Critical care - shock, sedation, respiratory support etc.
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| normal MAP | 70-100 mmHg
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| significance of lactic acid levels in critical care | indicates hypoperfusion and the resultant anerobic metabolism.
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| SVR in sepsis vs hypovolemic shock | will be low in sepsis and high in hypovolemic shock (compensatory mechanism)
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| normal pH | 7.4 (7.35-7.45)
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| normal pCO2 | 35-45mmHg
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| normal pO2 | 80-100 mmHg
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| normal HCO3- | 22-26 mEq/L
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| Normal SaO2 | 95-100%
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| metabolic acid base disorders are illustrated by changes in what blood gas measurement | HCO3-
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| respiratory acid base disorders are illustrated by changes in what blood gas measurement | pCO2 - elevated when acidiv, decreased in alkalosis
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| 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
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| how does metabolic acid base compensate for underlying respiratory acid base | in kidneys by regulating excretion and reabsorption of HCO3 or excretion.
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| MUDPILES | causes of anion gap metabolic acidosis:
Methanol, Uremia, DKA, Propylene glycol, Intoxication/Infection, Lactic acidosis, Ethylene glycol, Salycilates/Sepsis
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| 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
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| 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.
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| 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
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| Options other than phentolamine for extravasation. | nitroglycerin paste Q6H. or SQ terbutaline
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| 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.
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| 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.
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| monitoring for propofol | triglycerides, BP, calories from IV lipid 10% 1 kcal/ml. S/sx of PRIS
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| 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
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| What sedatives should you avoid loading doses with | propofol and precedex. Precedex can use load in surgery though.
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| infusion rate for precedex. | 0.2-0.7 mcg/kg/hr but some evidence supports going up to 1.5
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| what withdrawal symptoms are associated with precedex and when would they be likely to present? | nausea, vomiting, agitation. occur after prolonged use, 1 wk
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| what tools can be used to assess patients for delerium | CAM-ICU and ICDSC
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| drugs associated with delerium | benzos, opioids, anticholinergics
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| drug used to treat delerium | haloperidol - but no evidence to support
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| 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
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| risks with paralysis | bed sores and corneal ulcers, critical illness polyneuropathy, masks inadequate sedation and analgesia, masks seizure, inc risk for VTE
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| critical illness polyneuropathy | prolonged muscle weakness or paralysis once paralytic is removed
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| Train of four | a peripheral nerve stimulation tool. an awake and alert pt should have a TOF (4/4) and should get a baseline.
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| electrolyte disorders that potentiate nerve blockers | hypermag, hypo calcemia, hypokalemia
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| electrolyte disorders that antagonize nerve blockers | hypercalcemia, hyperkalemia
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| drugs that potentiate nerve blockers | aminoglycosides, corticosteroids, clinda, tetracyclines, CCBs, Type Ia antiarrhythmics, lasix, Lithium
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| drugs that antagonize nerve blockers | aminophylline and theophylline, CBZ, phenytoin.
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| treatment target for glucose in the ICU | <180
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| 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; )
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| 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
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| hypertensive urgency - time to controlled blood pressure | decrease BP over days
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| key difference between hypertensive urgency and emergency | end organ damage
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| 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
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| goal BP drop and timing in hypertensive emergency | decrease DBP to 100-110 or decrease MAP by 25% within 30-60 minutes
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| 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.
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| warfarin INR goal in patients with PAH for precention of catheter thrombosis and VTE | 1.5-2.5
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