Introduction: The Systems of Transport and Exchange
For a complex multicellular organism to survive, every cell must receive a constant supply of oxygen and nutrients, and have waste products removed. This immense logistical challenge is met by two closely integrated systems: the Cardiovascular System, which acts as the transport network, and the Respiratory System, which manages gas exchange with the environment. This lesson explores the structure and function of this vital cardiopulmonary partnership.
Part 1: The Cardiovascular System
1.1 Heart Anatomy: A Detailed Look
The heart is a four-chambered muscular pump located in the mediastinum. Its wall consists of three layers: the outer epicardium, the thick middle myocardium (the cardiac muscle), and the inner endocardium. The heart is enclosed in a double-walled sac called the pericardium.
The four chambers are the two upper atria (receiving chambers) and two lower ventricles (pumping chambers). The atrioventricular (AV) valves (tricuspid on the right, mitral/bicuspid on the left) are anchored to the ventricular walls by chordae tendineae and papillary muscles to prevent prolapse during ventricular contraction.
1.2 Blood Circulation: The Double-Loop System
- Pulmonary Circuit: (Right Heart → Lungs → Left Heart) Deoxygenated blood enters the right atrium → tricuspid valve → right ventricle → pulmonary valve → pulmonary artery → lungs. In the lungs, gas exchange occurs. Oxygenated blood returns via the pulmonary veins to the left atrium.
- Systemic Circuit: (Left Heart → Body → Right Heart) Oxygenated blood enters the left atrium → mitral valve → left ventricle → aortic valve → aorta → body tissues. Deoxygenated blood returns via the superior and inferior vena cavae to the right atrium.
Diagram: Pulmonary and Systemic Circulation
1.3 The Cardiac Cycle
The cardiac cycle describes the mechanical and electrical events of one heartbeat (average 0.8 seconds). It includes two main phases: systole (contraction) and diastole (relaxation).
- Ventricular Filling (Mid-to-Late Diastole): AV valves are open. Blood flows passively from the atria into the ventricles. Atrial systole then occurs, pushing the final volume of blood into the ventricles.
- Isovolumetric Contraction (Systole Phase 1): Ventricles begin to contract, increasing pressure. This closes the AV valves, producing the first heart sound (S1, "lub"). All four valves are briefly closed.
- Ventricular Ejection (Systole Phase 2): Ventricular pressure exceeds the pressure in the aorta and pulmonary artery, forcing the semilunar valves open and ejecting blood.
- Isovolumetric Relaxation (Early Diastole): Ventricles relax, pressure falls. Blood in the aorta/pulmonary artery flows back, closing the semilunar valves and producing the second heart sound (S2, "dub"). All four valves are again briefly closed.
1.4 The Heart's Electrical Conduction System
The heart's intrinsic conduction system coordinates the cardiac cycle. This can be visualized on an electrocardiogram (ECG or EKG).
Diagram: The Cardiac Conduction System
Diagram: The ECG and Electrical Events
- P Wave: Represents atrial depolarization, initiated by the SA node.
- QRS Complex: Represents ventricular depolarization, as the impulse spreads from the AV node through the Purkinje fibers. Atrial repolarization is masked by this event.
- T Wave: Represents ventricular repolarization.
1.5 Blood Vessels: Structure and Function
Vessel walls have three layers (tunics): the inner tunica intima (endothelium), the middle tunica media (smooth muscle and elastic fibers), and the outer tunica externa (connective tissue).
- Arteries: Have a thick tunica media to handle high pressure and maintain blood flow.
- Veins: Have thinner walls and larger lumens. They contain valves to prevent backflow, and blood return is aided by the muscular pump (skeletal muscle contractions).
- Capillaries: Consist only of a tunica intima, ideal for efficient diffusion.
1.6 Blood Components and Hemostasis
Blood is composed of plasma and formed elements.
Component | Sub-type | Primary Function |
---|---|---|
Formed Elements (45%) | Erythrocytes (RBCs) | Transport O₂ via hemoglobin. Their production is stimulated by the hormone erythropoietin (EPO) from the kidneys. |
Leukocytes (WBCs) | Immune defense. | |
Platelets (Thrombocytes) | Initiate blood clotting (hemostasis). | |
Plasma (55%) | Water, proteins (albumin, fibrinogen, globulins), electrolytes, nutrients, wastes. | Transport medium, osmotic balance, clotting. |
Hemostasis (Blood Clotting)
Hemostasis is the process to stop bleeding. It involves three steps: 1) Vascular spasm, 2) Platelet plug formation, and 3) Coagulation, a cascade of enzymatic reactions where soluble fibrinogen is converted into an insoluble fibrin mesh, trapping blood cells to form a stable clot.
Part 2: The Respiratory System
2.1 Anatomy of the Respiratory Passageways
Air travels through the conducting zone (nose → pharynx → larynx → trachea → primary bronchi → secondary bronchi → tertiary bronchi → bronchioles → terminal bronchioles) to the respiratory zone (respiratory bronchioles → alveolar ducts → alveoli).
2.2 Mechanics of Breathing (Ventilation)
Breathing is driven by pressure changes in the thoracic cavity, controlled by the diaphragm and intercostal muscles.
- Inhalation: An active process. The diaphragm contracts and moves down. The external intercostal muscles contract, lifting the rib cage up and out. This increases the volume of the thoracic cavity, which decreases the pressure inside the lungs below atmospheric pressure, drawing air in.
- Exhalation: A passive process at rest. The diaphragm and intercostal muscles relax. Elastic recoil of the chest wall and lungs decreases the thoracic cavity volume, increasing the pressure above atmospheric pressure and forcing air out. Forced exhalation is an active process involving abdominal and internal intercostal muscles.
Diagram: Mechanics of Breathing
2.3 Lung Volumes and Capacities
These are measured using a spirometer.
- Tidal Volume (TV): Air volume exchanged during normal quiet breathing.
- Inspiratory Reserve Volume (IRV): Maximum air that can be forcibly inhaled after a normal inhalation.
- Expiratory Reserve Volume (ERV): Maximum air that can be forcibly exhaled after a normal exhalation.
- Residual Volume (RV): Air remaining in the lungs after maximal exhalation (keeps alveoli open).
- Vital Capacity (VC): The maximum exchangeable air (VC = TV + IRV + ERV).
- Total Lung Capacity (TLC): Total air the lungs can hold (TLC = VC + RV).
Diagram: Lung Volumes (Spirogram)
2.4 Gas Exchange and Transport
Gas exchange is driven by partial pressure gradients.
- Oxygen Transport & Dissociation Curve: The S-shaped curve shows that in the high PO₂ of the lungs, hemoglobin has a high affinity for O₂ and becomes saturated. In the low PO₂ of tissues, affinity decreases, and O₂ is released.
- Bohr Effect: Increased CO₂ and H⁺ (lower pH) in active tissues weakens the Hb-O₂ bond, causing a rightward shift of the curve and enhanced O₂ delivery.
- Carbon Dioxide Transport: Most CO₂ is converted to bicarbonate (HCO₃⁻). The H⁺ produced by this reaction binds to hemoglobin (buffering the blood) and promotes O₂ release (the Bohr effect).
- Haldane Effect: Deoxygenated hemoglobin has a greater affinity for CO₂ and H⁺ than oxyhemoglobin. Thus, O₂ release in the tissues promotes CO₂ pickup, and O₂ pickup in the lungs promotes CO₂ release.
Graph: Oxygen-Hemoglobin Dissociation Curve
2.5 Control of Respiration
The respiratory centers in the medulla oblongata and pons control breathing. The primary stimulus is the level of CO₂ (and therefore pH) in the cerebrospinal fluid, detected by central chemoreceptors. Peripheral chemoreceptors in the aorta and carotid arteries also monitor CO₂, pH, and, to a lesser extent, large drops in O₂.
Clinical Correlations
- Myocardial Infarction (Heart Attack): Occurs when blood flow to a part of the myocardium is blocked (usually by a clot in a coronary artery), causing tissue death.
- Atherosclerosis: The buildup of fatty plaques within the arteries, which can lead to hypertension, thrombosis, and heart attacks.
- Asthma: A chronic inflammatory disease causing bronchoconstriction and airflow obstruction, often triggered by allergens.