Cardio: congenital defects, heart failure, pericarditis+ effusion, mitral valve disease, murmurs, DCM

what differences would you see PM on patient euthanised with intracardiac injection?

crystalline deposits on endocardium

acute hemopericardium

abnormal blood texture

myocardial pallor (chemical burn)

what is in the pericardial space and what is its function

lubricate layers of the heart during movement

the cardiac myocytes exist within _______ in the myocardium

fibrous connective tissue scaffold

left ventricle is ____x thicker than right ventricle

why is this?

3x thicker

because left ventricle sends blood to systemic circulation, which has increased volume and increased total resistance to blood flow relative to pulmonary circulation. so L ventricle has to work harder to send out blood

why are cardiac myocytes more susceptible to hypoxia / anoxia than skeletal myocytes?

they rely on aerobic glycolysis and have continuous activity

explain what happens when myocardial cells die

they are non-regenerative, so myocardial death results in fibrosis as there are no new cells to replace them

what is the impact of fibrosis on the heart

fibrosis to one part of the heart can effect the entire heart function due to synergy of the heart

what part of the endocardium looks different than the other parts?

the endocardium covering atria is thicker and whiter and more opaque than the endocardium than in ventricles

what would you look for in the pericardium on PM

thickening

adhesions between pericardium and other tissues (look at lung, mediastinum, thoracic wall)

adhesions between pericardium and epicardium

free fluid in pericardial sac

what would you look for in the myocardium on PM

size, weight, outline, color

expose all chambers, valves, great vessels

look at endothelium of great vessels- plaques? endarteritis?

measure R:L ventricular wall ratios (should be 1:3)

common appearances of heart on PM

R. ventricle can be flabby after death- do not mistake for DCM or dilation!

don't confuse PM blood clots with thrombi (clots wash away, thrombi stick to vessels)

in horses, chickenfat clots are common PM

the endocardium might be stained dark red due to haemoglobin imbibition- not pathological

pericardial fat may be seen in obese patients

serous atrophy of cardiac fat is seen in starved patients

clear, gelatinous fluid is common in epicardium

what is the AV ring?

segregation of atria and ventricles by fibrous ring

allows for synchronised cardiac conduction

only way to bypass the ring is through the AV node

how many bundle branches on right and left ventricles

one on right

two on left

what is function of bundle branches

rapidly conducting system

chicken fat clot in a horse (non-pathological, common PM finding in horses)

serous atrophy of cardiac fat. seen with starvation

dog euthanised by intra-cardiac barbituates, chemical burn of right ventricle

all congenital defects (talked about in this course) will result in a ________ due to turbulent / abnormal blood flow

heart murmur

in the fetus, the ____ side is the high pressure system

what happens to pulmonary vessel pressure?

right

at birth there is a drop in pulmonary vessel pressure as the lungs fill with air. this switches the high pressure system to the left side

atrial septal defect (image)

what determines the severity of atrial septal defect

the degree of failed closure of the septum

what is an atrial septal defect caused by

failure of the foramen ovale to close during fetal development

what type of shunt results from an atrial septal defect

left to right shunt

what causes the foramen ovale to close after birth (takes a few weeks)?

pressure switch (systemic circulation becomes the high pressure system at birth when lungs fill with air) pushes the septum primum over the foramen ovale, closing the hole

what are the long term consequences of an atrial septal defect?

right ventricle dilation and hypertrophy

dilation of both atria

audible murmur due to dilation of pulmonary artery

a severe / large shunt can result in secondary hypertension, fibrosis, increased pulmonary vascular pressure, and a right --> left second shunt --> cyanosis due to blood bypassing lungs

ventricular septal defect (image)

is ventricular septal defect common or rare in small animal?

one of the most common congenital abnormalities

is the ventricular septal defect more often cranial or caudal

cranial

what type of shunt results from a ventricular septal defect?

left to right shunt

what are the long term effects of ventricular septal defect?

small defect: can live normal life, asymptomatic

larger defect:

hypertrophy of both ventricles

secondary hypertension and fibrosis

LV overload ---> CHF

a right to left shunt, resulting in cyanosis

in a VSD, the intensity of a murmur is _______ to severity of the defect

inversely proportional

patent ductus arteriosus (image)

what is the ductus arteriosus and does it close?

vascular channel connecting fetal pulmonary artery to aorta

does not close in gestation. At birth, when L heart becomes high pressure system, the flow through the ductus arteriosus is prevented. It gradually fibroses, forming the ligamentum arteriosum

what causes the patent ductus arteriosus?

failure of formation of ligamentum arteriosum

what type of shunt results from PDA?

left to right shunt (aorta --> pulmonary artery)

what long term effects result from PDA?

secondary pulmonary hypertension

hypertrophy of LV

LV and LA dilation

predisposition from thromboses due to turbulent blood flow

what does PDA look similar to on an echo?

DCM

triple knuckle x-ray bulge

what happens if you don't correct a PDA?

animal will die in a year. Curative surgery is the treatment

what does PDA sound like on auscultation?

pathognomonic murmur, but requires echo to definitively diagnose

pulmonic stenosis (image)

what is the most common congenital heart disease in dogs?

pulmonic stenosis

what is pulmonic stenosis?

narrowing of the outflow of the pulmonary artery

what is the most common site of pulmonic stenosis?

narrowing is usually at the level of the valve, resulting in valvular stenosis (fusion)

what are long term effects of pulmonic stenosis?

hypertrophy of the right ventricle (narrowed pulmonary artery, RV pressure overload)

dilation of the pulmonary artery just outside the steonisis

mild stenosis can live normal life

even in severe stenosis, patients are often asymptomatic

occasionally you see exercise intolerance, syncope, RSHF

poor prognosis if the patient is a Frenchie

how do you determine the severity of pulmonic stenosis?

based on echo- the pressure difference across the lesion

also the murmur intensity is proportional to the disease severity

image PM of a VSD

in pulmonic stenosis, the murmur intensity is _______ to the disease severity

proportional

image PM of ASD

image PM of PDA

image PM of subaortic stenosis

subaortic stenosis (image)

what is a subaortic stenosis?

narrowing of the outflow of the aorta at or just below the aortic valves

what species is subaortic stenosis more common in?

pigs and dogs

what are long term effects of subaortic / aortic stenosis?

LVOT obstruction --> pressure loaded LV --> LV hypertrophy

post-stenotic dilation of the aorta

fibrosis and thickening of walls of arteries within myocardium --> reduced blood flow within the heart itself --> focal areas of myocardial necrosis

what does a murmur from subaortic/aortic stenosis sound like?

similar to pulmonic stenosis murmur: left basilar systolic

requires an echo

in subaortic/aortic stenosis, the murmur grade is _____ to disease severity

proportional

what is the prognosis of subaortic / aortic stenosis?

mild: asymptomatic

severe: exertional syncopy --> collapse, sudden death with exercise

which carries a worse prognosis- pulmonary stenosis or aortic/subaortic stenosis?

aortic/subaortic stenosis

which valve dysplasia is more common in cats?

left AV dysplasia

what are different ways that mitral and tricuspid/AV valve dysplasias present?

focal or diffuse thickening of leaflets

fusion of valves with cardiac wall

shortening of cordae tendinae

shortening of papillary muscles

what are long term results of mitral and tricuspid/AV valve dysplasias?

imcompetent / leaky valves

dilation of atria

secondary dilation of ventricle of the affected side

what is valve dysplasia not to be confused with?

endocarditis

image of valvular hematocyst

where do you commonly see valvular hematocysts and lymphocysts?

on the AV valves of young ruminants (found incidentally)

what is the clinical significance of valvular hematocysts and lymphocysts?

don't cause functional issues

may regress spontaneously

image of valvular lymphocyst

what are the 4 degrees of transposition of the aorta and pulmonary artery? which ones are compatible with life?

1. overriding aorta

2. partial transposition

3. overriding pulmonary aorta

4. complete transposition

only #1 is compatible with life because aorta receives blood from both ventricles

image of transposition of aorta and pulmonary artery

image of persistent right aortic arch (aka vascular ring anomaly)

what is a vascular ring anomaly?

when the ductus arteriosus entraps the esophagus against the trachea

when would you see a vascular ring anomaly clinical signs?

when the animal switches from milk to solid food, resulting in obstruction of the esophagus

clinical signs of vascular ring anomaly

dysphagia

regurgitation

megaoesophagus

image of tetralogy of fallot

what are the 4 features in tetralogy of fallot?

1. VSD

2. Pulmonary stenosis

3. secondary RV hypertrophy

4. Overriding aorta (aortic transposition)

will you see clinical signs of tetralogy of fallot?

always:

retarded growth rate

heart failure (due to RVH --> DCM)

cyanosis due to poor pulmonary perfusion

polycythemia (compensatory for hypoxia)

what are the 3 possible causes of heart failure?

1. lack of circulating fluid due to loss of blood or plasma (ex massive hemorrhage, dehydration)

2. failure of the blood vessels to maintain good tone, resulting in decreased blood pressure

3. heart damage resulting in insufficient blood flow

what is the definition of heart failure

when the heart is unable to pump blood at a rate sufficient to meet the oxygen demands of the body

what are the two subtypes of left sided CHF and what causes them?

systolic HF: caused by decreased contractility

diastolic HF: caused by increased afterload

what happens in systolic left CHF

left ventricle is dilated

left ventricle has decreased ejection

decreased CO due to low contractility

what happens in diastolic left CHF

left ventricle is hypertrophied, resulting in decreased ventricular filling

decreased cardiac output due to decreased preload

what two cell types respond to decreased CO?

baroreceptors

juxtaglomerular cells

what happens when the baroreceptors detect decreased CO?

they increase sympathetic activity (by increasing epi and norepi)

heart rate increases (beta receptors)

stroke volume increases (alpha receptors)

afterload increases as a result, worsening the heart failure by triggering hypertrophy

preload also increases as a result of baroreceptor response, causing dilation

what happens when the juxtaglomerular cells in the kidney detect decreased CO?

they increase production of renin, thus increasing aldosterone (which increases ADH, increasing reabsorption of sodium and water by the kidneys and resulting in fluid retention and oedema)

this is a compensatory response that overall increases stroke volume, increases afterload, and increases preload (further worsening the heart failure by causing hypertrophy and dilation)

what causes acute heart failure?

sudden big drop in blood flow that compensatory mechanisms can't cope with

what causes chronic (congestive) heart failure?

small drop in cardiac output that compensatory mechanisms can keep up with for a while, but as heart condition worsens decomposition occurs

clinical signs of acute heart failure

difficult to diagnose, difficult to see on PM

exercise intolerance

respiratory issues for a few hours or days before compensatory mechanisms fail

pale mucous membranes

cold extremities

oliguria (low urine output)

what are the compensatory mechanisms employed in chronic / congestive heart failure?

increased heart rate

increased force of contraction

increased peripheral vascular resistance

redistribution of blood away from non-vital organs

what is the reflex arteriolar constriction and when does it happen?

during acute heart failure, initiated by the baroreceptor triggering due to sudden drop in arterial BP

baroreceptors increase sympathetic tone

adrenaline released --> HR increased

reflex constriction of peripheral arterioles shunts the blood away from non-vital organs. Occurs in skin, GIT, kidneys

explain why acute heart failure results in dyspnoea?

left ventricle fails --> reduced ventricular output --> increased preload

pulmonary vascular congestion (exacerbated by the right ventricle still pumping to the lungs)

hydrostatic pressure in pulmonary capillaries increases, causing pulmonary oedema

pulmonary oedema is what causes clinical sign of dyspnoea

what does chronic left sided heart failure look like histologically in the lungs?

In addition to increased alveolar macrophages containing hemosiderin ----> heart failure cells

what does acute left sided heart failure look like histologically in the lungs?

Alveolar septae (arrows) are filled with blood. The alveolar spaces are filled with eosinophilic oedema fluid

how can chronic left sided heart failure affect the right side of the heart?

persistent increased pulmonary pressure can eventually result in interstitial lung fibrosis with subsequent right-sided heart

damage and failure (cor pulmonale)

more workload for the right side of the heart

what are some causes of left sided heart failure?

valve defects

myocarditis, pericarditis, endocarditis

cardiac tamponade

cardiomyopathies

systemic hypertension

infarction (uncommon in domestic animals)

how would right sided heart failure present differently from left sided heart failure?

left sided: lung oedema, dyspnea

right sided: liver congestion, ascites

how does right sided heart failure cause "damming back"?

reduced output to pulmonary circulation results in congestion of blood in the right atrium, vena cavae, systemic veins, liver, and spleen

why doesn't acute RSHF cause oedema despite congestion?

systemic veins can accomodate much more blood than pulmonary veins

what happens in acute RSHF? (response of body)

left side of heart is not receiving much blood because right side failed--> immediate drop in systemic arterial blood pressure --> peripheral arterial constriction reflex (mediated by adrenaline)

Heart rate increases

what pathological effects are seen with chronic RSHF?

prolonged damming of blood back in the liver --> liver oedema

hepatocellular hypoxia, necrosis, and fibrosis in the liver

results in the "nutmeg liver"

what are some causes of RSHF?

pulmonary disease

valvular disease and defects

myocarditis, endocarditis

cardiomyopathies

secondary to LSHF

what can cause biventricular failure?

myocarditis, myocardia toxins, acute cardiac tamponade