Pulmonary Hypertension, presented by Dr. Başar Ulaş Sayılkan

Dr. Veteriner Hekim Başar Ulaş Sayılkan: Pulmoner Hipertansiyon

In this blog post, we have compiled the key highlights from the session titled “Pulmonary Hypertension”, presented by Dr. Başar Ulaş Sayılkan, held as part of VetSummit 2025: New Horizons in Veterinary Clinical Sciences, sponsored by the Kito Healthy Pet Nutrition Ecosystem. We would like to thank our speaker for the presentation.

Pulmonary Hypertension (PH):

Not Just a Number — A Disease of the Pulmonary Vascular Bed

When you hear “pulmonary hypertension” in the clinic, it immediately makes you pause. It’s not something we diagnose every day. But when we do, it’s never something to take lightly.

As Dr. Başar Ulaş Sayılkan emphasizes:

First recognize PH, then understand which type it is, and only then intervene from the right angle.

Because PH is not a single disease. It is a final common pathway reached through different mechanisms.

1) What Does Pulmonary Hypertension Actually Mean?

The body has two major circulatory systems:

  • Systemic circulation (blood going to the body)
  • Pulmonary circulation (blood going to the lungs)

When the pressure balance (systole–diastole) in these systems is disrupted, organ perfusion suffers. Impaired perfusion leads to progressive tissue damage.

Pulmonary hypertension occurs when:

👉 Pressure in the pulmonary arteries rises above normal levels.

Under normal conditions, the pulmonary circulation is a low-pressure, low-resistance system. In PH, this system shifts from a “free-flow” state to a high-resistance state.

Numerically, PH is defined as:

  • Elevated systolic pulmonary arterial pressure
  • Elevated diastolic pulmonary arterial pressure
  • Mean pulmonary arterial pressure above 25 mmHg

But clinically, the real issue is this:

PH is not just a pressure disorder — it is a disease of the pulmonary vascular bed.

2) The Core Problem: Vascular Wall Thickening

At the heart of PH lies structural change:

  • The pulmonary vessel walls thicken.
  • The lumen narrows.
  • Vascular resistance increases.

The right heart must now pump against a much harder system to move blood into the lungs.

Initially, the body compensates. But over time:

  • Arteries, arterioles, and venules undergo remodeling.
  • Elasticity is lost.
  • Vessels become stiff, almost scar-like.

The feared endpoint?

👉 Right-sided heart failure.

3) Why Is PH So Insidious?

Pulmonary hypertension may not become clinically evident until approximately 60% of the pulmonary vascular bed is compromised.

That means a patient may appear stable for years.

Even more striking:

Up to 50% of dogs with moderate PH may show no obvious clinical signs.

This makes PH:

  • Late to declare itself
  • Capable of sudden deterioration
  • More difficult to manage once advanced

4) Which Pathways Drive Disease Progression?

Pulmonary vascular tone is regulated by three major systems:

1️⃣ Endothelin Pathway

  • Potent vasoconstrictor
  • Increased endothelin = worsening PH

2️⃣ Nitric Oxide (NO) Pathway

  • Vasodilator
  • Reduced NO allows vasoconstriction to dominate

3️⃣ Prostacyclin Pathway

  • Vasodilator
  • Anti-thrombotic

Reduced prostacyclin:

  • Increases thrombotic tendency
  • Worsens disease progression

In short:

When vasoconstrictors increase and vasodilators decrease, PH advances.

5) Cats or Dogs?

In Cats

  • Congenital abnormalities are more commonly implicated.

In Dogs

The most frequent cause is:

👉 Left-sided heart disease, especially degenerative mitral valve disease (DMVD).

Mitral valve disease is common. However, only a subset of these patients progresses to PH.

6) Classification: You Can’t Treat Without a Map

PH is not a primary diagnosis — it is a consequence. Classification guides therapy.

1️⃣ Pulmonary Arterial Hypertension (PAH)

  • Idiopathic
  • Secondary to left-to-right shunts (PDA, VSD)

2️⃣ PH Secondary to Left Heart Disease

  • Most common in dogs
  • DMVD is the key player

3️⃣ PH Secondary to Respiratory Disease

  • Chronic hypoxia
  • Pulmonary fibrosis
  • Chronic bronchitis
  • Pneumonia

4️⃣ PH Secondary to Pulmonary Thromboembolism (PTE)

  • Hypercoagulability
  • Endothelial injury
  • Blood flow stasis

5️⃣ Parasitic Causes

  • Heartworm disease (Dirofilaria)

6️⃣ Multifactorial

  • For example, DMVD plus chronic lung disease

Key clinical message:

It’s not enough to say “this patient has PH.”

You must determine which group.

7) Precapillary vs Postcapillary PH

A practical clinical shortcut:

Precapillary PH

Problem originates in the pulmonary vasculature.

(Heartworm, PTE, lung disease)

Postcapillary PH

Problem originates in the left heart.

Elevated left atrial pressure increases pulmonary pressure.

(DMVD is the classic example)

This distinction directly impacts treatment decisions.

8) Clinical Signs: The Language of the Right Heart

Signs are not specific, but patterns emerge:

  • Exercise intolerance
  • Dyspnea or tachypnea
  • Lethargy
  • Inappetence
  • Syncope (fainting episodes due to reduced cerebral perfusion)
  • Cough (more common in dogs)
  • Cyanosis
  • Jugular distension
  • Ascites
  • Hepatomegaly
  • Tricuspid regurgitation murmur

But again:

👉 Mild to moderate PH may be clinically silent.

9) The Diagnostic “Gold Trio” in Practice

1️⃣ Radiography

  • Right heart enlargement
  • Pulmonary artery dilation
  • Parenchymal lung changes
  • Pleural effusion or ascites

2️⃣ Laboratory Testing

  • CBC and biochemistry
  • Blood gas analysis
  • Coagulation profile
  • NT-proBNP, troponin (supportive)
  • Annual heartworm testing

3️⃣ Echocardiography (Most Powerful Tool)

Key parameters:

  • Tricuspid regurgitation jet velocity (Vmax)

3.4 m/s = strong suspicion

  • Pressure estimation: 4 × V²

50 mmHg = concerning

80 mmHg = critical

  • D-sign

Septal flattening due to right pressure overload

  • Main pulmonary artery to aorta ratio

1.2 suggests dilation

  • RPAD index

< 36% supports PH

  • Pulmonary artery flow notching

Characteristic in advanced PH

10) Treatment: Not Just “Start Sildenafil”

Yes, sildenafil is often the first drug that comes to mind.

But Dr. Sayılkan stresses:

Never start sildenafil blindly without distinguishing precapillary from postcapillary PH.

In Precapillary PH

Sildenafil is often appropriate and beneficial.

In Postcapillary PH (e.g., DMVD)

Sildenafil may reduce cardiac output and worsen the patient.

In these cases, priority should be:

  • Pimobendan
  • Management of left heart disease
  • Reduction of venous congestion

Additionally:

  • Oxygen for hypoxic patients
  • Anticoagulation for PTE
  • Guideline-based heartworm treatment when indicated

In short:

We do not treat “PH” in isolation.

We treat the pathway that led to PH.

Conclusion: Clarity Wins in PH Management

Pulmonary hypertension may sound like a single diagnosis, but it is the result of multiple potential mechanisms.

A structured approach is key:

1. Is PH present?

2. Which group does it belong to?

3. Precapillary or postcapillary?

4. What is the underlying cause?

5. How should treatment be tailored to this specific patient?

When you think clearly and systematically, pulmonary hypertension becomes less intimidating — and more manageable.

We will continue sharing key takeaways from the sessions of VetSummit 2025: New Horizons in Veterinary Clinical Sciences, sponsored by the Kito Healthy Pet Nutrition Ecosystem. See you in our upcoming content that will support your clinical practice.

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