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cardiovascular 6-8 Flashcards

1
Q

Why is arterial blood pressure important?

A
  • to provide a driving force
  • to ensure effective tissue perfusion
  • to keep vessels open
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2
Q

For which tissues is blood pressure critical and how?

Hint - the obvious and then the blood-cleaner

A
  • brain (if MAP < 60 mmHg, you become unconscious)

- kidneys

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3
Q

What value does blood pressure progressively reach once it reaches the RA?

A
  • falls to 0 mmHg
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4
Q

What is the formula for cardiac output?

A

cardiac output (L min-1) = heart rate x stroke volume

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5
Q

What does the distribution of cardiac output into the circulatory system depend on?

A

the pressure difference and resistance to blood flow in vessels

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6
Q

What is blood pressure?

A

the pressure blood exerts against a wall of the vessel/chamber

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7
Q

How is BP expressed?

A

systolic/diastolic i.e. 120/80

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8
Q

Where does blood flow from?

Hint - same direction as gases and water

A

high to low pressure

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9
Q

What is the formula for blood flow?

A

flow ∝ pressure difference/resistance

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10
Q

If there is a greater pressure difference what does it mean for blood flow?

A

greater blood flow

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11
Q

Describe blood pressure in terms of how constant it is.

A
  • is pulsatile (varies)

- and rises and falls with each heartbeat

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12
Q

Which 3 factors does vascular resistance (R) depend on?

Hint - BLB

A
  • lumen size – smaller diameter means greater resistance to flow
  • blood viscosity – thicker blood (i.e. by polycythaemia) can increase MBP
  • blood vessel length – longer vessels require higher resistance
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13
Q

What does systemic vascular resistance (SVR) oppose and what does it depend on?

A
  • opposes blood flow

- depends on smaller arterioles

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14
Q

What is the formula for mean blood pressure?

Hint - MCP

A

Mean Blood Pressure = Cardiac Output x Peripheral Resistance

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15
Q

With blood pressure:

a) what happens to CO if MBP decreases?
b) what happens to PR if MBP increases?
c) what must CO and PR do?

A

a) decrease in MBP means CO must decrease
b) increase in MBP means PR must increase
c) CO and PR must balance

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16
Q

What is venous return?

Hint - Venous return chamber

A

pressure generated by LV so blood can flow back to heart

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17
Q

What is the cardiac centre and what does it monitor?

A
  • cardio-acceleratory centre → increases HR via sympathetic innervation of SAN/AVN
  • cardio-inhibitory centre which slows heart
  • both monitor changes in BP, PO₂ and pH via baroreceptors and chemoreceptors
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18
Q

Where is the cardiac centre located and what is its input?

A
  • location → medulla oblongata

- input → nerve impulses from sensory receptors + higher brain centres

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19
Q

What is the vasomotor centre?

A
  • large group of cells → vasoconstriction

- small group of cells → vasodilation

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20
Q

Where is the vasomotor centre located and what is its input?

A
  • location → (also) medulla oblongata

- input → increased frequency of nerve impulses

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21
Q

Where are baroreceptors located?

Hint - all heart WAC

A

in carotid sinus, aortic sinus and wall of right atrium

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22
Q

Where are aortic baroreceptors located and what do they monitor?

(Hint - both parts to do with main aortic vessel)

A
  • ascending aorta

- monitor stretch within aorta (associated with adequate blood supply to systemic system)

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23
Q

What do carotid baroreceptors monitor and what is this associated with?

(Hint - carotid + it takes minutes)

A
  • blood pressure in carotid arteries

- associated with adequate blood supply to brain

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24
Q

Which receptors detect increased blood pressure and what does this initiate?

(Hint - all about feedback to slow HR + BP)

A
  • baroreceptors
  • initiate regulatory feedback signals to CV centre promoting:
    • inhibition of cardio acceleratory centre and stimulation of cardio inhibitory system
    • inhibition of vasomotor cells associated w/ vasoconstriction
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25
Q

What effect does parasympathetic stimulus have on blood pressure on a molecular level?

(Hint - NT and the effect it has at end of ECG)

A
  • releases Ach

- extends repolarization

26
Q

What effect does sympathetic stimulus have on blood pressure on a molecular level?

(Hint - a different NT and effect on ECG)

A
  • releases NA

- shortens repolarization

27
Q

Explain the Renin-Angiotensin-Aldosterone System including the effects of outside hormones.

A
  • low BP → renin secreted by kidneys
  • angiotensinogen (renin) → angiotensin I (ACE, or angiotensin-converting enzyme) → angiotensin II
  • angiotensin II:
    • vasoconstriction arterioles – increase peripheral resistance
    • increases aldosterone secretion - blood volume increases by renal reabsorption of Na⁺ + H₂O
  • hormones like E and NA increase HR by affecting SAN
  • epinephrine also affects contraction of cells

(see notes for diagram)

28
Q

How can blood flow be modified?

Hint - mechanisms of what by which parts of the vessel?

A

mechanisms of localised vasoconstriction + vasodilation of precapillary sphincter muscles

29
Q

Name some vasodilators.

Hint - three Os, breastfeeding hormone, what is taken for allergies

A

O₂, CO₂, NO, histamine, lactate

30
Q

Name some vasoconstrictors.

Hint - ETs both released by similar-sounding cells

A
  • thromboxains → released by platelets in a wound

- endothelins → released by damaged endothelial cells

31
Q

Name the 2 regions of the CV centre (functions already discussed).

A
  • cardiac centre (cardio acceleratory + cardioinhibitory centres which monitor changes in BP, PO₂, pH → baroreceptors + chemoreceptors)
  • vasomotor centre (large + small group of cells associated with vasoconstriction and vasodilation respectively)
32
Q

What is vasoconstriction achieved by and mediated with?

Hint - which CNS division + which receptors in which cell?

A
  • sympathetic system

- α-1 adrenoreceptors located in smooth muscle membranes

33
Q

What is vasodilation mediated via?

Hint - increasing dissertation vasodilator within the main type of muscle of body

A

via increasing NO within SM

34
Q

State the baroreceptor reflex.

Hint - about decreasing BP

A
  • increased BP is detected by baroreceptors which initiate regulatory feedback signals to CV centre promoting:
    • inhibition of cardioacceleratory centre and stimulation of cardioinhibitory system
    • inhibition of vasomotor cells associated with vasoconstriction
35
Q

Where are chemoreceptors which mediate reflexes located?

Hint - 2 types of bodies and then an oblong shape

A
  • carotid bodies
  • aortic bodies
  • medulla oblongata
36
Q

What are chemoreceptor reflexes sensitive to?

A

changes in blood O₂, CO₂ and pH

37
Q

How are vasodilation and vasoconstriction induced by chemoreceptor reflexes?

(Hint - 3 main increases/decreases)

A
  • vasoconstriction by:
    • low blood O₂ (vasodilation by high O₂)
    • low pH
    • high CO₂
38
Q

Which hormones are involved in hormonal (endocrine) control mechanism?

(Hint - AAAVE - last is a kidney hormone)

A
  • adrenaline
  • angiotensin
  • atrial natriuretic hormone (ANP)
  • vasopressin (ADH)
  • erythropoietin
39
Q

What effect does adrenaline have on the CV system?

A
  • activates cardio acceleratory centre

- increasing sympathetic stimulation of heart via NA

40
Q

What effects does the angiotensin-aldosterone system have on the CV system?

A

• decreased BP induces juxtaglomerular apparatus to secrete renin
• whole process of (renin + ACE) converting angiotensinogen to angiotensin I
• angiotensin II:
- vasoconstriction
- stimulates aldosterone secretion
- kindles thirst
- increases salt appetite + ADH secretion

41
Q

What is the reason for vasopressin (ADH) secretion and what effects does it have on the CV system?

(Hint - causes a move on blood vessels + urine volume modification)

A
  • caused by decreased BP

- causes vasoconstriction + decreased urine production

42
Q

Where is atrial natriuretic hormone released from and what effect does have on the CV system?

(Hint - clue-is-in-the-name cells + opposite effect of ADH)

A
  • released from atrial cells in response to increased atrial BP
  • causes increased urine production
43
Q

What is the fluid shift (hormonal) mechanism and what does this result in?

(Hint - movement of fluid between cells + opposite effect on BP)

A
  • BP increases fluid from blood vessels into interstitial space
  • results in decreased BP
44
Q

What is the stress relaxation response and what does this result in?

A
  • as BP decreases in vessels, reduction in force applied to vessel endothelium
  • SM cells → respond by slowly contracting
45
Q

How many long-term and short-term parts are three in the cardiovascular response to wounds/haemorrhaging?

(Hint - long response for the road)

A
  • two short-term responses

- one long-term response

46
Q

What are the short-term cardiovascular responses to wounds/haemorrhaging?

(Hint - BP sinuses and widening vessels, additional fight-or-flight)

A
  • decreased BP detected by baroreceptors in aortic + carotid sinuses → promotes vasoconstriction
  • stress-related responses further stimulate SNS
47
Q

What is the long-term cardiovascular response to wounds/haemorrhaging?

(Hint - more urine hormone, kidney/acne hormone, raas)

A

increasing:

  • activation of renin angiotensin system
  • ADH system
  • secretion of erythropoietin
48
Q

What can circulatory shock arise because of?

Hint - DDEE → blood escape, cardiac harm, cardiac force, too much vessel widening

A
  • drop in BP due to a major haemorrhage
  • damage to heart
  • external pressure on heart
  • extensive peripheral vasodilation
49
Q

State the symptoms of circulatory shock.

Hint - CIPHAC

A
  • confusion/disorientation
  • increased HR and weak pulse
  • pale cool skin
  • hypotension
  • acidosis
  • cessation of urination
50
Q

What can failure to stimulate sympathetic innervation to a patient in circulatory shock cause?

A
  • BP to decrease further → irreversible shock
51
Q

What is oxygen consumption (VO2)?

A

rate at which oxygen is delivered to tissues + extracted from blood by tissues

52
Q

What happens to oxygen consumption (VO2) during exercise?

A

increases to a maximal oxygen consumption

53
Q

Which changes in cardiac output occur during exercise?

Hint - anticipatory, abdomen + veins, VEDV

A
  • anticipatory increase in CO by SNS
  • decreased blood flow to abdominal arteries temporarily increasing venous return → increased ventricular EDV (RV contracts more forcefully during systole)
54
Q

How is respiration controlled and how can it be influenced?

Hint - meddys, what they do, how this can be influenced

A
  • controlled by medullary neurones which set basic rhythm of respiration
  • influenced by inputs from other parts of brain + peripheral sensory receptors
55
Q

Where is the respiratory centre located and which 2 regions does it consist of?

A
  • located in medulla oblongata with two regions:
    1. inspiratory centre
    2. expiratory centre
56
Q

Describe the inspiratory centre.

A
  • two dorsally-situated regions of medulla
  • neurones within centres show spontaneous rhythmicity and cyclic activity
  • action potentials derived from cells → along intercostal + phrenic nerves → supply inspiratory muscles
57
Q

Describe the expiratory centre.

A
  • two ventrally-situated groups of neurones

- mostly inactive but during heavy breathing they send action potentials to expiratory muscles

58
Q

Apart from the inspiratory and expiratory centre, which other 2 brain centres are associated w/ respiratory control and what are their effects?

A
  1. apneustic centre: scattered neurones in the pons send action potentials to inspiratory centre
  2. pneumotaxic centre: neurone within superior pons inhibitory effect on inspiratory and apneustic centre
59
Q

Which steady-state effects does exercise have on the CV system?

(Hint - resp increase + RR)

A
  • respiration starts to increase linearly with O₂ uptake

- respiratory rate is measured as ventilatory equivalent for oxygen (VE/VO₂)

60
Q

Which non-steady-state effects does exercise have on the CV system?

(Hint - disproportionate O₂, disproportionate VR, lactate + sodium bicarb)

A
  • RR increases disproportionately to oxygen uptake
  • disproportionate increase in ventilation rate at ventilatory threshold
  • accumulation of blood lactate + increased lactic acid buffered with sodium bicarbonate
  • lactic acid + NaHCO₃ → Na-lactate + H₂CO₃
61
Q

State 4 cardiovascular adaptive changes endurance training can result in.

A

changes in:

  • oxygen consumption
  • HR and SV
  • arteriovenous differences
  • BP and blood flow

CRR (11 decks)

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