Cardiovascular & Pulmonary Anatomy & Physiology

NORMAL CARDIOVASCULAR & PULMONARY ANATOMY & PHYSIOLOGY

Presenter: Angela Campbell

Course: PHTH 648 Cardiovascular & Pulmonary Physical Therapy

Institution: Springfield College

OBJECTIVES

• Refresh knowledge of the anatomy of the thorax and its contents.

• Review the mechanics of the chest wall during ventilation.

• Refresh knowledge of the physiology of the heart, vascular system, and lungs, emphasizing:

  • The cardiac cycle

  • The control of blood pressure

  • Oxygen transport

HEART & LUNG RELATIONSHIP

• Key Structures:

  • Pericardium: Tough fibrous sac surrounding the heart providing protection.

  • Great Vessels: Include internal jugular veins, phrenic nerve, subclavian arteries and veins, superior vena cava, pulmonary arteries, and more.

• Components:

  • Right internal jugular vein, right brachiocephalic vein, brachiocephalic trunk, arch of aorta, left common carotid artery, left internal jugular vein, left vagus nerve, pulmonary trunk, coronary sulcus, etc.

CARDIOVASCULAR ANATOMY & PHYSIOLOGY

CARDIAC MUSCULAR LAYERS

• Components:

  • Anterior (anterolateral) papillary muscle

  • Posterior papillary muscle

  • Medial (septal) papillary muscle

• Function: These muscles are vital for heart contraction and valve function.

CARDIAC FIBROSKELETON

• Structure: Composed of fibrous rings around the heart valves including:

  • Bicuspid ring

  • Aortic ring

  • Tricuspid ring

  • Pulmonary ring

• Significance: Provides structural support and a point of attachment for cardiac muscles.

CARDIAC PHYSIOLOGY

Automaticity & Rhythmicity

• Definition: Automaticity refers to the heart's ability to generate its own electrical impulses without external stimuli.

• Rhythmicity: The pace and regularity of these impulses as they spread through the heart tissue.

Excitation-Contraction Coupling

• Definition: The physiological process of converting an electrical stimulus into a mechanical response.

• Involves calcium ion influx and binding to troponin, resulting in muscle contraction.

Cardiac Output (CO)

• Formula: $CO = SV imes HR$

  • Where:

  • CO = Cardiac Output

  • SV = Stroke Volume

  • HR = Heart Rate

• Determinants:

  • Heart Rate Control: Influenced by the autonomic nervous system and catecholamines.

  • Stroke Volume Determinants:

  • Preload (Frank-Starling’s Law)

  • Afterload

  • Contractility

Stroke Volume (SV)

• Definition: The amount of blood ejected by the heart in one contraction.

• Determinants:

  • Preload: Tension on the heart muscle before contraction determined by venous return and end-diastolic volume.

  • Frank-Starling Law: Increase in preload increases force of contraction to a point.

  • Afterload: The load against which the heart must contract (end-systolic pressure).

  • Contractility: Muscle performance independent of preload and afterload.

CARDIAC CYCLE

• Flow Path: Blood moves sequentially through heart chambers from:

  • Vena Cava → Right Atrium (RA) → Right Ventricle (RV) → Pulmonary Arteries → Lungs → Left Atrium (LA) → Left Ventricle (LV) → Aorta → Body/Organs → Returns to Vena Cava.

STROKE VOLUME DETERMINANTS

• Factors Affecting Stroke Volume:

  • Increased: Preload through fast filling times, increased venous return, sympathetic stimulation, increased calcium, and hormonal influences.

  • Decreased: Afterload, decreased heart muscle performance, and various pathologies.

FACTORS AFFECTING HEART RATE (HR)

• Influenced by:

  • Autonomic innervation

  • Hormonal effects

  • Age and fitness levels.

AVERAGE RESTING ADULT CARDIAC OUTPUT

• Average Value: Approximately $5 ext{ L/min}$ for untrained individuals.

• Examples:

  • Men: $5000 ext{ mL} = 70 ext{ bpm} imes 71 ext{ mL}$

  • Trained: $5000 ext{ mL} = 50 ext{ bpm} imes 100 ext{ mL}$

CONTROL OF BLOOD PRESSURE

• Key Determinants:

  • Heart Rate: Average resting HR = $70 ext{ bpm}$

  • Stroke Volume: Average resting SV = $72 ext{ mL}$

  • Blood Volume: Average = $5 ext{ L}$

  • Peripheral/Systemic Vascular Resistance

• Basic Formula:

  • $BP ext{ (Blood Pressure)} = CO imes SVR ext{ (Systemic Vascular Resistance)}$

PULMONARY ANATOMY & PHYSIOLOGY

VENTILATION

• Definition: The process of air exchange in the lungs.

  • Involved structures: trachea, bronchi, lungs, ribs, diaphragm.

AIRWAYS & ALVEOLI

• Key Components:

  • Main bronchi: Right and Left mainstem bronchi.

  • Alveoli: Gas exchange sites.

• Alveolar Types:

  1. Type I cells: For diffusion.

  2. Type II cells: Produce surfactant.

RESPIRATORY VOLUMES & CAPACITIES

• Main Volumes:

  • Tidal Volume (TV)

  • Inspiratory Reserve Volume (IRV)

  • Expiratory Reserve Volume (ERV)

  • Residual Volume (RV)

  • Total Lung Capacity (TLC)

DEAD SPACES

• Definition: Volume not involved in gas exchange.

  • Types:

  • Anatomic Dead Space: Conducting airways.

  • Physiologic Dead Space: Increased in diseased alveoli.

ALVEOLAR VENTILATION

• Calculation:

  • $Va = (V<em>t – V</em>D) imes RR$

  • Where:

    • $V_t$: Tidal Volume

    • $V_D$: Dead Space

    • $RR$: Respiratory Rate

DIFFUSION

• Mechanism: Movement of gases across membranes (e.g., alveolar and capillary membranes).

• Factors Affecting Diffusion:

  • Surface area, thickness, and concentration gradient.

HEMOGLOBIN-O2 DISSOCIATION CURVE

• Demonstrates how oxygen is picked up and released from hemoglobin based on:

  • Partial pressure of oxygen (PaO2)

  • pH and temperature influence (Bohr Effect).

CONTROL OF BREATHING

• Neural Control: Stimulated by brainstem centers affecting pulmonary pacemaker.

• Chemical Control: Involves receptors that respond to H+, PaCO2, and PaO2 changes.

• Voluntary & Involuntary changes influence respiratory rate and depth.

CONDITIONS OF ACID-BASE IMBALANCE

• Respiratory Acidosis: Low pH due to hypoventilation.

• Respiratory Alkalosis: High pH from hyperventilation.

• Metabolic Acidosis: Poor buffering capacity.

• Metabolic Alkalosis: Excessive base accumulation.

SUMMARY: VENTILATION & PERFUSION MATCHING

• Efficient gas exchange relies on matching ventilation to perfusion.

• Factors affecting efficiency include lung compliance, surface tension, and pressures in alveoli and capillaries.