L18 - Physiology of blood pressure Flashcards

1
Q

Why are there valves present in the veins?

A

Prevention of back flow of blood

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2
Q

Why are the smooth muscle wall of arteries much thicker than that of veins?

A

Arteries carry blood from the heart to the rest of the body through the aorta at a very high pressure, therefore, the thicker walls withholds the high pressure and prevents the vessels to break.

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3
Q

What is the blood pressure dependent on?

A
  • Cardiac output (ml/min)
    (CO = Heart rate x Stroke volume)
  • autonomic control via baroreceptors (specifically control of rate + force)
  • Peripheral vascular resistance (PVR) (mmHg)
  • PVR dependent on diameter of arterioles
    • if arteriole dilated => low resistance to flow =>low PVR => low BP
  • PVR also dependent on blood volume
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4
Q

What is Systolic pressure (SP)

A

Maximum arterial pressure reached during peak ventricular ejection

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5
Q

What is Diastolic pressure (DP)?

A

Minimum arterial pressure just before ventricular ejection begins

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6
Q

What is Pulse pressure (PP)?

A

The difference between SP and DP

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7
Q

What is Mean arterial pressure (MAP)?

A

An average calculated blood pressure in an individual during a single cardiac cycle.

Although methods of estimating MAP vary, a common calculation is to take one-third of the pulse pressure, and add that amount to the diastolic pressure. A normal MAP is about 90 mmHg.

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8
Q

How is the blood flow like in the veins?

A
  • Little resistance to flow
  • At rest, ~60% of total blood volume is in veins
  • Valves direct blood towards the heart - prevents back flow away from heart
  • Aided by skeletal muscle pump
  • when calf muscles contract during exercise, blood is forced toward the heart, thus increasing venous return.
  • Respiratory pump aid venous return
  • when muscles contract and relax during the inspiration and expiration process, pressure changes occur in the thoracic and abdominal cavities. These pressure changes compress the nearby veins and assist blood return to the heart.
  • Sympathetic innervation - noradrenaline constricts veins, hence increases venous return to heart
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9
Q

Control of smooth muscle activity in blood vessels

A
  • Present in the tunica media layer of the blood vessels
  • Diameter of lumen changes due to contraction + relaxation of the smooth muscle layer – changes blood flow accordingly
  • Contraction + relaxation - controlled by nerve supply and endogenous chemicals released from endothelium.
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10
Q

What is the structure and role of the endothelium layer of blood vessels?

A
  • Single layer of endothelial cells lining the lumen of the vessels
  • Function: physical barrier to blood cells (e.g. inflammatory cells)
  • Without barrier - blood cells would be activated and start clotting (forming thrombus)
  • Physical barrier maintained by release of bioactive substances (factors)
    Because: *inhibition of platelet activation
    * cause relaxation/contraction of underlying smooth muscle
  • Endothelium derived relaxation factors:
  • Nitric oxide (NO)
  • Prostacyclin (PGI2)
  • Hyperpolarising factor
  • Endothelium derived contraction factors:
  • Endothelin (ET-1)
  • Thromboxane A2 (TxA2)

=> Factors released by endothelial cells into the smooth muscle cells to either contract or relax

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11
Q

Neuronal regulation of vascular smooth muscle activity

A
  • Primarily innervated by sympathetic nervous system
  • Act on adrenoceptors => alpha1, alpha2, beta2
  • Main agonist => noradrenaline (NA)
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12
Q

Activation of which adrenoceptor exerts vasoconstriction event?

A
  • Alpha1 receptor (binding of noradrenaline)
  • Alpha2 receptor also
  • Antagonist at alpha1 receptors cause vasodilation
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13
Q

Activation of which adrenoceptor exerts vasodilation event?

A
  • Beta2 receptor
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14
Q

What is the Baroreceptor reflex?

A
  • A short term reflex triggers in response to increase or decrease in BP
  • Homeostasis response to keep BP steady at all times
  • Baroreceptor => type of mechanoreceptors (pressure-sensitive) on arterial side of circulation – detect amount of stretch in blood vessel.
  • Relays information of change in BP to brain CV control centres via ANS
  • Exhibit adaptation - will acquire new “set point” in presence of persistently high arterial BP
  • Malfunction leads to medicinal intervention
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15
Q

Diseases concerning and drugs for control of BP

A
  • Hypertension (high blood BP) - main cause is result of increased PVR
  • Vasoactive drugs to control BP:
  • Diuretics - e.g. bendrofluazide => decreases circulating blood volume + total PVR
  • Alpha blockers - e.g. prazosin (alpha1 blocker) => prevent noradrenaline-induced decrease in vasoconstriction, which causes decrease in PVR
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16
Q

What non-drug advice can you give to patients with high BP?

A

Health promotion to patients:

  • weight loss + reduced salt intake
  • exercise
  • reduced alcohol consumption
  • smoking cessation
17
Q

Limiting factors of vasoactive drugs

A
  • Race
  • Age
  • Diabetes
  • Renal disease
  • Pregnancy
  • Oral contraceptives
18
Q

What the medication classes for the control of BP? (to reduce BP)

A
  • ACE inhibitors – ends with “pril”
  • E.g. enalapril, ramipril
  • Side effects - angioedema, increase in K+ level, hypotension
  • Beta Blockers – ends with “lol” or “olol”
  • E.g. atenolol, propanolol
  • Side effects - bradycardia, dizziness, hypoglycemia
  • Ca Channel Blockers - ends with “pine”, “amil” or “zem”
  • E.g. amlodipine
  • Diuretics
  • E.g. furosemide, bendrofluazide
  • Side effect - electrolyte imbalance