pulmonary Flashcards
Increase Capillary permeability (Kf, σ)
- Oxygen toxicity: too much O2 is bad for the lungs.
- Acute respiratory distress syndrome
- Inhaled or circulating toxins
Alveolar plateau of closing volume test [6]
This test is not usually done because it doesn’t work very well for the patients with high airways resistance.
shunt equation
-Ratio of shunted flow (mixed venous flow that goes directly to the left side of circulation) divided by (over) the total cardiac output (total blood flow) is = to (end capillary O2 content – arterial O2 content) divided by (over) the (end capillary O2 – mixed venous O2 content)
, the person has alveolar dead space.
If arterial pCO2 > end tidal pCO2 ,
Causes of Increased Alveolar-Arterial Oxygen Partial Pressure Gradient [17]
- The arterial oxygen difference can also be measured.
- Alveolar pO2 is calculated using the alveolar air equation, which provides an ideal alveolar pO2 value.
- Situations that increase the difference between alveolar and arterial pO2:
- Increased shunting (venous blood flowing to arterial side without picking up oxygen) will increase the difference between alveolar pO2 and arterial pO2.
- Both abnormal anatomic shunts and intrapulmonary shunts can increase this difference.
- Some level of V ̇/Q ̇ mismatch.
Everyone has some level of V ̇/Q ̇ mismatch, but larger mismatches can affect the alveolar-arterial O¬¬2 partial pressure gradient.
-Impaired diffusion due to fluid in lower portions of the lung. Interstitial fluid collects (especially in the lower parts of the lung) until it is removed by the lymph system.
- Increased inspired partial pressure of O2
- Decreased mixed venous partial pressure of O2
- Shift of oxyhemoglobin dissociation curve
Increased Capillary hydrostatic pressure (Pc)
Increased left atrial pressure resulting from left ventricular infarction or mitral stenosis.
Over-administration of intravenous fluids.
Decreased interstitial hydrostatic pressure (PIS)
Too rapid evacuation of pneumothorax or hemothorax.
Decreased oncotic pressure (π_pl)
- Protein starvation/dilution of blood proteins by intravenous solutions.
- Renal problems resulting in urinary protein loss (proteinuria).
C. Carbamino Compounds [28]
CO2 can bind to a terminal amine group in a protein in the blood to form a carbamino compound, but a hydrogen ion gets released in the process
Most carbamino compounds form with Hb, but some can form with other trace proteins and albumin, etc.
- Bohr Effect
a. Deoxyhemoglobin is a base, so it is willing to pick up the hydrogen ion, shifting the reaction forward, forming the carbamino compound.
b. Oxyhemoglobin is an acid, so it gives up that extra hydrogen or the CO2, and makes reaction go in the other direction
c. Much more CO2 will be carried as carbamino compounds in venous blood where there is more deoxyhemoglobin than in arterial blood
COPD (case 1) o Smoking history o Prolonged expiratory phase o Resonant chest, hyperinflation of lungs (Chest X-ray) o FEV1 = 0.55 low (13% predicted) o FVC = decreased FEV1:FVC ratio= decreased
Pulmonary Fibrosis (case 2)
o 5 year history of worsening dyspnea
o Nonproductive cough
o Rheumatoid arthritis autoimmune, causes pulmonary fibrosis in lungs
o Low RR
o Crackles and rails at bases of lungs, chest X-ray with white shit in lungs
o FVC = 55% low
o FEV1 = 52% low
o FEV1/FVC > 70%= normal (
o Increased resistive work (on expiration)
work to inflate and deflate the lungs (fat people- have to move a lot of tissue to breathe, and NO resistive work)
o Exercise = increased airway resistance, more trapped hair so FVR is increased with exercise compromising FVC
o Pulmonary function tests “sagging and wide” due to dynamic airway compression;
************
o All volumes low = restrictive disorder
o Diffusing capacity= doesn’t measure diffusion
measures uptake of carbon monoxide (CO
) CO comes into body and goes to Hb
forms carboxyhemoglobin. Can calculate how much CO is taken up. Binds to Hb in capillaries
measures effective capillary volume (which affects the diffusion capacity (anemia, or things that destroy pulmonary capillaries (fibrosis))
o Increases elastic work (stiff lungs= harder to inflate) – elastic recoil is high, no resistance (leather balloon), low compliance
o(elastic work-takes place when theres stiffness in the lungs or the chest wall)
Stiff lungs decreased compliance= pulmonary fibrosis
increased elastic work of breathing
Giving O2 will not help
*************
o Increase alveolar dead space = ventilation but not perfused
o High V/Q – increases with exercise (ventilation increases without recruitment of vessels)
**************
Negative intrapleural pressures during inspiration
Moving fluid also exerts less pressure
Cartilage prevents collapse with inspiration normally- but his trachea is damaged, allowing collapse
o Resistive work of breathing (on inspiration)
************** She’s just nervous tell her that there’s no disease or reason that she is getting SOB. She just needs to work on her exercise
o To see what it is, do a PFT with exercise! Brings out abnormal physiology that affects a disease process
o Pulmonary Function with Exercise Testing = abnormal
MVV – maximal amount of air you can breathe in and out in a min.
• Ventilation on exercise (VE) = 65% MVV (low)
• Ventilatory reserve (MVV – VE)
CO = normally limiting factor to exercise
OSA
- Collapse of the upper airway during normal inspiration is normally prevented by contraction of the pharyngeal dilator reflex
- Upper airway obstructions during sleep cause alveolar hypoxia and hypercapnia
- HPV occurs in response to the hypoxia and hypercapnia and increase PVR
- Repeated episode of pulmonary HTN may lead to vascular remodeling resulting in chronic pulmonary HTN
- Chronic alveolar hypoxia during the episodes of upper airway obstruction leads to hypoxemia,causing renal release of erythropoietin
The increased PAP and increased blood viscosity chronically increase the afterload of the RV, producing RV hypertrophy, which can be seen as right axis deviation in ECG
This could lead to cor pulmonale, RV failure secondary to pulmonary HTN
- Arterial hypoxemia and hypercapnia during episodes of upper airway obstruction cause increased cerebral BF, caused by dilation of cerebral blood vessels—-this repeated occurance causes HA
- increased RVEDP and volume lead to increased RA volume, which increases the secretion of atrial natriuretic peptide from atrial myocytes, increasing sodium excretion. The increased atrial volume also stretches receptors that suppress ADH secretion from the posterior pituitary gland and increases urine volume
physiologic dead space
is approximately equal to the anatomic deadspace in healthy lungs
minute volume is expressed as follows:
MV= VT X Breaths/min
Alveolar Ventilation is expressed as follows:
Alveolar ventillation= (VT-dead space) X Breaths/min
FEV1-
Obstructive d/o:
Restrictive lung d/o
A decreased FEV1= large airway problem
FEV1/FVC ratio is decreased
FEV1/FEC ratio is either normal or increased
