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Cardiovascular Block > L16 - The Cardiac Conduction system > Flashcards

L16 - The Cardiac Conduction system Flashcards

1
Q

Summarise the metabolic control concept

A
  • Increase in metabolic activity leads to…
  • Increased release of metabolic byproducts…
  • Causes increased resistance vessel dilation
  • Permitting increased BF
  • Resulting in increased Oxygen and nutrient supply
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2
Q

Resistance vessels are sensitive to metabolites found where?

A

Extracellular fluid and oxygen.

Vascular smooth muscle cells dilate, increasing blood flow

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3
Q

Myogenic control concept

A

IF

  • intraluminal pressures rise
  • then resistance vessels may constrict
  • contraction mediated by stretch activated Ca2+ channels in VSMC membranes
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4
Q

IF arterial pressure were to rise suddenly…

A

Flow will increase

  • metabolites washed away faster than produced
  • resistance vessels constrict reflexively
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5
Q

Sudden drop in arterial pressure may lead to…

A

Reflex vasodilation

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6
Q

Reactive hyperaemia

A

Period of increased BF that follows transient ischaemia, caused by arterial occlusion.

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7
Q

What hormones help control blood flow? (4)

A
  • Epinephrine
  • atrial natriuetic peptide
  • angiotensin II
  • ADH
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8
Q

Briefly, what modulated release of ADH?

A
  • released from posterior pituitary

- when tissue osmolarity rises or blood volume falls.

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9
Q

Where does ADH bind?

A

Binds to vasopressin V1a receptors n VSMC

V1a receptor couple to IP3 pathway

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10
Q

Angiotensin II

A

Potent vasoconstrictor.
Appears in blood stream when renal artery pressure falls.
Binds to angiotensin AT1 receptor on VSMC, which couple to the IP3 signaling pathway

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11
Q

Epinephrine

A

Adrenal medulla, SNS response.

Increase myocardial contractility and HR.

Binds:

  • A1 adrenergic receptor VSMC –> V. CCONSTRICTION
  • B2 adrenergic receptor –> V.DILATION
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12
Q

What is released by atrial myocytes if they are stretched by high blood volume?

A

Atrial myocytes will release ANP.

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13
Q

Role of ANP

A
  • vasodilation
  • binds to natriuretic peptide receptors, NPR1 on VSMCs
  • NPR1 is a guanyl cyclase that relaxes VSMCs by activating protein kinase G.
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14
Q

Summarise what chemicals contribute to endothelial control? (4)

A
  • nitric oxide
  • prostaglandins
  • endothelins
  • endothelium derived hyperpolarising factor
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15
Q

Vasodilators produced by the endothelium

A
  • NO
  • Prostacyclin
  • Endothelium-derived hyperpolarizing factors
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16
Q

Vasoconstrictors produced in the endothelium

A
  • endothelin
  • thromboxane A2
  • superoxide
17
Q

Describe how NO is produced and its action?

A
  • eNOS (constitutive endothelial NO synthase) produces NO.
  • diffuses into VSMC
  • activated guanylyl cyclase
  • causes release of cGMP
  • causes protein kinase G activation
  • PKG phosphorylated thereby inhibiting myosin light chain kinase
  • phosphorylates and increases activity of sarcoendoplasmic retriculum ATPase
  • VASODILATION and increased BF
18
Q

Angina

A

Caused by inadequate myocardial oxygen supply.

19
Q

What could be used as treatment for angina and why?

A
  • nitroglycerin (nitrate)
  • nitrates break down to release NO in vivo
  • causing arerial and venous vasodilation to lower ventricular afterload and preload
20
Q

Describe action of prostaglandins on vasculature

A
  • many PGE relax VSMC in vascular beds

- PGF and thromboxane A are vasoconstrictors

21
Q

Describe role of endothelium derived hyper polarising factor

A
  • EDHF opens K+ channels in the plasma membrane of VSMCs
  • ensuing membrane hyperpolarisation reducing calcium permeability
  • causing intracellular calcium levels to fall
  • vasodilation
22
Q

Action of endothelin

A
  • ET-1 = potent vasoconstrictor binds to ETa receptor on VSMC membrane
  • triggers intracellular Ca2+ release via IP3 pathway.
23
Q

Action of oestrogen on NO?

A

Oestrogen stimulates NO release from endothelium.

24
Q

How is Mean arterial pressure mediated?

A
  • changes in circulating BV by modifying renal function.
25
Q

What are Baroreceptor and where are they found?

HINT
what layer of carotid sinus?

A

Cluster of bare sensory nerve endings.

buried within elastic layer of the carotid sinus.

26
Q

How are information from baroreceptors relayed to the brain?

A
  • information to brain via sensory afferent travelling in sinus nerve
  • sinus nerve will join with glossopharyngeal nerve
27
Q

What occurs to the carotid sinus during systole?

A

Carotid sinus swells during systole.
Stretches the sinus wall and is embedded with nerve endings.

If there is no stretch, baroreceptors are inactive

28
Q

What occurs to aorta walls and carotid sinus when MAP increases?

A
  • aorta walls and carotid sinus expand
  • embedded nerve endings are stretched
  • if degree of deformation is sufficiently high, receptor potentials trigger spikes in sensory nerve.
29
Q

Compare the threshold values for carotid and aortic baroreceptors?

A

Carotid baroreceptors have a lower threshold that aortic baroreceptors, hence usually are inactive under resting conditions.

30
Q

Where are cardiopulmonary receptors found?

Where are the sensory nerve endings embedded?

A
  • found in low pressure regions of CVD system

- bare sensory nerve endings embeddded in walls of the vena cavae, the pulmonary artery and vein.

31
Q

Two types of baroreceptors found in atria

A

A-receptor

B-receptor

32
Q

A-receptor

A

Responds to tension that develops in the atrial wall during contraction

33
Q

B-receptor

A

Sensitive to atrial wall stretching during filing.

Also involved in raising HR when central venous pressure (CVP) is high - known as the Bainbridge reflex.

34
Q

The medulla contains a collection of nuclei known as the Cardiovascular centre. Describe the different subdivisions?

A
  1. Vasomotor centre
    - cells cause vasoconstriction when active
  2. Cardioinhibitory system
    - slows heart rate
  3. Cardioaccelatory centre
    - cells increase HR
    - increase myocardial inotrophy
35
Q

Describe the phases of cardiac action potential

A 
Phase 4 
- maintained by ATP dependent Na-K pumps 
Phase 0 
- AP arrives at neighbouring cell and triggers a rapid influx of Na+
Phase 1
- closure of the Na+ channels 
- brief opening of some K+
Phase 2
- plateau phase
- some K+ out some Ca2+ in 
Phase 3
- Ca2+ channels close and various K+ channels open leading to repolarisation.

Cardiovascular Block (16 decks)

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