Pulmonary Hypertension: 1. Identify Pulmonary Hypertension 2. Apply Required Collaborative and Nursing Care Plan

PULMONARY HYPERTENSION
LEARNING OBJECTIVES:
1. IDENTIFY PULMONARY HYPERTENSION
2. APPLY REQUIRED COLLABORATIVE AND NURSING
CARE PLAN
PULMONARY HYPERTENSION
 Chronically elevated mean PAP over 25mm Hg, at rest
 Primary or idiopathic pulmonary hypertension has no known cause.
 Its most common in women between ages 20 and 40 and is usually

fatal within 3 – 4 years .
 Mortality is highest in pregnant women

Pathophysiology
In Primary Pulmonary Hypertension (PH)
-the intimal lining of the pulmonary arteries
thickens, narrowing the lumen of the artery,
impairing distensibility, and increasing vascular
resistance
Alveolar hypoventilation can result from
disease causing alveolar destruction or diseases that
prevent the chest wall from expanding sufficiently
to allow air in to the alveoli. The resulting decreased
ventilation increases pulmonary vascular resistance
Hypoxemia resulting from the V/Q mismatch causes

vaso constriction, further increasing vascular
resistance and resulting in pulmonary hypertension
 Secondary Pulmonary hypertension results from existing cardiac or pulmonary
disease, or both
 Cardiac causes include;

 Left sided heart failure
 Ventricular septal defect
 Patent ductus arteriosus
 Pulmonary causes include:

 COPD and
 Vasoconstriction of the arterial
bed due to hypoxemia and acidosis
 If patient with PH does not receive
treatment, here's is what happens
 Hypertrophy occurs of smooth muscle

layer of arterioles worsening non
distensibility
 Increased pressure in the lungs is

transmitted to the right ventricles
(which supplies the pulmonary artery)
 The ventricles become hypertrophic

and eventually fails (corpulmonale)
 Impaired distensibility due to

hypertrophy can cause arrhythmias
Signs Look for signs of PH including:
 Patient with PH typically  Tachycardia

report  Tachycardia with mild exertion
 Increasing dyspnea on  Decreased BP
exertion  Changes in mental status from
 Weakness restlessness to agitation or confusion
 Syncope and fatigue  Signs of right sided Heart failure such as;
ascites and jugular vein distension
WHO Classification: Functional Status Of Patients With Pulmonary Hypertension
Classification Functional status of patient

of PH
1 Patient with PH but without resulting limitation of physical activity
Ordinary physical activity does not cause undue dyspnea or fatigue, chest pain or
near death syncope
2 Patient with PH resulting in slight limitation of physical activity
They are comfortable at rest
Ordinary physical activity causes undue dyspnea or fatigue, chest pain or near
syncope
3 Patient with PH resulting in marked limitation of physical activity
They are comfortable at rest. Less than ordinary activity causes undue dyspnea or
fatigue, chest pain or near syncope
4 Patient with PH with inability to carry out any physical activity without symptoms.
These patients manifest signs of right sided heart failure. Dyspnea and/ or fatigue
may even be present at rest. Discomfort is increased by any physical activity
 Tests
 ABG analysis reveals hypoxemia (PaO2 less than 80 mm Hg )

 ECG changes commensurate with Right Ventricular Hypertrophy (RVH),
include right axis deviation and tall or peaked P waves in inferior leads
 An easily palpable ventricular lift and a reduced carotid pulse
 PA catheterization reveals increased mean PAP above 25 mm Hg
 Pulmonary function studies may show decreased flow rates and increased
residual volume in underlying obstructive disease.
Collaborative care:
Treatment measures include;
 Oxygen therapy to correct hypoxemia
 Fluid restriction to decrease preload & minimize workload of right
ventricle
 Exercise training to improve peak oxygen consumption
 In severe cases with irreversible changes, heart –lung transplantation
maybe necessary
Diverse Drugs
 Inotropic drug such as Digoxin to increase cardiac output
 Diuretics to decrease intravascular volume and venous return
 Calcium channel blockers to reduce myocardial workload & oxygen
consumption
 Prostanoids, such as: epoprostenol (Flolan), Treprostinil (Remodulin), or
Iloprost ( Ventavis) to improve haemodynamic status and functional
capacity
 Phosphodiesterase type 5 inhibitors such as Sildenafil (Viagra Revatio),
Tadalafil (Cialis, Adcirca)to improve pulmonary dynamics and exercise
capacities
 Bronchodilators to relax smooth muscles and increase airway patency
 Anticoagulant therapy to reduce the risk for intrapulmonary thrombosis
and thromboembolism
Nursing management in general
 Assess cardiopulmonary status, auscultate heart and breath sounds
 Assess haemodynamic status including PAP & PAWP every 2hours or more often
depending on patients condition and report it
 Monitor intake and output closely and obtain daily weights. Institute fluid
restriction as ordered
 Administer medication as ordered to promote adequate heart and lung
function. Assess for potential adverse reactions, such as postural hypotension
with diuretics
 Administer supplemental oxygen as ordered and organize care to allow rest
periods

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PULMONARY HYPERTENSION

 Chronically elevated mean PAP over 25mm Hg, at rest

 Primary or idiopathic pulmonary hypertension has no known cause.

 Its most common in women between ages 20 and 40 and is usually

 Mortality is highest in pregnant women

Hypoxemia resulting from the V/Q mismatch causes

 Cardiac causes include;

 Pulmonary causes include:

 Hypertrophy occurs of smooth muscle

 Increased pressure in the lungs is

 The ventricles become hypertrophic

 Impaired distensibility due to

 Patient with PH typically  Tachycardia

Classification Functional status of patient

 ABG analysis reveals hypoxemia (PaO2 less than 80 mm Hg )

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