NRNP 6566 week 1 to 5 Key Concepts (VERIFIED)

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NRNP 6566 week 1 to 5 Week 1 1. Describe the cytochrome P450 system. Describe how inducers and inhibitors affect the cytochrome system and how that affects the half-life of medications. a. Cyt ... ochrome p450 system is a series of enzymes used to metabolize medications. b. Drugs that cause CYP450 metabolic drug interactions are referred to as either inhibitors or inducers. Inducers increase CYP450 enzyme activity by increasing enzyme synthesis c. Inhibitors block the metabolic activity of one or more CYP450 enzymes 2. Describe the affect on low and high albumin levels on active drug levels especially for drugs that are highly protein bound. a. Albumin is the plasma protein with the greatest capacity for binding drugs. i. Binding to plasma proteins affects drug distribution into tissues, because only drug that is not bound is available to penetrate tissues, bind to receptors, and exert activity. As free drug leaves the bloodstream, more bound drug is released from binding sites. b. Highly protein bound drugs, low albumin levels (w/ malnutrition, or chronic illness) may lead to toxicity because there are fewer than the normal sites for the drug to bind 3. Describe ways to lessen the hepatic first pass effect: metabolism during first pass through the liver a. Alternative routes (suppository, intravenous, intramuscular, inhalational aerosol, transdermal, and sublingual) avoid the first-pass effect  allow drugs to be absorbed directly into the systemic circulation 4. Be able to calculate creatinine clearance using the Cockgraft Gault equiation: a. Male  = ([140-age] × weight in kg)/(serum creatinine × 72) b. Female  = CrCl (male) × 0.85 5. Describe what determines the frequency of drug administration: a. Drug half-life, plasma concentration 6. Be familiar with the Beers criteria and how to use it: a. Potentially Inappropriate Medication Use in Older Adults i. to call attention to medications that are commonly problematic, and thus should be avoided in most older adults 7. Describe factors that affect absorption, distribution, metabolism and excretion: a. Absorption  low blood state (shock or arrest); contact time with GI tract too fast (diarrhea = can’t absorb); delayed stomach emptying (large meal = delayed absorption); drug-drug or drug-food interactions b. Metabolism  genetics, age, organ function c. Distribution  low albumin levels, body composition, cardiac decomp (HF), and age d. Excretion  affected by abnormal kidney or liver function; age, drug interactions 8. Define narrow therapeutic index How would you monitor a patient with a narrow therapeutic index? a. Therapeutic index: dose range where efficacy of med is optimized while side effects minimized b. Narrow therapeutic index (NTI) drugs are defined as those drugs where small differences in dose or blood concentration may lead to dose and blood concentration dependent, serious therapeutic failures or adverse drug reactions. c. Blood tests to monitor blood concentrations and dose adjustments accordingly 9. Describe how aging affect absorption, distribution, metabolism, and excretion a. Decreased organ function, poorly tolerate drugs that require metabolism, lower rates of excretion b. decrease in small-bowel surface area, slowed gastric emptying, and an increase in gastric pH, changes in drug absorption c. With age, body fat generally increases and total body water decreases. Increased fat increases the volume of distribution for highly lipophilic drugs (eg, diazepam, chlordiazepoxide) and may increase their elimination half-lives. d. Serum albumin decreases and alpha 1-acid glycoprotein increases i. Phenytoin and warfarin are examples of drugs with a higher risk of toxic effects when the serum albumin level decreases e. hepatic metabolism of many drugs through the cytochrome P-450 enzyme system decreases with age. For drugs with decreased hepatic metabolism clearance typically decreases 30 to 40%. i. Drugs metabolized in phase 1 reactions likely prolonged ii. First-pass metabolism (metabolism, typically hepatic, that occurs before a drug reaches systemic circulation) decreasing by about 1%/yr after age 40. 1. Thus, for a given oral dose, older adults may have higher circulating drug concentrations. f. Decreased renal elimination Week 2 and 3 1. Identify and describe 12 lead EKGs that demonstrate: a. 1st, 2nd, and 3rd degree AV blocks i. 1st degree HBcards consult ii. 2nd degree HB  type 1 & 2 1. Type 1: Echo (r/o structural dx), Thyroid levels, meds, lytes to identify and treat cause 2. Type 2: PPM, continuous tele with transcutaneous pacing if needed, determine cause; IV atropine if poor perfusion s/s q 3-5m with max 3mg if s/s poor perfusion; 3. If no response to atropine dopa, epi, isoproterenol iii. 3rd degree/ complete HB: PPM; tele and transcutaneous pace if neded; identify cause; IV atropine if s/s poor perfusion; If no response to atropine dopa, epi, isoproterenol b. STEMI in any lead (know what area of the heart is affected based on lead location) c. Atrial fibrillation: i. Stable  Rate control vs rhythm control strategy (AV nodal blockers, antiarrhythmics, anticoagulation); ablation if no response to meds; ii. unstable  DCC/CV d. Atrial flutter i. CV; rate control not as responsive as afib e. Ventricular fibrillation: i. Defibrillate and CPR f. VT: stable i. Stable/nonsustained  BB ii. Amiodarone, sotalol, mexiletine to reduce # shocks iii. Mg if torsades iv. EPS/ablation v. Unstable  CPR, epi vaso (2nd dose), amio, lidocaine, mg, airway management g. Tachycardia: i. Vagal maneuver, adenosine (6/12mg), BB or Ca channel; ablation; antiarrhythmics if no response to BB or don’t want ablation h. Asystole: CPR 2. Distinguish between dihydropyridine and non-dihydropyridine calcium channel blocker. Know what conditions each class would be used to treat. a. dihydropyridine calcium channel blocker: (e.g., nifedipine, amlodipine) primarily act on vascular smooth muscles i. use for HTN b. non-dihydropyridine calcium channel blocker: (diltiazem < verapamil) primarily act on the heart i. use for CP, SVT (verap); controlling irregular rapid HR and lowering BP (Diltiazem) 3. Describe the medications to treat atrial fibrillation (rate, rhythm, and embolus prevention). Know the side effects, needed monitoring, and interaction for each of these medications. a. 4. Calculate a CHADS2 score and describe treatment based on the score: a. 1 point for the following h/o: HF, HTN, DM, stroke/TIA (2 pt) and age >/= 75 i. 0 = low risk, 1-2 = mod risk, >3 = high risk  start anticoag 5. Calculate a HASBLED score and describe treatment based on the score: a. 1 point for each of the following: i. Hypertension ii. Uncontrolled, >160 mmHg systolic iii. Renal disease (Dialysis, transplant, Cr >2.26 mg/dL or >200 µmol/L) iv. Liver disease (Cirrhosis or bilirubin >2x normal with AST/ALT/AP >3x normal) v. Stroke history vi. Prior major bleeding or predisposition to bleeding vii. Labile INR (Unstable/high INRs, time in therapeutic range <60%) viii. Age >65 ix. Medication usage predisposing to bleeding (Aspirin, clopidogrel, NSAIDs) x. Alcohol use (≥8 drinks/week) b. Risk of major bleeding in one year: i. Score 0 points: Major bleeding risk 1% per year ii. Score 1 points: Major bleeding risk 3.4% per year iii. Score 2 points: Major bleeding risk 4.1% per year iv. Score 3 points: Major bleeding risk 5.8% per year v. Score 4 points: Major bleeding risk 8.9% per year vi. Score 5 points: Major bleeding risk 9.1% per year vii. Score >5 points: Major bleeding risk 12-15% per year 6. Describe the symptoms of hyperthyroidism, lab values that are altered, and medications to treat the disease and symptoms: a. s/s: hypermetabolism, heat intolerance , fatigue, anxiety, nervousness, manic, confusion/restless, emotional lability, fine tremors, diaphoresis, hyperreflexia of DTR, resting tachy/palpatations/afib, exertional dyspnea, low-grade fever, increased appetite, wgt loss, frew BM, smooth/warm/velvet skin, fine/thin hair, exopthalamus, eyelid lag, infreq blinking, Graves’ opthalmopathy (20-40% cases) b. Abnormal labs: i. LOW TSH ii. ELEVATED T3, T4, thyroid resin uptake, and free thyroxine index (FTI) 1. sometimes T4 is normal but T3 ALWAYS high iii. ELEVATED SED rate iv. ELEVATED antinuclear antibody (ANA) elevated, without evidence of lupus or autoimmune DO v. Hypercalcemia and low H/H c. RX: i. For s/s: 1. Propanolol (Inderal) 10mg 4 times/day (up to 80mg) 2. Metoprolol (Lopressor) 25 mg PO (up to 50 mg) q 6-8h ii. Antithyroid meds: 1. Methimazole (tapazole) intital = 30-60 mg/day in 3 doses; maintenance = 5-15 mg PO daily a. If intolerant  propylthiouracil initial dose = 300-600 mg /day in 4 doses; maintenance = 100-150 mg daily in 3 doses 7. Identify when cardioversion is indicated and relevant testing that should occur prior to it. a. Unstable afib/aflutter causing RVR, MI, hypotension, or HF; WPW syndrome in afib b. TEE should ALWAYS proceed DCCV to rule out valve dx or thrombus 8. Describe ACLS guidelines: Week 4 HYPERTENSION: 1. Know the diagnostic criteria for hypertension, hypertensive urgency, and hypertensive emergency. Describe goals of treatment (goal BP): a. HTN  sustained BP of =/> 140’s/90’s for a sustained period of time 1. Stage 1: 140-159/90-99 2. Stage 2: =/> 160/ =/> 100 ii. Primary  “essential” or “idiopathic” 1. Unknown cause, 95% of cases, onset age 25-55 iii. Secondary  r/t known cause or disease process 1. 5% of cases, etiology = estrogen use, renal dx, prego, endocrine DO iv. Isolated systolic HTN; SBP > 140/90 1. Common in the elderly; widening pulse pressure and Framingham point scale good indicator; 65-75% in elderly; 2. EFFECTIVELY treated with diruetics and long-acting Calcium channel blockers v. HTN s/s: may c/o occipital HA in AM, resolving by noon; epitaxis, LH, and visual disturbances; S4 present r/t LVH; retinal changes; hematuria (rare) b. Hypertensive urgency  severely elevated BP  180/110 or higher without progressive target organ dysfunction i. s/s: severe HA, SOB, epistaxis, or severe anxiety ii. RX: Clonidine (alpha-adrenergic stimulant) 0.2 mg PO, then 0.1 mg PO every hr until controlled or total of 0.8 mg admin 1. May experience sedation; possible rebound HTN once stopped iii. Captopril (capoten): ACE dose of 12.5-25 mg PO c. Hypertensive EMERGENCY: severely elevated BP > 180/120; can occur with lower BP if impending or progressive target organ dysfunction (encephalopathy, ICH, AMI, Pulm edema with acute LV failure, UA, dissecting AA or eclampsia i. RX: IMMEDIATE INTERVENTION  goal BP down to 160-180 or < 105 diastolic (no > 25% in 1-2 hr) then gradually lowered over several days with PO therapy ii. 1st DRUG OF CHOICE  Nicardipine 2.5-15 mg /hr IV 1. SE: HA, hypotension, tachycardia, N/V, fever, neck pain, indigestion iii. 2nd DRUG OF CHOICE  Nipride 0.25-10 mcg/kg/min IV 1. SE: brady or tachycardia, nausea, abd pain, twitching, dizziness, HA, flushing, sweating, IV site irritation 2. Can cause RAPID profound hypotension 3. DO NOT give for longer than 72h -> risk cyanide poisoning iv. Nitro (esp with ischemic pt’s) 5-220 mcg/min IV 1. SE: dizziness, HA, hypotension, ortho +, numbness/tingling, flushing, N/V v. Esmolol hydrochloride (Brevibloc) 500 mcg/kg IV over 1 min; maintenance 5-300 mcg/kg/min 1. No bolus unless HR > 100 2. SE: bradycardia, feet/hand edema, wheezing/chest tightness, IV irritation, cold extremities, hyperkalemia, hypoglycemia vi. Labetalol hydrochloride (Normodyne, Trandate) 1. Commonly used with prego; start 10-20 mg then  20-80 mg IV bolus over 10 min OR continuous infusion of 0.5-2 mg/min 2. SE: dizziness, tingling scalp/skin, LH, HA, tiredness, GI upset, stuffy nose vii. Hydralazine (apresoline) 5-20 mg IV, can be repeated in 20 min 1. SE: Headache, pounding/fast heartbeat, loss of appetite, nausea, vomiting, diarrhea, or dizziness 2. DO NOT GIVE to pts with CAD and aortic dissection 3. Vasodilator  reduces BP, may increase HR and retain fluid a. May need to combine with BB and diuretic 4. Must give QID= IV or PO 5. If give for too long  lupus like condition which goes away with withdrawal of med viii. Minoxidil: vasodilator 1. SE: dizziness, drowsiness, tiredness, temporary edema in hands/feet, wgt gain, HA, confusion, flushing 2. Decreases BP (good for ESRD) 3. Don’t use often 4. Can cause hair growth ix. Fenolodopam (Corlopam): 0.03-0.1 mcg/kg/min; increase or decrease by 0.05-1 mcg/kg/min NO SOONER than q15min; give up to 48 hr 1. SE: headache, cutaneous dilation (flushing), nausea, and hypotension, 2. May cause reflex tachy, hypotension, and increased IOP 2. Identify medications to treat hypertension based on ethnicity and co-existing conditions. Be very familiar with JNC guidelines. a. Non-African Americans  Thiazide type diuretic, CCB, ACEI, ARB (grade B) b. African Americans  Thiazides, CCB (grade B) ** grade C for pt with DM ** c. Adults =/> 18 with CKD  ACEI, ARB (grade B)  REAGRDLESS of race or other comorbidities 3. Be familiar with dosing and side effects of each medication class (ACE-I, ARB, Beta blockers, diuretics) a. Thiazide diuretics increase excretion of Na and H20: FIRST LINE DRUG for HTN i. SE: hypokalemia, hypomagnesia, hyperglycemia, hyponatremia, hypercalcemia ii. SCREEN for SULFA allergy prior to initiating b. ACE inhibitors  cause vasodilation and block Na and H2o retention i. SE: cough, rash, taste disturbances, hyperkalemia, renal impairment ii. May cause hyperkalemia if given with K sparing diuretic; may rise lithium levels iii. DO NOT use if K > 5.5; cant give to prego; DO NOT give with ARB c. Angiotension II-receptor blockers (ARBs)  cause vasodilation and block Na and H2o retention i. SE: cough, hyperkalemia, HA, taste disturbances, renal impairment ii. DO NOT use with ACE or if K > 5.5; cant give to prego d. Calcium channel blockers (CCB) i. SE: HA, flushing bradycardia ii. Can use for CP, arrythmias, and migraines e. Beta blockers  DIRECTLY relaxes heart muscle i. NOT FIRST line therapy ii. SE: dizziness, brady, heart block, fatigue, insomnia, nausea iii. AVOID in pts with asthma/COPD f. Peripheral alpha-1 antagonists (blood vessels)  vasodilators (prazosin, terazosin) i. Used as adjunct; take 1st dose at bedtime ii. SE: 1st dose hypotension/ syncope, dry mouth, ortho +, dizziness, HA, nausea iii. MOA: decreased BP due to vasodilation; typically used for BPH; can be used for PTSD g. Central alpha-2 agonsists (brain) reduces CO and PVR to lower BP; vasodilator, prevents vasoconstriction and slows HR i. Metyldopa  use for prego, clonidine transdermal ii. DO NOT d/c abruptly  rebound HTN and withdrawals iii. Can be used for opioid withdrawl iv. SE: dry mouth, sedation, depression, HA, brady h. Nitrates: veno-dilation  reduce pressures in RA (preload reduction) and increase flow to myocardium (increase coronary perfusion) and vaso-dilation to lower peripheral resistance/SVR i. Good for pt with HF with pulmonary edema ii. If cant tolerate BB  can use as alterantive with addition of hydralazine iii. DO NOT GIVE with RV infarction or RV failure iv. Should be nitrate free interval daily to minimize tolerance 4. Describe end organ damage related to hypertension a. End organ damage: classic manifestations include  vascular and hemorrhagic stroke, retinopathy, coronary heart disease/myocardial infarction and heart failure, proteinuria and renal failure and in the vasculature, atherosclerotic change including the development of stenoses and aneurysms Diagnosis of HTN: Normal Elevated Hypertension <120 mm Hg 120–129 mm Hg and and <80 mm Hg <80 mm Hg Stage 1 130–139 mm Hg or 80–89 mm Hg Stage 2 ≥140 mm Hg or ≥90 mm Hg 1. Identify what diagnostics are indicated and medications to treat hypertension a. Diagnostic testing for common cause: o Renal parenchymal dx: renal u/s o Renovascular dx: renal duplex, doppler u/s, MRA, abd CT o Primary aldosteronism: plasma aldosterone/renin ratio o OSA: polysonography o ETOH/drug: U-Tox o Pheochromocytoma/paraganglioma: CT or MRI of pelvis/abd o Cushings syndrome: overnight 1mg dexamethasome suppression test o Hypothyroidism/Hyperthyroidism: TSH, free tyroxine o Aortic coarctation: echo, CT or MRA thoracic and abd o Primary hyperparathyroidism: serum calcium and PTH o Congenital adrenal hyprplasia: HTN with hypokalemia and low or normal aldosterone and renin o Acromegaly: serum GH > 1 during oral glucose load SHOCK: 2. Identify the 4 types of shock and be able to distinguish between all four. Know the classic presentation (symptoms), medications to treat, and hemodynamic readings that would lead to diagnosis of each. a. Hypovolemic: r/t issue with vasculature/ not enough blood to maintain adequate circulation  r/t exogenous and endogenous loss of circulating volume  hemorrhagic (traumatic [ruptured spleen/liver, long bone fx] or non-traumatic [GIB, hemorrhagic pancreatitis]) OR Non hemorrhagic (GI losses +V/D, poor oral intake, fistulas); renal losses  excessive diuresis  DI, SIADH, addison’s DX; exudative lesions or burns; excessive diaphoresis i. S/S: increased HR, decreased BP, decreased CVP/CP/CI/PA/PCW pressures, postural hypotension, flat neck veins 1. s/s more prominent with more blood loss; < 10% may not have any s/s, some tachy; s/s start when 15-30% and > ii. RX: fluid repletion (crystalloids) via fluid challenges 250-500 cc of NS or LR; blood products, colloids (albumin); 1. MAST: military antishock trousers  external counterpressure device to redistribute peripheral circulation b. Cardiogenic: r/t heart failure (pump failure)  decreased SV and CO  inadequate tissue perfusion  tissue hypoxia i. Causes: AMI, arrythmias, HF, myocardial contusion, dissecting aortic aneurysm, hart valve damage/disease, myocarditis, end stage CM, septic shock with severe myocardial depression, any severe myocardial damage ii. s/s: Increased PAP/PCW/SVR; CVP may OR MAY NOT be elevated depending on RV involvement; DECREASED SV/CO/CI <1.8; reduced EF; pulm congestion: rales rhonchi, decreased PaO2/PaCO2, and mixed venous O2; S3/S4, possible palpable thrill, rapid/faint pulse, + murur systolic of MR or VSD; peripheral edema, JVD, s/s of decreased tissue perfusion  oliguria, clouded sensorium, cool/mottled skin 1. diagnosis made once myocardial dysfunction and exclusion of correlation of such factors hypovolemia/hypoxia/acidosis iii. RX: goal = improve contractility and CO 1. Fluids unless pulm edema present 2. Correct electrolyte abnormalities (esp hypokalemia/hypomag) 3. Drugs  a. intotropic agents Dopa, dobutamine, milrinone, vasodilating agents b. agents to reduce afterload  nipride, vasopressors c. agents to reduce preload  vasopressin, norepi, dopamine, epi, neo, nitro, diuretics 4. counterpulsation  IABP  increases pump efficiency via diastolic augmentation to increase coronary end-organ perfusion; reduces afterload, reduces MI demand; Impella; LVAD c. Obstructive: r/t obstruction of flow in the cardiac circuit leading to impairment of diastolic filling on increased afterload  r/t (tumors, high inthrathoracic pressures [tension pneumo, high PEEP], decreased cardiac compliance [constrictive pericarditis, tamponade], increased ventricle afterload [aortic dissection, PE, abd dissection, constricrive pericarditis, acute pulm HTN]. i. s/s and RX as per underlying etiology d. Distributive (Septic, neurogenic and anaphylactic): all types involve vasodilation and loss of vasomotor tone  venous pooling of blood and decreased venous return  decreased CO  inadequate tissue perfusion i. Sepsis  SIRS plus infection; overwhelming inflammatory response that allows for infective organisms in bloodstream that alter vasomotor tone  relative hypovolemia; coagulation and inflammation due to infection (bacterial [ gram +/-], viral, fungal) 1. Nosocomial infections major cause r/t malnutrition, invasive procedures, trauma, surgical wounds, advanced age, imunnosuppresive therapy, neoplastic diseases, immunosuppressive therapy (steroids, ctyotoxins), chronic Dx (DM, renal failure) 2. Sites of infection: GU, resp tract, wounds, invasive devices (catheters), meinges, GI tract 3. DX: leukocytosis, thrombycytopenis, elevated procalcitonin/CRP; C-xray to r/o PNA, UA, culture and sensitivity of wounds 4. RX: initial resusiciation (goals during first 6 hr)  CVP: 8-12, MAP >65, UO > 0.5 ml/kg/hr, SvO2 > 65% or ScvO2 > 70% a. Fluid/volume resuscitation b. NS or LR prior to pressors c. Antimicrobial therapy within FIRST HOUR: cefepime 1g IV with metronazole 500 mg IV every 8 hr; piperacillin/tazobactum 4.5g IV q6h PLUS  gentamycin/tobramycin/amikacin: consult pharm for dose; vanco: consult pharm d. IF IMMUNOSUPPRESSED  antiobiotic coverage for atypical recomm e. Hemodynamic support f. Vasopressors to keep MAP =/> 65 g. Cooling blanket/antipyretics h. Inotropic gents i. Dobutamine j. Corticosteroids if IVF and pressors not working ii. Neurogenic shock: disturbance of nervous system causing massive vasodilation due to interruption or loss of sympathetic innervation; normal blood volume; normal heart function 1. Spinal shock: sudden from damage to spinal cord tissue  temp or permanent interruption of neurotransmitter (loss of control or reflex below lesion) 2. Causes: injury/DX of spinal cord, high levels spinal anesthesia, vasomotor center depression, drug that block sympathetic activity 3. s/s: hypotension, bradycardia, hypothermia, warm/dry skin (due to venodialtion and pooling and loss of sweat response), decreased SVR/SV/ venous return (CVP), hyporeflexic/areflexia 4. RX: careful fluid admin to ensure adequate tissue perfusion; pressors once fluid is replaced a. If brady w/ decreased LOC, UO and BP  atropine iii. Anaphylactic shock: immediate hypersensitivity reaction antibody/antigen response leads to decreased tissue perfusion and initiation of shock response; includes one or both  resp difficulty with hypotension 1. s/s: a. cardiac: hypotension, tachy, arrythmias b. resp: brpnchospasm, laryngeal edema, patient describes “lump in throat” dysphagia, hoarseness, dyspnea, stridor, wheezing, rales/rhonchi, hypoxia c. cutaneous: pruritis, erythema, urticaria, angioedema (swelling) d. CNS: restlessness, uneasiness, apprehension, feeling of impending doom, anxiety, decreased LOC e. GI: +N/V/D, abd cramps, metallic taste f. Hemodynamics: decreased CO/CI/CVP/PA/SVR 2. RX: SPEED of treatment is ESSENTIAL  EPI IM or SQ 0.5-1mg (0.5-1 ml) should be given if hypotension or resp difficulty a. Inhaled epi  mild/mod laryngeal edema but NOT GIVEN if IM/SQ already admin as first line RX; not a substitute b. Give IV EPI if circulation comp  1 mg SLOW IV push c. May give ETT 2-2.5 times the normal dose (2-2.5 mg) if 1mg/10ml solution; use O2 valve reservoir bag or manually bag pt several times after admin d. 0.1-0.5 mg of 1 mg/10ml epi; repeat q10min until effect achieved e. Maintain airway f. H1 blocker Diphendydramine 50mg IV or PO x1 dose, may need up tp 100 mg, NO MORE than 400 mg/day  decrease urticaria, itching, flushing, angioedema g. H2 blocker  Ranitidine 50 mg IV  decrease flushing, HA h. Albuterol  bronchospasm i. LR infusion for volume j. Corticosteroids (Solu-medrol) 125-250 mg/IV or hydrocortisone 200 mg slow IV to decrease inflammation k. Inotropic agents l. Dobutamine m. Vasoconstrictor agents: Levo, Vaso, Epi, Dopa n. Neo NOT RECOMMENDED unless serious arrythmias/high CO/ or salvage states Vasculature (blood is stored)  heart pumps oxygenated blood choice of vital or non-vital organs (skin)  back to vasculature Normal ➔ blood from heart to VITAL and NONVITAL organs to oxygenate them If no O2 to vital organs b/c low volume states, heart not strong enough to pump or if blood is distributed improperly and less to vital organs  SHOCK! 3. Know the Surviving Sepsis guidelines for diagnosis, monitoring, and medications to treat: 4. Be able to distinguish the 4 stages of sepsis. Differentiate the stages by symptoms. a. Nonprogressive Stage 1: early changes at cellular level; no real s/s, normal VS b. Progressive Stage II: compensatory mechanisms begin to fail and circulatory and metabolic derangements more pronounced (pg. 737) i. s/s: decreased LOC, decreased pulse pressure, tachy, weak/thread pulse, decreased filling time decreased coronary perfusion  MI/arrythmia, decreased cellular metabolism  reduces temp and heat production; skin pale/cyanotic, cold/clammy; possible jaundice, decreased UO, increased RR, hypoventilation, rales/rhonchi, resonance leading to dullness; decreased or absent BS, possible paralytic ileus, if bleeding  increased BS c. Irreversible Stage III: final irreversible stage of shock  cardiac failure, acidosis, blood clot formation/ possible DIC, inadequate cerebral blood flow  ischemia of vital function of brain, severe decrease in HR/BP/tissue perfusion  DEATH 5. Interpret a WBC differential. Distinguish between a bacterial and viral infections based on the differential. a. WBC differential determines the percentage of each type of white blood cell present in your blood (neutrophils, bands, eosinophils, monocytes and lymphocytes) b. bacterial infection  increase of neutrophils and a decrease in lymphocytes. c. viral infection  decrease in neutrophils and an increase in lymphocytes. 6. Explain the mechanism of action and common side effects of dobutamine, norepinephrine, labetalol, and amiodarone a. Dobutamine  works by acting on the alpha-1, beta-1, and beta-2 adrenergic receptors which produces an inotropic effect increasing CO. i. SE: arrythmogenic, can cause hypokalemia, MI, hypotension and vasodilation. b. Norepinephrine (levo)  acts on the alpha-1 and alpha-2 adrenergic receptors causing vasoconstriction. This further causes increased heart rate and cardiac output. i. SE: of this medication include arrythmias and tissue or myocardial ischemia. c. Labetalol  acts by blocking the alpha-1, beta-1 and beta-2 adrenergic receptors activity decreasing peripheral vascular resistance. i. SE: dizziness, brady, heart block, fatigue, insomnia, nausea d. Amiodarone  antiarrhythmic works by blocking potassium currents that cause repolarization, prolonging cardiac action potential and delaying the refractory period. i. SE: bradyarrhythmia, hypotension, photodermatitis, photosensitivity, thyroid dysfunction, nausea, vomiting, increased liver enzymes, dizziness, paresthesia, visual disturbances, optic neuritis, fatigue, toxic epidermal necrolysis, and pulmonary fibrosis 7. Distinguish the actions and effects between dopamine and dobutamine. a. Dobutamine  cardioselective adrenergic agent that augments myocardial contractility, cardiac output and myocardial blood flow with only minimal changes in heart rate or arterial blood pressure b. Dopamine  a precursor to norepinephrine in noradrenergic nerves; neurotransmitter in certain areas of the CNS. i. produces positive chronotropic and inotropic effects on the myocardium, resulting in increased heart rate and cardiac contractility 8. Vasopressors  constrict certain pathways (brain/kidney/liver) to increase central BP a. Alpha 1 receptors: cause generalized/global vasoconstriction to increase BP; can cause issues with blood flow to end organ if significant enough b. Beta 2 receptors: smooth muscle relaxation to allow more blood flow to target organ; can cause drop in BP c. Beta 1 receptor: on heart  inotrope: beats faster (increased HR) and harder pump to increase blood flow; cardio stimulant d. Dopamine receptor: e. Drugs: MOST to LEAST constrictive i. Vasopressin 0.01 u-0.04u/min; acts on AVR1a receptor  PURE vasoconstriction to elevate BP and reduce perfusion to end organs (can cause anaerobic metabolism) ii. Phenylephrine (Neo) 20-200 mcg/min; stimulates alpha 1 receptor iii. Norepinephrine (levo) 5-30 mcg/min; stimulates alpha AND beta 1 AND beta 2 (a little bit)  vasoconstriction, increase in CO iv. Dopamine 1-20 mcg/kg/min; stim alpha/beta 1/beta 2  vasoconstriction/ little vasodilation/ increased contractility 1. Dopamine receptor activation: works on kidneys v. Epinephrine (adrenaline) 1- >5 mcg/min; stimulates alpha/beta 1/beta 2(little): more vasoconstriction; more cardiac stimulation (inotrope) vi. Dobutamine 2-20 mcg/kg/min; stimulates alpha 1(very small), beta 1 (a lot) and beta 2  more for vasodilation and increased contraction, increasing CO vii. Isoproterenol 0.5-30 mcg/min; stimulates pure beta 1 and beta 2  increased contractility and vasodilation Week 5 1. Be very familiar with the CHEST guidelines on anticoagulation management: a. VTE w/o associated cancer diagnosis  all direct oral anticoagulants (dabigatran, rivaroxaban, apixaban, or edoxaban) are recommended over vitamin K antagonist (VKA) (Warfarin) therapy (all Grade 2B); VKA therapy is recommended over low molecular weight heparin (LMWH; Grade 2C). b. VTE assoc. w/cancer  LMWH is recommended over VKA (Grade 2B) or any direct oral anticoagulants (all Grade 2C). c. Anticoagulants should stop after 3 months of therapy in patients with an acute, proximal deep venous thrombosis (DVT) provoked by surgery rather than shorter or longer treatment courses (Grade 1B). d. Anticoagulants should also be stopped after 3 months in patients with a proximal DVT or pulmonary embolism (PE) provoked by a nonsurgical transient risk factor over shorter or longer courses (Grade 1B for high bleeding risk patients, Grade 2B for low or moderate bleeding risk patients). e. Anticoagulation should be given for 3 months in patients with a first unprovoked VTE and a high risk of bleeding (Grade 1B), but should be extended without a scheduled stop date in patients with a low or moderate risk of bleeding (Grade 2B). f. Acute VTE and treated with anticoagulation  DO NOT USE an inferior vena cava filter g. Unprovoked proximal DVT or PE who are stopping anticoagulant therapy  use of aspirin over no aspirin to prevent recurrent VTE if there are no contraindications to aspirin therapy (Grade 2B). h. Acute DVT  DO NOT use compression stockings routinely to prevent the post- thrombotic syndrome (Grade 2B). i. Subsegmental PE and no DVT  clinical surveillance over anticoagulation when the risk of VTE recurrence is low (Grade 2C). j. Anticoagulation over surveillance when the risk of VTE recurrence is high (Grade 2C). k. Acute PE and hypotension (massive PE),  thrombolytic therapy (Grade 2B), preferring systemic therapy over catheter-directed thrombolytic therapy (Grade 2C). l. Recurrent VTE while treated with a non-LMWH anticoagulant, the guideline recommends changing to LMWH therapy (Grade 2C). If patients suffer a recurrent VTE while on LMWH treatment  increase the LMWH dose (Grade 2C). Contraindications to thrombolytics: Absolute contraindications: • Prior intracranial hemorrhage (any time) • Malignant intracranial tumor • Intracranial structural cerebral vascular lesion • Ischemic stroke within 3 months (exception for acute stroke within 3 hours) • Active bleeding or bleeding diathesis • Significant head or facial trauma within 3 months • Suspected aortic dissection Relative contraindications: • Severe uncontrolled hypertension (SBP > 180 mmHG or DBP >110 mmHg) • Nonhemorrhagic stroke >3 months • Major surgery < 3 weeks • Traumatic or Prolonged CPR (> 10 minutes) • Active peptic ulcer • Pregnancy • Noncompressible vascular punctures or Recent invasive procedure • For streptokinase/anistreplase – Prior exposure (more than five days ago) or prior allergic reaction to these agents • Recent internal bleeding (2 to 4 weeks) • Current use of anticoagulant 2. MORE INFORMATION  https://journal.chestnet.org/article/S0012-3692(12)60129-9/pdf or https://class.content.laureate.net/1b8a4c7f5c9c63b0fd76de0bb7cb4252.pdf 3. TREATMENT acute pulmonary embolism. Include the medications, dosages, and transition from injectable to oral medications a. Anticoagulation with IV unfractionated heparin (UFH), low molecular weight heparin (LMWH) or Fondaparinux (Arixtra [similar to LMWH  direcr inhibitor of factor Xa, but does not inhibit thrombin]). i. Most patients should have LMWH or fondaparinux instead of IV heparin ii. Use IV IF  conc of subq absorption, severe renal failure or if thrombolytic therapy is being considered iii. IV Heparin  initial bolus of 80 units/kg or 5000 units followed by an infusion of 18 units/kg/hr or 1300 U/h should be given, with the goal of rapidly achieving and maintaining the aPTT at levels that correspond to therapeutic heparin levels 4. Describe medications used to prevent PE in surgical, orthopedic, and trauma patients. Know dosages and length of treatment suggested: a. Pharmacological method include  i. Low dose unfractionated heparin (UFH): intermittent IV injection or gtt; 8000- 10,000 units IV initially, THEN 50-70 units/kg (5000-10,000 units) q4-6hr OR 1. Continuous IV infusion: 5000 units IV injection, followed by continuous IV infusion of 20,000-40,000 units/24 hr ii. Low dose low molecular weight heparin (LMWH): 5000 units SC q8-12hr, OR 7500 units SC q12hr (lovenox, dalteparin, iii. Oral direct thrombin inhibitors: lepirudin, desirudin, bivalirudin and argatroban iv. Xa inhibitors: 1. Xarelto: Start 6-10 hours after surgery once hemostasis has been established a. Knee replacement: 10 mg PO qDay for 12 days b. Hip replacement: 10 mg PO qDay for 35 days 2. Pradaxa: CrCl >30 mL/min: 110 mg PO 1-4 hr after surgery and after hemostasis has been achieved on first day, then 220 mg taken qDay for 28-35 days a. If dabigatran is not started on the day of surgery, after hemostasis has been achieved initiate treatment with 220 mg qDay 3. Eliquis: 2.5 mg PO 12-24 hr after surgery a. Duration of therapy (hip replacement): 2.5 mg PO BID for 35 days b. Duration of therapy (knee replacement): 2.5 mg PO BID for 12 days v. Admitted patients may be treated with a LMWH, fondaparinux, or unfractionated heparin (UFH). Warfarin 5 mg PO daily is initiated and overlapped for about 5 days until the international normalized ratio (INR) is therapeutic >2 for at least 24 hours. https://emedicine.medscape.com/article/1267714-medication#5 5. Describe how to manage warfarin (initiation, monitoring, and dose adjustments): a. Prophylaxis and treatment of venous thrombosis and its extension, pulmonary embolism (PE): i. Initial dose: 2-5 mg PO/IV qDay for 2 days, OR 10 mg PO for 2 days in healthy individuals ii. Initiate warfarin on day 1 or 2 of LMWH or unfractionated heparin therapy and overlap until desired INR, THEN discontinue heparin iii. Check INR after 2 days and adjust dose according to results iv. Typical maintenance dose ranges between 2 and 10 mg/day v. Initiate warfarin on day 1 or 2 of parenteral anticoagulation therapy (eg, LMWH or unfractionated heparin) vi. Overlap warfarin and parenteral anticoagulant for at least 5 days until desired INR (>2.0) maintained for 24 hours, then discontinue parenteral therapy vii. A nice "rule of thumb" for dose adjustments near the target range (generally works for INRs from the high 1s to low 4s): If you want to change the INR by 0.5- 1 unit, increase or decrease the weekly dose by a daily dose. 6. Identify what patients would not be eligible for oral anticoagulants: a. Pregnant b. Breast feeding c. Severe liver DX https://www.uwhealth.org/files/uwhealth/docs/anticoagulation/DOAC-chart.pdf 7. Describe how to bridge a patient taking warfarin that is undergoing a procedure: a. Discontinuation  typically omit warfarin for five days before elective surgery (ie, the last dose of warfarin is given on day minus 6) i. check the PT/INR on the day before surgery If the INR is >1.5, we administer low dose oral vitamin K (eg, 1 to 2 mg) to hasten normalization of the PT/INR and recheck the following day. ii. proceed with surgery when the INR is ≤1.4 b. Bridging  administration of a short-acting anticoagulant, typically a low molecular weight (LMW) heparin, during the interruption of a longer-acting agent, typically warfarin i. Initated 3 days pre procedure: 1. d/c LMWH 24 h pre procedure 2. UFH: d/c 4-5 h pre procedure https://www.uptodate.com/contents/perioperative-management-of-patients- receiving-anticoagulants#H753184 c. Resume warfarin  12 to 24 hours after surgery, typically the evening of the day of surgery or the evening of the day after surgery, assuming there were no unexpected surgical issues that would increase bleeding risk and the patient is taking adequate oral fluids [8]. We use the same dose the patient was receiving preoperatively. i. individuals at very high risk and some individuals with a high risk of thromboembolism with a heparin bridging agent d. individuals with renal insufficiency and/or those requiring hemodialysis, intravenous or subcutaneous unfractionated heparin can be used more easily because dosing is unaffected by renal clearance 8. Distinguish between HIT, TTP, ITP, and DIC. Describe diagnostics and treatment for all three a. ITP: Idiopathic thrombocytopenic purpura i. Causes: 1. Autoimmune DO that inhibits platelet productions/ increases platelet destruction 2. Isolated: 3. No apparent systemic assoc conditions: SLE & CLL 4. Classifications: primary (no identified cause), secondary (immune mediated with assoc DO), chronic (> 12mo), refractory (failure to respond, relapse post splenectomy) ii. Thrombocytopenia can be r/t  Heparin, sulfa, thiazides, quinine, cimetidine, gold iii. s/s: epistaxis, oral bleeding, menorrhagia, purpura, petechiae; usually systemically well; spleen nonpalpable iv. DX: thrombocytopenia < 20,000/ul = HALLMARK; diagnosis by exclusion 1. Megathrombocytes (enlarged platelets) present 2. 10% have autoimmune hemolytic anemia (Evan’s syndrome) 3. ANA testing  discover autoimmune 4. Testing  MAIPA (monoclonal antibody immobilization of platelet antigens) (igG present in 90%); bone marrow BX to r/o myelodysplasia; peripheral blood smear v. RX: WinRho or anti-D antibody therapy (in Rh positive pts to increase plt count 1. Prednisone 1-2 mg/kg/day 2. High dose IV sgamma globulin (1g/kg for 1 or 2 days) [for EMERGENCIES] 3. Splenectomy 4. Chemo for those who fail to respond to steroids or splenectomy 5. Thrombopoiesis stimulating agents 6. Platelet transfusion if LIFE-THREATENING BLEEDING vi. Complication: intracranial bleed b. HIT: Heparin-induced Thrombocytopenia i. Produces arterial and venous thrombosis ii. Occur with both LMWH and UFH, more common in surgical pts iii. s/s: often asymptomatic  may develop s/s r/t venous/arterial thrombosis; skin necrosis at injection site; anaphylactic reaction to IV or SQ heparin iv. DX: platelet fall of 50% from previous value 1. Tests  heparin-induced platelet aggregation assay (+/- serotonin release assay)  [together considered the standard]; platelet C serotonin release assay; heparin PF4 enzyme-linked immunosorbent assay 2. 4 T’s: extent of thrombocytopenia, timing of thrombocytopenia, presence of thrombosis, thrombocytopenia  score of 4 or > = IMMEDIATE to HIGH risk of HIT 3. RX: a. Hematology referral b. Discontinuation of heparin ASAP r/t high risk thrombus c. Switch to direct thrombin inhibitors as alternative to anticoagulation i. Danaparoid: adjust to wgt and renal function  bolus and maintenance infusion ii. Argatroban: intial infusion of 2 ug/kg/min 1. Hepatic impairment  start @ 0.5 ug/kg/min 2. No renal adjustment 3. PTT goal 1.5-3 times baseline, no > 100 (can reach therapeutic goal in 1-3h) 4. PTT draw 2 hr after initiation iii. Bivalirudin (angiomax): initiatie infusion @ 0.15 ug/kg/min 1. Adjust to PTT 1.5-2.5 baseline 2. Can adjust for renal/hepatic impairment iv. Fondaparinux: wgt based 1. Caution with renal impairment: CrCl 30-50 2. DO NOT give if CC less than 30 3. VTE: a. <50 kg: 5 mg SC once daily b. 50-100 kg: 7.5 mg SC once daily c. >100 kg: 10 mg SC once daily https://reference.medscape.com/drug/arixtra- fondaparinux-342172 4. TRANSITION TO WARFARIN WHEN the following conditions are met: • Properly anticoag with thrombin specific inhibitor, OVERLAP with Warfarin until INR is at goal • Platelet count has increased > 150,000 • Start with < 5mg /day for initial goal INR of 2.0-3.0 • MINIMUM 5 days overlap with thrombin inhibitor and warfarin before d/c thrombin inhibitor c. DIC: Disseminated Intravascular Coagulation i. ACQUIRED DO  hemorrhage and thrombosis secondary to patho disease or clinical state ii. Hemorrhagic syndrome: r/t consumption of many coagulation factors and platelets 1. Abnormal stimulus results in formation of excessive thrombin  fibrinogen consumption, irreversible platelet aggregation, activation of fibrinolytic system 2. AKA: consumptive coagulopathy, diffuse intravascular coagulation 3. Common cause = infection iii. s/s: oral/GI/GU bleeding; spont bruising, GIB, Resp bleed, hematuria, persistent bleeding at puncture sites, skin necrosis, VTE 1. acute  tachycardia, hypotension, edema 2. thrombosis  superficial or DVT (Trousseau syndrome); digital ischemia or gangrene is common, thrombosis most common with CACNER PATIENTS iv. DX: NO SINGLE LAB TEST 1. 5 step scoring system/algorithm to calulate DIC score 2. Fibrin degradation  D-dimmer 3. Hypofibrinogenemia is common 4. Acute decompensated DIC  active hemorrhage evident  thrombocytopenia < 150,000 ul, PT and aPTT prolonged by 70%, 50% respectively, fibrinogen, factor V and factor VII levels low, fragmented RBC (schistocytes) found on peripheral smear 5. Subacute DIC PT and aPTT normal, fibrinogen normal, thrombocytopenia and elevated d-dimer may be only abnormal finding 6. Chronic or COMPENSATED DIC: elevated fibrin degradation levels (FDPs > 45 ug/ml) a. d-dimmer used to differentiate from primary fibrinolysis 7. R/O DIFFERENTIAL DIAGNOSIS WITH: a. Blood cultures to r/o sepsis b. Repeat fibrinogen and PTT (initial fibrinogen is normal) – confirmed diagnosis with rapidly falling fibrinogen levels c. Factor VIII – usually in normal range in coagulopathy assoc with liver dx v. RX: hematology referral 1. Diagnosis and correction of underlying dx or cause 2. When risk of hemorrhagic complications are high  a. maintain blood volume w/ pRBCs b. platlet transfusion for goal 30,000-50,000/ul c. cryoprecipitate  goal plasma fibrinogen of 150 mg/dl; one unit increases fibrinogen by 6-8 mg/dl; 15 units  levels raise 50-150 mg/dl d. FFP q30 min in severe DIC 3. Supportive RX  prevention of hypoxemia and hemodynamic compromise 4. Heparin therapy controversial but considered approp with thrombosis or fibrin deposition producing acral cyanosis 500-750 units/hr a. NOT EFFECTIVE if antithrombin III depleted b. Should measure antithrombin III levels c. FFP or concentrates of antithrombin III should be used to raise levels > 50% d. If heparin used  no need to prolong PTT e. Success = raising fibrinogen and declining fibrin degradation products 5. Temperature has effect on coagulation enzyme factors  each decrease by 1 degree Celsius reduces activities by 10% 6. 5 new approaches to measure: a. Platelet factor analyzer (PFA-100) to distinguish Willebrand Dx from platelet function b. Waveform analysis  bleeding DO and hemophilias c. Thrombin generation test  monitor RX of hemophilia d. Overall hemostasis potential e. Thrombelastography 9. Describe appropriate labs and monitoring guidelines for all anticoagulant medications: a. Warfarin: Individualized doses and monitoring of PT/INR are necessary daily or every couple of days until stabilized b. Unfractionated heparin therapy  activated partial thromboplastin time (aPTT). c. Low dose SQ heparin = no labs d. LMWH: Lovenox  anti-Xa e. Dabigatran (pradaxa), Rivaroxaban (xarelto), and Apixaban (Eliquis) were developed and approved for use without the need for routine laboratory monitoring 10. Identify INR goals for all diagnosis: i. DVT/PE: 2.0-3.0 ii. Nonvalvular AF: 2.0-3.0 iii. Mitral bioprosthetic valve: 2.0-3.0 iv. Aortic mechanical valve: 2.0-3.0 v. MECHNICAL valves: 2.5-3.5 vi. Post MI: 2.0-3.0 vii. Rheumatic valve dx: 2.0-3.0 viii. Cryptogenic stroke and PFO with DVT: 2.0-3.0 ix. Cardioembolic stroke or TIA: 2.0-3.0 x. Systolic LV dysfunction: 2.0-3.0 xi. Antiphospholipid syndrome: 2.0-3.0 b. Lower starting doses with elderly, hepatic impairment, poor nutrition, CHF, high bleeding risk. Debilitated, valve replacement, concomitant meds known to increase effect c. https://reference.medscape.com/drug/coumadin-jantoven-warfarin-342182 11. Treatment recommendations for patients that had coronary stent placement and is on Plavix (duration of treatment): a. Drug-eluting stents  clopidogrel or ticagrelor for at least 6 months to one year after the stent is inserted b. Bare-metal stents DAPT is only recommended for one month after stent placement. [Show More]

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