Veterinary Cardiology – Clinical Manifestations & Cardiac Murmur Study Notes

Instructor & Lecture Context

  • Lecturer: Brady Little, DVM, MSc, Cert Vet Ed, FHEA
  • Topic Focus: Clinical Manifestations – Veterinary Cardiology
  • Over-arching theme: How to detect, interpret, and clinically act on abnormal heart sounds, structural disease, and radiographic evidence in small-animal practice.

Learning Objectives (What you must be able to do)

  • Cardiac auscultation – analyze normal vs. abnormal heart sounds.
  • Audible heart murmurs – describe common causes & acoustic characteristics.
  • Valvular insufficiencies – recognize underlying pathophysiology.
  • Cardiomyopathies – be familiar with common types & sequelae.
  • Cardiac radiology – comprehend diagnostic value, especially Vertebral Heart Score (VHS).

Cardiac Auscultation Essentials

  • Up to four heart sounds exist; two are normally heard in dogs/cats (large animals may reveal more).
    • S1 – AV valve (mitral & tricuspid) closure at onset of ventricular systole.
    • S2 – Semilunar valve (aortic & pulmonic) closure at end of systole.
    • S3 – Rapid ventricular filling in early diastole.
    • Not usually audible in small animals; when heard → suggests \text{congestive heart failure (CHF)} or dilated cardiomyopathy.
    • S4 – Atrial systole noise.
    • Audible only with non-compliant ventricles (e.g., feline hypertrophic cardiomyopathy [HCM]).

Describing Heart Murmurs

  • Definition: Sound of turbulent blood flow — always abnormal.
  • Key descriptive parameters (document all five in SOAP notes):
    1. Intensity (Absolute Grade I–VI)
      • I – almost imperceptible; prolonged S1
      • II – distinct yet very soft
      • III – low–moderate loudness
      • IV – very loud, no palpable thrill
      • V – very loud with palpable thrill
      • VI – audible without stethoscope touching skin / even without stethoscope
    2. Timing within cardiac cycle – systolic, diastolic, pansystolic, holosystolic, early, late, continuous.
    3. Point of Maximal Intensity (PMI) / Valve area – pulmonic, aortic, mitral, tricuspid.
    4. Quality (intensity profile) – plateau, crescendo, decrescendo, crescendo-decrescendo (diamond).
    5. Character (pitch/frequency) – blowing, musical, honking, harsh, noisy, etc.
  • Clinical truth: Murmur loudness ≠ disease severity; e.g., a tiny ventricular septal defect can be loud, while severe CHF may have a soft murmur.

Why Turbulence Happens (Three Mechanisms)

  1. Abnormal flow path – e.g., incomplete valve closure ⇒ regurgitant jet.
  2. Abnormal vessel diameter – e.g., congenital aortic or pulmonic stenosis.
  3. Abnormal blood viscosity – e.g., anemia ↓ viscosity → turbulence at lower velocities.

Refresher – Cardio-Renal Physiology

  • Cardiac Output (CO) \text{CO}=\text{HR}\times\text{SV}
  • Stroke Volume (SV) changes via:
    • Contractility (myocardial inotropy)
    • Preload (blood volume returned to heart, largely kidney-driven)
  • Clinical link: Any chronic cardiac disease eventually recruits renal mechanisms (RAAS), hence combined therapy often targets both organs.

Valvular Insufficiencies – Pathophysiology & Clinical Sequelae

Mitral Valve Insufficiency (Left-sided)

  • Initial event: Mitral leaflets fail to coapt → blood regurgitates into left atrium (LA) during systole.
  • Early compensation: ↓ CO sensed → reflex tachycardia restores CO ≈ normal.
  • Progression: Renal RAAS activation → water & Na⁺ retention ⇒ ↑ blood volume & preload.
  • Consequences
    • LA & LV dilation (acquired dilated cardiomyopathy phenotype).
    • Larger regurgitant volume perpetuates cycle (“snowball effect”).
  • De-compensation stages
    1. Congestive Heart Failure (CHF) – LA can’t enlarge further → LA & pulmonary venous pressures rise ⇒ pulmonary edema.
    • Clinical signs: ↑ respiratory rate/effort, cough, exercise intolerance.
    1. Myocardial failure – overstretched myocardium loses contractility.

Tricuspid Valve Insufficiency (Right-sided)

  • Mechanistic mirror of mitral disease but affecting systemic circulation.
  • High right-atrial & systemic venous pressures → capillary leak in serous cavities.
    • Peritoneum → fluid accumulation = ascites (pot-bellied abdomen).
    • Pleura → pleural effusion (dyspnea, muffled lung sounds).
  • Circulatory diagram parallels mitral schematic but congestion appears before pulmonary circuit.

Breed Predispositions for Acquired & Congenital Lesions

  • Mitral valve (degenerative) – Cavalier King Charles Spaniel, Dachshund, small breeds.
  • Mitral valve (congenital dysplasia) – Bull Terrier, Rottweiler.
  • Dilated cardiomyopathy (DCM) – Boxer, Doberman Pinscher, Great Dane, Irish Wolfhound, Labrador, Cocker Spaniel.
  • Patent Ductus Arteriosus (PDA) – Cocker Spaniel, Springer Spaniel, GSD, Maltese, Poodle.
  • Pulmonic stenosis – Boxer, Bulldog, Schnauzer, Samoyed, Mastiff, Westie.
  • Subaortic stenosis – Boxer, Golden, Newfoundland, Rottweiler, GSD.
  • Congenital tricuspid dysplasia – Labrador Retriever.
  • Ventricular septal defect (VSD) – English Springer Spaniel.

Cardiomyopathies

Dilated Cardiomyopathy (DCM)

  • Etiology: Primary genetic defect → ↓ myocardial contractility.
  • Signalment: Most common in Dobermans, Boxers (also Great Danes, Irish Wolfhounds, etc.).
  • Compensation: Tachycardia + volume retention mimic mitral disease; progressive LV dilation often distorts mitral annulus → secondary mitral regurgitation.

Feline DCM (Nutritional)

  • Cause: Taurine deficiency (rare today with commercial diets).
  • Pathology/Outcome: Similar to canine DCM; reversible if caught early & taurine supplemented.

Feline Hypertrophic Cardiomyopathy (HCM)

  • Genetics: Documented mutations in Maine Coon, Ragdoll cats.
  • Pathology: Concentric LV hypertrophy.
    • Systolic pump function can appear normal/supernormal.
    • Diastolic dysfunction (poor relaxation) → ↓ SV & CO.
    • Valve malalignment → systolic anterior motion (SAM) of mitral valve ⇒ audible systolic murmur, possible LVOT obstruction.
  • Complications: Atrial enlargement → risk of arterial thromboembolism (“saddle thrombus”).

Congenital Shunts & Defects

Patent Ductus Arteriosus (PDA)

  • Normal fetal vessel: Ductus arteriosus links pulmonary artery to aorta to bypass fetal lungs.
  • Post-natal failure to close ⇒ continuous machinery murmur (left heart base); blood shunts left → right (aorta → pulmonary artery).
  • Physiologic result: Volume overload of pulmonary circulation & left heart.
  • Imaging: Characteristic dilated descending aorta & pulmonary vessels.

Patent Foramen Ovale (PFO)

  • Incomplete closure of inter-atrial septum → potential right→left or left→right shunt depending on pressures.
  • Often incidental; becomes clinically relevant if concurrent pulmonary hypertension.

Cardiac Radiology & Vertebral Heart Score (VHS)

Imaging Views

  • Right Lateral & Ventro-Dorsal (VD) are standard; in cats VD especially reliable due to uniform thoracic conformation.
  • Normal cardiac silhouette width: \approx 60\text{–}65\% of thoracic width on VD.

How to Calculate VHS (Buchanan & Bücheler method)

  1. On lateral film, measure Long axis (L) – carina to apex.
  2. Measure Short axis (S) – widest heart diameter perpendicular to L at mid-heart.
  3. Place calipers against thoracic vertebrae starting at cranial edge of T4; count vertebrae to end of measurement lines.
  4. Formula: \text{VHS}=L+S\,(\text{in vertebral bodies})

Example Values (from lecture images)

  • Normal dog: L=5.2,\;S=4.4\;\Rightarrow\;VHS=9.6
  • Enlarged dog: L=7.2,\;S=6.4\;\Rightarrow\;VHS=13.6

Species-Specific Reference Ranges

  • Dogs
    • Average 9.7\pm0.5 v.
    • Normal range: 8.5\text{–}10.9 v.
    • Mild enlargement: 11\text{–}11.9 v.
    • Moderate: 12\text{–}12.9 v.
    • Marked: 13\text{–}14 v.
    • Extreme: >14 v.
  • Cats
    • Average 7.5\pm0.3 v.
    • Normal range: 6.8\text{–}8.1 v.
    • Mild enlargement: 8.2\text{–}8.5 v.
    • Moderate: 8.6\text{–}8.9 v.
    • Marked: 9\text{–}10 v.
    • Extreme: >10 v.

Clinical Application & Red Flags

  • Respiratory distress in a geriatric small-breed dog + left apical holosystolic murmur → think degenerative mitral valve disease; take thoracic rads & monitor RR at home.
  • Young Labrador with right apical systolic murmur & ascites → consider congenital tricuspid dysplasia.
  • Doberman with soft murmur but exercise intolerance → screen for occult DCM (ECG/echo), illustrating loudness ≠ severity.
  • Kittens with continuous murmur → rule out PDA early; surgery/coil closure is curative and ethically imperative.

Integrative Notes & Practical Pearls

  • Always interpret murmurs in context (signalment, radiographs, echocardiography).
  • Remember cardio-renal axis: diuretics & RAAS inhibitors form the cornerstone of CHF therapy; dietary sodium plays ethical/practical role (client compliance).
  • Thoracic point-of-care ultrasound (T-FAST) can detect pleural effusion & guide emergency thoracocentesis in right-sided CHF.
  • Genetic counselling (e.g., for Boxers, Maine Coons) has preventative value and ethical implications for breeding programs.