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SMP - Cardiopulmonary Exam 1 > Lecture 12 - Regulation of Cardiac Output > Flashcards

Lecture 12 - Regulation of Cardiac Output Flashcards

1
Q

Describe the speed and duration of the ANS effects on HR.

A
  1. Sympathetic: slow and last longer because the NTs must go through a slow reuptake mechanism
  2. Parasympathetic: fast onset and short because of the abundance of cholinesterase in synapses that can remove ACh quickly
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2
Q

Other name for sympathetic effects on the heart?

A

Beta-adrenergic effects

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3
Q

What compounds block beta-adrenergic effects on the heart? Resulting effect?

A

Beta-blockers = slight HR reduction because at rest the sympathetic effect on the heart is minimal

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4
Q

What compound blocks parasympathetic activation of the heart? Resulting affect?

A

Atropine = large increase in HR because at rest the parasympathetic effect on the heart is significant

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5
Q

Through what mechanism is ANS regulation of the CV system established? Example?

A

Reciprocal changes in sympathetic and parasympathetic NS activity

E.g. during exercise, you are increasing sympathetic activity and decreasing parasympathetic activity

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6
Q

Describe the regulation of BP via arterial baroreceptor reflex. Purpose?

A

Baroreceptors in the aortic arch and carotid sinus which monitor BP by detecting stretch and then trigger ANS activity adjustment

Purpose: keep arterial pressure constant to provide adequate perfusion to tissues

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7
Q

Describe the steps of the mechanisms of the regulation of BP via arterial baroreceptor reflex.

A
  1. Increase in BP
  2. Baroreceptors in aortic arch/carotid sinus are stretched
  3. Afferent sensory signals sent to medullary cardiovascular center
  4. Reciprocal adjustment of ANS by the medulla to decrease HR = increase in parasympathetic activity and decrease in sympathetic activity
    5a. Increased para => decreased HR
    5b. Decreased sympa => decreased venomotor tone => increased venous volume => decreased EDV + decreased contractility => decreased SV + decreased HR => decreased CO + decreased TPR
  5. Decreased arterial pressure
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8
Q

More NE or EPI released by sympathetic NS onto the heart?

A

NE

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9
Q

How does standing up affect BP?

A

Decrease in BP

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10
Q

What is the carotid sinus?

A

Dilated area at the base of the internal carotid artery just superior to the bifurcation of the internal carotid and external carotid

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11
Q

What is venomotor tone?

A

The degree of tension in the muscle coat of a vein that determines the shape of the vein

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12
Q

What is the bainbridge reflex?

A

Sudden IV infusion => increased RA pressure => stimulation of RA low pressure baroreceptors aka cardiopulmonary baroreceptors => bainbridge CNS reflex to increase HR to redistribute BV

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13
Q

What does the response to a physiological challenge depend on? E.g.?

A

Initial physiological state

  1. IV to patient who has a slow heart rate because normal BV (has NOT suffered a hemorrhage) => bainbridge reflex to increase arterial pressure until the baroreceptor reflex kicks in
  2. IV to patient who has a fast heart rate because dcreased BV (e.g. has suffered a hemorrhage) => instead baroreceptor reflex to decrease arterial pressure
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14
Q

Other name for baroreceptors?

A

Stretch receptors

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15
Q

Describe the regulation of the HR via peripheral chemoreceptors.

A

Chemoreceptors in aortic arch and carotid sinus that detect the quality of the arterial blood: PO2, PCO2, pH levels

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16
Q

Other name for peripheral chemoreceptors in aortic arch and carotid sinus?

A

Aortic and carotid bodies

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17
Q

How do PCO2, PO2, and pH levels vary in aortic and carotid bodies in a healthy normal individual? What does this mean for the peripheral chemoreceptor regulation of the heart?

A

They do not! Changes indicate a problem

Peripheral chemoreceptor regulation of the heart is an emergency system

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18
Q

Describe the mechanisms of the regulation of HR via arterial aka peripheral chemoreceptor reflex.

A

High PCO2/Low CO2/Low pH:

  1. Primary effect: chemoreceptors send signals to the medullary CV center to decrease HR to redirect blood flow to the brain (survival mode)
  2. Secondary effect: due to chemoreceptors sending a signal to the lungs and causing hypocapnia and increased lung stretch => inhibition of the medullary CV center to stop it from decreasing HR and make it go back to normal (bradycardia is transient if respiration is successfully increased)
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19
Q

Other name for medullary cardiovascular center?

A

Medullary vagal center

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20
Q

What is hypocapnia?

A

State of reduced carbon dioxide in the blood resulting from deep or rapid breathing, aka hyperventilation

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21
Q

Normal PO2?

A

95-100 mmHg

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22
Q

Normal PCO2?

A

40 mmHg

23
Q

Normal pH?

A

7.4

24
Q

How does respiration affect HR? What is this called in children?

A
  • During inspiration, there is negative thoracic pressure (decrease in pressure) and positive abdominal pressure to bring in the air => increase in venous blood return => increase in RA pressure and stretch => bainbridge reflex => increase in HR
  • During expiration, lung stretch receptors and arterial baroreceptors play a role in lowering the HR back

In children, this is called respiratory sinus arrhythmia = normal HR variation with respiration

25
Q

How can hormones affect HR?

A

EPI and TH raise HR

26
Q

How can temperature affect HR?

A

High temperatures cause a direct increase in SA nodal HR

27
Q

What are the limitations of HR increasing the CO?

A

If you electrically stimulate the heart of a patient and keep everything else constant:

CO will increase with HR pretty proportionally to a certain point = past diastasis (around 100 bpm) and into rapid passive filling

Past this point, CO will decrease because the ventricles do not have as much time to fill

28
Q

How did Frank-Starling figure out the Frank-Starling mechanism?

A

Experiments on dog hearts to investigate the effects of preload on SV by varying it using a venous reservoir to decrease/increase venous pressure and ventricular filling

29
Q

What is preload? What are 2 measures of it?

A

The degree of filling of the ventricle before contraction:

  1. EDV in an intact CV system
  2. Initial sarcomere length
30
Q

Describe the Frank-Starling mechanism.

A

Higher preload => higher filling => more optimal sarcomere length for subsequent contraction => greater SV and greater force of contraction (NOT a change in contractility)

31
Q

What does a change in heart contractility refer to?

A

Refers to inotropic effects on the heart which increase its inherent strength

32
Q

What is the difference between force of contraction and contractility?

A
  • Force of contraction = power exerted by the heart during contraction
  • Contractility = intrinsic ability of the myocardium to contract and create force (its “strength”) INDEPENDENT OF PRELOAD AND AFTERLOAD
33
Q

What is force of contraction dependent on?

A
  1. Preload
  2. Afterload
  3. Underlying contractility
34
Q

What is afterload? What is it loosely synonymous with?

A

Pressure against which the heart contracts (the force that the ventricle must pumo against) = arterial or ventricular pressure during contraction

Synonymous to force of contraction

35
Q

In what activity does the Frank-Starling mechanism play an important role?

A

During exercise to increase CO

36
Q

What is the driving gradient/force for blood flow in the CV system? How is this gradient increased?

A

The difference between end diastolic pressure and systolic pressure:

  • Increased EDV causes small increase in EDP
  • Increased EDV causes a MARKEDLY higher systolic pressure

=> therefore as EDV increases, the gap between these 2 gets bigger and bigger

37
Q

What is the Treppe effect? In what conditions is this true?

A

Increase HR => decreased time between myocyte contraction => decreased calcium sequestration intracellularly => increase in free calcium levels in the cardiac myocytes => increased contractility => increased force of contraction building up over several beats (staircase)

WITH PRELOAD AND AFTERLOAD HELD CONSTANT

38
Q

What is another name for the Treppe effect?

A

Staircase phenomenon

39
Q

What factors increase heart contractility?

A
  1. NE
  2. Dopamine
  3. Aerobic exercise aka conditioning
  4. Digitalis
40
Q

What factors decrease heart contractility?

A
  1. Infarction
  2. Ischemia
  3. Heart failure
41
Q

What is stroke work?

A

SV x systolic pressure

42
Q

To what receptors do NE and EPI secretion by the sympathetic NS bind to on the heart?

A

Beta 1 adrenergic receptors

43
Q

Does the parasympathetic NS affect contractility?

A

Barely because the ventricular myocardium lacks PNS innervation

44
Q

What does the slope of the Frank-Starling mechanism (of end diastolic pressure vs stroke volume) represent?

A

It’s a measure of contractility

45
Q

Where is the PNS innervation in the heart?

A

Pacemakers and atria

46
Q

How will myocardial infarction affect the sympathetic innervation of the heart?

A

MI => contractility is reduced => inadequate cardiac output => SNS activity increased

47
Q

What is mean circulatory pressure affected by?

A
  1. BV

2. Venous tone

48
Q

Through what 2 mechanisms is the heart’s contractility increased by conditioning?

A
  1. Hypertrophy

2. Increased intracellular Ca++ baseline

49
Q

What are all of the effects of a fall in systemic TPR IF CO is maintained constant?

A

Lower systemic arterial pressure => HIGHER CENTRAL VENOUS PRESSURE => higher venous return => increased preload on the RV (higher RVEDP) to maintain CO constant

50
Q

Why does exercise keep MAP constant but increases pulse pressure?

A

Increase in systolic due to sympathetic effects but decrease in TPR causes a decrease in diastolic: overall MAP is the same, but pulse pressure is higher

51
Q

How does increasing the heart rate affect the time spent in systole and diastole?

A

Both decrease, but time in diastole decreases more

52
Q

How will a person with aortic stenosis react to exercise?

A

Syncope because TPR decreases but no way of increasing CO enough to compensate so huge drop in pressure

53
Q

Role of stellate ganglion?

A

Site of SNS stimulation of the heart

54
Q

Is contractility dependent on preload and afterload?

A

NOPE

SMP - Cardiopulmonary Exam 1 (28 decks)

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