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BVM1 - Cardiovascular system > 4. Cardiovascular regulation > Flashcards

4. Cardiovascular regulation Flashcards

1
Q

What is heart failure?

A

Develops when the heart is unable to maintain a normal cardiac output at normal filling pressures
- leads to under filling of the arterial circulation

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2
Q

What does a rise in the LV pressure curve mean?

A

Pressure rising during systolic phase

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3
Q

What is end diastolic volume?

A

Maximum amount of blood either a left or right ventricle can hold

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4
Q

What is end systolic volume?

A

Blood left at the end of contraction - systolic phase

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5
Q

What is cardiac output?

A

Volume of blood pumped into the aorta per unit time

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6
Q

What is venous return?

A

volume of blood that comes back to the right atrium

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7
Q

What is the relationship between venous return + cardiac output in a normal heart?

A

They should be equal

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8
Q

What is the parasympathetic influence on heart rate?

A

Vagus nerve (parasympathetic) - innervates SA and AV nodes; small amount to the atria
- at rest predominates
- decreasing vagal tone
ACh release slows HR (muscarinic receptor antagonists increase HR)

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9
Q

What is the sympathetic influence on heart rate?

A

Innervate SA and AV, atria and ventricles

  • increasing sympathetic tone
  • NAd release accelerates heart rate (𝛃-adrenoreceptor anagonists slow HR)
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10
Q

What is the parasympathetic influence on regulation of heart rate?

A

Increases AV refractory period

Decreases AV conduction

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11
Q

What is the sympathetic influence on regulation of heart rate?

A

Decreases Av refractory period

Increases AV conduction

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12
Q

What is the Frank Starling mechanism?

A

Energy of contraction of a muscle fibre is proportional to initial fibre length at rest
- filling pressure can give us a good indication of what is happening in terms of stretch of the myocardium

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13
Q

What are some factors affecting venous return?

A
  1. Displacement of blood from the veins (sympathetic vasoconstrictor fibres) - increases venous return and stroke volume
  2. Skeletal muscle activity in lower extremities
  3. Thoracic pump - On inspiration, intrathoracic pressure falls; leads to reduction in central venous pressure
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14
Q

What is preload?

A

Filling pressure of the heart

- determined in vivo by venous volume and rate of venous return (determine central venous pressure)

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15
Q

What is afterload?

A

Pressure against which the heart ejects (resistance blood has to overcome to get blood moving)
- determined in vivo by the peripheral resistance which is proportional to arterial pressure

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16
Q

Do cardiac outputs need to be equal?

A

Right and left cardiac outputs do need to be equal under normal conditions
- can vary due to physiological and pathological factors

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17
Q

What is hypertension?

A

High blood pressure, heart needs to work harder to overcome the resistance
- sympathetic system causes an inotropic effect

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18
Q

What effect does stimulation rate have on stroke work and end diastolic pressure?

A

As sympathetic nerve stimulation is increased:

  • Stroke work = increased
  • end diastolic pressure = decreases
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19
Q

How do we increase stroke work?

A

Intrinsic regulation:
- movement along a Starling curve
- change in muscle filling pressure and resting length
Extrinsic regulation:
- movement from one starling curve to another due to sympathetic stimulation (improves contractibility without changing filling pressure)

20
Q

How is positive inotropism achieved?

A

Increased contractility at constant filling pressure

21
Q

What effect does sympathetic stimulation have on ventricular contraction and relaxation?

A

Increases in:

  1. Rate of force development
  2. Rate of relaxation
  3. Maximal force developed
22
Q

What is perfusion?

A

Flow of blood per unit of volume tissue

- energy generated in the arterial system by the aorta

23
Q

What is perfusion pressure?

A

Controlled variable in the circulation

- provides the energy for perfusion

24
Q

What is circulatory shock?

A

Failure to achieve adequate perfusion pressures

  • results in hypoxia = impaired metabolism = necrosis
  • severe haemorrage
25
Q

What is the result of excessive perfusion pressure?

A

Results in capillary damage, endothelial injury and fluid exudation
- can happen in some cases of heart failure

26
Q

What is systemic arterial pressure the major determinant of?

A

Tissue perfusion pressure

27
Q

How is blood pressure regulated short term?

A

Baroreceptor regulation

- autonomic nervous system

28
Q

What is a baroreceptor?

A

Mechanoreceptors located in the carotid sinus and aortic arch
- sense pressure changes in the tension of the arterial wall

29
Q

How is blood pressure regulated long term?

A

Control of fluid volume

  • vasopressin
  • renin-angiotensin-aldosterone system
30
Q

What is systolic arterial pressure?

A

SAP = peak pressure in the arteries when the left ventricle is ejecting blood during systole

31
Q

What is diastolic arterial pressure?

A

DAP = residual pressure in the arteries when the left ventricle is filling during diastole

32
Q

What is pulse pressure?

A

Difference between SAP + DAP

33
Q

How long are diastole and systole?

A 
Diastole = 2/3 of the time of the cardiac cycle 
Systole = 1/3 of the time of the cardiac cycle
34
Q

What is mean arterial pressure (MAP)?

A

Mean of arterial pressure but its not halfway between the two because diastole lasts 2x as long as systole

35
Q

How are flow, driving force and resistance linked?

A

Flow = driving force/resistance

Cardiac output = arterial pressure/total peripheral resistance

36
Q

How do MAP and CO link?

A

MAP = (HRxSV) x TPR

37
Q

What does long term regulation of blood pressure involve?

A

Body fluid balance

38
Q

What does effective regulation of MAP require?

A 
Sensors (ability to monitor pressure)
Integrating system (assess correctness of pressure)
Effectors (mechanisms to return pressure to required level)
39
Q

Describe the structure of a baroreceptor

A

Non-encapsulated nerve endings in adventitial layer of arteries = aortic arch and carotid sinus
Central axons terminate in medulla oblongata
- serve as mechanoreceptors - increase firing in response to distension

40
Q

How does BP affect the firing rate of baroreceptors?

A

↑ BP = ↑ firing rate

↓ BP = ↓ firing rate

41
Q

Describe the baroreceptor reflex

A

Acute rise in BP = Increased baroreceptor discharge in the brainstem (medulla oblongata) which results in either:

  • increased vagal output, ↓ heart rate and blood pressure
  • decreased sympathetic output, ↓ contracitility, heart rate and arteriolar tone, and decrease blood pressure
42
Q

What does the renin-angiotensin-aldosterone axis provide?

A

Immediate, potent control of BP via angiotensin II

Slower onset, prolonged regulation of BP via volume control (aldosterone ± vasopressin)

43
Q

What other receptors contribute to cardiovascular homeostasis by eliciting reflexes?

A

Atrial receptors in walls of atria act as volume receptors

44
Q

What mechanisms are used to decrease blood volume?

A

Inhibit sympathetic vasoconstrictor pathways to kidneys leading to diuresis
Reflex inhibition of ADH/vasopressin from posterior pituitary
As a result:
- ↓ central venous pressure
- ↓ stroke volume
- ↓ cardiac output
- ↓ arterial pressure

45
Q

Describe the role of renin in haemorrhage

A
  1. Renin release from juxtaglomerular apparatus
  2. Production of angiotensin II
  3. Constricts renal vasculature and causes secretion of aldosterone from adrenal cortex
  4. Urine volume falls/retention of Na+ and water
    - resulting in an increase in blood volume

BVM1 - Cardiovascular system (4 decks)

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