this process due to anatomical dead spaces where no gas exchange occurs.

Of the 500 ml of air inhaled with each breath, only about 350 ml participates in gas exchange. This highlights that some areas within the respiratory system do not have specialized membranes for gas exchange.

Anatomical Dead Space

The concept of anatomical dead space is defined as parts of the airway where air enters but does not undergo gas exchange. This space typically measures around 150 ml.

It’s noted that while anatomical dead space exists, effective areas for gas exchange include bronchioles and alveoli which contain specialized membranes necessary for this function.

Alveolar Dead Space

In healthy individuals, alveolar dead space—where air enters but does not participate in gas exchange—is minimal because most regions involved in respiration are equipped with appropriate membranes for effective gas transfer.

Pathological conditions may increase alveolar dead space; however, under normal circumstances, it remains negligible due to efficient alveolar structures facilitating oxygen uptake.

Physiological Dead Space Calculation

Physiological dead space combines both anatomical and alveolar components. In a healthy individual:

Anatomical dead space = 150 ml

Alveolar dead space ≈ 0

Thus physiological dead space also approximates to 150 ml.

When calculating effective ventilation:

Subtracting physiological dead space from tidal volume results in an effective ventilation value contributing to actual gas exchange (350 ml).

Understanding Alveolar Ventilation and Bronchial Dynamics

Alveolar Ventilation Calculation

The total ventilation is 6000 ml, but only 4200 ml contributes to alveolar ventilation due to the presence of dead space that does not participate in gas exchange.

To determine alveolar ventilation, it is essential to subtract the volume of dead space from the total ventilation. This emphasizes the importance of understanding dead space in respiratory physiology.

Structure and Function of Airways

The trachea and bronchi contain cartilage, while areas without cartilage are composed of smooth muscle, which plays a crucial role in bronchoconstriction and bronchodilation.

Smooth muscle receptors include beta-adrenergic receptors (sympathetic) and parasympathetic receptors, influencing airflow resistance through their respective actions on bronchial diameter.

Impact of Nervous System on Airflow

Bronchodilation leads to increased airflow due to reduced resistance, while bronchoconstriction results in decreased airflow due to increased resistance. Understanding this relationship is vital for managing respiratory conditions.

Adrenaline has a higher affinity for beta receptors compared to noradrenaline, promoting bronchodilation effectively during sympathetic activation. This highlights the pharmacological relevance of these hormones in respiratory therapy.

Pharmacological Interventions

Beta agonists like salbutamol stimulate beta-2 adrenergic receptors leading to bronchodilation; they are particularly useful during asthma attacks by increasing airflow and reducing airway resistance.

Conversely, parasympathetic stimulation via acetylcholine causes mild bronchoconstriction; antagonists that block beta receptors can lead to an increase in parasympathetic dominance resulting in constricted airways. Understanding these mechanisms aids in therapeutic decision-making for respiratory diseases.

Local Factors Influencing Bronchial Constriction

Local inflammatory substances such as histamine released during allergic reactions can cause significant bronchoconstriction; this aspect is critical when considering treatment options for asthma patients experiencing acute symptoms.

The balance between sympathetic and parasympathetic systems is crucial for maintaining normal airway function; medications affecting this balance must be used judiciously to avoid exacerbating conditions like asthma or COPD (Chronic Obstructive Pulmonary Disease).

Airway Clearance Mechanisms

The epithelium lining the airways features ciliated cells that play a key role in trapping particles with mucus and moving them towards the oropharynx for expulsion or swallowing—an essential defense mechanism against pathogens and irritants inhaled into the lungs.

Understanding Coughing and Sneezing

Commonalities Between Coughing and Sneezing

Both coughing and sneezing are reflex actions triggered by irritation in the respiratory pathways. The common factor is that both require some form of irritant to stimulate these responses.

For a cough to occur, there must be irritation in the lower airways, while sneezing is triggered by irritants in the upper airways, specifically within the nasal passages above the mouth.

Any irritant affecting the nasal airways can lead to sneezing, indicating that even minor disturbances can provoke this reflex.

Specialized receptors located throughout the trachea and even in alveoli play a crucial role in detecting irritants, leading to a nervous reflex response that results in coughing or sneezing.