Blood Pressure and Control Mechanisms Flashcards

1
Q

How is blood pressure generated and maintained?

A

*Ventricular Contraction
* Elastic rebound evens & maintains pressure

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2
Q

What are the factors affecting blood pressure?

A
  • Cardiac Output
  • Peripheral Vascular resistance
  • Volume
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3
Q

What are the important equations in regards to mean arterial pressure (MAP)?

A

*MAP = CO (Cardiac Output) x PVR (Peripheral Vascular Resistance)
*Cardiac Output = Stroke Volume x Heart Rate

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4
Q

What are the factors affecting cardiac output and their equations?

A

*Heart rate
*Stroke volume= end diastolic volume - end systolic volume
*Cardiac output (CO)= HR X SV

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5
Q

What are factors affecting heart rate?

A

*Autonomic innervation
*Hormones
*Fitness levels
*Age

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6
Q

What are factors affecting stroke volume?

A

*Heart size
*Fitness levels
*Sex
*Contractility
*Duration of contraction
*Preload (end diastolic volume)= amount of stretch during diastole when the ventricles fill with blood
*Afterload (resistance)= the pressure against which the heart must work to eject blood during systole

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7
Q

What are factors affecting contractility?

A

Starling’s Law of the Heart (The Frank-Starling Mechanism)

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8
Q

What does resistance depend on in a closed system?

A

*The length of the tube
*Radius of the tube
*Viscosity of the fluid

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9
Q

What is the effect of increased blood volume (hypervolemia)?

A
  • Increased BP
    *Increased preload = increased stroke volume= increased cardiac output= increased blood pressure
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9
Q

What is the effect of decreased blood volume (hypovolemia)?

A

*Decreased blood pressure
*Compensatory mechanisms
*Hypovolaemic shock

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10
Q

What are factors affecting blood volumes?

A

Oedema = accumulation fluid in interstitial space
Disruption in fluid exchange between blood and tissues
Factors disrupting balance
1. Increased hydrostatic pressure – eg heart failure – back pressure
2. Decreased plasma protein concentration – osmotic balance disrupted
3. Increase in interstitial proteins

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11
Q

What is vascular tone?

A
  • Refers to the degree of constriction experienced by ablood vessel relative to its maximally dilated state (max lumen= maxcapacity).
  • All arterial and venous vessels under basal conditions exhibit some degree of smooth muscle contraction that determines the diameter, and hence tone, of the vessel.
    *Vascular Tone: balance between contraction and dilatation in a vessel
    *Contraction and dilatation depends on:
    1) Composition of the vessels
    2) Control by Intrinsic and extrinsic factors
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12
Q

What effects smooth muscle contraction?

A
  • The mechanisms by which Extrinsic and Intrinsic mechanism influences either constrict or relax blood vessels involve a variety of signal transduction mechanisms that ultimately influence the interaction between actin and myosin in the smooth muscle promoting contraction/relaxation.
  • Calcium changes inside the muscle cells are coupled to contraction/relaxation of the cell.
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13
Q

What are the control mechanisms of the cardiovascular system?

A
  • Nervous/cytokine/autoregulatory
  • ANS/RAAS
  • NO, PGs etc..
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14
Q

How do baroreceptors regulate heart rate?

A

*Stretch-sensitive mechanoreceptors
*Found in Aortic arch and carotid sinus
Increased/Decreased Blood Pressure -> Increases/Decreases Stretch on Vessel Wall -> Increased/Decreased firing rate from Baroreceptor -> Medullary Cardiovascular Control Centre -> Altered Sympathetic / Parasympathetic Activity

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15
Q

What does the Sympathetic Nervous System do to the heart rate?

A
  • SNS increases (+) heart’s actions leading to:
  • Increased rate/chronotropy (tachycardia)
  • Increased force of contraction/inotropy
  • Increased relaxation during diastole (lusitropy)
  • Slight Increased impulse conduction (dromotropy)
  • Excitability is also increased
    *Postganglionic fibres from ganglion chain
  • Innervate atria, especially SA node, ventricles, including conduction system
16
Q

What does the Parasympathetic Nervous System do to the heart rate?

A
  • PNS decreases (-) heart’s actions leading to:
  • Decreased rate/chronotropy (bradycardia), dromotropy
  • Slight decreased inotropy, lusitropy
  • Vagus nerves (Xth)
  • Right to SA, Left to AV, but left/right innervation sometimes overlaps
  • Some atrial muscle, less so ventricles (hence why less control of inotropy/ lusitropy)
17
Q

What receptors are used in which nervous system?

A

*Sympathetic
Noradrenaline – adrenoreceptors
Alpha and Beta
*Parasympathetic
Acetylcholine - muscarinic receptors
*Ganglia (both)
Acetylcholine – Nicotinic receptors

18
Q

What effect does adrenaline have on adrenergic receptors?

A
  • α1 stimulated by noradrenaline –vasoconstriction
  • Neurotransmitter effect
  • Low [adren]: β2-selective -> mostly vasodilatation
  • High [adren]: also stimulates α1, andβ1 receptors, producing
  • vasoconstriction (mediated byα1 receptors)
  • increased heart rate & contractility
19
Q

What is the stimulus for renin release?

A

1 Decrease in sodium chloride concentration
2 Decreased rate of blood flow through the macula densa of kidneys
3 Baroreceptor detected decrease in blood pressure

20
Q

What is renin’s mode of action?

A

Converts angiotensinogen (synthesised in liver) into angiotensin I (ATI)

21
Q

What are the forms of Androtensin Converting Enzyme?

A

*ACE and ACE2
*Expressed predominantly in lung
*Converts ATI into Angiotensin II (ATII)
*Inhibited by ACE inhibitors (ACEI) e.g. captopril

22
Q

What is the actions of angiotensin II?

A
  1. Vasoconstrictor
  2. ADH (vasopressin) release
  3. Increased Sympathetic nervous system activity
  4. Increased sodium/water reabsorption
  5. Aldosterone Release
23
Q

What do ATI receptors do?

A

Vasoconstriction which increases the blood pressure

24
Q

What are the actions of ATII?

A

*Stimulates ADH (Vasopressin) release
*Stimulates AT1 receptors in hypothalamus -> Release of ADH -> Increased water reabsorption
*Increased SNS activity
*Aldosterone release

25
Q

What is aldosterone?

A

*Mineralocorticoid
*Steroid hormone released form adrenal gland
*From adrenal cortex (zona glomerulosa)

26
Q

How does hormonal/ paracrine regulation work?

A

*Release of a number of mediators e.g nitric oxide, endothelin , prostaglandins etc.
*Vascular endothelium

27
Q

What is the action of Nitric Oxide?

A
  • Vasodilation
  • Controls platelet aggregation, immunomodulatory
28
Q

What stimulates the production of Nitric Oxide?

A
  • Acetylcholine –
  • Histamine, bradykinin, serotonin
  • Shear stress on blood vessels
  • Synthesised from arginine by nitric oxide synthase (NOS)
29
Q

What is the action of Endothelin?

A

*Vasoconstriction
*Positive inotropic/chronotropic effects
*Opposite effect to NO

30
Q

What are the 3 isoforms of Endothelin and their receptors?

A

*Three isoforms - ET-1, ET-2, ET-3
*ET-1 main for cardiovascular effects(produced by endothelium and also VSMC (vascular smooth muscle cells) in inflammation)
*ETa and ETb

31
Q

What does ECE stand for?

A

Endothelin converting enzyme

32
Q

What is the action of Prostaglandin I2 (PGI2; prostacyclin) and what is it synthesised from?

A

*Vasodilator
*Inhibits platelet aggregation
*Anti-inflammatory effects
*PGI2 = synthesised from arachidonic acid

33
Q
A