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Pulmonology > Muthiah > Flashcards

Muthiah Flashcards

1
Q

How does pneumonia cause chest pain?

A

Pain receptors in the pleura

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2
Q

What are some indications for a chest x-ray?

A
  • Dyspnea, cough, hemoptysis (big 3 in pulmonology)
  • Chest pain (pneumothorax can cause chest pain and be seen on CXR)
  • Fever
  • Weight loss
  • Suspected pulmonary or CV involvement from systemic disease
  • Monitoring of previously defined pulm or CV abnormalities
  • Routine (i.e., places w/high rates of TB infection)
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3
Q

What are the ABC’s of reading CXR’s?

A
  • Address: make sure you’re comparing a pt’s x-ray to their x-ray, not comparing them to someone else; look at name and film characteristics, making sure they’re right
  • Bony cage
  • Cardiac silhouette
  • Diaphragm
  • ETT, esophagus, lines, etc. (confirm placement)
  • Fields of the lung
  • General impression
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4
Q

How can atelectasis and COPD affect the diaphragm?

A
  • Atelectasis: can cause it to be raised on one side
  • COPD: can cause it to be lower than normal
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5
Q

What are the 4 basic densities on an x-ray?

A
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6
Q

What is sepsis?

A
  • Sepsis: SIRS + Infection
  • Systemic inflammatory response syndrome (SIRS) due to infection -> proven OR suspected
    1. SIRS lacks sensitivity and specificity
  • NOT a positive blood culture
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7
Q

How common is sepsis? Epi?

A
  • Leading cause of death in critically ill patients in the US
    1. One patient w sepsis dies EVERY 3 MINUTES!
    2. 1 out of 3 admission to MICUs is sepsis!
    3. Rate of sepsis INC due to aging population -> total number of deaths INC
  • Rate of sepsis due to fungal orgs has INC by 207%
    1. HIV, overuse of antibiotics (which inhibit the normal flora and allow candida and o/fungi to overgrow)
  • Total in-hospital mortality rate has fallen and avg length of the hospital stay decreased
    1. Insurance companies want people out of hospital
  • Gram-positive bacteria - predom pathogens after 1987
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8
Q

What makes a patient SIRS (+)?

A
  • >2 of the following:
    1. Temp. >38o or <36o
    2. Pulse >90/min
    3. RR >20/min
    4. WBC >12,000 (leukocytosis), <4,000 (leukopenia), or >10% bands (bandemia)
  • Absolutely HAVE TO KNOW THIS
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9
Q

What are some things that can be associated with SIRS without infection?

A
  • Pancreatitis
  • Burns
  • Trauma
  • See attached table for more…
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10
Q

What patients may have sepsis w/o fever?

A
  • Extremes of age: immune response may be impaired (neonates or seniors)
  • Immunocompromised
  • Corticosteroid use
  • NSAID/acetaminophen use: antipyretics (i.e., for RA, gout, or osteoarthritis)
  • Chronic kidney disease (and patients with uremia): can get severe infections
  • Diabetes
  • Neurologic insults, i.e., strokes or brain malformations
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11
Q

Which vital sign in SIRS is particularly suspect?

A
  • RR because often not taken appropriately, and there is no machine that can do it for you (+ all the others, really)
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12
Q

What is severe sepsis?

A
  • Severe Sepsis = Sepsis + Organ Dysfunction
  • Sepsis + either organ dysfunction or evidence of hypo-perfusion or hypotension
    1. Neurologic: confused, less interactive
    2. Renal dysfunction: oliguric, INC creatinine
    3. Thrombocytopenia
    4. DIC: D-dimers up, platelets going down
  • End-organ hypo-perfusion and reduced O2 delivery -> anaerobic metabolism (can measure lactic acid)
  • Organs can fail even in the absence of hypoperfusion
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13
Q

What is septic shock?

A
  • Septic Shock: Sepsis + Hypotension not responding to Fluid Resuscitation
  • Sepsis-induced hypotension
    1. Persists despite adequate fluid resuscitation
  • Require vasopressors
  • Sepsis -> Severe sepsis -> Septic shock
    1. Continuum for most patients
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14
Q

How does the host response lead to sepsis?

A
  • Dysregulation: see attached image
  • Host response may be more important than what the pathogen itself does in some cases
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15
Q

What are the clinical manifestations of sepsis?

A
  • Fever
  • Tachycardia, tachypnea, increase in minute ventilation (i.e., if pt. is on ventilator and can’t measure RR)
  • Hypotension
  • Mental status change: can be important in neonates (will stop interacting)
  • Nausea/vomiting
  • Loss of appetite
  • ICU Patients: not tolerating feeds -> check to see how much is left in the stomach; if there is too much there, then there is something wrong
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16
Q

How do we treat septic patients? Why?

A

Empiric AB’s AS SOON AS YOU SUSPECT SEPSIS

  • Sooner the better bc each hour delay in AB’s increases mortality by 6-7%
    1. Immediate antibiotics: 20% mortality
    2. 1 hour delay: 27% mortality
    3. 3 hours delay: 44% mortality
    4. 5 hrs delay = 58% mortality
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17
Q

What is goal directed resuscitation?

A
  • MUST KNOW THESE:
    1. Central venous pressure: 8–12 mm Hg
    2. Mean arterial pressure > 65 mm Hg
    3. Urine output > 0.5 mL/kg/hr (500 CC’s/kg/hr.)
    4. Central venous O2 saturation > 70%
  • Early, goal directed resuscitation SAVES LIVES
  • Don’t forget source control: if it is an abscess, you need to drain it (same with a pleural effusion empyema)
  • Don’t stop when you have bacteremia, i.e., gram (-) rods, bc you need to know where they are coming from
  • Want arterial O2 saturation to be in the 90’s somewhere
  • Note: lactic acid elevation is a good surrogate for inadequate O2 delivery (low central venous O2 saturation)
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18
Q

Why does sepsis have variable outcomes?

A
  • It is diagnosed by the signs and symptoms of the host response to the septic event
  • This may only be evident hours to days after the inciting event
  • THE EARLIER YOU TREAT, THE BETTER THE OUTCOME
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19
Q

What lab work should you do in a suspected sepsis case? When should you do it?

A
  • Before giving antibiotics
  • Gram stain & culture of appropriate body fluids (i.e., UA)
    1. Blood cultures X 2 -> peripherally and through a vascular access device when present
  • Appropriate imaging -> CXR, CT scan, HIDA scan (used to diagnose problems in liver, gallbladder and bile ducts), etc.
  • A good H & P will direct our investigation
  • CBC, CMP
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20
Q

How many sepsis patients have a (+) blood culture? Why?

A
  • Minority of patients have a (+) blood culture because:
    1. Bacteremia is an episodic phenomenon (timing is important)
  • REMEMBER: do culture before giving antibiotics
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21
Q

What are some important elements of sepsis management (4)?

A
  • Nidus of infection: eradicate organisms
  • Blood stream invasion: neutralize microbial toxins
  • Host defense system activated and mediators released: modulate host response
  • Shock and multi-organ failure: provide intensive care life support
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22
Q

What is the most optimal and cost-effective fluid for resuscitation?

A
  • NORMAL SALINE
  • Even though: saline stays in circulation for only 40 minutes, which is why infusion has to be constant -> if you give albumin, it will stay about 6 hours
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23
Q

Should you give hydrocortisone to patients in septic shock?

A
  • Yes -> significant reduction in mortality with low-dose hydrocortisone
  • If they give you this option, do it
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24
Q

How can we prevent sepsis?

A
  • Hand-washing
  • DVT prophylaxis
  • Stress ulcer prophylaxis (H2 blocker Vs PPI)
  • Head of the bed elevation to prevent VAP/HAP
  • Chlorhexidine mouthwash? Pathogens in the mouth can get aspirated
  • Remove Foley cath & Central lines ASAP
  • Early ambulation & Physical therapy
  • Target Glucose < 150 mg/dL
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25
Q

What is the best fluid to give patients in sepsis? Why?

A
  • Balanced fluids: avoid the biochemical effects of normal saline -> giving these instead of NS may be a good thing
    1. Probably won’t be on test, but just in case, choose LACTATED RINGERS
    2. Reduced peri-operative mortality & ICU morbidity
  • Normal saline (NS): can cause hyperchloremia & metabolic acidosis bc pH is only 5.4
    1. Alterations in renal blood flow
    2. Potentially important effects on immune function
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26
Q

What vasopressor should you choose?

A
  • Levophed better than Dopamine
  • Wean Levophed first
  • Once > 20 mics/min – add Vasopressin
  • Then: stepwise reduction in Vasopressin
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27
Q

Severe sepsis is sepsis with..?

A

The presence of organ dysfunction

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28
Q

What is the key element of septic shock?

A

Hypotension not responding to fluid resuscitation

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29
Q

Pathogenesis of severe sepsis is associated with…?

A

Profound initial immune activation

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30
Q

Autopsy/immunohistochemical studies in sepsis have shown which cell lines to be dying?

A

Lymphocytes and GI epi cells -> this is why patients start to develop infections with bugs found in the gut

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31
Q

What is the resuscitation fluid of choice?

A

Crystalloids (saline/lactated ringers)

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32
Q

What is FASTHUG?

A
  • For sepsis treatment:
    1. Feeds
    2. Analgesics
    3. Sedation protocol
    4. Thrombo-embolism prophylaxis
    5. Head of bed elevated > 30o
    6. Ulcer prophylaxis
    7. Glucose control
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33
Q

How does early goal directed therapy impact sepsis treatment?

A

Improves mortality

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34
Q

What inflammatory levels are elevated in sepsis?

A
  • Sepsis is associated with profound immune activation
  • Pro-inflammatory cytokine levels are elevated along with neutrophilic leukocytosis
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35
Q

What is the difference between PPH and SPH? Prognosis?

A
  • Primary Pulmonary HTN (PPH) – IPAH (idiopathic pulmonary arterial hypertension)
    1. No identifiable reason
  • Secondary Pulmonary HTN
    1. Some other condition, i.e., left heart failure (pulm venous HTN -> back pressure on the arteries)
  • After dx, most people die within 3-5 years (mostly young F)
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36
Q

What are the pathophysiological mechs of PAH (image)? Name some of the associated therapies.

A
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37
Q

What is the difference between post-capillary and pre-capillary HTN?

A
  • Post-capillary HTN rules out IPAH b/c this means the PAH is most likely attributable to left heart failure
  • Pre-capillary HTN only -> PAH
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38
Q

What is the definition of PAH?

A
  • Mean PAP >25mmHg at rest >30mmHg w/exercise
    1. Schwann-Ganz catheter (RH catheterization) the only direct way to measure pulm HTN
    2. Mean PAP usually 10-15 mm Hg (>2x here)
  • Mean PCWP & LVEDP <15 mmHg (ruling out LH failure b/c common)
    1. INC LVEDP is gold standard for dx left heart failure (can do left heart catheterization, but dangerous, so PCWP is a surrogate)
  • Unclear etiology; absence of demonstrable cause
  • REMEMBER: systemic BP 120/80 (mean 65-70), PCWP = pulm cap wedge pressure, LVEDP = LV end diastolic pressure
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39
Q

What are some causes of SPH?

A
  • Parenchymal lung disease: alveolar hypoxia can stimulate vasoconstriction
  • Chronic thromboembolic disease: CTEPH
  • Left-sided valvular disease
  • Myocardial disease: left ventricular failure
  • Congenital heart disease: R to L shunting
  • Systemic connective tissue disease
  • Primary if you don’t find any of these
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40
Q

How is PH classified?

A
  • Groups 1-5: things to know are in BOLD
    1. Group 1: mutation-related (idiopathic, heritable, BMPR2), drug-, toxin-induced, HIV, CT disease -> look phenotypically the same

A. Plexiform lesions: endothelial proliferations in pulmonary circulation, causing occlusion of the arteries (seen in all conditions in group 1)

  1. Group 2: PAH due to heart disease
  2. Group 3: PAH due to lung disease
  3. Group 4: CTEPH
  4. Group 5: multifactorial etiology
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41
Q

What is this?

A
  • Plexiform lesion: single pulmonary arteriole
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42
Q

How can PAH lead to right heart failure?

A
  • INC in intimal thickness, fibroblasts, collagen, very small lumen -> obviously going to INC the pressure, so RV has to work harder, leading to RHF (i.e., lower extremity edema symptoms)
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43
Q

What do you see here? When might you see this?

A
  • Plexiform lesion: proliferation may be monoclonal
    1. PPH
    2. Familial PPH
    3. HIV-associated P HTN
    4. L-R shunts
    5. Toxins (Fen-phen, Aminorex, etc.)
    6. HHT (hereditary hemorrhagic telangiectasia) w/PHT
    7. CTEPH
    8. Mitral stenosis
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44
Q

Describe the pathogenesis of PAH. What vascular factors are involved?

A
  • Genetics + environmental trigger + imbalance of vascular effectors
  • Vascular factors:
    1. Prostacyclin and TXA2 (platelet factor)
    2. ET-1: most potent vasoconstrictor
    3. NO: locally produced, very short half-life (DEC in NO synthase)
    4. Serotonin: platelet aggregator, pulm vasoconstrictor
    5. VEGF: overexpressed in plexiform lesions
    6. Anorexiants: appetite suppressants (i.e., phen-phen associated with PAH in small minority of pts; mitral valve thickness and disease)
    7. CNS stimulants, including cocaine -> heart failure or brain hemorrhage first
    8. Adrenomedullin: vasodilator peptide
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45
Q

What conditions are associated with PAH?

A
  • Auto-immune: scleroderma, SLE, MCTD, RA (Raynaud’s)
  • HIV: 0.5%; HHV-8 (not sure why) -> always do good hx and HIV test
  • Portal HTN (~5%): relieve portal HTN, and 2/3rd’s of these pts get improvement in their PAH
  • Thrombocytosis: excess serotonin and TXA2 -> platelet plugs and vasoconstriction
  • Hemoglobinopathies (about 10% of sickle cell): may have to do with free heme (NO scavenger), which eats up NO
  • Hereditary hemorrhagic telangiectasia (HHT; 15%)

- KNOW: systemic sclerosis, HIV, and sickle cell

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46
Q

What is familial PPH?

A
  • Familial predisposition: observed in 6 - 10 %
  • Autosomal dominant with incomplete penetrance
  • A responsible gene (PPH1) - chromosome 2 at locus 2q33
  • Results in defective function of the bone morphogenetic protein receptor type II (BMPR2)
  • Asymptomatic carriers of PPH1 have abnormal pulmonary vascular responses to exercise
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47
Q

Nitric oxide in PAH

A
  • Made by vascular endothelium
  • Catalyzed by nitric oxide synthase
  • Promotes vasodilation and inhibits smooth-muscle growth
  • Endothelium from PPH patients showed negligible immunohistochemical staining for nitric oxide synthase
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48
Q

History of which class of meds is important to obtain in patient with PAH?

A
  • Fen-phen: especially in patients whose BMI is a little higher (they are not going to volunteer this information)
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49
Q

Endothelin-1 in PAH

A
  • Potent vasoconstrictor & mitogen for smooth-muscle cells
  • Produced by vascular endothelium
  • Localizes to muscular pulmonary arteries of patients with PAH
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50
Q

VEGF and PAH

A
  • Specific endothelial growth stimulant
  • Induced by various cytokines including PDGF &TGFβ
  • Expressed by endothelial cells in plexiform lesions
  • Role in pathogenesis is still speculative
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51
Q

Serotonin in PAH

A
  • Stored mainly in platelets
  • Associated with pulm vasoconstriction and proliferation of smooth muscle cells
  • Plasma serotonin concentrations are higher than normal in PPH
  • SSRI’s: small INC in PAH, but still not evidence-based
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52
Q

Voltage-gated K channels and PAH

A
  • Control the cell-membrane potential and the release of calcium via sarcolemmal voltage-gated channels
  • In PPH pulmonary artery smooth muscle cells have low mRNA for the potassium channels and low channel current, with a resultant increase in intracellular calcium
  • Blocked by the appetite suppressants -> thought this would help with therapeutic modalities, but not yet
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53
Q

What is the clinical presentation of PPH?

A
  • Mean age at dx: 36 (typically F in 20’s or 30’s); but can present at any age (Muthiah had a 72 y/o pt)
  • Diagnosis often delayed bc pts present with non-specific symptoms:
    1. Fatigue
    2. Exertional dyspnea (tx as asthma for a year sometimes)
    3. Exertional chest pain
    4. Exertional Syncope
    5. Edema
  • Treated as something else before dx of PAH entertained
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54
Q

How do you diagnose PPH?

A
  • Detailed H and P; high index of suspicion (rare, but bad)
  • Things to look for:
    1. Dyspnea of variable severity
    2. Apical impulse shifted outwards: same ICS, but in the axillary line (down and out LV, out RV)
    3. Parasternal heave: 2-3 fingers in L parasternal region (going to lift your fingers)
    4. Palpable P2: can hear accentuated P2 (loud)
    5. Accentuated P2; lungs may be clear
    6. Widely split S2
    7. SEM L 2nd ICS
    8. PFTs w/mildly DEC DLCO w/o evidence of airway obstruction or decreased lung volumes
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55
Q

Briefly describe PAH disease progression.

A
  • Nothing seems to stop disease course -> PROGRESSIVE
  • PVR: pulmonary vascular resistance
  • If sedentary lifestyle, may not have symptoms for awhile
  • Once RV starts to decompensate, PAP may come down -> PVR is what you are going to be looking for
  • CO stays okay in pre-compensation stage, but with symptoms and uncontrolled pulmonary pressure, CO starts to fall consistently
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56
Q

What is the screen for PAH? Confirmatory test?

A
  • Echo (TTE: transthoracic echo)
  • About 95% confidence -> if it looks like it, then do R heart catheterization to confirm
  • Pulmonary angiography: required when you are thinking about chronic thromboembolic PH
  • CT scan: when you think it is associated with interstitial lung disease (or if looking for a PE -> helical CT)
  • THIS WILL PROBABLY BE IN THE BOARDS
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57
Q

TTE: normal LV size and function, dilated RV, and RVSP of 70 mm Hg. V/Q scan normal. What do you do next?

A
  • R. heart catheterization: to confirm the diagnosis (do this bc also can be caused by left heart failure, so you have to check PCW pressure to make sure it is <15)
  • RV systolic pressure should be <15-20
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58
Q

In a right heart catheterization report, the thing that distinguishes PAH from PVH is?

A
  • PCWP: when left heart fails, left atrial pressure increase, but difficult and more invasive to do left heart cath, so you check pulmonary cap wedge pressure (PCWP) as an indirect measurement of L atrial pressure (Schwan Ganz catheter)
  • If <15, then patient does not have LHF (PAH, not PVH)
  • PVH = pulmonary venous HTN
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59
Q

What does vasoreactivity suggest in PAH? What can you use to test this?

A
  • Vasoreactive pts have a relatively (or much) better prognosis (only about 5-6% of pts) compared to pts w/o vasoreactivity
    1. Vasoreactivity: pulmonary vasculature constricted -> if I give vasodilators, will it give in to these
  • Inhaled NO is probs the best agent to test vasoreactivity
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60
Q

During RHC, what agent is used to test vasoreactivity?

A
  • Nitric oxide (NO)
  • Sometimes use adenosine: very important vasodilator, but short-acting, and can have unstable shelf-life
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61
Q

What will see you on a PPH echo?

A
  • Echo is usually the first diagnostic test -> good screen
  • Will show evidence of:
    1. Right heart chamber enlargement
    2. Paradoxical motion of the IVS
    3. Tricuspid insufficiency – 4V2+ RA Pressure
  • Look for tricuspid insufficiency: there will be tricuspid regurgitant jet (measured using echo -> formula above; don’t need to remember the equation, but know that this jet is used to measure pulmonary artery pressure)
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62
Q

How do you dx PPH?

A
  • CBC, CMP, TFTs (to test for hyperthyroidism), HIV
  • CXR
  • Connective tissue serology (ANA,Scl- 70, Anti-RNP)
  • PFTs, exercise oxymetry: only 2 conditions that can cause exercise desaturation in early stages -> PAH and pulmonary fibrosis
  • Echocardiography
  • V/Q scanning or CT angiography
  • Sleep studies
  • Complete cardiac catheterization
  • Go through most of these
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63
Q

What are the typical PFT findings in PAH?

A

Normal FVC, FEV-1, and TLC with reduced DLCO

  • Pulmonary vascular disease pattern (lung is normal; really a vascular disease, like PE)
    1. Isolated reduction in DLCO, unless some other comorbidity
  • Causes of reduction in DLCO: PAH, anemia, early/late stage emphysema (significantly DEC), chronic bronchitis (mildly decreased)
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64
Q

What agent should you give to a patient with PAH who is short of breath at rest (WHO class IV)?

A
  • Isoprostenol: IV; pretty unstable in ambient temperature (has to be refrigerated)
    1. Short half-life, so need an IV pump (venous access via indwelling catheter)
    2. Acute interruptions can lead to rebound increase in PAH -> if pump malfunctions, pt can drop dead
  • Class II or III, can start with Bosentan: endothelin-1 receptor antagonist available as a pill
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65
Q

What do you see here?

A

Normal CXR

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66
Q

What do you see here?

A

PPH CXR: proximal enlargement of the vasculature

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67
Q

What will you see on a PPH EKG?

A
  • Tall p wave: p-pulmonale -> R. atrial enlargement (if M-shaped or bifid, it looks like mitral or left atrial enlargement)
  • Evidence of R ventricular hypertrophy: dom R wave in V1 (and aVR), dom S wave in V5-6
  • R ventricular strain pattern: ST depression and T wave inversion in the right precordial (V1-4) and inferior (II, III, aVF) leads
  • S1Q3T3: bottom left -> acute = PE, chronic = PAH
  • Reference: http://lifeinthefastlane.com/ecg-library/basics/right-ventricular-hypertrophy/
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68
Q

What do these PFT’s show you?

A
  • Typical PFT from pt with PAH
  • FVC and FEV-1 normal, but DLCO reduced
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69
Q

What is inhaled vasoreactivity in PAH? What is used to test it?

A
  • ~5 percent of PAH pts are responders, defined as:
    1. >20% reduction in PAP & PVR
    2. INC or unchanged CO
    3. Minimally reduced or unchanged systemic blood pressure & SVR
    4. >10mmHg drop in MPAP (should drop to <40mmHg)
  • Inhaled NO: selective for the pulm vascular bed
    1. Binding w/Hgb in pulm caps makes it physiologically inactive
    2. Fall in PAP in response to inhaled NO is a good indicator the pt will respond to CCB’s
    3. Often better tolerated dx agent than IV vasodilators
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70
Q

What is the algorithm for the workup of PPH?

A
  • Start with echo, then depending on how pt looks, you can go through the rest of the work-up as needed
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71
Q

What are some of the vasodilatory treatments for PAH?

A
  • CCB’s: huge doses; most patients not compliant (for WHO III or IV, wait for RV failure, and start Ipoprostenol infusions)
  • Bosentan/Ambrisentan/Macitentan: can be given orally
  • Sildenafil: Viagra (PDE-5 INH that INC NO locally in pulmonary vasculature)
  • Treprostinil: prostacyclin analog (like Ipo; better shelf life and doesn’t have to refrigerated; oral form now too)
    1. Iloprost: inhaled, short half-life (9x per day)
    2. Epoprostenol
  • Riociguat: INC cGMP by stimulating Guanylate Cyclase
  • Adjuvant therapy
  • Advantage of different MOA’s is that you can use them in combination
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72
Q

How would you treat PAH based on severity of disease (flow chart)?

A
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73
Q

Epoprostenol

A
  • MOA: potent vasodilator that acts via receptors linked to adenylate cyclase -> vasodilation 2o to INC IC cAMP
    1. INH platelet aggregation and smooth m proliferation
  • Delivered by portable infusion pump: both responders and non-responders show improvements in exercise tolerance, hemodynamics, and survival
    1. Begin at doses of 1-2 ng/kg/min, and INC by 1 to 2 ng/kg/min every 1-2 days as tolerated
    2. Most pts require dose INC of 1-2 ng/kg/min every 2-4 weeks in order to sustain clinical improvement
  • Side effects: jaw pain, diarrhea, arthralgias, infection, thrombosis, pump malfunction, interruption of the infusion
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74
Q

Bosentan

A
  • Phase III trial: improved 6-min walk distance (Sildenafil showed similar walking improvements), INC CO, DEC mean PAP, and DEC PVR
  • AE’s: elev of serum aminotransferase levels, teratogenic, interaction with Cyclosporine
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75
Q

Why anticoagulants in PAH? What is the current anticoag of choice?

A
  • Several studies suggest they may improve survival
  • Pts with PPH at INC risk for intrapulmonary thrombosis and VTE, due to:
    1. Sluggish pulmonary blood flow (clots can form behind plexiform lesions)
    2. Dilated right heart chambers
    3. Venous stasis
    4. Sedentary lifestyle
  • Anticoagulant of choice is Warfarin (goal INR of 2)
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76
Q

What is the prognosis for PAH? What are some of the predictors?

A
  • Variable -> depends on the:
    1. Severity of hemodynamic derangement
    2. Response to vasodilator therapy
  • Echocardiographic findings associated w/poor outcome:
    1. Larger R atrial size
    2. Degree of septal shift in diastole (hypertrophied R. heart starts to shift septum to left side)
    3. Presence of a pericardial effusion
  • Patients with PAH are at risk for both progressive right heart failure and sudden cardiac death
  • CPR after CV collapse (code) in generally unsuccessful
  • Mean survival of ~ 3 yrs from diagnosis, but pts with severe PAH or Rt HF tend to die within one year (once RV failure sets in, hard to get these pts to turn back around)
  • Functional classes I and II tend to live far longer than those who fall into classes III and IV
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77
Q

What are some adjuvant therapies for PAH?

A
  • Hypoxemia at rest or during activity, due to a reduced CO, ventilation-perfusion inhomogeneity, or R-to-L shunting through a patent foramen ovale
    1. Try to break hypoxia-induced vasoconstriction
    2. Supplemental oxygen should be provided in this setting
  • Diuretics can be given for control of edema-> can get these pts from class IV to class II sometimes (but preload dependent, so take it slow)
    1. Avoid excessive preload reduction
  • Digoxin may be of some benefit with right ventricular dysfunction - controversial
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78
Q

What things are used in the current tx of PAH?

A
  • Coumadin, O2 (because they will desaturate when they walk), Digoxin, Aldactactone, Diuretic
  • CCB (seldom used), Bosentan/Ambri/Macitentan, Epoprostenol (IV), Iloprost (inhaled), Treprostinil (IV), Sildenafil, Riociguat
    1. Expensive
  • Transplantation – probably will cure PAH, but doesn’t make pts live much longer -> does improve quality of life (8-10% peri-operative mortality)
    1. Some may live up to 10 more years though
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79
Q

PAH summary

A
  • Insidious onset, progressive disease -> high index of suspicion necessary
  • Poor prognosis: ≤3year survival if untreated
    1. Epoprostenol, Bosentan proven to improve survival
    2. Anticoagulation also may add to survival
  • Oral ET antagonists may be an attractive choice
  • Inhaled Iloprost: also an attractive alternative
  • Macitentan/Riociguat – recently approved
  • Future (Already here!): combination therapy
  • Lung Transplantation in the appropriate setting
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80
Q

How can you tell if a PA view CXR is rotated?

A
  • Distance b/t spinous processes and the clavicles equal on both sides = not rotated
  • NOTE: if rotated, it can look like there are hilar infiltrates even though there are not
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81
Q

When might you use the AP view for a CXR? What is a disadvantage of this view?

A
  • This will be the view for patients that cannot stand up
  • One disadvantage is that the heart will look larger than it actually is (see attached image -> AP view on the right)
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82
Q

What does this line show?

A

Line is the minor fissure - normal CXR

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83
Q

What does this CXR show you?

A
  • Major fissure the diagonal, and the horizontal is the minor fissure -> helps you identify which lobe is infiltrated
  • Only a major fissure in the left lung
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84
Q

Where is the RUL on a PA and lateral CXR?

A
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85
Q

Where is the RML on a PA and lateral CXR?

A
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86
Q

Where is the RLL on a PA and lateral CXR?

A
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87
Q

Where is the LUL on a PA and lateral CXR?

A
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88
Q

Where is the LLL on a PA and lateral CXR?

A
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89
Q

What things might you see on a CXR to show air-space disease?

A
  • White-outs: pathognomonic for air-space disease
  • Air bronchograms (attached image): pathognomonic for air-space disease -> classic in pneumonia
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90
Q

What do you see here?

A

Air bronchograms (air-space disease)

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91
Q

What do you see?

A
  • White-out: air-space disease
  • Looks like left side pleural effusion as well (possible) - line on the left
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92
Q

What is this?

A
  • Pneumococcal pneumonia
  • Mostly neutrophils
  • Lower respiratory specimen bc minimal epithelial cells (light-colored ones)
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93
Q

What do you see?

A
  • Cardiomegaly with perihilar infiltrates (aka, central or bilateral alveolar)
  • Leads: AP view
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94
Q

What could cause this change (from left to right)?

A
  • Lasix for CHF patient
  • Note: transudative edema will clear much faster than exudative
95
Q

What is this?

A
  • “Bat wing” infiltrate -> pulmonary edema
96
Q

What are the radiologic signs of CHF?

A
  • Cephalization: rarely seen bc these pts present later
  • Cardiomegaly
  • Perihilar infiltrates
  • Peribronchial cuffing: looks like bronchus is surrounded by edema from side view
  • R. pleural effusion (more common on R side when unilateral, but most commonly bilateral)
  • Enlarged azygos vein
  • Kerley B lines (lymph lines -> transporting fluid when pts have chronic, not acute, pulmonary edema)
97
Q

What do you see?

A
  • Cardiomegaly -> sign of CHF
98
Q

What do you see?

A
  • Fluid in the fissures
  • Can be initial manifestation of CHF, but by no way the most common
99
Q

What is this?

A
  • Pulmonary hemorrhage, and in this case, renal (b/c Goodpasture’s)
100
Q

What are some examples of air-space disease?

A
  • Pulmonary edema: fluid
  • Pneumonia: exudate, or WBC’s
    1. Usually going to be pulm edema or pneumo -> think about white count, fever, etc. to distinguish bt the two
  • Pulmonary hemorrhage: blood
  • Tumor/bronchoalveolar cell carcinoma: looks like pneumo, but older pt w/o fever who won’t respond to tx
  • Idiopathic
101
Q

What do you see?

A
  • Reticulonodular pattern
  • Reticular: criss-crossed lines + nodular: dots = interstitial disease: sarcoidosis
102
Q

What do you see?

A
  • Reticulonodular pattern
  • Reticular: criss-crossed lines + nodular: dots = interstitial disease: sarcoidosis
103
Q

What is this?

A
  • Classic presentation of sarcoidosis: bilateral hilar adenopathy (enlarged lymph nodes)
    1. Should be at the bottom of your dx list, however, bc it is one of exclusion (think: lymphoma, histo, TB, etc.)
  • Paratracheal or bilateral hilar adenopathy with or w/o reticular infiltrates
104
Q

What do you see on the left?

A
  • Classic presentation of sarcoidosis: bilateral hilar adenopathy (enlarged lymph nodes)
    1. This should be at the bottom of your dx list, however, because it is a dx of exclusion (think: lymphoma, histo, TB, fen-phen use, etc.)
  • Paratracheal or bilateral hilar adenopathy with or w/o reticular infiltrates
105
Q

What things can cause bilateral hilar and mediastinal lymphadenopathy?

A
  • Lymphoma
  • Histo
  • Fen-phen use
  • TB
  • Castleman’s
  • HIV: pts with bilateral hilar adenopathy -> think TB
  • Sarcoidosis: at the bottom of the list because it is a diagnosis of exclusion
106
Q

What is this?

A
  • Well-formed, non-caseating granuloma -> sarcoid
107
Q

What is a honeycomb pattern? Examples?

A
  • Usually means advanced stage of interstitial disease
  • Air with cystic spaces separated by coarse reticular network
  • Grossly distorted parenchyma
  • Examples: IPF, RA lung
108
Q

What might be going on here?

A
  • IPF
  • Upper lobes less involved than lower lobes in this example
109
Q

What things might you see on a CXR for a pt w/COPD?

A
  • Similar chest radiographs for COPD/chronic bronchitis
    1. most pts have both
  • Hyper-inflated lungs
  • INC compliance and airway resistance
  • Flattened hemi-diaphragms
  • Narrow, vertical heart (in the absence of CHF)
  • Increased “lung markings”
  • Bullous disease
110
Q

What do you see here?

A
  • Flattened hemi-diaphragms
  • Characteristic of COPD
111
Q

What do you see?

A

Bullous emphysema

112
Q

MEMORIZE THIS. It will be on USMLE.

A

Good job!

113
Q

For emphasis: MEMORIZE THIS. It will be on USMLE.

A

Good job!

114
Q

What do you see?

A
  • Bronchiectasis: persistent dilatation of terminal bronchi with destruction of the elastic and muscle tissue of the bronchial wall
  • Plain CXR: bronchial wall thickening, parallel lines (tram lines), sometimes cysts
115
Q

What is this?

A

Cystic bronchiectasis

116
Q

What evidence will there be of a PE on a CXR?

A
  • Most common is a NORMAL CXR
    1. Atelectasis may be present (and pleural effusions, when present, are small)
    2. Portion of lung not getting blood flow will tend to divert air, probably via bronchospasm
  • In exam, if pt has acute onset SOB and no ronchi and normal breath sounds on both sides, then they have PE
117
Q

What do you see here?

A
  • PE in left lower lobe, so elevated hemi-diaphragm due to atelectasis
118
Q

What is this?

A
  • Hampton’s hump: infarcted part of the lung
  • Pretty rare -> probably won’t be tested on this
119
Q

What do you see?

A
  • Westermark’s sign
  • Don’t see vasculature at all -> R. pulmonary trunk embolus
  • We would also suspect pneumothorax (collapsed lung) in this case
    1. Know it’s not this because listen to the pt and hear good, bilateral lung sounds -> listening to lungs or ultrasound could help
  • Why doesn’t the lung infarct? Dual blood supply
120
Q

What are the features of benignity in a small pulmonary nodule (SPN)?

A
  • Signs of benignity:
    1. Well-defined (circumscribed) nodules
    2. No assoc lymph node or mediastinal masses
    3. No satellite lesions
    4. Calcified nodules
  • SPN’s: 3 cm’s in size or less, and 30-40% are malignant
    1. Smaller = nodules and larger = masses
  • MUST KNOW THESE
121
Q

What are the 3 types of benign calcifications?

A
  • Dense
  • Popcorn
  • Lamellar: onion-skinning
  • Some central can also be benign (less strong sign; top right example in attached image)
  • Note: spiculated or changing would be signs of malignancy
122
Q

What do you see here?

A

Popcorn calcification

123
Q

What are the features of malignancy for an SPN?

A
  • Spiculated nodules: larger on one side?
  • Non-calcified nodules
  • Associated mediastinal or lymph node masses
  • Presence of cavitation: blood supply not enough to keep up with fast growth, so necrosis -> usually squamous cell carcinoma
  • Large nodules: in general, 3-4 cm, suspect malignancy
124
Q

How do you diagnose an SPN?

A
  • Biopsy: surgical excision, transbronchial sampling during fiberoptic bronchoscopy, trans-thoracic needle aspiration
  • Sputum cytology (low yield): do this in patients with hemoptysis, esp. those that are poor bronchoscopy candidates
    1. Can help to avoid a procedure
125
Q

What might this be?

A
  • If there is fat in the nodule, it is a HAMARTOMA
  • Omstel units: water = 0 (things that float on water have negative value)
126
Q

What do you see?

A

TB

127
Q

What is this?

A

Well-circumscibed nodule (probably benign)

128
Q

What forms the right heart border on a CXR?

A

Right atrium (NOT the right ventricle)

129
Q

What do you see?

A
  • Silhouette sign
  • Can’t see the right heart border -> infiltration of the lung, changing contrast between heart and lung
    1. Right middle lobe infiltrative process
  • If there were no left heart border, this would suggest an invasive process in the lingula
  • If you are not able to see the hemi-diaphragm, the infiltrate is in the lower lobe
  • THIS WILL BE ON THE EXAM
130
Q

What do you see?

A
  • Carina is splayed -> cardiomegaly
  • Left atrial enlargement: described as an orange w/in the heart
131
Q

What do you see on the left? Right?

A
  • Left: pleural effusion (white out)
    1. Meniscus sign: crescent-shaped inclusion of air surrounded by consolidated lung tissue
    2. The larger the effusion, the more likely the mediastinum is going to be pushed to opposite side

A. If it shifts to the same side, you are going to assume there is some kind of atelectasis as well (like in this case)

B. Left lung looks hyperinflated here

  • Right: hydropneumothorax -> air and fluid (could be blood as well, or pyo, but not as common) in the pleural space (air:fluid straight line)
132
Q

What do you see?

A
  • Pneumothorax: 80-90% collapse of the left lung, but compared to Westermark’s sign, we are able to see the lung that has collapsed
  • Pleural pressure has increased, so there is no more negative pressure holding the lung open
133
Q

What do you see?

A

Large pneumothorax (pt w/bad emphysema)

134
Q

What do you see?

A

Lateral view of pneumothorax (more air in front, and maybe up in the apex as well)

135
Q

What do you see?

A

Ideally-placed chest tube -> negative suction to take the air out, allowing the lung to completely expand (post-pneumothorax, for example)

136
Q

What is the difference between respiratory and ventilatory failure?

A
  • Respiratory: hypoxic (respiratory failure will actually include ventilator failure)
  • Ventilatory: hypercapnic (decrease in alveolar respiration)
  • Clearly, these are often going to coexist, but we talk about them as separate issues
    1. Can be acute (hours to days) or chronic, or even acute on chronic (i.e., COPD exacerbation)
137
Q

How does increased PaCO2 stimulate breathing (flow chart)?

A
138
Q

What are some of the mechs of resp failure?

A
  • Hypoxemic failure
  • Ventilation/Perfusion (V/Q) mismatch: in airway obstruction (COPD), gas exchange not happening effectively even though it may look like pt is moving air
  • Shunt
  • Exacerbated by low mixed venous O2 (SvO2)
  • Hypercapnic failure
  • Decreased minute ventilation (MV) relative to demand, e.g., narcotics (hypoventilation)
  • Increased dead space ventilation
139
Q

What are the 5 causes of hypoxemia?

A
  • Normal A-a gradient:
    1. Hypoventilation
    2. Decreased PiO2
  • Increased A-a gradient:
    1. V/Q mismatch
    2. R-to-L shunt
    3. Diffusion limitation
140
Q

What are some causes of hypercapnic respiratory failure?

A
  • Central hypoventilation
  • Neuropathies
  • Muscle (pump) failure
    1. Muscular dystrophies
    2. Myopathies
    3. Myasthenia gravis
  • Airway Obstruction
141
Q

Why is this graph important?

A
  • Relatively large changes in O2 saturation do not dramatically change PO2 until you get to a PO2 of about 40 or O2 saturation of 70%
    1. For example, a minimal increase in O2 sat from pO2 of 60 to 100 due to hemoglobin loading
142
Q

What things cause the O2 curve to shift to the right?

A
  • TAP:
    1. Temperature
    2. Acidosis
    3. Phosphate – 2,3-DPG
    4. CO2
  • Decreases affinity for, and unloads oxygen
143
Q

What things cause the O2 curve to shift to the left?

A
  • Hypothermia (DEC temperature)
  • Alkalosis (INC pH)
  • Fetal hemoglobin
  • CO
  • These all cause increased affinity for O2
144
Q

How will a pt w/resp failure present? How do you evaluate them?

A
  • Pt will present with dyspnea and/or hypoxia
    1. Acute: think PE, acute MI (silent -> happen more often in F, and pts with uncontrolled diabetes)
  • Things to do:
    1. History and physical: JVD, S3, pulm crackles
    2. Vital signs, incl pulse oximetry
    3. CXR
    4. EKG: pts w/heart transplants may have MI and not know it bc denervated -> always do EKG on these patients when they come in short of breath

A. Also in pts w/suspected heart failure

  1. ABG
  2. CBC
  3. Electrolytes: e.g., bicarbonate -> if it is >30, you can begin to suspect these pts are retaining CO2

A. Pts retaining CO2 more likely to get into trouble

  1. Sputum and blood cultures: look for neutros
  2. UA: sepsis can cause resp failure (look for leukocyte esterase, nitrites to see if UTI -> esp. important in F, older M w/BPH, pts with catheters)
  3. Helical CT vs. V/Q scan: to avoid contrast (due to allergy or kidney damage), use V/Q scan

A. Helical CT: now test of choice if looking for PE bc global view (if you can’t find a PE, you can probably find out what is wrong)

B. PE: demonstrate V/Q mismatch

  1. Pulmonary function tests (PFT’s): don’t do these on pts in acute situations, but rather for chronic conditions like COPD or asthma
  2. 6-minute walk test: see how far patients can walk in 6 seconds
145
Q

How do you tx a pt with hypoxic resp failure?

A

Supplemental O2

146
Q

What is the most common mech of hypoxemia?

A
  • V/Q mismatch: readily corrects w/O2 supplementation
  • Note: shunt would NOT correct with O2
147
Q

What is the 6-minute walk test for?

A
  • To see how far patients can walk in 6 seconds
    1. Tests for interstitial disease and pulmonary arterial HTN (goal-directed therapy) -> these are the only 2 conditions w/desaturation on exercise in their early stages
    2. If this continues to drop, these patients have the worst prognosis
148
Q

How do you bust a PE clot?

A
  • Send them to the cath lab to break up the clot
  • Heparin helps prevent clots, but does not bust them up (if high suspicion, and no contraindications, start on anticoagulant while waiting for helical CT)
  • TPA will activate fibrinolytic process to help bust up clot -> bleeding is a big problem, so don’t want to use TPA on all patients; may be contraindicated
    1. Only use this in pts with acute PE and shock
149
Q

How do you treat bronchospasm?

A
  • Bronchodilators: Epinephrine, Theophylline, Albuterol
  • Beta 2 agonists:
    1. SABA: Albuterol
    2. LABA’s: Formoterol or Salmeterol -> don’t use these for rescue, even though Formoterol is fast-acting
  • Anticholinergic agents: Ipratropium
150
Q

How long does it take bronchodilators to work?

A
  • Albuterol and Ipatropium: 5 to 15 min.
  • Formoterol: fairly rapid onset of action, but still not used as a rescue inhaler
151
Q

What conditions result in bronchospasm?

A
  • Asthma, COPD exacerbations
  • Anaphylaxis
  • Acute bronchitis
  • Toxic inhalations
152
Q

How do you manage bronchospasm causing respiratory failure, i.e., asthma/COPD exacerbations?

A
  • Bronchodilators
  • Hydration: losing insensible water via breathing, so hydration is important for these patients (can lose a lot of water; sometimes up to 3 liters)
  • Systemic corticosteroids: reduce inflammation
  • Treat the precipitating cause
  • Infection/AB’s: err on side of caution by tx w/ AB’s if you are not sure if an infection is viral or bacterial
  • What if pt continues to get worse or get tired:
    1. BiPAP -> non-invasive positive pressure that doesn’t involve putting anything in pt. (mask you can put PEEP on -> pressure support for when pt takes a breath, DEC work of breathing, & keeping airways open when the pt is breathing out)

A. Decreases mortality by 30%

  1. If this doesn’t work, and pt. continues to retain CO2 and have bad O2 saturation, then intubate

A. Rarely intubate patients with COPD

  • How do you know if the patient is getting tired?
    1. Looks apprehensive
    2. Experienced nurse: “He is not looking good”
    3. Increased somnolence (sleepy, drowsy: CO2 is a narcotic)
    4. Decreasing RR or respiratory excursions
    5. Borderline O2 sats: may not be present while giving supplemental oxygen
    6. What is the ABG likely to reveal? INC CO2 -> need to IMPROVE VENTILATION
153
Q

How do we decrease work of breathing?

A
  • Assist breathing
  • Mechanical ventilation
  • Non-invasive (BiPAP) vs. endotracheal intubation
154
Q

Which of the following factors contribute LEAST to arterial oxygen content in humans?

A.Hemoglobin content of the blood
B.The amount of oxygen that is dissolved in plasma (PaO2)
C.The oxygen saturation of the hemoglobin in arterial blood (SPO2)
D.The amount of oxygen that is bound to hemoglobin (1.39 X Hb X % saturation of Hb)

A

B.The amount of oxygen that is dissolved in plasma (PaO2)

155
Q

A 47-year-old female undergoes an elective cholecystectomy. The surgery is completed without complications. The post op ward nurse notes an oxygen saturation of 92% on room air. The patient looks a little drowsy, hearing which the anesthetist orders a Blood gas, whose results are as follows: pH 7.26, PaCO2 60, PaO2 70. What is the reason for the mild hypoxia?

A

Alveolar hypoventilation

156
Q

Why does hypercapnia sometimes worsen with supplemental O2?

A
  • In chronic hypercapnia, PCO2 may rise in response to supplemental oxygen for 3 reasons:
    1. Worsening V/Q mismatch: supplemental O2 abolishes hypoxic-induced vasoconstriction of the pulmonary vasculature
    2. Release of hypoxic vasoconstriction in poorly ventilated areas of lung caused by INC in PaO2
    3. Consequence: increased blood flow to low V/Q areas and a worsening of V/Q inequality which exaggerates the degree of CO2 retention
157
Q

What is the Haldane Effect?

A
  • In hypoxic pts some CO2 is bound to hemoglobin as carboxyhemoglobin
  • Supplemental oxygen raises both PaO2 and SaO2
  • CO2 must be displaced from hemoglobin (carboxyhemoglobin becomes oxyhemoglobin)
  • CO2 can only dissolve in blood, raising PCO2
  • Succinctly: deoxygenation of blood INC its ability to carry CO2; conversely, oxygenated blood has a reduced capacity for carbon dioxide
158
Q

Pt in critical care with COPD gets ABG, which showed a pH of 7.18, and a PaCO2 of 90. The respiratory therapist on call tells you that oxygen should not be given to patients with COPD, since it makes patients retain CO2. What will be your response to the respiratory therapist, regarding hypercapnea in COPD patients?

A
  • The COPD V/Q inequality, along with the ‘Haldane effect’ are the most significant causes of hypercapnea; therefore continue 40% O2
  • Haldane effect: deoxygenation of blood INC its ability to carry CO2; conversely, oxygenated blood has a reduced capacity for carbon dioxide
159
Q

Which of the following statements are TRUE regarding Pulmonary Thromboembolism?

A.90% of the Emboli originate from the upper extremities
B.Bronchospasm and wheezing are seldom a part of the physical findings
C.The reason for hypoxia is usually alveolar hypoventilation
D.Anticoagulation therapy should not be initiated until the diagnosis is proven
E.The pathognomonic EKG finding of S1Q3T3 is seen only in a minority of patients

A

E. The pathognomonic EKG finding of S1Q3T3 is seen only in a minority of patients

  • About 10% from upper extremities, but INC due to obesity, lying in bed, IV’s from central venous catheters
  • Bronchospasm and wheezing can be seen because platelet products can provoke bronchoconstriction
  • Reason for hypoxemia is dead space ventilation
  • Anticoagulation therapy SHOULD BE initiated -> can save patient’s lives
  • S1Q3T3 is evidence of R ventricular strain
160
Q

What is unique about pulm blood supply?

A
  • Lung has dual blood supply
  • PA bringing in de-oxygenated blood, and veins take the oxygenated blood back to the left heart
161
Q

Is PE an emergency?

A
  • YES -> causes vital signs to go out of whack
  • We have rapid response teams for acute onset SOB
162
Q

What is the epi of PE?

A
  • Annual incidence more than 500,000
  • 11% die suddenly (autopsy -> saddle emboli)
  • 67% not diagnosed during life (autopsy)
  • Undiagnosed PE has a mortality of 30% to 55%
    1. Diagnosed PE has a mortality < 10% -> diagnosis saves lives
163
Q

What are the typical sources of PE?

A
  • > 90% from deep vein thrombosis (DVT) in the legs
    1. Pelvic veins in some (i.e., post-surgical)
    2. Upper extremity veins in others (central venous catheters)
  • Non-blood clot emboli:
    1. Air: from central venous lines (60-100 cc’s of air to kill the patient -> avoid this by placing patient in trendelenburg position)
    2. Tumor: renal cell carcinoma
    3. Amniotic fluid
    4. Talc
    5. Fat: bone break (typically in elderly)
164
Q

Acute onset SOB -> what should you always consider?

A

PE

165
Q

What are the predisposing factors for clot formation?

A
  • Virchow’s triad:
    1. Stasis
    2. Endothelial damage
    3. Hypercoagulable state (e.g., trauma or surgery)
166
Q

Which of the following are considered risk factors for venous thromboembolism?

A. Chemo

B. Factor V Leiden mutation

C. Marathon running

D. Progesterone admin

E. Visiting high-altitude area

A

B. Factor V Leiden

  • Factor V Leiden: resistance to activated protein C (a natural anti-coagulant)
    1. Homozygotes are most affected
    2. Prothrombin gene mutation also a risk factor
    3. Anti-cardiolipin Ab’s
    4. Protein C or S deficiency
    5. Antithrombin III deficiency
  • Chemo not a risk factor, but cancer causes hypercoagulable state, especially adenocarcinomas
  • Exertion not associated with VTE
  • Estrogen is associated, but progesterone is not
  • High altitude can cause pulmonary HTN, but not VTE
167
Q

What are some things that cause stasis?

A
  • Immobility
  • Bed rest
  • Anesthesia
  • Congestive heart failure/cor pulmonale
  • Prior venous thromboembolism
  • Central venous catheters
168
Q

What are some of the causes of hypercoagulability (heritable and acquired)?

A
  • Heritable:
    1. Factor V Leiden mutation
    2. Prothrombin G20210A mutation
    3. Protein C & Protein S deficiency
    4. Antithrombin III deficiency
    5. Dysfibrinogenemia
    6. Homocystinemia
    7. INC levels of factor VIII (newer info)
  • Acquired:
    1. Estrogen use: also INC during pregnancy (so hormonal changes while prego a factor)
    2. Malignancy
    3. Thrombocytosis: INC availability of platelets
    4. Disseminated intravascular coagulation (DIC)
    5. Heparin induced thrombocytopenia (HIT): if PLT count drops after starting heparin therapy (or clot forms), suspect HIT -> problem is if pt now has a clot or is going to, and need an anti-coagulant (will have to be something other than heparin)

A. Anti-platelet 4 antibodies (high sensitivity and low specificity)

  1. Antiphospholipid antibody syndrome: can be a stand-alone syndrome (aka, anti-cardiolipin)
  2. Nephrotic syndrome: loss of proteins (anti-coags lost in the urine, so pt more prone to VTE)
  3. Paroxysmal nocturnal hemoglobinuria (PNH)
169
Q

What are some causes of endo injury?

A
  • Homocystinemia
  • Autoimmune injury
  • Trauma
  • Surgery
  • Malignancy, and treatment for malignancy
170
Q

How does the # of risk factors you have affect your risk of DVT?

A
171
Q

What are some of the determinants of the physiologic consequences of PE?

A
  • Size of the embolus -> larger embolus = more problems
  • Cardiopulmonary status/reserve: has a lot to do with how the patient presents
  • Neurohormonal substances
172
Q

What are the physiological consequences of PE?

A
  • Increased pulmonary vascular resistance:
    1. Vascular obstruction
    2. Neurohumoral agents: serotonin, endothelin -> vasoconstriction, & further INC vascular resistance
  • Impaired gas exchange:
    1. Increased alveolar dead space ventilation from vascular obstruction (V/Q mismatch)
    2. Impaired carbon monoxide transfer (low DLCO) due to loss of gas exchange surface
    3. Right-to-left shunting (in massive PE)
  • Alveolar hyperventilation due to reflex stimulation of irritant receptors (J receptors)
  • Increased airway resistance due to broncho-constriction (resulting in wheezing)
  • Decreased pulmonary compliance due to lung edema, lung hemorrhage, or loss of surfactant
  • All of this can make your patient present with SOB after a pulmonary embolism
173
Q

How does the circulation try to compensate for PE?

A
  • Vasodilatation of uninvolved vasculature
    1. Pressure may not change at all, esp. if pt has healthy lungs
  • Helps DEC the INC in pulm vascular resistance (PVR)
    1. 1. If you block R pulm artery, pulm vascular resistance barely goes up bc, in general, about 25-30% of pulm capillaries aren’t participating (until you are exerting yourself, for example)
  • Also improves V/Q relationship in uninvolved areas
  • This improves overall oxygenation
    1. May not be very hypoxic -> pt may be tachypnic and tachycardic (hyperventilating)
174
Q

In which conditions will the trachea deviate toward the problem? Contralateral?

A
  • Trachea is index of upper mediastinal position:
    1. Pleural pressures on either side determine the position of mediastinum -> will shift to side with relatively higher (-) pressure relative to the other
  • Deviated towards diseased side:
    1. Atelectasis
    2. Agenesis of lung
    3. Pneumonectomy
    4. Pleural fibrosis
  • Deviated away from diseased side:
    1. Pneumothorax
    2. Pleural effusion
    3. Large mass
175
Q

What are the respiratory consequences of PE?

A
  • Increase in minute ventilation (tachypnea)
  • V/Q inequality (hypoxemia -> wide A-a)
  • Shunting (in massive PE)
  • Gas exchange abnormalities:
    1. Hypocapnia: because J receptors activated and hyperventilating
    2. Hypoxemia
    3. Wide (PA-Pa)O2 –> A-a gradient
176
Q

What is ARDS? CXR?

A
  • Severe ALI involving DAD, INC microvascular permeability and non-cardiogenic pulmonary edema
  • Acute refractory hypoxemia
  • High mortality: 40-60%
  • Bilateral, diffuse alveolar infiltrates (classic x-ray image attached)
177
Q

What is the Berlin criteria for ARDS?

A
  • Acute onset of resp failure (<1 week)
  • Bilateral infiltrates on CXR
  • No evidence of volume overload (new addition to the criteria)
  • PaO2/FiO2 < 300
178
Q

What is the mech of injury in ARDS?

A
  • Activation of inflammatory mediators and cellular components -> damage to cap endo and alveolar epi
    1. Neutros (instead of macros) predominate in BAL of these patients due to inflammation
  • INC permeability of alveolar capillary membrane
  • Influx of protein-rich edema fluid and inflammatory cells into air spaces
  • Dysfunction of surfactant: alveolar collapse -> very little gas exchange, but blood still coming into lungs
    1. If this happens to the whole lung, top to bottom, the patient will die (usually only about 80-90%, so patients end up on mechanical ventilation)
179
Q

What are some of the causes of ARDS?

A
  • Direct lung injury:
    1. Pneumonia/aspiration of gastric contents or other causes of chemical pneumonitis (inhaled smoke from a fire)
    2. Pulmonary contusion, penetrating lung injury
    3. Fat emboli: e.g., long bone fracture -> more common w/elderly than young people bc young people have more marrow and less fat
    4. Near drowning
    5. Inhalation injury
  • Indirect lung injury
    1. Sepsis: inflammation spreads via cytokines, and 100% of blood goes through lungs, so they are affected by sepsis (more than kidneys, even)
    2. Severe trauma w/ shock hypoperfusion
    3. Drug OD
    4. Cardiopulmonary bypass
    5. Acute pancreatitis: inflammation that can spread to lung, kidneys
    6. Tansfusion of blood products
    7. TRALI: transfusion-related lung injury
180
Q

What does this CT scan show about ARDS?

A
  • Consolidation usually most prevalent in posterior, or dorsal part of the lung -> excess lung water in the back of the patient when they are lying down (gravity)
  • Lying prone can help reduce mortality (rather than supine) -> diverts blood from poorly aerated to better aerated areas
    1. Can help improve gas exchange
181
Q

What are the stages of ARDS?

A
  • Exudative: 1-4 days
  • Proliferative: 4-8 days
  • Fibrotic: >8 days
  • Recovery
182
Q

What are the predictors of increased risk of death in ARDS?

A
  • Chronic liver disease
  • Non-pulmonary organ dysfunction
  • Sepsis
  • Advanced age
183
Q

What is the lung injury score?

A
  • Based on CXR, PaO2/FiO2, PEEP, and respiratory compliance
  • Add all of the points and divide by 4
    1. Mild-moderate: 1 - 2.5
    2. Severe: 2.5 - 4
  • Probably will not be tested on this -> know the concept, but not necessarily how it is calculated
184
Q

A patient with pneumonia is undergoing mechanical ventilation following the onset of ARDS. He is currently on 100% oxygen, and PEEP of 5. His oxygen saturation is at 75% What should be done in order to improve the patient’s oxygenation?

A

Increase the PEEP (+ end expiratory pressure)

  • To redistribute (NOT reduce) the lung water, pushing it away from the alveoli, and back into the non-alveolar portion of the interstitium
    1. Not going to stop the flow of air
  • INC tidal volume doesn’t work; can be detrimental bc the more you stretch your cells, the more they are going to get inflamed
  • Want to avoid O2 toxicity (i.e., from free radicals)
  • If you vasodilate portions of the lungs that are better aerated, you can improve function -> you can do this by giving inhaled NO (not shown to improve mortality, but can improve oxygenation; cost $300 per hour)
185
Q

What is the possible mechanism of improvement in oxygenation with the application of PEEP in patients with ARDS?

A

Recruiting atelectatic alveoli and increasing FRC

  • Residual volume + expiratory reserve volume = FRC; better the FRC, the better the reserve when you hold your breath
  • Pregnant women/obese patients, saturation drops when you intubate due to low FRC
    1. Better to have high FRC
    2. Pregnant women also have increased risk of PE
186
Q

What do pulmonary venous pressures look like in ARDS patients?

A

They are normal

187
Q

Which of the following is central to the pathogenesis of ARDS?

A.Cardiogenic pulmonary edema
B.Central pulmonary artery occlusion
C.High grade airflow obstruction
D.High grade inflammation
E.Neoplastic process of the endothelium

A

D. High grade inflammation

188
Q

Which of the following are criteria for diagnosis of ARDS?

A.Insidious Onset
B.Right upper lobe infiltrate
C.JVD with CVP 22 Cms.
D.Absence of evidence of Volume overload
E.Highly compliant lungs

A

D. Absence of evidence of Volume overload

  • Adaptive repair: can happen in younger patients, but some older patients will have lasting fibrosis
189
Q

In a pivotal study, a significant reduction in mortality in patients with ARDS was achieved with which of the following?

A.Chemotherapy
B.Deployment of a lower tidal volume than usual (6 cc /Kg predicted body weight).
C.Expedited antibiotic administration, within 4 hours of ARDS onset.
D.Nitric oxide administration in patients with refractory hypoxemia.
E.Rapid fluid resuscitation, with specific goals. (Early Goal-Directed Therapy)

A

B. Deployment of lower TV than usual (6 cc /Kg predicted body weight)

  • This will ABSOLUTELY be on the boards
  • Peak pressure: highest pressure that you see during inhalation in the respiratory system (flow + resistance)
    1. Plateau pressure: pressure taken when you pause at full inspiration
    2. If both peak and plateau pressures are high, then the problem is with compliance
    4. Peak high, plateau normal, resistance problem
190
Q

The incidence of pneumothorax as a complication of ARDS is usually seen:

A.In the first 48 hours after ARDS Onset
B.After two weeks of ARDS Onset
C.After two months of ARDS Onset
D.Pneumothorax has become a usual presentation of ARDS
E.After vasopressor therapy is begun

A

B. After two weeks of ARDS onset

-

191
Q

ARDS is characterized by which of the following?

A.Acute decrease in airway resistance
B.Acute increase in airway resistance
C.Acute decrease in pulmonary compliance
D.Acute increase in pulmonary compliance
E.ARDS has nothing to do with airway resistance, or pulmonary compliance

A

C. Acute decrease in pulmonary compliance

  • Increased lung water or consolidation will cause this
192
Q

What do you see?

A
  • Subcutaneous emphysema
  • Interstitial emphysema following inflammation rupture (due to necrosis?)
193
Q

Death in a pt due to ARDS is usually a result of?

A.Cerebrovascular accident
B.Multi-organ failure
C.Pulmonary embolism
D.Pulmonary hemorrhage
E.Refractory hypoxemia

A

B. Multi-organ failure

  • Because you can’t control inflammation -> give corticosteroids to help control this
  • This will probably be on USMLE
  • Decreasing tidal volume helps limit further damage to the lungs
194
Q

What do you see?

A
  • Gravity-dependent consolidation in ARDS
  • You can improve aeration of the dependent portions by having the patient lie prone
195
Q

36 y/o FM with acute onset dyspnea, L sided pleuritic chest pain, and purulent sputum since last night. Diagnosis?

A.Acute Pulmonary Embolism
B.CHF
C.Lung Abscess
D.Myocardial Infarction
E.Pneumonia
F.Pulmonary Arterial Hypertension

A

E. Pneumonia -> most likely etiologic agent is strep pneumo

196
Q

AIDS patient with pneumonia -> what is most likely etiologic agent?

A.Aspergillus fumigatus
B.Aceinetobacter baummanii
C.Burkholderia cepacia
D.Corynebacterium jeikeium
E.Mycobacterium tuberculosis
F.Pneumocystis jiroveci
G.Streptococcus pneumo

A

G. Strep pneumo

197
Q

The severe hypoxemia seen in ARDS does not adequately respond to supplemental oxygen, signifying the main mechanism of hypoxemia to be?

A.Diffusion defect
B.Hypoventilation
C.Shunt
D.V/Q mismatch

A

C. Shunt

  • Hypoxemia is not going to completely shut off this blood flow, but rather just limit it (shunt + V/Q mismatch)
198
Q

Management summary for ARDS

A
  • Medical emergency -> support breathing: intubation, mechanical vent, BiPAP
  • Tx underlying cause and give corticosteroids (most likely) to reduce inflammation and limit further damage to the lungs
  • Infection surveillance
  • Prone ventilation to redistribute lung water, and take weight off of the lungs (decreases mortality)
    1. Diuresis as needed to decrease lung water and avoid volume overload
  • Preventive care in ICU for: DVT, GI, infection
199
Q

When does fibrosis start in ARDS?

A

As soon as the injury happens

200
Q

What is a predictor of poor outcomes in ARDS?

A

Sepsis

  • Sepsis-associated ARDS mortality has decreased only minimally (predictor of bad outcomes)
201
Q

What is asthma?

A
  • Chronic inflammatory disorder of airways characterized by episodic, reversible bronchospasm resulting from exaggerated bronchoconstrictor response to various stimuli
    1. Airway inflammation contributes to airway hyper-responsiveness, airflow limitation, resp symptoms, and disease chronicity -> AIRWAY REMODELING
    2. Earlier stages completely reversible (but less so with more attacks)
  • Eosinophils, mast cells, T-cells
  • There is a link between obesity and asthma
  • Can’t be cured, but can be controlled
202
Q

Asthma Epi

A
  • 2-7% of pop
    1. We all have bronchospasm, but this protective mech goes overboard in asthma pts
  • 30-50% of children outgrow asthma
  • 20-30% of adult-onset asthma will have remission: may have no stimulus
  • Incidence more in F, but childhood prev more in M
  • Black race associated with higher rate of death (more arsenic-arsenic instead of arsenic-glycine)
  • Significant morbidity and mortality: attached graph shows INC prevalence (although deaths have been going down in the US since 2000 due to beta-agonist + inhaled corticosteroid therapy)
203
Q

Asthma types

​

A
  • Extrinsic: atopic/allergic
  • Intrinsic: idiosyncratic/non-allergic
  • Drug-induced: ASA, NSAIDS
  • Occupational
  • Cough-variant
  • Exercise-induced bronchospasm (EIC)
  • ABPA: anti-fungals seem to have no effect -> fleeting infiltrates bc coughed up and go somewhere else
204
Q

Asthma classification

A
  • Dx: intermittent vs. persistent
  • Follow-up: controlled, partially controlled, uncontrolled
205
Q

Asthma classification and tx

A
  • Intermittent: as-needed Albuterol (rescue medicine)
  • Persistent disease: requires controllers
    1. Mild: inhaled corticosteroids
    2. Moderate: inhaled steroids, LABA’s
    3. Severe: inhaled steroids, LABA’s, LTA’s
  • Note: LABA’s associated with increased mortality, so use with caution (black box warning, but clinicians still use these; make sure you f/u w/pt every 6 months, and more closely if you note any changes)
206
Q

Extrinsic asthma

A
  • Most common type of asthma, common in children
  • IgE-mediated response to enviro allergens (dust mites, cockroaches, animal protein, dusts, pollens, fungi, food)
    1. Acute response (minutes after exposure)
    2. Late response (hours after exposure)
  • Elevated serum IgE: significant (>40% or 2000; usually low, e.g., 40-50)
  • Family history
  • Control by: reducing exposure to house mites, cockroaches, pets, and mold -> cleaning up the envo critical to control
207
Q

Intrinsic asthma

A
  • Triggered by respiratory infection
  • Adult-onset
  • Non-allergic mediated -> serum IgE not elevated
  • skin antigen test usually negative
  • Family history non-contributory
  • Intrinsic asthma tends to be more year round than extrinsic asthma
208
Q

Can you alleviate asthma symptoms by moving?

A
  • YES
  • Moving to a different location can help alleviate asthma symptoms
  • For example, moving away from the pollen in Memphis to Denver -> get these people away from the allergen, and make the air less dense, e.g., by breathing a helium/oxygen mix, which eases the patient’s breathing
209
Q

What is vocal cord dysfunction?

A
  • 15-20% of patients with asthma
  • Psychosomatic, but not a manufactured attack
210
Q

Drug-induced asthma

A
  • Aspirin, NSAIDS
  • Affects adults -> do really well when you put them on LT antagonists
  • Samter’s Syndrome:
    1. Asthma
    2. Aspirin sensitivity (flushing, angioedema, urticaria)
    3. Nasal polyps
211
Q

Occupational asthma

A
  • Most common occupational disease
  • Exposure to fumes, organic and chemical dusts, gases at workplace
  • Occurs after repeated exposure and sensitization
  • 2-10% of adult-onset asthma due to occupational asthma
  • Mechs include IgE and non-IgE mediated reactions
  • Typical scenario: every evening, the person has asthma, but they are better on the weekends or when on vacation
212
Q

Exercise-induced bronchospasm

A
  • Asthma symptoms occur usually immediately after exercise
  • Symptoms and lung function changes usually peaks 5-10 minutes after exercise
  • Cooling and mucosal drying of airways during exercise thought to trigger mast cells to release histamine
  • Pre-treatment with B-agonist or cromolyn is effective
  • Also slow warm up period helps
  • Most patients with asthma will have an exercise-induced component (i.e., worse symptoms with exercise)
213
Q

Cough-variant asthma

A
  • Not all that wheezes is asthma and not all asthma wheezes
  • Cough may be the only presenting symptom of asthma without variable airflow obstruction
  • History of chronic cough with irritants (i.e. cigarette smoke, fumes, exercise)
  • Diagnosis may be a positive clinical response to tx
  • Methacholine inhalation challenge test may aid defining the diagnosis
214
Q

Nocturnal asthma

A
  • Asthma symptoms that predominantly occur at night during sleep
  • Common between midnight to 8AM thought to be due to decline of circulating catecholamines and cortisol
    1. Cortisol peak around 6-8 AM, and trough around 12 AM
215
Q

ABPA

A
  • Asthma due to specific fungi, Aspergillus fumigatus
  • IgE-mediated reaction and type III IgE mediated response
  • Criteria necessary for diagnosis:
    1. Poorly controlled asthma
    2. Eosinophilia
    3. A. fumigatus positive skin antigen test, IgG Ab
    4. IgE > 1000ng/ml
    5. Proximal bronchiectasis (see attached image)
    6. Fleeting chest infiltrates
    7. Peripheral eosinophilia with chest infiltrates
    8. Mainstay of treatment is prednisone
216
Q

Pathology of asthma

A
  • Airway hyperresponsiveness- exaggerated bronchoconstrictive response by the airways to a variety of stimuli (aeroallergens, cold air, environmental irritants, viruses, ozone, sulfur dioxide); airflow obstruction
    1. Airway Inflammation
    2. Epithelial Injury
    3. Neural Mechanisms
    4. Intrinsic Airway Smooth Muscle Function
  • Increase in goblet cells, mucous production, and peribronchial fibrosis -> all at the expense of the lumen
217
Q

Treatments for the pathogenic elements of asthma

A
  • Eosinophils: steroids
  • Basophils
  • Mast cells: cromolyn
  • CD4/TH2 lymphos
  • Major basic protein
  • Eosinophilic cationic protein
  • Histamine: H1 blockers
  • LT’s: LTRA’s
  • IgE: Omalizumab
  • Vagal afferent: anti-cholinergic
  • IL-5: Mepolizumab
  • PAF
218
Q

Charcot-leyden crystals

A
219
Q

What do you see?

A
  • Epi injury in asthma: disruption of the epi with loss of ciliated cells to complete denudation of the epithelium
  • INC permeability to inhaled allergens, irritants, and inflammatory mediators ultimately promoting hyperresponsiveness
  • Transudation of fluids and increased mucous and respiratory secretions
220
Q

What are the neural mechs involved in asthma?

A
  • ANS regulates airway tone, airway secretions, blood flow, microvascular permeability and release of inflammatory cells
  • Asthma patients have elevated parasympathetic tone and reflex bronchoconstriction
  • Partially responsible for bronchospasm due to inhaled irritants
221
Q

How is airflow obstruction determined in asthma?

A
  • Determined by the diameter of the airway lumen, which can be altered by:
    1. Edema
    2. Mucous
    3. Airway smooth m contraction and hypertrophy
    4. Inflammatory cell infiltration
    5. Airway remodeling
  • Airway remodeling causes permanent narrowing of airways due to subepithelial fibrosis
222
Q

What does this show?

A

Bronchoconstriction after allergen challenge

223
Q

Compare and contrast asthma and COPD (table).

A

KNOW THIS TABLE. Please. Thanks

224
Q

How do you diagnose asthma?

A
  • Symptoms: wheezing, chronic cough, nocturnal cough/wheeze, chest tightness, sputum production
    1. May be exacerbated by allergens, GERD, URI, exercise
  • SOB or wheezing that is seasonal/after exposure to allergens (may be more year-round in intrinsic)
  • Relief when medication is used
  • Viral tracheobronchitis may cause a post- infectious bronchial hyperresponsiveness for up to 6 weeks
  • Can actually make a dx of asthma based on symptoms
225
Q

Life-threatening asthma

A
  • Accessory muscle use on presentation (SCM and intercostal muscle retractions, pulsus paradoxus, signs of R heart strain, i.e., p-pulmonale on EKG), hypoxemia, hypercapnia
  • Death from asthma usually related to diffuse mucous plugging of airways
226
Q

What are the diagnostic PFT’s for asthma?

A
  • Peak flow meter – diurnal variation of PEFR >20% is considered diagnostic
    1. Normal: highest PEFR at 4PM and lowest at 4AM.
    2. Thought to be due to decline of circulating catecholamines and cortisol (JUST KNOW THIS)
  • Spirometry – reduction of FEV1, FEV1/FVC, FEF25-75 that reverses with bronchodilators
    1. Reversibility criteria: 12% improvement AND 200cc increase in FEV1 and/or FVC
  • Lung volumes – evidence of hyperinflation suggested by elevated RV, FRC, RV/TLC, TLC
  • Gas exchange – DLCO is normal; occasionally may be even be elevated
227
Q

How is this related to asthma?

A
  • Normal CXR vs. asthma attack
  • Count ribs when looking for hyperinflation
228
Q

Does this person have asthma?

A

Looks like it

229
Q

What does asthma flow-volume loop look like?

A

Peak and scoop improve with bronchodilators

230
Q

What is the methacholine challenge? Why is it important?

A
  • Give patient gradually increasing concentrations of methacholine, and do spirometry looking at FEV-1 until there is a 20% drop (at which point you stop the test)
  • PC = provocative concentration (the lesser it takes to cause bronchospasm, the higher the airway reactivity) -> positive test is less useful
  • NEGATIVE TEST RULES OUT ASTHMA bc high negative predictive value (this WILL BE ON EXAM)
231
Q

What are some of the triggers for asthma?

A
  • Changes in humidity and barometric pressure
  • Allergens: house dust mites, cockroaches, molds, pets, pollen, food (eggs, nuts, milk), aspirin, NSAIDS
  • Occupational fumes, gases, dust (ozone, sulfur dioxide)
  • Viral URI’s, Sinusitis
  • GERD: common cause of chronic cough, as well as difficult to control asthma
  • Hormonal: Menses, Hyperthyroidism, Pregnancy
  • Psychological factors
  • Cigarette smoking
232
Q

Asthma treatment

A
  • Patient education w/action plan to manage asthma
  • Objective measures of lung function to monitor and assess the disease severity and control: PFT’s
  • Pharmacologic therapy: anti-inflammatory, inhaled beta agonist, leukotriene inhibitors, immunotherapy, antibiotics (if infection was a trigger)
    1. Relievers: SABA, SAMA
    2. Controllers: inhaled corticosteroids, inhaled LABA, leukotriene modifiers, systemic steroids, anti IgE, and anti-IL-5
    3. Make sure you teach pt how to use inhaler
233
Q

Asthma summary

A
  • Asthma is an inflammatory disorder
  • Prevalence of asthma may be increasing
  • There are different types of asthma -> causes are multi-factorial and triggers are numerous
  • Airway hyperresponsiveness is due to several mechanisms causing airflow obstruction
  • Diagnosis: compatible symptoms and lung function tests (PEFR, Pulmonary Function Test)
  • Methacholine challenge test has a high NPV
  • Management of asthma: good patient education and appropriate pharmacologic treatments
    1. ICS -> LABA-> LTRA
    2. LABA are associated with increased Mortality – use cautiously, with regular follow up

Pulmonology (18 decks)

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