Respiratory Flashcards
How much do you expect pH to decrease with increase in CO2?
decrease 0.08 for every 10 mmHg CO2 rise
Infectious insult + Impaired bacterial clearance = dyspnea, hemoptysis, daily mucopurulent sputum, crackles, wheezing
Bronchiectasis
Etiologies of bronchiectasis
- cancer (airway obstruction)
- autoimmune (RA, Sjogrens)
- Aspergillosis, TB
- Hypogammaglobulinemia
- CF, a1at def (congenital)
most common causes of digital clubbing
- Cystic Fibrosis
- Lung Malignancies
- R to L cardiac shunts
most common adverse effect of inhaled steroids
oral thrush
Triad in obesity hypoventilation syndrome
- obesity
- hypercapnia (daytime)
- alveolar hypoventilation (hypoxmia/resp acidosis)
causes of transudate pleural effusions
CHF
Cirrhosis
Nephrotic Syndrome
Peritoneal dialysis
causes of exudative effusions
Infections
Malignancy
Pulmonary Embolism
Connective tissue dz
Inflammatory dz
Fluid from abdomen
CABG
Light’s criteria for exudative effusions
Having at least 1 of the following
Pleural fluid/serum ratio’s:
- -Protein >.5
- -LDH>.6
- -Pleural Fluid LDH > 2/3 of upper limit normal serum LDH
most common cause of pleural effusion
CHF (and thus transudative)
pt has severe asthma exacerbation with impending resp distress. why is a normal/elevated CO2 a poor sign?
asthma exac causes hyperventilation/increased resp drive = decreased CO2. if elevated/normal, shows respiratory muscle fatigue –> inability to meet respiratory demands.
–>these patients require intubation
whats the difference between enoxaparin, rivaroxaban, and fondaparinux?
Enoxaparin = LMWH Rivaroxaban = Oral Factor X inhibitor Fondaparinux = Injection Factor X inhibitor
None of these can be used in patients with poor renal f(x), use unfractionated heparin instead
Why do you need a heparin bridge before warfarin?
Warfarin inhibits Protein C and S, which are anti-thrombogenic..= state of thrombosis (heparin is anti-thrombin)
Criteria for ARDS (4)
- Acute onset (<1 week)
- Bilateral infiltrates on chest imaging
- Pulm edema not explained by fluid overload or CHF (i.e. PCWP <18) –>NONCARDIOGENIC PULM EDEMA
- Abnormal PaO2/FiO2 ratios (<300)
Pathophys behind ARDS
Massive Intrapulmonary shunting of blood, secondary to atelectasis, alveolar collapse and surfactant dysf(x)
–> Increase in lung fluid = stiff lungs, A-a gradient, ineffective gas exchange
Severe hypoxemia that does not improve on 100% oxygen
ARDS
an increase in ____________ causes ARDS, vs _____ causes cardiogenic pulmonary edema
Alveolar capillary permeability (ARDS)
Congestive Hydrostatic Forces (CHF/HF)
T/F: ARDS will have increase in lung fluid and signs of JVD, edema, hepatomegaly
False. ARDS will have increase in lung fluid without any of those cardiogenic signs
Patients with _____ have the highest risk of developing ARDS
sepsis/septic shock
T/F: Pulmonary vasodilators (nitroprusside) help improve tissue oxygenation
False…they should be removed in states of hypoxia
Does ARDS have respiratory alkalosis or acidosis?
Initially have Alkalosis (PaCO2 <40), which switches to acidosis as the work of breathing increases and thus PaCO2 rises
what is the most useful parameter in distinguishing ARDS from cardiogenic pulmonary edema?
PCWP…this refelcts Left heart filling pressures and indirect marker of intravascular V status….<18 points to ARDS
MAP> ____ (at rest) = Pulm HTN
25
clinical signs of pulmonary htn
- Loud P2 (pulmonic component of S2)
- Subtle lift of sternum (RV dilatation)
- if RV failure occurs, will show JVD/hepatomeg/edema etc