Exam 1: Things are Critical Flashcards
what is the intensive care unit?
-can be defined as a specialized section of a hospital that provides comprehensive care. for persons who are critically ill
–> around-the clock monitoring and treatment of critically ill patients, staffed with specially trained healthcare professionals & contains sophisticated monitoring equipment
Pharmacist role: direct patient care activities
-interdisciplinary pt care rounds
-code blue/code stroke response
-perform medication histories
-prevent and manage adverse drug events/medication errors
-pharmacokinetics/pharmacodynamic monitoring
-patient and caregiver education
Pharmacist role: indirect patient care activities
-policy and protocol development
-formulary management
-research
-participation in committees
PKPD changes in critically ill patients
-fluid shifts
-renal dysfunction
-hepatic dysfunction
Specific prophylaxis considerations in critically ill patients
-ventilator associated pneumonia
-stress ulcer prophylaxis
-venous thromboembolism prophylaxis
Nutrition considerations in critically ill patients
-enteral vs parenteral
FAST HUGS BID (what it is)
-emphasizes the important aspects of critical care medicine that can be applied twice daily to critically ill patients
-can serve as a “check-list” to ensure all elements of ICU care are being accounted for to provide safe, effective care in this setting
FAST HUGS BID (what it stands for)
-feeding
-analgesia
-sedation
-thromboprophylaxis
-head of bed (VAP prophylaxis)
-ulcer prophylaxis
-glycemic control
-spontaneous breathing trial
-bowel regimen
-indwelling catheters
-de-escalation of antibiotics
FAST HUGS BID: feeding
-malnutrition can lead to impaired immune function –> increased susceptibility to infection, impaired wound healing, bacterial overgrowth in the GI tract and an increased risk for development of decubitus ulcers
-feeding should be considered as soon as the pt is clinically stable
FAST HUGS BID: feeding considerations
-emphesis on an early feeding: enteral feeding is PREFERRED –> stimulated the gut to work, has been associated with less GI bleeding
-parenteral nutrition may become necessary if the pts gut it not working or enteral feeds are not being tolerated
FAST HUGS BID: Analgesia - why are they in pain and assessment
-pain due to underlying conditions (trauma, surgery), standard ICU care (lines, tubes, turning/repositioning, physical therapy )
Importance: providing adequate analgesia optimizes pt comfort and minimizes the acute stress response, hyper metabolism, increased oxygen consumption, hyper coagulability, and alterations in immune function- can also reduce the risk of developing agitation
FAST HUGS BID: Analgesia - type of pain and common meds used
–> type of pain: nociceptive vs neuropathic: helps to choose best agent to relieve pain
–> duration of pain: helps us determine whether we need long acting agents or as needed boluses for situation pain
–> account for home pain regimens: make sure underdosing isnt occurring in pts that receive high doses at home
Common meds: fentanyl, hydromorphone, morphine, oxycodone
FAST HUGS BID: Sedation
-pts in the ICU have multiple reasons to become agitated: anxiety, pain, lack of homeostasis, withdrawal, benzo use, sleep-wake cycle disruption
-sedative admin optimizes patient comfort and minimizes the acute stress response
FAST HUGS BID: Sedation - assessment and drug use
-sedation should be assessed and reassessed with a validated tool such as RASS or SAS
-propofol and dexmedetomide are the preferred sedative agents over continuous benzos as they have been associated with more delirium and neurocognitive implications
FAST HUGS BID: Thromboembolism Prophylaxis- importance & considerations
Importance: critically-ill pts have been shown to be at higher risk for VTE than general medical patients due to the additional risk factors for VTE acquired in the critical care setting
Considerations:
–> VTE prophylaxis should be given to ALL pts in the ICU
–> most common options: low molecular weight heparin (enoxaparin 40 mg SQ daily or 30 mg AQ BID) or unfractionated heparin in pts with renal dysfunction ( 500 units SQ Q8H)
-high risk pts: mechanical prophylaxis with graduated compression stockings or intermittent pneumatic compression devices should be initiated
FAST HUGS BID: head of the bed : ventilator associated pneumonia (VAP) prophylaxis
-importance: specific to pts receiving mechanical ventilation: elevating the head and thorax above the bed to a 30-45 degree angle reduces the occurrence of GI reflux and nosocomial pneumonia in pts who are receiving mechanical ventilation
–> maintain the head of the bed elevated at 30-45 degrees, apply antiseptic mouthwash (chlorhexidine 0.12%) topically to the oral cavity TID to maintain pts oral hygiene to prevent bacterial growth with the endotracheal tube
FAST HUGS BID: ulcer prophylaxis- importance
-critically ill pts develop stress-related mucosal damage (SRDM), potentially leading to clinically significant bleeding
(SRMD: an acute erosive, inflammatory upper GI insult to the upper GI tract associated with critical illness)
FAST HUGS BID: ulcer prophylaxis - risk factors for GI bleeding
–> major (need 1): mechanical ventilation > 48 hrs or INR > 1.5, PTT > 2x ULN or platelets < 50,000
–> minor (need 2 or more): drugs that increase bleed risk (steroids, warfarin, heparin), shock/sepsis/hypotension/vasopressors, hepatic/renal failure, multiple traumas, burns > 35% total body, organ transplant, head or spinal trauma, hx of upper GI bleeding or peptic ulcer disease
Drugs to use for prophylaxis: PPIs (pantoprazole), H2RAs (famotidine) - continue until risk factors have resolved
FAST HUGS BID: glycemic control
-hyperglycemia is common in critically ill pts due to meds (steroids, BBs, vasopressors), exogenous glucose (TPN)
-maintaining blood glucose at 140-180 mg/dL should be considered in the acutely ill patient
FAST HUGS BID: Spontaneous breathing trial
-a spontaneous breathing trial is performed on pts on mechanical ventilation and assesses the pts ability to breathe on minimal or no ventilatory support and is designed to assess whether the pts respiratory mechanics are favorable enough to consider liberation from mechanical ventilation
–> should be performed daily to determine a pts extubation readiness with the goal of weaning off of mechanical ventilatory support as early as possible
FAST HUGS BID: bowel regimen
-constipation can occur in many pts: regimen options = docusate, sennosides, polyethylene glycol for standing regimens, bisacodyl suppositories, enemas, magnesium citrate for rescue options
-diarrhea can also occur: infection, feeds, aggressive bowel regimen
FAST HUGS BID: indwelling Catheters:
-important to assess lines at least daily for signs of infection
-assessing the need for these lines or if they can be removed
peripheral venous catheters
a catheter placed into a peripheral vein for venous access to administer IV therapy
centeral venous catheters
lines that terminate in the superior vena cava, just above the right atrium
arterial lines
catheters that are placed into the lumen of an artery to provide a continuous display or accurate blood pressure and access frequent arterial blood sampling
foley catheters
a flexible tube that passes through the urethra and into the bladder to drain urine
rectal tubes
a soft catheter inserted into the rectum for fecal management to contain and divert fecal waste
FAST HUGS BID: De-escalation of antibiotics
-broad spectrum antibiotics are common in critical care units
-applying standard antimicrobial stewardship principles should be standard of care in the critical care setting
–> de-escalating antibiotics as appropriate based on culture results
–> setting appropriate antibiotic duration to avoid under or overuse of antibiotics
–> providing necessary dose adjustments based on PK changes
hypertensive crisis
an acute condition of very high BP with with either SBP > 180, DBP > 120, or both
hypertensive urgency
pts with acute condition of very high blood pressure without evidence of new or worsening target organ damage
hypertensive emergency
pts with acute condition of very high blood pressure and evidence of new or worsening target organ damage
risk factors for HTN crisis
-female sex
-obesity
-hypertensive/coronary heart disease
-presence of a somatoform disorder
-higher number of antihypertensive agents at baseline
common causes of hypertensive crisis
-non-adherence with prescribed rx
-abrupt withdrawal of certain antihypertensives = rebound hypertension (clonidine, BBs)
-substance abuse (cocaine, amphetamines, ecstasy)
-drug-drug interactions (serotonin syndrome)
-drug-food interactions (tyramine containing foods with monoamine oxidase inhibitors)
-drug-disease state interactions (NSAIDs, sympathomimetics in pts with HTN)
-withdrawal (alcohol, opioids, benzos)
Symptoms of hypertensive crisis
-headache
-nausea
-vomiting
-epistaxis
-SOB
-chest pain
-dizziness
-paresthesia
-vision changes
Signs of hypertensive crisis
-focal neurological deficits
-crackles on lung auscultation
-increased Scr/BUN, LFTs
-new/worsening hematuria/proteinuria
-EKG changes
-changes on fundoycopic examination of the eye
-changes on CT of the head (bleed)
-MRI evidence of CVA
Management of hypertensive urgency
-lower blood pressure slowly during the first 24-48 hrs using oral medication
-no need for ICU admission
Management of hypertensive EMERGENCY: 1st hour
requires IV antihypertensives and ICU admission
-decrease DBP by 10-15% or MAP by 25% with goal DBP > 100
Management of hypertensive EMERGENCY: 2-6 hrs, 6-24 hrs & 24-48 hrs
2-6: SBP 160 and/or DBP 100-110
6-24: maintain above goals
24-48: gradually decrease BP to normal (outpatient goal)
Management of hypertensive EMERGENCY: aortic dissection
-SBP < 120 within 1st hour, HR < 60
meds: esmolol then nicardipine
Management of hypertensive EMERGENCY: ischemic stroke
BP < 185/110 before tPA and < 180/105 during tPA infusion
-if no tPA SBP < 220
Meds: nicardipine, clevidipine, labetalol
avoid sodium nitroprusside
Management of hypertensive EMERGENCY: hemorrhagic stroke
SBP > 220: lower with infusion and monitor
SBP 150-220: < 140 in 60 mins
Meds: clevidipine, labetalol, nicardipine
avoid sodium nitroprusside
Management of hypertensive EMERGENCY: severe Pre-eclampsia or Eclampsia
SBP < 140 in 60 mins
Meds: hydralazine, labetalol, nicardipine
avoid RASS inhibitors and sodium nitroprusside
Meds used in hypertensive emergencies: sodium nitroprusside
-onset less than 2 mins, 1-10 min duration
-AEs: hypotension (potent), N/V, muscle twitching, cyanide toxicity
-caution in pts with high intracranial pressure, azotemia, CKD
Meds used in hypertensive emergencies: nitroglycerin
-immediate onset, 3-5 min duration
-AEs: hypotension, headache, methemoglobinemia, tolerance with prolonged use
-most often utilized in situations with coronary ischemia
Meds used in hypertensive emergencies: hydralazine
last line
-IV bolus, 10-80 min onset and up to 12 hr duration
-AEs: hypotension, tachycardia, flushing, headache
-concern with its unpredictable PK profile
-safe for use in pregnancy
Meds used in hypertensive emergencies: Labetalol
-most HTN emergencies, safe to use in pregnancy, caution in acute HF
AEs: hypotension, bradycardia/heart block, orthostatic hypotension
Meds used in hypertensive emergencies: Metoprolol
-only given as a bolus, caution in acute HF
AEs: hypotension, bradycardia/heart block
Meds used in hypertensive emergencies: esmolol
-drug of choice in aortic dissection, caution use in acute HF
AEs: hypotension, bradycardia/heart block
Meds used in hypertensive emergencies: clevidipine
-most hypertensive emergencies, caution with coronary ischemia CI with soy/egg allergy
AEs: hypotension, headache, tachycardia, hypertriglyceridemia
Meds used in hypertensive emergencies: Nicardapine
-most hypertensive emergencies
-not generally utilized in acute HF, caution with coronary ischemia
AEs: hypotension, tachycardia, headache, flushing, local phlebitis
Meds used in hypertensive emergencies: enalaprilat
rare usage
-use in caution with acute HF, AVOID in acute MI, eclampasia, AKI
Meds used in hypertensive emergencies: Fenoldopam
rare usage
dopamine receptor agonist
-avoid in pts with glaucoma (due to increased intraoccular pressure)
AEs: hypotension, tachycardia, headache, nausea, flushing
DKA + HHS
both have increased concentration of catecholamines, cortisol, glucagon and growth hormone –> leads to hyperglycemia via dec in glucose utilization, inc gluconeogenesis and inc glycogenolysis
Precipitanting factors of DKA/HHS
-infections (UTIS and pneumonia)
-#2 myocardial infarction
-medications (steroids)
-noncompliance with therapy
-poor “sick day” management
-pancreatitis
-drug/alcohol abuse
-inadequate dose of d/c of insulin
-new onset type 1 DM
Clinical Presentation of DKA
-onset: hours to days
-clinical pic: kussmaul respirations, N/V, abdominal pain
-glucose: > 250
-acidosis: < 7.3
-anion gap: > 12
-ketones: positive
-serum osmolality: < 320
Clinical Presentation of HHS
-onset: several days to weeks
-clinical picture: neurologic manifestations (seizures, hemiparesis)
-glucose: > 600
-acidosis: normal
-anion gap: variable
-ketones: negative
-serum osmolality: > 320
Treatment of DKA/HHS: fluid management
-initial: 15-20 ml/kg for the first hour
Severe hypovolemia: NS @ 1 l/hr
Mild dehydration:
–> Na+ normal or high: 0.45% NaCl (250-500 ml/hr)
–> Na+ low: 0.9% NaCl (250-500 ml/hr)
Cardiogeniic shock: utilize pressors and monitor hemodynamic closely
Treatment of DKA/HHS: fluid management & glucose levels
-when DKA BG: 200 and HHS BG 300 change to 0.45% NaCl/D5W at 150-250 ml/hr
Treatment of DKA/HHS: Insulin therapy
-regular infusions are the mainstay of treatment
can do: 0.1 unit/kg as IV bolus –> 0.1 unit/kg/he infusion OR 0.14 unit/kg/hr as an IV infusion (no bolus)
-decrease infusion rate to 0.02-0.05 unitd/kg/hr when DKA < 200, HHS < 300
GOAL BG: DKA: 150-200, HHS 200-300
Treatment of DKA/HHS: transition from IV to SQ insulin
-when pt shows resolution of crisis & able to eat: initiate SQ basal insulin and overlap with IV infusion for 1-2 hrs
–> HX of DM with insulin: PTA dosing if it was controlling their diabetic properly (however usually started off at a decreased dose)
–> insulin naiive: multidose regimen with basal and bolus started at a dose of 0.5-0.8 units/kg/day
Resolutions definitions: DKA and HHS
DKA: blood glucose < 200 AND 2 of the following: serum bicarb level > 15, venous pH > 7.3, anion gap < 12
HHS: normal osmolality AND normal mental status
Treatment of DKA/HHS: potassium management
*check K+ before initiating insulin therapy
-K+ < 3.3: HOLD insulin and replete @ 20-30 mEq/hr until the K+ > 3.3
-K+ 3.3-5.3: 20-30 mEq K+ should be given with every L of fluid
-K+ > 5.2: do not give until it falls below the upper limit of normal
Treatment of DKA/HHS: bicarbonate
only indicated in pts with a pH < 6.9: 100 mmol sodium bicarb ( 2 amplules) in 400 mL of H2O + 20 mEq of Kcl over 2 hrs
-repeat q2h until pH > 7
Treatment of DKA/HHS: Phosphate
-insulin therapy decreases serum phosphate as it causes a shift in phosphate
-careful phosphate replacement (20-30 mEq/l potassium phosphate added to replacement fluids) is indicated in: cardiac dysfunction, anemia, respiratory depression, serum phosphate concentration < 1.0 mg/dl
Complications of hyperglycemia crises
-hypoglycemia: glucose should be monitored q 1-2 hrs while in insulin IV infusion
-hypokalemia: BMPs should be monitored q 4-6 hrs while insulin infusion is running
-hyperchloremic non-anion gap metabolic acidosis: secondary to excess infusion of chloride containing fluids during tx
-cerebral edema: occurs in 1-3% of DKA episodes in children, prevent by avoidance of excessive hydration and rapid reduction of plasma osmolarity. treatment: mannitol infusion and mechanical ventilation
Opioid treatment for analgesia: Morphine
-onset is 5-10 min, can give bolus and infusion
-active metabolites & accumulates in renal impairment –> longer duration throughout the day
AEs: histamine release: hypotension, bronchospasm, urticaria
Opioid treatment for analgesia: Fentanyl
-onset in seconds, with 1-2 hours duration
-hepatic metabolism, CYP3A4 interactions
-can lead to tachyphylaxis: pt developed a resistance to drug –> switch to hydromorphone
Opioid treatment for analgesia: hydromorphone
-5 min onset with 2-4hr duration
-good in renal impairment, option for fentanyl tolerance
-available as patient-controlled analgesia (PCA)
Opioid treatment for analgesia: additional options
-acetaminophen: caution in acute liver failure
-NSAID: caution in acute kidney injury, increase risk of GI bleed
-methadone: slow titration to avoid QTC prolongation
-gabapentin
-ketamine
-patient centered analgesia (PCAs)
Richmond agitation sedation scale (RASS)
0: calm and alert
-1: drowsy
-2: light sedation
Sedation agitation scale (SAS)
4: calm and co-operative
3: sedated
Propofol
-stimulates GABA and inhibits NMDA receptors
-has hypnotic, anxiolytic, amnestic and anticonvulsant effects
-NO analgesic properties
-duration of action: 10-15 min (rapid hepatic and extra-hepatic clearance
-long term admin can lead to saturation of peripheral tissues (highly lipid soluble)
Propofol AEs
-respiratory depression
-hypotension
-bradycardia
-decrease cardiac output
-hypertriglyceridemia (acute pancreatitis)
-propofol related infusion syndrome (PRIS)
Propofol uses and clinical pearls
-potentially 1st line agent in: severe alcohol withdrawal, status epilepticus
-lipid emulsion therefore can provide 1.1 kcal/ml of nutrition
-avoid in patients with egg, sulfites, or soybean allergies
-monitor for BP, HR, triglycerides, anoin gap/lactate and CKD when using > 48 hrs
Dexmedetomidine
-decreases release of norepinephrine and dopamine in CNS (alpha-2 adrenergic agonist)
-FDA approve for procedural sedation and sedation for mechanical ventilation NOT > 24 HRS
-has sedative and analgesic properties
AEs: bradycardia, hypotension
Dexmedetomidine benefits
-no respiratory depression
-effects are similar to naturally occurring sleep
-opioid - sparing effects
-useful as adjunct therapy for alcohol withdrawal
Dexmedetomidine drawbacks
-risk of hypotension
-RASS score of -3 or less is unlikely (not for someone that needs heavy sedation)
-risk of withdrawal with prolonged use
-drug induced fever?
Benzos used for sedation: midazolam
-2-5 min onset, 1-2 hr duration
-lipophilic, active metabolites, accumulates in renal impairment
–> primary use for status epilepticus
Benzos used for sedation: Lorazepam
-5-20 min onset, 2-6 hr duration
-propylene glycol acidosis
-can use in renal/hepatic failure
Benzos used for sedation: Diazepam
-5-10. min onset, 1/2life of 44-100 hrs
-active metabolites
-can taper off quickly
-standing doses used in alcohol withdrawal
Benzos used for sedation: uses & drawbacks
-reserve for first line in: status epilepticus, extreme alcohol withdrawal syndromes, severe ARDs requiring deep sedation
-drawbacks: increase risk of delirium, increase time on ventilator & increase length of ICU stay
Ketamine indications and MOA
-indicated for: anesthesia, pain, rapid sequence intubation, acute severe agitation, status epilepticus, treatment resistant depression & PTSD
-MOA: NMDA antagonist, Mu and Kappa agonists, muscuranic acetylcholine receptor antagonist & inhibit reuptake of serotonin, NE and dopamine
Ketamine dosing for pain
0.15-0.5 mg/kg/hr
Ketamine dosing for anesthesia
0.5-2 mg/kg/hr
ketamine dosing for status epilepticus
> 2 mg/kg/hr
Ketamine advantages & common AEs
-advantages: favorable hemodynamic, bronchodilator effects, opioid sparing effects
-AEs: emergence reaction (pretreat with benzo or propofol), oral secretions, tachycardia, hypertension
effects of delirium sequalae (effects of delirium)
-increase mortality
-cognitive impairment
-functional decline
-increase health system costs
-prolonged mechanical ventilation
-increase length of stay
Delirium risk factors
-modifiable: benzo use, blood transfusions
-non-modifiable: increase age, dementia history, prior coma, pre-ICU emergency surgery/trauma, increase APACHE score
Non-pharm interventions for delirium
-re-orient the patient
-use of hearing aids or glasses
-limit noise and light at night (ear plugs etc)
-encourage natural sleep-wake cycle
-early mobilization
-family presence
-music therapy
-limit use of benzos and anticholinergic medications
Pharmacological options for delirium
-opioids, dexmedetomidine, melatonin receptor agonists, antipsychotics (quetiapine, haloperidol, olanzapine)
–> suggest using demedetomidine for delirium in mechanically ventilated adults where agitation is precluding weaning/extubation
indications of NMB
-facilitate mechanical ventilation
-minimize oxygen consumption (acute respiratory distress syndrome)
-increased muscle activity: tetany, neurolopetic malignant syndrome, anti-shivering agent
-increased intracranial pressures or intra-abdominal pressures
-surgical procedures
-rapid sequence intubation
neuromuscular blockers: advantages
-inhibit diaphragmatic function and reduce chest wall rigidity
-reduces oxygen consumption
-eliminates work of breathing
neuromuscular blockers: disadvantages
-patient CANNOT communicate
-no analgesic or sedative properties
-increase risk of DVT and skin breakdown
-corneal abrasion risk
-critical illness polyneuropathy
agents used in NMB
-non-depolarizing agents: cisatrasurium, rocuronium, vecuronium
-depolarizing agents: succinylcholine
what is cardiac arrest?
-unable to generate adequate cardiac output to support oxygen demands of tissue
-4 rhythms: ventricular fibrillation (VF), pulseless ventricular tachycardia (pVT), pulseless electrical activity (PEA), asystole
-survival depends on basic life support and or advanced cardiac life support
-immediate goal: return of spontaneous circulation
Cardiac arrest: CPR/treatment plan
-2 minute cycles of CPR
-end of cycle pulse and rhythm check
-understand when drug therapy is needed
-ONLY specific therapy proven to increase survival to discharge is defibrillation of VF and pulseless VT
what rhythm can you shock?
-VF and pulseless VT
VF or VT arrest steps
1- start CPR
2- shock
3- CPR 2 mins (IV access)
4- shock
5- CPR 2 mins, epinephrine every 3-5 mins, consider advanced airway capnography
7- shock
8- CPR 2 mins, amiodaraone or lidocaine, treat reversible causes
PEA/asystole arrest steps
*non-shockable –> epinephrine ONLY ASAP
1- epinephrine ASAP
2- CPR 2 mins, IV/IO access, epinephrine every 3-5 mins
–> if rhythm shockable: follow VF or VT arrest steps
–> if rhythm not shockable: if no signs of return of spontaneous circulation - consider appropriateness of continues resuscitation
Different types of medication administration
-IV
-IO: goes into the long bone and is circulated systemically
-ET (breathing tube): NAVEL- naloxone, atropine, vasopressin, epinephrine, lidocaine –> give 2 to 2.5 fold IV/IO dose down ET tube (dilute in 5-10ml sterile water or 0.9% saline
Epinephrine used in cardiac arrest
-helps to enhance organ perfusion by increasing arterial and aortic diastolic pressures resulting in increases in coronary and cerebral perfusion pressures
-indications: VF & pulseless VY, PEA & asystole
-administer as soon as feasible in PEA/asystole
Antiarrhythmics use in cardiac arrest
-no high - quality evidence to suggest that any antiarrhythmics drug given routinely during cardiac arrest increases survival to hospital discharge
-potentially normalize abnormally depolarizing and conducting myocardial cells
–> amiodarone, lidocaine, magnesium (torsades de pointes ONLY)
Antiarrhythmics use in cardiac arrest: Amiodarine
-indicated for VP, pulseless VT (stable VT with pulse)
-dose: VF/pulseless VT: 300mg IV bolus, may repeat 150mg IV bolus in 3-5 mins. Stable VT: 150 mg IV over 10 mins
-caution in bradycardia and hypotension
-arrhythmogenic potenial –> QT prolongation
-bolus followed by 20 ml normal saline flush
Antiarrhythmics use in cardiac arrest: lidocaine
-indications: VF, pulseless VT, stable VT (with pulse)
Dose: VF/pulseless VT: 1-1.5 mg/kg IV/IO, repeat 0.5-0.75 mg/kg q 5-10 mins. Stable VT: 0.5-0.75 mg/kg IV
-consider if: amiodarone unavailable, torsades de pointes due to minimal risk of QT prolongation
-with ROSC a continuous infusion of 1-4 mg/min may be initiated
Antiarrhythmics use in cardiac arrest: magnesium
-indicated for VF/pulseless VT, associated with torsade de pointes (wide-complex QRS)
-generally given 2 g IV bolus
-not to be used in VF/pulseless VT and normal QT internal
-flush with 10-20 ml saline
Reversible causes of arrest: H’s (6)
-hypovolemia: loss of effective circulating volume (trauma and blood loss)
-hypoxia: lack of adequate oxygen, give 100% oxygen by mask
-hydrogen ion: severe metabolic acidosis- routine use of sodium bicarb is NOT recommended
-hypothermia
-Hyperkalemia: 1- calcium chloride or calcium gluconate. 2- sodium bicarb or insulin & dextrose
Reversible causes of cardiac arrest: T’s (5)
-Toxins: opioids –> naloxone IV, local anesthetic toxicity –> lipid emulsion, TCAs –> sodium bicarb
-cardiac Tamponade
-Tension pneumothorax
-Thrombosis: pulmonary embolism –> alteplase (tenecteplase) or myocardial infarction –> tenecteplase, alteplase or PCI
deficits that are experienced after a stroke
-hemiparesis
-cognitive decline
-depression
-inability to ambulate without assistance
-PTSD
Ischemic stroke: risk factors
-hypertension
-cig smoking
-diabetes
-dyslipidemia
-arterial arrhythmias
-non-atrial arrhythmia cardiac conditions
-asymptotic carotid stenosis (> 60%)
-sickle cell disease
-postmenopausal hormone therapy
-oral contraceptives
-physical inactivity
-obesity
CHA2DS2-VASc Score
C: congestive HF or LV EEF < 40% -1
H: hypertension - 1
A: 65-74 (1), > 75 (2)
D: diabetes - 1
S: previous Stroke/TIA - 2
V: vascular disease - 1
S: female sex-1
-the higher the score the higher the need to use anticoagulants
Ischemic stroke: assessment/diagnosis
-time critical, accurate clinical assessment
-most important piece of information: time of symptom onset
-sudden onset of focal neurological deficit: dysphasia/dysarthria, hemianopia, weakness, ataxia, sensory loss, neglect
-symptoms are unilateral
-Primary goal: confirm the pts symptoms are due to ischemia rather than other neurological process, consider stroke mimics
–> neuro imaging: non-contrast head CT scan, MRI (more sensitive at detecting early ischemic changes)
Ischemic stroke mimics: neurological
-seizure/postictal state
-complicated migraine
-other intracranial process (abscess, infection, tumor, hemorrhage, MS)
-hypertensive encephalopathy
-vertigo
-cranial/peripheral neuropathies, bell’s palsy
-transient global amnesia
Ischemic stroke mimics: metabolic
-hypoglycemia/hyperglycemia
-hyponatremia
-hepatic encephalopathy
-drug overdose
Ischemic stroke mimics: psychiatric
-conversion disorder
-malingering
Ischemic Stroke Treatment: IV fibrinolytic –> ABSOLUTE CIs
–> approved for treatment of ischemic stroke presenting within 4.5 h of symptom onset
CIS:
-< 18 y/o
-ischemic stroke within 3 months
-intracranial/intraspinal surgery within 3 months
-GI malignancy or GIB within 21 days
-LMWH within 24 hrs
-Infective endocarditis
-intra-axial intracranial neoplasm
-unclear time of onset or > 4.5 h since symptoms onset
-current intracranial hemorrhage
-severe head trauma within 3 months
-subarachnoid hemorrhage
-platelet < 100,000, INR > 1.7, aPTT > 40 sec
-DOAC within 48 hr
-aortic arch dissection
Ischemic Stroke Treatment: IV fibrinolytic guideline recs
-seizure at onset: thrombolytics may be administered if residual impairment are believed to be secondary to stroke
-blood glucose < 50 or > 500: if corrected, can give
-arterial puncture in the last 7 days: uncertain
-recent major trauma (14 days): if not involving the head- may be considered
-recent major surgery (14 days): may be considered
Ischemic Stroke Treatment: Alteplase
-activate plasminogen leads to plasmin activation which dissolves fibrin
*dose: 0.9 mg/kg (max dose 90 mg)
–> bolus: 10% as IV bolus over 1 min, infusion: 90% of the total dose over 60 mins
-1/2 life: 5 mins
Ischemic Stroke Treatment: Tebecteplase
*dose: 0.25 mg/kg (max dose 25 mg) given as IV push
-1/2 life: 20-24 mins
-15 fols increase in fibrin specificity compared to alteplase
IV Fibrinolytics: blood pressure control
-blood pressure is often elevated int he setting of acute ischemic stroke
–> hypertension (> 220/120) is detrimental and increases the risk of hemorrhagic conversion
–> hypotension may worsen ischemia
**if pt meets exclusion criteria and alteplase is NOT given, permissive HTN is allowed: BP is NOT treated unless its > 220/110 in an effort to perfuse the injured brain
IV Fibrinolytics: BP required for thrombolytics bolus
< 185/110
IV Fibrinolytics: BP required for thrombolytics infusion
< 180/105
Blood pressure control in acute ischemic stroke
1st line: labetalol, nicardipine
2nd line: hydralazine, enalaprilat, celvidipine
Fibrinolytics complications: symptomatic ICH
step 1: d/c the alteplase infusion
step 2: cryoprecipitate 10 U infused over 10-30 mins (contains fibrinogen: increases fibrinogen level by 30-60 mg/dL
step 3: anti-fibrinolytics: displace plasminogen from fibrin which inhibits fibrinolysis: tranexamic acid 1000 mg IV
Fibrinolytics Complications: Angieodema
-rare by potentially life threatening (5% of pts), use of ACEi is a major risk factor
step 1: maintain airway
step 2: hold ACEi
step 3: treat with these options: methylprednisolone 80-100mg IV, diphenhydramine 50 mg IV, ranitidine 50 mg IV or famotidine 20 mg IV, epinephrine 0.3 mL
when is thrombectomy used?
for large vessel occlusions +/- intra-arterial thrombolytics
Post-fibrinolytic care
-neurologic and blood pressure monitoring for 24 hrs
-dysphagia and aspiration risk
-high dose statin in all pts
-antiplatelets (aspirin for all patients, dual-antiplatelets for low NIH stroke x 21 days OR those with intracerebral stent placement
-DVT prophylaxis ( > 24 h post alteplase)
-anticoagulation (if cardioembolic stroke or hx of atrial fib)
secondary stroke prevention
-lifestyle and nutrition
-smoking cessation
-limited alcohol consumption
-counsel on substance abuse
-hypertension
-dyslipidemia
-diabetes
reasons for a provoked seizure
-intoxication
-withdrawal (ETOH, benzos)
-trauma
-meningitis
-psychiatric
-metabolic derangements
-noncompliance with seizure medications
reasons for unprovoked seizures
-more difficult to determine cause
-may or may not need treatment with anti epileptic medications
–> true unprovoked first time seizure does not require medication therapy
Inhibitory and excitatory NTs:
inhibitory: GABA
Excitatory: glutamate, aspartate, acetylcholine
What agents are used to stop seizures?
Benzos: lorazepam, diazepam, midazolam
what agents are used to prevent more seizures from occuring?
anti-epileptics: phenytoin, fosphenytoin, leviteracetam, valproic acid
Benzos in seizure tx
1st line: lorazepam IV 4 mg
AEs: impaired consciousness, hypotension, respiratory depression
(Fos) phenytoin MAO and pk
-stabilizes neuronal membranes and decreases seizure activity by increasing efflux OR decreasing influx of Na ions across the cell membranes
LD: 20 mg/kg IV
MD: 4-6mg/kg/day
-highly protein bound
AEs: cardio, extravasation
Phenytoin AEs
P-450 interactions*
Hirsutism
Enlarged gums
Nystagmus
Yellow-browning of skin (hepatitis)
Osteomalacia (vit D deficiency)
Interference with folate metabolism (anemia)
Neuropathies: vertigo, ataxia, headache*
Rashes/fever/SJS*
Neutropenia, thrombocytopenia
Monitoring of Phenytoin
goal phenytoin level: 10-20 mcg/dl
-if seizing may target 15-25 mcg/dl
-levels > 30 are associated with seizures
-must correct level for low albumin (less than 3.5)
Levetiractem in seizures
-60 mg/kg IV bolun
AEs: agitation, drowsiness
Valproic acid in seizures
LD: 40 mg/kg, MD: 1 mg/kg IV q 8h
-goal level: 50-100 mcg/mL
AEs: drowsiness, headache, thrombocytopenia, pancreatitis, hyperammonemia
**important DDI with phenytoin (both strongly protein bound)
Lacosamide for seizures
-add on therapy
dose: 100-200 mg IV BID
AEs: dizziness, abnormal vision, diplopia, ataxia, ~generally well tolerated
Refractory SE
-if there is no response to the initial anticonvulsants, SE is considered to be refractory
–> seizures lasting > 2 hours OR
–> seizures recurring at a rate of 2 or more episodes per hour without recovery to baseline between seizures, despite treatment with conventional anti-epileptic drugs
- in general, these patients have respiratory and cardiovascular compromise and systemic complications: intubations/ventilation my be required, correct hypotension
Post-intubation treatment (seizures)
-a paralytic is used during intubation, therefore seizures are not going to be physcially observed
–> need to start an IV infusion of an antiepileptic such as propofol or midazolam
–> need to put the patient on a long term monitoring EEG to assess ongoing seizure activity
-at this point, patients are generally on 2 - 3 IV antiepileptics + at least 1 continuous IV infusion
Treatment of Refractory SE
-high dose benzo: midazolam bolus + infusion
-propofol IV infusion
-phenobarbital or pentobarbital coma
Phenobarbital/Phentobarnital coma
-suppresses the sensory context –> sedative hypnotic
AEs: respiratory depression - pts require inntubation, hypotension, lethargy, nystagamus, thrombocytopenia, suppress immune system, decreased GI motility
Goals of therapy for status epilepticus
-to attain burst suppression on the LTM
-generally burst suppression is maintained for 24-48 h
-after this time period, the IV infusions are slowly titrated off while monitoring the LTM for return of seizures
Super Refractory status epilepticus
-ketamine infusion
LD: 1.5-3 mg/kg IV once
MD: o.1-4 mg/kg/hr
After burst suppression is attained in seizure - now what?
-slowly ween the IV infusions based on the LTM reading
-usually wean agents that are causing adverse reactions or need for other interventions
-if LTM demonstrates seizure activity, agents doses are increased again
Define shock
-a potentially fatal physiologic reaction resulting from various conditions including infection, injury, hemorrhage, dehydration, heart failure
–> hypotension (SBP < 90 OR decrease by 40 from baseline BP)
-characterized by “cellular dysoxia” : diminished blood circulation, inadequate oxygen delivery to the tissues, results in anaerobic metabolism
Outcomes = multi-organ system failure & death
Clinical presentation of shock: cardiovascular organ compromise
-cardiac index < 2.2
-SBP < 90
-MAP < 65
Clinical presentation of shock: signs of tissue hypoperfusion
-cold. clammy, mottled skin
-lactate > 2
-SCVO2 < 65%
-SVO2 < 60%
clinical presentation of shock: signs of organ dysfunction
-encephalopathy, lethargy, confusion
-urine output < 0.5 ml/kg/hr
-liver dysfunction
equation for mean arterial pressure (MAP)*
1/3 SBP + 2/3 DBP
what are the goals for shock management?
-determine etiology (hypovolemic, cariogenic, distributive, obstructive)
-maintain adequate tissue perfusion
-restore mean arterial pressure: MAP > 65
-normalize lactate: < 2
Central venous catheter
measures: central venous oxygen saturation from venous blood gas
-can be used to administer fluids, antimicrobials, parenteral nutrition
Pulmonary artery catheter
measures: pulmonary capillary wedge pressure (preload), cardiac output/cardiac index, mixed venous oxygen saturation & systemic vascular resistance
–> no commonly used- several complications
arterial line
measures: mean arterial pressure, SBP and DBP, arterial blood gas
What are shock goals?
-hemodynamic optimization: MAP > 65
-maintain oxygen delivery
-reversal of oxygen dysfunction
-maintain urine output: > 0.5 ml/kg/hr
-reverse encephalopathy
Hypovolemic Shock- causes
-inappropriately low and sudden loss of intravascular volume
Causes: hemorrhage, GI loss, severe dehydration, 3rd spacing, burns
–> #1 cause of death in those under 45: trauma and hemorrhagic shock
Hypovolemic shock effects on the circulatory system
-decrease preload
-decrease cardiac output
-increase after load
-decrease tissue perfusion
hypovolemic shock management
-identify source of loss: surgical hemostasis may be required
–> hemorrhage: REPLACE BLOOD, packed red blood cells, may also need to give fresh frozen plasma and platelets
-anticoagulation reversal (DOACS)
-GI losses, burnd, 3rd spacing : give fluids (crystalloids)
Cardiogenic Shock
failure of left ventricle to deliver blood due to impaired stroke volume or HR, associated with cardiovascular disease
Causes: acute MI, arrhythmias, end-stage heart failure, valve failure, valve disease, dilated cardiomyopathy etc
Cardiogenic shock effect on the circulatory system
-failure of emptying left ventricle = increase preload
-decreased cardiac output
-decreased tissue perfusion
-compensatory increase in afterload
Cardiogenic shock management
-MI: revascularization: cardiac catheterization or coronary artery bypass grafting
-Arrhythmias: try to achieve sinus rhythm, heart dependent on perfusion goals
-Advanced methods: left ventricular assist devices, extracorporeal membrane oxygenation
Distributive shock
-characterized by pronounced vasodilation
septic shock is classic
other causes: anaphylaxis, neurologic, myxedema coma, adrenal and hepatic insufficiency
Distributive shock effect on circulatory system
-vasodilation =decreased afterload
-decreased preload (less volume returning to the heart)
- increased then decreased cardiac function and tissue perfusion
Obstructive Shock
-results from critical decrease in LV stroke volume or increase in left ventricle outflow obstruction
-common etiologies: pulmonary embolism, severe pulmonary hypertension, tension pneumothorax, pericardial tamponade
Obstructive shock effects on cardio system
see a decrease in LV stroke volume
-causes decrease cardiac out put and tissue perfusion
-preload will appear elevated due to the “obstruction”
-increase in afterload in attempt to compensate
Shock Pharmacotherapy: fluid therapy
-fluid challenge: generally with sepsis
–> *crystalloid 30 ml/kg over 15-30 mins then by 10,l/kg boluses
static variables
measure of current state of hemodynamic system
dynamic variables
measures responsiveness of cardiovascular system to therapy
Shock Pharmacotherapy: steps for treatment
initiation of vasoactive agents when MAP remains < 65 mmHg despite fluid administration
-arterial line should be placed if possible
Shock Pharmacotherapy: Norepinephrine
-potent alpha adrenergic agonist –> increases MAP via peripheral vasoconstriction, also has beta 1 properties
-use over dopamine in septic shock
-improved renal blood flow in fluid resuscitated pts
-significant SE: vasoconstriction
Shock Pharmacotherapy: Epinephrine
-low dose = beta 1, increases HR and stroke volume
-high dose = increased alpha 1, vasoconstriction
-3rd in line after NE and vasopressors
-my increase “aerobic lactate production* by stimulation of B2 skeletal muscle receptors
AEs: tachycardia, arrhythmias, cardiac ischemia, peripheral vasoconstriction, reduced renal blood flow, hyperglycemia and hypokalemia
-useful for anaphylactic shock
Shock Pharmacotherapy: dopamine
-dose-dependent pharmacology
–> < 5: vasodilation
–> 5-10: increase cardiac contractility, HR
–> > 10: vasoconstriction
-most effective in hypotensive pts with depressed cardiac function or cardiac reserve
-utilize when low risk for arrhythmia or with significant bradycardia
AEs: tachycardia, arrhythmogenesis, peripheral vasoconstriction at high doses
Shock Pharmacotherapy: Phenylephrine
-selective alpha-1 adrenergic agonist: peripheral vasoconstriction, purported reflex bradycardia
-not rec in septic shock unless:
–> NE produces significant tacharrhythmias
–>cardiac output is high and BP is persistently low
–> salvage therapy when standard therapies are ineffective
AEs: severe vasoconstriction, bradycardia, myocardial ischemia
Shock Pharmacotherapy: dobutamine
-considered an iontrope
-produces ionotropic action via beta 1
-added to treatment of shock when cardiac output or Sv)2/ScvO2 goals have not been achieved with vasopressor therapy –> often used for cardiogenic shock
Shock Pharmacotherapy: Vasopressin
V1: directly constricts smooth muscles
V2: ADH activity
V3: increase ACTH activity
-sepsis dose = 0.03 units/min
GOAL = reduce concurrent vasopressor doses - should not be used as the sole vasopressor in spesis
AEs: cardiac and mesenteric ischemia
Shock Pharmacotherapy: Angiotension II (Giapreza)
-indicated for tx of septic shock
-produces vasoconstriction and aldosterone release
-administered by continuous infusion via central line
-add to standard therapy
AEs: risk for thromboembolism
*shock: treatment goals
-hemodynamic goals: MAP > 65, HR < 100
-renal perfusion: urine output > 0.5 ml/kg/hr
-oxygen deficiency: lactate normalized to < 2 mmol/L
-brain perfusion: improved mental status
examples of cardiogenic shock
-myocardial infarction
-heart failure
-cardiac arrhythmias
examples of hypovolemic shock
-hemorrhagic
-dehydration
examples of distributive shock
-SEPSIS
-anaphylaxis
-neurogenic
-pancreatitis
examples of obstructive shock
-cardiac tamponade
-pulmonary embolism
-tension pneumothorax
ways to treat cardiogenic shock
- myocardial infarction: revascularization –> cardiac catheterization or coronary artery bypass grafting (CABG)
-arrhythmias: try to achieve sinus rhythm
Sepsis
-life threatening organ dysfunction caused by a dysregulated host response to infection
-clinically organ dysfunction can be recognized by using the SOFA
Septic Shock
-subset of sepsis with profound circulatory, cellular and metabolic abnormalities
–> requires vasopressors for MAP > 65 with serum lactate > 2 mmol/L in the absence of hypovolemia
qSOFA rapid bedside score
at least 2 of the following:
-SBP < 100
-RR > 22
-altered mental state
SIRS Criteria for SS*
at least 2 of the following:
-temp > 38 or < 36
-HR > 90
-RR > 20
-WBC > 12 x 10^9 or < 4 x 10^9
Antibiotic use in septic shock
-blood cultures should be drawn prior to antibiotic therapy initiation as long as this does not delay initiation of abx
-delay in abx in sepsis is associated with increased mortality
-harms of unnecessary antimicrobials: allergic reactions, kidney injury, thrombocytopenia, C diff and antimicrobial resistance
-empiric therapy should be narrowed once pathogen identification and sensitivities are established and/or clinical improvement is noted –> source control is ESSENTIAL
abx use: sepsis is definite or probable: shock is present or shock is absent
administer abx IMMEDIATELY, ideally within 1 hr of recognition
abx use: sepsis is possible & shock is present
administer abx IMMEDIATELY, ideally within 1 hr of recognition
abx use: sepsis is possible but shock is absent
-rapid assessment of infections vs noninfectious causes of acute illness
-administer abx within 3 hours if concern for infection persists
pt risk factors for high risk of MRSA infections
-prior hx of MRSA infection or colonization
-recent IV abx use
-hx of recurrent skin infections or chronic wounds
-presence of invasive devices
-hemodialysis
-recent hospital admissions
-severity of illness
patient risk factors for multi-drug resistant organisms (needing 2 gram - agents for empiric coverage)
-proven infection of colonization with resistant organisms within the preceding year
-recent broad spectrum IV antibiotic use within previous 90 day
-travel to highly endemic country within previous 90 days
-local prevalence of antibiotic resistant organisms
-hospital acquired infections
Fluid therapy in septic shock
-Crystalloid 30 ml/kg over 15-30 mins, followed by 10 mL/kg boluses as needed
-should be guided by hemodynamic parameters and assessment of volume status
Difference colloids that can be used in septic shock
-albumin: 5%: used for fluid resuscitation, 25% used for fluid mobilization
-starches: NOT recommended for resuscitations in septic shock –> increased risk of mortality, AKI and bleeding
-blood products: if Hgb < 7 mg/dL & active bleeding
Pharmacotherapy of shock
-initiation of vasoactive agents when MAP remains < 65 despite fluid administration
-arterial line should be placed if possible (more accurate blood pressure monitoring)
-central venous catheter generally required for administration
Vasopressors in Septic Shock (top 4)
1) norepinephrine: rec as the 1st choice vasopressor
2) vasopressin: can be added if pt has inadequate MAP while on NE; shown to help reduce NE req
3) epinephrine: can be added if blood pressure goals not achieves with NE and vasopressin
4) dopamine: has increased risk of tachyarrhythmias and is generally inferior to NE as a first line vasopressor, limited utility in septic shock
Vasopressors in septic shock (others)
-dobutamine: added to tx of shock when pts require cardiac output support, often used for cardiogenic shock (pump failure)
-angiotensin II: reserved for refractory distributive shock
-phenylephrine: used in clinical practice when tachycardia limits NE utility
Hydrocorticortisone (+ fludrocortisone) in septic shock
-cortisol improved the physiologic response to sepsis
-added after poor response to fluids and vasopressors (aka refractory shock)
–> hydrocortisone 50 mg q6h IV
–> fludrocortisone 50 mcg PO daily
-recommend in septic shock when there is ongoing need for vasopressors –> usually added when patient is hypotensive despite increasing NE dose and/or initiation of vasopressin
