Cardiopathology

Congenital Diseases
1. 1) Septal Defects (Chamber development/partitioning)
  1. Atrial Septal Defect
    1. Persistent foramen ovale
    2. 1) LA -> RA -> RV
      1. RA dilation
        Increased RV Preload => Eccentric RV Hypertrophy
    3. 2) Pulmonary overperfusion
      1. Increased pulmonary return => LA dilation
  2. Ventricular Septal Defect (VSD)
    1. 1) LV -> RV
      1. Increased RV Preload & Afterload => Eccentric RV Hypertrophy
    2. 2) Pulmonary overperfusion
      1. Increased pulmonary return => Dilation & Increased LV Preload => LV Eccentric Hypertrophy
    3. Development of ventricular septum: Ventral -> Dorsal (Opening Dorsal near Pulmonary valve or Mitral Valve)
2. 2) Great Vessel Vascular Anomaly (Great vessels & Valve origins)
  1. Pulmonic Stenosis
    1. 1) Increased RV Afterload
      1. => RV Concentric Hypertrophy
    2. 2) Pulmonary Artery Poststenotic Dilation
      1. Dilation of base of pulmonary artery
  2. Aortic Stenosis
    1. 1) Increased LV Afterload
      1. => LV Concentric Hypertrophy
    2. 2) Aortic Poststenotic Dilation
  3. Tetralogy of Fallot
    1. Uncommon
    2. Calves, Pigs, Dogs
    3. Multiple congenital abnormalities simultaneously
    4. 1) Pulmonic Stenosis
      1. Increased RV Afterload
        => 3) RV HYpertrophy
    5. 2) VSD: RV -> LV
      1. Systemic Hypoxia
    6. 4) Dextro-rotated aorta
  4. Patent Ductus Arteriosus
    1. Calves (Major vessels - Don't close until 2 weeks after birth (Normal))
    2. 3-5cm distal to Aortic & Pulmonary valves
    3. 1) Aorta -> Pulmonary artery (Blood flow)
      1. => Increased RV Afterload => RV Concentric Hypertrophy
    4. 2) Pulmonary Overperfusion
      1. => Increased Pulmonary return -> LA Dilation & LV Preload -> LV Eccentric Hypertrophy
  5. Shunting Sequelae
    1. Blood shunts from Left -> Right => Pulmonary Hyperperfusion
      1. => Sustained Pulmonary Hypertension
        => Vascular changes in lung & arteriosclerosis
        => Increased resistance (Increased pressure in RT) => SHUNT REVERSAL (Right -> Left => Cyanosis)
  6. Aortic Arch Syndrome
    1. Abnormal development of the Aorta from the foetal brachial arches
      1. Aortic Arch (LT side = Normal)
      2. Mechanical disruption
    2. Persistent Aortic Arch
      1. Most Common
      2. Aorta arises from anomalous right side (RT 4th brachial arch) + Persistent Ductus Arteriosus (ligamentum arteriosum)
        Consequence: Vascular ring formation => Stricture of the oesophagus => Megaoesophagus => Regurgitation (undigested)
    3. Double Aortic Arch
      1. Vascular ring formed by persistence of both 4th brachial arches around the oesophagus
      2. Very rare
    4. Anomalous Subclavian Arteries
      1. Aberrant origin of one or both subclavian arteries causes oesophageal stricture
3. 3) Valvular Dysplasias
  1. Usually atrioventricular valves affected
  2. Leaflets of endocardium
  3. 1) Valve leaflets replaced by web-like structure
  4. 2) Short chordae with small papillary muscles
  5. Combination of 2 forms possible
4. Result of impaired development during embryogenesis
  1. Genetics, Mother (issues during pregnancy), Chemicals, Infectious agent
5. Others: Coarctation of the aorta, Ectopia cordia, Endocardial fibroelastosis (Endocardium increases thickness), Pericardial abnormalities (absent or malformed)
Pathophysiological Mechanisms
1. Pump failure
  1. Heart not contracting as hard as it should
2. Obstruction to forward blood flow
  1. Systemic - Valves, Lungs (Increased PVR), Hypertension
3. Regurgitant Blood Flow
  1. Malformed valves not closing adequately - Esp. AV valves - Reflux back into Atria
4. Shunted Blood Flow
  1. Congenital defects (Septal defects, Persistant ductus arteriosus)
5. Rupture of Heart or Major
  1. Hypovolemia => Shock, fluid build-up in pericardium, Increase in P
6. Cardiac Conduction Disorders
  1. Arrhythmias - Unsynchronized contractions, blood not being pumped in proper direction
Myocardial Compensation
1. Responses of the myocardium to heart failure
2. Cardiomyocytes do NOT divide, can only undergo HYPERTROPHY, NOT Hyperplasia
3. Types
  1. Concentric Hypertrophy
    1. Response to increased Afterload (Ventricular volume </= Normal)
      1. HYPERTROPHY ONLY
        Increase in Mass (Thicker/larger wall)
  2. Eccentric Hypertrophy
    1. Response to increased Preload (Ventricular volume > Normal)
      1. HYPERTROPHY & DILATION
        Increase in Mass & Volume of chambers
4. Progression
  1. Chronic Hypertrophy => Myofibre degeneration + Interstitial fibrosis
  2. 1:1 Ratio of Cardiomyocytes to Blood not held => Cardiomyocytes not properly perfused => Degeneration
  3. Dilation can compensate up to a limit
    1. Frank Starling Mechanism
      1. Increase in Preload => Increase in SV (Functional)
        Congestion earlier for failing heart
Aquired Diseases
1. Pericardial Diseases
  1. Non-inflammatory
    1. Hydropericardium
      1. Excessive fluid accumulates in the pericardial cavity
        Cardiac tamponade
    2. Haemopericardium
      1. Blood accumulates in the pericardial sac
        Cardiac tamponade
    3. Idiopathic Effusions
  2. Inflammatory
    1. Pericarditis
      1. Causes:
        1) Haemotogenous
        Result of septicemia (Most Common)
        2) Extension from surrounding tissues
        Lungs, pleura, mediastinum > myocardium
        3) Traumatic
        Ex. Traumatic Reticulopericarditis
      2. Serofibrinous/haemorrhagic
        Purulent
        Staph, strep
        Leakage of fibrin
      3. Sequelae
        Resolution
        Adhesion
        Constriction
        Myocarditis
2. Myocardial Diseases
  1. Functional
    1. Ex. Concentric/ Eccentric Hypertrophy
  2. Metabolic Disturbances (Degeneration)
    1. Hydrophobic degeneration
      1. Fatty change/degeneration
        Fatty infiltration
        Hylaine degeneration
        Mineralization (Calcification - Metastatic vs. Dystrophic)
        Urate deposition (visceral gout)
        Dehydration/Infectious agent (Impairing renal function)
        Uric acid accumulates in tissues (not as soluble as urea)
        Diet (too much Vit. D)
        Parathyroid problems
  3. Infarction (rare in animals)
    1. Impairs contractability of heart
    2. Embolism
      1. Hyperthyroidism, Diabetes mellitus (Dogs)
    3. Acute
      1. Red (haemorrhage, hyperaemia)
      2. Grey
  4. Inflammation (Myocarditis)
    1. Acute & Suppurative
      1. Acute & Non-suppurative
        Chronic
        Lymphocytes, macrophages (No Neutrophils)
      2. Infectious lesion (elsewhere) => infectious embolis
  5. Parasitic
    1. Fibrous sacs
  6. Nutritional (deficiencies)
  7. Cardiomyopathies (Nutritional & Idiopathic)
    1. Nutritional (Vit. E/Se deficiency)
      1. Antioxidant function
      2. Mulberry heart disease
        White muscle disease
      3. Oxidative damage of myocytes => Necrosis
    2. Genetic
      1. Malignant hyperthermia (Pigs) - Point mutation in Ca2+ channel => Necrosis
    3. Endocrine
      1. Feline hyperthyroidism
        Sxs: Thin, tachycardia, hypertension, hyperactive, (possibly aggressive), Increased BMR, Increased appetite
        Pathology:
        LV Concentric Hypertrophy
        Uni/bi-lateral thyroid involvement
        Neoplasia (older)/ Hyperplasia (younger)
    4. Idiopathic
      1. Dilated cardiomyopathy (DCM)
        Cats (Taurine deficiency)
        Horses, Dogs (Toxicity)
      2. Hypertrophic cardiomyopathy (HCM)
        Cats
        LV Concentric hypertrophy
        Saddle thrombus (10-20% of cases)
        Myofibre disarray/ loss + fibrosis
        Point mutation in contractile proteins
        Turbulence in Atrium
        Thrombus of LA => Aortic arch
      3. Restrictive cardiomyopathy
        Fibrosis of endocardium
      4. Arrythmogenic RT ventricular cardiomyopathy
        Primarily Boxers (familial)
        Affects RV & S
        Myocardial replacement
        adipose tissue + fibrosis
        => Disruption of conduction tissue
3. Epicardial Disease
  1. Ex. Serous atrophy of Fat
4. Endocardial Disease
  1. Valvular Disease
    1. Consequences:
      1. Stenosis
        More common in AV or PV (Semi-lunar valves)
        Help flow to be unidirectional
        => Increased afterload > Concentric hypertrophy
      2. Insufficiency/ Incompetence
        AV Valves
        Large surface area
        => Regurgitation > upstream congestion > Increased preload > Eccentric Hypertrophy
    2. Valvular Endocardiosis
      1. Mostly Canine
        > 6 yrs old
        Small breeds (Ex. Cavalier King Charles Spaniel)
      2. Mostly arterioventricular: Mitral valve
      3. => Valvular Insufficiency (NOT Stenosis)
    3. Equine Valvulopathy
      1. Valvular lesions subtle in Horses
      2. Fibrosis
      3. AV valves => Insufficiency
        Aortic valve => Stenosis/Insuffiiciency
  2. Endocarditis
    1. Common: Cow, Sheep, Pig
      1. Rare: Horse, Dog, Cat
    2. Septicaemia/pyaemia from septic/purulent foci
      1. Colonize/infect endothelium
      2. Septic embolism -> deposit -> Thrombus
        Septic Thrombi (from leaflets of valves)
    3. Usually valvular (can extend to mural)
    4. RT side: Cow
      1. LT side: Other species
        Both sides: Pig
    5. Sequelae:
      1. Post endocarditis valvular obliteration
        Septic embolism
        Thromboembolic infarction (post LAV endocarditis -> Kidney)
        Pulmonary thromboembolism (post RAV endocarditis)
  3. Necrotising Mural Endocarditis
  4. Endocardial Calcification
  5. Valve " Cysts"
    1. Congenital
    2. Haematomas/lymphatic (AV)
  6. Jet lesions
    1. Valvular insufficiency
  7. Melanosis
    1. Non-significant
5. Cardiac Neoplasia
  1. Primary
    1. Arises in Heart itself
    2. Haemangiosarcoma
      1. Endothelum (Mesenchymal)
      2. RT Atrium
    3. Chemodectoma (Heart base tumor)
      1. Epithelial
  2. Secondary
    1. Lymphoma
    2. Metastasis
Secondary Cardiac Disease
1. Cor pulmonale
  1. => Pulmonary disease -> Cardiac disease
  2. Primary pulmonary disease
    1. Pulmonary Thromboembolism
      1. Mechanical vascular obstruction
        Resp. Impairment
        Altitude Disease (> 2000m)
        Pulmonary hypertension
        Increased Pulmonary resistance => Increased RT ventricle afterload
2. Systemic Disease
  1. LT side of Heart affected
    1. Ex. Cats: Renal failure => Hypertension
Vascular Disease
1. Arterial Disease
  1. Hypertension
    1. Intimal hypertrophy/ arteriosclerosis
      1. Obliterates lumen in artery
        Thickened tunica media
        Proliferation of tunica intima
        Decrease in size of lumen
  2. Intramural Substance Deposit
    1. Arteriosclerosis
      1. Plaque lesions, poorly demarcated
    2. Atherosclerosis
    3. Amyloidosis
      1. Spleen or Kidney
      2. Result of chronic inflammation
        Alpha sheet (soluble), Beta sheet (animals -> INSOLUBLE => Deposits in tissues)
        Acute phase proteins (SAA) -> Normally alpha helix + inflammation => Beta pleated sheet
        Systemic Reactive Amyloidosis (Most common), Heritary amyloidosis (sharpei, asian cats), AL amyloidosis (Increase in plasma cells (Tumor))
    4. Calcification
      1. Ca2+ deposits on walls of tissue
        Metastatic or Dystrophic
      2. Poor intestinal function
        Base of Aorta -> Not hypercalceamic (mimicing metastatic)
  3. Fibrinoid necrosis
    1. Looks like Fibrin, but is NOT fibrin (degeneration of cells)
      1. Wall has become necrotic & died
  4. Inflammation (Arteritis)
    1. Infectious (Generalized/local)
      1. Bacterial
        Thrombosis of vessels in skin (Infarcts)
      2. Viral
        Virus targeting endothelium -> infarction -> ulcers
      3. Mycotic
        Lush pasture/ High concentrates -> Dec. pH -> Inc. Lactic acid bacteria -> Mucosal erosion (Rumen/abomasum) -> FUNGAL INVASION (mucosa & vasculature) -> Thrombosis (obliteration of lumen) -> Necrosis
      4. Parasitic
        Upstream: Venacava -> obliteration
        Downstream: Arteriosclerosis
    2. Non-infectious
      1. Type III Hypersensitivity
        Ag-Ab complex (deposit in vasculature & glomeruli)
        Immune complex mediated inflammation & tissue injury
        Ex. Purpura haemorrhagica (Horses)
        Sequella of infection
      2. Idiopathic
        Ex. Polyarteritis nodosa, Beagle pain syndrome
  5. Mural/luminal changes
    1. Aneurysms
    2. Aortic rupture
    3. Thrombosis
2. Venous Disease
  1. Thrombosis/phlebitis
    1. Jugulars, Venacava, Portal vein
  2. Rupture
    1. Exercise induced (Horses)
3. Mural/Luminal Structural Chamges
  1. Aneurysm
  2. Rupture
  3. Thrombosis
    1. 1) Damage to Endothelium
      1. 2) Changes in BF
        3) Changes in coagubility
  4. Idiopathic (Ex. Hypertrophic cardiomyopathy)

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Cardiopathology

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	Created by melian.yates over 10 years ago