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Cardio > Cardio L7 Tissue blood flow > Flashcards

Cardio L7 Tissue blood flow Flashcards

1
Q

• The Key role of the vascular system is to

A

distribute the cardiac output according to the metabolic needs of the tissues.

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2
Q

• The distribution of blood flow is

A

is not fixed, for example at rest skeletal muscle receives about 20% of the cardiac output. During heavy exercise this may increase to 80%.

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3
Q

Arterioles: function

A
  1. Regulate local blood flow according to local metabolic need.
  2. Large amount of Smooth muscle
  3. Exhibit:
    a. Vasoconstriction
    b. Vasodilation
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4
Q

Vascular Smooth Muscle (VSM briefly allow

A

constriction dilation

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5
Q

VSM cell shape

A
  1. Spindle shaped cells
  2. Approx 50 nanometers x 4um
  3. Thick (myosin) and thin (actin) filaments.
  4. Actin → inserts into dense bands (inner membrane and dense bodies (cytoplasm)
  5. Function syncytium: cells are linked by gap junctions
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6
Q

VSM Contraction: process

A
  1. Calcium (from SR or calcium channels) forms a complex with calmodulin
  2. Ca-calmodulin regulates an enzyme called myosin light chain kinase (MLKC)
  3. MLCK regulates action myosin interaction by phosphorylating the light chain of the myosin head.
  4. Latch state of prolonged crossbridge formation (energy efficient tone).
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7
Q

VSM contraction stimuli:

A

VSM contraction stimuli:

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8
Q

VasoConstriction controlled by 3 and process

A

Noradrenaline (alpha 1 receptor)
Angiotensin (ATII receptors action)
Endothelin (act via ETA receptors)
Act via phosphplipase C (PLC) to produce vasoconstriction

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9
Q

Vasodilation controlled by

A

Adrenaline (Beta2) acts via a cAMP dependent pathway to inhibits MLCK and cause vasodilation

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10
Q

Beta 2 receptors

A

Found on skeletal muscle e.g. during exercise increase vasodilation to increase blood flow

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11
Q

Vasodilation controlled by

A

Endothelium derived relaxing factor (EDRF) and atrial natriuretic peptide (ANP) act via cGMP to produce vasodilation.

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12
Q

ANP acts via

A

Acts via cGMP = vasodilation

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13
Q

Alpha 1 receptor is for

A

Vasoconstriction

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14
Q

NO

A

Acts via cGMP causing relaxation

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15
Q

Control of Blood Vessels:

A

local and global control

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16
Q

local control

A

a. Mechanical
b. Metabolites
c. Autocoids

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17
Q

Global control

A

SNS

Hormones

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18
Q

Mechanical

A

A high external pressure may impede blood flow
E.g.
→ Left coronary flow pattern.
→ Pressure sores

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19
Q

Mechanical Process of action in arterioles

A

Raising the internal pressure in arterioles would initially distend them before they reacting by contracting i.e. myogenic response.

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20
Q

Metabolites: action

A

Many products of metabolism cause vasodilation and allow local blood flow to be matched to local metabolite rate

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21
Q

Metabolites: examples

A 
Carbon dioxide
Lactate
Adenosine
Potassium ions
Hypoxia
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22
Q

Metabolites: clinical

A

COPD → increase of Co2 pathologically

  1. Bounding pulse
  2. Headaches
23
Q

Active hyperaemia

A

Skeletal muscle during exercise. Metabolites increases and so vasodilation occurs and more blood flow.

24
Q

Reactive hyperaemia

A

After a period of ischemia. E.g cuff

Build up of metabolites that has occurined during ischemia

25
Q

Autocoids (local hormone) Function

A

These are vasoactive chemicals that are produce locally, released locally and act locally

26
Q

Autocoids (local hormone) Examples

A

Histamine
Serotonin (5-HT)
Bradykinin
Prostaglandins

27
Q

Thromboxane

A

Predominantly produce by platelets → platelet aggregation and vasoconstriction

28
Q

Prostacyclin

A

Produce by endothelium. Inhibits platelet aggregation and causes vasodilation

29
Q

Aspirin

A

Inhibit production of thromboxane. Acute treatment of MI

30
Q

Auto-regulation: function

A

Over a range of perfusion pressures blood flow remains remarkably constant.
2. Brain, kidney, myocardium, intestine → flow doesn’t obey straight line increase pressure increase flow

31
Q

auto-regulation 3. Underlying mechanisms

A

that changes resistance with change in pressure: Probably involves myogenic response and effects of local metabolites.

32
Q

Endothelial Derived Relaxing factor (EDRF):

A
  1. Shear stress, Ach and substance P will cause relaxation of arterial vessels.
    a. Achieved via: Stimulates endothelial production of EDRF (nitric Oxide)
    b. EDRF stimulates guanylate cyclase in VSM and produces relaxation.
33
Q

Patho: of EDRF

A

Septic shock → production of NO is abnormally elevated = abnormal dilation and therefore TPR falls and a fall in blood pressure.

34
Q

NO vasodilators

A

GTN (increased production of NO and so vasodilation).

35
Q

Sympathetic Nervous system:

A
  1. Tonic activity (noradrenaline release) contributes to the maintenance of vessel tone
36
Q
  1. A fall in sympathetic tone =
A

dilation

37
Q
  1. A rise in sympathetic tone =
A

arteriolar vasoconstriction (raises TPR and afterload) and venoconstriction (raises CVP and preload)→ therefore stroke volume.

38
Q

Hormones:

A
  1. Renin angiotensin aldosterone system
  2. Vasopressin (Anti-diuretic hormone
  3. Adrenaline
  4. ANP
39
Q

Renin-Angiotensin-Aldosterone Important in

A

Control of ECF and blood volume

40
Q

Renin-Angiotensin-Aldosterone Function

A

Decreased afferent arteriolar pressure

Increased renal sympathetic tone

41
Q

Renin-Angiotensin-Aldosterone Important in

A

Response to haemorrhage

42
Q

Renin-Angiotensin-Aldosterone Secreted by

A

The juxtaglomerular cells (afferent arterioles) in response to: decreased solute NaCL load at the macula densa.

43
Q

Renin-Angiotensin-Aldosterone Process

A

ACE converts Angiotensin 1 to angiotensin 2

44
Q

Angiotensin 2

A

Constricts vascular smooth muscle and so increases resistance and increased afterload.
Increased water and sodium retention via aldosterone stimulation → Increased preload.

45
Q

Vasopressin (ADH) Produced by

A

the magnocellular neurones of the supraoptic and paraventricular nuclei of the hypothalamus

46
Q

Vasopressin (ADH) Released from

A

The posterior lobe of the pituitary

47
Q

Vasopressin (ADH) Stiimulated by

A

Increased osmoarity or fall in BP

48
Q

Vasopressin (ADH) Outcome

A

Vasoconstriction (except cerebral and coronary vessles)

Renal water retention

49
Q

Adrenaline vs Noradrenaline Both function

A

Increases cardiac contractility and hert rate via the Beta 1 adrenoceptor → positive chronotrophs

50
Q

Adrenaline vs Noradrenaline Both Cause

A

Arteriolar vasoconstriction via the alpha 1 adrenoceptor

51
Q

Adrenaline alone

A

Has a high affinity for Beta 2 receptors and produces vasodilation in skeletal muscle, myocardial and liver vessels.

52
Q

Local Anaesthetics:

A
  1. A mixture of adrenaline and local anaesthetics is often used to cause vasoconstriction and reduced bleeding but should never be used in distal regions e.g.s fingers/toes (ischemia).
53
Q

Coronary Circulation:

A

LCA flow is greatest during diastole.

As myocardium contracting → the LCA perforating branches are occluded.

54
Q

Lewis Triple Response:

A
  1. Response to skin trauma → wheel and flare reaction

2. Abolished by sensory denervation.

Cardio (108 decks)

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