21. Regulation of Circulation Flashcards

1
Q

What is membrane potential?

A

Membranes of cells have a charge gradient. Membrane potential in resting state is more negative inside relative to outside

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2
Q

What is depolarisation?

A

Activation of cells caused by depolarisation. The charge difference switches to being more positive inside due to ion movement

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3
Q

What is hyper polarisation?

A

Inhibition of cells is caused by hyper polarisation. Charge difference becomes more negative than resting potential and therefore harder to depolarise

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4
Q

How does electric charge control the cardiac muscle?

A

Cardiac muscle is also controlled by changes in electrical charge across the membrane. A moving wave of change in electrical charge is called an action potential

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5
Q

What three things control rhythmic heart contraction?

A
  • Autorhythmicity
  • Gap junctions
  • Two groups of pacemaker cells: the sinoatrial node (SAN) and the atrioventricular node (AVN)
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6
Q

How does the atrioventricular node control rhythmic heart contractions?

A
  • Action potentials are sent to the ventricles via the bundle of His
  • They run to the ventricular apex via right and left bundle branches
  • Action potentials spread through ventricles via purkinje fibers
  • Ventricular sanctum
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7
Q

What is cardiac arrest?

A

The sudden loss of cardiac function, when the heart abruptly stops beating. Often referred to as “sudden death” or “sudden cardiac death”

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8
Q

What is the most common loss of function in cardiac arrest?

A
  • Loss of ventricular fibrillation
  • Caused by irregular electrical activity in the heart (arrhythmia)
  • When this happens the heart pumps little or no blood to the body
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9
Q

How is cardiac arrest treated?

A

Defibrillation using electricity to “shock” the heart to try and restore its regular rhythm

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10
Q

What do survivors of cardiac arrest have?

A

An implantable cardiac defibrillator (ICD)
- If the heart develops an abnormal rhythm, the ICD delivers an electrical shock to the heart to return the heart rhythm to normal

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11
Q

Why is mean arterial pressure used to calculate blood pressure in the body?

A

Because the diastolic part of the cycle is twice as long as systolic, therefore we calculate the weighted average

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12
Q

How is MAP calculated?

A

(systolic)+2(diastolic)
________________
3

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13
Q

What are the demands on the body?

A
  • Change in blood pressure and increased demand for oxygen
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14
Q

What is required in the response against a change in blood pressure?

A
  • Rapid response
  • Baroreceptros
  • Baroreceptor reflex
  • Autonomic nervous system
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15
Q

What is required in the response against an increased demand for oxygen?

A
  • Rapid resposne
  • Chemoreceptors
  • Autonomic nervous system
  • Hormones
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16
Q

In the autonomic nervous system how do systemic blood vessels change blood flow?

A
  • Arterioles can vasoconstrict and vasodilate and change blood flow and vascular resistance
  • Extrinsic (nervous and endocrine systems) factors alter arteriole and vein diameters by acting on the smooth muscle
17
Q

How does norepinephrine influence vasoconstriction and vasodilation?

A
  • Sympathic neurons
  • Neural type
  • Causes vasocontriction
18
Q

How does endothelin influence vasoconstriction or vasodilation?

A
  • Vascular enothelium
  • Paracrine
  • Vasoconstriction
19
Q

How does angiotensin influence vasoconstriction or vasodilation?

A
  • Sourced from plasma
  • Endocrine
  • Vasoconstriction
20
Q

How does CO2 affect blood flow?

A
  • Sourced from multiple tissues
  • Metabolite
  • Vasodilation
21
Q

How does nitric oxide influence blood flow?

A
  • Sourced from vascular endothelium
  • Paracrine
  • Vasodilation
22
Q

How does bradykinin influence blood flow?

A

Sourced from multiple tissues

  • Paracrine
  • Causes vasodilation
23
Q

How does noradrenalin affect vasomotor tone?

A
  • Arteriole diameter is controlled by tonic release of noradrenaline
  • If there is a change in signal rate either:
  • Increased noradrenaline release onto alpha receptors so there is an increase signal rate and the blood vessel constricts OR
  • Decreased noradrenaline release onto alpha receptors, decreased signal rate and the blood vessel dilates
24
Q

What is the process of vasoconstriction?

A
  • Noradrenaline, angiotensin II and Endothelin-1 act via different receptors (g-protein linked)
  • Phospholipase C activation causes the formation of inositol triphosphate
  • IP3 stimulates the release of calcium from the sarcoplasmic reticulum (SR)
  • Increased ca2+ causes smooth muscle contraction
25
Q

How is the contraction controlled by ca2+?

A

Myosin light chain kinase regulates the latch state of prolonged cross bridge formation (energy efficient tone)

26
Q

How does vasodilation occur?

A
  • Vasodilator binds to the receptor inside the endothelial cell which increases calcium production in that cell
  • increase in intracellular Ca2+ opens Ca2+ gated K+ channels
  • K+ flows out creating a difference in charges
  • Across the Smooth muscle cell there is an increase in positive charges, so the inside of the cell is more negative
  • The vascular SMC becomes hyper polarised; harder to start a contraction
27
Q

What factors alter heart rate?

A

Extrinsic (nervous and endocrine systems) factors alter heart rate by acting on the pacemaker cells (intrinsic) in the SAN
- SAN innervated by both sympathetic and parasympathetic autonomic neurons

28
Q

What factors cause autonomic innervation of the heart in sympathetic nerves?

A
  • Noradrenaline

- Beta1 receptors

29
Q

What factors cause autonomic innervation of the heart in the parasympathetic (vagal) nerves?

A

Acetylcholine

Muscarinic (M2) receptors

30
Q

What causes a decreasing heart rate?

A
  • Acetylcholine acts on muscarinic M2 receptors
  • SAN cells are hyperpolarised
  • The time for depolarisation takes longer
31
Q

What causes an increasing heart rate?

A
  • NA and adrenaline increased the heart rate and contractility
  • B1 adrenorecpotrs
  • Increased rate of depolarisation in the SAN
  • Increased ca2+ affects myocytes
32
Q

What is the baroreceptor reflex?

A

Initiates the response to bring MAP back to normal

33
Q

What is orthostatic hypotension?

A
  • When you stand up there is a pooling of blood in the lower body, decrease in venous return and a decrease in mean arteriole pressure
  • Gravity induced blood pooling in lower extremities causing decreased cardiac output and subsequently lowering of arterial pressure
  • Overall effect is a transitory insufficient blood perfusion in the upper part of the body, particularly the bria
34
Q

What do baroreceptors do?

A
  • They are stretch receptors in the walls of the large arteries going to the brain, carotid arteries and aorta
  • Send info to the brain stem about pressure in the vessels
35
Q

How does the brain regulate the ANS?

A
  • The baroreceptor reflex detects changes in blood pressure
  • Arterial chemoreceptors detect changes in blood chemical composition (CO2 and O2)
  • Medulalry chemoreceptors detect changes in increases in CO2 levels (brainstem)
36
Q

What happens when there is an increased demand for oxygen (exercise)?

A
  • Rapid response (central command, chemoreceptors, autonomic nervous system, hormones e.g. adrenalin)
  • Redistribution of blood flow – decreased flow to visceral beds; increased flow to skeletal muscle
  • Increased cardiac output – elevated heart rate
  • Increased breathing rate
37
Q

What is preeclampsia?

A

A pregnancy-specific cardiovascular disease that is characterized by hypertension > 20 week gestation and excess of serum protein levels in the urine ≥ 300 mg (proteinuria)

38
Q

What are the effects of preeclampsia on endothelium dependent relaxation?

A

Reduced sensitivity to bradykinin and abnormal vasorelaxation

39
Q

How does nitric oxide cause vasodilation?

A
  • Activating a receptor stimulates the production of nitric oxide inside the endothelial cell
  • Nitric oxide diffuses across to the vascular SMC
  • Activates cGMP
  • Causes hyper polarisation making it harder to contract