Drug
Levophed (norepi)
Receptors
Alpha 1&2 > Beta 1 >>> Beta 2
Effects
Vasoconstriction, increase SVR,
minimal increase in HR
Uses
Shock, especially sepsis
Dopamine
(Low dose 0.5-2 mcg/kg/min)
Dopaminergic
(Low dose)
Vasodilatation
(Low dose)
Renal dose
(Mod dose 2-10 mcg/kg/min)
Beta 1 >>> Beta 2
(Mod dose)
Inotrope and chronotrope –
increases HR, CO, contractility
(Mod dose)
Postop heart surgery
(High dose >10 mcg/kg/min)
Alpha 1
Alpha 1
(High dose)
Vasoconstriction, increase SVR
Vasoconstriction, increase SVR
Vasopressin
V1 and V2
Arterial vasoconstriction
Epinepherine
Alpha 1 & 2 (high dose = alpha >
beta)
Beta 1 & 2
Dobutamine
Beta 1, Beta 2 >>> Alpha 1
High dose = alpha receptor
vasoconstriction
B1 = inotrope, increase
HR/CO/contractility
Minimal B2 effects.
INOTROPE, NOT A PRESSOR
Minimal alpha
B1: Increases HR, CO, and
contractility
B2: Vasodilatation
Positive intropic, vasodilating, and
minimal chronotropic effects
(despite B1).
Neosynepherine
Milrinone
Isoproterenol
Cyclic-AMP specific
phosphodiesterase (PDE) inhibitor
Beta 1 and 2
B1: Increases HR, CO, and
contractility
B2: Vasodilation
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
Adverse Effects
Decreased tissue/organ perfusion.
Must ensure pt has adequate
intravascular volume.
Arrythmogenic, prone to
tachyarrythmias at higher doses
(High dose)
Shock
1)
Head bleeds to maintain CPP
goals
2) Neurogenic/spinal shock
3) To reverse hypotension with
anesthesia
Not titratable, either on or off.
Adjunct to levophed, usually start
when levo > 10.
1) Anaphylactic shock
2) CODES
3) All shock except cardiogenic
Reflex bradycardia (due to no beta
effects)
1)
2)
3)
Hypotension if used as a pressor.
1)
2)
3)
1)
2)
3)
Assist cardiac function
CHF
Adjunct in septic shock if
cardiac dysfunction of sepsis is
present
Assist cardiac function
CHF
Adjunct in septic shock if
cardiac dysfunction of sepsis
present
Assist cardiac function
CHF
Adjunct in septic shock if
cardiac dysfunction of sepsis
present
Decrease gut perfusion, do not use
in suspected mesenteric ischemia.
LAST RESORT
Avoid with cardiogenic shock as
increases myocardial O2 demand.
Most dysrhythmogenic
Ventricular arrhythmia
Electrolyte abnormalities
Long half-life (1-2 hours)
Angina, Adams-Stokes attacks,
pulmonary edema, hypertension,
hypotension, tachyarrhythmias (esp
ventricular)
Septic Shock
1) Check central venous O2 – less than 70% implies decreased DO2 and cardiac dysfunction of
sepsis can be implied if:
a.
CVP 8-12
b. HCT >= 30% or Hgb >= 10
c.
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)
a. pCO2
i. > 40 = primary respiratory acidosis
1. Acute (pH decrease by 0.08 for PaCO2
increase of 10mmHg)
2. Chronic (pH decrease by 0.03 for PaCO2
increase of 10mmHg)
ii. < 40
1. Respiratory compensation for metabolic
acidosis
PaCO2 >= [HCO3+] * 1.5 + 8
[+ or – 2.0]
2. Concurrent respiratory alkalosis
PaCO2 < [HCO3+] * 1.5 + 8
[+ or – 2.0]
b. HCO3
i. < 24
1. Primary metabolic acidosis (if PaCO2 <
40)
2. Concurrent metabolic acidosis (if PaCO2
> 40)
ii. > 24
1. Metabolic compensation
HCO3 <= 24 + 0.4 * (PaCO2 – 40)
2. Concurrent metabolic alkalosis
HCO3 > 24 + 0.4 * (PaCO2 – 40)
C) pH > 7.40 (Alkalosis)
a. pCO2
i. < 40 = Primary respiratory alkalosis
ii. > 40
1. Respiratory compensation to metabolic
alkalosis
PaCO2 <= 40 + [0.7 * (HCO3 –
24) ]
[+ or – 1.0]
2. Concurrent respiratory acidosis
PaCO2 > 40 + [0.7 * (HCO3 – 24)
]
[> + 1.0]
b. HCO3
i. > 24
1. Primary metabolic alkalosis (if PaCO2 >
40)
2. Concurrent metabolic alkalosis (if PaCO2
< 40)
ii. < 24
1. Metabolic compensation to respiratory
alkalosis
HCO3 >= 24 – 0.4 * (40 – PaCO2)
2. Concurrent metabolic acidosis
HCO3 < 24 – 0.4 * (40 – PaCO2)