Cardiovascular Physiology

Autorhymic cells

- Autorythmic system: means the heart creates and autoregulates its own electrical signal

- Pacemaker cells - Modified myocardial cells

- Create pacemaker potential - the electrical signal that spread via the intrinsic conductive system

- Causes myocardial cells to have cardiac potentials

- Electric current in the heart = intrinsic

- Generated by the pacemaker cells themselves

- Does not need brain signaling to occur; occurs on its own

Functional synctium

- the AV node is the connection between the atria and the ventricles; allows heart contraction to occur

- no AV node = death

- myocardial tissue acts as a single unit (within atria and ventricles separately) because of gap junctions

SA Node

- In the right atrium, superior to AV node

- Connected to fibers that spread the pacemaker potential throughout the atria (don't need to know their names)

- The spreaded pacemaker potential causes individual myocardial cells to generate cardiac action potentials

- The myocardial cells then spread the cardiac action potentials via intercalated disks: very fast

- Generates about 100 pacemaker potentials / minute

- NOT connected to the ventricles

- The atria contract first, so there must be a time delay between atrial and ventricle contraction

- Marginal edge - a line separating the atrium from the ventricles with NO gap junctions so that pacemaker potential cannot be shared between the atria and the ventricles

- Instead, the fibers coming off of the SA node spread to the AV node, causing the AV node to generate its own, separate pacemaker potentials

- Results in a .1 second delay

AV Node

- In right atrium directly superior to marginal edge

- Activated by pacemaker potential of SA node

- Genertaes its OWN pacemaker potential

- Spreads through AV Bundle (Bundle of His) fibers

- AV bundle splits into a left and right branch

- Fibers of the left and right branch are connected to purkinje fibers that distribute the pacemaker potential to each myocardial cell

- Myocardial cells generate cardiac potentials

- 30 pacemaker potentials / min

- Can function without the SA node, but contraction is very slow

the physiology of the pacemaker potential

a. Na+ influx (slow) offset by K+ efflux (slow)

b. K+ permeability gradually decreases

c. Influx of Na+ depolarizes the cardiac cells

d. Depolarization opens fast Ca2+ channels

e. Ca2+ influx from extracellular space causes rising phase of action potential

f. Repolarization causes K+ permeability to increase, cardiac cells repolarize

g. K+ channels inactivate

h. Cycle starts again

Purkinje fibers

• inferior terminal branches of the bundle

○ Fewer myofibrils, developed intercalated disks, and gap junctions → APs travel rapidly

• Process:

APs at SA node → adjacent cardiac cells → AV node → cardiac muscle of atrial wall contracts → AV bundles → left and right bundle branches → Purkinje fibers in myocardium → ventricular contraction begins at apex and progresses towards the base of the heart

Cardiac potential of myocardial cells

• APs in cardiac muscle last longer than those in skeletal muscle

○ Because cardiac muscle cells are smaller in diameter

• Membrane channels differ from those in skeletal muscle

• Process includes depolarization, early repolarization phase, plateau phase, and final repolarization phase

Depolarization phase

- Rising phase

- Na+ influx through fast Na+ channels

- Depolarizing Initiated by the pacemaker potential

- Spreads to every myocardial cell via gap junctions

Early repolarization phase

- Repolarization

- K+ channels open

- K+ efflux

- Slight repolarization as K+ leave, but then interrupted

Plateau Phase

- Cl- channels and Ca2+ channels open

- Repolarization is temporarily interrupted

- Cl- influx: -1 charge, influx makes inside more negative

- Ca2+ influx: +2 charge, influx makes inside more positive

(still from phase 1) K+ efflux: -1 charge, efflux makes the inside more negative

- SO, RESULTS = -2 + 2 = 0... NO CHANGE TO CHARGE

- This keeps the myocardial muscles contracted for an extended period of time, giving a chance for blood to be moved into the circulatory system

Final repolarization phase

- Repolarization

- Cl- and Ca2+ close

- K+ efflux repolarizes the myocardial cells

- Returns to phase four (rest)

EKG/ECG Trace

- a composite of all 4 electrical events that occur in the myocardium: atrial depolarization -> atrial repolarization -> ventricular depolarization -> ventiruclar repolarization

- Will never actually be observed in the way we draw it

- 12 different leads to look at; all show different EKG

- Depends on where from the body you're looking at

P wave

atrial depolarization

• stimulates atrium contraction

QRS wave

- ventricular depolarization

- Q = atria repolarization, not fully seen within an EKG as it occurs at (almost) the same time as R wave

- Electrical events of ventricles = much larger than those of atria

- Ventricular depolarization overrides atrial repolarization

T wave

ventricular repolarization (before ventricular relaxation)

• As the ventricles relax → the walls recoil and force the blood to flow back toward the ventricles → semilunar valves close

  • Therefore, ventricular volume does NOT change here

PR

interval that contains all atrial events, P -> Q -> R

• Atria contract and then relax

  • Ventricles start depolarization

  • If interval long, AP delay

QT

interval that contains all ventricular events, Q -> R -> T

• Ventricles contract and then relax

  • If interval is long, abnormal conduction of AP

    • May result in myocardial infarction

Atrial and ventricular diastole

Times when the chambers are in a relaxed state

Atrial and ventricular systole

Times when the chambers are contracting

Cardiac Cycle

1. Both start in diastole

2. Atria enters systole first - .1 second

3. Atria goes back to diastole, ventricles enter systole - .4 seconds

4. Ventricle returns to diastole - both are in diastole for about .3 - .4 seconds

NEVER BOTH ATRIA AND VENTRICLES CONTRACTING AT SAME TIME

how to calculate cardiac output (CO)

CO = SV X HR

Stroke volume formula (SV)

SV = EDV - ESV

End diastolic volume (EDV)

amount of blood accumulated in the ventricles at the end of ventricular diastole (relaxtion)

End systolic volume (ESV)

amount of blood leftover in the ventricle after contraction (systole)

Heart sounds

- Occur when the valves close

- Hence 2 sounds

- AV valve closes first, SL valve closes second

Ventricular pressure changes

- Increases as ventricles fill with blood

- Peaks as ventricles enter systole, contract

- Decreases as systole occurs and blood leaves

- Returns to low pressure

Ventricular volume changes

- Increases during atrial systole and blood is pushed into ventricle

- Stays the same during isovolumetric periods: no blood can enter or leave as both the valves are closed

- Decreases during ventricular systole and blood leaves the ventricles

Timing of valves opening and closing

- AV valve: closes when ventricular systole begins to prevent back flow back into the atria, opens when ventricular systole has ended and there is more pressure in the atria than there is in the ventricles

- SL valve: closes when there is more pressure in the aorta than in the ventricles to prevent back flow back into the ventricles, opens when ventricular systole begins and there is more pressure in the ventricles than there is in the aorta

Isovolumetric contraction

- blood volume in the ventricles cannot change because both the AV and SL valves are closed

- Occurs when the ventricle begins to contract

- AV valve has closed but semilunar valve has yet to open

- Ventricle is contracting but no blood leaves

Isovolumetric relaxation

- blood volume in the ventricles cannot change because both the AV and SL valves are closed

- Pressure in ventricles decreases to point where SL valve has closed but AV valve has not yet opened

- Ventircle is relaxed, no blood is moving

- Occurs because it only takes a little relaxation of the ventricles to have less aortic pressure

Sympathetic nervous system in cardiac function regulation

-- Increases heart rate

- Releases NE

- Causes depolarization of the pacemaker cells in the SA and AV nodes

- Reduces the time needed to reach threshold - so, the heart can initiate contractions at a faster rate

- Increasing HR increases CO

-- Increases strength of contraction

- NE also increases Ca+ levels in body

- Ca+ increases the contractile strength of the myocardium

Reduces ESV

- Less blood is left in the heart after it contracts because it is stronger and can exert more force to push the blood out

- Mediated by ß1 adrenergic receptors

Parasympathetic nervous system in regulating cardiac function

- Decreases heart rate

- Mediated by acetycholine

- Released by the vagus nerve

- Hyperpolarizes (inhibits) SA node

- This means that the it takes a longer amount of time for the pacemaker cells to reach threshold

- Hyperpolarization -> HR decreases -> CO decreases

- Inactivated in a stressful situation

Chemical regulation of cardiac function (Adrenal medulla)

- Epinephrine

- Sympathetic nervous system

- Increases HR and contractility (like NE) - same exact function; depolarizes pacemaker cells and increases Ca+ levels

- Mostly effects blood pressure

Physical factors: age

- Lose capacities with age

- Adverse relationship between age and CO

- Due to limits of highest possible HR; less in older people

Physical factors: Gender

- Men have more androgen/testosterone which increases the volume of red blood cells

- Women need to pump more blood to have the same amount of oxygen reach their body tissues

- So, women have a higher HR and therefore higher CO

Physical factors: Exercise

- Bradicardial = athletes have a lower resting HR due to physical activity

- Athletes have a stronger contractile strength, meaning their heart can fill with more blood before contracting which means their heart rates can be slower

Contractile Stength: Stretch Dependent

- Stretch dependent: more contraction

- Slower heart rate

- Heart waits longer to contract, fills with more blood (hence, it stretches more)

- Present in athletes: the heart muscle becomes stronger to the point where it always stretches more to hold more blood

- An increase in EDV

- Increase of volume of blood in the heart (EDV) -> increase stretch -> increase contractile strength -> decrease in ESV -> increase in SV

Contractile Strength: Stretch independent

- Based on Ca+ levels

- More Ca+ = more contraction

- NO increase in EDV

- Ca+ levels increase -> contractile strength increases -> ESV decreases -> SV increases

Preload

- the amount of mechanical force in the heart, increases the pressure of fluid

- Controls EDV and ESV

Afterload

not regulated by the body, outside of its ranges = pathology, hypertension

Normal CO vs. Athlete CO

- Normal SV & Heartrate: 70 mV x 70 beats/sec = 5L blood / min

- Athlete SV & Heartrate: 120 mV x 40 beats/sec = 5L blood / min

- Conclusion: becuase athletes can train their hearts to have higher contractile stength (stetch dependent), their resting heart rates can be lower as they can distribute the same amount of blood throughout their body with less beats