Cardiac Parameters and Regulation Notes

Cardiac Innervation, Regulation, and Hemodynamics

  • Adrenal medulla
    • Source of circulating catecholamines that affect heart function
  • Cardioregulatory center and chemoreceptors in medulla oblongata
    • Central control of autonomic output to the heart
  • Sensory nerve fibers / Baroreceptors / Chemoreceptors
    • Baroreceptors in walls of internal carotid artery and aorta detect blood pressure changes
    • Carotid body chemoreceptors respond to chemical changes (e.g., O2, CO2, pH)
  • Parasympathetic and Sympathetic efferents to the heart
    • Parasympathetic nerve fibers via the Vagus nerves
    • Sympathetic nerve fibers to cardiac tissue and to the adrenal gland
  • SA node and AV node as primary cardiac pacemakers and conductors
    • Innervation patterns influence heart rate and conduction velocity
  • Epinephrine and norepinephrine
    • Hormonal mediators of sympathetic activation affecting heart rate and contractility
  • Synoptic view of control pathways
    • Central reflexes and peripheral sensors coordinate the cardiac response to activity and environment

Cardiac Parameters

  • Heart Rate (HR)
    • Definition: number of heart beats per minute
    • Resting heart rate: approximately HRextrest ≈ 72 bpmHR_{ ext{rest}} \,\approx\,72\,\text{bpm}
    • Cardiac cycle duration: approximately Textcycle≈0.8 sT_{ ext{cycle}} \approx 0.8\ \text{s}
  • End-Diastolic Volume (EDV)
    • Volume of blood in each ventricle at the end of filling
    • Typical value: EDV≈120 to 130 mlEDV \approx 120 \text{ to } 130\ \text{ml}
  • End-Systolic Volume (ESV)
    • Volume of blood in each ventricle at the end of emptying
    • Typical value: ESV≈50 to 60 mlESV \approx 50 \text{ to } 60\ \text{ml}
  • Stroke Volume (SV)
    • Volume of blood ejected during each heartbeat
    • Formula: SV=EDV−ESVSV = EDV - ESV
    • Typical value: SV≈70 mlSV \approx 70\ \text{ml}

Cardiac Output and Cardiac Reserve

  • Cardiac Output (CO)
    • Definition: volume of blood ejected by the heart per minute; measure of heart performance
    • Formula: CO=HR×SVCO = HR \times SV
  • Resting CO (typical values)
    • Example: CO=75 bpm×70 ml/beat=5250 ml/min=5.25 L/minCO = 75\ \text{bpm} \times 70\ \text{ml/beat} = 5250\ \text{ml/min} = 5.25\ \text{L/min}
  • Exercise/Activity: CO increase capability
    • CO can increase markedly with physical activity to > 20 \text{–} 30\ \text{L/min}
  • Cardiac reserve
    • Definition: difference between resting CO and maximum CO achievable
    • Indicates the heart’s capacity to increase output during activity
  • Factors altering CO
    • CO is altered by factors that change either HR or SV (or both)

Regulation of the Heart: Intrinsic Regulation

  • Intrinsic regulation
    • Results from the heart’s own functional characteristics; does not depend on neural or hormonal input
  • Preload and venous return
    • Venous return equals end-diastolic volume (EDV)
    • EDV determines the stretch of ventricular walls (preload)
  • Starling’s law of the heart
    • Increased preload causes greater contraction force and greater SV
    • Mechanistic link: stretch of cardiac muscle cells enhances the force of contraction
  • Afterload
    • Definition: the pressure the contracting left ventricle must overcome to move blood into the aorta
    • Higher afterload reduces the ease of ejection and can affect SV

Regulation of the Heart: Extrinsic Neural Regulation

  • Neural control via SA and AV nodes
    • Innervated by both sympathetic and parasympathetic nerves
  • Cardioregulatory center
    • Located in the medulla oblongata; coordinates autonomic output
  • Parasympathetic control (via vagus nerve)
    • Innervates SA and AV nodes
    • Transmitter: Acetylcholine (ACh)
    • Effect: Slow HR; dominant at rest
  • Sympathetic control (thoracic spinal cord)
    • Innervates the SA node (and other cardiac tissues)
    • Transmitter: Epinephrine and Norepinephrine
    • Effect: Increase HR

Regulation of the Heart: Hormonal Controls

  • Epinephrine and norepinephrine from the adrenal medulla
    • Sympathetic stimulation increases their release
    • Effects: increase HR and the force of contractions
  • Triggers for secretion
    • Increased physical activity, emotional excitement, or any stressful situation
  • Mechanism and scope
    • Secretion is controlled by sympathetic stimulation
    • Hormonal actions complement neural inputs on SA/AV nodes
  • Other factors influencing HR (non-neural/hormonal)
    • Body temperature, drugs, sleep, psychological factors (stress, fear) can also affect HR

Factors Affecting Stroke Volume

  • The three primary determinants: preload, contractility, afterload

  • Preload

    • Definition: extent of ventricular wall stretch before contraction
    • Linked to EDV (end-diastolic volume)
    • Relationship to SV: the greater the EDV, the greater the SV (Starling mechanism)
    • Venous return is the major determinant of EDV

  • Contractility (inotropy)

    • Definition: the intrinsic strength of ventricular contraction at a given preload
    • Depends on Ca^{2+} availability in muscle fibers during contraction
    • Calcium effects: higher Ca^{2+} increases contractility; lower Ca^{2+} decreases contractility
    • Positive inotropes (increase contractility):
    • Sympathetic stimulation via ventricular innervation
    • Adrenaline and noradrenaline acting on β1 receptors
    • Digoxin
    • Negative inotropes (decrease contractility):
    • Decreased sympathetic stimulation
    • β-blockers

  • Afterload (restated)

    • Definition: the force opposing the ejection of blood from the ventricle
    • Left ventricle vs right ventricle: left ventricle faces a higher afterload
    • Pressures involved
    • Mean pulmonary arterial pressure for the right ventricle: PextRV≈15–20 mmHgP_{ ext{RV}} \approx 15 \text{–} 20\ \text{mmHg}
    • Aortic pressure for the left ventricle: PextLV≈100 mmHgP_{ ext{LV}} \approx 100\ \text{mmHg}
    • Consequences of higher afterload in LV
    • Higher workload
    • Greater muscle mass in LV
    • Higher O2 consumption requiring good coronary blood flow

Summary of Key Points

  • Cardiac parameters covered:
    • Heart rate (HR)
    • Cardiac volumes: EDV, ESV
    • Stroke volume (SV)
    • Cardiac output (CO)
  • Regulation of the heart:
    • Intrinsic regulation (Starling mechanism, preload, afterload)
    • Extrinsic regulation (neural and hormonal controls)
  • Neuronal factors
    • SA and AV nodes innervation
    • Medullary cardioregulatory center
    • Parasympathetic (ACh) vs sympathetic (epinephrine/norepinephrine) balance
  • Hormonal factors
    • Epinephrine and norepinephrine from adrenal medulla
    • Role in HR and contractility during stress/exertion
  • Factors affecting stroke volume
    • Preload, contractility, afterload
  • Preload relationships
    • EDV-dependent; Starling’s law explains SV changes with EDV
  • Contractility determinants
    • Ca^{2+} dynamics, sympathetic input, pharmacologic agents (Digoxin, β-blockers)
  • Afterload considerations
    • Higher in LV due to systemic circulation; lower in RV due to pulmonary circulation
  • Short references
    • Content and images referenced from Seeley’s Anatomy & Physiology (12th Ed), Van Putte, Regan, Russo (2020)
  • Seeley’s Anatomy & Physiology (12th Ed), McGraw-Hill
  • Seeley, Van Putte, Regan, Russo 2020 reference for content and images