respiratory Flashcards
neonatal respiratory distress: 1. pathophys 2. clin presentation 3. imaging+labs 4. risk factors 5. complications 6. trx
- surfactant deficiency –> alveolar collapse from inc surface tension aka “hyaline membrane ds”, essentially atelectasis of the neonate 2. severe hypoxemia from poor ventilation 3. ground glass appearance of all lung fields, inc pCO2, inc intrauterine insulin… 4. maternal diabetes (↑ insulin in fetus –> ↓ surfactant production ), C-section delivery (no release of natural steroids from stress of vaginal delivery) 5. PDA, necrotizing enterocolitis, [w trx of O2–>] **RIB**: Retinopathy of prematurity (can lead to blindness), Intraventricular hemorrhage, Bronchopulmonary dysplasia (w airway fibrosis)
at what embryologic point are the fetal lungs mature, and how is this defined? what is given for lung maturation for preterm babies born this point (be specific)
@ 35 weeks = where is enough surfactant betamethasone to stimulate surfactant production
how is the pulmonary A related to the bronchus at each lung hilum??
**RALS** pulm a is Anterior to R bronchus, Superior to L bronchus
what structures perforate the diaphragm and at what levels
**I ate ten eggs at twelve** T8= IVC and R phrenic N T10= esophagus + CN10 T12= aortia, thoracic duct, + azygos V **@ T-1-2, its red, white, and blue**
pain from the diaphragm can be referred to where?
shoulder = C5 trapezius ridge = C3-4
where are inhaled foreign bodies likely to land? be specific, depending on position @ time of aspiration
upright - inferior lobe, lower part of R lung supine= R inferior lobe, apex R upper lobe, posterior segment
define RV, ERV, IRV, TV, IC, VC, TC, FRC
RV= cannot be measured, the air still in lung after full expiration ERV= air that has to be forcefully exhaled IRV= air that has to be forcefully inhaled TV= quiet breathing volume= air brought in w each quiet inspiration TV+IRV = inspiratory capacity TV+IRV+ERV = vital capacity TV+IRV+ERV+RV = total capacity RV+ERV = Functional residual capacity = where lungs balance @ end of a quiet breath
define physiologic dead space, where is this primarily found?
= anatomic DS (nose/trachea) + volume of alveoli that don’t exchange gas (V/Q= infinity) mostly at apex of lungs
higher than normal lung tissue compliance ∝ what pathologies? lower than normal compliance ∝ what pathologies?
- high compliance ∝ emphysema, normal aging -low compliance ∝ pulmonary fibrosis, pneumonia, NRDS, pulmonary edema
what is the function of 2,3 BPG
exists in RBCs promote O2 release from Hgb ↑ levels in RBC –> ↓ affinity for O2 –> ↑ O2 released to tissues
what is methemoglobin how does it clinically present how can it be treated
- oxidized form of Hn (Fe3+) that doesn’t bind O2 –> left shift + makes remaining iron binding sites on that Hgb unable to release O2 to tissue 2. cyanosis and chocolate colored blood classic pt: endoscopy patient after BENZOCAINE spray was used for analgesia, now they have SOB post-op even tho their pulseOx is 80-90 and ABGs are normal 3. trx with methylene blue and Vit C **trx METHgb w METHylene blue**
what is carboxyhemoglobin how does it clinically present how can it be treated
- form of Hb bound to CO in place of O2–> cause left shift 2. presents with HA, dizziness, and cherry red skin (bright red lips: inc RR will delay cyanosis) ∝ w fires, car exhaust, gas heater 3. trx w 100% O2
how does cyanide poisoning present? how do you treat?
– hypoxia unresponsive to supplemental O2 -increased anaerobic metabolism present -almond breath order, pink skin, cyanosis trx by inducing methemoglobinemia (give nitrates, followed by thiosulfates) also give B12
what factors cause left vs right shift of teh O2-Hgb curve? HgF is shifted which way?
LEFT = hold on tighter ( **L for Lungs**) -less acidic (higher pH), lower pCO2, lower 2,3 BPG, lower Temp RIght shift: acidity (low pH), higher pCO2/2,3BPG/Temp HgF= shifted left= higher affinity to get O2 from maternal circulation
anemia vs polycythemia [Hb] %O2 sat PaO2 (dissolved O2) total O2 content
anemia: [Hb] ——————————- ↓ %O2 sat————————– n PaO2 (dissolved O2) ——- n total O2 content ————–↓ polycythemia: [Hb] ——————————- ↑ %O2 sat————————– n PaO2 (dissolved O2) ——- n total O2 content ————–↑
anatomically outline the pathway of blood through the lungs what 3 factors will change the pulmonary arterial pressure, potentially cause pulmonary HTN -what conditions affect these three parameters?
right ventricle –> pulmonary A –> capillaries of alveoli –> pulmonary V –> left atrium Pa= CO x PVR x P(LA) Cardiac Output (into the Pulm a) ∝ L–>R shunt (↑), ASD/VSD/PDA (BF asc aorta–>pulm A) PVR ∝ ↑ w ↑ ARTERIAL flow 1 °= rare= young F w inc endothelin and dec NO bc BHR2 mutation (trx w sildenafil) 2°= COPD, chronic pulm embol, pulm fibrosis (i.e. scleroderma), sleep apnea, high altitude, HIV P(LA): most common cause Pulm HTN ∝ HF, valvular ds
clinical presentation of pulmonary HTN
loud P2 heart sound (= 2nd heart sound @ left upper sternal border) –> dyspnea if untrx, can lead to cor pulmonale
CAUSES OF HYPOXIA hypoxemia vs HF vs anemia vs CO poisoning O2 content Pa(O2) %O2 sat
hypoxemia: O2 content —–↓ Pa(O2) ————↓ %O2 sat ———-↓ HF: (but dc BF–> hypoxia) O2 content —–n Pa(O2) ————n %O2 sat ———-n anemia: O2 content —–↓ Pa(O2) ————n %O2 sat ———-n CO poisoning O2 content —–↓ Pa(O2) ————n %O2 sat ———-↓
in what situations do you have hypoxemia with a normal A-a (arterial-alveolar) gradient? in what situations do you have hypoxemia with a high A-a gradient?
n A-a gradient = -high altitude, hypoventilation (opiates) high A-a gradient= (alveoli no working, get O2 into blood OR the wrong alveoli are being ventilated) -V/Q mismatch = -via shunting= pulmonary edema (no hypercapnia, 100% O2 no help hypoxemia, need to resolve obstruction) -via inc deadspace = pulm embolism (hypercapnia present, will improve w 100%O2) -diffusion limitation = pulmonary fibrosis -R–>L shunt
describe the ventilation and perfusion (V/Q) ration throughout the lung
-apex= v dec perfusion = ↑ (V/Q) -base= v inc perfusion= ↓(V/Q)
what lab values are and are not reliable for the determination of whether a patient is hypoventilating? in what situations do patients often need mechanical ventilation support?
-hypoventilation can be masked by normal PaO2 levels with O2 administration -check PaCO2 levels to determine more accurately (↑ CO2 ∝ w hypoventilation) -mechanical ventilation helpful in pneumonia, COPD, and asthma -NSMK ds (i.e. ALS) where resp M are no reliable may also need
what are the ways in which CO2 are transported in the blood
-bicarb (carbonic anydrase.. Cl-HCO3 membrane antiporter). [inc Cl- in venous blood as it is brought in to transport HCO3 out of lungs) =in RBCs -carboxyhemoglobin =in RBCs -dissolved CO2
what is the physiologic response to high altitude what medication can be given to help with compensation efforts
–increased ventilation–> respiratory alkalosis –renal excretion of HCOs (met acid) to compensate *can give acetazolamide to augment the compensation* –inc EPO–> inc Hct and Hgb – chronic –> pulm HTN+ RV hypertrophy
how does cerebral BF react to changes in O2 and CO2 levels explain how a panic attack affects CBF
O2 levels do not change CBF ↑ CO2 levels -> inc CBF panic attack: hyperventilation –> hypocapnia –> cerebral vasoconstriction to ↓ CBF –> dizziness, blurred vision, etc
head and neck CAs are mostly what type of CA?? risk factors
mostly squamous cell carcinoma risk: tobacco, alc, HPV-16 for oropharyngeal, EBV for nasopharyngeal carcinogen damage
epistaxis most commonly occurs in what part of the nostril and is related to what BVs?? life threatening hemorrhages occur in what part of the hemorrhages and is related to what BVs?? clin presentation of nasal angiofibromas?
epistaxis= mostly anterior segment Kiesselback plexus= superior Labial a, ant+post Ethmoidal a, Greater palatine a, Sphenopalatine a **kiesselbach drives his lexus w his L.E.G.S** life-threatening = posterior segment sphenopalatine A nasal angiofibromas= common cause of bleeding= common in adolescent males
examples of pathologies with dull vs hyperresonant percussion of the lungs
dulls= pleural effusion, pneumonia (consolidation) hyperresonant= pneumothorax, emphysema
rales heard at the bases are ∝
∝ pulmonary edema (gravity pulls fluid down)
rales heard diffusely throughout the lungs are ∝
interstitial fibrosis =sticky, fibrous tissue
classic pathology associated w wheezes? can also be ∝ w?
asthma (during an exacerbation) ∝HF (“cardiac asthma”), chronic bronchitis, localized obstructions (tumors)
rhonchi diffusely heard in all lung fields are classically ∝ w?
COPD exacerbation
bronchial breath sounds = what? +longer than normal expiratory wheeze is ∝ w?
pneumonia w consolidation
stridor is classically ∝ w ?
laryngotracheitis (aka croup) epiglottitis (rare but in unvaccinated kids) retropharyngeal abscess diphtheria (membrane of inflamed tissue at back of throat)
(+) pectoriloquy (bronchophony, whispered, egophany) are associated with what pathologies?
fluid in lungs =pleural effusion =consolidations (pneumonia)
who are the potential culptrits of drug induced interstitial lung disease, and how does it present
describe the pathogenesis of high output cardiac failure
what does each wave in the below jugular venous pressure tracing represent
clinical presentation of aortic dissection
complications of a dissection
aortic aneurysm vs aortic dissection
An aortic aneurysm occurs when a weak spot in the wall of your aorta begins to bulge . This can occur anywhere in your aorta. Having an aneurysm increases the risk of an aortic dissection — a tear in the lining of the aorta,
