Transcript Cor pulmonale - The Medical Post | Trusting Medicine

Cor pulmonale
ALOK SINHA
Department of Medicine
Manipal College of Medical Sciences
Pokhara, Nepal
Cor pulmonale is defined as an alteration
in the structure and function of the right
ventricle caused by a primary disorder of
the respiratory system – lung
parenchyma, lung vasculature or thoracic
cage
.
Right sided heart disease secondary to lung disease
Pulmonary hypertension is the common link between
lung dysfunction and the heart in cor pulmonale
Pathophysiology
1.Pulmonary vasoconstriction due to
a.Hypoxia
b.Blood acidemia
2. Obliteration of the pulmonary vascular
bed secondary to lung disorders –
a. emphysema
b. pulmonary thrombo embolism
c. interstitial lung disease
3. increased blood viscosity secondary to
blood disorders
 polycythemia
vera
 sickle cell disease
 macroglobulinemia
4. idiopathic primary pulmonary
hypertension
Pul art pressure – dilatation of R V –
reduced C O & septal displacement-decrease L.V. volume – decresed coronary
blood to R V – further detoriation of R V
function
Septum pushed to left
Reversed Bernmeim’s effect
patient with acute pulmonary hypertension
due to pulmonary embolism
After clot lysis
Acute cor pulmonale
a. massive pulmonary embolism (more
common)
b. acute respiratory distress syndrome (ARDS).
is associated with R V dilatation
Chronic cor pulmonale
 C O P D > 50% of cases
Disorders with primary involvement of
pulmonary vasculature and circulation
Repeated pulmonary emboli
Pulmonary vasculitis
Pulmonary veno-occlusive disease
Sickle cell disease
High altitude disease with pulmonary
vasoconstriction
Primary pulmonary hypertension
Disorders with secondary involvement of
pulmonary vasculature and circulation

Parenchymal lung diseases
Chronic
 interstitial

obstructive pulmonary diseases
lung diseases
Neuromuscular disorders
 myasthenia
gravis
 Poliomyelitis
 amyotrophic lateral sclerosis
Obstructive and central sleep apnea
 Thoracic deformities

 Kyphoscoliosis
 Ankylosing
spondylitis
CLINICAL FEATURES
Clinical manifestations of cor pulmonale
nonspecific
symptoms subtle in early stages of the disease
mistakenly attributed to underlying pulmonary
pathology which are:
Easy fatigability
 Tachypnea
 Exertional dyspnea
 Cough
Followed by
1. Anginal chest pain
 Right
ventricular ischemia (does not respond
to nitrates)

Rt. coronary artery stretching in dilated A-V groove following RVH
2. Hemoptysis
because of rupture of a dilated or
atherosclerotic pulmonary artery
3. A variety of neurologic symptoms may
be seen due to decreased cardiac output
and hypoxemia
 impaired
cognitive & higher mental functions
4. Rarely hoarseness due to compression of
the left recurrent laryngeal nerve by a
dilated pulmonary artery
5. In advanced stages, passive hepatic
congestion secondary to severe right
ventricular failure lead to
 anorexia
 right
upper quadrant abdominal discomfort
 jaundice
6. Syncope with exertion
seen in severe disease
reflects a relative inability to increase
cardiac output during exercise with a
subsequent drop in the systemic arterial
pressure
7. Peripheral edema
Physical findings
may reflect
a. The underlying lung disease
b. pulmonary hypertension
c. RVH
d. RV failure
On inspection
1.An
increase in chest diameter
2.Laboured respiratory efforts with
retractions of chest wall
3.distended neck veins with prominent
“a” or giant “v” waves
4.cyanosis may be seen
 RVH
- characterized by
 Epigastric
pulsation
 left parasternal heave
 Apex beat: in 5th ICS outside MCL diffuse, ill
suatained
 + Hepatojugular reflex and pulsatile liver
are signs of RV failure with systemic
venous congestion
 On
percussion, hyper resonance of the
lungs may be a sign of underlying COPD
 ascites seen in severe disease
On auscultation of the chest
wheezes & crackles: signs of underlying lung
disease
in early stages
1. Splitting of the S2
2. Loud P2
in advanced disease
1. sharp ejection click (single or multiple)
over the pulmonary artery
2. Followed by ejection systolic murmur
3. Latter on: diastolic pulmonary
regurgitation murmur (Graham steel)
4. may be S3 &/or S4
5. systolic murmur of tricuspid
regurgitation
DIFFERENTIAL DIAGNOSIS
Congestive (biventricular) heart failure
Primary pulmonic stenosis
Primary pulmonary hypertension
Right-sided heart failure due to congenital heart
diseases
Right heart failure due to right ventricular
infarction
INVESTIGATIONS
Routine investigation:

Hematocrit
> 50 polycythemia
 > 60 – indication for phlebotomy

To confirm diagnosis
ECG
 X ray chest
 Echocardiography
 Right heart catheterization

E C G in Cor pulomale
Electrocardiography (ECG)
RVH or RV strain
a. right axis deviation
b. R/S amplitude ratio in V1 greater than 1
R/S amplitude ratio in V6 less than 1
c. P-pulmonale -increase in P wave
amplitude in leads 2, 3, and aVF
d. incomplete or complete right bundle
branch block (RBB), especially if
pulmonary embolism is the underlying
etiology
e. low-voltage QRS because of
underlying COPD with hyperinflation and
increased AP diameter of the chest.
Chest roentgenography
enlargement of the central pulmonary arteries
with oligemic peripheral lung fields- per. pruning
 right descending pulmonary artery > 16 mm
 left pulmonary artery >18 mm in diameter
RVH

Elevated brain natriuretic peptide (BNP) level
Earliest evidence of CCF
a natural mechanism to compensate for elevated pulmonary hypertension
and right heart failure by
a. promoting diuresis and natriuresis,
b. vasodilating systemic and pulmonary vessels
Arterial blood gas tests
provide important information about the level of
oxygenation and type of acid-base disorder
To know the etiology
P F T to confirm underlying lung
disease
To exclude pulmonary thromboembolism
Ventilation/perfusion (V/Q) scan or CT chest
Hypercoagulability states evaluated by levels of
 proteins
C and S
 antithrombin III
 factor V Leiden
antinuclear antibody (ANA) level for collagen
vascular disease such as scleroderma
 serum alpha1-antitrypsin

Oxygen therapy
Diuretics
Vasodilators
Digitalis
Anticoagulation therapy
are all different modalities used in the long-term
management of
Chronic cor
pulmonale
long-term oxygen therapy can be
considered even if
PaO2 is greater than 55 mm Hg or
O2 saturation is greater than 88%.
( because of vasodilator effect on pulmonary
arteries)
DIURETICS
Right ventricular filling volume markedly elevated
Diuretics may result in improvement of function of
both the right and left ventricles
adverse effects.
a. Excessive volume depletion can lead to a
decline in cardiac output
b. hypokalemic metabolic alkalosis lead to
cardiac arrhythmia
Diuretics needs to be used with caution
Vasodilator drugs
In long-term management of chronic cor pulmonale
have modest results
1.Calcium channel blockers
 oral
sustained-release nifedipine
 diltiazem
2.beta blockers
3.Nitrates
4.angiotensin-converting enzyme (ACE) inhibitors
 not routinely used. A trial of vasodilator therapy
considered in patients with COPD with
disproportionately high pulmonary blood pressure –
more than 40 mm Hg
NEWER VASODILATORS
endothelin receptor antagonist
(Bosentan)
prostacyclin PGI 2 analogues
Epoprostenol -i.v.
iloprost - M D I
THEY HAVE SHOWN A PROMISING EFFECT IN
REDUCING THE PULMONARY HYPERTENSION
CARDIAC GLYCOSIDES
NOT ROUTINELY INDICATED
Beneficial effect not as obvious as in LVF
 modest effect of digitalis on failing right ventricle in chronic
cor pulmonale
Must be used cautiously
should not be used during the acute phases of
respiratory insufficiency
Patients with hypoxemia or acidosis are at
increased risk of developing arrhythmias
Theophylline

bronchodilatory effect

reduce pulmonary vascular resistance and
pulmonary arterial pressures

weak inotropic effect and thus may improve
right and left ventricular ejection

Strenghtens diaphragm

Stimulates the respiratory centre
Phlebotomy
 Mean
Pul art press and PVR decrease in
polycythemic patients after phlebotomy
(hematocrit of >60 or 65)
 The
reduction of markedly elevated hematocrit
level to about 50% by phlebotomy leads to
1. Reduction of blood viscosity
2. Reduction in PVR and pulmonary art pr
3. Improve gas exchange & increases exercise
tolerance