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Semester 2 > cardiovascular 2 > Flashcards

cardiovascular 2 Flashcards

1
Q

coronary circulation how much cardiac output, what are the 2 main arteries of heart and and what 3 smaller branches do they supply

A

1) left coronary artery
2) right coronary artery
1. ventricular 2. septal 3 . atrial arteries

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2
Q

what does the left coronary artery and right coronary artery divide into

A 
Left coronary artery 
1. Left (or paraconal) interventricular artery
○ Lies in the left I-V groove
2. Left circumflex artery (bends around the heart)
Lies in the circular coronary groove
right coronary artery
1. Right (or subsinuosal) I-V artery
○ Lies in the right I-V groove, and
2. Right circumflex artery
○ Lies in the circular coronary groove
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3
Q

what does the left and right coronary artery supply and which is larger for dogs, ruminants

A 
Dog and ruminant 
○ Left coronary artery supplies:
§ All I-V septum
§ All L. ventricle
§ Regions of R. ventricle adjoining the L. and R. interventricular groove
○ Right coronary artery supplies:
§ Remainder of R. ventricle
- L. coronary a. carries 80% of coronary arterial flow
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4
Q

what does the left and right coronary artery supply and which is larger horses, pig

A 
horse and pig 
- Left coronary a. supplies:
○ Most of the I-V septum
○ Most of the L. ventricle
○ Little of the R. ventricle
- Right coronary artery supplies:
○ Part of I-V septum
○ Regions of L. ventricle adjoining the R. interventricular groove
○ Most of R. ventricle
- Both coronary arteries similar in size
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5
Q

what does the left and right coronary artery supply and which is larger for cats

A

○ 50% similar to dogs and ruminants - Left over the right
○ 30% similar to horses and pigs - about even with left and right
○ 20% showing other variations

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6
Q

coronary blood flow how increased and effect of mechanical compression

A
  • Increased activity produces more metabolic byproducts (e.g. adenosine) - indirect effect
    ○ These act as local vasodilators
    ○ This is called active hyperaemia - during increase in activity increase in blood flow
  • (Sympathetic NS increases cardiac activity and therefore acts indirectly to increase coronary blood flow)
    left ventricle - systole blood vessels squashed so flow occurs in diastole
    right ventricle - systole causes blood flow
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7
Q

hypoxic vasoconstriction where does it occur and what happens

A
  • Hypoxia (poor oxygenation - poor circulation) causes vasoconstriction
  • This helps to adjust blood flow to the level of ventilation in that part of the lung
  • Increase flow in areas that are hypoxic
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8
Q

what are the 2 main arterial supplies to the head

A
  1. L. and R. common carotid arteries - come off brachsephalic trunk
  2. L. and R. vertebral arteries
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9
Q

skin blood flow what vascular beds are present, what is an important type and function

A

superfical and deep vascular beds
- Arteriovenous anastomoses
○ Very low resistance to flow so increase flow
○ Countercurrent heat exchange for heat conservation
On hot days increase blood flow through increase heat exchange - thermoregulation

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10
Q

what are the two main common carotid arteries and what does each supply

A

○ Internal carotid a. - intracranial circulation

○External carotid a. - extracranial circulation - face, head, tongue etc.

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11
Q

external carotid artery what are the major branches and where terminates

A 
- Major branches:
○ Cranial laryngeal, occipital, ascending pharyngeal, lingual, facial (artery that can feel the pulse), caudal auricular and parotid aa.
- Terminates in:
○ Superficial temporal a.
○ Maxillary a.
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12
Q

vertebral artery where branch from, what supply and what does it fuse with

A
  • First branch of subclavian a.
  • Supplies segmental arteries to the spinal cord, meninges and vertebral bodies
  • fuses with cerebrospinal artery
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13
Q

cerebrospinal artery what type of circulation and how occurs

A
  • L. and R. cerebrospinal aa. Fuse - ensure - collateral circulation
    ○ Basilar a. - cranially
    ○ Ventral spinal a. - caudally
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14
Q

basilar artery what does it form and function

A
  • Forms Circle of Willis - where all vessels come together
    ○ Supplies brain
    ○ Internal carotid also supplies
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15
Q

cycle of willis what type of circulation how occur

A

Artery to artery anastomosis - collateral circulation

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16
Q

functional end arteries where preset and structure, how different to true end arteries

A

brain micro-circulation
arteries anastomose wit nearby arteries but too small to be functionally effective so still get local ischaemia if blockage
- true end arteries no anastomotic connections - if artery closed area of tissue dies

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17
Q

what are the 4 parts of the blood-brain barrier

A
  1. Endothelial cells have closed intercellular (tight) junctions - physical
  2. Thick basement membrane -physical
  3. Surrounded by ‘end feet’ from astrocytes (supporting cells) -physical
    ○ pseudopodia
  4. Specific enzymes also contribute - chemical
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18
Q

what are the major veins draining from the head

A
  • External jugular v.
  • Internal jugular v. - runs close to carotid
  • Vertebral v.
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19
Q

In what circumstances does active hyperaemia develop?

A

1) increased blood flow to gastrointestinal tract following ingestion of food - physiological
2) increased blood flow to skeletal muscles during exercise
3) increased blood flow to skin during exercise or hot weather to augment heat loss
4) inflammation - local active hyperaemia is responsible for the redness (rubor, erythema) and heat (calor) of acute inflammation - pathological

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20
Q

Why is active hyperaemia a localised phenomenon?

A

there is insufficient blood volume to permit generalised active hyperaemia whilst maintaining adequate systemic blood pressure

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21
Q

examples of when localised passive congestion can develop

A

localised

1) intestinal strangulation due to torsion or volvulus - compression of mesenteric veins - obstruction of venous outflow
2) hypostatic or dependent congestion = gravitational pooling of venous blood in dependent (down-side) areas in recumbent or inactive animals (especially large animals) or as a post mortem change

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22
Q

examples of when generalised passive congestion can develop

A

1) left-sided congestive heart failure - venous blood pulls in pulmonary veins, venules
2) right-sided congestive heart failure - blood pools in systemic veins and venules - liver

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23
Q

grossly distinguish between active hyperaemia and passive congestive of live animal

A

active - oxygenated blood so bring red, warm, pulse sometimes palpable at inflammatory sites
passive - red-purple to black-blue (cyanosis), enlargement of veins, no associated increase in temp so cooler than normal

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24
Q

potential consequences of passive congestion of tissues

A

1) hydrothorax
2) hydropericardium
3) congestion of spleen, kidneys, stomach, intestines etc
4) hepatic congestion
5) bottle jaw

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25
Q

what gross lesions occur in left-sided congestive heart failure and why

A
  • lungs wet, heavy, do not fully collapse due to pulmonary oedema
  • stable white or pink (blood-stained) foam from lungs - mixture oedema fluid with pulmonary surfactant
  • tan-brown discolouration (“bronzing” or haemosiderosis) of the lungs
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26
Q

what gross lesions occur with right-sided congestive heart failure

A
  • liver swollen and dark red-purple
  • film of coagulated fibrin (“sugar-frosting”) may be present due to increase hydrostatic pressure, increase lymph formation, overfollowing around liver - present in blood
  • undergo hydropic of fatty degeneration, necrosis or atrophy
  • zonal necrosis - nutmeg liver
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27
Q

what are the 5 main mechanisms that can lead to oedema development and which is likely to be responsible for localised and generalised oedema

A

1) increased plasma hydrostatic pressure
2) decreased plasma colloid osmotic pressure - generalised
3) lymphatic obstruction - localised
4) increased vascular permeability
sodium retention - less likely

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28
Q

what is likely to lead to increase plasma hydrostatic pressure within a capillary bed

A
  • dependent on pressure at venular end
    1. local obstruction of venous flow resulting in congestion upstream
    2. impaired venous return to the heart - cirrhosis, right-sided congestive heart fialure
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29
Q

Why is extracellular oedema NOT expected in animals with systemic hypertension (increased arterial pressure)

A

this is because increased arteriolar blood pressure (and/or increased blood volume) causes reflex vasoconstriction of the pre-capillary arteriolar sphincter in order to protect the delicate capillary bed downstream

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30
Q

what are the main gross appearances of oedema

A

excess watery, colourless to pale, clear, fibrin (as a gel), swollen, heavy or rubbery
- oedematous tissue “pits” on pressure (i.e. finger pressure displaces the interstitial fluid into surrounding tissues to leave a transient indentation = “pitting oedema”) - tumour causes swelling but doesn’t pit

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31
Q

what are possible consequences of oedema and where in the body can it prove fatal

A
  • impaired wound healing, susceptible to secondary bacterial infection, friboplasia and permanent fibrosis
  • cerebral and pulmonary oedema may be fatal
    cerebral
  • increased intra-cranial pressure and cerebral dysfunction - may push through foramen magnum
    pulmonary
  • drowning from within - stable foam formation within airways comprimised ventilation, secondary bacterial infection
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32
Q

how does thrombus differ from a physiological blood clot that develops after injury to a blood vessel

A

thrombosis grows into the lumen of the blood vessel as there is damage to the endothelial cells and therefore can compromise flow (intra-vascular)
blood clot grows from damage vessel wall to outside vessel (extravascular)

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33
Q

What are the three major mechanisms that predispose to thrombosis? Which of these is the most important predisposing mechanism?

A

1) endothelial injury - most important
2) abnormal haemodynamics (blood stasis or blood turbulence)
3) hypercoagulability of the blood

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34
Q

how does endothelial damage promote thrombosis

A

normally possess both procoagulant and anticoagulant properties
- injured or activated endothelial cells adopt a procoagulant phenotype that promotes local coagulation of blood and hence thrombosis

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35
Q

where in cardiovascular system is their natural tendency for blood turbulence to develop and how does this and blood stasis predispose to thrombosis

A

areas of hydraulic stress (e.g. sharp bends, changes in vessel lumen diameter, valves and branching points, abnormal vessel wall dilation or stenosis
blood turbulence - direct endothelial injury, accereates intravascular procoagulant cellular and enzymatic reactions
blood stasis - increase blood viscosity, blood hypercoagulability, hypoxic injury to endothelial cells as decrease blood flow

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36
Q

what are some circumstances that can lead to blood hypercoagulability

A

1) increase hepatic synthesis of coagulation factors with decreased of antithrombin
2) severe burns, tissue trauma, snake bites, pancreatic necrosis release procoagulants into circulation
3) severe protein losing glomerulopathies - increase loss of antithrombin in urine
4) cirrhosis - decreased hepatic synthesis of antithrombin

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37
Q

what are 3 basic events in thrombus formation

A

1) circulating platelets adhere to subendothelial collagen and become activated releasing recruiting molecules
2) platelets then aggregate via binding soluble fibrinogen
3) activation of coagulation cascade convert fibrinogen to fibrin anchor platelets

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38
Q

thrombus propagation

A

continued flow of blood over a mural thrombus may permit its gradual enlargement (propagation) by allowing repeated layering of platelets and fibrin on its surface and entrapment of erythrocytes and leukocytes within it
- start off non-occlusive and can become occlusive

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39
Q

what are lines of Zahn and why do they signify

A

during thrombus propagation blood coagulates in series resulting in gross and microscopic laminations - lines of Zahn
- significant only that they indicate that the thrombus was initially non-occlusive with continued blood flow over it

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40
Q

what is the expected gross appearance of thrombus in an artery of within the heart

A
  • thrombi also attached to vessel wall or endocardium - often heart valves
  • firm and pale yellow (pale or white thrombi) and have a dull, dry, rough surface because they are chiefly composed of platelets and fibrin
  • vegetations - branched
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41
Q

what is expected gross appearance of a thrombus in a vein

A
  • tend to form perfect casts of vessels and have smooth, shiny surface
  • moister and dark red
  • do not generate strong points of attachment and generally fragile
  • larger with longer tails
42
Q

how to tell the difference between post mortem and anti mortem blood clots

A

detection of the (albeit weak) point of anchorage to the vessel wall, by detection of fine tangled strands of pale grey-yellow fibrin on their cut surface grossly, and especially by detection of evidence of congestion and oedema of tissues upstream (venous infarction tissue)

43
Q

are venous or arterial thrombi more likely to thromboemolise and why

A

venous thrombi

1) don’t form as strong attachments and usually fragile
2) much larger with longer tails so more to break off

44
Q

how do thrombi undergo organisation

A
  • older thrombi not removed by fibrinolysis tend to become organised by phagocytosis by leukocytes (especially macrophages
  • viable cells from margins of the thrombus attach and grow on surface ultimately insulating it from circulating blood - preventing propagation
45
Q

what is meant by recanalisation of thrombus

A

capillaries growing into occlusive thrombus from either end may reach and restore blood flow

46
Q

what is the most common type of embolus and what is meant by saddle thromboembolism

A
  • thromboembolism

- saddle thromboembolism commonly lodge at sites of vessel bifurcation such as distal end of aorta

47
Q

how would you distinguish grossly between thrombus and thromboembolus

A

difficult - need to search for a possible thrombus upstream to distinguish

48
Q

where do most venous thromboemboli become trapped

A
  • from gastrointestinal, splenic or pancreatic mesenteric veins or the portal vein itself are likely to become trapped in the liver
  • rest of the systemic system - the vascular beds of the lungs
49
Q

consequences of pulmonary thromboembolism

A
  • may occlude the main pulmonary artery, impact across the bifurcation of the right and left pulmonary arteries, or pass into the smaller arterial branches
  • sudden obstruction of ≥ 60% of the pulmonary circulation - sudden death
  • dual blood supply (pulmonary and bronchial) usually no pulmonary infarction
  • hypertensive right heart disease (cor pulmonale
50
Q

list 8 other times of emboli besides thromboemboli

A

1) bacterial colonies
2) malignant neoplastic cells
3) lipid - diabetes mellitus
4) gas bubbles - more than 100ml of gas - decompression sickness
5) foreign bodes
6) parasites
7) fibrocartilage
8) clumps of erythrocytes - immune-mediated haemolytic anaemia

51
Q

List 4 other causes of ischaemia apart from thrombosis

A

1) congestive heart failure
2) shock
3) impaired venous return to right heart - GDV
4) sustained vasoconstriction - frost bite

52
Q

why is infarction commonly referable to arterial obstruction than to venous obstruction and which organs is infarction often fatal

A
  • arterial infarcts are far more common than venous due to collateral circulation more numerous in veins
  • cerebral, myocardial, intestinal(sterile - can be absorbing bacteria into circulation) and pulmonary infarcts can be fatal
53
Q

what are the 6 main factors that determine the prognosis for an animal with reduction in blood flow

A

1) presence of an alternative oxygen supply
2) rate of development of occlusion
3) size of the affected vessels
4) cell vulnerability to hypoxia and duration of hypoxia
5) oxygen content of blood
6) miscellaneous factors

54
Q

what organs are less likely to develop infarcts and why

A

lungs and liver as both have dual supply
lungs - pulmonary and bronchial
liver - hepatic and portal

55
Q

what type of necrosis occurs with an infarct and what happens to necrotic debris in infarct overtime if patient survives

A

coagulative type
with the basic microscopic outline of the dead cells persisting for at least several days until they are liquefied or phagocytosed by leukocytes

56
Q

difference between acute, sub-acute and chronic infarct grossly

A

acute - tissue is friable, narrow zone of acute inflammation
subacute - peripheral inflammation becomes more prominent, fibroplasia in the margins
chronic - leukocyte invasion progressive liquefaction and phagocytosis of necrotic debris, ultimately replaced with scar tissue

57
Q

Dilated cardiomyopathy what is the primary problem and what does that lead to

A

decreased contractility - decreased stroke volume - decrease cardiac output - decrease tissue perfusion (poor excercise tolerance)
ALSO decreased blood pressure - RAAS activation - retention of sodium + water - increase preload - concentric hypertrophy ALSO decrease ejection fraction - increase EDV - congestion in pulmonary veins etc - pulmonary oedema

58
Q

why in dilated cardiomyopathy do you get ventricular tachycardia (ventricular premature complexes VPCS)

A

large amount of QRS which have high altitude - “rogue” pacemaker in ventricle due to:
1. Stretched heart (struggles with perfusion)
2. Blood pressure low
3. High heart rate (200 beats per minute) -
Therefore - coronary perfusion decreased - decreased oxygen and ability to make ATP within the myocardial cells - results in decreased Na+/K+ ATPase activity - abnormal resting potential - random depolarisation of the ventricular muscle

59
Q

vascular tone

A
  • amount of constriction in a blood vessel
  • there is a basal degree of vascular smooth muscle contraction
  • controls contraction and therefore blood pressure
60
Q

steps in contraction within smooth muscle cells

A

1) increase in [Ca2+] mainly from extracellular but also SR
2) Ca2+ + calmodulin
3) binds to myosin light chain kinase
4) phosphorylation of myosin light chains
5) cross-bridge forms between myosin and actin filaments
6) myosin phosphatase removes phosphate from myosin and inactivates it to allow relaxation of the cell

61
Q

List 7 differences about smooth muscle contraction

A

1) Constant ‘tone’
2) Slower contraction, Lower energy requirements
3) Electrical connections between cells
4) No T tubules and no Voltage operated Na channels
5) Limited SR
6) nward movement of calcium through voltage operated and receptor operated (hormones and calcium itself) calcium channels
7) Different regulatory protein- calmodulin

62
Q

list some molecules that control vascular smooth muscle tone

A

vasoconstriction
- Noradrenalin sympathetic nerves- macro control
- angiotensin and thromboxane, endothelin - local
vasodilation
-parasympathetic nerves ACh
- endothelial cells release NO, adenosin,- local
- sensory nerve release local substance P in response to inflammation

63
Q

sympathetic nervous system control of vascular smooth muscle how differs in different organs

A

fine control through receptor types
- most blood vessels have majority alpha receptors so undergo vasoconstriction with sympathetic stimulation
Eg - skin, uterus, GI tract
- some have majority beta receptors and therefore undergo vasodilation
Eg - skeletal muscle and heart muscle

64
Q

how does the alpha and beta receptor work in terms of contraction or relaxation

A

alpha receptor:
1) NA binding –> IP3 & DAG increased
2) increased intracellular Ca++ from SR
3) Ca++ binds to cytoplasmic regulatory protein- Calmodulin
- CONTRACTION
beta receptor:
1) NA binding –> increased adenylate cyclase
2) increased cAMP
3) Inactivates myosin light chain kinase (MLCK) which phosphorylates myosin
4) cGMP also activates phosphatase that inactivates myosin by removing phosphate group
- RELAXATION

65
Q

autoregulation of vascular tone how achieved

A

1) Stretch induced myogenic response (contraction)

2) Flow induced endothelial relaxation

66
Q

myogenic response what is its function and how does it achieve this

A
  • Preserves organ flow in face of changing arterial pressure
  • “protects” capillaries from excessive hydrostatic pressure
    1. Stretch activates ion channels and membrane-bound enzymes
    2. Also get changes in cell cytoskeleton (stiffening)
  • CONTRACTION
67
Q

what is metabolic control of blood flow and 2 ways it is achieved

A
  • Matching blood flow to the metabolic demands of the tissue
    1) Metabolic (Active) hyperaemia
  • Increase in tissue flow in response to an increase in metabolic rate
  • Metabolic products include: adenosine (heart), K+ and lactic acid (skeletal muscle) and CO2 (brain)
    2) Reactive hyperaemia
  • Temporary increase in blood flow immediately after period of flow restriction
  • Reactive oxygen species can be generated and interact with nerve endings causing pins and needles
68
Q

what are the 6 functions of endothelium of smooth muscle

A

1) Blood vessel tone control - via the production of both vasoconstrictors and vasodilators
2) Selective barrier - transports H2O, lipids, gases, proteins etc. according to demand
3) Maintenance of fluidity - via anti-thrombosis and monitoring of shear stress.
4) Angiogenesis - growth of new capillaries.
5) Inflammatory mediators - platelet adhesion, prostacyclins etc.
6) Ecto-enzymes- Antithrombin III, nucleotidases.

69
Q

endothelium-induced flow dependent what is its function and how to achieve

A

Increased blood velocity
- Increased sheer stress (friction)
- More sheer stress indicates faster blood flow so need to slow it down
• Activation of endothelial receptors
- Release of smooth muscle relaxants
• Dilation of the vessel ( artery or vein)

70
Q

what is Nitric oxide released in response to and how does it exert its effect

A
  1. sheer stress
  2. Metabolic change e.g. hypoxia
  3. Endogenous NO release stimulated by bradykinin, acetylcholine, adenine nucleotides
    1) NO causes increase in cGMP by diffusing from endothelial cell into smooth muscle cell
    2) cGMP inactivates myosin by activating a phosphatase that removes the phosphate from the myosin inactivating it
    3) No cross-linkages therefore no contraction
71
Q

what are the two types of baroreceptors

A

1) high pressure (Arterial)

2) Cardiopulmonary (low pressure)

72
Q

high pressure (arterial) baroreceptors are what, what do they respond to, location

A
  • Are stretch receptors
  • Respond rapidly to changes in pressure (within one heart beat)
  • Buffer sudden changes in pressure
  • If pressure remains elevated for longer periods of time firing rate of receptors decreases leading to new “set point
    Location
    1. Aortic arch - respond to pulsatile flow
    2. Carotid sinus - respond to non-pulsatile stretch
73
Q

Cardiopulmonary (low pressure) baroreceptors where found and what respond to

A
  • Pressure (stretch) receptors in atria, at junctions of great veins and atria, ventricles and pulmonary veins
  • Respond to absolute pressure (rather than change in pressure)
    ie respond to changes in blood volume in heart and great veins (VENOUS RETURN)
    Location
  • Nerve fibres run in vagus nerve to the medullary cardiovascular centre in the brain
74
Q

what is unloading and what results

A

(decreased stretch) of cardiopulmonary receptors by reducing central blood volume –> increased sympathetic drive to heart and blood vessels and decreased parasympathetic drive to heart

75
Q

what is the effect of vasoconstriction in the arterioles and veins

A

1) Arterioles
- Vasoconstriction leads to increased TPR and increased diastolic pressure
2) Veins
- Vasoconstriction leads to increased venous return –> increased EDV –> increased stroke volume

76
Q

what are the two main compensatory mechanisms that occur within the heart

A

1) eccentric hypertrophy

2) concentric hypertrophy

77
Q

eccentric hypertrophy what occurs in response to what and examples of what causes it

A
  • increases the volume within the heart by increasing size of ventricular lumen without increasing diameter
  • in response to increase volume, elevated ventricular end diastolic volume
    EG
    1) mitral valve leak - back flow from ventricle to atrium
    2) hole in interventricular septum - blood flow from left to right ventricle
    3) PDA - blood from left to right and looping around lungs
78
Q

concentric hypertrophy what occurs, in response to what and examples of what causes it

A
  • increase in muscular mass of the heart ventricular wall decreasing the lumen
  • response to chronic pressure overload - increased afterload (MAP)
  • therefore decrease volume but can increase ability to push that volume with change in pressure
    Eg - pulmonic/aortic stenosis
  • wont see on X-ray just ultrasound
79
Q

what is different between getting mitral problem first or DCM first and mitral valve problem second

A
  • End stage mitral problem dogs -at the beginning would get increase contractility (A) due to eccentric hypertrophy causing length-tension relationship to be at peak, eventually get reduced contractility as myosin and actin are pulled too far apart
    DCM - contractility is the problem at the beginning - later stages get mitral regurgitation as pulled apart - low grade murmur
80
Q

relationship between heart disease and blood pressure

A
  • Heart disease doesn’t cause high blood pressure
    ○ Causes low blood pressure and trying to increase
  • High blood pressure can cause heart disease
    Heart increase workload - leads to concentric hypertrophy
81
Q

What is the result of eccentric and concentric hypertrophy of the heart and treatment

A

1) end diastolic pressure will increase due to decrease cardiac capacity
2) MAP will fall so body correct by
1. increase stroke volume or heart rate - sympathetic
2. vessels contract increase TPR sympathetic nerves
3. vasopressin released activates RAAS causing increase retention of fluid
3) increase volume going back to heart with increase resistance so heart have to work harder - make disease worse
treatment - relax vascular and increase fluid loss - diruetic, block RAAS

82
Q

why do you see cardiac cachexia with heart disease

A
  • Increase workload of heart
  • Increase metabolic requirements
  • Heart uses protein substrate for energy
  • Cardiac cachexia - animal increase but still losing weight
83
Q

what occurs with hydrostatic pressure and heart disease

A
  • hydrostatic pressure increases at venule end (congestion) so fluid moves out into tissues
    • Right sided failure - ascites, pleural effusion - dogs
    •Left-sided failure - pulmonary oedema dogs - cats can get pleural effusion
    CONGESTIVE HEART FAILURE
84
Q

what circumstances does venous hypertension develop

A
  • impairment of outflow of venous blood responsible for passive congestive
  • increased plasma hydrostatic pressure
  • congenital or acquired arteiovenous anastomosis
85
Q

cor pulmonale what is it and what does it result in

A

right heart disease caused by pulmonary hypertension

  • as ventricle contracts need to contract against extra resistance - increase work load
  • leads to chronic concentric hypertrohpy of right ventricle
86
Q

causes of pulmonary hypertension in domestic animals

A

1) congenital cardiac anomalies causing left-to-right shunting
eg - ventricular septal defect, atrial septal defect, PDA (patent ductus arteriosus)
2) increased resistance to pulmonary arterial blood flow
eg - heartworm infestation wtihin pulmonary arterial branches
eg - pulmonary thromboembolism

87
Q

what physiological factor contribute to systemic arterial blood pressure

A

= cardiac output x total peripheral vascular resistance = (heart rate x stroke volume) x total peripheral vascular resistance

88
Q

what is meant by primary or essential hypertension and what factors contribute to this in older humans

A
  • multifactorial cause of systemic hypertension in middle age humans
  • genetics, smoking, stress, arteriosclerosia, lipid-rich diets, obesity
89
Q

what diseases may be responsible for systemic hypertension in dogs and cats

A 
- generally secondary to other diseases 
EG
- renal disease
- hyperadrenocorticism - dgs
- hyperthyroidism - cats 
- hypothyroidism - dogs
90
Q

how does systemic hypertension become self-perpetuating if not treated

A

1) persistent arteriolar vasoconstriction - smooth muscle hypertrophy of the tunica media - arteriolosclerosis with decreased elasticity/compliance and narrowing of the vessel lumen - a further increase in vascular resistance
2) decrease autoregulation in glomerular, lead to glomerulosclerosis - excerabation of increased resistance

91
Q

what are the organs that are most susceptible to systemic hypertension and clinical manifestations in domestic animals

A

eyes, kidneys, heart and brain

1) sudden onset blindness - retinal haemorrhage or detachment
2) polyuria/polydipsia
3) systolic cardiac murmur
4) epistaxis
5) strokes - weakness, collapse, seizures, sudden death

92
Q

what characterises shock

A
  • s characterised by systemic hypoperfusion and systemic hypotension
  • if shock persists, impaired tissue perfusion - irreversible hypoxic tissue injury, organ failure and death
93
Q

list 3 causes of cardiogenic shock

A

1) primary disorders of myocardium - cardiomyopathy
2) acute heart valvular dysfunction - rupture of chordae tendineae
3) intra-cardiac obstruction to blood flow - heavy heartworm infestation

94
Q

list 3 causes of hypovolaemic shock

A

1) severe, acute, chronic internal or external haemorrhage
2) severe loss through diarrhoea or vomiting
3) severe fluid loss through burns

95
Q

what can trigger neurogenic shock and why does effective circulation blood volume decrease

A

animals that are severely frightened, emotionally stressed or suffering severe pain
triggered by electrocution (including lightning strike), acute brain spinal cord injury, or through use of anaesthetics or vasodilator drugs
- inappropriate peripheral vasodilation and bradycardia

96
Q

what can trigger septic shock, why does EBV decrease and what happens within microcirculation to contribute to poor prognosis

A
  • Gram-negative bacterial infection with release of endotoxins into the circulation (endotoxic shock) - overwhelming bacterial infections
  • LPS released which activates cytokines activating vasodilators, also decrease contractility, decrease cardiac output, platelet activation and endothelial injury resulting in widespread microthrombosis
97
Q

what are some neurohumoral mechanisms that are activated during shock

A

1) release of catecholamines - adrenalin
2) generalised stimulation of autonomic sympathetic nerves system
3) activation of RAAS - blood shunted from non-vital organs to vital and if under perfusion continues results in hypoxic injury to those areas

98
Q

what happens during stage 2 (progressive stage) of shock

A

glomerular filtration rate declines - oliguria (decreased urine volume)
sustained vasoconstriction in “non-essential” organs - tissue hypoxia, forcing cells to switch from aerobic metabolism to anaerobic glycolysis - production of lactic acid - dilation of arterioles and venules - pooling blood in microcirculation - further decrease in cardiac output as decrease in blood pressure and ECBV

99
Q

what occurs in stage 3 of shock

A

irreversible stage

- wide spread tissue hypoxia, cell necrosis, multiple organ failure as neurological reflexes fail and vital organs fail

100
Q

what are the clinical signs that suggest animal is in shock and what shock as best prognosis

A

1) increased HR, weak and rapid pulse, dry or clammy skin, peripheral cyanosis,
hypovolaemic shock
Paramedics often refer to the 30mins - “golden half-hour” or 1 hour - “silver hour” during which therapeutic intervention

101
Q

what is the result of low blood pressure for an animal losing blood rapidly

A

1) Normally - 37mmHg is the arteriolar end of capillary - hydrostatic pressure - this dog arteriolar pressure is 40mmHg - no net filtration - poor exchange of nutrients - net reabsorption - DECREASE PCV
2) reduced blood pressure and volume - decrease MAP - detected by baroreceptors - angiotensin activates which activates RAAS - retention of sodium and water - increase blood volume without increasing red blood cell count
ALSO decrease MAP - increase vasoconstriction and heart rate - trying to restore MAP

102
Q

why do anemic patients have haemic systolic murmur, is it reversible

A

Anaemia - decreased PCV - less viscus blood - increased turbulence (murmur)
- Clear up once restore normal PCV and protein levels in the blood

Semester 2 (17 decks)

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