Cardiovascular Physio Exam 2

Front 1

Term

Back 1

Definition

Front 2

Positive chronotopic effects

Back 2

Things that *increase* heart rate. Ex: sympathetic n.s., where Norepi stimulates Beta-1 receptors in SA Node and activate AC through G-protein. This increases I[funny], which in turn icreases rate of Phase 4 depolarization.

Hint 2

None

Front 3

Positive chronotopic effects

Back 3

Things that decrease heart rate. Ex: parasympathetic n.s. releases ACh to activate muscarinic (M2) receptors in the SA node. Activates G-protein, G[k] that inhibits AC and decreases I[funny]. G[k] also increases potassium channels K+-ACh and increases outward K+. Hyperpolarizes.

Front 4

Dromotropic effect

Back 4

changes the conduction velocity of heart. Positive effect increases it, Negative effect decreases it. Ex: sympa increases conduction velocity through AV Node and I[calcium], parasympa decreases it through decreased I[calcium] and increased I[K-ACh].

Front 5

Conduction velocity factors

Back 5

depends on the size of the inward current. The larger this current, the more rapidly the current spreads. This also correlates with dv/dt (the rate of rise of upstroke of Acction potential), since dv/dt correlates with size of inward current.

Front 6

EKG: P wave

Back 6

The depolarization of atria. The P duration correlates with conduction time through atria. Ex: If conduction velocity decreases, P wave spreads out.

Front 7

EKG: PR interval

Back 7

The time from initial depolarization of atria to initial depolarization of ventricles. This flat part of curve is the “PR segment” and corresponds with “AV Node Conduction.” Normally 160ms. If increase conduction velocity, decreases the PR interval length.

Front 8

EKG: QRS complex

Back 8

The depolarization of ventricles. This time length is similar to P-wave because conduction velocity in His-Purkinje system is much faster than atrial conducting system.

Front 9

EKG: T wave

Back 9

The repolarization of ventricles.

Front 10

EKG: QT interval

Back 10

Represents 1st ventricular depolarization to last ventricular repolarization.

Front 11

Heart Rate

Back 11

On EKG: count the QRS complexes (or also R waves). …..Heart rate = 1/cycle length , where cycle length is one R to the next R. units is beats/sec. If heart rate changes, so does the duration of action potential, and thus the refractory periods and excitability.

Front 12

If Heart Rate increases, results in:

Back 12

Decreases the duration of action potential and its refractory period. But increase in number of action potentials per given time. This may cause arrhythmias.

Front 13

Inotropic effect

Back 13

Positive inotropic effect—increases contractility. Positive results in high peak tension, increased rate of tension development, and faster relaxation, so contraction twitch is shorter. Ex: Sympa n.s. works on Beta-1 receptors that activate AC, then cAMP, etc.

Front 14

phospholambdan

Back 14

Protein that regulates Calcium ATPase in sarcoplasmic reticulum. When phosphorylated, it stimulates Calcium ATPase, results in uptake and storage of calcium, so faster relaxation.

Front 15

Mean arterial pressure (P[a]) equals?

Back 15

P[a] = (cardiac output) x (Total peripheral resistance)

Back 16

where CO is units mL/min and TPR units is mm Hg/mL/min

Back 17

*Be aware: the units are not independent. If you change TPR, it also changes CO, etc.

Front 18

Baroreceptors

Back 18

Found in carotid artery, which detects both increase and decrease in P[a], the mean arterial pressure and sends info to brain center via Carotid Sinus Nerve (of CN 9), to NTS Nucleus Tractus Solitarius, which either sends out positive info to parasym system or has an inhibitory pathway to sympa system. Also found in aortic arch, which detects only increase in P[a] and sends info via Vagus CN 10.

Front 19

Brainstem CV centers

Back 19

In reticular formation of medulla and the lower third of pons.

Back 20

1) Vasoconstriction center, 2) Cardiac accelerator center, 3) cardiac decelerator center

Back 21

Set-point normal pressue is about 100 mmHg.

Back 22

It has tonically active control over sympa and parasympa. Parasympa sends info via Vagus nerve to SA Node.

Back 23

Sympa has 4 effects: (1) to SA Node, (2) on cardiac muscle to increase contractility and stroke volume, (3)acts on arterioles for vasoconstriction to increase TPR, (4) and acts on veins for venoconstriction to decrease unstressed volume.

Front 24

What is baroreceptor reflex’s response to increased arterial pressure?

Back 24

The NTS receives info. Wants to reduce P[a] to normal, so NTS directs increase in parasympa activity, and to decrease sympa activity to the heart. Heart rate decreases (slows). This slow heart rate also decreases contractility. These lead to decreased cardiac output, which tends to reduce P[a] back to normal (since P[a] = cardiac output x Total Peripheral Resistance).

Back 25

Also, sympa’s effects: less constriction of arterioles, so decrease TPR and thus P[a]. Also decrease constriction of vessel, so increases the Unstressed volume.

Front 26

What is baroreceptor reflex’s response to hemorrhage?

Back 26

Hemorrhage -> low P[a] and decreased stressed volume.

Back 27

The reflex response is exactly opposite to that of an increased arterial pressure. Baroreceptors sense less stretch on their mechanoreceptors.

Back 28

Sympa activity is increased in response. Heart rate and contractility increase. Results in increased cardiac output and constriction of arterioles (which increases TPR) and veins (which decreases unstressed volume but increases venous return and works via Frank-Starling.)

Front 30

What is the Renin-angiotensin II-Aldosterone system’s response to hemorrhage?

Front 31

Valsalva Maneuver

Back 31

This tests the baroreceptor reflex.

Back 32

Expire against a closed glottis (during coughin, defecation or heavy lifting). When doing this, increased intrathoracic pressure decreases venous return to heart. Low return leads to decreased CO and consequent decrease in P[a].

Back 33

If baroreceptor reflex works, heart rate shows an increase, and when patient stops, heart rate decreases.

Front 34

What is the Renin-angiotensin II-Aldosterone system? What’s its mxn?

Back 34

It controls blood volume, and is a slower response than baroreceptor reflex.

Back 35

Activated when P[a] decreases. So attempts to raise it to normal. Steps: 1) Decreased P[a] leads to low renal perfusion, sensed by mechanoreceptors in afferent arterioles in kidney. Renin thus made by JG cells.

Front 37

Renin level influenced by?

Back 37

1)      P[a] sensed by mechanoreceptors in afferent arterioles in kidney 2) Increased by sympa and by Beta-1 agonists like isoproterenol. 3) Decreased by Beta-1 antagonists like propanolol.

Front 39

Action of Angiotensin II

Back 39

An octopeptide. Acts on adrenal cortex, vascular smooth muscle, kidneys and brain: 1) zona glomerulosa of adrenal cortex: to increase synthesis & secretion of aldosterone (which acts on distal tubule and collecting duct to increase Sodium reabsorption to increase ECF volume and blood volume) 2) Arterioles: vasoconstricted, thus increase TPR and P[a].

Front 40

Aldosterone

Back 40

Acts on distal tubule and collecting duct to increase Sodium reabsorption to increase ECF volume and blood volume.

Back 41

Production is Stimulated by Angiotensis II.