Chapter 53: Acute and Critical Care Medicine Flashcards
Crystalloids
- D5W
- NS
- LR (contains NaCl, KCl, CaCl2, Na-lactate)
Colloids
Albumin 5%, 25% (Albutein, AlbuRX)
Stay in intravascular space and increase oncotic pressure
Hyponatremia
Na<35meq/l
Correcting more rapidly than 12meq/l over 24 hours can cause osmotic demyelination syndrome (ODS) or central pontine myelinolysis which can cause paralysis, seizures, and death.
Hypotonic Hypovolemic Hyponatremia
Can be cause by diuretics, blood-loss, vomiting, diarrhea.
Treatment is to correct cause and administer NaCl IV solutions
Hypotonic Hypervolemic Hyponatremia
Cause by fluid overload (cirrhosis, HF, or renal failure)
Treatment is diuresis with fluid restriction
Arginine Vasopressin (AVP) receptor antagonists
Conivaptan and Tolvaptan
May be used to treat SIADH and hypervolemic hyponatremia.
They increase excretion of free water while maintaining sodium
Tolvaptan
Limited to <=30 days use due to hepatoxicity
Boxed warning: Should be initiated in a hospital, rapid over correcting can cause ODS
SE: thirst, nausea, dry mouth, polyuria
Hypernatremia
NA>=145meq/l
Associated with water deficit and hypertonicity
Hypokalemia
K<3.5meq/l
In general a drop of 1 meq/l in serum K below 3.5 represents a total body deficit of 100-400 meq
K replacement
Safe administration through a peripheral IV line include a max infusion rate of <=10 meq/hr and a max concentration of 10 meq/100ml
IV K can be fatal if administered undiluted or through IV push
Magnesium is necessary for K uptake
Hypomagnesium
Mg<1.3 meq/l
When serum Mg is <1 meq/l with life-threatening symptoms (seizures, arrhythmias) IV replacement is recommended. Magnesium Sulfate is used for IV replacement.
When serum Mg is >1 meq/l and <1.5 Mg can be replaced orally, most commonly with Mg Ox
Hypophosphatemia
Considered severe and is usually symptomatic when serum PO4 is < 1 mg/dL, IV PO4 is used for replacement.
Intravenous Immunoglobulins
Carimune NF, Flebogamma DIF, Gammagard, Gamunex-C, Octagam, Privigen
-Use slower infusion rate in renal and CV disease
APACHE II
The Acute Physiologic Assessment and Chronic Health Evaluation II: scoring tool used to determine prognosis and ICU mortality risk
Vasopressors
Most work by stimulating alpha receptors which causes vasoconstriction and increases systemic vascular resistance (SVR) which increases BP
Dopamine MOA
Dependent on dose
- Low (renal) dose: 1-4mcg/kg/min (dopamine-1 agonist)
- Medium dose: 5-10mcg/kg/min (beta-1 agonist)
- High dose: 10-20mcg/kg/min (alpha-1 agonist)
Epinephrine
Adrenaline
Alpha-1, Beta-1, and beta-2 agonist
Norepinephrine
Levophed
Alpha-1 agonist activity > beta-1 agonist activity
Phenylephrine
Neo-synephrine
Alpha-1 agonist
Vasopressin
Vasostrict
Vasopressin receptor agonist
Vasopressors warnings, SE, notes
Boxed warnings: all vasopressors are vesicants, when administered IV, treat extravasation with phentolamine
SE: arrhythmias, tachycardia, necrosis (gangrene), bradycardia (phentolamine), hyperglycemia (epinephrine)
Notes: solutions should not be used if they are discolored or contain a precipitate, should be administered through central line, epinephrine used for IV push is 0.1mg/ml (1:10,000) and IM is 1mg/ml (1:1,000)
Phentolamine
Alpha-1 blocker that antagonizes the effects of the vasopressor
Nitroglycerin uses
Often used when there is active myocardial ischemia, or uncontrolled HTN but effectiveness may be limited to 24-48 hrs due to tachyphylaxis (tolerance)
Nitroprusside MOA and uses
It is a mixed (equal) arterial and venous vasodilator at all doses.
Should not be used it active myocardial ischemia because it can cause blood to be diverted away from diseased coronary arteries (“coronary steal”)
Nitroprusside toxicity
Metabolism results in thiocyanate and cyanide formation which can cause toxicity. Hydroxocobalamin can be administered to reduce risk and sodium thiosulfate + sodium nitrite (Nithiodote) is used for cyanide toxicity
Nitroglycerin MOA, CI, SE
MOA: low doses is a venous vasodilator; high doses is a arterial vasodilator
CI: SBP<90, use with PDE-5 inhibitor
SE: HA, tachycardia, tachyphlaxis
Notes: requires non-pvc container (glass, polyolefin)
Nitroprusside warnings, SE, notes
Boxed warning: metabolism produced cyanide, excessive hypotension, must be diluted (D5W preferred)
Warning: increased ICP
SE: HA, tachycardia, thiocyanate/cyanide toxicity (increased risk in renal and hepatic impairment)
Note: requires light protections, use only clear solutions, blue color indicates degradation to cyanide
Inotropes
They increase the contractility of the heart
Dobutamine MOA
MOA: beta-1 agonist with some beta-2 and alpha-1 agonism. It increases HR and force of contraction which increases CO
(may turn slightly pink due to oxidation but potency is not lost)
Milrinone MOA
Selective PDE-3 inhibitor in cardiac and vascular tissue. It produces inotropic effects with significant vasodilation
Hypovolemic Shock
To treat fluid resuscitation with crystalloids is generally recommended as 1st line therapy for hypovolemic shock that is not caused by hemorrhage.
Vasopressors will not be effective unless intravascular volume is adequate
Distributive Shock
Include septic, anaphylactic, and neurogenic shock
Sepsis and Septic Shock
Sepsis is life-threatening organ dysfunction cause by a dysregulated host response to infection
Septic shock is sepsis in the presence of persistent hypotension requiring a vasopressor to maintain a MAP >=65
Early administration of broad-spectrum abx and crystalloids. Norepinephrine is the vasopressor of choice for septic shock.
General Principles for treating Septic Shock
Target MAP of >= 65
MAP = [(2 x DBP)+SBP]/3
“fill the tank:” optimize preload with IV crystalloid fluids (prn)
“squeeze the pipe and kick the pump:” alpha-1 agonist activity (peripheral vasoconstriction) to increase systemic vascular resistance; beta-1 agonist activity to increase myocardial contractility and CO
Two common causes of ICU infections
- ventilation
- foley catheters
Acute Decompensate and Cardiogenic Shock
Patients with HF may experience episodes of worsening symptoms (sudden weight gain, unable to perform daily routine), this is called acute decompensated HF (ADHF) and when hypoperfusion and hypotension are also present it is called cardiogenic shock
ADHF Clinical presentation
BB should only be stopped in ADHF episode if hypotension or hypo-perfusion is present
ADHF presents with volume overload, hypo-perfusion or both
ADHF Assessment
Sometimes invasive monitoring with a catheter that is guided through the right side of the heart into the pulmonary artery called a Swan-Ganz or Pulmonary Artery (PA) catheter.
This provides measurements of pulmonary apaillary wedge pressure, cardiac output
ADHF tx
Patients with edema, JVD, and/or ascites are volume overloaded tx options include:
- loop diuretics
- vasodilators
Pts with decreased renal fx, altered mental status, and/or cool extremities have hypo-perfusion tx includes:
- inotrope (dobutamine, milrinone)
- if pt becomes hypotensive consider vasopressor
Pain
Opioids given IV, such as morphine, hydromorphone, and fentanyl, are 1st line for analgesia
Analgesia based sedation or analgosedation is a sedation strategy that uses analgesia first to relieve pain and discomfort.
Sedation
Sedation is necessary for some ICU patients to maintain synchronized breathing with the ventilator (prevent “bucking” the ventilator
Agitation management
agitation is managed with benzodiazepine or non-benzos (propofol and dexmedetomidine) which are preferred and are associated with improved ICU outcomes
Dexmetomidine (precedex) is the only sedative approved for use in intubated and non-intubated patients
Delirium
Sedation with non-benzos may reduce incidence of delirium and/or shorten duration in patients who already have it
Dexmedetomide MOA, SE, notes
Precedex
MOA: Alpha-2 adrenergic agonist
SE: hypo/hypertension, bradycardia
Notes: does not require refrigeration, duration of infusion should not exceed 24 hours, used for sedation in intubated and non-intubated patients
Propofol MOA, SE, notes
Diprivan
MOA: short-acting general anesthetic
SE: hyptension, apnea, hypertriglyceridemia, green urine/hair/nail beds, propofol-related infusion syndrome (PRIS) rate but fatal
Notes: oil in water emuslion (1.1kcal/ml)
Lorazepam
Propylene glycol toxicity (acute renal failure and metabolic acidosis)
Midazolam CI, Notes
Versed
CI: use with potent CYP3A4 inhibitors
Notes: Can accumulate in patients with renal impairment (active metabolite)
Etomidate monitoring
Amidate
Monitoring: s/sx of adrenal insufficiency (hypotension, hyperkalemia)
Ketamine warnings
Ketalar
Warnings: Emergence rxs (vivid dreams, hallucinations, delirium)
Stress Ulcers Tx
H2RAs and PPIs for prophylaxis
PPIs have been associated with increased risk for GI infections (C.Diff), fractures, and nosocomial pneumonia
Risk factors for development of stress ulcers
- mechanical ventilation >48hrs
- coagulopathy
- sepsis
- TBI
- major burns
- acute renal failure
- high dose systemic steroids
Local anesthetic
Lidocaine (xylocaine)
Inhaled anesthetic
Desflurane (suprane), sevoflurane (ultane)
Injectable anesthetic
Bupivicaine, ropivacaine
Anesthetic warnings
Can cause malignant hypothermia (MH)
Bupivicaine, used in epidurals, can be fatal if administered IV
Lido/epi
Epi keeps lido localized
Neuromuscular blocking agents (NMBA)
Cause paralysis of the skeletal muscle, including those used for respiration.
Patients can require NMBA in surgery conducted under general anesthesia to facilitate mechanical ventilation, to treat muscle spasms (tetany).
NMBAs have to effect on pain so patients should receive adequate sedation and analgesia prior to starting an NMBA
Patients must be mechanically ventilated
Types of NMBA
-Depolarizing and non-depolarizing
Succinylcholine
- Succinylcholine is the only available depolarizing agent and is reserved for intubation
- Short acting, fast onset (30-60sec)
Non-depolarizing NMBA SE
SE for all: flushing, bradycardia, hypotension, tachyphylaxis
- Cisatracurium (nimbex): metabolized by Hoffman elimination (independent of renal and hepatic fx)
- Pancuronium: long-acting
Hemostatic agents MOA
Systemic hemostatic drugs work by inhibiting fibrinolysis or enhancing coagulation.
Topical hemostatic agents
Recothrom, Thrombin-JMI
names often include -throm
Tranexamc acid
hemostatic agent
Cyklokapron (injection)
Lysteda (oral) approved for use in heavy menstrual bleeding (menorrhagia)
Recombinant Factor VIIa
NovoSeven RT
fda approved for hemophilia and factor VII deficinecy
Intravenous Immunoglobulins Warnings, SE
Boxed warnings: acute renal dysfunction can occur, usually occurs within 7 days (more likely with products stabilized with sucrose), thrombosis
SE: HA, nausea, diarrhea, injection site rx, infusion rx (facial flushing, chest tightness, fever, chills, hypotension-slow/stop infusion