CVS Physiology 1-5 Flashcards

1
Q

Define the function of the cardiovascular system.

A

Function of the CVS - bulk flow system: transports Oxygen and Carbon dioxide, nutrients, metabolites, hormones and provides heat.
The heart can vary it’s output - vessels can redirect blood-flow to where it is needed most and vessels can store blood.

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2
Q

Indicate the significance of vascular beds being arranged in parallel or in series.

A

Pumps are in series output=input, therefore:
Output of right side of heart must be equal to left side to prevent accumulation of blood in pulmonary and systemic circulations.

Most vascular beds are in parallel (receive blood at the same time) therefore:
All tissues get oxygenated blood
Allows regional redirection of blood

Most vascular beds are arranged in parallel however there are some exceptions to this rule, most notably the gut and the liver which are arranged in series.

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3
Q

Describe the importance of resistance with respect to the cardiovascular system.

A

Resistance is a measure of how difficult it is for blood to flow through the circulation.
To allow redirection of blood flow there must be a change in resistance. The main thing that influences this is the diameter of the blood vessel that you’re trying to push blood through. Resistance controlled by radius^4, selectively redirects flow. Arterioles act as the taps, controlling resistance and therefore flow to each vascular bed.

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4
Q

Justify the significance of pressure with respect to the cardiovascular system.

A

To allow fluid to be transported through a tube there must be a difference in pressure. High pressure side on the left and lower pressure side on the right. High pressure side on the left pushes blood into the arteries out of the left side of the heart and into systemic circulation. Lower pressure on the right to allow blood to return to the right side of the heart.

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5
Q

What is darcy’s law

A

Flow = Difference in Pressure/Resistance
Pressure difference = mean arterial pressure - central venous pressure, affects all tissues.

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6
Q

What does regional distribution of blood describe?

A

This describes the ability of the body to constrict and dilate arterioles supplying different vascular beds to redirect blood flow to different body regions.

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7
Q

Describe the importance of capacitance with respect to CVS.

A

In electrical circuits, capacitance describes the ability of a component to store electrical charge. By analogy, capacitance vessels (the venules and veins) have the ability to store blood and may contain two thirds of the total blood volume.

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8
Q

Explain the functions of elastic arteries, muscular arteries, resistance vessels, exchange vessels and capacitance vessels.

A

Aorta - elastic arteries, wide lumen, thick elastic wall, damp pressure variations.

Arteries - Muscular arteries, wide lumen, strong, thick, non-elastic wall, low resistance conduit.

Arterioles - resistance vessels, narrow lumen, thick contractile wall, control resistance and therefore flow, allow regional redirection of blood.

Capillaries - exchange vessels, narrow lumen, thin wall.

Veins and Venules - Capacitance vessels, wide lumen, thin, distensible wall, low resistance conduit and reservoir, allows fractional distribution of blood between veins and rest of circulation.

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9
Q

Describe the flow of blood through the heart.

A
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10
Q

List the sequence of events occurring during excitation-contraction coupling.

A

When a motor neurone fires an action potential, you get release of the neurotransmitter acetylcholine from its axon terminal, that will diffuse across the synaptic cleft where it binds to cholinergic nicotinic receptors on the end plate. This triggers endplate potential and that is enough to get muscle cell membrane to threshold to evoke an action potential. This is propagated along the sarcolemma, that’s mediated by voltage gated sodium channels and it will be propagated down into these T-tubules. Then calcium is released from these stores in the sarcoplasmic reticulum. That calcium binds to binding sites on troponin, and that then allows the actin and myosin filaments to interact with each other and they form cross-bridges. Essentially myosin grabs actin and pulls it which causes muscle contraction.

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11
Q

List the differences between excitation contraction coupling in cardiac muscle and skeletal muscle.

A

Cardiac muscle forms a functional syncytium:
- Electrically connected via gap junctions
- Physically connected by desmosomes
- These form the intercalated discs

Cardiac muscle has a long action potential (~250 ms vs. ~2 ms in skeletal muscle)
- Long refractory period, so cannot exhibit tetanic contraction
- Ca2+ entry from outside cell can regulate contraction
- - Ca2+ release does not saturate the troponin, so regulation of Ca2+ release can be used to vary the strength of contraction

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12
Q

What is the function of pacemakers.

A

Send electrical signals to heart to make it beat at the correct pace.

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13
Q

Describe the basis of the action potential in non pacemaker tissue.

A

Non pacemaker:
- Resting membrane potential
High resting PK+

  • Initial depolarisation
    Increase in PNa+
  • Plateau
    Increase in PCa2+ (L-type) and decrease in PK+
  • Repolarisation
    Decrease in PCa2+ and increase in PK+
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14
Q

Describe the basis of the action potential in pacemaker tissue.

A

Action potential
Increase in PCa2+ (L-type)

Pacemaker potential (= pre-potential)
Gradual decrease in PK+
Early increase in PNa+ (= PF)
Late increase in PCa2+ (T-type)

Pacemaker explains autorhythmicity
Also a basis for understanding modulation of the activity of the heart (see directed work)

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15
Q

Describe the functions of the components of the special conducting system.

A

Sinoatrial node
- Pacemaker
~0.5 m/s

Annulus fibrosus
- Non-conducting

Atrioventricular node
- Delay box
~0.05 m/s

Bundle of His and Purkinje fibres
Rapid conduction system
~5 m/s

Ensures coordinated contraction of the heart

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16
Q

Describe the initiation and spread of electrical activity throughout the heart.

A

An action potential in a single myocyte evokes a very small extracellular electrical potential.
However, lots of small extracellular electrical potentials evoked by many cells depolarising and repolarising at the same time can summate to create large extracellular electrical waves.
These can be recorded at the periphery as the electrocardiogram.

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17
Q

Correlate the various components of the electrocardiogram with the electrical events in the heart.

A
18
Q

Describes the various degrees of heart block.

A

1st degree heart block - conduction occurring from atria to ventricles just taking longer.

2nd degree heart block - some failure of conduction - PR interval increasing and conduction fails.

3rd degree heart block - complete heart block - no atrioventricular conduction.

19
Q

Define the terms atrial flutter, atrial fibrillation and ventricular fibrillation.

A

Atrial flutter - atria depolarise and contract a lot faster than they should,

Atrial fibrillation - Failure of pacemaker to spread wave of depolarisation through atria.

Ventricular fibrillation - uncoordinated contraction but this time in ventricles.

20
Q

Identify the P-wave, QRS-complex and T-wave in a normal ECG and what heart events they respond to.

A
21
Q

Identify the PR interval, QT interval, PR segment and ST segment

A
22
Q

Describe what the PR interval corresponds to, and state the normal range for this

A

The PR interval = time from atrial depolarisation to ventricular depolarisation, mainly due to transmission through the AV node (normally about 0.12-0.2 s)

23
Q

Describe what the duration of the QRS complex corresponds to, and state the normal
range for this

A

QRS = time for the whole of the ventricle to depolarise
(normally about 0.08 s)

24
Q

Describe what the QT interval corresponds to, and state the normal range for this

A

QT interval = time for ventricles to depolarise and repolarise (varies with heart rate, but normally about 0.42 s at 60 bpm)

25
Q

Why cant you see atrial repolarisation?

A

Because atrial repolarisation coincides with ventricular depolarisation. Ventricular depolarisation involves much more tissue depolarising much faster so it swamps any signal from atrial repolarisation.

26
Q

Describe how to measure heart rate from an ECG

A

Heart rate:
Measure the RR interval and work out how many occur in 60 s, or better…
Count the R waves in 30 large squares (= 6 s) and multiply by 10

27
Q

Describe normal sinus rhythm, sinus tachycardia and sinus bradycardia

A

60-100 bpm = normal
Below 60 bpm = bradycardia
Above 100 bpm = tachycardia

28
Q

Recognise what is meant by the terms STEMI and non-STEMI

A

STEMI = ST segment elevation myocardial infarction
NSTEMI = non-ST segment elevation myocardial infarction

29
Q

Illustrate the sequence of changes in pressure and volume in the chambers of the heart throughout the cardiac cycle.

A
30
Q

Interpret and label a pressure-volume loop.

A
31
Q

Define a, c and v waves

A

a wave - caused by atrial contraction

c wave - left ventricle contracts, exceeds pressure of left atrium causing the mitral valve to close. When mitral valve closes it bulges into left atrium increases pressure of left atrium.

v wave - during systole blood return from the lungs to the left atrium. Atrium has very low volume so when blood flows into it the pressure within that atrium is going to gradually increase, when pressure of left atrium exceeds pressure of left ventricle mitral valve will open so blood flows to ventricle causes decrease in pressure.

32
Q

Explain the generation of the heart sounds (phonocardiogram).

A

Heart sounds occur due to turbulence in blood flow caused by…
1st = closure of the AV (mitral and tricuspid) valves
2nd = closure of the semi-lunar (aortic and pulmonary) valves
3rd = rapid passive filling phase
4th = active filling phase
These are normal
Additional heart sounds are called murmurs (physiological or pathological)

33
Q

Explain the effects of the sympathetic system on heart rate.

A

Sympathetic nervous system
Sympathetic nerves release noradrenaline
Plus circulating adrenaline from adrenal medulla
Both act on β1 receptors on sinoatrial node
Increases slope of the pacemaker potential
Increases heart rate = tachycardia

34
Q

Explain the effects of the parasympathetic system on heart rate.

A

Parasympathetic nervous system
Vagus nerve releases acetylcholine
Acts on muscarinic receptors on sinoatrial node
Hyperpolarises cells and decreases slope of pacemaker potential
Decreases heart rate = bradycardia

35
Q

Explain the effects of the sympathetic system on stroke volume.

A

Sympathetic nervous system
Sympathetic nerves releasing noradrenaline
Plus circulating adrenaline from adrenal medulla
Both act on β1 receptors on the myocytes
Increases contractility (an inotropic effect)
Gives stronger, but shorter contraction

36
Q

Explain the effects of the parasympathetic system on stroke volume.

A

Parasympathetic nervous system
Little effect
Probably because the vagus nerve does not innervate the ventricular muscle

37
Q

What is starling’s law?

A

Starling’s Law states - the energy of contraction is proportional to the initial length of the cardiac muscle fibre

38
Q

Explain the effects of preload on stroke volume.

A

In vivo, preload is affected by the end diastolic volume

Increased venous return, increases EDV and therefore increases stroke volume
Decreased venous return, decreases EDV and therefore decreases stroke volume
Ensures self-regulation – matches SV of left and right ventricles

39
Q

Explain the effects of afterload on stroke volume.

A

Afterload is the load against which the muscle tries to contract
In vivo, afterload is determined by the arterial pressure against which the blood is ejected - this in turn depends on the total peripheral resistance (TPR)
If TPR increases, stroke volume will go down (more energy is “wasted” building up enough pressure to open the aortic valve)

40
Q

How is cardiac output calculated.

A

Cardiac output = heart rate x stroke volume

41
Q

Why does an increase in heart rate cause a decrease in filling rate?

A

The shortened cardiac interval cuts into the rapid filling phase
The reduced end diastolic volume reduces preload
So according to Starling’s law, stroke volume is reduced

42
Q

Describe how different factors combine and work together to keep cardiac output stable.

A

In the body, physiological increases in heart rate, e.g. in exercise, are accompanied by several things that offset decrease in stroke volume.

HR increases
Via decreased vagal tone
Increased sympathetic tone

Contractility increases
Via increased sympathetic tone
Alters inotropic state and shortens systole

Venous return increases
Via venoconstriction and skeletal/respiratory pumps
Maintains preload

Total peripheral resistance falls
Due to arteriolar dilation in muscle, skin and heart
Reduces afterload

CO increase 4-6 times