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Fellowship revision > ICU > Flashcards

ICU Flashcards

1
Q

What’s the normal anion gap?

A

12+/-4

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2
Q

What’s the compensation rule for expected PaCO2 with a metabolic acidosis?

A

1.5x[HCO3-] + 8 (+/-2)

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3
Q

What are the causes of NAGMA?

A

Addisons, Bicarb loss (GI or renal), Chloride, Drugs (acetazolamide, acids)

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4
Q

What are the causes of HAGMA?

A

Acids we can’t see, either exogenous or endogenous not counted (ketoacids, lactic acids, uraemia)
Lactate
Toxins (eg. metformin, paracetamol, ethylene glycol, methanol, salicylate)
Ketones
Renal

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5
Q

What’s a central line?

A

One that terminates in one of the great vessels or in or near the heart

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6
Q

What are indications for central venous access?

A 
intravenous access (eg. if difficult IV access)
infusion of irritant substances
CVP monitoring
central venous oxygen monitoring
Advanced haemodynamic monitoring (eg. PICCO, PA catheter)
extracorporeal therapies (ECMO, RRT)
IVC filter placement
venous stenting
transvenous pacing
catheter-guided thrombolysis
repeated blood sampling
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7
Q

What are some contraindications to central venous access?

A 
contaminated site/infection over site
traumatised site
burned site
occluded vessel
stenotic vessel
severe coagulopathy (eg. INR >1.5, plt <50, APTT >50, clopidogrel or ticagrelor)
raised ICP (for IJV)
respiratory failure with high FiO2
uncooperative awake patient
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8
Q

Advantages & disadvantages of subclavian insertion site for central venous access?

A

Advantages: lowest infection rate (lowest risk CLABSI), suitable for longer-term use (eg. 14 days)
disadvantages: non-compressible, highest PTx rate, not suitable for vascaths (may kink off, risk subclavian stenosis which may sabotage future AV fistulae), pt needs to be supine & head down for insertion, insertion interferes w CPR,

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9
Q

Advantages & disadvantages of internal jugular insertion site for central venous access?

A

Pros: convenient, easy to access during surgery for short-term use, best site for vascath, compressible, no “pinch-off” phenomena, least acute complications (unlikely to result in haemothorax or pneumothorax)

Cons: unsuitable for long-term use, may be better to save this site for vascath/PA catheter/ECMO, contra-indicated if raised ICP, requires pt to be supine & head down for insertion, if pt develops IJ thrombus may cause raised ICP, can’t use if c-spine collar needs to be in situ, not ideal if tracheostomy planned

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10
Q

Advantages & disadvantages of femoral insertion site for central venous access?

A

Adv: no haemo/pneumothorax risk, no need for supine/head down (suitable for pts in resp distress), able to be used if c-spine collar or tracheostomy planned, no need for CXR confirmation (can use immediately), compressible (unless to above inguinal ligament in which case may get external iliac vein, retroperitoneal & non-compressible)
cons: highest infection risk, poor choice if previous DVT in the limb, poor choice in morbid obesity (pannus), risk retroperitoneal haematoma, circulation of drugs relatively delayed, unsuitable for PA catheter placement, impairs patient mobility

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11
Q

Advantages & disadvantages of PICC site for central venous access?

A

Adv: very low risk serious complications, suitable for prolonged use (up to 6/52 in many cases), no need to position the pt supine
Cons: highest risk of thrombus, more difficult to assure correct tip position, unsuitable for high-volume or highly-viscous infusions (too much resistance to flow), unsuitable for CVP monitoring or central venous blood sampling (too much risk of lumen obstruction or poor waveform fidelity)

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12
Q

For whom should antibiotic-impregnated CVCs be reserved?

A

Immunosuppressed
Those requiring prolonged CVC
Those at high risk CLABSI (eg. burns pts)
If the unit has high rates of CLABSI despite good insertion technique & attention to routine maintenance

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13
Q

What’s the flow rate of a 16g CVC line? 14g? 18g?

A

2.7L/hr. 5L/hr. 1.4L/hr

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14
Q

What risks should be discussed with informed consent for CVC insertion?

A

Failure of technique/resiting/repositioning
discomfort- failure of LA & need for sedation
haemo/pneumothorax & chest drain
damage to heart or great vessels or other surrounding structures
cardiac arrhythmias
air embolism
death

later complications:
blocked line
wound or bloodstream infection

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15
Q

What are the basic pre-conditions for informed consent?

A

Legally capable of giving consent (competent)

Consent must be informed (risks/benefits/alternatives), specific, freely given, must cover what’s actually done

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16
Q

What environment is required for CVC insertion?

A

Adequate lighting & spake
Ability to maintain aseptic technique
Skilled assistant
immediate access to cardiac resuscitation equipment & drugs
electrical safety support (cardiac protected electrical area with RCDs & LIMs & equipotential earthing)

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17
Q

Why lie the pt trendelenburg for upper limb lines?

A

making the vein of interest the most dependent vein dilates it
Less risk air embolus (air flow through a 14g needle is 100mL/second, all that’s required to fill the RVOT (life-threatening)

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18
Q

What monitoring is essential for CVC insertion?

A

ecg
pulse ox
pressure transducer (to confirm in right place)

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19
Q

At what level should the tip of the CVC be on chest radiograph?

A

level of carina

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20
Q

What’s the (approximate) insertion depth for a R) & L) IJ CVC?

A

12-13 cm in males and 11-12 cm in females in the right IJV
13-14 cm in males and 12-13 cm in females in the left IJV

R) is age/10 -1
L) is age/10 +4

21
Q

For how long (max) should central lines stay in?

A

Femoral- 7
IJV- 7-10
subclavian- 10-14

22
Q

What are the indications for stress ulcer prophylaxis? best options?

A

Very high risk factors= mechanical ventilation >48hrs, coagulopathy, PHx UGI bleeding in the past 12/12, trauma (TBI, SCI, burns), 2+ of: ICU >1/52, occult GI bleed, steroids (hydrocortisone equivalent >250mg/week)

PPI (potent, long-lasting & don’t have tolerance after 72hrs as do H2 antagonists, no difference nosocomial pneumonia, risk C diff enterocolitis, long-term ass’d with fractures, hypoMg++, hypoCa++, rarely risk interstitial nephritis) but maximal effect takes 48hrs) superior to H2 antagonist, early enteral feeding

23
Q

What’s the main source of infection leading to sepsis?

A

Lung
Abdomen
bloodstream

genitourinary tract, skin & vascular access devices= 5-15%

24
Q

What’s sepsis?

A

Sepsis= a life-threatening organ dysfunction caused by a dysregulated host response to infection. The new definition (Sepsis 3 taskforce) de-emphasises SIRS criteria & places emphasis on organ failure. A change in SOFA score of 2 or greater is stipulated to evaluate pts likely to have sepsis in ICU.

25
Q

What are shortcomings of the SIRS criteria?

A

lack sensitivity & specificity for the detection of sepsis
12% on septic pts don’t have 2 or more SIRS criteria
almost half of all hospital inpatients meet SIRS criteria at some point during their admission; the SIRS criteria lacks specificity

26
Q

What’s the quick SOFA (qSOFA)?

A 
any 2 of:
SBP <100mmHg
altered mentation (GCS <15)
RR 22/min
prompts Ix for organ dysfunction or escalate Rx for infection
27
Q

What’s septic shock & it’s mortality?

A

sepsis causing persistent hypoT (requiring vasopressors to maintain MAP >65mmHg) AND with serum lactate >2mmol/L despite adequate volume resuscitation
mortality 40%

28
Q

what are the elements of sepsis pathophysiology?

A

interplay of both pro- and anti-inflammatory states:
eg. pro-inflammatory includes toll-like receptors which recognise bacterial, fungal & viral elements, bind & release pre-inflammatory cytokines including TNF alfa, interleukins & interferon-y. This may lead to a cytokine storm. Most early deaths due to this.
anti-inflammatory mechanisms occur concurrently- leads to immunosuppression, often later in the course of sepsis, apoptosis of lymphocytes & dendritic cells. T-cell anergy occurs & CD4 T cells move from pro- to anti-inflammatory, “immune paralysis” where the host becomes susceptible to viral re-activation or secondary nosocomial infection with organs that may not have been pathogenic in an immunocompetent host.

coagulopathy:
up regulation of procoagulant mechanisms (eg. during the pro-inflammatory phase, tissue factor expressed on circulating mono-nuclear cells–> activation of coagulation & platelets. Platelets may also be activated by presence of bacteria), down-regulation of anticoagulant mechanisms (consumption & degradation of tissue factor pathway inhibitor, reduction in activation of protein C, increased consumption & down-regulated synthesis of antithrombin).
Thrombin formation & fibrin deposition in microvascular bed may be a key factor in the development of multi-organ dysfunction syndrome in sepsis.
consumption of platelets & clotting factors may also lead to DIC (micro thrombosis & haemorrhage)

endothelial injury:
inflammatory mediators–> oxidative stress & shedding of endothelial glycocalyx

29
Q

what are the elements of sepsis pathophysiology?

A

interplay of both pro- and anti-inflammatory states:
eg. pro-inflammatory includes toll-like receptors which recognise bacterial, fungal & viral elements, bind & release pre-inflammatory cytokines including TNF alfa, interleukins & interferon-y. This may lead to a cytokine storm. Most early deaths due to this.
anti-inflammatory mechanisms occur concurrently- leads to immunosuppression, often later in the course of sepsis, apoptosis of lymphocytes & dendritic cells. T-cell anergy occurs & CD4 T cells move from pro- to anti-inflammatory, “immune paralysis” where the host becomes susceptible to viral re-activation or secondary nosocomial infection with organs that may not have been pathogenic in an immunocompetent host.

coagulopathy:
up regulation of procoagulant mechanisms (eg. during the pro-inflammatory phase, tissue factor expressed on circulating mono-nuclear cells–> activation of coagulation & platelets. Platelets may also be activated by presence of bacteria), down-regulation of anticoagulant mechanisms (consumption & degradation of tissue factor pathway inhibitor, reduction in activation of protein C, increased consumption & down-regulated synthesis of antithrombin).
Thrombin formation & fibrin deposition in microvascular bed may be a key factor in the development of multi-organ dysfunction syndrome in sepsis.
consumption of platelets & clotting factors may also lead to DIC (micro thrombosis & haemorrhage)

endothelial injury:
inflammatory mediators–> oxidative stress & shedding of endothelial glycocalyx
endothelial glycocalyx plays a key role in regulation of haemostasis & vascular permeability & the vasomotor response to fluid shear stress through eNOS release
endothelial glycocalyx damage–> increased vascular permeability, capillary leakage, tissue oedema
In the lung, this–> protein-rich fluid accumulation in interstitium, arterial hypoxaemia & reduced pulmonary compliance consistent with ARDS

microcirculatory dysfunction:
due to heterogenous dysregulated expression of iNOS (inducible nitric oxide synthase) in different vascular beds, leads to hypoperfusion of areas which are iNOS deficient
alterations in microvascular blood flow is a proposed mechanism for sepsis-associated AKI
Excessive NO production through production of iNOS is responsible for a loss of adrenergic sensitivity & vascular tone in arteriolar & venous beds. This, along with relative vasopressin deficiency, is believed to cause vasoplegic shock characteristic of sepsis.

30
Q

Which element of sepsis pathophysiology has prognostic significance?

A

glycocalyx shedding- blood levels of glycocalyx components higher in non-survivors vs survivors of septic shock

31
Q

What’s the microcirculation?

A

vessels <100microm diameter

32
Q

what’s thought to cause the vasoplegic shock characteristic of sepsis?

A

excessive NO due to production of iNOS and relative vasopressin deficiency

32
Q

what’s thought to cause the vasoplegic shock characteristic of sepsis?

A

excessive NO due to production of iNOS and relative vasopressin deficiency

33
Q

What’s monocyte distribution width validated as?

A

a marker of sepsis severity (but not a diagnostic test)

34
Q

what’s lactate elevation useful for?

A

a marker of tissue hypoperfusion
elevated serial measurements are associated with mortality in sepsis but it’s not sensitive or specific for sepsis diagnosis

35
Q

What’s CRP? what’s it’s use?

A

acute phase protein
released in response to rising IL-6 levels
aids complement binding & phagocytosis of pathogens & inactivation of toxins
begins to rise 4-6hours after an inflammatory stimulus, peaks at 24-72hours (half-life 19hrs)

is sensitive but not specific for infections, useful to track course of infection or inflammation & responses to therapy

36
Q

Which is the only sepsis biomarker that has been implemented in sepsis guidelines?

A

procalcitonin

pro-hormone for calcitonin, released into the blood in inflammatory states (particularly bacterial & parasitic)

can’t be used as a single diagnostic test for sepsis as it can be elevated after trauma or major surgery

PCT becomes detectable after 3-4hrs & peaks 6-14hours after inflammatory stimulus- long half-life of 25-30hrs

37
Q

What are the cornerstones of sepsis treatment?

A

SOURCE CONTROL
-early identification & management- improves mortality

ANTI-INFECTIVE THERAPY

  • effective empirical antimicrobials should be instituted asap- likely reduce mortality & sepsis progression
  • SSC recommends ABx within 1 hour of recognition of sepsis or septic shock- mortality increases 12% for every hour effective ABx were delayed from onset of septic shock
  • ideally cultures before but ABx shouldn’t be delayed for cultures

SUPPORT FAILING ORGANS

Fluids:

  • avoid starch (renal impairment)
  • albumin may result in less volume administered but doesn’t improve pt outcomes
  • both crystalloid & albumin are safe resus fluids- possible mortality benefit towards albumin in severe sepsis (substudy of SAFE trial: albumin vs saline didn’t impair renal or other organ function & may decr risk of death in severe sepsis).

Vasopressors:

  • NAdr= most robust research for use as first-line
  • dopamine associated with increased arrhythmias (but no difference in mortality cf NAdr)
  • Adr is as effective & safe as NAdr but it can increase lactate, HR & affect glycemic control
  • vasopressin & Adr are safe 2nd line agents

Inotropes:

  • dobutamine has the most clinical data suggesting safety for use in sepsis
  • Doesn’t appear to be an increased incidence of serious adverse events when comparing Adr alone vs NAdr & dobutamine
  • role of inodilators levosimendan & milrinone in sepsis is unclear

Transfusion:
-target of 70g/L non-inferior for septic shock- TRISS study: conservative (70g/L) vs liberal (90g/L) in septic shock pts- no difference in mortality @ 90 days, incl in pts with cardiac disease, older age, severe physiological derangement.

Steroids:

  • hydrocortisone reduces vasopressor duration & may reduce time in ICU in pts with septic shock.
  • hydrocortisone & fludrocortisone may reduce mortality, shorten length of organ failure & days on vasopressor & the duration of mechanical ventilation.

Anticoagulation:
-safe, but no convincing evidence of mortality benefit.

MANAGE DYS-REGULATED HOST RESPONSE
There are currently no conclusive trials on immunomodulatory drugs in sepsis

38
Q

What did the ALBIOS trial find?

A

For pts with severe sepsis, alb 20% + crystalloid vs crystalloid alone with alb targets >30g/L resulted in less overall fluid (alb group) with closer to neutral fluid balance. No difference in mortality.

39
Q

what did the SAFE trial conclude?

A

no mortality difference when 4% albumin used for fluid resus cf 0.9% NaCl but should avoid 4% albumin in head injuries (incr mortality at 28 days in pts with brain injury)

40
Q

What’s the bottom line on vasopressors for organ support for sepsis?

A

NAdr first line (most robust research base)
Dopamine= more arrhythmias (but no diff in mortality when cf NAdr)
Adrenaline= as effective & safe as NAdr but incr risk lactataemia, HR & impaired glycaemic control (transient insulin use)
Vasopressin & Adr are safe 2nd line agents (VASST trial showed no difference in mortality if Adr or vasopressin added as 2nd line agent to NAdr. VANISH trial showed no difference in mortality or renal complications with NAdr vs vasopressin)

41
Q

What did the VASST trial show?

A

in pts with septic shock on NAdr, when adding either vasopressin or Adr as a 2nd line agent, no difference in mortality, MI, mesenteric ischaemia & other important outcomes although a post hoc analysis found lower rates of progression to renal failure & less RRT in pts with vasopressin as their 2nd line vasopressor.

42
Q

What did the VANISH trial show?

A

Vasopressin vs NAdr in septic shock: no difference in mortality, incidence & severity of AKI, rates of renal failure, requirement for RRT

43
Q

What’s dopamine & it’s evidence base in sepsis?

A

synthetic analogue of dopamine

small RCTs: no strong evidence of benefit cf Adr or dopamine

44
Q

What was the bottom line of the TRISS trial?

A 
2014, NEJM
compared conservative (70g/L) vs liberal (90g/L) Hb targets in pts with septic shock
no difference in 90 day mortality & ischaemic event rate, including for pts with cardiac disease, older age & more severe physiological derangement. Less transfusion in the conservative group.
45
Q

What’s the bottom line regarding early goal-directed therapy?

A

while pts with sepsis may require organ support, early aggressive & invasive haemodynamic management (eg. the CVP, MAP & SvO2 goals of the 2001 Rivers trial) are associated with significant costs without significant benefit; more recent multi-centre RCTs: PROCESS, PROMISE & ARISE, haven’t reporduced mortality benefits of The Rivers trial.

46
Q

What’s the bottom line on steroids in sepsis?

A

relative adrenal insufficiency or glucocorticoid resistance exists in sepsis
pts with septic shock, on steroids, have improvement in vasopressor response
Pts with septic shock receiving hydrocortisone plus fludrocortisone had lower 90-day mortality & shorter duration of mechanical ventilation & vasopressor therapy & days with organ failure.
Higher rates hyperglycaemia.

47
Q

What proportion of pts with sepsis have DIC?

A

30-50%

48
Q

What may be benefits of anticoagulation in sepsis?

A

reduce disordered coagulation
reduce the inflammatory signals that result from the coagulation cascade
many pts with sepsis often have other risk factors for VTE

Fellowship revision (78 decks)

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