Control of Cardiac Output (Stroke Volume & Heart Rate)

Control of Cardiac Output (Stroke Volume & Heart Rate)

Learning Objectives

  • Understanding Cardiac Output (CO): By the end of this session, students should be able to describe:

    • The variables that determine cardiac output

    • How heart rate is controlled by the autonomic nervous system

    • The role of veins in determining cardiac output

    • Intrinsic and extrinsic mechanisms that alter stroke volume (SV) and affect cardiac output

Key Equations

  • Cardiac Output (CO) = Heart Rate (HR) x Stroke Volume (SV)

  • Alternate Representation: CO = HR x (End Diastolic Volume (EDV) - End Systolic Volume (ESV))

  • Typical cardiac output is about ~5L/min

Control of Heart Rate

  • Cardiac muscle cells can depolarize and contract without neural input, known as myogenic rhythmicity or autorhythmicity.

  • The SA node (Sinoatrial node) acts as the heart's pacemaker located in the right atrium.

Autonomic Control of the Heart

  • The autonomic nervous system has two branches that control heart rate antagonistically:

    • Parasympathetic System:

    • Decreases heart rate

    • Uses acetylcholine (Ach) at M2 receptors leading to a hyperpolarizing effect (increases K+ permeability)

    • Sympathetic System:

    • Increases heart rate

    • Increases Na+ and Ca2+ permeability via norepinephrine (NorAd) at beta-1 receptors, causing depolarization and a positive chronotropic effect

Variables Affecting End Diastolic Volume (EDV)

  • EDV: Volume of blood in the ventricle at the end of diastole, approximately 120 ml. It is influenced by:

    1. Venous Return

    2. Central Venous Pressure (CVP)

Factors Affecting Venous Return

  1. Skeletal Muscle Pump: Muscle contractions pushing blood towards the heart against gravity.

  2. Respiratory Pump: Changes in thoracic pressure during breathing affecting venous return.

  3. Blood Volume: Increased blood volume raises venous return while decreased blood volume lowers it (e.g., due to hemorrhage or dehydration).

  4. Venous Tone: The compliance of veins, affected by sympathetic stimulation, controls the capacitance of veins (60-80% of total blood volume).

  5. Gravity: Affects venous return significantly when standing due to hydrostatic pressure.

Stroke Volume (SV) Control

  • SV = EDV - ESV

  • Increased EDV leads to increased SV through:

    • Frank-Starling Mechanism: Increased ventricular filling leads to a greater force of contraction (according to the length-tension relationship).

    • Contractility (Inotropy): Increased sympathetic stimulation boosts contractility via beta-1 receptor activation leading to more cross-bridge formation between actin and myosin, enhancing force of contraction and thus increasing SV while decreasing ESV.

Afterload Effects on Stroke Volume

  • Afterload is the pressure the heart must work against to eject blood:

    • Left Ventricle Afterload: Primarily the aortic pressure which relates to systemic vascular resistance (Total Peripheral Resistance - TPR).

    • Right Ventricle Afterload: Affected by pulmonary pressure, generally lower than left ventricular afterload.

Summary of Key Points

  • Control of HR: SA node's activity is the primary control point for heart rate changes influenced by autonomic input.

  • Increasing Stroke Volume: Achievable via enhancing EDV (venous return) or contractility, keeping ESV in mind to maintain an optimal output.

  • Autonomic Regulation: Both sympathetic and parasympathetic systems play crucial roles in adjusting heart rate dynamically to meet physiological demands.

Conclusion

  • Understanding the interaction between heart rate and stroke volume is crucial for appreciating changes in cardiac output during various bodily demands such as exercise, stress, and overall cardiovascular health.