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66 Cards in this Set

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Nodal conducting tissues include...
SA Node, Atrial conducting fibers, AV node, His-Purkinje fiber system

And finally, cardiac myocytes themselves.
Nodal cells
SA and AV node cells.

Rate of depolarization is greatest in SA node.
Conducting fibers are made up of...
nodal tissue, bundle of His and Purkinje fibers.
Ca induced Ca release...
When Ca influx from intersitital fluid causes SR to release Ca into the cytoplasm.
Positive Inotropic effect
Increases myocardial contractility. (Ca+2 release increases, resulting in increases contractility)
Effect of cardiac glycoside...
Stronger contraction

Cardiac glycoside inhibits Na/K pump ---> Higher Na concentration inside ----> Inhibits Na/Ca pump ----> Higher Ca concentration inside and stronger contraction.
Phospholamban activates..

Phospholamban is activated via...
Activates the Ca-ATP pump in the SR.

Adenylyl-cyclase cAMP secondary pathway. (NE activates this pathway via beta receptors on the sarcolemma)
DHP receptors

Ryanodine receptors
Found on L-type channels

Ca+2 release channels which are activated when mechanically coupled with DHP receptors.
How does increasing conduction velocity in AV node impact the cardiac function?
This increases shortens the delay between P and R waves. The ventricles are given less time to fill.

EDV decreases, Stroke Volume decreases, CO decreases.
Decrease in PR interval correlates with...
Increased conduction velocity of the AV node.

SNS simulation (PSNS would increase PR interval)
Explain the effect of Phospholamban on cardiac muscle contraction.
Phosporylated phospholamban activate SRCa-ATPase and so more Ca is stored into the SR faster.

This does two things
(1) Faster relaxation (more filling time)
(2) Stronger contraction (more Ca in the SR so next cycle the contraction would be stronger).
Explain why blood flows from Aorta to large arteries when Large arteries are at higher pressure than aorta?
Because the diastolic pressure in larger arteries is smaller than aorta. Since more time is spent in diastole, the mean pressure in large arteries is also lower. Hence, blood can go from aorta to large arteries.
Norepinephrine is released by...

Epinephrine is released by...
Postganglionic SNS

Adrenal glands.
Lidocaine
Class Ib anti-arrythmia drug.

Blocks Na channels.
Verapamil and Diltiazem
Shutdown calcium channels.
Verapamil and Diltiazem
Shutdown calcium channels.
Sustained cardiac arrest..
By raising extracellular K.
What supplied blood to AV and SA nodes?
Right coronary arteries (occlusion here result in server arrythmias)
When do cardiac myocytes start beating on their own?
During Hypoxia. Myocyte foci are created.
Chronotropic effect
SNS and PSNS inputs as they refer to heart rate.
Dromotropic effects
ANS factor that effect the change in conduction velocities through cardiac tissue.
Adrenergic response
Increase Ica currents
Increases the rate of phase 4 depolarization
Lowers threshold potentials.
Atenolol and Lopressor
Selective beta-blockers.
PSNS (vagal)innervation
Only to SA and AV. Not to atrial and ventricular myocytes.
Atropine
Blocks PSNS response by blocking Ach response
Name three calcium channel blockers..
Verapamil
Nifedipine
Diltiazem

They all block L-type channels (in the T-tubule)
Which cardiac tissues have pacemaker activity?

Which cardiac cells do not have pacemaker activity?
SA Node (approx 70/min highest rate)
AV node (approx 40/min)
His-Purkinje system (approx 20/min)

Ventricular and Atrial myocytes (unless its pathologic and then there will be foci within atrial and ventricular myocytes)
What is responsible for unstable resting membrane potential in pacemaker cells?
If (funny current) - Is allowing Na to flow in slowly, which results in slow depolarization and eventual firing of an AP.
T-Type Ca channels

L-Type Ca channels
Responsible for phase 0 in SA node.

Responsible for plateau phases in atrial and ventricular APs.
Heart rate is determined by...
Phase 4 depolarization
Which medicine can be used to treat bradycardia?
Atropine (PSNS antagonist)
Frank-Staarling relationship...
As sarcomere length increases (EDV increases), tension, cardiac output, SV, pressure increases.
Preload is dependent on...

VR is dependent on...
EDV, which is dependent on VR and RAP.

VR is dependent on TRP, Heart rate, Orthostatic differences etc...
Ways to increase VR...

Ways to decrease VR....
Increase - blood volume, Higher systemic pressure (veno-constriction)

Decrease - Bleeding, lower systemic pressure (veno-dilation)
List three ways to control size of vessels locally...
(1) Myogenic - When smooth muscles responds to stretch or distenstion.
(2) Interstitial tissue pressure or temperature
(3) Vasoactive substance - locally released substances. Endothelial cells released substances.

(NOTE: Local vasocontrol only DILATES the vessels).
Sympathetic innervation controls the size of the blood vessels in three ways....
(1) density of innervation
(2) receptor type
(3) rate of discharge

(compare this to local control - myogenic, intersititial pressure, vasoactive substances)
Define delivery vessels.
Carry blood before the capillary level and include aorta and large vessels.
Describe exchange vessels
capillaries. Substance exchange happens here. Not innervated by adrenergic nerves (because no smooth muscle)
List three characteristics of arterioles...
smaller diameter
thicker walls
large content of smooth muscle
What physiological change is vital DEFENSE mechanism (during exercise, thermoregulation)...
venoconstriction (helps return more blood to heart and Q goes up, hence maintaining BP and coronary and cerebral perfusion).
How does B2 receptor work?
Vaso-dilator.

via adnyly cyclase, cAMP and protein Kinase A, it does four things..
(1) Protein Kinase A phosphorylates MLCK and MLCK-P is unable to bind to Ca-Calmodulin.
(2) Activate Ca2+ atpase pump, so more calcium leaves.
(2) inhibit calcium release (from ca storage)
(3) Increase internal calcium storage

(so less free calcium in the cytoplasm for the MLCK).
What is unique about splanchnic and renal adrenergic receptors?
Concentration of alpha receptors is higher than beta receptors.

So when EPI is released as part of sympathetic tone, vasoconstriction occurs.
Where is epi released from?
Adrenal medulla
What does "tonically active" mean?

Which nerve fibers are not tonically active?
Tonically active - having a basal firing rate. Adrenergics have this. NE is always being release.

Cholinergics do not have this. There is no basal constant release of ACh.
What are pacemaker neurons?
They go from RVLM to Pregangionic fibers in IML horns.

They have a basal firing rate, hence called pacemaker neurons.
Which neurons are tonically active? And which are not?
Tonically active - Pacemaker and adrenergic

No basal firing rate - Cholinergic
What is the primary cause of blood flow during diastolic run-off?
elastic recoil of aorta
Firing rate of baroreceptors increases during _____ and decreases during _______.
Systole, Diastole
During SA node firing....

(1) Phase 0 is due to....
(2) Phase 1 and Phase 2...
(3) Phase 3 is due to...
(4) Phase 4 is due to...
Phase 0 - Rapid depolarization. Due to inward Ca currents via T-Type channels.

Phase 1 and 2 - don't exist (because no plateau)

Phase 3 - Is due to the outflow of K.

Phase 4 - Unstable due to continued Funny current, Na flowing in.
Inotropic effects impact...

Chronotropic effects impact...

Dromotropic effects impact...
Contractility

HR

Conduction velocity
Contractility can be changed by these receptors...
Beta 1 (SNS and Muscaranic (PSNS)
List five changes that will cause the VR to increase....
(1) Veno-constriction
(2) Vaso-dilation (decrease in TPR)
(3) Increased BV
(4) Supine Postural change
(5) More negative intra-thoracic pressure (during inspiration)
What defines steady state (on the cardiac and vascular function curve)?
When CO equals to VR. (This steady state moves up and to left when VR increases).
Change in PR interval on the EKG is an indication of....
change in the conduction velocity. (Positive or negative dromotropic effect)
Which neurotransmitter has the greatest effect on following recepors?

B1
B2
M2
Alpha
B1 - NE (SNS)
B2 - Epi (SNS)
M2 - Ach (PSNS)
M1 - Ach (PSNS)
Alpha - NE (SNS)
Desribe the two sensory afferent nerve fibers that are involved in Peripheral reflex mechanism of muscle contraction response.
Type III - Small diameter, Myelinated, Fast (2.5-30m/sec), Mechanoreceptors (some are chemo)

Type IV - C fibers - Small diameter, unmyelinated, slow, Chemoreceptors .
SBP is a function of...

DBP is a function of...
SBP - SV, Distensibility of the vessel (aorta...), Velocity of ejection (strength of contraction of the heart)

DBP - Afterload, TPR, HR (the amt of time spent in Diastole)
What is an indicator of intensity of the dynamic exercise?

What is an indicator of intesntiy of static exercise?
Maximum O2 consumption (Vo2)

% maximum voluntary contraction.
How does change in temperature effect O2 extraction?
As Temp goes up, O2 disociates easily from the Hb. (Remember Bohr effect). Hence, As T increases, O2 extraction increases.
Nitroprusside

How is this different from Ach?
Dilates vessels. Endothelial cell independent. Effects SMCs.

Ach dilates via NO which is endothelial dependent mechanism.
Phospholipase C
Alpha Receptor pathway

Binding of chemical activator to G-protein (guanine nucleotide)activates PL-C. Which in turn causes PIP2 to go to IP3 and DAG.

IP3 causes release of Ca from SR.
Over perfused vs. under perfused
Over perfused - When CO is high and O2 extraction is low (as in kidney)

Under perfused- When CO is low but O2 extraction is high as in heart.
Why is heart supplied during diastolic phase?
Because coronary arterioles are at very high pressure during ventricular contraction and so pressure gradient is for retrograde flow.

Contracting cardiac muscle shuts or collapses small arterioles of the coronary arteries during systole.
Potent dilators for coronary arteries AND for cerebral arteries?
Adenosine

Hydrogen Ions (CO2, which is converted to H+ via carbonic anhydrase)
Bradykinin
potent vasodilator in the non-apical skin.

It is released by sweat glands when activated by Acetylcholine.
What is triple response?
Skin's response to mechanical stress -- (1) Contraction of arterioles (white reaction) (2) Subsequent dilation and spreading of dilation (red streak) (3) Alternation in capillary permeability (swelling) AND flare dilation of arterioles.