Cardiovascular III

Cardiac Output

• Cardiac output is the volume of blood ejected by the heart per minute.
• It can be calculated by multiplying heart rate by stroke volume.
• Cardiac output is influenced by sympathetic and parasympathetic nervous systems, contraction strength, and end-diastolic volume.
• End-diastolic volume is the volume of blood in the ventricles at the end of diastole.

Heart Rate Regulation

• Denervated heart rate is intrinsically dictated by the SA node.
• The heart rate is primarily controlled by sympathetic/adrenal medulla and parasympathetic nervous systems.
• Sympathetic stimulation and adrenal medulla increase heart rate while parasympathetic stimulation decreases it.

Stroke Volume Regulation

• Stroke volume is the volume of blood ejected per heartbeat, determined by the difference between end-diastolic volume (EDV) and end-systolic volume (ESV).
• EDV, also known as preload, is the volume of blood in the ventricles at the end of diastole.
• ESV, also known as afterload, is the amount of blood remaining in the ventricle after systole.

Effect of End-Diastolic Volume

• An increase in EDV leads to an increase in stroke volume.
• The Frank-Starling Law of the Heart describes the relationship between preload and contractility.
• Increased preload causes increased contractility and stroke volume.
• Stretching of the cardiac muscle fibers at the end of diastole improves calcium binding to troponin-C, enhancing contractility.

Factors Affecting Preload

• Venous return is the primary determinant of preload (EDV).
• Increased venous return leads to increased EDV.
• Decreased venous return leads to decreased EDV.

Venous Return

• The pressure difference between the large veins and the right atrium drives venous return.
• The skeletal muscle pump and respiratory pump contribute to venous return.
• Increased blood volume raises venous return.
• The autonomic nervous system regulates venous return through sympathetic innervation of smooth muscle in veins.

Factors Affecting Afterload

• Afterload is the resistance the ventricles face during ejection.
• During exercise, afterload is regulated by sympathetic nervous system-induced increased contractility, resulting in lower ESV.
• During rest, arterial vasomotor tone, known as total peripheral resistance (TPR), is the main determinant of afterload.
• Blood pressure is a surrogate indicator of afterload.

Blood Vessels

• Key properties of blood vessels include diameter, elasticity, and contractility.

Blood Flow

• Flow refers to the fluid volume transported per unit time.
• Flow is influenced by pressure difference between two points and resistance to flow.
• Arteries have higher pressure than veins.
• Arterioles serve as the "bottlenecks" and are crucial for pressure and flow regulation due to their abundance of smooth muscle.

Significance of Pressure Difference

• The pressure difference between two points, rather than the absolute pressure, is the primary driver of flow.
• Initial pressure originates from heart contraction.

Resistance to Flow

• Vessel's length contributes to resistance, but is often constant within an individual.
• Vessel's radius is the most important factor influencing resistance.
• Viscosity of blood, determined by cells and protein concentration, also affects resistance but is not the primary regulator.

Arterial Pressure During a Cardiac Cycle

• Aortic valve opening during ventricular contraction results in rapid blood flow, increased arterial pressure, and temporary energy absorption by aorta's elasticity.
• Aortic valve closure during diastole stops blood flow from the ventricle, causing stored energy release from aorta and gradual pressure decrease.

Arteries

• Arteries are compliant due to their elastic, large diameter walls.
• This elasticity limits pressure drop after systole, ensuring more continuous blood flow.

Aortic Blood Pressure Profile

• Systolic pressure is high during contraction.
• Diastolic pressure is lower during relaxation.
• Mean blood pressure (MBP) represents the average pressure over a cardiac cycle.

Factors Influencing Arterial Pressure

• Elasticity of arteries: Low elasticity leads to high pressure.
• Cardiac output: A higher cardiac output results in increased pressure.
• Respiration: Inspiration decreases thoracic pressure and increases abdominal pressure, affecting blood flow. Expiration reverses this effect.
• Resistance to flow (TPR): Vasoconstriction of arterioles increases TPR and pressure.
• Blood volume: Primarily affects cardiac output (minimal direct effect on pressure due to vein absorption).

Control of Vascular Resistance

• smooth muscle in arteriole walls:
  • Arterioles possess less elasticity and more smooth muscle fibers.
  • Myogenic tone (basal tone) creates a baseline level of constriction, allowing for diameter changes.
  • Constriction increases resistance.

Blood Pressure Control: Local vs. Extrinsic

• Local (Autoregulation)
  • Controls flow to critical organs (heart, brain, liver, kidneys)
  • Metabolic regulation: Responses to changes in metabolism, like CO2, pH, K+, and NO, lead to dilation.
  • Myogenic regulation: Vessels respond to stretching by adjusting diameter, maintaining flow despite pressure changes.
• Extrinsic:
  • Regulates systemic pressure.
  • Vasoconstrictors: Sympathetic stimulation, angiotensin II, and arginine vasopressin.
  • Vasodilators: Parasympathetic stimulation (mainly in penis and clitoris).

Veins and Venous Pressure

• Blood pressure is low in the veins (around 10 mm Hg) yet blood continues toward the right atrium due to sufficient pressure difference.
• The heart's sucking action during relaxation helps draw blood upwards.
• Skeletal muscle activity assists in propelling blood back to the heart.
• Veins have smooth muscles but minimal resistance.
• High pressure in veins can cause fluid leakage and tissue edema.

Blood Pressure Control Mechanisms

• Key variables include:
  • Heart rate
  • Stroke volume
  • TPR (extrinsic regulation)
• Blood pressure reflexes involve:
  • Baroreceptors
  • Sensory fibers
  • Integration center
  • Motor fibers
  • Effectors

Baroreceptors

• Stretch receptors in arterial walls (aortic arch and carotid sinus) that sense pressure changes.
• Increased stretching causes increased action potential frequency.
• Decreased stretching causes decreased action potential frequency.

Sensory Fibers

• Transmit signals from baroreceptors via the vagus nerve to the integration center.

Integration Center

• Located in the cardiovascular (vasomotor) center in the medulla oblongata.
• Compares incoming signals to a reference value.

Motor Fibers

• Transmit signals via the autonomic nervous system (both sympathetic and parasympathetic) to effectors.

Effectors

• Heart: Regulates heart rate and stroke volume.
• Arterioles and veins: Modulate TPR.

Baroreceptor Action

• High pressure:
  • Increased stretch of baroreceptors
  • Increased action potential frequency to integration center
  • Integration center triggers parasympathetic nervous system and reduces sympathetic activity
  • Decrease heart rate, stroke volume, TPR, and overall blood pressure.
• Low pressure:
  • Decreased stretch of baroreceptors
  • Decreased action potential frequency to integration center
  • Integration center triggers sympathetic nervous system and reduces parasympathetic activity
  • Increase heart rate, stroke volume, TPR, and overall blood pressure.

Test your knowledge on cardiac output, heart rate regulation, and stroke volume. This quiz covers essential concepts such as the role of sympathetic and parasympathetic systems and the definitions of key terms like end-diastolic volume. Challenge yourself with questions that explore how these factors interact to influence cardiovascular health.