Pulmonary Flashcards
Acute respiratory failure
Respiratory dysfunction resulting in abnormalities of oxygenation ofr ventilation severe enough to threaten vital organs
What blood gas paO2 level is it considered ARF
<60
What PCO2 level is considered ARF
> 50
What all is included in an arterial blood gas (ABG)
pH
PaO2
PaCO2
HCO3
Normal blood pH
7.35-7.45
Normal PaO2
80-100
Normal PaCO2
35-45
Normal HCO3
22-26
How to shorthand ABG
pH/pCO2/pO2/HCO3
Symptoms and signs of acute respiratory failure
Hypoxemic or hypercapnic
DYSPNEA
HEADACHE
Cyanosis
Restlessness
Confusion
Tachypnea
What to give someone that is hypoxemic
Nasal cannula 1-3 liters
Then Venturi mask
Number one step in treating patient in respiratory distress
Get an ABG
Hypoxemic and hypercapnic causes
Airway disorders (asthma, COPD, obstruction)
Pulmonary edema (ARDS, left heart dysfunction, acute leg injury)
Lung disorder (pneumonia, interstitial lung disease, aspiration, lung contusion)
Pulmonary vasculature problems
Chest wall, diaphragm, and pleural disorders (rib fracture, pneumothrax, pleural effusion, flail chest)
Neuromuscular problems
CNS problem
Increased CO2 production
ARF diagnosis
Stabilize aireay
ABG
CPK to check for rhabdo
Toxicology
BMP
CMP
Common findings in pts with hypercapnia
History of sedative use
History of COPD
Obesity
Snoring
Postop
ARF BIPAP
8-12 cm H2O inspiratory pressure (pushing O2 in)
3-5 cm H2O expiratory pressure (pulling CO2 out)
CPAP vs BiPAP
BIPAP changes pressure to help with inspiration and expiration (higher pressure during inspiration).
CPAP has the same constant pressure
BIPAP contraindications
AMS
Throwing up
Upper airway obstruction
Moderate to severe ARDS
Ventilator
Maintains airway
Ensures adequate alveolar ventilation
Might be done through tracheal intubation (noninvasive positive pressure ventilation
Noninvasive positive pressure ventilation (NIPPV)
Full facemask or nasal mask for COPD with hypercapnic respiratory.
Pt must be able to protect and maintain patency of airway, handle own secretions, tolerate mask apparatus
Uses BIPAP-like changes in pressure
Tracheal intubation indications in ARF
Hypoxemia even with supplemental oxygen
Upper airway obstruction
Impaired airway obstruction
Inability to clear secretions
Respiratory acidosis
BIPAP and NIPPV doesn’t work
Meds to give before intubation for ARF
Etomidate or ketamine
Tidal volume
Quantity of gas delivered with each breath
Positive end-expiratory pressure (PEEP)
Prevents lungs from collapsing after exhaling
Pressure support
Suppport provided by ventilator in breathing
Normally 5-8
Inspiratory time
Period over ventilator delivers a breath
Fraction of inspired oxygen (FiO2)
Fraction of inhaled air that is O2
We increase it on ventilator when can’t get pts O2 levels up
Peak inspiratory pressure
Highest pressure in lungs during inspiration
Two most common primary control variables on ventilator
Volume
Pressure
Complications often caused by ventilator
Barotrauma
Volutrauma
Acute respiratory alkalosis
Hypotension
Ventilator associated pneumonia
What to do when pt is in respiratory failure but an endotracheal tube can’t be placed
Cricothyrotomy (going through cricothyroid cartilage into airway
ARF caused by opioid overdose treatment
Nalaxone (narcan)
ARF caused by benzo overdose treatment
Flumazenil (romazicon)
pCO2 of pregnant
30-32
Acute respiratory distress syndrome (ARDS)
Causes severe diff breathing.
Usually happens in people already critically ill or major injuries
ARDS diagnosis
NONCARDIAC PULMONARY EDEMA
Resp failure within one week of known clinical insult
New bilateral radiographic pulm opacities that aren’t PE, atelectasis, or nodules
Resp failure not explained by HF or volume overload.
Impaired O2 with PaO2 to FiO2 ratio less than 300mmHg and PEEP >5cm H20
What determines severity of ARDS
PaO2/FiO2 ratio
Mild: 201-300
Moderate 101-200
Severe <100
Acute lung injury
Used to describe pts wht hypoxemia (PaO2/FiO2=201-300)
(Mild ARDS)
ARDS risk factors
Sepsis
Aspiration
Pneumonia
Trauma
Blood transfusion
Lung and stem cell transplantation
Pancreatitis
Drug OD
Alcoholism
Genetics
Tobacco
Pulmonary causes of ARDS
Pneumonia
Aspiration og gastric contents
Pulmonary contusion
Inhalation injury
Fat emboli
Non-pulmonary causes of ARDS
Sepsis
Trauma
Drug OD
Pancreatitis
Cardiopulm bypass
ARDS pathophys
Damage to capillary endothelium
Protein escapes from vascular space
Fluid shift into interstitium (third spacing)
Edema with proteinaceous fluid
Loss of surfactant
All this causes impaired gas exchange, decrease lung compliance, and pulmonary HTN
ARDS symptoms
Dyspnea
Increased O2 requirement
Cough, wheeze
Chest pain
Hemoptysis (blood spit)
Confusion, resp distress, cyanosis, diaphresis
ARDS physical exam findings
Tachypnea, tachycardia
Raised JVP, crackles, S3/S4 gallop
Dullness to percussion, egophony , enlarged lymph nodes
Check skin turgor an d mucus membranes for volume status
ARDS imaging
CXR shows bilateral diffuse alveolar opacities with dependent atelectasis and usually bronchograms
Chest CT shows widspread patchy opacities (ground glass)
ARDS labs
ABG shows hypoxemia
Acute respiratory alkalosis
Pneumonia or sepsis may have elevated WBC
BNP <100
ARDS EKG
Maybe arrhythmias or ST changes
ARDS common complication
Organ failure (Kidney, liver, gut, CNS, Cardiovascular)
ARDS treatment
Treat underlying cause
Mechanical ventilation
Low tidal volume (4-6 ml/kg) to avoid volutrauma (lung overdistension)
Prostacyclin
Nitric oxide
PDE4 inhibitors
ARDS supportive care
Sedation
Hemodynamic monitoring
Nutritional support
Fluid management
Prone positioning
Normal setting for CPAP
5cm H2O
Maximium setting of CPAP
20cm H2O
Transudates
Clear fluid low in protein and cell content
Exudates
Cloudy fluid high in protein and cell content
Pleural effusion causes
Increased production of fluid with nromal capillaries (transudative)
Increased production of fluid with abdnormal capillary permeability (exudates)
Decreased lymphatic clearance from pleural space (exudates)
Infection in pleural space (empyema)
Bleeding in pleural space (hemothorax)
Pleural effusion treatment options
Thoracentesis (drain)
Observe
Diuretics
Pleural effusions symptoms and signs
Dysnpnea
Cough
Chest pain
Physical findings usually absent in small ones
Dullness to percussion
Atelectasis may cause bronchial breath sounds adn egophony above effusion
Pleural friction rub
Empyema
Purulent fluid drained from some pleural effusion.
pH<7.2
Glucose<40
Positive Gram stain
Chylothorax
Lymph causing pleural effusion
TG>100
Hemorrhagic pleural effusion
Mixture of blood and pleural fluid
Hemothorax
Presence of gross blood on pleural space
Lab findings that show pleural fluid is exudative
Pleural fluid protein to serum protein ratio >0.5
Pleural fluid LDH to serum LDH ratio >0.6
Pleural fluid LDH >2/3 upper limit of normal serum LDH
If none of these are met, that means its transudative
Thorocostomy
Putting in a chest tube
Thorocotomy
Opening the chest
Transudates pH
7.4-7.55
Most common transudative effusion
Heart failure
Most common bacterial exudative effusion
Bacterial pneumonia and cancer
What does elevated amylase in pleural fluid suggest
Pancreatitis
Pancreatic pseudocyst
Adenocarcinoma of lung or pancreas
Esophageal rupture
TB pleural effusiion findings
Adenosine deaminase
Interferon-gamma
Granulomatous inflammation in 60% of pts
Paramalignant effusino
Efussion in pt with cancer when repeated attempts to identify tumor cells in pleural fluid or pleura but continues to be nondiagnostic but there is a solid tumor somewhere.
No evidence of cancer but you know there’s malignancy
How much fluid must be present on standard upright CXR to be visible
175-200 ml
How much fluid must be present on lateral CXR to be seen
50 mL
How much fluid must be present to be seen on on CT scan
10 mL
Pleurvac
Drains pleural effusion.
Helps reestablish normal neg pressure
Facilitates lung re-expansion
Prevents air and fluid from reentering chest cavity
Malignant pleural effusion treatment
Thoracenesis if symptomatic
If fluid remains, place indwelling catheter pt can access at home
Simple/uncomplicated pleural effusion
Free flowing sterile exudates of modest size resolved quickly with abx
Complicated pleural effusion
Larger
More inflammatory stimuli (low glucose, low pH, loculation)
Hemothorax treatment
Close observation for small and asymptomatic
Drain existing blood clots
Keep track of bleeding
Reduce risk of fibrothorax
Permit getting edges close together to reduce hemorrhage
Three categories of pneumothorax
Spontaneous (primary or secondary)
Traumatic
Iatrogenic
Primary spontaneous pneumothorax
Occur in the absence of underlying lung disease
Secondary spontaneous pneumothorax
Complication of preexisting pulmonary disease
Tension pneumothorax causes
Trauma
Infection
CPR
Pressure of pleural space excedes alveolar vanous pressures
Tension pneumothorax signs and symptoms
Increased JVP
Systemic HTN
Pulsus paradoxus
Tachycardia
Mediastinal/tracheal shift
Tension pneumothorax treatment
IMMEDIATE needle decompressions in 2 intercostal space at midclavicular line
Pneumothorax treatment
Chest tube
Very small ones can resolve spontaneously
Indications for sthoroscopy or open thoracotomy
REcurrence of spontaneous pneumothorax
Bilateral pneumothorax
Failure of tube thoracosotomy for first episode
Pleuritis
Localized, sharp, fleeting pain from acute pleural inflammation
Pleuritis causes
Viral respiratory infections
Pneumonia
Pleural effusion
Pleural thickenin
Air in pleural space
Simple rib fractures
Pleuritis treatment
Treat underlying disease
Analgesis and anti-inflammatory meds for pain
Pneumonitis
Inflammatin of lung tissue
Usually noninfectious
Inflammation makes it hard for gas exchange in aveoli
Pneumonia
Type of pneumonitis
INfection causes inflammation.
Infection causes alveoli to fill with purulence and can become solid
Bacterial, fungal, viral, aspiration pneumonia
Types of pneumonitis
Aspiration (aspiration pneumonia)
Hydrocarbon (lipoid pneumonia)
Hypersensitivity
Radiation
Vaping
Acute aspiration of gastric contents
One of the most common causes of ARDS
The more acidic the material, the greater the degree of chemical pneumonitis
Signs and symptoms of acute aspiration event
HYPOXEMIA (first)
Cough
Wheezing
Fever
Tachypnea
Patchy alveolar opacities on radiograph
Leukocytosis
Acute aspiration of gastric contents treatment
O2
Maintain aireway
Use rebreather mask
Fluids to avoid hypotension but careful bc pulm edema
No antibiotics unlesss aspiration pneumonia develops (usually 2-3 days after aspiration in 1/4 of pts)
Chronic aspiration of gastric contents
Achalasia
Esophageal stricture
GERD
Systemic sclerosis (scleroderma)
Esophageal carcinoma
Esophagitis
GERD
Relaxation of tone of the lower esophageal sphincter allows reflux of gastric contents into esophagus and can eventually cause aspiration
Things other than GERD that relax lower esophageal sphincter
Cig smoking
Alcohol
Caffeine
Theophylline
Pulmonary disorders linked to GERD
Asthma
Chronic cough
Bronchiectasis
Pulmonary fibrosis
Modified Barium Swallow study
Looking to see how pt is swallowing solids or liquids.
Have them drink something with barium and can watch it through floroscopy.
Watches oral, pharyngeal, and upper esophagus
Aspiration pneumonia
Infection caused by less virulent bacteria usually found in upper airways or stomach
Aspiration pneumonia clinical presentation
Depends on what causes it
Cough
Purulent sputum
Dyspnea
Fever
NOT rigors or chills
Hospital acquired aspiration pneumonia
Staph aureus
Sputum has putrid odor
Infectious process is faster in infections with anaerobes
Aspiration pneumonia labs
Blood cultures
Sputum gram stain and culture
Respiratory viral panel
Urine streptococcal antigen testing
Sputum or urine Legionella testing
Procalcitonin
Elevated with bacterial infections, not viral infections
Aspiration pneumonia imaging
CXR may be negative early on
Can be caught early on CT
Aspiration pneumonia treatment
Antibiotics
5 days for community acquired aspiration pneumonia
7 days for hospital acquired aspiration pneumonia
Café Coronary
Sudden death by obstruction of upper airway by food
Associated with elderly, dental problems, babies
Associated with sedative drugs and alcohol
Need heimlich maneuver
What chronic conditions can be caused by rentention of aspirated foreign body in tracheobronchial tree
Atelectasis
Post-obstructive hyperinflation
Acute and recurrent pneumonia
Bronchiectasis
Lung abscess
Best diagnostic test for retention of aspirated foreign body
CXR DO THIS FIRST (two views)
Retention of aspirated foreign body treatment
Bronchoscopy
Remove
Aspiration of inert material
Soil, sand, rock, etc (no chemicals)
Can cause asphyxia if amount aspirated is massive and cough is impaired.
Need suction if this is the case
Hydrocarbon pneumonitis
Aspiration of toxic materials into lungs (usually gasoline) usually causing pneumonia.
As soon as gas gets into mouth you cough increasing risk of aspiration
Lungs injured from vomiting gas
Hydrocarbon pneumonitis treatment
Supportive
Lung protected from repeated aspiration with CUFFED endotracheal tube
Lipoid pneumonia
Chronic syndrome related to repeated aspiration of oily materials.
Occurs in elderly with impaired swollowing
Lipoid pneumonia signs and symptms
Patchy opacities
Lipid-laden macrophages in expectorated (coughed up) sputum
Hypersensitivity pneumonitis cause
AKA extrinsic allergic alveolitis
Exposure to iinhaled organic antigens leads to acute illness
(moldy stuff, sawdust, deetergents)
Hypersensitivity pneumonitis signs in imaging
Interstitial infiltrates of lymphocytes and plasmacells with noncaseating granulomas in interstitial and air spaces
Can be acute, chronic, recurrent
Hypersensitivity physical exam findings
Tachypnea
Crackles
Midinspiratory squeeks (chirping or squawks)
Digital clubbing
Initial imaging of Hypersensitivity of pneumonitis
CT scan of chest
What is used to stage functional lung damage in hypersensitivity pneumonia
PFTs
Hypersensitivity pneumonitis labs
IgG
Acute radiation pneumonitis
AKA radiation induced lung injury
Occurs in people that have had radiation for treatment of lung, breast, or hematologic malignancies
How long does it take symptoms of acute radiation pneumonitis to start
4-12 weeks after irradiation
How long does it take for symptoms of late or fibrotic radiation pneumonitis to star
6-12 months after radiation
Acute radiation pneumonitis symptoms
Nonproductive cough
Dyspnea
Fever
Chest pain
Malaise and weight loss
Acute radiation pneumonitis physical exam
Crackles or pleural rub
DUllness to percussion
Skin erythema may outline radiation port
Tachypnea, cyanosis, HTN
Acute radiation pneumonitis diagnosis
Chest CT preferred
PFTs to rule out COPD flare up or interstitial process
Tidal volume and total lung capacity lowered.
O2 may be low
Bronchoscopy to see infection, bleeding, malignancy
Acute radiation pneumonitis treatment
Glucocorticoids (no benefit with pts with established fibrosis)
Prednisone
Medication toxicities
Asthma with beta blockers, NSAIDs, and nebulized drugs
Pulmonary edema with beta blockers
Ecigarette or vaping product use associated lung injury (EVALI)
Acute lng injury with actue fibrinous pneumonitis, diffuse alveolar damage, or organizing pneumonia
EVALI symptoms
SOB
Cough
Chest pain
Hemoptsis
Fever and chills
NVD
Abd pain
EVALI physical exam
Fever
Tachycardia
Tachypnea
Hypoxemia
Progression to respiratory failure common
EVALI labs to get
CBC
BUN/Cr
Check LFTs if pt has GI symptoms
EVALI imaging
Diffuse bilateral opacities
Ground glass
Sometimes subpleural
EVALI treatment
Hospitalization if bad.
Emi[iric antibiotics
Maybe antiviral
SARS-CoV-2 pathophys
occurs due to development of prolonged inflammatory cascade clled cytokine storm
Uncontrold amplication of IL- leads to multiorgan failure and death
SARs Cov-2 symptoms and signs
Many asymptomatic
Symptoms start 2-14 days after exposure
Cough
Fever
Chills/rigors
Myalgias
Dyspnea
SARS CoV-2 lab findings
Neutrophillia
Absolute lymphtocytosis
Increased LDH
Increased LFT
Elevated D-dimer
Elevated fibrin
Platelet counts usually neffected
SARS CoV-2 imaging
Diffuse ground glass opacities and/or multilobular infultrates that often turn into consolidation.
May appear on CXR or CT scan
SARS-CoV-2 complications
ARDS
Pulmonary embolus
HF
Myocarditis
Acute coronary syndrome
Sudden death
Stroke
Encehphalopathy
Multisystem inflammatory syndrome
Complication of SARS COV-2 in kids
Mimmics kawasaki
SARS COV-2 treatment
Usually mild and require no treatment
Early course antivirals
Later cytokine storm phase needs anti-inflammatory
Remdisivir
Remdisivir
used to treat SARS COV-2
When to admit someone with SARS CoV-2
Respiratory failure and ARDS
High risk category
COVID-19 outpatient treatment
Nirmatrelvir/Ritonavir (paxlovid)
Oral tablets taken over 5 days
Respiratory Syncytial Virus (RSV)
Paramyxovirus that causes annual outbreaks during winter
Happens in wet months outside of US
Leading cause of hospitalization in children
Causes upper and lower respiratory tract infections in adults
RSV symptoms
Bronchiolitis
Fever
Tachypnea
Wheezing
APNEA is common presenting symptom
Lung hyperinflation causing decreased gas exchange
Pulmonary hemorrhage
Most common cause of acute lower respiratory infection and otitis media
RSV
RSV lab diagnosis
ELISA
Imunoflluorescent
PCR
RSV treatment
Supportive (hydration, humidification, ventilatory support)
Ribavirin
Plavizumab for infants
NO bronchodilators or corticosteroids
CDC recomendations for RSV vaccine
60 yrs and older
50-59 with underlying conditions
INfants and young children
Pregnant (32-36 weeks sep-jan)
Human Metapneumovirus clinical presentation
Muld upper respiratory infection or severe lower respiratory tract infection with bronchiolitis, croup (barking seal), pneumonia
Human metapneumovirus treatment
Ribavirin for lung transplant pts
Human metapneumovirus diagnosis
PCR
Human parainfluenza virus
Most common in children
HIPIV-1 causes croup
HPIV-2 causes croup
HPIV-3 causes bronchiolitis and pneumonia
HPIV-4 causes less frequently reported pathogen
Human parainfluenza virus diagnosis
ELISA
Immunofluorescence
PCR
Culture
Nipah virus
Southeast asia
Fruit bat is natural host
Pigs, cows, human transmission
Causes acute encephalitis with high fatlity raes
Rspiratory symptoms
Cranial nereve palsies, encephalopathy, dystonia
Nipah virus diagnosis
ELISA
PCR
Three types of seasonal influenza
Type A (human, swine, horse, bird)
Type B (humans)
Type C (humans) more mild
Seasonal influenza signs and symptoms
Asymptomatic
Fever
Chills
Headache
malaise
Myalgias
Confusion in elderly
Resp symptoms
GI symptoms (usually in children with type B)
Lymph node enlargement
Seasonal influenza diagnosis
Positive rapid flu test
PCR
People at high risk of hospitalization from seasonal influenza
Astma pts
Nursing home
>65y/o
Obese
Underlying conditions
Immune deficiency
Pregnancy
Seasonal flu complications
Pneumococcal pneumonia
Staphylococcal pneumonia
Necrosis of respiratory epithelium
Increased adherence of bacteria to infected cells
Ciliary dysfunction
Reye syndrome
Giving aspirin to child causes hepatic failure and encephalopathy.
Seasonal influenza treatment
Supportive
-mivir
Baloxavir (causes diarrhea and bronchitis)
Who should get flu vaccine
Everyone over 6 months old with no contraindications
Types of flu vaccine
Inactivated
Recombinant
Live attenuated
Flu vaccine contraindication
Past severe allergic reaction.
Wait until healthy
When to admit someone with seasonal influenza
Pneumonia
Decreased O2
Changes in mental status
Consider with pregnancy
Avian influenza
Zoonotic influenza
Comes from birds (chickens)
Can get from eating or handling chickens
H5, H7, H9
H5N1 or H7N9 avian influenza symptoms
Fever
Lower respiratory (cough, dyspnea)
Upper respiratory symptoms less common
Avian influenza signs ans symptomc
Conjunctivitis (H7)
Encephalopathy
Seizure
Liver impairment
Prolonged febrile states
General malaise
Resp failure, multiorgan dysfunction, septic shock is usual cause of death
Avian influenza diagnosis
RT-PCR
Need to test within 7 days of onset
Avian influenza treatment
-mivir
Severe acute respiratory syndrome (SARS)
Caused by coronavirus
Natural reservoir is horseshoe bat
SARS symptoms and sign
Atypical pneumonia
Affects persons in all age groups
Ranges from asymptomatic to severe respiratory illness
Incubation 2-7 days
Can be spread for 10 days
Fever
Chills
Cough
SOB
Rales
Rhonchi
Diarrhea
Delerium in elderly
SARS lab findings
Leukopenia
Low DIC
High ALT and CPK
O2 <95 with pulmonary infiltrates
SARS diagnosis
RT-PCR usually negative in first week of illness
Serum serologies
SARS complications
ARDS with bilateral consolidations (requires intubation and ventilaion)
SARS treatment
Supportive
Lopinaver/rotinavir
Ribavirin
Interferon
IVIG
Systemic corticosteroids
Middle eastern respiratory syndrome-coronavirus (MERS-CoV)
Get it from cammels in saudi arabia
MERS-CoV signs and symptoms
Acute respiratory syndrome
Fever
Chills
GI symptoms
MERS-CoV lab findings
Thrombocytopenia
Lymphopenia
Lymphocytosis
High LDH, AST, ALT
MERS-CoV imaging
CXR with increased bronchovascular markings, patchy infiltrates, opacities, pleural effusions, ground glass, consolidation
MERS-CoV diagnosis
Rt-PCR
Serum serologies
Test lower respiratory tract specimens and sputum
MERS CoV case definition
Fever
Pneumonia or ARDS
History of travel to arabian peninsula 14 days before symptoms
Faster respiratory failure than SARS
MERS-CoV treatment
Respiratory support
No vaccine
Interferons
Ribavirin
Lopinavir-ritonavir
Mycophenolate mofetil
Adenovirus symptoms and signs
Worse in native americans
Chronic lung disease
Hepatitis Hemorrhagic cysts
Adenovirus diagnosis
Fluorescence immunoassay
PCR
Adenovirus imaging
Multifocal consolidation or ground glass opacity without airway inflammatory findings on chest CT
Adenovirus treatmen
Ribavirin or cidofovir in immunocompromised
IVIG
Acute bronchitis
Lower respiratory tract infection causing inflammation in large airways
Acute bronchitis pathophys
epithelial infection of bronchitis to inflammation and thickening of bronchial and tracheal mucosaI decreasing airflow and bronchial hyperrresponsiveness
Acute bronchitis signs and symptoms
Wheezing or mild dyspnea with cough
Hemoptysis
Fever is rare
Ronchi
Usually clears with coughing
Acute bronchitis imaging
Don’t need imaging
Acute bronchitis treatment
Nonpharm: throat lozenges, hot tea, stop smoking
Pharm: Dextrometorphan, Guaifenesin if >2 y/o
Pulmonary embolism (PE) presentation
Dyspnea
Chest pain
Hemoptysis
Syncope
Tachypnea
Tachycardia
Hypoxia
Pulmonary embolism (Pulmonary venous thromboembolism) cause
Deep vein thrombus
Superficial vein
Closer to skin
Smaller
Tend to move blood more slowly bc no muscle near
Deep veins of lower extremities examples
Anterior tibial
Posterier tibial
Peroneal
Femoral veins
Superficial veins in lower extremities examples
Great sephenous vein
Small (short) saphenous vein
Where do pulmonary embolisms usually come from
Iliac, femoral, and popliteal veins
DVTs below popliteal or superficial veins don’t usually get to pulm circulation
Substances that can embolize to pulmonary circulation
Fat (long bone fractures)
Septic emboli (acute inefective endocarditis)
Risk factors for PE that are risk factors from thrombus formation
Virchow triad
1. Venous stasis
2. INjury to vessel wall
3. Hypercoagulability
Common cause of hypercoagulability
WHite people
Resistance to activated protein C (Factor V Leiden)
PE physiologic effects
Physical obstruction of vascular beds
Vasoconstriction
Thrombus occlusion greater than 20-25%
Vascular obstruction causing hypoxemia
Reflex bronchoconstiction promotes wheezing and increased work of breathing
PE pathophys
Usually multiple with lower lobes involved more commonly than upper lobes
Saddle PE
Located at bifurcation of main pulmonary artery
PE signs and smptoms
Dyspnea
Pain on ispiration
Cough
Wheezing
Anginal pain
RR>16
Tachycardic
S4
Temp
Homans sign
S3
Cyanosis
Symptom of massive PE
Syncope and obstructive shock with circulatory collapse (saddle embolus)
PE EKG
S1Q3T3 pattern bc of right heart dysfunction
Nonspecific ST and T wave changes
New RBB
Right axis deviation
Tachycardic
PE labs
Alkalosis bc hyperventilation
Elevated D-dimers
Troponin and BNP elevated
CBC and coagulation studies
PE imaging
Helical CT-PA scan GOLD STANDARD
CXR needed to rule out stuff and could see Westermark sign or Hampton hump
Pulmonary CT angiography
V/Q can be used if CT-PA can’t be used bc of contrast
Echocardiogram
Venous ultrasound to check for DVT
Westermark sign
PE CXR finding
Decreased vasularization of lung periphery causes sharp cut off of pulmonary vessls with avascular marksings ins egmental distribution distal to PE
Hampton hump
PE CXR finding
Wedge or dome shaped, pleural based opacification in periphery of lung
High risk PEs
Massive
SBP<90mmHg or a drop in over 40mmHg for longer than 15 minutes
Intermediate risk PEs
Submassive PE
Hemodynamically stable but strainsof right ventricular dysfunction seen in imaging or in troponin/BNP
Low risk PEs
Normotension without signs of right ventricular dysfunction
PE treatment
Unfractioned heparin
LMW heparin
DOACs
IVC filter
Catheter directed thrombolysis via angiography
Surgical embolectomy
IVC filter
Used to treat recurrent PE
Stops clot from entering RA
Thrombolytic therapy
Streptokinase, urokinase, recombinant tissue plasminogen cativator.
Increases plasmin levels and directly lyse intravascular thrombi accelerating resolution of thrombi
IV
PE treatment in pregnant
Low molecular weight heparin (Lovenox) (-parin) bc doesn’t cross placenta
PE treatment for people with malignancy
LMWH (lovenox) (-parin)
Apixiban (DOAC)
PE prophylaxis drugs
DOAC
Warfarin
Unfractioned heparin
Pulmonary HTN diagnosis value
Pulmonary arterial pressure of 20 mmHg
Pulmonary HTN clinical presentation
Dyspnea, fatigue, chest pain, syncope on exertion
Split S2 with loud pulmonary component
Tricuspid regurgitation murmur
Systolic ejection click
RV hypertrophy
Elevated RV systolic pressure
JVD
Hepatomegaly
Lower extremity edema
Normal pulmonary artery systolic pressure
15-30 mmHg
Groups of pulmonary HTN
Group 1 primary
Group 2 PVH from Left heart disease
Group 3 PHTN due to lung disease or hypoxemia
Grop 4 PHTN due to pulmonary obstruction
Group 5 PHTN secondary to unclear or multifactorial mechanisms
Group 1 pulmonary arterial hypertenson causes
Diseases that localize directly to pulmonary arteries leading to structural changes, smooth muscle hypertrophy, endothall dysfunction.
Idiopathic
Heritable
Drug induced
Portal HTN
HIV
Connective tissue disorders
Congenital heart disease
Schistosomiasis
Group 1 pulmonary HTN diagnosis
Mean pulm arterial pressure of 20 mmHg
Wedge pressure of 14mmHg or less.
Pulmonary vascular resistance of 2 Wood units or moreGrou
Group 2 pulmonary HTN
Caused by left heart disease
Includes LV systolic or diastolic dysfunction and valvular heart disease
Group 3 pulmonary HTN
Caused by lund disease or hypoxemia
Group 4 pulmonary HTN
Caused by pulmonary obstruction
Includes chronic thromboembolic pulmonary HTN, sarcoma, metasttic alignancies, congenital pulmonary artery stenosis.
Group 5 pulmonary HTN
Secondary to unclear multifactorial mechanisms like hematoligic, systemic, metabolic, and other orders
Pulmonary HTN lab findings
BNP may be elevated
Check liver
EKG normal except in bad cases RV hypertrophy, right axis deviation, RA enlargement, right BBB
Pulmonary HTN imaging
Pulm arteries enlarged on CXR and CT
RV and RA enlargement seen
CT good to find cause in group 3
Echocardiogram with bubble study (does not diagnose pulmonary HTN)
V/Q
CT-PA
Group 2 pulmonary HTN treatment
Decrease pulmonary venous rpessure
Diuretics
Group 3 pulmonary HTN treatment
Assessed for hypoxemia
Give O2 if needed
Focus on supportive care in COPD
Group 4 pulmonary HTN treatment
Long term anticoagulation
Undergo thromboendoarterectomy if able and have surgicallly accessible lesions
Cor pulmonale signs and symptoms
Chronic productive cough
Exertional dyspnea
Wheezing
Fatigue
Cyanosis
JVD
Dependent edema
Low cardiac output and reduced LV filling, preload, and stroke volume
Cor pulmonale treatment
Oxygen
Sodium restriction
Diuretics
Ionotropic agents
Alveolar hemorrhage syndromes
Alveolar infiltrates on chest radiograph
Dyspnea
Anemia
Hemoptysis
Rapid clearing of diffuse lung infultrates within 2 days
Lavage aliquots progressivel more hemorrhage in bronchoalveolar lavage bronchoscopy
Alveolar hemorrhage syndrome cause
Anti-basement membrane antibody disease
Granulomatosi with plyangiitis
Systemic necrotizing vasculitis
Lupus
Coagulopathy
Mitral stenosis
Necrotizing pulonary infection
Drugs
Idiopathic pulmonary hemosiderosis
Good pasture syndrome
Idiopathic recurrent alveolar hemorrhage
Mediated by antiglomerular basement membrane antibodies
Good pasture syndrome symptoms
HEMOPTYSIS
Dyspna, cough, hypoxemia, diffuse bilateral infultrates
Pulmonary edema causes
Acute MI
Ischemia
Exacerbation of HF
Acute severe hypertension
Acute kidney injury
Acute volume overload of LV
Mitral stenosis
High salt intake
Pulmonary edema clinical findings
Dyspnea
Pink frothy sputum
Diaphoresis
Cyanosis
Rales
Pulmonary edema imaging
CXR has blurriness of vascular outlines
INcreased interstitial markings
Butterfly pattern alveolar edema
enlarged heart maybe
Pulmonary edema teatment
O2
IV Morphine
IV Diuretic
Nitrate
IV Nesirtide
What lab to meaasure when on a heparin drip
aPTT (activated partial thromboplastin time)
Anticoagulation for pre-MI cath lab
Start unfractionated heparin (IV)
Leave on ASA/Plavix if alreadyy on it
Hold Warfarin and DOACs
Meds post MI cath lab
Dual antiplatelet therapy (like ASA+Plavix)
Off fractionated heparin now
Indications of low molecular weight heparin
DVT prophylaxis in hospital
DVT/PE initially while bridging pt to daily oral anticoagulant
DVT prophylaxis for low risk pts
Compression stockings
What do we need to check when someone is on warfarin
PT/INR (prothrombin time/international normalized ratio
Prothrombin time
Measures activity of extrinsic and common pathways of coagulation.
Measures prothrombin (factor II) and factors I, V, VII, X
International normalized ratio (INR)
Value we base changes ot warfar on.
Normla is 1
Goal is 2-3
What to do if PT is elevated on warfarin
Give vitamin K.
Could mean wrong dosage, vitamin K deficiency, or liver disease
What to do if INR is 3-5
Lower dose or omit dose
Monitor more frequently
What to do if INR is betweeen 5-9
Hold next 1-2 doses
Monitor more frequently and
Pneumonia
Infection that inflames alveoli in one or both lungs.
Can be viral, bacterial, or fungal
Pneumonia pathway
Failure of protective mechanisms–>
Infiltration–>
Inflammation–>
Hypoxia
Bronchopneumonia
Affects lungs in patches around bronchi or bronchioles instead of whole lobe.
Much more common than lobar.
Usually bacterial
Lobar pneumonia
Fills up the lobe
Usually bacterial
Interstitial pneumonia
Involves areas between alveoli
Progressive scaring
Mostly viral or atypical
Nosocomical pneumonia
Acquired in hospital/nursing home
occurs >48 hrs after admission.
Most common bacterial causes of pneumonia
STREP PNEUMO
H. influenza
Staph aureus
Moraxella catarrhalis
Legionella (Legionnaire’s disease)
Reportable pneumonia
Bad in immunocompromised
Typical Pneumonia symptoms
SOB
Pleuritic chest pain
Fever
Cough (productive or nonproductive)
Dyspnea
Fatigue
GI
Headache
Atypical pneumonia symptoms
Nonproductive cough
Scanty sputum
Fatigue
Malaise
Headache
Pneumonia physical exam findings
Tachypnea
Tachycardia
Hypoxemia
Hypotension
Hyperthermia
Accessory muscle use
Dullness to percussion
Craakles/bronchial breath sounds
Enhanced tactile fremitus
Egophony
Bronchial breath sounds
Best imaging for pneumonia
AP and lateral CXR is gold standard
CT if CXR not diagnositic
UA for legionella
Indications for thoracentesis in pneumonia
Effusion >10mm
Bronchoscopy indications in pneumonia
INconclusive CT scan
Suspected mass
Labs needed in pneumonia
CBC with differential
Procalcitonin
2 sets of blood or sputum culture
Pneumonia treatment for healthy <65 yo with no comorbidities or risk factors for MRSA or P aeruginosa
Amoxicillin 1000 mg TID 5 days
or Doxycyclin 100mg BID 5 days
or Macrolide (-mycin) for 5 days
Pneumonia treatment for someone with comorbidities (CHF, CKD, liver disease, T2DM, EtOH, immunosuppression) or recent antibiotic use
COombo therapy
Macrolide (-mycin) or doxycycline with amoxixillin/clavulanic acid or 3rd gen cephalosoprin
Doxycycline adverse effects
Can’t use in pregnant
Macrolide adverse effects
Prolong QT interval
Fluoroquinolone adverse effects
Prolong QT interval
Tendon rupture
C. diff colitis
Outpatient community acquired pneumonia treatment
Abx for At least 5 days continue until afebrile for 48 hours
Acetaminophen and NSAIDs for pain
Guaifenesin (mucinex)
PSI risk stratification
Risk I: 0 points outpatient oral abx
Risk II: 1-70 points outpatient oral abx
RIsk III: 71-90 observation admission
Risk IV: 91-130 hospital admission
RIsk V: >130 hospital admission
Inpatient community acquired pneumonia abx treatment
Combo of beta-lactam and macrolide.
Will be IV at start
Add vancomycin or linezolid if MRSA suspected
Use combo of antipseudomonal beta-lactam and fluoroquinolone if Pseudomonas expected
Additional inpatient community acquired pneumonia treatment
Pulmonary exercise
SUpplemental hygene
Prone positioning
Maybe mechanical ventilation
Hospital acquired pneumonia treatment
Abx for at least 7 days
Prevnar 13`
S. pneumo vaccine for all children younger than 2 yo
Pneumovax 23
S. pneumo vaccine for those over 65 yo
Most common cause of community acquired pneumonia
S. pneumonia
S. pneumoniae pneumonia symptoms
Abrupt onset
Sever rigor
Rusty sputum
Fever
Bronchial breath sounds in early stages
S. pneumoniae pneumonia imaging
CXR with lobar infiltrates, air bronchograms
H. flu pneumonia
G- Coccobaciillus
Common in COPD and smokers
H. flu pneumonia imaging
CXR lobar patchy infiltrates
Staph aureus pneumonia
Usually from preceding flu infection.
Infect multiple lobes of lungs quickly
Staph aureus pneumonia imaging
CXR shows cavitary lung lesions that mimic TB
MSSA pneumonia treatment
Cephalexin, dicloxacillin, Trimethoprim/sulfamethoxazole
IVV nafcillin or cafazoline
MRSA pneumonia treatment
IV vancomycin, linezolid, cefaroline, or daptomycin
Staph aureus pneumonia complications
Lung abscess
Pneumothorax
Empyema
Moraxella catarrhalis pneumonia
Gram negative diplococci
Usually in upper respiratory
Mycoplasma pneumoniae
Young kids
Bullous myringitis
Papular rash or erythema multiform
Mycoplasma pneuomniae treatment
Azithromycin
Doxycycline
Levofloxacin
Moxifloxacin
Chlamydophila pneumonia
Children and overcrowded
CXR nonspecific
PCR needed
Clamydophila pneumonia treatment
Macrolinde
Tetracycline
Resp fluoroquinolone
Legionella pneumophila pneumonia symptoms
NVD
Legionella pnemophilia pneumonia imaging
CXR lbar pneumonia
Can form cavities in immunocompromised
Legionella pneumophila treatment
Levofloxacin
Azithromycin
Doxycycline
Klebsiella pneumonia
Gram negative rods
Associated with aspiration
Currant jelly colored sputum
Chlamiydophila psittaci
Birds
Pneumonia
Tetracyclines or macrolide
Coxiella burnetti
Q fever
farm animals
Pneuomnia
Microaerophilic bacteria anaerobes (aspiration pneumonia)
Usually in pts with poor oral hygeine
Usually in right lower lobe
What usually causes pneumonia in cystic fibrosis pts
Pseudomonas
Histoplasmosis pathophys
IN soil with berd or bat droppings.
Spores inhaled then engulfed by macrophages in alveolar space causing granuloma formation
Histoplasmosis epidemiology
North american fungus
Usually seen in chicken coops, farms, caves
Histoplasmosis clinical findings
Erythema nodosum
Erythema multiform
Pericarditis
Histoplasmosis diagnosis
CXR with patchy infiltrates
Reticulonodular pattern
Fungal culture
Antigen assay
Histoplasmosis treatment
Itraconazole
Amphotericin. B only for extremely ill
Blastomycosis pathophys
Inhale spores and immune system inhibits conversion of spores into pathogenic yeast form (thermal dimorphism).
Blastomycosis epidemiology
Immunocompetent men
Major soil disruption in endemic ariesa
Drainage systems
Warm, moist soil in he woods
Blastomycosis clinical findings
Cough fever dyspnea pleuritic chest pain
Prurulent sputum, pleurisy
Fever, chills, weight loss
Ulcers (look like squamous cell carcinoma)
Osteomyelitis
Epididymitis
CNS involvement
Blastomycosis diagnosis
Failed trial of abx
CXR
Fungal culture
Antigen assay
Blastomycosis treatment
Itraconazole
Amphotericin in immunocompromised
Coccidioidmycosis Pathophys
Inhale spores.
Spores evade immune system and enarge into spherules that make endospores
Coccidioidomycosis epidemiology
Southwest US
Dry climates
Coccidioidomycosis clinical findings
Meningitis
Erythema nodosum
Erythema multiform
Fever, night sweats, weight loss, fatigue, arthralgia
Coccidioidomycosis diagnosis
CXR with patchy infiltrates, lobar consolidation, hilar adenopathy, diffuse, reticulonodular pattern, interstitial fluid
Serologic enzyme immunoassay
Antigen assay
Coccidioidmycosis treatment
Fluconazole or itraconazole
Amphotreicin B for severe
Aspergilosis
Allergic reaction to fungus in pts with asthma and CHF
Aspergillosis pathophys
Inhale spores
Toxins inhibit phagocytes and T cell function
Very bad in immunocompromised
Allergic aspergillosis clinical fidings
Bronchopulmonary
Rhinosinusitis
Hypersensitivity
Mucoid impaction
Acute asthma exacerbation with bronchial obstruction
Chronic aspergillosis clincial findings
Cavitary, fibrosing, necrotizing
Aspergilloma
Weight loss, productive cough
SOB
Fatigue
Invasive aspergillosis clinical findings
Sinusitis
Tracheobronchitis
Progressive, acute
Fever, chest pain, hemoptysis
Aspergillosis extrapulmonary clinical findings
Cutaneous infiltration
Endocarditis
Endophthalmitis
Cutaneous lesions
Branin abscess
Hemorhagic infarction
Aspergillosis imaging
CXR shows aspergilloma
Lung nodule
Allergic aspergillosis diagnosis
Asthma, cystic fibrosis
Elevated IgE
Elevate IgG
Pulmonary opacities on CXR
Chronic aspergillosis diagnosis
Presence of cavitation on CXR (one large or two small)
Fever, weight loss, fatigue, cough, sputum, hemoptysis, SOB (three of those for more than 3 months)
INvasive aspergilllosis diagnosis
Fungal culture
Aspergillosis treatment
Itraconazole
Prednisone taper over months
Voriconazole for invasive
Pneumocystis pneumonia epidemiology
Opportunistic infection in immunocompromised
Common in HIV/AIDS
Pneumocystis pathophys
Proliferates in alveoli tissue causing alveolar damage
Pneumocystis clinical findings
acute pneumonia in immunosuppressed pt..
Potential to progress to ARDS
Pneumocystis imaging
CXR showing diffuse bilateral interstitial infiltrates
Chest CT showing ground glass opacities
Pneumocystis diagnosis
Pathogen identification with sputum o r bronchoalveolar lavage.
Stain wright giems
Can’t be cultureed
PCR
Pneumocystis treatment
Trimethoprim-sulfamethoxazole (bactrim)
Obstructive lung disease characteristics
Narrowing of lower airway
Bronchoconstriction ]
Inflammation
Mucous production
Alveolar damage
Air trapping
Restrictive lung disease characteristics
Decreased lung compliance
Fibrosis
Infiltration
Hemoptysis
Coughing up blood
Spirometry
Measures volume of air exhaled at poins during forceful complete expiration
Records:
FVC (forced vital capacity)
FEV1 (forced expiratory in one second)
FEV1/FVC ratio
Normal FVC/FV1 ratio
80%
Obstructive pulmonary disorder spirometry
Decreased FV1
Decreased FVC
FEV1/FVC <80%
Restrictive pulmonary spirometry
Normal or decreased FEV1
Decreased FVC and TLC
FEV1/FVC normal (>80%)
Obstructive pulmonary disorder examples
Asthma
Emphysema
Chronic bronchitis
COPD
Pre and post Bronchodilator spirometry
Identifies reversible vs irreversible obstructive lung disease
Positive test shoes increase >10% in FEV1 or FVC (reversible)
Bronchoprovocation
Used if spirometry alone was not diagnostic.
Stimulus (methacholine) administered to assess airway constriction, hyperresponsiveness via spirometry
Positive test is FEV1 decline >20% and PD20<200
PD20
Provocation dose.
Dose of methacholine that causes significant drop in FEV1 >20%
Flow volume loop
Graphs out pattern of breath
Obstructive volume loop
scooped out
Restrictive volume loop
Reduced overall volume
Asthma
Reversible obstructive variable inflammatory airway disorder
Asthma pathophys
Airways narrow excessively in response to stimuli
Caysed by release of IgE, mast cells, leukotrientes, histamine, eosinophils obstructing airway
Goblet cell hyperplasia
Over time causing hypertrophy (remodeling)
Asthma risk factors
FAM HISTORY
Atopic triad (atopy)
NSAID allergy
Atopic triad
Eczema (atopic dermatitis)
Allergic rhinitis
Asthma
Asthma clinical presentation
Wheeze
Cough
Dyspnea
Could have silent chest in exacerbation
Asthma supporting physical exam findings
Allergic shiners
Morgan-Dennie lines
Allergic crease (salute)
Nasal drainage
Boggy turbinates
Nasal polyps
Atopic dermatitis
AMS shows resp distress
Tripod
Asthma vital signs
Tachycardic
Tachypnic
Hypoxic
Pulsus paradoxus (>10mmHg fall in systolic blood pressure during inspiration)
Asthma diagnostic
Pulmonary function testsd (spirometry with or without bronchodilation, DLCO, lung volumes)
Spirometry best initial test
DLCO in asthma
Normal or increased
DLCO in emphysema
Lowered
Lung volume in obstructive disease
Increased TLC suggest hyperinflation
Increased compliance
Increased RV suggests air trapping
Lung volume in restrictive disease
TLC is less than 80% what was expected
Asthma Peak expiratory flow rate test
> 20% increased in PEF after treatment showing that it is reversible
Asthma treatment for 6-11 y/o
Stepwise
1: Low dose ICS when SABA taken
2: Daily low dose ICS
3: Low dose ICS-LA A or medium dose ICS or very low dose ICS
4: Medium dose ICS-LABA or low dose ICS and refer to expert
5: Refer for phenotypic assessment and maybe higher dose ICS LABA or add-on therapy
Asthma treatment for adult
1-2 (symptoms less than 4-5 days/week): As needed low dose ICS-formoterol as needed
3 (symptoms most days or walking asthma once/week): Low dose ICS-formoterol daily
4 (daily symptoms or walking asthma once/week and low lung function): Medium dose daily ICS
5: add on LAMA and refer for assessment of phenotype and consider high dose ICS
Long acting Beta 2 agonists (LABA)
Asthma first line reliever in GINA
Bronchodilation starting at 15 mins and lasting up to 12 hours
Decreases exacerbations
Not monotherapy
Ex. formoterol, salmeterol
Short acting beta 2 agonist
Asthma second line reliever in GINA
First line in NAEPP
Onset in 5 mins and lasts up to 6 hrs
ex. albuterol
Overuse can cause increased exacerbations
Leukotriene receptor antagonists
-lukast
Long term controller for add on therapy in asthma not well controlled by ICS
Long acting muscarinic antagonist (LAMA)
Used in step 5 Gina asthma with ICS
Tiotropium
Monoclonal antibody agents
-zumab
Used in step 5 GINA asthma
Omalizumab
Humanized monoclonal antibody blocks IgE from binding in asthma
Used in asthma with blood eosinophilia >260
Dupilumab
Anti-IL4 agent used in asthma
Givn to pt with severe eosinophilic asthma >150 and 6 yrs or older
Exercise induced asthma treatment ad adverse effects
SABA prior to exercise
Muscel tremor
Tachycardia
Hypokalemia
Restlessness
Mild asthma exacerbation treatment
PEF is 50-80% personal best
Administer SABA by nebulizer
Titrate oxygen to >92
Prednisone 40mg PO x 7 days
Want to get PEFR>80% personal best
Severe asthma exacerbation treatment
PEF is <50% personal best
Administer nebulized SABA and maybe ipatropium
Titrate O2>92
IV methlyprednisolone
Mag sulfate IV in life threatening
Want PEFR>80% personal best
Oral corticosteroid indications in asthma
Severe, not well controlled asthma presentation, asthma, exacerbation
Short term use for acute exacerbations
COPD
Chronic obstructive pulmonary disease
Irriversible
Includes emphysema and chronic bronchitis
COPD Risk factors
Smoking
Coal
Biomass fuel cooking
Alpha-1 antitrypsin deficiency
COPD pathyphys
Inflammation of airway
Alveolar wall destruction leading to airway collapse
Fibrosis narrowing airway
Mucus gland hyperplasia
Vasoconstriction of pulmonary artery causing arterial HTN, hypoxemia, hypercapnia
Centriacinar COPD
Most common
Usually in upper lobes of smokers
Panacinar COPD
Associated with ALpha-q antitrypsin dficiency
Effects lower lung zones and exacerbated by smoking
Paraseptal COPD
Found near pleura and septum of lungs often adjacent to areaas of fibrosis or scaring
Irregular COPD
LEss common and can happen anywhere in lungs
COPD symptoms
Dyspnea
Chronic cough
Sputum production
Wheezing
Fatigue
Pink puffers and blue bloaters
Alpha antitryspin-1 deficiency treatment
IV alpha 1 antitrypsin
Lung transplant is the definitive treatment
Emphysema pathophys
Loss of alveolar walls causing enlargement of air
Resistance of blood flow due to capillary loss
Loss of elastic recoil
Airway collapse makes expiration active process
Hyperinflation leading to air trapping and flattening of diaphragm
Emphysema symptoms
Dyspnea
Exertion usually first sign
Chronic cough
Fatigue
Emphysema physical exam findings
Pink sometimes or cyanotic
Usually noncyanotic at rest
Barrel chest
Hyperresonant to percussion bc hyperinflation
Decreased breath sounds
Expiratory wheezing
Chronic bronchitis pathophys
Chronic inflammation leads to mucous gland hyperplasia, goblet cell mucous production, dysfunctional cilia, infiltration of neutrophils and CD8 T cells
Increased susceptibility to infection
Chronic bronchitis symptom
Chronic cough
Sputum production
Dyspnea
Chronic bronchitis physical exam
Blue bloaters from cyanosis (hypoxia)
COPD diagnosis
Spirometry is GOLD (scooped out graph)
Post bronchodilator shows irreversible
FEV1 and FVC lowered
FEV1/FVC<80%
RV, TLC, and FRC increased
Emphysema has low DLCO
6 min walk test and get O2 sat
Emphysema (COPD) CXR
Decreased lung markings
Large bullae
Flattened diaphragm from hyperinflation
COPD ECG changes
Tachycardic with 3 different P wave morphologies (multifocal) is main one
Could also show low amplitude, right axis deviation, right atrial enlargement, RBBB
COPD CBC
Increaesd HGB, HCT, chronic hypoxia
More in chronic bronchitis
Elevated eosinophils
COPD ABG
Respiratory acidossi
Decreased pH
Increased pCO2 from CO2 from rentention in lungs
Hypercapnia
Severity of airflow obstruction GOLD criteria
GOLD 1: Mild FEV1>80
GOLD 2: Moderate FEV1 50-80
GOLD 3: Severe FEV1 30-50
GOLD 4: Very severe FEV1 <30
COPD GOLD group A
mMrc 0-1
CAT <10
0-1 exacerbations/yr
COPD GOLD group A treatment
LABA daily (aformoterol, formeterol, salmeterol)
LAMA alternative
SABA for acute breathlessness
COPD GOLD group B
mMRC>1
CAT>9
0-1 exacerbations/yr
COPD GOLD group B treatment
LAMA+LABA dual bronchodilator daily (umeclidinium/vilanterol)
SABA PRN for acute breathlessness
COPD GOLD Group E
> 1 exacerbations/yr
COPD GOLD Group E treatment
LAMA+LABA daily
SABA PRN for acute breathlessness
Refer to pulmonary rehab
If have hospitalizations or eosinophils >300 add ICS
Refractory Gold E COPD
Continuous exacerbations while on LABA+LAMA+ICS
Give roflumilast in chronic bronchitis with FEV1<50
Give Dupilumab if eosinophills >300
Give azithromycin in bbronchiectasis or recurrent bacterial infections in nonsmoker
Toflumilast
PDE4 inhibitor
Givee pt with chronic bronchitis with FEV1<50 refractory COPD with LABA+LAMA+ICS
Antiinflammatory
Dupilumab
Monoclonal antibody that blocks shared receptor in IL-4 and IL-13 (antiinflammatory)
Give to pts with eosinophils >300 with recurrent COPD on LAMA+LABA+ICS
Azithromycin in COPD
Macrolide with antiinflammatory properties
Give in refractory COPD with LABA+LAMA+ICS with bronchiectasis or recurrent bacterial infections in nonsmoker
What is the only treatment that lowers mortality in COPD
Oxygen therapy
When to refer COPD pt
Onset before 40 yo
Two or more exacerbations per year
Rapidly progressive
Symptoms disproportionate to severity of airflow obstruction
Triggers for COPD exacerbation
Respiratory infections
Pollution
Pulmonary embolism
When to admit someone having COPD exacerbation
FEV1<50%
New symptoms
Signs of respiratory distress
Hemodynamic instability
COPD bronchodilator treatment
Mild: SABA: albuterol or levalbuterol
Moderate/severe: SABA+ SAMA: ipratropium+albuterol
COPD steroid treatment
Indicated for moderate to severe exacerbations
Prednisone
Methylprednisolone
When to give antipseudomonas abx for COPD
Previous psudomonas infection
FEV1<30
Abx use in last 3 months
CHronic glucocorticoid treatment
Restrictive lung disease pathophys
Decreased lung distensibility–>
Compromised lung expansion–>
Reduced lung volumes
Interstitial lung disease
Destruction of lung parenchyma
Infiltrates
Toxins
Extraparynchymal conditions that cause restrictive lung disease
Scoliosis
Kyphosis
Neuromuscular causes
Marked obesity
Interstitial lung disease examples
Idiopathic pulmonary fibrosis (IPF)
Silicosis
Asbestosis
Coal worker’s pneumoconiosis
Sarcoidosis
Interstitial lung disease symptoms
Progressive DOE
Persisitent nonproductive cough
Interstitial lung disease labs
CMP for hepatic or renal involvement
CBC for anemia, polycythemia, eosinophilia
UA
Rheumatic labs(Antinuclear antibody, rheumatoid factor, anticyclic citrullinated peptide)
HIV test
Idiopathic pulmonary fibrosis
Restrictive lung disease usually in 60-70 yo
Idiopathic pulmonary fibrosis risks
Smoking
Dusts
Agent orange
GERD maybe
Idiopathic pumonary fibrosis physical exam findings
Bibasilar crackles
Idiopathic pulmonary fibrosis clinical manifestation
Gradual DOE and nonproductive cough over months.
Idiopathic pulmonary fibrosis testing and imaging
Pulmonary function testing (PFT) to see restrictive pattern and severity
CXR with increased reticular markings and ground glass opacities (not diagnostic)
CT to congirm presence and see distribution (diagnostic)
Possible biopsy
Diagnosis of idiopathic pulmonary fibrosis without biopsy
Pt>60yo AND
insidious cough AND
Diffuse patchy fibrosis with pleural based honeycombing on CT AND
Other potential causes ruled out
Gold standard biopsy for idiopathic pulmmonary fibrosis
Open procedure using video assisted thoracoscopic surgery (VATS)
Diagnostic on its own
Mild idiopathic pulmonary fibrosis
Asymptomatic or mild nonproductive cough and DOE
<10% lung parenchyma involvement
PFT normal or mild reductions
Moderate idiopathic pulmonary fibrosis
DOE with some activity maybe needing O2
Nonproductive cough
Mild-moderate PFT changes
20-30% lung parenchyma involvement and honeycombing of 5%
Advanced idiopathic pulmonary fibrosis
DOE with little activity
O2
Extensive honeycombing
pFT moderate to severe FCV reduction
Idiopathic pulmonary fibrosis treatment
Referral to pulmonologist
No cure
Antifibrotic meds help (nintedanib, pirfenidone)
Supplemental O2 as needed
Lung transplant is definitive treatment (usually die in 5.2 years)
Silicosis
Restrictive
Chronic fibrotic lung disease caused by inhalation of inorganic dusts.
Usually work with rocks/mining
Silicosis imaging
CXR diffuse nodular opacities, egg shell calcification
Often found in upper lungs
Asbestosis
Caused by inhaled asbestos fibers
Can be asymptomatic or severe. symptomatic life-shortening disorders.
Usually found in people that work in shipyards, construction, insulation
Asbestosis imaging
CXR diffuse nodular opacities
Pleural calcifications
Honeycombing CT
CT is best
Asbestosis symptoms
Progressive dyspnea
Clubbing
Cyanosis
Inspiratory crackles
Asbestosis diagnosis
PFTs show restrictive dysfunction adn reduced diffusing capacity
CT images
Ferruginous body (asbestos body) in tissue
Asbestosis treatment
No treatment
Coal worker’s pneumoconiosis
Restrictive lung disease caused by inhaling coal dust
Coal worker’s pneumoconiosis imaging
2-5 mm opacities of upper lung
Coal worker’s pneumoconiosis symptoms
Cough
SOB
Chest tightness
Black sputum
Hypoxemia
COal worker’s pneumoconiosis diagnosis
Mostly history (work in coal)
Smoking makes it worse
Coal worker’s pneumoconosis treatment
O2
Inhalers
Pulmonary rehab
Transplant in severe
Sarcoidosis
Restrictive lung disease
Usually in african americans and northern europeans 30-40yo
Sarcoidosis symptoms
Parotid gland enlargement
Malaise
Fever
Dyspnea
Erythema nodosum and lupus pernio
Iritis
Peripheral neuropathy
Arthritis
Cardiomyopathy
Sarcoidosis imaging
CXR Bilateral hilar and right paratracheal lymphadenopathy
Sarcoidosis labs
ACE levels elevated
Leukopenia
Elevated ESR
Hypercalcemia
Hypercalciuria
Sarcoidosis diagnosis
NONCASEATING GRANULOMAS in flexible bronchoscopy and biopsy
BAL fluid high CD4/CD8 ratio
Opthalmology exam
Sarcoidosis treatment
Oral corticosteroids (prednisone 1mg/kg/day)
Long term therapy
Immunosuppressive therapy (methotrexate, azathioprine, infliximab
Small cell carcinoma
Lung cancer
Early widespread metastasis
Most common in heavy smokers
Centrally located
Dark blue cells with rosette formation
Associated with Lambert Eaton syndrome, SIADH, Cushing syndrome
Adenocarcinoma
Most common lung cancer
Minimally invasive or in situ
Usually in peripheral location
Neoplastic gland formation
Squamous cell carcinoma
Lung cancer
Usually arises in mucous membrane of proximal bronchi
Strongly associated with smoking
Centrally located cavitary lesions
Widened mediastinum
Causes hypercalcemia
Large cell undifferentiated carcinoma
Rare lung cancer
Rapidly growing in peripheral lung tissue
Lung cancer risk factors
Smoking
Radon
Air pollution
Asbestos
Family history
Lung cancer symptoms
Asymptomatic
Cough
Hemoptysis
Dyspnea
Hoarseness
Pleural effusion
Weight loss
Lung cancer diagnosis
CXR
CT
Biopsy
Occult stage of cancer
Cancer cells picked up in mucus but tumor not found
Stage 0 cancer
Very small tumor
Canccer cells haven’t spread (in situ)
Stage I cancer
Cancer is in the lung tissue but not lymph nodes
Stage II cancer
Cancer has spread to lymph nodes near lungs
Stage III cancer
Cancer has spread to lymph nodes in middle chest
Stage IV cancer
Cancer has spread widely
Maybe into bones, brain, or liver
Small cell lung cancer treatment
Chemotherapy
Who qualifies for lung cancer screening
50-80 yo
20 pack-year history or quit in the last 15 years
Most common primary lung cancer
Adenocarcinoma
Adenocarcinoma symptoms
Asymptomatic
cough
dyspnea
hemoptysis
Weight loss
Adenocarcinoma treatment
Surgery
Chemo
Squamous cell carcinoma treatment
Surgery
Chemo
Large cell carcinoma treatment
Surgery
Chemo
Small cell carcinoma treatment
Chemotherapy and immunotherapy
Usually relapses within months
Bronchial carcinod tumor
Secrete serotonin, ACTH, ADH, MSH
Slow growing
Slow metastasis
Bronchial carcinoid tumor symptoms
Asymptomatic
Cough
Hemoptysis
SIADH
Cushing syndrome
Carcinoid syndrome
Caused by serotonin and histamine release
Diarrhea, flushing tachycardia, hypotension, bronchoconstriction.
5-HIAA in urine
Carcinoid syndrome treatment
Octreotide
Superior sulcus (Pancoast tumor) symptoms
Horner syndrome (ipsilateral ptosis with arrowing of palpebral fissure
Shoulder pain
Fushing and sweating
Weakness in arm involved
SUPRACLAVICULAR lymph node enlargement
Weight loss
Superior sulcus tumor treatment
Chemo
Radiation
Surgery f no metastasis
Superior vena cava syndorome
Obstruction of blood flow in SVC
Usually tumor but could be medical device
Most common n non-small cell lung cancer
Superior vena cava syndrome symptoms
Facial swelling or head fullness
Neck swelling
Dyspnea
Resp distress
Superior vena cava syndrome physical exam
Distention of neck
Edema
Cyansosis
Superior vena cava syndrome imaging
CXR with mediastinal widening and pleural effusion
CT
Superior vena cava syndrome treatment
Radiation to treat underlying malignancy
Head elevation and fluid reduction
Paraneoplasic syndromes
Caused by production of hormones, cytokines, or other substances
Commonly cushings, hypercalcemia, SIADHm, neuropathy
Pulmonary nodule
> 3cm
Usually infectious granuloma (not cancer)
Could be adenocarcinoma (cancerous)
Usually no symptoms
Get good medical and social history
Pulmonary nodule imaging
Found on CXR
Get CT
Compare to old CXR and CT
Maybe PET
Biopsy or resection
What to do if pulmonary nodule >8mm found
Get PET scan
Biopsy or resection
What to do if pulmonary nodule <8mm found
Get another CT later on
Subsolid nodule on CT
Ground glass
More likely to be adenocarcinoma than solid
At what point does a nodule need no further workup
If it is sable for two years with no growth
Benign calcification pattersn
Central, diffuse, fat, lamellated
More worrisome calcifaction patterns
Puntuate
Eccentric
amorphous
More suspicious characteristics of nodules
Spiculated or lobulated borders
Worse in upper lobe
Gold standard for pulmonary nodule diagnosis
Surgical biopsy and if you need to take it out go ahead and do it at same time
A-a gradient
PAO2-PaO2
Difference in O2 in alveoli and arteries
A-a gradient increased with hypoxemia
Shows intrapulmonary cause
Caused by dead space ventilation (pulm embolism) or diffusion disorder (pulm fibrosis) that are fixable with 100% oxygen.
Also caused by shunt (pneumonia) not fixable with 100% oxygen bc problem is blood flow to alveoli
A-a gradient normal with hypoxemia
Shows extrapulmonary cause
Caused by hypoventilation, low inspired O2 (altitude)
Correctible with 100% oxygen
Respiratory alkalosis
Hyperventilation
Hypoxemia most commmon cause
Anxiety
Stimulants
Can cause hypocalcemic symptoms (treussau and chvostek)
Metabolic compensation for respiratory acidosis
HCO3 must increase 3.5 mEq/L for every 10mmHg PaCO2 is increased
Metabolic compensation for respiratory alkalosis
HCO3 should decrease by 5mEq/L for every 10mmHg decrease in PaCO2
Respiratory compensation for metabolic acidosis
PaCO2 should decrease by 1.2mmHg fro every 1mEq/L decrease in bicarb
Respiratory compensation for metabolic alkalosis
PaCO2 should increase by 0.7mmHg for every 1mEq/L increase in HCO3
Obstructive sleep apnea
Cessation of airflow during sleep with persistent respiratory effort
Most common sleep apnea
Central sleep apnea
Cessation of airflow bc brain stops sending signals to muscles of respiration
Rare
Mixed sleep apnea
Apnea that begins as central apnea and ends as obstructive
Apnea
Drop in airflow of at least 90% lasting longer than 10 seconds
Hypopnea
Drop in airflow at least 30% lasting longer than 10 seconds
Apnea/Hypopnea index
Apneas and hypopneas per hour
5 or more diagnostic for sleep apnea of OSA
>30 is severe OSA
Sleep apnea risk factors
Men
Family history of snoring or OSA
Nasal congestion
Obesity
CHF
Pulm HTN
Kidney disease
Lung disease
Sleep apnea clinical presentation
Tired
Snoring, choking, gasping during sleep
Morning headaches
Nocturia
Sleep apnea physical exam
Obesity (BMI>30)
Crowded airway from tonsils, uvula, or other stuff
Large neck (>17 males and >16 females) and/or waist
Obesity hypoventilation syndrome
Awake alveolar hypoventilation and hypercapnea
Need PAP device
First line treatment for sleep apnea in KIDS
Tonsillectomy
NOT for adults
Epworth sleepiness scale
Pt ranks likelyhood of falling asleep in certain scenarios.
10-15 is very sleepy
16-24 needs medical attention
STOP-BANG sleepiness scoring
Snore
Tired
Observed apnea
Pressure (blood)
BMI
Age
Neck
Gender
Best diagnostic test for sleep apnea
In-lab polysomnography sleep study
Hooked up head to toe with monitors
When to give home sleep apnea test
When you think pt has uncomplicated sleep apnea
Shows severity of sleep apnea, O2, position
Box strapped to chest, oximeter on finger, canular under nose.
Mild obstructive sleep apnea
AHI 5-15 and one or more of these:
Sleepiness, waking up gasping, snoring, HTN, mood problems, Afib, T2DM
Severe obstructive sleep apnea
AHI>30
Falling asleep during daily activities
Obstructive sleep apnea treatment
Behavioral modifications
Weight loss (GLP-1 (tirzepetide))
PAP devices
Avoid alcohol
Sleep position
Oral devices for mild
What pts usually require higher CPAP pressure
Heavier pts with short, thick neck
Mycobacterium
Aerobic acid fast bacilli
Slow growth
Often acquired through municipal water sources
Non-TB mycobacterium presentation
Persistent fever and weight loss
Pulm exam usually normal
Non-TB mycobacterium treatment
Azithromycin
Rifampin
Ethambutol
Types of tuberculosis
Primary
Primary progressive
Latent
Reactivation
Primary TB pathophys
Inhale airborne droplet
Bacilli ingested but not destroyed by mø
Pulmonary granulomas formed to isolate infection and regional lymphadenopathy (Ghon complex)
Can be dormant for years
Primary progressive TB pathophys
Immune response inadequate to contain infections.
Will develop pulmonary symptoms
Latent TB pathophys
NOT active disease.
Reactivation can occur if immune system impaired (can be triggered by meds)
Reactivation TB pathyophys
Usually associated with waining immune system.
Lesions usually localized in lung apices due to increased O2 in apices.
Contagious
TB clinical findings
Very slowly progressive
Fever, malaise, anorexia, weight loss, night sweats
Chronic cough
Malnourished
Cervical lymphadenopathy
Can effect vertebral bodies, adrenals, meninges, GI
TB diagnosis
Sputum culture or acid fast bacilli
Primary TB imaging
CXR shows small unilaterla infiltrates.
Hilar and paratracheal lymphadenopathy
Segmental atelectasis
Pleural effusion
Reactivated TB imaging
Fibrocavitary apical disease
Nodules
Upper and superior segment of lower lobe infiltrates.
Millet seed nodules
Miliary pattern
What is measured to find if TB skin test is positive
Induration (raised area) not red area 48-72 hrs after test
What to do if TB skin test is positve
Get CXR
Interferon gamma release assays
High sensitivity and specificity for TB
Fewer false positives but more expensive
Number one cause for TB treatment failure
Nonadherence to medication regimen.
So every person gets case manager to watch them take meds
TB treatment
4 total months
First 2: isoniazid, rifapentine, pyrazinamide, moxifloxacin
Second 2: isoniazid, rifaapentine, moxifloxacin
No pyrazinamide in pregnant
Drug resistant is different for 6 months
Monthly follow up until sputum and culture negative (should only take 3 months)
Latent TB treatment
Isoniazid and rifampan 3 months
or
Isoniazid and rifapentine 3 months
or
Isoniazide alone 9 months