Cardiac Diseases

Blood cells can be reproduced

Causes:

Haemorrhage (loss of blood cells) - wounds, parasites, rodenticide toxicity, inherited coagulopathies (von willebrands disease/ haemophillia), Disseminated intravascular coagulation (clots).

Haemolysis (destruction of blood cells)- immune mediated haemolytic anaemia, drug reaction/ toxicity, Infection (e.g. mycoplasma haemofelis)

Blood cells are not being reproduced

Causes:

Medullary Disorders - Inherited disorders, Myelosuppression (Feline Leukaemia virus, lead toxicity, B12 deficiency), infiltration (neoplasia)

Extramedullary Disorders - Chronic disease (liver failure, neoplasia, inflammation e.g. pyometra), renal failure (drop in erythropoeitin)

• Pale mucous membranes
• Poor coat quality
• Exercise intolerence
• Lethargy
• Collapse
• Slow Capillary Refill Time
• Poor Appetite
• Tachycardia
• Dyspnoea
• Hypothermia
• Petechiae (spotting of bruising if there is a bleeding disorder)

Causes: Tumour in the bone marrow

Clinical signs: see anaemia

Diagnosis: PCV, Bone marrow aspiration, haematology and biochemistry, blood smear.

Treatment: Limited depending on type, blood transfusion, chemotherapy

Nursing Care: Symptomatic (temperature control, regular checks, tempt to feed/ tube feed, O2 therapy)

Bleeding disorder: Patient's body has an inability to clot

Clotting disorder: Patient's body has an increased tendancy to form clots

Primary haemorrhage = initial bleed

Reactionary haemorrhage = bleeding reoccurs 24-48 hours later (slipped ligatures, dislodged clot, blood pressure normalised)

Secondary haemorrhage = rebleeding occurs 3-10 days later due to infection of wound site.

Causes: inherited (von willebrands disease, haemophillia), aquired (rodenticide toxicity, liver disease, DIC, immune mediated thrombocytopaenia 

Clinical Signs: Petechiae (pinpoint haemorrhage)/ Ecchymosis (patchy haemorrhage), anaemia and clinical signs associated with anaemia

Diagnosis: Radiography of body cavities, buccal mucosal bleeding time, platlet counts, activated clotting time, prothrombin time, activated partial thromboplastin tim, fibrin degradation products

Sound of abnormal blood flow

Causes: Heart disease (irregular structure or blood flow), changes in blood consistency (anaemia, hypervolaemia), high blood pressure (hyperthryroidism)

Acute:

Sudden onset of symptoms - Emergency

Clinical Signs: Collapse, Pale MM, Slow CRT, weak pulse

Chronic:

Develop over time, signs dependant on cardiac compensation

Causes: Congenital disease (present at birth, early signs of murmer), Aquired (present later in life, breed predispositions for degenerative disease)

Classification: Forward (inability to pump blood, often in acute cases, leads to congestive heart failure), Congestive (build up of fluid in heart)

•  Mitral valve insufficiency (leakage from LV to LA = murmer)
• Enlargement of LA and increased HR to compensate reduced outflow
• Congestion from pulmonary vein to lung tissues

Clinical signs:

• Pulmonary oedema
• Coughing
• Tachypnoea / Dyspnoea
• Tachycardia / Weak Pulse
• Lethargy/ Exercise intolerence
• Murmers/ Dysrhythmias
• Cyanosis if severe

• Pulmonic stenosis causing outflow resistance
• RA enlargement
• Congestion of vena cava

Clinical Signs:

• Ascites
• Hepatomegaly (liver enlargement)/ Splenomegaly
• Exercise intolerence/ lethargy
• Pale MM
• Tachycardia/ weak pulse
• Tachypnoea/ Dyspnoea
• Murmers/ Dysrhythmias
• USUALLY CAUSED BY LEFT SIDED CHF

• History and clinical exam
• Imaging: Radiography, Echocardiography
• ECG
• Blood Pressure Monitoring
• Blood Tests:
  • Cardiac biomarkers
  • T4
  • Haematology
  • Biochemistry  

Mitral Valve Endocardiosis:

• Thickening of mitral valves
• Most common heart disease in canines (small breeds predisposed)
• Backflow of blood from LV to LA

Endocarditis:

• Bacterial Infection of the endocardium and heart valves
• Rare in small animal patients

Dilated Cardiomyopathy:

• Dilation of the heart chambers
• Reduction of systolic function
• Large dogs predisposed, cats with taurine deficiency
• Often associated with arrythmias (atrial fibrillation)

Hypertrophic Cardiomyopathy:

• Thickening of the heart muscles
• Reduction of diastolic function
• Cat breed dispositions or secondary hyperthyroidism
• Often asymptomatic and present with CHF
• May lead to aortic thromboembolism

• Fluid build up in the pericardial sac
• Pericardial effusion compresses heart (Cardiac tamponade)
• Leads to R sided CHF
• Cardiac tamponade prevents contraction and diastolic filling
• Requires emergency drainage (pericardiocentesis)
• Monitor using ECG

Atrial Septal Defects:

• Foramen ovale present in foetus remains open (should close at birth)
• Causes a L to R shunt if remains open
• Asymptomatic if minor defect
• Corrected surgically or CHF managed medically

Ventricular Septal Defects:

• Idiopathic
• Terriers predisposed
• Causes L to R shunt and blood mixing
• Symptoms depend on size of defect
• Corrected surgically or CHF managed medically

Pulmonic Stenosis:

• Common congenital disease in canines
• Obstruction to pulmonary artery = resistance to outflow
• Increased pressure on right side of heart
• Clinical Signs: Syncope, R CHF, exercise intolerence
• Treatment: Medically, balloon valvuloplasty

Aortic Stenosis:

• Narrowing of aortic valve
• Obstructs LV outflow = increased pressure
• Clinical Signs: Syncope to CH, aorta rupture (sudden death) 

Subaortic Stenosis:

• Narrowing of LV beneath aortic valve = Obstructs LV outflow
• Surgery to cure

• Mitral Valve Displasia = Common in cats
• Leads to heart failure depending on severity of lesion
• Diagnosis: endocardiography
• Treatment: Valve replacement
• Mitral valve = Left
• Tricuspid valve = Right

• Heart malformation in dogs
• Females predisposed
• Ductus arteriosus = normal foetal blood vessel, directs blood away from lungs. Closes after birth to form ligamentum arteriosum
• Diagnosis: Causes L to R shunt (endocardiography) and continuous murmer
• L sided CHF
• Treatment: Surgical ligation, catheter based occlusion (early surgery required as high risk)

Caused by 4 heart defects: Pulmonary stenosis, thickening of RV wall, ventricular septal defect, overriding aorta

Treatment for Chronic: reduce stress, reduce exercise, drug therapy, weight management

Treatment for Acute (Emergency): O2 therapy, strict rest, glyceryl trinitrate, diuretics, strict monitoring, temperature control, reduce stress.

Aims: Improve QOL and exercise tolerence, reduce effects of maladaptive compensation mechanism, control arrhythmias

Diuretics: Furosemide (Dimazon, Lasix) - Mainstay of treatment: reduce oedema

Inodilators: Pimobendan (Vetmedin) - Dilates venous return to the heart, reduces preload. Increases calcium sensitivity and heart contraction.

ACE Inhibitors: Benazapril (Fortekor), Enalapril - Reduces maladaptive RAAS effects, May reduce remodelling of heart tissue by aldesterone, Spironolactone blocks aldosterone directly