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Semester 2 > cardiovascular 1 > Flashcards

cardiovascular 1 Flashcards

1
Q

what are the two parts of the extracellular fluid and function

A

1) Blood plasma
2) Interstitial fluid - (site of metabolic exchange) - middle man - take fluid from capillaries to the cells as some cells don’t have direct access to the circulation (unlike liver (hepatocytes and heart cells)
- Exchange takes place between intracellular fluid and interstitial fluid

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2
Q

list 4 factors effecting diffusion rate

A
  1. Concentration difference
  2. Surface area
  3. Diffusion distance - very rapid over 5-7um not 1cm - need thing cell wall
  4. Permeability to that substance
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3
Q

interstitial fluid where released, where reabsorbed

A
  • Released from the arterial ends of capillaries
  • 90% reabsorbed at venous end of capillaries
  • 10% returned to CVS via the lymphatics
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4
Q

what is needed for flow to occur and what can flow be altered by

A
  • pressure difference
    Therefore blood flow can be altered by:
    1) changing the pressure difference across its vascular bed
    2) or by changing its vascular resistance.
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5
Q

vessels in series and parallel how does resistance occur

A

largest pressure drop will occur in the part having the greatest resistance to flow: arterioles
parallel - resistance to flow in a parallel network of vessels is given by Ohm’s law - overall resistance for any parallel network will always be less than the resistance of any of the elements of the network

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6
Q

heart and circulation in a fish what is the greatest advantage and greatest disadvantage

A

advantage is that the blood passing through the gills is fully oxygenated when it moves into the tissues.
limitation is that in passing through the gills, blood loses much of its pressure developed by contraction of the heart
- This limits rate of oxygen delivery to the rest of the body as limits flow

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7
Q

what occurs with systole and diastole

A

Systole:•Muscle contraction → increased pressure→ blood flow from heart into blood vessels
Diastole:•Muscle relaxes → pressure falls below atrial pressure → ventricle fills through AV valve

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8
Q

what are the 3 things needed for effective functioning of the heart

A

1) conductivity
2) contractility
3) autorhythmicity

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9
Q

position of the heart, size of heart and shape of the heart

A
  • Between 3rd and 6th rib
  • 3rd, 4th or 5th intercostal space
  • Slightly towards the left side
    size - 0.6% of total body weight
    shape - cone shape in horses and ruminants, more globular in small animals
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10
Q

pericardium how many walls and function

A 
Inner wall -
- Single layer of flattened mesothelium
- Visceral pericardium (inner pericardial sac layer)
•Outer wall - two layers
1. Inner parietal pericardium
2. Outer fibrous pericardium - hard to tear 
•Pericardial cavity
- Occupied by thin film of serous fluid - lubricant
Functions of the pericardium
•Protective
•Help maintain position
•Minimise friction during cardiac cycle
•Prevent over-distension of the heart
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11
Q

where is the site for performing pericardiocentesis

A

Typical site - 4th or 5th intercostal spaces

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12
Q

what is the auricle, where is it found and what is the most cranial part of the heart

A

auricle - blind diverticulum
right and left auricles curve around the origin of the pulmonary trunk
right auricle most cranial part of the heart

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13
Q

what is the left surface and right surface of the heart called and what parts of the heart are in those areas

A

•Left lateral surface of the heart (auricular surface)
- Left atrium and left ventricle
- Right ventricle and right auricle extend around the cranial border
•Right lateral surface of the heart (atrial surface)
- Right atrium and right ventricle
- Left ventricle and left atrium extend around the caudal border

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14
Q

what are the grooves within the ventricle and what do they mark

A

○ Left interventricular groove (or paraconal)
○ Right interventricular groove (or subsinuosal)
- mark the interventicular septum

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15
Q

what are the four main openings in the right atrium and where do they come from

A

1) cranial vena cava - drains neck, head, forelimb
2) caudal vena cava - abdominal viscera, hindlimbs, abdominal wall
3) coronary sinus - from heart itself - ventral to caudal vena cava
4) right atrio-ventricular opening - guided by A-V valve

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16
Q

small coronary veins and azygous vein where drain and when present

A 
coronary - heart supply 
azygous - part of lumbar region, bronchial circulation and oesophagus 
right in carnivores 
left usually in pigs 
both in ruminants
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17
Q

what are the 3 vestigaes of the fetal circulation in right atirum

A

1) fossa ovalis - depression on interatrial septum
2) intervenous ridge (tubercle) - directs blood from cranial vena cava into ventricle
3) cista terminalis - muscular ridge on internal surface of right atrium

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18
Q

entry into the right ventricle what guarded by and what made from

A
  • guarded by the tricuspid valve - prevent backflow of blood back into atrium
    ○ Three thin flap-like cusps
  • Cusps are composed of a layer of collagen fibres between two layers of endothelium
    ○ Free edge of cusp - restrained by chordae tendineae
    ○ Chordae tendineae arise from papillary muscles
  • Fan out to attach to the cusps of the A-V valve
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19
Q

where is the right septomarginal trabeculae found and what parts

A

right ventricle
2 functional components
1) inflow channel - 3 papillary muscles
2) outflow channel - (conus arteriosus) - directs blood into pulmonary trunk

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20
Q

pulmonary valve structure

A

3 semi-lunar valves

3 buldges in the wall of hte pulmonary trunk

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21
Q

left ventricle what valve guarding entry and structure

aortic valve what enter into and structure

A

atrioventricular (mitral) valve
2 cusps and 2 papillary muscles arise from outer wall
3 semi-lunar valves
left coronary artery from left aortic sinus
right coronary artery from right aortic sinus

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22
Q

list the openings into the left atrium

A

1) 6 pulmonary veins
2) small coronary veins
3) left A-V orifice into left ventricle

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23
Q

what is the cardiac skeleton made up of and function

A

fibrous rings to which valves are tethered

1) ensure heart doesn’t tear with force of pressure
2) blocks electrical impulses so only one way for impulses to move through to ventricle via AV node - stops random contraction of ventricle when not filled

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24
Q

where are the valves of the heart positioned in terms of ribs

A 
Left hand side
- 3rd intercostal space- pulmonic 
- 4th intercostal space - Aortic 
- 5th intercostal space - Mitral - most caudal - hear heart sound the loudest
Right hand side 
- Tricuspid valve
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25
Q

what are the 3 parts of the aorta and what comes off where

A

ascending aorta - supplies blood to wall of heart - left and right coronary arteries
aortic arch - 1-3 major branches (species variation)
1) brachiocephalic trunk
branches - left and right common carotid artery and right subclavian artery
2) left subclavian artery
descending aorta

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26
Q

left and right subclavian arteries what 4 main branches do they give rise to and what do they supply

A

1) vertebral artery - cervical muscle, spinal cord and brain
2) costocervical artery - muscles at base of neck, intercostal spaces
3) internal thoracic artery - thoracic wall
4) superficial cervical artery

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27
Q

how do ions move into cardiac myocytes and what ions are important to action potentials

A

1) receptor operated ion channels
2) voltage operated ion channels - once opened almost immediately inactivated
- depends on the entry of Na+ and Ca2+ into the cell

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28
Q

what are the phases of an action potential

A

Phase 0
- entry of Na through voltage gated sodium channels
• Phase 1
- Early repolarisation due to efflux of K+
• Phase 2
- Plateau due to entry of Ca through voltage gated Ca channels
• Phase 3
- Repolarisation with efflux of K+
• Phase 4
- Restoration with exchange of Na for K+

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29
Q

describe the refractory period in cardiac myocytes

A

cells in absolute refractory period fro most of action potential as Na+ voltage gates channels inactive quickly and don’t reactivate until voltage more -ve than -65mV - cannot be tetanized
-relativew refractory period can be present at more negative potentials as channels reactive and large stimulus can activate

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30
Q

where are pacemaker cells present, what does the AP depend on and characteristics of the AP

A 
sinoatrial node and atroventricular node 
Ca2+, Na+ and K+ movement 
1. Slow depolarization
2. Lower amplitude AP
3. Shorter plateau
4. Unstable resting potential
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31
Q

what is the ionic basis of the pacemaker AP

A

1) increased permeability to Na+ so RMP tends towards threshold
2) no voltage operated Na+ channels
3) depolarisation occurs due to entry of Ca2+ through VO Ca2+ channels
4) threshold for depolarisation more positive due to dependence on VO Ca2+ channels

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32
Q

autorhytmic tissues in heart, are they all the same, if not what does this mean

A

different rates of depolarization - faster decay - faster rate
SA node fastest rate of decay therefore set the rate for other tissues before they decay themselves - SINUS RHYTHM

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33
Q

purkinje cells histology

A

very large diameter, pa,e central area due to glycogen and marginalisation of myofibrils around the periphery

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34
Q

what does conduction velocity of an AP depend ion

A
  1. Shape of action potential: faster upswing generates greater local currents and more rapid conduction
  2. Diameter of muscle fibre- larger diameter eg Purkinje fibres lead to faster conduction
  3. Disease states ( with changes in plasma electrolyte levels) change ionic conductance ( eg hyperkalaemia in renal disease)
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35
Q

What are the 3 layers of the heart

A

1) Endocardium
1. Endothelium - layer protects blood
2. Inner subendothelial layer
3. Outer subendothelial layer
2) Myocardium
- Bundles of cardiac muscle cells
3) Epicardium
- Mesothelial cells of visceral pericardium
- Subepicardial connective tissue
Adipose tissue is found under the epicardium

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36
Q

how does cardiac myocotyes differ from skeletal muscle

A
  • Intercalated discs, central nuclei (usually one but sometimes two) with perinuclear space, branched fibres, good blood supply (respiration is aerobic at all times)
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37
Q

calcium source percentages for cardiac myoctyes and what stimulates calcium release

A

○ 20% of the rise in intracellular Ca enters cell through VO (voltage operated) channels
○ 80% of the rise in intracellular Ca contributed by release from sarcoplasmic reticulum - initiated by Ca sensitive release channels- ryanodine receptor channels

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38
Q

what contributes to cardiac muscle refractory period and how does muscle relaxation occur

A
  • Ca release from SR contributes to the plateau phase of the AP, and hence to the refractory period - ensuring tetanus doesn’t occur
    Relaxation
    1) Active pumps return Ca to :
  • Sarcoplasmic reticulum
  • Extracellular fluid
    2) Calcium exchanged for extracellular Na
    3) Intracellular Calcium concentration falls
    4) Myocyte relaxes
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39
Q

length-tension relationship what generates tension and what effects does it have

A

1) intracellular Ca2+ levels
2) length of myocyte - overlap of thick and thin filaments (determined by amount of blood in ventricle)
- at certain length overlap is optimal however if increase more fibres no longer overlapping so can no longer increase tension
- normal cell length is less than maximal so can increase if need b e

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40
Q

difference between isotonic and isometric contraction

A

isotonic - activating unrestrained muscle shortens without force development
isometric - muscle develops force at fixed length so able to develop tension - cardiac contraction before valves open

41
Q

contractility define, how to change

A
  • The amount of tension that can be developed at any given stretch of cardiac muscle
  • adjusted physiologically and pathologically
  • Inotropes are agents (physiological or pharmacological) that alter contractility
  • increased by an increase in intracellular calcium concentration
  • Intracellular calcium can be modulated by
    ○ Receptor Operated Ca channels on cell membrane
    ○ Ryanodine channels on SR
  • Modulation can be
    ○ Physiological (Noradrenaline, adrenaline at B receptor)
    ○ Pharmacological (inotropic drugs)
    +ve ionotrophic increase
    -ve ionotrophic decrease
42
Q

electrocardiogram what occurs when cardiac muscle depolarizes

A

extracellular currents between depolarised and resting cells cause potential differences that can be measured at the body surface
- therefore records charge difference of one cell compared with another cardiac cell from different area

43
Q

electrocardiogram when get positive, negative or no wave with resting cell, depolarisation, depolarised and repolarisation

A

resting cell - protein within negative so cell positive - no flow as no dipole
depolarisation - surface relatively negative so dipole between cells not depolarised and cell that are - current flow from -ve to +ve therefore positive wave
depolarised - no current flow all -ve so isoelectric point
repolarisation - some repolarised +ve others repolarising -ve dipole but negative wave

44
Q

the magnitude of the wave or dipole in electrocardiogram depends on what 2 things

A
  1. how many cells are depolarising at that instant - heart mass
  2. vector analysis of simultaneous dipoles (produced by movement of AP from SA node and the separation)
45
Q

einthovens hypothesis what are the 5 interpretations that are needed and limitations to these

A

1) body conducter - not true homogenous conducter
2) arms and legs to trunk are equal length - not so much in quadrupeds
3) limbs behave as linear conducters
4) heart at center of leads on limbs - often not at centre
5) difference in potentials recorded between leads represent dipoles orginating from dipole in the heart - moving limbs in quadrapeds alters amplitude and direction of potentials

46
Q

what does each part of the ECG represent: P wave, QRS complex, T wave, P-R, S-T, T wave

A

P wave - depolarisation of the atria
QRS complex - ventricular depolarisation
T wave - ventricular repolarisation
P-R - delay through the AV node
S-T plateau of ventricular muscle AP potential
T wave - repolarisation of ventricles - variable (-ve or +ve) as can be masked from depolarising ventricle

47
Q

what is the mean electrical axis of the heart

A
  • Is the orientation of the ECG vector at its maximum amplitude - from right arm to left leg
48
Q

what is a sinoatrial and atrioventricular block

A

Sinoatrial block: impulse blocked before it enters atrial muscle so no P wave - SA node not working
• Atrioventricular block:
- transmission through AV node either slowed or completely impeded
- P waves (seen but) not always related to QRS complex - need to have ECG to figure out

49
Q

what are the degrees of atrioventricular block and what characterised by

A

first degree - slow conduction through AV node - abnormally long PR internal
second degree - some but not all impulse transmitted through AV node - atrial rate often faster than ventricular
third degree - complete block without P wave and QRS complex - area in ventricle assumes pacemaker role

50
Q

what occurs with premature atrial and ventricular contractions

A

atrial - area or atrium escapes normal pacemaker control - may or may not be followed by ventricular contraction
ventricular - not preceeded by P wave - reduced stroke volume and reduced cardiac output

51
Q

paroxysmal tachycardia what is it and where may aris e

A

a tachycardia arising from ectopic pacemaker
onset and termination generally abrupt
1) atrial or AV node
2) ventricles more serious as ventricular filling and contraction incomplete - may progress to fibrillation

52
Q

what is fibrillation and what does atrial and ventricular fibrillation lead to

A

rapid completely disorganised conduction pathways
atrial - disorganised atrial activity and conduction, irregular ventricular rhytm, no P waves on trace - reversible with medication
ventricular - more serous as may result from major myocardial infarction, loss of consciousness within a few seconds
resuscitate with electric shock - defibrillation as give chance for pacemaker to take over again

53
Q

Development of submandibular oedema in the cow with hardwire disease

A
  1. penetration of pericardial sac by foreign body
  2. inflammatory response to contaminated foreign body
  3. fibrinopurulent discharge accumulates in pericardial space
  4. reduced capacity of pericardium to distend during cardiac filling and/or compression of right ventricle during filling
  5. reduced filling of right ventricle during diastole
  6. increased hydrostatic pressure in great veins
  7. distension of jugular veins
  8. increased hydrostatic pressure at venous end of capillary
  9. reduced reabsorption of fluid at venous end of capillary
  10. increased net filtration in capillary beds
  11. increased fluid content in extracellular space- oedema
54
Q

heart valve function and how does it open and close and what are the papillary muscle function

A
  • Movements of valve leaflets are essentially passive - blood pressure makes them close
  • Orientation of valves is responsible for unidirectional flow.
  • Valve opens when pressure in proximal chamber exceeds pressure in the distal chamber.
  • Valve closes when pressure in the distal chamber exceeds pressure in the proximal chamber.
  • Papillary muscles do not help close valvular orifice, but prevent excessive bulging of valves into atrial chambers during ventricular contraction.
55
Q

what are the general steps in the cardiac cycle

A

1) SA node initiates AP
2) atrial systole
3) ventricular systole
1. isovolumetric contraction
2. rapid ejection
3. reduced ejection
4) ventricular diastole
1. isovolumetric relaxation
2. rapid ventricular filling
3. reduced ventricular filling
5) end of diastole

56
Q

what occurs with atrial systole

A

contraction of atria completes ventricular filling
80% of ventricular filling occurs due to venous pressure (direct flow from veins to ventricle)
no valves between atria and great veins so some regurgitation
EDV - end diastolic volume

57
Q

what occurs with ventricular systole

A

1) isovolumetric systole - QRS complex - increase in pressure causing AV valves to close and bulge into atria causing atrial pressure wave (c wave)
2. rapid ejection - ventricular pressure above diastolic arterial pressure (80mmHg) so semilunar valves open flow into aorta - rapid
3. reduced ejection - no blood flow but ventricle still contracting, aortic pressure begins to decline and blood reverses briefly to close aortic and pulmonary valves, muscle beings to repolarise T wave and blood from veins fills up atria - v wave

58
Q

what occurs within ventricular diastole

A

isovolumetric relaxation - following closure of valves ventricle relaxes rapidly but ventricle still higher than atrial so AV valve closed

  1. rapid ventircular filling - ventricular pressure falls below atrial so AV valves open and rapid ventricular filling - assisted by elastic recoil of ventricular walls that suck in blod
    3) reduced ventricular filling - ventricles completely relax and refilling slows
59
Q

what occurs at the end of diastole

A

all chambers are relaxed
AV valves open
pulomnary and aortic valves closed

60
Q

why get pressure waves in the systemic arteries

A
  • Ejection of blood from the heart results in pulsatile flow in the arteries
61
Q

what is the major difference between the right and the left heart

A 
stroke volume must be equal but pressure are a lot different 
systolic 
right - 25mmHg 
left - 125mmHg
diastolic 
right - 8mmHg 
left - 80mmHg
62
Q

heart sounds what does all correspond to

A

1st and 2nd are start and end of venticular systole
1st - closure of AV valves
2nd - closure of outlet valves
3rd - mid diastole entry of blood into ventricle - can only really hear in horses
4th - atrial contraction

63
Q

define murmur, stenosis, incompentence and gallop rhythm in terms of abnormal heart sounds

A

murmurs - turbulent blood flow - hole in heart, thin blood, valve defects
stenosis - narrowing of orifice flow become turbulent
incompetence - valve leaks blood while closed, regurgitation hear as dull roar
gallop rhythm - a duplication of splitting of the first or second heart sound - triple sound - normal in dairy cows

64
Q

what can cyanosis be due to

A

severe respiratory compromise - blue tinge
- In cardiac disease this usually indicates severe pulmonary oedema or pleural effusion - problem with oxygen transfer in the lungs
Congenital shunts
pulomary stenosis or hypertension
differential cyanosis

65
Q

what is differential cyanosis

A

normal cranial membranes & cyanotic caudal membranes (vaginal) - cyanosis to the caudal part of the body, abdominal flow of blood through patent ductus arteriosus (pulmonary artery to the aorta as when in foetus don’t need to go the lungs - some dogs don’t have the muscle to contract and close off this hole so blood doesn’t go to the lungs and less oxygenated to the caudal part of the body (blood already gone to the head before PDA which is why its caudal)

66
Q

what can cause a bounding pulse and a weak pulse

A
  • Bounding pulse
    ○ PDA - Patent ductus arteriosus - some blood goes from aorta to pulmonary artery - drop in diastolic pressure
    ○ Aortic insufficiency - leaky aortic valve - drop in diastolic pressure
  • Weak pulse
    ○ Shock - poor cardiac contractility
    ○ Cardiac tamponade - fluid between pericardial sac and heart - pushing on the heart
    ○ Aortic stenosis - narrowing of aorta - hard to push out blood
    ○ Clot - rare in dogs not so rare in cats
67
Q

respiratory rate what is normal for cats and dogs, what is sign of congestive heart failure and what does cough mean

A
  • Dogs and cats sleeping respiratory rate is normally
68
Q

where does systole and diastole occur in terms of heart sounds therefore when hear systolic and diastolic murmur

A

S1 to S2 = systole - systolic murmur (same time as pulse)

S2 to S1 = diastole - diastolic murmur (between pulses) - rare

69
Q

what is the point of maximal intensity

A

The PMI is usually described by the hemithorax, valve area or base/apex location where the murmur is the loudest.

70
Q

timing of the murmur changes the type of murmur what are the 4 times

A
  • Holosystolic - both S1 and S2 still audible - between S1 and S2 still - lupp shh dupp
  • Pansystolic - both S1 and S2 not discernible - just hear the murmur - shh shh shh
  • Diastolic - To and Fro (systolic and diastolic but with gap) - continuous sounds generally caused by PDA
  • Continuous - occur throughout systolic and diastolic
71
Q

how to grade cardiac murmurs

A

mild - hear both S1 and S2
moderate - don’t hear S1 and S2 but don’t feel vibration
severe - feel vibration

72
Q

what are the 3 types of murmur classified with character and what generally caused by

A

1) systolc ejection - begin and end abruptly, cresendo and decresendo
- narrowing of valve - pulmonary or aortic
2) systolic plateau - begin and end abruptly, no change in frequency
- leaky valve - generally mitral or tricuspid regurgitation
3) musical - high frequency - mitral valve tiny leaks causing vibration

73
Q

what is resistance determined by, and what is pressure maintained by modulation

A

resistance to flow throughout the vascular tree- mainly determined by resistance in the arterioles
need to modulate cardiac output and arteriolar resistance

74
Q

what are the 2 ways to increase stroke volume

A
  1. Increasing muscle length ( venous return).. The Frank Starling principle
  2. Increasing contractility ( force generated for any given length) .. By increasing intracellular Ca during contraction by giving positive ionotrophs
75
Q

difference between increasing force of contraction between cardiac muscle and skeletal muscle

A

In skeletal muscle – force is increased by increasing
○ Frequency of action potentials
○ Number of fibres stimulated ( recruitment)
- In cardiac muscle:
○ Action potential frequency is determined by SA node - beat
○ Increased force of contraction (at any given fibre length) depends on intracellular Calcium concentration
§ Intracellular calcium concentration:
1. depends on entry of Ca through VOCC
2. release of Ca from sarcoplasmic reticulum
- Both of these are modulated by cell surface receptors

76
Q

list 4 rules of thumb for the canine cardiac size on radiographs

A

1) lateral view cardiac length should be about 70% of the dorsal to ventral distance of the thoracic cavity
2) lateral view the width of the heart should be 2.5-3.5 intercostal spaces wide
3) DV view cardiac width 60-65% thoracic width
4) sternal contact 2.5-3 sternebrae

77
Q

what is the rule of thumb with cardiac size in cats

and the vertebral heart scale for both

A

1) lateral width no more than 2-2.5 intercostal spaces width
normal range 9.7 vertebrae +/- 1 vertebrae

78
Q

what look for with lateral and ventrodorsal projection with cardiomegaly

A

lateral
- elevation of the trachea
- increased craniocaudal diameter of heart
- cranial bulging of right heart border and increased sternal contact
ventrodorsal
- increased transverse diameter (width) of heart
- increase rounding and elongation of heart borders
- valentine shape heart (cat) or bulging left heart (dog)

79
Q

Echocardiography what are the 3 tests to run and what do they achieve

A

1) B mode - image of the heart
2) droppler or spectral - can be added to B mode to see movement through the heart
3) M mode - movement of the heart walls - measure contractility of the heart

80
Q

horse atrial fibrillation what causes it and why are horses predispose

A
  • Spontaneous - no evidence of cardiac disease - common in horses
    ○ Predispose as heart is already large
  • Large vagal tone - Random contraction of atrial muscle as less likely to cause depolarisation of the AV node due to the space from the conduction pathways
    ○ Therefore the heart rate only increases moderately
81
Q

why is there an irregular rhythm with atrial fibrillation

A
  • SA node not undergoing its pacemaker activities
  • At some point there is a high enough coordinated AP within the atrium to depolarise AV node and therefore cause a heart beat
  • However the F waves and absence of P waves are due to the uncoordinated contraction of the atrium due to the absence of pacemaker activity from the SA node
82
Q

dog atrial fibrillation what causes it

A
  • Generally with dogs atrial fibrillation is caused by underlying cardiac disease resulting in increase in heart size
  • Dilated cardiomyopathy - abnormally large left ventricle resulting in decrease in ventricular filling
    ○ Atrial fibrillation generally occurs in larger hearts
  • Almost all contraction of the atrial muscle all can depolarise AV node and therefore increase in heart rate - inadequate heart filling - wearing out of the heart - decrease prognosis
83
Q

goal of treatment of horse with atrial fibrillation, treatment options and will it occur again

A
  • Goal is to restore normal sinus rhythm provided there is no underlying cardiac disease (generally not in horses)
    ○ Achieved using drug quinidine - administered orally, blocks the sodium channels on the muscle cell membrane
    ○ Toxic side effects - anorexia, depression, incoordination, colic
  • Likelihood of horse getting back into atrial fibrillation is much greater if it has been going on for more than 3 months
84
Q

goal of treatment for dog with atrial fibrillation and what drug used

A
  • Goal is to slow impulses through AV node in order to slow heart rate, allowing more time for ventricular filling and increasing cardiac output
  • Generally not possible to restore normal sinus rhythm due to it commonly being caused by underlying cardiac pathology
  • Digoxin - first line of treatment can also use calcium channel blockers and beta blockers
85
Q

what are the 3 layers of blood vessels and what vessels don’t have all 3 layers

A

1) tunica intima
2) tunica media
3) tunica adventitia
capillaries on;y have one layer of endothelial cells

86
Q

arteries what are involved with each wall layer

A

1) tunica intima - endothelial cell, basement membrane, subendothelial connective tissues, internal elastic membrane
2) tunica media - layers of smooth muscle and elastic fibres, external elastic membrane
3) tunica adventita - collagen and elastic fibres that bends with surrounding connective tissues

87
Q

difference between veins and arteries structure

A
  • The internal and external elastic membranes are absent.
  • The amount of smooth muscle and elastic fibres in the t. media is relatively small
  • collagen fibres are relatively abundant.
    Many collagen fibres in the adventitia - often the thickest layer of the wall
88
Q

what are the functional significance of components of blood vessel walls

A

1) endothelium - confers low frictional resistance to blood flow, immune system, prevent clotting
2) elastic membranes tunica intima and tunica media provide elasticity during pulsatile pressure change or distension
3) smooth muscle cells in tunica media regulate internal calibre of lumen
4) collage fibres in adventita provide protection against longitudinal circumferential stress

89
Q

what are the 9 type of blood vessels based accordingly to function

A

1) elastic arteries
2) muscular arteries
3) arterioles
4) metarterioles
5) capillaries
6) sinusoids
7) postcapillary venules
8) muscular venules
9) veins

90
Q

what are the two types of arteries and what is their function

A

1) conducting arteries - low volume, high pressure, arising from heart eg - aorta
2) distributing arteries - contractile ability enabling them to distribute blood selectivity to various components of the body

91
Q

arterial compliance why important how compared to veins

A

○ Arterial compliance is important in converting pulsatile flow from the heart into steady flow through peripheral vascular beds - stronger but less compliant than veins as cannot burst
- Elastic arteries therefore act as a pressure reservoir – during systole more blood is ejected into them than is drained off into narrow high resistance arterioles. Elastic recoil of arteries during diastole continues driving blood forward when the aortic valves are closed.
Arterial compliance decreases with age

92
Q

what are resistant vessels, what are there main functions and what structure

A

large and small arterioles (metarterioles - after the larger arteriole before the precapillary sphincters
regulate total peripheral resistance - arteriole blood pressure and flow through capillaries
arterioles have a much larger resistance, due to their high wall thickness to lumen ratio and relatively low cross sectional area (400cm2)

93
Q

what are exchange vessels and what is increased and decreased

A

capillaries, sinusoids and postcapillary venules
total cross sectional area of capillary beds is much greater than that of other vessels
○ Due to the high cross sectional area of the capillary beds, blood velocity is lower.
- This maximises time available for capillary exchange.

94
Q

what are the essential components of a capillary

A

1) thin endothelial cell
2) basement membrane
3) sometimes a pericyte (can turn into endothelial cell)

95
Q

postcapillary venules structure and function

A

several capillaries drain into one postcapillary venule.

  • Very low pressure and very low flow rates
  • white blood cell migration during inflammatory response
96
Q

arterio-venous shunts structure and function

A

Shunt vessels (arteriovenous anastomoses) directly connect arterioles with venules, bypassing capillaries and causing a local diversion of flow.

  • glomeriform arteriovenous anastomosis have highly convoluted segments enclosed by a dense connective tissue capsule. ‘
  • important for thermoregulation
97
Q

what are veins also called and main function and characteristics

A

capacitance (reservoir) vessels

  • large volume and low pressure
  • serving as blood volume reservoirs - their compliance and volume means they can hold 70% of blood volume - increase return of blood to the heart - increase cardiac filling
  • During exercise or hypotensive states, venoconstriction displaces blood to essential organs, and helps to increase blood pressure.
  • generally not pulsatile
98
Q

what are the ways to enhance venous return of blood to the heart

A

1) sympathetically induced vasoconstriction
2) valves - especially in the limbs, one way
3) skeletal muscle activity - contraction of muscle in limb - blood move towards teh heart - muscle pump
4) respiratory activity and cardiac suction - increasing the pressure gradient between the veins and the heart

99
Q

lymphatic vessels what is pressure and flow, does it have valves, what is wall structure

A
  • very low pressure and slow flow
    = valves to increase flow - semilunar
    1. tunica intima - elongated endothelial cells supported on an elastic membrane.
    2. tunica media - smooth muscle cells and fine elastic fibers.
    3. tunica adventitia - connective tissue
    no muscular or elastic fibres

Semester 2 (17 decks)

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