Pulm Deck 2 Flashcards
where are alveolar (A) PO2 & PCO2 set?
where are arterial (a) PO2 & PCO2 set before they enter the alveoi?
PAO2= 100 mmHg PACO2= 40 mmHg
PaO2= 40 mmHg PaCO2= 46 mmHg
what happens in shunt alveoli? what happens in dead space alveoli?
shunt- perfused but not ventilated (PaO2= 40, PaCO2= 45); V/Q= 0
dead space- ventilated but not perfused- PaO2= 150, PaCo2= 0); V/Q= infinity
what happens to the V/Q ratio in the bottom of the lung?
- have more blood flow than ventilation; V/Q ratio is very low
what does a high V/Q ratio represent?
- high alveolar ventilation; low alveolar perfusion
- like dead space alveolus
- ventilation exceeds perfusion
what happens to the V/Q ratio at the top of the lungs?
- have more ventilation than blood flow (but still less ventilation than the bottom of the lung)
- however, the relative ratio causes a high V/Q ratio
- get over-ventilation & dead space
(alveolar PaO2 is higher and CO2 lower)
The majority of oxygenated blood leaving the lung comes from the _____, this causes the arterial PO2 to be ______ than atmospheric pressure
base, lower
what is the AaDO2 and what is normal?
- alveolar-arterial PO2 difference; - - normal is less than 15
what are the two reasons for AaDO2?
1) V-Q inequality
2) Anatomic shunt- veins that go directly into LV
how do you calculate AaDO2?
alveolar PO2 (gas equation= 100 mmHg) - arterial PO2 (blood draw)
what is hypoxemia?
when arterial blood oxygen (PaO2) is below 80 mmHg
what are the four causes of hypoxemia?
- hypoventilation
- diffusion limitation
- shut (anatomic or physiologic)
- V/Q mismatch
what 2 things happen during hypoventilation? What happens to AaDO2? What is the arterial PO2 response to 100% oxygen? what is hypoventilation caused by?
- alveolar PO2 decreases
- alveolar CO2 increases
- AaDO2 is normal (gas exchange is normal)
- arterial PO2 increases with 100% O2
- caused by drugs that depress central drive to breathe
With diffusion limitation, what happens to AaDO2? What is the arterial PO2 response to 100% oxygen? what is diffusion limitation caused by?
- AaDO2 increases (have more alveolar, less arterial)
- arterial PO2 increases with 100% O2
- caused by lung edema, fibrosis, capillary block
With an anatomic/physiological shunt, what happens to AaDO2? What is the arterial PO2 response to 100% oxygen? what happens to arterial PCO2?
- AaDO2 increases (have more alveolar, less arterial)
- additional O2 will not increase arterial PO2 b/c shunted blood isn’t exposed to enriched O2 (a physiological shunt will decrease O2 on 100% O2)
- PCO2 does not change b/c chemoreceptors which increase ventilation
what is the main cause of hypoxemia in patients with respiratory disorders?
V/Q inequality with LOW V/Q ratio
In V/Q inequality, what happens to AaDO2? Does 100% O2 help?
- AaDO2 is increased (high alveolar, low arterial)
- 100% O2 helps
2 ways O2 is transported in blood, and which does blood gas analysis measure?
- dissolved (= blood gas, PaO2)
2. bound to hemoglobin
what is Henry’s law?
the concentration of a solute gas in a solution is directly proportional to the partial pressure of that gas above the solution (C=khP)
dissolved PaO2 measured as mL/min
3mL O2 dissolves/ 1L blood X 5 L/min= 15 mL O2/min
At partial pressures
< 60 mmHg: small changes in pressure lead to _______
release of large amounts of O2
what is the normal P50 for O2? what happens if it’s higher?
27 mmHg
- if higher, have right shift of the curve, less affinity for O2, and lower saturation
what is the Bohr effect?
decreased P50= increased affinity and a left shift is caused by
- decreased temp
- decreased PCO2
- decreased DPG
- increased pH
what is CO’s affinity for hemoglobin like?
- affinity of CO for Hb is 200 times greater; all binding sites are occupied at 1 mmHg CO
- affinity for O2 is also enhanced and unloading prevented
what is SO2? what is is normally and what is the PaO2 at 90%?
oxygen saturation- the amount of O2 combined with hemoglobin/capacity OR O2 binding sites occupied normal- 97.5 hyoxemia (80mm Hg PO2)- 94.5 90%= 60 mmHg= danger
what is the concentration of O2 when SO2= 100%?
1 g hb= 1.34 mL O2
15 g hb= 20.1 mL O2/ 100 mL blood
what is the SO2 in tissue? how much O2 is extracted from the blood?
SO2= 75% (15.1 mL O2/100)
= 19.5-15.1= 4.4 mLO2/100 mL blood (or 220mL O2/min)
how is CO2 transported in the blood?
- dissolved (10%)
- ** as bicarb (HCO3-) (60-70%)
- as carbamino compounds with proteins (carbaminohemoglobin) (20-30%)
dissolved Co2 per 1 mmHg of PCO2
0.067 mL Co2/100mL of blood (20x more than O2)
equation for bicarbonate
Co2+H20 H2CO3 H+ + HCO3-
what is the haldane effect?
- free Hb can bind more CO2 than HbO2
- SO lower O2 saturation, larger CO2 concentration
what’s the chloride shift caused by?
an increase in H+ or HCO3- causes HCO3- to diffuse out and Cl- to move in to maintain electrical neutrality
what happens when you get a decrease in pH?
H+ shifts equation left, increase CO2, causes right shift of O2 dissociation curve (higher P50), facilitates offloading, Hb carries more CO2
what are the 4 major types of tissue hypoxia?
- hypoxic hypoxia (cyanosis from decreased PaO2)
- circulatory hypoxia (reduced blood flow to tissues)
- anemic hypoxia (blood can’t carry O2)
- histotoxic hypoxia (cell can use O2 due to poison)
T/F- CO2 dissociation curve is directly proportional to PCO2
T
what is tissue hypoxia?
insufficient O2 is available to maintain adequate aerobic metabolism
2 factors determining O2 delivery to the tissues?
O2 content
blood flow
where are the respiratory centers responsible for generating and controlling the rhythmic pattern located?
generating- medulla (automatic)
controlling- pons
major sites of respiratory control for autonomic respiration
- control center- brainstem
- central chemoreceptors
- peripheral chemoreceptors
- pulmonary mechanoreceptors/sensory nerves
major sites of respiratory control for voluntary respiration
- motor cortex (hyper/hypoventilation)
2. output to CST
two groups of cells in the medulla that generate breathing pattern
dorsal respiratory group- inspiration
ventral respiratory group- expiration (and a little inspiration)
two groups of cells in the pontine respiratory group
- apneustic center- lower pons- excitatory effect on DRG (stimulates inspiration)
- pneumotaxic center- higher pons- inhibits DRG (inhibits inspiration)- associated with fine control of the frequency of breathing
where are the central chemoreceptors located? what are they sensitive to?
- ventrolateral surface of the medulla oblongata;
- sensitive to changes in pH in CSF (PCO2)
- responsible for most of min-by-min control (60-70% of response)
- H+ can cross BBB at low pH
2 sites of peripheral chemoreceptors? what do they respond to?
- carotid body*** (CN9) & aortic arch (vagus)
- respond to decreases in PO2**, decreases in pH (carotid only), increases is PCO2
- carotid body has robust firing when PaO2 < 70 mmHg; not important during normal conditions; has fast response
- CB responds to arterial PO2
what is the Hering-Breur inflation and deflation reflex? what receptors does it involve?
- inflation of the lung inhibits inspiratory muscle activity (CN10)
- deflation initiates inspiratory activity
- pulmonary stretch receptors
what are irritant receptors?
- rapidly adapting stretch receptors
- respond to irritants- smoke, dust, cold air
- cause bronchoconstriction
- asthma?
what are J receptors and bronchial C fibers?
- juxtacapillary receptors- endings are in capillary walls- inject something into pulmonary circulation, get rapid response
- cause rapid shallow breathing (e.g. pulmonary edema)
- bronchial C- supplied by bronchial circulation
other receptors
- nose/upper airway receptors
- joint/muscle pain
- pain/temperature
- arterial baroreceptors
what happens to the ventilatory response to CO2 (slope of response curve) when you lower PaO2? what are some things that lower the ventilatory response?
- ventilation at a given PaCO2 is higher
- ventilatory response to CO2 become steeper than 2-3 mL/min
- lowered by sleep, aging, drugs, COPD (increased work of breathing)
what happens to ventilation at a fixed high PCO2 when O2 is decreased? what is this called? when does it become important?
- as PO2 drops, ventilation increases rapidly - (occurs when PaO2 is below 100 mmHg, versus 50-70 mmHg normally)
- called hypoxic stimulation; is important in patients with chronic CO2 retention
what happens to PaO2, PCO2, and pH during moderate exercise? severe exercise?
moderate exercise- gases don’t change but ventilation is still increased
severe exercise- cross anaerobic threshold, lactic acid released, pH decreased, ventilation increases
what is the difference between obstructive sleep apnea and central sleep apnea?
- with both, see depressed airflow for a period of time
- with central sleep apnea, also see decreases in pleural pressure, signifying that the diaphragm is not receiving signals to contract
what does Kussmaul breathing look like and what is it a sign of?
- deep breathing with reduced frequency
- typical in metabolic acidosis
what does apneustic respiration look like?
- sustained periods of inspiration followed by brief expiration
- losing input from vagal nerve/pneumotaxic center (inhibits DRG (inhibits inspiration)- associated with fine control of the frequency of breathing)
what are two examples of end of the line, shakey breathing? what are they mostly due to?
cheyne-stokes (rapid bouts of hyperventilation), biots (slow bouts of hyperventilation)
- brain injury, neuronal damage
what happens to barometric pressure and inspired PO2 with higher altitude?
both decrease
- low PO2 is the most important problem at high altitude
how does acclimatization occur when climbing mt everest?
- hyperventilation, reducing the PaCO2 via hypoxic stimulation of peripheral chemoreceptors
what allows the PO2 of mixed venous blood at higher altitudes to be only 7mmHg lower?
- polycythemia- increase in red blood cell concentration over time
- erythropoietin from kidney increases Hb/O2 carrying capacity
parts of the physiological response to high altitude
- hyperventilation
- polycythemia
- shift of binding curve due to changes in 2,3 DPG
- maximal breathing capacity increases with less dense air
- alveolar hypoxia results in pulmonary vasoconstriction, right heart hypertrophy and pulmonary edema
what is the diving response?
- peripheral vasoconstriction due to sympathetic activity induced by apnea and enhanced by cold water on face
- results in initial hypertension (sympathetics)
- then vagally induced bradycardia
- lower HR gives a higher O2 saturation
when does hypoxic loss of conciousness occur?
PO2: 20-25 mmHg
3 preventable pathophysiological mechanisms that lead to death in divers
1) hyperventilation- reduces CO2 drive to breath, hypoxic signal is voluntarily overridden
2) ascent blackout- PO2 in lungs decreases as you ascend, exacerbated b/c less O2 left
3) carbohydrate depletion- less CO2 production reduces hypoxic drive to breathe
what happens to the lungs as you descend?
- when mechanical compression of the wall has occurred, maintenance of pressure equilibrium is achieved by redistribution of blood volume from extra-throacic to intra-thoracic
- leads to edema and capillary rupture
when does decompression sickness occur?
- decreased breathing over-saturates tissues with nitrogen
- decreased pressure causes it to leak out too quickly
- N2 can form bubbles which cause pain in joints
what is inert gas narcosis?
- increased N2 causes euphoria/loss of coordination, coma
what are the effects of high O2 for prolonged periods of time?
- in CNS- vomiting/dizzy/vision/hearing impairment (confusion/seizures/coma @ 4ATM)
- in Lung- lower tolerance- high O2 can cause damage of endothelial cells/pulmonary capillaries/ substernal pain, impaired gas exchange, etc.
what can hyperbaric O2 therapy be used for?
- CO poisoning
- anemic crisis
- gas gangrene
- impaired bone/wound healing
