Critical Care Resuscitation Flashcards

Resus topics, critical care/ICU

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1
Q

What is your approach to RSI intubation (8 P’s)

A

Preparation: Room, airway equipment, suction, monitor, IV access
Personnel: RT
Pre-oxygenation: NRB mask for spontaneously breathing patient, ventilate if hypoxic
Positioning
Plan A
Plan B: ?emergency airway
Paralysis
Post intubation management/confirm placement, Vent settings

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2
Q

For an RSI what is the dose for: (avg 80 kg)

  • Propofol
  • Ketamine IV
  • Ketamine IM
  • Etomidate
A
  1. Propofol: 1.5-2 mg/kg (120mg)
  2. Ketamine IV: 1.5 mg/kg (120 mg)
  3. Ketamine IM: 3 mg/kg (240 mg)
  4. Etomidate IV: 0.3 mg/kg (24 mg)
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3
Q

For an RSI what is the paralytic dose for Suxx and Roc?

assume 80 kg

A

Succ: 1.5 mg/kg = 120 mg
Rocc: 1.2 mg/kg = 96 mg (standard dose nonRSI is 0.6mg/kg)

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4
Q

Physiology: What are the actions of Alpha 1 and Alpha 2 receptors?

A

Alpha-1 agonists cause vasoconstriction

Alpha-2 agonists causes vasodilatation esp of coronary arteries

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5
Q

Physiology: What are the actions of Beta 1 and 2?

A

Beta-1 agonists increases HR and cardiac contractility –> increased CO

Beta-2 agonists dilate small coronary A’s, visceral organ A’s, skeletal muscle A’s
and increase bronchodilation

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6
Q

Physiology: What are the actions of Dopamine receptors?

A

There are 7 types of dopamine receptors.
D4 agonists increase cardiac contractility.
D1 and D2 agonists increase renal diuresis and naturesis

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7
Q

Physiology: What is the action of vasopressin receptors?

A

V1 agonists cause vasoconstriction mostly in peripheral arterioles

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8
Q

What is the preferred vasoactive agent for Anaphylactic shock?

A

Epinephrine
alternative is Norepi
Dose:

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9
Q

What is the preferred vasoactive agent for Cardiogenic shock? (LV dysfunction)

A

If SBP 90 - Dobutamine (for ionotropy B1, B2)

2nd line Alternative: Milrinone (not in MI)

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10
Q

What is the preferred vasoactive agent for Cardiogenic shock secondary to PE?

A

Dobutamine

Alternative: Norepi

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11
Q

What is the preferred vasoactive agent for Hemorragic shock?

A

Volume/ blood resusitation

Dopamine for temporizing

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12
Q

What is the preferred vasoactive agent for Neurogenic shock?

A

Dopamine
NE is most commonly used..
2nd line Alternative: Norepi, Phenylephrine

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13
Q

What is the preferred vasoactive agent for Septic shock?

A

Norepinephrine
Epinephrine
Dobutamine
Dopamine* (only in bradycardia + low risk for arrythmias)

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14
Q

When is dopamine recommended to be used in septic shock?

A

Dopamine is suggested to not be used as an alternative to norepinephrine in septic shock, except in highly selected patients such as those with inappropriately low heart rates (absolute or relative bradycardia) who are at low risk for tachyarrhythmias (Grade 2C). Dopamine is recommended to not be used in low doses in a so-called renal-protective strategy (Grade 1A).
(Surviving sepsis guidelines)

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15
Q

What is the mechanism and effects of Epinephrine?

A

Vasopressor, Inotrope
incr a1, a2, b1, b2
Incr HR, SV, CO, vasoconstriction at higher doses

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16
Q

What is the mechanism and effects of Norepinephrine?

A

Vasopressor + Inotrope
Incr a1 +/- a2, B1, B2
Incr vasoconstriction and mild increase in CO

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17
Q

What is the mechanism and effects of Phenylephrine?

A
Vassopressor
Pure alpha agonist - vasoconstriction
Incr BP (SVR)

Only temporizing has risk of tachyphylaxis can’t use long term

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18
Q

What is the mechanism and effects of Dopamine?

A

Vasopressor + Inotrope
DA at low doses (incr renal perfusion)
Incr a1, a2, B1
Incr CO, Vasoconstriction at higher doses

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19
Q

What is the mechanism and effects of Dobutamine?

A

Inotrope
incr B1, B2
Increases CO, SV

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20
Q

What is the mechanism and effects of Milrinone?

A

Inotrope
Inhibits PDE3 preventing breakdown cAMP incr intracellular Ca causing nice contractility

Incr diastolic relaxation, CO, vasodilation

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21
Q

What is the mechanism and effects of Vasopressin?

A

Vasopressor
Incr levels of IP3 and DAG which cause in intracellular Ca
Incr peripheral vasoconstriction

22
Q

Sepsis: Fluid resuscitation end points/ thing you monitor - name 5

A
  1. lactate clearance
  2. Physiologic parameters
  3. u/o want minimally 0.5cc/kg/hr
  4. IVC - not great indicator
  5. CVP
  6. Mentation/ Signs of reperfusion
  7. Can look at pulse pressure variation
23
Q

Name main findings of the Kumar 2006 and 2009 studies

A

Kumar 2006 N= 2731
- Incr mortality 10% delay first hour. Every hr incr 7.5% mortality

Kumar 2009
4000 pts. Regardless of etiology 5x mortality if inappropriate Abx so choose wisely

24
Q

What are indications for intubation?

A
  1. Failure to ventilate
  2. Failure to oxygenate - needing positive pressure to improve oxygenation
  3. Failure to maintain airway (secretions, decr GCS)
  4. Anticipated clinical course (OR, inevitable airway compromise)
  5. Evidence of neck, airway or vascular injury (similar to pt 4)
25
Q

What factors assist in predicting difficult larygnoscopy? (5)

A

LEMON
Look externally for signs of difficult intubation (by gestalt, c-spine)
Evaluate the “3-3-2 rule”
(pt’s fingers - 3 fingers between incisors, 3 fingers submandibular space, 2 fingers from cricoid to floor of mandible ‘thyroid-hyoid distance)
Mallampati
Obstruction or obesity
Neck mobility

26
Q

How do you evaluate for difficult BVM?

A
MOANS
Mask seal (beard)
Obesity/obstruction
Age
No teeth
Stiffness (to ventilation - stiff lungs)
BOOTS
Beard
Obese
Old
Toothless
Snoring
27
Q

How do you evaluate for difficult insertion and use of an extraglottic device?

A
RODS
Restricted mouth opening
Obstruction or obestity
Deformity of anatomy (wont get good esophageal seal and indirect oxygenation..)
Stiffness (to ventilation)
28
Q

How do you evaluate for a difficult Cricothryoidotomy?

A
SMART
Surgery
Mass (abcess, hematoma)
Access/Anatomy distorted (obesity, edema)
Radiation
Trauma (distortion, subQ air)
29
Q

In an RSI, what is the purpose of pre-oxygenation?

A

It washes out the nitrogen in the alveoli/ functional residual capacity of the pt so that they will have a longer ability to be apneic without getting hypoxic.

30
Q

Even in an unconscious patient, why do we use induction agents?

A
  1. Enhances effect of paralytic and improves intubating conditions because it is being done at the earliest phase of the neuromuscular blockade.
  2. May help attenuate response to airway manipulation
31
Q

ddx of hypovolemia and bradycardia?

A

Elderly
BB, CCB
Intra-abdominal pathology stimulating vagal tone
Neurogenic shock

32
Q

What are the SIRS criteria?

A

Temp >38 or 20 or paCO2< 32

WBC >12 or 90

33
Q

What are 6 complications of sepsis?

3A’s 3 D’s

A
Acute Renal failure (Pre-renal --> ATN)
ARDS
Acute hepatic dysfunction
DIC
Decr. LOC
Death
34
Q

What lab values do you expect in DIC?

A
  • Incr PT/INR, PTT, D-dimer
  • Low fibrinogen
  • Decr. RBCs, platelets (due to consumption)
35
Q

What antibiotics cover Pseudomonas?

A
  • Piptazo
  • Ceftazidime, Cefepime
  • Ciprofloxacin
  • Aminoglycosides (tobramycin, gentamicin)
  • Meropenum, imipenem
  • Aztreonam
36
Q

Which antibiotics cover anerobes?

A
  • Metronidazole
  • Ciprofloxacin
  • Piperacillin/Tazobactam
  • Ampicillin/Sulbactam
  • Amoxicillin/Clavulanate
37
Q

Whats the ‘Rosen’s’ definition of shock?

A

Need 4 criteria

  1. Decr LOC or looks ill
  2. HR >100
  3. RR>22 or PCO2
  4. Base def 4
  5. U/O 20 minutes duration
38
Q

Of the physiologic parameters that we monitor when treating shock +/- sepsis which is best?

A

Urine output. want minimum 0.5 cc/kg/hr.

in peds 1cc/kg/hr. if less than 1 y.o target is 2 cc/kg/hr.

39
Q

With regards to Acid base status what is the natural progression in shock?

A
  • start off with respiratory alkalosis
  • mild metabolic acidosis
  • severe metabolic acidosis with severe lactatemia (due to inadequate tissues perfusion)
40
Q

What is the equation for the buffer system in the blood?

A

CO2 + H2O H2CO3 HCO3- + H+

41
Q

At what pressure are you worried about intra-abdominal compartment syndrome?

A

> 12 mmHg

42
Q

What are 5 contraindications for NIPPV?

A
  1. Inability to protect airway or clear secretions.
  2. Impaired consciousness (including agitated/uncooperative patients).
  3. Cardiac or respiratory arrest.
  4. Hemodynamic instability.
  5. Facial surgery/trauma/deformity.
  6. Pneumothorax.
  7. Upper airway obstruction.
  8. Complicated multi-organ failure.
  9. Recent esophageal anastomosis
43
Q

In which conditions is there strong evidence for the use of NIPPV?
intermediate evidence? weak evidence?

A
  1. Severe COPDE
  2. CHF - cardiogenic pulmonary edema
  3. Respiratory failure in the immunocompromised

Intermediate evidence: Asthma, Community-acquired pneumonia, DNR/DNI patients.

Weak evidence: Trauma, Neuromuscular diseases (e.g., myasthenia gravis), Cystic fibrosis.

44
Q

What are 10 causes of elevated lactate?

A
Think of increased production and decreased clearance. 
OR categories
1. Shock
- Distributive, Cardiogenic, Hypovolemic, Obstructive.
2. Post cardiac arrest
3. Regional tissue ischemia
- Mesenteric ischemia
- Limb ischemia
- Burns
- Trauma
- Compartment syndrome
- Necrotizing soft tissue infections
4. DKA (lactate irrelevant for prognosis)
5. Drugs/Toxins
- Alcohols
- Cocaine
- CO/CN
- Metformin, propofol, Linezolid, B2 agonists, INH
6. Anaerobic muscle activity
- Seizure
- Heavy exercise
- Excessive WOB (severe asthma - lactate irrelevant for prognosis)
7. Thiamine Def
8. Malignancy
9. Liver failure
10. Mitochondrial disease
45
Q

Trouble shooting with difficult airway with failed intubation (BBBARS)

A
Best look larygnoscopy
Bougie, Blade change
Alternative (VL)
Rescue ( Supraglottic/LMA)
Surgical (Circothyroidotomy)
46
Q

The use of albumin has associated increased mortality in which patient population?

A

Patients with traumatic brain injury.

  • assoc with incr ICP.
  • May have benefit in early sepsis.

SAFE study in new Zealand and Australia found this.

In general albumin should not be used for resuscitation per se.

47
Q

Why is HES (Hydroxyethyl starch) NOT recommended for resuscitation?

A

HES has been associated with incr incidence of renal failure and subsequent renal replacement therapy.

  • this is because older agents had high molecular weight and would accumulate in the skin, liver and kidney
  • some trials have shown incr risk of mortality also.
48
Q

Why is there lactate in Ringer’s Lactate?

A

Bicarbonate is unstable in plastic containers so lactate acts as an anion and is metabolized into bicarb by the liver.

49
Q

What is the pH of Ringers lactate?

A

pH 6.5

  • however it is an alkalizing solution.
  • Note RL is more hypotonic than extracellular tissues
50
Q

What is the pH of Normal saline?

A

pH 5.5
- is an isotonic solution to the extracellular tissues
(therefore if stays intra-vascularly there wont be a large gradient resulting in worsening interstitial edema)

51
Q

What are the components of Normal saline and Ringers lactate?

A

NS (isotonic)
Osm 308 (blood 291)
Na- 154 mmol/L
Cl- 154 mmol/L

RL (hypotonic)
Osm 280
Na - 131 mmol/l
Calcium - 2.2
Cl - 111
K - 4
Lactate 28
52
Q

What is the difference between a mixed venous saturation (ScO2) and a central venous saturation (ScVO2)?

A
  1. Mixed venous (ScO2)- need a swan ganz cath to get it. our usual target is greater than 70%. Is blood from both the upper and lower extremities.
  2. Central venous (ScVO2) - get from central line. Target greater than 60%, but may be 70% by some…?
    represents blood from the upper half of body. The brain extracts more O2 because of its high metabolic demands.