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BCPS study guide

Critical care - shock, sedation, respiratory support etc.

normal MAP 70-100 mmHg
significance of lactic acid levels in critical care indicates hypoperfusion and the resultant anerobic metabolism.
SVR in sepsis vs hypovolemic shock will be low in sepsis and high in hypovolemic shock (compensatory mechanism)
normal pH 7.4 (7.35-7.45)
normal pCO2 35-45mmHg
normal pO2 80-100 mmHg
normal HCO3- 22-26 mEq/L
Normal SaO2 95-100%
metabolic acid base disorders are illustrated by changes in what blood gas measurement HCO3-
respiratory acid base disorders are illustrated by changes in what blood gas measurement pCO2 - elevated when acidiv, decreased in alkalosis
what is the compensatory mechanism for metabolic acid base disorders respiratory acid base via slowing or increasing respiratory rate to alter pCO2. blow off CO2 to increase pH. or decrease pCO2. alternate is true to decreasing pH
how does metabolic acid base compensate for underlying respiratory acid base in kidneys by regulating excretion and reabsorption of HCO3 or excretion.
MUDPILES causes of anion gap metabolic acidosis: Methanol, Uremia, DKA, Propylene glycol, Intoxication/Infection, Lactic acidosis, Ethylene glycol, Salycilates/Sepsis
F-USED CARS causes of non-anion gap metabolic acidosis: Fistula, Uteroenteric conduits, saline excess, Endocrine, diarrhea, carbonic anhydrase inhibitors, arginine/lysine/chlorine, renal tubular acidosis, spironolactone
Hypovolemic shock - first line treatment fluid resucitation. either blood, colloids or crystalloids. if still hypotensive may need pressor support but this wont work without adequate fluid replacement.
protocol to achieve goals in pts with sepsis fluid resuscitation to achieve HR, MAP and CVP goals. if SvO2 still not at goal may give more fluid. vasopressors to achieve MAP of 65+ if needed. place ART line rather than BP cuff for monitoring. if cardiac dysfunction may need inotropes
Options other than phentolamine for extravasation. nitroglycerin paste Q6H. or SQ terbutaline
preferred vasopressors for septic shock norepi is first line. can add vasopressin to achieve a pressor sparing effect. both are equivalent efficacy. phenylephrine if need BP support or tachyarrhythmias. dopamine no better than norepi and can cause arrhythmias.
preferred inotropes for septic shock milrinone and dobutamine but only if cardiac function is compromised or persistently low CO or MAP after adequate fluid resucitation.
monitoring for propofol triglycerides, BP, calories from IV lipid 10% 1 kcal/ml. S/sx of PRIS
What is PRIS? what causes it and what are the symptoms. Propofol related infusion syndrome. associated with infusion rates of >50mcg/kg/min. results in metabolic acidosis, rhabdomyolysis, hyperkalemia, kidney failure, cardiac arrest, bradycardia
What sedatives should you avoid loading doses with propofol and precedex. Precedex can use load in surgery though.
infusion rate for precedex. 0.2-0.7 mcg/kg/hr but some evidence supports going up to 1.5
what withdrawal symptoms are associated with precedex and when would they be likely to present? nausea, vomiting, agitation. occur after prolonged use, 1 wk
what tools can be used to assess patients for delerium CAM-ICU and ICDSC
drugs associated with delerium benzos, opioids, anticholinergics
drug used to treat delerium haloperidol - but no evidence to support
uses for paralytics in icu intubated pts with persistent hypoxia despite adequate sedation and analgesia. control intracranial hypertension in pts with neurological injury from TBI
risks with paralysis bed sores and corneal ulcers, critical illness polyneuropathy, masks inadequate sedation and analgesia, masks seizure, inc risk for VTE
critical illness polyneuropathy prolonged muscle weakness or paralysis once paralytic is removed
Train of four a peripheral nerve stimulation tool. an awake and alert pt should have a TOF (4/4) and should get a baseline.
electrolyte disorders that potentiate nerve blockers hypermag, hypo calcemia, hypokalemia
electrolyte disorders that antagonize nerve blockers hypercalcemia, hyperkalemia
drugs that potentiate nerve blockers aminoglycosides, corticosteroids, clinda, tetracyclines, CCBs, Type Ia antiarrhythmics, lasix, Lithium
drugs that antagonize nerve blockers aminophylline and theophylline, CBZ, phenytoin.
treatment target for glucose in the ICU <180
risk factors for stress ulcers that ALONE warranting drug therapy respiratory failure with mechanical ventilation >48 hours, coagulopathy (plt<50,000; INR>1.5; aPTT>2xcontrol; )
risk factors for stress ulcers that if two+ present warrants drugs head or spinal cord injury, 35%+ burn, hypoperfusion, acute organ dysfunction, GI bleed in last year, high dose corticosteroid, liver failure with associated coagulopathy, postop transplant, AKI, major surgery, multiple trauma
hypertensive urgency - time to controlled blood pressure decrease BP over days
key difference between hypertensive urgency and emergency end organ damage
what are the end organ complications that can occur with hypertensive emergency encephalopathy, ICH, unstable angina/MI, acute decompensated heart failure, pulmonary edema, aortic dissection, retinopathy/papilledema, decreased urine output or acute renal failure, eclampsia
goal BP drop and timing in hypertensive emergency decrease DBP to 100-110 or decrease MAP by 25% within 30-60 minutes
drugs of choice for hypertensive emergency - tailored by disease state CHF - NTG or ACEi with diuretics; intracranial hemorrhage - labetalol or nicardipine; MI - beta blocker and nitrate; acute renal failure - nicardipine, clevidipine or fenoldopam; ecclampsia - hydralazine, labetalol or nicardipine.
warfarin INR goal in patients with PAH for precention of catheter thrombosis and VTE 1.5-2.5
Created by: mjuhlin



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