New York-Presbyterian Hospital Weill Medical College of Cornell

New York-Presbyterian Hospital
Weill Medical College of Cornell University
Medical Intensive Care Unit
Medical Student Orientation Manual
April 2005
For exclusive use by students and house-staff physicians at the New York Presbyterian Hospital 5 South Intensive
Care unit.
Table of Contents
Part I: Policy and Procedures
2
Part II: Patient Care
How to Round in the ICU
Daily Presentations
Vascular Catheter Management
Naso/orogastric Tubes
2
Part III: ICU Curriculum
Airway Management
How to be a Code Leader
Shock
Interpretation of Hemodynamic Data
Introduction to Mechanical Ventilation
Principles of Sedation in the ICU
Selected Abstracts
9
Part IV: Medicated Drips used on 5 South
30
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Part I: Introduction
Welcome to the MICU critical care rotation. We hope find the rotation educational and enjoyable. Please read this
manual prior to starting on 5 South. This manual is an excerpt of the one written for housetaff physicians. Part II of
the manual contains information about patient care. The section “How to round in the MICU” is especially
important for students and junior house officers. It is designed to guide your evaluation of critically ill patients
during your morning pre-rounds. Each student should try to pick a patient to pre-round on and then present to the
team during Attending rounds. Please follow the standardized flow sheet for presenting data on morning rounds.
Section III of the manual is a basic critical care curriculum. It has a small collection of important abstracts.
Please remember to dress professionally while in the MICU. Please do not wear T-shirts or sweat shirts unless
under scrubs. You may assist on invasive procedures performed by credentialed providers.
Part II: Patient Care
How to Round in the MICU
Step 1: Data Collection
1.
Review overnight events with nurse and post-call intern or resident (e.g. spontaneous breathing trials, major
tests, episodes of hypotension, changes in antibiotics, dialysis sessions)
2
Degerm your hands and follow appropriate isolation procedure.
3
Global assessment (aka “Look around the room.”)
• Look for patient distress and level of sedation.
• Look at the drips and lines. Does the patient have appropriate IV access and monitors (e.g. A-line and
Foley)?
• Is the patient restrained? If so, can they be discontinued? If not, why?
4
Hemodynamics:
• Note rhythm and rate on monitor
• Record BP, HR, and, (for patients with right heart catheters) CO, PCWP, and PA pressure. Note all
trends.
• If a RHC is in place does the monitor show an appropriate PA tracing?
• Record doses of vasoactive drips and note all trends (dopamine and dobutamine recorded in mcg/kg/min;
norepinephrine and phenylephrine in mcg/min).
5
Fluid balance:
• Record I/O’s and weight for past 24hrs. Note the trend for the past few days.
• Record volume loss by ultrafiltration.
• Record all IVF the pt is receiving (including KVO lines and medications).
6
Respiratory status:
• Record ventilator settings: Mode, FIO2, machine rate, tidal volume, PEEP
• Record O2 sat, respiratory rate, exhaled tidal volume, and peak airway pressures
• Look for secretions.
• Record last ABG; note the vent settings when ABG was drawn.
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7
Focused physical examination:
• Look at the eyes (does pt. need corneal protection?)
• Examine neck veins
• Note ETT position
• Do the central venous catheters; PEG and trach sites look infected?
• Heart, lung, abdomen exam
• Are extremities cool or well perfused? Is there asymmetric limb enlargement (think DVT)?
• Look for dependent edema in sacrum, legs or flanks
• Note mental status.
 Is the head of the bed appropriately elevated if not contraindicated (greater than 30 degrees prevents
pneumonia)
8
ID:
• Record fever curve and WBC trend
• Review old cultures and sensitivities
• Record current ABX, duration of treatment and ABX levels
9
Review other labs:
• Especially note drug levels and trends in creatinine/Hgb
10 Review CXR
• Note position of all tubes; look for effusions, infiltrates, and pneumothorax
11. Record all meds
Step 2: Putting it all together; Systems
1.
Cardiovascular:
• Is the pt hypotensive, on pressors or in shock? If yes, why? (cardiogenic, volume depletion, vasodilatory,
or obstructive)
• Will the patient benefit from trial of intravascular volume expansion or inotropes?
• What is the purpose of each of the vasoactive drips? Can they be discontinued?
• What is the purpose of the each cardiac med?
2.
Pulm:
• Is oxygenation (pAO2: FiO2 ratio) normal? If no, why? Can FiO2 or PEEP be lowered?
• Is ventilation adequate? (pH, pCO2, end-tidal CO2)
• Are the peak airway pressures high (>32cmH2O)? If yes, why? (bronchospasm, edema, pneumonia, PTX,
secretions, excessive tidal volume)
• Is the patient tachypneic? If yes, why? (hypoxia, acidemia, pain, sepsis, anxiety, etc.)
• Why is this patient still on the ventilator? (e.g. weakness, secretions, airway protection)
• Can this patient have a trial of spontaneous ventilation? (Answer should be yes in most patients).
• If pt. is on spontaneous mode, note the rapid shallow breathing index: Resp Rate/TV in liters (RSBI >105
predicts extubation failure)
3.
Assessment of volume status:
• Is pt. euvolemic, volume overloaded or depleted? Determine by synthesis of data:
a) BP, pulse, CO and cardiac filling pressures (CVP, PCWP)
b) Urine output (oliguria = < one-half cc/kg/hr) and renal function
c) Assessment of "lung water” (rales, cxr, oxygenation, compliance)
d) Presence of dependent edema
• Goal of today's fluid balance (net in, out, or even)
• Change IVF and diuretics accordingly
4.
ID:
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•
•
•
•
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Is there an active infection? Is it resolving?
What is the role of the current ABX and their planned duration?
Are ABX doses correct for renal/liver function?
When is the next dose or level of intermittently dosed ABX due (e.g. vanc/aminoglycoside)?
For unexplained fever think: pneumonia (new infiltrate, secretions, decreased oxygenation), UTI, line
infection, DVT/PE, sinusitis, drug fever, C. diff
5.
Renal:
• Review renal function and trend
• Why is pt. azotemic? (e.g. volume depletion, shock induced ATN, Aminoglycosides/NSAIDS,)
• When is HD scheduled?
• ARE MEDS DOSED FOR RENAL FUNCTION?
6.
Heme:
• Is there bleeding or hemolysis?
• Is patient coagulopathic? If yes, why? Does pt. require blood products prior to a procedure today?
• If pt requires any blood product transfusions, is there an active type and screen listed in Cisyphus? (They
only last 48 hours.)
7.
Can patient be fed enterally? If yes, do it. If no, why not?
• Is the current feeding preparation adequate?
• Check serum Na; if elevated add free H2O enterally or hypotonic IV fluids.
8.
DVT prophylaxis: Heparin 5000 units tid or enoxaparin 40mg sc qd unless contraindicated
9.
Endo:
• Is the current diabetic regimen appropriate? If feeds will be held, should diabetic meds be changed?
10. GI prophylaxis indications: If intubated >48 hrs, burn, coagulopathy, neurosurgical disease, peptic ulcer disease
• Enteric PPI unless cannot take enteric medications (i.e. don’t waste money on IV meds)
11. Sedation:
• Can it be discontinued to allow wean?
• Should analgesia be added if pt in pain?
• Turn off sedation/paralytic and awaken patient at least daily; this decreases duration of intubation (NEJM
342; 2000: 1471-1477)
12. Other issues prn
13 Change meds from IV to enteric as soon as possible
14. Prognosis and code status and health care proxy
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Daily Presentation on Attending Rounds
1) Review events of previous 24 hours (e.g. procedures, intubation, extubation, spontaneous
breathing trials, dialysis, hypotension,)
2) Current BP, Pulse
3) Current drips (Levophed in mg/min; Dopa and DBA in mcg/kg/min; Neo in mcg/min,
vasopressin in units/min)
4) List central and arterial lines, drains and tubes
5) CVP
6) If Swan-Ganz catheter in place: PA pressure, PCWP, Cardiac Index, Mixed venous sat
7) Oxygen saturation, Respiratory rate and FiO2
8) Current vent settings: Mode of ventilator, Tidal Volume, RR set on machine, PEEP, Peak
airway pressure
9) ABG
10) Max and current Temp
11) Type and rate of IV fluid
12) Urine output last 2 hours
13) Total amount in and out past 24 hours
14) Last 4 Finger sticks
15) Type of Dialysis
If on CRRT: Ultra filtration rate, component and rate of replacement
fluid, component and rate of dialysate
16) Type and rate of nutrition
17) Abnormalities on physical examination
18) CBC, Chem-7, LFT
19) Drug levels and other pertinent labs
20) Blood, urine and sputum culture results
21) List each medication and the reason you are prescribing it (antibiotics with length of
therapy)
22) Type of DVT prophylaxis
23) GI prophylaxis
24) Head of bed elevated/not elevated at 45 degrees
25)
Type of advance directives
-5-
Vascular Catheter Management
Department of Medicine Protocol For Insertion and Maintenance of
Intravascular Catheters
(Applies to arterial, central venous, PICC and dialysis catheters)
•
Protocol designed to comply with the standard of care established by consensus by the CDC, ATS, SCCM, IDSA, ACCP (MMWR
2002; 51 No.RR-10)
I)
II)
III)
IV)
V)
VI)
VII)
VIII)
IX)
X)
XI)
XII)
XIII)
•
•
•
•
•
•
•
•
•
•
•
Choose appropriate catheter and location. Internal jugular and subclavian sites are preferred for
venous access (see below for merits of different sites) Get appropriate consent and supervision for
insertion
Have non-sterile assistant present
Degerm hands with Purell (wash hands first if soiled)
Clip hair at insertion site (do not shave)
Wear surgical mask, cap, and sterile gloves
Prep site with ChloraPrep
a) Release antiseptic by pinching wings on applicator to break ampule
b) Wet sponge by repeatedly pressing and releasing the sponge against the treatment area until liquid is
visible on skin (do not touch sponge)
c) Cleanse the site with repeated back and forth strokes of the sponge for a minimum of 30 seconds
d) Allow antiseptic to air dry for 30 seconds
Wear sterile gown and new pair of sterile gloves
Place large (full body) fenestrated drape for venous access. For radial arterial access place half size
blue sterile drape on table under arm and white fenestrated sheet over radial site
Flush catheter with sterile saline
Insert catheter, check for blood return, flush ports and suture in place
Remove sterile drape
Replace sterile gloves with a new pair from dressing change kit. Re-prep insertion site with ChloraPrep
from kit. Allow 30 seconds to dry
Place Tegaderm over site. Initial and date label
Remove catheters within 24 hours if they are not placed using above sterile technique
Remove femoral catheters within 24 hours unless there is no suitable alternative
Promptly remove catheter if local or systemic signs of infection are present or as soon as the
catheter is not essential
Guide-wire exchange is permitted if there is a low suspicion of catheter related infection and
there is high risk of mechanical complication from new catheter insertion
No routine catheter changes
Examine dressing and insertion site daily (after degerming hands) for signs of infection or loss of
dressing integrity
Degerm hands and wear mask and sterile gloves when changing dressing (follow step XII and XIII)
Degerm hands and swab access port with alcohol before accessing connector tubing for blood draws or
injecting medication. Clean cap and access port with alcohol before replacing cap.
Degerm hands and wear mask and sterile gloves when drawing blood directly from a central catheter
hub. Swab connections with alcohol before replacing cap or reconnecting tubing
Use dedicated port of a catheter for TPN
Gauze dressings are acceptable alternatives to Tegaderm
-6-
Advantages and Disadvantages of Different Approaches to Central Venous Catheters
The best approach is the one you are most skilled at. For the placement of a Right Heart catheter, the Right IJ and
then the Left SC are the preferred approaches. To limit the impact of a pneumothorax, consider using the side where
there is already lung disease (pneumonia or large effusion).
The internal jugular vein is accessible and can be compressed if bleeding occurs. The pneumothorax risk is lower
than with the subclavian approach, although the infection risk is slightly higher. The subclavian vein is resistant to
collapse during hypotension; however it is not easily compressible if bleeding or arterial puncture occurs. The
femoral vein approach is associated with higher risk of infection and thrombosis and prevents the patient from
getting physical therapy. It is easily compressible and may be used if the patient is coagulopathic or cannot lie flat.
Always make certain arterial puncture has not occurred; inspect the color of the blood and look for pulsatile flow.
The signs can be confusing if there is significant hypoxia or elevated venous pressure. If you are uncertain,
simultaneously measure blood gas from the puncture you have made and a true arterial puncture. If you have
punctured an artery remove the needle and compress the site (may need to compress for 15minutes. If the
subclavian artery was punctured compress above and below the clavicle. If an artery was cannulated with a large
bore catheter, leave the catheter in place and consult vascular surgery.
Venous air embolism can occur if a negative gradient exists. This is more likely to occur when patient is upright,
hypotensive, or during deep inspiration. To prevent this place the patient in trendelenberg position for neck lines
and always occludes the proximal opening of the needle and catheter with your sterile gloved finger when they are
in the vessel lumen. Always be sure the hub locks and tubing are tightly connected. Air embolism can cause
hypoxia, hypotension and CNS findings. If you suspect its occurrence inspect the entire catheter and tubing for
loose connections. Place the patient in the left lateral decubitus position and attempt to aspirate the air with a
pulmonary artery catheter
Swan-Ganz Catheters (RHC)
The RHC is a diagnostic rather than therapeutic tool. Place all right-heart catheters under the direct supervision of
the ICU attending or fellow. Review the proper placement and use of RHC at www.PACEP.org. When a RHC is in
use make sure a PA tracing is displayed at all times (because RV placement causes VT). Check PCWP by slowly
inflating the balloon with air; stop inflating when you see a PCWP tracing. If inflation with less than 1.5 cc of air
creates a PCWP tracing the RHC is “over-wedged” (i.e. advanced too far into the pulmonary artery) and must be
withdrawn. Inflation of the balloon with more air than is required to create a PCWP can cause pulmonary artery
rupture. The RHC is in good position when a PCWP tracing occurs with inflation of 1.5cc of air. Leaving a RHC
over-wedged can cause pulmonary infarcts. Always collect data by printing out a tracing after leveling and zeroing
the transducer. Obtain a printout by pressing “real-time record” and “wedge plug-in” on the monitor prior to balloon
inflation. Always evaluate pressure waveforms at end-expiration.
Guide Wire Changes
Guide wire exchange of vascular catheters is reserved for those patients at high risk of mechanical complications
from attempted line placement and who have suspected line sepsis. Do not attempt a guide wire exchange by
threading the wire through the distal hub! The indwelling catheter should be withdrawn to expose a sub-cutaneous
segment; the catheter should be cut with sterile scissors in the withdrawn segment; and the guidewire threaded
through the largest lumen (distal port). Once the guidewire has been advanced a sufficient distance, withdraw the
old catheter and culture the intravascular portion. Then, thread the new catheter over the guidewire and proceed as
usual. If the old catheter has a positive culture with > 15 colonies, the catheter site must be changed.
A chest radiograph must be ordered after a catheter is replaced via guide wire exchange to verify placement.
Antimicrobial Triple Lumen Catheter
The Cook antimicrobial catheter is impregnated with rifampin and minocycline for patients on TPN or who are at
high risk for infection and mechanical complication and who are not allergic to the impregnated antibiotics.
Nasogastric Tubes (NG Tubes)
-7-
Placement Technique
Optional: Anesthetize the nasal passage with 3-5 cc of 2% Viscous lidocaine.
Bend the patient’s head forward in a chin tuck position, the opposite of what you would do to open the airway.
If the patient is awake and alert, ask him to swallow. This will draw the tube into the esophagus
Measure the NGT from the nares to the TMJ to just below the sternum. Place the tube in only this far then check the
CXR. Do not remove the stylet of the silastic tube until the tube has been advanced into the stomach. In addition,
never replace the stylet once it has been removed. If the tube is perpendicular below the sternum you can advance it
into the stomach without checking another film. If the tube has gone into the airway, it will only be in as far as the
mainstem bronchi. As long as it is not used in this position, it should not cause harm
REMEMBER TO PRIME THE SILASTIC TUBE WITH 3-5 CC OF SALINE TO ACTIVATE THE LUBRICANT
AND ALLOW EASY REMOVAL OF THE STYLET.
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Part III: ICU Curriculum
Airway Management
The first priority in managing any critically ill patient is to secure the airway. Foreign bodies can obstruct the
airway as occurs during choking on food (treated with the Heimlich maneuver or extraction with Magill forceps).
The most common cause of airway obstruction in an unconscious patient, however, is occlusion by the tongue and
soft tissues of the pharynx. The following protocol enumerates steps to maintain a patent airway in an unconscious
patient. This protocol emphasizes manual ventilation and delays endotracheal intubation until adequate preoxygenation and ventilation have been performed. One of the most common errors made by physicians in
emergency situations is proceeding directly to endotracheal intubation without first establishing a temporarily secure
airway and manual ventilation.
Unconscious Patient with Stable Cervical Spine
I)
Determine if airway is patent by physical examination
• Assess for stridor
• Assess if chest wall rises and falls with each breath
• Assess breath sounds
II)
If airway is patent
• Provide supplemental oxygen if indicated
• Continue with general assessment of patient
III) If airway is not patent or inadequate spontaneous breathing
• Head tilt and chin lift to open airway
• Ask someone to set up suction apparatus with rigid suction catheter
• Attach bag-valve mask (BVM) to high flow (10L/min) oxygen
• Place BVM over patient’s face
• Press down with your thumbs on cephalad portion of mask against the bridge of the nose
• Press down with your index fingers on the portion of the mask covering the chin
• Gently lift the mandible toward the ceiling with your remaining three fingers on each hand
• A second operator compresses the bag to deliver tidal volume
• Adequate ventilation occurs when the chest wall rises with each breath delivered and condensation
forms in the mask upon exhalation. Excessive amounts of air should not leak out from the sides of the
mask.
• Ventilate at appropriate rate: e.g. 20/min if patient has severe metabolic acidosis or at slower rate (e.g.
12/min) if patient has chronic CO2 retention
IV) If chest wall does not rise with manual ventilation
• Repeat head tilt and chin lift
• Reposition seal with mask and re-attempt manual ventilation
IV) If chest wall still does not rise with manual ventilation
• Ask for an appropriate sized oral pharyngeal airway (should reach from tragus to ipsilateral angle of
the mouth when held against the side of the face)
• Temporarily remove BVM and inspect airway for secretions or foreign bodies
• If no foreign bodies found, insert an oral pharyngeal airway. The oral airway’s curved tip should face
the palate during insertion. Advance the oral airway between the palate and tongue until
approximately 2/3 of it lies within the mouth. Next, rotate the oral airway 1800 around its long axis so
that the curved tip points caudad. Advance the oral airway until the proximal end lies anterior to the
teeth and the distal end lies posterior to the tongue. A properly placed oral airway prevents the tongue
from occluding the airway.
• Repeat head tilt/jaw lift and replace BVM with a good seal
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II)
•
•
The above steps should secure the airway and provide adequate ventilation in the overwhelming
majority of patients
Manually ventilate the patient until he/she is adequately pre-oxygenated and someone skilled in
intubation is present and has equipment properly assembled
If you cannot manually ventilate a patient with a BVM, a true airway emergency exists. Get as much
help as possible and proceed to endotracheal intubation
Checking oral
airway for
correct size
Inserting the
oral airway
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Rotating the oral
airway into
position
Two operator
technique for
manual mask
ventilation
- 11 -
How to be a Code Leader
1)
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2)
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Pre-code responsibilities
Know and understand all ACLS algorithms
Know how to operate the defibrillator/pacer
Ensure properly operating defibrillator/pacer each shift
You don’t need to bring the defibrillator or transport medication box, although the latter may be useful if the
patient is stabilized for transfer to the MICU.
Always listen overhead for cardiac arrest announcements.
General responsibilities
Clearly identify yourself as code leader
Speak loudly in a calm voice
Determine if patient is DNR
Assign people, by name, to specific tasks (e.g. “Dick control the airway, Jane perform chest compressions,
Ishmael operate the defibrillator”)
Code leader should not perform specific tasks but should stand back, observe entire situation and direct the team
Constantly verify that ABCD goals are met (airway, breathing, circulation and early defibrillation)
Most treatable codes are secondary to ventricular tachyarrhythmias or respiratory arrest; therefore, you must
administer adequate ventilation and, if indicated, defibrillation within seconds of your arrival
•
Generate hypothesis about why patient coded (and treat underlying problem if possible)
3)
Principles of airway management (see attached document)
4) Basics of ventricular tachyarrhythmias (see ACLS handbook for details)
• Clinically stable, sustained VT: Consider synchronized electrical cardioversion or anti-arrhythmic therapy
(choice of agent depends on clinical situation; e.g. sotalol, procainamide, lidocaine 1mg/kg IV load; amiodarone
150mg IV over 10minutes is preferred in setting of LV dysfunction)
• Unstable VT with pulse: synchronized cardioversion 100/200/300/360J; consider additional anti-arrhythmic
drug therapy
• Pulseless VT or VF: Defibrillate 200/300/360J
• Biphasic defibrillator in select locations in hospital; use 150 J
• Shock refractory pulseless VT or VF: Epinephrine 1mg IV (or vasopressin 40 units IV); repeat defibrillation
then amiodarone 300mg IV (or lidocaine 1mg/kg IV); repeat defibrillation
• Success of code inversely proportional to time to defibrillation
• If successfully cardioverted/defibrillated, start appropriate maintenance infusion
• Polymorphic VT with long QTc (torsades): Mg infusion and overdrive pace if pause dependent
• VF and polymorphic VT are often caused by acute coronary syndromes; consider Aspirin, b-blocker (if
stabilized) and reperfusion therapy
• Can give repeat doses of lidocaine (q 3-5minutes twice), epinephrine (q 3-5minutes), and amiodarone
(additional 150mg)
5)
•
•
•
Principles of supraventricular tachycardias: (see ACLS handbook for details)
If unstable: synchronized cardioversion 50/100/200/300J
If stable: rate control; consider chemical/electrical cardioversion
Be careful when treating wide complex tachycardias as supraventricular with aberrancy (could be disastrous if
actually VT)
6)Brady/asystole (see ACLS handbook for details)
• Ventilate patient
• R/O “fine VF” by checking second lead (if in doubt: defibrillate)
• Epinephrine and Atropine (1mg q3-5min)
- 12 -
•
Consider pacing
7) Pulseless electrical activity (see ACLS handbook for details)
• Ventilate
• Epinephrine 1mg q 3-5 minutes
• Treat possible underlying cause (e.g. PE, tamponade, metabolic disarray)
8) Outcome of CPR
• Success defined as neurologically intact patient who survives to hospital discharge
• Significantly better for tachyarrhythmias
• Prognosis dismal for patients for patients with asystole, PEA, unwitnessed arrest, severe underlying disease or
poor functional status
9) Terminating CPR
• Terminate if patient is DNR
• Terminate when you judge efforts futile; use your assessment of prognosis and reversible pathology, not rigid
rules about duration of effort.
10) Miscellaneous
• Sodium bicarbonate not routinely indicated (unless known hyperkalemia, acidemia or tricyclic overdose)
• No known benefit to escalating doses of epinephrine
• NAEL drugs can be administered via endotracheal tube (narcan, atropine, epinephrine, lidocaine) at one and
one-half dose
11) Post Code
• Transfer patient to appropriate monitored setting
• Chart note should include: events immediately preceding code, initial rhythm, and estimation of time from loss
of pulse to CPR and to restoration of spontaneous circulation
• Contact responsible team/attending and patient’s next of kin
• Consider therapeutic hypothermia for anoxic brain injury (NEJM Feb 21, 2002: 549)
- 13 -
Shock
Definition: Acute circulatory disturbance associated with ineffective tissue perfusion and
cellular injury.
Cellular injury manifests as organ dysfunction, called multi-system organ failure, which
is initially reversible. Persistent shock leads to irreversible organ dysfunction and death. The
physiological derangements of shock occur on many levels:
a) circulatory failure
b) micro vascular dysfunction manifested by a failure of auto-regulation (causing
misdistribution of blood flow) and endothelial disruption (causing interstitial edema)
c) cellular injury and dysfunction including loss of cell membrane function and
apoptosis
The mediators of these derangements include cytokines (TNF, interlocking, interferon’s),
immunologic injury, free radical injury, cellular ischemia and activation of the clotting cascade.
A limitation of this definition is that there is no practical way to evaluate the
effectiveness of tissue perfusion. We, therefore, use surrogate markers for tissue perfusion to
diagnose and monitor shock.
Blood pressure is the best surrogate marker for the adequacy of the circulation.
Hypotension, however, is not equivalent to shock; compensatory mechanisms may maintain
adequate tissue perfusion. One reasonable clinical definition of shock is: hypotension (SBP <
90mmhg, or >30mmhg below baseline, or MAP <60mmhg, or requirement of vasopressors) and
signs of organ dysfunction (e.g. oliguria, acidemia, encephalopathy).
BP is governed by:
BP α cardiac output x systemic vascular resistance
where cardiac output (CO) is determined by pulse and stroke volume
Therefore:
BP α pulse x stroke volume x SVR
Another surrogate marker for perfusion is oxygen delivery (DO2).
DO2 =CO x content of oxygen in arterial blood
Where the content of oxygen in arterial blood is determined by: 1.36 ml O2 x Hgb x SaO2
Therefore:
DO2 = CO x 1.36 ml O2 x Hgb x SaO2
Substituting in the normal values (CO=5L/min at rest, Hgb 15gm/dl, 100% saturation) we find
that the normal resting oxygen delivery approximates 1000 ml/min. But how much oxygen
delivery is adequate for a critically ill patient? Clinicians try to answer this question indirectly
by measuring the oxygen saturation in a sample of blood obtained from the pulmonary artery
- 14 -
(using a PA catheter). This is called SvO2 or "mixed venous sat", because it represents a
summation of the oxygenation of blood returning from all the various tissues of the body. If the
SvO2 is below normal (68%) it is presumed that DO2 is inadequate for the current metabolic
requirement. Many clinicians will then attempt to increase the various components of DO2 until
SvO2 normalizes. The problems with this commonly used approach include:
a) SvO2 is decreased in normal states when oxygen consumption is increased (e.g. exercise)
b) Sepsis is often associated with a normal SvO2 despite profound shock
c) Interventions to increase the components of DO2 (i.e. transfusion, high FiO2, inotropes) can
be harmful
In summary, surrogate markers for perfusion (BP, DO2, SvO2) are useful in the appropriate
clinical context. However, abnormal values for any of them do not diagnose shock because
compensatory mechanisms can prevent organ dysfunction. Moreover, normal values of these
variables do not mean the patient is not in shock (e.g. the septic patient with a BP of 100/50 on
levophed with a CO of 7 L/min and SvO2 of 70% can still be dying of shock).
Classification of Shock
Four categories
I) Hypovolemic shock: Caused by decreased ventricular preload due to loss of intravascular
volume. Decreased preload reduces stroke volume which reduces cardiac output. The BP
equation predicts that the compensatory mechanisms of hypovolemia are tachycardia and
elevated SVR. Therefore, the patient in hypovolemic shock will be cool and clammy due to
peripheral vasoconstriction.
The clinical correlates of ventricular filling (preload) are called the "filling pressures". They
are:
a) Central Venous Pressure (CVP): this is the pressure in the right atrium and is obtained by
transducing any neck vein catheter or measuring the jugular venous pressure
b) Pulmonary Capillary Wedge Pressure (PCWP): This value is obtained by pulmonary artery
catheterization (Swan-Ganz) estimates the left atrial pressure which approximates left
ventricular end diastolic pressure which estimates left ventricular end diastolic volume (LV
preload)
The classic hemodynamic profile of hypovolemic shock is decreased CVP, PCWP, CO, SvO2
and increased SVR.
Hypovolemic shock is caused by hemorrhage or fluid loss (GI losses, or loss of fluid into
the interstitial space such as occurs in pancreatitis, traumatic tissue injury and sepsis).
II) Cardiogenic Shock The primary disturbance is an inadequate cardiac output despite adequate
preload. In fact, the filling pressures are usually pathologically elevated resulting in JVD and
pulmonary edema (typically occurring when PCWP is > 19 mmHg). The BP equation predicts
an elevated SVR as the compensation for decreased CO; therefore, the skin will be cold and
clammy. The typical hemodynamic profile is elevated CVP, PCWP, SVR and decreased CO and
SvO2.
Etiologies include massive MI, cardiomyopathy, acute valvular disease, tachycardia and
bradycardia.
- 15 -
III) Obstructive shock Many consider this a variant of cardiogenic shock. The primary
disturbance is a low cardiac output due to an obstruction of diastolic filling (e.g. tension
pneumothorax, pericardial tamponade) or an outflow tract obstruction (massive pulmonary
embolism).
The typical profile is decreased CO and SvO2 and elevated SVR and CVP. PCWP may
be elevated but is typically normal with pulmonary emboli.
IV) Vasodilatory shock also called distributive shock. The primary circulatory disturbance is
decreased SVR. This failure of vascular smooth muscle to contract occurs despite extremely
elevated levels of endogenous catecholamines and can persist despite infusions of massive doses
of exogenous catecholaminies (i.e. pressors). The pathogenesis of this phenomenon includes
activation of ATP sensitive potassium channels in vascular smooth muscle as well as vasopressin
deficiency and elevated NO activity (see Landry and Oliver N Engl J Med 2001; 345:588-595,
Aug 23, 2001).
The causes of vasodilatory shock include sepsis, the systemic inflammatory response
syndrome (SIRS) due to pancreatitis and massive trauma, and anaphylaxis. Importantly,
vasodilatory shock is a common endpoint of prolonged shock of any etiology such as massive
hemorrhage or after prolonged cardiopulmonary bypass or cardiac arrest.
Because of vasodilation and loss of intravascular fluid to the interstitium (capillary leak),
most cases are initially complicated by hypovolemia which can diminish CO. Volume
resuscitation can restore preload and allow the typical compensation for vasodilation: increased
CO. The patient in vasodilatory shock will be warm and flushed (due to peripheral vasodilation)
and have a hyperdynamic precordium.
Prolonged vasodilatory shock results in progressively diminished cardiac function in part
due to myocardial underperfusion and circulating myocardial depressant factors (including
TNF).
The typical profile of vasodilatory shock is decreased SVR, and elevated CO (if volume
resuscitated). CVP and PCWP vary depending on volume status. SvO2 may be normal in
vasodilatory shock as DO2 is often elevated and the tissues are unable to utilize the delivered
substrate.
End Organ Dysfunction in Shock Virtually any organ can be involved. Important
abnormalities include:
Respiratory system: Patients in shock will be tachypneic or in respiratory distress even if
oxygenation is normal. Minute ventilation increases in response to the metabolic acidosis of
shock, but a respiratory alkalosis will also occur due to cytokines and hypoperfusion of
medullary receptors. Hypoperfusion of respiratory muscles at a time of increased demand can
lead to respiratory failure requiring intubation to prevent sudden death. As shock progresses,
ventilation/perfusion mismatches and non-cardiogenic pulmonary edema from endothelial
dysfunction commonly cause severe hypoxia (ARDS).
Renal: oliguria (<1/2 ml/kg/hr) is an important early sign of hypoperfusion. As shock progresses
ATN and ARF may develop.
Metabolic acidosis: due to accumulation of lactate and other unmeasured anions
CNS: encephalopathy manifested as agitation or obtundation
- 16 -
Other abnormalities include: hepatic cholestasis, ischemic hepatopathy (shock liver), ileus,
erosive gastritis, bacterial translocation from the gut, pancreatitis, myocardial depression, DIC,
thrombocytopenia, hypergylcemia, immune dysfunction.
General Approach to Management
Prompt recognition of shock and diagnosis of its etiology are essential if the patient is to
survive. The airway must be secured. If respiratory distress or severe acidemia is present the
patient will require mechanical ventilation to assume the work of breathing. Nearly all patients
require a foley catheter to follow hourly urine output, continuous cardiac and oxygen saturation
monitoring, and most will require an arterial line. CVP or Swan Ganz catheters are indicated if
volume status or cardiac function is unclear. Supplemental oxygen is given for hypoxemia.
The most important intervention is prompt and adequate volume resuscitation with
isotonic crystalloid (NS or LR). Most patients with vasodilatory shock will require 4-5 L of
volume in the first few hours (and may ultimately require three times this amount). Patients
must be re-evaluated after each fluid bolus to ensure that additional fluid is required. Typical
end points of volume resuscitation include restoration of blood pressure without the need for
vasoconstrictors and restoration of normal urine output (although urine output may not correct if
patient is in oliguric ATN). For hemorrhagic shock many intensivists continue volume
resuscitation until the acidosis is corrected. If a Swan Ganz catheter is placed consider
resuscitation guided by normalization of SvO2 (goal > 68%). Other end points include evidence
of pulmonary edema or markedly elevated filling pressures. Patients in cardiogenic shock
should receive much more cautious fluid boluses (100-200cc) or none at all if there is evidence
of pulmonary edema.
Although it remains controversial we do not routinely resuscitate patients with colloid.
An exception is blood transfusion; we generally correct the Hgb to around 10mg/dl for shock.
Correct choice of intravascular catheters is essential. Flow through the catheter is
independent of the size of the vein but inversely proportional to the length of the catheter. Flow
is proportional to the fourth power of the radius of the catheter. Therefore short, large bore
catheters are essential for rapid fluid administration. For example:
22 gauge angiocath: maximum infusion rate:
20 gauge angiocath: maximum infusion rate:
18 gauge angiocath: maximum infusion rate:
16 gauge angiocath: maximum infusion rate:
14 gauge angiocath: maximum infusion rate:
35 ml/minute
60 ml/min
105 ml/min
205 ml/min
333 ml/min
Therefore, small IV's and long PICC lines are inadequate for rapid volume resuscitation.
Long triple lumen central lines may also be inadequate (large lumen allows 34 ml/min, other two
lumens each allow 17 ml/min). Large bore central venous introducers (cordis) are ideal. Electric
pumps and micro-drip IV tubing will slow infusion rates through large bore catheters (maximum
rate 1L/hr). Rapid infusions require only gravity and plain IV tubing (the way blood products
are infused). Place central venous access if adequate peripheral access is not possible or the
patient requires vasopressors, or CVP or Swan-Ganz monitoring.
Prompt treatment of the underlying cause of the shock is essential: antibiotics and
drainage of infected foci for sepsis, thrombolysis for PE, pericardiocentesis for tamponade,
control of bleeding, re-perfusion therapy in acute MI, tube thoracostomy for tension
- 17 -
pneumothorax, cardioversion or pacing of arrhythmias, and placement of intra-aortic balloon
pump or left ventricular assist device for refractory cardiogenic shock. Also consider using
activated protein C for patients in septic shock (Bernard, NEJM 344; 20001: 699-709). Consider
low dose steroid replacement (JAMA 288; 2001:862-871) and early normalization of
hemodynamic variables (i.e. ScvO2, CVP, UO, BP as in NEJM 345; 2001: 1368-1377) for septic
shock. Consider low tidal volume ventilation if the patient develops ARDS (NEJM 2000; 342:
1301-1306) as well as tight glucose control (NEJM 345; 2001:1359-1367) for all critically ill
patients.
Vasoactive drips: There is little evidence from clinical trials to guide the use of vasoactive
drips. Vasoconstrictors can restore the blood pressure to a normal value without normalizing
perfusion and they do not correct the misdistribution of blood flow that characterizes shock.
Vasoactive drips should never be used in place of adequate volume resuscitation or treatment of
the underlying etiology of the shock. The patient who is on these vasoactive drips is unstable
and the clinician should constantly attempt to liberate the patient from the drips.
Vasoactive drips target various receptors:
Alpha Predominantly found in the vasculature; activation causes vasoconstriction
Beta1 Predominantly found in heart; activation causes increased inotropy and chronotropy
Beta2 Predominantly found in vasculature; activation causes vasodilation
Dopaminergic: One subtype causes vasodilation of splanchnic, cerebral and coronary
vasculature; another subtype causes vasoconstriction
Phenylephrine (Neosynephrine): Pure alpha agonist causes vasoconstriction (increases SVR).
May cause reflex bradycardia. Useful in vasodilatory shock especially in setting of
tachyarrhythmias
Norepinephrine (Levophed) potent alpha agonist (vasoconstrictor) also some B1 activity which
may increase CO. Used in vasodilatory shock, it is generally agreed that it is the most potent
vasopressor. Patients who remain hypotensive on dopamine or phenylephrine may have BP
restored by norepinephrine.
Dopamine dose responses for various receptors vary;
1-3 mcg/kg/min dopaminergic receptors predominate with dilation of renal and splanchnic
vessels. Some vasodilation and tachycardia
5-10 mcg/kg/min : Beta predominates with some alpha activity
>10 mcg/kg/min: alpha predominates with some Beta activity
In summary, at mid doses dopamine causes tachycardia and modest increase in CO.
Vasoconstriction increases with increased dose. Dopamine is used in virtually all shock states to
support the circulation. Controversy exists over the use of renal dose dopamine (1-3
mcg/kg/min) to preserve renal perfusion. Dopamine does increase urine output at low doses that
is likely transient and due to naturesis. However, it is relatively certain that it does not improve
renal function (GFR) or mortality [Lancet 356; 2000]
- 18 -
Epinephrine At low doses epinephrine activates B receptors and alpha. The net result is
increased CO with variable vasoconstriction and effect on BP. At higher doses alpha effects
predominate increasing vasoconstriction and BP. Epinephrine is used in anaphylaxis and for
circulatory support immediately after coming off bypass.
Vasopressin Used in vasodilatory shock to replace vasopressin deficiency and cause
vasoconstriction. May preserve renal perfusion. Can decrease CO as well as cause
hyponatremia.
Mix 25 units/250cc D5W infuse at 0.04 units/minute (24ml/hour), do not titrate to higher dose;
must taper off slowly.
Dobutamine Potent stimulator of _ receptors causes increased cardiac output and vasodilation.
Commonly used in cardiogenic shock. Causes vasodilation and hypotension as well as
tachyarrhythmias. Long-term isotropic support increases mortality; it is presumed that shortterm isotropic support does not increase mortality although there is no clinical trial data to
support this.
Start at 2.5mcg/kg/min if no adverse effects increase to 5mcg/kg/min, if the patient tolerates this
dose but inadequate response increase to 7.5mcg/kg/min
Interpretation of Hemodynamic Waveforms
Waveforms seen on insertion of pulmonary artery catheter
Images from Pulmonary Catheter Education Web site (www.pacep.org)
- 19 -
Images from Pulmonary Catheter Education Web site (www.pacep.org)
- 20 -
Cardicac output by thermodilution: Room air saline is injected into right atrium via PA
catheter. A thermistor at the distal tip of the swan measures the fall and recovery of the
temperature of blood in the pulmonary artery. The area under the idealized thermodilution curve
is proportional to the cardiac output.
Image adapted from Hugo Sacks Electronik website http://www.hugo-sachs.de/haemo/car_ou.htm
Commonly Used values
Normal Range
CO=pulse x stroke volume
CI=CO/Body surface area
CVP
PCWP (also called PAOP)
Pulmonary artery pressure
SVR= MAP-CVP x 80
CO
4-7 L/min
2.6-4L/min/m2
2-8 mmHg
5-12 mmHg
mean<25mmHg
800-1300 dynes/sec/cm
Arterial oxygen content:
CaO2 = 1.36 ml O2 x SaO2 x Hgb g/dl + (0.003 ml O2/mmHg x PaO2 mmHg)
Oxygen Delivery
DO2 = CO x CaO2
1000 ml/min (rest)
Fick determination of Cardiac output
CO = VO2
CaO2-CvO2
4 – 7 L/min
Oxygen consumption VO2
250mlO2/min at rest
- 21 -
20 ml O2/dl
Introduction to Mechanical Ventilation
I)
Modes of Mechanical Ventilation
A) Assist Control (AC also erroneously called CMV): Machine delivers a guaranteed number of breaths
each minute; each breath delivers the full tidal volume set on the control panel. If the patient attempts
additional breaths the machine will deliver the full tidal volume for each additional effort.
You set: FiO2, PEEP, respiratory rate, inspiratory flow rate, tidal volume
Variables: respiratory rate, exhaled tidal volume, peak airway pressure
Common uses: to completely support the ventilation
B) Synchronized Intermittent Mandatory Ventilation (SIMV): Machine delivers a guaranteed number of
breaths each minute; each breath delivers the full tidal volume set on the control panel. If the patient
attempts additional breaths the machine will not deliver the full tidal volume; instead the machine will
augment these spontaneous breaths with positive pressure called pressure support. The tidal volumes
of the spontaneous breaths vary according to the patient's strength and the amount of pressure support
added by the machine.
You set: FiO2, PEEP, Respiratory rate, inspiratory flow rate, tidal volume, and pressure support
Variables: respiratory rate, exhaled tidal volume, peak airway pressure
Common uses: to support the ventilation or as a weaning mode
C) Spontaneous Mode (erroneously called CPAP): No guaranteed rate or tidal
volume (i.e. no machine generated breaths). All spontaneous breaths are augmented by the amount of
pressure support added by the machine.
You set: FiO2, PEEP, pressure support
Variables: respiratory rate, exhaled tidal volume, peak airway pressure
Common uses: usually a weaning mode; can also be a comfortable way of supporting ventilation if
generous pressure support is given
D) Pressure Control (technically not a mode of ventilation): Potentially useful in patients with very poor
lung compliance (i.e. very high airway pressures) Ventilator settings similar to AC except that the machine
delivers tidal volume during each breath until a certain peak airway pressure limit is reached
II)
Basic steps to Improve Oxygenation (measured by SaO2, PaO2)
A) Treat underlying pulmonary pathology (e.g. diurese pulmonary edema)
B) Increase FiO2 (FiO2 >50% probably toxic to lungs)
C) Increase Positive End Expiratory Pressure (PEEP) [this may decrease cardiac preload and increase
peak airway pressure]
III)
Basic Steps to Improve Ventilation (measured by minute ventilation, pH and PCO2)
A) Increase respiratory rate
B) Increase tidal volume (or increase pressure support on spontaneous breaths)
IV)
Causes of Common Ventilator Alarms
A) High Peak Airway Pressure (usually >36 cmH2O) caused by:
Decreased compliance (pneumonia, fibrosis, pulmonary edema, chest wall abnormalities, ascites, tension
pneumothorax)
Increased resistance to airflow (secretions, obstructed endotracheal tube, bronchospasm)
Patient-ventilator asynchrony
•
•
•
B) Low Exhaled Tidal Volume
- 22 -
•
•
On machine generated breaths: leak around ET tube cuff or in ventilator tubing, broncho-pleural fistula,
high pressure cutoff terminating breath before complete tidal volume delivered, patient-ventilator
asynchrony
On spontaneous breaths: inadequate patient effort or pressure support
V)
Weaning Strategies
• Probably no such thing as "weaning": patient will tolerate extubation or not
• No proof that you can train respiratory muscles with exercise/rest
• Your job is to treat all reversible medical problems, remove impediments to extubation (such as
malnourishment) and quickly identify patients capable of tolerating extubation
• Protocol based daily interruption of continuous sedation, regardless of whether or not you are planning to
wean the patient that day, decreases time to extubation (NEJM 342; 2000: 1471-1477)
• Protocol of daily trials of spontaneous ventilation is superior to strategies of slowly lowering SIMV or
CPAP support (NEJM 332; 1995: 345-350)
• Our protocol: If patient hemodynamically stable, adequate mental status, FiO2 requirement <45%, PEEP <
5cmH2O, then perform daily trials of spontaneous ventilation (either on T-piece or spontaneous mode with
pressure support 5cmH2O). If rapid shallow breathing index (respiratory rate/tidal volume in liters) >105
patient likely will not tolerate extubation
VI)
Mechanical Ventilation Strategy for ARDS
• Use of low tidal volume (6cc/kg of ideal body weight) reduces mortality compared to use of traditional
tidal volumes (10-15cc/kg) [absolute risk reduction 8.8% NEJM 2000; 342: 1301-1306]
• Increase PEEP to allow decrease of FIO2 to less toxic levels (<60%)
- 23 -
Principles of Sedation in the Intensive Care Unit
I)
II)
III)
•
•
IV)
V)
VI)
VII)
VIII)
IX)
X)
XI)
Problems: Pain, agitation, anxiety, confusion
Treatments: Analgesia, hypnotics, anxiolytics, anti-psychotics
Drug therapy should include:
Induction: Rapidly achieve desired effect; in general requires bolus of short-acting agent (i.e.
for rapid onset)
Maintenance of desired effect; in general requires constant infusion or intermittent dosing of
longer acting agents.
Sedatives (especially intravenous agents) can cause life threatening respiratory depression.
Only physicians credentialed by the moderate sedation committee are permitted to administer
intravenous sedatives for the purpose of performing procedures.
Under-treatment of pain and over-sedation of mechanically ventilated patients are common
ICU problems
In general, you should interrupt continuous sedation every day and allow the patient to
awaken. This prevents over-sedation and decreases the duration of mechanical ventilation
Hypnotics and sedatives (such as benzodiazepines, zolpidem and anti-cholinergics) can
precipitate agitation in patients with delirium (so called “paradoxical response”)
Frail, elderly and debilitated patients are much more sensitive to sedatives and the lowest
possible doses should be used. (You can always give more if the dose is ineffective)
A combination of agents may be helpful (e.g. combining an opiate with a benzodiazepine)
Titrate sedative to objective endpoints using minimum effective dose. Order sedatives with a
goal Ramsay score (mandatory for continuous infusions)
Ramsay Sedation Scale
Level
Patient Response
1
Anxious, agitated, restless
2
Cooperative, oriented, tranquil
3
Responds to commands only
4
Asleep, brisk response to stimulus
5
Asleep, sluggish response to stimulus
6
Unarousable
Sedative agents commonly used in the ICU
• Opiates: Superlative analgesics; also cause sedation. All opiates cause respiratory
depression, constipation and mild hypotension
• Morphine sulfate: Start with an intravenous bolus of 1-4mg to rapidly induce analgesia
and sedation. Morphine causes more severe hypotension than other opiates (because of
histamine release).
• Fentanyl: Very short acting agent; administer intravenous bolus to intubated patients
(usually 50mcg) up to q3minutes to rapidly induce sedation and analgesia. Use
continuous infusion for maintenance of sedation and analgesia. This is our preferred
sedative infusion for mechanically ventilated patients in shock. If a patient on a fentanyl
infusion becomes agitated give repeated boluses of 30-50 mcg or bolus of midazolam in
addition to increasing the drip rate by 30-50mcg/hr. Lorazepam (1-2mg q 4-6 hours) can
be used in addition to the fentanyl infusion for maintenance of sedation.
• Meperidine (Demerol): avoid in the ICU because of drug interactions and an eleptogenic
active metabolite that accumulates in renal failure.
• Hydromorphone (Dilaudid): Use in place of morphine when concerned about
hypotension
- 24 -
B. Benzodiazepines: Excellent hypnotics and anxiolytics, also causes useful amnesia. NO
ANALGESIC PROPERTIES. Cause respiratory depression and mild hypotension
• Midazolam (Versed): Very short onset to and duration of effect. Excellent for
conscious sedation and immediate treatment of agitation. Administer intravenous
bolus (1-2mcg) q 3-5minutes to intubated patients to rapidly induce sedation. With
prolonged use (i.e. infusion) in critically ill patients active metabolites can
accumulate causing prolonged sedation
• Lorazepam (Ativan) Compared with midazolam it has a much longer time to onset
and duration of action (starts within 15-30 min and lasts hours). INEFFECTIVE
FOR RAPID INDUCTION OF SEDATION BUT EXCELLENT FOR
MAINTANANCE. Dose intermittently IV or PO to maintain sedation. A frequent
mistake is to repeatedly bolus lorazepam for agitation or rapidly titrating up the
infusion rate. If a patient becomes agitated on a lorazepam infusion you can increase
the drip rate by 0.5-1mg/hr but you will need to bolus with an induction agent for
rapid effect (e.g. versed, fentanyl, morphine). Order lorazepam drip to begin at 0.5
–1mg/hr but specifically order that the infusion should not be increased without MD
approval.
C. Propofol (Diprivan) An intravenous short acting sedative. Has no analgesic properties.
Excellent induction of sedation with repeated 20-30mg boluses. Also used for
maintenance by continuous infusion. Discontinuation of the infusion causes more rapid
emersion from anesthesia than other agents (except midazolam). Causes severe
hypotension and should be avoided in all hemodynamically unstable patients. Other side
effects include severe respiratory depression (and should only be used in intubated
patients), pain on injection and hypertriglyceridemia/pancreatitis. Provides 1 kcal/ml .
D. Etomidate A potent intravenous hypnotic that rapidly induces sedation with bolus
injection. (0.1mg/kg). Not used for maintenance of sedation. Minimal cardiovascular
effects and is useful for inducing anesthesia for intubation in patients in shock. Causes
myoclonus and inhibition of adrenal corticosteroid synthesis.
E Paralytics: These agents supply neither analgesia nor sedation. They are only used in
patients who are fully sedated to Ramsay 6 to facilitate either endotracheal intubation by
attending physicians or control of patients difficult to manage on mechanical ventilation.
Used with extreme caution under direct supervision of MICU fellow/attending. Cisatracurium (Nimbex) as bolus/continuous infusion is the best agent for patients with
tachycardia or renal failure. Causes complete apnea. Causes severe polyneuropathy
(synergistic with aminoglycosides or corticosteroids). Risk decreased by using lowest
effective dose and assessing depth of paralysis each shift with a twitch monitor.
Selected Abstracts
- 25 -
- 26 -
- 27 -
- 28 -
- 29 -
- 30 100 mg/100 mL D5W
20 mg/100 mL D5W
250 mg/250 mL D5W
50 mg/250 mL D5W
50 mg/250 mL D5W
4 mg/250 mL D5W
8 mg/250 mL D5W
1200 mcg/250 mL D5W
20 mg/250 mL D5W
2 g/250 mL NS
500 mg/50 mL
100 Units/100 mL D5W
100 mg qs to 100 mL D5W
Midazolam (Versed)
Milrinone (Primacor)
Morphine
Nitroglycerin
Nitroprusside (Nipride)
Naloxone (Narcan)
Norepinephrine (Levophed)
Octreotide (Sandostatin)
Phenylephrine (Neosynephrine)
Procainamide (Pronestyl)
Propofol (Diprivan)
Vasopressin (Pitressin)
Vecuronium (Norcuron)
100 mg/100 mL D5W
Furosemide (Lasix)
100 g/ 1000 mL (10%)
1 mg qs to 100 mL NS
Fentanyl
Mannitol
2.5 g/250 mL (0.59% NS)
Esmolol (Brevibloc)
20 mg/250 mL D5W
4 mg/250 mL D5W
Epinephrine
Lorazepam (Ativan)
400 mg/250 mL D5W
Dopamine
2 g/250 mL D5W
500 mg/250 mL D5W
Dobutamine
Lidocaine
125 mg qs to 125 mL D5W
Diltiazem (Cardizem)
400 mg/200 mL D5W
100 mg/100 mL D5W
Cisatracurium (Nimbex)
Labetalol
10 mg qs to 100 mL D5W
Bumetanide (Bumex)
100 Units/100 mL NS
250 mg/250 mL NS or D5W
Argatroban
Insulin
100 mg/100 mL SW = 1 mg/mL
Alteplase (Activase)
25,000 Units/250 mL D5W
450 mg/250 mL D5W
Amiodarone (Cordarone)
Heparin
Standard
Concentration
Medications
(mechanically ventilated patients only )
50 mcg IVP for hypotensive shock
(Varices bleeding) 50 mcg IV
Not recommended
Not recommended
Not recommended
2 – 10 mg IVP over 2 min
50 mcg/Kg in 50 mL D5W over 10 min
10 – 50 mcg/Kg
1 g/Kg IVP (max=100 g) over 10 min
0.5 – 2 mg IVP over 2-3 min
1 – 1.5 mg/Kg IVP over 2-3 min
20 mg IVP over 2 min
0.1 Units/Kg IVP for DKA
80 Units/Kg IVP (DVT/PE)
20 – 40 mg IVP over 2 min
50 – 100 mcg IVP over 2 min
500 mcg/Kg over 30 sec
ACLS: 1 mg IVP
Not recommended
Not recommended
May re-bolus (in 15 min) w/ 0.35 mg/Kg IVP over 2 min.
0.25 mg/Kg IVP over 2 min (max 20 mg).
0.1 mg/Kg IVP
0.5 – 1 mg IVP over 2 min
150 mg/50 mL D5W over 10 min
Bolus Dose
Start at 0.06 – 0.075 mcg/Kg/min
0.04 Units/min (2.4 Units/hr)
Start at 0.3 mg/Kg/hr
Start at 1 – 2 mg/min
Start at 0.2 mcg/Kg/min
IV infusion of 50 mcg/hr
0.015 mcg/Kg/min or 2 mcg/min
0.25 – 0.3 mcg/Kg/min
2 – 20 mcg/min
1 mg/hr
1 mg/hr
1 mg/hr
2 mg/min
0.5 – 2 mg/min
5 mg/hr
50 – 100 mcg/hr
50 – 300 mcg/Kg/min
1 – 3 mcg/min
1- 5 mcg/Kg/min (renal perfusion) OR 5 – 15
mcg/Kg/min (Beta 1) OR > 15 mcg/Kg/min (Alpha)
2.5 mcg/kg/min
10 mg/hr
1 – 3 mcg/Kg/min and titrate
0.5 – 2 mg/hr
2 mcg/Kg/min
Stroke: 0.9 mg/Kg (max 90 mg) IV over 1 h
1 mg/min (33 mL/h) for 6 h, then
0.5 mg/min (17 mL/h) for 18 h
Maintenance Dose