Cardiac Output, Blood Flow, and Blood Pressure

Cardiac Output, Blood Flow, and Blood Pressure

Cardiac Output

• Definition: The volume of blood pumped each minute by each ventricle.

  • Formula: \text{cardiac output} = \text{stroke volume} \times \text{heart rate} \quad (\text{ml/min}) \quad (\text{ml/beat}) \quad (\text{beats/min})

• Average Values:

  • Average heart rate = 70 beats per minute (bpm)

  • Average stroke volume = 70-80 milliliters (ml/beat)

  • Average cardiac output = 5,500 ml/minute

Cardiac Output Increases During Exercise

• At Rest:

  • Cardiac output = 5.8 L/min.

• During Vigorous Exercise:

  • Cardiac output = 25.6 L/min.

• Distribution: Blood flow distribution at rest vs. vigorous exercise

  • Brain: Rest: 13%, Exercise: 3%

  • Kidneys: Rest: 4%, Exercise: 1%

  • GI Tract: Rest: 19%, Exercise: 9%

  • Skin: Rest: 2.5%, Exercise: 0.5%

  • Other Tissues: Rest: 10%, Exercise: 88% to Skeletal Muscles

Regulation of Cardiac Output

• Heart Rate: Determined by the rate of depolarization in autorhythmic cells.

  • Increases/Decreases:

  • Increase: Due to sympathetic innervation

  • Decrease: Due to parasympathetic innervation

• Stroke Volume: Function of:

  • Force of contraction in ventricular myocardium

  • Influenced by contractility and end-diastolic volume (EDV)

  • Influenced by:

    • Epinephrine (increases contractility)

    • Venous constriction (increases EDV)

• Venous Return: Aided by skeletal muscle pump and respiratory pump.

Autonomic Regulation of Heart Rate

• Increase in Heart Rate (HR) can be achieved by:

  • Decreasing parasympathetic activity

  • Increasing sympathetic input: Norepinephrine (NE) or Epinephrine (E) act on b1-receptors to speed up depolarization rate of autorhythmic cells.

• ACh (Acetylcholine): Slows the conduction of action potentials (APs) through the AV node (increases AV node delay).

Action Potentials in Autorhythmic Cells

• Nature of Autorhythmic Cells: Ability to generate action potentials spontaneously.

  • Membrane Potential:

  • Starts from a less negative state,

  • Threshold reached when Ca²⁺ channels open leading to depolarization.

  • Ion Movements During an Action Potential:

  • Lots of Ca²⁺ channels open, then close as K⁺ channels open leading to repolarization.

• Pacemaker Potential:

  • Gradually becomes less negative until threshold is reached, triggering an action potential.

Modulation of Action Potentials

• Influence of Ion Permeability:

  • Increased permeability to Na⁺ and Ca²⁺ speeds up depolarization (positive chronotropic effect).

  • Increased permeability to K⁺ causes hyperpolarization (negative chronotropic effect).

Autonomic Effects on the Heart

• Table of Autonomic Nerve Activity:

  • Sympathetic Effects:

  • SA Node: Increased conduction rate and rate of diastolic depolarization; increased cardiac rate.

  • AV Node: Decreased conduction rate.

  • Atrial Muscle: Increased strength of contraction.

  • Ventricular Muscle: Increased strength of contraction.

  • Parasympathetic Effects:

  • SA Node: Decreased rate of diastolic depolarization; decreased cardiac rate.

  • AV Node: Decreased conduction rate.

Factors Regulating Cardiac Output

• Stroke Volume Regulation:

  • End-Diastolic Volume (EDV) – Preload. Higher EDV results in increased contractility.

  • Total Peripheral Resistance – Afterload (End-Systolic Volume, ESV).

  • Ejection Fraction: Percentage of EDV that is ejected during ventricular contraction.

Frank-Starling Law of the Heart

• Definition: Stroke volume is proportional to end-diastolic volume (EDV).

• Length-Force Relationship: Muscle length (determined by volume of blood in ventricle) affects contraction strength.

• Preload: Degree of stretch of myocardial fibers before contraction begins.

Control of Contraction Strength

• Intrinsic Control:

  • Actin-myosin cross-bridging influences tension production.

  • Stretch of myocardium results in sensitivity of Ca²⁺ release channels.

Extrinsic Control of Contractility

• Iotropic Effect: Increases in contraction strength via increased calcium availability to sarcomeres.

Venous Return

• Definition: Amount of blood entering the heart from the venous circulation.

• Factors Affecting Venous Return:

  • Blood Volume.

  • Negative intrathoracic pressure (respiratory pump).

  • Venous pressure.

Laws of Blood Flow

• Poiseuille's Law: Describes blood flow through vessels.

  • \text{blood flow} = \frac{AP \cdot \pi r^4}{8nL} where AP = pressure, r = radius, n = viscosity, L = length of vessel.

Velocity of Blood Flow

• Determinant for Velocity: Total cross-sectional area of vessels.

• Slowest Flow: Occurs in capillaries and venules, allowing sufficient time for diffusion to reach equilibrium.

Blood Pressure Dynamics

• Pressure Differences in systemic circulation:

  • Highest pressure in arteries (e.g., aorta) decreasing throughout circulatory system to lowest in vena cavae.

• Main Factors Affecting Blood Pressure:

  • Cardiac Output (Stroke Volume, Heart Rate)

  • Total Peripheral Resistance (via vasoconstriction/dilation)

  • Blood Volume

• Resistance: Greatest in arterioles, which are narrower than larger arteries.

Baroreceptor Reflex

• Function: In response to increased blood pressure, baroreceptors in the walls of vessels produce more action potentials.

• Information Integration: Relayed to the medulla oblongata to control cardiac rate and total peripheral resistance.

• Sensitivity: Reflex is more sensitive to decreases in pressure.

Abnormal Blood Pressure Conditions

• Hypotension:

  • BP falls too low, impairing blood flow and oxygen supply (can cause dizziness or fainting).

• Hypertension:

  • Chronic elevation of BP may lead to vascular damage, e.g., cerebral hemorrhages or arterial rupture.

• Treatment Measures:

  • Lifestyle modifications (e.g., smoking cessation, exercise).

  • Medications: Diuretics, Beta blockers, ACE inhibitors, ARBs (angiotensin receptor blockers).