Cardiovascular system Flashcards
what is the difference between heart disease and heart failure?
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.
clinical signs of heart disease
altered heart rate - tachy or bradycardia
altered heart rhythm - arrhythmia
altered audibility of heart sounds
presence of auditory vibrations - heart murmur
define cardiac arrhythmia
= a disturbance in the normal cardiac rhythm due to an abnormality in impulse initiation and or impulse propagation. Can be physiologic or pathologic
define cardiac murmur
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.
what are the two main types of cardiac failure?
diastolic - heart is unable to fill appropriately
systolic - heart is unable to pump out the blood appropriately
signs of systolic heart failure
- Weak pulses
- Pale mucus membranes
- Prolonged CRT
- Tachycardia
- Cold extremities
signs of left-sided diastolic heart failure
- Pulmonary oedema
- Adventitial sounds - wheezing, crackles etc.
- Cyanosis
- Tachypnoea (rapid breathing rate
signs of right-sided heart failure
- Ascites
- Pleural effusion
- Peripheral oedema
- Jugular distension and pulses
- Hepatojugular reflex – small animals
Frank-Starling mechanism
increased preload increases myocyte stretch, increases contractility, and thus increases stroke volume
compensatory mechanisms in heart failure
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
counter-compensatory mechanisms
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
mechanisms of heart failure
- Sustained pressure overload
- Sustained volume overload
- Altered cardiac muscle contractility – systolic dysfunction
- Altered cardiac muscle compliance – diastolic dysfunction
- Altered normal cardiac rate and rhythm
what type of hypertrophy is caused by sustained pressure overload
concentric hypertrophy
(heart muscle has to push harder against the pressure and so it thickens - parallel addition of sarcomeres)
what type of hypertrophy is caused by sustained volume overload
eccentric hypertrophy
(more blood filling the chambers means that walls are stretched and so sarcomeres are added in series)
sustained pressure overload
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
clinical signs of pulmonary hypertension
tachypnoea
syncope
split S2 heart sounds
hypertrophy of the right ventricle
sustained volume overload
due to increased preload
abnormal patterns in blood flow
mitral valve disease
systolic dysfunction
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
dilated cardiomyopathy
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
diastolic dysfunction
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
restrictive cardiomyopathy
associated with diastolic dysfunction
thick-walled, stiff ventricles that cant relax
due to increased myocardial fibrosis / leukocyte infiltrates / endomyocardial fibrosis
may be post-inflammatory
hypertrophic cardiomyopathy
associated with diastolic dysfunction
big, thick-walled ventricles that cant relax properly
most common heart disease in cats
automaticity
- 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
Disorders of impulse formation – automaticity
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
disorders of impulse conduction - bradyarrhythmias
slow rhythm
conduction delays or blocks
sinoatrial blocks / atrioventricular blocks
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
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
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
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
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
bradydysrhythmias - atrial standstill
QRST complexes without P waves (assuming atrial fibrillation not present)
pathologic due to atrial muscle loss and fibrosis
hyperkalaemia in cats
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
bradydysrhythmias - 1st degree AV block
prolonged PR interval
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
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
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
sinus tachycardia
higher than normal rate with regular rhythm
pain, anxiety, hypoxia, acidaemia, hyperthyroidism, drugs
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
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
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
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
ventricular tachycardias
3 or more successive PVCs
sustained if more than 30 seconds
monomorphic or polymorphic (more serious)
most are regular
ventricular fibrillation
pre-terminal event
fatal if not treated
make sure electrodes are properly connected
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
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
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)
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
how does sepsis cause shock?
reduces systemic vascular resistance = malperfusion
how can brain injury cause shock? (neurogenic shock)
damage to sympathetic nuclei of medulla - > whole body vasodilation
what happens after a large haemorrhage?
fluid redistribution - hours-day
protein reconstitution - days
RBC regeneration - weeks
vasoconstricting agents
ergot alkaloids, adrenaline
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
vasculitis
inflammation of blood vessels
often systemic or immune-mediated
results: haemorrhage, oedema, necrosis
may induce DIC
causes: MCF, hendra, drugs, immune-mediated
hyperaemia
an increase in blood flow to a region
active - increased metabolic activity
passive - obstruction or restriction of blood flow
reactive - post-obstruction resolution
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
what factors can cause localised oedema?
increased vascular permeability
increased venous hydrostatic pressure
decreased lymphatic drainage
what factors can cause generalised oedema?
decreased osmotic pressure
increased vascular permeability
increased venous hydrostatic pressure
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
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
jet lesions
fibrosis seen in the heart due to continuous turbulent blood flow (seen with congenital heart defects)
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
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
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
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)
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
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)
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)
cardiomyopathy in poultry
idiopathic cardiomyopathy of broilers / ascites syndrome
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
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
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
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
morphology of endocarditis
caseous exudate
marked nodular thickening of valves
hyperaemia of tissues
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
morphology of pericarditis
thickened pericardium
fibrinosuppurative exudate
most common causative infectious agents of endo or pericarditis in horses
strep equi, actinobacillus equuli, E. coli
most common causative infectious agents of endo or pericarditis in cattle
trueperella pyogenes, strep, mannheimia haemolytica
most common causative infectious agents of endo or pericarditis in sheep
strep, mannheimia haemolytica, pasteurella multicoda
most common causative infectious agents of endo or pericarditis in dogs and cats
strep, staph aurueus, e. coli
most common causative infectious agents of endo or pericarditis in pigs
erysipelothrix rhusiopathiae, haemophilus parasuis (Glasser’s disease), strep suis, pateurella multicoda, mcyoplasma
most common causative infectious agents of endo or pericarditis in poultry
e.coli, mycoplasma, salmonella, pasteurella multicoda
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
calcification and mineralisation
e.g. chicken visceral gout, horse with metastatic hypercalcaemia due to vit D toxicosis
pericardial effusion
accumulation of fluid within the pericardial space
dirofilariasis
(heartworm)
most common in dogs
prophylaxis most important thing
vascular blockage -> pulm hypertension -> RV hypertrophy -> RSCHF
most common primary cardiac neoplasias
rhabdomyoma (PIGS)
rhabdomyosarcoma (dogs - rare)
Schwannoma / neurofibroma (cattle)
haemangiosarcoma (dog - most common in small animals)
most common secondary cardiac neoplasias
lymphoma (cattle)
aortic body tumour (dogs- brachycephalics)
ectopic thyroid / parathyroid neoplasia (dogs)
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)
feline infectious peritonitis (FIP)
infection with a mutation of feline enteric coronavirus
systemic infection + host immune response
strong response = virus cleared
weak response = vasculitis
african and classical swine fever
separate viruses but very similar lesions
(exotic to aus)
lymph node, splenomegaly, infarction of the spleen
DIC
intermediary mechanisms of disease - not a disease itself but it is a way that many diseases manifest
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
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
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
splenomegaly - congested
Bloody appearance
Circulatory disturbances, sepsis, barbiturates, haemolytic anaemia, infectious diseases e.g. anthrax
splenomagaly - non-congested
meaty appearane
subacute/chronic infectious disease, cellular proliferation (diffuse neoplasia), amyloidosis
splenic nodules in the dog
common
incidental finding or acute collapse due to haemorrhage
differentials: haemangiosarcoma, nodular hyperplasia, lymphoma, haematoma
