cor pulmonale.pptx

Salale University College of Health Sciences
Department of Adult Health Nursing MSc Program
Group Seminar Presentation on:
Cor Pulmonale
Present to Mr Melese
October, 2023
Fitche, Oromia, Ethiopia
11/4/2023 Cor Pulmonale 1

Group Name
1. Mesfin Assefa............................................186/15
2. Merga Wakweya........................................184/15
3. Mulnesh Mosisa........................................187/15
4. Nugussie Wendimu...................................188/15

Presentation Outline
Case scenario .
Definition
Epidemiology
Causes
Pathophysiology
Clinical features
Diagnosis and Management of Cor Pulmonale
Summary
Cor Pulmonale 3

OBJECTIVES
Review the anatomy and physiology of the respiratory system and
cardiovascular system
Interpret the term cor pulmonale
Describe the etiologic of cor pulmonale
Discuss the pathogenesis involved in the disease process and C/M
Differentiate the various diagnostic measures
Explain the medical management

Patients biographic data
• Patient Name: Damo Dame Hordofa Age : 52 Sex ; F
• MRN; 318077
• Date of admission: 02/02/2016
• Referral Source: Self
• Data Source: Patient

Chief Complaint:
 SOB
 Bilateral Pitting Edema
 palpitation

History of Present Illness
This is 52yrs old female patient admitted in female medical ward
presented with hx of bilateral pitting edema of 05 days duration and
the swelling is started from the feet which is gradually increased to
the knee joint. And associated to this she has hx of shortness of
breathing and chest pain which is aggravated by lying sleeping and
relieved by using extra pillow.
She has hx of cough, weakness, palpitation and loss of appetite
She has no hx of abdominal swelling, vomiting and syncope.

Past medical history
• She has no hx of: DM ,HTN ,Asthma ,Malaria and jaundice, Blood
transfusion
• She has no hx previous admission to the hospital.
• She has no past surgical history.
• She has hx of took anti TB the 15 yrs ago
• She has no hx past allergies to drug and other food.
Family history:
• She has no hx of DM, HTN and asthma.

Physical examination
General appearance :
• acute sick looking.
• V/S: BP- 85/54, PR-98 , RR-24 , -SPO2, 52% off 02
HEENT:
• No scar over the head
• Pink of conjunctiva
• No jaundice and no redness of the eye.
• No ear discharge, no accumulation of wax
• No nasal discharge , obstruction and polyp
• Dry and cyanosis of buccal mucosa
• No lip cyanosis and throat sore
• No neck swelling .no goiter and JVD

Physical examination....
Integumentary system
• No scar ,rash, nodules, skin cyanosis.
• There is Bilateral pitting edema over the feet.
LGS
• No enlarged lymph node

Respiratory System
Symmetric chest shape, no scar and deformity
No tenderness over the chest.
Resonant sound on percussion
Wheezing and crackles on ant. And pos. Chest

Cardio Vesicular System
 No distended neck veins
 S1 and S2 is well heard no gallop but there is systolic murmur over right side 3rd inter costal space
 GIS
 No scar, no distention,
 28/min abdominal sound
 No tenderness, no mass, no enlargement of organ
 Tympanitic sound

GUS
No costo vertebilal angle tenderness
MSS
Grade II bilateral pitting edema
No deformity, no fracture, no restriction
All range of motion is normal

CNS
 Oriented to PPT
Glasgow coma Scale 15/15

Assessment: Cor Pulmonale
Plan: CBC, CXR, ECG, ECO, RFT
Treatment:
Lasix 40mg IV BID
Ceftriaxone 1gm IV BID
Spironolactone 25mg po daily
Put on INO2

Investigation
CBC:
 WBC: 19.95X103
/uL
 Neu%: 88.1 %
 Hgb: 17g/dl
 PLT: 271X 103
/uL
Chemistry
 BUN: 34.2 mg/dl
 Creatine: 1.37mg/dl
CXR
• Pulmonary fibrosis
• Rt lung volume loss (? Rt upper lobe
Atelectasis)
ECG
 Sinus tachy cardiac with PVC
 Possible bilateral enlargement
 Marked right ventricular hyphertrophy
Echo report
RV Systolic dysfunction with moderate
Pulmonary Hypertension?

Nursing Diagnosis:
1. Decreased Cardiac Output related to restricted cardiac muscle
contractility as evidenced by, ECG showing right ventricular
hypertrophy, and fatigue
2. Impaired Gas Exchange related to expiratory air flow obstruction as
evidenced by decreased oxygen saturation level (63%).
3. Excess fluid volume related to sodium retention as evidenced by
pitting edema.
4. Activity intolerance related to imbalance between oxygen supply
and demand as evidenced by shortness of breath.

Expected Outcome
1. W/r Damo will be able to maintain adequate cardiac output
2. W/r Damo will have improved oxygenation and will not show any
signs of respiratory distress.
3. W/r Damo will be free from edema
4. W/r Damo will demonstration active participation in necessary and
desired activities and demonstrate increase in activity levels.

Planning
 To administer oxygen
 To administer ordered medication
 To facilitate positioning of the patient by elevate bed
 To monitor vital sign closely.
 To monitor input & out put
 To measure daily weight
 To educate patient on salt free diet

Nursing Intervention
 We administer oxygen
 We administer Lasix 40mg IV BID, Ceftriaxone 1gm IV BID
 Patient position on up right , elevate bed
 We monitor vital sign every 4 hours
 Monitor input & out put
 We measure daily weight
 We educate patient on salt free diet

Evaluation
• Edema completely subside
• Return of activity tolerance
• She is on oxygen intermittently.
• Her saturation is improve when compare with previous result(82%).
• All IV medication is change to PO.

Anatomy of Human Heart
Pericardium
 The heart sits within a fluid-filled cavity called the pericardial cavity.
 The walls and lining of the pericardial cavity are a special
membrane known as the pericardium.
 Pericardium is a type of serous membrane that produces serous
fluid to lubricate the heart and prevent friction between the ever
beating heart and its surrounding organs.

 The heart wall is made of 3 layers:
 Epicardium- is the outermost layer of the heart wall.
 Myocardium- is the muscular middle layer of the heart wall
that contains the cardiac muscle tissue and is the part of the
heart responsible for pumping blood.
 Endocardium.- is the simple squamous endothelium layer
that lines the inside of the heart.
Structure of the Heart Wall

Chambers of the Heart
 The heart contains 4 chambers:
 The right atrium,
 Left atrium,
 Right ventricle, and
 Left ventricle.

Valves of the Heart
• Atrioventricular valves- are located in the middle of the
heart between the atria and ventricles and only allow
blood to flow from the atria into the ventricles.
• TheAV valve on the right side of the heart is called the
tricuspid valve because it is made of three cusps (flaps).
• Semilunar valves. are located between the ventricles and
the arteries that carry blood away from the heart.
• The semilunar valve on the right side of the heart is the
pulmonary valve, so it prevents the backflow of blood
from the pulmonary trunk into the right ventricle.

Conduction System of the Heart
 The conduction system starts with the
pacemaker of the heart—a small bundle of cells
known as the sinoatrial (SA) node.
 The AV node is located in the right atrium in the
inferior portion of the interatrial septum.
 The AV node picks up the signal sent by the SA
node and transmits it through the
atrioventricular (AV) bundle.

REVIEW OF ANATOMY & PHYSIOLOGY
LOWER RESPIRATORY TRACT Upper RESPIRATORY TRACT

Respiratory process

 The lungs are located in the chest on either side of the heart in the
rib cage.
 They are conical in shape with a narrow rounded apex at the top and
a broad base that rests on the diaphragm.
 The apex of the lung extends into the root of the neck, reaching
shortly above the level of the sternal end of the first rib.
 The lungs are surrounded by the pulmonary pleurae.
 The pleurae are two serous membranes.
Lungs

 Between the pleurae is a potential space called the pleural cavity
containing pleural fluid.
 Each lung is divided into lobes by the invaginations of the pleura as
fissures. The fissures are double folds of pleura that section the
lungs and help in their expansion.
 The lobes of the lungs are further divided into bronchopulmonary
segments based on the locations of bronchioles .
Lungs Cont...

Lungs Cont...
 Right Lung- has both more lobes and segments than the left. It is
divided into three lobes, an upper, middle, and a lower, by two
fissures, one oblique and one horizontal.
 Left lung- is divided into two lobes, an upper and a lower, by the
oblique fissure, which extends from the costal to the mediastinal
surface of the lung both above and below the hilum.

INTRODUCTION
 Pulmonary hypertension is often the common link between lung
dysfunction and the heart in cor pulmonale.
 cor pulmonale commonly has a chronic and slowly progressive
course, acute onset or worsening cor pulmonale with life-
threatening complications can occur.

Definition of Cor Pulmonale
 It is the hypertrophy of the right ventricle resulting from diseases
affecting the function and/or structure of the lung, (WHO, 1963)
It is a condition in which the right ventricle of the heart enlarges (with
or without right sided heart failure) as a result of diseases that affect
the structure or function of the lung or its vasculature

Epidemiology
• Cor pulmonale is estimated to accounts for 6% to 7% of all types of adult
heart disease in the united state.
• The incidence of the condition varies widely among different countries
and depends on air pollution, the prevalence of cigarette smoking and
other risk factor for lung diseases.
• Cor pulmonale accounts for 10-30% of decompensated heart failure
related to admission in the united state and also 50,000 death in the
united state (Mar 14, 2023 Derek Leong).

Etiology
 Pulmonary Vascular disease
 COPD
 Chronic bronchitis.
 Acute respiration syndrome(ARDS).
 Cystic fibrosis.
 Chronic blood clot in the lung: Pulmonary embolism.
 Severe bronchiectasis.

Sub types of cor pulmonale
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
COPD, Obliterans subtype is
pulmonary thromboembolic disease

PATHOPHYSIOLOGY
Due to etiological factors ( hormonal, mechanical & others)
Pulmonary endothelial injury
 smooth muscle proliferation.
 vascular scarring
Sustained Pulmonary Hypertension
Right Ventricle Hypertrophy
Cor Pulmonale Right sided heart failure

CLINICAL MANIFESTATIONS
 Fatigue ,Tachypnea Exertional dyspnea and Cough.
 Cyanosis can be seen in chest and Chronic Hypoxemia
 Anginal pain -due to right ventricular ischemia
 Hemoptysis - due to rupture of a dilated or atherosclerotic
pulmonary arteriole.
 Right upper quadrant abdominal discomfort, and jaundice.
 Swelling of the feet or ankles

Diagnostic evaluation
 History Collection
 PE-increase in chest diameter, JVD and cyanosis may be seen.
 Auscultation: the lungs, wheezes and crackles may be heard .
 Percussion: hyper-resonance of the lungs may be a sign of underlying
COPD.
 Pulmonary function tests
 ABG analysis- Reveals decreased PaO2 & pH and Increased PaCo2.

Diagnosticevaluation....
 Hematocrit count- It is done for polycythemia,
 Serum alpha1-antitrypsin, if deficiency is suspected
 Antinuclear antibody (ANA) level for collagen vascular disease,
 Coagulations studies to evaluate hypercoagulability states

Diagnosticevaluation....
 Doppler Echocardiograph
 ECG – ECG changes can be seen due to Right Ventricle Hypertrophy.
 Magnetic Resonance Imaging
 Right Cardiac Catheterization
 Lung Biopsy

Management
A. Pharmacological Management
 Diuretics: to decrease the elevated right Ventricular filling volume
 Calcium channel blockers: Vasodilate the pulmonary arteries
 Bronchodilators- Theophylline
 Anticoagulation & Thrombolytic therapy for massive pulmonary
embolism
 Inotropes with vasodilatory properties

Management...
B. Non Pharmacological Management
 Oxygen Therapy
C. Surgical Management
 Phlebotomy: for Chronic Cor pulmonale & chronic hypoxia
causing severe poly
 Pulmonary embolectomy: for Acute pulmonary embolism
 Lung transplantation

 Determine if the patient has experienced orthopnea, cough, fatigue, epigastric
distress, anorexia, or weight gain or has 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.
 Evaluate the rate, type, and quality of respirations.
 Observe the patient for dependent edema: ascites, buttocks & down both legs.
Inspect the patient's chest and thorax for the general appearance and
anteroposterior diameter.
 Look for the use of accessory muscles in breathing.
Nursing Management: Assessment

 Impaired gas exchange related to excess fluid in lungs; increased
pulmonary vascular resistance.
 Decreased cardiac output related to an ineffective ventricular pump
 Excess Fluid volume related to right sided heart failure
 Acute pain related to right ventricular ischemia & decreased oxygen
supply
 Activity intolerance related to abnormal pulse, ECG changes & chest
pain.
Nursing Diagnosis

 Exertional syncope.
 Hypoxia.
 Peripheral oedema.
 Peripheral venous insufficiency.
 Tricuspid regurgitation.
 Hepatic congestion and cardiac cirrhosis.
 Death.
Complications

 The overall five-year survival rate for cor pulmonale complicating
COPD is approximately 50%.
 Prognosis also appears to be significantly improved by smoking
cessation and correct use of long term O2 therapy.
Prognosis

 Advice patient to take protein rich diet.
 Educate patient regarding his disease condition.
 Modification in lifestyle like cessation of smoking & alcohol 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 follow-up & care.
Health Education

TheoryApplication
Modified wholly compensatory system
Accomplishes patient’s therapeutic self-care
Compensates for patient’s inability to engage in self-care
Supports and protect patient
Nurse action
 Oxygenation
 Suctioning
 Input & output
maintenance
 Ventilator care
 Postop care etc.

 Cor pulmonale commonly has a chronic and slowly progressive
course, acute onset or worsening cor pulmonale with life-threatening
complications can occur. Cor pulmonale has poor prognosis.
 Pulmonary heart disease, also known as cor pulmonale is the
enlargement and failure of the right ventricle of the heart as a
response to increased vascular resistance (such as from pulmonic
stenosis) or high blood pressure in the lungs.
 Cor pulmonale is failure of the right side of the heart.
Summary

References
 Mason R.J, Braaddus V.C.Murray and Nadel`s :Textbook of Respiratory Medicine.
6th edn. Philadelphia: Saunders;2015.
 George R.B,Light R.W. Chestmedicine:Essentials of Pulmonary and Critical Care
Medicine. 5th edn . Philadelphia: Lippincott;2015.
 Fauci AS, Braunwald E, Kasper DL, Hauser SL, Longo DL, Jameson JL, et al.,
editors. Harrison’s principles of internal medicine. 20th ed. New York: McGraw Hill;
2018
 Crawform M.H. Current Diagnosis and Treatment in cardiology. 2nd edn . New York:
McGraw Hill;2013.
 Michael H.C,Paulus W.J.Cardiology. 3rd edn.Philadelphia:Elsevier;2015.

THANKYOU

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