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normal structure + function > cardiovascular > Flashcards

cardiovascular Flashcards

1
Q

what is the thorax + what does it contained

A

sealed cavity that contains the heart, thoracic oesophagus, thymus, blood vessels, nerves, lymph nodes and lungs.

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2
Q

How is the thorax contained

A
  • Laterally = the ribcage
  • Cranially = the thoracic inlet
  • Dorsally = the thoracic vertebrae
  • Ventrally = the sternum
  • Caudally = the diaphragm
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3
Q

How many ribcages does a dog have

A

13

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4
Q

What does each rib join onto

A

thoracic vertabrea and hypaxial muscle

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5
Q

What is the rib made of

A

dorsal 2/3 = bone
ventral 1/3 = cartialage

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6
Q

How do the rib bones join together

A

First 9 ribs join the sternum ventrally, the bottom 4 join their cartilage together to from the costal arch, with the last rib not connecting to anything (floating rib).

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7
Q

How many bones is the sternum made up of + what are they called

A

8 sternabrae

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8
Q

What is the diaphragm

A

sheet of skeletal muscle extending from the sternum, ribs and vertebrae and inserts on a central aponeurotic tendon

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9
Q

What is the thoracic inlet

A

Not an enforced boundary, where blood vessels and other things like the trachea and oesophagus enter and leave the thorax.

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10
Q

What is the pleura

A

Thorax is lined by shiny serous membrane = pleura. Seals off the thorax, very thin and smooth mesothelial sheet. It is separated into two parts

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11
Q

What are the two parts of the pleura

A
  • Visceral pleura = attaches to the lungs
  • Parietal pleura = where it lines everything else. Mediastinal = oragans in midline. Diapragmatic = diaphragm at caudal extent. Costal = laterally on ribs
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12
Q

How does the pleura create a potential space

A

Layers form a potential space, separated by thin layer of fluid to allow lungs to move over ribs. Maintains negative pressure so lungs pulled open when breathing in

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13
Q

Describe the trachea

A

tube that contains rings of cartilage for structure and a muscle at each dorsal aspect

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14
Q

what are the lungs split into

A

lobes

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15
Q

How are the lobes subdivided

A
  • Left lung = 2 lobes. Cranial (split into cranial and caudal) and the caudal
  • Right lung = 4 lobes. Cranial, middle, caudal and accessory. In most domestic animals except horses, who lack a middle lobe.
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16
Q

What is the base of the heart

A

fatter bit at the top where blood vessels enter and leave the heart sits cranially and dorsally to the apex

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17
Q

What is the apex of the heart

A

point at the bottom which consists of the left ventricle, sits caudally and ventrally to the base

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18
Q

What is the pericardium

A

invaginated sac of serous membrane that covers heart, is an extension of the pleura

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19
Q

What is the structure of the pericardium

A

contains two layers : parietal and visceral layers, fluid filled gap in the middle to allow movement.

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20
Q

What is muscular contraction of the heart stimulated by

A

electrical impulses (action potentials) that orginate rom the SAN

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21
Q

How does the action potential spread across the heart

A

spread cell to cell by branching of the cells and communicated by intercalculated diiscs

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22
Q

How do intercalated discs work

A

contain gap junctions that allow cations to move in-between cells to depolarise, so the cardiac muscle contracts at the same time

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23
Q

What does functional syncytium mean

A

means the cardiac muscle acts as one cell and all contract as one unit as the action potential is transmitted cell to cell very quickly

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24
Q

Which nervous system does the heart receive input from

A

autonomic nervous system - causes changes in the heart rate and contractility to change cardiac output

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25
Q

Which nerve does the sympathetic nervous system access the heart from

A

cardiac nerves (also piggy backs on the vagus nerve)

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26
Q

Which nerve does the parasympathetic nervous system access the heart rom

A

vagus nerve

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27
Q

What does automaticity

A

cells in the san node spontaneously depolarise and create action potentials

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28
Q

Which cells of the hearts possess automaticity

A

sinoatrial and atrioventricular nodes, faster cells are in the SAN - they are the pacemaker .

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29
Q

Can av node become pacemaker

A

they have a slower depolarisation so only take over if signal from AV node is disrupted. Other cells in myocardium can become pacemaker cells if they are damaged (develop automaticity)

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30
Q

What are ectopic pacemakers

A

damaged myocardium cells not in the AV or SA nodes that develop automaticity after being damaged, can be responsible for abnormal rhythms (arrhythmias)

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31
Q

What is the electrical pathway

A

1) Action potential generated from the SAN in the right atrium
2) wave of depolarisation spreads across both atria via the intercalated discs causing simultaneous contractions of all atria cells (happens relatively slowly)
3) wave of depolarisation collects at the AVN where it is delayed - as fibres are narrow - before being passed onto the ventricles. Allows atrial systole to optimise ventricular filling – atria and ventricles are electrically isolated from each other by annulus fibrosus
4) action potential passed from the AVN to the bundle of his which goes down the interventricular septum into the left and right ventricles by left and right branch. Right bundle branch crosses right ventricle by septomarginal band to free wall. Left branch divides into anterior+ posteriorfasicles for thick walls
5) causes contraction from the apex up to push blood out of the ventricles back into circulation

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32
Q

why doesn’t the action potential spread straight from the atria to the ventricles

A

they are electrically isolated by the annulus fibrosus which is the fibrosus skeleton of the heart

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33
Q

Wherre do sympathetic nerves arise from

A

thorcolumbar spinal segments

34
Q

where does the postganglionic sympathetic supply arise from

A

the ganglions C5-T3 which combine to form two larger ganglia == stellate ganglion and middle cervical ganglion

35
Q

How do postganglionic fibres innervate the heart wall

A

cardiac nerves

36
Q

Where do the parasympathetic nervous system arrive from

A

brainstem and sacral spinal segments

37
Q

what role does innervation of the heart play

A

changes contractility, rate of depolarisation

38
Q

what type of nerves supply the heart

A

autonomic

39
Q

what ganglia supply the heart

A

T1 T2 T3 (thoracic segments) from one mega ganglion called stellate ganglion
and cervical ganglia (C7 andC8) communicate by two legs o C6 and C5 (no spinal segments)

40
Q

How does the parasympathetic nervous system affect the heart

A

at rest, moderates heart rate and contractility, opposes action of sympathetic NS. Acts at a more local level, only genital and coronary dilatation, other effects are fue to lack of sympathetic stimulation rather than direct parasmpathetic effects

41
Q

what effect will a generalised vasodilation have on cardiac output

A

Vasodilation will mean arterioles dilate so there is less blood pressure in the capillaries and veins. This means decreased preload and therefore decreased EDVP so decreased stroke volume and cardiac output,

Could say that if overall pressure too high (afterload too high, so cardiac output was too high) so vasodilation allows ventricle to empty easier so cardiac output increases

42
Q

What effect will sympathetic stimulation have on blood vessels

A

blood vessels only receive sympathetic innervation, effect depends on the vessel concerned. most constrict (to non-essential organs) but vasodilate to brain, heart and skeletal muscles to increase perfusion and preload.

43
Q

What are the effector organ receptors in parasympathetic

A

parasympathetic
blood vessels –M3 cholinergic
heart - M2 cholinergic

44
Q

What are the effector effector receptors in the sympathetic nervous system

A

blood vessels = alpha 1,2 and beta androgenic (plus M3 cholinergic at skeletal muscle arterioles)
heart = beta 1 adrenergic

45
Q

Where do the alpha 1 and alpha 2 receptors affect, what neurotransmitter and what effect

A

site - arterioles
neurotransmitter - circulation noradrenaline (from sympathetic neurones) /adrenaline
causes vasoconstriction to increases total peripheral resistance and decrease blood flow to the organs

site - veins
neurotransmitter - noradrenaline (from sympathetic neurones) and adrenaline
causes vasoconstriction which moves venous blood towards the heart

46
Q

Where do beta one receptors affect, what neurotransmitter and what effect

A

site - cardiac myocytes (include nodal tissue)
neurotransmitter - noradrenaline (from sympathetic neurones) and adrenaline
causes increased heart rate, faster conduction, shorter refractory period and increased contractility
so increased cardiac output

47
Q

where do beta two receptors affect, what neurottransmitter and what effect

A

coronary and skeletal muscle arterioles,
noradrenaline and adrenaline
causes vasodilation to increase coronary and skeletal muscle blood flow

48
Q

what are the adrenergic receptors

A

alpha and beta (sympathetic nervous system#0

49
Q

what are the cholinergic receptors

A

muscarinic

50
Q

Where does the muscarinic 2 receptors affect, what neurotransmitter and what effect

A

site - cardiac myocytes (SA and AV nodes) less direct innervation of ventricular cells
neurotransmitter - -acetylcholine (parasympathetic neurones)
causes decreased heart rate, slower conduction, longer refractory period and decreased contractility

51
Q

Where does the muscarinic 3 receptors affect, what neurotransmitter and what effect

A

affect coronary, genital and skeletal arterioles. All acetylcholine, coronary and genital are from the PARAsympatehetic whereas skeletal muscles come from the sympathetic neurones.
all causes vasodilation and increased blood flow

52
Q

difference in responding to neurotransmitters for cholinergic and adrenergic receptors

A

Cholinergic receptors respond to acetylcholine from the presynaptic neurone.
Adrenergic receptors respond to noradrenaline from the presynaptic neurone, and circulating noradrenaline or adrenaline from the adrenal gland.

53
Q

After exercise how does cardiac output and heart rate return to normal

A

parasympathetic activation of M2 cholinergic receptors at sympathetic nerve endings in heart and on cardiac myocytes causes reduced heart rate and contractility via M2
Parasympathetic nervous activation of the M3 receptor maintains coronary blood flow

54
Q

What 5 systems manage blood pressure during exercise

A

1) metabolic autoregulation of blood flow (chemoreceptors detecting CO and O levels)
2) psycogenice response
3) baroreflex
4) exercies reflex
5) skeletal and respiratory pumps

55
Q

How does the psychogenic response work

A

before exercise, body prepares
increases sympathetic activity, decreases parasympathetic
causes increased cardiac output (up HR, contractility and conduction speed)
increased total peripheral resistance due to vasoconstriction of non-essential organs (increases preload - increased venous return)
is a graded response, modified throughout exercise

56
Q

What is the exercise reflex

A

Joint and muscle receptors have specialised nerve endings to assess the intensity of exercise, and feedback to the autonomic nervous system

57
Q

What is the baroreflex

A

Stretch receptors detect blood pressure in the carotid sinuses and aortic arch, and sends a continuous stream of action potentials to the cardiac centre in the brain. Decreased blood pressure means there is a decreased frequency of action potentials so cardiac centre compares to refernce value and will increase sympathetic output

58
Q

How does the respiratory pump work

A

increased depth of respiration (exercising) causes the diaphragm to push onto the lumbar so veins contract, creating negative and positive pressure as breathe in/out = pump to increase preload

59
Q

How does the skeletal muscle pump work

A

during exercise movement of muscles causes blood to be pushed up through the veinss to the heart so increases preload

60
Q

What is hypovolaemia

A

decreased volume of circulating blood,

61
Q

what is hypovolaemic shock

A

acute drop in mean arterial pressure due to reduced blood volume

62
Q

Why does hypovolaemic shock occur

A

haemorrhage (loss of blood, cells proteins and water)
severe dehydration (plasma c=volume reduced due to water loss, cells + proteins don’t change, very concentrated )
sequestration of blood - blood stuck somewhere

63
Q

What is the first compensatory mechanism for hypovolaemia

A

baroreflex, first seconds
causes increased sympathetic stimulation - increases contractility, heart rate and conduction speed

64
Q

how does increased sympathetic stimulation affect the circulatory system when blood pressure drops

A

heart - increased contractility, increased heart rate and speed conduction
blood vessels -vasoconstrict
spleen - contracts to expel blood in spleen into circulation (replace lost blood, and also lost cells, higher than normal rbc count)

65
Q

how does starling’s law of capillaries work to oppose hypovolaemia

A

less hydrostatic pressure in capillaries so increased absorption of ISF into capillaries so increased blood volume

66
Q

How does RAAS oppose hypovolaemia

A

replaces fluid by aldosterone released from adrenal gland causing the kidney to release sodium into blood so water enters. also makes you feel thirsty so dink more, causes powerful vasoconstriction and releases anti-diuretic to stop peeing

67
Q

What happens if blood is lost by haemorraghe

A

mechanisms don’t replace proteins or blood cells lost. Haematocrit (PCV) and plasma protein levels drop as fluid replaced so more dilute = becomes anaemic. Protein levels restored by liver in several days. Bone marrow replaces blood cells in a few weeks.

68
Q

What are the two types of heart failure

A

forward and backward

69
Q

What is forward heart failure

A

heart failure caused by reduced blood being pumped out of heart. Reduced cardiac output, could be because afterload in the arteries is too high or reduced stroke volume (dilated cardiomyopathy) . This means there is reduced blood flow in the circulation and therefore reduced mean arterial pressure.

70
Q

What are signs of forward heart failure

A

reduced perfusion
- cold extremities
- slow capillary refill time
- pale mucous membranes
- weak pulses
- unable to exercise
- weak / lethargic
- fainting (vasovagal syncope)

71
Q

What is dilated cardiomyopathy and how can it lead to forward heart failure

A

condition when muscle wall of heart is stretched and thinned, so ventricles are unable to contract effectively = reduced stroke volume , so reduced cardiac output = forward heart failure

72
Q

what is backwards heart failure also known as

A

congestive heart failure

73
Q

What is backwards heart failure

A

when the heart annot cope with the preload, de to excessive preload and failing heart. This causes the venous pressure to increase due to the backup and therefore also increased pressure in the capillaries (hydrostatic) which causes increased filtration of the blood into the ISF. Can have either right or left heart failure

74
Q

What is backwards left heart failure

A

in the left it causes increased venous pressure in the lungs which leads to pulmonary oedema causing an increased respiratory rate (tachypnoea) and sometimes respiratory difficulty (dsypnoea) and audible crackles

75
Q

what is backwards right heart failure

A

increased systemic venous pressure so fluid leakage leads to effusions (fluid build-up in body cavities) and potentially subutaneous oedema. Can cause visible distension of the jugular veins and enlargement of the liver and spllen

76
Q

what is hepatomegaly

A

enlargement of the liver

77
Q

what is splenomegaly

A

spleen enlargement

78
Q

How does forward failure lead to backwards failure e.g.

A

forward leads eventually to backwards as reduced output means increasing atrial pressure which increases the venous pressure.
backward may lead to forward failure if regurgitation of blood from ventricle to atrium is big enough to reduce stroke volume and therefore cardiac output

79
Q

How does body compensate for forwards heart failure

A

starling’s mechanism, baroreflex, RAAS
starling’s mechanism - reduced cardiac output results in venous + atrial pressure rising giving a greater preload which increases the EDVV and cardiac output
barorelfex - activated from drop in arterial BP, leads to sympathetic stimulation of heart and blood vessels to increase contractility, heart rate and conduction – so increases cardiac output
sympathetic activation results in RAAS activation which causes vasoconstriction
this is just in the early stages of heart disease to try and maintain CO and BP but only work for a while but can have bad effects that outweigh the benefits

80
Q

What does backwards heart failure compensation result in

A

ask friends

normal structure + function (9 decks)

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