Drug / Receptors / Effects / Uses / Adverse Effects
Levophed (norepi) / Alpha 1&2 > Beta 1 > Beta 2 / Vasoconstriction, increase SVR, minimal increase in HR / Shock, especially sepsis / Decreased tissue/organ perfusion. Must ensure pt has adequate intravascular volume.
Dopamine / (Low dose 0.5-2 mcg/kg/min)
Dopaminergic
(Mod dose 2-10 mcg/kg/min)
Beta 1 > Beta 2
(High dose >10 mcg/kg/min)
Alpha 1 / (Low dose)
Vasodilatation
(Mod dose)
Inotrope and chronotrope – increases HR, CO, contractility
(High dose)
Vasoconstriction, increase SVR / (Low dose)
Renal dose
(Mod dose)
Postop heart surgery
(High dose)
Shock / Arrythmogenic, prone to tachyarrythmias at higher doses
Neosynepherine / Alpha 1 / Vasoconstriction, increase SVR / 1)Head bleeds to maintain CPP goals
2)Neurogenic/spinal shock
3)To reverse hypotension with anesthesia / Reflex bradycardia (due to no beta effects)
Vasopressin / V1 and V2 / Arterial vasoconstriction / Not titratable, either on or off. Adjunct to levophed, usually start when levo > 10. / Decrease gut perfusion, do not use in suspected mesenteric ischemia.
Epinepherine / Alpha 1 & 2 (high dose = alpha > beta)
Beta 1 & 2 / High dose = alpha receptor vasoconstriction
B1 = inotrope, increase HR/CO/contractility
Minimal B2 effects. / 1)Anaphylactic shock
2)CODES
3)All shock except cardiogenic / LAST RESORT
Avoid with cardiogenic shock as increases myocardial O2 demand.
Dobutamine / Beta 1, Beta 2 > Alpha 1 / INOTROPE, NOT A PRESSOR
Minimal alpha
B1: Increases HR, CO, and contractility
B2: Vasodilatation / 1)Assist cardiac function
2)CHF
3)Adjunct in septic shock if cardiac dysfunction of sepsis is present / Hypotension if used as a pressor.
Most dysrhythmogenic
Milrinone / Cyclic-AMP specific phosphodiesterase (PDE) inhibitor / Positive intropic, vasodilating, and minimal chronotropic effects (despite B1). / 1)Assist cardiac function
2)CHF
3)Adjunct in septic shock if cardiac dysfunction of sepsis present / Ventricular arrhythmia
Electrolyte abnormalities
Long half-life (1-2 hours)
Isoproterenol / Beta 1 and 2 / B1: Increases HR, CO, and contractility
B2: Vasodilation / 1)Assist cardiac function
2)CHF
3)Adjunct in septic shock if cardiac dysfunction of sepsis present / Angina, Adams-Stokes attacks, pulmonary edema, hypertension, hypotension, tachyarrhythmias (esp ventricular)

Confirm the following:

A – Airway established and secured

B – Breathing adequate and work of breathing appropriate (sedation, analgesia, ventilation)

C(a) – Circulation optimization – fluids, inotropes, pressors, ensure appropriately resuscitated (crystalloids). Pressors are ineffective without adequate volume.

C(b) – Control O2 consumption – (sedation, fever, seizure control)

D – Delivery of O2 adequate. (O2 sats, Hgb, lactate, SmVO2) – Consider fluids, transfusion, pressors, inotropes.

E – Extraction of O2. Consider cyanide, met-Hgb, SEPSIS

Septic Shock

1)Check central venous O2 – less than 70% implies decreased DO2 and cardiac dysfunction of sepsis can be implied if:

  1. CVP 8-12
  2. HCT >= 30% or Hgb >= 10
  3. Lactate is normal (implying adequate resuscitation)

2)If CVO2 < 70%, may need inotrope. Start dobutamine in conjunction with pressor (Levophed). Titrate dobutamine to CVO2 sat > 70% and titrate Levophed to MAP affected by dobutamine.

Ventilator Management

(All kg-based calculations should be based on ideal body weight (IBW), not actual body weight, as lungs do not increase in size in relation to adipose tissue.)

Typically start off with A/C volume control, rate 12-14, FiO2 100%, PEEP 5, tidal volume 8-10mL/kg. As you titrate, you should become uncomfortable with any rate > 22, PEEP > 15, or tidal volume > 10mL/kg. Ask for help. Your friendly respiratory therapists are an excellent resource in the absence of staff.

Titrate down FiO2 to 30-40% if ABG’s show a reasonable pO2 and O2 sats are correlating. Don’t need to check an ABG after each change if O2 sats are reasonable.

If pCO2 high or low, adjust rate and/or tidal volume.

If pO2 high or low, adjust FiO2 and PEEP.

Difficulty ventilating/oxygenating despite adjustments of rate, TV, FiO2, and PEEP (i.e. refractory low pO2, high peak/plateau pressures):

  • Consider mucous plug, severe pneumonia (needs bronch?)
  • PE???
  • Consider pressure control ventilation to manage peak/plateau pressures – accept whatever tidal volume you can get and adjust rate accordingly
  • Consider starting nebulized Flolan – theoretically matches perfusion with ventilation by vasodilating vessels around alveoli which are being ventilated
  • Consider rotating patient to prone position – re-distributes atelectasis and secretions to better ventilate healthy lung (???)
  • Consider ultimate low-tidal-volume ventilation: THE OSCILLATOR!!! - Allows for oxygenation by diffusion, does not achieve ventilation so there is nothing you can do about pCO2.

ARDS – low tidal volume ventilation – decrease tidal volumes to be no more than 6mL/kg, keep plateau pressures < 30mmHg. Ok to have higher pCO2 due to lower minute ventilations as long as pO2 is adequate (permissive hypercapnea). Adjust rate accordingly.

  • Acute lung injury (ALL) = PaO2/FiO2 ratio of < 300
  • ARDS = PaO2/FiO2 ratio of < 200

ABG Interpretation

A)Check internal consistency of ABG (is the test calibrated correctly, do the values make sense?)

[H+] = 24 * (PaCO2 / [HCO3+] )

pH / 7.10 / 7.20 / 7.30 / 7.40 / 7.50 / 7.60
[H+] / 84 / 63 / 50 / 40 / 30 / 20

B)pH < 7.40 (Acidosis)

  1. pCO2
  2. > 40 = primary respiratory acidosis
  3. Acute (pH decrease by 0.08 for PaCO2 increase of 10mmHg)
  4. Chronic (pH decrease by 0.03 for PaCO2 increase of 10mmHg)
  5. < 40
  6. Respiratory compensation for metabolic acidosis

PaCO2 >= [HCO3+] * 1.5 + 8

[+ or – 2.0]

  1. Concurrent respiratory alkalosis

PaCO2 < [HCO3+] * 1.5 + 8

[+ or – 2.0]

  1. HCO3
  2. < 24
  3. Primary metabolic acidosis (if PaCO2 < 40)
  4. Concurrent metabolic acidosis (if PaCO2 > 40)
  5. > 24
  6. Metabolic compensation

HCO3 <= 24 + 0.4 * (PaCO2 – 40)

  1. Concurrent metabolic alkalosis

HCO3 > 24 + 0.4 * (PaCO2 – 40)

C)pH > 7.40 (Alkalosis)

  1. pCO2
  2. < 40 = Primary respiratory alkalosis
  3. > 40
  4. Respiratory compensation to metabolic alkalosis

PaCO2 <= 40 + [0.7 * (HCO3 – 24) ]

[+ or – 1.0]

  1. Concurrent respiratory acidosis

PaCO2 > 40 + [0.7 * (HCO3 – 24) ]

[> + 1.0]

  1. HCO3
  2. > 24
  3. Primary metabolic alkalosis (if PaCO2 > 40)
  4. Concurrent metabolic alkalosis (if PaCO2 < 40)
  5. < 24
  6. Metabolic compensation to respiratory alkalosis

HCO3 >= 24 – 0.4 * (40 – PaCO2)

  1. Concurrent metabolic acidosis

HCO3 < 24 – 0.4 * (40 – PaCO2)