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VET377 (SPAM) > Cardiovascular system > Flashcards

Cardiovascular system Flashcards

1
Q

what is the difference between heart disease and heart failure?

A

Heart disease = the presence of an abnormality in cardiac function or structure (can reduce performance but doesn’t cause complete failure).

Heart failure = the clinical manifestation of heart disease, when the heart is unable to maintain sufficient cardiac output to satisfy the needs of the body. Heart failure is not an aetiological diagnosis, but the end product of numerous causes.

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2
Q

clinical signs of heart disease

A

altered heart rate - tachy or bradycardia
altered heart rhythm - arrhythmia
altered audibility of heart sounds
presence of auditory vibrations - heart murmur

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3
Q

define cardiac arrhythmia

A

= a disturbance in the normal cardiac rhythm due to an abnormality in impulse initiation and or impulse propagation. Can be physiologic or pathologic

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4
Q

define cardiac murmur

A

an auditory vibration of longer duration than the normal heart sounds created when laminar flow is disrupted (grade 1-6). Can be physiologic or pathologic.

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5
Q

what are the two main types of cardiac failure?

A

diastolic - heart is unable to fill appropriately
systolic - heart is unable to pump out the blood appropriately

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6
Q

signs of systolic heart failure

A
  • Weak pulses
  • Pale mucus membranes
  • Prolonged CRT
  • Tachycardia
  • Cold extremities
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7
Q

signs of left-sided diastolic heart failure

A
  • Pulmonary oedema
  • Adventitial sounds - wheezing, crackles etc.
  • Cyanosis
  • Tachypnoea (rapid breathing rate
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8
Q

signs of right-sided heart failure

A
  • Ascites
  • Pleural effusion
  • Peripheral oedema
  • Jugular distension and pulses
  • Hepatojugular reflex – small animals
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9
Q

Frank-Starling mechanism

A

increased preload increases myocyte stretch, increases contractility, and thus increases stroke volume

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10
Q

compensatory mechanisms in heart failure

A

sympathetic NS - increases HR, increases contractility, neurogenic vasoconstriction
- improves CO initially, later increases afterload, reduced peripheral tissues perfusion, increases heart muscle oxygen requirements

RAAS - improved CO, increased preload, maintains BP
- eventually increases thirst, vasoconstriction, water retention and congestion

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11
Q

counter-compensatory mechanisms

A

Atrial natriuretic peptide
- Released in response to atrial stretch
- Natriuretic and diuretic properties
- Response to ANP blunted in chronic heart failure

Brain natriuretic peptide
- From ventricular stretch
- Can be used as a clinical biomarker

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12
Q

mechanisms of heart failure

A
  1. Sustained pressure overload
  2. Sustained volume overload
  3. Altered cardiac muscle contractility – systolic dysfunction
  4. Altered cardiac muscle compliance – diastolic dysfunction
  5. Altered normal cardiac rate and rhythm
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13
Q

what type of hypertrophy is caused by sustained pressure overload

A

concentric hypertrophy
(heart muscle has to push harder against the pressure and so it thickens - parallel addition of sarcomeres)

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14
Q

what type of hypertrophy is caused by sustained volume overload

A

eccentric hypertrophy
(more blood filling the chambers means that walls are stretched and so sarcomeres are added in series)

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15
Q

sustained pressure overload

A

is due to increased afterload - ventricular outflow tract lesions e.g. subaortic stenosis, pulmonic stenosis

pulmonic hypertension - affects right ventricle

systemic hypertension - affects left ventricle

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16
Q

clinical signs of pulmonary hypertension

A

tachypnoea
syncope
split S2 heart sounds
hypertrophy of the right ventricle

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17
Q

sustained volume overload

A

due to increased preload
abnormal patterns in blood flow
mitral valve disease

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18
Q

systolic dysfunction

A

altered cardiac muscle contractility
reduced ejection fraction and enlarged end-diastolic chamber volume
CO is decreased but diastolic filling is normal

insufficient myocytes - anything that causes myocardial damage (inflammation, toxins)

dysfunctional myocytes - unknown, hereditary, iatrogenic

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19
Q

dilated cardiomyopathy

A

thin-walled, weak ventricles
associated with systolic dysfunction (muscle is thin and flaccid so cant contract appropriately)

manifests as L-sided heart failure - lethargy, weakness, syncope

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20
Q

diastolic dysfunction

A

altered cardiac muscle compliance
increase resistance to filling

slowed or incomplete relaxation - increased myocyte calcium, decreased ATP, activation of angiotensin II

reduced left ventricular filling

altered passive elastic properties - wall stiffness due to endomyocardial fibrosis

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21
Q

restrictive cardiomyopathy

A

associated with diastolic dysfunction
thick-walled, stiff ventricles that cant relax
due to increased myocardial fibrosis / leukocyte infiltrates / endomyocardial fibrosis
may be post-inflammatory

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22
Q

hypertrophic cardiomyopathy

A

associated with diastolic dysfunction
big, thick-walled ventricles that cant relax properly
most common heart disease in cats

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23
Q

automaticity

A
  • spontaneous depolarisation without an external stimulus
  • SA node is dominant – fastest rate of depolarisation
  • The remaining portions are latent pacemakers – fail-safe system
  • If the SA node fails to depolarise, lower order pacemakers take over, but a slower heart rate ensues
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24
Q

Disorders of impulse formation – automaticity

A

depressed automaticity - slowing rate of pacemaker cell discharge

enhanced automaticity - faster rate of pacemaker cell discharge

abnormal automaticity - damaged cells that arent normally automatic become so or cells that have a slow rate become faster

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25
Q

disorders of impulse conduction - bradyarrhythmias

A

slow rhythm
conduction delays or blocks

sinoatrial blocks / atrioventricular blocks

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26
Q

disorders of impulse conduction - tachyarrhythmias

A

fast rhythm

can be caused by re-entry - the re-stimulation of a cell by nearby tissue after it has been depolarised
does not normally occur due to the refractory period

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27
Q

clinical consequences of arrythmias

A

often no consequences unless we increase the systolic demands of the body
signs related to tissue or organ ischaemia
weakness
syncope
death

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28
Q

bradydysrhythmias - sinus arrhythmia

A

phasic variation in sinus cycle length
resp form - P-P interval shortens during inspiration due to reflex inhibition of vagal tone, and lengthens during expiration
can occur without influence of respiration
regularly irregular rhythm
should not require treatment

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29
Q

bradydysrhythmias - sinus bradycardia

A

regular sinus rhythm but has sinus firing that is too slow
high vagal tone, drugs, hypothermia, intrinsic conduction disease
typically no clinical signs
response to atropine

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30
Q

bradydysrhythmias - sinoatrial block and sinoatrial arrest

A

absence of electrical activity - nothing on ECG
typically asymptomatic
long periods are interrupted but junctional or ventricular escape complexes

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31
Q

bradydysrhythmias - atrial standstill

A

QRST complexes without P waves (assuming atrial fibrillation not present)
pathologic due to atrial muscle loss and fibrosis
hyperkalaemia in cats

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32
Q

bradydysrhythmias - sick sinus syndrome

A

degenerative disease of the sinus node
persistent bradycardia; paroxysms of rapid regular or irregular atrial tachycardia and SA block or arrest
pacemaker implant

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33
Q

bradydysrhythmias - 1st degree AV block

A

prolonged PR interval

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34
Q

bradydysrhythmias - 2nd degree AV block

A

some sinus depolarisations conduct through the AV node to depolarise the ventricles while others do not
regularly irregular rhythm
P-wave without following QRST complex

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35
Q

bradydysrhythmias - 3rd degree AV block

A

complete AV dissociation - none of the atrial pulses are conducted to the ventricles

no relationship between P waves and QRST complexes

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36
Q

tachydysrhythmias

A

differentiated on the basis of the width of the QRS complexes - normal(narrow) or wide

and on the location - supraventricular or ventricular

normal width implies conduction through the AV node -> ventricular tachydysrhythmias are wide

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37
Q

sinus tachycardia

A

higher than normal rate with regular rhythm
pain, anxiety, hypoxia, acidaemia, hyperthyroidism, drugs

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38
Q

supraventricular premature depolarisations

A

premature beat arising from an ectopic focus from within the atria, AV junction

on ECG: single premature beat, often abnormal P wave but normal QRS complex

single events - do not require treatment

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39
Q

supraventricular tachycardia

A

ectopic focus - increased automaticity
can be very difficult to distinguish from sinus tachycardia

ECG: QRS complexes very narrow, P waves and QRS altogether

40
Q

supraventricular tachyarrhythmias - atrial fibrillation

A

most common pathophysiologic arrhythmia in horses

irregularly irregular rhythm
erratic cardiac rhythm
variable pulse quality
in horses, signs are only present during exercise

no P waves, fibrillation waves

41
Q

ventricular tachyarrhythmias - premature ventricular contractions

A

premature ventricular depolarisations - often wide and bizarre QRS complexes
no related P wave, large bizarre T wave
present in normal animals
non-cardiac diseases = electrolyte abnormalities, post-trauma, post-surgery, colic
treatment not necessary with single PVCs

42
Q

ventricular tachycardias

A

3 or more successive PVCs
sustained if more than 30 seconds
monomorphic or polymorphic (more serious)
most are regular

43
Q

ventricular fibrillation

A

pre-terminal event
fatal if not treated
make sure electrodes are properly connected

44
Q

mulberry heart disease

A

vitamin E / selenium deficiency in pigs
many pigs death over a short period
multifocal areas of necrosis in heart +/- liver
epicardial haemorrhage esp RA
arrhythmias of ventricular origin - cause of death

morphology: pale areas of necrosis within heart muscle

45
Q

compensatory mechanisms for shock

A

baroreceptor response = within seconds
- sympathetic nervous stimulation
- increased HR and contractility
- vasoconstriction

salt and water reabsorption = min to hours
- to restore blood volume
- angiotensin 2 - vasoconstriction
- aldosterone - salt retention
- ADH - water retention

46
Q

types of circulatory shock

A

hypovolaemic - haemorrhage, severe dehydration e.g. diarrhoea, third spacing of fluids

obstructive - something stopping blood from going in or out of the heart e.g. pulmonary embolism

distributive - anaphylaxis, septic, neurogenic

cardiogenic - acute heart failure (not chronic)

47
Q

what is third spacing of fluids?

A

too much fluid moves from intravascular space into interstitial (third) space - can be due to hypoalbuminaemia, which causes fluids to move out of vessels

48
Q

how does sepsis cause shock?

A

reduces systemic vascular resistance = malperfusion

49
Q

how can brain injury cause shock? (neurogenic shock)

A

damage to sympathetic nuclei of medulla - > whole body vasodilation

50
Q

what happens after a large haemorrhage?

A

fluid redistribution - hours-day
protein reconstitution - days
RBC regeneration - weeks

51
Q

vasoconstricting agents

A

ergot alkaloids, adrenaline

52
Q

aortic thromboembolism

A

saddle thrombus in cats
common complication of feline hypertrophic cardiomyopathy
increased risk with left atrial enlargement

obstructs blood flow to pelvic limbs - acute posterior paresis

53
Q

vasculitis

A

inflammation of blood vessels
often systemic or immune-mediated

results: haemorrhage, oedema, necrosis
may induce DIC
causes: MCF, hendra, drugs, immune-mediated

54
Q

hyperaemia

A

an increase in blood flow to a region
active - increased metabolic activity
passive - obstruction or restriction of blood flow
reactive - post-obstruction resolution

55
Q

what are the 4 mechanisms of oedema formation?

A

1) increased hydrostatic pressure
2) increased vascular permeability
3) decreased colloidal osmotic pressure
4) decreased lymphatic drainage

56
Q

what factors can cause localised oedema?

A

increased vascular permeability
increased venous hydrostatic pressure
decreased lymphatic drainage

57
Q

what factors can cause generalised oedema?

A

decreased osmotic pressure
increased vascular permeability
increased venous hydrostatic pressure

58
Q

ventricular septal defect

A

failure of complete development of the interventricular septum
allows blood to shunt from left to right ventricle - often causes biventricular hypertrophy due to volume overload
loud hollow systolic murmur over right thorax
wide range of species

59
Q

patent ductus arteriosus

A

the ductus arteriosus is a link between the aorta and pulmonary artery present in foetuses to allow blood to bypass the lungs
in some animals it fails to close and blood can flow from aorta back into the pulm. artery - overcirculation of lungs, pulmonary hypertension, L-sided congestive heart failure
or if pulmonary resistance increases then the shunt can reverse -> sudden death, lethargy, cyanosis

60
Q

jet lesions

A

fibrosis seen in the heart due to continuous turbulent blood flow (seen with congenital heart defects)

61
Q

patent foramen ovale (PFO) / atrial septal defect

A

hole between the right and left atria
excessive flow from left to right atrium causes volume overload of right atrium and pulmonary hypertension
right-sided congestive heart failure
affects a range of species

62
Q

dysplasia of the tricuspid valve

A

common in cats, rare in other species
valve leaflets become thickened
(congenital/hereditary)
regurgitation of blood causes volume overload, leading to atrial dilation and eccentric ventricular hypertrophy

63
Q

subaortic stenosis

A

(lesion below the aortic valve usually)
most common in dogs and pigs
the most common congenital anomaly in large breed dogs
most patients present with lethargy, exercise intolerance and syncope

64
Q

pulmonic stenosis

A

(lesion usually at the level of the pulmonary valve)
most common in dogs
variable presentation
outflow tract obstruction of right ventricle, leads to pressure overload of RV and concentric hypertrophy (also R congestive heart failure)

65
Q

persistent right aortic arch

A

most common in dogs, rare in other species
ligamentum arteriosum that passes over the oesophagus and the trachea forms a vascular ring that can constrict around the oesophagus
this causes dilation of the cranial oesophagus, as well as dysphagia, regurgitation, aspiration pneumonia

66
Q

transposition of the aorta and pulmonary artery

A

the two main arteries leaving the heart are reversed
this diagnosis is usually made on a stillborn animal (don’t usually survive)

67
Q

hypertrophic cardiomyopathy in cats

A

young to middle-aged cats, males more often than females
pathogenesis: LV hypertrophy -> unable to relax during diastole -> increased pressure -> dilation of LA -> blood backing up to lungs -> LSCHF (pulmonary oedema, pleural effusion)

68
Q

cardiomyopathy in poultry

A

idiopathic cardiomyopathy of broilers / ascites syndrome

69
Q

toxic cardiomyyopathies

A

range of drugs, plants and other toxins
most common: ionophores in horses and dogs
plants: cottonseed, white snakeroot, fluoroacetate toxicity in ruminants

causes myocardial degeneration and necrosis +/- cardiac conduction disturbances
if the animal survives may progress to fibrosis

70
Q

nutritional myopathy / white muscle disease

A

ruminants
affects skeletal and cardiac muscle
polyphasic myopathy, usually in juveniles
may be subclinical, present as lameness, inability to suckle, exercise intolerance, sudden death
heart lesions are often myocardial necrosis and fibrosis with some mononuclear inflammation

71
Q

myxomatous valvular degeneration (endocardiosis)

A

progressive mitral valve degeneration
the most common CVS lesion of the dog
mitral insufficiency -> regurgitation into LA -> LA dilation -> eccentric LV hypertrophy -> LSCHF
toy/small breeds and old dogs

72
Q

endocarditis

A

inflammation of the valves and endocardium
occurs in all species, often neonates/juveniles
most often bacterial
mitral > aortic > tricuspid > pulmonary

infectious focus elsewhere in the body e.g. peridontal disease/mastitis can lead to bacteremia = increased risk of endocarditis

73
Q

morphology of endocarditis

A

caseous exudate
marked nodular thickening of valves
hyperaemia of tissues

74
Q

pericarditis

A

inflammation within the pericardium, also often involving the epicardium
common in production animals esp. pigs and chickens
rare in small animals
often haematogenous
e.g. traumatic reticuloperitonitis in cattle (hardware disease)
often results in sudden death due to highly virulent bacteria

75
Q

morphology of pericarditis

A

thickened pericardium
fibrinosuppurative exudate

76
Q

most common causative infectious agents of endo or pericarditis in horses

A

strep equi, actinobacillus equuli, E. coli

77
Q

most common causative infectious agents of endo or pericarditis in cattle

A

trueperella pyogenes, strep, mannheimia haemolytica

78
Q

most common causative infectious agents of endo or pericarditis in sheep

A

strep, mannheimia haemolytica, pasteurella multicoda

79
Q

most common causative infectious agents of endo or pericarditis in dogs and cats

A

strep, staph aurueus, e. coli

80
Q

most common causative infectious agents of endo or pericarditis in pigs

A

erysipelothrix rhusiopathiae, haemophilus parasuis (Glasser’s disease), strep suis, pateurella multicoda, mcyoplasma

81
Q

most common causative infectious agents of endo or pericarditis in poultry

A

e.coli, mycoplasma, salmonella, pasteurella multicoda

82
Q

myocarditis

A

less common than endocarditis and pericarditis but often occurs with them
even small lesions may be fatal if they involve the conduction system
outcomes: resolution, myocardial scarring, progressive myocardial damage

83
Q

calcification and mineralisation

A

e.g. chicken visceral gout, horse with metastatic hypercalcaemia due to vit D toxicosis

84
Q

pericardial effusion

A

accumulation of fluid within the pericardial space

85
Q

dirofilariasis

A

(heartworm)
most common in dogs
prophylaxis most important thing
vascular blockage -> pulm hypertension -> RV hypertrophy -> RSCHF

86
Q

most common primary cardiac neoplasias

A

rhabdomyoma (PIGS)
rhabdomyosarcoma (dogs - rare)
Schwannoma / neurofibroma (cattle)
haemangiosarcoma (dog - most common in small animals)

87
Q

most common secondary cardiac neoplasias

A

lymphoma (cattle)
aortic body tumour (dogs- brachycephalics)
ectopic thyroid / parathyroid neoplasia (dogs)

88
Q

morphological appearance of cardiac neoplasia

A

areas of pallor through myocardium that look like necrosis, but the heart is swollen (tissue added, so cannot be necrosis)

89
Q

feline infectious peritonitis (FIP)

A

infection with a mutation of feline enteric coronavirus
systemic infection + host immune response
strong response = virus cleared
weak response = vasculitis

90
Q

african and classical swine fever

A

separate viruses but very similar lesions
(exotic to aus)
lymph node, splenomegaly, infarction of the spleen

91
Q

DIC

A

intermediary mechanisms of disease - not a disease itself but it is a way that many diseases manifest

92
Q

farcy (glanders disease)

A

bacterial infection (Burkholderia mallei) that is ingested and infected through the pharynx, and then spreads haematogenously to form ulcerated nodules in the skin that track along lymph vessels

93
Q

anthrax

A

Bacillus anthracis
acute septicaemia and death in herbivores
variable presentation in other species
exposure via ingestion, inhalation or skin
spores germinate in macrophages to local lymph nodes, lymphatics and blood, spleen, tocin production
ZOONOTIC

94
Q

diseases of the spleen

A

Congenital disease e.g. asplenia, accessories spleens etc
Degenerative disease e.g. senile atrophy, siderosis, amyloidosis
Rupture - trauma, massas, volvulus (GDV)
Infection e.g. tularaemia, leishmania, anthrax
Neoplasia

95
Q

splenomegaly - congested

A

Bloody appearance
Circulatory disturbances, sepsis, barbiturates, haemolytic anaemia, infectious diseases e.g. anthrax

96
Q

splenomagaly - non-congested

A

meaty appearane
subacute/chronic infectious disease, cellular proliferation (diffuse neoplasia), amyloidosis

97
Q

splenic nodules in the dog

A

common
incidental finding or acute collapse due to haemorrhage
differentials: haemangiosarcoma, nodular hyperplasia, lymphoma, haematoma

VET377 (SPAM) (13 decks)

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