Resp - Cor Pulmonale Flashcards

1
Q

Define Cor Pulmonale

A

Enlargement of right ventricle/ Right heart hypertrophy due to increased right ventricular afterload from lung/ airway diseases, chest wall disorder, poor ventilation control or pulmonary circulation

Associated with pulmonary hypertension

Manifests as right heart failure

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2
Q

Pathophysiology of cor pulmonale

A

1) Respiratory diseases with Hypoxia > Hypoxic vasoconstriction and polycythaemia > Increased pulmonary vascular resistance
2) Disorders of pulmonary vessels > Increase pulmonary vascular resistance

>> Pulmonary Hypertension
>> Right ventricular hypertrophy/ dilatation due to increased RV workload
>> RV failure

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3
Q

Clinical features of Cor Pulmonale

A

□ Underlying lung condition

Pulmonary hypertension: SOB, loud P2

Right ventricular hypertrophy and RH failure: oedema, chest pain, fatigue, syncope, palpitation, ↑JVP, parasternal heave, RV S3

→ Often manifest during acute exacerbation of chronic respiratory problem
→ Also prone to LV failure (reason unknown, may be due to pro-inflammatory state)

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4
Q

First-line investigations for diagnosis of Cor Pulmonale

A

Arterial blood gas: hypoxaemia ± hypercapnia

CXR:
→ Dilated pulmonary trunks with peripheral pruning
→ RV dilatation

ECG: p pulmonale, right atrial dilatation, right ventricular hypertrophy

Echocardiography – doppler for pulmonary hypertension, right ventricular function

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5
Q

Management of Cor pulmonale

A

□ Treat underlying respiratory disease
Diuretics for Right heart failure, Low salt diet and fluid restriction
Anticoagulation for ↓risk of thromboembolism
Digoxin if atrial tachyarrhythmia

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6
Q

Underlying diseases that cause Cor Pulmonale

A
  1. Respiratory diseases with hypoxia causing pulmonary hypertension
    - COPD
    - Bronchiectasis
    - ILD
  2. Disorder of pulmonary circulation:
    - Chronic pulmonary thromboembolism
    - Massive acute PE
    - Primary PHTN
  3. Chest wall dysfunction: - Kyphoscoliosis, Obesity hypoventilation syndrome
  4. Acute exacerbations of chronic respiratory diseases
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7
Q

Define respiratory failure and define gas tension in arterial blood gas

A

Respiratory failure = Failure of the lungs to meet the metabolic demands of the body
□ Hypoxaemia → failure in tissue oxygenation
□ Hypercapnia → failure in carbon dioxide homoeostasis

Type 1: ↓pO2 <60mmHg (8kPa) + ↓/-pCO2 ≤ 50mmHg (6.5kPa)

Type 2: ↓pO2 <60mmHg (8kPa) + ↑pCO2 > 50mmHg (6.5kPa)

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8
Q

Define normal limits of PaO2, PaCO2 and pH

A

PaO2 10.6-14.0 kPa
PaCO2 4.7-6.0 kPa
pH 7.35-7.45

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9
Q

3 main pathophysiological causes of Type 1 respiratory failure

List examples of respiratory diseases a/w each pathophysiological process

A

V/Q mismatch: hypoxaemia and CO2 retention

e.g. COPD, asthma, bronchiectasis, pulmonary embolism

Shunting: Mixed venous blood passes through lungs without oxygenation (alveoli not ventilated)

e.g. pneumonia, collapsed lung, ARDS, acute pulmonary oedema

Diffusion impairment: = failure of pulmonary capillary blood to fully equilibrate with alveolar gas

e.g. ILD, pulmonary oedema, emphysema

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10
Q

4 main pathophysiological causes of Type 2 respiratory failure

A

Depressed respiratory drive (TV and RR increase): e.g. sedative overdose, CNS depression, metabolic alkalosis, hypothermia, hypothyroidism

Neuromuscular (Low TV, High RR): spinal cord injury, GBS, phrenic nerve injury, myasthenia gravis…

Thoracic cage disorder (Low TV High RR): kyphoscoliosis, flail chest, OHS

Global lung hypoventilation: upper airway obstruction, decompensated diffuse lower airway disorder (COPD, asthma)

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11
Q

Clinical features of Type 2 respiratory failure

A

Hypercapnia/ CO2 retention: headache (from vasodilation), altered mentation, flushing, papilloedema, HTN, flapping tremor

Acidosis: Kussmaul breathing, gasping

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12
Q

Clinical features of Type I respiratory failure

A

Hypoxia and Hypocapnia

  • *Increase respiratory effort**: tachypnoea, use of accessory respiratory muscles
  • *Diaphragmatic fatigue**: paradoxical breathing of abdomen
  • *Sympathetic discharge**: ↑HR, ↑BP, sweating, agitation
  • *Hypoxaemia**: central cyanosis, confusion
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13
Q

Pathophysiology of respiratory failure

A

respiratory failure is defined in terms of gas tension
of blood leaving the lungs i.e. arterial blood gases

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14
Q

Formulas for oxygen saturation, DO2 and Minute Volume

A

Minute ventilation or minute volume = tidal volume (TV) x respiratory rate (RR)

O2 delivered to body / mls/min (DO2): (O2 binding capacity of Hb x SaO2) x cardiac output = 1.34 x Hb x SaO2 x C.O.

Oxygen saturation = Oxy Hb / (Oxy Hb + reduced Hb) = % of oxy Hb

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15
Q

Causes of increased respiratory load

A

Airway resistive loads: Bronchospasm; Airway edema, secretions, scarring; Upper airway obstruction; OSA

Lung elasticity: Alveolar edema, atelectasis, infection…etc

Chest wall elasticity: Pneumothorax, rib fracture, effusion, tumor, ascites…etc

Minute ventilation load: Sepsis, PE, hypovolemia

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16
Q

Causes of decreased respiratory strength

A

Depressed respiratory drive: drug, brainstem lesion, hypothyroidism

Neuromuscular diseases: spinal cord lesion, GBS, ALS, MG, Botulism…etc

Muscle weakness: Fatigue, Electrolyte disturbance, Malnutrition, Myhopathies…etc

17
Q

Clinical picture:

Long history of cough and exertional dyspnea

bilateral leg swelling for one day

Physical examination:
o Cyanotic, tachypnoeic
o Bilateral pitting ankle oedema
o Inspiratory retraction of intercostal muscles

Hyperinflated chest with diffuse expiratory rhonchi

Oxygen saturation on
supplemental oxygen at 1 L/min
through nasal cannula: 94%

Interpret following profile

A

Clinical diagnosis:
o Chronic obstructive pulmonary disease (COPD) – chronic bronchitis, pulmonary emphysema
o Acute on chronic type 2 respiratory failure – hypoxaemia ± hypercarbia, respiratory acidosis with inadequate renal metabolic compensation

o Cor pulmonale (right heart failure)

o Precipitated by respiratory infection

18
Q

Pathophysiology of chronic bronchitis and emphysema (COPD)

A
  1. Destruction of alveoli - loss of capillary bed and loss of elastic support of airways
  2. Inflammation of airway - collapse of distal poorly supported airways
  3. Excess secretion with mucus plugging
  4. Increased airway smooth muscle contraction - Airflow obstruction, gas trapping, hyperinflation
19
Q

Describe the lung function test profile for COPD

A

o Obstructive: LOW FEV1 / FVC
o Air trapping: High residual volume
o Hyperinflation: High total lung capacity
o Destroyed capillary bed: Low DLCO

20
Q

Pathophysiology of respiratory failure in COPD

A

Mixed type 1 and 2 Respiratory failure:_

V/Q mismatch:
 Destruction of alveoli: loss of capillary bed
 Airflow obstruction

Alveolar hypoventilation:

Respiratory muscle fatigue: Increase work of breathing due to increased airway resistance

Blunted central drive: severe hypoxaemia and hypercarbia

Shunting: pneumonia or congestive heart failure

21
Q

Management of acute (on chronic) respiratory failure in COPD

A
  1. Treat airflow obstruction in COPD:

 Inhaled bronchodilators (beta-agonists, anticholinergics)
Systemic steroids in acute exacerbation of COPD

  1. Identify the trigger of exacerbation and treat, e.g. infections, pneumothorax
  2. Supportive measures for respiratory failure:
    Oxygen supplement
    Ventilatory support (invasive or non-invasive)
  3. Treat heart failure – diuretics
  4. Identify any other comorbidities e.g. arrhythmia, ischemic heart disease
22
Q

Long-term management of COPD with chronic respiratory failure

A
  1. Stop smoking
  2. Treat airway obstruction and inflammation - Bronchodilator and ICS
  3. Pulmonary rehabilitation
  4. Influenza and pneumococcal vaccines
  5. Long-term home oxygen/ LTOT
  6. Home nocturnal ventilation
23
Q

A COPD patient was admitted for acute onset of shortness of breath. He has an oxygen saturation of 75% on 3 liters/min of oxygen supplement, and arterial blood gas confirms severe hypoxemic respiratory failure with no carbon dioxide retention. CXR shows hyperinflation and a 3 cm lung mass in RLZ suspicious of lung malignancy. What is the cause of this severe hypoxaemia?

A. Acute exacerbation of COPD
B. Pulmonary embolism
C. Pleural effusion

A

B: CXR shows lung mass in this patient with COPD (likely heavy smoking history) suspicious of lung cancer. Malignancy predisposes to deep vein thrombosis and pulmonary embolism which gives rise to further hypoxemia.

24
Q

Severe kyphoscoliosis may lead to type 2 respiratory failure with high carbon dioxide retention due to the pathophysiologic mechanism of:

A. Ventilation:perfusion mismatch
B. Shunting
C. Hypoventilation

A

(C: Chest wall restriction leads to limited lung expansion and hypoventilation)

25
Q

Which of the following among the three is the first line treatment in COPD, and why?

A. Inhaled bronchodilator
B. Oral beta agonists
C. Inhaled corticosteroids

A

(A: COPD only has partial and limited reversibility of airways obstruction, given the structural destruction of alveolar tissue. But the small degree of bronchodilatation can lead to less air-trapping and lung hyperinflation, thus resulting in lower work of breathing and less dyspnea and better exercise tolerance.)