Volume Ventilation NS (isotonic): Uses- ^ circulating plasma volume when RBCs adequate. Shock.

Fluid replacement in pts c

CMV- Ventilator controls all breaths. Delivers breaths @ set Vt and rate. Pt may require sedation/neuro DKA. Hyponatremia. Blood tx. Resuscitation. Metabolic alkalosis. Hypercalcemia. // Do not use in pts c HF,
blockade to tolerate. If pt attempts to breathe, ventilator dyssynchrony occurs causing ^ intrathoracic edema, hypernatremia because NS replaces extracellular fluid & can lead to fluid overload. Replaces
pressures and barotrauma. losses w/out altering fluid concentrations. Helpful for Na+ replacement.
LR (isotonic): NS c electrolytes (K+, Ca2+) & (lactate) buffer. Uses- Replaces fluid & buffers pH.
AC- Senses pt’s inspiratory effort & completes inspiration of basis on the set Vt. Ventilator supports every Hypovolemia r/t third spacing. Dehydration. Burns. Lower GI tract fluid loss. Acute blood loss. // Similar
inspiratory effort. If pt unable to assist c inspiratory effort, ventilator will deliver controlled breath. Pt electrolyte content c serum but doesn’t containing Mg. Has K, therefor don’t use c renal failure. Don’t use in
breathing rapidly may need a different mode or sedation to prevent hyperventilation. liver disease because the pt cant metabolize lactate; a functional liver converts it to bicarbonate; don’t give
if pts pH >75
SIMV- Delivers set # of breaths @ set Vt and synchronizes with pt’s effort. Breaths the pt takes between ½ NS (hypotonic): Use- water replacement. Raises total fluid volume. DKA after initial NS & before
ventilator-delivered breaths are not assisted with a set Vt. dextrose infusion. Hypertonic dehydration. Na+ & Cl- depletion. Gastric fluid loss from NGT
Pressure Ventilation suction/vomiting. // Caution- may cause CV collapse or ^ I ICP. Don’t use in pts c liver disease, trauma, or
PCV- Delivers preset # of breaths augmented by a preset amount of inspiratory pressure. Time cycled to burns. Helpful for establishing renal function. Fluid replacement for clients who don’t need extra glucose
end inspiration & begin expiration. Used to provide full ventilator support in pts c noncompliant lungs & poor (diabetics)
oxygenation (ARDS, rising PIP & plateau pressures). Can be used c reversed inspiratory to expiratory (I:E) D5W (hypotonic): Use- raises total fluid volume. Helpful in rehydrating & excretory purposes. Fluid loss and
ratio & is called pressure controlled/inverse ratio ventilation (PC/IVR). Pts on PC and PC/IVR may need dehydration. Hypernatremia. // can cause hyperglycemia. Caution in pts c CV or renal disease, may cause
sedation/neuromuscular blocks. fluid overload.
D5NS (hypertonic): Use- hypotonic dehydration. Replaces fluid Na+, Cl-, & cals/ temp tx of circulatory
PSV- Provides set amount of inspiratory pressure when pt initiates spontaneous breath. RR & Vt insufficiency & shock if plasma expanders not available. SIADH. Addisonian crisis. // Do not use in pts c
completely dependent on pt. *This mode may be used alone or added to SIMV to support pt-initiated, non- cardiac or renal failure because of danger of HF & pulmonary edema. Watch for fluid volume overload.
Vt supported breaths, or pts ready to wean, or discomfort r/t ^ airway resistance, D51/2NS (hypertonic): Use- DKA after initial tx c NS & ½ NS, prevents hypoglycemia & cerebral edema
(occurs when serum osm. Decreased rapidly). // In DKA, use only when glucose falls <250. Most common
PEEP/CPAP- Maintains preset pressure within ventilator circuit @ end of expiration. Prevents closure of postop fluid. Useful for daily maintenance of body fluids & nutrition, & for rehydration.
small airways & terminal alveoli during expiration, maintaining functional residual capacity & improving D5LR (hypertonic): Use- same as LR plus provides about 180 cals per 1000mL. source of water,
oxygenation. *Prevents atelectasis, improves lung volume. Set between 5-15 cm H20 (>10 caution!) electrolytes, & cals or as an alkalinizing agent.

Adrenergic Location/Response to Stimuli Cholinergic Location/Response to

Dexmedetomidin Sedation; may cause bradycardia & hypotension! 200 mcg/50 mL NS
Receptor Receptor Stimuli
e Conc: 4 mcg/mL
Site Sites
(Precedex)
Sedative/Hypnotic Onset: Rapid Peak: Unknown Maintenance: 0.2-0.7 a1 Arteries & veins (constriction) Nicotinic All ANS ganglia
a2 agonist Duration: Unknown Half-Life: 2 h mcg/kg/hr Bladder neck (contraction) (N) (stimulation of SNS &
Eyes (mydriasis/dilation of pupil) PSNS)
Propofol Short-acting hypnotic; produces amnesia. No 500 mg/50 mL or 1000
Male sex organs (ejaculation) Adrenal medulla (release
(Diprivan) analgesic properties. mg/100 mL
Prostatic capsule (contraction) of epinephrine)
General Anesthetic Conc: 10 mg/mL
Shake vial first. Do not filter. Change IV tubing a2 CNS (inhibits release of norepinephrine) Nicotinic Neuromuscular junction
Q12h. monitor VS Q5min X 30 min initial. 5 mcg/kg/min for minimum B1 Heart (increased rate, +inotrope, ^AV (M) (contraction skeletal
of 5 min; Titrate 5-10 conduction) muscle)
mcg/kg/min Q5min Kidneys (release of renin)
Onset: 40 sec Peak: Unknown B2 Arterioles (dilation) Muscarinic Eye (miosis/constriction,
Duration: 3-5 min Half-Life: 3-12 hour Range: 5-50 mcg/kg/min Bronchi (dilation) accommodation)
Fentanyl Pain relief, sedation 1250 mcg/250 mL NS Liver (glycogenolysis) Heart (decreased HR,
(Sublimaz) Conc: 5 mcg/mL Skeletal muscle (contraction) contractility, conduction)
Opioid Analgesic Uterus (relaxation) Lung (bronchoconstriction,
Onset: 1-2 min Peak: 3-5 min Maintenance variable. Dopamine Vessels (peripheral vasodilation) ^ bronchial secretions)
Duration: 0.5-1 h Half-Life: 2-4 h Start @ 10-20 mcg/hr 1 Proximal tubule (maintain/^ GFR) Blood vessels
Midazolam Short-term sedation, post-op amnesia 100 mg/100 mL NS Renal tubules (natriuresis & diuresis) (vasodilation, hypotension)
(Versed) Conc: 1 mg/mL Dopamine Vessels (peripheral vasodilation) GU (micturition)
Benzodiazepine 2 Glomerulus (decreased renal blood flow) GI (^ salivation, tone,
Maintenance: 0.5-1 mg/hr Renal nerves (decreased GFR) motility, secretions,
(>60 y/o); 0.5-2 mg/hr (<60 Adrenal cortex (decreases Na & H20 defecation)
Onset: 1.5- 5 min Peak: Rapid y/o); 1-5 mg/hr (mech vent excretion & decreased aldosterone) Sweat glands (^sweating)
Duration: 2-6 h Half-Life: 2-6 h pt) Sex organ (erection/
vasodilation)

Dopamine Indication: shock states: cardiogenic, sepsis; post- 400 mg/250 mL D5W Epinephrine Indication: low output states, cardiac arrest, shock 8 mg/500 mL
Inotropic/ cardiac sx. Immediate precursor of Conc: 1600 mcg/mL a & b agonist states, asthma, anaphylaxis Conc: 16 mcg/mL
Vasopressor norepinephrine. Neurotransmitter in CNS & PNS. Typical: 1-2 mcg/kg/min *Cardiac effects are mediated though B receptors:
a1, dopaminergic Decreases aldosterone secretion in the adrenal 0.005-0.02 mcg/kg/min = ^HR + inotropic effect, Start at 0.5 to 1.0 mcg/min
agonist cortex. Inhibits TSH, prolactin release, & insulin Duress: 2mcg/kg/min vasodilation = decreased SVR Maintenance: 1-4 mcg/min
secretion. (B>alpha); ^HR, *Vascular effects mediated through a receptors @
Admin via PICC or CVC if possible. Max: 20 mcg/kg/min CO, SVR high doses: ^SVR, ^BP, renal artery
vasoconstriction
2-10 mcg/kg/min = ^ contractility (B stim) Side Effect: restless, ^HR,
Side Effect: nausea, *B2 stimulation = bronchodilation
>10 mcg/kg/min = vasoconstriction (a stim) ^BP, CVA, angina,
emesis, tachyarrhythmia, hypokalemia,
profound vasoconstriction Onset: Rapid Peak: 20 min
Onset: 1-2 min Peak: 10 min hypophosphatemia
Duration: 20-30 min Half-Life: Unknown
Duration: <10 min Half-life: 2 min Norepinephrine Indication: hypotensive states, cardiogenic shock, 8 mg/500 mL NS
Dobutamine Indication: CHF, shock states: cardiogenic, 500 mg/250 mL D5W (Levophed) GI bleeding. Dose dependent; low dose = B stim, Conc: 16 mcg/mL
Inotropic sepsis. Synthetic catecholamine, directly stim B1, Conc: 2000 mcg/mL Vasopressor high dose = a stim. Vasoconstriction, ^SBP & Typical: 2 mcg/min
a1, (B1), B2 B2, a receptors. Directly ^ myocardial contractility Typical: 1-2 mcg/kg/min a1, mild B1 agonist coronary blood flow; a1 effects > B1 effects.
agonists & HR while lowering PVR. Stimulates B1 with ^contractility + ^HR= ^CO Duress: 5-10 mcg/min
minor effect on HR or peripheral blood vessels. ^ Duress: 2mcg/kg/min
contractility & HR; some B2 effect can be more Start @ 0.05-0.1 mcg/kg/min & titrate up.
Max: 20 mcg/min
(B1>B2); B2 can pronounced than a1 effect; resulting in some Max: 20 mcg/kg/min
sometime vasodilation (monitor for initial hypotension), Onset: Immediate Peak: Rapid
decrease SVR & decreases CVP. Admin via PICC or CVC if Duration: 1-2 min Half-life: 2 min Side Effect:
BP possible. Do not administer in alkaline solutions tachyarrhythmias, h/a,
Side Effect: dysrhythmias tremor, restless, ^BP
Onset: 1-2 min Peak: 20 min
Duration: Brief Half-life: 2 min

Phenylephrine Pure a stim; effects primarily vascular, causing 50 mg/500 mL NS Nitroglycerin Indication: cp r/t MI, preload reduction, afterload 25 mg/250 mL D5W
(Neo-synephrine) vasoconstriction resulting in ^SBP and ^DBP, Conc: 100 mcg/mL Vasodilator reduction. Systemic & pulmonary venodilation, decreased Conc: 100 mcg/mL
Vasopressor ^PAP. Coronary & renal arteries constrict. If Typical: 10-20 mcg/min LV and RV filling pressures. Decreased LV pressure
a1 agonist vasoconstriction severe, blood flow to vital organs volume relationship, decreased aortic impedance, Maintenance: 5-50
could decrease. Indirect effect: release of Duress: 50-100 mcg/min decreased RV & LV afterload, dilation of coronary mcg/min
norepinephrine from storage sites. @ large doses, arteries, improvement of ischemic zone, ^ CO, decreased
could stim B1 receptors. Max: 200 mcg/min BP. Side Effect: low BP,
nitrate tolerance
Onset: Immediate Peak: Unknown Onset: Immediate Peak: Unknown
Duration: 15-20 min Half-Life: 2.5 h Duration: Several min Half-Life: 1-4 min
Vasopressin Larger doses: a stim causing vasoconstriction. 20 units/100 mL NS Sodium Indication: severe HF c ^SVR, mitral regurgitation to 50 mg/250 mL
Antidiuretic Alters permeability of renal collecting ducts, Conc: 0.2 unit/mL Nitroprusside decrease afterload & improve forward flow out of the Conc: 200 mcg/mL
Hormone allowing reabsorption of water; ^ SVR and MAP Typical: 0.01 units/min (Nipride) ventricle, low CO syndrome with ^SVR, hypertensive
Vasodilator crisis.// Direct vasodilator c balanced effect on the Maintenance: 0.3-5
Onset: Unknown Peak: Unknown Max: 0.04 units/min arteriolar & venous systems. Rapid lowering of BP, mcg/kg/min
Duration: 30-60 min Half-Life: 10-20 min decrease cardiac preload & afterload.
Side Effect: cyanide
Milrinone Indication: low CO state, acute CHF, 40 mg/200 mL or 20
Onset: Immediate Peak: Rapid poisoning
(Primacor) cardiomyopathy. Positive inotrope. ^ myocardial mg/100 mL
Duration: 1-5 min Half-Life: 2 min
Inotrope contractility, decreases preload & afterload by a Conc: 200 mcg/mL
direct dilating effect on vascular smooth muscle. Nesiritide Brain natriuretic peptide, identical to endogenous BNP. 1.5 mg/250 mL NS
Maintenance: 0.375 - 0.75 (Natrecor) Effects: vasodilation, natriuresis. Smooth muscle cell Conc: 6 mcg/mL
mcg/kg/min Vasodilator; BNP relaxation; dilates veins & arteries. Dose dependent Infusion: 0.01
reduction in PAOP & systemic arterial pressure in pts c mcg/min
HF c resultant decrease in dyspnea.
Onset: 5-15 min Peak: Unknown Onset: 15 min Peak: 1 h Side Effect:
Duration: 3-6 h Half-Life: 2.3 h Duration: 60 min Half-Life: 18 min hypotension