ABIM 2015 - Pulm Flashcards
Patients with DYSPNEA, those with KNOWN LUNG disease or to establish a BASELINE prior to a treatment or new job with potential LUNG injury, during PRE-OP period (thoracic surgery or LUNG resection), usually undergo what testing?
PULMONARY FUNCTION TESTS (PFT’s)
Most widely used pulmonary function test which measures the FORCED EXPIRATORY VOLUME (FORCED VITAL CAPACITY - FVC) over TIME after a patient has taken a DEEP INSPIRATION?
SPIROMETRY
After a patient takes a MAXIMAL (as much as they can), DEEP INSPIRATION, they are told to EXHALE FORCEFULLY, their ENTIRE BREATH, OVER 6-12 SECONDS. This is known as what component of SPIROMETRY?
FORCED VITAL CAPACITY (FVC)
What is FEV1 in spirometry?
The FORCED EXPIRATORY VOLUME (FVC) in ONE SECOND
The smaller the FEV1 is the smaller the FEV1/FVC will be, and if FEV1/FVC is
AIRWAY OBSTRUCTION
When a BRONCHODILATOR is given (to try and relieve an AIRWAY OBSTRUCTION that is caused by INFLAMMATION or IRRITATION of the AIRWAYS (bronchi), what is considered a “REVERSIBLE” airway obstruction?
An increase of FEV1/FVC ≥12% (or ≥200 mL)
What is best to review when performing SPIROMETRY testing in a patient in order to rule out poor test results such as due to a SLOW START, HESITATION or COUGH while a patient tries to perform the test?
FLOW-VOLUME CURVE (flow volume loop)
Conditions such as ASTHMA, ALLERGIES, VIRAL INFECTIONS, SMOKING, BRONCHITIS and CYSTIC FIBROSIS affect the airways in what way?
Make them HYPERRESPOSIVE
What test is performed to assess airway HYPERRESPONSIVENESS which is VERY SENSITIVE (rules OUT disease) for ASTHMA but NOT SPECIFIC (rules IN disease) - meaning if the test is negative, its NOT asthma, however if the test is positive, it CAN be asthma, but it can also be lots of other things like allergies, viral infections, the effects of smoking, bronchitis and cystic fibrosis)?
Bronchial Challenge Testing
In performing this test, SERIAL SPIROMETRY measurements are obtained while the patient is given INCREASING concentrations of an INHALED medication that causes BRONCHOCONSTRICTION - irritation of the airways (bronchi)?
Bronchial Challenge Testing
When is a Bronchial Challenge Test considered POSITIVE?
When the FEV1/FVC is DECREASED by ≥20% from BASELINE
What happens to the Bronchial Challenge Test if a patient with ASTHMA used their BRONCHODILATOR medication recently OR the test was IMPROPERLY PERFORMED OR the patient has SEASONAL/OCCUPATIONAL ASTHMA WITHOUT recent exposures?
FALSE NEGATIVE TEST
What is the ONLY USE for the Bronchial Challenge Test?
To RULE OUT or “exclude” (high SENSITIVITY) ASTHMA in patients with NORMAL SPIROMETRY and symptoms consistent with but not typical of ASTHMA
What are the agents METACHOLINE, HISTAMINE and MANNITOL used for?
These are DIRECT BRONCHIAL IRRITATING agents used in BRONCHIAL CHALLENGE TESTING (used to EXCLUDE ASTHMA)
HOW is MANNITOL a different and BETTER agent to use in BRONCHIAL CHALLENGE TESTING when attempting to EXCLUDE a diagnosis of ASTHMA?
Because it is an INDIRECT BRONCHOCONSTRICTING agent in that is causes the release of ENDOGENOUS mediators when inhaled, which cause airway (bronchial) smooth muscle constriction (more accurate in determining an underlying airway inflammation)
The volume of air contained in the lung after a FULL INHALATION? What is the normal volume?
TOTAL LUNG Capacity (TLC)
Normal volume is 6 L
The volume of air that can be INSPIRED AFTER a NORMAL INSPIRATION?
INSPIRATORY Capacity (IC)
The MAXIMAL volume of air that can be EXPELLED from the lungs AFTER a NORMAL EXPIRATION?
EXPIRATORY RESERVE Volume (ERV)
The volume of air LEFT in the lungs AFTER a FORCED EXHALATION (cannot be measured, only calculated)?
RESIDUAL Volume (RV)
The most amount of air a person can INHALE and EXHALE are called?
INSPIRED VITAL Capacity (IVC) and EXPIRED VITAL Capacity (EVC)
The TOTAL volume of air DISPLACED during a normal INSPIRATION and EXPIRATION WITHOUT any additional EFFOR is called? What is the normal volume for inspiration?
TIDAL Volume (TV) Normal is 500 mL or 7 mL/kg
When the Total Lung Capacity (TLC) is
CHEST RESTRICTION (parenchymal - pulmonary fibrosis or respiratory muscle weakness - neuromuscular disease)
What happens to ALL lung volumes in RESTRICTIVE lung disease (pulmonary fibrosis or neuromuscular disease)?
They are ALL reduced in parallel
Describe DLCO?
A patient has his nose pinched and is connected to a machine via his mouth. He is asked to take a deep breath (of carbon monoxide - CO), hold for one second, then exhale all of it out again. A computer measures HOW MUCH CO was INHALED and SUBTRACTS from this volume HOW MUCH CO was EXHALED. The resulting DIFFERENCE is HOW MUCH CO was DIFFUSED from the ALVEOLI into the BLOOD
In what TYPE of RESTRICTIVE LUNG DISEASE is the DLCO reduced?
In those that affect the PARENCHYMA of the lung (destruction of the alveolar-capillary bed)
What type of lung disease is suspected in a patient with REDUCED BOTH FVC and FEV1 with a NORMAL or HIGHER than NORMAL FEV1/FVC ratio?
RESTRICTIVE LUNG DISEASE
How is CHEST RESTRICTION confirmed, with what LUNG VOLUME test?
Total Lung Capacity (TLC)
In what diseases is there a LOSS of SURFACE for GAS EXCHANGE?
EMPHYSEMA, Pulmonary FIBROSIS, Pulmonary EDEMA and PNEUMONIA (infiltration)
When can the DLCO be LOW in the ABSENCE of LUNG DISEASE?
If there is something wrong with the VASCULATURE or BLOOD (ANEMIA, PULMONARY HTN)
When can the DLCO be HIGHER than NORMAL?
ASTHMA (increased blood volume and inflammation), Pulmonary HEMORRHAGE (faster uptake by RBC’s in the airspaces)
How much does the DLCO have to be REDUCED by in order to result in SYMPTOMS of DYSPNEA on EXERTION and potential need for supplemental OXYGEN?
DLCO
Why should PULSE OXIMETRY NOT be used in patients with FIRE/SMOKE or CO INHALATION?
BECAUSE the Pulse Oximeter CANNOT distinguish between OXYhemoglobin (O2-Hb complex) and CARBOXYhemoglobin (CO-Hb complex)
When a patient with suspected DECREASE in Partial Pressure of Oxygen (PO2) due to ALTITUDE SICKNESS or in a patient with HYPOventilation (increasing CO2), what MUST be done to get an ACCURATE measure of patient OXYGENATION (oxygen saturation)?
Arterial Blood Gas (ABG), CANNOT use Pulse Oximetry
An imaging test that is BEST for quickly assessing the DISTRIBUTION and PATTERN of PARENCHYMAL LUNG DISEASE as well as assessing short-term RESPONSE to TREATMENT (as in pneumonia, pneumothorax or CHF) is?
CXR
Where would the DISTRIBUTION of LUNG OPACITIES be demonstrated on a CXR in diseases such as SARCOIDOSIS, SILICOSIS, CYSTIC FIBROSIS, LANGERHANS CELL HISTIOCYTOSIS and REACTIVATION TB?
UPPER LUNG LOBES
Where would the DISTRIBUTION of LUNG OPACITIES be demonstrated on a CXR in diseases such as PULMONARY FIBROSIS, CRYPTOGENIC ORGANIZING PNEUMONIA, ASBESTOSIS and HEART FAILURE (CHF)?
LOWER LUNG LOBES
Diagnosis of Idiopathic Pulmonary Fibrosis, distinguishing between PULMONARY LN’s and Vessels (especially in hilar areas), evaluation of LIVER and ADRENAL GLANDS for METASTASES, identifying vascular abnormalities such as DISSECTION or THROMBOSIS and evaluating for suspected PE, is best made with this IMAGING MODALITY?
CT-scan (CT-angiography for PE)
Cancer cells have a HIGHER rate of glycolysis (however so are TB, FUNGAL diseases, Infections, Sarcoidosis and other Inflammatory conditions - FALSE POSITIVES) compared to non-neoplastic cells and can be detected EXCEPT for when they are
PET-CT
Although suggested on PET-CT scans, BEFORE deciding on SURGERY CANDIDACY for a LUNG or other CANCER, a POSSIBLE DISTANT METASTATIC FOCUS needs to be evaluated how?
BIOPSY
What IMAGING MODALITY is best for RIB Fractures, Pneumothorax, Pleural Effusion, HF, Pneumonia, Device/Line/Tube placement, Follow-Up or a recognized disorder?
CXR
What IMAGING MODALITY is best for Diffuse Parenchymal Lung Disease, Bronchiolitis, Bronchiectasis, Lung Masses, Lymphadenopathy, Lung Nodules, PE and Guidance for Fine Needle Aspiration Biopsy?
CT-scan
What IMAGING MODALITY is best for LUNG CANCER STAGING and DETAILED evaluation of a MASS/NODULE?
PET-CT
What is an effective method for sampling CENTRAL airway lesions, MEDIASTINAL LN’s and parenchymal MASSES?
Bronchoscopy
What Diagnostic Imaging modality can be used for lung cancer staging that is COMPARABLE to MEDIASTINOSCOPY?
Endobronchial Ultrasound (EBUS)
What does it mean when a BRONCHOALVEOLAR LAVAGE is performed and 95% of the cells are alveolar macrophages?
NORMAL LAVAGE
What does it mean when a BRONCHOALVEOLAR LAVAGE is performed and there is LEUKOCYTOSIS, NEUTROPHILIA or EOSINOPHILIA?
Infection (can further characterize by Bronchoscopy w/biopsy)
What are the THERAPEUTIC ROLES of Bronchoscopy?
Mucus PLUG Clearance, Foreign Body REMOVAL, DEBULKING central tumors, AIRWAY DILATION and STENT placement
Airway inflammation related to allergies, increased airway responsiveness with EPISODIC COUGH (productive of THICK SPUTUM), CHEST TIGHTNESS, SOB and WHEEZING?
ASTHMA
When patients with this disease are EXPOSED to an ALLERGEN, they develop an EARLY RESPONSE (15-30 minutes AFTER EXPOSURE) that resolves in 1-2 HOURS and 50% of these patients will also develop a LATE RESPONSE (3-8 HOURS AFTER EXPOSURE)?
ASTHMA
What can uncontrolled inflammation and repeat exacerbations in ASTHMA lead to?
AIRWAY REMODELING (structural airway changes)
The majority of ASTHMA patients have what underlying triggers for the disease?
Allergies (demonstrated by skin testing)
What occurs over time in the lung function of asthmatic patients?
It declines over time
Biopsy of an affected airway with this disease demonstrates eosinophils, mast cells, lymphocytes and neutrophils with sub-epithelial fibrosis, mucus gland hyperplasia and increased smooth muscle mass in the airways?
ASTHMA
Increased sub-epithelial fibrosis, increased smooth muscle mass and mucus gland hyperplasia are together signs of what?
Airway REMODELING in ASTHMA
A patient with EPISODIC cough, productive of thick sputum, without fever, usually late at night or in the early morning, triggered by viral URI’s, COLD air, STRESS and exercise besides allergies likely has?
ASTHMA
What can OSA, GERD, OBESITY, and Vocal Cord Dysfunction do to Asthma?
Worsen it
What does SPIROMETRY demonstrate in ASTHMA?
Airway Obstruction (LOW FEV1/FVC) with REVERSIBILITY (>12% improvement in FEV1 with bronchodilator)
If suspecting ASTHMA in a patient with NORMAL SPIROMETRY, what should be done NEXT?
Bronchial CHALLENGE test (HIGH SENSITIVITY)
How should you test an ASTHMA patient for allergies?
SKIN testing or if not available, RAST testing (IgE)
In a patient with ASTHMA, when during the day is their highest LUNG function and when is the lowest (diurnal)?
Highest lung function is in the mid-afternoon and lowest is in the MORNING
An occupational ASTHMA (cough, dyspnea, chest tightness) disorder that occurs MINUTES to HOURS after a SINGLE accidental EXPOSURE to high levels of irritant vapors, gases or fumes (chlorine gas, bleach, ammonia) leading to airway injury with PERSISTENT inflammation, dysfunction and hyperresponsiveness?
Reactive Airway Dysfunction Syndrome (RADS) - positive bronchial challenge test but may or may not have obstruction demonstrated on spirometry
Do patients with Reactive Airway Dysfunction Syndrome (RADS) have a history of ASTHMA or allergic sensitization to the offending irritant PRIOR to the accidental exposure?
NO!!
What can happen to ASTHMA control in a patient who gets a VIRAL URI (rhinovirus, RSV, influenza)?
Loss of control
What should a patient with ASTHMA with a MILD exacerbation due to a VIRAL URI?
Increase FREQUENCY of inhaled bronchodilator, START inhaled CORTICOSTEROIDS or ADDING a LONG-ACTING INHALED β-2 AGONIST BRONCHODILATOR
What should a patient with ASTHMA with a SEVERE exacerbation due to a VIRAL URI?
SYSTEMIC CORTICOSTEROIDS (5-7 DAYS)
After a VIRAL URI, how long does the exacerbated airway hyperresponsiveness last?
4-6 WEEKS
What is DIFFERENT about “COUGH-VARIANT” ASTHMA?
The cough is DRY
An older patient who smokes presents with COUGH and some asthma type symptoms, SPIROMETRY shows
Likely COPD
ABRUPT onset of MONOPHONIC WHEEZE, in younger patients?
Vocal Cord Dysfunction
A patient presents with DYSPNEA and a WHEEZE, CRACKLES on auscultation, LIMITED response to asthma therapy, CARDIOMEGALY, EDEMA, ELEVATED BNP (except for in OBSESE patients due to aromatase action), what do they have?
CHF
A cough productive of a LARGE amount of PURULENT sputum, RHONCHI and CRACKLES with WHEEZING and MAY HAVE CLUBBING?
BRONCHIECTASIS
RECURRENT infiltrates on CXR, EOSINOPHILIA, HIGH IgE levels and frequent need for CORTICOSTEROID TREATMENTS?
Allergic Bronchopulmonary Aspergillosis (ABPA)
A cough productive of a LARGE amount of PURULENT sputum, RHONCHI and CRACKLES and PROMINENT CLUBBING, MAY HAVE WHEEZING?
Cystic Fibrosis
LOCALIZED WHEEZING?
Mechanical Obstruction
When a patient has ASTHMA that is difficult to control and has typically more COUGH symptoms than other symptoms, what should be considered?
GERD
Would patients with GERD that is not symptomatic and ASTHMA benefit from GERD treatment as far as ASTHMA treatment is concerned?
NO!!
A patient who has difficulty ACHIEVING control of their ASTHMA with usual therapy or who has FREQUENT EXACERBATIONS requiring SYSTEMIC CORTICOSTEROIDS should be tested with a CXR for what?
Allergic Bronchopulmonary Aspergillosis - ABPA - (recurrent pulmonary infiltrates or bronchiectasis on CXR)
The UBIQUITOUS fungus that colonizes the ABNORMAL AIRWAYS in patients with ASTHMA or CYSTIC FIBROSIS with development of immune responses that cause pulmonary INFLAMMATION, BRONCHIECTASIS and FIBROSIS?
Aspergillus Fumigatus
Diagnosing this disease requires an elevated serum IgE (total and specific for this particular pathogen), POSITIVE SKIN test for the pathogen and EOSINOPHILIA?
Allergic Bronchopulmonary Aspergillosis (ABPA) - Aspergillus Fumigatus
CT scan shows MUCUS occlusion of the PROXIMAL airways with atelectasis?
BRONCHIECTASIS
How is Allergic Bronchopulmonary Aspergillosis treated?
SYSTEMIC corticosteroids + INHALED corticosteroids WITH bronchodilator RESCUE therapy with TAPER of SYSTEMIC corticosteroids once disease is under control
What can happen if Allergic Bronchopulmonary Aspergillosis is left untreated or POORLY controlled?
Progressive PULMONARY FIBROSIS (restrictive disease - with reduced DLCO) that leads to LOSS of lung function
A patient with ASTHMA breathing COLD, DRY air during INTENSE EXERCISE can cause what?
Exercise-Induced Bronchospasm (EIB) - bronchial obstruction that PEAKS 5-10 MINUTES after CESSATION of exercise and RESOLVES within 30 minutes
When are the SYMPTOMS of Exercise-Induced Bronchospasm (EIB) at their worst?
Immediately following CESSATION of EXERCISE
How are patients with Exercise-Induced Bronchospasm (EIB) prophylactically treated so that they CAN exercise without SYMPTOMS?
They are given a SHORT-ACTING INHALED β-2 AGONIST 15 MINUTES BEFORE exercise which lasts for ~3 HOURS
Gradual WARM-UP before INTENSE exercise, using a MASK over the NOSE & MOUTH during COLD weather and AVOIDING HIGH-INTENSITY INTERMITTENT exercise are non-pharmacological measures to prevent what?
Exercise-Induced Bronchospasm (EIB)
What should be suspected when a patient with ASTHMA presents with an ABRUPT-ONSET of an episode with LOUDER WHEEZING on INSPIRATION (stridor) and ABRUPT TERMINATION?
Vocal Cord Dysfunction (monophonic wheezing, loudest over the neck)
Monophonic wheezing, loudest over the neck?
Vocal Cord Dysfunction (VCD)
Polyphonic Wheezing, loudest over the chest?
ASTHMA
How can you diagnose vocal cord dysfunction?
Laryngoscopy (shows vocal cords coming TOGETHER - adduction - when the patient is trying to breath - they are SUPPOSED to move apart)
How is Vocal Cord Dysfunction treated?
Patient EDUCATION, BEHAVIOR modification and SPEECH therapy
How are ACUTE attacks of Vocal Cord Dysfunction treated?
Inhaled Helium-Oxygen mixture and/or CPAP (Continuous Positive Airway Pressure)
What is the SAMTER TRIAD in those patients who have ASPIRIN-SENSITIVE ASTHMA?
SEVERE asthma, ASPIRIN sensitivity and NASAL POLYPS
How OFTEN does a patient with “OPTIMAL” asthma control use their inhaler?
What types of ASTHMA medications are the following: INHALED SHORT-ACTING β-2 AGONISTS, SHORT-ACTING ANTICHOLINERGICS?
Asthma RELIEVERS (used INTERMITTENTLY as needed)
What types of ASTHMA medications are the following: INHALED CORTICOSTEROIDS, LEUKOTRIENE-modifying drugs, ANTI-IgE therapy (anti-inflammatories); INHALED LONG-ACTING β-2 AGONISTS, SUSTAINED-RELEASE THEOPHYLLINE (methylxanthine - a bronchodilator)?
Asthma CONTROLLERS (used on a REGULAR BASIS)
What are the TWO (2) main CLASSIFICATIONS of ASTHMA?
Intermittent and Persistent
What MODE of drug administration is preferred for ASTHMA to achieve the HIGHEST CONCENTRATION and MINIMIZE SYSTEMIC side effects?
INHALED (pressurized Metered Dose Inhalers - MDI’s OR Dry Powder Inhalers - DPI’s - require fast inhalation of drug)
What is the function of a SPACER when using Metered Dose Inhalers (MDI’s)?
Provides better coordination of inspiration and activation of the MDI (the device containing the aerosolized drug)
What should be evaluated BEFORE starting or ADJUSTING INHALED asthma medications?
Proper INHALER TECHNIQUE (whether MDI - metered dose inhaler with spacer or DPI - dry powder inhaler)
What MEDICATIONS should ALL ASTHMA patients have with them at ALL times?
INHALED SHORT-ACTING β-2 AGONISTS (most effective bronchodilators available - prevent exercise/cold-induced asthma and relieve bronchoconstriction caused by exposure to allergens)
If asthma symptoms are NOT adequately-controlled by allergen avoidance and OCCASIONAL use of INHALED SHORT-ACTING β-2 AGONISTS, what other medication is given?
INHALED LONG-ACTING β-2 AGONISTS (salmeterol/formoterol) are ADDED to INHALED CORTICOSTEROIDS - rapid onset, long duration (12-HOURS)
Is it proper to use INHALED LONG-ACTING β-2 AGONISTS as single-agent therapies in ASTHMA?
NO!! (because they have NO anti-INFLAMMATORY properties) - so they have to be ADDED AFTER inhaled corticosteroids achieve optimal control
What is IPRATROPIUM BROMIDE?
An INHALED, SHORT-ACTING ANTICHOLINERGIC drug (reliever) used in ASTHMA patients EITHER to ENHANCE the bronchodilator effect of INHALED SHORT-ACTING β-2 AGONISTS OR as a RESCUE INHALER in patients with EXCESSIVE SENSITIVITY to β-2 AGONISTS
What is TIOTROPIUM BROMIDE?
An INHALED LONG-ACTING ANTICHOLINERGIC DRUG (controller) that can be ADDED to INHALED CORTICOSTEROIDS INSTEAD of an INHALED LONG-ACTING β-2 AGONIST (salmeterol/formetorol)
What is ALBUTEROL?
An INHALED SHORT-ACTING β-2 AGONIST (reliever)
What are BECLOMETHASONE, FLUTICASONE, MOMETASONE, CICLESONIDE, BUDESONIDE, TRIAMCINOLONE?
INHALED CORTICOSTEROIDS (controllers) used in ASTHMA therapy
What are the MAINSTAY CONTROLLER therapy for ASTHMA?
INHALED CORTICOSTEROIDS
What are the TWO VERY important functions of INHALED CORTICOSTEROIDS?
BLUNT the LATE-PHASE inflammatory response to ALLERGENS in asthma and ENHANCE the EFFECTIVENESS of β-2 AGONISTS
REGULAR used of these medications REDUCE asthma exacerbations, hospitalizations and asthma-related mortality?
INHALED CORTICOSTEROIDS (controllers)
What are the side effects of INHALED CORTICOSTEROIDS?
Cough, Hoarseness and Oral THRUSH (reduced by using inhalational aids - MDI’s - rinsing mouth after each use and using the LOWEST effective dose)
What are side effects that can be seen PARTICULARLY in the ELDERLY with REGULAR use of HIGH-DOSE INHALED CORTICOSTEROIDS?
SYSTEMIC side-effects: weight gain, adrenal gland suppression, osteopenia, skin thinning, glaucoma and cataracts - need to evaluate periodically and STEP-DOWN therapy
These ASTHMA drugs are also controllers and are used PRIMARILY as ADD-ON or ALTERNATIVE therapy to CORTICOSTEROIDS or β-2 AGONISTS and most appropriate for patients with MILD, PERSISTENT asthma who are INTOLERANT of INHALED CORTICOSTEROIDS or have an ASPIRIN SENSITIVITY?
Leukotriene-Modifying DRUGS (montelukast, zafirlukast, zileuton)
What ASTHMA drugs have the side-effects of AGITATION, ANXIETY, HALLUCINATIONS, DEPRESSION, SUICIDAL IDEATIONS and LIVER TOXICITY?
Leukotriene-Modifying DRUGS
Use of this OLD asthma drug requires STRICT DRUG LEVEL monitoring, PREVENTION of drug-drug interactions (with fluoroquinolones) and TOXICITY (TREMOR, HA, NAUSEA, PALPITATIONS, CARDIAC ARRHYTHMIAS, SEIZURES)?
Theophylline (methylxanthine - a bronchodilator)
This ASTHMA drug is used as a SECOND LINE alternative to INHALED CORTICOSTEROIDS for chronic asthma management and should NOT be used in ACUTE asthma exacerbations?
Theophylline (methylxanthine - a bronchodilator)
In patients with SEVERE asthma who have EVIDENCE of ALLERGIES, have ELEVATED IgE levels and remain SYMPTOMATIC in spite of treatment with INHALED corticosteroids and long-acting β-2 agonists, can be treated with what?
OMAlizumab (an IgE blocker)
What is the MOST serious risk with the use of the IgE-blocking asthma drug OMALIZUMAB?
Anaphylactoid Reactions
An asthma patient receiving this anti-IgE DRUG must be monitored for at LEAST 2 HOURS for their first 3 doses and for 1 HOUR after subsequent doses?
OMAlizumab
WHEN is the ONLY time INHALED, LONG-ACTING β-2 AGONISTS be added to asthma therapy?
ONLY AFTER INHALED-CORTICOSTEROID therapy has been optimized
What CLASS/SEVERITY of ASTHMA does a patient have if they have SYMPTOMS ≤2 days/week, awaken at night with symptoms ≤2 x/month, use SHORT-ACTING β-2 AGONIST for SYMPTOM CONTROL (not Exercise-Induced Bronchospasm prevention) ≤2 days/week, have NO interference with normal activity and have a NORMAL FEV1 between exacerbations, NORMAL FEV1/FVC and an FEV1 >80% of predicted and have EXACERBATIONS 0-1/YEAR?
INTERMITTENT (not PERSISTENT - which is further subdivided into mild/moderate/severe))
What CLASS/SEVERITY of ASTHMA does a patient have if they have SYMPTOMS ≥2 days/week but NOT DAILY, awaken with symptoms at night 3-4 x/month, use SHORT-ACTING β-2 AGONIST for SYMPTOM CONTROL (not Exercise-Induced Bronchospasm prevention) >2 days/week but NOT >1 x/day, have MINOR limitations to normal activity, NORMAL FEV1/FVC and an FEV1 >80% of predicted and have EXACERBATIONS >2/YEAR?
PERSISTENT/MILD
What CLASS/SEVERITY of ASTHMA does a patient have if they have SYMPTOMS DAILY, awaken with symptoms at night >1 x/week but NOT NIGHTLY, use SHORT-ACTING β-2 AGONIST for SYMPTOM CONTROL (not Exercise-Induced Bronchospasm prevention) DAILY, have SOME limitations to normal activity, FEV1/FVC REDUCED by 5% and an FEV1 >60% BUT 2/YEAR?
PERSISTENT/MODERATE
What CLASS/SEVERITY of ASTHMA does a patient have if they have SYMPTOMS THROUGHOUT THE DAY, awaken with symptoms at night NIGHTLY, use SHORT-ACTING β-2 AGONIST for SYMPTOM CONTROL (not Exercise-Induced Bronchospasm prevention) SEVERAL TIMES/DAY, have EXTREME limitations to normal activity, FEV1/FVC REDUCED by >5% and an FEV1 2/YEAR?
PERSISTENT/SEVERE
What should be considered in ALL patients with PERSISTENT ALLERGIC asthma?
Subcutaneous ALLERGEN IMMUNOTHERAPY
BEFORE initiating ANY therapy for a patient with ANY CLASS/SEVERITY of ASTHMA, what should be ADDRESSED FIRST?
Education, Environmental control, Management of co-morbidities
What is the preferred treatment for patients who have INTERMITTENT ASTHMA?
SHORT-ACTING β-2 AGONISTS PRN
What is the preferred INITIAL treatment for patients who have PERSISTENT asthma?
LOW-DOSE INHALED CORTICOSTEROIDS (if need more control, ONLY THEN sequentially add LONG-ACTING β-2 AGONISTS or MEDIUM-DOSE INHALED CORTICOSTEROIDS, or HIGH-DOSE INHALED CORTICOSTEROIDS or ORAL CORTICOSTEROIDS, etc.
What are the ALTERNATIVES for INHALED CORTICOSTEROIDS?
Cromolyn (anti-inflammatory, mast-cell destabilizer and anti-histamine), LEUKOTRIENE RECEPTOR ANTAGONISTS (zafirlukast, montelukast), Theophylline (methylxanthine - a bronchodilator)
Can LONG-ACTING β-2 AGONISTS be used as ALTERNATIVES to INHALED CORTICOSTEROIDS?
NO!!! (Cannot be used as single-agents)
What is the STRONGEST REGIMEN for SEVERE ASTHMA CONTROL as an OUTPATIENT?
HIGH-DOSE INHALED CORTICOSTEROIDS + LONG-ACTING β-2 AGONISTS + ORAL (systemic) CORTICOSTEROIDS + OMALIZUMAB
What should be done for ALL PERSISTENT asthma patients who begin to require more and more medications for control?
CONSULTATION by ASTHMA specialist
How many SHORT-ACTING β-2 AGONIST treatments should be given prior to considering a course of ORAL corticosteroids?
3 TREATMENTS, 20-MINUTES APART
In a patient with ASTHMA, what indicates INADEQUATE CONTROL and need for STEPPING UP treatment?
USE of SHORT-ACTING β-2 AGONISTS >2 days/week for SYMPTOM relief NOT prevention of Exercise-Induced Bronchospasm
What would you advise a patient who called and complained of an acute ASTHMA exacerbation?
Increase SHORT-ACTING β-2 AGONISTS and possibly a short-course of SYSTEMIC CORTICOSTEROIDS
If SPIROMETRY is not available, what other test can be done in a clinical setting for an ACUTE asthma exacerbation?
Peak Expiratory Flow Rate (PEFR)
What should be the OUTPATIENT treatment for a patient who scores 40%-69% (moderate exacerbation) or
SHORT-ACTING β-2 AGONISTS and ORAL (SYSTEMIC) CORTICOSTEROIDS (can add inhaled IPRATROPIUM - short-acting anticholinergic drug used to enhance bronchodilator effect or as a rescue med)
How should CORTICOSTEROIDS be administered in SEVERE ASTHMA ATTACKS?
IV
When can a patient with a MILD or SEVERE asthma exacerbation be discharged from the hospital rather than be admitted?
IF Peak Expiratory Flow Rate (PEFR) is >70% 1 HOUR POST treatment and SUSTAINED for AN HOUR (checked again)
Patients with asthma that DO NOT ADHERE to inhaled medications, continue SMOKING, have co-morbidities and severe allergies or chronic sinusitis usually require what type of ASTHMA therapy?
CHRONIC ORAL (SYSTEMIC) CORTCOSTEROID therapy (needs to be addressed with education, close follow-up and an asthma specialist)
What is the ONLY testing MODALITY approved for diagnosing ASTHMA in PREGNANCY?
SPIROMETRY
Low birth WEIGHT, PREMATURE labor, PREECLAMPSIA and increased INFANT MORTALITY can all be seen if this respiratory disease is not well CONTROLLED during pregnancy?
ASTHMA
As INHALED corticosteroids are the MAINSTAY medications for ASTHMA therapy, which is the SAFEST to use during PREGNANCY?
BUDESONIDE (HOWEVER, if a pregnant patient is ALREADY on another inhaled corticosteroid, they can REMAIN on that as NO studies show adverse effects)
What rescue INHALERS should be used by PREGNANT patients for ASTHMA?
SHORT-ACTING β-2 AGONISTS
What is the RECOMMENDED second-line therapy for pregnant patients with ASTHMA ALREADY on INHALED CORTICOSTEROIDS?
LONG-ACTING β-2 AGONISTS
How is an ACUTE, SEVERE ASTHMA attack treated in ANY patient whether PREGNANT or NOT?
SHORT-COURSE of ORAL (SYSTEMIC) CORTICOSTEROIDS
A SLOWLY-PROGRESSIVE INFLAMMATORY disease of the AIRWAYS and LUNG PARENCHYMA characterized by a gradual LOSS of LUNG FUNCTION and increasing OBSTRUCTION to EXPIRATORY airflow?
Chronic Obstructive Pulmonary Disease (COPD)
INFLAMMATORY NARROWING of the small airways (BRONCHOLITIS) with eventual FIBROSIS and proteolytic digestion of supportive lung tissue adjacent to these airways (EMPHYSEMA) causing loss of elasticity which keeps the airways open are seen in lung disease?
COPD
What types of HYPERINFLATION of the lungs are seen in EMPHYSEMA (COPD)?
STATIC (more air STAYS in the lungs after exhalation due to decreased elasticity of the lung) and DYNAMIC (a NEWly inhaled breath begins BEFORE a full EXHALATION has been completed therefore TRAPPING air in the lung with EACH breath)
When is HYPERINFLATION of the lung worsened in a patient with EMPHYSEMA (COPD)?
During COPD EXACERBATION or EXERTION
The VOLUME of GAS INHALED or EXHALED from a person’s LUNGS per MINUTE is known as?
MINUTE ventilation
In this LUNG disease, during a disease exacerbation or during exertion, the Tidal Volume and Respiratory Rate INCREASE, the available time for EXHALATION becomes INSUFFICIENT beginning a vicious CYCLE of AIR TRAPPING and HYPERINFLATION?
EMPHYSEMA (COPD)
This PROCESS FLATTENS and REDUCES the EFFECTIVENESS of the DIAPHRAGM making the use of the ACCESSORY MUSCLES of BREATHING more crucial while also MARKEDLY INCREASING the WORK of BREATHING as CHEST WALL COMPLIANCE DECREASES?
HYPERINFLATION of the lungs (COPD - EMPHYSEMA)
What happens to the DLCO in EMPHYSEMA?
It DECREASES and correlates with the degree of disease
EXPOSURE to ANY TOBACCO smoke, DUSTS and CHEMICALS, POLLUTION as well as GENETIC factors (α-1 anti-trypsin deficiency) are all RISK factors for this LUNG disease?
COPD
Pulmonary HTN, Cor Pulmonale, PNA, PTX, Bronchiectasis, Atelectasis, Lung Cancer are all complications of this LUNG disease?
COPD
What LUNG VOLUME is increased in patients with COPD due to HYPERINFLATION and air trapping?
Residual Volume (RV)
SMOKING, h/o TB, h/o CHRONIC ASTHMA, AIR POLLUTION (burning of wood, charcoal, coal, particulate matter, NO2, CO), OCCUPATIONAL EXPOSURES (crop farming dusts - grain dust, animal farming dusts - organic, ammonia and hydrogen sulfide dusts, mining, concrete manufacturing, construction, iron and steel, plastics, textile, rubber and leather industries, automotive and automotive repair) are RISK factors associated with what LUNG disease?
COPD
How are SMOKING and COPD related?
DOSE related
How are smoking PACK-YEARS calculated?
PACKS smoked/day X YEARS smoked (where one pack is 20 cigarettes and 10 cigarettes is 1/2 pack, etc. ROUNDED UP)
What is the SINGLE most EFFECTIVE way to PREVENT COPD, SLOW PROGRESSION of established disease and IMPROVE SURVIVAL?
SMOKING CESSATION
How are ASTHMA and COPD related?
CHRONIC, POORLY-CONTROLLED ASTHMA ca cause a degree of FIXED airflow OBSTRUCTION similar to COPD
How are TB and COPD related?
TB can cause a degree of LUNG destruction and therefore EXPIRATORY airflow OBSTRUCTION similar to that seen in COPD
PROLONGED inhalation of SMOKE caused by BIOMASS FUELS (wood, charcoal, vegetable matter, animal dung) can cause what LUNG disease?
COPD
The DEFICIENCY of this circulating INHIBITOR of SERINE PROTEASE can cause COPD in patients ≤45, in NON-SMOKERS and in patients with OTHER underlying chronic lung or LIVER disease?
α-1 anti-trypsin deficiency
WEIGHT LOSS, MUSCLE WASTING, WEAKNESS as a result of deconditioning and malnutrition, are EXTRAPULMONARY manifestations of this LUNG disease?
COPD (result in decreased functional status and survival)
What is the FEV1/FVC value that is DIAGNOSTIC for airway OBSTRUCTION (such as seen in asthma and COPD)?
What should EARLY INTERVENTIONS focus on in the TREATMENT of COPD?
PREVENTING and AGGRESSIVELY treating co-morbidities and complications of COPD
What should be suspected in a patient that presents with dyspnea, chronic productive (sputum) cough, intermittent wheezing, DECREASED EXERCISE TOLERANCE, h/o SIGNIFICANT SMOKING or other INHALATIONAL EXPOSURES?
COPD (dyspnea, chronic productive cough, intermittent wheezing - are also seen in patients with ASTHMA)
Hyperresonance and Distant breath sounds are noted in more ADVANCED stages of this LUNG disease?
COPD
How should DIAGNOSTIC SPIROMETRY testing be performed for a patient SUSPECTED of having COPD?
AFTER the administration of an INHALED BRONCHODILATOR because it will IMPROVE the ACCURACY of the study results
How CLOSE measurements made are to a “TRUE” (previously established and recognized) VALUE is called what?
ACCURACY (how close to the BULL’s eye on a target you are)
How CLOSE measurements made are to EACH OTHER is called what?
PRECISION (your grouping on a target)
Post-bronchodilator FEV1/FVC (GOLD - scale of 1 to 4), Dyspnea scale measuring clinical symptoms and frequency of exacerbations (MMRC) and Factors such as BMI (the lower the worst as in ≤21), Obstruction, Dyspnea and Exercise (BODE index) are used for what?
Classification of COPD severity (risk for hospitalization, long-term prognosis and assessment for interventions such as surgery or transplantation)
What is the 4-year survival prediction for a patient with COPD and a BODE index score of ≥7 (BMI, Obstruction, Dyspnea, Exercise)?
≤20% (0-10)
Flattening of the diaphragm on CXR indicates what about a patient with COPD?
CHRONIC and worsening disease
What can a CT of the chest demonstrate about a patient with COPD - EMPHYSEMA?
Destruction of the pulmonary parenchyma
- An FEV1 ≥80% of predicted is a GOLD scale of COPD severity of what?
- An FEV1
- GOLD-1 (mild)
- GOLD-2 (moderate)
- GOLD-3 (severe)
- GOLD-4 (very severe)
What TYPE of medications are the MAINSTAY of COPD management?
INHALED
What should always be evaluated BEFORE considering an adjustment of therapy in a patient with COPD?
INHALER technique used by patient
What should be done for patients diagnosed with COPD that are
Refer to a PULMONARY SPECIALIST
What medication has been shown to reduce the progressive decline in LUNG function in COPD?
NONE
For MILD COPD (FEV1/FVC ≥60% of predicted), for “breakthrough symptoms” and for exacerbations, what is the FIRST-LINE treatment?
SHORT-ACTING β-2 AGONISTS or ANTICHOLINERGIC meds (IPRATROPIUM) either alone or in combination, used on a PRN basis
In patients with COPD, WHEN should a DAILY BRONCHODILATOR treatment be used?
When they are SYMPTOMATIC AND their FEV1/FVC
What medications CAN be used for MONOTHERAPY when treating COPD in a symptomatic patient with FEV1/FVC
EITHER a LONG-ACTING β-2 AGONIST (cannot be used as monotherapy in asthma and must be used as co-therapy with inhaled corticosteroids) or a LONG-ACTING ANTICHOLINERGIC
Salmeterol, Folmoterol, Bambuterol, Indacaterol? Adverse effects?
LONG-ACTING β-2 AGONISTS
Tremors, Tachycardia, Overdose: FATAL
Tiotropium?
LONG-ACTING ANTICHOLINERGIC
After switching classes of MONOTHRAPY drugs used for the treatment of COPD (LONG-ACTING β-2 AGONISTS or ANTICHOLINERGICS) and pt still remains symptomatic or not adequately controlled, what is the NEXT STEP?
COMBINATION therapy (β-2 AGONIST + ANTICHOLINERGIC or INHALED CORTICOSTEROID with EITHER a β-2 AGONIST or ANTICHOLINERGIC or ALL THREE COMBINED if advanced, poorly-controlled disease)
Which INHALED DRUG DELIVERY DEVICES are easiest to use in the elderly with COPD?
NEBULIZERS
Albuterol, Fenoterol, Levabuterol, Metaprotenerol, Pirbuterol, Terbutaline? Adverse effects?
INHALED, SHORT-ACTING β-2 AGONISTS
Tremors, Tachycardia
Ipratropium? Adverse effects?
INHALED, SHORT-ACTING ANTICHOLINERGIC
Dry mouth, Mydriasis (dilation of pupil), tremors, tachycardia, acute narrow-angle glaucoma
Tiotropium, Aclidinium? Adverse effects?
INHALED, LONG-ACTING ANTICHOLINERGIC
Dry mouth, Mydriasis (dilation of pupil), tremors, tachycardia, acute narrow-angle glaucoma
What is the MOST serious SIDE EFFECT of LONG-ACTING β-2 AGONISTS?
DEATH (can be fatal in an OVERDOSE)
Theophylline, Aminophylline? Adverse effects?
Both LONG and SHORT-ACTING METHYLXANTHINE BRONCHODILATORS
Tachycardia, N/V, Sleep disturbance, Narrow therapeutic index (can be TOXIC - FATAL with seizures and anemia)
What is the MOST serious SIDE EFFECT of SHORT or LONG-ACTING METHYLXANTHINE BRONCHODILATORS?
DEATH (can be fatal with anemia and seizures in an overdose due to its NARROW therapeutic index) - Theophylline, Aminophylline
Roflumilast? Adverse effects?
Oral Phosphodiesterase-4 Inhibitor
Diarrhea, Nausea, Backache, Dizziness, Decreased appetite
This medication is an ORAL agent used to REDUCE the RISK of EXACERBATIONS in patients with SEVERE COPD with CHRONIC BRONCHITIS and h/o exacerbations and SHOULD NOT BE USED with METHYLXANTHINES (Theophylline, Aminophylline) due to potential toxicity?
Roflumilast
These medications act by RELAXING the smooth MUSCLES of the airways resulting in WIDENING of the airways which IMPROVES EMPTYING of the LUNGS during EXHALATION and reduces DYNAMIC HYPERINFLATION?
Bronchodilators (PREFERRED: β-2 AGONISTS, ANTICHOLINERGICS) METHYLXANTHINES can also be used
What is the strongest and longest-lasting RESCUE therapy for ASTHMA or COPD?
COMBINATION of a SHORT-ACTING β-2 AGONIST + IPRATROPIUM - a short-acting anticholinergic)
What is the duration of a typical SHORT-ACTING β-2 AGONIST? SHORT-ACTING ANTICHOLINERGIC?
SHORT-ACTING β-2 AGONIST: 3-6 HOURS
SHORT-ACTING ANTICHOLINERGIC: 4-5 HOURS - slower onset of action
What is the duration of a typical LONG-ACTING β-2 AGONIST? LONG-ACTING ANTICHOLINERGIC?
LONG-ACTING β-2 AGONIST: 12 HOURS
LONG-ACTING ANTICHOLINERGIC: 24 HOURS
Are INHALED CORTICOSTEROIDS preferred MONOTHERAPY for COPD?
NO!! (for asthma, yes)
Is COMBINATION treatment with INHALED CORTICOSTEROIDS recommended for COPD patients?
NO!! (for asthma, yes) - in COPD, this can result in PNA, especially in oder patients - however, sometimes TRIPLE combined therapy with inhaled corticosteroids is used
In patients with SEVERE EXACERBATIONS of COPD warranting HOSPITALIZATION, what medication is used?
IV CORTICOSTEROIDS (unlike oral corticosteroids used for acute exacerbations not requiring hospitalization)
What two medication types are RESERVED for COPD patients that continue to do poorly EVEN after combined therapy with long-acting bronchodilators ± inhaled corticosteroids?
Methylxanthines (theophylline, aminophylline) or phosphodiesterase-4 inhibitor (roflumiLAST)
What is the duration of METHYLXANTHINES (Theophylline, Aminophylline)?
24-HOURS (used only as a last resort)
This COPD drug is to be used ONLY as an ADD-ON in SEVERE COPD associated with CHRONIC BRONCHITIS patients with FREQUENT exacerbations and a h/o exacerbations. It is NOT to be used for EMPHYSEMA-COPD or as a rescue medication?
Phosphodiesterase-4 Inhibitor roflumiLAST (NOT to be used in patients with liver impairment or in combination with STRONG cytochrome P-450 inducers (rifampin, carbamazepine, phenytoin, phenobarbital)
How is α-1 anti-trypsin deficiency - related disease (COPD-emphysema) treated?
With α-1 anti-trypsin REPLACEMENT therapy
What is the recommendation for the use of antitussive agents and pulmonary vasodilators (phosphodiesterase-5 inhibitors - sildenafil) in COPD patients?
NOT RECOMMENDED - no benefit (cough serves a very important protective role)
When a patient with COPD presents with increased DYSPNEA associated with increased SPUTUM VOLUME and sputum PURULENCE, what should be suspected and treated?
INFECTION (bacterial OR viral - because thought to be colonized with bacteria anyway)
When should ANTIBIOTICS be used to treat a patient with a COPD exacerbation?
When INFECTION is suspected AND when they require MECHANICAL VENTILATION (invasive or not)
What are the most common pathogens responsible for INFECTION-related COPD EXACERBATIONS? What is the recommended antibiotic treatment?
H. influenzae, S. pneumoniae, Moraxella catarrhalis
FLUOROQUINOLONES (levofloxacin) OR 3rd gen cephalosporin + macrolide (CEFTRIAXONE + AZITRHOMYCIN)
What vaccinations are recommended in ALL COPD patients?
INFLUENZA and PNEUMOCOCCAL vaccines
What are the ONLY two interventions known to REDUCE COPD risk and POSITIVELY affect DECLINE in pulmonary FUNCTION?
SMOKING CESSATION and OXYGEN THERAPY
What should be considered for ALL SYMPTOMATIC patients with an FEV1
Pulmonary Rehabilitation (education, nutritional counseling, exercise - ≥30 min 3x/week for 6-8 weeks, assessment and follow-up to reinforce behaviors and techniques)
What is considered RESTING HYPOXEMIA and how is it treated?
PO2 ≤55 mm Hg OR an arterial O2 saturation ≤88%, treated with OXYGEN THERAPY (at rest, while sleeping and during exercise)
How long should patients with RESTING HYPOXEMIA be treated with OXYGEN THERAPY throughout the day?
≥15 HOURS/day (IMPROVES SURVIVAL)
In hospitalized patients with COPD, receiving OXYGEN therapy to raise their PO2 levels ≥60 mm Hg and OXYGEN SATURATION ≥90%, what should be MONITORED every 30-60 minutes throughout the therapy and WHY?
To check for CO2 RETENTION and PREVENTION of acidosis
What can be used in a HOSPITALIZED patient with an ACUTE EXACERBATION or INFECTION with SEVERE COPD that is spontaneously breathing to improve their breathing PATTERN, reduce DYSPNEA, improve OXYGENATION and AVOID INTUBATION?
Non-invasive Positive Pressure Ventilation - NPAP - (BiPAP or CPAP), especially while sleeping
In a patient presenting with VERY SEVERE PULMONARY DISEASE and/or LIFE-THREATENING HYPOXIA, PROGRESSIVE HYPERCAPNIA, SOMNOLENCE or SIGNIFICANTLY AMS, what should be done?
Endotracheal Intubation
Resecting up to 30% of diseased or non-functioning lung parenchyma to reduce hyperinflation and allow remaining lung to function more efficiently is called?
Lung Volume Reduction Surgery (LVRS)
In patients with ADVANCED COPD, FEV1 >20% of predicted, DLCO >20% of predicted with B/L UPPER LOBE EMPHYSEMA who remain symptomatic despite MAXIMAL therapy should be considered for what?
Lung Volume Reduction Surgery (LVRS)
A hospitalized patient with MODERATE-to-SEVERE dyspnea, with use of ACCESSORY muscles and paradoxical abdominal motion OR MODERATE-to-SEVERE acidosis (pH 45 mm Hg) OR RR >25/min should be treated with what?
Non-invasive Positive Airway Pressure (NPAP)
SEVERE ACIDOSIS (pH 60 mm Hg) or RR >35 breaths/min (despite aggressive medical treatment) are an indication for what?
Immediate Endotracheal Intubation
Which procedure, Lung Volume Reduction Surgery or Lung Transplantation (single or double) has been shown to confer an overall survival benefit?
NEITHER (they only improve functional capacity and quality of life)
What is Obliterative Bronchiolitis?
Chronic Lung Allograft Rejection in lung transplant patients
- B/L upper lobe EMPHYSEMA, post-bronchodilator TLC >150% and RV >100% of predicted with MAX FEV1 >20% but ≤45% of predicted, PCO2 ≤60 mm Hg & PO2 ≥45 mm Hg, what’s the next step?
- H/o ACUTE HYPERCAPNIA (PCO2 >50% mm Hg), pulmonary HTN, Cor Pulmonale, FEV1
- Consideration for Lung Volume Reduction Surgery
2. Consideration for Lung TRANSPLANT
Continued smoking, substance addiction (alcohol, tobacco, narcotics - current or active over the past 6 MONTHS), malignancy in the last 2 years, significant chest wall/spinal deformity, poor social support system, untreated psychiatric issues, untreated advanced dysfunction of another organ system are ABSOLUTE contraindications for what?
Lung TRANSPLANT
PO2 ≤55 mm Hg, Oxygen Saturation ≤88%?
HYPOXEMIA (requires OXYGEN therapy)
What is the GREATEST predictor of future COPD exacerbations in a particular patient?
≥2 exacerbations in the PAST YEAR OR an FEV1
Cardiovascular Instability (hypotension, arrhythmia, MI), AMS/uncooperative patient, Viscous or Copious secretions, Recent Facial or Gastro/Esophageal surgery, Craniofacial trauma or burns or Fixed Nasopharyngeal abnormalities are all contraindications to this method of preventing Endotracheal Intubation?
Non-invasive Positive Airway Pressure (NPAP) - BiPAP/CPAP
What medication should be started prophylactically for OLDER patients who have COPD?
PPI’s to prevent GERD-related exacerbations common in this group
How is a CHF exacerbation differentiated from a COPD exacerbation?
BNP (except in morbidly obese pts), CXR, Physical Exam, ECHO
When should an ORAL corticosteroid be added to a patient’s COPD management?
When FEV1 ≤50% of predicted
What is the risk of DEATH correlated in a patient with a COPD exacerbation?
Development of RESPIRATORY ACIDOSIS, co-morbidities and requirement for VENTILATORY support
What should be done when a hospitalized patient with an ACUTE COPD exacerbation no longer needs their SHORT-ACTING β-2 AGONIST more frequently than Q4 HOURS, are clinically stable AND their ABG has been stable for 12-24 HOURS?
Can be DISCHARGED with a FOLLOW-UP visit in 2-4 weeks
Why is EALRY follow-up post discharge from hospital for a COPD exacerbation IMPORTANT?
To REDUCE hospital RE-ADMISSION rates
PO2 60 mHg, pH
IMMEDIATE ICU ADMISSION with ENDOTRACHEAL INTUBATION
DISEASES that affect the TISSUE and SPACE around the ALVEOLI are known as?
Diffuse Parenchymal Lung Disease (DPLD) or Interstitial Lung Disease (ILD)
NON-INFECTIOUS diseases that affect the lung parenchyma (airways, vasculature, pleura, tissue and space around the alveoli) AND that appear DIFFUSE on IMGING studies with main presentation of EXERTIONAL DYSPNEA & FATIGUE and do NOT INCLUDE copd or pulmonary HTN are called?
Diffuse Parenchymal Lung Disease (DPLD) or Interstitial Lung Disease (ILD)
EXERTIONAL DYSPNEA & FATIGUE that eventually leads to symptoms of RIGHT HEART FAILURE - RV hypetrophy (exertional chest pain or syncope and congestion including peripheral edema, ascites, and pleural effusion) and INABILITY to INCREASE CARDIAC OUTPUT (CO) during EXERCISE is caused by what?
Pulmonary HTN (PH)
Why can Pulmonary HTN (PH) present with HOARSENESS?
Because hoarseness is caused by compression of the left recurrent laryngeal nerve by a dilated main pulmonary artery
How does Diffuse Parenchymal Lung Disease (ILD) present?
Progressive, with gradually-worsening cough and SOB ≥3 MONTHS with FAILURE to respond to antibiotic or diuretic therapy (for presumed infectious or cardiogenic edema)
Occupational exposures, Medications, Viral illnesses, Radiation therapy, Family history are all possible risks for this rare, progressive lung disease?
Diffuse Parenchymal Lung Disease (DPLD) or “Interstitial Lung Disease (ILD)”
Inspiratory Crackles, Wheezing (suggestive of airflow obstruction), cardiac features of Pulmonary HTN and RIGHT heart failure with digital CLUBBING, presence of RA or Systemic Sclerosis are present in this rare, progressive lung disease?
Diffuse Parenchymal Lung Disease (DPLD) or “Interstitial Lung Disease (ILD)”
Can Diffuse Parenchymal Lung Disease (DPLD) or “Interstitial Lung Disease (ILD)” occur ACUTELY?
YES!! (Interstitial PNA, Eosinophilic PNA, Hypersensitivity Pneumonitis - hot tub, birds, farmers - Drugs - amiodarone, nitrofurantoin, chemo - Bronchiolitis Obliterans Organizing Pneumonia, Diffuse Alveolar Hemorrhage and Vasculitis, otherwise check for infectious/cardiogenic cause)
What is the GOLD standard IMAGING test for LUNG PARENCHYMA?
High-Resolution CT (especially in symptomatic patients with a NORMAL CXR)
If a High-Resolution CT scan cannot make the diagnosis of Diffuse Parenchymal Lung Disease (DPLD) or “Interstitial Lung Disease (ILD)” what should be done next?
Open-LUNG Biopsy
Connective Tissue Diseases (RA, polymyositis, systemic sclerosis), Hypersensitivity Pneumonitis (farmer’s lung, hot tub lung, Bird Fancier’s lung), Pneumoconioses (asbesosis, silicosis, coal workers), Drugs (chemo, amiodarone, nitrofurantoin), Smoking (Langerhans cell histiocytosis, bronchiolitis, desquamative interstitial pneumonia), Acute Eosinophilic Pneumonia, Radiation and Toxic Inhalation (cocaine, zinc chloride - “smoke bombs,” ammonia) can all cause this progressive lung disease?
Diffuse Parenchymal Lung Disease (DPLD) or “Interstitial Lung Disease (ILD)”
CT demonstrating a PATTERN of SEPTAL, RETICULAR, NODULAR, RETICULONODULAR or GROUND-GLASS, the most likely diagnosis also based on DISTRIBUTION of disease is?
Diffuse Parenchymal Lung Disease (DPLD) or “Interstitial Lung Disease (ILD)”
What imaging “window” on high-resolution CT can further narrow the differential of Diffuse Parenchymal Lung Disease (DPLD) or “Interstitial Lung Disease (ILD)”?
SOFT-TISSUE window (can better visualize the pleura and mediastinum for lymphadenopathy, effusions, etc.)
What are the IDEAL biopsy sites for LUNG biopsies?
Upper and Lower lobes as well as Normal and Abnormal-appearing areas
What kind of disease is Idiopathic Pulmonary Fibrosis?
An Idiopathic Interstitial Pneumonia
On CT, a pneumonia with PERIPHERAL or BASAL predominant distribution in an older patient with progressive pulmonary symptoms (inspiratory crackles at the bases), biopsy revealing SUB-PLEURAL COLLAGEN deposition and FIBROBLASTIC foci in between NORMAL lung as well as CYSTIC areas forming a HONEYCOMB pattern and Pulmonary HTN late in the disease?
Idiopathic Pulmonary Fibrosis
CT: RETICULAR opacities and HONEYCOMBING with a PERIPHERAL or BASILAR predominance and MINIMAL GROUND-GLASS opacification?
Idiopathic Pulmonary Fibrosis
What is the treatment for Idiopathic Pulmonary Fibrosis?
VERY poor prognosis (3-5 years), treat CO-MORBIDITIES (OSA, GERD, Pulmonary HTN, Obesity, Emphysema) Supportive treatment with Pulmonary REHABILITATION and OXYGEN therapy (if oxygen saturation is
DO CORTICOSTEROIDS HELP in Idiopathic Pulmonary Fibrosis?
NO!!
What is the ONLY intervention shown to IMPROVE SURVIVAL for patients with Idiopathic Pulmonary Fibrosis?
Lung TRANSPLANTATION
CT showing a SEPTAL lung disease PATTERN (short lines extending to the pleura) is commonly seen in?
Lymphatic enlargement from pulmonary edema or cancer
CT showing a RETICULAR lung disease PATTERN (interlacing lines as in a mesh or lattice) is commonly seen in?
Diffuse Parenchymal Lung Disease (DPLD) or “Interstitial Lung Disease (ILD)”
CT showing a NODULAR lung disease PATTERN (spherical
Sarcoidosis
CT showing a RETICULONODULAR lung disease PATTERN (intersection of reticular lines or nodules) is commonly seen in?
Sarcoidosis, Langerhans Cell Histiocytosis and Lymphangitic carcinomatosis
CT showing GROUND-GLASS lung disease PATTERN (hazy opacities that DO NOT obscure underlying vascular markings) is commonly seen in?
Desquamative Interstitial Pneumonia (and in Idiopathic Pulmonary Fibrosis when MINIMAL)
CT showing HONEYCOMB lung disease PATTERN (septal lines adjacent to cystic areas in the periphery of the lung) is commonly seen in?
Idiopathic Pulmonary Fibrosis
What is the DISEASE DISTRIBUTION expected on a CT of a patient with Idiopathic Pulmonary Fibrosis?
BASILAR or PERIPHERAL
What is the DISEASE DISTRIBUTION expected on a CT of a patient with Hypersensitivity Pneumonitis?
UPPER-LOBE
What is the DISEASE DISTRIBUTION expected on a CT of a patient with Eosinophilic PNA and Cryptogenic Organizing PNA?
PERIPHERAL
What is the DISEASE DISTRIBUTION expected on a CT of a patient with Alveolar Proteinosis?
CENTRAL
What is the DISEASE DISTRIBUTION expected on a CT of a patient with Sarcoidosis?
UPPER LOBE & CENTRAL
How is Idiopathic Pulmonary Fibrosis palliated?
OPIOIDS
Connective tissue diseases (systemic sclerosis, RA, polymyositis) can present with what type of lung involvement?
Nonspecific Interstitial PNA
CT with BASILAR disease PATTERN and GROUND-GLASS predominance (not “minimal”) with associated connective tissue disease such as Systemic Sclerosis or RA or Polymyositis, is likely showing?
Nonspecific Interstitial PNA
What is necessary to make the diagnosis of Nonspecific Interstitial PNA?
Lung BIOPSY (a UNIFORM lymphoplasmacytic interstitial infiltration disrupting the normal lung architecture)
How is Nonspecific Interstitial PNA treated besides treating the underlying Connective Tissue Disease (systemic sclerosis, RA, polymyositis)?
Systemic CORTICOSTEROIDS
What are potential causes of Bronchiolitis Obliterans Organizing Pneumonia (BOOP)?
Infections, Collagen vascular diseases, Drugs
What is the IDIOPATHIC form of Bronchiolitis Obliterans Organizing Pneumonia (BOOP)?
Cryptogenic Organizing Pneumonia (COP)
If a patient presents with symptoms suggestive of a community-acquired pneumonia, undergo a couple of antibiotic regimens but 6-8 weeks later still have the disease, what is the diagnosis most likely?
Cryptogenic Organizing Pneumonia (COP)
How long does Cryptogenic Organizing Pneumonia (COP) persist for?
3-6 MONTHS
How is Cryptogenic Organizing Pneumonia (COP) diagnosed?
Lung BIOPSY
How is Cryptogenic Organizing Pneumonia (COP) treated?
Systemic CORTICOSTEROIDS
RAPID-ONSET PNEUMONIA over days-to-weeks with PROGRESSIVE, HYPOXEMIC RESPIRATORY FAILURE with BIOPSY demonstrating DIFFUSE ALVEOLAR DAMAGE with an appearance like ARDS (but without sepsis or inhalational injury)?
Acute Interstitial Pneumonia
How is Acute Interstitial Pneumonia treated?
Systemic CORTICOSTEROIDS and low Tidal Volume ventilation
A pulmonary disease with CT findings of Thin-Walled Cysts that are UPPER-LUNG predominant with NODULES, found in SMOKERS with cough and dyspnea and in more severe disease, Pulmonary Function Tests demonstrate an OBSTRUCTIVE (FEV1
Langerhans Cell Histiocytosis (smoking-related)
How is Langerhans Cell Histiocytosis treated?
SMOKING CESSATION and systemic CORTICOSTEROIDS
Langerhans Cell Histiocytosis, Respiratory Bronchiolitis and Desquamative Interstitial Pneumonia are all caused by what?
SMOKING (treatment is smoking cessation)
How is Connective-Tissue associated LUNG Disease treated?
By treating the UNDERLYING connective tissue disease (RA, Polymyositis, Systemic Sclerosis)
What is the leading cause of DEATH in patients with Systemic Sclerosis (scleroderma)? Treatment?
Progressive Diffuse Parenchymal Lung Disease (ILD)
Treated with CYCLOPHOSPHAMIDE (steroids don’t help)
In which TWO Diffuse Parenchymal Lung Diseases (DPLD) or “Interstitial Lung Diseases (ILD)” do systemic corticosteroids have no effect and thus NOT used for treatment?
Idiopathic Pulmonary Fibrosis and in Systemic Sclerosis (scleroderma) - associated lung disease
Repeated INHALATION of FUNGAL (actinomycets), BACTERIAL, PROTOZOAL, ANIMAL/INSECT PROTEINS (bird droppings) or CHEMICAL COMPOUNDS can cause this lung disease?
HYPERSENSITIVITY PNEUMONITIS
Pt that works around FUNGI or ANIMALS/INSECTS, CHEMICALS, that develops FLU-LIKE symptoms (fever, chills, malaise, anorexia, weight loss, HA, arthralgia/myalgia) 4-8 HOURS after INTENSE exposure with dyspnea, chest tightness and a dry cough with CT demonstrating B/L UPPER and MID-LING distributed hazy ground-glass opacities with resolution in 24-48 hours but RECUR with re-exposure most likely has?
HYPERSENSITIVITY PNEUMONITIS
How is HYPERSENSITIVITY PNEUMONITIS treated?
REMOVAL of the offending AGENT + systemic CORTICOSTEROIDS (if severe)
How can it be determined that a particular LUNG DISEASE is being caused by a DRUG or THERAPY?
There would be a TEMPORAL (time of onset from initiation of drug) relationship between drug and development of disease
Lung disease that usually presents within the FIRST YEAR of treatment with this DRUG?
AMIODARONE (HIGH-incidence of toxicity) - poor prognosis
What is the mainstay of treatment of DRUG-induced LUNG disease AFTER REMOVAL of offending DRUG?
Systemic CORTICOSTEROIDS
This drug can RARELY cause LUNG disease with peripheral EOSINOPHILIA and BIOPSY shows GRANULOMAS?
METHOTREXATE
Lung disease that occurs within DAYS of starting this DRUG with a CUTANEOUS RASH with peripheral EOSINOPHILS with imaging showing KERLEY B lines (faint, discrete bi-basilar markings) and pleural EFFUSIONS?
NITROFURANTOIN
Pneumonitis, Sub-pleural masses, Pulmonary Fibrosis, Pneumonia, Diffuse Alveolar Damage and Alveolar Hemorrhage are all seen in LUNG DISEASE associated with this DRUG?
AMIODARONE
6 weeks after this treatment, patients present with cough and dyspnea, CT shows hazy ground-glass opacities around the area of treatment and resolve in 6 MONTHS however may need CORTICOSTEROIDS if severe?
Radiation Therapy
In this disease, there is tissue infiltration by MONONUCLEAR PHAGOCYTES, LYMPHOCYTES and NONCASEATING GRANULOMAS?
SARCOIDOSIS
ACUTE disease with ERYTHEMA NODOSUM, FEVER, ARTHRALGIA and HILAR LYMHADENOPATHY?
Löfgren Syndrome (ACUTE Sarcoidosis)
What is the TREATMENT of CHOICE for SARCOIDOSIS?
Systemic CORTICOSTEROIDS
How many people with SARCOIDOSIS have PULMONARY involvement?
90%
A RARE, CYSTIC lung disease that occurs in WOMEN of CHILDBEARING AGE or in association with TUBEROUS SCLEROSIS (genetic disease that causes benign tumors to grow in the brain and the kidneys, heart, eyes, lungs, and skin. Symptoms include seizures, intellectual disability, developmental delay, behavioral problems) with pulmonary parenchymal INFITRATION of SMOOTH MUSCLE CELLS - a LOW GRADE METASTATIC NEOPLASM that targets the LUNG?
LYMPHANGIOLEIOMYOMATOSIS
A young woman with DYSPNEA presents with SPONTANEOUS PNEUMOTHORAX and/or CHYLOTHORAX with CXR demonstrating HYPERINFLATION and CT shows DIFFUSE, THIN-WALLED, SMALL CYSTS and labs show elevated VASCULAR ENDOTHELIN FACTOR-D (VEGF-D)?
LYMPHANGIOLEIOMYOMATOSIS
What is the treatment for LYMPHAGIOLEIOMYOMATOSIS?
Lung TRANSPLANT
Ship builder, b/l pleural plaques, restrictive lung disease with basilar-predominant interstitial opacities?
ASBESTOSIS
What MUST you do for a patient that mentions a potential INHALATION EXPOSURE at work but has no symptoms?
MUST INVESTIGATE ANYWAY
Patients with work-related exposure to this substance, can develop accelerated OBSTRUCTIVE lung disease MANY YEARS AFTER exposure even if they are ASYMPTOMATIC and have NO SMOKING HISTORY?
COAL
When after exposure to ASBESTOS does ASBESTOS-RELATED disease usually present? Mesothelioma?
15-35 YEARS later
30-40 YEARS
Construction, Automotive industry and Ship-building?
ASBESTOS exposures
Fiber deposition in the lung parenchyma elicits a CHRONIC INFLAMMATORY response leading to proliferation of mesenchymal (connective tissue) cells, intra-alveolar fibrosis and loss of alveolar capillary units?
ASBESTOSIS
Partially calcified, WELL-CIRCUMSCRIBED pleural PLAQUES (asymptomatic) and DIFFUSE pleural THICKENING (associated with RESTRICTIVE disease)?
ASBESTOSIS
What can present as a MASS-LIKE PULMONARY (not pleural) lesion in a patient with ASBESTOSIS?
ROUNDED ATELECTASIS caused by progressive pleural fibrosis with atelectatic areas beneath the pleural thickening and MUST be distinguished from malignancy by radiology
Exposure to this substance can cause SMALL CELL and NON SMALL CELL LUNG CANCER?
ASBESTOS (often with pleural effusions)
ASBESTOS is SYNERGISTIC with this substance to INCREASE the RISK of LUNG CANCER x 60!!!?
TOBACCO SMOKE
Exposure to this mineral poses an INCREASED RISK for mycobacterial & fungal infections (TUBERCULOSIS), RA, Systemic Sclerosis (scleroderma) and SLE and treatment for LUNG DISEASE is SYMPTOMATIC and consists of BRONCHODILATORS, OXYGEN or TRANSPLANT?
SILICOSIS
Exposure to this mineral and development of lung disease demonstrates small 1 cm with LOWER-LUNG HYPERINFLATION as disease PROGRESSES (PROGRESSIVE MASSIVE FIBROSIS?
SILICOSIS
What are the THREE (3) most common causes of PLEURAL EFFUSIONS?
- HF, 2. PNA, 3. CA
Dyspnea, PLEURITIC CHEST PAIN, NON-PRODUCTIVE cough are the most COMMON symptoms of this condition?
PLEURAL EFFUSION
Can you obtain a diagnosis for the cause of pleural effusion if the effusion is aspirated and tested?
NO! (it would be Exudative - CA, PNA, TB, PE or Transudative - HF, Cirrhosis, Nephrotic Syndrome, Dialysis, Hypoproteinemia)
When should a PLEURAL EFFUSION be aspirated?
When it is UNEXPLAINED and >1 cm displaced from LUNG
What differentiates an EXUDATIVE pleural fluid from a TRANSUDATIVE one?
PROTIEN content and LDH levels
PLEURAL PROTEIN : SERUM PROTEIN > 0.5 and/or PLEURAL LDH > 2/3 upper limit of normal = ?
EXUDATIVE PLEURAL EFFUSION
What conditions cause BLOODY PLEURAL EFFUSIONS?
TRAUMA, CA, TB
When is a PLEURAL EFFUSION INFECTED?
When WBC (leukocyte) count is >10,000 (usually an exudative effusion)
What does the presence of NEUTROPHILS (predominant WBC’s “segs”) in a PLEURAL EFFUSION most commonly imply?
ACUTE INFECTION or INFLAMMATION
When does an EXUDATIVE PLEURAL EFFUSION caused by PNA require DRAINAGE?
When COMPLICATED (bacterial presence) - called an “EMPYEMA” or puss (also requires ANTIBIOTICS)
What does the presence of LYMPHOCYTES (B and T cells) in a PLEURAL EFFUSION most commonly imply?
CA or TB
What is done NEXT if an EXUDATIVE PLEURAL FLUID sample with predominant LYMPHOCYTES does not yield a diagnosis?
PLEURAL BIOPSY
What does a TRANSUDATIVE effusion with predominant LYMPHOCYTES signify?
NOTHING (transudative effusions are not worrisome for directly-affected LUNG disease)
LOW GLUCOSE levels (
Likely caused by TB, CA, PNA or RA - NEED for DRAINAGE and POOR PROGNOSIS
What does a PLEURAL FLUID Triglyceride level >110 mg/dL signify?
CHYLOTHORAX (milky white appearance)
What is the WORLD-WIDE LEADING cause of a EXUDATIVE PLEURAL EFFUSION?
TB
LYMPHOCYTE Predominant PLEURAL FLUID EXUDATE in the presence of a POSITIVE PPD test?
TB
What Laboratory test is POSITIVE in >70% of cases of TB?
ADENOSINE DEAMINASE (high NPV - if test is negative, there’s no disease)
A MASSIVE, UNILATERAL PLEURAL EFFUSION is most likely caused by what?
MALIGNANCY (checked with cytology)
A MASSIVE, UNILATERAL PLEURAL EFFUSION is most likely caused by malignancy, if sampled pleural fluid cytology is negative, prior to a THORASCOPIC PLEURAL BIOPSY (not a “CLOSED” pleural biopsy) what should be done next?
Repeat Thoracentesis and obtain more fluid (up to 3 times)
If LYMPHOMA is a diagnostic consideration, what test should be run on fluid obtained from an EXUDATIVE PLEURAL FLUID sample?
FLOW CYTOMETRY
How are SMALL (
Antibiotics alone
What is meant by “complicated” effusions that REQUIRE ANTIBIOTICS + DRAINAGE?
LARGE (>1 cm), LOCULATED, SEPTATED, LOW pH (
What is done for EFFUSIONS that are REFRACTORY to ANTIBIOTICS or DRAINAGE?
SURGICAL DEBRIDEMENT
How are SLOW and FAST-accumulating MALIGNANT PLEURAL EFFUSIONS managed?
SLOW - periodic thoracentesis with drainage
FAST - chemical pleurodesis with TALC
Wha is meant by Primary SPONTANEOUS PNEUMOTHORAX?
A spontaneous PNEUMOTHORAX that occurs in ABSENCE of disease (caused commonly by smoking)
What is the most COMMON cause of Primary SPONTANEOUS PNEUMOTHORAX?
SMOKING (others are MARFAN syndrome and Thoracic Endometriosis)
What is the most COMMON RISK factor for SECONDARY (due to presence of a disease) SPONTANEOUS PNEUMOTHORAX?
COPD (others are Cystic Fibrosis, TB, Pneumocystis Jirovecii)
When is a PNEUMOTHORAX not spontaneous?
When it is caused by trauma or iatrogenic
How should a LARGE, HEMODYNAMICALLY-SIGNIFICANT PNEUMOTHORAX be treated?
HIGH-FLOW OXYGEN, EMERGENT NEEDLE Thoracostomy and CHEST TUBE placement
How is a SMALL PRIMARY PNEUMOTHORAX (
OBSERVATION with SERIAL CXR With CHEMICAL (TALC) PLEURODESIS to prevent recurrence
When does a PNEUMOTHORAX require SURGERY?
When there is a persistent air leak
What type of management is necessary for a SECONDARY SPONTANEOUS PNEUMOTHORAX?
INPATIENT (whether SMALL or LARGE) WITH CHEMICAL (TALC) PLEURODESIS to prevent recurrence
A patient presents with DYSPNEA and CHEST PAIN in the setting of HEMODYNAMIC INSTABILITY with possible TRACHEAL DEVIATION, JUGULAR VENOUS DISTENTION and SUBCUTANEOUS CREPITUS?
TENSION PNEUMOTHORAX
Where is the NEEDLE THORACOSTOMY made for a TENSION PNEUMOTHORAX?
At the SECOND INTERCOSTAL SPACE along the MID-CLAVICULAR LINE
Where do MOST PE’s come from?
DVT’s at or above the POPLITEAL FOSSAE
ACUTE INCREASES in PULMONARY ARTERY and RV PRESSURES, DECREASE in CARDIAC OUTPUT and VENTILATION/PERFUSSION MISMATCHING?
PE
What is the RISK for DVT in persons >60 with each 2-HOUR segment of air travel?
18% (HIGH)
Tachypnea, TACHYCARDIA, Chest Pain, DYSPNEA, Anxiety, Crackles, Cough and Increased Pulmonic S2?
PE
What do ALL of the following have in common? (Antithrombin deficiency, Protein C & S Deficiency, Factor V Leiden, Dysfibrogenemia, Prothrombin Gene Mutation, Cancer, Pregnancy, Hormone Replacement Therapy, Oral Contraceptives, Polycythemia Vera, Smoking, Antiphospholipid Syndrome and Chemotherapy)
Hypercoagulable states that can cause DVT/PE
Hypercoagulability, Endothelial Damage (trauma, surgery) and Venous Stasis are the VIRCHOW TRIAD for what?
PE
What patients should be tested with a D-dimer test for PE?
Those with LOW likelihood for PE (negative test rules out)
What does a NEGATIVE D-dimer test mean in a HOSPITALIZED patient or in a patient with INTERMEDIATE (moderate) or HIGH likelihood for PE?
NOTHING
Are ECG or CXR findings helpful in diagnosing PE?
NO (very non-specific)
What are the RARELY-SEEN WESTERMARK sign and HAMPTON HUMP suggestive of on CXR?
PE
Signs of RIGHT-HEART strain on ECG (right axis deviation, RBBB, S1Q3T3 pattern) may be suggestive of what?
PE
What determines a patients RISK stratification for PE?
Scoring systems (Wells Prediction Score or the Revised Geneva Score) - age, presence of cancer, h/o past DVT/PE, recent surgery, immobilization or LE fracture, hemoptysis and tachycardia
What is the PRIMARY diagnostic method that should be used for a patient with an INTERMEDIATE (moderate) or HIGH RISK for PE?
CT-angiography (CTA) - beware of contrast nephropathy/allergy
What diagnostic method should be used for a patient with an INTERMEDIATE (moderate) or HIGH RISK for PE with a CONTRAST ALLERGY?
MAGNETIC RESONANCE ANGIOGRAPHY (MRA)
What diagnostic method that should be used for a patient with an INTERMEDIATE (moderate) or HIGH RISK for PE however neither CTA (CT-angio) nor MRA (MR-angio) are available?
V/Q Scan (suited for patients WITHOUT COPD or HEART/LUNG DISEASE
Which are the ONLY meaningful diagnostic results of a V/Q Scan?
Normal (negative) or Abnormal (positive)
What should be done for a patient with PRESUMED PE but POSITIVE for DVT on LE Ultrasound?
Treat for both DVT and PE (no need for other imaging)
What should be done for a patient with PRESUMED PE but NEGATIVE for DVT on LE Ultrasound?
Need for further imaging with either CT-angio (CTA) or MR-angio (MRA)
What should be done for a patient with DIAGNOSED PE on CT-angio/MR-angio or V/Q Scan?
Can treat, no need for DVT evaluation
What test can be done to diagnose PE for patients who are too unstable for CT-angio or V/Q Scan?
ECHO (elevated pulmonary artery pressure, RV dilation, paradoxical septal motion, diminished LV size)
How is a PE treated in a HEMODYNAMICALLY STABLE patient treated?
Anticoagulation ONLY (start IMMEDIATELY and achieve therapeutic levels within 24 HOURS!!)
What is the anticoagulation medication used to treat an ACUTE PE?
Unfractionated HEPARIN or LMWH or FONDAPARINUX
What are contraindications to using LMWH or FONDAPARINUX for treatment of PE?
Obesity and Kidney Dysfunction
In the setting of Heparin-Induced Thrombocytopenia (HIT), what agents CANNOT be used to treat PE, what can?
Cannot use Unfractionated HEPARIN nor LMWH, CAN use HIRUDIN, BIVALIRUDIN, ARGATROBAN
When is WARFARIN started for the treatment of ACUTE PE?
AT THE SAME TIME as the HEPARIN or FONDAPARINUX and continued until a THERAPEUTIC INR is reached and documented for 2 CONSECUTIVE DAYS
How should patients with PE presenting with REFRACTORY HYPOTENSION (high-grade PE) not responsive to IVF (NS) or vasoconstrictors be treated?
With THROMBOLYTIC therapy or SURGICAL/CATHETER EMBOLECTOMY FOLLOWED by ANTICOAGULATION
When should a PE be treated with THROMBOLYTIC therapy or SURGICAL/CATHETER EMBOLECTOMY FOLLOWED by ANTICOAGULATION?
ONLY when there is CLEAR EVIDENCE of HEMODYNAMIC INSTABILITY not amenable to medical therapy alone
How long after an INITIAL episode of PE must a patient be treated for with WARFARIN anticoagulation?
3 MOTNHS with an INR 2.0-3.0
If a patient has a RECURRENT PE, or an INITIAL PE but h/o PRIOR DVT’s or ACTIVE CANCER, how long should they be anticoagulated with WARFARIN for?
INDEFINITELY
What are the ABSOLUTE CONTRAINDICATIONS to THROMBOLYTIC THERAPY for PE or CVA?
H/o IC bleeding, CVA or HEAD/FACIAL TRAUMA in past 3 MONTHS, suspected AORTIC DISSECTION, ACTIVE INTERNAL BLEEDING, UNCONTROLLED HTN (SBP >180 mm Hg or DBP >100 mm Hg ALL OTHERS ARE RELATIVE
How are patients with PE/DVT treated if they are NOT candidates for ACUTE/CHRONIC anticoagulation or have had unsuccessful anticoagulation and are at HIGH RISK for recurrent emboli?
REMOVABLE IVC FILTER (because chronic use of filter can cause DVT formation AROUND or BELOW the filter)
Elevation of PULMONARY ARTERY PRESSURE of 25 mm Hg or HIGHER during REST?
Pulmonary HTN (Pulmonary Artery HTN, LEFT Heart Disease - associated, Lung Disease - associated, Chronic Thromboembolism - associated)
Restricted FLOW through the pulmonary vasculature with elevation in vascular resistance?
Pulmonary Artery HTN (PAH)
How does the management of Pulmonary Artery HTN (PAH) vary from the treatment of other causes of Pulmonary HTN?
Because PAH is treated with VASODILATOR therapy
What causes the MAJORITY (>80%) of Pulmonary HTN and how is that treated?
Conditions causing elevation of LEFT HEART filling pressures or PULMONARY DISEASE (COPD, ILD, OSA, Chronic High-Altitude) TREATMENT is of the UNDERLYING CAUSE
What test can rapidly and efficiently and non-invasively determine RIGHT-HEART function, pressures and functional status of the patient and is a better predictor of PROGNOSIS than the actual value of the PULMONARY ARTERY PRESSURE?
6-MINUTE WALK test
Methamphetamines, Scleroderma, HIV, Portal HTN, Schistosomiasis and Chronic Hemolytic Anemia can all cause this PULMONARY disorder?
Pulmonary Artery HTN
Fatigue, Dyspnea with exertion, Syncope, Edema, Ascites and Hepatomegaly?
Pulmonary HTN with RIGHT VENTRICULAR decompression
LEFT parasternal LIFT, Augmentation of the JUGULAR a-wave as well as the pulmonic component of S2 or a SINGLE S2, murmurs of TRICUSPID REGURGITATION or PULMONIC INSUFFICIENCY and RV S3 or S4 GALLOPS?
RIGHT-HEART failure with Pulmonary HTN
What is the ONLY CONFIRMATORY DIAGNOSTIC TEST for PULMONARY HTN?
RIGHT-HEART CATHETERIZATION
What PULMONARY ARTERY PRESSURE is SUGGESTIVE of RIGHT-HEART FAILURE and PULMONARY HTN?
≥40 mm Hg
What TEST can confirm the DIAGNOSIS of PULMONARY HTN and is REQUIRED PRIOR to therapy?
RIGHT HEART CATHETERIZATION
How is response to therapy for PULMONARY HTN and PROGRESSION of disease regularly measured?
Combination of Cardiac US and 6-MINUTE WALK test
What is the recommended INITIAL test for diagnosing potential CHRONIC THROMBOEMBOLIC PULMONARY HTN in a patient who has a h/o PE with development of Pulmonary HTN symptoms?
V/Q Scan (if not sufficient, can do CTA or RIGHT-HEART CATHETERIZATION and angiography
How is CHRONIC THROMBOEMBOLIC PULMONARY HTN treated?
Supportively and with INDEFINITE ANTICOAGULATION to prevent further PE
What is the DEFINITIVE treatment of CHRONIC THROMBOEMBOLIC PULMONARY HTN?
Surgical THROMBOENDARTERECTOMY to remove the organized clots
A patient has a h/o PE and develops ORGANIZATION of acute THROMBOEMBOLI with PULMONARY VASCULAR REMODELING, persistently elevated D-dimer and symptoms of Pulmonary HTN, what have they developed?
CHRONIC THROMBOEMBOLIC PULMONARY HTN
What is considered NORMAL Pulmonary Capillary Wedge Pressure?
≤15 mm Hg
What happens if Pulmonary Artery HTN is left untreated?
It progresses and pt dies on average in 2.8 years
PRIOR to INITIATING VASODILATOR therapy for PRESUMED Pulmonary Artery HTN, what MUST be done?
RIGHT-HEART CATHETERIZATION to CONFIRM diagnosis
What are the FINDINGS of RIGHT-HEART CATHETERIZATION in patients with Pulmonary Artery HTN?
ELEVATED Pulmonary Artery Pressure (RESTING ≥25 mm Hg), NORMAL Pulmonary Capillary Wedge Pressure (≤15 mm Hg) and ELEVATED Pulmonary Vascular Resistence
What are the MAIN VASODILATORS used for the treatment of Pulmonary Artery HTN?
Calcium Channel Blockers (can also use epoprostenol, iloprost, bosentan and SILDENAFIL, TADALAFIL)
What is the ONLY treatment for ADVANCED Pulmonary Artery HTN?
LUNG or HEART-LUNG TRANSPLANTATION
A focal nodular opacity in the lung, ≤3 cm, surrounded by NORMAL lung tissue and NOT associated with LYMPHADENOPATHY? What if ≥3 cm?
Pulmonary NODULE (single or multiple, SMOOTH borders) Pulmonary MASS (high-likelihood of MALIGNANCY - SPICULATED borders))
What is the MOST important feature of a LUNG NODULE in predicting MALIGNANCY?
SIZE (≥2-3 cm)
What is the follow-up for an incidentally-noted LUNG NODULE
NO FOLLOW-UP necessary
What should be done for a NON-CALCIFIED PULMONARY NODULE >8 mm for which no PRIOR imaging exists?
Further imaging and possibly BIOPSY
What are PULMONARY NODULES considered if they have remained STABLE in SIZE for 2 YEARS on CXR or CT?
BENIGN with NO FURTHER Follow-Up necessary
What does the PATTERN of CALCIFICATION (better seen on CT) predict about a LUNG NODULE?
Malignant (Eccentric or Off-Center) vs Benign (Central, Diffuse, Lamellar)
A pulmonary nodule with “satellite” nodules is likely FUNGAL not malignant and one that contains FAT and calcification is likely what?
A benign HAMARTOMA
What size must PULMONARY NODULES be in order for a PET-CT scan to be able to diagnose malignancy?
> 1 cm (used if CT still can’t determine etiology and BEFORE considering biopsy)
What should be done for a PULMONARY NODULE withot REGIONAL or DISTANT spread with INTENSE ACTIVITY on PET-CT? What if NO or LOW ACTIVITY?
Intense Activity - RESECT nodule
NO or Low Activity - Monitor with CT for 2 years
What do GROUND GLASS OPACITIES which are ONLY visible of CT SCANS mean?
ADENOCARCINOMA or INFLAMMATION/FIBROSIS
What is DONE if a GROUND GLASS OPACITY visualized on CT is felt to be potentially malignant (adenocarcinoma)?
WEDGE-RESECTION (not lobectomy) - because these tend to have a LOW LIKELIHOOD of RECURRENCE
What should be done for follow-up in a patient with an incidentally found lung nodule
Repeat imaging in 12 months, if no change, STOP
What should be done for follow-up in a patient with an incidentally found lung nodule 4-6 mm who NEVER SMOKED and has NO OTHER RISK FACTORS for MALIGNANCY?
Repeat imaging in 12 months, if no change, STOP
What should be done for follow-up in a patient with an incidentally found lung nodule 4-6 mm but has RISK factors (smoking, prior h/o malignancy, family history, etc.)?
Repeat imaging in 6-12 months, if no change in 18-24 months
What should be done for follow-up in a patient with an incidentally found lung nodule 6-8 mm who NEVER SMOKED and has NO OTHER RISK FACTORS for MALIGNANCY?
Repeat imaging in 6-12 months, if no change in 18-24 months
What should be done for follow-up in a patient with an incidentally found lung nodule 6-8 mm but has RISK factors (smoking, prior h/o malignancy, family history, etc.)?
Repeat imaging in 3-6 months, if no change in 9-12 months AND at 24 months
What should be done for follow-up in a patient with an incidentally found lung nodule >8 mm WITH or WITHOUT other RISKS for MALIGNANCY?
CT w/contrast, PET scan or BIOPSY
Although adenocarcinomas of the lung have a good prognosis if found early because the grow very slowly, how do they show up on CT imaging?
As GROUND-GLASS Opacities (single or multiple)
What is the MOST COMMON cause of CANCER DEATHS WORLD-WIDE?
LUNG CANCER
80% of LUNG CANCERS are of what type?
Non-Small Cell Lung Cancer (adenocarcinoma, squamous cell carcinoma and large-cell carcinoma)
What are 90% of LUNG CANCERS caused by?
SMOKING
Pulmonary Fibrosis, Radon, Arsenic, Chromium, Nickel, Ionizing Radiation and Polycyclic Aromatic Hydrocarbons (oil, coal, benzene) are associated with what disease?
LUNG Cancer
For high-risk patients, what has been shown to be a potentially effective LUNG CANCER screening modality?
LOW-DOSE SPIRAL CT scan
The symptoms of COUGH, HEMOPTYSIS and DYSPNEA present in a HIGH-RISK patient should raise the concern of what possibility?
LUNG CANCER
What labs should be considered in a patient being evaluated for possible metastatic lung cancer?
CBC, LFT’s and serum Calcium
CT scanning in a patient with possible metastatic LUNG cancer should include what structures besides the lungs?
LIVER, ADRENAL GLANDS and BRAIN (if symptoms of NEW HA’s, Visual Changes, Unsteadiness)
ALL patients with LUNG cancer who are being considered for SURGICAL or RADIATION treatment should undergo what testing PRIOR to THERAPY?
Pulmonary Function Testing (PFT’s)
If a CT or PET-CT identifies a 4 cm LUNG MASS and Mediastinal LYMPHADENOPATHY, what should be biopsied FIRST and why?
THE LYMPH NODES, because this would establish the DIAGNOSIS as well as STAGING instead of just the diagnosis if the mass were biopsied first
What is the appropriate NEXT step if a SINGLE 2 cm growing peripheral NODULE in a former SMOKER with a PET-CT shows uptake ONLY in the NODULE?
RESECTION, no biopsy necessary (because in this setting, the likelihood of a benign lesion is LOW and would eventually still need resection)
What is the appropriate NEXT step if a SINGLE 2 cm growing peripheral NODULE in a NEVER-SMOKER?
CT-GUIDED BIOPSY or BRONCHOSCOPY with BIOPSY (no PET-CT would have been done because of the LOW likelihood for malignancy in this setting)
What CANCER is LAMBERT-EATON (myasthenic-like only opposite) Syndrome associated with?
Small Cell Lung Cancer
What CANCER are SIADH and Cushing Syndrome associated with?
Small Cell Lung Cancer
What LUNG CANCER is HYPERCALCEMIA associated with?
Non-Small Cell Lung Cancer - NSCLC - (Squamous Cell type)
How is a STAGE I or II (neg PET-CT for other involvement) CONFIRMED Non-Small Cell Lung Cancer (NSCLC) nodule/mass treated?
RESECTION (Radiation if NOT surgical candidate)
How is Non-Small Cell Lung Cancer (NSCLC) with Mediastinal LN’s treated?
CHEMO if EBUS/EUS w/FNA confirm POSITIVE nodes
How is Non-Small Cell Lung Cancer (NSCLC) with METASTATIC disease treated?
CHEMO AFTER confirmatory BIOPSY
How is Non-Small Cell Lung Cancer (NSCLC) with PAINFUL BONE METS treated?
CHEMO/RAD AFTER confirmatory BIOPSY - PALLIATIVE
How is Non-Small Cell Lung Cancer (NSCLC) with LOCALIZED MASS with PLEURAL EFFUSION treated?
THORACENTESIS FIRST!! (CHEMO if POSITIVE or RESECTION if NEGATIVE)
How is Non-Small Cell Lung Cancer (NSCLC) with a SINGLE BRAIN METASTATIC LESION treated?
RESECTION, IF the LUNG CANCER is RESECTABLE
How is Small Cell Lung Cancer staged (besides TNM)?
LIMITED (one HEMIthorax - one radiation port “treatment area”) or EXTENSIVE (beyond one HEMIthorax)
What imaging modality to assess RESECTABILITY is MOST important in Non-Small Cell Lung Cancer (NSCLC)?
PET-CT
What should be done for ALL patients with an FEV1
MUST calculate the Predicted POST-OP Pulmonary Function - FEV1 & DLCO (to assess feasibility for resection)
- Once the Predicted POST-OP Pulmonary Function (FEV1 & DLCO) is calculated (to assess feasibility for LUNG surgery), what is accepted as the CUTT-OFF value below which LUNG surgery should NOT be done? 2. What would be the NEXT step IF FEV1 & DLCO were indeed BELOW the CUTT-OFF?
- FEV1 & DLCO of AT LEAST 40%
2. Perfusion Scan or Exercise Assessment could determine if surgery is still an option
Instead of a LOBECTOMY (standard surgical approach for resection of a STAGE I or II Non-Small Cell Lung Cancer), what would be an alternative surgery in a patient with MARGINAL pulmonary reserve (reduced FEV1 & DLCO)?
SEGMENTECTOMY or WEDGE resection
In what patients with Non-Small Cell Lung Cancer who will be undergoing LUNG surgery should also have surgical NODE DISSECTION performed?
ALL PATIENTS undergoing surgery
What are SURGICAL ALTERNATIVES in patients with STAGE I Non-Small Cell Lung Cancer who are NOT surgical candidates or REFUSE surgery?
Radiation (standard or stereotactic “focused”), RFA, Cryoablation
What should ALL STAGE II patients with Non-Small Cell Lung Cancer (NSCLC) be OFFERED AFTER SURGICAL RESECTION?
ADJUVANT CHEMOTHERAPY
How should a patient with STAGE IIIA Non-Small Cell Lung Cancer (NSCLC) be treated?
NEO-ADJUVANT CHEMOTHERAPY FIRST, and if resectable thereafter, then surgery
How should a patient with STAGE IIIB or IV Non-Small Cell Lung Cancer (NSCLC) be treated?
CHEMO (radiation only for local bone or brain involvement)
How is LIMITED stage Small Cell Lung Cancer treated?
COMBINATION CHEMO & RAD
How is EXTENSIVE stage Small Cell Lung Cancer treated?
CHEMOTHERAPY ONLY (no radiation)
What are the TWO (2) most important factors in the prognosis of a patient with lung cancer?
STAGE at presentation AND PERFORMANCE status of that patient
This LOW-GRADE lung malignancy has cells of neuroendocrine origin, favors an ENDOBRONCHIAL location (presents w/ hemoptysis, atelectasis or focal bronchiectasis) with TYPICAL (better prognosis) or ATYPICAL types, BOTH treated by RESECTION?
CARCINOID tumors (not associated with carcinoid syndrome - flushing & diarrhea)
A LUNG CANCER that presents with an UNRELENTING, DULL PLEURITIC PAIN with a relatively poor prognosis, originates from the surfaces of the PLEURA (large effusion and thickening) and PERITONEUM and is associated with a chemical exposure with a very long LATENCY of 30-40 YEARS!!
MESOTHELIOMA - inhalation of ASBESTOS
How is MESOTHELIOMA treated?
CHEMOTHERAPY + removal of the ENTIRE PLEURAL SURFACE and LUNG (in very few patients with limited disease)
When is METASTATIC disease to the LUNG resectable?
When its a SOLITARY lesion with NO evidence of SPREAD ELSEWHERE (found with sarcomas, renal cell carcinomas, colon and breast cancers)
What’s the NEXT step if a MEDIASTINAL MASS is found but DIAGNOSIS cannot be made by imaging?
BIOPSY or RESECTION
What’s the NEXT step if a MEDIASTINAL CYST is found?
FOLLOW-UP of the CYST with IMAGING
How is an ANTERIOR MEDIASTINAL tumor such as a THYMOMA treated?
Surgical RESECTION
What NEUROLOGICAL condition is caused by the PARANEOPLASTIC syndrome of a THYMOMA?
Myasthenia Gravis (elevated serum acetylcoline-receptor Ab’s)
A mass in the POSTERIOR mediastinum most likely arose from which of two tissues?
ESOPHAGUS or NEURAL TISSUE (neurofibroma)
A sense of exhaustion that PREVENTS MENTAL or PHYSICAL activity at the intensity or pace desired is called?
FATIGUE
What should be done BEFORE additional testing or TREATMENT for a patient presenting with c/o Excessive Daytime Sleepiness?
1-2 WEEK SLEEP DIARY (normal sleep is 7-8 hours daily)
What is meant by Mean Sleep Latency Time and what is considered NORMAL/ABNORMAL?
Time it takes an individual to fall asleep. NORMAL is >15 minutes, ABNORMAL
How are OSA and Narcolepsy treated (after trial of counseling to maintain a firm sleep-wake schedule that allows for 8 hours of sleep)?
OSA - CPAP
Narcolepsy - STIMULANTS
What is the most common cause of Excessive Daytime Sleepiness?
Insufficient Sleep Duration (sleep deprivation)
HTN, HF, Cardiac Arrhythmias and DM are risk factors OF what sleep disorder?
OSA
What is the most IMPORTANT RISK factor FOR developing OSA?
OBESITY (especially in the trunk and neck)
What is the GOLD STANDARD diagnostic test for SLEEP APNEA (both OSA and CSA)?
POLYSOMNOGRAPHY
Can a patient with NORMAL OVERNIGHT OXIMETRY AND LOW-PRETEST probability for OSA have OSA?
NO
What is the STRONGEST indication for TREATMENT of OSA?
Excessive Daytime Sleepiness (especially in truck drivers, pilots)
What is the difference between CPAP and BiPAP?
CPAP (used mainly to treat OSA) delivers “CONSTANT” positive airway pressure during BOTH inspiration and expiration. BiPAP delivers SEPARATE inspiratory and expiratory pressures to augment ALVEOLAR ventilation for patients with underlying HYPOVENTILATION syndrome or for patients in whom the constant pressure of CPAP is uncomfortable
What are the two components of abnormal breathing in a patient with OSA?
Apnea and Hypopnea (overly shallow breathing)
What factor is MOSLTY responsible for influencing the success of CPAP therapy for OSA patients?
Patient COMPLIANCE (address claustrophobia, comfort, etc.)
What INDEX is used in OSA to gauge the SEVERITY of this condition? What is considered MILD/SEVERE?
Apnea Hypopnea INDEX
MILD: 5-15, SEVERE >30
When should SURGERY be used for the treatment of OSA?
As a last resort, if weight loss or CPAP are refused or suboptimal (pt should undergo REPEAT polysomnography in 3-6 months after surgery to check for benefit)
Are MEDICATIONS or OXYGEN therapy recommended as treatments for OSA?
NO!
What are the TWO (2) sleep apnea syndrome TYPES?
OBSTRUCTIVE sleep apnea (OSA) and CENTRAL sleep apnea (CSA)
What is HYPERCAPNIA?
Excessive carbon dioxide (CO2) in the bloodstream, typically caused by inadequate respiration
What is VENTILATION controlled by DRUING SLEEP and where is the RESPIRATORY CENTER?
Controlled by BLOOD CO2 content (tension) as well as BLOOD pH, the center is in the BRAIN STEM (pons & medulla)
In which SLEEP APNEA type is HYPERVENTILATION noted?
CENTRAL sleep apnea (CSA)
In what two (2) sleep situations is SLEEP APNEA most prominently seen?
SUPINE sleeping position (worsened by gravity) and REM sleep (physiologic muscle paralysis “atonia”)
HF, a-fib, Stroke, Brainstem Lesions, Kidney Failure and the use of OPIATE analgesics are high RISKS for which TYPE of SLEEP APNEA?
CENTRAL sleep apnea (CSA) - also seen in patients who live at HIGH ALTITUDES and in SOME who use CPAP for treating OSA
In patients with HF, this type of breathing pattern observed with CENTRAL sleep apnea (CSA) worsens HF and worsens survival?
Cheyne -Stokes Breathing (crescendo-decrescendo pattern of ventilation) with an EXAGGERATED breathing response to CO2
Patients with CNS disease or HF are more likely to have what TYPE of SLEEP APNEA?
CENTRAL sleep apnea (CSA)
How should CENTRAL sleep apnea be treated?
By FIRST addressing the UNDERLYING conditions (HF, CNS disease and other co-morbid conditions)
WHEN should SLEEP APNEA be treated?
WHEN there are SYMPTOMS (often reported by patient bed-partner, anesthesiologist after a procedure)
HOW is CENTRAL sleep apnea (CSA) treated DIFFERENTLY than OBSTRUCTIVE sleep apnea (OSA)?
CSA is treated by ADAPTIVE ServoVentilation (ASV) as it promotes ventilatory stability with TIMED delivery of PRESSURE SUPPORT SYNCHRONIZED to the patient’s breathing EFFORT
Is CPAP used to treat CENTRAL sleep apnea (CSA)?
RARELY (usually if there is an overlapping OSA component) (can exacerbate it, can sometimes cause it in patients using CPAP to treat OSA)
What is required to DIAGNOSE SLEEP-RELATED HYPOVENTILATION?
HYPERCAPNIA DURING SLEEP (increased BLOOD CO2 levels) - OXYHEMOGLOBIN
What DISTINGUISHES HYPOVENTILATION syndromes from SLEEP APNEA?
SUSTAINED REDUCTION in OXYHEMOGLOBIN SATURATION rather than the repetitive deoxygenation-reoxygenation cycles typical of sleep apnea (OSA & CSA)
How is SLEEP-RELATED HYPOVENTILATION caused by COPD treated besides OPTIMIZING COPD THERAPY?
BiPAP with supplemental OXYGEN
Are MILD reductions in BLOOD OXYGEN and increases in blood CO2 normally seen in the PHYSIOLOGIC sleep state?
YES!! (however, MILD) these are EXAGGERATED in COPD
30% of OBESE patients with a BMI of 35+ and 50% of those with a BMI of 50+ experience this sleep disorder?
SLEEP-RELATED HYPOVENTILATION (OBESITY HYPOVENTILATION SYNDROME - OHS)
What is the CARDINAL SIGN of the Obesity Hypoventilation Syndrome (OHS)?
Daytime Hypercapnia (PCO2 >45 mm Hg) signifying reduced ventilation during wakefulness as well as sleep
What is considered a NORMAL ABG (pH, PCO2, HCO3)?
pH - 7.4
PCO2 - 40 mm Hg
HCO3 - 24 mmol/L
How is Obesity Hypoventilation Syndrome (OHS) treated besides WEIGHT LOSS?
Initially with CPAP (OSA component often present) but if suboptimal results, SWITCH to BiPAP + OXYGEN
In patients with NEUROMUSCULAR DISEASE related BREATHING disorders AND in those with Pulmonary HTN (PH), RIGHT-HEART failure and POLYCYTHEMIA, how should the SYMPTOMATIC SLEEP-RELATED BREATHING DISORDER be treated?
BiPAP ± OXYGEN
WHY should SUPPLEMENTAL OXYGEN NOT be prescribed WITHOUT adjunctive VENTILATORY SUPPORT in patients with NEUROMUSCULAR-DISEASE SYMPTOMATIC SLEEP-RELATED BREATHING DISORDERS?
Because supplemental OXYGEN by itself can FURTHER depress ventilation in patients with RESPIRATORY MUSCLE WEAKNESS
Kyphoscoliosis and Neuromuscular diseases can cause what TYPE of LUNG DISEASE that result in SLEEP-RELATED HYPOVENTILATION?
RESTRICTIVE lung diseases
How is ALTITUDE sickness (sleep disturbances and periodic breathing) PREVENTED and treated?
Acclimatization with a GRADUAL rather than an ACCELERATED ascent to higher altitudes (2,500 m - 7,500 m and greater) as well as ACETAZOLAMIDE (accelerates the acclimatization process) - metabolic acidosis and kidney stones
What treatment is used to RELIEVE SYMPTOMS of disrupted sleep and paroxysmal nocturnal dyspnea associated with HIGH-ALTITUDE sickness?
Supplemental OXYGEN
What treatment is used PROHYLACTICALLY in patients with a h/o HIGH-ALTITUDE sickness to prevent SYMPTOMS?
ACETAZOLAMIDE (metabolic acidosis and kidney stones)
Symptoms of HA, Fatigue, N/V and DISTURBED SLEEP that develop 6-12 HOURS after a patient who lives at a LOW ALTITUDE and has ASCENDED to a HIGH ALTITUDE (>2,000 m) that RESOLVE in 24 HOURS if there is NO FURTHER ASCENT?
Acute Mountain Sickness
What can happen in a patient with Acute Mountain Sickness (lives at low altitude and recently ascended to a high altitude >2,000 m) that is an EMERGENCY and requires IMMEDIATE intervention (symptoms of AMA & ATAXIA - loss of full control of body movements)?
High-Altitude Cerebral EDEMA (vasogenic brain SWELLING) with RISK of COMA and DEATH
How is High-Altitude Cerebral EDEMA (vasogenic brain SWELLING) with RISK of COMA and DEATH treated EMERGENTLY?
- DESCENT from high altitude
- TREATMENT with DEXAMETHASONE
- Supplemental OXYGEN
- HYPERBARIC therapy
BRAIN swelling due to EDEMA (vasogenic - due to high-altitude) or due to TUMOR is INITIALLY treated with what?
DEXAMETHASONE
BRAIN compression/swelling due to an Intra-Cranial Hemorrhage (ICH) is INITIALLY treated with what?
MANNITOL (a diuretic) prior to craniotomy
After 2-4 days at high altitude, a patient develops cough, dyspnea, chest tightness, fatigue and a decreased exercise tolerance with tachypnea, tachycardia, crackles and wheezing with PINK FROTHY sputum or HEMOPTYSIS followed by RESPIRATORY FAILURE?
High-Altitude PULMONARY EDEMA
How do you treat HIGH-ALTITUDE PULMONARY EDEMA in a patient with symptoms of cough, dyspnea, chest tightness, fatigue and a decreased exercise tolerance with tachypnea, tachycardia, crackles and wheezing with PINK FROTHY sputum or HEMOPTYSIS 2-4 days after a hike to HIGH-ALTITUDE?
Supplemental OXYGEN and DESCENT (to avoid RESPIRATORY FAILURE
If ya aint got supplemental oxygen and your mule died so you can’t get to lower altitude after a nice bromance hike up the mountain, how do you treat your buddy who is wheezing, breathing rapidly, coughing, can’t breath well, is yammering about chest tightness and fatigue and can’t walk much without getting out of breath tachypnea, is frothing pink at the mouth and spitting up blood?
Give him your VIAGRA (sildenafil) or NIFEDIPINE (ca-channel blocker for HTN) - vasodilators - and tell his ass that he owes you big time and a date with his fine-ass sister!
Normal OXYGEN tension at SEA LEVEL is 150-160 mm Hg, what are COMMERCIAL AIRLINE CABINS pressurized to during air travel?
110-120 mm Hg (equivalent of an altitude of 1500 - 2500 m)
What can happen to a patient with COPD or Pulmonary HTN during a COMMERCIAL AIRLINE FLIGHT and why?
They may experience a SUBSTANTIAL REDUCTION in ARTERIAL OXYGENATION due to the DECREASED OXYGEN TENSION in PRESSURIZED AIRLINE CABINS
A PULSE OXIMETRY value AT SEA LEVEL BELOW what level is an INDICATION for IN-FLIGHT SUPPLEMENTAL OXYGEN in a patient with COPD or Pulmonary HTN who is planning a FLIGHT?
SpO2
What testing should be done for patients with SpO2 92%-95% or PaO2
Hypoxia-Altitude Simulation Testing
How should patients at risk for in-flight HYPOXIA (COPD) be treated?
Supplemental OXYGEN and if already on that, INCREASE in FLOW RATE
Patients with LUNG BULLAE, BLEBS, CYSTIC LUNG DISEASE, or a COPD EXACERBATION should be questioned/tested for WHAT with a possibly DELAY in planned air travel?
PNEUMOTHORAX and h/o PNEUMOTHORAX (ABSOLUTE CONTRAINDICATION to FLYING - can result in TENSION PNEUMOTHORAX
Can a patient with a TINY pneumothorax not requiring hospitalization NOR active therapy plan AIR TRAVEL?
NO!! ABSOLUTE CONTRAINDICATION - can result in TENSION PNEUMOTHORAX
Cyclic CENTRAL apneas and hyperpneas associated with REPETITIVE arousals from sleep with SUDDEN and PERIODIC (paroxysmal) difficulty breathing is seen in this condition?
HIGH-ALTITUDE “PERIODIC” BREATHING
ABRUPT, SEVERE decline in OXYHEMOGLOBIN saturation that does NOT correlate with supplemental oxygen given to a patient when the patient’s ambient air PaO2 ≤60 mm Hg and the Carrico Index (PaO2/FiO2) ≤ 200 mm Hg with either NORMAL or REDUCED PCO2 implies what and how is this TREATED?
HYPOXEMIA (ongoing perfusion of portions of the lungs that are NO LONGER receiving VENTILATION due to ALVEOLAR COLLAPSE or FLOODING with blood/pus/edema that DOES NOT CORRECT with increased alveolar ventilation or supplemental oxygen. This (HYPOXEMIC RESPIRATORY FAILURE or ARDS) is treated with Positive End Expiratory Pressure (PEEP) which OPENS UP flooded or collapsed alveoli - ENDOTRACHEAL INTUBATION AND ICU ADMISSION
What is AMBIENT AIR FiO2 (Fraction of inspired Oxygen in the air breathed)?
21% (this is what naturally occurs in the ambient air)
A NON-CARDIOGENIC form of PULMONARY EDEMA characterized by ACUTE, PERSISTENT LUNG INFLAMMATION causing INJURY to ALVEOLAR epithelial cells and CAPILLARY endothelial cells with resulting INCREASED VASCULAR PERMEABILITY and LEAKAGE of protein, fluid and neutrophils into the interstitium and alveoli?
Acute Respiratory Distress Syndrome (ARDS) - MILD, MODERATE and SEVERE
What is the term for a PARTIAL (lobe) or COMPLETE COLLAPSE of the LUNG at the ALVEOLAR level?
ATELECTASIS
What is a normal Carrico Index (PaO2/FiO2) in ambient air?
100%-98%/0.21 (portion of oxygen in room air) = 476-466 mm Hg
ACUTE onset of RESPIRATORY SYMPTOMS within ONE WEEK of CLINICAL INSULT, B/L opacities on CXR not explained by other pathology (effusions, atelectasis or nodules) AND RESPIRATORY FAILURE NOT explained by HF or VOLUME OVERLOAD are required to diagnose what?
Acute Respiratory Distress Syndrome (ARDS)
What SYNDROME is graded with a patient receiving PEEP of AT LEAST 5 cm H2O (given with CPAP or intubation), a Carrico Index of PaO2/FiO2 measured at 201-300 mm Hg (MILD), 101-200 mm Hg MODERATE) and ≤100 mm Hg (SEVERE)?
Acute Respiratory Distress Syndrome (ARDS) - this method does not require Pulmonary Artery Wedge Pressure measurement
What is the MAJOR cause of Acute Respiratory Distress Syndrome?
SEVERE SEPSIS from ANY source (not just pneumonia)
When does Acute Respiratory Distress Syndrome (ARDS) manifest itself after RISK FACTOR exposure (SEPSIS)?
48-72 HOURS after
The MORTALITY rate in Acute Respiratory Distress Syndrome (ARDS) is very high (40%) and is generally caused by what?
The UNDERLYING cause of the lung INJURY (sepsis) not the lung injury itself (best prognosis with trauma-associated lung injury and worst prognosis with PNA-associated lung injury)
What is the PRIMARY treatment for Acute Respiratory Distress Syndrome (ARDS)?
VENTILATOR support with PEEP, treatment of the UNDERLYING pathology that caused it AND LIMITING FLUIDS (as this decreases volume of capillary leak)
What effect do NITRIC OXIDE and PROSTAGLANDINS (vasodilators) have in Acute Respiratory Distress Syndrome (ARDS)?
DRAMATIC short-term increases in oxygenation but NO DIFFERENCE in MORTALITY
What effect do CORTICOSTEROIDS have on Acute Respiratory Distress Syndrome (ARDS)?
NONE, DO NOT USE
PNA, aspiration, near-drowning, inhalational injury, trauma/lung contusion, SEPSIS, MULTIPLE BLOOD TRANSFUSIONS and pancreatitis can all cause this SEVERE lung-injury associated syndrome?
Acute Respiratory Distress Syndrome (ARDS)
What are the only TWO (2) NON-VENTILATOR treatments that have shown promise for IMPROVING MORTALITY of patients with Acute Respiratory Distress Syndrome (ARDS)?
Neuromuscular Blockade for 48 HOURS EARLY in the course and WhaExtra-Corporeal Membrane Oxygenation (machine that oxygenates the blood for the patient, bypassing the lungs) “ECMO”
What tests can be used to RAPIDLY distinguish PULMONARY EDEMA caused by SYSTOLIC/DIASTOLIC HF or Valve Disease from Acute Respiratory Distress Syndrome (ARDS)?
ECHO (also helpful are BNP, ECG, Cardiac Enzymes)
What is the most common cause of Acute Respiratory Distress Syndrome (ARDS) in non-hospitalized patients?
PNEUMONIA
Why is PEEP NOT INDICATED when a patient has UNILATERAL presentation of Acute Respiratory Distress Syndrome (ARDS) with FOCAL flooded, atelectatic or consolidated areas of lung? How is this best treated?
Because of OVERDISTENTION of NORMAL lung tissue causing ALVEOLAR INJURY
Best treated by positioning the patient in a LATERAL DECUBITUS position with the “GOOD” lung DOWN (“DEPENDENT” - meaning the LOWEST part of the lung in relation to GRAVITY where gravity is the STRONGEST the closer to the earth’s surface an object is) and the INJURED lung UP, to reduce the shunt (made by the fluid in the injured lung)
Why is there INCREASED CO2 production in CRITICALLY ILL patients?
Due to INCREASED METABOLIC DEMAND from FEVER or INCREASED MUSCLE ACTIVITY related to the patient’s RESPIRATORY EFFORTS or AGITATION
What is meant by “WASTED VENTILATION” that is seen in patients with COPD and SEVERE Acute Respiratory Distress Syndrome (ARDS)?
Ventilation of lung spaces that have INJURED CAPILLARY BEDS which do not benefit from GAS EXCHANGE
SEDATING drugs and drug OVERDOSES are the most common cause of what ventilatory issue?
Respiratory Failure due to INSUFFICIENT RESPIRATORY DRIVE (especially OPIOIDS)
What should be done for ALL OBTUNDED patients suspected of OPIOID INTOXICATION BEFORE considering INTUBATION with INVASIVE MECHANICAL VENTILATION?
ATTEMPTED REVERSAL with NALOXONE
MIOSIS (constricted pupils), ENCEPHALOPATHY (AMS), HYPOTENSION, HYPOTHERMIA and HYPOREFLEXIA are all features seen in what INTOXICATION?
OPIOID intoxication
In an OBTUNDED patient with suspected OPIOID INTOXICATION (miosis, encephalopathy, hypotension, hypothermia, hyporeflexia) who does NOT respond to UP TO 10 mg dose of NALOXONE, what should be done?
CONSIDER ALTERNATIVE DIAGNOSIS
A CHRONIC OPIOID user presents obtunded and is placed on a CONTINUOUS INFUSION of NALOXONE because frequent, repeat dosing became necessary for recurrent respiratory depression. Naloxone was stopped and pt became delirious, agitated and developed diaphoresis, tremulousness, hypotension, fever and seizures, why?
They are experiencing WITHDRAWAL
What is the antidote for RESPIRATORY depression caused by BENZODIAZEPINES (-“azolam”, -“azepam”)
FLUMAZENYL (only given when strongly suspecting benzodiazepine overdose, not routinely as it can precipitate seizures in chronic benzodiazepine users)
A patient that uses their accessory muscles of respiration , has a weak cough, orthopnea, a rapid, shallow breathing pattern and paradoxical inward motion of the abdomen with inspiration likely has what condition?
Neuromuscular disease with IMPAIRED respiratory muscle strength
What type of tests should patients with respiratory muscle weakness due to NEUROMUSCULAR DISEASE (ALS, Spinal Cord Injury, Guillain-Barre (acute inflammatory demyelinating polyneuropathy) and Myasthenic Crisis) have in order to detect declining strength over time?
Serial Pulmonary Function Tests
Spinal Cord Injuries, Guillain-Barre Syndrome (acute inflammatory demyelinating polyneuropathy) and Myasthenic Crisis are all examples of what process, that can result in RESPIRATORY FAILURE?
Respiratory Muscle Weakness
Complete spinal cord injury to what levels requires initial and potential life-long mechanical ventilation due to loss of ventilatory muscle function?
C3-C5 (above or at this level - phrenic nerve which innervates the diaphragm)
What are the dangers of chronic mechanical ventilation?
Atelectasis, Mucus Plugging and Pneumonia
What can a Myasthenic Crisis with respiratory failure be triggered by?
Infection, Surgery, Medications or Pregnancy
How is ACUTE respiratory failure treated in Guillain-Barre Syndrome and Myasthenic Crisis?
Plasmapheresis and IVIG
Which SYNDROME benefits from treatment with CORTICOSTEROIDS, Myasthenia Gravis or Guillain-Barre?
Myasthenia Gravis ONLY, no role for corticosteroids in Guillain-Barre
In patients with EXTRAPULMONARY conditions such as KYPHOSCOLIOSIS (hypercapnia), a RESTRICTIVE pattern of lung disease is seen. How do you treat this in adults?
Non-invasive Positive Airway Pressure ventilation (CPAP or BiPAP)
What gas exchange abnormality is seen in patients with ACUTE respiratory failure due to RSTRICTIVE pulmonary fibrosis?
HYPOXEMIA (not hypercapnia) - give supplemental oxygen
What is ACUTE VENTILATORY FAILURE caused by in patients with exacerbations of ASTHMA or COPD?
FATIGUE due to the INCREASED Mechanical WORK of breathing (resulting in AIR-TRAPPING due to incomplete expiration between breaths due to worsening airflow obstruction and elevated minute ventilation causing auto-PEEP and risk of pneumothorax)
What hemodynamic abnormality can occur due to the severe air-trapping seen in ASTHMA or COPD exacerbations with INCREASED INTRA-THORACIC PRESSURE?
HYPOTENSION (reduced venous return to the right heart)
Epiglottitis, Infections of the Neck, Retropharyngeal Abscess, Peritonsillar Abscess, Trauma, Thermal Injury, Anaphylaxis and Angioedema (ACE-I therapy) can cause what type of airway emergency?
Upper Airway Obstruction (inspiratory STRIDOR, retractions, cyanosis) - IMMEDIATE need for ENDOTRACHEAL INTUBATION
How are COPD and ASTHMA exacerbations READILY treated?
Supplementary OXYGEN
A patient with a presumed COPD or ASTHMA exacerbation that does not respond as expected to supplementary OXYGEN and requires a LARGE amount of oxygen to maintain saturations >90% should have what done?
CHECK for OTHER factors (HF, PNA, PTX, PE)
An ABNORMALLY LARGE DECREASE in SBP (normal ≤10 mm Hg) and PULSE-WAVE AMPLITUDE during INSPIRATION is seen in?
SEVERE ASTHMA/COPD exacerbations, CARDIAC TAMPONADE, PERICARDITIS and CHRONIC SLEEP APNEA (pulsus paradoxus)
What should be done for a patient with PERSISTENT FEV1 or PEAK EXPIRATORY FLOW
ADMIT to ICU
A patient presents with a COPD or ASTHMA exacerbation with RESPIRATORY ALKALOSIS (ELEVATED pH, normal or low HCO3, PCO2
IMMINENT RESPIRATORY ARREST - INTUBATE IMMEDIATELY (this does NOT indicate recovery)
DECREASED levels of consciousness, AGONAL respirations, ESCALATING work of breathing and FATIGUE despite aggressive bronchodilator therapy are indications for?
Invasive Mechanical Intubation
What should be done IMMEDIATELY for a patient with an ACUTE ASTHMA EXACERBATION who presents with HYPOXEMIA (4)?
- Inhaled SHORT-ACTING β-2 AGONISTS (albuterol)
- ADDITION of Inhaled anticholinergics (ipratropium)
- Supplemental OXYGEN
- Systemic Corticosteroids (treat the underlying inflammation) - methylprednisolone 60 mg/day IV
* . Can consider “adjunctive interventions” (Magnesium Sulfate IV and HELIOX)
What does a SLIGHTLY ELEVATED or NORMAL PCO2 in a patient with an ACUTE ASTHMA or COPD exacerbation mean?
IMPENDING RESPIRATORY ARREST - INTUBATE NOW!!!
The state of DECREASED TISSUE PERFUSION resulting in INADEQUATE OXYGEN DELIVERY for cellular needs (tissue ischemia) with organ and system dysfunction is called?
SHOCK (Cardiogenic, Distributive, Hypovolemic)
What do IVF (NS) + Vasopressors + Inotropic Agents do?
Restore PERFUSSION (such as during a state of SHOCK)
An AGENT that INCREASES the STRENGTH of CARDIAC MUSCLE CONTRACTION is called what?
A POSITIVE INOTROPIC AGENT
What type of shock can a LARGE PE cause?
CARDIOGENIC SHOCK (treat by lysis or removal of clot)
When should a patient with CHRONIC STABLE ANGINA NOT receive a Calcium Channel Blocker?
If they have HF, because it INCREASES MORTALITY (calcium channel blockers are NEGATIVE inotropic agents)
What role does PCI play in the treatment of CHRONIC STABLE ANGINA?
SYMPTOM REDUCTION (improvement of quality of life) ONLY!! with NO effect on improving survival or mortality
Are PULMONARY ARTERY CATHETERS recommended for diagnosis or routine care of patients with SHOCK?
NO!!
The following are INDICATIONS for what?
- Unexplained or unknown volume status in shock
- Severe cardiogenic shock (acute valvular disease, pericardial tamponade)
- Suspected or known pulmonary artery hypertension
- Severe underlying cardiopulmonary disease (congenital heart disease, left-to-right shunt) who are undergoing corrective or other surgery
Placement of a Pulmonary Artery Catheter
The following are CONTRAINDICATIONS for what?
- Infection at the insertion site
- The presence of a right ventricular assist device
- Insertion during cardiopulmonary bypass
Placement of a Pulmonary Artery Catheter
SEPSIS (infection), Systemic Inflammatory Response Syndrome (SIRS) - infection, pancreatitis, trauma, TOXIC SHOCK SYNDROME, ADRENAL INSUFFICIENCY, DRUGS, TOXINS, HEAVY METAL POISONING, HEPATIC INSUFFICIENCY and CNS damage can all cause what TYPE of SHOCK?
Distributive SHOCK - DECREASED SYSTEMIC VASCULAR RESISTANCE (abnormal distribution of blood flow in the smallest blood vessels even though CARDIAC OUTPUT is NORMAL or above normal)
What is considered NORMAL Mean Arterial Pressure (MAP) - which is the average arterial pressure during a single cardiac cycle
70-100 mm Hg (an MAP of ≥60 mm Hg is REQUIRED to maintain ORGAN PERFUSSION
SBP 40 mm Hg and the LACK of MAP response (increase) to IVF (NS) bolus suggests what?
SHOCK
Decreased URINE OUTPUT, AMS, Increased Serum LA level suggest what?
END-ORGAN DYSFUNCTION due to HYPOPERFUION (SHOCK)
Decreased CARDIAC OUTPUT in the setting of ACUTE HF or MASSIVE PE suggests what TYPE of SHOCK?
CARDIOGENIC
Decreased SYSTEMIC VASCULAR RESISTANCE in the setting of SEPSIS or ANAPHYLAXIS suggests what TYPE of SHOCK?
DISTRIBUTIVE
Decreased PRELOAD to the HEART in the setting of ACUTE HEMORRHAGE or DEHYDRATION suggests what TYPE of SHOCK?
HYPOVOLEMIC
What TYPES of SHOCK respond FAVORABLY to AGGRESSIVE VOLUME EXPANSION with IVF (NS)?
HYPOVOLEMIC and SEPTIC (distributive) SHOCK
Should you worry about precipitation of HF or Pulmonary Edema when a patient in SHOCK needs LARGE IVF BOLUSES?
NO!!
Since VASOPRESSORS affect multiple RECEPTORS, what are EXPECTED adverse effects?
ARRHYTHMIAS, MESENTERY or EXTREMITY ISCHEMIA
Why MUST VASOPRESSORS be administered via CENTRAL LINES ONLY?
Because they can cause LOCAL TISSUE ISCHEMIA if given peripherally or if they extravasate into surrounding tissues
When is the ONLY time LOW-DOSE CORTICOSTEROIDS are recommended for the treatment of SEPTIC SHOCK?
When SEPTIC SHOCK does NOT RESPOND TO VASOPRESSORS
How should you treat HYPOVOLEMIC SHOCK due to HEMORRHAGE?
IVF (NS) + PRBC’s Transfusions
What Hb level is the threshold for transfusion in a patient who is NOT ACTIVELY BLEEDING?
Hb ≤7 g/dL
What are the FIRST LINE VASOPRESSORS used for the treatment of SEPTIC and ANY REFRACTORY SHOCK?
NOREPINEPHRINE (levophed) and DOPAMINE (HIGH-DOSE)
What two VASOPRESSORS have the HIGHEST risk for ARRHYTHMIA?
DOPAMINE (HIGHEST), EPINEPHRINE
Is low-dose dopamine still recommended for kidney failure?
NO!! (no evidence of benefit)
What TYPE of SHOCK is MEDIUM-DOSE DOPAMINE (vasopressor) be used for?
CARDIOGENIC
What SECOND VASOPRESSOR can be added for the treatment of SEPTIC SHOCK but ONLY after the addition of NOREPINEPHRINE?
VASOPRESSIN
What is the ONLY TYPE of SHOCK VASOPRESSIN is recommended for and ONLY as an ADJUNCTIVE agent to NOPREPINEPHRINE (vasopressor)?
SEPTIC SHOCK
What VASOPRESSOR is used for MILD SHOCK STATES?
PHENYLEPHRINE
WHEN is EPINEPHRINE used as a VASOPRESSOR for treating SHOCK?
ONLY as a SECOND-LINE agent (septic, cardiogenic or any refractory shock)
What should be done for ANY patient with ANY DEGREE of SHOCK (mild, moderate, severe)?
ICU ADMISSION
Why are these agents used in treating SHOCK? (AMIODARONE, CALCIUM, DOPAMINE, DOBUTAMINE, EPINEPHRINE, NOREPINEPHRINE, DIGOXIN, MILRINONE, AMRINONE, THEOPHYLLINE, GLUCAGON, INSULIN)
POSITIVE INOTROPIC AGENTS (INCREASE the STRENGTH of HEART MUSCLE CONTRACTILITY)
What TYPE of agents are the following? (β-blockers, Ca-channel blockers, CLASS IA antiarrhythmics - quinidine, procainamide, disopyramide, CLASS IC antiarrhythmics - flecainide)
NEGATIVE INOTROPIC AGENTS (DECREASE the STRENGTH of HEART MUSCLE CONTRACTILITY)
What are the TWO (2) components of Non-invasive Positive Pressure Ventilation (NPPV) which is different than Non-invasive Positive Airway Pressure “NPAP” (CPAP and BiPAP)?
INSPIRATORY Positive Airway Pressure (IPAP) and EXPIRATORY Positive Airway Pressure (EPAP)
What portion of the Non-invasive Positive Pressure Ventilation (NPPV) helps maintain upper-airway patency thus increasing end-expiratory volume which is impaired in COPD and ASTHMA?
EXPIRATORY Positive Airway Pressure (EPAP)
The expiratory portion of Non-invasive Positive Pressure Ventilation (NPPV) - EXPIRATORY Positive Airway Pressure (EPAP) is the same as CPAP used for OSA and PEEP used in intubated patients. What component of NPPV do CPAP and PEEP lack, which NPPV provides in order to reduce INSPIRATORY effort as well?
INSPIRATORY Positive Airway Pressure (IPAP) - can be set to be triggered ONLY by the patient when they SPONTANEOUSLY initiate a breath or set at a PRESET rate in case patient is too weak
What is Non-invasive Positive Pressure Ventilation (NPPV) used for in patients with SEVERE COPD exacerbations besides AVOIDING INTUBATION for which Non-invasive Positive Airway Pressure (NPAP) is also used?
It is ALSO used for WEANING patients OFF of IVASIVE MECHANICAL VENTILATION
What is the STANDARD of CARE for managing VENTILATION in patients with MODERATE to SEVERE COPD EXACERBATIONS?
Non-invasive Positive Pressure Ventilation (NPPV) which has pressure support for BOTH INSPIRATION and EXPIRATION thus reducing the effort of breathing
Is Non-invasive Positive Pressure Ventilation (NPPV) recommended for ASTHMA exacerbations?
NO
In what conditions is Non-invasive Positive Pressure Ventilation (NPPV) INDICATED?
COPD, IMMUNOCOMPROMISED (to AVOID intubation) and IMMEDIATELY following EXTUBATION in patients with CHRONIC LUNG DISEASE and HYPERCAPNIA
Patients with ACUTE RESPIRATORY FAILURE who do NOT require IMMEDIATE INTUBATION with an UNDERLYING condition such as COPD and in whom a PROLONGED PERIOD of VENTILATORY SUPPORT is NOT anticipated, are most likely to BENEFIT from what therapy?
Non-invasive Positive Pressure Ventilation (NPPV)
What should be DONE NEXT for a patient who does NOT RESPOND to a 1-2 HOUR trial of Non-invasive Positive Pressure Ventilation (NPPV)?
ELECTIVE MECHANICAL INTUBATION
What type of VENTILATORY support is recommended in scenarios such as RESPIRATORY or CARDIAC ARREST, SEVERE ACIDOSIS (pH
INVASIVE Mechanical Intubation
What is the most COMMON VENTILATOR MODE used for patients with ARDS?
ASSIST/CONTROL (AC)
This VENTILATOR MODE delivers a PRESET VOLUME (TV breath) or PRESET PRESSURE for EACH DETECTED inspiratory effort and if there is no effort, it is delivered at a PRESET RATE?
ASSIST/CONTROL (AC)
This VENTILATOR MODE assures MAXIMAL diaphragm REST and MAXIMAL CONTROL of minute ventilation through a PRESET VOLUME and RESPIRATION RATE however can be UNCOMFORTABLE, can cause OVERVENTILATION in patients with HIGH RESPIRATION RATES and AIR TRAPPING?
ASSIST/CONTROL (AC)
This VENTILATOR MODE is used to ASSIST SPONTANEOUSLY-BREATHING patients as it delivers a HIGH RATE of FLOW to achieve a PRESET PRESSURE for each DETECTED INSPIRATORY EFFORT made by the patient HOWEVER, if the patient FAILS to INITIATE a BREATH or the PRESET PRESSURE is not sufficient to support the inspiratory flow, the delivered minute ventilation may be inadequate?
PRESSURE SUPPORT (PS)
This VENTILATOR MODE is a MIXTURE of BOTH ASSIST/CONTROL and PRESSURE SUPPORT modes which UNLIKE ASIST/CONTOL has LESS AIR TRAPPING and OVERVENTILATION and UNLIKE PRESSURE SUPPORT, it allows delivery of a certain MINUTE VOLUME however the breaths TRIGGERED by the PATIENT are PRESSURE-SUPPORTED not VOLUME SUPPORTED as in the ASSIST/CONTROL mode?
Synchronized Intermittent Mandatory Ventilation (SIMV)
What is the PHYSIOLOGIC HALLMARK of ARDS?
HYPOXEMIA (corrected with INVASIVE MECHANICAL VENTILATION COMBINED with OXYGEN and PEEP)
Delivering TIDAL VOLUMES of limited size (6 mL/kg of IDEAL BODY WEIGHT), MINIMIZING PLATEAU PRESSURE (
Limiting Ventilator-Associated Lung Injury (caused by trauma to alveoli)
This VENTILATOR feature, when exceeding a certain NUMBER, can cause HYPOTENSION by INCREASING INTRA-THORACIC PRESSURE resulting in DECREASED VENOUS RTURN to the RIGHT HEART, INCREASING PULMONARY VASCULAR RESISTANCE and DECREASED CARDIAC OUTPUT as well as PTX and ALVEOLAR BAROTRAUMA?
PEEP >15 cm H2O
What are the TWO (2) endpoints that SHOULD be achieved with PEEP regardless of pressure used?
Achieving ADEQUATE OXYGENATION with an FiO2
LOW MINUTE VENTILATION and PERMISSIVE HYPERCAPNIA with HIGH-FLOW RATE (delivery of the INSPIRATORY breath VERY QUICKLY allowing the rest of the breathing cycle for EXPIRATION) are best used in what patients?
Those with SEVERE OBSTRUCTIVE LUNG DISEASE (COPD or ASTHMA) that require INVASIVE MECHANICAL VENTILATION (because NPPV is preferred for COPD)
How is potential AUTO-PEEP avoided when a patient is anxious and “overbreaths” the vent due to hypercapnia (potent stimulus to increase respiration rate) by triggering breaths more FREQUENTLY than the set rate?
SEDATION
Because patients with OBSTRUCTIVE LUNG DISEASE present with ACUTE on CHRONIC RESPIRATORY ACIDOSIS (CO2 retention “hypercapnia”), when requiring INTUBATION, their MINUTE VENTILATION should be set to achieve what level of PCO2 in order to PREVENT IMMEDIATE RESPIRATORY CORRECTION which will result in LIFE-THREATENING METABOLIC ALKALOSIS?
The patient’s BASELINE LEVEL, NOT NORMAL PCO2
A patient that is INTUBATED becomes hemodynamically stable, recovered from respiratory failure, has a cough strong enough to clear their own secretions, has a low secretion burden and a patent upper airway, what’s the NEXT STEP?
WEANING OFF the VENT and EXTUBATION
What TEST is performed DAILY in an INTUBATED patient in order to assess their READINESS for WEANING off of an INVASIVE MECHANICAL VENTILATOR?
Rapid Shallow-Breathing Index (with interruption of sedation and spontaneous breathing trial)
What MUST the RATIO between the RESPIRATION RATE and TIDAL VOLUME be for a patient to have an 80% chance of SUCCESS of WEANING off of an INVASIVE MECHANICAL VENTILATOR?
RR/TV 105, 95% chance of FAILURE)
When should a tracheostomy be performed in an INTUBATED patient?
AFTER 14-21 DAYS of INVASIVE MECHANICAL VENTILATION?
Which patients benefit from DIRECT EXTUBATION to Non-invasive Positive Pressure Ventilation (NPPV) for WEANING off the INVASIVE MECHANICAL VENTILATOR?
Those with OBSTRUCTIVE LUNG DISEASE with HYPERCAPNIC RESPIRATORY FAILURE ONLY (COPD) - not asthma patients who have hypoxemic respiratory failure
What is PNA called when it occurs 48 HOURS AFTER ENDOTRACHEAL INTUBATION?
Ventilator-Associated Pneumonia
How can you diagnose Ventilator-Associated Pneumonia as STANDARD methods (CXR showing pulmonary infiltrates, colonized trachea secretions and blunted fever/leukocytosis) are not useful?
Sampling the LOWER RESPIRATORY TRACT with ENDOTRACHIAL TUBE suctioning and BRONCHOALVEOLAR LAVAGE (BAL) or via BRONCHOSCOPY (with brush sampling and lavage)
An exaggerated inflammatory response to an infection with dysfunction in coagulation resulting in vasodilation and capillary leak, hypotension and end-organ damage that significantly increases after the age of 65 is called?
SEPSIS (SIRS + Infection) - hypotension, decreased urine output, metabolic acidosis (lactic acid)
Altered Temperature, Tachycardia, HYPERventilation and Abnormal Leukocyte Count regardless of cause, are the findings in?
Systemic Inflammatory Response Syndrome (SIRS)
WHEN should BROAD-SPECTRUM ANTIBIOTICS be started in a patient with suspected SEPSIS?
AFTER blood & suspected infection source CULTURES are taken and WITHIN ONE HOUR of DIAGNOSIS
What happens when there is EITHER a DELAY or initiation of INAPPROPRIATE ANTIBIOTICS in a patient with suspected SEPSIS?
SIGNIFICANT INCREASE in MORTALITY
What is considered NORMAL central venous pressure (CVP) which is the pressure of the THORACIC VENA CAVA near the RIGHT atrium?
Normal CVP 3-8 mm Hg
What should the Central Venous Pressure (normal 3-8 mm Hg) be raised to when treating SEPSIS?
8-12 mm Hg
When should VASOPRESSORS be used when treating SEPSIS to avoid onset of SEPTIC SHOCK?
When the Mean Arterial Pressure is ≤65 mm Hg (
What should be done in a SEPTIC patient if the VENA CAVA OXYGEN SATURATION (SCVO2) is
- BLOOD TRANSFUSION to raise Hct >30%
2. START POSITIVE INOTROPIC AGENTS
When should COLLOID solutions (ALBUMIN) be used to treat SEPSIS instead of the much less expensive CRYSTALLOID solutions (NS, Lactated Ringer’s, etc.)?
Low oncotic pressure states (Burns, Liver Failure)
When should VASOPRESSORS be started when treating SEPSIS?
If the initial fluid challenge FAILS to adequate blood pressure for organ perfusion (Mean Arterial Pressure >70 mm Hg)
What should PLASMA GLUCOSE levels be reduced to in ICU patients, ESPECIALLY those recovering from SEPSIS?
GLUCOSE
How should antibiotics be managed in the treatment of SEPSIS?
NO MORE than 7-10 days unless there are abscesses, DAILY reassessment of antibiotic regimen to otptimize efficacy, COMBINED ANTIBIOTICS for neutropenia and pseudomonas
Why do MOST patients with SEPTIC SHOCK require INVASIVE MECHANICAL VENTILATION (intubation) and not NPPV?
Because they develop ARDS and thus a lung-protective strategy with LOW TIDAL VOLUMES must be used
WHEN is the ONLY TIME in which HCO3 (BICARBONATE) should be USED when treating LACTIC ACIDOSIS?
ONLY WHEN pH is
When SHOULD LOW-DOSE corticosteroids (IV hydrocortisone) be used in treating SEPSIS?
ONLY as a LAST RESORT if blood pressure does not respond to fluids and vasopressors
BESIDES the thermal and chemical injury of SMOKE inhalation, what other toxicity exists that must be addressed and recognized IMMEDIATELY?
Carbon Monoxide poisoning (CO) - carboxyhemoglobin
What BACTERIAL infections are BURN victims especially susceptible to?
PSEUDOMONAS and STAPHYLOCOCCUS (aureus)
In a case of CARBON MONOXIDE POISONING, what would you use to determine the patient’s BLOOD OXYGEN SATURATION LEVEL?
ABG (CANNOT USE PULSE OXIMETRY - false values)
What is the ANTIDOTE for SMOKE-INHALATION associated CYANIDE TOXICITY?
SODIUM THIOSULFATE (using nitrites can cause methemoglobin formation)
In a SMOKE-INHALATION injury patient, after INTUBATING them, giving them ANTIBIOTICS, IVF’s, Chest Physiotherapy and performing Bronchoscopic Debridement and Suctioning, what agent is given to treat BRONCHOSPASM and UPPER AIRWAY EDEMA?
INHALED RACEMIC EPINEPHRINE and other BRONCHODILATORS
How is RADIOCONTRAST ALLERGY different than other ALLERGIES?
The radiocontrast agent ITSELF activates MAST CELL degranulation without activating IgE on the surface of basophils and mast cells (as in typical anaphylaxis)
This type of ANGIOEDEMA is not associated with the typical cause (ACE-I use) and is rather FAMILIAL, caused by C1-inhibitor deficiency and ANGIOEDEMA episodes typically start early in life and occur after what situations?
TRAUMA or ILLNESS
What is the MOST COMMON cause of DEATH due to ANAPHYLAXIS?
AIRWAY CLOSURE due to LARYNGEAL EDEMA
What are the TWO (2) essential therapies for ALL patients with ANAPHYLAXIS due to ANY cause?
OXYGEN and IVF’s
An episode of ELEVATED BLOOD PRESSURE associated with ACUTE end-organ damage or dysfunction is called?
Hypertensive Emergency
Stroke, Acute Kidney Injury, Ischemic Chest Pain, Acute HF are examples of end-organ damage/dysfunction in patients with what condition?
Hypertensive Emergency
A DIASTOLIC blood pressure of ≥120 mm Hg WITHOUT evidence of END-ORGAN damage or dysfunction is called what?
Hypertensive Urgency
When a patient presents with POTENTIAL Hypertensive URGENCY/EMERGENCY, what should be RULED OUT FIRST?
Evidence of END-ORGAN damage or dysfunction (Hypertensive EMERGENCY)
AMS, Seizures, Muscle Rigidity with Rhabdomyolysis and resulting Kidney Failure in the setting of a body temperature >40ºC (>104ºF) with potential ARDS and DIC are seen in what condition?
HYPERthermic Emergencies (HEAT STROKE, MALIGNANT HYPERTHERMIA and NEUROLEPTIC MALIGNANT SYNDROME)
What TWO (2) medication types are commonly seen in patients with HYPERTHERMIC Emergencies as they can facilitate dehydration and HYPERTHERMIA?
Diuretics and Anticholinergics
What is the MOST effective way to COOL a patient with HYPERTHERMIA due to HEAT STROKE?
EVAPORATIVE COOLING (ICE PACKS or gastric/peritoneal lavage)
What medication is used as a FIRST CHOICE for controlling HYPERTENSIVE CRISIS?
IV NITROPRUSSIDE (risk is cyanide toxicity) - vasodilator
What medication is used for controlling HYPERTENSIVE CRISIS where the END-ORGAN damage/dysfunction is MYOCARDIAL ISCHEMIA?
IV NITROGLYCERIN - vasodilator
What medication is used for controlling HYPERTENSIVE CRISIS in PREGNANT patients?
IV HYDRALAZINE - vasodilator
What medication is used for controlling HYPERTENSIVE CRISIS in a patient with STROKE?
IV ENALAPRILAT - ACE-I (can also use IV LABETALOL)
What medication is used for controlling HYPERTENSIVE CRISIS in PHEOCHROMOCYTOMA?
PHENTOLAMINE (α-blocker)
Anesthetics HALOTHANES (inhaled gases) and depolarizing neuromuscular blockers (Succinylcholine, Decamethonium) can cause a reaction in which there is MARKEDLY INCREASED INTRACELLULAR CALCIUM with SUSTAINED MUSCLE TETANY resulting in muscle rigidity, masseter spasm, and HYPERTHERMIA with core temperatures up to 45ºC (115ºF) with cardiac arrhythmias and rhabdomyolysis for which there isa GENETIC SUSCEPTIBILITY?
MALIGNANT HYPERTHERMIA
Does previous exposure to agents that cause MALIGNANT HYPERTHERMIA suggest that RE-EXPOSURE will not result in this condition?
NO, it can happen ANYTIME
How is MALIGNANT HYPERTHERMIA treated?
DISCONTINUE OFFENDING AGENT, give DANTROLENE, IVF’s and COOLING measures + benzodiazepines for agitation
Can DANTROLENE be given PROPHYLACTICALLY to patients with HISTORY of MALIGNANT HYPERTHERMIA to avoid repeat reaction when receiving anesthesia with potentially offending agents (HALOTHANE gases or depolarizing neuromuscular blockers Succinylcholine and Decamethonium)?
YES!!
Muscle RIGIDITY, HYPERTHERMIA (can be very mild), AUTONOMIC DYSREGULATION and DELIRIUM seen in a patient after receiving a NEUROLEPTIC drug (haloperidol, chlorpromazine, thioridazine, fluphenazine) or in PARKINSON patients when HIGH-DOSE medications are discontinued abruptly?
NEUROLEPTIC MALIGNANT SYNDROME
How is NEUROLEPTIC MALIGNANT SYNDROME treated?
DISCONTINUE OFFENDING AGENT, give IVF’s and COOLING measures + benzodiazepines for agitation (dantrolene and bromocriptine may also be used)
What is the DIFFERENCE in the treatment of MALIGNANT HYPERTHERMIA and NEUROLEPTIC MALIGNANT SYNDROME?
DANTROLENE is usually used ONLY in MALIGNANT HYPERTHERMIA, all other measures (IVF’s, COLLING, Stopping the offending agent and benzodiazepines for agitation) are the same
In order to avoid triggering NEUROLEPTIC MALIGNANT SYNDROME, when using a neuroleptic such as HALOPERIDOL or CHLORPROMAZINE, you should avoid ADDING this particular DRUG as well as AVOID DEHYDRATION?
LITHIUM (can cause NEUROLEPTIC MALIGNANT SYNDROME when used concomitantly with another neuroleptic in the setting of dehydration)
WHEN can a patient who developed NEUROLEPTIC MALIGNANT SYNDROME on a drug (haloperidol, chlorpromazine, thioridazine, fluphenazine) be restarted on this drug, though at a LOWER DOSE initially?
AFTER 2 WEEKS
CORE temperatures below 35ºC (95ºF) from exposure to COLD weather or SUBMERSION in COLD WATER that is most commonly seen in the ELDERLY, ALCOHOL-INTOXICATION and PROLONGED SURGICAL PROCEDURES is called?
HYPOTHERMIA
What dysfunction is seen with HYPOTHERMIA?
HYPERKALEMIA, Shivering, AMS, Ataxia, Polyuria, decreased Heart Rate and Cardiac Output, Cardiac Arrhythmias, Pulmonary Edema, Coma, Hypotension, Areflexia and Cardiac Arrest
What ECG ABNORMALITY is seen in HYPOTHERMIA?
J-Wave (right after the S-wave of the QRS complex which will look like a “W”) best seen in the INFERIOR (II, III, aVF) and LATERAL (I, aVL, V5, V6)
How should patients with SEVERE HYPOTHERMIA (CNS depression, cardiac dysfunction) be re-warmed?
INVASIVELY (gastric, peritoneal or pleural space lavage)
WHEN is THERAPEUTIC HYPOTHERMIA used?
After CARDIAC ARREST, to improve neurologic outcomes
When can patients with HYPOTHERMIA rewarm THEMSELVES if REMOVED from the COLD environment and kept dry?
If they are SHIVERING (body’s natural treatment to hypothermia)
Because alcohol is a depressant, chronic abuse with dependence causes WITHDRAWAL if alcohol is SUDDENLY stopped. How does this manifest?
Diaphoresis, Anxiety, Insomnia, TREMMOR, PALPITATIONS, HA
What symptoms suggest DELIRIUM TREMENS?
SEIZURES, HALLUCINATIONS (occurs 2-4 days after cessation)
A patient in WITHDRAWAL from ALCOHOL with cardiac dysfunction and arrhythmias due to HYPOKALEMIA, HYPOMAGNESEMIA and HYPOPHOSPHATEMIA has likely developed what?
Delirium Tremens
How are ALCOHOL WITHDRAWAL and DELIRIUM TREMENS treated?
BENZODIAZEPINES, IVF’s, ELECTROLYTE correction, THIAMINE, GLUCOSE and FOLATE as well as nutrition
Poisoning with what ALCOHOL form causes KIDNEY INJURY?
Ethylene Glycol (antifreeze) - ANIONIC GAP METABOLIC ACIDOSIS
Poisoning with what ALCOHOL form causes RETINAL TOXICITY?
METHANOL - ANIONIC GAP METABOLIC ACIDOSIS
What is seen when a patient ingests ISOPROPYL ALCOHOL (rubbing alcohol)?
ELEVATED KETONE LEVELS (acetone) and CNS DEPRESSION but no kidney or retinal injury, no metabolic acidosis
What is used to treat POISONING with Ethylene Glycol (antifreeze), Methanol and Isopropyl Alcohol (rubbing alcohol)?
FOMEPIZOLE, ETHANOL or DIALYSIS
At what Hb-BOUND percentage does CARBON MONOXIDE (carboxyhemoglobin) reach TOXIC levels?
> 20% (shifts oxyhemoglobin dissociation curve to the LEFT, reducing oxygen transfer to tissues resulting in dysfunction of brain and heart)
HA, Disorientation, Nausea, Chest Pain, AMS, Dyspnea, Arrhythmia, Muscle Weakness, Coma and Death occur with prolonged exposure to this gas?
CARBON MONOXIDE
What happens DAYS to MONTHS in 40% of patients who recover from ACUTE Carbon Monoxide Toxicity?
Delayed Cognitive Impairment Syndrome
How can patients with Carbon Monoxide Toxicity be treated to PREVENT the Delayed Cognitive Impairment Syndrome that can be seen in up to 40% of such patients after recovery?
HYPERBARIC OXYGEN
How is Carbon Monoxide Toxicity treated?
100% OXYGEN (if carboxyhemoglobin is >20%, use HYPERBARIC OXYGEN in available)
In addition to 100% OXYGEN for CARBON MONOXIDE TOXICITY, what ELSE must be given to a SMOKE-INHALATION victim for treatment?
SODIUM THIOSULFATE for concomitant CYANIDE TOXICITY
Hypoxia, Lactic Acidosis with HA, Nausea, Chest Pain, Abdominal Pain and Anxiety and ORGAN DYSFUNCTION occur with exposure to this TOXIN?
CYANIDE (INHALED OR INGESTED)
What is used to treat CYANIDE TOXICITY?
SODIUM THIOSULFATE (for inhalational toxicity) or NITRITES or Sodium Thiosulfate (if ingested) or Hydroxocobalamin
What toxicity can be seen if NITROPRUSSIDE is given at a HIGH-RATE and for a PROLONGED period of time?
CYANIDE TOXICITY (treat with either sodium thiosulfate or nitrites - since not inhalational)
What DRUG of ABUSE increases CATECHOLAMINES causing ANOREXIA, tachycardia, hypertension, hyperthermia and agitation with potential MYOCARDIAL ISCHEMIA, MI, STROKE, SEIZURES, ACUTE KIDNEY and LIVER FAILURE and PSYCHOSIS?
AMPHETAMINES (3,4-methylinedioxy-methamphetamine “ecstasy”) - STIMULANT
What DRUG of ABUSE can specifically cause BRUXISM (severe dental damage and hyponatremia leading to cerebral edema)?
(3,4-methylinedioxy-methamphetamine “ecstasy”) - STIMULANT
How is TOXICITY with AMPHETAMINES treated?
BENZODIAZEPINES and supportive measures (IVF’s and nutrition)
What DRUG of ABUSE causes tachycardia, MYDRIASIS (pupillary DILATION), hyperthermia and agitation, ATRIAL/VENTRICULAR ARRHYTHMIAS, myocardial ischemia, AORTIC DISSECTION/RUPTURE, seizures, stroke, BRONCHOSPASM, PULMONARY EDEMA, ALVEOLAR HEMORRHAGE and RHABDOMYOLYSIS?
COCAINE - STMULANT
How is TOXICITY with COCAINE treated?
BENZODIAZEPINES and Calcium Channel Blockers (to control HR and BP) or COMBINED α & β - blocker like LABETALOL
What is MYOCARDIAL ISCHEMIA due to COCAINE TOXICITY treated with ?
NITROGLYCERIN + ASPIRIN
TOXICITY (overdose) with this MEDICATION produces BOTH a ANION GAP METABOLIC ACIDOSIS and RESPIRATORY ALKALOSIS by stimulating CENTRAL RESPIRATORY CENTERS?
ASPIRIN (salicylate) TOXICITY (overdose)
How is ASPIRIN (salicylate) TOXICITY treated?
ACTIVATED CHARCOAL, IV GLUCOSE and IV NaHCO3 (sodium BICARBONATE)
SEVERE ABDOMINAL PAIN
Pancreatitis, Aortic Aneurysm
What should be done to treat a patient in which abdominal pain is suspected to be from thrombosis or ischemia (diffuse pain out of proportion to physical exam)?
ANTIBIOTICS and EMERGENCY SURGERY
What does FREE AIR under the diaphragm on an abdominal film suggest?
INTESTINAL PERFORATION
CRAMPY abdominal pain, HIGH-PITCHED HYPERACTIVE bowel sounds and diarrhea, suggest what condition?
Partial small bowel obstruction
What is the typical duration of abdominal pain in an ACUTE ABDOMEN event?
INTOXICATION with these DEPRESSANTS cause symptoms of SALIVATION, LACRIMATION, POLYURIA, DIARRHEA, GI upset, EMESIS, CONFUSION, bradycardia, MIOSIS (pin-point pupils)?
CHOLINERGICS (organophosphates - insecticides, sarin; Physostigmine, NICOTINE)
INTOXICATION with these STIMULANTS cause symptoms of hyperthermia, DRY skin and mucus membranes, agitation, DELIRIUM, tachycardia, tachypnea, hypertension and MYDRIASIS (wide pupils)?
ANTICHOLINERGICS (antihistamines, TCA’s, Antiparkinsonian drugs, Atropine, Scopolamine)
INTOXICATION with these DEPRESSANTS cause symptoms of MIOSIS (pin-point pupils), RESPIRATORY DEPRESSION, LETHARGY, CONFUSION, hypothermia, bradycardia, hypotension?
MORHINE, HEROIN
How do pupils react to STIMULANTS (toxicity)?
WIDE (mydriasis)
How do pupils react to DEPRESSANTS (toxicity)?
CONSTRICT - PIN POINT (miosis)
How do you reverse a β-blocker toxicity/overdose (heart block, bradycardia, hypotension)?
GLUCAGON + CaCl (or pacing)
What ACETAMINOPHEN dose taken within 8 HOURS is considered TOXIC (ACUTE/FULMINANT HEPATITIS/FAILURE)?
≥7.5 g (treat with N-acetylcysteine, PO or IV within 8 hours)
How do you reverse a Ca-Channel Blocker toxicity/overdose (heart block, bradycardia, hypotension)?
GLUCAGON + CaCl (or pacing)
How do you reverse a DIGOXIN toxicity (tachy/brady arrhythmias, CNS/GI symptoms)?
Digoxin-specific Ab (hemodialysis does NOT WORK)
How do you reverse a SULFONYLUREA toxicity/overdose - seen in CHILDREN/ELDERLY - (HYPOGLYCEMIA)?
DEXTROSE, OCTREOTIDE, GLUCAGON
What can occur with SULFONYLUREA toxicity/overdose (seen in children/elderly) after initial treatment and reversal (dextrose, octreotide, glucagon)?
Can RECUR after initial response to treatment and patients must be MONITORED for this
WHYS is OCTREOTIDE used in SULFONYLUREA toxicity/overdose?
BECAUSE it INHIBITS INSULIN SECRETION
How do you reverse a LITHIUM toxicity/overdose (tremor, SEIZURES, nausea, diabetes insipidus with polyuria, arrhythmias, cardiogenic shock, photosensitivity)?
YOU CAN’T!! MUST TREAT arrhythmias, seizures and hypotension or HEMODIALYSIS
How do you reverse a SALYCILATE (aspirin) toxicity/overdose (anion-gap metabolic acidosis AND respiratory alkalosis, HYPERVENTILATION, dehydration, seizures)?
IV NaHCO3 (sodium BICARBONATE) or HEMODIALYSIS
For what TWO (2) DRUG TOXICITIES can you NOT use HEMODIALYSIS to treat as it is INEFFECTIVE!!!?
DIGOXIN, TCA’s
What DRUG TOXICITY does NOT HAVE an ANTIDOTE and the ONLY TREATMENT is SUPPORTIVE/HEMODIALYSIS?
LITHIUM
How do you reverse an ANTICHOLINERGIC (theophylline) toxicity/overdose (nausea, nervousness, tachycardia, CNS stimulation, DRYNESS, SEIZURES, ARRHYTHMIAS)?
ACTIVATED CHARCOAL/HEMODIALYSIS
How do you reverse a TCA toxicity/overdose (SEIZURES, SEVERE ARRHYTHMIAS, RHABDOMYOLYSIS & KIDNEY FAILURE)?
IV NaHCO3 (sodium BICARBONATE) + BENZODIAZEPINES
What should be done with ALL SEDATED PATIENTS on CONTINUOUS INFUSIONS in an ICU setting?
DAILY sedation interruptions
What is the BEST treatment for BOTH AGITATED and LETHARGIC DELIRIUM?
HALOPERIDOL
These TWO (2) conditions can be seen in up to 50% of patients in the ICU for PROLONGED CRITICAL ILLNESS?
- Critical Illness MYOPATHY - complicates vent weaning
2. Critical Illness POLYNEUROPATHY
How long can WEAKNESS from Critical Illness MYOPATHY persist for?
YEARS or INDEFINITELY
How many patients get COGNITIVE IMPAIRMENT (acquired dementia) that can persist for YEARS after PROLONGED ICU STAY for CRITICAL ILLNESS or INDEFINITELY that decreases quality of life and are associated with AGE, DURATION of MECHANICAL VENTILATION and degree of HYPERGLYCEMIA?
75% (some develop DEPRESSION, ANXIETY and POST-TRAUMATIC STRESS DISORDER)
Is there ANY benefit to post-pyloric enteral feeding for ICU patients with critial illness vs gastric feeding?
NO!! (enteral feeding is ALWAYS preferred, and when feasible, gastric feeding is recommended)
Overfeeding an ICU CRITICALLY ILL patient with this NUTRIENT can cause EXCESSIVE CO2 production resulting in DIFFICULTY with VENTILATION?
HIGH-FAT formulations
ICU patients with KIDNEY FAILURE NOT on DIALYSIS should have what NUTRIENT LIMITED?
PROTEIN (if on dialysis, INCREASE!!)
ICU patients with KIDNEY FAILURE ON DIALYSIS should have what NUTRIENT INCREASED?
PROTEIN (if NOT on DIALYSIS, DECREASE!!)
ICU patients with HYPERCARBIC (CO2) RESPIRATORY FAILURE should have which NUTRIENT LIMITED and which NUTRIENT INCREASED?
LIMIT CARBOHYDRATES
INCREASE FAT
ICU patients with BURNS should have what NUTRIENT INCREASED?
PROTEIN
ICU patients with PANCREATITIS should have what types of ENTERAL/TOTAL PARENTERAL NUTRITION with what NUTRIENT LIMITED?
ENTERAL - ELEMENTAL formulation
TOTAL PARENTERAL - LIMIT FAT (keep triglycerides
What serum level of PRE-ALBUMIN indicates a SEVERE PROTEN and CALORIC MALNUTRITION?
Groups of best practices that improve patient care are called BUNDLES (ventilator bundle, central line bundle, delirium bundle, etc.), CLOSED ICU MODELS, implementation of RAPID RESPONSE TEAMS, CARE ALGORITHMS are all systems put in place for what purpose?
Providing BEST PRACTICE
