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Cardiovascular Week 1 & 2 2016/17 > 2: Force generation by the heart > Flashcards

2: Force generation by the heart Flashcards

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1
Q

Cardiac muscle has a streaky appearance - what are these streaks called?

A

Striations

So cardiac muscle is described as ‘striated’

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2
Q

Why is cardiac muscle striated?

A

Alternating actin and myosin proteins

(Actin has a lighter colour and myosin has a darker colour)

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3
Q

Do muscles have a nerve supply?

Why?

A

No

Autorhythmicity - heart can generate its own nerve impulses

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4
Q

What allows for cell-to-cell conduction of impulses between cardiac myocytes?

A

Gap junctions

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5
Q

What property of gap junctions allows for electrical communication between cardiac myocytes?

A

Low resistance

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6
Q

What is the All-or-none Law of the Heart?

A

All cardiac myocytes will respond to an action potential, no matter its strength

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7
Q

The low resistance of gap junctions ensures that excitation reaches ___ cardiac myocytes.

A

all

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8
Q

What is the function of desmosomes?

A

Provide mechanical adhesion - sticks cardiac myocytes together so they all tense up together

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9
Q

Within a muscle fibre, fascicles contain ___ which are made up of sarcomeres.

A

myofibrils

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10
Q

Myofibrils have alternating __ and __ protein segments.

A

thick , thin

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11
Q

What is the smallest unit of contractile muscle?

A

Sarcomere

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12
Q

What are the thin, lighter segments of myofibril made of?

A

Actin

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13
Q

What are the thicker, darker sections of myofibril called?

A

Myosin

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14
Q

What are the smaller functional units found within myofibrils called?

A

Sarcomeres

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15
Q

Actin filaments ___ along myosin filaments to cause muscle ___.

A

slide along

muscle contraction

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16
Q

The interactions between actin and myosin are dependent on what two molecules?

A

ATP

Ca2+

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17
Q

ATP binds to myosin to trigger what?

A

Detachment of myosin cross bridge from actin

Cross bridge then slides along actin and rebinds

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18
Q

Ca2+ triggers (binding / detachment) of myosin-actin.

A

Binding

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19
Q

What ion is required to switch on myosin cross-bridge formation?

A

Ca2+

So ATP binds to myosin to detach it from actin, it then slides forward and if calcium is present, it rebinds (and the muscle has contracted)

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20
Q

Name the two regulatory proteins found on actin filaments.

A

Tropomyosin

Troponin

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21
Q

What is the name of the rope-like protein structure found on actin filaments?

A

Tropomyosin

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22
Q

What protein blocks myosin binding sites on actin filaments until it is disabled by calcium ions?

A

Troponin

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23
Q

Calcium binds to troponin causing a _____ change, moving the protein away and exposing the ___ binding sites on the ___ filaments.

A

conformational change

myosin-binding sites on actin filaments

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24
Q

Ca2+ is released from the ____ ____ depending on the extracellular presence of Ca2+.

A

sarcoplasmic reticulum

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25
What triggers the **release** of **Ca2+ ions** from the **sarcoplasmic reticulum** of myofibrils?
**Extracellular calcium** - i.e Calcium-dependent Calcium release
26
During systole... 1. Contractile machinery activated 2. Ca2+ influx during plateau phase of action potential 3. Ca2+ released from the sarcoplasmic reticulum 4. Ca2+ binds to troponin and allows myosin-actin cross-bridge binding **Arrange these statements in the correct order.**
**2 → 3 → 4 → 1**
27
What is the **refractory period**?
The **period following an action potential** in which **it is not possible to produce another action potential**
28
During the plateau phase, how do **Na+ channels** ensure that another action potential (i.e depolarisation) does not take place?
They **close**
29
In the descending phase, how do K+ channels ensure that another depolarisation does not take place?
They **open** bringing membrane back down to K levels
30
Why is the **refractory period** of the heart important?
It prevents generation of **tetanic contractions** of cardiac muscle (i.e constant heartbeats)
31
What are **tetanic contractions** of the heart?
Sustained muscle contraction when the **rate of action potentials in cardiac muscle is too high**
32
**Contraction of ventricular muscle** ejects the ___ volume.
stroke
33
What is the definition of **stroke volume**?
The volume of blood ejected by **each** ventricle per heart beat
34
What is the equation for **stroke volume**?
Stroke volume (SV) = End diastolic volume (EDV) - End systolic volume (ESV) ## Footnote **SV = EDV - ESV**
35
Which **two types** of mechanism regulate the stroke volume of the heart?
**Intrinsic** and **extrinsic** mechanisms
36
What is **intrinsic** control of stroke volume?
Controls found **within** the heart muscle itself
37
What is **extrinsic** control of stroke volume?
Control by the **nervous system** and **hormones**
38
Intrinsic changes in **stroke volume** are brought about by...
**end diastolic length of myocardial fibres** (preload)
39
Which **volume** determines the **preload** of myocardial fibres?
**End Diastolic Volume (EDV)**
40
What is the **cardiac preload**?
The **stretching of myocardial fibres at the end of diastole** (which **determines the stroke volume** of the next heart beat)
41
What determines the **end diastolic volume**?
**Venous return**
42
1. End diastolic volume determines 2. Diastolic length of myocardial fibres determines 3. Venous return determines 4. Cardiac preload **Arrange the numbers 1-4 in the correct order.**
**3** → **1** → **2** → **4**
43
What is **Starling's Law of the Heart?**
The more the ventricle fills with blood during diastole (**greater** **end diastolic volume**) the greater the volume of ejected blood will be (**greater stroke volume**) during the resulting systolic contraction i.e **greater EDV = greater stroke volume**
44
Which **law** does this graph show?
**Starling's Law of the Heart** (increased EDV = increased stroke volume)
45
Increased **stretch** has an effect on a regulatory protein found on actin. What is this effect?
**Increased stretch** \> increased **affinity of troponin for Ca2**+
46
According to Starling's Law of the Heart, **optimum length in cardiac muscle** is achieved by _____ the muscle.
**stretching**
47
1. Increased stroke volume into the pulmonary artery by Starling's Law 2. Increased venous return to left atrium from pulmonary vein 3. Increased venous return to right atrium 4. EDV of left ventricle increases 5. EDV of right ventricle increases **...causing increased stroke volume into the aorta by Starling's Law.** **Arrange 1-5 in the correct order.**
3 → 5 → 1 → 2 → 4
48
What is **afterload**?
The **resistance into which the heart is pumping**, imposed **after** the heart has contracted Determined by **TPR**
49
What happens if afterload increases?
**1. The heart is unable is eject its full stroke volume, so some is left over** **2. Thus EDV of the ventricles increases** **3. So force of contraction increases by Starling's Law** **4. If chronic, ventricular hypertrophy may occur to overcome the resistance**
50
Which **autonomic nervous division** supplies ventricular muscle?
**Sympathetic** (remember that parasympathetic impulses have no effect on contractility)
51
Which post-synaptic **neurotransmitter** acts on ventricular muscle?
**Noradrenaline** (sympathetic division supplies heart muscle)
52
Stimulation of sympathetic nerves **(increases / decreases) force of contraction**.
**increases**
53
Sympathetic stimulation **increases** the force of contraction of ventricular muscle. What name can be given to this effect?
**Positive **_ino_**tropic effect**
54
Stimulation of the sympathetic nerves in the heart produces **two different effects**, what are they called?
**Positive chronotropic effect** (increased heart rate) **Postivie inotropic effect** (increased force of contraction) Remember sympathetic stimulation also **reduces AV nodal delay**
55
Why does sympathetic stimulation increase the force of contraction of ventricular muscle?
**Activation of Ca2**+ **channels** causes greater Ca2+ influx
56
What molecule mediates the activation of calcium channels associated with sympathetic stimulation of the heart?
**cAMP**
57
The activation of calcium channels associated with sympathetic stimulation of the heart also reduces the durations of ___ and \_\_\_.
**systole** and **diastole** | (Thus increasing heart rate)
58
What effect does sympathetic stimulation have on the Frank-Starling curve and why?
**Shifts curve to the left** **_Contractility of the heart at a given EDV increases_**
59
Explain the trends seen on this Frank-Starling curve.
Positive inotropic effect is an increase in the force of contraction so stroke volume increases and the opposite
60
**Heart failure** causes a shift to the ___ on a Frank-Starling curve.
**right**
61
What effect does **parasympathetic** stimulation have on the **force of contraction**?
**No effect** Parasympathetic stimulation influences rate, not force, of contraction
62
Where in the body are **adrenaline** and **nonadrenaline** released?
**Adrenal medulla**
63
What is cardiac output?
The volume of blood pumped by **each ventricle** per **minute**
64
Write an equation for cardiac output.
Cardiac output = Stroke volume x Heart rate ## Footnote **CO = SV x HR**
65
What is the resting cardiac output in a healthy adult?
Approx. **5L** 70ml SV x 70bpm = 4900ml CO

Cardiovascular Week 1 & 2 2016/17 (19 decks)

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