Consequences of Elevated Pulmonary Artery Pressure Flashcards
What are abnormalities of the pulmonary circulation?
- increased leakage across the pulmonary capillaries
- increased pressure in pulmonary arteries
Describe Asbestosis?
- A form of diffuse interstitial lung disease (DILD) due to exposure to asbestos.
- Progressive, diffuse inflammation and fibrosis of lung parenchyma causing disruption and destruction of the A-C membrane
- Gas exchange and mechanical defects with ↑ PaO2, ↓ A-a gradient, ↓ lung volumes (restrictive ventilatory defect), ↓ compliance and ↑ work of breathing.
- Present with progressive exertional breathlessness and cough
- Clubbing, crepitations +/- cyanosis on examination
What are some of the Clinical Findings of Pulmonary hypertension, right ventricular hypertrophy and tricuspid valve incompetence?
Clinical Findings:
- Tachypnoea, finger clubbing & cyanosis
- Increased JVP with v waves
- Basal crepitations
- Tender pulsatile hepatomegaly
- Ascites
- Peripheral oedema
Cardiac Findings:
- Sinus tachycardia
- Right ventricular heave
- Loud P2 and 4th heart sound
- Pulmonary systolic ejection murmur
- Tricuspid pansystolic murmur
- Increased JVP with v waves
- tricuspid regurgitation is due to ventricular dilation
What is pulmonary hypertension likely to be broadly caused by?
- destruction of pulmonary capillaries
2. spasm of pulmonary arterioles
What are the effects of pulmonary hypertension?
Pulmonary hypertension will increase the right atrial pressure and systemic venous pressures. Increasing systemic venous pressures will cause peripheral oedema, ascites and pleural effusions in the systemic capillary beds
What are the causes of pulmonary hypertension?
- Increased Left Atrial Pressure
- mitral stenosis, LV failure - Increased Pulmonary Blood Flow
- left to right shunts, high flow rates, excess central volume - Increased Pulmonary Vascular Resistance
a. vasoconstriction - low alveolar oxygen (including hypoventilation)
b. Obstruction - embolism, primary pulmonary hypertension
c. Obliteration - arteritis, emphysema, pulmonary fibrosis
Describe the Outcomes of Right Ventricular Failure.
Pulmonary Hypertension
↓
RV Dilatation & Hypertrophy
↓
EITHER A) Increased Systemic Venous Pressure
↓
Extravasation of Fluid into Tissues, peritoneal space and pleural spaces
OR B) Poor Cardiac Output → Lassitude Breathlessness
In summary, Respiratory Pathophysiology includes what types of conditions?
- Conditions that cause airflow obstruction (such as asthma and COPD) can affect:
– mechanics ( ↑sensation of breathlessness, ↑ resistive WOB, obstructive spirometry)
– gas exchange (esp because of V/Q mismatch) → ↓PaO2, ↓ SaO2 - Conditions that involve the lung parenchyma (such as pneumonia, alveolitis and fibrosis and pulmonary odema), can affect:
– mechanics (↑sensation of breathlessness, ↑ elastic WOB, restrictive spirometry)
– gas exchange (V/Q mismatch, shunt, diffusion impairment) → ↓ PaO2, ↓ SaO2 - Conditions primarily affecting the pulmonary arteries (emboli, idiopathic pulmonary hypertension) can affect gas exchange.
- All of these conditions, if severe can result in type 1 (gas exchange) respiratory failure, and in some cases type 2 (ventilatory) failure.
- All of the conditions above, if severe, can also result in pulmonary hypertension and right heart failure.
Describe the surface area of the AC membrane?
A-C Membrane Surface Area: 50-100 square metres
–> to accomodate tissue oxygen requirements
The problem of packaging large surface area into thoracic volume of 6L is solved by spreading the area over 300 x 106 alveoli. What follow on problems does this cause?
- How can all A-C units be ventilates and perfused equally?
- How can the alveoli be kept dry?
- How can alveolar collapse be prevented?
How can all AC units be ventilated and perfused equally?
- Approximately even distribution of ventilation and perfusion are achieved through-out the lungs because the bronchial and pulmonary arterial trees have fractal structures.
- They divide dichotomously for 23 generations so that the distance that air or blood travels to any part of the lung is about equal.
- V/Q scans can be used to show even distribution of ventilation and perfusion throughout the lungs.
How can the alveoli be kept dry?
- Fluid in the alveoli (and to a lesser extent, interstitial spaces) adversely affects gas exchange and lung mechanics.
- The juxtaposition of air filled alveoli and a wet capillary membrane creates the risk of capillary fluid flooding the air spaces.
- Normally there is a small flow of fluid out of the capillaries.
- Lymphatics drain fluid moving from the capillaries into the interstitial spaces before it can pass into the alveoli
- The normal rate of flow is a few ml per hour but this can increase if necessary
- Movement of fluid between alveoli and the interstitium is prevented by tight junctions and surfactant
- Alveolar cells can pump ions and water to the interstitium
How can alveolar collapse be prevented?
- Alveoli vary in size and as a result pressure generated by surface tension will vary
- In accordance with Laplace’s Law (P = 4T/r), pressure will be greater in smaller alveoli than larger ones, causing air to empty out of the smaller ones, with subsequent collapse of parts of the lung and over expansion of other areas, adversely affecting lung function.
- Surfactant reduces T inversely proportional to size of alveoli (r) and therefore equalises pressure –> prevents the collapse of regions of the lung (esp. the bases)
What is surfactant?
- A group of closely related phospholipids secreted by type 11 pneumocytes
- Lower surface tension (T) at air fluid interfaces with the unique property of lowering T in proportion to thickness of layer of surfactant
- Functions
– Prevents collapse of alveoli
– Increases lung compliance
– Helps to keep alveoli dry
What is acidosis?
Acidosis - DECREASE IN pH
- Either respiratory or metabolic
- Primary abnormalities:
- Respiratory due to CO2 retention (hypoventilation)
- Metabolic due to loss of HCO3 or consumption due to addition of acid
