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What is a Swann-Gans catheter?
a pulmonary artery catheter
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What is stroke volume (SV)?
the volume of blood ejected during systole
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What is cardiac output?
HR x SV (L/min)
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What is Cardiac Index?
total blood flow from the heart (L/min) divided by BSA (Body Surface Area)
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What is Systemic Vascular Resistance (SVR)
estimates the degree of peripheral vascular contraction/dilation (vascular tone)
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What is Pulmonary Capillary Wedge Pressure (PCWP)?
measures the left ventricular end diastolic volume
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What is Central Venous Pressure (CVP)?
- can be used to estimate fluid status of a patient, although affected by pulmonary vascular resistance changes
- most commonly used to measure the LV preload
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What is Mean Arterial Pressure (MAP)
- more reliable measure of perfusion of blood in the organs than blood pressure
- calculated: [systolic BP + 2(diastolic BP)]/3
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What is the normal range and goal for MAP
- 80-100 mmHg
- goal: at least 65 mmHg
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What is ischemia?
- organs need more O2 than they are getting
- lactate levels are a good marker of O2 deficiency
- keep liver fx in mind
- once blood flow is returned to an organ, you will see a spike in lactate b/c it's being cleared now
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What is hemodynamic shock?
- unsufficient circulating volume
- Hypovolemic Shock
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What are the causes of hemodynamic shock?
- dehydration
- bleeding (gunshot would is most common cause)
- diuretics
- fluid shifts (3rd spacing: burns, cirrhosis, CHF)
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What are the effects of hemodynamic shock?
- PCWP: down
- SVRI: up or same
- MAP: down
- CVP: down
- CI: down
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What is the treatment for hemodynamic shock?
- fluids
- crystalloids (usually first-line)
- colloids (only if there is 3rd spacing occuring - to draw fluids into the vascular space)
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What crystalloids can be used to treat hemodynamic shock?
- 0.9% saline
- 3% saline
- lactated ringers solution
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What colloids can be used to treat hemodynamic shock?
- 5% albumin
- 25% albumin
- Hetastarch in 0.9% NS
- blood
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What is cardiogenic shock?
- ticker ticking poorly
- may be combined with other types of shock
- this is the only shock syndrome that you don't jump to adding fluids
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What are the effects of cardiogenic shock?
- PCWP: up
- SVRI: up
- MAP: down
- CVP: down or up
- CI: down
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How do you treat cardiogenic shock?
- dobutamine (B1 specific)
- milrinone (potent inotrope, potent vasodilator - probably need a vasopressor, usually NE, to stop this from causing hypotension)
- vasopressors (NE, phenylephrine - usually only with milrinone)
- dopamine (not specific enough)
- avoid fluids in most cases
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What is anaphylactic shock?
often associated with peanuts and bee stings
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What are the effects of anaphylactic shock?
- PCWP: up or same
- SVRI: down
- MAP: down
- CVP: same
- CI: up or same
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How do you treat anaphylactic shock?
- epinephrine followed up by antihistamines and/or steroids
- very acute and short-lived
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What is septic shock?
- Sepsis + hypotension despite adequate fluid resuscitation(adding fluids)
- release of cytokines (TNF-a, IL-1, IL-6) d/t damage to tissues or response to toxins
- cytokines mediate inflammation and may activate coagulation (chemotaxis of leukocytes, vasodilation, capillary leak, activation of coag. cascade)
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What are the criteria for SIRS?
- 3 of the following
- hyper/hypothermia (>38 or <36)
- tachycardia (HR > 90 bpm)
- tachypnea (RR > 20 bpm or PaCO2 < 32 mmHg)
- leukocytosis/leucopenia (WBC >12,000/mm3; <4,000/mm3 or >10% bands)
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What are the sequelae of SIRS?
- may progress to shock
- may progress to Acute Respiratory Distress Syndrome (ARDS)
- may progress to Multiple Organ Dysfunction Syndrome (MODS)
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What is sepsis?
infection + 2 SIRS criteria
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What is the definition of severe sepsis?
- sepsis + organ dysfunction
- hypotension
- hypoxemia
- acute lung injury (ALI)
- PaO2/FiO2 <200 w/ pneumonia or <250 w/o pneumonia
- Oliguria (UO < 0.5 mL/kg for > 2h
- metabolic acidosis
- platelets < 100,000/mm3obtundation
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How do you treat septic shock?
- antibiotics (will usually get worse initially d/t toxin release)
- check CVP
- check MAP
- check Scv O2
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Norepinephrine
- a and B agonist
- 1st-line, especially in septic shock
- by far, the most effective vasoconstrictor
- dose-dependent increase in SVR
- does not adversely effect CO
- more potent than dopamine
- can cause arrhythmias, but not as bad as other catecholamines
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dopamine
- dose-dependent action of adrenergic and dopaminergic receptors
- gets kidneys back online quickly
- increase in CO and SVR before you see a1 effects (DA -> B -> a1)
- 1-3 mcg/kg/min = dopaminergic activity
- 3-10 mcg/kg/min = B activity
- 10-20 mcg/kg/min = a activity
- arrhythmogenic effects often precede sufficient vasopressor effects
- tachyarrhythmias
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epinephrine
- primarily B agonist at low doses and a agonist at high doses
- used for pulseless cardiac arrest to restore perfusion
- most arrhythmogenic and can shut off areas of periphery completely!
- coronary eschemia - can cause MI
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phenylephrine
- the only pure a agonist
- little or no effect on HR - good option if severe tachycardia or tachyarrythmias
- dose-related increase in MAP and SVR
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vasopressin
- V1 receptor agonist
- increases response to catecholamines
- will increase urine output despite it being an ADH b/c it increases blood flow to the kidneys
- coronary steal
- CAD
- myocardial dysfunction
- used for septic shock
- highly increases SVR
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dobutamine
- mainly B1 but some B2 agonism
- inotrope with vasodilatory properties
- used for distributive and cardiogenic shock
- increases CO, SV and DO2
- tachyarrhythmias
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milrinone
- PDE inhibitor
- far more vasodilatory than dobutamine (nearly always requires concurrent vasopressor to maintain pressure)
- inotrope with vasodilatory properties
- used for cardiogenic shock
- increases CO, SV, and DO2
- highly decreases SVR
- Hypotension
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steroids
- consider when hypotension does not respond to fluids
- hydrocortisone has the best data
- remove as soon as not needed
- relative adrenal insufficiency
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Drotrecogin alpha (Xigris) (activated protein C = APC)
- anti-inflammatory
- anti-coagulation
- pro-fibrinolytic
- very expensive
- must start within 48h of organ dysfunction/failure starting
- benefit: may not die
- prophylactic UFH can be co-administered with APC (do not dc heparin)
- can increase PT, aPTT times and increase INR
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How is a stress ulcer created?
d/t shunting away of blood from the GI tract
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When should stress ulcer prophylaxis be given?
- coagulopathy > 24h (plt < 50,000, INR > 1.5) or any 2 of the following:
- neurologic trauma
- hypoperfusion (sepsis, shock)
- severe burns (> 35% BSA)
- multiple organ failure
- PMH GI ulcers/bleed within 1 yr
- high dose steroids (> 200mg HCT eq.)
- multiple trauma
- postoperative transplant
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What agents are used in stress ulcer prophylaxis?
- H2 blockers
- PPIs
- sucralfate
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How do pts get deep venous thrombosis (DVT)?
damage done to vessel endothelium during invasive monitoring
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What agents are used in DVT prophylaxis?
- heparin 5,000u q 8
- LMW heparin 40mg qd (usually enoxaparin)
- fundaparinox
- coumadin
- sequential compression devices
- IVC (intravena caval) filter to catch embolism before it gets to the lungs
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What risks can cause ileus?
- opioid use
- immobilization
- decreased blood flow
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What agents are used in bowel prophylaxis to prevent ileus?
- docusate sodium
- senna
- bisacodyl
- polyethylene glycol
- Milk of Magnesia, etc.
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What are the stages of sedation?
- analgesia
- conscious sedation
- amnesia
- paralysis
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What is analgesia in the sedation cascade?
- first and primary goal before instituting a sedative (want to know the pain is being blocked before we make them unable to tell us so)
- always reassess before increasing any other sedative
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What is conscious sedation?
- comfortable but interactive
- anxiolysis
- ICU psychosis
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What is amnesia in the sedation cascade?
- mandatory for paralysis
- utilize for procedures which may be unpleasant
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What is paralysis in the sedation cascade?
- NOT a sedative!!!!
- used only for rare indications
- necessary for intubation and difficult ventilation
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What agents are used in sedation?
- Morphine
- hydromorphone
- fentanyl
- methadone
- lorazepam
- midazolam
- diazepam
- chlordiazepoxide
- succinyl choline
- pancuronium
- vecuronium
- cisatracurium
- ketamine
- chloral hydrate
- propofol
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Morphine
- agent of choice
- onset < 5 min
- peak in 1/2 to 1 hr
- duration 3-7h (mostly 3)
- may exacerbate hypotension d/t histamine release
- may cause itching
- decreases respiratory drive
- decreases GI motility
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hydromorphone
- not used much
- no histamine release
- no active metabolites
- little cross-reactivity w/morphine
- greater potency than morphine
- onset 15-30 min
- peak 1/2 to 1h
- duration 4-5h (mostly 5)
-
fentanyl
- #2 analgesic (for CV unstable instead of morphine)
- less histamine release
- short DOA
- no cross-reactivity w/morphine
- lipophilic
-
methadone
- long terminal half-life
- dose q 6h at low doses but may decrease to bid or qd after prolonged tx
- lipophilic
- high inter-patient variability
- high risk for overdose
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What are the advantages of benzodiazepines in sedation?
- sedation
- anxiolysis
- hypnosis
- some amnesia
- multiple routes of administration
- intermittent dosing possible
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lorazepam
- DOC for long-term sedation
- glucuronidated in liver
- good amnestic qualities
- poor solubility
- no active metabolites
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midazolam
- preferred benzo for short-term sedation (< 72h)
- water soluble/ lipid soluble (long term sedation if used over 72h - can't get out of it d/t depot effect)
- quick onset 1-3 min
- short DOA 1-3h
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diazepam
- generally reserved for status epilepticus
- very poor solubility
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chlordiazepoxide
- generally used for alcohol w/d
- many active metabolites - long DOA
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When are neuromuscular blockers used?
when pt is breathing against intubation to prevent pneumothorax
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What concurrent therapies should be used with NM blockers?
- eye lubrication
- body repositioning
- suction
- train of four monitoring
- anticoagulation
- adequate sedation!!!!
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succinyl choline
- depolarizing NM blocker
- causes contraction and then you're stuck there
- mimics ACh
- lasts 3-5m (ideal for intubation)
- CI in renal failure, burns, trauma
- tachyphylaxis
- bradycardia
- fasciculation
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pancuronium
- nondepolarizing NM blocker
- generally 1st line agent
- many patients cannot tolerate CV effects (hypotension and reflex tachycardia)
- very cheap
-
vecuronium
- MOST USED nondepolarizing NM blocker
- hepatically eliminated
-
cisatracurium
- nondepolarizing NM blocker
- for patients with multiple organ dysfunction
- Hoffman degradation
- patients often require far higher doses than those recommended for infusion
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What is the Train of 4 testing?
- twitch response
- goal is 2 twitches per 4 shocks
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What are the other problems associated with NM blockers?
- prolonged myopathy (inability to move)
- critical illness myopathy (incoordination - increased risk with steroids and AGs)
-
ketamine
- NMDA antagonist
- useful in peds (adults get emergence phenomenon - hallucinations, altered mood)
- causes less respiratory depression
- some bronchodilation (useful in asthmatics)
-
chloral hydrate
- NOT an ideal agent (many cases of overdose)
- often used for conscious sedation in peds
-
propofol
- extremely short DOA
- must be given as infusion - titrate to effect
- in a lipid base - infections, pancreatitis a problem
- used in pts needing frequent removal of sedation (brain injury pts)
- not much amnesia
- very sedative at proper doses
- hypertriglyceridemia
- hypotension
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What are the treatments for delirium in the ICU?
- haloperidol
- AAP
- etomidate
- dexmedetomidine
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