phys exam 3

atria

upper chamber of the heart

ventricles

lower chambers of the heart

2 circulations

pulmonary and systemic

O2 poor blood

blue - pulmonary arteries

O2 rich blood

red - pulmonary veins, systemic arteries

valves

prevent blood from going backward

four valves of the heart

2 AV valves

2 SLV (semilunar valves)

what are the 2 AV valves

tricuspid and bicuspid/mitral

what are the 2 SLV

pulmonary and aortic

what is the pressure gradient

the difference in pressure

how does pressure gradient affect flow

Fluid flow = directly related (DR) to pressure gradient
Flow rate or flow DR pressure gradient

how does distance affect pressure of a fluid in motion

distance is IP to pressure

how does resistance affect flow

flow is IP to R

how does viscosity affect resistance and flow

viscosity (thickness) DR to R, IP to flow

hows does the vessel radius affect resistance and flow

radius is IP to R is DR to flow

vasoconstriction

decreases radius, increases R, decreases flow

vasodilation

increase radius, decrease R, increase flow

what is flow rate (Q)

volume that passes a certain (fixed) point (the number)

what is velocity (V)

speed (how fast)

what is the relationship between flow rate and velocity

V=Q/A

velocity, flow rate, cross-sectional area

what is the relationship between velovity and the cross sectional area of the tube

as A decreased V increases

what is poiseuille’s law

R related to Lη/r^4

length

L = DR to R, IP to flow.

viscosity

η = DR to R, IP to flow.

radius

r^4 = IP to R, DR to flow

has the biggest impact on R and flow

autorhythmic cells

creates their own EPP

less than 2%

contractile cells

contracts to create pressure

more than 98%

how does the contractile cardiac cell contract

1. Signal travels into T tubule.

2. In T tubule, there is an L-type Ca++ channel.

   • Voltage.

   • When open, calcium influx from the ECF.

3. Calcium binds to the RyR.

   • RyR opens.

   • Calcium influx from sarcoplasmic reticulum.

4. Calcium-induced calcium signal — a calcium spark.

5. Calcium binds to troponin — power stroke.

To relax: get rid of Ca from ICF.

1. Ca pump in sarcoplasmic reticulum.

2. NCX in plasma membrane.

   • Antiport.

   • Ca efflux to ECF.

   • Na+ influx.

Electrical signal → calcium enters from outside the cell → calcium causes more calcium to leave the SR → calcium binds to troponin → contraction.

steps of an action potential of a cardiac contractile cell

1. Start at RMP = −90 mV (resting).

2. No threshold.

3. For depolarization, Na+ voltage gates open.

4. Max depolarization = +20 mV.

5. Na voltage close; fast K voltage gates open, repolarization begins.

6. Fast K voltage close. Repolarization stops.

   • Ca voltage open — plateau begins.

7. Plateau ends.

   • Ca gates close.

   • Slow K gates open; repolarization continues.

8. Returns to RMP.

The cardiac contractile cell starts at −90 mV. Sodium entering makes it depolarize. Potassium leaving helps repolarize it. Calcium entering creates the plateau. Slow potassium channels help finish repolarization and return the cell to resting potential.

(Na⁺ → fast K⁺ → Ca²⁺ plateau → slow K⁺ → resting potential)

membrane potential

the electrical difference across a cell membrane

Action potential of contractile cell: Start at RMP = −90 mV (resting).
Action potential of autorhythmic cell: No RMP; has a pacemaker potential around −60 mV.

threshold for contractile cell

no threshold

threshold for autorhythmic cell

at threshold -40mV

when are gates open for contractile cells

• Na+ voltage gates open for depolarization.

• Fast K voltage gates open for repolarization.

• Ca voltage gates open when the plateau begins.

• Slow K gates open when the plateau ends.

when are gates open for autorhytmic cells

• At −60 mV, If channels open.

• Before threshold, If channels close and Ca++ channels open.

• At −40 mV, Ca++ voltage gates open.

• When Ca++ gates close, K+ gates open for repolarization.

when are gates closed for contactile cells

Na voltage gates close; fast K voltage gates close; Ca gates close; slow K gates open.

when are gates closed for autorhythmic cells

If channels close before threshold; Ca++ voltage gates automatically close; K+ gates close after repolarization.

what is the plateau

Ca voltage open — plateau begins

the extended stage of the cardiac contractile cell’s action potential when calcium channels are open

why is there a plateau

1. More Ca to enter sarcoplasm (ICF).

2. Prevents tetanus.

3. Lengthens refractory period for entire muscle twitch.

Tetanus = sustained contraction.

refractory times between cardiac contractile cells and skeletal muscle cells

the cardiac contractile-cell plateau “lengthens refractory period for entire muscle twitch.”

why is comparing the refractory times between cardiac and skeletal muscle cells important

prevents tetanus
lengthens refractory period for entire muscle twitch

steps of an action potential in a cardiac autorhythmic cell

1. No RMP.

   • Has a pacemaker potential = around −60 mV.

2. At −60 mV, If channels open.

   • Na+ influx.

   • K+ efflux.

3. Before threshold:

   • If channels close.

   • Ca++ channels open — brings to threshold.

4. At threshold = −40 mV.

   • Ca++ voltage opens — depolarization.

5. No max depolarization.

   • Ca++ voltage automatically closes.

6. When Ca++ gates close, K+ gates open — repolarization.

7. When K+ gates close, back at pacemaker potential.

The cell slowly moves toward threshold on its own. Calcium entering causes depolarization, and potassium leaving causes repolarization. The cell then starts the cycle again.

pacemaker potential

No RMP. Has a pacemaker potential = around −60 mV

the gradual change in voltage that brings an autorhythmic cell toward threshold so it can generate another action potential.

what gates are involved when pacemaker potential open

At −60 mV — If channels open.

Na+ influx

K+ efflux.

what gates are involved when pacemaker potential closes

Before threshold:

If channels close

Ca++ channels open — brings to threshold.

what gates are involved when pacemaker potential is at threshold

at threshold — −40 mV.

- Ca++ voltage open — depolarization.

action potentials of skeletal muscle

action potentials cardiac contractile cells

• RMP = −90 mV.

• No threshold.

• Na+ voltage gates open — depolarization.

• Max depolarization = +20 mV.

• Na voltage close; fast K voltage gates open — repolarization begins.

• Fast K voltage close; Ca voltage open — plateau begins.

• Ca gates close; slow K gates open — repolarization continues.

• Returns to RMP.

sodium causes the initial depolarization, calcium creates the plateau, and potassium helps repolarize the cell

action potentials cardiac autorhythmic cells

• No RMP; pacemaker potential around −60 mV.

• If channels open: Na+ influx and K+ efflux.

• If channels close; Ca++ channels open.

• Threshold = −40 mV; Ca++ voltage opens — depolarization.

• No max depolarization.

• Ca++ gates close; K+ gates open — repolarization.

• K+ gates close; back at pacemaker potential.

autorhythmic cells slowly reach threshold on their own, depolarize with calcium, and repolarize with potassium

cardiac conduction system

• SA node = upper right atrium; main pacemaker; leads to atrial contraction (systole).

• Internodal pathway.

• AV node → leads to ventricular contraction (systole).

• AV bundle — in interventricular system.

• AV bundle branches.

• Purkinje fibers.

Purkinje fibers = in trabeculae carneae and papillary muscle.

When papillary muscle contracts, AV valves stay closed

SA node → internodal pathway → AV node → AV bundle → bundle branches → Purkinje fibers.

waves of ECG what they rep

• P wave = atrial depolarization.

• QRS complex = ventricular depolarization.

• T wave = ventricular repolarization.

what do waves of an ECG lead to

• P wave → atrial systole.

• QRS complex → ventricular systole.

• T wave → ventricular diastole.

mechanical events of the cardiac cycle

• Late atrial diastole:

  • AV valves open because atrial pressure is higher than ventricular pressure.

  • 80% of ventricular filling is passive.

• Atrial systole:

  • 20% of ventricular filling.

  • AV valves open.

• Early ventricular systole:

  • AV valves close.

  • SLV are still closed — isovolumic ventricular contraction.

• When ventricular pressure is higher than pulmonary and aortic pressure:

  • SLV open.

  • Full ventricular contraction.

• At the end of ventricular systole, ventricular diastole starts:

  • SLV closed.

  • AV valves still closed — isovolumic ventricular relaxation.

• When ventricular pressure drops below atrial pressure:

  • AV opens and relaxation phase ends.

The heart fills, the atria contract to finish filling, the ventricles begin contracting with all valves closed, blood is ejected, the ventricles relax with all valves closed, and the AV valves reopen to allow filling again.

what happens during atrial/ventricular

• Atrial systole: 20% of ventricular filling; AV valves open.

• Early ventricular systole: AV valves close; SLV are still closed.

• When ventricular pressure exceeds pulmonary and aortic pressure, SLV open and full ventricular contraction occurs.

what happens during diastole/systole

Diastole = relaxing/filling (with blood) (while muscles are repolarizing).
P wave leads to atrial systole.
QRS complex leads to ventricular systole.
T wave leads to ventricular diastole.

• Systole: Contraction.

  • Diastole: Relaxation and filling.

what happens during isovolumic contraction

AV valves close; SLV are still closed.

what happens during isovolumic contraction/relaxation

SLV close; AV valves are still closed

when do the valves open and close

• Late atrial diastole: AV valves open because atrial pressure is higher than ventricular pressure.

• Early ventricular systole: AV valves close; SLV are still closed.

• When ventricular pressure is higher than pulmonary and aortic pressure: SLV open.

• At the end of ventricular systole: SLV close; AV valves are still closed.

• When ventricular pressure drops below atrial pressure: AV opens.

what is stoke volume

SV = volume ejected/heartbeat.
average 70 mL

how is stroke volume calculated

SV = EDV − ESV.
EDV average 135 mL.
ESV average 65 mL.
SV = 135 − 65 = 70 mL.

what is cardiac output

CO = volume ejected/min

how much blood a ventricule pumps in one min

how is cardiac output calculated

CO = SV × HR.
70 mL × 70 bpm = 4900 mL/min = 4.9 L/min.

parasympathetic control of heart rate

• Decreases HR or sets normal.

• Makes SA node depolarization harder by opening K+ channels (makes more negative), closing Ca++ channels.

sympathetic control of heart rate

• Increases HR.

• Makes depolarization easier by opening Ca++ or Na+ channels.

what are the different factors that influence stroke volume

• Contractility: ability to contract; amount of Ca++ in sarcoplasm directly related.

• Sarcomere length is directly related to force/tension and preload.

• Preload is directly related to volume entering ventricles and EDV.

• Inotropes affect contractility.

• Venous return factors: skeletal muscle pump, respiratory pump, sympathetic innervation.

what is the length tension relationship

Sarcomere length is directly related to contractile force.
Sarcomere length is directly related to force/tension and preload.

frank starling law of the heart

“Volume of blood that enters the heart is the same volume that leaves the heart.”

what are inotropic effects

affect contractility.

• Positive inotropes increase contractility.

• Example: catecholamines — epinephrine/norepinephrine.

how do inotropic influence stroke volume

Positive inotropes increase contractility.
Increase Ca++ concentration in SR for faster Ca diffusion into sarcoplasm.

what are the factors that affect venous return to the heart

• Skeletal muscle pump (flex/extend).

• Respiratory pump (diaphragm; inhale decreases thoracic cavity pressure).

• Sympathetic innervation (decreases lumen area; A inverse to velocity).

anatomy of blood vessels

1. Arteries — conduct blood away; pressure reservoirs.

2. Arterioles — small arteries.

3. Metarterioles — in the middle of the capillary bed.

4. Capillaries — smallest; exchange vessels.

5. Venules — small veins.

6. Veins — lead to heart.

arteries

• Conduct blood away.

• Pressure reservoirs.

• Most elastic content.

• Highest BP.

arterioles

• Small arteries.

• Well-defined tunica media.

• Variable resistance vessels.

• Diameter directly related to MAP.

capillaries

• Smallest.

• Exchange vessels.

• Only tunica intima.

• Slowest velocity.

• Pericytes surround and control exchange.

venules

• Small veins.

• 3 tunics.

• Can do some exchange.

veins

• Lead to heart.

• Larger lumens.

• Lowest BP.

• Mostly connective tissue.

• Limb veins have valves.

• 60% circulating blood.

• Volume reservoirs.

metarterioles

in the middle of the capillary bed

precapillary sphincters

Metarterioles have valves called precapillary sphincters.
Must be open for blood to enter the bed.

pericytes

Pericytes surround and control exchange.

what is systolic pressure

working blood pressure.
Pressure exerted on vessel wall during ventricular systole.

what is diastolic pressure

resting pressure.
Pressure that remains in artery during ventricular diastole.

what is pulse

feeling the blood flow through an artery during ventricular systole.

what is pulse pressure (PP)

systolic pressure − diastolic pressure.
120 − 80 = 40.

what is MAP

mean arterial pressure = blood flow driving force

MAP = diastolic + ⅓ (of systolic − diastolic) or ⅓ (pulse pressure).

80 + ⅓(40) = 93 MAP.

Normal range for MAP is between 70 and 110.

Above 110 — hypertension (high BP).
Below 70 — hypotension (low BP).

how does cardiac output and peripheral resistance affect MAP

MAP related to CO × R (arterioles).

• If cardiac output increases, then MAP increases.

• If cardiac output decreases, then MAP decreases.

• If R (arterioles) increases, vasoconstriction, then MAP increases.

• If R (arterioles) decreases, vasodilation, then MAP decreases.

• R (arterioles) is TPR.

how do chnages in blood volume affect blood pressure

Blood volume is DR to MAP.
If blood volume increases, then MAP increases.

what factors influence MAP

• MAP related to CO × R (arterioles).

• CO = SV × HR.

• HR increases, MAP and CO increase.

• Blood volume is DR to MAP.

what are the compensation mechanisms for increased blood volume

Cardiovascular compensation:

• Decrease CO by decrease HR.

• Decrease R (arterioles) by vasodilation.

• Fastest method.

Renal compensation:

- Decrease blood volume by increasing urine production.

what is myogenic autoregulation

• When smooth muscle stretches, Ca++ gates open.

• Makes smooth muscle contract.

mechanisms of active hyperemia

due to an increase in metabolism.
Example: exercise.

mechanisms of reactive hyperemia

due to a blockage.

When the blockage is removed, normal blood flow is restored.

how does the sympathetic branch control most vascular smooth muscle

• Monitors arteriolar R.

• Sends constant frequency of signals to arteries.

• The frequency of signals is IP to diameter.

• If frequency of signals increases, then vasoconstriction (increase R).

• If frequency of signals decreases, then vasodilation.

what is the baroreceptor reflex

• Cardiovascular control center (CVCC) controls mean arterial pressure.

• Baroreceptor reflex.

• Carotid artery = CN IX.

• Aortic arch = CN X.

• Tonic receptors.

• Baroreceptors send a constant frequency of signals to the CVCC.

what are the steps of a baroreceptor reflex

If MAP increases:

• Frequency of signals increases.

• Parasympathetic = stimulated.

• Sympathetic = inhibited.

If MAP decreases:

• Frequency of signals to CVCC decreases.

• Parasympathetic = inhibited.

• Sympathetic = stimulated to increase heart rate, increase CO, and vasoconstrict (increase R).

what are the 3 kinds of capillaries

Continuous capillaries

• Most common and least permeable.

• Skeletal muscle and skin.

• Have gaps between endothelial cells called intercellular clefts. Fenestrated capillaries

• Small intestines.

• Kidneys.

• Have larger clefts and true fenestrations (pores).

Sinusoids

• Most permeable.

• Largest clefts.

• Larger pores.

• Bone marrow, spleen, liver.

why is the velocity of blood flow lowest in capillaries

Velocity of blood in capillaries is slowest.
V = Q/A.

• Total area of all capillaries to an organ.

• Highest area.

what are the methods of capillary exchange

• Bulk flow = down a pressure gradient.

• Gases.

• Diffusion = down a concentration gradient.

• Paracellular = between the cells.

• Transcellular = through cells.

• Transcytosis = vesicular transport.

compare the methods of capillary exchange

• Bulk flow = down a pressure gradient.

• Diffusion = down a concentration gradient.

• Paracellular = between the cells.

• Transcellular = through cells.

• Transcytosis = vesicular transport.

diffusion

down a concentration gradient.

transcytosis

vesicular transport.

bulk flow

down a pressure gradient.