Flashcards in Pathology of the Cardiovascular System 3 Deck (34):
DISEASES OF THE ENDOCARDIUM
(Wall of the heart)
1. INFLAMMATION- MURAL ENDOCARDITIS- necrotising endocarditis
2. DEGENERATION- calcification, fibrosis.
Associated with uraemia of acute or chronic renal failure.
Degeneration and necrosis of the LEFT ATRIAL endocardium (not particularly understood why)
Yellow-white plaques on atrial wall, may see associated ulceration and calcification
-Signs seen due to presumed toxic damage to small blood vessels and necrosis of the overlying cells.
-May be release of ammonia and pro-inflammatory cytokines.
INHERITED ARRHYTHMIAS AND CONDUCTION DISORDERS
In humans and animals, inherited arrhythmias and cardiac conduction system disease occur in very young patients.
Can be congenital heart disease, or occur in a structurally normal heart.
Mutations responsible for the majority of inherited arrhythmias occur in genes encoding for CYTOSKELETAL PROTEINS, SARCOMERIC PROTEINS, ION CHANNELS.
Variation in rhythm
Abnormality in the conduction system of the heart.
PRIMARY ARRHYTHMIAS/CONDUCTION DISORDERS
NO MORPHOLOGICAL ABNORMALITIES.
May be normal in some species/breeds- often disappear with increased activity (horses)
SECONDARY ARRHYTHMIAS/CONDUCTION DISORDERS
Seen secondary to underlying disease.
eg. Atrial fibrillation in cardiomyopathy.
eg. Ventricular tachycardia in ventricular hypertrophy.
eg. Heart block following myocardial damage.
Transmitted through genetic line, but may not be seen at birth. Can manifest when the animal is older.
Hereditary. Transmitted from parent to offspring.
Present at birth, may not be inherited.
Congenital anomaly or defect.
INHERITED ARRHYTHMIAS IN DOGS
-Arrhythmogenic Right Ventricular Cardiomyopathy- Boxers. Generally only seen in adult/older dogs.
Signs include ventricular premature contractions (VPCs) or ventricular tachycardia (VT)
-Dilated Cardiomyopathy in the Doberman. Increased VPCs or VT are evidence of occult disease.
-Inherited Ventricular Arrhythmias in German Shepherd Dogs- Sudden death syndrome at approximately 4-20 months. Check heart/lung/brain- true sudden death may not have obvious developed pathology.
SICK SINUS SYNDROME
aka. BRADYCARDIA-TACHYCARDIA SYNDROME.
A group of conduction disorders involving the sino-atrial node.
May or may not involve the atrio-ventricular node and bundle of His/branches.
Potentially life threatening- Periods of ventricular standstill cause syncope.
-Paroxysms of supraventricular tahcycardia cause syncope.
Usually idiopathic (spontaneous), but may have ischaemia of SA node.
Possibly inherited in some breeds- miniature Schnauzer (especially bitches)
FIRST DEGREE- DELAY of impulse through AV node.
SECOND DEGREE- Intermittent FAILURE of conduction through AV node, with dropped beats.
Normal in the horse.
First degree can progress to second degree.
THIRD DEGREE- Complete failure of conduction (complete block)
Heart blocks are associated with areas of myocardial scarring in the horse and dog.
Present in some families and not others, or occurs more in family members than would be expected by chance.
Usually but not always inherited.
Originating after birth- not caused by hereditary or developmental factors, but instead by a reaction to environmental influences outside of the organism.
HEART AND GREAT VESSEL DEVELOPMENT
3 basic development stages.
3. Separation of common truncus arteriosus in to aorta and pulmonary artery
STRUCTURES OF FOETAL CIRCULATION
FORAMEN OVALE- opening between left and right atria.
Allows blood to flow from RIGHT to LEFT- right-left shunt bypasses lungs.
DUCTUS ARTERIOSUS- connects pulmonary artery and aorta.
DUCTUS VENOSUS- Portal and umbilical veins are connected to the vena cava (liver)
Pressure changes at birth should force the foramen ovale shut immediately, allowing blood to reach the lungs for oxygenation.
CONGENITAL DEFECTS- 3 MAIN CATEGORIES
1. FAILURE OF CLOSURE OF FOETAL STRUCTURES
2. SEPTAL DEFECTS
3. GREAT VESSEL DEFECTS (defects of outflow tracts- aortic or pulmonary valves- dysplasia, stenosis or malposition/fusion)
PATENT FORAMEN OVALE
Failure of closure of opening between atria.
Right to left shunt allows deoxygenated (right atrium) and oxygenated (left atrium) blood to mix.
PATENT DUCTUS ARTERIOSUS
Pulmonary artery (deoxygenated) and aorta (oxygenated) remain connected.
Oxygenated blood is shunted from left to right VENTRICLE.
This causes pulmonary hypertension -> thickened right ventricle.
Normal flow from portal vein is diverted to systemic circulation, bypassing the liver.
Normal hepatic detoxification of portal flow is incomplete.
Build up of toxins, especially ammonia, causes HEPATIC ENCEPHALOPATHY.
Can be intra- or extra-hepatic.
-Intrahepatic- Persistent ductus venosus (portal/umbilical vein and vena cava)
-Extrahepatic- Portocaval shunt, Portazygos shunt.
Represents prominent dilation of various portosystemic shunts that are usually quite small vessels.
SEPTAL (ENDOCARDIAL CUSHION) DEFECTS
Atrial Septal Defect
Ventricular Septal Defect
ATRIAL SEPTAL DEFECT
Opening between right and left atria allows mixing of oxygenated and deoxygenated blood.
Opening is not always where the foramen ovale would be.
Signs depend on size of defect and how much blood can flow through.
Risk of pulmonary vascular damage- increased pulmonary arterial pressure (due to mixed blood in pulmonary artery- oxygenated blood from left atrium mixes with deoxygenated blood in right atrium -> RV -> pulmonary artery)
Risk of endocarditis (will also cause pulmonary vascular damage)
A large defect will cause bilateral atrial distension, as the atria are working harder to counteract the blood mixing.
VENTRICULAR SEPTAL DEFECT
Seen in cattle, can be an incidental finding at PM- no clinical signs.
Blood flows from left to right (left ventricle is more muscular).
in CHRONIC/SEVERE VSD, SHUNT REVERSAL can occur.
Blood flow from left to right moves more blood to the lungs (pulmonary artery), causing pulmonary hypertension.
This allows REVERSAL of the shunt -RIGHT TO LEFT.
This only occurs in very chronic/sever/large ventricular septal defects.
GREAT VESSEL DEFECTS
VALVULAR DEFECTS- insufficiency (regurgitation)- MITRAL or TRICUSPID DYSPLASIA
STENOSIS- outflow obstruction- AORTIC (subaortic) or PULMONIC STENOSIS (semilunar valves)
Some anomalies can produce both insufficiency and stenosis.
ATRIOVENTRICULAR VALVE DYSPLASIA
Improper formation of valve.
Remnants are small and dysfunctional- distorted leaflets, short chordae (restrict valve movement)
Can occur in mitral (left) or tricuspid (right) valve.
Sever incompetence will lead to atrial distension.
Obstruction of outflow from left ventricle to aorta.
-Subaortic fibrous ridge- MOST COMMON
-Subaortic stenosis- Second most common inherited heart disease in dogs. Mostly seen in large, purebreed dogs.
Blood struggles to leave the heart and enter the systemic circulation.
There is dramatic enlargement (hypertrophy) of the heart to try and push the blood out.
Turbulent flow causes dilation of the aorta and jet lesions (fibrosis, some mineralisation)
Obstruction of outflow from right ventricle to pulmonary artery.
Can be valvular, subvalvular (fibrous ridge below valve) or infundibular (not involving valve)
Narrowing of valve/below valve
-> Dilation of pulmonary artery above obstruction
-> Thickened right ventricle
LEFT TO RIGHT SHUNTS
Can be caused by:
Patent ductus arteriosus
Atrial septal defects
Ventricular septal defects
Atrioventricular canal (endocardial cushion defect)
Extra blood flows through the lungs, causing pulmonary hypertension and right ventricular hypertrophy.
A collection of symptoms, including cyanosis (due to decreased oxygen in blood), pulmonary hypertension, erythrocytosis (due to decreased blood oxygen), caused by LEFT TO RIGHT SHUNT.
RIGHT TO LEFT SHUNT
TETRALOGY OF FALLOT.
Severity depends on extent of pulmonary stenosis.
Deoxygenated blood enters systemic circulation (RV -> LV -> aorta)
Causes cyanosis -'blue babies' (human).
Too LITTLE blood is flowing through the lungs.
TETRALOGY OF FALLOT
1. RIGHT VENTRICULAR OUTFLOW OBSTRUCTION due to pulmonary stenosis.
2. VENTRICULAR SEPTAL DEFECT allows blood to flow from left to right ventricle.
3. DEXTRAPOSED AORTA- shifted from left to right (overlies the ventricular septal defect instead of the left ventricle, so can receive blood from left and right ventricles)
4. RIGHT VENTRICULAR HYPERTROPHY- to compensate for right ventricular outflow obstruction.
SPECIES SUSCEPTIBILITY TO CONGENITAL DEFECTS
DOGS- patent ductus arteriosus, pulmonic stenosis, subaortic stenosis.
CATS- mitral dysplasia, atrioventricular canal
CATTLE- atrial septal defect, ventricular septal defect, transposition of great vessels.
HORSES- congenital defects are uncommon.
CONGENITAL VASCULAR ANOMALIES
Abnormal arterial or venous connections.
-Persistent right aortic arch
-Portosystemic shunts (including persistent ductus venosus in the liver)