Summary
Highlights
The respiratory system is highlighted as one of the four most important systems in physiology, along with CVS, CNS, and kidneys, due to its clinical applications and complex concepts. The approach to studying the respiratory system is divided into five major sections: mechanism of breathing, pulmonary circulation, gas transport (especially oxygen), regulation of breathing, and applied respiratory physiology. Special emphasis is placed on mechanisms of breathing and gas transport as 'last minute revision' topics due to their high chances of appearing in exams as long questions.
The mechanics of breathing involve inspiration and expiration, with inspiration being an active process and expiration passive in quiet breathing. Key muscles include the diaphragm (vertical diameter increase) and external intercostals (anterior-posterior diameter increase). Different breathing types are noted for males (abdominothoracic) and females (thoracoabdominal), with clinical correlations for conditions like peritonitis and pleurisy. Two main movements of the thoracic cage are described: bucket-handle and pump-handle. Pressures involved include intra-thoracic/intra-pleural (mostly negative, crucial for lung distension) and intra-alveolar (oscillates between -1 and +1 mmHg during quiet breathing). Transpulmonary pressure (alveolar pressure - intrapleural pressure) is the driving force for lung distension.
Surfactant, a surface-active agent, reduces surface tension in alveolar fluid, decreasing lung collapsibility and increasing distensibility (compliance). It is synthesized by Type II pneumocytes. Its composition includes DPPC, surface apoproteins (SP-A, SP-B, SP-C, SP-D), and calcium ions. Functions include reducing surface tension, keeping alveoli dry, and stabilizing the alveolar system of interdependence, preventing collapse of smaller alveoli into larger ones as per Laplace's Law. Clinically, surfactant deficiency leads to Acute Respiratory Distress Syndrome (ARDS) in adults and Hyaline Membrane Disease (IRDS) in infants, often treated with corticosteroids to stimulate production.
Lung compliance measures the distensibility or stretchability of the lungs. It is inversely related to surface tension. Three types are discussed: static (200 ml/cm H2O for lungs alone, 100-110 ml/cm H2O for lungs + thorax), specific (compliance divided by FRC), and dynamic (changing compliance during inspiration and expiration). Dynamic compliance is high at the start of inspiration (lower lung volumes) and low at the end of inspiration (higher lung volumes), illustrated by the hysteresis curve. Decreased compliance occurs in restrictive lung diseases (e.g., pulmonary edema, interstitial lung disease), while increased compliance is seen in emphysema (early stages). COPD and restrictive lung diseases affect breathing patterns: shallow and rapid breathing at lower lung volumes for restrictive diseases, and slow and deep breathing at higher lung volumes for COPD patients.
This section covers four lung volumes (Tidal Volume, Inspiratory Reserve Volume, Expiratory Reserve Volume, Residual Volume) and four capacities (Inspiratory Capacity, Functional Residual Capacity, Vital Capacity, Total Lung Capacity). FRC is the equilibrium position of the respiratory system. Vital capacity and FRC are often affected in lung diseases; for instance, vital capacity decreases in restrictive diseases. Timed vital capacity (FEV1, FEV2, FEV3) and FEV1/VC ratio are crucial PFTs. FEV1 below 70% indicates airway obstruction (COPD), while an increased FEV1/VC ratio might indicate restrictive disease due to reduced vital capacity. Other PFTs include Peak Expiratory Flow Rate (PEFR) and Maximum Mid-Expiratory Flow Rate (MMFR), which help diagnose and characterize airway obstructions, especially in small airways.
Dead space is the volume where gas exchange does not occur. It includes anatomical dead space (conducting airways, measured by Fowler's method) and alveolar dead space (non-functioning alveoli). Physiological dead space is the sum of both (measured by Bohr's method). Factors like forced inspiration can increase anatomical dead space but decrease alveolar dead space. Tracheostomy significantly reduces dead space. Pulmonary circulation, also known as lesser circulation, is a low-resistance, high-compliance system, making the lungs a blood reservoir. It also has a dual blood supply (pulmonary for gas exchange, bronchial for lung tissue oxygenation). Hypoxia causes vasoconstriction in the lungs, unlike systemic circulation, due to O2-sensitive potassium channels.
Oxygen transport is critical, occurring in two main ways: bound to hemoglobin (97%) and dissolved in plasma (3%). PO2 in atmospheric air is 159 mmHg, decreasing to 149 mmHg in inspired air (due to humidification) and 104 mmHg in alveolar air (due to CO2 exchange). Arterial blood PO2 is typically 95 mmHg due to mixing with deoxygenated bronchial venous blood (physiological shunt). The Alveolar-Arterial (A-a) PO2 difference (normal 9-11 mmHg) increases in significant right-to-left shunts or diffusion abnormalities but remains normal in hypoventilation. Oxygen utilization coefficient shows that resting tissues use about 25% of delivered oxygen, with variations (e.g., heart 75%, kidneys lowest).
The oxygen dissociation curve describes the relationship between arterial PO2 and hemoglobin saturation. Its 'S' shape is crucial: initial slow saturation (hemoglobin in T-state, low O2 affinity) followed by rapid saturation (hemoglobin in R-state, high O2 affinity) due to positive cooperativity. The flatter upper portion ensures stable oxygen loading despite PO2 fluctuations, while the steeper lower part facilitates rapid oxygen release to tissues. The curve can shift right (easier O2 liberation) due to increased H+, PCO2, temperature, or 2,3-Bisphosphoglycerate (Bohr effect), or left (tighter O2 binding) due to opposite conditions, fetal hemoglobin, or carbon monoxide poisoning.
Breathing is controlled both voluntarily (motor cortex) and involuntarily (brainstem respiratory centers). The involuntary control involves four groups of neurons: DRG and VRG in the medulla, and Apneustic and Pneumotaxic centers in the pons. The DRG generates the inspiratory ramp signal, initiating and regulating inspiration, while the VRG primarily controls forceful expiration. The Pre-Bötzinger Complex acts as the pacemaker for spontaneous breathing. Apneustic and Pneumotaxic centers fine-tune the rate and depth of breathing. Damage to these centers or their connections leads to abnormal breathing patterns, such as apneustic breathing (slow, deep), Cheyne-Stokes breathing, or Biot's respiration.
Chemical regulation involves peripheral and central chemoreceptors. Peripheral chemoreceptors (carotid and aortic bodies) respond primarily to hypoxia (PO2 below 60 mmHg) and arterial H+. Central chemoreceptors (in the medulla) respond to H+ ions in the CSF, which primarily reflect arterial PCO2 levels. Elevated PCO2 and H+ stimulate ventilation, while decreased levels depress it. This explains why CO2, not O2, is the primary driver of ventilation, as over-ventilation in response to hypoxia can lead to washout of CO2, further depressing ventilation.
Hypoxia, defined as reduced oxygen supply to tissues, is classified into four types: hypoxic (low atmospheric O2, e.g., high altitude), anemic (reduced O2 carrying capacity, e.g., anemia, CO poisoning), stagnant (reduced blood flow, e.g., heart failure), and histotoxic (tissues unable to utilize O2, e.g., cyanide poisoning). High altitude physiology involves adaptation to low barometric pressure and hypoxic hypoxia. Acclimatization mechanisms include increased 2,3-BPG (shifting O2 curve right), increased peripheral chemoreceptor sensitivity, and decreased central chemoreceptor sensitivity. Deep sea diving physiology deals with high barometric pressure. Nitrogen narcosis (due to high N2 dissolving in lipids of neuronal membranes, causing alcohol-like symptoms) and Caisson's disease (decompression sickness, due to rapid ascent causing N2 bubbles where they shouldn't be, leading to bends, chokes etc.) are key concerns. Prevention involves slow ascent and curative measures use decompression chambers.