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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
disorders of impulse conduction - bradyarrhythmias
slow rhythm conduction delays or blocks sinoatrial blocks / atrioventricular blocks
26
disorders of impulse conduction - tachyarrhythmias
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
27
clinical consequences of arrythmias
often no consequences unless we increase the systolic demands of the body signs related to tissue or organ ischaemia weakness syncope death
28
bradydysrhythmias - sinus arrhythmia
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
29
bradydysrhythmias - sinus bradycardia
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
30
bradydysrhythmias - sinoatrial block and sinoatrial arrest
absence of electrical activity - nothing on ECG typically asymptomatic long periods are interrupted but junctional or ventricular escape complexes
31
bradydysrhythmias - atrial standstill
QRST complexes without P waves (assuming atrial fibrillation not present) pathologic due to atrial muscle loss and fibrosis hyperkalaemia in cats
32
bradydysrhythmias - sick sinus syndrome
degenerative disease of the sinus node persistent bradycardia; paroxysms of rapid regular or irregular atrial tachycardia and SA block or arrest pacemaker implant
33
bradydysrhythmias - 1st degree AV block
prolonged PR interval
34
bradydysrhythmias - 2nd degree AV block
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
35
bradydysrhythmias - 3rd degree AV block
complete AV dissociation - none of the atrial pulses are conducted to the ventricles no relationship between P waves and QRST complexes
36
tachydysrhythmias
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
37
sinus tachycardia
higher than normal rate with regular rhythm pain, anxiety, hypoxia, acidaemia, hyperthyroidism, drugs
38
supraventricular premature depolarisations
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
39
supraventricular tachycardia
ectopic focus - increased automaticity can be very difficult to distinguish from sinus tachycardia ECG: QRS complexes very narrow, P waves and QRS altogether
40
supraventricular tachyarrhythmias - atrial fibrillation
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
ventricular tachyarrhythmias - premature ventricular contractions
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
ventricular tachycardias
3 or more successive PVCs sustained if more than 30 seconds monomorphic or polymorphic (more serious) most are regular
43
ventricular fibrillation
pre-terminal event fatal if not treated make sure electrodes are properly connected
44
mulberry heart disease
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
compensatory mechanisms for shock
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
types of circulatory shock
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
what is third spacing of fluids?
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
how does sepsis cause shock?
reduces systemic vascular resistance = malperfusion
49
how can brain injury cause shock? (neurogenic shock)
damage to sympathetic nuclei of medulla - > whole body vasodilation
50
what happens after a large haemorrhage?
fluid redistribution - hours-day protein reconstitution - days RBC regeneration - weeks
51
vasoconstricting agents
ergot alkaloids, adrenaline
52
aortic thromboembolism
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
vasculitis
inflammation of blood vessels often systemic or immune-mediated results: haemorrhage, oedema, necrosis may induce DIC causes: MCF, hendra, drugs, immune-mediated
54
hyperaemia
an increase in blood flow to a region active - increased metabolic activity passive - obstruction or restriction of blood flow reactive - post-obstruction resolution
55
what are the 4 mechanisms of oedema formation?
1) increased hydrostatic pressure 2) increased vascular permeability 3) decreased colloidal osmotic pressure 4) decreased lymphatic drainage
56
what factors can cause localised oedema?
increased vascular permeability increased venous hydrostatic pressure decreased lymphatic drainage
57
what factors can cause generalised oedema?
decreased osmotic pressure increased vascular permeability increased venous hydrostatic pressure
58
ventricular septal defect
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
patent ductus arteriosus
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
jet lesions
fibrosis seen in the heart due to continuous turbulent blood flow (seen with congenital heart defects)
61
patent foramen ovale (PFO) / atrial septal defect
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
dysplasia of the tricuspid valve
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
subaortic stenosis
(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
pulmonic stenosis
(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
persistent right aortic arch
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
transposition of the aorta and pulmonary artery
the two main arteries leaving the heart are reversed this diagnosis is usually made on a stillborn animal (don't usually survive)
67
hypertrophic cardiomyopathy in cats
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
cardiomyopathy in poultry
idiopathic cardiomyopathy of broilers / ascites syndrome
69
toxic cardiomyyopathies
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
nutritional myopathy / white muscle disease
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
myxomatous valvular degeneration (endocardiosis)
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
endocarditis
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
morphology of endocarditis
caseous exudate marked nodular thickening of valves hyperaemia of tissues
74
pericarditis
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
morphology of pericarditis
thickened pericardium fibrinosuppurative exudate
76
most common causative infectious agents of endo or pericarditis in horses
strep equi, actinobacillus equuli, E. coli
77
most common causative infectious agents of endo or pericarditis in cattle
trueperella pyogenes, strep, mannheimia haemolytica
78
most common causative infectious agents of endo or pericarditis in sheep
strep, mannheimia haemolytica, pasteurella multicoda
79
most common causative infectious agents of endo or pericarditis in dogs and cats
strep, staph aurueus, e. coli
80
most common causative infectious agents of endo or pericarditis in pigs
erysipelothrix rhusiopathiae, haemophilus parasuis (Glasser's disease), strep suis, pateurella multicoda, mcyoplasma
81
most common causative infectious agents of endo or pericarditis in poultry
e.coli, mycoplasma, salmonella, pasteurella multicoda
82
myocarditis
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
calcification and mineralisation
e.g. chicken visceral gout, horse with metastatic hypercalcaemia due to vit D toxicosis
84
pericardial effusion
accumulation of fluid within the pericardial space
85
dirofilariasis
(heartworm) most common in dogs prophylaxis most important thing vascular blockage -> pulm hypertension -> RV hypertrophy -> RSCHF
86
most common primary cardiac neoplasias
rhabdomyoma (PIGS) rhabdomyosarcoma (dogs - rare) Schwannoma / neurofibroma (cattle) haemangiosarcoma (dog - most common in small animals)
87
most common secondary cardiac neoplasias
lymphoma (cattle) aortic body tumour (dogs- brachycephalics) ectopic thyroid / parathyroid neoplasia (dogs)
88
morphological appearance of cardiac neoplasia
areas of pallor through myocardium that look like necrosis, but the heart is swollen (tissue added, so cannot be necrosis)
89
feline infectious peritonitis (FIP)
infection with a mutation of feline enteric coronavirus systemic infection + host immune response strong response = virus cleared weak response = vasculitis
90
african and classical swine fever
separate viruses but very similar lesions (exotic to aus) lymph node, splenomegaly, infarction of the spleen
91
DIC
intermediary mechanisms of disease - not a disease itself but it is a way that many diseases manifest
92
farcy (glanders disease)
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
anthrax
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
diseases of the spleen
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
splenomegaly - congested
Bloody appearance Circulatory disturbances, sepsis, barbiturates, haemolytic anaemia, infectious diseases e.g. anthrax
96
splenomagaly - non-congested
meaty appearane subacute/chronic infectious disease, cellular proliferation (diffuse neoplasia), amyloidosis
97
splenic nodules in the dog
common incidental finding or acute collapse due to haemorrhage differentials: haemangiosarcoma, nodular hyperplasia, lymphoma, haematoma

VET377 (SPAM) (13 decks)

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