Respiratory (11%) Flashcards
PE (everything but treatment)
• Risk factors – venous stasis, immobility, recent surgery, malignancy, hx of VTE
• Virchow’s triad – inflammation, hypercoagulability, and endothelial injury
• Symptoms – abrupt onset of chest pain, SOB, and hypoxia are classic symptoms
o Other – anxious, wheezing, hemoptysis, tachypnea, diaphoretic
• Diagnostics – CTA (PE protocol)
PE Treatment
o Respiratory support
o Hemodynamic support – cautious IVF (can overload RV), levophed, ECMO?
o Anticoagulation
o Reperfusion
o Chronic phase – 3 months anticoagulation if provoked or indefinite anticoagulation if unprovoked (rivaroxaban, dabigatran, apixaban)
Pulmonary Edema
Excess fluid collects within the lungs, leading to impaired gas exchange and respiratory distress
Cardiogenic causes – typically r/t volume overload – valve disorders, acute MI, left-sided HF
Non-cardiogenic causes – typically r/t injury to endothelium – ARDS, PE, opioid overdose, TRALI
Symptoms – acute dyspnea, anxiety, increased WOB, tachycardia, crackles, pink frothy sputum
Treatment – reduce pulmonary fluids – oxygen (non-invasive or invasive helps reduce fluid in vasculature), loop diuretics, nitrates, inotropes
Acute Respiratory Distress Syndrome (ARDS)
An inflammatory lung condition caused by direct or indirect injury to the lungs (infection, trauma, hypotension)
Diagnostic inclusion criteria – acute onset of: bilateral diffuse infiltrates not caused by pulmonary edema, PAWP/PCWP < 19, PaO2/FiO2 ratio of ≤ 200
Treatment – treat underlying cause, support oxygenation and ventilation
Initial vent management strategies – calculate predicted body weight, select vent mode, initial tidal volume of 8 ml/kg (will have to come down to 6 ml/kg), set initial RR at approximately baseline
Goals of vent therapy – minimum PEEP of 5, plateau pressure ≤ 30
Check plateau pressure every 4 hours – if > 30, decrease TV by 1 ml/kg (minimum of 4 m/kg), if < 25, increase by 1 ml/kg (until plateau pressure > 25 or TV is 6 ml/kg)
Monitor pH – if pH 7.15-7.30 increase RR; if pH < 7.15 increase RR to 35 and consider increasing TV by 1 ml/kg until pH > 7.15; if pH > 7.45 decrease RR if able
Respiratory Failure
Hypoxemic – PaO2 < 60 mmHg and PaCO2 normal or < 50 mmHg
Hypercapneic – PaO2 < 60 mmHg and PaCO2 > 45 mmHg
Can be caused by numerous things – COPD, drug overdose, asthma, obesity, chronic bronchitis, rib fractures, neuromuscular disease, PE, ARDS, pulmonary edema, shunting
Stable – treat underlying cause, aggressive respiratory care
Unstable – BiPap or intubate, aggressive respiratory therapy, treat underlying cause
Pneumothorax
Can be caused by trauma (blunt is most common) or spontaneous (COPD, asthma, tall/thin males
Air-trapping and increased pressure can cause mediastinal shift → compression of great vessels and heart (aka tension pneumothorax)
Symptoms – acute onset of SOB, tachypnea, pleuritic chest pain, hyperresonance to percussion, absent breath sounds on injured side
Tension pneumo findings – severe respiratory distress, signs of obstructive shock, hypotension, distended neck veins (late sign), tracheal deviation (late sign)
Diagnostics – CXR is diagnostic of choice, will see air in the pleural space with absence of lung markings
Treatment – needle decompression (first line for primary pneumo, minimal symptoms), chest tube placement (definitive treatment for those with symptoms)
Tension pneumo treatment – emergent needle compression in 2nd ICS MCL followed by chest tube insertion
Angioedema
- An allergic reaction that affects parts of the face like eyes and lips
- Symptoms – swollen face (especially eyes, mouth, lips, tongue), swelling in mouth, throat, or airway
- Management – ABCs!, a definitive airway must be established if edema is extensive or progressing; antihistamines (diphenhydramine, loratadine), H2 blockers (ranitidine or cimeditine), epinephrine, steroids
COPD
- Airflow limitation that is not fully reversible
- Risk factors – tobacco smoke, environmental exposures, occupational exposures, genetics
- Symptoms – chronic cough, chronic sputum production, activity intolerance, symptom progression
- Individuals with COPD with a hx of ≥ 2 exacerbations in the last year, FEV1 < 50%, and/or hospitalization for COPD in the last year are at highest risk for COPD exacerbation and COPD death
- Diagnosis – spirometry is required – FEV1:FVC < 0.70 (70%) post-bronchodilator
- Severity of COPD is determined by FEV1 (GOLD category)
- Initial treatment – low risk/less symptoms – SABA; low risk/more symptoms – LABA + long-acting muscarinic antagonist (tiotropium [Spiriva])
Indications for hospital admission in COPD exacerbation
- Marked increase in symptom intensity
- Acute respiratory failure
- New onset of physical signs
- Failure to respond to initial treatment
- Insufficient home support
Indications for ICU admission in COPD exacerbation
- Severe dyspnea not responding to initial therapy
- Change in mental status
- Worsening hypoxemia (PaO2 < 40 mmHg)
- Worsening acidosis (pH < 7.25)
- Invasive mechanical ventilation
GOLD categories for COPD
- GOLD 1 (mild): FEV1 ≥ 80%
- GOLD 2 (moderate): 50% ≤ FEV1 < 80% predicted
- GOLD 3 (severe): 30% ≤ FEV1 < 50% predicted
- GOLD 4 (very severe): FEV1 < 30% predicted
COPD Exacerbation
- Symptoms – chronic symptoms increase – cough increases in frequency and severity, sputum production increases in volume or changes, dyspnea increases
- Exam findings – diffuse wheezing, tachypnea, features of respiratory distress (pursed lip breathing, accessory muscle use), signs of impending respiratory arrest
- ABG: PaO2 < 40 mmHg or PaCO2 >45 and pH < 7.35 indicates respiratory failure
- Treatment – SABA (albuterol), corticosteroids (prednisone 40 mg daily x5 days), +/- mechanical ventilation, +/- antibiotics
- Give antibiotics if – increased dyspnea, sputum production, and/or increased sputum purulence; and give to anyone mechanically vented
- Antibiotics to give – azithromycin 500 mg BID x3 days, cephalosporin, or Cipro if vented (500-750 mg BID x 7-14 days)
Asthma
- Bronchial hyper-responsiveness and underlying inflammation
- Symptoms – recurrent cough, wheeze, SOB, chest tightness, symptoms can worsen at night or with exercise, airflow obstruction is partially reversible after SABA
- Diagnosis – spirometry is needed to make diagnosis – increase in FEV1 ≥ 12% from baseline after SABA
- Peak flow meter is used for monitoring
- Treatment consists of SABA (acute reliever) + controller for persistent asthma (inhaled corticosteroid – fluticasone, bedusonide))
- Step-up therapy if not well controlled on current regimen
Asthma Exacerbation
- Moderate – dyspnea interferes with usual activity, peak flow 40-69%, requires provider evaluation, SABA, systemic corticosteroids (prednisone 40-60 mg/day x 3-10 days [average 5-7 days])
- Severe – dyspnea at rest, to ED, likely hospitalization, peak flow < 40%, SABA + systemic corticosteroids + adjunct therapies
- Warning signs of impending respiratory arrest – confusion, absence of wheezing, bradycardia, paradoxical thoracoabdominal movement, peak flow < 25%
Interstitial Lung Disease
- Lung tissue becomes damaged and scarred, thick/stiff lung tissue
- Risk factors – environmental toxins (ex: pesticides, asbestos), agriculture and farming, sand/silica, genetics (RA, sarcoidosis), medication-induced (nitrofurantoin, chemo [bleomycin])
- Symptoms – CHRONIC EXERTIONAL DYSPNEA, CHRONIC DRY COUGH, fatigue, bilateral Velco-like crackles, clubbing of nails
- CXR – may look normal in early stages and may progress to reticulonodular infiltrates (ground glass)
- CT – diagnostic of choice, “HONEYCOMBING” is characteristic of pulmonary fibrosis
- Acute management – high dose steroids, antitussives, and antibiotics are ineffective but are still the mainstay of treatment; ABCs – supplemental O2; anxiolytics/morphine