Pulmonary Hypertension

RUSSELL J LEADSOM – BVSc CertVC MRCVS

A review ohypertension-dogf the pathophysiology, symptoms, diagnosis and available treatment of pulmonary hypertension in veterinary patients.

In the last decade pulmonary hypertension (PH) has become well recognised in veterinary patients, but remains an elusive condition that is infrequently diagnosed. Despite many (human) advances in the research of PH, there still remain many mechanisms of this multifactorial condition that are poorly understood.

The definition of PH is a mean pulmonary artery pressure (PAp) that exceeds 25mmHg when resting. This elevated pressure is the result of increased pulmonary vascular resistance, and leads to compensatory changes to the right side of the heart, right heart side dysfunction and ultimately failure.

There are now many groups and sub-groups in the classification of PH; in veterinary medicine it may usefully be limited to 4 main groups.

Group I Pulmonary arterial hypertension (PAH)

This occurs in the setting of congenital cardiac defects that produce left to right shunts including patent ductus arteriosus, atrial and ventricular septal defects. The distal pulmonary arteries are particularly affected with intimal proliferation, medial hypertrophy, fibrotic and inflammatory infiltrates and vasoconstriction, resulting in increased vascular resistance and increased PAp. Pulmonary veins are largely unaffected.

Group II Pulmonary venous hypertension (PVH)

This is probably the most frequently encountered group in veterinary medicine. Sustained elevated left atrial pressure with backward pressure into the pulmonary veins eventually leads to a cascade of deleterious vascular changes. The condition is reversible in its early (passive) stages, but local activation of agents such as endothelin and angiotensin, together with hypoxia leads to irreversible (reactive) thickening of the alveolar-capillary membrane which impedes gas transfer. Hypertrophy and thickening of the vessels is characterised by collagen deposition and causes increased pulmonary vascular resistance.

Conditions leading to PVH include dilated cardiomyopathy and mitral valve disease (systolic dysfunction), and hypertrophic and restrictive cardiomyopathies (diastolic dysfunction).

Group III Pulmonary hypertension due to hypoxaemia

This group is also well represented in veterinary medicine with conditions including chronic bronchitis, chronic obstructive airway disease, collapsed trachea, laryngeal paralysis and brachycephalic syndrome. Hypoxia is a powerful vasoconstrictor, which together with vascular proliferative changes and variable fibrosis and inflammation leads to increased vascular resistance.

Age related changes of reduced pulmonary vascular compliance might also be an additive factor.

Group IV Thromboembolic diseases including tumours and foreign bodies.

Hypoxaemia leads to a reflex vasoconstriction, PH, and increased right ventricular afterload. Sometimes the clinical examination may reveal muffled heart sounds due to pleural effusion.

Diagnosis

Symptoms include dyspnoea, exercise intolerance, coughing, murmurs that are commonly from tricuspid and mitral valves, increased pulmonary sounds and crackles, syncope, arrhythmias, increased jugular distension, and ascites.

Diligent cardiac auscultation may detect a loud and `split` second heart sound (S2). This is because the pulmonic valve closure is delayed beyond the aortic valve closure, and requires more energy in the face of increased pulmonary pressure.

pul-1

Fig 1. Right lateral radiograph of an old dog showing significant right side cardiomegaly and pulmonary changes.

Radiographic changes include right-side heart cardiomegaly, and variable pulmonary changes (Figure 1). In the case of PVH there will also be left side enlargement.

Haematology may reveal an elevated haematocrit in response to sustained hypoxia. This increases the risk of developing thrombi in the small pulmonary arteries; due to both increased viscosity and altered endothelial function.

ECG changes are non-specific, expected findings include a right shift in the electrical axis, and tall P waves (P.pulmonale). Arrhythmias may originate from the atria or ventricles.

Echocardiography can often provide concurring evidence with an enlarged right atrium, an enlarged hypertrophied right ventricle with `flattening` of the interventricular septum and possibly paradoxical septal movement. A dilated pulmonary artery may also be visualised.

Doppler flow studies remain the diagnostic method of choice in veterinary patients. Continuous wave Doppler shows documents significant velocity elevations in tricuspid valve regurgitant flows (Figure 2) or in pulmonary valve incompetence flows.

The tricuspid regurgitant flow may be the result of responsive changes to PH that include ventricular hypertrophy, altered geometry of the right ventricle with dilation of the valve annulus, and/or endocardiosis.

pul-2

Fig 2. Continuous wave Doppler of a tricuspid valve regurgitant flow showing a characteristic shape and very high velocity consistent with PH.

There are often multiple contributing factors to the development of PH e.g. an older brachycephalic dog with advanced mitral valve disease that develops chronic bronchitis. Diagnosis requires a high index of suspicion together with a careful appraisal of all clinical and investigative findings.

Treatment

There is no single curative therapy for PH; treatment is aimed at reducing dyspnoea and coughing, improving exercise tolerance, and overall quality of life. Identifying likely causes and targeting these should be the priority; this will involve agents that improve ventilation, reduce volume overloads, assist failing ventricles and decrease PAp.

There is an inexhaustible list of medications used to treat PH in both human and veterinary patients; some of the more available and applicable veterinary ones are listed below.

  • Basic therapy includes rest, oxygen supplementation and warmth.
  • ACE inhibitors are indicated for their vasodilatory actions, and their modifying affects on the deleterious changes to the pulmonary vessels.
  • Spironolactone is an aldosterone antagonist that has been shown to reduce inflammation and fibrosis, together with improved endothelial function.
  • Theophylline, a xanthine derivative, is not only a bronchodilator, but also reduces inflammation and pulmonary fibrosis, and has been shown to increase the response to corticosteroids.
  • Corticosteroids may be especially useful in the hypoxic group (Chronic Bronchitis)
  • Diuretics (frusemide) are useful to reduce the volume overload of right side congestive heart failure, and are also beneficial earlier in the process of PH when there may be non cardiac areas of pulmonary oedema, but care must be exercised not to cause excessive drying and thickening of mucous so hindering its clearance.
  • Aspirin and /or clopidogrel should be considered where thromboemboli formation is suspected or anticipated.
  • Beta-2- agonists such as terbutaline improve pulmonary function, but no long-term benefits have been documented.
  •  Vasodilatory calcium channel blockers such as nifedipine or amlodipine have been used to limited effect in humans.
  • Propentofylline is a non specific PDE inhibiting xanthine derivative with bronchodilatory and anti-inflammatory effects, and reduces blood viscosity.
  • Cough suppressants such as codeine are used are non-productive coughing.
  • Pimobendan often proves beneficial due to several effects including positive inotropic support to a failing myocardium, and also (pulmonary) vasodilatory effects of both PDE3 and probably PDE5 inhibition.
  •  At present the most promising medications available to veterinary practice are the phosphodiesterase (PDE) 5 inhibitors Sildenafil or Tadalafil.

Summary

Clinicians presented with a dog (or cat) that shows e.g. exercise intolerance, coughing, murmurs, dyspnoea and inspiratory crackles – but that only shows a negligible or moderate response to standard congestive heart failure therapy should be aware of the possibility of PH.

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