Critical Care Flashcards
Hypovolemic Shock
GI bleed, hemorrhage
Low CI
Low PCWP
High SVR (reflex)
Treat with fluid resuscitation
Blood products if Hgb <7 or actively bleeding
Pressors if hypotension not improved after fluids
Cardiogenic Shock
Acute MI, ADHF, valvular injury
Low CI
High PCWP (impaired blood flow causes congestion)
High SVR (reflex vasoconstriction)
Treat based on acute cardiovascular diseases
Obstructive Shock
Massive PE, Tamponade
Low CI
Low PCWP, if tamponade
High PCWP, if massive PE, aortic stenosis)
High SVR
Treat obstruction to reverse shock
PE: thrombectomy or thrombolytics
Tamponade: remove fluid
Fluids & vasopressors may improve symptoms but not outcomes
Distributive Shock
Sepsis
Early:
High CI
Low PCWP
Low SVR
Late:
Low CI
High PCWP
Low SVR
Antibiotic & fluid resuscitation in first hour
Sepsis
life-threatening end organ dysfunction caused by dysregulated response to infection
Do not use qSOFA as only screening tool
Septic shock
subset of sepsis
profound circulatory, cellular, and metabolic abnormalities are associated with greater mortality risk than sepsis alone
criteria: vasopressor need for MAP >65 and lactate > 2 despite fluid resuscitation
Surviving Sepsis Campaign 1 hour bundle
1) Baseline lactate
2) Obtain blood cultures prior to antibiotics
3) Administer broad spectrum antibiotics
4) 30mL/kg crystalloid infusion (LR may be > NS)
5) Initiate vasopressors if hypotensive during or after fluids for MAP > 65
6) Reassess if persistent arterial hypotension
Vasopressor extravasation
Get central venous access ASAP but may start peripherally to not delay administration
If extravasation occurs, stop immediately and switch to another site
Inject phentolamine (alpha receptor antagonist) around site ASAP to reduce tissue necrosis
Alternatives in shortage: nitroglycerin ointment or SC terbutaline
Vasopressor treatment cascade
1) DOC: Norepinephrine
2) Vasopressin may be added if needed at 0.03 units/minute
3) Epinephrine can be added if inadequate MAP on norepi + vasopressin
Alternative: Dopamine
Phenylephrine
Norepinephrine vs Dopamine
No difference in 28-day mortality
Dopamine associated with higher risk of arrhythmia, more days on vasopressor therapy, and needed another pressor.
Norepi does not improve mortality but is safer and more effective.
Norepinephrine (dose, receptors, info)
0.01-3 mcg/kg/min
alpha»_space; B1
No activity at B2 or DA
Decrease renal perfusion
Increase SVR, MAP
No change or increase CO
May cause peripheral ischemia
Can induce tachyarrhythmia & Myocardial ischemia
Vasopressin (dose, receptors, info)
0.03-0.04 unit/min - no titration
No adrenergic activity at alpha, B1, B2, or DA
V1 agonism = peripheral vasoconstriction
No adrenergic activity = effective during acidosis & hypoxia
High dose = coronary vasoconstriction, peripheral necrosis
Epinephrine (Dose, receptors, info)
0.04-1mcg/kg/min
alpha»_space;>B1=B2
No activity at DA
low doses = beta adrenergic
Positive inotrope/chronotrope = tachyarrhythmia & myocardia ischemia
May increase lactate (type B lactic acidosis) and blood glucose
May reduce splanchnic circ = gut ischemia
Used in refractory hypotension
Phenylephrine (dose, receptors, info)
0.5-8 mcg/kg/min
alpha only (no B1, B2, DA) - minimal cardiac activity
Reduce renal perfusion
Increase SVR, MAP
Primarily used to raise BP. Can rapidly inc SBP, DBP which may cause bradycardia = reduction in CO.
Low dose dopamine (dose, receptors, info)
1-3 mcg/kg/min = lower inotropic dose
+/- alpha
+ B1
+/- B2
++++ DA
Causes renal, coronary, mesenteric, and cerebral arterial vasodilation & natriuretic response
Do not use for renal protection. No evidence to support
Complements vasoconstrictive effects of norepi
May induce arrhythmia. May cause endocrine changes.
Immediate precursor to norepi. Prolonged infusion can deplete norepi stores = loss of vasopressor response
Moderate dose dopamine (dose, receptor, info)
3-10 mcg/kg/min
+ alpha
++ B1
0 B2
++ DA
May increase contractility and SVR
Can induce arrhythmia. Can cause endocrine changes.
Immediate precursor to norepi. Prolonged infusion can deplete norepi stores = loss of vasopressor response
High dose dopamine (dose, receptors, info)
10-20 mcg/kg/min
alpha +++
B1 ++
B2 0
DA +
Vasodilatory effect on renal blood flow may be lost due to predominant alpha1 vasoconstrictive effects
Can induce arrhythmia. Can cause endocrine changes.
Immediate precursor to norepi. Prolonged infusion can deplete norepi stores = loss of vasopressor response
Dobutamine (dose, receptor, info)
2-20 mcg/kg/min
B1»_space;> alpha = B2
0 DA
Positive inotrope = increased CO
B2 stimulation = possible hypotension
Higher doses can cause tachyarrhythmia and changes in BP which may cause myocardial ischemia
Milrinone (dose, receptor, info)
50 mcg/kg load over 10 min, then 0.375-0.75 mcg/kg/min
*Load often omitted due to increased risk of vasodilation - vasodilation can cause hypotension, arrhythmia
Nonadrenergic
PDE type 3 inhibitor
Positive inotrope = increased CO
Renally adjust
Angiotensin II (dose, receptor, info)
10-80 ng/kg/min then 1.25-40 ng/kg/min
Nonadrenergic
Causes smooth muscle contraction & vasoconstriction
Increased thrombotic risks
May cause increased HR, LA, infections, delirium
ACE-I = exaggerated response
ARB = reduced response
Antibiotic cascade in SSC
Broad spectrum abx initiated within an hour (septic shock) after 2 sets of blood cultures and other cultures obtained
Each 1 hour delay = increase risk of mortality by 7.6%
Infuse broadest antibiotic first as rapidly as possible
Limit empiric antibiotic to 3-5 days
SSC steroid recommendation
Hydrocortisone 200mg/day
Unsure if mortality benefit, but has short term benefits
Do not use corticotropic stimulation test
Initiate when norepinephrine needs of > 0.25mcg/kg/min for at least 4 hours
Ascorbic acid in septic shock
Possible anti-inflammatory, antioxidant properties
2021 guidelines recommend against use of ascorbic acid
Metabolic acidosis
pH <7.35
pHCO3 <22
Compensation: increase RR to decrease pCO2
Metabolic alkalosis
pH > 7.45
pHCO3 > 26
Compensation: decrease RR to increase pCO2
Respiratory acidosis
pH < 7.35
pCO2 > 45
Compensation: increase HCO3 (kidneys regulate this)
Respiratory alkalosis
pH > 7.45
PCO2 < 35
Compensation: decrease in HCO3 (kidneys regulate this)
Anion gap calculation
Na - [Cl + HCO3]
Normal: 6-12
>12: primary metabolic acidosis
For every 1 decrease in albumin less than 4, AG decreases by 2.5-3
Respiratory acidosis causes
Think - Decreased respirations
Bronchospasm
Cardiac arrest
CNS depression
PE
Pneumonia
Pulmonary edema
Spinal cord injury
Sedatives
Stroke
Respiratory acidosis treatment
Correct cause
Invasive/noninvasive ventilation
Respiratory alkalosis causes
Think - increased respirations
Anxiety, pain
CNS tumor
Stroke
Head injury
Hypoxia
Stimulants
Reduced oxygen-carrying capacity
Reduced alveolar oxygen extraction
RR stimulation
Extracorporeal removal
Respiratory alkalosis treatment
Correct cause
O2 supplement
Invasive/noninvasive ventilation
Hypoventilation
Sedation
Anion gap metabolic acidosis causes
MUDPILES
Methanol
Uremia
DKA
Propylene glycol
Intoxication, infection
Lactic acidosis
Ethylene glycol
Salicylate
Non-anion gap metabolic acidosis causes
F-USED CARS
Fistula (pancreatic)
Uteroenteric conduits
Saline excess
Endocrine (hyperparathyroid)
Diarrhea
Carbonic anhydrase inhibitors
Arginine, lysine, chloride
Renal tubular acidosis
Spironolactone
Metabolic acidosis treatment
Correct cause
Base use (sodium bicarbonate) may be considered but controversial
Metabolic alkalosis Urine Cl > 25 causes
Chloride resistant
Hyperaldosteronism
Increased mineralocorticoid
Metabolic alkalosis Urine Cl < 25 causes
Chloride responsive
Vomiting
NG suction
Diuretic
Metabolic alkalosis Urine Cl > 25 treatment
Correct cause
Potassium
Aldosterone antagonist
Acetazolamide
Metabolic alkalosis Urine Cl < 25 treatment
Correct cause
0.9% NaCl
Consider acetazolamide
Consider HCl if severe
Vfib or pulseless Vtach in CPR
shock therapy
PEA or asystole in CPR
epinephrine
Med admin in CPR
Do not stop compressions
Central venous access preferred
IO > ET administration
Peripheral: follow with 20 ml of IV fluid
Meds that can be administered in ET tube
ET “LANE” during CPR
2-2.5x IV dose, diluted in 5-10 ml sterile water
Lidocaine
Atropine
Naloxone
Epinephrine
General post cardiac arrest care
- Sao2 >= 94%
- Hypotension (SBP <90) treated w/ fluid bolus, pressors
- Avoidance of fever
- TTM for first 24 hours to 32-37.5 C (0.3-0.5 C every hour)
Complications of TTM
- Shivering
- Reduced drug metabolism - use lower doses
- Bleeding risk
- Dehydration thru renal loss of water
- Arrhythmia, hypotension
- Hyperglycemia during cooling, hypoglycemia in rewarming
- Infection
- Hypokalemia/magnesemia/phosphatemia during cooling
Meds to reduce shivering
Sedatives (precedex, ketamine)
Anesthetics
Analgesics (meperidine, tramadol, fentanyl)
Dexamethasone
Clonidine
Buspirone
Ondansetron
Magnesium
Avoid paralytics
Potassium in TTM
Decreases during cooling phase
Increases during warming phase due to electrolyte shift
Do not over-replete during cooling.
Behavioral Pain Scale (BPS)
Use to monitor pain in adults in ICU
Takes into account facial expression, upper limb movements, and compliance with mechanical ventilation
> =6: significant pain
Critical Care Pain Observation Tool (CCPOT)
Use to monitor pain in adults in ICU
Takes into account facial expression, body movements, muscle tension, compliance with ventilator, and vocalization (if extubated)
> =3: significant pain
Richmond Agitation-Sedation Scale (RASS)
Assesses quality & depth of sedation
Individualize goal but typically 0 (alert & calm) to -2 (light sedation)
Sedation Agitation Scale (SAS)
Assesses quality & depth of sedation
Individualize goal but typically 3 (sedated) - 4 (calm & cooperative)
Propofol-related infusion syndrome
Rates of 80mcg/kg/min for at least 48 hours
Metabolic acidosis, cardiac failure, bradycardia, cardiac arrest, rhabdomyolysis, hyperkalemia, kidney failure
Calories from propofol
1.1 kcal/mL (in 10% lipid emulsion)
Propofol dosing, AE
Preferred sedative
5 mcg/kg/min, increase by 5 mcg/kg/min every 5 minutes to achieve certain RASS
Avoid bolus dosing = hypotension
Sedative only, does not provide pain relief.
AE: Respiratory depression (must be intubated), Elevated trigs (stop if 500-800), propofol-related infusion syndrome
Dexmedetomidine dosing, AE
0.2-0.7 mcg/kg/hr (possible up to 1.5 mcg/kg/hr), max 24 hours
Does not cause respiratory depression (do not need to be intubated)
ADR: bradycardia, hypotension (do not bolus in ICU)
Noninferior to propofol for sedation
Can use clonidine to help wean off
Ketamine place in therapy, AE
Analgesic & sedative properties
May use w/ opioid in postsurgical patients, no other routine role
hypertension, tachycardia, delirium
Lorazepam dosing, ADR
1-4mg q2-6 hours
1mg/hr continuous infusion but RISK of proplyene glycol toxicity (“P” in mudpiles)
Preferred in hepatic dysfunction - lack of active metabolites
Midazolam dosing, ADR
1-4mg q15min - 1 hour or 1mg/hr continuous infusion
May accumulate in renal & hepatic dysfunction, has active metabolites
Must be mechanically ventilated for continuous infusion
IV Diazepam place in therapy
alcohol withdrawal - long half-life, fast onset
May cause hypotension, thrombophlebitis
Analgesia cascade in critically ill
1) Opioids are first line therapy for pain
2) May add gabapentin > carbamazepine for nerve pain
3) Tylenol and ketamine can be added for multimodal pain relief, keep doses lower
4) Avoid NSAIDs (risk of bleed, kidney injury in critically ill)
5) Non-benzo > benzo sedatives
Delirium
Acute change in cognitive function characterized by disorganized though, altered level of consciousness, and inattentiveness
Associated w/ increased mortality, prolonged length of stay in ICU, and cognitive impairment after ICU discharge
Nonpharm»_space;> pharm treatment!
Confusion Assessment Method for ICU (CAM-ICU)
Intensive Care Delirium Screening Checklist (ICDSC)
Validated delirium screen
CAM-ICU: detect delirium at time of testing
ICDSC: detect delirium during nursing shift
Pharm treatment for delirium
Haloperidol
Quetiapine
Olanzapine
Ripseridone
Ziprasidone
All have QTc risk, less with olanzapine and risperidone
Atypicals besides risperidone have sedative benefit
Nonpharm preferred
Cisatracurium dosing, place in therapy
0.1mg/kg load then 2-10 mcg/kg/min
May use in severe ARDS x 48 hours – persistently hypoxemic or risk for ventilator injury
MUST be completely sedated with adequate pain control
Precedex should not be used for sedative
Neuromuscular blockade concerns
Masks seizure activity
Critical illness poly-neuromyopathy
Masks insufficient analgesia, sedation
Increased risk of VTE
Increased risk of skin breakdown, decubitus
Corneal abrasion due to lack of blinking
Paralytics prolonged in renal, hepatic failure
Vecuronium
Rocuronium
Electrolyte disorders on paralytics
Hypermagnesemia, hypocalcemia, hypokalemia: potentiate blockade
Hypercalcemia, hyperkalemia: antagonize blockade
Meds that may potentiate blockade
Steroids
Antibiotic (aminoglycosides, clinda, tetracycline, polymyxins)
CCBs
Type Ia antiarrhythmics
Furosemide
Lithium
Meds that may antagonize blockade
Aminophylline
Theophylline
Carbamazepine
Phenytoin
Glucose control in ICU
Insulin infusion to maintain blood glucose 140-200
Avoid SC insulin if on vasopressor, significant edema, or need for rapid correction
Draw whole blood glucose instead of finger prick
Stress ulcer prophlyaxis warranted in these pts
Mechanical ventilation for > 48 hours
Plt < 50,000
INR > 1.5
PTT > 2x normal
Recent GI bleed
Risk of PPIs for stress ulcer prophylaxis
Ventilator-associated pneumonia
Cdiff infection
VTE prophylaxis in critically ill
LMWH or LDUH better than mechanical or no ppx
Choose pharm or mechanical - not both
LMWH all therapeutically equivalent and less risk of HIT than LDUH
Rivaroxaban approved for medically ill ppx, not critically ill
VTE ppx if CrCl < 30
Dose adjust LMWH. If <20, avoid
May use dalteparin if <30 due to minimal renal metabolism
Avoid fondaparinux
LDUH safe to use in reduced kidney function
VTE ppx in major trauma
Enoxaparin 30mg q12h
Caloric requirements in critically ill
non obese: 12-25 kcal/kg ABW
BMI >30: 11-14 kcal/kg ABW
Protein requirements in critically ill
nonobese: 1.2-2 g/kg ABW
BMI >30: 2-2.5 g/kg IBW
Glasgow Coma Scale
Assesses level of consciousness
Higher the score = more conscious
15 is highest score
ICH Blood pressure control
If SBP 150-220, lower to 140 using nicardipine or clevidipine (or other IV titratable agent)
Aminocaproic acid
Antifibrinolytic therapy recommended if delay of 72 hrs to intervention for intracranial hemorrhage
4-5g load followed by 1g/hr
Preferred over TXA
Monitor VTE
Vasospasm prevention in aneurysmal SAH
Nimodipine 60mg q4H for 21 days. May cause hypotension.
Types of intracranial hemorrhage
Intraparenchymal hemorrhage
Subarachnoid hemorrhage (worst headache of life)
Subdural hematoma
Epidural hematoma
