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BVETMED2 > CVRS > Flashcards

CVRS Flashcards

1
Q

define heart failure

A

When the heart is unable to maintain cardiac output, leading to underfilling of the arterial circulation

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2
Q

What determines preload

A
  • Circulating fluid volume
  • venous tone
  • myocardial compliance
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3
Q

What is starlings theory

A

strength of contraction of the cardiac muscle is proportional to the initial fibre lenth at rest

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4
Q

What is dilated cardiomyopathy

A

Sacromeres add in series due to increased volume of blood. Thinning of the cardiac muscle leads to a loss in contractility

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5
Q

What alters central venous pressure

A
  • Volume of blood
  • Distribution of blood
  • Sympathetic nerve activity
  • gravity and movement
  • Thoracic pump - On inspiration, abdominal pressure increases and intra thoracic pressure drops. Pressure gradient favours venous return
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6
Q

Where does the baroreceptor reflex feedback to

A

Medullary cardiovascular centre

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7
Q

What are atrial natruretic peptides (ANP’s)

A

Released from atrial walls when stretched.

  • Antagonist to RAAS
  • relaxes vascular smooth muscle
  • Excretes salt
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8
Q

How does norepinephrine effect heart rate

A
  • Acts on B1 adrenoreceptors of the cardiomyocytes
  • Binds to receptor causing activation of Gs
  • Upregulates adenyl cyclase elevating cAMP levels.
  • Increase in PKA, which phosphrylates Na+ and Ca+2 channels. causes faster repolarisation and increased Ca+2 levels

An increase in intracellular cAMP in Vascular smooth muscle will cause vasodilation!

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9
Q

How does Ach affect heart rate

A
  • Binds to muscarinic receptor
  • Gk subunit opens K+ channels and Gi subunit inhibits adenycl cyclase
  • Also inhibits norepinephrine release from nerve endings
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10
Q

Describe initial stages of heart development

A
  • Cells from primary heart field differentiate into cardiace cells and zip together to form a outflow and inflow tract
  • early looping occurs to get correct orientation of inflow and outflow tracts.
  • Late looping gives rise to one ventricle and one atrium
  • Secondary heart field differentiates and myocardium is added to the outflow tract and ventricle
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11
Q

How are atria and ventriles alligned

A
  • Endocardial cushons fuse
  • This defines left and right atrial ventricular canal
  • Endocardial cushons also give rise to valves
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12
Q

How are left and right atria defined

A
  • Septum primum initially grows down leaving a space known as ostium primum.
  • Ostium primum closes and ostium secundum forms in the middle of the septum
  • Septum secundum grows down adjacent, covering the ostium secundum
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13
Q

How are ventricles divided

A

Muscular septum grows down the middle. A mesenchymal cap fuses with the AV cushons

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14
Q

Describe septation of outflow tract

A

Neural crest cells migrate and cause seperation into aortic and pulmonary trunks

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15
Q

Which aortic arches are retained and what are they’re purposes

A
  • 3rd - Forms left and right carotid arteries
  • 4th - Forms aorta and subclavian artery
  • 6th - Forms left and right pulmonary arteries. Also forms ductus arteriosus
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16
Q

what are the 3 foetal shunts

A
  1. Ductus venosus - Connects umbilical artery to the caudal vena cava. Allows limited blood to go to the liver and is controlled by sphincter
  2. Ductus arteriosus - Connect pulmonary trunk to the distal aorta. Allows only 10% of blood to flow to lungs. Also allows right ventricle adequate excercise
  3. Foramen Ovale - Opening connecting the two atria. Allows high pressure blood from right atrium into left instead of travelling to lungs. closes at birth when pressure equalises
17
Q

What are possible congenital defects with the heart

A
  • Septum primum fails to grow down to av cushons. or septum secundum doesnt cover ostium secundum
  • Muscular septum in ventricle doesnt grow or fails to fuse with endocardial cushons
  • neural crest fails to migrate leading to failure of the outflow tract development
  • Patent foramen ovale - Failure of blood clots to be filteres. could become lodges in brain capillaries and cause a stroke
18
Q

explain how changes in contractility are regulated by calcium

A
  • calcium travels down t-tubules & through DHDP channel.
  • This causes calcium induced calcium release from the SR throu ryanodine recepter 2
  • Increased sensitization of Ca+2 to troponin = stronger contraction
  • relaxation achieved by CaATPase pump and ca/na pump
19
Q

What are the factors altering contractility

A
  • increase in preload
  • sympathetic innervation
  • change in troponin affinity to Ca+2
  • Reduced 02 supply leads to reduced arterial pressure and reduced coronary blood
20
Q

What is concentric hypertrophy

A
  • Pressure overload causes sacromers to be added in parallel
  • volume of ventricle decreases and so does compliance
21
Q

What adaptation does the carotid sinus have and where is it located

A
  • Contains baroreceptors
  • tunica media - Converted into elastic tissue enabling expansion in response to increased arterial pressure
  • tunica adventitia - Thickened to accomodate rich network of affert nerve endings
22
Q

What is empysema

A

Alveolar membrane damaged by respiratory burst of immune cells, leading to rupture of the alveoli. Decrease in compliance

23
Q

What are the non respiratory functions of the lung

A
  • Mucociliary escalater
  • IgA secretion
  • Alveolar macrophages
  • Mast cells
  • Release ACE
  • Uptake of norepinephrine/histamine
24
Q

Explain surface tension and how pulmonary surfactant influences this and where its released from

A

Surface tension occurs because of the force created by the intracellular fluid and dry surface of the alvoeli

  • Pulmonary surfactant is synthesised by type 2 alveoli
  • Has polar phospholipid heads which repel eachother preventing collapse
25
Q

What are factors affecting airway resistance

A
  • Lung volume
  • Contraction of brochial smooth muscle
  • Tissue resistance
  • Density
26
Q

Describe Babesia’s Life cycle , pathogenesis & epidemiology

A

Life cycle

  • Tick feeds on infected animal and becomes infected
  • Sexual repro in intestines followed by asexual repro forming vermicules
  • Vermicules migrate to salivary glands and are transmitted
  • Asexual reproduction in RBC’s

Pathogenesis

  • Multiply in RBC’s by budding and forming 2 or 4 daughter cells
  • These cause Haemolytic anaemia Or Hameoglobinuria & fever

Epedemiology

  • Occurs sporadicly
  • Immunity occurs quickly but dissapears in the abscence of infection (Enzootic instability) Whereas constant exposure leads to high levels of immunity (Enzootic stability)
  • Calves <9months are refractory to disease, so develop disease with no clinical signs
    *
27
Q

Describe life cycle, pathogenesis & epidemiology of Leishmania

A

Life cycle

  • Transmitted via sand fly
  • Invades macrophages and forms Amistigote
  • picked up by new sandfly when feeding and miltiplys in gut.

Pathogenesis

  • Very long incubation period
  • Cutaneos form - ulcers on pinnae
  • Visceral form - wasting condition, generalised eczema and intermittent fever

Epidemiology

  • Dependant on distibution of sand flys
  • No sandflys in england but can be caught on holiday
  • Can be diagnosed by skin smeer or LN biopsy
  • Treated via chemotherapy and prevented by vaccination and vector control
28
Q

What is dirofilaria’s & whats it life cycle and clinical signs

A

Canine heartworm diesease which is a serious cause of canine morbidity and mortality. Prepatent period of 6-7months

Life
cycle

  • adults release microfilaria into blood ( 2 years)
  • Microfilaria are ingested by mosquito and develop L1-L3 within 14 days
  • L3 transmitted by mosquito into dog
  • L3-L4-L5 in dog before migrating to the heart where it can survive for 5-7 years

Clinical signs

  • Excercise intolerance
  • chronic heart failure
  • acute collapse
29
Q

where does bronchial circulation return blood to

A

Bronchial circulation has a low volume and high pressure. Blood is returned to the left side of the heart via pulmonary vein and the right side of the heart via bronchial vein and azygous vein

30
Q

What two factors effect perfusion

A
  • Hypoxia - Blood vessels constric allowing for blood to reach where its needed
  • Excercise - Increase number of open capillaries. Increase pulmonary arterial pressure
31
Q

What would happen if the pulmonary artery is blocked

A

Diameter of bronchial arteries would increase. in addition, angiogenesis would occur to obstruc the obstruction

32
Q

Explain the terms shunt and physiological dead space

A

Shunt

  • Blockage of the airway preventing adequate ventilation but blood is normal

Physiological dead space

  • Block in blood flow but normal ventilation
33
Q

Why does the lower regions of the lung ventilate/perfuse better than upper regions ?

A

Lower regions of the lung have higher forces of gravity. This reduces intra pleural pressure at the base of the lung. Alveolar are also smaller at the base and have a higher compliance. Also gravity increase hydrostatic pressure at the base increasing perfusion

34
Q

What is the bohr effect

A

Shift of the Hb-02 concentration curve to the right due to increased C02 concentration. Reduces affinity of HB for 02, meaning its more readily released

35
Q

What is the haldane effect

A

When 02 binds to HB displacing C02. This increases the amount of co2 removed from the lungs

36
Q

Why are peripheral chemoreceptors important

A
  • Central chemoreceptors only detect changes in C02
  • Peripheral chemoreceptors capable of detecting a decrease in 02. This leads to an increase in inspiration. Key in chronic conditions showing great plasticity
37
Q

Why is lead 2 commonly used during ECG

A

Lead II runs from Right forlimb to hind left limb. Meaning it runs parallel to the heart therefore will give best trace.

38
Q

What are the possibilities if there is no P wave for every QRS?

A
  • Premature complex - area of mycardium prematurely depolarising. due to irritation
  • Sinus arrest with escape complexes - SA node stops depolarising
  • No organised atrial depolarisation - Not depolarising in a organsied way. Atrial standstill or atrial fibrilation
39
Q

What are the possible reasons for a P with no QRS

A
  • Failure of AV conduction
  • Second degree of AV block - Intermittent failure of AV to initiate ventricular depolarisation
  • Third degree AV block - Complete failure of AV to initiate ventricular contraction (Accessory pacemaker will have to generate escape complexes)

BVETMED2 (10 decks)

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