CVS regulatory mechanisms Flashcards

1
Q

What is the relationship between metabolic rate and blood flow?

A

Linear

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2
Q

How can blood flow by increased locally?

A

Autoregulation via myogenic responses

Locally produced vasodilator metabolites

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3
Q

How can blood flow by controlled systemically?

A

Nerves to control arteriole or circulating vasoactive substances
(short term)

In the long term there are changes to the size and number of blood vessels in the tissue

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4
Q

What are the local factors that cause a blood vessel to constrict?

A

Drop in temperature
Injured vessels
Autoregulation (myogenic response)

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5
Q

What are the local factors that cause a blood vessel to dilate?

A
Increased temp
Hypoxia
Increased pCO2
Lactate
Cells leaking K+
Breakdown of ATP
Histamine
(adenosine is a vasodilator in cardiac muscle but not skeletal)
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6
Q

What are the endothelial products that cause constriction of blood vessels?

A

Endothelin-1
Locally released platelet serotonin
Thromboxane A2

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7
Q

What are the endothelial products that cause dilation of blood vessels?

A

Nitrous oxide
Kinins
Prostacylin

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8
Q

Which circulating hormones cause constriction of blood vessels?

A
Adrenaline (except in skeletal muscle and liver)
Noradrenaline
Angiotensin 2
Circulating Na/K ATPase inhibitor
AVP
Neuropeptide
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9
Q

Which circulating hormones cause dilation of blood vessels?

A
Adrenaline in skeletal muscle and liver
CCRP-alpha
Substance P
Histamine
ANP
VIP
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10
Q

What are the neural factors which increase constriction of blood vessels?

A

Increased discharge of noradrenergic vasomotor nerves

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11
Q

What are the neural factors which increase dilation of blood vessels?

A

Decreased discharge of noradrenergic vasomotor nerves

Activation of cholinergic dilator fibres to skeletal muscle

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12
Q

How do additional blood vessels grow into tissue?

A

Endothelial cell growth factors
Fibroblast growth factor
Angiogenin

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13
Q

Where is prostacyclin produced?

A

Produced by endothelial and smooth muscle cells in blood vessels

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14
Q

What does prostacyclin do?

A

Inhibits platelet aggregation and promotes vasodilation ->increasing blood flow
Increases renin secretion by acting on juxtaglomerular cells

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15
Q

What makes thromboxane A2?

A

Made in platelets
Comes from common precursor arachnidonic acid via COX pathway
Promotes platelet aggregation and vasoconstriction

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16
Q

What is the action of aspirin?

A

Irreversible inhibition of cylooxygenase, shifts the balance more towards prostacyclin and causes bleeding

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17
Q

What is another name for nitric oxide?

A

Endothelium derived relaxing factor

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18
Q

What makes nitric oxide?

A

Made from arginine

Crosses cell membrane readily

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19
Q

What increases/decreases production of nitric oxide?

A

+ by products of platelet aggregation

- by Hb

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20
Q

What are the key functions of nitric oxide?

A

Vasodilation
Tonic release of NO is necessary to maintain BP
Helps penile erection
Vascular remodelling and angiogenesis
Important for brain function
Important for cytotoxic ability to kill cancer cells

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21
Q

What increases production of endothelin-1?

A
Stretched wall
Hypoxia
Ang II
Catecholamines
GF
Insulin
LDL, HDL
Thrombin
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22
Q

What decreases the production of endothelin-1?

A

Nitric oxide
ANP
PGE2
Prostacylin

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23
Q

What are the key actions of endothelin-1?

A

Potent vasoconstrictor (particularly coronary arteries)
Decreases renal blood flow, decreases GFR and increases renin and aldosterone
Positive chronotrope and inotrope
Increases ANP
Increases Glucononeogenesis
Bronchoconstriction
IV injection causes transient hypotension then sustained rise in BP

24
Q

Where are kinins formed?

A

Sweat glands
Salivary glands
Exocrine pancreas

25
What do kinins do?
Increase permeability of capillaries chemotaxic for leukocytes Relaxation of vascular smooth muscle Contraction of visceral smooth muscle
26
What increases release of atrial natriuretic peptide?
``` Raised CVP (hypervolemia, over infusion of fluids) Raised HR (increased venous return) Immersion of body in water Will generally rise when aldosterone falls ```
27
What are the actions of atrial natriuretic peptide?
Inhibits release of ADH Increases GFR-> increase sodium loss Inhibit release of renin-> reduce Na retention Lowers BP by inhibiting actions of several vasoactive substances May have a role in central control of BP in the brain
28
Where is serotonin found?
``` Derived from tryptophan Platelets Chromaffin tissue in gut Brain Retina ```
29
What are the actions of serotonin?
``` Constriction of some vessels Contraction of ileum Potentiates effect of NA May be involved in vasospasm in migraine Also a central neurotransmitter NO effect on stimulation of cardiac muscle or secretion of saliva ```
30
How is serotonin excreted?
Active reuptake mechanism Inactivated by monamine oxidase Forms 5-hydroxyindoleacetic acid which is excreted in urine
31
Where is histamine produced and what does it do?
Basophils and mast cells Released in response to trauma and allergy Dilates arterioles Increases capillary permeability
32
What are the clinical features of carcinoid syndrome?
Flushing Diarrhoea Cough, wheeze dyspnoea Nodular liver (in the case of hepatic metastases)
33
Which substances are released in carcinoid syndrome?
Serotonin Bradykinin + kallikreins Prostaglandin Histamine
34
How does sympathetic activation affect blood vessels?
``` Releases noradrenaline Increases HR and SV Inotropic and chronotropic Constrict arterioles and veins Inhibits affects of parasympathetics via neuropeptide Y ```
35
What happens to blood vessels when sympathetic nerves are cut?
Vessels dilate
36
What affect does parasympathetic release have on heart rate?
Releases ACH Decreases heart rate Blocked by atropine
37
What is the difference between the areas of inhibitory and excitatory input on blood vessels?
Both have input from cortex via hypothalamus and carotid and aortic chemoreceptors Excitatory only comes from pain and muscles Inhibitory only comes from lungs
38
Where are the 4 baroreceptors located?
Carotid sinus and aortic arch receptors: monitors arterial circulation Wall of right atrium: monitor venous return Wall of left atrium: monitor pulmonary circulation
39
Describe the baroreceptor reflex
Too much volume Increased wall stretch Afferent fibres pass via glossopharyngeal and vagus nerves to medulla Reach nucleus tractus solitarius Inhibits tonic discharge of vasoconstrictor nerves Excites vagal innervation of heart producing vasodilation, drop in BP, bradycardia and dropped CO
40
List some key things that increase HR via baroreceptors
``` Reduced cardiac output Reduced venous return Hypoxia, inspiration Emotions Hormones( adrenaline) ```
41
List some key things that decrease HR via baroreceptors
``` Increased CO Noradrenaline Emotions Stimulation of pain fibres from trigeminal nerve Raised ICP ```
42
What are some of the characteristics of coronary artery blood flow?
High oxygen extraction fraction of 70% at rest Flow through coronary arteries occurs mainly diastole because myometrium is relaxed so pressure is low Therefore reduced flow during tachycardia During exercise O2 extraction is almost 100% Flow is increased to 5 or 6 times Increase limited in the case of proximal stenosis
43
What are the two types of receptor on coronary vessels?
Alpha adrenergic-> vasoconstriction | Beta adrenergic-> dilation
44
Why does noradrenaline dilate the coronary arteries?
Because although its cellular action is to cause constriction, it simultaneously increases HR, CO and SBP. This causes an accumulation of vasodilator metabolites in the coronary vessels If you remove chronotropic and inotropic affect of NA bia betablockers and gave NA this would cause vasoconstriction. Therefore the direct affect of NA on the heart is vasoconstriction, clinically it causes vasodilation
45
Why do we use NA and not adrenaline in ICU?
In slow IV adrenaline infusion: HR and CO increases, SBP increases, but DBP and TPR decrease In slow NA infusion: SBP and DBP increase, TPR increases. But HR and CO decrease. Adrenaline causes a widened pulse pressure
46
Which 5 factors influence cerebral blood flow?
1. Intracranial pressure 2. Mean arterial pressure at brain level 3. Mean venous pressure at brain level 4. Local constriction and dilation of cerebral arterioles 5. Viscosity of blood
47
What is normal cerebral blood flow?
Arterial pressure of 65-140mmHg | Cerebral metabolism always remains constant
48
Why does increased ICP cause hypertension and bradycardia?
Stimulation of vasomotor centre due to local accumulation of CO2 with increased ICP
49
How does blood travel from mother to foetus?
Umbilical vein -80% oxygenated Blood then enters the baby's liver and gets directed into IVC via ductus venosus -67% oxygenated Enters heart through iVC and diverted directly into LA via patent foramen ovale Gets pumped into LV then aorta then to head -65% oxygenated
50
How does the fetus ensure that the better oxygenated blood (from the IVC) enters the brain and lower oxygenated blood (from the SVC) goes to its lower limbs?
Blood coming from SVC preferentially enters the RV and is expelled into pulmonary circulation Blood in the pulmonary artery gets shunted into aorta via ductus arteriosus and therefore to trunk and lower body of fetus
51
How much of the fetal carbon dioxide goes back through the placenta?
55%
52
What is the oxygen saturation of the portal and systemic venous blood of the fetus?
26%
53
Which 3 things close at birth?
Umbilical vein is cut off->ductus venosus shuts off Fetal lungs expands-> blood flows into lungs and returns to LA-> pressure in LA rises-> closure of foramen ovale Aortic pressure increases-> closure of ductus arertiosus
54
What are the features of a congenital ventricular septal defect?
Pansystolic murmur Increased pulmonary blood flow Possible late right ventricular failure Possible late pulmonary hypertension
55
What are the most important mechanisms for maintaining high blood flow to skeletal muscles?
a fall in pO2 Accumulation of vasodilator metabolites Also but less important: decrease in tonic vasoconstrictor discharge
56
What affect do sympathetic nerves have on blood flow?
Blood flow in resting muscles doubles after sympathectomy but once exercise is commenced there is no difference in flow