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Cor Pulmonale Chronicum

dr. Jesly Charlies


CPC - Definition

 pulmonary heart disease


 altered RV structure (i.e., dilation with or without
hypertrophy) and/or function in the context of chronic
lung disease and is triggered by the onset of pulmonary
hypertension
 develops in response to chronic changes in the pulmonary
vasculature and/or the lung parenchyma that are
sufficient to cause pulmonary hypertension
CPC - Etiology
CPC – Pathophysiology

Parenchymal
lung diseases,
primary Circulatory bed  Pulmonary
pulmonary vascular artery pressures
vascular remodeling, and RV afterload
disorders, or vasoconstriction, increase  Cor
chronic and destruction Pulmonale
(alveolar)
hypoxia
ACUTE COR PULMONALE
• occurs after a sudden and severe stimulus
(e.g., massive pulmonary embolus), with RV
dilatation and failure but no RV hypertrophy

CHRONIC COR PULMONALE


• more slowly evolving and progressive
pulmonary hypertension that leads to initial
modest RV hypertrophy and subsequent RV
dilation.
 Acute decompensation of previously compensated chronic
cor pulmonale, can trigger by:
 Worsening hypoxia from any cause (e.g., pneumonia)
 Acidemia (e.g., exacerbation of COPD)
 Acute pulmonary embolus
 Atrial tachyarrhythmia
 Hypervolemia
 Mechanical ventilation that leads to compressive forces on
alveolar blood vessels.
CPC – Pathophysiology of cor pulmonale
in COPD

Abbreviations: NO, nitric oxide; ET-1, endothelin-1; PVR, pulmonary vascular resistance; PH, pulmonary hypertension.
CPC - Symptoms

 Fatigue
 Exertional dyspnea
 Cough
 Anginal chest pain (due to right ventricular ischemia or pulmonary artery
stretching, typically do not respond to nitrates)
 A variety of neurologic symptoms may be seen due to decreased cardiac
output and hypoxemia.
 Hemoptysis (due to rupture of a dilated or atherosclerotic pulmonary
arteriole)  tumors, bronchiectasis, and pulmonary infarction, should be
excluded
 Hoarseness (rare, due to compression of the left recurrent laryngeal nerve by
a dilated pulmonary artery)
 In advanced stages, passive hepatic congestion secondary to severe right
ventricular failure may lead to anorexia, right upper quadrant abdominal
discomfort, and jaundice.
 Syncope with exertion (seen in severe disease)
 Elevated pulmonary artery pressure can lead to elevated right atrial,
peripheral venous, and capillary pressure.
 peripheral edema
 by increasing the hydrostatic gradient
 decrease in glomerular filtration rate (GFR) and filtration of sodium as well as
stimulation of arginine vasopressin (which decreases free water excretion) by
hypoxemia
CPC - Signs

 tachypnea
 elevated jugular venous pressures
 hepatomegaly
 lower-extremity edema
 tricuspid regurgitation (prominent v waves in the jugular venous pulse)
 RV heave palpable along the left sternal border or in the epigastrium.
 the increase in intensity of the holosystolic murmur of tricuspid regurgitation
with inspiration (“Carvallo’s sign”) may be lost eventually as RV failure
worsens.
 cyanosis is a late finding
CPC – Signs and Symptoms
CPC - Diagnosis

 ECG
 Right axis deviation
 RV hypertrophy (R/S amplitude ratio in V1 > 1, R/S amplitude ratio in V6 < 1)
 P-pulmonale pattern (an increase in P wave amplitude in leads 2, 3, and aVF)
 Low-voltage QRS because of underlying COPD with hyperinflation

 Chest X Ray
 enlargement of the main central pulmonary arteries and hilar vessels

 Spirometry
 Shows obstructive and/or restritive defects

 Arterial blood gases


 Hypoxemia and/or hypercapnia
CPC - Diagnosis

 Spiral CT scans of he chest


 Identify acute thromboembolic disease or intestitial lung disease
 2D echocardiography
 measuring RV thickness and chamber dimensions
 Doppler echocardiography
 assess pulmonary artery pressures
 MRI
 assessing RV structure and function, particularly in patients who are difficult to
image with 2-D echocardiography because of severe lung disease
CPC - Management

 General principles:
 Treatment of the underlying pulmonary disease
 Improving oxygenation and right ventricular (RV) function by
increasing RV contractility and decreasing pulmonary
vasoconstriction.
CPC - Management

 Oxygen therapy
 Administered on a continuous basis
 Relieves hypoxemic pulmonary vasoconstriction, which then
improves cardiac output, lessens sympathetic vasoconstriction,
alleviates tissue hypoxemia, and improves renal perfusion
 recommended when the PaO2 is <55 mmHg or the SaO2 <88%
 Diuretics
 decrease the elevated right ventricular (RV) filling volume, and in
the management of associated peripheral edema.
 Vasodilators
 Calcium channel blockers, particularly oral sustained-release
nifedipine and diltiazem, can lower pulmonary pressures
 Beta – selective agonist drugs (i.e. Theophylline)
 as bronchodilator and mucociliary clearance effect
 reduce pulmonary vascular resistance and pulmonary arterial
pressures acutely in patients with CPC secondary to COPD.
 Anticoagulation (i.e. Warfarin)  high risk for thromboembolic event
or PAH
 Digitalis  give if there is an altered of left ventricle function.