83 - Physiological Consequences of Elevated Pulmonary Pressure Flashcards
What does airflow obstruction result in?
Gas exchange difficulties, especially if there is low V/Q.
Abestosis
A form of diffuse interstitial lung disease from exposure to asbestos fibres.
When inhaled, asbestos fibres can’t be broken down, can lead to progressive, diffuse inflammation and fibrosis.
Arises ~8-10 years after heavy exposure.
Pathology of asbestosis
Causes a gas exchange and mechanical defect at capillary-alveoli membrane.
Decreased PaO2, increased A-a gradient, decreased lung volumes (restrictive ventilatory defect), decreased compliance, increased work of breathing.
How do people with asbestosis present?
Clubbing, crepitations, +/- cyanosis.
Exertional breathlessness, cough
What can sinus tachycardia mean?
Reduced stroke volume. Increase contraction rate to compensate
What does right ventricular heave mean?
Right ventricle is contracting at a higher pressure than it is used to.
What does tricuspid pansystolic murmur mean?
Incompetent tricuspid valve (can be from defective valve or from dilated ventricle, pulling on valve leaflets)
What is spasm of pulmonary arterioles?
Lack of ventilation of bronchioles can lead to contraction of smooth muscle in arterioles leading to these gas exchange units.
Does oxygen desaturation normally occur with exercise?
No
Interstitial lung disease
A problem at the alveolar-capillary membrane
How can you tell if someone has interstitial lung disease?
Shows up on a chest X-ray and can hear crepitations
Diagnostic tests for pulmonary arteries
1
2
1) Pulmonary angiogram (dye is injected into a peripheral vein, a CT scan is performed to see where in the pulmonary circulation the dye goes)
2) Ventilation/perfusion scan (breathe in a radioactive substance, and inject radioactive substance. Injected substance gets lodged in pre-capillary arterioles). See if areas of ventilation and perfusion match up.
What can a ventilation/perfusion test tell you?
If a problem with the lungs is due to a blockage of pulmonary vessels or obstruction of airways.
What is the effect of pulmonary hypertension on right atrial and systemic venous pressures?
They increase
Effect of increased systemic venous pressure on the systemic capilary bed
If severe enough, leads to peripheral oedema, ascites, pleural effusions
Cor pulmonalae
Right heart failure from excessive pulmonary circulation pressure
Causes of pulmonary hypertension
1
2
3
1) Increased pulmonary vascular resistance
2) Increased left atrial pressure
3) Increased pulmonary blood flow
Causes of increased pulmonary vascular resistance
1
2
3
1) Vasoconstriction (low alveolar O2, EG: hypoventilation)
2) Obstruction (embolism, primary pulmonary hypertension)
3) Obliteration of vascular bed (arteritis, emphysema, pulmonary fibrosis)
Right ventricular failure effects 1 2 3 4 5
1) Pulmonary hypertension leads to
2) Right ventricular dilation and hypertrophy, leading to
3) Increased systemic venous pressure, which leads to
4) Extravasation of fluid into tissues, peritoneal space, pleural spaces.
5) Right heart failure also leads to decreased cardiac output, which results in lassitude, tiredness.
Primary abnormalities of acidosis
1
2
Respiratory acidosis from CO2 retention (hypoventilation)
Metabolic due to loss of HCO3 or addition of acid
Compensatory mechanisms behind acidosis
1
2
1) Bicarbonate retention for respiratory acidosis (days)
2) Hyperventilation (low PaCO2) for metabolic acidosis (seconds)
Examples of metabolic acidoses
Keto-acidosis (from starvation)
Lactic acid buildup
Diarrhoea (causes loss of bicarbonate)
Which part of the body is responsible for bicarbonate retention
Kidneys
Normal bicarbonate compensation for increasing CO2
~3.5mmol/L per 10mmHg increase CO2
Primary alkalotic disorders
1
2
1) Respiratory due to low CO2 (hyperventilation)
2) Metabolic due to increased HCO3 or loss of acid
Way for body to lose acid
Vomiting
Compensation for respiratory alkalosis
Bicarbonate excretion (kidneys) for respiratory alkalosis
Compensation for metabolic acidosis
Mild hypoventilation (can’t be much, as you still need to breathe in oxygen)
Why is the body’s response to severe metabolic alkalosis limited?
Can’t reduce breathing rate much
Normal serum bicarbonate concentration
22-29mmol/L
If there is high PaCO2, does HCO3 have to be high from renal compensation?
Not necessarily, as elevated HCO3 can come about from elevated CO2 being in the blood (increased carbonic acid being made)
How can you tell if an acid/base disorder is compensated from wither acidosis or alkalosis?
pH doesn’t return completely to normal. If a compensated alkalosis, pH will be at high end of normal, if compensated acidosis, will be at low end of normal.
