Pulmonary Hypertension

Pulmonary hypertension (PHT) is characterized by high pulmonary artery

pressure (PAP) that leads to impaired right ventricular performance and right-sided
failure.

Hypertension in horses is defined as an increase in systolic blood pressure in the

pulmonary artery greater than 40 mm Hg and an increase in mean blood pressure
(pulmonary artery) over 35 mm Hg

Cor pulmonale is characterized by right ventricular enlargement secondary to

PHT due to pulmonary parenchymal or vascular disease, in the absence of left
ventricular failure, a congenital malformation (e.g. VSD) or an aquired valvular
disorder.

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Normal Pressure mmHg Systolic Diastolic Mean

Right Atrium – – 5 – 10

Right Ventricle 40 – 60 10 – 14 (end diastoli) 19 – 25

Pulmonary artery 32 – 38 15 – 22 25 – 30

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 Classification of Pulmonary Hypertension
(PHT)
1. Pulmonary arterial hypertension: idiopathic, drug, toxin

2. PHT caused by left-sided heart diseases: congenital and acquired heart

disease

3. PHT caused by lung disease and/or hypoxia

4. Chronic thromboembolic PHT

5. PHT with unclear multifactorial mechanisms (hematologic, systemic,

metabolic and other disorders) 6
 1. Pulmonary arterial hypertension
1. Pulmonary venous hypertension

2. Pulmonary overcirculation (volume overload)

3. Increased pulmonary vascular resistance

Pulmonary idiopathic arterial hypertension is a diagnosis of exclusion and has

not been characterized in the horse.

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 2. PHT caused by left-sided heart diseases
Causes are:

- Severe mitral valve regurgitation

- Aortic regurgitation
- Left ventricular dysfunction ↑ LA or LV end diastolic pressure
- Cardiomyopathy
- Constrictive pericarditis
- Left atrial masses
- Congenital cardiac disease:
Left to right shunts: PDA, VSD, ASD
↑ Pulmonary venous hypertension

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 3. PHT caused by lung disease and/or hypoxia
• Hipoxia – induced vasoconstriction
• Loss of vascular surface area from lung distruction
• Loss of vascular compliance from hyperinflation-induced vascular compression
• Vascular remodeling caused by chronic hypoxic vasoconstriction

Recurrent airway obstruction is the most commonly recognized pulmonary disease

leading to pulmonary hypertension and cor pulmonale in the horse.

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 Persistent Pulmonary Hypertension of the
newborn
Causes: imbalance of endothelin – 1 (vasoconstrictor) and nitric oxid (vasodilator)

↑ PAP

Presence of shunting of blood from right to left through the foramen ovale and
ducturs arteriosus

Hypoperfusion of the lung and severe hypoxemia 11

 4. Chronic thromboembolic PHT
Pulmonary hypertension secondary to pulmonary thromboembolization
can be considered in horses that are predisposed to thrombus formation by:
1. Hipercoagulability state
2. Circulatory stasis
3. Endothelial injury.

Acute or peracute onset of respiratory distress is the usual presenting

sign and horses with severe involvement may have completely circulatory
failure.

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 Clinical Signs
The clinical diagnosis is difficult to establish due to the non-specific
clinical signs, dominated by the symptoms of the primary disease.

1. Accentuated or split second heart sound

2. Murmurs holosystolic of tricuspid valve
3. Jugular vein distension
4. Peripheral edema
5. Generalized venous distension develop once right-sided heart failure
develop.
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 Echocardiography
Two-dimensional echocardiography allows the evaluation of:
- the size of the right atrium
- right ventricular size
- pulmonary artery dilation
- tricuspid valve morphology
- size and functionality of the left ventricle

In PAH are observed: dilation of the pulmonary artery, right atrium and
ventricle and flattening of the interventricular septum
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In PAH are observed:
1. Dilation of the pulmonary artery,
2. Dilation of right atrium and ventricle, and
3. Flattening of the interventricular septum, paradoxic septal motion
4. Decreased size of the left ventricle

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• Color Doppler echocardiography allows visualization of regurgitations in
the tricuspid valve or pulmonary artery valve.

• Pulsed Doppler echocardiography allows the calculation of velocity and

pressures in the tricuspid valve or pulmonary artery.

• In the case of the latter two methods, the parallel alignment of the Doppler
beam interrogation with the blood jet is required.

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 Treatment
The goals of therapy are:
- treatment of the underlying disease
- correction of hypoxemia
- treatment of acidosis

Nitric Oxide
Phosphodisterase Inhibitors: PDE – 5 Inhibitor (Sildenafil)

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