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BVMS 2 > Module 10 Wk1 > Flashcards

Module 10 Wk1 Flashcards

1
Q

T/F Ventricles recieve blood and atriums distribute blood systemically and pulmonary

A

False - The 2 atrias recieve blood and the 2 ventricles are more muscular and distribute the blood systemically or pulmonary

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2
Q

Describe Pulmonary circulation

A
  • The right artrium recieves deoxygenated blood from systemic circulation
  • This blood is directed to the right ventricle exiting pulmonary trunk to pulmonary arteries to lung
  • The return of oxygenated blood from lungs goes into left atrium via pulmonary veins
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3
Q

Describe systemic circulation

A
  • blood comes into left atrium then to left ventricle and exits via aorta
  • Arterial blood then goes onto head, neck and forelimb via subclavian and commen carotid arteries
  • arterial blood to body tissues via decending and abdominal aorta
  • then the venous return via cranial and caudal vena cava into right atrium
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4
Q

In a left lateral view describe the position of the heart

A

lies between ribs 3-6 at an angle with its base lying cranial and dorsal to the apex which lies caudal and ventral

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5
Q

In dorsolateral view of the heart where is it positionsed?

A

lies to the left of the midline
Apical heart beat tends towards left

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6
Q

What is the hearts own serous sac called?

A

The pericardium

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7
Q

T/F the mediastinum is two layers

A

True it is two layers of mediastinum pleura

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8
Q

What does the pericardium consist of?

A

Viscera and parietal layers

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9
Q

What seperates the viceral and parietal layers?

A

The pericradial cavity filled with serous fluid

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10
Q

What is the visceral layer continyous with and where does it go after this?

A

The outer layer of the heart and reflexts over the great vessels at the base of the heart

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11
Q

What does the parietal layer of the pericardium consist of?

A
  • partial pericardium, CT layer and mediastinal pleura
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12
Q

What does the parietal layer form ventrally?

A

sternopericardial ligament

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13
Q

What limits the stretch of the parietal layer?

A

CT and mediastinal pleura

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14
Q

What are the three layers of the heart wall?

A
  • epicardium
  • myocardium
  • endocardium
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15
Q

What is the inner layer of the heart? what kind of epithelium covers this?

A

Endocardium and is covered by a special type of simple squamous epithelium called endothelium

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16
Q

What is the function of this epithelium covering the endocardium?

A

it allows low resistance to blood flow

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17
Q

What is the middle layer of the heart wall?

A

the myocardium

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18
Q

The myocardium is a ct layer in the middle what is its function?

A

It brings blood vessels to nourish and support cardiac muscle and the impulse conducting system is controlled through it aswell

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19
Q

What is the outer layer of the heart wall?

A

It is called the epicardium made up of deep fiberelastic CT

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20
Q

What is the myocardium made up of?

A

It is made up of cardiac muscle with CT running between muscke fibers

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21
Q

What is the CT making up the myocardium called?

A

endomysium

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22
Q

How would you distinguish between cardiac and skeletal muscle in histological section?

A

Skeletal muscle has multiple nuclei at periphery of very long unbranched muscle fibres (myofibrils)
Little endomysium between myofibrils
No intercalated discs

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23
Q

Describe the Histology of cardiac muscle?

A
  • Striated muscle with centrally located nuclei
  • Branching myofibres
  • Intercalated discs – connections between myofibres that allow for unified contraction of sarcomeres – specialised jusctional complexes allowing impulse to move between the individual cells
  • Endomysium- CT running between the myofibres – bvs
  • Purkinje fibres - modified fibres that conduct electrical stimuli through the heart
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24
Q

What are features of the right or atrial surface?

A
  • The base and apex
  • The coronary groove
  • The Right inter-ventricular (subsinuosal) groove
  • The major blood vessels entering the right atrium
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25
Q

What is the coronary groove and what does it define?

A

It is usually fat filled and contains coronary blood vesseks and defines postition of atria versus ventricles

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26
Q

What does the right inter-ventricular groove and what does ir define?

A
  • contains coronary blood vessels and defines position of right and left ventricles
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27
Q

what are the major blood vessels enetering the right atrium?

A

caudal vena cava, cranial vena cava and right axygous vein

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28
Q

What are the features of the left surface?

A
  • The auricles
  • the coronary groove
  • the left inter-ventricular groove
  • the apex
  • the aorta
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29
Q

what is an auricle and which is more prominent?

A

the left auricle is more prominent
an auricle is a blind ended sac associated with each atrium

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30
Q

t/f the apex is formed bu the right ventriicle

A

false left

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31
Q

where does the aorta arise from?

A

from the middle of the base of the heart

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32
Q

what interrups the coronary groove on the left side of heart?

A

The pulmonary trunk

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33
Q

Describe the pattern of blood flow in the right atrium?

A

Venous return from systemic circulation via Cr. Vena cava & Cd. vena cava

venous return lumbar region via The Azygos vein

venous return from the coronary circulation via The Coronary sinus

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34
Q

What limits turbelence from the different blood flows from the vessels into right atrium?

A

The intervenous tubercle limits by directing blood flow towrads the right ventricle

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35
Q

what are the key interial features of the right atrium?

A
  • main chamber
  • fossa ovalis
  • inter-venous tubercle
  • terminal crest
  • right antrioventriular valve
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36
Q

What is the fossa ovalis?

A

It is a remenent of foetal circulation

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37
Q

Describe the right atrioventricular valve?

A

It is the AV valve, has 3 cusps, hence the other name being tricuspid

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38
Q

Describe how the right AV valve work

A

Flaps arent tiggered to stop blood entering back into ventricle when it is contracting as you wnat blood out of heart so they flick up and dont invert so blood cant get back in
In advance of the contraction of the ventricle the papillary muscles have already received impulse to start to contract and take up the tension that’s about to be exerted on the rest of the valve from blood going behind valve flaps and then flicking them up but chordae teninea stop the flaps of the velve flicking right up

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39
Q

what are the main featires of the right ventricle?

A
  • wall
  • trabecular septomargilanis
  • Trabeculae carnae roughened surface
  • right ventricle arount the cranial margin of heart
  • pulmonaru trunk
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40
Q

what is the trabecular septomarginalis?

A
  • It is a moderator band that runs from the septal to the marginal surfaces of the heart across the chamber
  • It is most evident in right ventricle
  • It is important as inside the structure we have some of the fibers for the impulse conduction system coming away from the main fiberous structures travelling doewn inberteeen ventriclesas the bundle of hiss, side group coming off here to inervate the papillary mmuscles of the valve
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41
Q

Descrbe the pulmonary semilunar valve?

A

when ventricle contracts the little pockets will be pushed flat allowing blood to enter the pulmonary trunk, when ventricle relax blood will back down pulmonary tunk and pools behind the little pockets and flciks it into the mid lline

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42
Q

(anatomy and blood flow through foetal heart)
What are the main features of the interoir of left atrium and ventricle

A
  • mitral valve
  • left ventricle
  • aortic semi-lunar valve
  • aorta
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43
Q

Describe the blood flow in the left atrium and vventrics

A

o2 blood eneterl L atrium and auricle via pulmonary veins and then mitral valve garurds enterence to the L ventricle

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44
Q

what guards enterence to aorta?

A

aortic semilunar valve

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45
Q

what is the difference between the R and L AV valve?

A

The L has fewer flaps and is much thicker

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46
Q

T/F As blood coming out of left ventricle the heart itself is ciphering off highly oxygenated high pressure blood in order to sustain itself and rest goes round the body

A

True

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47
Q

what is the Puncta maxima?

A

points on the chest wall where each heart valve is heard best- consistent between species

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48
Q

what is the Puncta maxima
of the pulmonic valve?

A

at the ventral part of left 3rd intercostal space

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49
Q

What is the Puncta maxima of the aortic valve?

A

The dorsal part of the left 4th intercostal space

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50
Q

what is the Puncta maxima of the mitral valve?

A

At the dorsal part of the left 5th intercostal space

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51
Q

what is the Puncta maxima of the tricuspid valve?

A

at the mid right 4th intercostal space

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52
Q

Where are the SA and AV nodes located?

A

In the right atrium

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53
Q

What does the AV bundle travel in?

A

Within the intraventricular septum and directs the impulse to the apex

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54
Q

what does the autonomic innervation of the heart modify?

A

The rate and strength of contraction

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55
Q

what does the sympathetic chain in the thoracic wall form at heart?

A

A couple of ganglia sending off symapthetic nerve fibers off up vagosympathetic trunk and also through nerve roots at the base of the heart that find their way to SA node and modulate the rate and strength of contraction

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56
Q

where do the parasympathetic fibers that modulate beats come from?

A

come from vagus nerve travelling over the base of heart

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57
Q

T/F in the foetus the lungs are completely non functional so don’t want a four chamber working heart until birth so no blood gets in

A

Trueeeee bitch

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58
Q

Describe the steps involved in the formation of the 4 chambered heart

A
  • Starts with just 2 chambers
  • Subdivision of the primitive atrium and ventricle
  • Single atrioventricular canal between the primitive atrium and ventricle also begins to divide
  • Subdivision of the primitive ventricle continues-via -interventricular septum
  • The interventricular foramen will eventually close
  • The atrioventricular canal is now splits into two
  • The interatrial septum continues to form but separation is never complete- communication between the two atria continues until birth (foramen ovale)
  • Ventricles are now separate
  • AV valves form between the atria and ventricles on each side of the heart
  • The left and right atria continue to intercommunicate (RA to LA) via foramen ovale
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59
Q

What are special features associated with foeatl circulation before birth?

A
  • Lungs are not functional- high resistance pulmonary circulation
  • Blood flows mainly through the low resistance systemic circulation and the placenta
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60
Q

what are Two important shunts associated with the Foetal heart that make the before birth features possible?

A

foramen ovale
ductus arteriosus

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61
Q

what is A third shunt in the liver maximises the pO2 of blood entering the heart from the placenta?

A

Ductus venosus

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62
Q

Foetal circulation- Ductus venosus

A

Blood moves from the umbilicus towards the liver via umbilical vein
Ductus venosus - Shunt in liver prevents mixing of oxygenated blood from placenta with foetal hepatic venous return from gut
Blood enters Right atrium via caudal vena cava has high pO2 in the foetus

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63
Q

Foetal circulation- Foramen ovale

A

Blood entering Right Atrium (RA) passes through foramen ovale into LA and into aorta via LV (high pO2)

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64
Q

Foetal Circulation: Ductus arteriosus

A

Blood entering RA from cranial vena cava flows into RV (as in adult)
2nd Shunt links pulmonary trunk to aorta -ductus arteriosus
Allows blood entering Right ventricle to bypass the lungs and pass into the aorta
Exercises right ventricle -in prep for delivering entire output to lungs after birth
pO2 in aorta flowing to rest of body lower due to mixing

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65
Q

what are the 3 main catorgies of congenital defects?

A
  • failure of closure of foeatal structures
  • septal defects
  • great vessel defects
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66
Q

What is an ECG?

A

The ECG is a record of the average electrical potential generated in the heart muscle and graphed in terms of voltage against time during the different phases of the cardiac cycle

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67
Q

describe the electrical conduction system of the heart

A
  • The electrical activity of this conduction system is passed to the muscle cells (cardiomyocytes) which then contract via the process of excitation-contraction coupling.
  • The SA node in the right atrium has action potentials that have the spontaneous depolarisation membrane potential that will suddenly reach threshold and kicks off.
  • The pacemaker cells pass the activity to the right atrium, and then to the left atrium and to the AV node.
  • It passes down the bundle of hiss and to the atrioventricular septum and to the right and left bundle branches.
  • The bundle branches end up in the endocardium (inner wall of the heart) and in the purkinje fibres.
  • It then goes to the epicardium (outer wall of the heart).
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68
Q

Describe the dipole concept using a cardiomyocytes

A

1) A cardiomyocyte has a resting membrane potential (approx. -80 mV), the inside of the cell is negative and the outside is positive

2) During depolarisation positive ions enter the cardiomyocyte – the inside becomes positive and the outside becomes negative

3) During repolarisation the interior of the cardiomyocyte becomes negative again and the outside becomes positive

4) If the positive end of the dipole is nearer the (+) electrode then an upward deflection in the voltage trace occurs, and vice versa

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69
Q

Describe atrial depolarisation

A

(1) The SAN cells in the RA spontaneously depolarise and result in depolarisation of the adjacent RA cells

(2) The wave of depolarisation moves towards the left as demonstrated by the arrow

(3) The cells in the LA are at rest hence a dipole is created

(4) The positive end of the dipole is closer to the (+) electrode hence an upward deflection occurs in the ECG trace

(5) When all the RA and LA is depolarised the trace returns to base-line

(6) The next delay is the wave of depolarisation passing through the AVN to the ventricles

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70
Q

Describe early ventricular depolarization

A

(1) Wave of depolarisation passes down the interventricular septum

(2) Wave of depolarisation spreads from left to right creating a dipole

(3) The negative end of the dipole is closer to the (+) electrode hence a downward deflection in the ECG trace occurs

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71
Q

Describe ventricular depolarization

A

(1) The endocardium depolarises before the epicardium

(2) A dipole is created which is very large since the number of cardiomyocytes within the left ventricle are numerous

3) The positive end of the dipole is closer to the (+) electrode hence a upward deflection in the ECG trace occurs

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72
Q

Describe late ventricular depolarization

A

(1) The wave of depolarisation finishes spreading from the endocardium to the epicardium of both ventricles

(2) The ECG returns to the baseline point and sometimes goes negative

(3) The negative end of the dipole is closer to the (+) electrode hence a downward deflection in the ECG trace occurs

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73
Q

describe ventricular repolarisation

A

(1) The epicardium is the last to depolarise but the first to repolarise

(2) The epicardial cells are now positive on the extracellular surface and create a dipole with the endocardial cells which are still depolarised

(3) The positive end of the dipole is closer to the (+) electrode hence a upward deflection in the ECG trace occurs

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74
Q

what is the P wave om ECG?

A

arterial depol

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75
Q

What is the QRS complex on ECG?

A

Ventricular depol - early norm and late

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76
Q

What is the T wave om ECG?

A

Ventricular repol

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77
Q

what is the PR interval?

A

It is the time fro atrial depol to electricle activity reaching the ventricle as the Q wave is early vent depol

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78
Q

T/F if you have someting wrong with your atria it might be reflected in your PR interval

A

True

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79
Q

What might be altered if you have something wrong with your ventricles(ECG)?

A

The distance between Q and T

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80
Q

What is the QT interval?

A

The length of time that the ventricles remain depolarised

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81
Q

What is the PP interval?

A

The time between atrial depolarisations

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82
Q

What are RR intervals?

A

Time between ventricular depolaristaion

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83
Q

Describe the cardiac cycle - the two parts

A

(a) Ventricular systole: period of ventricular contraction
(b) Ventricular diastole: ventricular relaxation during which ventricle fills with blood

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84
Q

is LVP low or high at the start of systole?

A

Low

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85
Q

What causes a back flow of blood from left ventricle to left atrium and what does this cause?

A
  • Contraction of muscles causes a rapid increase in pressure momentarily
  • causes closure of the mitral (left AV) valve
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86
Q

Describe what iso-volumetric contraction is

A

where there is no change in ventricular volume (or aortic blood flow) in early systole despite an increase in ventricular pressure.

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87
Q

As pressure in ventricle drops just after peak what happens to aortic valve?

A

the pressure in ventricle is slightly below aortic but blood flowing out (momentum) keeps aortic valve open.

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88
Q

what begins ventricular diastole?

A

As blood flow slows there is a momentary back flow of blood from the aorta which closes the aortic valve

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89
Q

while Muscles relax, pressure continues to decline and there is no refilling occuring, why is this?

A

due to pressure inside the ventricle being greater than atrial pressure

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90
Q

when the pressure in ventricle drops below arterial pressure what happens?

A

the mitral valve opens

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91
Q

once the mitral valve opens what occurs?

A

a phase of rapid ventricular filling followed by a period of slow filling until atrial contraction occurs (atrial systole).

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92
Q

Describe ventricular filling ( this is more of a note but didnt know how to split it up)

A
  • So there is 2 pumps in series, 1 pump propels blood through the lungs for oxygen and carbon dioxide exchange (pulmonary circulation) and the other propels blood through other tissues (systemic circulation)
  • The tubes or ducts are made up of distributing tubes (a) exchange vessels (b) and collecting vessels (c).
  • So oxygenated blood pumped from LV to AO which branches to supply all parts of body (except lungs)
    There is a parallel arrangement of vessels to each organ in that each organ receives the same composition.
    Blood passes through capillaries in organ to enter veins which combine until we have 1 large vein - vena cava.
    Blood then passes to RA, to RV which pumps it to the pulmonary artery.
    From there to capillary system of lungs and is collected in pulmonary veins and returned to LA.
    Pulmonary and systemic circulation are in series, blood must pass through one before reaching the other.
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93
Q

What is splanic circulation

A

It is blood from splenic, gastric and mesenteric capillaries enters portal vein to liver where it passes another bed of capillaries before returns to heart.

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94
Q

what does the splanic system allow

A

allows nutrients from GI tract to be delivered direct to the liver (liver also has own blood supply).

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95
Q

what is atrial systole?

A

It is the last phase of a diastole during which the ventricular filling is completed

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96
Q

do ventricles empty in artial systole?

A

nope

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97
Q

how much do ventricles contain just before ventricular systole in dog and what is this volume called?

A

40-60ml and it is called the end-diastolic volume which is the max volume of blood

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98
Q

what the blood called that is ejected at rest?

A

ejection fraction

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99
Q

what is the min volume that you are left with?

A

the end-systolic volume

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100
Q

what does the ED and ES create?

A

the stroke volume ie the volume ejected

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101
Q

T/F in heart failure you tend to get lower stroke volume?

A

True

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102
Q

Pressure-volume loops - again need to go look at the graph to understand this IMPORTANTTTTT

A

Start at A: This is diastolic filling which finishes at B with only a small increase in pressure
Iso-volumetric (B-C) occurs as systole begins with no change in volume.
At C the aortic valve opens and in first phase (C-D) there is a large reduction in volume with a continued but less marked change in pressure.
During D-E there is a reduced ejection and a small drop in ventricular pressure. Aortic valve closes at E and you get the rapid drop in pressure with little change in volume

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103
Q

T/F Left hand side of hearts pressure is lower

A

False it is higher at 120mm compared to 20mm

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104
Q

Describe the 4 heart sounds you hear

A
  • LUB - this is when the mitreal valve shuts when pressure within the ventricle exeeds pressure in atria
  • DUB is when the aortic valve shuts and the turbulance created by blood makes noise
  • WHOOSH is when the ventricles are rapidly filling
    -STP is the sound of the atria contracting
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105
Q

when might you hear a WHOOSH between LUB DUB

A

if the mitreal valve damaged and cant shut and blood started running back into the left atria as its not shut

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106
Q
A
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107
Q

T/F there is smooth muscle in blood vessel walls

A

True - the amount varies between types of vessels

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108
Q

What is the function of this smooth muscle in the walls of the blood vessels?

A

Can control the level of constriction which regulates the amount of blood flowing

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109
Q

T/F small chnages of the diameter of the lumen in arterioles has big impact on the pressure

A

True

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110
Q

What is the flow of blood matched to?

A

Metabolic requirements of that organ

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111
Q

what is the cardiac output?

A

It is the colume of blood ejected by one ventricle in one min

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112
Q

What is the cardiac index?

A

It is the cardiac output taking into consideration the size of the animal?

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113
Q

Does chnages in CO involve changes in both HR and SV?

A

Yes since CO = HR x SV

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114
Q

What are the two opposing factors stroke volume is influenced by?

A
  • High energy of contraction increases SV
  • A high arterial pressure opposes ejection and hence SV
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115
Q

What is the energy of contraction increased by?

A

Stretching the myocardium in diastole through a rise in end-diastolic pressure

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116
Q

The strength of contraction at a given stretch can be increased by what?

A

By sympathetic stimulation and circulating hormones

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117
Q

What effect does arterial pressure have on stroke volume?

A

It depresses it since ejection cannot behin until ventricular pressure exeeds aortic pressure

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118
Q

What is the consequences of high arterial pressure?

A

Much of the contractle energy is consumed in raising ventricular pressure during isovolumetric contraction phase, leaving less energy for the ejection phase

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119
Q

What are the two different scenarios(experiments) diastolic stretch can be considered in?

A
  • isolated myocardium - cardiac tissue that has been taken from the whole organ
  • intact myocardium - whole heart invitro or invivo
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120
Q

When looking at contractile properties of isolated myocardium what is the pre load?

A

Preload is the force that stretches the cardiac muscle prior to contraction

121
Q

What is the isometric length tension relationship?

A

Shows that the active tension increases with stretch

122
Q

what is the afterload in the heart?

A

It is the amount of resistance the heart must overcome to open the aortic valve and push the blood volume out into the systemic circulation

123
Q

what does an increase in the afterload cause and what is this called?

A
  • Causes reduction in both rate and degree of shortening
  • this is called after-load shortening action
124
Q

What is the length of the sarcomere in the cardiomyocytes like during preload?

A

It is lengthened

125
Q

Length - tension relation - GO

A

If you start to stretch muscle the actin and myosin have more bonds and form more muscle contraction - if you keep pulling them appart there is less cross linking therefore less contraction

126
Q

Describe the relationship between calcium and tension?

A

It is sigmoidal - Stretch increases the fraction of cross bridges activated by a given calcium

127
Q

What would you see if there is a sudden increase in the height of the venous resovoir?

A

See a trace where the amplitude of those contractions are much higher than when you had venous resovoir lower down

128
Q

What do you increase when you increase that venous pressure?

A

The amount of blood going into that ventricle and out increasing its stretch and pre load so more force generated

129
Q

T/F a rise in CVP results in an increase in the output of both ventricles

A

True

130
Q

What is a venticular function curve?

A

A plot of stroke volume versus filling pressure

131
Q

starlings law of the hearts can be summerised as? ad what does this mean in an intact heart?

A

The energy of contraction of a cardiac muscle fibre, like that of skeletal muscle fibre, is proprtional to the initial fibre length at rest

In an intact heart this means the greater the stretch of the ventricle in diastole, the greater the stroke work achieved in systole

132
Q

What is central venous pressure?

A

It is the pressure at the enterence to the right atrium which determines the right ventricular end-diastolic pressure and resting distention

133
Q

What does the CVP depend on?

A
  • The total volume of blood in circulation
  • How the volume is distributed between the peripheral and central veins
134
Q

What is the mechanism called in which the CVP will alter SV through?

A

Frank-starling mech

135
Q

Name the 6 factors affecting CVP and hence SV

A
  • lower blood volume - due to 2/3 of blood in body is in venous system so heamorrphage or dehydration will recuce CVP and SV
  • sympathetic nerves regulate peripheral venous tone
  • venous muscle pump - rythmic excercise repeatedly compresses the deep veins of the limbs and displaces their blood centrally due to venous valves whihc increases CVP and SV
  • Increases CO reduces filling pressure
  • respirations effect on extramural cardiac pressure
  • increased extramural pressure impairs filling - this can occur with damage to pericardium like hardwire disease where infection causes pus to put pressure on heart
136
Q

Anything that increases systemic resistance (TPR) will oppose what?

A

The force generated by the heart to eject blood - this means the heart has to contract harded to get the aortic pressure up

137
Q

In the muscle strip experiment the greater the afterload the more shortening what is the equivelent of this in the intact heart?

A

Is an increase in arterial pressue and equivelent of shortening is a fall in SV

138
Q

What does chronic increase in arterial pressure result in?

A
  • LV undegoes concentric hypertrophy (chmaber wall enlarges but there is no chnage in chmaber size) induced by angiotension 2 and endothelin
  • Hypertrophy increases the contractile force for a while helping the ventricle to cope with hypertension
  • in longer terms however the overload ventricle often goes into failure
139
Q

What is intrinsic regulation of the heart?

A

It is the chnage in contractile energy caused by chnages in resting fibre length

140
Q

What is extrinsic regulation of the heart?

A

It is the change in contractile energy by external chemical factors

141
Q

when is sympathetic activity increased?

A

excercise
orthostatis
stress
heamorrhage

142
Q

What do left symapthetic fibers innevate at the heart?

A

Innervates atrial and ventricular myocardium

143
Q

What do the right fibers innervate at the heart?

A

The pacemaker conduction system

144
Q

What is the effect of noradrenaline on heart?

A

Rate of rise and total pressure are increased and rate of relaxation is much faster

145
Q

When is the only time the heart is fed with oxygen?

A

When it is relaxed due to the heart twisting as it contracts so closes off the coronary arteries that supplu the heart with o2 blood

146
Q

What is the functional classification of elastic arteries?

A

conduction (usually away from the heart)

147
Q

what is the functional classification of muscular arteries?

A

Distributing

148
Q

what is the functional classification of arterioles?

A

Resistance (to flow/regulate)

149
Q

what is the functional classification of metartioles?

A

Resistance (to flow and arterioles)

150
Q

what is the functional classification of capillaries and sinusoids?

A

Exchange

151
Q

what is the functional classification of post capillary venules, muscular venules and veins?

A

capacitance (reservoir)

152
Q

what are the 3 layers that make up a blood vessel?

A

intima, media and adventitia

153
Q

what is the vessel that is the exception to the 3 layers?

A

capillaries as they only have intima

154
Q

what are all blood vessels lined with?

A

endothelium

155
Q

Why is the tunica intima smooth?

A

To allow blood to travel with low resistance, covered in endothelium

156
Q

What does the mix of elastic tissue and smooth muscle determine in the tunica media?

A

Determines the recoil and constriction of the vessel

157
Q

what are the three subdivisions of afferent vessels in arterial system?

A
  • elastic arteries ie aorta and major branches
  • muscular arteries
  • arterioles
158
Q

What is the function of an elastic artery?

A
  • Conduction of blood at high pressures
  • the elastic component is like a shock absorbant to make blood more streamlined
159
Q

what is the vasa vasorum?

A

Small blood vessels in the adventia which nourish outer 2/3 of media and adventitia

160
Q

describe the structural components of the muscular artery?

A
  • intima
  • prominent internal elastic lamina between intima and media
  • media - mainly sm muscle under control of symapthetic system and elastic fibres
  • adventitia - composed of CT and vasorum
161
Q

Describe the structure assocaited with function of arterioles

A
  • peripheral resitance to slow rate of flow and cause drop in blood pressure
  • reguation of amount of blood enetering capillary bed via contraction
  • nourished by diffusion
162
Q

what is microcirculation?

A

varying the blood flow through capillary bed and the role of precapillary sphincters

163
Q

Where would you find Precapillary arteriovenous anastomosis microcirculation?

A

The skin and the small intestines

164
Q

what does the Precapillary arteriovenous anastomosis microcirculation consist of?

A
  • artery
  • vein
  • arteriovenous anastomosis
  • capillary plexus
165
Q

what two structural things do capillaries have to maximise exchnage?

A
  • thin wall
  • 2 way exchange between plasma and tissue fluid
166
Q

what is a pericyte? what are they omportnat for?

A

It is a cell that is associated with capillaries that is undifferentiated but can differentiate if needed. It is important in tissue repair

167
Q

what type of capillary is seen mainly?

A

continuous

168
Q

T/F continuous capilllaries are variably permeable depending on leakiness of cell junctional complexes

A

True

169
Q

Describe fenestrated capillaries

A
  • They have pores in the walls
  • you can get open and closed fenestrae which have a thin film over them
170
Q

what type of capillarys are seen at the liver and spleen?

A

sinusoids which have discontinuous endothelium and absent basal lamina

171
Q

what is the function og the efferent vessels in the venous system?

A

capasitance and storage

172
Q

what is the transition in function from post capillary to muscular venules?

A
  • exchanage to capacitance
173
Q

how would you distinguish venules from arterioles in histological section?

A

arterioles have thicker wall and 3-2 layers if sm musle
venules have thinner walls as it is lower pressure

174
Q

How would you distinguish arteries from veins in histological section?

A
  • Veins are designed for capacitence
  • have a thinner eall
  • they dont have internal elastic laminae
  • they have a thinner media
  • they have valves in larger veins
175
Q

what are the function of the valves in bigger veins?

A

Prevents back flow and pressure while acting as muscular pumps

176
Q

Describe the inter-relationship between the blood vascular and the lymphatic system

A

Lymphatic capillaries- blind ending – return excess tissue fluid to the blood vascular system

177
Q

describe what you would see histologically when looking at lymphatic vessels

A
  • lined with endothelium
  • lack basal lamina
  • thin walled
  • contains valves
  • carry lymph
178
Q

(heart and lung worms in cats and dogs)

How do animals become infected with Dirofilaria immitis?

A

By adult worms

179
Q

How does Dirofilaria cause pathology?

A
  • pathology is associated with the adults in heart as they impede blood flow giving rise to chronic congested right-sided heart failure
  • they can cause pulmonary embolisms (aduclt blcoking vessel), vena cava blockage, endocardidtis in valves and glomerulonephritis
180
Q

What are the clinical signs of D. immitis?

A
  • cadiovascular dysfunction
  • listless/gradual loss of condition
  • excercise intolerence
  • chronic soft cough
181
Q

Although there are clinical signs of D.immitis it is importnat to diagnose, how would you go about doing this?

A
  • radiography or echocardiography
  • detection of Microfilaraie in blood
  • detection of circulating antigen by ELISA - can detect single female byt not male worm (as antigen secreted by F)
    (best to test both)
182
Q

How would you control dirofilaria infection?

A
  • Prophylaxis is the basis of control
  • treated with macrocyclic lactones whihc kill L3/L4
  • in tropics treat all year round as there will be mosquitos all year
  • in temperate only treat in mosquito seasons 1 month before and till 2 months after
183
Q

what is an adverse effect of treating Microfilaraie positive dogs and what can counteract this?

A

can induce anaphylactic shock if high Mf counts and topical mocidectin seems to limit this

184
Q

How do animals get infected with Angiostrongylys vasorum?

A

infected by contact with slugs or snails (and usually from eating these)

185
Q

How does Angiostrongylus vasorum cause pathology

A
  • Pathology associated with adults in large vessels and eggs in pulmonary capilleries
  • chroni congestive cardiac failure
  • fibrosis in arteries
  • lung mottles
  • bleeding - coagulation defcets
186
Q

what are the clinical signs of A. vasorum?

A
  • Early on - asymptomatic
  • Later - increased respiratory rate/ cough on exercise

Can be associated with brain and spinal cord haemorrhage
Sub-cutaneous haematomas
Parasite excretory/secretory products interfere with blood clotting

187
Q

Although there are clinical signs of D.immitis it is importnat to diagnose, how would you go about doing this?

A
  • diagnossi baermann on a fecal sample after 3days
  • antigen test detects antigen in blood stream of infected dog
188
Q

( cardiac pathology 1+2)

what is preload and what is it dependent on?

A

Pre load is the initial stretch of cardiac muscle prior to contraction and dependent on venous return ie blood returning to the heart

189
Q

What is the afterload and what does it depend on?

A

It is pressure that chmabers must develop to eject blood during systole and depends on resistance

190
Q

Describe briefly in terms of output and congestion what happens during heart failure?

A

There is decreased output as less blood pushed into aorta or pulmonary artery
There is increased congestion due to inability to empty venous reservoirs

191
Q

T/F heart disease can be present without heart failure

A

True

192
Q

what are the 6 pathophysiological mechanisms of heart failure?

A
  • pump failure
  • obstruction to forward flow
  • regurgitant blood flow
  • shunted blood flow due to congenticla defects
  • heart/mahor vessel rupture
  • cardiac conduction disorders
193
Q

What is systolic heat failure?

A

normal filling of the ventricle and decrease in forward stroke volume

194
Q

what are the mechanisms leading to systolic heart failure?

A
  • failure of myocardium so decreased contractibility
  • volume overload increasing ventricular volume
  • pressure overload increasing ventricular colume
195
Q

what is diastolic heart failure?

A

improper filling of ventricles

196
Q

what are the mechanisms that lead to diastolic heart failure?

A
  • poor ventricular function
  • blockage of vesels preventing ventricular filling
  • pericardial abnormalities
197
Q

Give examples of myocardium failure?

A
  • dilated cardiomyopathy
  • mycarditis
  • doxorubicin toxicity
  • myocardial infarcts
198
Q

What are examples of causes of volume overload?

A
  • valvular diseases
  • ventricular septum defects, Patent ductus arteriosus or artrial septal defect
  • chronic anemia
199
Q

what examples can cause pressure overload in the heart?

A
  • subaortic stenosis
  • pulmonic stenosis
  • systemic hypertension
  • pulmonary hypertension
200
Q

what can ventricular hypertension be caused by?

A

HCM, subaortic stenosis, pulmonic stenosis, obstruction (heartworm), systemic hypertension

201
Q

what things can contribule to poor ventricular function?

A
  • ventricular hypertrophy
  • dilated cardiomyopathy
  • myocardial infarct
  • restrictive cardiomyopathy
202
Q

what does acute heart failure look like clinically?

A

May see intermittent weakness and syncope (not enough blood flow to the cerebrum) due to significant drop in cardiac output

203
Q

why would there be sudden death due to acute heart failure?

A
  • decreased cardiac output due to cardiogenic shock, failure to pump blood effectively
  • colume overload due to acute pulmonary congestion and/or systemically congestion
204
Q

what are the mechanisms of odema formation?

A
  • increased vascular permeability
  • increased hydrostatic pressure
  • decreased oncotic pressure
  • decreased lymphatic drainage
205
Q

what is congestive heart failure?

A

failure to empty veins leading to congestion and odeama. There is a gradual loss of myocardial pumping ability due to pressure overload or myocardial damage

206
Q

what is seen with right sided congestive heart failure?

A
  • increased right atrial pressure
  • systemic venous congestion
207
Q

clinically what is observed with right sided congestive heart failure?

A
  • jug distention
  • hepatic and splenic emlargement
  • ascites
  • periperal odeama
208
Q

what would you see with let sided congestive heart failure?

A
  • dilated left atrium
  • pulmonary congestion and odeama
209
Q

what are clinical signs you would see when left sided congestive heart failure is present?

A
  • dyspnoea and cough
210
Q

What does right sidead heart failure mean?

A

Failure of the right side of the heart means blood isn’t being pumped out to the lungs leading to hypoperfusion and therfore back pressure

211
Q

What might you see with left sided heart failure?

A

hypotrophy of systemic organs, back pressure in lungs, pulmanory oedema

212
Q

what is cardiogenic shock?

A

It s circulatory failure

213
Q

cardiac shock is an uncommen presentation of cardica disease, what are more commen types of shock?

A

hypovolaemic, vasogenic, neurogenic

214
Q

what happens in pulmonary oedema?

A

Macrophages move in and remove protein and extravasated red blood cells.

215
Q

what do you see in chronic pulmonary oedema?

A

In chronic pulmonary oedema, haemosiderin-laden macrophages within the alveoli may be numerous

216
Q

what are the siderophages (haemosiderin-laden macrophages) also known as?

A

Heart failure cells

217
Q

need to come back to this but its the 3 cycles of pulmonary oedema

A
218
Q

what are the different types of neuroendocrine responses to cardiac failure?

A
  • sympathetic activation
  • RAAS (renin-angiotensin-aldosterone system)
  • thromboxane
  • endothelin
  • Natiuretic peptides
219
Q

what is the mechanism of symp activation, RAAS, thromboxane and endothelin?

A

increase in rate & contractility, Salt & water retention and Vasoconstriction occurs.

220
Q

what is the mechanism of Natriuretic peptides (ANP;BNP)?

A

Counteract RAAS, diuresis and natriuresis and Vasodilation occurs.

221
Q

what is the benifit of the Sympathetic activation, RAAS, Thromboxane and Endothelin neuroendocrine responses?

A
  • increase in cardiac output
  • increase in preload > increase in cardiac output
  • increase in BP
222
Q

what is the benifit of the Natriuretic peptides neuroendocrine responses?

A
  • They increase tissure perfusion
  • inhibit maladaptive cardic/hypertrophy
223
Q

What harm can neuroendocrine responses to cardic failure cause?

A

Cardiac remodelling and myofibre dysfunction and a decrease tissue perfusion

224
Q

what can incresed pressure in the lungs cause?

A
  • failure of the right side of the heart
  • cardiac dilation and hypertrophy
225
Q

what are possible causes of increased pressure in the lung?

A
  • pulmonary disease
  • vascular disease
226
Q

Describe how hypoxia can cause cor pulmonale?

A

chronic hypoxia, pulmonary vasoconstriction and pulmonary hypertension causes cor pulmonale

227
Q

what is dirofilariasis?

A

physical obstruction in the vessels

228
Q

Describe accute cardiac compression

A
  • cardiac tampnade
  • rapid fluid accumulation
229
Q

Describe chronic cardiac compression?

A

Gradual accumulation of fluid causing constrictive pericarditis, +/- herniated tissue

230
Q

What are the 4 diseases of the pericardium?

A

Hydropericardium
Haemopericardium
Pericarditis
Hernia

231
Q

What is Hydropericardium?

A

When there is transudate in the pericardium

232
Q

Describe what you might see with hydropericardium?

A
  • generalise oedema
  • pulmonary hypertension
  • renal failure
  • hyperproteinamia
  • systemic diseases
233
Q

Describe primary conduction disorders and arrythmias

A

No morphological abnormality
May be ‘normal’ in some species / breeds- Often disappear with increased activity (horses, sighthounds)

234
Q

What is hemopericardium and what is caused by?

A

blood in the pericardial sac of the heart due to alteration in hydrostatic pressure between pericardial cavity, circulatory system and lymphatic system.

235
Q

Describe secondary conduction disorders and arrythmias

A

Atrial fibrillation in cardiomyopathy
Ventricular tachycardia in ventricular hypertrophy
Heart block following myocardial damage

236
Q

Give examples of inherited arrythmias in dalmations, mini schnauzers, german shepherds and alaskan sled dogs

A

dalmations - intermittent sinus arrest in deaf ones
mini schnauzers - in femals can have sinoatrial syncope
german shepherds - ventricular arrythmias and sudden death
alaskan sled dogs - conduction lesion that manifests as sudden death

237
Q

what is a syncope?

A

temporary loss of consciousness due to cerebral hypoperfusion

238
Q

what is sick sinus syndrome?

A

It is a group of disorders involving sino-atrial node with sometimes atrio-ventricular, the bundle of his

239
Q

Give an example of a neoplasia that can cause hemopericardium

A

hemangiosarcoma

240
Q

describe what you would see with chronic constrictive pericarditis

A

The heart is encased by dense fibrous tissue i.e. organised inflammatory exudate – fibrin (from blood fibrinogen) has been replaced by collagen from fibroblasts.
Pericardial sac is distended and pericardial wall is thickened. Epicardium = visceral pericardium.

241
Q

what are condruction dissorders?

A

abnormalities in the conduction pathways of the heart

242
Q

what is an arrythmia

A

It is a variation from the normal cardiac rhythm

243
Q

Mutations responsible for most inherited arrhythmias occur in genes encoding what?

A
  • cytoskeletal proteins
  • sarcomeric proteins
  • ion channels
244
Q

Describe what you would see with Bovine traumatic reticulopericarditis

A

Fibrinous debris lines the pericardial surfaces. On opening the pericardial sac the soft fibrinous adhesions break down revealing “Bread and Butter” heart

245
Q

What can cause Hemopericardium in dogs?

A

atria rupture

246
Q

(branching of the aorta part 1)

Development of the aorta, pulmonary arteries and ductus arteriosus

A
  • There are 6 aortic arches surround primitive pharynx in the foetus
  • Aorta develops left 4th aortic arch (Mammals) which curves around and forms definitive aorta
  • Pulmonary trunk develops ventral parts of R & L 6th aortic arch
  • Ductus arteriosus develops dorsal part of left 6th aortic arch the right doesn’t last as long

come back to this!!!

247
Q

Describe the pattern of coronary circulation in different species

A
  • Dogs and ruminants - the right interventricular branch is a continuation of the left coroanry artery
  • horse and pigs - the right interventricular brnach is a continuatuion of the left coronary artery
248
Q

List the major branches of the aorta as it leaves the base of the heart

A

carnivore
- one major trunk called brachiocephalic trunk
- coming off of this is 3 branches - L and R common carotid artery and R subclavia
- L subclavia makes seperate branch coming off distal to the initaial branch

Horse and cow
- alll 4 maojor branches come off the one branch (brachiocephalic trunk)

Pig
- Has a pattern in which subclavia both come off at slighty diff positions

249
Q

T/F each common carotid artery divides into an external and internal carotid artery above the larnyx in the dog

A

True

250
Q

What are the main branches of the external carotid artery?

A

Facial and superficial temporal artery

251
Q

What so the branches of the internal cartotid artery contribute too?

A
  • enters cranial cavity (via gutteral pounch in horse)
  • contributes to arterial circle of brain (horses and carnivores so not ruminants)
252
Q

what does the branching of the R and L subclavian artery supply?

A

Forelimb and structures of neck and cervico-thoracic region

253
Q

What are the 4 branches of the subclavian artery?

A
  • Vertebral artery
  • Costocervical artery
  • superficial cervical artery
  • internal thoracic artery
254
Q

Where does the L vertebral artery run?

A

Runs Cranio-dorsally via transverse foramina to enter vertebral canal within the atlas.

255
Q

what arteries does the left L vertebral artery form?

A
  • basilar artery
  • ventral spinal artery
256
Q

what does the L costocervical artery form?

A

Forms 1st few dorsal Intercostal aa. & Deep Cervical a.

257
Q

what doe sthe L superficial cervical artery supply?

A

Supplies ventral neck muscles, cranial shoulder and upper forelimb.

258
Q

Describe the two ways the L internal thoracic artery goes and what does it form?

A
  • Passes bet. sternum and transversus thoracis m. which forms ventral intercostal aa/ Musculo-phrenic a.
  • Tunnels beneath diaphragm into abdomen. which forms Cr. Superficial /deep Epigastric aa.
259
Q

After branching what does the L subclavian continue as?

A

L axillary a.

260
Q

what does the L Axillary a. supply?

A

Supplies lateral chest wall and forelimb

261
Q

(Branching of the abdominal aorta & the origins of the vena cavae & azygos veins)

List the visceral branche sof the abdominal aorta and comment on the structures or areas of the body they supply

A

visceral branches
- celiac artery - foregut
- cranial mesenteric artery - hindgut
- renal aa. - kidneys
- testicular or ovarian aa. - gonads
- caudal mesenteric a. - hindgut

262
Q

List the partial branches of the abdominal aorta and comment on the structures or areas of the body they supply

A
  • Phrenico-abdominal aa
    caudal phrenic aa - diaphragm, cranial abdominal aa - cranial lateral wall of abdomen
  • 4th lumbar aa.
  • 5th lumbar aa.
  • deep circumflex iliac aa. - caudal abdom, flank and cr thigh
  • median sacral a. - tail
  • External iliac aa.
    femoral aa (hindlimb)
    deep femoral aa (adductor muscles of thigh)
  • Internal iliac aa.
    Caudal gluteal aa.
    internal pudendal aa.
263
Q

Describe the origins of the vena cavae - dog, cat and pig

A

Beyond the enternace to the thoracic cavity the cranial vena cava will already be formed
- external and internal jugular veins join with R and L subclavian veins which from the R and L braciocephalic veisn that come together to form vena cava

264
Q

Describe the origins of the vena cavae - ruminant and horse

A

The difference here is the external and internal jugular vein fuse together before joining the R and L subclavian veins which goes onto form vena cava without brachiocepahlic veins

265
Q

How is the external jugular vein formed

A

maxillary vein and linguofacial vein join here to form ext jug that continue down neck

266
Q

comment on the pattern of venous return to the heart

A
267
Q

Describe the path of the gut venous system?

A

the gut venous system passes through the liver via the hepatic portal veins and then after the liver the venous blood is brought to the caudal vena cava by hepatic vein and heads straight to the right atrium

268
Q

(Control of Blood Vessel Function)

Why is basal tone important?

A

If vessel fully constricted can’t constrict more and fully dilated vessel wont dilate anymore

269
Q

what tissues have the highest basal tone?

A

Ones with the highest blood flow

270
Q

what influences basal tone?

A
  • local and extrinsic factors - dominace is dependent on the tissue
271
Q

where does local control dominate?

A

critical tissues where there must be enough blood to meet metabolic needs on a second to second basis for survival

272
Q

what are critical tissues?

A

Brain, heart, skeletal muscle

273
Q

where does extrinsic control dominate?

A

Tissues that can withstand a temporary decrease in blood flow

274
Q

What tissues can withstand a temporary decrease in blood flow?

A

Kidneys, splanchnic, resting skeletal muscle

275
Q

T/F skin is an example of both local and extrinsic control?

A

True babes

276
Q

How is local temp importnat in skin?

A
  • Heating the cutaneous arteriole and veins will cause dilation
  • cooling them will cause constriction
277
Q

what can mechnical compression lead too?

A

Can lead to ischemia and infarction

278
Q

What are the physiological examples of mechanical compression?

A
  • coronary flow - when heart contracts it constricts coronary muscles therefore only recieves blood during diastole
  • skeletal muscle contraction - as you walk these contract meaning the blood goes back to heart rather than falling back down to feet
279
Q

what is myogenic response?

A

the contraction of a blood vessel that occurs when intravascular pressure is elevated

280
Q

what is metabolic vasodilatation?

A

Where many by-products of normal tissue metabolism cause vascular relaxation – thus any increase in metabolic rate of a tissue causes arteriolar dilatation and increases local tissue perfusion.

( organ feeds back to the blood vessel so when more metabolically cative produce more bi products to ie liver give more blood )

281
Q

What are autocoids and what do they do?

A

They are vasoactive chemicals produced, released and act locally
Have differing effects on VSM some causing vasodilatation (bradykinin, PGE/I) some vasoconstriction (5HT,PGF) some mixed histamine dilates arterioles, constricts veins.

282
Q

Local mechanisms serve only local needs so what happens to serve general needs?

A

The CNS imposes control system over the circulation.

283
Q

When are the endocrine secretion important in terms of control of circulation?

A

If neural control is impaired or in pathological conditions

284
Q

what is the most important hormone in cardio and why?

A

adrenaline - Secretions are made in response to exercise, fear, fight, flight reactions, hypotension, hypoglycaemia

285
Q

What is the end effect of the baroreflex?

A

The response is usually aimed at stabilising blood pressure

286
Q

What does increaes pressure in artery cause?

A

distension and this excites the receptors

287
Q

Describe the BR response to stretch

A
  • The BR response shows similarities to responses seen in type 1a fibres from muscle spindles with a greater response during the change in pressure
  • Increased firing during pressure rise, no firing during reduction

(So normally their response is bursts of firing during systole)

288
Q

T/F sick sinus syndrome is usally Idiopathic?

A

True - they may have ischeamia of heart or fibrosis of SA node and potentailly inherited in some breeds

289
Q

Describe first degree heart block

A

A delay of impulse through AV node

290
Q

Describe second degree heart block

A

Intermittent failure to conduct through AV node with dropped beats

291
Q

What animal is a second degree heart block normal?

A

Horse

292
Q

Describe third degree heart block and what is it assocaited with?

A

Complete block through AV node and is associated with areas if myocardial scarring in horses and dogs.

293
Q

Describe the normal microanatomy of the heart

A
  • straited muscle with centrally located nuclei
  • myofibers are branching
  • purkinje fibers
  • intercalated discs
294
Q

What do intercalated discs form?

A

They form a zigzag interconnection between each cardiac muscle cell and are observed to cut across the muscle fibers.

295
Q

what are purkinjie fibers?

A

Modified fibres that conduct electrical stimuli through the heart

296
Q

what are physiological changes to myocardium that can be seen?

A
  • atrophy - where cells get smaller
  • hypertrophy - Where cells grow in size
297
Q

Describe concentric hypertrophy

A
  • increase in myocyte width due to addition of sarcomeres in parallel
  • pressure overload
298
Q

What are examples

A

BVMS 2 (18 decks)

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