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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 -1- 26 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. -2- 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: -3- • • • • • 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 -4- 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. -8- 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 -9- 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 - 10 - Rotating the oral airway into position Two operator technique for manual mask ventilation - 11 - How to be a Code Leader 1) • • • • • 2) • • • • • • 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