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2024 - Élo - LMCC > Pulmonary > Flashcards

Pulmonary Flashcards

1
Q

Definition of hemoptysis and how much blood is needed for massive hemoptysis?

A

Coughing up blood from the lower resp tract (distal to larynx). Massive hemoptysis is production of ≥ 600 mL of blood (about a full kidney basin’s worth) within 24 hours.

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2
Q

Etiology of hemoptysis?

A

Airway Disease

  • Inflammatory – bronchitis (most common), bronchiectasis
  • Neoplasia: Primary: bronchogenic carcinoma, carcinoid. Secondary: endobronchial metastases
  • Foreign Body/Trauma

Pulmonary parenchymal disease
- Infectious - CF, necrotizing pneumonia, TB, fungus, lung abscess

Cardiac/Vascular – pulmonary thromboembolism, primary and secondary pulmonary HTN, cardiac failure, AV malformation, systemic coagulopathy

Immunological: Goodpasture’s (fatigue, weight loss, often hematuria, sometimes edema), Wegener’s

Idiopathic – 10-20% of cases

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3
Q

Risk factors for hemoptysis?

A

HIV infection, use of immunosuppressants (TB, fungal infection); exposure to TB; long smoking history (cancer); and recent immobilization or surgery, known cancer, prior or family history of clotting, pregnancy, use of estrogen-containing drugs or anticoagulants, and recent long-distance travel (pulmonary embolism).

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4
Q

Physical exam for hemoptysis?

A

o Vital signs, level of patient distress
o Lung exam + LN
o Heart + legs (edema)
o Skin, mucous membranes (ecchymoses, petechiae, telangiectasia)

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5
Q

Investigations for hemoptysis?

A
  • CXR (70-80% will have an abnormal CXR), CT sometimes indicated (known hx of bronchiectasis)
  • Bronchoscopy – direct visualization, acquisition of specimens for diagnostic studies, therapeutically
  • Labs: CBC, PT/PTT, TB skin test, urinalysis
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6
Q

Patients with normal results, a consistent history, and nonmassive hemoptysis can undergo empiric treatment for?

A

Bronchitis

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7
Q

Patients with abnormal results and patients without a supporting history for hemoptysis should undergo?

A

CT and bronchoscopy

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8
Q

What are the two objectives of hemoptysis?

A
  • Prevent aspiration of blood into the uninvolved lung (which can cause asphyxiation)
  • Prevent exsanguination due to ongoing bleeding
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9
Q

Ways to prevent aspiration of blood into the uninvolved lung (which can cause asphyxiation) in hemoptysis?

A

Positioning the patient with the bleeding lung in a dependent position and selectively intubating the uninvolved lung and/or obstructing the bronchus going to the bleeding lung.

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10
Q

Ways to prevent exsanguination due to ongoing bleeding in hemoptysis?

A
  • Clotting deficiencies can be reversed with fresh frozen plasma and factor-specific or platelet transfusions.
  • TXA
  • Laser therapy, cauterization, or direct injection with epinephrine or vasopressin can be done bronchoscopically.
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11
Q

Should you use rigid or flexible bronchoscopy in massive hemoptysis?

A

Rigid

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12
Q

If bronchoscopy doesn’t work for control of bleeding in hemoptysis?

A

Bronchial Artery Embolization
Thoracotomy + Lung Resection - Today many cases can be managed with bronchoscopy + embolization + medical therapy for the underlying cause. Surgery continues to be used when there is a structural problem with the lung that is not treatable with more conservative therapy (localized, severe bronchiectasis not responding to medical therapy)

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13
Q

What is the definition of pleural effusion?

A

Excess amount of fluid in the pleural space (up to 25mL)

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14
Q

What is the pathophysiology of pleural effusion?

A

Disruption of normal equilibrium between pleural fluid formation/entry and/or pleural fluid absorption/exit

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15
Q

Pleural effusions can be broken into which 2 categories?

A

Transudate

Exudate

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16
Q

Are transudate pleural effusions usually bilateral or unilateral

A

Usually bilateral, not unilateral

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17
Q

Ddx for transudate pleural effusion?

A

CHF (most common), liver cirrhosis (causing hypoalbuminemia or hepatic hydrothorax), nephrotic syndrome, hypothyroidism, cardiac valvular disease, peritoneal dialysis, Rheumatoid arthritis (green fluid)

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18
Q

Are exudate pleural effusions usually bilateral or unilateral

A

Can be bilateral or unilateral

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19
Q

Ddx for exudate pleural effusion?

A
  • Infectious: parapneumonic effusion - pneumonia (most common), TB pleuritis, viral infection, fungal, empyema
  • Malignancy: lung carcinoma, lymphoma, metastases, mesothelioma, myeloma
  • Inflammatory: RA, SLE, pancreatitis, pulmonary embolism, drug reaction
  • Trauma: hemothorax, pneumothorax, chylothorax, iatrogenic
  • Other: drug-induced, hypothyroidism
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20
Q

What is Light’s criteria?

A

Lights (exudative if);
• Pleural LDH: >2/3 ULN for serum LDH
• Pleural fluid:serum total protein ratio >0.5
• Pleural fluid:serum LDH ratio >0.6

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21
Q

What would be found on analysis of complicated exudative effusion

A

pH <7.2, LDH >1/2 serum, glucose <2.2, positive Gram stain

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22
Q

What should you send the fluid analysis for if pus + microorganisms

A

pH

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23
Q

What color would the fluid be if chylothorax?

A

White

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24
Q

Signs and symptoms of pleural effusion

A

o Often asymptomatic
o Dyspnea: varies with size of effusion and underlying lung function
o Orthopnea
o Pleuritic chest pain

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25
Q

Questions on history for pleural effusion

A

o Symptoms: OPQRST, previous episodes
o Exertional dyspnea, PND, orthopnea, leg swelling (CHF)
o Cough, hemoptysis, infectious symptoms (fever), hx of aspiration (pneumonia)
o Constitutional symptoms and risk factors for malignancy
o Jaundice, ascites, easy bruising, fatigue, weight loss, risk factors for liver cirrhosis (EtOH use, Hx hepatitis or fatty liver)
o Recent immobility (surgery, travel), hypercoagulability (pregnancy, hormone use, malignancy), unilateral leg swelling, hemoptysis, previous DVT/PE
o Recent infections, exposure to infectious/TB contacts, travel Hx, chest trauma
o Red Flags: Always consider PE-induced pleural effusions have unilateral effusions and pleuritic CP

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26
Q

What would be the expected findings on respiratory exam for pleural effusion

A

 Inspection: asymmetric chest expansion
 Percussion: dullness to percussion
 Palpation: decreased tactile fremitus
 Auscultation: reduced vocal resonance (bronchophony, whispered pectoriloquy, egophony), lung sounds (reduced), pleural friction rub

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27
Q

What are 5 things that differentiate the JVP from carotid

A

o Biphasic
o Non-palpable
o Occludable
o Abdominal-jugular reflex, pt positioning changes
o Decreases on inspiration (increased intrathoracic pressure causes more RV filling and moves septum towards LV)

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28
Q

What is the abdominojugular reflex?

A

Abdominojugular reflex = apply midabdomen pressure for 30s, positive if sustained (>10s) 4cm rise in JVP

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29
Q

Besides respiratory exam on physical what else should be performed for pleural effusion?

A
  • Vitals, LN (TB, malignancy)
  • CV
  • ABDO - Liver
  • Extremities: Unilateral leg swelling (PE), pedal edema (CHF)
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30
Q

What lab investigations should be sent for pleural effusion?

A

CBC-D, lytes, serum LDH, total protein, glucose, LFTs, liver enzymes, Cr

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31
Q

Is PA or lateral more sensitive for pleural effusion on CXR?

A

Lateral

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32
Q

What usually causes chylothorax?

A

Caused by traumatic or neoplastic (most often lymphomatous) damage to the thoracic duct

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33
Q

How much fluid needs to be present to detect pleural effusion on PA and lateral CXR?

A

On PA there needs to be 200 mL, on lateral 50 mL

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34
Q

When is CT indicated for pleural effusion?

A

CT is not routinely indicated but is valuable for evaluating the underlying lung parenchyma for infiltrates or masses when the lung is obscured by the effusion or when the detail on chest x-rays is insufficient for distinguishing loculated fluid from a solid mass.

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35
Q

What are the indications for thoracentesis?

A

Indications: Should be done in almost all patients who have pleural fluid that is ≥ 10 mm in thickness on CT, ultrasonography, or lateral decubitus x-ray and that is new or of uncertain etiology. In general, the only patients who do not require thoracentesis are those who have heart failure with symmetric pleural effusions and no chest pain or fever; in these patients, diuresis can be tried, and thoracentesis avoided unless effusions persist for ≥ 3 days.

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36
Q

What should the fluid from thoracentesis be sent for?

A

Fluid analysis: LDH, total protein, pH, cell count and differential, gram stain and culture

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37
Q

If fluid appearance is bloody what should you order and what’s your ddx?

A

Get HCT/RBC count > DDx: malignancy + trauma + PE + hemothorax

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38
Q

If fluid appearance is cloudy/white what should you order and what’s your ddx?

A

Get TG’s > DDx: chylothorax

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39
Q

If fluid has putrid odor what should you order and what’s your ddx?

A

Get Gram Stain & C&S > DDx: anaerobic infection

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40
Q

When is pleural bx indicated?

A

Indicated if suspect TB, mesothelioma, or other malignancy

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41
Q

When should tube thoracostomy be done?

A

If associated pneumothorax, empyema, hemothorax, chylothorax, or complicated parapneumonic effusion (persistent, recurrent, under tension or bilateral)

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42
Q

For treatment, thoracentesis should be done for?

A

Symptomatic effusions should be drained independent of cause

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43
Q

Treatment for empyema?

A

In patients with adverse prognostic factors (pH < 7.20, glucose < 60 mg/dL (< 3.33 mmol/L), positive Gram stain or culture, loculations), the effusion should be completely drained via thoracentesis or tube thoracostomy.

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44
Q

What surgical options exist for recurrent pleural effusions?

A

Pleurodesis for recurrent effusions, intrapleural fibrinolysis for loculated effusions

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45
Q

Approach to cough?

A
  • Start -> Medical history plus examination.
  • First determine if cough is reflection of serious illness (PE, pneumonia), exacerbation of RTI (common cold, URTI), exacerbation of pre-existing condition (COPD, UACS, Asthma or bronchiectasis) or secondary to exposure.
  • If subacute -> Post-infectious? If yes -> secondary to UACS, asthma, pertussis or acute exacerbation of chronic bronchitis?
  • If non-infectious – manage as chronic cough.
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46
Q

Approach to management of chronic cough?

A

Chronic cough -> systematically direct empiric treatment to most common causes (UACS, asthma, NAEB, GERD) in sequential and additive steps to account for multiple possible causes. Smokers should be counseled and assisted with cessation. ACE-inhibitors should be stopped.

  • Start with first-generation A/D - antihistamine/decongestant (UACS treatment).
  • If still present – proceed to perform spirometry (may be nondiagnostic) then BPC. Asthma treatment should follow.
  • If still present – NAEB – sputum test for eosinophils. CS follow. Treatment with inhaled corticosteroids is recommended
  • If still present – GERD – antireflux therapy, proton pump inhibitors, dietary regimen, surgery if all else fails
  • If undiagnosed after all this -> referral to cough specialist is indicated. ONLY diagnose psychogenic cough if ALL unusual, somatic and genetic causes have been eliminated.
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47
Q

Ddx for acute cough?

A
  • Upper respiratory infection (URTI) – including acute bronchitis - rhinitis, no red flags, sore throat
  • Pneumonia – febrile. ↑HR, ↑RR, signs of consolidation. Can persist and become chronic.
  • Influenza – febrile. No signs of consolidation.
  • Pertussis – whopping cough, cough-emesis
  • Exacerbations of asthma, COPD, CHF
  • Allergic rhinitis – allergy symptoms
  • Foreign body – new onset in children
  • Sinusitis – facial pressure/pain
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48
Q

Ddx of chronic cough?

A
  • Chronic bronchitis
  • Post-viral cough can last up to 6 weeks after the acute infection, especially in the context dx of asthma;
  • Post-nasal drip (UACS)
    ▪ Chronic rhinitis
    ▪ Chronic sinusitis
    ▪ Vasomotor rhinitis
  • Whooping cough
  • GERD
  • COPD
  • ACE-inhibitor induced cough.
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49
Q

Physical exam for cough?

A

O2 saturation, respiratory exam, HEENT (lymph nodes, ears) and precordial exam

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50
Q

Red flags of cough?

A
  • Systemic symptoms: persistent fever (pneumonia, TB); night sweats, weight loss (TB, lung cancer)
  • Dyspnea (asthma, congestive heart failure, COPD, interstitial lung disease)
  • Hemoptysis (TB, lung cancer); copious sputum production (bronchiectasis)
  • Severe thoracic pain/pleurisy (pneumonia, TB, pulmonary embolism)
  • Change in character of a chronic cough (esp. in a smoker’s cough)
  • History of contact with TB and/or HIV
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51
Q

Risk factors for cough?

A

Risk Factors: smoking, occupation, exposure, family history of lung CA or other CA, TB status, recent travel

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52
Q

What is chronic bronchitis?

A

Chronic bronchitis: Persistent cough for at least 3 months per year for ≥ 2 consecutive years. Most common cause in smokers. Most also have COPD.

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53
Q

What is post-nasal drip (UACS)?

A

Abnormally increased nasal mucus secretion that drips down the back of the throat and can lead to coughing, a feeling of obstruction in the throat, and throat clearing, tickle in throat

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54
Q

History of cough?

A
  • Onset and duration of cough
  • Characteristics of the cough: Productive (cough with production of phlegm/mucus), Non-productive (dry cough)
  • Timing: Nocturnal cough, Seasonal/geographical variation
  • Associated symptoms
  • Red Flags
  • Medications: ACEI, β-blockers
  • Allergies: any known
  • PHx: lung (asthma, COPD, CF), heart (CHF, MI, arrhythmias), chronic illness, GI (reflux)
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55
Q

Possible causes of productive cough?

A

Pneumonia (rust coloured), bronchitis, bronchiectasis (large volume of foul smelling, pulmonary edema (pink, frothy), tuberculosis

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56
Q

Possible causes of non-productive cough?

A

Asthma, interstitial lung disease, viral pneumonia (e.g., adenovirus. RSV, influenza virus)

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57
Q

Possible causes of nocturnal cough?

A

Asthma; upper airway cough syndrome (UACS); GERD

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58
Q

Cough; symptoms that would make you consider URI?

A

URI: rhinorrhea, odynophagia, myalgia, fever: suggestive of UR

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59
Q

Cough; symptoms that would make you consider GERD?

A

GERD (3rd most common cause of chronic cough) : heartburn or reflux

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60
Q

Cough; symptoms that would make you consider allergic origin?

A

Allergic origin: itching and watering of eyes, rhinorrhea, pruritus

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61
Q

Cough; symptoms that would make you consider cough-variant asthma?

A

Cough-variant asthma: exacerbation of cough with activity

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62
Q

Labs for cough?

A
  • Complete blood count: indicated in patients with chronic cough/red flag symptoms if an infective etiology (e.g., neutrophilic leukocytosis in pneumonia, lymphocytosis in TB) or allergic etiology (e.g., eosinophilia in asthma) is suspected
  • Tuberculin skin test: patients with suspected TB
  • Sputum examination
    ▪ Sputum culture: suspected bacterial pneumonia, TB
    ▪ Sputum examination for acid-fast bacilli: suspected TB
  • Nasopharyngeal swab/deep nasopharyngeal aspirate culture and PCR for pertussis: indicated in patients with subacute/chronic cough, esp. if associated with an inspiratory whoop and/or post-tussive vomiting
  • Blood culture: suspected pneumonia
  • Arterial blood gas analysis: patients with dyspnea and those with suspected life-threatening causes of acute cough
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63
Q

Chest CT scan for cough?

A
  • Suspected bronchiectasis (diagnostic test)
  • Recurrent pneumonia
  • Chest x-ray findings suggestive of lung cancer (e.g., mass, hilar lymphadenopathy)
  • Inconclusive chest x-ray findings in patients with foreign body aspiration
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64
Q

Chest x-ray for cough?

A
  • Suspected pneumonia or TB
  • Chronic cough with abnormal physical examination findings or prolonged history of nicotine abuse
  • Red flag symptoms
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65
Q

Bronchoscopy for cough?

A
  • Foreign body aspiration
  • Lung cancer
  • Suspected tracheoesophageal fistula
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66
Q

X-ray of paranasal sinuses for cough?

A

Patients with UACS secondary to suspected sinusitis

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67
Q

Test to differentiate between obstructive lung disease (e.g., asthma, COPD) and restrictive lung disease (e.g., interstitial lung disease)?

A

Spirometry

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68
Q

Treatment of non-life-threatening acute cough (URI, acute bronchitis)?

A
  • Nonpharmacological treatment: Honey,Menthol (vapors), Hydration, lozenges, and humidifiers
  • NSAIDs: for myalgia, headaches, fever
  • Antibiotics: usually not recommended
  • Hypersensitivity pneumonitis: antigen avoidance with/without glucocorticoid therapy
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69
Q

Treatment of life-threatening acute cough?

A
  • Inhalation injury: secure airway (endotracheal intubation/tracheostomy); administer high-flow oxygen; administer aerosolized bronchodilators and N-acetylcysteine with/without heparin; chest physiotherapy
  • Treat the underlying cause: See congestive heart failure, pulmonary embolism, asthma, COPD, and acute pericarditis.
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70
Q

Test to differentiate asthma from other obstructive lung disease?

A

Bronchial challenge test (metacholine challenge test; bronchodilator reversibility test)

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71
Q

Treatment of chronic cough with no abnormal physical examination findings and no history of ACE-inhibitor use?

A
  • Empirical trial of treatment with first-generation antihistamines (e.g., dimetindene, diphenhydramine)- improvement of symptoms within 2 weeks - diagnostic of UACS; treat the underlying cause
  • No/partial improvement with antihistamines
    o Empirical trial of inhaled bronchodilators or corticosteroids - symptomatic improvement - diagnostic of cough-variant asthma - bronchodilators, corticosteroids, leukotriene receptor antagonists
    o Empirical trial of proton pump inhibitors and anti-reflux lifestyle modification - symptomatic improvement - continue PPIs for 8-12 weeks
  • Treat the underlying cause
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72
Q

Definition of cyanosis?

A

Physical sign of bluish coloration of the skin due to the presence of >50 g/L of deoxygenated hemoglobin in blood vessels near the skin surface. O2 saturation of arterial blood falls below 85%

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73
Q

Definition of hypoxemia?

A

An abnormal deficiency in the concentration of O2 in arterial blood. PaO2 <60mmHg or SaO2 < 90

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74
Q

Definition of hypoxia?

A

Total body is deprived of O2.

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75
Q

What is central cyanosis?

A

Due to a circulatory or ventilatory problem that leads to poorer blood oxygenation in the lungs or greater O2 extraction due to slowing down of blood circulation in the skin’s blood vessels

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76
Q

Etiology of central cyanosis?

A

High alveolar-arterial (A-a) gradient

  • Shunting: Physiological – atelectasis, ARDS. Anatomical: pulmonary AVM, R-L intracardiac shunt
  • V/Q (ventilation-perfusion) mismatch: Obstructive (asthma, COPD), PE, Restrictive
  • Diffusion impairment (e.g., restrictive lung disease)

Hypoventilation (elevated PCO2, normal A-a gradient)

  • Central control: stroke, narcotics, obesity, hypothyroid
  • Peripheral: neuromuscular, chest wall
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77
Q

Define Type 1 Hypoxemic Respiratory Failure?

A

PO2 < 50 mmHg on room air. These disorders interfere with the lung’s ability to oxygenate blood as it flows through the pulmonary vasculature. A-aDO2 gradient.

78
Q

Which causes of hypoxemia fully correct with 100% O2?

A
  • V/Q Mismatch

- Diffusion Impairment

79
Q

Treatment for acute hypoxemic respiratory failure

A

Oxygen, PEEP, Diuresis, Prone Position, Permissive hypercapnia, Inverse Ratio Ventilation or Pressure Control Ventilation, Nitric oxide

80
Q

Define Type 2 Hypercapneic Respiratory Failure?

A

PCO2 > 50 mmHg (if not a chronic CO2 retainer). This is usually seen in patients with an increased work of breathing due to airflow obstruction or decreased respiratory system compliance, with decreased respiratory muscle power due to neuromuscular disease, or with central respiratory failure and decreased respiratory drive.

81
Q

Define Type 3 Mixed Respiratory Failure?

A

A-a gradient + increased PaCO2

82
Q

What is peripheral cyanosis?

A

Blood reaching the extremities is not O2 rich causing the skin to the appear blue. All factors contributing to central cyanosis can also cause peripheral symptoms to appear; however, peripheral cyanosis can be observed without there being heart or lung failures

83
Q

Etiology of peripheral cyanosis?

A

Decreased O2 delivery, low cardiac output, arterial/venous obstruction

84
Q

Causes of hypoxemia (Type 1)?

A
  1. Decreased Alveolar O2:
  2. V/Q Mismatch
  3. Shunt: Alveolar collapse or infiltration - alveolar capillary perfusion is much greater than alveolar oxygenation due to collapse and derecruitment of alveoli
  4. Diffusion Impairment
85
Q

Causes of decreased alveolar O2 for Type 1?

A
  • Decreased FiO2 (Check if oxygen is plugged in)
  • Increased PaCO2 – will have a normal A-a gradient (even though both values will decrease)
    Look at RR, there is not enough space in the alveolar for O2
86
Q

Causes of V/Q mismatch for Type 1?

A
  • Airway – asthma, COPD
  • Alveolar – pus, water, blood - Pneumonia, alveolar edema, pulmonary hemorrhage, cancer
  • Vascular – PE, pulmonary HTN
  • Interstitial – CHF, ILD
    CXR – Rules out alveolar and interstitial
87
Q

Causes of shunt for Type 1?

A

Causes: Cardiogenic pulmonary edema, Noncardiogenic pulmonary edema (ARDS), Pneumonia, Lung hemorrhage, Atelectasis

88
Q

Approach to hypoxemia?

A

Q1: Decreased FiO2 – Rarely

Q2: Increased PaCO2?

  • No: must be A-a gradient – Q4
  • Yes – Q3

Q3: Is there an A-a gradient?

  • PAO2 = 150 – (PaCO2/0.8)
  • A-a gradient = PAO2 – PaO2 = difference between alveolar and arterial O2
  • Normal A-a gradient = (age/4) + 4

Q4: Is O2 sat easily correctable with oxygen?

  • Yes: V/Q or diffusion impairment
  • No: Shunt
89
Q

Causes of hypercapnia (Type 2)?

A
  • Increased CO2 production (fever, sepsis, burns, overfeeding) – secondary to increased metabolism
  • Decreased alveolar ventilation
90
Q

Signs of decreased alveolar ventilation?

A

Decreased RR, decreased tidal volume (Vt), increased dead space (Vd)

91
Q

Causes of decreased alveolar ventilation?

A
  • Decreased CNS drive (CNS lesion, overdose, anesthesia) “won’t breathe”.
  • Neuromuscular disease (Myasthenia Gravis, ALS, Guillian-Barre , Botulism, spinal cord disease, myopathies, etc.). “can’t breathe”.
  • Increased Work of Breathing leading to respiratory muscle fatigue and inadequate ventilation.
    o Asthma/ COPD
    o Pulmonary fibrosis
    o Kyphoscoliosis
  • Increased Physiologic Dead Space (Vd) - pulmonary embolus, hypovolemia, poor cardiac output, and alveolar over distension.
92
Q

Respiratory compensation through ventilatory control of PaCO2 occurs ____

A

Immediately

93
Q

Treatment for hypoxia/cyanosis?

A

ABCs (c-spine!), Tx underlying cause, supportive O2 therapy (nasal cannula, BIPAP, CPAP)

94
Q

Signs/symptoms of hypoxia/cyanosis?

A

Dyspnea, fatigue, headache, anxiety, confusion, tachypnea, bradypnea, altered mental status, cyanosis, accessory muscle use, indrawing, paradoxical abdominal breathing

95
Q

Metabolic compensation occurs over ___ reflecting altered renal HCO3- production and excretion

A

2-3 d

96
Q

What is Winter’s Formula?

A

1.5 x HCO3 + 8 (+/- 2) used to calculate expected pCO2

97
Q

ABG clinical purposes?

A
  • To determine oxygenation and
  • To determine acid-base status.
  • To determine alveolar ventilation
98
Q

What is increased physiologic dead space?

A

When blood flow to some alveoli is significantly diminished, CO2 is not transferred from the pulmonary circulation to the alveoli and CO2 rich blood is returned to the left atrium

99
Q

In metabolic acidosis, if actual pCO2 > than predicted range, there is also ____

A

Respiratory acidosis

100
Q

In metabolic acidosis, if actual pCO2 < than predicted range, there is also ____

A

Respiratory alkalosis

101
Q

What is the anion gap and its baseline?

A

[Na+]–([Cl–]+[HCO3–]); baseline 12 (10-14)

102
Q

Increased anion gap (metabolic acidosis) suggests an increased number of ____

A

Increased anion gap (metabolic acidosis) suggests an increased number of unmeasured anions (like LACTATE from hypoxia, methanol from poison, or others…).

103
Q

What is the osmolar gap help with?

A

Helps to determine if there is an osmotically active particle that is not normally found in plasma, usually toxic alcohol such as ethanol, methanol, or isopropyl alcohol

104
Q

What is the calculation of osmolar gap?

A

Osmolar gap = measured osmolarity – calculated osmolarity.

105
Q

How do you calculate osmolarity?

A

Calculated Osmolality: (2*Na) + Glucose + Urea (all in mmol/L); normal ≤10 mmol/L

106
Q

If all three variables (HCO3 + pCO2 + pH) move in the same direction =

A

Metabolic

107
Q

If any of the three variables (HCO3 + pCO2 + pH) are discordant =

A

Respiratory

108
Q

How do you determine acid-base status on ABG?

A
  1. Is the pH acidemic (pH <7.35), alkalemic (pH >7.45), or normal (pH 7.35-7.45)?
  2. What is the primary disturbance? metabolic or respiratory
  3. Is there appropriate compensation?
  4. if there is metabolic acidosis, what is the anion gap and osmolar gap?
  5. if anion gap is increased, is the change in bicarbonate the same as the change in anion gap? If not, consider a mixed metabolic picture
  6. If NAGMA then distinguish renal causes from non-renal causes, use Urine AG = (Na+ + K+) - Cl-
109
Q

Adequate compensation of metabolic alkalosis?

A

Metabolic Alkalosis (0.6): PCO2 rises ⅔ the rise in HCO3 - PCO2 should increase 0.6 for every increase in 1 HCO3

110
Q

Does the change in AG = the change in HCO3. If so then the metabolic acidosis is purely an ___.

A

AG

111
Q

Adequate compensation of acute respiratory alkalosis?

A

0.2: 2 (mmol fall in HCO3):10 (fall in pCO2)

112
Q

Adequate compensation of chronic respiratory alkalosis?

A

0.5: 5 (mmol fall in HCO3):10 (fall in pCO2)

113
Q

Adequate compensation of acute respiratory acidosis?

A

0.1: 1 (mmol rise in HCO3):10 (rise in pCO2)

114
Q

Adequate compensation of chronic respiratory acidosis?

A

0.3: 3 (mmol rise in HCO3): 10 (rise in pCO2)

115
Q

If change HCO3&raquo_space; change AG =

A

AG acidosis and non-AG acidosis

116
Q

If change HCO3 &laquo_space;change AG =

A

AG acidosis and metabolic alkalosis

117
Q

If UAG <0, suggests adequate NH4+ excretion in urine, likely?

A

Likely nonrenal cause: diarrhea

118
Q

If UAG >0, suggests problem is lack of NH4+ in urine, likely?

A

Renal cause

119
Q

Ddx for respiratory acidosis - Increased PaCO2 secondary to hypoventilation?

A
  1. Respiratory Centre Depression (Decreased RR)
  2. Neuromuscular Disorders (Decreased Vital Capacity)
  3. Lung Disease
120
Q

Ddx of respiratory centre depression (Decreased RR) causing respiratory acidosis?

A
  • Drugs (anesthesia, sedatives, narcotics)
  • Trauma
  • Encephalitis
  • Stroke
  • Central apnea
  • Supplemental O2 in chronic CO2 retainers (e.g. COPD)
121
Q

Ddx of lung disease causing respiratory acidosis?

A
  • COPD
  • Asthma
  • Pulmonary edema
  • Pneumothorax
  • Pneumonia
  • ILD (late stage)
  • ARDS
122
Q

Ddx of neuromuscular disorders causing respiratory acidosis?

A
  • Myasthenia gravis
  • Guillain-Barré syndrome
  • Botulism
  • Poliomyelitis
  • Muscular dystrophies
  • ALS
  • Myopathies
  • Chest wall disease (obesity, kyphoscoliosis)
123
Q

Ddx of respiratory centre stimulation causing respiratory alkalosis?

A
  • Drugs (ASA, progesterone, theophylline, catecholamines, psychotropics, nicotine, salicylates)
  • Chest wall disease (obesity, kyphoscoliosis) Hepatic failure
  • Gram-negative sepsis Pregnancy
  • Anxiety
  • Pain
124
Q

DDx of respiratory alkalosis - Decreased PaCO2 secondary to hyperventilation

A
  • Pulmonary disease (pneumonia, edema, PE, interstitial fibrosis)
  • Severe anemia
  • Heart failure
  • High altitude
  • Respiratory Centre Stimulation
125
Q

Precipitating factors of metabolic alkalosis?

A
  • GI (vomiting, NG tube) or renal loss of H+
  • Exogenous alkali (oral or parenteral administration), milk alkali syndrome
  • Diuretics (contraction alkalosis): decreased excretion of HCO3-, decreased ECF volume, therefore increased [HCO3-]
  • Post-hypercapnia: renal compensation for respiratory acidosis is HCO3- retention, rapid correction of respiratory disorder results in transient excess of HCO3-
126
Q

Maintenance factors of metabolic alkalosis?

A
  • Volume depletion: reduced GFR and increased proximal reabsorption of NaHCO3- and increased aldosterone
  • Hyperaldosteronism (1o or 2o): distal Na+ reabsorption in exchange for K+ and H+ excretion leads to metabolic alkalosis; aldosterone also promotes hypokalemia
  • Hypokalemia: transcellular K+/H+ exchange, stimulus for ammoniagenesis and HCO3- generation
127
Q

Ddx of increased AG metabolic acidosis

A
  • M - Methanol
  • U - Uremia
  • D - DKA/Alcohol Ketoacidosis
  • P - Paraldehyde
  • I - Isoniazid
  • L - Lactic Acidosis
  • E - EtOH/Ethylene Glycol
  • R - Rhabdo/Renal Failure
  • S - Salicylates (ASA, Aspirin)
128
Q

What is type A lactic acidosis?

A

Due to tissue hypoperfusion (any cause of shock), ischemic bowel, profound hypoxemia

129
Q

What is type B lactic acidosis?

A

Non-hypoxic - multiple causes; the most common is failure to metabolize normally produced lactic acid in the liver due to severe liver disease

130
Q

Ddx of normal AG metabolic acidosis (hyperchloremic acidosis)

A
  • Hyperalimentation
  • Acetazolamide
  • RTA*
  • Diarrhea*
  • Ureteroenteric fistula
  • Pancreaticoduodenal fistula
131
Q

What is hyperchloremic acidosis?

A

Involves increased bicarbonate excretion that is replaced with Cl

132
Q

Ddx of acute dyspnea?

A
  1. Cardiac
  2. Pulmonary
  3. Neurologic/Psychogenic
133
Q

5 most common causes of chronic dyspnea?

A
  • Asthma
  • COPD
  • ILD
  • Myocardial dysfunction
  • Obesity/deconditioning
134
Q

Ddx of chronic dyspnea?

A
  1. Cardiac
  2. Pulmonary
  3. Metabolic
  4. Neuromuscular and chest wall disorders
135
Q

Cardiac causes of acute dyspnea?

A
  • Acute myocardial infarction
  • CHF exacerbation
  • Pericardial disease - cardiac tamponade
  • CAD
  • Arrhythmia
136
Q

Pulmonary causes of acute dyspnea?

A
  • Upper airway (e.g., foreign body, anaphylaxis, aspiration, croup)
  • Airway disease (e.g., asthma, chronic obstructive pulmonary disease)
  • Parenchymal lung disease (ARDS, pneumonia)
  • Pulmonary vascular disease (PE, vasculitis)
  • Pleural disease (pneumothorax, tension pneumothorax)
137
Q

Neurologic/Psychogenic causes of acute dyspnea?

A
  • Respiratory control (metabolic acidosis, trauma)

- Anxiety, panic attack

138
Q

Cardiac causes of chronic dyspnea?

A
  • Myocardial dysfunction - ischemic cardiomyopathy

- Valvular heart disease

139
Q

Pulmonary causes of chronic dyspnea?

A
  • Airway disease (asthma, COPD)
  • Parenchymal lung disease (interstitial disease)
  • Pulmonary vascular disease (pulmonary HTN)
  • Pleural disease (effusion)
140
Q

Metabolic causes of chronic dyspnea?

A
  • Medication
  • Severe anemia
  • Hyperthyroidism
141
Q

Neuromuscular and chest wall disorders causes of chronic dyspnea?

A
  • Deconditioning, obesity, pregnancy, neuromuscular disease
142
Q

Investigations for dyspnea?

A
  • Labs: CBCd, glucose, BUN, creatinine, lytes, troponin, CK
  • ABG
  • Chest Xray, 12 lead ECG
  • D-dimer
  • PFT, methacholine challenge test, shunt test, pulse oximetry, sleep study
  • Plasma BNP
143
Q

Management of dyspnea?

A
  • Hypoxemia (in the absence of compensatory hyperventilation) is treated with supplemental oxygen as needed to maintain oxygen saturation > 88%
  • Morphine 0.5 to 5 mg IV helps reduce anxiety and the discomfort of dyspnea
144
Q

Definition of COPD

A

Progressive, non-reversible lung diseases characterized by limited airflow with variable degrees of air sac enlargement and lung tissue destruction

145
Q

Causes of COPD?

A

Caused mainly by exposure to cigarette smoke/pollution.

146
Q

Only known genetic defect causing COPD

A

Alpha-1-anti trypsin deficiency (A1AT)

147
Q

Screening for A1AT deficiency should be considered in individuals diagnosed with COPD before age ___ or with a smoking history of ____

A

65 years

< 20 pack years

148
Q

What are the two subtypes of COPD?

A
  • Emphysema

- Chronic bronchitis

149
Q

Clinical presentation of COPD?

A
  • Smoker or ex-smoker >=40 yo
  • Cough regularly. May be intermittent.
  • Cough up phlegm regularly
  • SOB with simple chores. Progressive over time.
  • Wheezing with exertion, or at night
  • Frequent colds that persist longer
150
Q

Definition of chronic bronchitis?

A

Defined as cough that produces sputum repeatedly on most days for at least 3 consecutive months in 2 successive years. When chronic bronchitis involves airflow obstruction, it qualifies as chronic obstructive bronchitis.

151
Q

What causes the obstruction in chronic bronchitis?

A

Obstruction is due to narrowing of the airway lumen by mucosal thickening and excess mucus

152
Q

Clinical/physical exam findings of chronic bronchitis?

A

Chronic productive cough, purulent sputum, hemoptysis, cyanosis (2o to hypoxemia/hypercapnia), peripheral edema from cor pulmonale (RHF), crackles, wheezes, prolonged expiration if obstructive, frequently obese

153
Q

What is referred to as “Blue Bloaters”

A

Chronic bronchitis

154
Q

What would be seen on PFT for chronic bronchitis?

A

See decreased FEV1, normal/increased TLC

155
Q

What would be seen on CXR for chronic bronchitis?

A

Normal AP diameter, increased bronchovascular markings, potentially enlarged heart

156
Q

Definition of emphysema?

A

Defined as widespread and irreversible destruction of the alveolar walls and enlargement of many of the alveoli.

157
Q

Pathophysiology of emphysema?

A

Dilation and destruction of air spaces distal to the terminal bronchiole without obvious fibrosis + decreased elastic recoil of lung parenchyma causes decreased expiratory driving pressure, airway collapse, and air trapping

158
Q

What is referred to as “Pink Puffers”

A

Emphysema

159
Q

What are the types of emphysema?

A
  • Type 1 – Centriacinar (Respiratory Bronchiole): typical in smokers, primarily affects upper lobes
  • Type 2 – Panacinar (All Parts of Acinus): 1%, alpha-1-antitrypsin deficiency, primarily affects lower lobes
160
Q

What would be seen on PFT for emphysema

A

Decreased FEV1, increased TLC (hyperinflation), increased RV (gas trapping)

161
Q

What would be seen on CXR for emphysema

A

Increased AP diameter, flat hemidiaphragm (lateral CXR), decreased heart shadow, increased retrosternal space, bullae, peripheral vascular markings

162
Q

Clinical/physical exam findings of emphysema?

A

Dyspnea (+/- exertion), minimal cough, tachypnea, decreased exercise tolerance, pink skin, pursed-lip breathing, accessary muscle use, cachexia, hyperinflation/barrel chest, hyperresonant to percussion, decreased breath sounds/diaphragmatic excursion

163
Q

Physical exam findings of COPD?

A

Barrel chest, pursed lip breathing, accessory mm use, hyperresonance in upper lungs, pulsus paradoxus, diminished breath sounds, wheezing, prolonged forced expiratory time >9s (auscultate over trachea), costal paradox/Hoover sign, tripod pose, laryngeal height <4cm, early inspiratory crackles, absent cardiac dullness, subxiphoid cardiac impulse

164
Q

Diagnostic criteria for COPD?

A
  • If FEV1/FVC ratio <0.7 or <88%s → diagnose obstruction.

- If after bronchodilator, FEV1 is <80% → COPD.

165
Q

Treatment for COPD?

A

All patients should have VACCINATIONS (flu/pneumococcal every 5-10yrs)/smoking cessation/exercise/self-management/education and short acting bronchodilators (PRN)!

166
Q

What is the only intervention that can improve the disease state and affect the long-term decline in FEV1 in COPD?

A

Smoking cessation

167
Q

Entrance criteria for home O2 for COPD?

A

Stable over 3 months, PO2 <55 mmHg or PO2 <60 mm Hg and end-organ injury (cor pulmonale or polycythemia)

168
Q

Initial bronchodilator pharmacotherapy for COPD?

A

Initially SABA/SAMA/Combo -> LABA -> LAMA -> LABA+LAMA/LABA+ICS

169
Q

Bronchodilator pharmacotherapy for symptomatic COPD without exacerbations?

A

LABA + LAMA

170
Q

Bronchodilator pharmacotherapy for symptomatic COPD patient with frequent exacerbations?

A

LABA + ICS + LAMA

171
Q

Other drugs to prevent COPD exacerbations?

A
  • PDE4 inhibitor - Oral PDE4 inhibitors eg. Roflumilast (ICS preferable due to fewer side effects)
  • Macrolide anti-inflammatory (azithromycin)
172
Q

COPD complications?

A

Polycythemia 2o to hypoxemia, chronic hypoxemia, pulmonary HTN from vasoconstriction, cor pulmonale, pneumothorax due to rupture of emphysematous bullae, depression, pneumonia

173
Q

Precipitants of COPD exacerbation?

A

Infections, lifestyle/environmental (10%, cigarette smoke, dust, pollutants, cold air), non adherence, pulmonary embolism, pulmonary edema, pneumothorax, progression of COPD

174
Q

Investigations of COPD exacerbation?

A

Basic:
- LABS CBCD, lytes, urea, Cr, troponin/CK, Ca, Mg, PO4
- MICROBIOLOGY sputum Gram stain/AFB/C&S/fungal
- IMAGING CXR
- ECG left atrial enlargement, atrial fibrillation, sinus tachycardia
- SPIROMETRY/PFT FEV1/FVC <0.7, partially reversible. Severity based on FEV1
- ABG if acute respiratory distress
Special:
- BNP if suspect HF
- D dimer if suspect PE
- ECHOCARDIOGRAM

175
Q

Give antibiotics for acute exacerbation of COPD if any two of three symptoms

A

Increased sputum purulence, increased dyspnea or increased sputum volume.

176
Q

Management of acute exacerbation of COPD

A
  • ABCs → O2 to keep sat >90%, or 88 92% if CO2 retainer
  • BRONCHODILATORS salbutamol 2.5 5 mg NEB q4h ATC + q1h PRN and ipratropium 0.25 0.5 mg NEB q4h. Puffers preferable for acute management if proper technique used
  • STEROIDS prednisone 40 60 mg PO daily x14 days (tapering dose not necessary in all cases) or methylprednisolone 60 125 mg IV daily (inpatient)
  • ANTIBIOTICS bacteria cause 50% of COPD exacerbations! Doxy, amox, or amox-clav are best choices.
  • MECHANICAL VENTILATION Non-invasive Positive Pressure Vent (NIPPV): reduced need for invasive ventilation/ICU and shortens hospital time.
177
Q

Definition of asthma

A

Chronic, reversible airway inflammation characterized by periodic attacks of wheezing, SOB, chest tightness, and coughing; often FHx of atopy (asthma, allergic rhinitis, eczema)

178
Q

Can you diagnose asthma on first presentation?

A

Cannot diagnose at first presentation; called reactive airway disease until recurrent presentations

179
Q

Pathophysiology of asthma?

A

Airways hyper-responsive to triggers/antigens leading to acute obstructive symptoms by bronchoconstriction, mucous plugs, and increased inflammation; reversible airway obstruction

180
Q

Diagnosis of asthma?

A
  • Spirometry FEV1/FVC < 0.8 or improvement of FEV1 by 12% after trialling SABA (Ventolin)
  • Methacholine challenge or other PFTs rarely used but can be if high index of suspicion and normal spirometry
181
Q

Asthma severity?

A
  • Intermittent Asthma: exacerbations x2/week
  • Moderate Persistent Asthma: daily symptoms
  • Severe Persistent Asthma: continuous symptoms & frequent exacerbations
182
Q

Signs of poorly controlled asthma

A 
D: aytime  sx => 4x/week
A: ctivities reduced
N: ighttime sx => 1x/week
G: P visits
E: R visits
R: escue puffer (SABA) >4x/week
S: chool and work absences
183
Q

Management of intermittent asthma (Step 1)?

A

Patients with intermittent asthma have traditionally been treated with a SABA (salbutamol (100mcg) MDI, ideally with aerochamber (MDI), taken as needed for relief of symptoms. Could consider low-dose glucocorticoid and the fast-acting long-acting beta agonist (LABA).

184
Q

Environmental control of asthma?

A

Avoidance of out door/indoor allergens, irritants, and infections; home environment cleanliness (e.g. steam cleaning)

185
Q

Management of mild persistent asthma (Step 2)?

A
  • Regular (daily) use of a low-dose inhaled glucocorticoid or a combination glucocorticoid-LABA inhaler (ADVAIR – can use in all age groups. SYMBICORT – can’t give to children <12).
  • Patients receiving long-term controller therapy should continue to use their SABA as needed for relief of symptoms and prior to exposure to known triggers of their symptoms
186
Q

Management of moderate persistent asthma (Step 3)?

A
  • For moderate persistent asthma, the preferred controller therapies are either low-doses of an inhaled glucocorticoid plus a LABA, or medium doses of an inhaled glucocorticoid. *IF <12 yo increase ICS 1st, if >12 yo add LABA
  • Addition of an inhaled long-acting muscarinic antagonist (LAMA; tiotropium) to an inhaled glucocorticoid has proven equally effective compared to the combination of an inhaled glucocorticoid and LABA. Most effective in asthma complicated with sinus disease and exercise induced asthma)
187
Q

Management of severe persistent asthma (Step 4 or 5)?

A
  • For severe persistent asthma, the preferred controller treatments are medium (Step 4) or high (Step 5) doses of an inhaled glucocorticoid in combination with a LABA. Consider pulm referral and LTRA
188
Q

Red flags of acute exacerbations of asthma?

A

Severe tachypnea/tachycardia, respiratory distress, muscle fatigue, diminished expiratory effort, cyanosis (SaO2 <85%), silent chest, decreased LOC

189
Q

Treatment of mild acute exacerbations of asthma?

A
  • Use a nasal cannula or face mask to ensure oxygen saturation is above 94%. Furthermore, give inhaled salbutamol 1-3 doses every 20 min.
190
Q

Treatment of moderate acute exacerbations of asthma?

A
  • Start oral corticosteroids early, ensure O2 sat are above 94%, give inhaled salbutamol 3 doses every 20 minutes also known as ‘back-to-back’ salbutamol, and consider giving ipratropium (Atrovent) (3 doses in 1 hr)
191
Q

Treatment of severe acute exacerbations of asthma?

A
  • Severe exacerbations, similarly start oral corticosteroids (prednisone 40-60mg) early or consider IV steroids (methylprednisolone 125mg – if you are thinking ICU), consider giving 100% oxygen which may require a different mask, give continuous aerosolized salbutamol and back-to-back ipratropium 3 doses every 20 minutes, keep the patient NPO and consider IV magnesium sulphate (2g IV over 20m as bolus, good at dilating smooth muscles - S/E – hypotension). CALL PICU

2024 - Élo - LMCC (23 decks)

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