Cardio Physiology 5 - Factors effecting cardiac output, Arteries

3 factors that effect stroke volume

End diastolic volume (preload, EDV)
Contractility of ventricular myocardium
Afterload

What is end diastolic volume

Volume of blood in the ventricles at the end of ventricular diastole (volume of blood in ventricles after filling is complete)

Intrinsic mechanism to alter stroke volume

Ventricles contract more forcefully when they have been stretched prior to contraction

Increased ventricle stretching causes increased stroke volume. What causes increased ventricular stretching?

Ventricles filled more fully with blood

How to fill ventricles with more blood

Increase venous return (blood flowing back to the heart through veins)

Effect of increased venous return

Increased end-diastolic volume, which increases stroke volume, which increases cardiac output

Why is end diastolic volume called the preload

Is the tension/load of ventricular myocardium before contraction

Extrinsic mechanism to increase filling of ventricles

Sympathetic stimulation of venous smooth muscle

Parasympathetic system effect on venous volume

No effect - system does not constrict/dilate veins

Frank Starling Mechanism

Independent mechanism that displays relationship between EDV and SV

Relationship between EDV and SV

Increased EDV, increased SV

Why does increased EDV lead to increased SV

Ventricles fill with more blood, stretching out the sarcomeres, causing more forceful contraction

Frank-starling mechanism matches output of the two ventricles - what does this ensure?

Ensures the ventricles pump the same volume in blood, so blood does not accumulate in one circuit

Mechanism of how increased blood volume impacts sarcomeres

More blood = more sarcomere stretch. The myosin cross bridges will connect to their correct actin. Titin protein is stretched out, and sarcomere is not crowded (high tension) = more forceful contraction

How to increase strength of contraction of ventricular myocardium

Increased sympathetic stimulation, allowing ventricles to eject more than the normal % of their blood volume

Effect of parasympathetic innervation on strength of ventricular myocardium contraction

No impact, ventricular myocardium does not receive parasympathetic innervation

How does sympathetic stimulation increase stroke volume

Stroke volume is greater at a given end-diastole volume with innervation = increase cardiac output

Ejection fraction

measurement of the volume percentage of left ventricular contents ejected with each contraction. = SV/EDV

Increased contractility on ejection fraction

Increased ejection fraction

Impact of sympathetic activity on rate of contraction/relaxation

Heart contracts and relaxes faster, giving more time for ventricles to fill (despite increase in heart rate)

How is myocardial contractility regulated

G protein coupled mechanism

Sympathetic neurotransmitters for heart

Norepinephrine, epinephrine

Impact of sympathetic innervation on myocardial contractility regulation

Proteins involved in excitation-contraction coupling become phosphorylated, enhancing contractility

What proteins are phosphorylated leading to increased contractility

- L-type calcium channels (sarcolemmea)
- Ryanodine receptor in SR membrane
- Thin filament proteins (troponin)
- Thick filamens proteins associated with cross bridges
- Proteins that pump Ca2+ back into SR

Afterload

Tension against which ventricle must eject blood, related to arterial pressure

Effect of afterload on stroke volume

more ventricular afterload, lower stroke volume. Ventricle uses it's pressure to overcome the afterload

Endothelium continuity

Endothelium in blood vessels is continuous with the endocardium of the heart

Role of the endothelium in blood vessels

Provides smooth surface for blood to flow over

Why are pressures in the systemic circulation higher than the pulmonary circulation

Pressure needs to be generated to deliver blood to the entire body, and has to work against gravity (in legs)

Why is the pulmonary vascular resistance much lower than systemic resistance

Larger vessels throughout the pulmonary system, and the arterioles have less smooth muscle

Artery wall composition

Smooth muscle, elastic fibers, connective tissue

Use of muscular wall in artery

Contraction and diameter change

Use of artery wall elasticity

Allows for passive changes in vessel diameter in response to changes in blood pressure (no contracting smooth muscle)

Vasoconstriction

Contraction of arterial smooth muscle, decreases artery diameter

Vasodilation

Relaxation of arterial smooth muscle, increases artery diameter

Types of arteries

elastic, muscular, arterioles

Elastic arteries

Contain elastic fibers and few muscle cells. Inside pulmonary trunk and aorta - tolerate pressure changes during cardiac cycle

Elastic artery stretch/contraction in cardiac cycle

Expand when stroke volume ejected

Recoil to original dimension in diastole

Muscular arteries

Contain smooth muscle cells, few elastic fibers. Makes most of the arterial system vessels.

Function of muscular arteries

Distribute blood throughout body

Arterioles

Smallest arteries in body

Role of arterioles

Regulate blood flow to organs by regulating blood flow to capillary beds. Determine mean arterial pressure (blood pressure)

Arterioles composition

Smooth muscle forms rings around endothelium - allows for constriction of arteriole

Use of arteriole's small diameter + constriction

Increases resistant to flow, allows less blood to reach organs

Role of arterioles in exercise

Muscular arterioles dilate, allowing more blood to flow to capillary beds to oxygenate muscles. GI arterioles contract to prevent blood from entering

Vasoconstriction of arterioles

Contracts arteriolar smooth muscle = decreased blood flow

Vasodilation of arterioles

Relaxes arteriolar smooth muscle = increased blood flow

Arteriole intrinsic tone

Partial contraction in absence of neural/hormonal stimuli

Increased arteriole tone =

Constriction

Decreased arteriole tone =

Dilation

Extrinsic factors that effect arteriole tone

External to the organ/tissue. Alter whole body needs. Includes nerves and hormones

Intrinsic factors that effect arteriole tone

Nerves and hormones that organs/tissues use to alter their own blood flow

Sympathetic innervation to arteriolar smooth muscle

Sympathetic nerve fibers release norepinephrine to cause vasoconstriction. Always discharge at basal level (but can be increased/decreased)

Importance of sympathetic innervation of arteriolar smooth muscle

Regulates blood pressure by influencing arteriolar resistance

Noncholinergic, noradrenergic neurons impact on arteriolar smooth muscle (No Ach, No NE)

Release nitric oxide, a vasodilator, onto smooth muscle

Role of epinephrine on arteriolar smooth muscle

Can cause vasoconstriction or vasodilation depending on which receptor it binds to

Examples of local controls effecting arteriolar resistance

Active hyperemia, reactive hyperemia, flow autoregulation

Active hyperemia

Local control acts to increase blood glow when metabolic activity of organ/tissue increases

Hyperemia

Excess of blood in vessels supplying organ or tissue

Steps of active hyperemia

1. Increased metabolic activity of organ

2. Decreased O2 (due to metabolism), Increased metabolites in organ interstitial fluid

3. Arteriolar dilation in organ

4. Increased blood flow to organ

How does the active hyperemia pathway get activated

Arteriolar smooth muscle is sensitive to local chemical changes in ECF surrounding arterioles - sensitive to O2, CO2, pH (changed by metabolism)

Where is active hyperemia most developed

Skeletal muscle, cardiac muscle, glands (where metabolic conditions are most altered)

Flow autoregulation

Locally mediated changes in arteriolar resistance do to organ/tissue experiencing change in blood pressure - occurs at constant metabolism

Steps of flow autoregulation at low pressure

1. Low arterial pressure in organ causes decreased blood flow to organ
2. Decreased oxygen, excess metabolites, decreased vessel wall stretch in organs
3. Arterioles dilate in organ
4. Restoration of blood flow to normal in organ

Steps of flow autoregulation at high pressure

1. High arterial pressure in organ causes increased blood flow to organ
2. Increased oxygen, decreased metabolites, increased vessel wall stretch in organ
3. Arterioles constrict in organ
4. Blood flow is constricted, restoration to normal flow

What mediates flow autoregulation

Changes in local chemical factors, and by myogenic response (direct smooth muscle response to stretch)

Are nerves/hormones involved in flow autoregulation

No - done by changes in chemical factors due to muscle wall response to stretch (myogenic response)

Reactive hyperemia

Form of flow autoregulation caused by occlusion (blockage) of blood flow. Allows for increased blood flow

Steps of reactive hyperemia

1. Occlusion of blood flow decreases O2 levels and increases metabolites
2. Arterioles dilate
3. Blood flow increases when occlusion is removed

Example of reactive hyperemia

When you remove a tightly tied string from finger, finger turns red due to blood rushing in (arterioles dilated)