Components of the Cardiovascular System
Heart – four chambers: right atrium (RA), right ventricle (RV), left atrium (LA), left ventricle (LV).
Valves – tricuspid (RA–RV), pulmonary (RV–pulmonary artery), mitral (LA–LV), aortic (LV–aorta).
Vessels – arteries, arterioles, capillaries, venules, veins.
Pulmonary circulation – RV → lungs → LA.
Systemic circulation – LV → body → RA.
Key Functions
Basic Physiologic Concepts
1. Heart Failure
Heart failure = inability of the heart to pump enough blood to meet metabolic demands at normal filling pressures.
Systolic failure: impaired contraction → reduced stroke volume (e.g., dilated cardiomyopathy).
Diastolic failure: impaired relaxation/filling (e.g., hypertrophic cardiomyopathy, pericardial effusion).
Left-sided failure: pulmonary venous congestion → pulmonary edema, cough, dyspnea.
Right-sided failure: systemic venous congestion → ascites, pleural effusion, peripheral edema, jugular distension.
2. Volume and Pressure Overload
Volume overload: from valvular regurgitation or shunts → chamber dilation (eccentric hypertrophy).
Pressure overload: from stenotic valves or systemic/pulmonary hypertension → concentric hypertrophy (thickened walls).
3. Arrhythmias
Abnormal impulse formation or conduction can result in:
Tachycardia (too fast)
Bradycardia (too slow)
Irregular rhythms (premature beats, fibrillation)
Arrhythmias may be primary or secondary to structural heart disease, metabolic disorders (electrolytes, hypoxia), systemic disease (e.g., sepsis).
4. Congenital vs Acquired Disease
Congenital: present at birth (PDA, VSD, pulmonic stenosis).
Acquired: develop later (degenerative valve disease, cardiomyopathies, heartworm disease, endocarditis).
1. Degenerative Mitral Valve Disease (DMVD)
Species: Primarily small-breed, older dogs (e.g., Cavalier King Charles Spaniels).
Pathogenesis: Progressive myxomatous degeneration of mitral valve → valve thickening and prolapse → mitral regurgitation → left atrial and ventricular dilation → left-sided heart failure over time.
Clinical signs:
Early: asymptomatic murmur (left apical systolic).
Progressive: cough (from left atrial enlargement compressing mainstem bronchus), exercise intolerance, tachypnea, dyspnea, possible syncope.
Advanced: signs of pulmonary edema, cachexia.
Diagnostics:
Auscultation: characteristic systolic murmur over left apex.
Thoracic radiographs: cardiomegaly, pulmonary venous congestion, pulmonary edema.
Echocardiography: regurgitant jet, valve lesions, chamber enlargement.
Blood pressure, BNP/NT-proBNP may aid staging.
Treatment principles:
Preclinical stages: monitored; some patients benefit from early Pimobendan (per guidelines where evidence supports).
Symptomatic CHF:
2. Dilated Cardiomyopathy (DCM)
Species: Large and giant breed dogs (Doberman Pinschers, Great Danes, Boxers, etc.).
Pathogenesis: Primary myocardial disease → ventricular dilation and systolic dysfunction → reduced CO and arrhythmias.
Clinical signs:
Exercise intolerance, weakness.
Cough, dyspnea from pulmonary edema.
Syncope or sudden death (ventricular arrhythmias).
Possible ascites in right-sided failure.
Diagnostics:
Auscultation: soft systolic murmur ± gallop rhythm.
ECG: ventricular arrhythmias, atrial fibrillation.
Radiographs: cardiomegaly, pulmonary edema.
Echocardiography: dilated chambers, reduced fractional shortening/ejection fraction.
Treatment:
Pimobendan to improve systolic function.
ACE inhibitors.
Diuretics for CHF.
Antiarrhythmic drugs (e.g., sotalol, mexiletine) if ventricular arrhythmias.
Dietary considerations (e.g., check for taurine deficiency in some breeds or diet-related DCM suspicion).
3. Hypertrophic Cardiomyopathy (HCM)
Species: Cats (most common primary heart disease).
Pathogenesis: Thickening (hypertrophy) of the LV wall → impaired relaxation (diastolic dysfunction) → increased filling pressures → LA enlargement → risk of CHF and thromboembolism.
Clinical signs:
Often asymptomatic; may be detected by murmur or gallop rhythm.
Signs when decompensated: tachypnea, dyspnea (pleural effusion, pulmonary edema), lethargy.
Aortic thromboembolism (ATE): acute hindlimb paralysis, pain, cold limbs.
Diagnostics:
Auscultation: systolic murmur ± gallop rhythm.
Echocardiography: LV wall thickening, LA enlargement.
Radiographs: variable heart enlargement, pulmonary edema/pleural effusion.
ECG: may show arrhythmias.
Treatment:
CHF management: diuretics, oxygen, thoracocentesis (for effusions).
Beta-blockers or calcium-channel blockers in some cases to improve diastolic filling (patient-dependent).
Antithrombotic therapy in high-risk cats (e.g., clopidogrel) to reduce thromboembolism risk.
4. Heartworm Disease (Dirofilariasis)
Species: Dogs (primary), cats more rarely affected.
Pathogenesis: Adult worms in pulmonary arteries and sometimes right heart → pulmonary hypertension, vascular damage, right-sided heart strain; severe cases → caval syndrome.
Clinical signs:
Cough, exercise intolerance, weight loss.
In advanced disease: dyspnea, ascites, syncope.
Caval syndrome: acute collapse, hemoglobinuria, severe anemia.
Diagnostics:
Antigen tests (detect adult female worms).
Microfilaria tests.
Radiographs: enlarged pulmonary arteries, right heart enlargement.
Echocardiography: visible worms in heart/pulmonary artery in some cases.
Treatment:
Adulticide therapy (melarsomine) per protocol.
Microfilaricide and macrocyclic lactone preventives.
Strict exercise restriction during treatment.
Doxycycline (to target Wolbachia bacteria) as part of multi-step regimens.
Surgical removal of worms in caval syndrome.
Prevention:
Regular heartworm prophylaxis is key; client education is crucial.
1. Valvular Disease & Endocarditis
Species: Ruminants, horses, pigs.
Endocarditis often bacterial (e.g., from septicemia, umbilical infections, mastitis, respiratory disease).
Signs:
Fever, weight loss, decreased performance.
New or changing murmur.
Signs of CHF (jugular distension, edema, exercise intolerance).
Possible embolic disease: lameness (septic emboli to joints) or organ dysfunction.
Diagnostics:
Auscultation: loud murmur, sometimes “to-and-fro.”
Blood cultures for bacteremia.
Echocardiography when available.
CBC (inflammatory profile).
Treatment:
Long course of appropriate antibiotics.
Supportive care.
Prognosis often guarded–poor in food animals.
2. Congenital Defects (All Species)
Common lesions:
Patent ductus arteriosus (PDA) – continuous murmur, volume overload of LV.
Ventricular septal defect (VSD) – pansystolic murmur, left-to-right shunt, pulmonary overcirculation.
Pulmonic or aortic stenosis – systolic ejection murmurs, pressure overload of RV or LV respectively.
Diagnosis:
Echocardiography is key; murmurs often detected in young animals.
Treatment:
Some defects are surgically or interventionally correctable (e.g., PDA ligation, balloon valvuloplasty for pulmonic stenosis).
Others managed medically or monitored if mild.
3. Cardiomyopathies & Arrhythmias in Horses
Atrial fibrillation – common arrhythmia in performance horses; may be lone AF or associated with structural disease.
Signs:
poor performance, exercise intolerance, irregularly irregular rhythm.
Diagnosis:
ECG, auscultation.
Treatment:
cardioversion (e.g., quinidine) in suitable cases; rate control in others.
Myocarditis – from viral, bacterial, or toxic causes; leads to decreased performance, arrhythmias, possible heart failure.
4. Pericardial Disease
Species: Dogs, cattle, horses.
Pericardial effusion (dogs – often neoplastic or idiopathic; cattle – traumatic pericarditis from hardware disease).
Beck’s triad (in tamponade): muffled heart sounds, jugular distension, weak pulses/hypotension.
Treatment:
Pericardiocentesis (dogs).
In ruminants, hardware disease management (magnet, surgery where appropriate).
Key Signs of Cardiovascular Disease
Physical Exam Focus
1. History & Signalment
Age, breed (e.g., predisposition to HCM, DCM).
Onset and progression of cough, exercise intolerance, syncope, respiratory signs.
Past illnesses, diet, medications, travel history.
2. Auscultation & Basic Exam
Characterize murmurs: location, timing, intensity, radiation.
Identify additional sounds: gallops, clicks, rubs.
Check for arrhythmias (confirm with ECG).
3. ECG (Electrocardiography)
Detects arrhythmias (AF, ventricular arrhythmias, AV block).
Provides information on chamber enlargement in small animals (less useful in large animals for size).
4. Imaging
Thoracic radiographs – cardiac size, pulmonary circulation, edema, vascular patterns.
Echocardiography – gold standard for structural assessment: chamber size, wall thickness, systolic and diastolic function, valve function, congenital defects, pericardial effusion.
5. Laboratory Tests
CBC/biochemistry: assess systemic disease.
Cardiac biomarkers: NT-proBNP, troponins (where available).
Blood pressure measurement for systemic hypertension.
1. Stabilize the Patient
Oxygen therapy if dyspneic.
Cage rest, minimal stress.
Diuretics for pulmonary edema/effusions.
Careful IV fluids (if shock, but avoid fluid overload in CHF).
2. Disease-Specific Management
CHF:
Diuretics (furosemide).
ACE inhibitors.
Pimobendan (dogs with systolic dysfunction).
+/- Spironolactone.
Arrhythmias:
Underlying cause treatment (electrolytes, systemic disease).
Antiarrhythmic drugs (e.g., sotalol, diltiazem, lidocaine, amiodarone depending on rhythm and species).
Cardioversion in selected cases (AF in horses/dogs).
Congenital defects:
Surgical or interventional correction when possible.
Medical palliation in non-correctable or mild lesions.
Pericardial effusion:
Pericardiocentesis.
Treat underlying cause (neoplasia, traumatic pericarditis, idiopathic).
Heartworm disease:
Adulticide protocols and prevention as outlined earlier.
3. Long-Term Management
Regular rechecks with auscultation and imaging.
Client education on signs of decompensation (increased respiratory rate at rest, reduced appetite, collapse).
Dietary considerations (moderate sodium restriction in CHF).
Exercise restriction tailored to severity.
Dogs: DMVD, DCM, heartworm disease, pericardial effusion, congenital defects.
Cats: HCM, restrictive cardiomyopathy, sometimes DCM (e.g., nutritional taurine deficiency historically), thromboembolism.
Horses: AF, valvular insufficiencies, congenital defects, myocarditis.
Cattle & Small Ruminants: Endocarditis, pericarditis (hardware disease), congenital defects, cor pulmonale in chronic pulmonary disease (“brisket disease” at high altitude).
Swine: Congenital heart defects, heart failure secondary to systemic disease.
Breeding programs to reduce congenital defects or hereditary cardiomyopathies.
Heartworm prevention in endemic areas.
Regular health checks in older animals to detect preclinical disease.
Manage systemic conditions that stress the heart (hyperthyroidism in cats, systemic hypertension).
Avoid rapid ascents/high altitude for susceptible animals.
Clinical Hints
Resting respiratory rate at home is a sensitive indicator of impending CHF in dogs and cats—excellent for monitoring.
Not all murmurs mean significant disease, but all new murmurs should be investigated, especially in young animals or those with clinical signs.
Cats can have significant cardiac disease with a very soft or no audible murmur—echocardiography is essential in suspicious cases.
In large animals, jugular distension and peripheral edema are key signs of right-sided failure or pericardial disease.
Early diagnosis and staged treatment (using standardized staging systems where available) significantly improve quality and length of life.
Home