sedation & paralytic therapy in the icu leanna r. miller, rn, mn, ccrn-csc, pccn-cmc, cen, cnrn,...

Post on 26-Mar-2015

231 Views

Category:

Documents

3 Downloads

Preview:

Click to see full reader

TRANSCRIPT

Sedation & Paralytic Therapy in the ICU

Leanna R. Miller, RN, MN, CCRN-CSC, PCCN-CMC, CEN, CNRN, NP

Education Specialist

LRM Consulting

Nashville, TN

Objectives

Identify the purpose for pain, sedation, & paralysis management in the ICU patient

Analyze and compare assessment methods for determining appropriate pain, sedation & paralysis management.

Recognize and apply the different pharmacotherapeutics used in the ICU for pain, sedation, & paralysis.

Goals of Critical Care Management

Save the salvageable and relieve suffering Peaceful & dignified death without prolonging life Curative therapy should not supplant palliation of

pain Use of state-of-the-art interventions Aggressive & fast paced therapy according to need Quality pain management mandatory for all

patients

The Balance of Analgesia, Sedation, and Paralytics to promote comfort

Consciousness/SedationConsciousness/Sedation

What is Sedation?

Several Clinical Definitions: process of establishing a state of calm promoting a sense of well-being reduction of anxiety and agitation through the

use of pharmacotherapy

Sedation is NOT analgesia 80% of Doctors and 40% of ICU nurses

answered that benzodiazepines provided analgesia (1990s)

Pathophysiology Response of Stress and Anxiety Cardiovascular

Release of systemic epinephrine and norepinephrine

Elevated HR and BP Increased cardiac O2 demand Decrease end-organ perfusion

Endocrine Release of Cortisol, Glucagon, Glucose

Hyperglycemia

Pathophysiology Response of Stress and Anxiety Neurological

Increased response and activation of peripheral pain fibers

Increased sensation to pain Release of neurotransmitters in the brain

Pain Agitation Delirium

Pathophysiology Response of Stress and Anxiety

Immune Increased levels of prostaglandins,

cortisol, glucose, cytokines, Increase anti-inflammatory response Decrease wound healing

SIGNIFICANT STRESS IN THE ICU PATIENT OVERALL CAUSES ORGAN ISCHEMIA AND DECREASED HEALING

Analgesia

Clinical Definition: The absence of pain through the use of

pharmacotherapy

Acute and chronic pain in the ICU activates the stress response

Patients with analgesia can still experience anxiety

PAIN THERAPY - Myth

“One size fits all or

Set and forget therapy.

Its essentially a maintenance therapy”

Truths

Majority of ICU patents suffer moderate/severe pain 40% are delirious & cannot communicate 50% are either physically/emotionally distressed 10-20% have no hopes of cure --- end-of-life in ICU Balance between pain relief & maintaining alertness Multidisciplinary team for multimodal therapies.

Pain in ICU Repeated episodes of acute pain localized Surgery/tissue inflammation immobility catheter/ apparatus discomfort/ nasogastric

& orogastric tubes endotracheal intubation/ suctioning/ chest

tubes phlebotomy/vascular access/physiotherapy routine turning & positioning the patient

Types of pain in ICU

Somatic – most common –localized opiates Visceral – cramping & colicky anticholinergics Neuropathic – burning / shooting antidepressants Mixed type combination therapy Sustained or chronic pain of varying degrees

Inherent Problems

difficult to differentiate due to lack of communication

untreated pain affects all body systems synergistic effect of pain on anxiety,

depression, sleep all modalities are unpredictable & have

adverse effects pain therapy to be tailored to individual

needs.

Assessment of pain in ICU

Pain as the 5th vital sign- requires frequent evaluation

Cognitive impairment/delirium markers• Behavioral (facial, FACS)• Physiological (BP, HR, RR)

Creative assessments (teaching hand movements, blinking

Subjective quantification (numeric/graphic scales –W-B faces)

Assessment of pain in ICU

Treatment of Pain treatment of perceived & prevention of

anticipated pain Opiates – principal agents in ICU

- potent / lack ceiling effects - mild anxiolytic & sedative - relieves air hunger & suppresses cough in

respiratory failure - improved patient – ventilator synchrony - effective antagonist – naloxone lack amnesic effects /additional sedatives

required

Treatment of Pain

adjuvant / non-pharmacological / multimodal therapies• Simple Relaxation – must begin preoperatively

Jaw relaxation Progressive muscle relaxation Simple imagery Music (either patient – preferred or “easy listening” are

effective in reducing mild to moderate pain• Complex Relaxation – must begin preoperatively

Biofeedback imagery

Causes of Pain in the ICU?

The Messengers of Pain

• Direct tissue damage stimulates pain fibers• Local Inflammatory mediators

• Bradykinin, Prostaglandins, Cytokines• Tissue Injury

• Histamine• Serotonin• TNF

WHY IS THIS IMPORTANT?

Common Analgesic Drugs in the CVICU

A Focus on Morphine

First narcotic to be used Narcotic standard Relies on good kidney function for excretion Stimulates mast cells to release histamine

Itching Rash Hypotension Acute Asthma episode

No longer used frequently due to newer drugs

A Focus on Fentanyl

100x stronger then Morphine Fastest metabolizing narcotic used in the

CVICU Chest Wall Rigidity

can cause shortness of breath and difficulty weaning

occurs most often with high IV bolus doses Decreases BP and HR

A Focus on Remifentanil

Newest synthetic narcotic derived from Fentanyl Eliminated by plasma esterases

Metabolism not dependent on liver or kidney function Elimination not dose dependent

Advantages Organ independent metabolism Lack of accumulation Provides analgesia and sedation in ventilated patient

Disadvantages Expensive Severe withdrawal Rebound hyperalgesia

A Focus on Toradol

Is a potent IV/IM NSAID Decreases sternal incision pain and

inflammation Like many NSAIDs can be nephrotoxic

Know your patients BNP and Creatinine Can cause GI bleeding Usually not given if the patient is…

Age >75 Elevated creatinine Chest tube bleeding Low platelets

Sedation in ICU

used in the agitated, ventilated & for procedure discomfort

to avoid self extubation & removal of catheters

NM blockade mandates analgesia & sedation

control of pain before sedation all have side effects – dose dependent analgesics are not sedatives/ Sedatives

are not analgesics

Common Sedatives in the ICU

A Focus on Precedex

Only sedative used that does not cause respiratory depression

Patients can be weaned and extubated while on Precedex

Usual titration range 0.2 – 0.7mcg/kg/hr MD order >0.7mcg/kg/hr

Titrate by 0.1-0.2mcg/kg/hr q30-45min Can cause SEVERE bradycardia and

hypotension Very expensive!

A Focus on Ketamine

dissociative anesthetic light sedation & amnesia

used as an adjunct for patients with uncontrolled pain or inadequately sedated

rarely used in the CVICU due to myocardial depressant properties

monitor for hallucinations and vivid dreams

Assessment of Pain and Sedation

Sedation scoring systems

Assess levels to vary according to course of ICU stay

Observational scales - 4 levels – min, mod, deep, GA

Addenbrooke sedation scale 0-7 (vocal, tracheal suction)

Ramsay sedation scale 1-6 (vocal, glabellar tap)--aim for 3-4

Direct information- ideal to assess analgesia & sedation

BIS – for deep sedated & paralyzed

RASS ASSESSMENT

+4 Combative, violent, danger to self/staff +3 Very agitated, pulls lines, tubes, aggressive +2 Agitated frequent non-purposeful movement, fights the vent +1 Restless / Anxious but not aggressive or vigorous 0 Alert and calm -1 Drowsy, not fully alert but can stay awake, eyes open to voice for >10sec -2 Light sedation, wake and makes eye contact for < 10 sec -3 Moderate sedation, moves/opens eyes to voice but no eye contact -4 Deep sedation, no response to voice but moves or opens eyes to physical

stimulation -5 Unarousable, no response to stimuli

BIS monitor

BIS Monitoring

BIS Monitor

BIS monitor utilizes EEG waveforms. reading is monitored from the patient’s

forehead. excessive muscle activity can interfere with

EEG detection

Bispectral Index

BIS – an attempt to objectively monitor patients sedation

processed EEG measurement that gives a score to help determine the patient’s response to sedation

useful to help titrate medication proper sensor placement is key to

accurate monitoring

Sensor ApplicationSensor Application

Apply sensor on forehead at angle

Circle #1: Centered, 2 inches above nose

Circle #4: Directly above eyebrow

Circle #3: On temple, between corner of eye and hairline

Press around the edges of each circle to assure adhesion

Press each circle for 5 seconds

BIS Placement

Make sure the forehead is clean and dry!

Label the sensor with date/time Replace sensor every 24 hours and

PRN

BIS Monitor

implement BIS monitoring on all patients with paralytic drips infusing

purpose of BIS monitor is to provide a direct measurement of the SEDATIVE effects on the brain.

goal for BIS Monitoring will be 40 – 60. studies have indicated that this is a safe range

for no memory recall.

BIS Monitoring

Troubleshooting the BIS

If the BIS increases suddenly or is higher than expected: Consider:

Is the sedative dose sufficient? Is there an increase in stimulation? When was the last analgesic given? Is the patient adequately paralyzed? TOF? Is the patient having a seizure

Troubleshooting the BIS

If the BIS decreases suddenly or is lower than expected: Consider:

Has there been a decrease in stimulation or increase in sedation/analgesia?

Is the patient significantly hypothermic? Has there been a sudden significant drop in BP?

BIS Monitoring

Always consider the overall picture of the patient Ex: if nothing significant has changed with

patient and BIS number suddenly reflects very different readings then fall back to your overall assessment of the patient

REMEMBER!

Look at the BIG PICTURE!

Do Not Forget

You are treating a patient not just the number

“Sedation Vacation”

Assess for daily awakening• Exclusions

Increased ICP Neuromuscular blockade Significant ventilation support CABG, immediate post-op

“Sedation Vacation”

Is patient awake and calm?• SAS 3 – 4• RASS 0 to -1

If no, restart sedation @ ½ previous dose

If yes, proceed to spontaneous breathing trial (SBT)

“Sedation Vacation”

Assess for SBT• Calm & co-operative• Hemodynamically stable• PEEP < 8• FiO2 < 0.60

• pH > 7.34• SpO2 > 90%

“Sedation Vacation”

SBT Termination Criteria• RR > 35/min for > 5 minutes• SpO2 < 90% for > 2 minutes

• New ectopy• HR change 20% from baseline• BP change 20% from baseline• Accessory muscle use• Increased anxiety/diaphoresis

“Sedation Vacation”

Conduct SBT for 1 minute• Mode CPAP• PEEP = 0• PS @ least 5 – 10• FiO2 unchanged

Paralytics in the ICU

Paralysis – the loss of voluntary muscular function due to the administration of a paralytic

Neuromuscular Blockade Agent (NMB) – Drugs that obstruct transmission of nerve impulses to the muscle

Neuromuscular Blockade agents DO NOT BLOCK THE TRANSMISSION OF PAIN!!!!

Paralytics in the CVICU

Sedation and Analgesics must always be given FIRST

Must use sedatives with an Amnesic affect Benzodiazepines (VERSED) High dose Propofol

Paralytics are always given LAST

Why Do We Paralyze?

Decreases O2 demand ARDS

Prevent Patient-Ventilator dysynchrony VDR ventilators BiVent

Prevents Shivering in hypothermia patients Shivering increases O2 demand Raises patients temperature

Open chest

Checklist for chemical paralysis

Must be adequately sedated first before paralytic administered

Must have anxiolytic drip that has amnesic properties

Must have analgesic drip infusing Must have lubrication for eyes/eye bubbles

Common CVICU Paralytics

Drug Dose Onset Peak Duration

Vecuronium .08 - .1 mg/kg 1 min 3-5 min 15-25 min

Pancuronium .04 -.1 mg/kg 30-45 sec 3-4 min 35-65 min

Succinylcholine .6 mg/kg 30-60 sec 1-2 min 4-10min

Nimbex 3 mcg/kg/min 1-2 min 2-5 min 25-44 min

A Focus on Vecuronium

A non-depolarizing NMB Will NOT increase K+ Full recovery from paralytic 25-40min Frequently used in the CVICU for intubation

or as a bolus drug before Nimbex Rarely used as a drip in the absence of

Nimbex 0.8-1.2mck/kg/min

A Focus on Succinylcholine

A depolarizing NMB Can increase K+ ~ 0.5-1mEq/L

KNOW YOUR PATIENTS K+ before administering

Does your patient have any renal disease? Metabolized by plasma cholinesterase

Very rapid metabolism ~5min Does not rely on kidney or liver function

A Focus on Nimbex

Is our primary titrating NMB used in the CVICU

Is also metabolized in the blood Standard dose is 3mcg/kg/min

Titrate range: 0.5-5mcg/kg/min Metabolism ~45min

Changes with hypothermia?

Successful Paralysis: How do we know? Assessment

Movement Spontaneous Breaths Peripheral Nerve Stimulator

Peripheral Nerve Stimulators

Peripheral Nerve Stimulator – A device that delivers a determine electrical current to create a muscular contraction

Used to determine the amount of neuromuscular blockade a patient has

An increase in NMB will show a decrease response to a peripheral nerve stimulator at a set current

Train of Four

Train of Four – 4 consecutive impulses generated from the peripheral nerve stimulator resulting in 4 muscular twitches

# of twitches seen = degree of NMB No blockade – 4 twitches Total blockade – 0 twitches GOAL IS 1-2 TWITCHES

Increase drip by 10% if >2 twitches Decrease drip by 10% if <1 twitch

Train of Four: Facial Nerve

Place one electrode on the face at the outer canthus of the eye (positive/red electrode)

Place the second electrode 2 cm below and parallel with the tragus of the ear (negative/black electrode)

Watch and feel for facial nerve contraction

Train of Four: Ulnar Nerve

Train of Four

Must have 2x baseline TOFs before starting NMBs

Ulnar nerve is more preferred but facial nerve is easier to see/assess

Use alcohol pad to wipe clean and dry the skin before applying electrode

Electrodes must be changed 24 hrs Possibly inaccurate in hypothermia patients…

Helpful tips for TOF

If checking the thumb – ensure the leads are placed on the ulnar side of the arm(this is where the nerve lies)

Be careful with applying maximum MA’s when leads are placed on the face – this can lead to burns/scarring

Check your battery Change your electrodes q24h

Putting it all Together

1. start BIS Monitoring

2. get a Baseline TOF on two locations

3. start Sedation and Analgesic Drips

4. titrate medication up until BIS 40-60

5. bolus paralytic

6. start paralytic drip

7. check TOF q30min until 1-2 twitches

8. monitor TOF and BIS and titrate drips to endpoints

***** CRUCIAL POINT ******

Prior to the administration of any paralytic agent - sedation MUST be administered first. If paralytic will be continued as an infusion, sedation MUST also be continued.

Sedation MUST be a drug that has amnesic properties.

Drugs that have amnesic effects

Benzodiazepine class

Examples: Versed

Propofol (in high doses) dose will be individual to patient

Intravenous Medicines commonly used in CVICU SEDATION

Ativan * Versed * Propofol ** Precedex ***

• * Amnesic properties• ** Amnesic in high

doses only• *** DOES NOT have

amnesic properties

ANALGESIA Morphine Fentanyl Dilaudid Toradol

Case Study

You are caring for a patient that has an open chest, they are on a Nimbex, Fentanyl & Versed gtts: VS’s:

BP 160/90 HR 128 Vent Settings: SIMV 12, TV 450, PEEP 5, PS 10,

Spontaneous RR 12, 02 saturation 98%, TOF 2/4 Is anything wrong here?

Case Study

Patient has open chest, Nimbex, Fentanyl & Versed gtts: VS’s

105/68 HR 80 Paced Vent settings: SIMV 12, TV 600, PEEP 5, PS 10,

Spontaneous RR 16 TOF 2/4

Is anything wrong here?

Case Study

Patient has open chest, has experienced excessive blood loss through chest tubes, Nimbex & Propofol gtts(5 mcg/kg/hr)

VS’s BP labile 70’s to 100’s systolic HR 80’s paced Vent settings: SIMV 12, TV 400, PEEP 5,

PS 5, Spontaneous RR 14, 02 saturation 98% TOF 0/4

Is anything wrong here?

SCCM task force recommendations

Benzodiazepines most popular for sedation Short term sedation

• Midazolam <3h (amnesic/ hypotension)• propofol – infusion syndrome/ pancreatitis

Long term – lorazepam <20h /diazepam>96h (not for infusion)

Delirium – haloperidol - neuroleptic syndrome/ torsade pointes

Antagonist- flumazenil 0.2mg-1mg (withdrawal seizures)

ReCap of Key Points

Sedation: Patient may still experience pain, goal is anti-

anxiety/ – relaxation, goal is usually to give amnesia

Analgesia: Used to treat pain, no anti-anxiety properties

Paralytics: Used to decrease skeletal muscle movement,

imperative that amnesic drugs be used in combination with analgesic meds, MUST sedate before paralyzing

ReCap of Key Points

BIS Monitor: Used to strictly assess patient’s sedation level Goal is 40-60

Peripheral Nerve Stimulator: Used to strictly assess patients paralytic state TOF goal is 1-2/4

Putting it all Together

1. start BIS Monitoring

2. get a Baseline TOF on two locations

3. start Sedation and Analgesic Drips

4. titrate medication up until BIS 40-60

5. bolus paralytic

6. start paralytic drip

7. check TOF q30min until 1-2 twitches

8. monitor TOF and BIS and titrate drips to endpoints

Final Thoughts

give sedation/analgesia before paralyticsBIS assess for sedationTOF assess for adequate NMBIf in doubt it never hurts to ask!

References

Gelinas C. Management of pain in cardiac surgery ICU patients: have we improved over time? Intensive Crit Care Nurs. 2007;23(5):298-303.

Girard TD, Shintani AK, Jackson JC, et al. Risk factors for post-traumatic stress disorder symptoms following critical illness requiring mechanical ventilation: a prospective cohort study. Crit Care. 2007;11(1):R28.

Jacobi J, Fraser GL, Coursin DB, et al. Clinical practice guidelines for the sustained use of sedatives and analgesics in the critically ill adult. Crit Care Med. 2002;30(1):119-141.

Pandharipande PP, Pun BT, Herr DL, et al. Effect of sedation with dexmedetomidine vs lorazepam on acute brain dysfunction in mechanically ventilated patients: the MENDS randomized controlled trial. JAMA. 2007;298(22):2644-2653.

top related