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
how will EKG/Echo help assist in dx of Pulm HTN?
Pulm HTN can lead to RV failure…
-EKG will show RV hypertrophy (Right axis deviation/right atrial abnormality)
-ECHO = dilated pulm artery, dilatation of RA and RV, abnormal movement of ventricular septum
which vasoactive agents can be used in tx of PAH (after R heart cath and trial of vasodilators tried first)
They lower pulm vascular resistance
- PDE inibitors (sildenafil)
- CCB
- Prostacyclins (Epoprostenol)
- Endothelin receptor antagonists (bosentan)
what is cor pulmonale usually secondary to?
COPD!
Defined as RV hypertrophy/failure from pulm htn secondary to pulm disease
PE/Asthma/CF/OSA/ILD also can cause it
Clinical features of cor pulmonale
- decrease exercise tolerance
- Cyanosis and digital clubbing
- RV failure (JVD, edema, hepatomegaly)
- Parasternal lift (RV dilatation)
why is there tachypnea in PE ?
PE causes dead space in areas of the lung because there is ventilation but no perfusion (dec blood flow)
–> causes Hypercarbia and Hypoxemia, which drive respiratory effort
T/F: Most often, PE is clinically silent
True
–>Recurrences are common, leading to chronic pulm HTN and cor pulmonale
What causes most PE-related deaths?
Recurrent PE within first few hours of inital PE…tx with anticoagulatns decreases mortality
Signs of PE
-Tachypnea, Rales, Tachycardia, S4, Increased P2
PaO2 and PaCO2 levels in PE?
Both are low…PaCO2 is low due to hyperventilation (because dec perfusion= hypoxemia and hypercarbia = stimulation to respiratory drive)
=Resp ALKalosis
Initial study of choice for PE
CTa (spiral ct)…only contraindicated if renal dz, for whom V/Q scan works well
Pulmonary angiography = gold standard, but is invasive (rarely performed)
PE clinically likely, do a ______study
PE clinically unlikely, do a ______ study
likely: Spiral CT. if inconclusive, LE ultrasound
Unlikely: D-Dimer. If abnormal, Spiral CT
what should you consider as long term prevention in a patient who had PE but has CI to anticoagulation
IVC filter
Tx for PE
- Heparin drip: start as soon as their is any clinical suspicion (prevent recurrent PE)
- Oxygen
- Consider thrombolytic therapy (not always given tho)
- Consider IVC filter if anticoag CI
where is aspiration most likely to go?
lower portion RUL
upper portion of RLL
most common causes of acute dyspnea
CHF exacerbation pneumonia bronchospasm PE anxiety
causes of high DLCO
- Asthma (increases pulm capillary blood V)
- Obesity
- Intracardiac L-R shunt
- Exercise
- Pulmonary hemorrhage
causes of low DLCO
- Emphysema
- Sarocoidosis
- Fibrosis
- Pulmonary vascular dz
- Anemia (reduced binding of CO to Hgb)
For every 10mm Hg change in PaCO2, there should be a change in pH by ___
.08
- if change is in same direction as change in PaCO2, its metabolic
- if inverse, respiratory
T/F: Restrictive dz has reduced FEV1 and reduced FEV1/FVC ratio
False.
Restrictive has reduced FEV1.
However, ratio is actually normal or increased because of FVC decrease
signs of ILD
- Inspiratory crackles, digital clubbing
- Progressive exertional dyspnea, persistent dry cough
- CXR = reticular/nodular opacities
Pulmonary function tests in ILD
- normal or increased FEV1/FVC
- decreased DLCO
- decreased TLC
- decreased RV
will also see increased A-a gradient
What is the pathophys behind changes to A-a gradient and DLCO in ILD (i.e. pulmonary fibrosis)?
Get peri-alveolar collagen deposition
=decreased gas exchange (A-a) and reduced diffusion capacity of CO
Tx of SIADH
FLUID RESTRICTION +/- salt tablets
Hypertonic saline is only used for severe hyponatremia (sxs of coma, seizure, etc)
Progressive exertional dyspnea + dry cough
ILD ILD ILD ILD ILD ILD ILD ILD
Low FEV1/FVC ratio + increased or decreased DLCO
Low ratio = Obstructive dz
Increased DLCO = Asthma (inc. pulm capillary blood V)
Decreased DLCO = COPD
Normal/high FEV1/FVC ratio + increased or decreased DLCO
Normal/high ratio = Restrictive dz
Increased DLCO = Chest wall weakness
Decreased DLCO = ILD
why is there pulmonary hypertension in ARDS?
hypoxic vasoconstriction
2 ways by which oxygenation can be improved in ARDS pt
- Increasing fraction of inspired O2 (FiO2)
- PEEP (via mechanical ventilator)
–>You want to wean FiO2 to <60% asap to avoid risk of oxygen toxicity (free radicals), so once you’re higher than this you should increase PEEP
most common trigger of COPD exacerbation
URI
Why is FVC decreased in COPD
Air Trapping due to progressive airflow limitation
solitary nodule > ____ likely malignancy
2cm
most common primary lung cancer in smokers and nonsmokers
Adenocarcinoma
non-allergic vs allergic rhinitis
Allergic: predom eye sxs, itching, sneezing, identifiable triggers
NAR: Predominant nasal congestion w/o obvious triggers. antihistamine or glucocorticoids.
in patient tx for CAP (esp in pt >65)
Fluoroquinolone or beta lactam/macrolide (cef/azithro)
Name the mediastinal mass by location:
- Anterior mediastinum
- Middle
- Posterior
Anterior: THYMOMA, retrosternal thyroid, teratoma
Middle: Bronchogenic Cyst, Aortic arch aneurysm
Posterior: all neurogenics i.e. neuroblastoma, esophageal tumor
t/f: panacinar emphysema of a1-antitrypsin def is present diffusely throughout the lungs
false, it is predominantly in the lower bases (vs smoking emphysema which is in upper lobes). Presents in 30-40s
Whats the next step if you suspect CAP based on sxs (few days of fever, cough, and crackles on exam)?
Need CXR to make dx!! Then you can do empiric antibiotics (don’t need cultures)
3 most common causes of chronic cough
- Upper-airway cough syndrome (POSTNASAL DRIP)
- ->responds to anti-histamines - Asthma
- GERD
Simple rule of thumb for pleural effusions (exudative vs transudative)
Transudative: Organs failure…heart (chf), liver (cirrhosis, low albumin), lung (PE, atelectasis), kidneys (nephrotic, low albumin)
Exudative: Infectious, Cancerous (ICE ICE Baby)
If someone has a parapneumonic effusion, what should you be looking out for?
Empyema. Look for a pt who has received antibiotics but continues to be ill.
Empyema vs parapnuemonic effusion
- pH
- Glucose
- Protein
- wbcs
Parapneumonic: Glucose dec, protein inc, pH >7.2, wbc <50k
Empyema: Glucose dec, protein inc, pH <7.2, wbc >50k
orthostatic hypotension usually presents in elder patients, due to _______ ; which lab value should you follow?
Hypovolemia Urine Na (hypovolemia = dec renal perfusion = RAAS = decreased urine Na)
classic triad of fat emboli
Hypoxemia
NEURO dysf(x)
RASH
Why would an asthmatic have elevated wbc’s after an acute exacerbation?
Most likely will get some glucocorticoid therapy, which causes leukocytosis (by released marginated neutrophils)