Pulmonology- Step Up To Medicine

Front 1

Sarcoidosis
1. definition
2. What population does it mostly affect
3. prognosis

Back 1

1. a chronic granulomatous disease characterized by non-caseating granulomas, involving multiple organ systems-- lungs are almost always affected
2. African Americans, especially women, usually <40 yo
3. usually good

Front 2

Symptoms of Sarcoidosis

Back 2

a. constitutional sx- malaise, fever, anorexia, weight loss
b. dry cough, dyspnea (esp with exercise)
c. skin (25%)- erythema nodosum, plaques, subQ nodules, maculopapular eruptions
d. eyes (25%)- anterior uveitis (75%), posterior uveitis (25%), conjuctivitis
e.heart (5%) -- arrhythmias, condution abn (heart block etc), sudden death
f. MSK- arthralgias, arthritis, bone lesions
g. nervous system- CNVII (bell's palsy), optic nerve dysfunction, papilledema, peripheral neuropathy

Front 3

Diagnosis of Sarcoidosis
1. radiographic findings
2. lab findings
3. histiologic findings

Back 3

Based on clinical, radiological, and histiological findings
1. CXR- BILATERAL HILAR ADENOPATHY is hallmark, but not specific and only seen in 50% of cases-- 4 stages depending on what you see on CXR- stge 1 has no parenchymal infiltrates
2. Increased Angiotensin Converting Enzyme (ACE) levels in 50-80%--> not sensitive or specific, hypercalciuria and hypercalcemia are common
3. definitive dx requires transbronchial bx-- must see non-caseating granuloma (can be seen in other diseases)
4. PFTs- decreased lung volumes (VC and TLC), dec DLco, decreased FEV1/FVC

Front 4

Treatment of Sarcoidosis and indications for tx

Back 4

- most cases resolve or significantly improve spontaneously within 2 years and do NOT require treatment
- systemic corticosteroids are the tx of choice- indications for treatment are unclear- but if symptomatic, lung disease, cardiac disease or severe skin or eye involvement then treat

Front 5

Histiocytosis X
1. definition
2. what patients is this typically seen in?
3. variants

Back 5

1. Chronic Interstitial pneumonia caused by abnormal proliferation of histiocytes
2. 90% are cigarette smokers
3. variants are eosinophilic granuloma, Letterer-Siwe disease, Hans-Schuller-Christian syndrome

Front 6

Histiocytosis X
1. common findings
2. other manifestations
3. CXR and CT appearance
4. prognosis
5. treatment

Back 6

1. dyspnea and nonproductive cough
2. spontaneous pneumothorax, lytic bone lesions, diabetes insipidus (excessive thirst and huge amounts of dilute urine)
3. CXR - honeycomb appearance, CT- cystic lesions
4. prognosis is highly variable
5. corticosteriods are sometimes effective, lung transplant may be necessary

Front 7

Wegener's granulomatosis
1. general characteristics- how common, histology?
2. what is affected?
3. clinical manifestations?
4. gold standard for diagnosis?
5. treatment

Back 7

1. rare disease of unknown origin characterized by necrotizing granulomatous vasculitis
2. affects vessels of lungs, kidneys, upper airway, and sometimes other organs
3. upper and lower respiratory infections, glomerulonephritis, and pulmonary nodules
4. gold standard for dx = tissue bx, but if patient has c-ANCA antibodies then probability of dz is high
5. tx- usually immunosuppression and glucocorticoids

Front 8

Churg-Strauss Syndrome
1. definition
2. typical presentation
3. Labs
4. Treatment

Back 8

1. granulomatous vasculitis seen in patients with asthma (allergic vasculitis)
2. pulmonary infiltrates, rash, eosinophilia- systemic vasculitis may result in skin, muscle and nerve lesions
3. eosinophilia, p-ANCA
4. glucocorticoids

Front 9

Back 9

Sarcoidosis- bilateral hilar adenopathy

Front 10

Coal worker's pneumoconiosis
1. definition
2. presentation
3. cause

Back 10

1. accumulation of dust in the lungs and the tissue reaction to its presence
- most of the time there is no significant respiratory disability
- some patients may develop complicated pneumoconiosis, which is characterized by pulmonary fibrosis
- causes- inhalation of coal dust which contains carbon and silica

Front 11

Asbestosis
1. characteristics
2. disease course
3. what are patients with this disease at increased risk for?
4. sx and physical exam findings
5. diagnosis
6. CXR
7. treatment

Back 11

1. diffuse interstitial fibrosis of the lung caused by inhalation of asbestos- predilection for the lower lobes
2. develops insidiously many years after exposure (>15-20 yrs)
3. increased risk for bronchogenic carcinoma (smoking is synergistic), and malignant mesothelioma
4. sx and physical findings are non-specific, restrictive lung disease
5. diagnosis is based on clinical findings and history of exposure to asbestos
6. CXR shows hazy infiltrates with bilateral linear opacities - PLEURAL PLAQUES
7. no specific tx

Front 12

Silicosis
1. definition
2. clinical course
3. associated with risk of what?
4. sources
5. symptoms
6. treatment

Back 12

1. restrictive lung disease with localized AND nodular peribronchial fibrosis - upper lobes most common
2. can be acute- massive exposure leading to rapid onset and death or chronic- symptoms years after exposure- up to 15 yrs or longer
3. associated with increased risk of TB
4. sources- mining, stone cutting, glass manufacturing
5. exertional dyspnea, cough productive of sputum can be seen
6. removal from exposure to silica

Front 13

Berylliosis
1. features
2. clinical course
3. dx
4. tx

Back 13

- like silicosis- has acute and chronic forms
- acute disease is a diffuse pneumonitis caused by massive exposure to beryllium, chronic disease is similar to sarcoidosis- granulomas, skin lesions, and hypercalcemia
- dx -beryllium lymphocyte proliferation test
- tx: glucocorticoids for both acute and chronic disease

Front 14

Hypersensitivity Pneumonitis (extrinsic allergic alveolitis)
1. definition
2. causes
3. dx
4. acute vs chronic forms
5. treatment

Back 14

1. inhalation of antigenic agent to the alveolar level induces immune-mediated pneumonitis- chronic exposure may lead to restrictive lung disease
2. variety of organic dusts and chemicals- farmer's lung (moldy hay), bird-breeder's lung (avian droppings), air conditioner etc-- often caused by spores of thermophilic actinomycetes
3. increased IgG and IgA to the inhaled antigen- some may have these antibodies with no disease
4. acute- flu like illness- fever, chills, cough, dyspnea, CXR- shows pulmonary infiltrates
5. chronic- insidious and difficult to diagnose
6. treatment- removal of offending agent, glucocorticoids

Front 15

Goodpasture's Disease
1. cause
2. clinical features
3. complications
4. diagnosis
5. prognosis
6. treatment

Back 15

1. autoimmune disease caused by IgG antibodies directed against glomerlar and alveolar basement membranes (type II hypersensitivity reaction)
2. hemorrhagic pneumonitis and glomerulonephritis-- hemoptysis, dyspnea, hematuria
3. renal failure as result of proliferative glomerulonephritis
4. dx by tissue biopsy- serologic evidence of antiglomerular basement membrane antibodies
5. prognosis is poor
6. treatment is plasmapheresis, cyclophosphamide, and corticosteroids

Picture = immunofluorescence - anti-glomerulobasement membrane antibodies-- ribbon-like

Front 16

Pulmonary Alveolar Proteinosis

Back 16

- rare condition caused by accumulation of surfactant-like protein and phospholipids in the alveoli
- usually presents with dry cough, dyspnea, hypoxia, and rales
- CXR typically has ground glass appearance with bilateral alveolar infiltrates that resembles the shape of a bat
- lung biopsy needed for definitive diagnosis
- lung lavage is the mainstay of treatment, but granulocyte-colony stimulating factor is a new tx
- patients are at increased risk for infection so steroids should NOT be given

Front 17

Idiopathic pulmonary fibrosis
1. cause
2. who is most commonly affected?
3. presentation
4. clinical course

Back 17

1. etiology is unknown but it is more common in men and smokers
3. gradual onset of progressive dyspnea with nonproductive cough
4. devastating and unrelenting, however prognosis is variable- mean survival is 3-7 yrs after first diagnosis

Front 18

Diagnosis of idiopathic pulmonary fibrosis (IPF)

Back 18

1. CXR- ground glass or honeycombed appearance, but may be normal
2. definitive diagnosis requires open lung biopsy, but even this may show non-specific findings
3. other causes of ILD must be excluded

Front 19

Treatment for idiopathic pulmonary fibrosis

Back 19

1. No effective treatment is available- the majority of patients (>70%) do not improve with therapy and experience progressive and gradual respiratory failure... however the following may be of some benefit
- supplemental oxygen
- corticosteroids with our without cyclophosphamide- taper after 1 year of use
- lung transplant

Front 20

Cryptogenic Organizing Pneumonitis (COP)
1. definition
2. associations
3. symptoms
4. CXR
5. efficacy of abx?
6. treatment
7. relapse?

Back 20

1. inflammatory lung disease with similar clinical and radiographic features to infectious pneumonia
2. associated with many entitities-- viral infections, medications, connective tissue disease-- but MOST are idiopathic
3. features- cough, dyspnea, and flu-like symptoms
4. CXR- bilateral patchy infiltrates
5. antibiotics are ineffective
6. Spontaneous recovery may occur- but corticosteroid are used most commonly (>60% recover)
7. Relapse may occur after cessation of steroids - necessitating resumption of steroids

Front 21

Radiation pneumonitis
1. definition
2. what determines morbidity and mortality?
3. acute vs chronic form
4. clinical features
5. CXR
6. CT
7. treatment

Back 21

1. interstitial pulmonary inflammation -- occurs in 5-15% of patients that undergo thoracic radiation for lung cancer, breast cancer, lymphoma, or thymoma
2. mortality and morbidity are related to the irradiated lung volume, dose, patient status and concurrent chemotherapy
3. acute form- occurs 1-6 months after irradiation, chronic form develops 1-2 years later-- characterized by alveolar thickening and pulmonary fibrosis
4. low grade fever, cough, chest fullness, dyspnea, pleuritic chest pain, hemoptysis, acute respiratory distress
5. CXR is usually normal
6. CT is best study- diffuse infiltrates (hallmakr), ground glass density, patchy/homogenous consolidation, pleural/pericardial pleural effusions-- excellent for detecting recurrent cancer in irradiated area
7. treatment of choice = corticosteroids- prophylaxis is not helpful

Front 22

Acute Respiratory Failure
- definition-- cutoffs for hypoxia and hypercapnia

Back 22

- results when there is inadequte oxygenation of blood or ventilation (elimination of CO2) or both
- Hypoxia (PaO2 < 60 mmHg and PaCO2 > 50 mmHg)
- Hypercapnia- partial pressure of CO2- > 50 mmHg

Front 23

Potential causes of respiratory failure by system

Back 23

1. CNS- brain or spinal cord depression or insult- drug overdose, stroke, trauma
2. neuromuscular disease- myasthenia gravis, polio, guillan barre, ALS (amyotrophic lateral sclerosis- lou guerigs)
3. upper airway- obstruction due to a number of causes including stenosis, spasm and paralysis
4. thorax and pleura- mechanical restriction due to kyphoscoliosis, flail chest-broken rib, hemothorax
5. cardiovascular system and blood- CHF, valvular diseases, PE, anemia
6. lower airways and alveoli- asthma, COPD, pneumonia, ARDS

Front 24

Two major types of acute respiratory failure

Back 24

there is often overlap
1. hypoxemic respiratory failure
2. hypercarbic respiratory failure

Front 25

hypoxemic respiratory failure
- PaO2 and PaCO2
- causes
- pathophysiology

Back 25

- low PaO2 with a PaCO2 that is either low or normal-- present with oxygen sat less than 90% despite FiO2- >0.6 (fraction of inspired oxygen)
- causes include disease processes the involve the lung itself - ARDS, severe pneumonia, pulmonary edema
- V/Q (ventilation to perfusion) mismatch and intrapulmonary shunting are the major pathophysiologic mechanisms

Front 26

Hypercarbic respiratory failure
- pathophysiology
- respiratory causes
- non pulmonic causes

Back 26

VENTILATORY respiratory failure
- decrease in minute ventilation or an increase in physiologic dead space leads to CO2 retention and eventually results in hypoxemia
- may be caused by underlying lung disease (COPD, asthma, CF, severe bronchitis)
- may occur in patients with no underlying lung disease who have impaired ventilation due to neuromuscular disease, CNS depression, mechanical restriction of lung inflation (extreme obesity), or any cause of respiratory fatiure (prolonged hyperventilation in DKA)

Front 27

Ventilation vs oxygenation

Back 27

Ventilation is monitored by PaCO2- to decrease paCO2 you must either increase respiratory rate or increase tidal volume-- minute ventilation = RR x VT

Oxygenation is monitored by O2 saturation and PaO2- to decrease PaO2 in a ventilated patient you must decrease FiO2 or PEEP (positive end-expiratory pressure)

Front 28

Young patient presents with constitutional symptoms, respiratory complaints, erythema nodosum, blurred vision. On CXR she is found to have bilateral hilar adenopathy. What is the most likely diagnosis?

Back 28

Sarcoidosis

Front 29

what type of respiratory failure does a V/Q mismatch typically produce?

Back 29

Hypoxia without hypercapnia- PaCO2 levels are usually low to normal
- most common mechanism of hypoxemia (especially in chronic lung disease)
- responsive to supplemental oxygen

Front 30

Intrapulmonary shunting
1. definition
2. causes

Back 30

little or no ventilation in perfused areas- due to collapsed or fluid-filled alveoli- venous blood is shunted into the arterial circulation without being oxygenated
- causes of shunts- atelectasis or fluid buildup in the alveoli (pneumonia or pulmonary edema), direct right to left intracardiac blood flow in congenital heart disease
- hypoxia due to a shunt is NOT responsive to supplemental oxygen-- the area is not ventilated so it does not matter how much oxygen is getting into the lungs-- it won't cross into the blood

Front 31

What type of respiratory failure does a diffusion impairment lead to?

Back 31

hypoxemic respiratory failure-- oxygen cannot get into the blood-- but the CO2 can get out--> no hypercapnia.

Front 32

clinical features/symptoms of acute respiratory failure

Back 32

1. dyspnea- first symptom
2. cough may or may not be present depending on the underlying cause

Front 33

clinical features/physical exam signs of acute respiratory failure

Back 33

- inability to speak in full sentences, use of accessory muscles of respiration
- tachypnea, tachycardia
- cyanosis
- impaired mentation (due to fatigue or hypercapnia- or if cause of respiratory failure is CNS depression)

Front 34

Diagnosis of Acute Respiratory Failure

Back 34

1. ABG - arterial blood gas- analysis- may confirm diagnosis and help determine the severity of the condition- should be obtained in most cases of respiratory failure
- hypoxemia- mechanisms include V/Q mismatch, intrapulmonary shunting or hypoventilation
-hypercapnia- caused by hypoventilation - secondary to a variety of causes
- arterial pH- respiratory acidosis occurs when hypercapnia is present-- however if respiratory failure is chronic- renal compensation occurs and acidosis is less severe
- CXR or CT chest
- CBC and metabolic panel
- If cardiogenic pulmonary edema is suspected--> cardiac enzymes-- CK-MB, troponins + ECG

Front 35

Treatment of acute respiratory failure

Back 35

1. treat the underlying disorder- bronchodilators, corticosteroid, antibiotics etc
2. supplemental O2- if the patient is hypoxemic-- remember this will not help if the patient has an intrapulmonary shunt
3. Apply NPPV- non-invasive positive pressure ventilation via CPAP or BIPAP ONLY for conscious patients with possible impending respiratory failure-- if the patient cannot breathe on his or her own--> intubate
4. intubation and mechanical ventilation may be needed in both types of respiratory failure

Front 36

Supplemental oxygen use in hypoxemic respiratory failure

Back 36

use the lowest concentration of oxygen that provides sufficient oxygenation to avoid oxygen toxicity due to free radical production

Front 37

supplemental oxygen use in hypercarbic respiratory failure

Back 37

- traditionally, it has been taught that high concentractions of oxygen can cause retention of CO2- especially in patients with COPD because hypoxia drives breathing so when a patient is no longer hypoxic, hypoventilation can result and hypercapnia can worsen-- causing respiratory acidosis-- however the validity of this theory is now in question

Front 38

Techniques to improve tissue oxygenation

Back 38

- increase Fio2- fraction of inspired oxygen
- increase PEEP (positive end expiratory pressure)-- keep airways open
- extend inspiratory time fraction
- decubitus, upright or prone positioning bronchodilation
- improve oxygen delivery - increase cardiac output, increase hemoglobin
- decrease oxygen requirements - decrease work of breathing, fever, agitation
- remove pulmonary vasodilators such as nitroprusside

Front 39

Oxygen delivery system for Low Flow

Back 39

- nasal cannula (1-6 L/min) , FiO2 up to 40%- easy to use and comfortable
- simple face mask (1-10 L/min)-, FiO2 40-60%- can deliver higher flow rates than nasal cannula

Front 40

Oxygen Delivery Systems for High Flow needs

Back 40

Venturi Mask- 4-10 L/mn, up to 50% FiO2 but can determine exact FiO2 to deliver- preferred in CO2 retainers because one can precisely control oxygenation

Non-rebreathing Mask- up to 15 L/min- variable FiO2 up to 70-80%, can achieve higher FiO2 at lower flow rates

Front 41

What is the Alveolar-arterial oxygen gradient (A-a gradient) like in hypoxemia due to hypoventilation?

Back 41

Normal-- all the oxygen that is getting into the lungs is getting into the blood-- there just is not enough
- A-a gradient is high in most other causes of hypoxemia

Front 42

ARDS (Adult Respiratory Distress Syndrome)
1. definition
2. mechanism

Back 42

1. diffuse inflammatory process that is not necessarily infectious involving both lungs. Due to neutrophil activation in the systemic or pulmonary circulations
2. Not a primary disease but rather a disorder that arises due to other conditions that cause a widespread inflammatory process. It is a CLINICAL DIAGNOSIS

Front 43

Pathophysiology of ARDS

Back 43

- Massive intrapulmonary shunting of blood is key pathologic event in ARDS- severe hypoxemia with NO significant improvement on 100% oxygen
- shunting is due to widespread atelectasis, collapse of the alveoli and surfactant dysfunction
- interstitial edema and alveolar collapse are due to increase in lung fluid, which leads to stiff lungs, an increase in alveolar=arterial oxygen difference (A-a gradient) and ineffective gas exchange
- Note: the effects of the increase in pulmonary fluid are identical to those seen in cardiogenic pulmonary edema, but the cause is different: An increase in alveolar capillary permeability causes ARDS, whereas congestive hydrostatic forces cause cardiogenic pulmonary edema
- Decreased pulmonary compliance-- leads to increased work of bleeding
- increased dead space-- secondary to obstruction and destruction of pulmonary capillary bed
- Low Vital Capacity, Low FRC

Front 44

Causes of ARDS

Back 44

1. Sepsis is the most common risk factor- can be secondary to a variety of infections (e.g. pneumonia, urosepsis, wound infections)
2. aspiration of gastric contents
3. Severe trauma, fractures (e.g. femur, pelvis), acute pancreatitis, multiple or massive transfusions, near-drowning
4. drug overdose, toxic inhalations
5. Intracranial HTN
6. Cardiopulmonary bypass

Front 45

Clinical features of ARDS

Back 45

1. dyspnea, tachypnea, and tachycardia due to increased work of breathing
2. progressive hypoxemia- not responsive to supplemental oxygen (ration of PaO2 to FiO2 < 200)
3. Patients are difficult to ventilate because of high peak airway pressures due to stiff, noncompliant lungs

Front 46

Diagnosis of ARDS
1. CXR findings
2. ABG findings
3. Pulmonary artery catheter
4. bronchoscopy- when used? What do you send the lavage fluids for?

Back 46

1. CXR - shows diffuse bilateral pulmonary infiltrates- there i variable correlation between findings on CSR and severity of hypoxemia or clinical response. Diuresis improves and volume overload worsens the pulmonary infiltrates. CXR improvement follows clinical improvement by 1-2 weeks or more
2. ABG- Hypoxemia (PaO2 < 60 mmHg), Initially, respiratory alkalosis (PaCO2 < 40 mmHg) is present which gives way to respiratory acidsosis as the work of breathing increases and the paCO2 increases. if the patient is septic ,metabolic acidosis may be present with or without respiratory compensation
3. pulmonary artery catheter- enables determination of pulmonary capillary wedge pressure (PCWP- LA Filling Pressure)- an indirect marker of intravascular volume status. PCWP is the most useful parameter in differentiating ARDS from cardiogenic pulmonary edema. If PCWP is low (<18 mmHg), ARDS is more likely, whereas if PCWP is high (>18mmHg) then cardiogenic pulmonary edema is more likely
4. bronchoscopy with bronchoalveolar lavage- this may be considered if patient is acutely ill and infection is suspected. Fluid collected can be cultured and analyzed for cell differential, cytology, gram stain, and silver stain

Front 47

Treatment of ARDS

Back 47

1. Oxygenation- try to keep O2 saturation > 90%
2. mechanical ventilation with PEEP is usually required. It serves to increase lung volume by opening collapsed alveoli and decreasing shuting
3. Fluid management- volume overload should be avoided. A low-normal intravascular volume is preferred, the goal should be a PCWP of 12-15 mmHg. Vasopressors may be needed to maintain BP. On the other hand, patients with sepsis have high fluid requirements, so determining in the appropriate fluid management may be difficult
4. Treat the underlying cause (e.g. infection)
5. Do not forget to address the patient's nutritional needs. Tube feedings are preferred over parenteral nutrition-- always use the gut when you can

Front 48

Complications of ARDS

Back 48

1. Permanent lung injury- resulting in lung scarring or honeycomb lung
2. complications associated with mechanical ventilation- barotrauma secondary to high pressure mechanical ventilation possibly causing a pneumothorax or pneumomediastinum. Nosocomial pneumonia
3. Line-associated infections- central lines and pulmonary artery catheters (line infection sepsis), urinary catheters (UTI), and nasal tubes (sinus infection)
4. renal failure- may be due to nephrotoxic medication, sepsis with hypotension, or underlying disease
5. Ileus, stress ulcers
6. Multiple organ failure
7. Critical illness myopathy

Front 49

Mechanical Ventilation- what are the 2 major goals of mech vent?

Back 49

1. maintain alveolar ventilation
2. correct hypoxemia

Front 50

When should patients be initiated on mechanical ventilation?

Back 50

The decision to initiate mechanical ventilation should be a clinical one. Generally, patients with the following require mechanical ventilation:
1. Significant respiratory distress (e.g. high RR) or respiratory arrest
2. Impaired or reduced level of consciousness with inability to protect airway (look for absent gag or cough reflex)
3. Metabolic acidosis (if the patient is unable compensate with adequate hyperventilation to blow off CO2)
4. respiratory muscle fatigue
5. Significant hypoxemia (paO2 <70 mmHg) or hypercapnia (PaCO2 > 50 mmHg), respiratory acidosis (pH < 7.2) with hypercapnia
- ABGs are used to assess response to initiation of mech vent. Acceptable ranges of gas values include a PaO2 of 50 to 60 with PaCO2 of 40 to 50, and pH between 7.35 and 7.50.

Front 51

General principles of mechanical ventilation

Back 51

1. Initial settings should rest the respiratory muscles
2. The goal is to reduce the likelihood of barotraumas (high static airway pressures, overinflation) and atelectasis (low static airway pressures, underinflation)
3. A volume-cycled ventilator is most commonly used

Front 52

Ventilator Settings- Assisted Controlled (AC) Ventilation

Back 52

1. Assisted controlled (AC) Ventilation - this is the initial mode used in most patients with respiratory failure. Guarantees a "backup" minute ventilation that has been preset. The ventilator delivers a breath (of a predetermined tidal volume) when the patient initiates a breath. If the patient does not initiate a breath, the ventilator takes control and delivers a breath at a predetermined rate. In other words, the patient can go over the determined rate, but not under it. And every breath over the determined rate delivers the same predetermined tidal volume.. All breaths are delivered by the ventilator (in contrast to intermittent mandatory ventilation).

Front 53

Ventilator Settings - synchronous Intermittent Mandatory Ventilation (SIMV)

Back 53

- patients can breathe on their own above the mandatory rate without help from the ventilator (i.e. tidal volume of these extra breath is NOT determined by the ventilator, as it is in the assisted control mode)
- when the patient breathes spontaneously, there is no present volume of breath that is triggered, but he or she still gets the guaranteed predetermined rate
- this method delivers the mandatory breath in synchrony with the patient's initiated breath so that the two do not overlap, which is possible with the intermittent mandatory ventilation alone
- if no spontaneous breath is initiated by the patient, the predetermined mandatory breath is delivered by the ventilator
- this is the appropriate mode for both support of ventilation and weaning

Front 54

Continuous Positive Airway Pressure (CPAP)

Back 54

- Positive pressure (0-20 cm H2O) is delivered continuously (during expiration and inspiration) by the ventilator, but no volume breaths are delivered (patient breathes on his or her own)
- the only parameters to set are PEEP and pressure support
- If the patient is being weaned, one can use CPAP to assess whether the patient is ready to be extubated

Front 55

Pressure-Support Ventilation (PSV)

Back 55

- This is mostly used during weaning trials. Pressure is delivered with an initiated breath to assist breathing (pressure is not continuous-- only responds to initiated breath)
- It enhances respiratory efforts made by the patient
- PEEP may be added

Front 56

Key Ventilator Parameters
1. Minute Ventilation -components
2. FiO2
3. Inspiratory:Expiratory (I:E ratio)
4. PEEP

Back 56

1. Minute Ventilation (RR x tidal volume)- this should be adjusted to achieve the patient's baseline PaCO2. An initial tidal volume of 8-10 mL/kg is appropriate in most cases (lower tidal volumes are recommended for patient with ARDS and COPD). A rate of 10-12 breaths/min is appropriate
2. FiO2- fraction of inspired oxygen- the initial FiO2 should be 100% and should be quickly titrated down and use the lowest possible FiO2 to maintain a PaO2 of 50 to 60 or higher (or saturation > 90%) to avoid oxygen toxicity. FiO2 of less than 60% is generally safe. If an FiO2 of 0.5 does not result in adequate PaO2 add either PEEP or CPAP, both of which allow one to reduce FiO2 (i.e. to support PaO2 at a lower FiO2)
3. I:E ratio- the duration of time allotted to inspiration compared with the time allotted to expiration in one delivered breath. Remember that the duration of each breath is determined by the set RR. Therefore, increasing the time spent inspiration will proportionately decrease the time spent in expiration and vice versa. 1:2 is the usual ratio used.
4. PEEP- positive pressure maintained at the end of passive exhalation- keeps alveoli open. 2.5-10 cm H2) is appropriate initial setting. Can be added to any of the modes of ventilation, used mostly in patients with hypoxemic respiratory failure (ARDS). It allows for increased lung compliance and oxygenation (improves gas exchange), Prevents alveolar collapse and atelectasis. Side Effects: barotrauma (injury to the airway = pneumothorax), Low cardiac output due to decreased venous return, especially in the setting of hypovolemia.-- PEEP- like any form of positive intrathoracic pressure, lowers venous return and increases pulmonary vascular resistance

Front 57

Complications of Mechanical Ventilation

Back 57

1. Anxiety, agitation, discomfort- sedation is important, benzodiazepines are the preferred agents. Other options are opiods or induction agents such propofol. use opiods for analgesia.
2. Difficulty with tracheal secretions-- suction on a regular basis
3. Nosocomial pneumonia (especially if intubated for more than 72 hours)
4. Accidental extubation
5. Barotrauma- caused by high airway pressures
6. Oxygen toxicity- when FiO2 of >0.6 is required for prolonged period (2-3 days).
7. Hypotension- positive pressure ventilation results in creased intrathoracic pressures, leading to decreased venous return
8. trachelomalacia- softening of the tracheal cartilage- due to the prolonged presence of an endotracheal tube (ET)
9. Laryngeal damage during intubation
10. Gastrointestinal effects- stress ulcers and cholestasis- increased risk in mechanically ventilated patients.

Front 58

What patients have the highest risk of developing ARDS?

Back 58

Patients with sepsis or septic shock

Front 59

classic clinic criteria for diagnosing ARDS

Back 59

1. hypoxemia- that is refractory to oxygen therapy: ratio of PaO2/FiO2 </= 200
2. bilateral diffuse pulmonary infiltrates on CXR
3. No evidence of CHF: PCWP </= 18mmHg

Front 60

After placing an ET (endotracheal tube) what should you always do?

Back 60

Confirm correct placement by listening for bilateral breath sounds and checking a postintubation CXR
- On CXR- the tip of the ET tube should be approximately 3-5 cm above the carina

Front 61

Parameters to consider in extubation or weaning from a ventilator- the more criteria that are met, the more likely that extubation will be tolerated

Back 61

- whether the patient has an adequate respiratory drive
- intact cough (when suctioning secretions)
- PaO2 > 75, PaCO2< 45
- O2 saturation of > 90% with PEEP of 5 cm H20 or less and FiO2 < 40% to 50%
- Tidal volume > 5 mL/kg
- RR < 30 breath per min
- Vital Capacity > 10 to 15 mL/kg
- Negative inspiratory pressure <-20 cm H20 or more

Front 62

When should a tracheostomy be performed?

Back 62

When a patient is ventilator dependent for 2 or more weeks, a tracheostomy should be done to prevent tracheomalacia

Front 63

PEEP vs CPAP

Back 63

PEEP is positive end expiratory pressure that is applied during mechanical ventilation, whereas CPAP is positive pressure during spontaneous breathing. Both serve to increase the PaO2 at a constant FiO2 (by lowering intrapulmonary shunting and V/Q mismatch)

Front 64

What things should you always remember when assessing a patient with ARDS? (4)

Back 64

1. Physical findings are usually non-specific
2. Because the patient is usually intubated and on a ventilator, decreased unilateral breath sounds may be due to the endotracheal tube being in the right main bronchus or possibly a pneumothorax
3. Look for potential sources of sepsis and check for any signs of infection: acute abdomen, IV lines, wounds, decubiti etc
4. Keep in mind that cardiogenic pulmonary edema has to be distinguished from ARDS- look for signs of volume overload, CHF, JVD, edema, and hepatomegaly

Front 65

Pulmonary Hypertension definition

Back 65

1. Mean pulmonary arterial pressure > 25 mmHg at rest or 30 mmHg during exercise

Front 66

Classifications of causes of pulmonary hypertension from a physiologic standpoint

Back 66

1. passive type- resistance to pulmonary venous drainage, no active disease in the pulmonary vascular bed ( passive reflection of a process further down) - e.g. mitral stenosis, LV failure, atrial myxoma, pulmonary veno-occlusive disease
2. hyperkinetic type- caused by high pulmonary blood flow (left-to-right shunt)- ventricular septal defect, atrial septal defect, PDA
3. Obstructive type- resistance to flow through large pulmonary arteries (E.g. PE, stenosis of pulmonary artery)
4. Obliterative type- resistance to flow through the small pulmonary arterioles due to some parenchymal inflammation that leads to fibrosis (e.d. primary pulmonary hypertension, collagen vascular disease, CREST syndrome)
5. Vasoconstrictive type- resistance to flow due to hypoxia-induced vasoconstriction (e.g. anything that causes chronic hypoxemia-- COPD, OSA etc)
6. Increased intrathoracic pressure- the increased intrathoracic pressure is transmitted to the pulmonary vasculature (e.g. mechanical ventilation with PEEP, COPD).
7. Increased blood viscosity (e.g. polycythemia vera)

Front 67

Classification of causes of pulmonary hypertension from an anatomic standpoint (2)

Back 67

1. Postcapillary causes - associated with diseases of the left side of the left side of the heart that increase pulmonary venous pressures- ex- mitral stenosis, left ventricular dysfunction, atrial myxoma, constrictive pericarditis, pulmonary veno-occlusive disease)
2. Mixed capillary and pre-capillary causes associated with diseases of lung parenchyma or pulmonary vessels-- all obstructive and parenchymal diseases (e.g. COPD, ILD, PE, Primary pulmonary hypertension, kyphoscoliosis)

Front 68

Symptoms of pulmonary hypertension

Back 68

1. Dyspnea on exertion
2. fatigue
3. chest pain
4. syncope- exertional (with severe disease)

Front 69

Signs of pulmonary hypertension

Back 69

1. Loud pulmonic component of the second heart sounds (P2) and subtle lift of sternum- sign of RV dilitation-- these may be the only findings and the patient may have devastating disease
2. When RV failure occurs-- JVD, hepatomegaly, ascites, and peripheral edema

Front 70

Diagnosis of pulmonary hypertension
1. ECG
2. Echo
3. Right heart catheterization

Back 70

1. ECG- often suggest RV hypertrophy-specifically right axis deviation and right atrial abnormality
2. Echo - dilated pulmonary artery, dilatation/hypertrophy of RA and RV, abnormal movement of the IV septum-- due to increase right ventricular volume
3. right heart catherization- increased pulmonary artery pressure

Front 71

Treatment of pulmonary hypertension

Back 71

No specific treatment plan because it depends largely on the cause

Front 72

Primary Pulmonary Hypertension
1. definition
2. pathophysiology
3. Cause and who is usually affects?
4. prognosis and course of disease

Back 72

1. Pulmonary hypertension in the absence of diseases of the heart or lung-- DX OF EXCLUSION
2. An abnormal increase in the pulmonary ateriolar resistance leads to thickening of the pulmonary arterioral walls. This worsens the pulmonary hypertension, which in turn causes further wall thickening (due to increases wall stress, this leading to a vicious cycle
3. the cause is unknown and it usually affects young to middle aged women
4. prognosis is poor- mean survival is 2-3 years from the time of diagnosis. By the time a patient seeks medical attention, the disease is often irreversible.

Front 73

Clinical features of primary pulmonary hypertension

Back 73

1. signs and symptoms similar to those from pulmonary HTN from another cause (dyspnea, CP, fatigue, syncope, RVH, edema, ascites, JVD, hepatomegaly)
2. exertional syncope is particularly common and is found in up to 50% of cases

Front 74

Diagnosis of Primary Pulmonary Hypertension

Back 74

1. Cardiac catheterization establishes the diagnosis
2. CXR shows enlarged central pulmonary arteries, enlarged RV, and clear lung fields
3. PFTs show a restrictive pattern
4. ECG shows right axis deviation and RVH

Front 75

Treatment of Primary Pulmonary Hypertension

Back 75

1. pulmonary vasodilators such IV prostacyclins (epoprostenol) and calcium channel blockers can lower pulmonary vascular resistance.
- perform a vasodilator trial - using inhaled nitric oxide, IV adenosine, or oral CCB under hemodynamic monitoring to predict response before initiating treatment.
-Sildenafil (Viagra) may also be useful as a vasodilator
2. Anticoagulation with warfarin is generally recommended (keep INR around 2.0) due to venous stasis, physical inactivity, and increased risk of microvascular thrombosis
3. lung transplantation may be an option in qualified patients

Front 76

Cor pulmonale
1. definition

Back 76

1. Right ventricular hypertrophy with eventual RV failure resulting from pulmonary hypertension, secondary to pulmonary disease
2. this does NOT encompass any causes of pulmonary HTN due to left-sided heart disease (such as MS, or left to right shunts)

Front 77

Causes of cor pulmonale
1. most common
2. others

Back 77

1. most commonly due to COPD
2. other causes- recurrent PE, ILD, asthma, CF, sleep apnea, and pneumoconioses

Front 78

Clinical features of cor pulmonale

Back 78

1. decrease in exercise tolerance
2. cyanosis and digital clubbing
3. signs of RV failure-- hepatomegaly, ascites, JVD, edema
4. parasternal lift
5. polycythemia is often present if COPD is the cause (secondary to chronic hypoxemia)

Front 79

Diagnosis of cor pulmonale
1. CXR
2. ECG
3. Echo

Back 79

1. CXR- enlargement of the RA, RV, and pulmonary arteries
2. ECG- right axis deviation, P pulmonale (peaked P waves), RVH
3. Echo- RV dilitation, but normal LV size and function-- useful in excluding LV dysfunction

Front 80

How do you determine the cause of pulmonary hypertension?

Back 80

1. Perform a series of tests (CXR, PFTs, ABGs, serology, echo and cardiac cath). These tests will give you enough information to recognize heart or lung disease as the causes
2. If the cause is not revealed - neither heart nor lung cause, then obtain a V/Q scan- this indicates either PE or PPH-- PPH is a diagnosis of exclusion

Front 81

What is the right-sided heart disease that is pretty much equivalent to left-sided heart disease due to systemic hypertension?

Back 81

Cor pulmonale-- secondary to pulmonary hypertension

Front 82

What cardiac condition to patients with COPD often die from?

Back 82

Right ventricular failure secondary to chronic pulmonary hypertension

Front 83

Sources of emboli to the lungs

Back 83

1. fat emboli- long bone fracture
2. amniotic fluid embolism- during or after delivery
3. air embolism- trauma to thorax, indwelling venous/arterial lines
4. septic embolism (IV drug use)
5. schistosomiasis- parasitic disease

Front 84

If patient with a long-bone fracture develops dyspnea, mental status changes and petechia, what diagnosis should you think of?

Back 84

Fat embolism- respiratory failure and death can ensue rapidly

Front 85

Pulmonary Embolism - general characteristics (pathophysiology etc)

Back 85

A PE occurs when a thrombus in another region of the body embolizes to the pulmonary vascular tree via the RV and pulmonary artery. Blood flow distal to the embolus is obstructed.
- consider PE and DVT as a continuum of one clinical condition (venous thromboembolism)- diagnosis either PE or DVT is an indication for treatment

Front 86

Sources of emboli in PE

Back 86

1. Lower extremity DVT- most pulmonary emboli arise from thomboses in the deep veins of the lower extremities above the knee (iliofemoral DVT)
2. pelvic venous thromboses
3. calf vein thrombi have a low incidence of embolizing to the lungs, however in many patients, these thrombi progress into the proximal veins, increasing the incidence of PE
4. Upper extremity DVT are a rare source of emboli (may be seen in IV drug users)

Front 87

Risk Factors for PE/DVT

Back 87

1. Age >60
2. Malignancy--> hypercoaguability
3. Prior h/o PE/DVT
4. hereditary hypercoaguable states (Factor V Leiden, Protein C and S deficiency, antithrombin III deficiency)
5. prolonged immobilization, bed rest, long-distance travel
6. cardiac disease, especially CHF
7. obesity
8. nephrotic syndrome
9. major surgery- especially orthopedic e.g. pelvic surgery (immobility etc)
10. major trauma
11. pregnancy, estrogen use (OCPs)
12. smoking

Front 88

Pathophysiology of PE

Back 88

- emboli block a portion of pulmonary vasculature, leading to increased pulmonary vascular resistance, pulmonary artery pressure, and RV pressure. If it is severe (large blockage)- acute cor pulmonale may result
- Blood flow decreases in some areas of the lung creating dead space (ventilation without perfusion). The resulting hypoxemia and hypercarbia drive respiratory effort leading to tachypnea
- If the size of the dead space is large 9large PE), clinical signs are more overt (SOB and tachypnea)

Front 89

Clinical Course and Prognosis of PE

Back 89

1. Most often PE is clinically silent. Recurrences are common, which can lead to development of chronic pulmonary hypertension and chronic cor pulmonale
2. when PE is undiagnosed, mortality approaches 30%. A significant number of cases are undiagnosed (50%)
3. When PE is diagnosed, mortality is 10% in the first 60 minutes. Of those who survive the initial event, approximately 30% of patients will die of a recurrent PE if left untreated. Most deaths are due to recurrent Pe within the first few hours of the initial PE. Treatment with anticoagulant decreases the mortality to 2% to 8%.

Front 90

Symptoms of PE

Back 90

1. Dyspnea (73%)
2. Pleuritic Chest Pain (66%)
3. Cough (37%)
4. Hemoptysis (13%)
5. only 1/3 of patients with PE will have signs and sx of DVT
6. Syncope may be seen in large PEs

Front 91

Physical Exam Findings with PE

What is the most common finding?

Back 91

1. tachypnea (70%)
2. rales (51%)
3. tachycardia (30%)
4. S4
5. Increased P2
6. Shock with rapid circulatory collapse in massive PE
7. Other signs- low-grade fever, decreased breath sounds, dullness on percussion

Front 92

Diagnosis of PE
1. ABG
2. CXR
3. Venous Duplex US of LE

Back 92

1. ABG levels are not diagnostic- PaO2 and PaCO2 are low (PaCO2 is low due to hyperventilation) and pH is high from blowing off all the CO2-- respiratory alkalosis. The A-a gradient is usually elevated. A normal A-a gradient makes PE less likely, but cannot be relied upon for exclusion
2. CXR- usually normal. If any findings-- atelectasis, pleural effusion. The main utility is in excluding alternative diagnoses. Classic CXR signs like Hampton's hump and Westermark's sign are rarely present.
3. Venous duplex US of LE- If there is a positive result, treat with IV anticoagulation (heparin), treatment of DVT is the same as for PE. Keep in mind that with this approach, a false positive will lead to tx of some pts with no DVT or PE. A negative result is not helpful as this is the case in 50% of patients with proven PE. This test is very helpful when positive, but of little value when negative.

Front 93

Diagnosis of PE
1. V/Q scan
2. Helical CT chest with IV contrast
3. Pulmonary Angiography
4. D-Dimer assay

What is the test of choice in most medical centers?

What is the gold standard for diagnosis?

Back 93

1. V/Q scan- traditionally this WAS the most common test used when PE was suspected, but it has been replaced by helical CT as the initial study of choice in most medical centers unless there is C/I to CT. Is particularly useful when CXR is clear and there is no underlying cardiopulmonary disease. results-- either normal, low-probability, intermediate or high prob (see other card for interpretation of results).
2. Helical (spiral) CT chest with IV contrast- good sensitivity (90%) and specificity. can visualize very small clots (as small as 2 mm), but may miss clots in small subsegmental vessels (far periphery). Used to guide treatment in conjunction with clinical suspicion based on modified wells criteria. C/I in patients with significant renal insufficiency because of the IV contrast.
3. Pulmonary angiography- gold standard. Definitively diagnoses or excludes PE but is invasive. Contrast is injected into the pulmonary artery after percutaneous catherization of femoral vein. Consider this when noninvasive tests are equivocal and risk of anticoag is high or if the patint is hemodynamically unstable and embolectomy may be required. Angiography is rarely performed because it carries a 0.5% mortality
4. D-dimer assay- D-dimer is a specific fibrin degradation product so level can be elevated in patients with PE or DVT. It is fairly sensitive (90-98%). If results are normal and clinical suspicion is low, PE is very unlikely. Specificity is LOW- D-dimer results may also be elevated in MI, CHF, pneumonia, and post-op state. Any cause of clot or increased bleeding may elevate d-dimer level

Front 94

Interpretation of V/Q scan results
1. normal scan
2. high probability
3. Low to intermediate probability

Back 94

1. Normal scan- virtually rules out PE- no further testing is needed- but a scan is almost never normal in anyone
2. high probability- very high sensitivity for PE- treat with heparin
3. low to intermediate probability-- clinical suspicion determines the next step. If suspicion is high pulmonary angiography is indicated. if low then LE duplex US. If duplex positive then heparinize. if duplex negative--pulmonary angio. Basically the LE US allows you to avoid angio sometimes.

Front 95

Complications in patients with PE who survive the initial event (2)

Back 95

1. Recurrent PE
2. Pulmonary HTN (up to 2/3 of patients)

Front 96

Reliability of signs and symptoms of PE?

Back 96

NOT reliable. Often leads confusion and delay in treatment. However, if patient has signs and sx of PE and a DVT is found then one can make the diagnosis of PE without further testing.

Front 97

What tests provide an adequate basis for treating PE with anticoagulation?

Back 97

1. intraluminal filling defects in the central, subsegmental or lobular pulmonary arteries on helical CT (or high probability with a V/Q scan) and clinical suspicion.
2. DVT diagnosed with US and clinical suspicion
3. positive pulmonary angiogram (definitely proves PE)

Front 98

What tests can r/o PE?

Back 98

1. low probability V/Q scan (or normal helical CT scan) and low clinical suspicion
2. Negative pulmonary angiography (definite)
3. Negative D-dimer and low clinical suspicion

Front 99

What if a CT- pulmonary angio is negative for PE but there is high clinical suspicion?

Back 99

there is still a 5% chance that there is a PE-- so negative results should always be interpreted with caution in a patient with high clinical suspicion.

Front 100

Modified Wells Criteria for suspected Acute Pulmonary Embolism

Back 100

1. Symptoms and signs of DVT - 3.0
2. Alternative diagnosis less likely than PE - 3.0
3. Heart Rate > 100 bpm - 1.5
4. Immobilization > 3 days or surgery in the past 4 weeks - 1.5
5. Previous PE/DVT - 1.5
6. Hemoptysis - 1.0
7. Malignancy (current therapy, or in previous 6 months, or palliative) - 1.0

Calculators will tell the % chance of having a PE based on these factors/total score

> 4 then PE is likely

Front 101

PE Treatment based on modified wells criteria
1. Score of <4
2. Score > 4

Back 101

1. Score <4 then do D-dimer-- if negative then no treatment, if positive then do CT if possible
2. Score > 4 then do CT with contrast. If positive then treat. If negative then do not treat. If inconclusive or cannot be performed then do LE US. If this is positive then treat. If negative then do V/Q scan or pulmonary angio and treat if positive

Front 102

What is this ?

Back 102

Saddle Embolism-- PE

Front 103

Treatment of PE

Back 103

1. Supplemental Oxygen to correct hypoxemia. Severe hypoxemia or respiratory failure requires intubation and mechanical ventilation.
2. Acute anticoagulation therapy with either unfractionated of LMWH to prevent another PE. Anticoagulation prevents further clot formation. It does NOT lyse the existing emboli or diminish the thrombus size. Start immediately on basis of clinical suspicion. DO NOT WAIT FOR STUDIES TO CONFIRM PE IF CLINICAL SUSPICION IS HIGH. Give one bolus of heparin, followed by continuous infusion for 5-10 days. The goal is get an aPTT of 1.5-2.5 times control.
3. Oral warfarin for long term treatment- start with heparin on day 1. Therapeutic INR is 2-3. Continue for 3-6 months of more, depending on risk factors. Some patients at significant risk for recurrent PE (malignancy, hypercoaguable state) may be considered for lifelong anticoagulation
4. Thrombolytic therapy- e.g. streptokinase, tPA- speeds up lysis of clots. There is no evidence that thrombolysis improves mortality rates in patients with PE. However, its use should be considered in patients with massive PE who are hemodynamically unstable (persistent hypotension), patients with evidence of Right heart failure
5. IVC filter placement- use has become more common but reduction in mortality has not been conclusively demonstrated. Patients who have IVC filter placed are at a higher risk of recurrent DVT (but lower risk of recurrent PE). Complications of placement are rare but include- filter migration or misplacement, filter erosion, and perforation of IVC wall, and IVC obstruction due to filter thrombosis. Indications include- C/I to anticoagulation in a patient with DVT or PE, complication of current anticoagulation, failure of adequate anticoagulation as reflected by recurrent PE or DVT, a patient with low pulmonary reserve who is at high risk for death from PE

Front 104

Mechanism of action of heparin

Back 104

promotes the action of antithrombin III

Front 105

Back 105

Mech of action of anticoagulants

Front 106

Contraindications to heparin

Back 106

1. active bleeding
2. uncontrolled HTN
3. recent stroke
4. Heparin-induced thrombocytopenia (HIT)

Front 107

low molecular weight heparin (LMWH) vs unfractionated heparin (UFH)

Back 107

LMWH- better bioavailability and lower complication rates than UFH.
At least as effective if not more than UFH
- longer half-life
- given at weight adjusted doses-- do not need routine aPTT measurement

Front 108

Pretest probability and PE

Back 108

If pre-test probability of PE is low then D-Dimer is a good non-invasive test to rule out PE. so if D-Dimer is negative then you can rule out clot. But if positive it does NOT help you because many things can cause an elevated D-Dimer

Front 109

INR

Back 109

- way of reporting PT in standardized fashion
- warfarin increases INR values
- therapeutic INR is usually between 2-3. Notable exceptions are prosthetic mechanical heart valves, prophylaxis of recurrent MI, and treatment of antiphospholipid antibody syndrome, for which 2.5-3.5 is recommended

Front 110

What can you do if anticoagulation is contraindicated in a patient with a PE or DVT?

Back 110

Vena cava filter

Front 111

3 different types of pulmonary aspiration

Back 111

1. acidic gastric content, which are especially damaging to the lungs
2. aspiration of oropharyngeal flora, which can lead to infection
3. foreign body fluids (e.g. chemicals)

Front 112

Which lung is usually affected if someone aspirates?

Back 112

The right lung is most often involved due to anatomy- - the right main bronchus follows a more straight path down-- particularly the lower segments of the right upper lobe and upper segments of the right lower lobe

Front 113

Predisposing factors to pulmonary aspiration

Back 113

1. reduced level of consciousness (e.g. seizures, stroke, sedating drugs)
2. alcoholism
3. Extubation- impaired pharyngeal or laryngeal function
4. excessive vomitting, ileus
5. tube feeding, tracheostomy tubes
6. anesthesia, surgery
7. neuromuscular diseases
8. esophageal disorders (e.g. achalasia, GERD, cancer)

Front 114

Clinical features of pulmonary aspiration

Back 114

1. Presentation is variable- some patients develop acute onset of respiratory distress. However, most often, the patient appears well, but later develops respiratory dysfunction (cough, SOB, fever, tachypnea, hypoxemia, or frothy sputum)
2. it may be initially silent, with development of acute respiratory failure with no obvious cause
3. fever may or may not be present
4, may lead to obstruction of the airways with localized wheezing

Front 115

Diagnosis of pulmonary aspiration

Back 115

Findings on CXR are variable and resemble infiltrates that mimic bacterial pneumonia. Atelectasis and local areas of collapse may also be present

Front 116

Treatment of pulmonary aspiration
1. if witnessed
2. if suspected
3. if obstruction
4. prevention
5. complications if untreated?

Back 116

1. If aspiration is witnesses- Airway, Breathing and circulation, supplemental oxygen and supportive measures
2. If aspiration pneumonia if suspected, give antibiotics (penicillin G or clindamycin). Although many patients who aspirate will go on to develop aspiration pneumonia-- antibiotic treatment is controversial as it may select for resistant organisms
3. if obstruction is present- early bronchoscopy is indicated
4. prevention is critical in patients at high risk for aspiration- keep the head of the bed elevated and place an NG tube to decompress the stomach
5. abscess formation

Front 117

How likely is aspiration pneumonia in the event of aspiration?
- which organisms are implicated?

Back 117

40% of patients who aspirate will develop pneumonia--usually 2-4 days after aspiration
- organisms are often mixed (aerobic and anaerobic)
- foul smelling breath often indicates anaerobic infection
- poor oral hygiene increases risk of infection

Front 118

Dyspnea- general characteristics
1. what should you assess on history?
2. most common causes of acute dyspnea
3. what elements of a history make lung disease more likely?

Back 118

1. distinguish acute from chronic
2. patients with chronic dyspnea usually have either heart or lung disease or both. It may be difficult to distinguish between the two
3. the most common causes of acute dyspnea include- 1. CHF exacerbation, pneumonia, bronchospasm, PE and anxiety
4. assess the patient's baseline level of activity, whether the dyspnea is new in onset and its association with exertion
5. If the patient has a history of smoking, cough, sputum, repeated infections or occupational exposure--> lung disease is likely the reason for the chronic dyspnea

Front 119

4 most common causes of acute dyspnea

Back 119

1. CHF exacerbation
2. pneumonia
3. bronchospasm - as in asthma
4. anxiety

Front 120

What tests may be helpful in distinguishing lung and heart disease? (6)

Back 120

1. CXR
2. Sputum gram stain and culture
3. PFTs
4. ABGs
5. ECG
6. echocardiogram

Front 121

Causes of dyspnea (ddx)

Back 121

1. cardiovascular
a. CHF
b. ischemic heart disease, acute MI
c. pericarditis, cardiac tamponade
d. arrhythmias
e. valvular disease
f. congenital heart disease

2. Pulmonary causes
a. obstructive lung diseases- COPD, asthma, bronchiectasis
b. PE
c. ARDS
d. Pneumonia, TB, bronchitis
e. pleural effusion, pulmonary edema
f. pneumothorax
g. upper airway obstruction, foreign body aspiration (FBA)
h. ILD
i. chest wall abnormalities (kyphoscoliosis, rib fracture)

3. psychiatric disease- generalized anxiety disorder (GAD), panic attacks, hyperventilation,

4. systemic causes- severe chronic anemia, sepsis, DKA, GERD, medication (narcotic overdose)

5. chest wall abnormalities- kyphoscoliosis, rib fracture, ankylosing spondylitis

6. neuromuscular disease-- weaken respiratory muscles (myasthenia gravis, muscular dystrophy

Front 122

Diagnosis of dyspnea

Back 122

1. thorough history and physical exam, vitals
2. pulse ox- normal is 96-100% on room air. Be aware that the baseline oxygen sat is chronically low in many cOPD patients
3. ABG- may be indicated if oxygen saturation is low on pulse ox-- if hypercarbia is suspected or to evaluate for acid-base abnormalities
4. CXR- can reveal pneumothorax, pleural effusion, pulmonary vascular congestion secondary to CHF, infiltrates due to pneumonia, ILD and so on
5. CBC- evaluate for anemia, infection
6. ECG- may show ventricular hypertrophy or evidence of ischemic heart disease
7. Echo- - for further evaluation of CHF, valvular heart disease
8. PFTs- perform if all of the above are normal or if an obstructive lung disease is suspected
9. V/Q Scan or spiral CT- perform if PE is suspected
10. bronchoscopy- indicated if foreign body aspiration is suspected

Front 123

treatment of dyspnea- general characteristics- when to use mech vent etc

Back 123

1. treat the underlying causes
2. use mechanical ventilation in the following situations
- impending respiratory failure is suspected
- patient is unable to protect airway (e.g. decreased mental status, stroke, drug overdose)
- severe hypoxia despite supplemental oxygen (PO2 < 50 to 60)
- severe hypercarbia (PCO2 > 50)
- exercise and conditioning may improve perception of dyspnea

Front 124

Hemoptysis- general characteristics
1. definition
2. amount and what it indicates

Back 124

1. expectoration of blood, hemoptysis varies widely in severity and medical significance. The amount of blood does not necessarily correspond with the gravity of the underlying cause

Front 125

Differential diagnosis for hemoptysis
1. most common causes
2. other causes

Back 125

1. bronchitis (50% of cases), lung cancer (bronchogenic carcinoma), TB, bronchiectasis, pneumonia, many times the etiology is unclear after thorough eval (up to 30%)
2. goodpastures syndrome, PE with pulmonary infarction, aspergilloma within cavities, mitral stenosis-- elevated pulmonary venous pressure- vessels rupture, hemophilia

Front 126

Diagnostic evaluation of hemoptysis

Back 126

1. verify that the hemoptysis has truly occurred. For example- superficial mouth lacerations and hematemesis may be confused with hemoptysis
2. history and physical - fever, night sweats, weight loss suggest TB or cancer. Fever and chills or history of HIV- suggest pneumonia or TB, look for risk factors for PE, in the presence of acute renal failure or hematuria, goodpastures syndrome should be considered
3. diagnostic studies
a. CXR- may be a clear indicator of a pathogenic process or even diagnostic -- e.g. if fungus ball, irregular mass, granuloma, opacity consistent with pulmonary infarction is present. A normal CXR does not exclude a serious condition, especially PE or lung cancer
b. fiberoptic bronchoscopy- should be performed even if CXR is normal if there is a significant clinical suspicion for lung carcinoma. look for small tumor that may not be evident on radiograph. May localize the site of bleeding.
4. CT of chest- performed as a complement to bronchoscopy or as a substitute if there are contraindications to bronchoscopy

Front 127

treatment of hemoptysis

Back 127

1. treat the underlying cause
2. suppress the cough if it is aggravating the hemoptysis
3. correct bleeding diathesis (although anticoagulation is the treatment for PE)

Front 128

Why do patients with COPD sometimes have PND?

Back 128

Their excessive airway secretions accumulate at night causing airway obstruction, resulting in dyspnea that awakens the patient and forces him or her to clear the airway. Therefore PND is not specific to heart disease

Front 129

chronic CO2 retainers vs acute

Back 129

common in COPD patients-- usually have a normal pH and increased HCO3 levels-- compensatory.

- If CO2 retention is acute, pH will be decreased and HCO3 will be near normal levels

Front 130

massive hemoptysis

Back 130

- defined as more than 600 mL of blood in 24 hours
- the most common causes are bronchiectasis and bleeding diathesis
- airway protection is key- intubate if necessary
- bronchoscopy can help identify the source of the bleeding
- use bronchial artery embolization or balloon tamponade of the airway if indicated.

Front 131

What is the oxygen saturation cutoff for receiving home oxygen?

Back 131

</= 88%

Front 132

ABG
1. what does it measure?
2. What is the normal range of blood pH?
3. How does PaO2 change with age?
4. What is the normal PaCO2 range?

Back 132

1. the partial pressures of oxygen and carbon dioxide along with the pH of arterial blood
2. Normal pH is 7.35 - 7.45
3. Normal PaO2 decreases with age
4. Normal PaCO2 is 35-45 mmHg

Front 133

For every 10 mmHg increase or decrease in PaCO2 what should the corresponding increase or decrease e?

- How do you determine whether the pH change is metabolic or respiratory?

Back 133

0.08. In general if the change in pH is in the same direction as the change in PaCO2 then the primary disorder is metabolic.
- when there is an inverse relationship then the primary relationship is respiratory (as when CO2 is retained--goes up then the pH should go down)

Front 134

Spirometry
1. What is it?
2. What is it used for?

Back 134

1. From maximum inspiration the patient exhales as forcibly as possible to maximum expiration-- PFTs. Spirometer plots the change in lung volume against time

2. Helps to distinguish obstructive from restrictive lung disease.
- useful in assessing degree of functional impairment as well as monitoring effectiveness of treatment (during asthma exacerbation). May detect respiratory impairment in asymptomatic patients (e.g. smokers)

Volumes are measured as percentages of predicted values based on age, height, and sex.
- incorrect measurement of technique may lead to false positives.

Front 135

What are complications of obtaining an ABG?

Back 135

It is painful and can cause radial artery spasm which may lead to ischemic in patient with a radial dominant circulation

Front 136

DLco
1. explanation of test
2. what is it used for?

Back 136

1. The patient breathes in a small specific amount of CO, and the amount transferred from alveolar air to pulmonary capillary blood is measured. CO is a diffusion limited gas, so other variables are eliminated. Essentially measures the surface area of the alveolar capillary membrane.
2. Can often distinguish between asthma, emphysema and COPD. Useful in monitoring various conditions, such as sarcoidosis and emphysema

Front 137

Causes for low DLco (diffusing capacity for CO)

Back 137

1. Emphysema
2. sarcoidosis
3. Interstitial fibrosis
4. pulmonary vascular disease
5. also lower with anemia due to reduced binding of CO

Front 138

Causes for high DLco

Back 138

1. asthma-- increased pulmonary capillary blood volume
2. obesity
3. intracardiac shunt-- left to right shunt- inc pulm blood flow
4. Exercise
5. pulmonary hemorrhage (alveolar RBCs bind with CO)

Front 139

What does a high V/Q ratio indicate?
What is a normal V/Q ratio?

Back 139

Inadequate perfusion (more ventilation than perfusion)

Normal is 0.8 (so there is normally more ventilation than perfusion)

Front 140

What is a methacholine challenge and what is it used for?

Back 140

Methacholine induces bronchospasm, which can thus determine the degree of airway hypersensitivity.
- Useful in patients in whom asthma or COPD is suspected
- Sensitive in detecting airway hyperresponsiveness in mild asthma