ZSFG AM Report 8/21/2017: Oxygen Delivery Systems and Use of PA Catheters in Undifferentiated Shock

Thank you to Megan Lockwood and the ICU team for presenting an interesting case of a women with a history of HFrEF who presented with undifferentiated shock who where a mixed picture of septic and cardiogenic shock developed into a management challenge.

Top Pearls:

  1. There are diminishing returns on FiO2 above 6L NC, and you should switch to a different delivery device at that point.
  2. Think about checking Co-ox to rule out Met-Hemoglobinemia or Carbon Monoxide poisoning in refractory hypoxemia
  3. Pulmonary arterial catheterizations, although never linked with outcomes in large studies, may be helpful in cases of mixed shock or undifferentiated shock (although this remains an area of HOT debate)


Oxygen Delivery Systems and Approximate FiO2:

Supplemental O2

Notes on High-Flow Oxygen (Courtesy of Teja Kompala):

  • What is it? Heated and humidified air that allows for comfortable delivery of higher flow oxygen
  • No specific threshold that absolutely warrants ICU level care (institution dependent) but an escalating requirement is worrisome and should prompt ICU evaluation
  • Liters per minute (LPM) and FiO2 are the two variables that can be manipulated, again this is institution dependent
  • High flow oxygen also provides a small amount of positive pressure. Also found to have decreased 90-day mortality in pts with nonhypercapnic acute hypoxemic respiratory failure.


Pulmonary Arterial Catheterization – Use and Interpretation:

  • Pulmonary arterial catheterization (PAC) has never been shown to improve patient-important outcomes.
  • However, when the diagnosis or the type of shock remains undetermined or mixed, hemodynamic measurements obtained by PAC can be helpful
  • Additional patients that may benefit from PAC are those with unknown volume status despite adequate fluid resuscitation, those with severe cardiogenic shock (eg, acute valvular disease), or those suspected to have severe underlying pulmonary artery hypertension or cardiac tamponade.
  • The major hemodynamic indices measured on PAC are
    • cardiac output (ie, cardiac index)
    • systemic vascular resistance
    • pulmonary artery occlusion pressure (ie, pulmonary capillary wedge pressure)
    • right atrial pressure
    • mixed venous oxyhemoglobin saturation (SvO2).
  • These measurements are most useful diagnostically but can also be used to guide fluid resuscitation, titrate vasopressors, and assess the hemodynamic effects of changes in mechanical ventilator settings

Interpreting PA Catheter

aThere is significant patient-to-patient variation. Pressure may be normalized if cardiac output is low.

bForrester et al classified nonreperfused MI patients into four hemodynamic subsets. (From JS Forrester et al: N Engl J Med 295:1356, 1976.) PCW pressure and CI in clinically stable subset 1 patients are shown. Values in parentheses represent range.

c”Isolated” or predominant RV failure.

dPCW and pulmonary artery pressures may rise in RV failure after volume loading due to RV dilation and right-to-left shift of the interventricular septum, resulting in impaired LV filling. When biventricular failure is present, the patterns are similar to those shown for LV failure.

Abbreviations: CI, cardiac index; MI, myocardial infarction; P/SBF, pulmonary/systemic blood flow; PAS/D, pulmonary artery systolic/diastolic; PCW, pulmonary capillary wedge; RA, right atrium; RVS/D, right ventricular systolic/diastolic; SVR, systemic vascular resistance.

  • Hochman JS, Ingbar DH. Cardiogenic Shock and Pulmonary Edema. In: Kasper D, Fauci A, Hauser S, Longo D, Jameson J, Loscalzo J. eds. Harrison’s Principles of Internal Medicine, 19e New York, NY: McGraw-Hill; 2014. http://accessmedicine.mhmedical.com/content.aspx?bookid=1130&sectionid=79745930. Accessed August 21, 2017.
  • Mimoz et al. (1994). Pulmonary artery catheterization in critically ill patients: a prospective analysis of outcome changes associated with catheter-prompted changes in therapy. Crit Care Med. 22(4): 573.
  • Frat et al. (2015). High-flow oxygen through nasal cannula in acute hypoxemic respiratory failure. NEJM. 372:2185-2196.


  • Supplemental Oxygen & Oxygen Delivery: https://www.evernote.com/shard/s509/sh/f1c45977-e455-4b4b-85c5-ba4b6b27dc0b/b1de1faa22ff233b903583b688ab3be4
  • Pulmonary Arterial Catheterization: https://www.evernote.com/shard/s509/sh/9fdbc91f-34df-4663-9692-0a6ecd201086/ad851155dcdd877aa0f449087c19550c

Moffitt Pearls – Rheumatology Report – 8.21.2017 – Evan’s Syndrome and SLE

Thank you to Leah for presenting a very interesting case of a young man with history of lupus c/b APS and DVT presenting with thrombocytopenia+ hemolysis found to have Evan’s Syndrome (ITP + AIHA)!


Key Pearls

  1. Although the term is falling out of favor Evan’s syndrome describes the combo of ITP & AIHA.
  2. For unclear reasons, lupus flares are often accompanied by a dissociation between ESR (high) and CRP (nl or minimal elevation). Other findings of flare (vs. infection) include drop in complement, recued leukocyte count and + RBC casts and/or proteinuria.
  3. Direct oral anticoagulants have not been studied nor are they recommended as anticoagulants in patients with lupus and known DVT. Treat with warfarin or LMWH only!


More on Evan’s Syndrome

  • Combination of Coombs-positive warm AIHA and immune thrombocytopenia (ITP).
  • Antibodies that cause platelet destruction are unique from those that cause AIHA.
  • Differential Diagnosis:
    • Infectious (eg, HCV, HIV)
    • SLE
    • Lymphoproliferative disorders
    • Common Variable immunodeficiency
  • Treatment (similar to ITP, however azathioprine and cyclophosphamide are used)
    • First line therapy: Glucocorticoid @ 1-2 mg/kg +/- IVIG
    • Second line: Azathioprine or rituximab
    • Third line: Splenectomy
    • Under investigation: Eltrombopag –> a TPO receptor agonist stimulating platelet formation

American College of Rheumatology Classification of SLE

[Always verify all prior diagnoses of rheumatological conditions]

  • SLE Criteria > 3 of 11 ( Se & Sp > 95% and all DO NOT have to be at the same time)
    • Cutaneous Manifestations
      • Malar Rash
      • Photosensitivity
      • Discoid Rash
      • Oral ulcer
    • MSK
      • Nonerosive arthritis – oligioarticualr; symmetrical, migratory
    • Cardiopulmonary
      • Serositis – pleuritic or pericarditis
    • Renal
      • Proteinuria or cellular Casts – > 500 mg/dL on UA or 3+ on dip


    • Neurological
      • Seizures OR psychosis


    • Hematological
      • Hemolytic anemia or leukopenia, or lymphopenia or thrombocytopenia
    • Serologies
      • +ANA
      • +anti-dsDNA or antiphopholipid Abs


Review of Hemolytic Anemias based on Smear


VA ICU Report 8.18.17 – STEMI equivalents and the “subtle STEMI”

Case summary

Thanks to our excellent ICU team for presenting a fascinating case of a 70M who had an lumbar drain after spinal surgery who develop abdominal pain and AMS raising concern for ACS and low CSF pressure.

Top pearls

  1. While ST elevation in aVR does not technically meet STEMI criteria, it can provide key information about apical ischemia and is a marker of poor prognosis in ACS.
  2. ST elevations in two contiguous leads raises concern for total occlusion of the corresponding coronary vasculature. Other EKG manifestations of total occlusion are rare but include: (1) Wellen’s EKG (2) new LBBB and (3) De Winter’s EKG – see below
  3.  Suspect intracranial hypotension in patients who present with orthostatic headaches. This is a rare disease than occurs due spontaneous CSF leak or excessive removal of CSF in patients with a lumbar drain.

aVR in ACS

  • In patients diagnosed with ACS, ST elevation in aVR does not meet true “STEMI” criteria, but
    • Strongly predicts proximal LAD occlusion
    • ST elevation in aVR > ST elevation in V1 suggests acute left main occlusion
  • In patients with inferior STEMI, ST depressions in aVR suggests left circumflex infarction or large RCA infarction.

STEMI equivalents

ST elevations in two contiguous leads raises concern for acute total occlusion of the corresponding coronary artery.  While this is the most common EKG pattern of total occlusion, several other “STEMI equivalent” can also occur.

  • Wellen’s T waves (https://lifeinthefastlane.com/ecg-library/wellens-syndrome/)
    • Deep, symmetric (Type B, 75%) or Biphasic (+ then -, 25%) V2-3 (may extend to V1-6)
    • Isoelectric or minimally-elevated ST segment (< 1mm)
    • No precordial Q waves
    • Preserved precordial R wave progressions
  • De Winter’s pattern (https://lifeinthefastlane.com/ecg-library/de-winters-t-waves)
    • Concave ST depressions into tall, symmetric T waves in the anterior precordial leads
  • ST depressions in the anterior leads + tall R waves
    • Get posterior EKG looking for posterior STEMI
  • LBBB in the setting of acute chest pain
  • Subtle STEMI
    • 1/20 of all acute coronary occlusions do not meet criteria for STEMI, instead cause 0.7 – 0.9 mm ST elevations termed “subtle-STEMI”
    • In this setting, look for reciprocal depressions
    • The RCA is usually involved
      • ST depressions in inferior leads —> scrutinize the high lateral leads (I and aVL) for subtle ST elevations
      • ST elevations in inferior leads, scrutinize, the high lateral leads to ST depressions (>0.5 mm)

Subtle STEMI: Wei, Margaret, Daniel R. Sanchez, and Ivan Rokos. “Nondiagnostic ST Elevations With Chest Pain: The Subtle STEMI.” JAMA Internal Medicine177.4 (2017): 577-578.


VA Ambulatory Report 8.16.17 – Falls in the Elderly and Urinary Retention in Women

Thanks Beth for the awesome case of a 90 yo F with pmhx of HTN, CKD presenting after multiple falls who developed urinary retention and fecal incontinence found to have cervical spine myelopathy from spinal stenosis.

Key Learning Points

  • Approach to a patient with falls:  Consider a physiologic approach thinking about the systems that need to be functioning properly to walk: cognition, motor strength, sensation, musculoskeletal apparatus, cardiovascular fitness, navigable environment
  • Use the CHIP rule for determining which patients presenting to urgent care or the ambulatory setting need a head CT.  The Canadian head CT rule is for patients with loss of consciousness
  • The Timed Get-Up and Go test is helpful for assessing falls risk


Falls in the elderly

Step 1– Assess if the fall is consistent with syncope or pre-syncope vs. mechanical cause.

Step 2 – Assess the patient for injuries related to the fall.

  • When to get a head CT?
  • Decision rules to help us decide who needs a head CT after a fall.  The Canadian CT Head Rule is often applied in the Emergency setting and only applies to patients with loss of consciousness.  The Canadian head CT rules are the most widely validated.
  • For the ambulatory and urgent care setting you could consider using the CHIP rule because it applies to patients without loss of consciousness. Note that the CHIP rule recommends head CT in patients over 60 years of age.  This is a nice reminder that our older patients are at a much higher risk of subdural hematomas due to cerebral atrophy even with minor head trauma.


Step 3 – Evaluate for the etiology of the fall

Falls in the elderly are multifactorial and each fall could have a different etiology so needs to be evaluated separately.

You can use a physiologic approach to falls.  Think about all the systems you need to walk (which is actually a very complex task!):

  • Cognition
    • Dementia from any cause
    • Dementias associated with decreased physical functioning: parkinsons, spinal muscle atrophy
    • Normal pressure hydrocephalus
    • Drugs and toxins: alcohol, medications (see below)
  • Motor strength
    • Primary muscle disease
    • Stroke
    • Myelopathy
    • Neuromuscular junction disorder
  • Sensation
    • Peripheral neuropathy
    • Poor vision
    • Vestibular dysfunction
  • Musculoskeletal apparatus
    • Osteoporosis
    • Fracture
    • Ligamentous Injury
  • Cardiovascular fitness
    • Orthostatic hypotension
    • Arrythmias
  • Navigable environment
    • Lighting, irregular floor surfaces, unsafe stairs, cords and carpets
  • Medications (always include as a category of your differential in the elderly!)
    • Sedative-hypnotics, TCAs, antihypertensives, cardiac medications, corticosteroids, NSAIDs, anticholinergic meds, hypoglycemic agents


Timed Up and Go Test

  • Can be used to help with the global gait assessment
  • How to perform: Instruct the patient to get out of the chair (without using armrests), stand up, walk forward 10 feet, turn around and walk back to chair, sit down.
  • Normal is < 10 seconds and indicates the patient is mobile.  > 20 seconds indicates the patient is variably mobile.  > 30 seconds indicates impairments in mobility
  • Aside from timing, observing the patient’s ability to perform each maneuver of the test can help you determine what area the patient is deficient .

Interventions for abnormal results of the Timed Up and Go test (Table copied from Preventing Falls in the Geriatric Population reference below)

Observation Significance Intervention
Difficulty rising from chair Proximal muscle weakness PT referral for lower extremity strengthening
Staggering or reported dizziness upon rising Possible orthostasis Check orthostatic vital signs; review medications that may contribute to orthostasis
Pill-rolling tremor, stooped posture, shuffling/festinating gait Possible parkinsonism Consider neurology referral
Increased sway, magnetic gait Possible normal pressure hydrocephalus Ask about urinary incontinence and memory issues. If these are highly suspected, consider head CT
Path deviation Possible peripheral neuropathy, cerebrovascular disease Consider neuropathy workup, examination of feet, PT referral for assistive device
Slow, antalgic gait Pain from osteoarthritis, peripheral neuropathy, podiatric disorders Pain control, examination of feet


Differential for Urinary Retention in Women

  • Detrusor underactivity: aging, DM, neurologic disease (stroke, spinal cord compression),
  • Outflow obstruction: pelvic organ prolapse, pelvic masses
  • Functional: Dysfunctional voiding, Detrusor sphincter dyssynergia, bladder neck obstruction
  • Meds: Most common: anticholinergic and sympathomimetic
  • Infection – UTI, genital herpes


Smits M, et al. Predicting intracranial traumatic findings on computed tomography in patients with minor head injury: the CHIP prediction rule. Ann Intern Med. March 20, 2007;146(6):397–405.

AAFP article on falls in the elderly: http://www.aafp.org/afp/2000/0401/p2159.html



ZSFG AM Report Pearls 8/16/2017 – Acute Polyarthritis and Fevers

Thank you to Lev Malecanchik for presenting a very interesting, and mysterious case of a young woman with acute, progressive symmetric polyarticular arthritis whose underlying diagnosis remains shrouded in mystery and intrigue.

Top Pearls:

  1. The presence of synovitis is key in diagnosis an arthritis vs. arthralgia
  2. Acute etiologies of polyarthritis include infectious (viral, bacterial especially) as well as reactive
  3. Choosing Wisely campaign recommends a ANA prior to sub-serologies (including antibodies to double-stranded DNA, Smith, RNP, SSA, SSB, Scl-70, centromere)


“Perhaps no disease is more painful than acute polyarthritis. The inability to change the posture without agonizing pain, the drenching sweats, the prostration and utter helplessness, combine to make it one of the most distressing of febrile afflictions. A special feature of the disease is the tendency of the inflammation to subside in one joint, while developing with great intensity in another.”

-Sir William Osler, the Principles and Practice of Medicine

Approach to Polyarthritis:

  • The Differential is BROAD, but thinking about a few factors can help you narrow
  • Acute presentations should raise concern for infectious etiologies (especially bacterial and viral) as well as a reactive arthritis
  • Confirming the presence of synovitis helps you identify an arthritis vs. arthralgia.
  • “Inflammatory pain” (i.e. AM stiffness lasting than more than 1 hour) can also help you get to the right category of diseases as well


  • Assess the number of joints involved
    • Consider whether there is a presence of systemic symptoms
    • Systemic symptoms makes Rheum etiology much more likely
  • Presence of synovitis is also important in moving along algorithm
  • Don’t forget to think about subacute bacterial endocarditis


Discriminating Factor
Possible Diagnoses
Temperature >40.0 C
Still’s disease, bacterial arthritis, SLE
Fever preceding arthritis
viral arthritis, lyme disease, reactive arthritis, Still’s disease, endocarditis
Migratory arthritis
Rheumatic fever, gonococcus, meningococcus, viral arthritis, SLE, acute leukemia, Whipple’s disease
Effusion disproportionate to pain
TB arthritis, endocarditis, IBD, GCA, lyme disease
Pain disproportionate to effusion
Rheumatic fever, FMF, acute leukemia, AIDS
Positive RF
RA, viral arthritis, TB arthritis, endocarditis, SLE, sarcoidosis, systemic vasculitis
Morning stiffness
RA, PMR, Still’s disease, some viral and reactive arthritis
Symmetric small joint
RA, SLE, viral arthritis
Leukocytosis (>15K)
Bacterial arthritis, endocarditis, Still’s disease, systemic vasculitis, acute leukemia
SLE, viral arthritis
Episodic recurrences
Lyme disease, crystal-induced arthropathy, IBD, Whipple’s disease, FMF, Still’s disease, SLE




  • Polyarthritis: https://www.evernote.com/shard/s509/sh/6c94512c-3834-4e0b-b050-7dd274ec36a8/1851f230f437dedfc5625850309308a5


Moffitt Pearls 8.16.17 – Endocrine Report – Central AI & Hypothyroidism

Case Summary

Thank you to Emma for presenting a fascinating case of a middle aged man with SCC of the head and neck treated with a PD-1 inhibitor p/w hyponatremia found to have SIADH 2/2 hypothyroidism and central adrenal insufficiency (AI)!!!


Key Pearls

  1. Remember that replacement of thyroid hormone without replacement of glucocorticoids can precipitate acute adrenal insufficiency.
  2. Nonthyroidal Illness (formerly known as Euthyroid Sick Syndrome) is a normal response to illness and is a relative hypothyroid state marked by elevated TSH and depression of Free T4 and T3.
    • NOTE: Thyroid function should not be assessed in seriously ill patients unless there is a strong suspicion of thyroid dysfunction (thanks Brad Monash!).
  3. A standard stimulation test is 250 mcg of IV Cosyntropin which tests ability of ACTH -> increase cortisol (more details below)


Evaluation of Adrenal Insufficiency

The HPA Axis

  • A primary adrenal disorder resulting in deficiency of cortisol = 1° AI or Addison’s disease
  • A pituitary disorder resulting in deficiency of corticotropin (ACTH) secretion = 2° AI
  • A hypothalamic disorder resulting in deficiency of corticotropin-releasing hormone (CRH) and secondarily of ACTH = 3° AI

Evaluation of HPA Axis Response to ACTH

  • Early am cortisol < 3 is virtually diagnostic of primary OR secondary AI; >17 rules this out
    • If unclear (often the case) then go to stim testing!
  • Standard Stim test is 250 mcg of IV Cosyntropin
    • Measure cortisol before, 30 & 60 min after intravenous (IV) injection
    • If f/u cortisol is greater than 18, this indicates normal adrenal function
    • A inadequate response suggests EITHER primary or secondary AI
      • Measure ACTH:
        • High = primary AI
        • Low = secondary or tertiary AI


Copyright © 2000-2015 The Cleveland Clinic Foundation. http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/endocrinology/

VA morning report 8.15: VBG vs ABG and CXR infiltrates

Case Summary

Thanks to Anne Rohlfing for presenting an interesting case of a 66M with severe COPD who presented with dyspnea found to have likely CAP and severe hyponatremia

Top pearls

  1. The FEV1% classifies disease severity in patients with COPD. Other supportive information includes –  (1) need for home O2 (2) frequency of exacerbations (3) history of intubation (4) medications (e.g rofllumilast – only approved for severe COPD)
  2. A VBG is a less precise test than an ABG but is more convenient. Get a VBG when you need a sense of the pH and PCO2. An ABG is important when this information is critical to the management
  3. Consolidation on CXR usually represents an infection. In rare causes, mimickers of this can be considered by the nature of the fluid. See below for details.

VBG versus ABG

Where can a VBG be obtained from?
  • Peripheral
  • Central
What numbers can be obtained?
Converting a VBG to an ABG
General principles
While there are some subtle differences between central and peripheral VBG’s, but as a general rule:
  • pH –  add 0.05 to VBG —> ABG
  • CO2 – subtract 5mm to VBG —> ABG
  • Central venous blood gases correlates much better with ABGs that peripheral VBGs
  • Peripheral VBGs are even less reliable in
    • Hypotensive patients
    • Issues with technique
      • Prolonged tourniquet application
      • Delayed sample collection
    • In these situations, the venous pH is more accurate than the pVCO2
Putting this together
  • The ABG is the gold standard test for assessing pH, pCO2 and pO2
  • While VBGs are less reliable, there are more convenient


  • For most clinicians, convenience of VBGs outweighs their imprecision when a sense of the pH and acid base status is needed (e.g. non-severe COPD exacerbation, mild acidosis)
  • Get an ABG where this information is critical to decision making (e.g intubation, severe acidosis/alkalosis)

Alveolar infiltrate on imaging
The vast majority of alveolar infiltrates ( = consolidation) represent bacterial, or viral, pneumonia. Mimickers of this clinical syndrome can be generated by considering the nature of the fluid
  • Complicated bacterial pneumonia – the radiologic abnormalities resolves in a delayed manner (~ 2 months) but failure to improve/recurrent alveolar infiltrates in the same distribution prompts consideration of (1) obstruction (malignancy) (2) immunodeficiency (HIV) or anatomic pulmonary pathology (bronchiectasis)
  • In immunosuppressed patients broaden the infection DDX to consider (1) atypical bacterial infections (Tb, Nocardia) or fungi (PCP, Crypto, aspergillus)


  • Cardiogenic pulmonary edema
    • Unilateral pulmonary edema has been described in CHF – more so with mitral regurgitation
  • Non-cardiogenic edema -> ARDS


  • Bland pulmonary hemorrhage (e.g. as a complication anti-coagulantion)
  • Inflammatory (vasculitis)

Sterile inflammation (cells without organisms)

  • Interstitial lung disease
    • Acute or chronic eosinophilic pneumonia
    • Hypersensitivity pneumonitis
    • Autoimmune pulmonary disease (scleroderma, dermatomyositis)
  • Drug-induced pulmonary disease
    • Amiodarone
    • PD-1 inhibitors
  • Radiation induced
  • Inhalational injury
    • Crack lung


  • Infiltrating adenocarcinoma
  • Lymphangitic spread of tumor


  • Pulmonary alveolar proteinosis


  • Lipoid pneumonia