• Pulse oximetry (which measures oxy-hemoglobin saturation), chest X-ray (CXR), and on occasions arterial blood gas (ABG), are important initial diagnostic tools to evaluate the severity and the cause of respiratory compromise.
Bilevel positive airway pressure (BiPAP) is a noninvasive method of ventilation that can deliver up to 100% oxygen with application of positive airway pressure through a tight-fitting mask. The mask is very easy to put on and take off (since it is a mask), in contrast to invasive intubation. In acute pulmonary edema, BiPAP has the added benefit of decreasing preload. BiPAP increases intrathoracic pressure and decreases venous return to right heart.
Minimal PEEP of 5 cm H2O is used in all patients on mechanical ventilation to prevent end expiratory alveolar collapse. As PEEP is increased, it helps to recruit collapsed alveoli to improve gas exchange and oxygenation. Higher levels of PEEP (15–20 cm H2O) may be required to improve oxygenation, with the goal to reduce higher FiO2 to prevent oxygen toxicity.
or narrow endotracheal tube).
3 To prevent auto-PEEP in COPD/asthma, it is recommended to use lower TV and RR, even at the expense of mild hypoventilation and respiratory acidosis, as long as pH is > 7.2. This strategy is known as permissive hypercapnia.
In this case, the lungs do not have enough time to expire the inhaled air, and hence, more and more air gets trapped in each consecutive respiratory cycle, incrementally increasing the intrathoracic pressure. This can result in barotrauma and hypotension, similar in pathophysiology to high PEEP.
An intubated patient is found to be hypoxic and hypotensive. Exam reveals severe wheezing. It appears that ventilator settings needs to be adjusted. What is the likely cause of hypoxia and hypotension in this patient?
If patient’s own breathing rate is 15, then the extra 3 breaths that patient initiates, he/she will get 500 cc of preset TV in each breath (minute ventilation = 0.5 × 15). In this case, patient is said to be breathing over the vent.
b Reducing FiO2 is the first step to reduce risk of oxygen toxicity. But note that if PEEP was mistakenly set at 20 and FiO2 is set at 60%, and if oxygenation is adequate then NSIM is to decrease PEEP in this case; but this is an extreme example only.
6. A 65-year-old female with asthma exacerbation is currently intubated. RR of 20. ACMV mode is set at RR of 13 per minute and TV of 500 cc. ABG shows pH of 7.26, PaCO2 of 60 mmHg, PaO2 70 mm Hg. What is the NSIM?
To determine whether patient is ready for extubation, a spontaneous breathing trial is used with ventilation mode changed to low-pressure support ventilation. It is very similar to BiPAP, with positive pressure given during inspiration and expiration and TV/RR is completely dependent on the patient’s own respiratory effort.
During the first few hours of low-pressure support ventilation, rapid shallow breathing index (RSBI) ratio is calculated.RSBI = RR/TV (in liters). It is a ratio that is used to assess readiness of a patient to get extubated.
A 65-year-old male patient is on 5 PEEP and 40% FiO2 on ACMV mode. ABG done showed PaO2 of > 60 mmHg. Prior to morning intensive care unit (ICU) rounds the ventilator setting is changed to lowpressure support ventilation. During rounds he is found to have RR of 30 per minute and TV of 200 cc.
When perfusion is decreased to a well-ventilated area of the lung, then that part of the lung is defined as a dead space, where the ventilated volume of air will not participate in gas exchange. Think of this as dead air (space), which is useless. Classical example is pulmonary embolus
Anatomic or vascular shunts: blood passes from right side of heart to the left side bypassing the lungs/alveoli. This is known as right to left shunt
aHypoxemia due to anatomic/vascular shunts canot be corrected by supplemental oxygen. Physiologic shunting, on the other hand, is usually not a pure shunt. Supplemental oxygen will help in these cases.
6 On the other hand, chronic hypercapnia +/- hypoxemia can occur in COPD, obesity hypoventilation syndrome and extrinsic lung disease (e.g., severe kyphoscoliosis). It is usually well compensated by chronic metabolic alkalosis.
bA-a gradient = Alveolar (PAO2) – arterial (PaO2) gradient. As alveolar (PAO2) is not easily obtainable, clinically the following formula is used to calculate A-a gradient = (150 – 1.25 × PaCO2) – PaO2 (the normal value is < 15 mmHg). Increased gradient (in between the oxygen content of the alveoli and the oxygen content of the systemic arteries) means that there is intrinsic lung pathology. A-a gradient is not increased in hypoventilation or high altitude.
Background: Any severe local lung injury (e.g. drowning) or severe extrapulmonary pathology (e.g. severe sepsis) can cause oversecretion of inflammatory mediators into the blood stream that can activate neutrophils, which in turn release proteases and free radicals, damaging the endothelial and epithelial layers of alveoli. This leads to high protein vascular fluid leakage into the alveoli which eventually fills most of the intra-alveolar space, thereby causing significant areas of shunting. This condition is called ARDS. Histopathological picture is of diffuse alveolar damage.
Work-up: Transthoracic echocardiogram (TTE), and serum Brain natriuretic peptide (BNP) are good initial tests, as the major differential dx for ARDS is cardiogenic pulmonary edema. TTE is generally adequate to assess for evidence of heart failure. If large body habitus makes it hard to get a good quality TTE images and if assessment of volume status is needed, a Swan-Ganz catheter can help in direct measurement of cardiac pressures.
Rx: Always treat the underlying etiology. Mechanical ventilation is usually necessary. Recommended TV is 6 mL/kg of predicted body weight and plateau pressure (end inspiratory) of ≤ 30 cm H2O, even if it results in mild hypercapnia and respiratory acidosis (permissive hypercapnia is tolerated until pH is < 7.2).
A 41-year-old male admitted to ICU for severe pancreatitis now develops acute onset of respiratory symptoms with increasing SOB. ABG in 100% non-rebreather mask reveals PaO2 of 40 mmHg. CXR shows diffuse bilateral infiltrates (see picture).
9 If a patient presents with vague respiratory complaints and has hx of smoking as well as high-risk occupation (such as working in mining industry), test of choice is spirometry. It can differentiate between obstructive (COPD) and restrictive (asbestosis associated interstitial lung) disease.
One of the classic examples of restrictive lung diseases is interstitial lung fibrosis. Imagine the lung as a thick, stiff, small balloon which is very hard to inflate (to inhale) and easy to deflate (exhale), as the recoil pressure of the stiff-fibrosed lung is very high
Emphysema, bronchiolitis obliteransc and bronchiectasis
Asthmad and chronic bronchitis
Extraparenchymal lung disorderse
c Bronchiolitis obliterans (aka obliterative bronchiolitis) is inflammatory condition of smallest airways. It can be either sudden in onset or slowly progressive. It presents with dry cough, SOB, and wheezing. Etiologies include lung, or bone-marrow transplantation, infection, connective tissue disorders, toxic fume inhalation, etc. Treatment is supportive as disease is irreversible and patients may go on to require lung transplantation.
d NSIDx after PFTs suggest obstructive airway disease is to do bronchodilator challenge (e.g., albuterol). If FEV1 increases by ≥ 12% and/or increases by 200 mL from baseline, it indicates reversible airway obstruction suggestive of asthma.
Note: These values (FEV1, FVC, etc.) obtained from PFT are used for diagnosis, prognosis, evaluating progression of disease, and treatment response. So, PFT is “the” diagnostic test of choice for most of the chronic respiratory disorders.
First trick is to look only at percentage of predicted value. The normal value is usually 80 to 120% (100 +/- 20). Low is <80%. The only exception is forced expiratory volume1/forced vital capacity (FEV1/FVC) ratio, where the cut off for low value is < 70%.
If FEV1 or FEV1/FVC is reduced (in moderate to severe asthma), NSIM is bronchodilator challenge (e.g., albuterol). If repeat PFT shows ≥ 12% increase in FEV1 and/or increase in 200 mL from baseline, this indicates reversibility of airway obstruction, suggestive of asthma.
LDIS + LABAa
aIn asthma, LABA is not used alone and is always given in combination with inhaled steroids. Using LABA alone has been shown to increase risk of asthma-related complications. In contrast, LABA can be given alone in COPD.
bWhen patients are on HDIS evaluate for appropriateness of omalizumab (monoclonal IgG antibody to IgE). Omalizumab is indicated in patients who have evidence of allergy in skin testing and IgE levels between 30 and 700 IU/mL. If IgE levels are too low, giving antibody to IgE is useless. If IgE levels are too high, antibodies to IgE are overwhelmed by the amount of IgE .
cSome patients with severe asthma might require chronic use of systemic steroids. In these patients an FDA approved procedure, called bronchial thermoplasty can be considered, which consists of bronchoscopy-mediated application of heat to reduce smooth muscle hypertrophy and obstruction.
In patients with persistent asthma, alternative therapies such as mast cell stabilizers (cromolyn or nedocromil), theophylline, and leukotriene receptor antagonist (zafirlukast and montelukast) can also be considered.
14. Patient has hx of asthma and is on LDIS+ long-acting β2 agonist (LABA). Currently patient reports that for the last few months, he has had to use his rescue inhaler (albuterol) only two times per week. What is the NSIM?
15. Patient has hx of asthma and is on LDIS. Patient has FEV1 of 50 in office. She reports that this is her baseline and feels SOB throughout the day. What is the severity of asthma? What is the NSIM?
Example CCS: Patient with hx of asthma comes to emergency department (ED) with acute onset of shortness of breath(sob). Exam reveals diffuse wheezing. Peak expiratory flow rate (PEFR) at beside is 220 L/minute. Patient’s predicted PEFR value is 350. Patient’s PEFR is 62% of predicted (as 220/350 = 0.62).
15 There is so much lung hyperinflation that it is increasing the intrathoracic pressure, leading to greater than expected drop in systolic pulse pressure (> 20 mmHg) on inspiration. (The pathophysiology is similar to auto-PEEP.)
• PaCO2 is N or ↑ : PaCO2 is low in acute asthmatic attack, due to tachypnea and hyperventilation, but if PaCO2 is N or ↑ then it is either due to severe obstruction or patient’s respiratory muscles are tiring.
16 Decision to intubate should not be made based on ABG alone. If ABG shows PaO2 of > 60 mmHg and high PaCO2, but patient is speaking in full sentences and clinically appears better, then intubation is likely not necessary. In this case, patient is likely improving from severe asthma attack and is responding to treatment.
Prior to discharge remember the indications for vaccination which include flu and pneumococcal vaccination (same schedule as in COPD). Also, assess underlying severity of asthma (to prescribe LDIS or MDIS or LABA, if needed).
Pathophysiology: Long-term exposure to irritants, such as tobacco smoking, air pollution, exposure to poorly ventilated cooking and heating fires (particularly in developing world), and genetic factors can lead to an inflammatory response in the lungs, causing COPD.
Patients have normal oxygenation (pink) but as the lungs are hard to deflate (due to poor lung recoil and diaphragmatic flattening), patients typically must puff out the air (puffers). Hence known as “Pink puffers”
Early stage: chronic sputum production (look for this to make a clinical dx of chronic bronchitis)
Main differentiating feature in PFTa
Vaccination: flu vaccine is given every year. For pneumococcal vaccine give PPSV23 alone at diagnosis. After 5 years or at the age of 65 (whichever comes late) give PCV13 followed by PPSV23 (booster dose).
aLAMA is generally preferred because it is associated with reduced rate of exacerbation and it is also a once daily medication. Unlike asthma, in COPD inhaled steroids isn’t the 1st line therapy. In COPD, inhaled steroids have not been shown to alter long-term decline in FEV1; in-fact in old patients with advanced disease, inhaled steroids may actually increase the risk of pneumonia.