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Human Physiology 2 > Unit 1 - CV System The Heart PART H > Flashcards

Unit 1 - CV System The Heart PART H Flashcards

1
Q

What are the 2 factors affecting Heart Rate (HR)?

A

a. Neural Control
- PSNS control
- SNS control

b. Hormonal Control

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2
Q

What is heart rate intrinsically controlled by?

A

Heart rate is intrinsically controlled by the frequency of action potentials (APs) in SA node autorhythmic cells which is normally ~100 APs/min.

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3
Q

However, the heart is exposed to neural and hormonal factors that…

A

modify the rate of AP generation in the SA node

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4
Q

What can heart rate be modified by?

A

The rate can be modified by neural control via the antagonistic effects of the parasympathetic (PSNS) and sympathetic (SNS) branches of the autnonomic nervous system and through the effects of hormones.

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5
Q

Both divisions of the ANS are active at ___ times

A

ALL

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6
Q

Both divisions of the ANS are active at all times, however antagonistic tonic control means…

A

increased signaling in the PSNS leads to decreased signaling in the SNS and vice versa.

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7
Q

At rest, the ____ is dominant, resulting in an HR that is ____ (__ bpm) than the intrinsic rate of the SA node (___ bpm).

A

PSNS

LOWER

72

100

As a result, heart rate can be increased either by decreasing PSNS signaling or by increasing SNS signaling.

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8
Q

As a result, heart rate can be increased either by ______ PSNS signaling or by _______ SNS signaling.

A

DECREASING

INCREASING

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9
Q

The _____ division modulates HR

A

AUTONOMIC

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10
Q

Average HR in an adult

A

70 bpm (highly variable though)

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11
Q

Trained athletes resting HR

A

50 bpm or less

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12
Q

Someone excited or anxious’ HR

A

125 bpm or higher

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13
Q

Children have ______ average HR’s than adults

A

HIGHER

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14
Q

HR is initiated by _________, but it is modulated by ________

A

AUTORHYTHMIC CELLS IN THE SA NODE

NEURAL & HORMONAL INPUT

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15
Q

PSNS ____ HR

A

SLOWS

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16
Q

SNS _____ HR

A

SPEEDS UP

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17
Q

What are the 2 forms of Neural Control?

A

i. Parasympathetic (PSNS) Control

ii. Sympathetic (SNS) Control

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18
Q

Describe the Parasympathetic (PSNS) Control mechanism

A

1) PSNS neurons from vagus nerve release acetylcholine.
2) ACh binds to muscarinic receptors of SA node cells, initiating signal transduction.
3) Result is an INCREASE in K+ permeability, which hyperpolarizes the pacemaker potential and a DECREASE in Na+ and Ca2+ permeability which SLOWS the rate at which the pacemaker potential depolarizes.
4) Hyperpolarization and slow depolarization of pacemaker potential, DELAYS the time required to reach threshold, which in turn DECREASES the rate of action potentials and therefore the heart rate.

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19
Q

Describe the Sympathetic (SNS) Control mechanism

A

1) SNS neurons from thoracic nerve release norepinephrine (NE).
2) NE binds to b1 adrenergic receptors of SA node cells, stimulating the cAMP second messenger system.
3) Result is a DECREASE in K+ permeability, which depolarizes the pacemaker potential and an INCREASE in Na+ and Ca2+ permeability, which SPEEDS UP the rate at which the pacemaker potential depolarizes.
4) FASTER depolarization, SHORTENS the time required to reach threshold, which in turn INCREASES the rate of action potentials and therefore the heart rate.

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20
Q

Explain what increases HR

A

MORE RAPID cation entry SPEEDS UP the rate of the pacemaker depolarization, causing the cell to reach threshold FASTER & INCREASING the rate of AP firing

When the pacemaker fires APs MORE RAPIDLY, HR INCREASES

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21
Q

Describe the Hormonal Control mechanism

A

EPINEPHRINE secreted by the adrenal medulla as a result of increased sympathetic activity reinforces the the effects of the SNS action on the heart. The mechanism of action of hormonal epinephrine is the same as that for norepinephrine released by neurons.

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22
Q

Describe Tonic Control (of HR)

A

dominated by the PS branch

  • this control can be shown experimentally by blocking all autonomic (S & PS) input to the heart
  • now, the spon. depol rate of the SA node is 90-100 times per min
  • to get a HR of 70 bpm, tonic PS activity must SLOW the intrinsic rate DOWN from 90 bpm
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23
Q

An INCREASE in HR can occur in 2 ways:

A
  1. DECREASE PS activity
    - as PS influence is withdrawn from the autorhythmic cells, they resume their intrinsic rate of depol., & HR INCREASES to 90-100 bpm
  2. Sym. input is req. to increase HR ABOVE the intrinsic rate
    - NE or E on B1-receptors SPEEDS up the depol. rate of the autorhythmic cells & INCREASE HR
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24
Q

BOTH autonomic branches also alter the rate of conduction through the AV node:

A
  • ACh SLOWS the conduction of APs through the AV node, INCREASING AV node DELAY
  • Contrasty, E & NE ENHANCE conduction of APs through the AV node & through the conducting system
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25
Q

What are the Factors affecting Stroke Volume (SV)?

A

Any factor (INOTROPIC AGENT) that increases the force (strength) of ventricular contraction (= contractility) will increase SV. This involves the contractile cells of the myocardium as opposed to the autorhythmic cells of the conduction system.

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26
Q

Stroke Volume

A

volume of blood pumped per ventricle per contraction, is directly related to the force generated by cardiac muscle during a contraction

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27
Q

Define Inotropic agent & Inotropic effect

A

any chemical that affects contractility, & its influence is called an INOTROPIC EFFECT

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28
Q

If a chemical increases the force of contraction, it is said to have a ___ inotropic effect

A

+

vice versa with (-) inotropic effects

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29
Q

Contractility…

A
  • increases as the amount of Ca2+ available for contraction increases
  • is enhanced by catecholamines & certain drugs
30
Q

Increasing sarcomere length also makes cardiac muscle more sensitive to Ca2+ thus…

A

linking contractility to muscle length

31
Q

What 2 parameters is the force of ventricular contraction affected by?

A
  1. Length of muscle fibers @ the beginning of contration

2. The contractility of the heart

32
Q

The volume of blood in the ventricle @ the beginning of contraction (the ____) determines the ____ of the muscle

A

EDV

LENGTH

33
Q

Contractility

A

is the intrinsic ability of a cardiac muscle fiber to contract at any given length & is a function of Ca2+ interaction with the contractile filaments

34
Q

_____ is distinct from the length-tension relationship

A

Contractility

35
Q

What are the 5 factors affecting SV?

A
  1. Neural Control
  2. Hormonal Control
  3. Intrinsic Control
  4. Venous Return
  5. Afterload
36
Q

What are the two branches of Neural Control?

A

i. Parasympathetic (PSNS) Control

ii. Sympathetic (SNS) Control

37
Q

Parasympathetic (PSNS) Control (for SV)

A

none (little to no vagal innervation of contractile cells)

38
Q

What is the Sympathetic (SNS) Control mechanism (for SV)?

A

1) SNS neurons release norepinephrine

2) NE binds to B1 adrenergic receptors on CONTRACTILE
cells, stimulating the cAMP second messenger system.
- to phosphorylate specific intracellular proteins

39
Q

What are 4 effects of the Sympathetic (SNS) Control mechanism for SV?

A

a) Phosphorylation of L-type calcium channels causes them to open wider. This increases flow of Ca2+ into contractile cells following the action potential on the contractile cell membrane.
b) Increased release of Ca2+ from the sarcoplasmic reticulum (SR) (increased calcium induced calcium release).
c) More Ca2+ in the cytosol, increases the number of crossbridges between actin and myosin, and increases the speed of crossbridge cycling.
d) Phosphorylation of phospholamban, increases activity of Ca2+ ATPase in SR membrane, increasing the speed of relaxation.

40
Q

a) to c) ______ ventricular contractility - _______________

A

INCREASE

AT ANY GIVEN END DIASTOLIC VOLUME (i.e. SNS stimulation operates independently of length tension relationships)

41
Q

Phospholamban

A

is a regulatory protein that alters sarcoplasmic reticulum Ca2+-ATPase activity

  • catecholamine INCREASE Ca2+ storage through the use of this regulatory protein
42
Q

What does Figure 14.22 show?

A

mech. by which catecholamines INCREASES Ca2+ entry of storage & exert their (+) inotropic effect

43
Q

What do Catecholamines (E & NE) do? Why?

A
  1. INCREASE the FORCE of cardiac contraction (when they bind to B1-adrenergic receptors)
  2. SHORTENS the DURATION of contraction

b/c the enhanced Ca2+-ATPase speeds up removal of Ca2+ from the cytosol
- which, shortens the time that Ca2+ is bound to troponin & decreases the active time of the myosin crossbridges (therefore, briefer muscle twitch)

44
Q

Cardiac glycosides:

A
  • INCREASE contractility by SLOWING Ca2+ removal from the cytosol (opp. of catecholamines)
  • pharmacological effect
  • remedy for heart failure (unable to contract forcefully)
  • depress Na+-K+-ATPase activity in all cells, NOT just in heart
  • in the myocardial cell, cardiac glycosides DECREASE the cell’s ability to remove Ca2+ by means of the Na2+-Ca2+ exchanger
  • the resultant INCREASE in cytosol Ca2+ causes more forceful myocardial contractions
45
Q

What is the Significance: SNS stimulation:

A

1) Increases force of ventricular contraction, which increases the proportion of EDV ejected from the ventricle (ejection fraction), which increases SV.

2) Increases contraction/relaxation speed, which decreases duration of SYSTOLE and increases duration of DIASTOLE.
a) Each cardiac cycle takes ~0.8 sec at rest (72 bpm), but only 0.3 sec at 200 bpm.
b) Shortening systole during SNS stimulation lengthens diastole, which ensures sufficient time for ventricles to refill during intense exercise, despite the higher HR.

3)
SNS also increases:
a) the force of atrial contraction
b) vasoconstriction of peripheral veins (which increases venous return to heart).

46
Q

Why is, “Increases contraction/relaxation speed, which decreases duration of SYSTOLE and increases duration of DIASTOLE,” important?

A

This is important, since the SNS also increases heart rate, which decreases the time for ventricular filling (diastole). This decrease in diastole due to increased HR must be compensated for, or else EDV will be too low to maintain or increase (SV).

47
Q

Each cardiac cycle takes ~___ sec at REST (72 bpm), but only __ sec at 200 bpm.

A
  1. 8

0. 3

48
Q

Shortening _____ during SNS stimulation lengthens ______, which __________

A

SYSTOLE

DIASTOLE

ensures sufficient time for ventricles to refill during intense exercise, despite the higher HR.

49
Q

SNS also increases:

A

a) the force of atrial contraction

b) vasoconstriction of peripheral veins (which increases venous return to heart).

50
Q

As a result (of SNS increasing)…

A

blood enters the ventricles faster, ensuring sufficient filling and further compensating for the effects of increased heart rate. which help to maintain/increase EDV, and help to maintain, if not increase SV.

51
Q

Hormonal Control Mechanism:

A

The mechanism of action of hormonal epinephrine is the same as that for norepinephrine released released by the SNS (cAMP second messenger is activated, etc).

52
Q

Intrinsic Control

A
  • The force of ventricular contraction also varies in response to how much the ventricular myocardium is stretched upon filling (length tension relationship).
  • At REST, cardiac fibers are at LESS than optimal length (which is 2.2 μm). When Increasing EDV, (by for example, increasing venous return) will cause cardiac cells to stretch and approach optimal length. This allows more crossbridges to form between actin and myosin and therefore increases the force of contraction and as a result the stroke volume.
53
Q

At REST, cardiac fibers are at ____ than optimal length (which is 2.2 μm)…

A

LESS

When Increasing EDV, (by for example, increasing venous return) will cause cardiac cells to stretch and approach optimal length. This allows more crossbridges to form between actin and myosin and therefore increases the force of contraction and as a result the stroke volume.

54
Q

EDV affects ventricular ______.

A

preload

55
Q

Ventricular preload

A

the degree of myocardial stretch before contraction begins

56
Q

EDV & preload are determined by _________

A

venous return

57
Q

Length-tension relationship

A
  • the longer the muscle fiber & sarcomere when a contraction begins, the greater the tension developed, up to a maximum
  • seen in the heart: as stretch of the ventricular wall increases, so does SV
  • if additional BF’s into the ventricles, the muscle fibers stretch, then contract more forcefully, ejecting more blood
58
Q

The _____ a muscle fiber is when it begins to contract, the _______ the force of contraction

A

LONGER

GREATER

59
Q

Frank Starling’s Law of the Heart.

A
  • Force of ejection (SV) is directly proportional to the EDV (which determines the degree of stretch in the cardiac muscles.
  • i.e. the more blood in during diastole (increased EDV) (heart contracts more forcefully), the more blood comes out during systole (increased SV) and vice versa.
60
Q

What does a Starling curve show?

A

shows that SV is proportional to EDV

x-axis: Stretch: indicated by ventricular EDV (this volume is a measure of stretch in the ventricles, which in turn determines sarcomere length)

y-axis: Force: indicated by SV (indicator of the force of contraction)

61
Q

Venous Return

A

Venous return (the amount of blood returning to the heart from veins) has direct effects on EDV and therefore on stroke volume and cardiac output..

62
Q

What 3 factors are determining EDV?

A

i. Neural control (sympathetic innervation of veins AKA constriction of veins by symp. activity)
ii. Skeletal muscle pump (contraction or compression of veins returning blood to the heart)
iii. Respiratory pump (pressure changes in the abdomen & thorax during breathing)

63
Q

Neural control (1 factor determining EDV)

A
  • SYMpathetic neurons innervate the smooth muscle in the walls of veins. NOREPINEPHRINE released from these neurons binds to a1 adrenergic receptors.
  • VASOCONTRICTION in response to decreased mean arterial pressure (or exercise) strongly increases venous pressure and therefore venous return.
  • Increased tension in the vein wall decreases compliance (i.e. blood will not be able to pool in veins), which also will INCREASE VENOUS RETURN and therefore increase EDV, SV, and cardiac output.
  • if not understanding look on slide 45
64
Q

Skeletal muscle pump (1 factor determining EDV)

A
  • Large muscle groups compress deep veins in the legs (and arms) when they contract.
  • This compression, combined with the valves in large veins that PREVENT backflow of blood, ensure that when muscles are contracting (like during exercise) more blood is moved towards the heart.
  • So exercise and contracting muscles PUSHES blood back toward the heart, increasing venous return, which increases EDV, which increases SV and cardiac output.
  • Note: at rest (sitting), the skeletal muscle pump is usually NOT working (unless you are doing calf raises or other exercises while seated).
65
Q

Respiratory pump (1 factor determining EDV)

A

is created by movement of the thorax during inhalation (breathing in)

  • Venous return depends on the pressure gradient (∆P) between peripheral veins and the right atrium.
  • Right atrial (and thoracic vena cava) pressure is affected by changes in thoracic cavity pressure.
  • During inspiration, contraction of the diaphragm decreases pressure in the thoracic cavity and increases pressure in the abdominal cavity.
  • Result, is compression of abdominal veins (increasing their pressure) and distension of thoracic cavity veins and the right atrium (decreasing their pressure). The larger difference in pressure between the abdominal and thoracic veins/right atrium (i.e. larger ∆P) causes more blood to flow into thoracic veins and into the right atrium (i.e. increases venous return).
  • The LARGER the inhalation, the greater the ∆P, and the greater the venous return. So every time you yawn while studying for Physiology, you are increasing your venous return, and for a brief moment your stroke volume and cardiac output.J
66
Q

Afterload definition

A

the combined load of blood in the ventricle (the EDV) & arterial resistance during ventricular contraction

  • reflects the preload & the effort req. to push the blood out into the arterial system
  • the load placed on the ventricle as it contracts
67
Q

Afterload

A
  • SV depends on the arterial pressure against which it is pushing.
  • Semilunar valves only open once ventricular pressure becomes greater than aortic pressure.
  • Therefore, if MAP increases, aortic pressure increases, and more force will be needed to eject the same volume of blood against the greater pressure in the arteries.
  • Increased afterload only becomes a problem in diseased states:
    i. Chronic hypertension (>140/90 mmHg)
    ii. STENOSIS of the semilunar valves
    iii. COARCTATION of the aorta
68
Q

Afterload Analogy

A

waiters carrying trays of food through a swinging door

  • tray = blood in the ventricles at the beginning of contraction
  • door = additional load that the waiter must push against to leave the kitchen (relatively minor)
  • if someone piled furniture against the other side of the door (increased afterload), the waiter must expend more force to push through
  • ventricular contraction must push a load of blood through a semilunar value & out into the blood-filled arteries
69
Q

To eject blood from the ventricle,…

A

the heart must create force to displace the blood in the aorta, pushing it further downstream

70
Q

Review Ex on page 48 of notes

A

done

71
Q

Review graph on page 48 of notes

A

done

72
Q

Review control of cardiac output review on page 49 of notes

A

done

Human Physiology 2 (37 decks)

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