ch 14 pt 1

Blood Vessels, Blood Flow, and Blood Pressure

Physical Laws Governing Blood Flow and Pressure

  • These laws apply to any liquid flowing through pipes, relevant to blood flow in the cardiovascular system.

Flow Rate

  • Definition: Volume of liquid flowing per unit of time.
  • Units: Milliliters per minute (mL/min) or liters per minute (L/min).
  • Directly proportional to the pressure gradient (\Delta P).
  • Inversely proportional to resistance (R).
  • Equation: Flow = \frac{\Delta P}{R}

Pressure Gradient

  • Driving force pushing liquid flow through a pipe.
  • In cardiovascular system, blood flow is an example of bulk flow.

Bulk Flow

  • Movement of a mass of fluids (or gases) down its pressure gradient.
  • Direction: Always from high to low pressure.

Resistance

  • Measure of factors hindering liquid flow in a pipe.
  • Inverse relationship to flow rate: Increased resistance decreases flow (if pressure is constant).

To increase blood flow to an organ/tissue:

  • Increase the pressure gradient.
  • Decrease resistance (primarily via vasodilation, increasing blood vessel radius).

Blood Flow Through Systemic Circuit

  • Flow rate is directly proportional to pressure gradient.
  • Pressure gradient is the difference between pressures at two ends of the "pipe".

Simplified Model:

  • Beginning pressure: Mean Arterial Pressure (MAP) in the aorta.
  • MAP ≈ 85 mmHg.
  • Ending pressure: Central Venous Pressure (CVP) in the thoracic cavity's large veins returning blood to the heart.
  • CVP ≈ 0 mmHg (simplified).
    Pressure\ Gradient = MAP - CVP = 85\ mmHg

Blood Flow Through Pulmonary Circuit

  • Pressure gradient is the difference between pulmonary artery and vein pressures.
  • Pulmonary arterial pressure = 15 mmHg.
  • Pulmonary venous pressure = 0 mmHg.
  • Pressure gradient = 15 mmHg.
  • The same volume of blood must circulate in both circuits.
  • Lower pressure in pulmonary circuit is compensated by lower resistance, to maintain equal flow.

Factors Determining Resistance

  • Determined by physical dimensions of blood vessels and properties of blood itself.

Physical Dimensions of Blood Vessels

  • Length: Longer pipes have greater resistance; however, it's not adjustable in the body.

  • Radius/Diameter: Adjustable and the main way to alter resistance.

    • Vasoconstriction: Decreases radius, increases resistance, decreases flow.
    • Vasodilation: Increases radius, decreases resistance, increases flow.

  • Properties of blood, blood viscosity (thickness) is not changeable in the short term under normal conditions.

  • Systemic circuit resistance is higher than in the pulmonary circuit.

Resistance of an entire blood vessel network is the combination of individual vessel resistances within that network.

  • Vasoconstriction/vasodilation anywhere affects the whole network.
  • Total Peripheral Resistance (TPR): Total resistance in the systemic circuit.

Applying the Flow Rule to the Systemic Circuit

  • Substitute cardiac output for flow.
  • Substitute mean arterial pressure for pressure gradient.
  • Substitute total peripheral resistance (TPR) for resistance.
    Cardiac\ Output = \frac{Mean\ Arterial\ Pressure}{Total\ Peripheral\ Resistance}
  • Bulk Flow Law for the cardiovascular system.

Blood Vessel Classification and Structure

  • Arteries: Carry blood away from the heart.
  • Veins: Return blood to the heart.
  • Capillaries: Sites of material exchange (oxygen, nutrients, waste).

Blood Vessel Wall Layers (Arteries & Veins)

  • Outer layer: Fibrous connective tissue (collagen).
  • Middle layer: Smooth muscle.
  • Inner layer: Endothelium (simple squamous).
  • Collagen provides strength; elastic tissue allows expansion/recoil.

Capillaries

  • Endothelium and basement membrane only; very thin walls for rapid diffusion.

Artery Structure

  • Large arteries have thick walls with much elastic and fibrous connective tissue, and thick muscular layers as well.
  • Arteries serve as a pressure reserviour.
  • Smaller arteries and arterioles have less elastic tissue but more smooth muscle for radius regulation.
  • Arterioles are where resistance is most regulated.

Veins structure

  • Veins have thinner walls and less smooth muscle, serving as volume reservoirs.
  • Veins hold more blood than arteries.

Capillary Beds

  • Require relaxed precapillary sphincters to be open.
  • Blood is diverted through metarterioles if sphincters are closed.
  • About 75% of capillary beds are shut down at any time.

Overview of Blood Flow Through Blood Vessels

  • Continuous movement due to arteries acting as pressure reservoirs.
  • Blood flows through the path of least resistance.
  • Highest resistance occurs in smaller arteries and arterioles.
  • Arterioles control tissue blood flow.
  • Capillaries have high cross-sectional area, slowing blood flow for material exchange.
  • Veins serve as volume reservoirs returning blood to the heart.

Arteries: Pressure Reservoirs

  • Elastic connective tissue (elastin fibers) allows expansion and recoil.
  • Elastic force stored during systole propels blood during diastole.
  • Walls are thick with smooth muscle, fibrous tissue, and elastic tissue.
  • Low compliance: Large pressure increases cause small volume changes.

Arterial Blood Pressure

  • Pressure exerted by blood on artery walls (typically in the aorta).
    • Systolic Pressure: Maximum pressure during systole.
    • Diastolic Pressure: Minimum pressure during diastole.
    • Mean Arterial Pressure: Average pressure during one cardiac cycle, an average aortic pressure during the cardiac cycle.
  • Usually measured in the brachial artery as an estimate of aortic pressure.

Blood Pressure Measurement

  • Two numbers: Systolic/Diastolic.
  • Measured in millimeters of mercury (mmHg).
  • Healthy average: 110/70 to 120/80 mmHg.
  • Sphygmomanometer: Inflatable cuff with pressure gauge.
  • Stethoscope: Listens for Korotkoff sounds.
    • Cuff inflated above systolic pressure collapses the artery (no sound).
    • Pressure lowered below systolic allows brief opening with each heartbeat, causing turbulent flow (Korotkoff sounds).
    • First sound indicates systolic pressure.
    • Sounds disappear when cuff pressure is below diastolic, as laminar flow returns.

Determining Pulse Pressure and Mean Arterial Pressure:

Pulse Pressure

Is the difference between systolic and diastolic pressure.
Pulse\ Pressure = Systolic\ Pressure - Diastolic\ Pressure

  • Normal value = 40 mmHg.
  • Affected by stroke volume, speed of ejection, arterial compliance.
  • High pulse pressure may indicate hardening of arteries.

Mean Arterial Pressure (MAP)

  • Average arterial pressure during one cardiac cycle.
  • Weighted mean to emphasize time spent in systole vs diastole.
    MAP = Diastolic\ Pressure + \frac{1}{3}(Pulse\ Pressure)
  • Acts as driving force for blood through the systemic circuit.

Arterioles: Gatekeepers to Capillaries

  • Connect small arteries to capillary beds.
  • Contain rings of smooth muscle to alter vessel radius and resistance.
  • Contraction decreases the radius, and increases resistance.
  • Relaxation increases the radius and decreases resistance.
  • Major site of resistance regulation (over 60% of total peripheral resistance).
  • Cause the largest drop in blood pressure.

Major Roles

  • Control blood flow to individual capillary beds.
  • Regulate mean arterial pressure.
  • Smooth muscle tone: Partially contracted state due to inherent activity and sympathetic input.
    • Intrinsic Control Mechanisms: Local metabolites and gases regulate blood flow to match metabolic needs.
      • Extrinsic Control Mechanisms: Autonomic nervous system and hormones regulate smooth muscle contraction and mean arterial pressure.
        Vasoconstriction: Contraction of smooth muscle cells decreases the radius (decreasing flow).
        Vasodilation: Relaxation of smooth muscle cells increases the radius (increasing flow).

The contraction and relaxation of the circular smooth muscle.

Control Mechanisms

  • Organs and tissues can regulate their own blood flow through local contros, and this depends on their metabolic needs.
  • Local Control: Paracrine regulators and myogenic autoregulation act locally.
  • Extrinsic Factors: Sympathetic activity and hormonal influence regulate mean arterial pressure.

Intrinsic Control Mechanisms of Blood Flow Distribution

  • Blood is distributed based on metabolic needs.
  • Organs regulate their own flow via local controls.
    Organ\ Blood\ Flow = \frac{Mean\ Arterial\ Pressure}{Organ\ Resistance}
  • Vascular resistance altered by smooth muscle contraction/relaxation.
  • Intrinsic controls are important for the heart, skeletal muscles, and the brain.
  • Smooth muscle is sensitive to extracellular fluid conditions and responds to metabolic activity, changes in blood flow, stretch, and local chemical messengers.

Smooth Muscle Response to Metabolic Activity

  • Increase in metabolic activity
  • Decrease in metabolic activity

Increase Metabolic Activity

  • Decrease in oxygen levels
  • Increase in carbon dioxide levels
  • Decrease in pH.

These changes cause smooth muscle relaxation and vasodilation.

Decrease in Metabolic Activity

Increase in oxygen levels.
Decrease in carbon dioxide levels.
Gases and metabolites act on smooth muscle to induce vasoconstriction.

Blood Flow Changes with Increased Metabolic Activity

  • Initially, blood flow is insufficient, leading to ischemia: Blood flow is inadequate.
  • Decreased oxygen, increased carbon dioxide, and decreased pH result.
  • Smooth muscle relaxes resulting in vasodilation lowering vascular resistance.
  • Active Hyperemia: Increased blood flow following increased metabolic activity.
  • Increased oxygen delivery, increased carbon dioxide removal.
    Metabolites act directly on arterioles (intrinsic).

Reactive Hyperemia

  • Local increase in blood flow following a previous reduction in blood flow.
  • Response to reduced oxygen levels and increased carbon dioxide due to occlusion.
    The metabolites stimulate vasodialtion and try to remove blocakge.
  • The cause is an occlusion.

Comparing Active and Reactive Hyperemia

  • Hyperemia: Higher than normal blood flow.
  • ACTIVE hyperemia is caused by increase in metabolic activity as a result of a higher rate of metabolism.
  • REACTIVE hyperemia is caused by a previous reduction in blood flow.
  • Vasodilatation is increased due to a reduction in flow during reactive hyperemia, in an effort to remove the blockage.

Myogenic Repsonse to Stretch.

  • Inherent ability of arterial smooth muscle to contract when it gets stretched.
  • To maintain a constant blood flow through the tissue.
    Flow autoregulation: Local regulation maintaining constant blood flow.
    Increase in perfusion pressure caused by an increase in mean arterial pressure causes an increase in stretch causing contaction of smooth muscles and therefore vasoconstriction and an increasing blood resitance in turn decreasing blood flow.
    Flow autoregulation, that is a local flow control.

Regulation of Local Chemical Messengers

  • Local chemical substances can affect the contractile activity of vascular smooth muscle.
  • Substances secreted by: blood vessel endothelial cells, or local tissues:
    • Nitric Oxide (NO): Vasodilation from endothelial cells.
    • Bradykinin and histamine: Stimulates nitric oxide
    • Prostasyclin: An eicosanoid, and strong vasodilator.
    • Adenosine: Coronary artery vasodilator.
    • Endotherlin-1: Promotes vasoconstriction.

The Intrinsic mechanisms (Response to touch, local, blood flow, local chamical messengers) regulate local blood flow.

Extrinsic Control Mechansims

Very improtant for the regulation of mean arterial pressure.
Establish a base line arterial resistance.

Sympathetic Control and Hormonal Control
Sympathetic Control (Autonomic Nervous System Division) and Hormonal Control regulate the radius of arterioles in turn regulating total peripheral resistance influencing the mean arterial pressure.
The parasympathetic division isn't very effective at controlling the arterial smooth muscles and therefore doesnt contribute much to the control of the arterial blood pressue.

Vascular tone is a state of partial constriction that is maintained by: open calcium channels and arteriolar smooth muscles with continued input of norepinephrine.

The process of Nor-epinephrine

Nor-epinephrine is secreated by the sympathetic postganglionic neurons. The norepinephrin than binds to the alpha 1 adrenergic receptors starting the phosphatidylinositol bisphosphate second messenger system. In this system the protein Phospholipase C activates the breakdown of PIP2 into DAG and IP3. IP3 increases the Calcium that gets released to the cytosol from the sarcoplasmic reticulum. And the DAG activates the open and closing of multiple ion channels and depolarizations to increase muscle contractions causing vasoconstriction.
The effect is to increase vasoconstriction, total peripheral resistance, and mean arterial pressure.

Sympathetic Control by the sympathetic Division

The blood cells that the sympathetic division regulates:

  • Tonic release of norephinephrine maintaing partial constriction of muscles.
  • To undergo vasoconstriction you need to increase norephinephrine.
  • To undego vasodilatation you need to decrease norephinephrine.
    Beta 2 adernergic receptors:
    These respond to Epinephrine, and are in cardiac muscles, and skeletal muslce cells, allowing muscles to under go a vasodilation.
    Epinerphrine will activate the cyclic admp second messenger system allowing muslces to under go muscle relaxation.

Vasodialation can occur when epinerphrine binds to beta 2 receptors.

In low does the epinephrine primarily binds to beta 2 to encourage vasodialation.
If we have high amounts of epinephrine at high enough amounts the epinephrine can bing to beta 1 (promoting vasoconstriction, increasing total peripheral resistance) and beta 2 adrenergic receptors. These higher doses give cardiac and skeletal muscles more blood. These large doeses of epinephrine are realted to the fight or flight response.

Parasympathetc effects of the arteriol Smooth muscle.

These are only found in the Digestive tract, external genitalia, and salivary glands, and use accetylcholine and promote vasodialation, but don't largely affect anything since they do not come into contact with most smooth muscle cells from anterioles.
Epinphrine and other sources:
Anigotensin II (produced from kidneys), and Vasopressin increase mean arterial pressure.

The Process for Angiotesin II

There is anginotesinogen which is created from proteins in plasma. That gets turned into Angiotesin I from renin (an enzyme from the blood). Angiotesin II is then created by a conversion of Angiotesin I from ACE(Angiotensin Converting Enzyme), which is found on inner surfaces of the blood vesels.
Angiotesin has an effect to promote vasconstriction, that helps to increase total peripheral resistance.
Vasopressin or anti-diuretic hormone
From the posterior pitutiary gland. that can limit urine uptput from increased water reobsorption through the kidneys. The hormone also can promote vasoconstriction increasing arterial pressure and blood pressure.

Local controls and systemic extrinsic controls act in deviations from normal arterial tone, in order regulate mean antieral pressure.