Respiratory Physiology

Ventilation: Inspiration and Expiration

Ventilation, or breathing, consists of two phases: inspiration (air intake) and expiration (air expulsion). Inspiration is driven by contraction of the external intercostal muscles and the diaphragm, which increases thoracic volume and creates a partial vacuum, drawing air into the lungs. Expiration is usually passive, but during forced expiration, abdominal muscles and internal intercostal muscles contract to expel air more forcefully.

Respiratory Volumes and Capacities

Respiratory volumes are measurements of air movement during breathing. Key volumes include:

• Tidal Volume (TV): Amount of air inspired and expired during normal breathing (approx. 500 ml).

• Inspiratory Reserve Volume (IRV): Maximum air that can be inspired after a normal inspiration (male: 3100 ml, female: 1900 ml).

• Expiratory Reserve Volume (ERV): Maximum air that can be expired after a normal expiration (male: 1200 ml, female: 700 ml).

• Residual Volume (RV): Air remaining in lungs after forced expiration (male: 1200 ml, female: 1100 ml).

Capacities are calculated from volumes:

• Total Lung Capacity (TLC): (male: 6000 ml, female: 4200 ml)

• Vital Capacity (VC): (male: 4800 ml, female: 3100 ml)

• Forced Vital Capacity (FVC): Maximum air expelled after deep inspiration.

• Forced Expiratory Volume (FEV1): Amount of VC expired in first second of FVC test (normally 75–85%).

Equipment Used in Respiratory Experiments

• Simulated human lungs in a glass bell jar

• Rubber diaphragm to seal and change volume/pressure

• Adjustable airflow tube

• Oscilloscope

• Three breathing patterns: TV, ERV, FVC

Pathophysiology: Emphysema and Asthma

Emphysema reduces elastic recoil in lung tissue, increasing airway resistance and making expiration difficult. Acute asthma attacks cause bronchial smooth muscle spasms and mucus secretion, narrowing airways and increasing resistance.

Breathing During Exercise

During exercise, metabolic demand increases, leading to increased breathing rate and tidal volume. Heavy exercise further increases respiration to meet extreme metabolic demands.

Surface Tension and Surfactant

Surface tension at the gas-liquid boundary in alveoli resists inflation. Surfactant (a detergent-like mixture of lipids and proteins) reduces surface tension, facilitating lung inflation.

Intrapleural Pressure and Pneumothorax

Intrapleural pressure is lower than atmospheric pressure, creating a partial vacuum. If the pleural membrane is breached, air enters the pleural cavity (pneumothorax), potentially causing lung collapse (atelectasis).

Equipment Used in Pleural Pressure Experiments

• Simulated human lungs in a glass bell jar

• Rubber diaphragm

• Valve for intrapleural pressure equalization

• Surfactant (dipalmitoylphosphatidylcholine, phosphatidylglycerol)

• Oscilloscope

Cardiovascular Physiology

Blood Vessel Radius and Blood Flow

Blood vessel radius is a principal method of controlling blood flow. Contraction or relaxation of smooth muscle in vessel walls alters radius (vasoconstriction/vasodilation). Laminar flow describes blood flow in vessels, with central flow moving faster than peripheral flow.

Blood Viscosity and Flow

Viscosity is fluid thickness; higher viscosity increases resistance and decreases flow. Blood viscosity is affected by plasma proteins and formed elements (leukocytes, erythrocytes, platelets). Homeostatic balance maintains blood viscosity; dehydration or altered cell numbers can change viscosity.

Blood Vessel Length and Flow

Longer vessels increase resistance due to greater surface area contact. Vessel length increases with growth and weight gain, and decreases with weight loss.

Pressure Gradient and Blood Flow

The pressure difference between vessel ends drives blood flow (pressure gradient). The heart's contraction provides initial pressure; vessel resistance affects the gradient. Large arteries near the heart have elastic tissue to accommodate changes.

Cardiac Cycle and Heart Function

The heart beats about 70 times per minute, with chambers filling during diastole and pumping during systole. Key volumes:

• End Diastolic Volume (EDV): Volume in ventricles at end of diastole.

• End Systolic Volume (ESV): Volume remaining after contraction.

• Stroke Volume (SV): Blood ejected per beat ().

The heart consists of two pumps: right (pulmonary circuit) and left (systemic circuit).

Cardiac Output and Blood Pressure

Cardiac output (CO) is the product of heart rate (HR) and stroke volume (SV):

• Blood pressure equation:

• Substituting:

To maintain blood pressure, the cardiovascular system can alter HR, SV, or resistance.

Factors Affecting Stroke Volume

• Preload: Degree of ventricular filling (stretch).

• Contractility: Strength of cardiac muscle contraction.

• Afterload: Back pressure from blood in aorta/pulmonary trunk.

Frank-Starling law: Increased venous return increases EDV and stroke volume.

Equipment Used in Cardiac Function Experiments

• Left beaker: simulates blood from lungs

• Flow tube: simulates pulmonary veins

• Pump: simulates left ventricle

• Flow tube: simulates aorta

• Right beaker: simulates systemic circuit

Cardiovascular Compensation and Disease

If a vessel is compromised (e.g., aortic valve stenosis), the heart compensates by increasing contractility or stroke volume. Atherosclerosis (arterial hardening) increases resistance and can lead to heart disease.

Experimental Compensation Mechanisms

• Increasing left flow tube radius (preload)

• Increasing pump pressure (contractility)

• Decreasing right beaker pressure (afterload)

These mechanisms are tested to predict improvement in flow rate.

Summary Table: Respiratory Volumes and Capacities

Summary Table: Cardiac Volumes and Output

Key Equations

Additional info:

• Some details about surfactant composition and function were inferred for completeness.

• Cardiac compensation mechanisms and disease context were expanded for academic clarity.