COR PULMONALE
SUBMITTED BY
Anmol Prashar
Bsc.Nursing 4th year
(Intern)
Roll no 6

CONTENTS
 Definition
 Subtypes of Cor Pulmonale
 Mortality Associated with Cor Pulmonale
 Etiology
 Clinical Presentation
 Pathophysiology
 Diagnosis & Diagnostic Tests

Medical Management
Nursing Management
Complications
Health Education
References

DEFINITION
 Cor pulmonale is a latin word means "pulmonary heart“
 The world Health Organizaton in 1963 adopted this definition of
cor pulmonale :" hypertrophy of the right ventricle resulting from
diseases affecting the function and/or structure of the lungs,
except when these pulmonary alterations are the result of
diseases that primarily affect the left side of the heart , as
congenital heart diseases.”

 Cor pulmonale is a disease of the right ventricle characterized
by hypertrophy and dilation that results from diseases directly
affecting the lung parenchyma or lung vasculature. Of
note ,right heart failure need not be present in cor pulmonale

SUBTYPES OF COR PULMONALE
 Cor pulmonale can be either acute or chronic in development.
 Acute cor pulmonale is the result of a sudden increase in right
ventricular pressure, as seen in massive pulmonary embolism or
acute respiratory distress syndrome.
 Chronic cor pulmonale can be further characterized by hypoxic or
vascular obliterans pathophysiology.
 The most common disease process associated with hypoxic subtype
is chronic obstructive pulmonary disease (COPD).The most common
process associated with obliterans subtype is pulmonary
thromboembolic disease.

The Mortality Associated with Cor Pulmonale
 Patients with COPD have a 5-year survival rate, whereas patients with
COPD and pulmonary artery pressure in excessof 25 mmHg have a
survival of only 36%.
 The 5-year survival rate for patients with COPD who develop
preipheral edema is approximately 30%.
 It is unclear whether pulmonary artery hypertension is the cause of
death or whether it is a marker of increased motality.

ETIOLOGY
 Conditions that restrict or compromise ventilatory function,
leading to hypoxemia or acidosis e.g. deformities of the
thoracic cage, massive obesity.
 Conditions that reduce the pulmonary vascular bed e.g.
primary idiopathic pulmonary arterial hypertension,
pulmonary embolus.
 Disorders involving nervous system, respiratory muscles,
chest wall , and pulmonary arterial tree may also be
responsible for cor pulmonale.

CLINICAL PRESENTATION
 Dyspnea. the most common symptom: usually the result of the
increased work of breathing secondary to changes in elastic
recoil of the lung (fibrosing lung diseases) or altered
respiratory mechanics
 Orthopnea and nocturnal dyspnea are rare symptoms of right
HF, reflect the increased work of breathing in the supine
position that results from compromised excursion of the
diaphragm.
 Tussive or effort-related syncopebecause of the inability of the
RV to deliver blood adequately to the left side of the heart

 Abdominal pain and ascites
 Lower extremity edema
 Shortness of breathwheezing
 Tachypnea
 Elevated jugular venous pressures
 Hepatomegaly
 Lower-extremity edema.
 Cyanosis is a late finding

 Chronic wet cough
 Chest discomfort
 Distention of neck veins

PATHOPHYSIOLOGY

PATHOPHYSIOLOGY
 Hypoxic pulmonary vasoconstriction and arterial occlusion
are the major causes of pulmonary hypertension.
 Both produce reduced blood flow with increased vascular
resistance.
 Acute hypoxic pulmonary vaso —constriction optimizes
ventilation — perfusion relationships when regional
ventilation demands in the lung are not met.

 However, chronic hypoxemia leading to chronic
vasoconstriction produces smooth ms proliferation in small
pulmonary arteries.
 Decreased luminal cross sectional diameter leads to
increased resistance and increased pulmonary artery
pressure.
 These architectural changes in pulmonary arteries may
promote platelet aggregation and activation.
 This leads to thrombi formation that further increases
pulmonary vascular resistance and pulmonary hypertension.

 Hypoxemia produces changes in vascular mediators such as Nitric
Oxide, Endothelinl (ET 1) and platelet derived growth factors (PDGf A
and B).
 Nitric oxide is a vasodilator; hypoxemia reduces endothelial cell
production of nitric oxide and results in impaired smooth ms relaxation.
 Hypoxemia increases ETI production and PDGF A and B
 ETI is apotent vasoconstrictor, and PDGF A and B results in
pulmonary vascular remodeling.
 All causes increased pulmonary artery resistance and causes
pulmonary hypertension.

DIAGNOSIS
 History Collection
 Physical Examination-increase in chest diameter, distended neck veins
and cyanosis may be seen.
 On auscultation of the lungs, wheeæs ard crackes may be heard
 On percussion, hyper-resonance of the lungs may a sign of underlying
COPD.
 Pulmonary function tests
 ABG analysis- Reveals decreased Pa02 & pH and Increased
 Hematocrit: It is done to rule out polycythemia.

DIAGNOSTIC TESTS
Electrocardiography criteria of right ventricular hypertrophy
 Right axis deviation.
 P Pulmonale (large P wave ) in the inferior and anterior leads " right
atrial enlargement
 Right bundle branch block.
 Right precordial T-wave inversions.
 Delayed interinsicoid deflection of right precordial leads.

 QR pattern in lead VI or V3R.
 An R wave in VI or V3R.
 An R/S ratio > 1 in VI or <1 in or /6.

Chest Radiograph:
 Enlarged pulmonary artery.
 Enlarged right ventricle.
 Distended azygous or other central vein.
 Westermark sign "oligemia of lung lobe or entire lung
 Hampton's hump "wedge shaped opacity
 COPD signs as anterior-posterior diameter , flattening of
diaphragm , honeycombing and hyperlucency.

sensitivity of 84 % and specificity of 75% for the diagnosis of pulmonary
hypertension.
 There are data to suggest that an enlarged main pulmonary artery
diameter and ratio of segmental pulmonary artery diameter to
corresponding bronchus diameter > 1 increases the specificity of a
pulmonary hypertension diagnosis.

 An adequate examination is reported in up to 65 — 80 % of patients with
COPD because of the technical difficulty associated with hyperinflation.
 A better examination can be obtained with transesophageal
echocardiography.
 Doppler echocardiography has aided in the assessment of pulmonary
artery pressure by measuring the flow of regurgitant blood across the
tricuspid valave or by measuring right vetricular ejection flow.

Right heart catheterization:
 This is the gold standard for thorough evaluation and diagnosis of
pulmonary hypertension.
Radionuclide angiography (gated blood pool scan):
 This test is most useful for measuring right and left ventricular
ejection fraction.
Magnetic resonance imaging:
 This non invasive technique yields highly accurate dimensions of the
right ventricle.

MEDICAL MANAGEMENT
Non pharmacological treatment:
 Oxygen therapy
 Phlebotomy
 Non invasive positive pressure ventilation (NIPPV)
Pharmacological treatment:
 Diuretics
 Anticoagulation
 Vasodilators

 This is considered a mainstay of treatment for patients with COPD.
 Large controlled trials demonstrate that long term administration of
oxygen improves survival in hypoxemic patients with COPD.
 Oxygen therapy decreases pulmonary vascular resistance by diminishing
pulmonary vasoconstriction and improves right ventricular stroke volume
and cardiac output

Phlebotomy
 In patient with pronounced polycythemia (hematocrit
>60 %), phlebotomy may provide symptomatic relief
 In resting patients , phlebotomy can affect a mild
decrease in pulmonary artery pressure and pulmonary
vascular resistance.
 In general , blood viscosity has less effect than blood
volume on pulmonary arterial pressure.
 Phlebotomy , with a goal hematocrit of 50 %, may
improve exercise tolerance in patients with polycythemic
COPD.

PHARMACOLOGIC
Diuretics
 Diuretic therapy with salt restricted diet may be needed in congestive
heart failure to take care of the excessive water that the lungs share
and to improve alveolar ventilation and gas exchange.
 However, the use of diuretics may produce hemodynamic adverse
effects, such as volume depletion, decrease venous return to the right
ventricle, and decreased cardiac output.
 Another complication is the production of hypokalemic metabolic
alkalosis, which diminishes the c02 stimulus to the respiratory center,
decreasing ventilatory drive.

Anticoagulation
 Chronic anticoagulation with Warfarin may provide benefit for those
patients with Cor Pulmonale resulting from thromboocclusive
pulmonary disease.
Vasodilators
 Vasodilators improve cardiac output in many patients with cor
pulmonale.
 However, treatment with vasodilators may be associated with
adverse effects, including systemic hypotension that coronary
perfusion pressure, blunting of hypoxic pulmonary vasoconstriction
and circulatory collapse.

Different classes of vasodilators used in Cor Pulmonale
Nonspecific vasodilators:
 Hydralazine increases cardiac output in patients with COPD; however,
its ability to decrease pulmonary artery pressure is unpredictable.
 Nitroprusside may provide benefit but also runs the risk of systemic
hypotension and compromise of adequate coronary perfusion pressure.
 Calcium channel blockers such as Nifedipine reduce pulmonary vascular
resistance and increase cardiac output only for the short term.
 Verapamil and Diltiazem have not proved effective in dilating pulmonary
vasculature.

 Prostaglandins decrease pulmonary artery pressure and increase right
ventricular ejection fraction and cardiac output.
 Aerosolized prostacyclin causes pulmonary artery vasodilatation and
improves cardiac output and arterial oxyhemoglobin saturation in
patients with chronic pulmonary hypertension.
 3. Nitric oxide provides a real clinical scenario. It reliably decreases
pulmonary vascular resistance without causing systemic hypotension
and preserves or improves optimal ventilation-perfusion match. Its
drawbacks are difficult administration, high cost, and a welldocumented
tachyphylactic effect. Multiple studies have shown that its benefits are
most significant for only 1-3 days, especially in patients with acute
respiratory distress syndrome.

Inotropes with vasodilatory properties:
 Dobutamine is an inotropic agent with vasodilatory effect which
improves right ventricular function and cardiac output, but its effect
on systemic blood pressure is unpredictable.
 Amrinone lowers pulmonary artery pressure and rises cardiac output
and systemic blood pressure.
Endothelin receptor antagonist:
 Bosentan is an endothelin receptor antagonist that produces
pulmonary vasodilation and attenuates ventricular remodeling and
improve survival on chronic use.

Role of digoxin in treatment
 Cardiac output improves in about 10% of patients with primary
pulmonary hypertension who receive digoxin.
 This rate is similar to that in patient with left ventricular dyfunction.
 Patients who receive digoxin also show a modest increase in
pulmonary pressure, perhaps due to increase in cardiac output.
 Clinical studies show improvement in right ventricular function only in
those patients who have reduced left ventricular ejection fraction.
 Recently, digoxin has fallen out of favor in the setting of left ventricular
dysfunction; the trend in clinical medicine has been its continued use
in rate control.

NURSING MANAGEMENT

Assessment
 Determineif the patient has experienced orthopnea, cough, Eytigue, epigastric
distress, anorexia, or weight gain Or has a history of previously diagnosed lung
disorders.
 Ask if the patient smokes cigarettes, noting the daily consumption and duration.Ask
about the Color and quantity of the mucus the patient expectorates.
 Determine the type Of dyspnea if it is related only to exertion oris continuous.
 Observe if the patient has difficulty in maintaining breath while the history is taken.
 Evaluate the rate, type, and quality of respirations.
 Observe the patientfor dependent edema fromthe abdomen (ascites) and
buttocksanddown both legs.
 Inspect the patient's chest and thorax forthe general appearance and
arteroposterior diameter.Look for theuse of accessory musdes in breathing.

NURSING MANAGEMENT
Nursing Diagnosis
 Impaired tissue perfusion related to decreased cardiac contractility and
expiratory airflow obstruction as evidenced by increased capillary refilling
time >3 seconds
 Activity intolerance related to decreased cardiac activity and laboured
respirations as evidenced by difficulty in performing activities of daily
living.

respirations as evidenced by difficulty in performing activities of daily
living
 Anxiety related to breathlessness as evidenced by patient's
verbalization and facial expressions
 Imbalanced nutrition less than body requirement related to
breathlessness as evidenced by weight loss.
 Disturbed sleep pattern related to shortness of breath as evidenced
by presence of dark circles around the eyes.

COMPLICATIONS
 Exertional syncope.
 Hypoxia and significantly limited exercise tolerance.
 Peripheral edema.
 Peripheral venous insufficiency.
 Tricuspid regurgitat ion.
 Hepatic congestion and cardiac cirrhosis.
 Death.

HEALTH EDUCATION
 Advice patient to take protein rich diet.
 Educate patient regarding his disease condition.
 Educate patient regarding modification in lifestyle like cessation of
smoking & alcohol consunWion.Advice patient to reduce spicy &
fatty foods.
 Instruct patient to avoid caffeine intake which can increase pulse
rate & produce angina.
 Educate patient to minimize level of activities to prevent strain.
 Advice patient for regular followup & care.

REFERENCES
 Page 26-30, 92 -154 Oxford handbook of clinical medicine 10th
Edition
 Fishman AP. Chronic cor pulmonale. American Review of
Respiratory Disease. 1976 Oct;114(4):775-94.
 Jardin F, Dubourg O, Bourdarias JP. Echocardiographic pattern of
acute cor pulmonale. Chest. 1997 Jan 1;111(1):209-17.
 Weitzenblum E. Chronic cor pulmonale. Heart. 2003 Feb
1;89(2):225-30.