Acute care Flashcards

1
Q

Absorption

A

Oral:
Impaired and unpredictable in critically ill patients

Alterations in gastric emptying and motility–>opioids, C.diff
Interactions with enteral feeding and tubing–>fluoroquinolines, phenytoin, GI injury/disease

IV: preferred in many of those cases

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2
Q

Distribution

A

Relates to fluid and hydration status
-Hydrophilic drugs have high Vd in critically ill patients than regular medical floor patients

Alterations in protein binding
-Decreased albumin–>less protein binding of drugs
-Increased acute phase proteins–>more protein binding of drugs
Ex: lidocaine

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3
Q

Metabolism (hepatic)

A

Enzyme expression and activity may be decreased in critically ill patients

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4
Q

Metabolism (renal)

A

Renal dysfunction and HD/CRRT is common

Decreased: shock, sepsis, nephrotoxic drugs

Increased: burn, trauma

How to assess?
CrCl–>delayed
Urine output–>immediate

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5
Q

Sepsis

A

Life threatening dysfunction caused by dysregulated response to infection
-Immune dysregulation
-Coagulation and thrombosis leading to endothelial injury

Occurs in response to any pathogen–>bacterial is most common
Occurs in any site of injection–>lungs, bloodstream, urinary tract

Treatment: early detection and supportive care + broad spectrum IV antibiotics/antifungals and source control

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6
Q

Septic shock

A

Sepsis associated with cardiovascular collapse and hypotension
-Hypotension caused by decreased vascular tone

Treatment:
Fluids
+
Vasopressors–> increase vascular tone and cardiac output via vasoconstriction
1st line: norepinephrine
others: epinephrine, phenylephrine, dopamine, add- on vasopressin, dobutamine
Target MAP > 65 mmHg

If refractory–>IV hydrocortisone

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7
Q

Respiratory failure

A

MECHANICAL VENTILATION IS COMMON

Causes: airway compromise, hypoventilation, hypoxic failure, inability to protect airways

Acute Respiratory Distress Syndrome (ARDS)
Characterized by acute, diffuse inflammatory lung injury
1st phase: mucous
2nd phase: fibrotic

Risk for ARDS: pneumonia, sepsis, trauma, aspiration

Treatment: mechanical ventilation + sedation +/- neuromuscular blockade
Corticosteroids may be used

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8
Q

Analgesia treatment

A

Preemptive analgesia in advance to painful procedures (dressing changes, chest tubes, insertion of lines)

IV opioids: Bolus or continuous infusion or both
SE: sedation, respiratory depression, do not have to worry about respiratory depression if on vent

Non-opioids: Tylenol
NSAIDS–>procedural
Ketamine–>post-surgery
Gabapentin/pregabalin/carbamazepine–>neuropathic

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9
Q

Underlying causes of agitation

A

Pain
Mechanical ventilation
Hypoxia
Delirium
Hypotension
Withdrawal

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10
Q

Non-pharmacological treatment of agitation

A

Maintain patient comfort
Provide adequate analgesia
Reorient the patient–> where and why they are in the hospital
Optimize environment for sleep patterns

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11
Q

Pharmacologic treatment of agitation

A

Sedatives
-Adjunct for anxiety and agitation
-Adjunct to non-pharmacological
-Many mechanical ventilation patients

ANALGESIA-FIRST SEDATION

Goal: Less is best–>light sedation
Desire a calm arousable patient, able to purposefully follow simple commands

Methods: spontaneous awakening trial, nursing-protocolized targeted sedation

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12
Q

Lorazepam MOA

A

Binds to the allosteric site of GABAa receptor increasing frequency of Cl- channel opening

Inhibits GABA activity on neuron impulses–>hyper-polarizes cells leading to resistance to excitation

IV contains propylene glycol solvent that can cause lactic acidosis and nephrotoxicity after high doses or prolonged infusions–>MONITOR OSMOL GAP

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13
Q

Lorazepam side effects

A

Respiratory depression

Hypotension, tachycardia

Withdrawal (seizures)–> gradually taper dose

Delayed sedation: prolonged infusion, advanced age, hepatic/renal insufficiency (midazolam)

DELIRIUM

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14
Q

Lorazepam properties

A

Anxiolysis
Sedation
Amnesia
Anticonvulsant and muscle relaxant

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15
Q

Lorazepam pearls

A

Tolerance with chronic administration

Metabolized into inactive metabolite via glucuronidation–>less accumulation

Least lipid soluble crossing the BBB more slowly leading to delayed onset and prolonged duration of action (long t1/2 life)–>LESS TITRATABLE

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16
Q

Midazolam

A

IV only

Hepatically metabolized by CYP3A4–> increased t1/2 in elderly, hepatic disease, drug interactions

At physiological pH, very high lipid solubility leading to rapid onset (short 1/2 life)–> TITRATABLE

After 48 hours, t1/2 becomes prolonged or unpredictable especially in renal disease due to metabolite accumulation

Recommended for short term use only, not for long term sedation because of unpredictable awakening time

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17
Q

Propofol MOA

A

Binds sites on multiple receptors (GABA, glycine, nicotinic, M1 muscarinic) interrupting neural transmission leading to global CNS depression

IV

Diprivan–>contains EDTA that can cause electrolyte abnormalities, recommended drug holiday after > 7 days treatment

Sodium metabisulfate–>allergic reactions in asthmatics

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18
Q

Propofol Indications

A

General anesthetic
Procedural sedation
Neurosurgical–>may reduce ICP and rapid offset of sedative effects

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19
Q

Propofol side effects

A

Hypertriglyceridemia–>check q48 hours

Apnea

Hypotension, bradycardia

Pain with infusion

Withdrawal–> gradual taper if > 7 days of therapy

Propofol Infusion Syndrome–>acidosis, bradycardia, lipidemia
**sustained treatment > 48 hours
**high doses >75-80 ug/kg/min
**metabolic acidosis
**rhabdomyolysis
**hypotension, arrhythmias
**asystole (rare)

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20
Q

Propofol PK

A

Hepatically metabolized with no active metabolite

No changes in renal or hepatic function

High protein bound

Large Vd

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21
Q

Propofol pearls

A

Easily penetrates BBB–> rapid onset
Rapidly redistributes tissues and rapid hepatic clearance–>rapid offset
Provides some amnesia
Phospholipid emulsion–>1.1 kcal/mL
DO NOT HANG > 12 hours–>risk of infection

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22
Q

Dexmedetomidine MOA

A

selective alpha-2-agonist within CNS inhibiting norepinephrine release

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23
Q

Dexmedetomidine ROA

A

IV

Avoid loading dose

May push doses higher than guidelines due to weak sedation

May use for longer than > 24 hours compared to guidelines

24
Q

Dexmedetomidine properties

A

Patients readily arousable with gentle stimulation–>not used for deep sedation

Anxiolysis

Analgesic sparing effects

No respiratory depression

No anticonvulsant

25
Dexmedetomidine Side effects
Increase in blood pressure with rapid administration Hypotension, bradycardia **more common in volume depleted patients with high sympathetic tone-->AVOID IN HEMODYNAMIC UNSTABLE PATIENTS
26
Dexmedetomidine PK
Highly protein bound High Vd Short t1/2 Hepatically metabolized and eliminated in urine as glucuronide **no changes in renal dysfunction **decrease dose by 40-70% in hepatic dysfunction
27
Monitoring-->hourly assessment
Subjective: assessment is difficult due to inability to outward express anxiety Richmond-agitation-sedation scale (RASS) Sedation-agitation scale (SAS) Objective: Bispectral index (BIS) -Utilizing EEG to find objective number -Guidelines suggest using in patients who other measures are not feasible (sedation, NMBA) NOT RECOMMENDED IN ALL PATIENTS
28
Thromboprophylaxis
Receive unless sufficiently mobile, low risk of VTE, contraindications
29
Enoxaparin
DOC 30 mg SQ q12h or 40 mg SQ q24h monitor s/sx of bleeding, CBC CrCl < 30 mL/min: 30 mg SQ q24h
30
Daltaparin
5000 units SQ q24h monitor s/sx of bleeding, CBC No renal adjustment
31
Unfractionated heparin
5000 units SQ q8-12 hours monitor s/sx of bleeding, CBC No renal adjustment
32
Ulcer risk factors
Shock, coagulopathy, chronic liver dx Neurotrauma, burn injury, extracorporeal life support Mechanical ventilation Drugs: antiplatelets, anticoagulants, NSAIDS
33
Glycemic control
Causes: stress, TPN Balance risk between hypo/hyperglycemia BG goal: 144-180 mg/dL > 180 mg/dL: initiate insulin Avoid long-acting agents due to long t1/2 life
34
Two subtypes of delirium
Hyperactive (agitated)-->hallucinations, delusions Hypoactive (calm, lethargic)-->confusion, sedation
35
Modifiable risk factors of delirium
Benzodiazepines Blood transfusions
36
Non-modifiable risk factors of delirium
Older age Preexisting dementia Prior coma Pre-ICU emergency surgery or trauma High severity of illness at admission
37
Other risk factors of delirium
HTN Psychoactive drugs Prolonged physical restraint, immobility Sepsis Hypoglycemia, hyponatremia Metastatic disease of the brain, head injury, CNS infections
38
Assessment of delirium
ICDSC CAM-ICU
39
Non-pharm treatment of delirium
Early mobilization Optimize sleep Optimize hearing and vision Improve cognition
40
Pharmacological treatment of delirium
NOT RECOMMENDED FOR PREVENTION NOT RECOMMENDED FOR ROUTINE THERAPY
41
Haloperidol MOA
Short-term treatment typical antipsychotic-->D2 antagonist IV, PO
42
Haloperidol properties
Mild sedation without analgesia Minimal CV effects
43
Haloperidol PK
long t1/2 life
44
Haloperidol SE
QTc prolongation and TdP -Avoid in high risk patients -Avoid with other Qtc prolonging agents -D/C if QTc >450 msec or > 25% increase from baseline Lower seizure threshold EPS Neuroleptic Malignant Syndrome
45
Atypical antipsychotics
Risperidone, olanzapine, quetiapine, aripiprazole, ziprasidone MOA: 5HT2A and D2 antagonist
46
Atypical antipsychotic SE
Lower EPS QTc prolongation: avoid in high risk patients, avoid with other QTc prolonging agents, D/C if QTc > 450 msec NMS-->olanzapine most common Hypotension-->olanzapine most common
47
Dexmedetomidine for delirium
May be used for delirium-related agitation precluding weaning off vent/extubating
48
Depolarizing NMBA
initial inactivation of Ach receptors then inhibition
49
Non-depolarizing NMBA
Competitively block the action of Ach Amino steroidal Benzylisoquinolinium
50
Reversal agents
Pyridostigmine, neostigmine-->Ach inhibitors Sugammadex: modified A cyclodextrin for reversal of rocuonium/vecuronium
51
Succinylcholine MOA
physically resembles Ach to bind to Ach and activate receptors-->depolarization of neuromuscular junction-->muscle contraction blocked
52
Succinylcholine indication
Rapid sequence intubation (RSI) NOT USED FOR SUSTAINED NEUROMUSCULAR BLOCKAGE
53
Succinylcholine SE
Initial muscle contractions: may pre-administer with non-depolarizing MNDA agent APNEA-->MUST BE READY TO INTUBATE IMMEDIATELY Prolonged apnea-->impaired pseudocholinesterase activity or lower levels Muscle fasciculations-->deep aching muscle pain lasting for days Hyperkalemia: contraindicated in major burns, crash injury, and upper motor neuron disease
54
Succinylcholine PK
onset: 1 minute Duration: 3-5 minutes Elimination: rapidly hydrolyzed by pseudocholinesterase
55
Non-depolarizing agents indications
Immediate/sustained paralysis Mechanical ventilation Muscle relaxation operations RSI if contraindicated to succinylcholine -Rocuonium if CI to succinylcholine Increased ICP Hypothermia
56
Non-depolarizing NMBA SE
Paralysis of respiratory muscles/apnea Inadequate pain/sedation: NMDA do not provide analgesic, sedative, or anxiolytic effects, assessment can be hard when they cannot talk, MUST BE OPTIMIZED ON SEDATIVE AND ANALGESIC DRUGS PRIOR Prolonged paralysis: caused by accumulation of medication and chronic administration Solution: drug holidays Drug interactions: corticosteroids
57
Toxicity endpoint-->peripheral nerve stimulation
Twitch monitoring or train-of-four 4/4--> < 75% suppression 3/4--> 75% suppression 2/4--> 80% suppression 1/4--> 90% suppression 0/4--> 100% suppression Goal: 1-2 out of 4