7) congenital cardiac diseases, diseases of the pericardium Flashcards
When do we consider a case congenital?
- Sudden death of new-born puppy
- Cyanosis, dyspnoea, exercise intolerance and restricted development in young animals, less than 1 year
- Cardiac murmur, III/VI grade in young dogs, less than 1-2 years (but distinguish from innocent cardiac murmur in young animals
Diagnosis of congenital heart disease
- Listen to the heart at the first visit (vaccination) → often cause audible murmurs
- Pathological murmur:
➢ Has a point of maximum intensity that indicates location of heart disease
➢ Loud, often with fremitus, permanent, can be conducted
➢ Timing and quality help to determine the origin
Types of congenital heart disease and their prevelance
- Patent ductus arteriosus (PDA) 27%
- Aortic stenosis 25%
- Pulmonic stenosis 21%
- Ventricular septal defect 10%
- Tricuspid dysplasia 5%
- Tetralogy of Fallot 4%
- Persistent right aortic arch 3%
- Mitral dysplasia 1,7%
- Atrial septal defect 1,3%
- Peritoneal-pericardial diaphragmatic hernia (PPDH) 0.5%
Types of congenital heart disease and their prevelance
- Patent ductus arteriosus (PDA) 27%
- Aortic stenosis 25%
- Pulmonic stenosis 21%
- Ventricular septal defect 10%
- Tricuspid dysplasia 5%
- Tetralogy of Fallot 4%
- Persistent right aortic arch 3%
- Mitral dysplasia 1,7%
- Atrial septal defect 1,3%
- Peritoneal-pericardial diaphragmatic hernia (PPDH) 0.5%
- Anomalies causing concentric hypertrophy:
Aortic stenosis → left ventricular hypertrophy
➢ Pulmonic stenosis → right ventricular hypertrophy
(everything that causes pressure overload)
Anomalies causing eccentric hypertrophy:
Mitral dysplasia → insufficiency on left side
➢ Tricuspid dysplasia → insufficiency on the right side
➢ Ventricular septal defect → right or left side
➢ PDA → usually left side
Aortic stenosis
Predisposed: boxer, newfoundland, German shepherd, golden retriever, rottweiler, bull terrier, bouvier de Flanders, bernese mountain dog, dogue de Bordeaux
Location:
- Subvalvular/subaortic (SAS/subaortic stenosis) → most common
- Valvular
- Supravalvular
Pathogenesis:
- Fibrous tissues or fibrous nodules causing stenosis → left ventricular pressure rises → left ventricular concentric hypertrophy + the pressure in the left atrium will rise as well eventually
➔ Leads to a decrease in left ventricular output + myocardial ischemia due to hypertrophy (remember: needs more oxygen!) →arrhythmias → can be life-threatening
Clinical Findings:
- Lethargy, exercise intolerance, syncope
- Ejection-type (crescendo-decrescendo) systolic murmur→ aorta at 3-4 IC, left side- heart base
- Femoral pulse strength decreased
- ECG → might see left ventricular hypertrophy = tall R-wave
- Radiograph → enlarged left ventricle and dilated aorta (but enlarged aorta rarely seen!)
Definite diagnosis→ doppler echocardiography
Treatment:
- Mild cases might not need any treatment
- Medical:
➢ beta-blocker e.g. atenolol → decrease myocardial oxygen demand, prolongs diastole, decreases wall stress
➢ antiarrhythmic drugs
- surgery: balloon vulvoplasty, cardiopulmonary bypass
Pulmonic stenosis
Predisposed: boxer, English bulldog, Scottish terrier, fox terrier, Samoyed, miniature schnauzer, chihuahua, beagle
Location: usually valvular
Pathogenesis:
- dysplasia of the pulmonic valve → obstruction of the right ventricular outflow → increased systolic pressure → concentric right ventricular hypertrophy
➔ compliance decreases → increased right atrial pressure and venous congestion → right sided congestive heart failure in severe cases
- Turbulent blood flow → deformation of the vessel wall of the pulmonary artery → post-stenotic dilation
Clinical findings:
- Exercise intolerance, failure to thrive
- Right-sided congestive heart failure → ascites, peripheral edema, jugular distension, pulsation
- Ejection-type systolic murmur → arteria pulmonalis at 3rd ICS, left side, heart base + corresponding pericardial thrill
- ECG → might show right ventricular enlargement = deep S wave
- Radiograph: right ventricular enlargement (increased sternal contact!), dilation of the main pulmonary artery, diminished pulmonary perfusion
Definite diagnosis → echocardiography →turbulent blood flow over stenosis
Treatment:
- Balloon vulvoplasty is highly effective here (in comparison to SAS, where it is not a long-term option0
- Some can be managed with beta-blocker
- Antiarrhythmic drugs if arrhythmia present
Atrioventricular dysplasia
Predisposed: large breed dogs
Can be mitral or tricuspid, rarely both, will usually cause valve insufficiency → Clinical signs are similar to those of chronic Endocardiosis!
- Mitral valve involved → signs of left sided HF
➢ Pulmonary oedema
➢ Tachypnoea, dyspnoea
➢ Cough
- Tricuspid valve involved → signs of right sided HF
➢ Ascites
➢ Jugular vein distension and pulsation
- Holosystolic or systolic murmur
- Systolic click (3rd heart sound
- ECG:
➢ Left atrial enlargement → widened P wave
Pathogenesis:
- Dysplasia of the valve leaflets → turbulent systolic flow from the ventricle back into the atrium i.e. regurgitation → increased atrial volume → increased atrial chamber size and pressure → HF
- Mitral valve involved → increased pulmonary pressure → cardiogenic pulmonary pressure
- Tricuspid valve involved → increased venous pressure → right-sided congestive HF signs
- Jet flow will cause lesions → rupture in severe cases?
Diagnosis → echocardiography
Treatment: valvuloplasty
Mitral valve dysplasia
Predisposed:
- German shepherd, newfoundland, golden retriever, bull terrier great Dane, mastiff, dalmatian;
- usually young dogs
Tricuspid valve dysplasia
Predisposed:
- German shepherd, Labrador retriever, bobtail, dog de Bordeaux
- usually young dogs
- more common in male
Patent ductus arteriosus
Predisposed:
- miniature poodle, German shepherd, collie, sheltie, Pomeranian, Maltese, poodle
- young age
- female 3 times as much
Physiological in foetus → shunts blood from the pulmonary artery to the descending aorta
After birth → inflation of the lungs = remodelling of foetal vasculature → change in pulmonary circulation from high-pressure/ high-resistance to low-pressure/ low resistance → closure of ductus arteriosus → becomes ligamentum arteriosum
Pathogenesis:
- persistence of ductus arteriosus with otherwise normal circulation → shunting blood-flow from aorta to pulmonary artery, and this is continuous! Because aortic pressure is always higher, In diastole and systole! → there is always some blood staying in the lung-left heart side circulation→ pressure in pulmonary arteries and veins, left ventricle and atrium rises → left atrial and left ventricle dilation
- decrease in diastolic BP and increase in systolic BP → increased difference between systolic and diastolic BP → bounding femoral pulse, increased pulse pressure → left sided congestive HF
- reverse-PDA: pulmonary pressure exceeds aortic pressure → right-to-left back-flow from pulmonary artery to aorta → caudal hypoxemia! (pink mm cranially and cyanosis caudally → subsequent polycythaemia due to increased erythropoietin release)
Clinical findings:
- continuous machinery (locomotive) murmur
- bounding femoral pulse, “steam-hammer” pulse
- often first no clinical signs → then when older sings of left-sided CHF
- ECG → wide P wave and tall R wave
- Radiographs → generalized enlargement of the heart, especially left-sided
- Reverse-PDA: lethargy, exercise intolerance, collapse due to severe pulmonary hypertension and venous admixture, differential cyanosis
- Continuous murmur, at apulmonary artery, left side, machinery
Diagnosis: echocardiography → continuous turbulence in the main pulmonary artery, left-sided dilation
Treatment:
- Closure and medical management of CHF before surgery
- BUT contraindicated in reverse-PDA → pulmonary hypertension would increase even more → can just do medical management and bad long-term prognosis
Tetralogy of Fallot
- Combination of 4 congenital diseases:
➢ Pulmonic stenosis
➢ Large ventricular septal defect
➢ Right ventricular hypertrophy ( consequence of the pulmonic stenosis
➢ Dextroposition and overriding of the aorta; i.e. aorta receives some blood from the right ventricle!
Pathogenesis:
- Depends on severity of pulmonic stenosis, i.e. Depends on pressure relation, i.e. depends on where the blood goes between the ventricles (N.B: without pulmonic stenosis, septal defects usually lead to left-to-right shunts due to higher pressure in the left side of the heart)
➔ Hight right ventricular pressure → venous blood gets to left side of the heart and aorta, right-to-left shunt → decreased pulmonary blood flow (part of blood flows to left heart side before it even reaches the lungs) and generalized cyanosis (venous blood mixes into the oxygenated blood delivered to the body)
Clinical Findings:
- Fatigue, shortness of breath
- Generalized cyanosis leading to polycythemia and weakness
Eisenmenger syndrome:
- When a long-standing left-to-right cardiac shunt causes pulmonary hypertension and eventually leads to reverse right-to-left shunt
Peritoneopericardial diaphragmatic hernia (PPD)
- Abnormal development of the dorsolateral septum transversum/ failure of the lateral pleuroperitoneal folds and the ventromedial pars sternalis to unite → herniation of the abdominal viscera into the pericardial sac
- Most commonly herniated: liver > SI > spleen > stomach
Clinical signs: - Often none, with sudden death and then detected during necropsy
- Cardiac tamponade, dyspnoea, tachypnoea, exercise intolerance, coughing, vomiting, GI obstruction
- Radiographs should be diagnostic
Treatment: surgery
Congenital heart diseases in cats
- Less common
- No overall breed or sex predilection
- Frequency:
➢ Atrioventricular valve insufficiency 17%
➢ Ventricular septal defect 15%
➢ Endocardial fibroelastosis 11% (fibrosis of the ventricular endocardium → short coursed → rapid death)
➢ PDA 11%
➢ Aortic stenosis (Subvalvular) 6%
➢ Tetralogy of Fallot 6%
