SinoAtrial Node

SA node

generates pacemaker potentials

generates action potentials - generates atrial systole

autorhythmicity (depolarizes spontaneously)

gradual Na influx through Na leak channels - this creates the action potential

what is ectopic pacemaker?

what cells generate them?

Ectopic focus/pacemaker is a potential or beat that is generated slower than the pacemaker (SA node)

cardiocyctes near the SA node and AV bundle generate ectopic focus

describe the pathway  of the electrical conduction through the heart.

How does this relate to the actual pumping of the heart?

the SA node spontaneously depolarizes at 100bpms, creating atrial systole

this electrical impulse is sent to the AV node where it is stalled for a moment

this ensures time for ventricles to completely fill with blood

electrical impulse is then sent to AV bundle and perkinje fibers, creating ventricular systole

before the next action potential, the heart relaxes (DIASTOLE)

The AV delay occurs when the electrical impulse sent to the AV node by the SA node is held or stalled for a moment

this is important because it allows for complete filling of the ventricles with blood

slow through the contractile cells

rapid through the internodal tracts that connect SA and AV nodes

slow and decremental through the AV node (the AV delay)

approximately a .1 second delay

timeline of events in a cardiac cycle

(see slide 4 of cardiovascular physiology)

1: late diastole; all chambers relaxed, ventricles passively filling

2: atrial systole; overlapping with ventrical diastole. AV valves open , Atrial contraction force small amount of additional blood into ventricles

3: End diastolic volume; max amount of blood in ventricles

4: isovolumic ventricular contraction; beginning contraction pushes AV valves closed to prevent backflow (however, not enough pressure to open the semilunar valves)

5: ventricular ejection; ventricular pressure rises, exceeds that of arteriole pressure, semilunar valves open, blood is ejected

6: end systolic volume is reached; This is the minimum amount of blood in ventricles

7: isovolumic ventricular relaxation; ventricles relax causing ventricle pressure to decrease. Blood flows back towards semilunar valves and snaps them closed

(back to diastole of both ventricles and atria) 

Timeline of cardiac events

(electrical AND muscular activity)

1. during the pacemaker potential (the small slope from -60 to - 40) the If channels open and allow a slow leak of inward Na+. This allows the cell to reach it's threshold potential (-40)

2. Once the influx of Na+ allows for the potential to reach -40, the action potential begins and there is a calcium influx. This happens through the Ca++ channels and it increases up to the peak of the potential.

3. After the peak is reached (about 0 volts), K+ channels open and K+ goes out of the cell to start reastablishing the resting potential. All the while, during the repolarization phase, the Ca++ channels are closing.

1. AV valves are open during the combination of ventricular and atrial diastole

2. Passive ventricular filling occurs as blood naturally flows through the atrium, AV valves and into the ventricles

3. Electrical activity spreads across the sarcolemmas and through gap junctions of contractile cardiocytes of the atria

4. pacemaker potential generates action potential in the SA node

5. Electrical activity spreads through the internodal and interatrial tracts

6. ejection phase of atrial systole (only small amount of blood is pumped through, the rest had already passively filled)

7. AV node conducts electical activity to AV bundle and bundle branches

8. electrical activity spreads from base to apex through the contractile cordiocytes of the interventricular septum

9. electrical activity spreads through the contractile cardiocytes of the ventricular walls from apex to base

10. WHILE 8 and 9 ARE HAPPENING: Isovolumetric contraction of ventricles which causes...

11. the AV to Valve close

12. electrical activity spreads through purkinje fibers

13. semilunar valves open as ventricles continue to contract

14. ventricular ejection through the semi-lunar valves

15. isovolumetric relaxation of ventricles

16. blood pulses (in a backwash fashion) in the aorta and pulmonary trunks which causes

17. semilunar valves to close/AV valves re-open

Atrial and Vetricle Diastole

AV valves open and passive filling, electricle activity spreading through sarcolemms etc etc all the way to the point where the electrical activity is spreading through the internodal and interatrial tracts.

Atrial Systole/Ventricles still in Diastole

Once the atria start to contract we are in atrial systole all the way righ up to when the electrical activity gets into the bundle branches and purkinje fibers. When this happens...

Atrial Diastole/Ventricle Systole

The AV valves snap shut and atria relax while the ventricle starts its isovolumetric contraction. this phase continues until blood is actually ejected through the semi-lunar valves from the ventricles.

Atrial and Ventricular Diastole

The atria are still relaxed, but after ventricular ejection the ventricles relax too and backwash blood closes the semilunar valves and the AV valves re-open and we are back at he begining.

during the cardiac cycle, when is intraventricular pressure the highest? lowest?

when are systolic and diastolic bp measured?

intraventricular pressure is the highest right before the semi-lunar valves open and blood is ejected from the ventricles

intraventricular pressure is the lowest after the ventricular blood is ejected and the ventricles are relaxing but blood has yet to start passively filling the ventricles yet

systolic blood pressure is measured during the ejection phase when the pressure in the arteries is at it's highest due to all the blood being pumped through it

diastolic blood pressure is measured right before the ejection phase and it is the arterial BP at this point

ESV: 65mLs

SV: 70 mLs

EDV: 135 mLs

1. the pacemaker potentials of the SA node cause na+ influx through If channels and once they reach the threshold value, Ca++ channels begin to activate and AP

2. Ventricular contractile cardiocytes prolong repolarization (way longer than APs for skeletal muscles) by allowing Ca++ and Na+ channels to remain open and creates a really long absolute refractory period

extracellular (10%) from the sarcolemma

intracellular (90%) from sarcoplamic reticulum

for an AP in contractile cardiocytes, prepare a graph of time (mSec) and membrane potential (mV). About how long is the absolute refractory period? What is the peak membrane potential? Resting membrane potential?

In the diagram provided ignore the blue line.

first, slow Na+/ Ca++ channels open allowing Na+ into the cell

the Na+ influx is regulated once a certain mV is hit, by the Na+ gates closing. this causes the sharp peak at the top of the plateau potential

All this time Ca++ channels have been slowly opening and allowing Ca++ allowing calcium in. this causes the flat platuea portion of the potential

finally the Ca++ channels close and K+ channels open allowing K+ out during the repolarization phase and bring the potential back down

the slow ca++ influx makes a crazy long absolute refractory period in comparison to a muscle twich.

the fast na+ gates of a plateau potential make the steep incline in comparison to the muscle twitch which doesn't initiate as quickly,

it roughly characterizes the plateau phase of depolarization.

when the entire ventricle is depolarized.

time for ventricular depolarization and repolarization.

roughly the time for ventricular action potential.

what is tachycardia and how can it be seen on an ecg?

bradycardia?

this is when the hear beats abnormally fast at rest. this can be seen by looking at the RR distance on an ecg.

bradycardia would have a smaller distance between R and R because bradycardia is when the heart beats abnormally slow during rest.

bradycardia: because the heart rate is abnormally slow, the sympathetic nervous system helped keep the HR up as much as possible. sympathetic division increases heart rate.

tachycardia: during tachycardia the parasympathetic division is at work.

L/min

5L/min

CO=heart rate x stroke volume

CO=HR x SV

As exertion increases (in the begining) the heart begins to pump faster creating an increase. However as heart rate continues to increase, the heart can't beat as efficeintly, meaning that as it pumps faster, it isn't pumping as much blood each time. for this reason, plot of CO and exertion would have a peak and then drop a little.

CO=HR x SV

HR and SV will increase together at the begining of exertion but after the body begins to work hards HR keeps increasing but SV starts decreasing.  

explain how resting and maximum cardiac output vary between the average person and a runner.

based on this, what would causes the difference, time? or volume?

AT REST: the runners heart rate is lower and stroke volume is higher. at rest, a marathoner and a regular person have about the same CO

MAX: the runner has a lower max heart rate and a much higher stroke volume. As a result the runner's max cardiac output is much greater than the non-runners

VOLUME

stroke volume is the variable that is the most influential

↑end diastolic volume =↑stretching=↑contractility=↑SV

aka: the greater volume entering the ventricle (EDV) the greater ejected during contraction

draw a quick plot of frank sterling law

in given plot (ignore line B and C), just note that LVEDV=end diastolic volume

1. frank starling law

2. the AV delay

1. Sarcomere length/tension relationship

---the sarc. length is shortest right before the filling the heart with blood. makes it hard to generate tension.

---if we increase the EDV, then there will be an increase in sarc. length which allows for CB cycling

2. Passive tension increases with stretching by a larger EDV

3. troponin's affinity for Ca++ increases with stretching

it shows the relationship between cardiac output and the Central Venous Return.

*CVR is directly related to the CVP (central venous pressure)

how does the franks staling law effected by CVR/CVP?

what is an example of this?

increased CVR=increased blood volume=increased SV

an example of increase blood volume would be during intense liquid uptake or some sort of blood/fluid transfusion

what is TPR?

what causes TPR?

how is the frank sterling law related to TPR?

TRP is total peripheral resitance=sum of all vessels resistances to blood flow

it is usually caused by vasoconstriction

when ↑vasoconstriction causes ↑TPR, this TPR backs up arterial blood causing the semi-lunar valves to close sooner which causes an  ↑ESV

as a result of the increased ESV, in the next cardiac cycle, there will be a higher stroke volume (assuming vasoconstriction is over)

1. PSD

2. SD

3. Stroke Volume (positive and negative ionotropic effects)

firstly: cerebrum gets message from baroreceptors, sends them to the cardiac control center of medulla oblangata which initiates autonomic regulation as follows:

-the info comes from the vagus nerve

-it is a cholinergic input to the SA/AV nodes and atrial contractile cells

-heart slows down a bit

firstly, just as with the PSD: the cerebrum gets a message from the baroreceptors saying that CO is not enough, the cerebrum sends a message to the cardiac centers of medulla oblangata which start and autonomic response

then....

-the neurons from the chain ganglia secrete and adrenergic input to the SA/AV nodes and atrial AND ventricular contractile cells

-at the same time the adrenal medullae secretes NE and E

combined, these things increase heart rate

1. Positive Ionotropic Effect

---increased contractility resulting from  ↑SD input to contractile cells

a)  NE/E sent to beta1 receptors -> gprotein slide that activate Ca++ VG channels which  ↑CB formation and thus contractility

b) also the beta1 causes activation of cAMP which also increases active Ca++ pumps in sarcolemma and sarc. recticulum.

--all this results in a lower duration of plateau phase=decreased sytole and  ↑diastolic filling and by frankstarling law  ↑edv= ↑co

2. Negative Ionotropic Effect

---mostly decreased sympathetic input to ventricles and a little increased parasympathetic

after a heart gets either a psd or sd input what is the regulatory mechanism of heart rate? or how do sympathetic and parasypathetic divisions regulate heart rate?

1. Chronotropic Effect

a.) neg: big increase in PSD  input to SA node by ACh to M2 receptors. message goes then to Gprot which delays inactivation of K+ channels. causes prolonged hyperpolarizations and thus an interval twix contractions. also a little decrease in sypathetic input.

b.) posi: decrease in psd input to SA node and increase in sd input. NE/E to beta1 receptors to gprots inacativate k+ gates more quickly and plateau potentials become more frequent

too much positive chronotropic effect can cause tachycardia (abnormally high HR)

too much negative chrono. effect can cause brady. (abrnormally low HR)

secreted by adrenal glands

NE and E can cause either positive ionotropic effect or positive chronotropic effect

N and NE bind to beta1 receptors on contractile cardiocytes

metabotropic

secreted in neurons

causes negative ionotropic effect that decreases sympathetic input to ventricles

M1 receptors

they are metabotropic

this was described in a previous card....but just for kicks and giggles.....

ACH binds to M1 receptors which cause a gproteing slide which causes a DELAYED inactivation of K+ channels (that is to say that it now takes longer for all the K+ channels to inactivate during repolarization) this slows the HR down 

once again!

E and NE are recieved by beta1 receptor. this acts on gprotein, causing the gprot slide which ultimately speeds up the inactivation of K+ channels making the heart rate go faster.

in the knee jerk response

what is the sensor, afferent pathway, integrator, efferent pathway and effector

sensor=spindle

afferent pathway=neuron

integrator=spinal chord

efferent pathway: motor neuron

effector: quadricep

the tendon is stretched when hit by the hammer

the tendon is connected to the spindle which acts as the stretch receptor and sends an afferent message to the spinal chord

where are the somae and dendrites in the knee jerk reflex?

where is the ganglia?

sensory soma is in the spindle

sensory dendrite is in the gray matter of spinal cord

motor soma is in the gray of spinal cord

and the motor dendrite is attached to muscle

the ganglia is on the dorsal root/sensory side