Ventilation PDF - Functions, Process, and the Balloon Model

Ventilation: the process of gas (air) moving in and out of the lungs. This process can be affected by the lungs and thorax compliance Pressure gradients: generated by the respiratory muscles: elastic properties of airways, alveoli and chest wall and produced by the thoracic expansion/contraction; i...

Ventilation: the process of gas (air) moving in and out of the lungs. This process can be affected by the lungs and thorax compliance Pressure gradients: generated by the respiratory muscles: elastic properties of airways, alveoli and chest wall and produced by the thoracic expansion/contraction; it is responsible for the gas flow (movement of gas) in and out of the lungs — either during inspiration or expiration. Pleural Pressure (Ppl): Pressure within the pleural cavity: The space between Visceral pleura (lining of the lungs) and the Parietal Pleura (lining the chest wall). At rest, Ppl is NEGATIVE (Subatmospheric) this pressure keeps the lungs expanded against the chest wall. Transrespiratory Pressure Difference (PTR) FORMULA: PTR = PAO-PBS (PAO is always higher than PBS) Function: Gas flow in and out of the lungs Def: The difference between body surface pressure (PBS) and Airway opening pressure (PAO); Everything that exists between pressure measured at airway opening and pressure measured at body surface. Components: Airway, Lungs, and Chest wall. Transpulmonary Pressure (PTP) FORMULA: PTP = PA-Ppl Function: Maintains alveolar inflation; prevents collapse of alveoli which can cause atelectasis. Def: The difference between Alveolar pressure (PA) and Pleural pressure (Ppl). A higher PTP. expands the lungs while a lower one allows passive recoil. Inspiration: Ppl become MORE NEGATIVE, increasing PTP resulting in lung expansion. Negative pressure maintains the alveoli inflated. Expiration: Ppl becomes LESS NEGATIVE, reducing PTP resulting in lungs to recoil. Indication: A reduced transpulmonary pressure can indicate stiff lungs (ARDS or FIBROSIS). Excessively high PTP due to over distension can cause lung injury. Transthoracic Pressure Difference (PTT) FORMULA: PTT = PA-PBS Function: it causes gas to flow into and out of alveoli during breathing. Def: The difference between Alveolar pressure and atmospheric pressure. INSPIRATION PROCESS. ​ Thoracic expansion → Pleural pressure decreases  ​ Pleural pressure decreases → Transpulmonary pressure increases ​ Increased transpulmonary pressure → Lungs expand ​ Alveolar pressure drops → Air flows into the lungs ​ Airflow slows as alveolar pressure approaches equilibrium with atmospheric pressure. During forced inspiration (big downward movement of diaphragm) Ppl can drop up to -50 cm EXPIRATION PROCESS ​ Inspiratory muscles relax, and the thorax/lungs recoil ​ Pleural pressure increases, reducing lung expansion. (decrease Ptp) ​ Alveolar pressure rises above atmospheric pressure. ​ Air is forced out of the lungs. ​ Expiration is usually passive, requiring no muscular effort. In cases of forced expiration (e.g., during exercise or coughing), the internal intercostal and abdominal muscles contract to actively push air out faster. Spontaneous breathing (SB) & Positive Pressure Ventilation (PPV) SB and PPV inflate lungs by increasing PTP (T.Pulmonary Pressure) expanding the alveoli and drawing air in. ​ SB and PPV have opposite effects on blood flow of the heart; Spontaneous Breathing (SB) during inspiration PPL becomes more negative, helping to pull more blood back to the heart (Increase in venous return) that improves cardiac output. ​ Positive pressure ventilation (PPV): The ventilator pushes air into the lungs which raises PPL. This higher pressure compresses the veins, reducing blood return to the heart, lowering cardiac output. Both SB and PPV increase transpulmonary pressure (PL) to inflate the lungs. SB helps the heart by improving blood return, while PPV reduces flow to the heart by increasing PPL. Balloon Model of ventilation The balloon model demonstrates how changes in thoracic cavity dimensions affect lung pressure and gas flow during breathing. ​ Inspiration is caused by the diaphragm's downward movement. ​ Expiration is driven by the diaphragm's upward movement. ​ Inspiration creates negative pleural pressure, pulling air into the lungs. ​ Expiration causes positive pleural pressure and pushes air out as the lung recoils. Flail chest When the patient inhales, the PTP (PA-PPL) and Transthoracic (PA-PB) pressures causes the lungs to sink in that leads to inspiratory volume decrease. When the patient exhales, the pressure gradients cause the broken ribs to bulge outward. This causes some of the air from the unaffected lung to move into the affected lung directly under the broken rib rather than be exhaled out. What to do? Put the patient on a positive pressure ventilator to eliminate the negative intrapleural pressures changes during inspiration. This stops the adverse effects of PTP and Transthoracic. Forces Opposing Lung Inflation The lungs and chest wall have a natural tendency to move in opposite directions. The lungs want to pull inward, while the chest wall wants to push outward. These opposing forces keep the lungs at their resting volume, which is called Functional Residual Capacity (FRC). There are two main ways that these opposing forces can keep the lungs at their resting volume: 1. Elastic forces: These forces come from the tissues of the lungs, thorax, and abdomen, as well as surface tension in the alveoli. 2. Frictional forces: These forces come from the resistance that the airways (natural and artificial) and tissues move during breathing create. Elastic opposition to ventilation: Elastic and collagen fibers provide resistance to lung stretch which is achieved by the application of air pressures into lungs. Deflation is a passive recoil and less force is required to maintain the same volume. Surface Tension Forces ​ Hysteresis Cause: Partly caused by surface tension, which opposes lung inflation. ​ Surfactant Function: Reduces lung surface tension, stabilizes alveoli, and prevents collapse. ​ Surfactant Production: Produced in alveolar type II pneumocytes. Hooke’s Law Elastance is like a rubber band’s natural ability to stretch and snap back to its original shape. It’s all about how matter responds to force and bounces back. In the lungs, when you breathe in, the tissue stretches out. But the lungs and chest wall have this special elastic property that pushes back against the stretch. So, to make the lungs bigger, you need to apply more pressure. In the world of pulmonary physiology, elastance is all about how much pressure changes when the volume of the lungs changes. When pressure increases so does volume; When applied to the lungs, volume is substituted for length and pressure is substituted for force. Hooke’s law helps explain why hazards such as pneumothorax can occur with the increased pressure of mechanical ventilation. Lung compliance Def: A measure of the lung’s ability to stretch and expand; a change in volume per unit of change if pressure difference across structure. ​ Increase compliance = Easy to inhale, hard to exhale ​ Decrease compliance = Hard to inhale, easier to exhale If the lungs have increased compliance they expand easily with minimal pressure. ​ Emphysema (COPD): Destruction of elastic lung tissue reduces lung recoil. Patients can inhale easily but struggle to exhale due to poor elastic recoil ​ Fibrosis: Restrictive lung disease, decreases CL. ​ Decrease in compliance may be caused by pulmonary fibrosis which affects the connective tissue making them stiff and unable to take in more volume. ​ Anatomical malformations such as Ankylosing spondylitis and Severe Kyphoscoliosis can cause decrease in lung compliance. Frictional Resistance to Ventilation Friction opposition happens only when the system is moving. Here are some ways it can occur: ​ Tissue viscous resistance ​ Impeded motion caused by tissue displacement (like the lungs, rib cage, diaphragm, and abdominal organs) ​ Obesity fibrosis and ascites can also increase resistance ​ Friction accounts for about 20% of the total resistance that causes tissues to become obese. Patients who have emphysema can directly influence the EPP in the airways to reduce collapse and closure. Airway collapse may occur in patients who have emphysema. Work of Breathing (WOB) Pulmonary diseases can increase WOB: -​ Restrictive diseases work is greater due to elastic tissue recoil -​ Obstructive disease work is greater due to airway resistance. -​ Patients with stiff lung will breathe faster because of the increased elastic WOB  -​ Patients with airway obstruction will take on a different pattern to reduce frictional WOB. ; May use pursed lip to minimize airway resistance. Metabolic Impact of Increased WOB ​ The rate of O2 consumption (Vo2) reflects energy requirements, and can indirectly measure WOB ​ In shock, intubation and mechanical ventilation may indicate to decrease excess O2 consumption of respiratory muscles. WOB ​ Muscle weakness — at higher risk for muscle fatigue (if lungs muscle weakens, it can cause respiratory arrest). ​ Electrolyte imbalance, shock, sepsis or disease that causes muscle weakness play a role in WOB ​ VT decreases, RR increases, Muscle fatigue, Gas exchange does not function well. Distribution of Ventilation In upright lung, ventilation and perfusion (V/Q) are matched best at bases (called dependent area). -​ IN HEALTHY LUNGS: Neither ventilation (V) or perfusion (Q) are distributed evenly. Result: uneven ventilation to perfusion ratio of 0.8 -​ In local disease, place good lung down for better V/Q matching (Lobar pneumonia) Time Constants ​ Time (in seconds) necessary to inflate a particular lung region to approx. 60% of its potential filling capacity. ​ Lung regions that have increased airway (RAW) or increased compliance require more time to inflate. Alveoli has a long time constant. ​ Lung regions that have decreased airway (RAW) or decreased lung compliance require less time to inflate. ​ Lung unit has a long time constant (TC) if compliance and airway is high. ​ Lung unit has a short time if compliance and airway (RAW) is low. Efficiency of Ventilation ​ To be effective: O2 uptake, CO2 removal ​ To be efficient: consume little O2, produce maximum CO2 ​ Healthy lungs waste gas due to: Anatomic dead space of conducting airways, alveoli that have little or no perfusion. Dead space Ventilation Dead space Ventilation: Usually related to defects in pulmonary circulation — Pulmonary embolism (blocks a portion of pulmonary circulation) Apical alveoli have minimal or no perfusion in normal upright subject at rest. ​ Alveolar dead space: Volume of gas ventilating unperfused alveoli. The alveoli receive gas but no perfusion.