Cardiology Anatomy, Function, & Disease Flashcards
What is the function of the cardiovascular system?
1) To pump blood, delivering oxygen, nutrients, and water while removing carbon dioxide and metabolic waste
2) To provide thermoregulation (vasoconstrict and dilation)
3) To support body functions (urine formation in kidney, gas exchange in lings, digestive processes and absorption, reproductive system functions
fibrous sac that surrounds the heart
contains a trivial amount of fluid for lubrication
pericardium
Track the flow of blood:
Right Ventricle > ________> Lungs > _________>Left ventricle >____>Tissues >_______
Pulmonary artery
Pulmonary vein
Aorta
Cranial/Caudal vena cava
Do the atrium or ventricles have higher pressure
ventricles
the auricular appendages have
numerous muscle bundles- pectinate muscles
What is significant about the auricular appendage in a cat with heart disease
If a cat has advanced heart disease there might be static blood flow and a dilated left auricular appendage
this makes it so that blood sits there and can lead to an arterial thromboembolism
What three vessels enter into the right atrium
1) Cranial Vena Cava
2) Caudal Vena Cava
3) Coronary sinus (venous return from the myocardium)
Provides venous return from the myocardium to the right atrium
coronary sinus
where do the pulmonary veins go
they go into the left atrium where blood will then go into the mitral valve into the left ventricle
how many papillary muscles does the left ventricle have?
What about the right ventricle
LV: 2 papillary muscles connecting chordae tendineae to the mitral valve
RV: 3-5 papillary muscles connecting chordae tendineae to the tricuspid valve
Pressures on the right side of the heart are generally ______ to _____ the pressures of the left size
1/5 to 1/6 the pressures of the left sides
LV=130mmHg
RV: 25mmHg
LA=0-10mmHg
RA=0-5mmHg
Aorta 130/105/90 mmHg
Pulmonary artery 25/18/12mmHg
the valve that separates the RA from RV
tricuspid
the valve that separates the RV from PA
pulmonary
the valve that separates the LA from LV
mitral valve
the valve that separates the LV from Ao
Aortic valve
How many leaflets does the mitral valve have?
2
Anterior leaflet: short circumference, long length
Posterior leaflet: large circumference, short length
How many leaflets does the tricuspid valve have
2 to 3 leaflets, larger circumference
Atrioventricular valves (Mitral and Tricuspid) must be _______ during diastole and __________ during systole
open in diastole (when ventricle is relaxing, allowing filling of ventricles)
closed in systole (when ventricles contract, valves closed, preventing backflow)
What is the most important heart disease of the dog
Myxomatous mitral valve degeneration
-degeneration of the mitral valve -> causes backflow from LV to the LA
How many leaflets do they semilunar valves have?
Three
What do the left and right aortic valve cusps have
coronary ostia
when diseases, semilunar valves may either be stenotic (not open fully) or be regurgitant (leaky)
Semilunar valves are ______ during systole and _____ during diastole
open in systole
closed in diastole
What is the most common congenital heart defect in dogs
Pulmonary Valve Stenosis
stenosis of the pulmonary valve where the leaflets are fused and fail to open properly
cant get blood out of the right ventricle -> creates more problems for right ventricle, working harder
where do the left and right coronary arteries arise from
from the aorta
flow occurs during diastole
when does left and right coronary artery blood flow occur
during diastole
arises from the right ventricle and delivers deoxygenated blood to the left and right lungs
pulmonary artery
brings oxygenated blood back from the lungs to the left atrium
pulmonary veins
inlet throught the mitral valve and outlet through the aortic valve
V shaped chamber: mitral and aortic valves are in fibrous continuity
left heart
inlet through the tricuspid valve
outlet through the pulmonary valve
geographically separate valve U-shaped chamber
right heart
the right heart is ____ shaped while the left heart is ____ shaped
R: U
L: V
where do cardiac impulse start
Sinoatrial (SA) node
propagate cell to cell
and are rapidly disbursed through the specialized conduction pathways
what are the two primary difference between fetal and adult circulation
-Flow across the atrial septum
-Flow between the aorta and pulmonary artery
In the fetal circulation: deoxygenated blood goes from the pulmonary artery to the ________ and then to the _______ where it becomes oxygenated. This then returns through the _________and travels across the __________ to the left heart and body
pulmonary artery to the aorta (via ductus arteriosus) and then to the placenta to be oxygenated. Returns through the umbilical vein and then across the atrial septum (foramen ovale) to the left heart and body
The heart develops initially as a _______
linear tube
has a venous pole (inflow) and arterial pole (outflow)
the heart tube undergoes looping as it bends to the right and primitive chambers begin to take shape
Septation then occurs as the atrial chambers, ventricular chambers, and great vessels twist and divide to result in final cardio anatomy
What are the different diagnostics that you can do for the heart
1) auscultate
2) Electrocardiography
3) Radiography
4) Echocardiography
5) Ambulatory monitoring
6) Cardiac catherization
What are the general therapies for heart disease (Broad)
medical treatment
surgery
transcatheter intervention
Phases the cardiac cycle
1) Atrial contraction
2) Isolvolumic contraction
3) Rapid ejection
4) Reduced ejection
5) Isovolumic relaxation
6) Rapid (early) filling
7) Reduced filling (diastasis)
Systole: 2-4
Diastole: 5-7
Systolic pressures are markedly different between the right and left ventricles but what is the same between them?
Volumes
closure of what valves defines the onset of systole
Atrioventricular valves
-Mitral (Left Atrioventricular)
-Tricuspid (Right Atrioventricular)
*closure prevents flow from atria into ventricle
*First heart sound
closure of what valve defines the onset of diastole
Aortic/Pulmonic valve
What makes the noise of the first heart sound (S1)
Closure of the Atrioventricular valves
-Mitral (Left Atrioventricular)
-Tricuspid (Right Atrioventricular)
creating the abrupt stop in blood flow
What makes the noise of the second heart sound (S2)
Closure of the aortic and pulmonic valves creating abrupt change in blood flow
the volume of blood ejected from ventricle in one cycle/contraction
Stroke Volume
End-Diastolic Volume (EDV) - End Systolic Volume (ESV)
aka
What you start with (End Diastolic is after filling) minus the end-systolic volume (after ejection of the ventricle)
the percent of blood that leaves the ventricle in each cycle
the ejection fraction
= SV (EDV-ESV) / EDV
What is the equation for stroke volume
End-Diastolic Volume (EDV) - End Systolic Volume (ESV)
aka
What you start with (End Diastolic is after filling) minus the end-systolic volume (after ejection of the ventricle)
What is a normal ejection fraction
> 50-60% is normal
ex: if lower- you are not ejecting enough (ex- DCM)
cardiac output equation
Stroke volume x heart rate
Total volume of blood pymped into the Aorta and Pulmonary artery in 1 minute (L/min)
Cardiac output
T/F: cardiac output is equal for right and left ventricle
True
What is the gold standard method for measuring cardiac output
invasively via a catheter in the pulmonary artery
not really done
where is the catheter for cardiac output measurement placed
Pulmonary artery
-extremely invasive
cardiac index
a method used to normalize cardiac output in regards to body size (weight, body surface area)
Right sided systolic pressures are generally _____ the left
1/5 the left
if hole in ventricle, there will be flow from left to right
What occurs during filling (diastole)
the mitral valve opens and passive filling and due to compliant left ventricle you get filling.
What occurs during isovolumic contraction
after the mitral valve closes and ventricle is full of blood, the ventricle begins to contract to generate enough pressure to force the aortic valve open
The period in which the ventricle is at its max volume of blood
End-diastolic volume is fulfilled once the mitral valve closes. isovolumic contraction then occurs
what occurs during ejection
after isovolumic contraction, the aortic valve will be forced open. Volume plummets and there is a gradual rise in pressure
Ventricles start to relax
What occurs during isovolumic relaxation
after ejection (now at end-systolic volume), the aortic valve closes (S2 heart sound) the ventricle then relaxes
If ESV is 50 and EDV is 120. what is the stroke volume
70mL
If ESV is 50 and EDV is 120. what is the ejection fraction
70/120 = 58%
> 50% is normal
What is the area of the pressure-volume work
external work of the heart
diastolic wall stress or pressure just prior to contraction (related to sarcomere length)
volume effects this
Preload
systolic wall stress or pressure (load or force on contracting cardiomyocyte)
afterload
the degree the muscle fibers shorten independent of the laod
Contractility (inotropy)
the degree of ventricular compliance and diastolic function
relaxation (lusitrophy)
How does an increase in preload affect stroke volume
Increased preload
increases stroke volume (increased EDV)
How does an increase in afterload affect stroke volume
Increased afterload decreases the stroke volume (Increased ESV)
Why does heart rate only increase cardiac output up to a point
because less diastolic filling time leading to less stroke volume
CO starts to fall at HR >180-200bpm in dogs
CO begins to decrease once HR reaches (dogs)
above 180-200 because there is less diastolic filling time
T/F: Increases in HR increases contractility of the
true
treppe and Bowditch effect
What factors influence preload
*Venous Return is most important
more blood returning to ventricles
increased end-diastolic volume and therefore pressure (up to a point) increases stroke volume (independent of contractility)
Frank-Starling’s Law
-assumes afterload and contractility remain constant
Intrinsic property of cardiomyocytes where increase in sarcomere length increases optimizes overlap of actin and myosin AND TnC Ca2++ sensitivity -> increases rate of cross bridge complex formation and velocity of myofiber shortening
Frank-Starling’s law
How can you increase preload and therefore cardiac output
give a fluid bolus
What affects afterload
*Think impedance to ejection
1) Systemic vascular resistance (and thus arterial blood pressure)
2) Compliance of the aorta and arteries
3) Left Ventricular outflow tract anatomy (subaortic stenosis)
4)
How does subaortic stenosis affect afterload
it increases afterload
decreases stroke volume
increases ESV
What is LaPlace’s Law
Wall stress = (Pressure x Radius) / (2x wall thickness)
if there is an increase in systolic pressure (increased afterload) the
heart compensates will compensate and get thicker to overcome that increased pressure
ex: Subaortic stenosis leads to a marked increase in LV systolic pressure and the wall thickens to reduce wall stress (more fibers share that load)
Normal RV is _____ the thickness of the normal LV
1/3
How can you decrease afterload and therefore increase stroke volume
Give a vasodilator
drugs that increase the contractility (degree/velocity muscle fibers shorten) due to increase Ca2+ influx or sensitivity to Ca2++
Positive inotropes
What are clinical surrogates used to measure heart contractility (inotropy)
Gold standard: Slope of end-systolic pressure volume relation (ESPVR) line
ejection fraction, shortening fraction are influenced by load and are therefore called indices of systolic function
What is the gold standard of heart contractility (inotropy)
Slope of end-systolic pressure volume relation (ESPVR) line
-Increased contractility affects SV (increased), EDV (-), ESV (decreased)
Do changes in preload and afterload influence contractility
No they all affect cardiac output but preload and afterload do not influence contractility
How does impaired relaxation (lusitropy) affect stroke volume
Decreased stroke volume because there is decreased EDV from diastolic dysfunction aka there is less compliance and ability to take to fluid from the atria
When is the energy in blood delivered the muscle cells via the cornoary arteries
during diastole
What determines myocardial oxygen consumption/demand (MVO2)
1) Heart rate (increased creates more oxygen demand)
2) Wall stress/pressure- hypertrophied hearts require more energy
3) Contractility - increased inotropy consumes more oxygen
What drugs decrease the MVO2
Beta-blockers (blocking sympathetic)
Drugs that increase the parasympathetic
Is there more blood in the veins or arteries
Of the 84% of total blood volume in the systemic circulation
-64% in veins
-13% in arteries
-7% in arterioles and capillaries
*Veins are a major pressure volume
the major volume reservoir
easily expand and contract to meet demands
high compliance
systemic veins
the major pressure reservoir
preserve pressure to propel blood
low compliance
systemic arteries
do arteries or veins have high compliance
veins
Blood flow is going to increase if you have
a low vascular resistance
pressure = flow (Q) x resistance (R)
Ohm’s law of fluod
Change in Pressure = Flow (Q) x Resistance
Blood flow through a blood vessel is dependent on
1) Pressure difference gradient across the vessel
2) Vascular resistance (friction of blood as passes along endothelium )
measured as displacement of volume per unit time
blood flow
ex: cardiac output
How can you measure cardiac output non-invasively
via echo estimation (freeze image during systole and at diastole)
What does Poieuille’s law tell you
you can predict the flow (or resistance) based on the geometry of the tube
1) Flow is directly proportional to r^4 Blood vessel radius/diameter has a huge impact on flow and resistance
altering blood vessel diameter is a powerful tiil to alter blood flow
2) Flow inversely proportional to blood viscosity
How does blood viscosity affect blood flow
it is inversely proportional to blood flow
As you increase driving pressure of blood it will change from
laminar blood flow to the turbulent blood flow
radius, blood densityand viscosity are all factors that influence this
turbulent blood flow across a heart valve
murmur
why might animals with anemia have heart murmurs when their heart is fine
murmurs are the turbulent blood flow across a heart valve
you are affecting the blood properties (density and viscosity)
anemia reduces viscosity (inverse relationship) and increased velocity
Why might you auscultate a physiologic murmur in moderate to severely anemic animals
1) decreased viscosity (indirect relationship with blood flow) less viscous -> more turbulent flow
2) increased velocity
Where is the largest pressure difference in the circulation
High pressures in aorta, large arteries, small arteries but once you get to arterioles pressure plummets and remains low in capillaries, vein, small & large veins and the venae cavae
What do we typically measure as a surrogate of mean arterial pressure (MAP)
MAP - CVP = CO s SVR
*We measure systolic blood pressure as a surrogate of MAP
the difference between systolic and diastolic pressure
the pulse pressure “pulse”
When we refer to blood pressure it is always the
pressure difference between the aorta and the right atrium
How is MAP calculated
it is the mean between systolic and diastolic blood pressures but it is accounted for the duration of time you are in each phase
why your MAP is closer to you systolic blood pressure
Why is your MAP closer to your systolic blood pressure
Diastole is a longer period of your time
At faster Heart rate your MAP is closer to your systolic blood pressure
ex: 120/80 ;Mean is 93 and its closer to diastolic
Ways to measure blood pressure
1) Invasively via art line
2) Sphygomanometry- doppler vs oscillometric
What is the Windkessel effect
the effect at which the aortic/arterial blood flow continues due to the recoil of aorta’s elastic wall after ventricular contraction and propels blood during ventricular diastole
helps maintain organ perfusion pressure during diastole
What impacts the pulse pressure
1) HR
2) Stroke Volume (mostly)
ex: reduced stroke volume from DCM will have weak pulses and cool limbs
If pressure at the aorta and left ventricle are the same, what is it that influences the blood flow to organs
organs modulate local arteriole diameter to increase/decrease flow based on needs
ex: exercise
What are the organs that are the best regulators of blood flow
brain and heart
vascular resistance is changes to maintain blood flow
the net resistance of the entire systemic circulation
Systemic Vascular Resistance (SVR) or Total Peripheral Resistance (TPR)
difficult to calculate
estimate CO or BP instead (assumes blood flow is at a steady state)
What are the differences between capillaries in series vs parallel
When capillaries are arranged in parallel it reduces their resistance
how you maintain blood flow in these really small beds, despite small diameter (and youd think high resistance)
the gatekeepers that control flow to specific tissues via changes in vascular resistance
arterioles - they are the sight of the steepest pressure change due to their high resistance
it is also the most variable
Why arent capillaries the site of the highest resistance, given their smaller radius
each arterioles distributes blood to many capillaries in parallel resistance
net resistance of all capillaries less than resistance of single arteriole
What does the pulmonary circulation do in response to hypoxia
pulmonary arterioles actively vasoconstrict in hypoxic regions of lung
this is to match the ventilation to perfusion
the process of making more cardiomyocytes
hyperplasia (not what we are doing in disease) you are born with only a certain number of heart cells
increase synthesis of cardiomyocyte components, enlargement. not in the number of cardiomyocytes
hypertrophy
T/F: cardiomyocytes multiply as a result of heart disease
false they do not divide (hyperplasia is not possible)
instead the existing cardiomyocytes undergo hypertrophy (increased synthesis of cell components)
What are the different types of cardiac hypertrophy
1) Concentric
2) Eccentric
3) Mixed
T/F: Hypertrophy is reversible
true
What is a stimulus for concentric hypertrophy
high blood pressure or aortic stenosis- increased afterload. the resistance the heart must overcome to pump blood.
undergoes hypertrophy and gets a donut appearance (lumen gets smaller as the wall gets thicker)
A response to increased afterload
Concentric Hypertrophy
high blood pressure or aortic stenosis- increased afterload. the resistance the heart must overcome to pump blood.
undergoes hypertrophy and gets a donut appearance (lumen gets smaller as the wall gets thicker)
A response to increased preload
Eccentric Hypertrophy
valve regurgitation or congenital shunts - increased preload- volume of blood distending heart before contraction
get an onion ring appearance (thin wall with dilated lumen)
Does patent ductus arteriosus cause concentric or eccentric hypertrophy
if remains open there is excess blood returning to the left heart causing eccentric hypertrophy
mass of the heart is increased in eccentric hypertrophy even though the wall appears thin
T/F: The mass of the heart is increased in eccentric hypertrophy
true- despite the wall appearing to be thin
sarcomeres added in series (lengthwise)
If you close a PDA, will you reverse the caused eccentric hypertrophy
yes it is reversible over time
How are the sarcomeres added in concentric hypertrophy
they are added in parallel (width)
How are the sarcomeres added in eccentric hypertrophy
they are added in series (lengthwise)
still more mass but the walls look thinner
Cardiac hypertrophy adds sarcomeres to help normalize wall stress lessening the work of the heart. It is generally okay in the short term but what can occur during long-term?
Blood supply cannot keep up
muscles become ischemic resulting in degeneration, necrosis, replacement fibrosis
How might the loss of cardiomyocytes (myocardial necrosis occur)
1) ischemia/hypoxia
2) catecholamine exces
3) oxidative injury
4) toxins
5) pathogens
how does ischemic necrosis of the heart occur
impaired coronary blood flow to the heart
1) Coronary narrowing (arteriosclerosis)
2) Coronary thrombosis (heart attack)
3) Impaired coronary flow (hypertrophy, reduced time in diastole, increased wall stress/pressure)
What part of the heart is the myocardium most susceptible to ischemic necrosis
the subendocardial myocardium (the most inner)
coronary arteries perfuse out to inner and this is the last part to be perfused and under the greatest stress
How do cattle, sheep, and pigs typically get nutritional myocardial necrosis
vitamin E/selenium deficiency creating free-radical injury
“White muscle disease)
White Muscle Disease
diffuse myocardial necrosis in cattle, sheep, and pigs due to Vitamin E/Selenium deficiency generating free radical injury
What are some causes toxic myocardial necrosis
1) Doxorubicin
2) Inophores (monensin)
3) Cardiac glycosides (digoxin)
4) Gossypol
5) Thallium
6) Blister beetle
What occurs after myocardial necrosis
Replacement fibrosis in the response to loss of cardiomyocytes
Interstitial fibrosis: interstitial deposition of collagen between/around cardiomyocytes
Fibrosis causes
impaired contractile function
impairs relaxation/filling
disrupts electrical activity (blocks conduction, cause premature or abnormal activity)
may impact perfusion
How can myocardial fibrosis impact the functionality of the heart
-impaired contractile function
-impairs relaxation/filling
-disrupts electrical activity (blocks conduction, cause premature or abnormal activity)
-may impact perfusion
form of cardiomyopathy in cats where there is exuberant fibrous tissue that spans/obstructs the left ventricle leading to impaired myocardial relaxation filling resulting in heart failure
Endomyocardial fibrosis
Endomyocardial fibrosis
form of cardiomyopathy in cats where there is exuberant fibrous tissue that spans/obstructs the left ventricle leading to impaired myocardial relaxation filling resulting in heart failure
The most common cardiac disease of the cat
common among Maine Coon, Ragdoll, and Sphynx
Severe concentric hypertrophy of the left ventricle resulting in impaired filling and reduced compliance
Hypertrophic Cardiomyopathy
What breeds of cats commonly get hypertrophic cardiomyopathy
Maine Coon, Ragdoll, and Sphynx
What form of hypertrophic cardiomyopathy do cats typically get
Severe concentric hypertrophy of the left ventricle resulting in impaired filling and reduced compliance
What are the causes for dilated cardiomyopathy
1) Primary: genetic- Dobermann, Irish Wolfhound, GSD, St Bernard, Great Dane
2) Secondary due to taurine deficiency (cats) or grain free diets in dogs
Cats with taurine deficiency can develop
Dilated Cardiomyopathy:
dilated chambers leading to poor function of the heart
What breeds of dogs are genetically prone to Dilated Cardiomyopathy (DCM)
Dobermann Pinschers*, Irish Wolfhound, German Shephards, St Bernard, Great Dane
Non-traditional, grain free diets in dogs could cause
dilated cardiomyopathy
What would you see on histo of heart tissue with dilated cardiomyopathy
the chamber is dilated, walls appeas thin and fibers are thin and appear attenuated
What kind of diets could cause DCM in dogs
atypical breeds fed grain free diets with carbohydrate sources of lentil, peas, chickpeas, and potatoes
there is a correlation but not necessarily a causation
What breeds typically get Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)
Boxers and Bulldogs
replacement of cardiomyocytes with fat and fibrous tissue
typically in the right ventricle
results in abnormal heart rhythms related to the islands of abnormal tissue
can result in heart failure
Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)
What causes the abnormal heart rhythms in Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)
there is a replacement of cardiomyocytes with fat and fibrous tissue (genetic-desmosome protein)
resulting in the abnormal heart rhythms related to islands of abnormal tissue
can result in heart failure
a rare condition associated with the replacement fibrosis throughout the atria leading to loss of atrial electrical activity
progressive heart failure
typically in the english springer spaniel
Atrial Myopathy
What breed is predisposed to atrial myopathy (replacement fibrosis throughout atria leading to loss of atrial electrical activity)
English Springer Spaniels
What are some secondary cardiomyopathy diseases that may cause myocardial changes
1) anemia
2) hyperthyroidism
3) systemic hypertension
4) acromegaly
5) diabetes mellitus
6) cor pulmonale (lung)
7) steroid administration
degeneration of what valve is very common in dogs
Atrioventricular valve degeneration
-valve becomes thick, increased chordal laxity causing leakage of valve
-regurgitation is common
what kind of valve degeneration is common in older horses ?
aortic valve degeneration resulting in diastolic heart murmur
What are the consequences of chronic mitral regurgitation
Increased left atrial pressure and backup into the pulmonary veins and lung interstitial
leakage of high protein fluid (edema) into the lung alveoli causing respiratory symptoms
*rare- left atrial rupture
large vegetative growths on affected valves
-yellow (fibrin) and red (hemorrhage) on fresh postmortem speciments
infective endocarditis
cattle typically get infective endocarditis on their ____________ but all other species get them more commonly on their _____________
cattle- right sided valves
other species- left side valves
What is the most common heart tumor of the dog
Hemangiosarcoma (Right auricle)
What are different types of cardiac neoplasia
1) Lymphoma (feline and cattle-right atrium)
2) Hemangiosarcoma (canine in right auricle)
3) Chemodectoma (canine- heart vase/aorta)
4) Mesothelioma
shunts that bring deoxygenated blood to the arterial circulation resulting in hypoxemia
right to left shunts
shunts that cause volume overload and excess blood from the artial side passing to venous side
left to right shunts
Stages of ACIM heart disease
Stage A: at risk for heart disease (ex: cavalier, maine coon)
Stage B: structural heart disease no congestive failure
Stage C: pasot or current CHF
Stage D: CHF refractory to standard therapy
Why are rabbits a good model for heart attacks in humans
When fed high fat diets they develop a metabolic syndrome (hypercholesterolemia, systemic hypertension, and vascular disease
*the coronary arteries have limited collateral circulation and they can get myocardial infarctions
How can rabbits get myocardial infarctions
When fed high fat diets they develop a metabolic syndrome (hypercholesterolemia, systemic hypertension, and vascular disease
*the coronary arteries have limited collateral circulation and they can get myocardial infarctions
What is unique about the vena cava or rabbits
they normally have a right and left cranial vena cava (the left drains into the coronary sinus)
What drains into the coronary sinus in the rabbit
the left cranial vena cava
(keep in mind that they have two cranial vena cavas- right and left)
Why is there a high incidence of respiratory disease in rabbits
relatively small lungs and the diaphragm is the only muscle used for breathing
T/F: cough is an uncommon sign of CHF in rabbits
true
What is normal rabbit HR
200-300/min
*give midazolam for cardiac exams as it has limited effects on CV system
What can you give rabbits during cardiac exam because it has limited effects on CV system
Midazolam
How might a rabbit have a non-pathological heart hurmur
if you push too hard, can lead to gallop but its hard to hear due to fast heart rate
breathing might mimic a heart murmur
Rabbit thoracic radiography
Used to rule out CHF, cardiomegaly (respiratory disease is more common vs CHF)
1) Cranial cardiac silhouette is often obscured (fat, persistent thymus)
2) tiny thorax vs trunk size
3) Obese rabbits can give you false positive cardiomegaly
4) Compare lungs with healthy rabbit if inexperienced
How might you have false positive cardiomegaly on thoracic radiography in a rabbit
if they are obese
How do you rule out CHF in rabbits on radiography
-Interstitial or alveolar pulmonary pattern
-pleural effusion (wont see with heart)
-overt cardiomegaly
How are ECGs performed in rabbits
based on CV exam findings
-sternal recumbency
-fast sweep speed >50mm/sec and increase amplitude (20mm/mV)
T/F: rabbit right heart size is normally closer to left heart size on echo
True
What CV disease do rabbits typically get
1) Endocardioisis- older rabbits. mitral > tricuspid
2) Infectious- Endocarditis
3) Cardiomyopathies- DCM, hypertrophic, restrictive, stressed induced
4) Arrhythmias
5) Congenital is rare
6) Vascular- arteriosclerosis and systemic hypertension from renal disease
Is mitral or tricupsid endocardioisis more common in rabbits
Mitral >tricuspid
*older rabbits- acquired AV valve disease
In NZ white rabbits, what might induce myocardial necrosis and fibrosis
Alpha-2 agonists
What should you not use when sedating a rabbit
A-2 agonists- might induce myocardial necrosis and fibrosis
*NZ White Rabbits
How do you treat CV in rabbits
-centesis for thoracocentesis and oxygen
-same as dogs and cats: furosemide, enalapril, digoxin, pimobendan, dilitiazem, lidocaine
What cardiac disease do ferrets typically get
DCM
What cardiac diseases do ferrets typically get
-Full spectrum possible
1) DCM
2) Arrhythmias
3) Acquired valvular disease (Mitral or aortic regurg)
4) Definitive host for Dirofilaria immitus
Do ferrets cough with CHF
yes
Normal ferret heart rate
180-250/min
notorious for bradycarrhythmias 2nd or 3rd degree AV blocks
Healthy (calm) ferrets are possible to get what arrhythmias
1) Sinus arrhythmias
2) Mobitz type I 2nd degree AV (pauses)
What is unique about the normal ferret heart on radiography
it has a floating heart appearance
-not pneumothorax or effusion
What do you need when doing ferret echocardiography
smaller transducer footprint, high frequency probe because their rib spaces are smaller
What is unique about ECG in ferret
-largely indicated based on physical exam
-ften need restraint or sedation
-Use fast paper speed (>50mm/sec)
-Low amplitude P-waves
-High amplitude QRS but <3mV
Commonly get:
a) 2nd Degree AV block
b) 3rdDegree AV block
DCM in ferret
most common cardiac disease in ferret
systolic dysfunction leading to eccentric LV hypertrophy
adult onset
may result in CHF
Do ferrets have a low or high heartworm burden
low burden
*Ag +Ab testing is ideal
Do you treat heartworm in ferrets with Melarsomine?
NO, unlike the dog, it will kill them
How do you prevent heartworm in ferrets
all macrocyclic lactones/preventatives
Chinchillas commonly get
physiologic/stress related murmurs (like cats)
Mice typically get:
naturally occuring myocardial mineralization
Hamsters normally have
right and left cranial vena cava (like rabbits)
guinea pigs have
spectacular collateralization of coronary arteries (not good for studying heart attacks in humans)
captive african hedgehodgs have:
high incidence of CV disease (>40%)
What is unique about avian cardio anatomy
1) Muscular right AV valve (no chordae)
2) Right and left vena cava
3) Coelomic cavity (lack diaphragm)
4) RA > LA (normal)
What is unique about the right AV valve in birds
Muscular right AV valve (no chordae)
T/F: avians do not have diaphragm
true
what is unique about vena cava of birds
they have a right and left vena cava
Is the RA or LA bigger in the bird
RA > LA (different from dog and cat)
What species have Type B purkinje fibers
horse, cow/ruminants, pig, birds
2 phases: apex -> base in very rapid succession
Main wavefront = sternum to spine
What species have Type A Purkinje fibers
Dog, cat, ape, man
3 phases: Septum -> Apex -> Base
main wavefront is caudal and ventral
How do Type A and Type B Purkinje fibers differ
Type A: 2 phases: apex -> base in very rapid succession
Main wavefront = sternum to spine
Type B: 3 phases: Septum -> Apex -> Base
main wavefront is caudal and ventral
deeply penetrating
Why do birds have a normally negative QRS
Because they are Type B: completely penetrating Purkinje fibers
Depolarize from the apex up to the base
Why do ruminants have a normally negative QRS
Because they are Type B: completely penetrating Purkinje fibers
Depolarize from the apex up to the base
Why do horses have a normally negative QRS
Because they are Type B: completely penetrating Purkinje fibers
Depolarize from the apex up to the base
How do you recognize CV in birds
Hard- because fast HR
nonspecific signs: lethargy, weakness, hyporexia, breathing difficulty
pulse challenging to palpate
Clinical signs of avian CHF
pericardial or coelomic effusion, pulmonary edema
-intra-coelomic air sac compression
-poor coelomic detail
-cardiomegaly
-pulmonary edema
-dilation or mineralization of great vessels
There are limited acoustic window for echo in birds. Where should you go
under the keel
What are important avian cardiovascular diseases
1) Arteriosclerosis in older pet or captive birds on high fat/cholesterol diets and inactivity
stenosis and occasionally mineralization of great vessels
2) Cardiomyopathies (DCM-turkeys), vitamin E/Selenium deficiency
What causes arteriosclerosis in birds
older or captive birds on high fat/cholesterol diets or inactivity
leading to stenosis and occasionally mineralization of arteries/great vessels (AScAo, BT, PA)
What CV disease do young turkeys (poults) tend to get
DCM
T/F: Degeneration (endocardiosis) of the mitral valve is the most common heart disease of dogs
true
T/F: Congenital pulmonary valve stenosis results in an increased right ventricular afterload (pressure overload); therefore, the right ventricle will show eccentric hypertrophy
False
T/F: Infective endocarditis of a cardiac valve appears as a red/hemorrhagic and yellow/fibrin vegetation on the valve surface when evaluated at post mortem
True
T/F: Valvular disease in the horse is most commonly degeneration of the pulmonary valve, resulting in a diastolic heart murmur
false
A hypokinetic pulse can occur due to ________ , while a hyperkinetic pulse may be present in the setting of ________.
hypovolemia ; bradycardia
You examine a 6-month-old dog with a palpable thrill and a heart murmur (grade V/VI) heard best at the left heart base. Congenital heart disease is likely and your top differentials include subaortic stenosis and _________________ , while a less likely cause of the murmur based on the point of maximal intensity would be _____________.
Pulmonary valve stenosis
tricuspid valve dysplasia
What is a normal vertebral heart score
9.7 +/- 0.5
What is the patient’s fractional shortening with the following echo measurements
LV chamber (d): 10.9mm
LV chamber (s): 5.4mm
50%
What should you do before initiating ACE-inhibitor and diuretic
Measuring blood pressure and submitting a chemistry profile (BUN, creatinine, electrolytes) should optimally be performed before and after initiation of these drugs
Dysfunction of the right-side of the heart may lead to elevated
[ Select ]
venous pressures and cavitary effusions.
systemic
Dysfunction of the left-side of the heart may lead to elevated
[ Select ]
venous pressures and pulmonary edema
pulmonary
The heart responds to hemodynamic challenges in a predictable fashion. Match the underlying disease with the most likely response.
Chronic pulmonary hypertension
Concentric RV hypertrophy
The heart responds to hemodynamic challenges in a predictable fashion. Match the underlying disease with the most likely response.
Chronic systemic hypertension
Concentric LV hypertrophy
The heart responds to hemodynamic challenges in a predictable fashion. Match the underlying disease with the most likely response.
Myxomatous mitral valve disease
Eccentric LV hypertrophy
Which statement best describes pimobendan’s primary mechanism of action; and how does this compare to that of digoxin?
Pimobendan increases the sensitivity of the contractile apparatus to available Ca++ and increases inotropy whereas digoxin leads to an increase in the intracellular Ca++ concentration and increases inotropy
Furosemide is an important medication in the management of heart disease. Furosemide reduces __________ and therefore lowers ventricular filling pressures. Amlodipine as an arterial vasodilator primarily reduces ________ and therefore lessens myocardial oxygen demand.
preload ; afterload
Furosemide is an important medication in the management of heart disease. Furosemide reduces __________ and therefore lowers ventricular filling pressures.
preload
Amlodipine as an arterial vasodilator primarily reduces ________ and therefore lessens myocardial oxygen demand.
afterload
A 10 year old female spayed Chihuahua presented to your clinic for a heart murmur evaluation. The patient is asymptomatic at home. On physical examination, the patient has a grade II/VI left apical systolic heart murmur. You perform thoracic radiographs to evaluate for cardiomegaly. You suspect degenerative mitral valve disease (stage B1) based on signalment, physical examination, and thoracic radiographs.
What treatment is indicated?
No treatment
Causes of dilated cardiomyopathy (DCM) or a DCM- phenotype in the dog include:
a. Genetic mutations
b. Hyperthyroidism
c. Myocarditis
d. Doxorubicin (Adriamycin)
A, C, D
Causes of left ventricular hypertrophy in the cat include:
a. Primary cardiomyopathy (hypertrophic cardiomyopathy)
b. Hyperthyroidism
c. Systemic hypertension
d. Pulmonary hypertension
A, B, C
ophthalmologic examination of a 13-year-old cat with chronic kidney disease. The ophthalmology report described retinal vessel tortuosity, focal areas of retinal hemorrhage, and a mottled appearance consistent with areas of retinal detachment. Which of the following medications might be prescribed in the management of this patient’s disease (please choose all correct responses)?
Amiodarone
Amlodipine
Thyroxine
Telmisartan
Furosemide
Pimobendan
Amlodipine
Telmisartan
Which of the diagnostic findings listed below would be compatible with pericardial effusion in a dog (select 3)?
a) Variable pulse quality associated with respiration
b) Loud S2 heart sound
c) Variable amplitude of the QRS complexes on a beat-to-beat basis
d) Small cardiac silhouette and reduced pulmonary markings on thoracic radiographs
e) Dilation of the jugular veins
A, C, E
What heart disease so dobermans typically get
DCM
What are differential causes of Mitral regurgitation
1) Degenerative mitral valve disease
2) DCM- genetic, nutritional, arrhythmia undced
3) Mitral valve endocarditis
4) Mitral valve dysplasia
5) volume overload from L-R shunt causing functional MR
Differentials for irregular heart rhythm
1) Sinus arrhythmia
2) Atrioventricular block
3) Premature atrial complexes
4) Atrial fibrillation
5) Atrial tachycardia or flutter with variable conduction
6) Paroxysmal ventricular tachycardia
You have a dog with DCM that is in congestive heart failure, atrial fibrillation, and cardiogenic shock. What should you initially do for therapy
1) Furosemide to reduce preload; reduce filling pressure
2) Oxygen therapy
3) +/- Nitroglycerin
4) Dobutamine- beta agonist, catecholamine to improve cardiac output and blood pressure
Drugs that slow conduction down the AV node to limit the ventricular repsonse rate
1) Digoxin (indirect = increases vagal tone)
2) Calcium channel blockers (diltiazem, verapamil)
3) Beta blockers
What are drugs for rhythm control
oral quinidine in horses
transcutaneous shicked timed to the R wave
