IP2 test 2 AF/VTE/DVT/HF

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Terms in this set (157)
Preload
volume of blood in ventricles at end of diastole
- amount of blood coming into the heart. We can impact this by giving or getting rid of fluid
- The ability of the heart to alter the force of contraction depends on changes in preload. In normal hearts, the preload response is the primary compensatory mechanism such that a small increase in EDV results in large increase in CO. While preload response is the primary compensatory mechanism in normal hearts, the chronically failing heart has exhausted its preload reserve. The increase in preload can only increase SV to a certain point.
Afterload
The force or resistance against which the heart pumps.
- pressure at which the heart is pumping against; If there is arterial hypertension, this would be a sign of high after load.
What are the symptoms and signs of heart failure?
- Dyspnea
- Fatigue
- Exercise intolerance - "not able to walk as far as I used to"
- Fluid overload (peripheral edema, pulmonary congestion) - weight gain; Jugular venous distention (JVD)
- Hypoperfusion (end organ damage, cool/clammy skin)
Brain Natriuretic Peptide (BNP)
- Normal: <100 pg
- Intermediate: 100-500 pg/mL "grey area"
- >500 pg/mL likely HF
- This is released from stretching of ventricles. This acts as your body's own diuretic. This peptide increase the amount of sodium in your urine. Water will follow the sodium into urine.
HFpEF
- symptoms and signs of HF
- LVEF ≥ 50%
- Cardiac structural and/or functional abnormalities - includes elevated natriuretic peptides
HFrEF
- Symptoms and signs of HF
- LVEF < 40%
Goals of heart failure therapy
- Reduce mortality
- Prevent HF hospitalizations
- Improve clinical status, functional capacity, quality of life
HFpEF treatment
manage risk factors (mainly hypertension, obesity, etc) and minimize symptoms/exacerbations (predominantly with diuretic therapy)

In general, for the purposes of class, there have not been therapies to date that have reliably proven to reduce mortality in HFpEF. Therefore, it is less important to have all four therapies on board, but rather adding therapies as needed to control hypertension or other modifiable risk factors.
HFrEF treatment
HFrEF - 4 pillars: ACEi/ARB/ARNI, beta blocker, MRA, SGLT2i
What are the four pillars of heart failure?
- ARNI (or ACEi/ARB)
- BB
- MRA
- SGT2i
- Diuretic prn
LVEF persistent HFrEF → For persistently symptomatic Black patients despite ARNI/beta blocker/ aldosterone antagonist/ SGLT2i NYHA class III-IVHydralazine + isosorbide DinitrateAldosterone antagonistFor patients with eGFR ≥ 30 mL or creatinine ≤ 2.5 mg mg/dL in females or K ≤ 5.0 mEq/LBeta blockers- Metoprolol succinate (when just targeting the heart metoprolol succinate is go to), bisprolol, carvedilol (bisprolol and carvedilol can be useful if you have concurrent HTN that is resistant) - Start low, go slow - Titrate every 2 weeks to target or maximally tolerated doses (we are not going above max doses) - Monitoring: + HR, BP, symptoms worsening after initiation (overaggressive initiation of BB in HF patients can lead to HF exacerbation) - Caution: Do not initiate until stable - Metoprolol tartrate does not reduce mortality in those patients.ARNIEntresto (sacubitril/valsartan) - titrate dose at two weeks based on tolerability - starting dose may be dependent on baseline ACEi/ARB dose - Monitoring: +BP, electrolytes (potassium), kidney function, angioedema (usually happen if started without wash out period) Caution: + 36 hr washout REQUIRED when switching from ACEi - may reduce diuretic requirementACE inhibitors/ARBS- Lisinopril, catopril - titrate every 2 wks to target or maximally tolerated dose - Monitoring: + BP, potassium, serum creatinine, angioedema, dry cough - Caution: + impaired renal function (unstable/acute renal function), hyperkalemia + NSAID drug interaction - risk for kidney injury should be avoidedMRAs- Spironolactone, Eplerenone - Titrate every 2 wks to target or maximally tolerated dose - Monitoring + BP, potassium, renal function, gynecomastia - Eplerenone has much lower risk for gynecomastia - Caution: + Hyperkalemia, renal insufficiency:check frequently - In HFrEF, aldosterone is a big player in ventricular remodeling. Primary purpose of Aldosterone is sodium retention. That's an issue with someone without a good functioning heart. Blocking that helps omit some of the fluid retention.BiDil (hydralazine/isosorbide dinitrate)- Persistently symptomatic Black patients on optimized therapy - More generally as an alternative to ACEi/ARB therapy - Monitoring + BP - Pearls + Give individual agents to reduce cost - Lower level recommendation than previous therapies - If you are having problems on optimized medications, this may be an alternative agent. - Also, may be used in patients who cannot tolerate ACE or ARB.Diuretics- Reduce signs and symptoms of congestion - Titrate dose to relief over days to weeks - May need to reduce dose if ARNI therapy initiated (make sure you aren't over diuresis someone) - Monitoring: + BP, electrolytes (K, NA), renal function - BUN/SCr (acute kidney injury can happen) - If BUN:SCr ratio is above 20, we've push the patient too far. - Diuretic resistance - consider addition of thiazide type - Diuretics don't improve mortality. They help control symptoms and reduce hospitalizations. - Commonly done with loop diuretics: Furosemide, Torsemide, Budesemide - titrate to reliefEquivalent of 80 mg BID furosemide1. change to different loop 2. add thiazide - will block distal convoluted tubule - where your body starts picking up saltFurosemide 40 mg PO is EQUIVALENT to:Furosemide 20 mg IV = Bumetanide 1 mg IV/PO = Torsemide 20 mg IV/POSGLT2 inhibitorsDapagliflozin (Farxiga), Empagliflozin (Jardiance) - Flat dosing (10 mg daily for both, some renal considering) - Renal considerations - mainly if renal function isn't "strong enough", it is not "technically" recommended to use because of reduced efficacy. - ADRs: + hypovolemia (diuretic effects)/hypotension (AKI if severe) + GU infection (related to increase concentration of glucose in urine) - Significant benefits in HFpEF and HFrEF - IRRESPECTIVE OF DIABETES STATUSDigoxin- Fib with rapid ventricular rate to other options: if other agents limited by hypotension - Monitoring: + serum levels: <1.2, electrolytes (K+), kidney function, visual disturbances nausea/vomiting - caution + narrow therapeutic index: especially elderly, kidney dysfunction, hypokalemiaCalcium Channel Blockers- NonDHP + DO NOT USE in HFrEf - associated with worse outcomes - DHP + may muddy picture with edema adverse effectsHF exacerbation- dietary indiscretion - medication non-adherence - non cardiac illness - recent dose titrationsWhere do we want most patients in HF?Warm and dryHF exacerbation management- Determine etiology - Alleviate symptoms. (improve congestion, improve perfusion) - target 1 liter net loss per day via diuresis (don't forget about insensible losses ~700mL/day [0.7L]) - Initiate and/or up-tirate disease modifying therapy when stable - Investigate opportunities to reduce cost or increase adherenceManagement of diuretic therapy in patients with acute heart failure- Y - you want to give at least give their home medication, but more frequently we double their home meds (because if they have been taking their home meds it's obvious it hasn't been working for them)Pharmacist impact/ role HF- address barriers to medication titration - diet advice (sodium, potassium) - Improve adherence (20-50% of patients) + patient's perspective + simplify + cost/access + monitor and follow upWhen should a HF call their provider?- More than 2-3 pounds of weight gains in one day - More than 5 pounds of weight gain in a weekNormal venous circulation- gravity - muscle contraction (particularly in legs) - one-way valves - Heart pumps → LV contracts → blood to body (through arteries) → blood returns through the venous system through a more passive system → gravity works against this so calf muscle contraction moves blood back to heart → we have one way valves in our veins. This will allow blood to move back to the heart → When the muscle contraction ends, we don't want the blood to just fall back. The problem with one way valves is they create abnormal blood flow. This is where clots start to form.Hemostasis- Physiologic process to maintain vessel integrity after injury - maintenance of vessel integrity; blood should not be pouring out - maintenance of normal circulatory systemThrombosis(a process) clotting in an unbroken blood vessel - usually a vein - blood moves faster through arteries, so usually doesn't happen in arteries - Thrombus - clotEmbolusa blood clot, air bubble, fat from broken bones, or a piece of debris transported by the bloodstream - something that is moving in circulatory systemthromboembolism- vascular obstruction resulting from a dislodged thrombus - pulmonary emboli originate in the venous circulation (mostly from deep veins of the legs) or in the right heart.normal hemostasis and thrombosis introA. vasoconstriction: reduce amount of volume through vessel B. Primary hemostasis: Platelets are sensing clotting factors (collagen and VWF) that are now inside of the blood vessels. This cause the platelets to become sticky and form a temporary plug. C. Secondary hemostasis: fibrin is activated and strengthens plugs made by platelets D. THROMBUS INTRO: Thrombus and antithrombotic events: plug is bigger than it needs to be - unnatural and occludes vesselsClinical presentation DVTSymptoms + typically unilateral and localized to the affected area + swelling + pain + redness + tenderness + heat Signs + superficial veins dilated (palpable cored) + Homan's signs: calf pain during dorsiflexion (backward bending) of the foot - If you flex foot, pt will have severe foot pain.Clinical presentation of PE- can be rapidly fatal (thrombus in lungs) Symptoms (NB: some PE patients are asymptomatic) + Most common: shortness of breath and fatigue - missing functionality of one or both lungs + chest pain + palpitations + hemoptysis + syncope + easily can be confused with MI Signs: + Tachypnea (abnormally rapid breathing) + tachycardia + diaphoresis + hypoxiaComplications of VTE- death (cannot live without lungs for more than a few minutes) - PE secondary to DVT if untreated - Post-thrombotic syndrome (PTS) - pain, swelling, discoloration (from damage to vein) - Chronic thromboembolic pulmonary hypertension - VTE recurrence - history of VTE is one of the strongest risk factors of VTEDVT risk complications- rarely fatal - postthrombotic syndrome - can lead to PEPulmonary embolism- often fatal (minutes) - chronic thromboembolic pulmonary hypertensionVTE epidemology- Occurs more frequently in women than men - May be more prevalent in Blacks > Whites > Asians - Heriable risk factors (Factor V Leiden, Prothrombin G20210A) - The rate of recurrent VTE is higher in the 180 days following the initial event - The 10 yr cumulative risk of recurrent VTE ~25%Factor V LeidenMost common hypercoagulable state, mutated factor V that is resistant to , Protein C and Protein S cleavage.Prothrombin G20210A mutation- *prothrombin* gene mutation results in *mRNA that is resistant to degradation* - excess prothombin. - correlates toward *venous thrombosis* - HypercoagulabilityVirchow's triad- Hypercoagulable state - increase tendency of blood to clot + Transient (drug induced, pregnancy, malignancy) + Acquired (genetic risk factors - coagulation factor abnormalities) - Vessel wall injury - any penetrative trauma not at the time of thrombus e.g. trauma, vascular injury, venous catheters surgery, trigger, etc - Venous Stasis - abnormal blood flow e.g. immobility, obesity - All three must be present for thrombus formationHypercoagulability disorder- a state of increase clot formation - increase likelihood of DVT - Primary - genetic + common - Caucasian prevalence 2% - 7% + activated protein C (aPC) resistance - Factor V mutation (Arg to Glucose substitution at 506) = factor V Leiden"; 3x increase risk of VTE + Prothrombin mutation (G202101A mutation - increased prothrombin levels) + increase levels of factor VIII, IX, XI, or fibrinogen Rare - inherited deficiencies of plasma protein that inhibit thrombus formation - antithrombin III, protein C and S deficienciesHypercoagulability disorder - Acquired High risk for thrombosis- Prolonged bed rest or immobilization - Myocardial infarction; Atrial fibrillation - Tissue injury (surgery, fracture, burn) - Cancer ( tumors can disrupt veins. Tumors can also build their own vasculature. They express regulatory proteins that tend to be prothrombotic) - Prosthetic cardiac valves - Disseminated intravascular coagulation - Heparin-induced thrombocytopenia - Anti-phospholipid antibody syndrome - common with history of SLE (lupus related syndrome - auto immune issues)Hypercoagulability disorder - Acquired Low risk for thrombosis- Cardiomyopathy - Nephrotic syndrome - Hyperestrogenic states (pregnancy) - Oral contraceptive use - Sickle cell anemia - SmokingVenous statis- stasis occurs with immobility of an extremity or the entire body - Bed rest & immobilization →↓ blood flow, venous pooling in the lower extremities, & ↑ risk of DVT - patients immobilized by hip fracture, joint replacement, or spinal cord injury - Impaired cardiac function ↑ the risk of DVT - high incidence in MI & CHF - Obesity - Older adults are more susceptible than younger people - Long airplane travel - prolonged sitting & ↑ blood viscosity because of dehydrationEndothelial damageEndothelial damage can result from: - trauma and surgery - infection or inflammation of the vessel wall - vascular injury from venous catheters A lot of risk when being hospitalized e.g. thinking a bout being a cancer patient with catheters, surgeries, tumors, etcRisk factors for VTE- Advanced age - Prior VTE - strongest known risk factor - Cancer -Chronic illnesses - Family history - Genetic disorders - Major surgery - Medications - Obesity - Pregnancy - Prolonged immobility/inactivity - Tobacco use - Traumaplatelet aggregation- Endothelial surface disruption exposes von Willebrand factor (vWF). (first triggering event) - GpIb receptor on the platelet adhere to vWF on the endothelium → platelet adhesion. - The platelet releases ADP immediately after adhesion. - Triggers: VWF and collagenOverview of Hemostasis- Von willebrand factor, collagen, tissue factor: spark that kicks off coagulation cascade - Plasminogen activator inhibitor-1, ⍺-antiplasmin: destruction of clot - Cascade of activations: allows us to very rapidly turn on an enormous amount of enzyme activity; It allows us to have some type of regulation because we don't want clots everywhere. We want to build the clot very fast, so all the blood won't flowout of the body. We also need to stop it very quickly, just as fast as it started. When you are start to form a clot in a healthy vessel, we need to be able to inhibit that clot formation (right side of flow chart).Pathologic VTE- occurs n the absence of vessel wall damage - may be triggered by tissue factor (TF) Brough to the clot formation site by circulating microparticles I. An impaired blood vessel activates platelets & initiates the clotting factor cascade*. II. coagulation cascade - intrinsic, extrinsic & common pathways* III. Thrombin is activated → formation of a clot*. IV. The clot may enlarge & can block the vein. V. Impaired hemostasis → hypercoagulability(theoretical) pathologic formation of thrombusA. activated platelets adhere to vascular endothelium; B. activated platelets express P-selectin; C. microparticles express active tissue factor (TF) present in circulation - accumulate by binding to activated platelets expressing P-selectin; D. TF can → thrombin generation → fibrin clot formation.Coagulation cascade intrinsic pathway- Xa and Va activates thrombin. We cleave prothrombin (factor II) to thrombin (IIa). Tissue factor is also activating the intrinsic pathway. The intrinsic molecules are bigger in qty and can do a lot more work. - factor 12 activates 11 → 11 activates 9 → 9 + 8 partner and they are intrinsic 10-ase. They are activating factor Xa which activate factor V which cleaves prothrombin into thrombin.Cellular coagulation cascade model extrinsic pathway1. Initiation TF + VIIa (extrinsic tenase) activate IX and X → Xa and Va form prothrombinase complex → prothrombinase complex cleaves II to IIa → IXa moves to surface of activated platelet → Tissue factor pathway inhibitors (regulator of TF/VIIa induced coagulation) terminations initiation 2. Amplification IIa activates V and VII → Va and VIIa bind to platelet surface to support thrombin generation IIa also activates XI 3. Propagation (bulk of thrombus formation happens here) VIIIa/IXa (intrinsic tenase) and prothrombinase complex assemble on activated platelets → acclerate the generation of factor Xa and IIa → burst of thrombin productionThe coagulation cascade- Thrombin generation is further supported by factor XIa bound to platelet surfaces, which activates factor IX to form additional intrinsic tenase. - Thrombin then converts fibrinogen to fibrin monomers that precipitate & polymerize to form fibrin strands. - Factor XIIIa (activated by thrombin) covalently bonds these strands to form an extensive meshwork that encases the aggregated platelet thrombus & red cells to stabilize the fibrin clot.Antithrombotic substances- secreted by intact endothelium adjacent to damaged tissue - control hemostasis 1. Thrombomodulin - secreted by healthy endothelium - modulates thrombin activity by converting protein C to its activated form (aPC) - aPC joins with protein S to inactivate factors Va & VIIIa. - This prevents coagulation reactions from spreading to uninjured vessel walls. 2. Circulating Antithrombin - inhibits thrombin & factor Xa. 3. Heparan sulfate (endogenous - helps to prevent overgrowth of clot) - secreted by endothelial cells and accelerates antithrombin activity. - Factor V is cofactor to Factor XFibrinolysis- end of our process when we are finished with out clot - Endothelial cells secrete t-PA at sites of injury - t-PA binds to fibrin & converts plasminogen to plasmin, which digests fibrin - Plasminogen activator inhibitor-1 (PAI-1) & PAI-2 inactivate t-PA - α2-AP inactivates plasmin. - After we are finished with our clot, we need to dissolve it. - Plasminogen is inactive. It gets activated by T-PA. Now, it will be plasmin. Plasmin will help to dissolve the cross linked fibrin into plasmin. Plasmin will help to dissolve the cross linked fibrin into a soluble protein. That will soluble protein is known as D-Dimer. When you have a clot, you will have detectable D-dimer from destruction of the clot.D - dimer test- Specific for lysis of fibrin thrombi - Detects cross-linked insoluble fibrin monomers in a fibrin clot - Positive (>500 ng/mL) D-dimer does not confirm diagnosis of DVT/PE (indicated follow up testing is indicated) - Negative (<500 ng/mL) D-dimer excludes diagnosis of DVT/PEWells scoreclinical prediction rule that incorporates signs, symptoms, & risk factors used to categorize patient as at low, intermediate, or high probability of having acute DVT or PE. PE: - ≤ 4 pts (pe unlikely) → D - dimer test - > 4 pts (pe likely) → imaging: CTPA or V/Q DVT: - < 2pt DVT unlikely → D-dimer test - ≥ 2 pt DVT likely→ CUSWhat are the times you may have high D-Dimer without a clot?- D-dimer - fibrin clot degradation product - levels ↑ in acute thrombosis - Conditions associated with D-dimer elevations - recent surgery or trauma, pregnancy, ↑ age, cancer - *Appropriate use of D-dimer should include initial risk stratification using a validated clinical assessment tool - D-dimer almost never gives you a false negative, but it will give you a false positive (age, MI, surgery, trauma, pregnancy, etc cause cause higher risk of positive dimer test)Diagnostic test for DVT1. D-dimer test 2. compression ultrasound - CUS + 1st line testing for DVT - highly sensitive and specific (pushing down on vein - If you can collapse it, it is not a clot. If it doesn't compress, there is something blocked (clot). - uses sound waves to visualize vasculature - DVT diagnosis→ veins do not compress from pressure applied with ultra sound probe + risk: If we have clot in our blood vessels and we push on it, there is some risk you may dislodge that clot. After you find the lot, you should stop compressing.Diagnostic test for PE1. D-Dimer Test 2. Computed tomographic pulmonary angiography (CTPA) + 1st-line testing for PE - highly sensitive & specific + Contrast dye is used to visualize thrombus in lungs (coloring veins) + PE Diagnosis → filling defect (vein appears dark against white contrast dye) + Disadvantages: Radiation exposure (serious with patients who are young because you are going to test them multiples times throughout their lives), Renal toxicity & anaphylaxis from contrast dye, Expensive 3. Ventilation-perfusion (V/Q) scan - alternative diagnostic test for patients allergic to contrast media, renal impairment, high radiation exposure risk - measures the distribution of blood & air flow in the lungs.What is an abnormal SpO2?lesss than 94% - pulse will compensate for poor oxygen delivery by being hypoxic (heading toward respiratory failure)Acute episode assessment for respiratory patient- ABC - appearance, breathing, circulation - Appearance - LOC - tone, interactiveness, gaze, cry/console (peds) - Work of Breathing - positioning (Patients prefer to sit up rather than lie down; Hunched shoulders), RR>30, accessory muscle use/retractions, airway sounds - Circulation - Cyanosis, pallor, tachycardia - "Labs" - Pulse oximetry (<90%), end tidal CO2 (normally 35-45 mm HG), blood gas, chest X-ray; Peak expiratory flowChronic assessment with a respiratory patient- History - Symptoms - albuterol use, activity limitations, night- & daytime symptoms, cough/sputum - Risk - respiratory flareups (exacerbations), medication side effects, loss of lung function - Validated tools - Asthma control test (ACT); COPD Assessment Test (CAT) - Pulmonary function testnasal cannula- Low-flow - less than 10 lpm - FiO2 could be as low as 0.21; Max 29%; depends upon fit/nose breathing fraction/nasal obstruction, etc - Benefits: easy, cheap, connects to tank for ambulatory/home use - Drawbacks: not very effective O2 delivery; nasal dryness/irritation - Patient type: ambulatory, minimal O2 requirement; COPD, former premature infants with chronic lung diseaseSimple mask- Low-flow device - oxygen concentration: Best case use is FiO2 0.3-0.4 - Easy to use, cheap, non-invasive - Must have holes punched in side for safety to avoid asphyxiation - Not a commonly used device in acute care, but widely available; often in non-emergent settings (post-op, Labor & Delivery)Non-rebreather mask- Low-flow - oxygen concentration: 95% if totally sealed... in reality, probably 50% at best case because of vent holes, poor seal, dead space - benefits - fast/easily deployed, cheap, non-invasive - Drawbacks - lower O2 conc; suffocation risk - especially if holes obscured - Patient types - conscious; spontaneously breathing; EMS/ER patients with acute problems as first choice of deviceHigh flow nasal cannula- it's high-flow! Can be 60 L/min! - Oxygen can be dialed with oxygen blender from 0.21 to 1.0 - Benefits: Higher oxygen concentrations can be delivered; tighter fit with flexible nose piece & head band; humidification/warming of air; - risks/drawbacks: More invasive; humidity can fill tubing where there is a gush of water up the nose - Patients: Higher acuity patients! More in ICU setting; NICU, ER and acutely ill patients; last step before non-invasive ventilationCPAP or BiPAP non-invasive ventilation maks- High-flow - Attached to a device like a ventilator - can be 100% O2 (FiO2 of 1) - Benefits: Less invasive that intubation; can offer positive pressure to recruit (open up) atelectatic airways; mask or scuba mask - Risks: Less invasive, but still can be claustrophobic - Patients: Used in CPAP and BPAP (BiPAP) for OSA treatment; severely ill patient where there is a significant risk of complications from intubationBag valve mask (ambu- or self-inflating bag)- High-flow - oxygen concentration: Attached to a device like a ventilator - can be 100% O2 (FiO2 of 1) - Benefits: Less invasive that intubation; can offer positive pressure to recruit (open up) atelectatic airways; mask or scuba mask Risks: Less invasive, but still can be claustrophobic Patients: Used in CPAP and BPAP (BiPAP) for OSA treatment; severely ill patient where there is a significant risk of complications from intubationEndotracheal tube- High flow device - O2 concentration: Any concentration of Fi02 can be delivered Complete airway control; can do complicated vent settings (PEEP, high-peak pressures, pressure controlled breathing) - Drawbacks - highly invasive, uncomfortable, trauma of ET tube insertion - Patients: If having complete failure, this is almost the only optionadminsitering meds via O2 delivery devices- Nebulization is traditional method: Mask, Endotracheal tube, High-flow nasal cannula (new) - MDI/respimat: + Requires adaptor + Many factors affect lung depositionAsthma steroid dosageChild: 1-2 mg/kg/day for 3-5 days; max 40 mg/day; Adult: 40-50 mg/day x5-7 daysSystemic steroid therapy- Topical or inhaled - designed to limit systemic side effects Ex: prednisone (-solone), methylprednisolone, dexamethasone - Most commonly as short burst; minimizes known side effects - Short means <3 weeks of ≤20 mg prednisone equivalent - Recommendation for asthma & COPD flare is short, oral burst; NO TAPERCOPD steroid dosage40 mg oral daily for 5-7 daysCOVID steroid dosageDexamethasone 6 mg po/iv x10 days (stop upon discharge from hospital)Post-extubation stridor (adult) steroid dosageusually initiate 4 hr before if no cuff leak - Methylprednisolone 20 mg every 4 hours for 4 doses - DexamethasoneGuidelines for long term glucocorticoid therapy- Initiate only if there is published evidence of objective therapeutic benefit - Use only after other specific therapies fail - Identify a specific therapeutic objective - Use objective criteria of response - Administer sufficient dose for sufficient time to achieve desired response - Administer for no longer than necessary to achieve the desired response - Terminate if therapeutic benefit achieved, not observed or complications arisepolymyalgia rheumatica steroid tapering (long term systemic steroid tapering)15 mg/d x2-4 wks; taper to 10 mg over a month; then ↓1mg/moNephrotic syndrome (long term systemic steroid tapering)3-5 monthsLong term Systemic Steroid taperingDisease Taper vs. HPA-axis suppression taper - Some diseases flare back up if tapered too rapidly (polymyalgia rheumatic and Nephrotic syndrome) - Tapering not needed for: + Regimens (even high-dose) of up to 3 weeks + HPA axis suppression uncommon in doses below Prednisone 5 mg/day - Minimal published evidence on optimal regimen to avoid adrenal insufficiency - Disease-related tapers must be based upon patient response - Some patients have psychological dependenceGeneral guide for Long term Systemic Steroid tapering- Reduce dose by 10-20% every 1-2 weeks, slowing to q2-4 weeks at 3rd step - If disease recrudesces, increase back up by 10-15% for 2-4 weeks - If no response, double dose, stabilize and taper more slowlyRetractions (Breathing)Skin pulling around the ribs or above the clavicles during inspirationasthma action plana written plan that the person develops with his or her healthcare provider that details daily management of the condition as well as how to handle an asthma attackWhat are the goals of AF therapy?1. prevent stroke 2. control of ventricular rate 3. restore normal sinus rhythm (NSR)Stroke prevention in AF1. Calculate the stroke and bleeding risks - CHA2DS2-VASc score - HASBLED: Score ≥3 follow up more often - Treatment based on CHA2DS2-VASc scoreCHA2DS2-VASc score- Basically, If someone' score is over 1, add an anticoagulant unless their value is only 1 due to being a female. - 0 = omit therapy - 1 (female) = omit therapy - 1 (male) = consider oral anticoagulant - ≥ 2 (male) - oral anticoagulant - ≥ 3 female - oral anticoagulantWarfarin A. Fib- Dose: 2-5mg daily; adjust based on INR - administration: Take with food in evening - Monitoring: Efficacy: s/sx stroke Safety: CBC, INR (goal 2-3), s/sx bleeding - Comments: · Only option for valvular AF · DOC if severe renal disease DOC if pt can't afford DOACDabigatran (Pradaxa) A. Fib- Dose: Avoid if CrCl <15 - Administration: Don't crush, chew, or open capsules Keep in original container - Monitoring: Efficacy: s/sx stroke Safety: CBC, SCr, ALT/AST, s/sx bleeding, GI side effects - comments: · Careful in >80 yo &/or ↓ body weight · On Beer's Criteria: Use with caution if ≥75yo due to ↑ risk of GI bleed · ↑ risk of MIs versus warfarin - All DOACs on Beers Criteria for warning regarding kidney function (lack of evidence of efficacy/safety at CrCl <30 (D, E, R), <25 (A) or higher if presence of drug interactionsRivaroxaban (Xarelto) A. Fib- Dosing: Avoid if CrCl<15 - Administration: take with food - Monitoring: Efficacy: s/sx stroke Safety: CBC, SCr, ALT/AST, s/sx bleeding - Comments: · Consider DOAC first line for many pts · Can switch to DOAC if fluctuating INRs from warfarin, difficulty getting to AC, side effects from warfarin, or lots of short-term warfarin drug interactions · Rivaroxaban on Beers Criteria: Use with caution if ≥75yo due to ↑ risk of GI bleed - All DOACs on Beers Criteria for warning regarding kidney function (lack of evidence of efficacy/safety at CrCl <30 (D, E, R), <25 (A) or higher if presence of drug interactionsApixaban (Eliquis)Monitoring: Efficacy: s/sx stroke Safety: CBC, SCr, ALT/AST, s/sx bleeding (least risk of GI bleeding) - - Comments: · Consider DOAC first line for many pts · Can switch to DOAC if fluctuating INRs from warfarin, difficulty getting to AC, side effects from warfarin, or lots of short-term warfarin drug interactions · Rivaroxaban on Beers Criteria: Use with caution if ≥75yo due to ↑ risk of GI bleed - All DOACs on Beers Criteria for warning regarding kidney function (lack of evidence of efficacy/safety at CrCl <30 (D, E, R), <25 (A) or higher if presence of drug interactionsEdoxaban (Savaysa) A. Fib- Dosing: avoid if CrCl < 15 - monitoring: Efficacy: s/sx stroke Safety: CBC, SCr, ALT/AST s/sx bleeding - - Comments: · Consider DOAC first line for many pts · Can switch to DOAC if fluctuating INRs from warfarin, difficulty getting to AC, side effects from warfarin, or lots of short-term warfarin drug interactions · Rivaroxaban on Beers Criteria: Use with caution if ≥75yo due to ↑ risk of GI bleed - All DOACs on Beers Criteria for warning regarding kidney function (lack of evidence of efficacy/safety at CrCl <30 (D, E, R), <25 (A) or higher if presence of drug interactionsOAC duration with A.Fibusually a lifetimePatients AF and CAD who undergo PCI- CHA2DS2VASc = 0-1: aspirin + clopidogrel - CHA2DS2VASc = ≥2: Triple therapy (OAC/aspirin 81/clopidogrel) X4-6 wks (when they are at the highest risk of having an even after placing that stent in vessels) → OAC/clopidogrel, Consider adding a PPI (pantoprazole) {protect stomach}, INR goal 2-2.5 (decrease risk of bleeding)watchman procedure- Sometimes patients cannot be on OAC for long periods of time because of their increase risk of bleeding. There are various devices that can be used for AF> When a blood clot happens in A.Fib, it mostly happens in the Left atrial appendage. One solution to this is walling it off with a device called the watchman device. By walling that off, the blood cannot pull in that area. When the patient first has this installed, the patient needs to be on both warfarin and baby aspirin for a month and a half. After that, the warfarin and aspirin will be stopped, and DAPT therapy will be started for 6 months. Afterwards, the patient can just be on aspirin indefinitely. This gives the patient a much less likely bleeding risk. -Rate control A. FIb- reduce conduction through Av node to help protect the ventricles 1. Necessary to prevent ventricular arrhythmias and cardiomyopathy 2. Mechanism of drug action: reduce AV node conduction and ventricular heart rate 3. Onset of drug action: IV - minutes, PO - hours Choices: - BBL - CCB - Digoxin - AV node ablation - AmoidarioneBeta Blockers in AF- Atenolol (tenormin) (beta 1), Esmolol (brevibloc) (beta 1), Metoprolol (lopressor; Toprol XL) (beta 1); Propranolol (inderal) (beta 1+2) - Effects on Heart: ↓ BP, HR, and AV node conduction (help with A.Fib by reducing HR) - Side Effects: · CV: hypotension/dizziness, bradycardia/heart block, aggravation of acute heart failure, peripheral vasoconstriction · Bronchospasm, ↓ exercise tolerance/fatigue, depression, impotence, glucose and lipid abnormalities - Warnings: Don't abruptly discontinue (risk of rebound adverse CV effect - taper); Do not use ISA beta blockers - DI: many are CYP 2D6 substrates Place in therapy: most effective rate control drug class in AFFIRM trial, preferred over CCBs in HFrEF - If you need to use in COPD, make sure you use a β1 specific blocker. - If patient has asthma, try your best to avoid and use something like beta blocker.NDHP CCB In AF- Diltiazem (used most commonly) - Verapamil - Effects on Heart: decrease BP, HR, AV node conduction, and contractility (reason why we dont use in HF) - Side effects: · CV: hypotension/dizziness, bradycardia/heartblock · Peripheral edema, headache, nausea, constipation - DI: · Metabolized by CYP 3A4 (careful with grapefruit juice) · Inhibits CYP 3A4 (warfarin, DOACs, amiodarone) [we still use together just have to monitor therapy] · Other drugs that ↓ conduction through AV node CI: other arrhythmias, hypotension, HFrEF Warnings: don't abruptly discontinue (risk of rebound adverse CV effects) Place in therapy: IV diltiazem (can be given as a drip) preferred for hospital rate control; PO CCBs preferred over BBLs in asthma/COPDDigoxin In AF- not preferred; can be used if necessary - Effects on heart: ↓ HR and AV node conduction, ↑ contractility; Na+/K+ pump inhibitor→ ↑ intracellular calciumAV node ablation in AF- burns the abnormally firing atrial tissue and pace maker will be inserted a. Prevents atrial impulses from getting to the ventricles b. Creates need for permanent pacemaker and still requires anticoagulation because atria continue to fibrillate c. No mortality benefit, but ↓ hospitalizations and ↑quality of lifeAmiodarone in AFa. Last line recommendation due to side effects b. Consider in acute systolic HF, hypotensionMonitoring in AFa. Heart rate: goal 60-80 bpm at rest, 90-115 with exercise b. Blood pressure ≤ 130/80 c. Other: drug interactions, side effects, electrolytes, kidney function, serum drug levels (digoxin)Rhythm control in Afib- restore back to normal sinus rhythm - not every patient needs this. It is used when patient is symptomatic despite rate control - can be issued through meds or shocking Indications: persistent symptoms, inability to attain rate control, patient preference - two choices: convert to normal sinus rhythm (NSR) or maintain NSR - Whether we use rhythm control or not patients still need to be addressed for chronic coagulation - If CHASVASC score is 0, and we immediately cardiovert they still need temporary anticoagulant in cause of clot in heart.Convert to NSR- If converted, pt needs to be coagulated (clot could go to the brain). - Immediate: · Direct current cardioversion (DCC): indicated when pt is hemodynamically unstable; requires deep sedation or general anesthesia · Antiarrhythmics: conversion rate < DCC, but don't require sedation · Anticoagulate before and after to prevent "throwing a clot" - Delayed: · DCC, antiarrhythmics, atrial ablation (cauterization of cardiac tissue in atria that is responsible for triggering or maintaining an arrhythmia) · Anticoagulate with OAC 3 weeks before and ≥4 weeks after cardioversion · Rate control should be achieved before conversionMaintain NSR in AF- have to use oral antiarrhymics - Antiarrhythmics, pacemaker, implantable atrial defibrillator, surgery, ablation proceduresIC antiarrhythmicsFlecainide Propafenone - can be used for converting and maintaining NSRIII antiarrhythmics- Dronedarone; Sotalol = not helpful for converting - Ibutilide (corcvert): could use to convert to NSR, but is IV only - Amiodarone; Adofetilide: used to converted and maintain NSRCompare Amiodarone and DronedaroneAmoidarone: - cheap - elimination: 14-75 days - less CI - more side effects - Pulmonary fibrosis - Not used in any antiarrthmic in permanent A.F Dronedarone: - expensive - Elimination: 13-19 hrs - more CI - less Side effects - Safest: dronedarone - Most effective for AF: AmoidaroneAmoidaroneDI: Moderately inhibits CYP 1A2, 2C9, 2C19, 2D6, 3A4 - CI: + 2nd/3rd degree heart block + Bradycardia (HR<50bpm) + Prolonged QT interval + Caution in liver disease Side effects: + Hepatic (BBW) + Renal + Arrhythmias/torsades de pointes (BBW) + Phototoxicity, blue-gray skin color + Nausea + Thyroid + Pulmonary (BBW) + Ocular + Polyneuropathy Managing SE: + Hypothyroidism: levothyroxine + Hyperthyroidism: antithyroid meds or d/c + Corneal microdeposits: nothing + Optic neuritis: d/c + Pulmonary fibrosis: d/c + Hepatotoxicity: lower dose or d/c if LE >2X ULN + Bradycardia/heart block: lower dose or d/c + Neuropathy: lower dose or d/c Monitoring: - ECG - Liver enzymes (may stop if these go out of wack) - Chemistry panel/SCr - Other proarrhythmic drugs - Thyroid function - Chest X-ray, PFTs - Eye exam Depending on pt characteristics, 1st line to convert/maintain NSR, esp. in pts with HFDronedaroneDI: Moderately inhibits CYP 3A4; Weakly inhibits P-gp, CYP 2D6 CI: - 2nd/3rd degree heart block - Bradycardia (HR<50bpm) - Prolonged QT interval - Severe liver impairment - Concurrent strong 3A4 inhibitors - NYHA Class II-IV HF (BBW) - Permanent AF (BBW) SE: - Hepatic - Renal: SCr by 0.1 mg/dl - Arrhythmias/torsades de pointes - Phototoxicity, rash - N/V/D/abdominal pain Manage SE: - Hepatotoxicity: d/c if LE >2X ULN - Bradycardia/heart block: d/c Monitoring: - ECG - Liver enzymes: baseline, frequent in 1st 6 mo - Chemistry panel/SCr - Other proarrhythmic drugs: phenothiazines, TCAs, macrolides, other antiarrhythmics Can be used to maintain NSR in pts without HF who have paroxysmal or persistent AF Recurrence of AF higher with dronedarone, but less side effects"Pill in the pocket" strategy AFa. For paroxysmal AF <4 episodes/year b. High dose class 1c antiarrhythmic given at onset of episode to acutely convert c. Choices: propafenone 600 mg, flecainide 300mg PO PRN d. 70-80% convert within 12 hours e. Patient should also be on anticoagulation and rate control - Cardiologist may give patient a IC antiarrthymic and dose will be PRN. They are given this basically to relieve symptoms without going to ER.VTE goals of therapy1. to treat active VTE 2. To prevent VTE, stroke, complications - VTE can be DVT. It can be in arms, legs, brain, etc. If it travels from legs to lungs and lodges there, it is a called a PE.What anticoagulant can be started initially in VTE treatment in hospital?LMWH, UH, Rivaroxaban, ApixabanWhat anticoagulant can a patient be discharged on in VTE treatment?Apixaban, rivaroxaban, warfarin, Dabigatran, edoxabanVTE treatmentWarfarin specifics: - Start warfarin when aptt is therapeutic (1.5-2.5) - Stop initial anticoagulant when reach therapeutic INR (with a minimum of 5 day overlap)UH in treatment of VTE- acute treatment of vte - Dose: 80 units/kg IV LD, 18 units/kg/hour IV infusion (actual body weight) - length of treatment: D/c when INR therapeutic X 24 hrs (minimum 5 day overlap) Monitoring - Parameter: aPTT - Baseline level: 20-30 seconds (need to measure) - Therapeutic treatment level: 1.5-2.5 X baseline (corresponds to 0.3-0.7 IU/ml heparin anti-Xa activity) - Indication/Frequency of monitoring: Monitor for patients on treatment doses; Baseline, Q6 hrs until therapeutic; then daily - CBC: Baseline, then Q2-3 days (in hospital)LMWH in treatment of VTE- Acute and short/long-term treatment of VTE - Dose (enoxaparin): 1mg/kg SQ BID (actual body weight) CrCl < 30ml/min: 1mg/kg SQ once daily (use UH if <20ml/min) - Length of treatment: D/c when INR therapeutic X 24 hours (minimum 5 days overlap) Monitoring: - Parameter: anti-Xa levels (obese, children, renal impaired, pregnant pts) - baseline level: <0.5 U/ml (don't need to measure) - Indication/frequency of monitoring: Consider monitoring anti-Xa in obesity, renal impairment, pregnancy, or children on treatment doses; Check 4-hour post dose at steady state - CBC: Baseline, then Q2-3 days (in hospital)Adverse effects of heparins1. Bleeding (avoid in active bleeding) a. Major bleeding = intracranial, requires transfusion/hospitalization, GI bleed, blood in urine/stool b. Minor = nose bleed, bruises, etc. c. Reversible with IV protamine sulfate (1 mg neutralizes 100 units heparin) or fresh frozen plasma 2. Injection site reactions (hematomas) 3. Spinal hematoma if concurrently given with spinal anesthesiaThrombocytopenia type I- decrease platelets - Patiophysiology: Early, reversible, non-immune; associated with a direct interaction between heparin and platelets; this can cause: bleeding -Decrease in platelet count: ~30%; <100,000 - Incidence in herapin treated patients: ~10-20% - time course: Usually occurs ~1-2 days after treatment begins with heparin - Treatment: Discontinue heparin Next step depends if VTE treatment or prophylaxisThrombocytopenia type II- Immune mediated rxn; due to antibodies - Patiophysiology:Serious allergic reaction; Late, more serious IgG-mediated; heparin-platelet interaction results in platelet and coagulation cascade activation; this can cause:clots -Decrease in platelet count:~30-50%; 20,000-150,000 (platelets clump up and cause clots) - Incidence in herapin treated patients: < 3%; occurs with UH > LMWH - time course:Usually occurs ~4-14 days after beginning heparin therapy (can occur within 12 hours of re-exposure) - Treatment: - Discontinue heparin (need to also stop warfarin if platelets <150K) - Start argatroban or fondaparinux - Start low dose warfarin when platelets >150K and aPTT therapeutic (argatroban)Heparin DI, monitoring, and patient educationDrug Interactions 1. Drugs that potentiate bleeding Monitoring 1. Signs/symptoms bleeding/VTE 2. CBC (watch for bleeding) 3. aPTT: UH 4. LMWH: SCr (adjust doses with levels), maybe Anti-Xa level Patient Education 1. Anticipated duration of therapy 2. Side effects (what signs of bleeding to look for, what to do, how to prevent) 3. Technique of SQ injectionFondaparinux (Arixtra) VTEindirect factor Xa inhibitor -Place in therapy: Acute VTE treatment, HIT (rarely used) - dosing: Avoid if CrCl<30 - Lab monitoring: CBC, SCr - Adverse Effects: bleedingRivaroxaban (Xarelto) VTEdirect factor Xa inhibitor - Place in therapy: Acute and short/long-term VTE treatment - Dosing: Avoid if CrCl <15 - Lab monitoring: CBC, SCr, ALT/AST - ADR: bleeding PK: substrate of CYP 2A4 and PGPApixaban (Eliquis) VTEdirect factor Xa inhibitor - Place in therapy: Acute and short/long-term VTE treatment - Lab monitoring: CBC, SCr, ALT/AST - ADR: bleedning - PK: substrate of CYP 2A4 and PGPEdoxaban (Savaysa) VTEdirect factor Xa inhibitor - Place in therapy: Short/long-term VTE treatment - Dosing: avoid if CrCl <15 - ADR: bleeding - PK: substrate of PGPArgatroban VTE- Acute VTE treatment when HIT present (only indication) - IV - lab monitoring: APTT Q6H until therapeutic, then Q24H; Goal APTT is 1.5-2.5 X control; CBC - ADR: BleedingDabigatran (Pradaxa) in VTEShort/long-term VTE treatment - dosing: Avoid if CrCl<30 - Lab monitoring: CBC, SCr , ALT/AST - increase incidence of GI bleeds - increase risk of bleed in elderly - increase risk of MI compared to warfarin - ADR: Bleeding, dyspepsia (25-40%) Substrate of PGPGuidelines for DOACs· Guidelines recommend DOAC usually first line based on studies but recommend also that oral anticoagulant choice depends on patient factors (financial, adherence, other medications, kidney function, valvular disorder, pregnancy/breastfeeding) · Contraindications: active bleeding, valvular heart disease, pregnancy/lactation · Drug interactions: less than warfarin; avoid some other drugs; other drugs that cause bleeding · PK: OOA <30 min, DOA 1-2 days · $$$ · Hold 1-5 days before invasive procedures, depending on drug, CrCl, and procedure bleed riskManagement of severe bleeding in DOACso All: stop drug, supportive care o Dabigatran: idarucizumab (Praxbind), 4-factor prothrombin complex concentrate (PCC, i.e. KCentra, FEIBA), hemodialysis o Factor Xa inhibitors: Andexxa, KCentraWarfarin VTE- onset of anticoagulant effect:24-48 hours (Related to half-life of clotting factors) - time to therapeutic effect: 10-14 days (Related to half-life of clotting factors) Avail:PO: 1,2,2.5,3,4,6,7.5,10mg tabs, 5mg IV injectionWarfarin monitoring VTEINR 1. CBC: baseline, then annually 2. Signs/symptoms of bleeding or VTE 3. Drug interactions 4. Adherence 5. Duration of treatmentWarfarin dosing VTE1. Acute dosing: 5-10mg daily (based on age) a. Start when APTT therapeutic from UH or same day as LMWH b. Adjust dose daily based on magnitude of change c. Example 53 year old patient with baseline INR of 1.0 has new DVT; start with warfarin 7.5mg daily 2. Chronic dosing: a. Adjust dose by ~10% of weekly dose b. If INR low, increase weekly dose or give an extra dose; then recheck INR in 1-2 weeks c. If INR high, decrease weekly dose or hold doses; then recheck INR in 1 day-2 weeks a. Questions to ask patient before adjusting the dose include: · What dose of Coumadin are you taking? · Have you missed any doses? · Have you had any bleeding/VTE s/sx? · Have you have had any changes in your diet? Other medicines? Alcohol?Warfarin VTE dosing age- 50-65: 7.5 mg QD - <50: 10 mg QD - >65: 5 mg QDWarfarin dosing INR 4 or aboveHold dose for today and come back in a week. This is why we have them take their warfarin in the evening.What is the anticoagulant drug of choice when a patient is pregnant?LMWHWhat anticoagulant can be used in breastfeeding?WarfarinINR between 10-20 and/or minor -moderate bleeding at any INRHold warfarin; consider vitamin K 2.5 - 5mg PO; recheck INR Q24h (until INR 2-3); repeat vitamin K if necessary; resume therapy at lower dose - vitamin k PO/IV $30Serious bleeding with warfarinHold warfarin; vitamin K 5-10mg IV infusion; recheck INR q6-12h; may repeat vitamin k IV q12h; supplement with PCC(Kcentra)>FFP, resume therapy at lower doseWarfarin side effects1. Bleeding (Contraindicated in active bleeding) a. Major - go to ER b. Minor - call doctor/anticoagulation clinic Hold for 5 days prior to invasive procedures 2. Purple toes syndrome (rare): cholesterol emboli in toes (occurs within 3-8 weeks) 3. Warfarin-induced skin necrosis (rare): micro clots in vessels of SQ fat at initiation of higher dose (>10mg daily, occurs within 3-8 days, due to ↓ in Protein C) 4. Teratogenicity (Category X): contraindicated in pregnancy (DOC is LMWH); compatible with breastfeedingHow long is warfarin held prior to surgery?5 daysWhat are the drugs that interfere with warfarin?The 10A's: 1. antibiotics (all antibiotics increase INR by messing with gut flora; some increase INR by messing with the CYP450 [bactrium and flagyl]. Check INR in about 5-7 days) 2. Azole antifungals 3. antidepressants (increase risk of bleeding) 4. Antiplatelets (don't increase INR - increase risk of bleeding) 5. Anti-inflammatory agents (can increase the bleeding risk, even at a therapeutic INR) 6. Amiodarone (inhibits almost every CYP 450) 7. APAP (If you're just using it as needed, it does not increase the INR. If you take it regularly at two grams or more a day for at least five days it might increase the INR.) 8. Alternative remedies - herbals (ginkgo biloba, St. john's wort - lower INR) 9. antiepileptic (Phenobarb, phenytoin, carbamazepine induce CYP - decrease INR) 10. Alcohol (Acute binge will increase INR. INR may go down after that binge. The problem is when we see it is high, we want to lower the dose. Also, when it is high and pt is drunk, they may stumble around and hit their head. This could cause a severe brain bleed. Drink in moderation - no more than 2 drinks a day.) This does not mean the pt cannot get these. It means we have to monitor INR. We do not preemptively lower the warfarin dose. All we do is we have to check the INR sooner, and if it goes up, then we lower the warfarin dose. This is because DI do not always occur. If we preemptively lower warfarin and INR stays low, pt could have a stroke or a blood clot.When a patient is having pain while on warfarin, which pain medication would be best to give them between Motrin (NSAID) or APAP?Between APA and ibuprofen, the one that's preferred for minor aches and pains or headaches is APAP. Because if they take it as needed, it has zero effect.How should warfarin DI be managed?1. Always check to see if new drug interacts with warfarin 2. Consider non-interacting alternative 3. Interacting drugs are not contraindicated 4. When adding warfarin to an interacting drug, consider starting at a lower warfarin dose 5. When adding an interacting drug to warfarin, increase frequency of monitoring INR (check in 2-3 days, within a week, in 1-2 weeks, Q1 week, etc.), then adjust warfarin dose if necessary 6. Review medications each time INR monitored, including RX, OTC, herbal, PRNWhat are some other factors that may impact warfarin?- Increase warfarin effect: decrease vitamin K intake; Food: grapefruit (juice), cranberry (juice); extra doses; liver disease (you cannot make your clotting factors normally, you are going to have less clotting factors around), heart failure - decrease warfarin effect: increase vitamin K intake, Foods high in vitamin K (green leafy vegetables - spinach, collard green, cabbage, broccoli, etc) green tea, vitamins with ↑ vitamin K; missed doses; bowel resection (cut out part of your bowel where warfarin is absorbed)VTE treatment - reversible risk factor present (surgery, trauma, estrogen, car accident, etc)OAC duration: 3 monthsVTE treatment: idiopathic (we don't know the reason)OAC duration: > 3 monthsVTE treatment: post-orthopedic (the spine, joints, and muscles) surgery prophylaxisOAC duration: 10-35 daysVTE treatment: coagulopathies (Protein C or S deficiency; Factor V Leiden deficiency; gene mutation)OAC duration: 12 months - lifetimeVTE treatment: recurrent VTE (more than one DVT)OAC duration: lifetimeOAC patient education (highlighted parts are for all OAC)1. Need for strict compliance with frequent blood draws (taking doses as directed, follow-up visits, what to do for missed doses - let Coumadin clinic know at next visit, don't double up) (warfarin) 2. Take dose in the evening (warfarin) 3. Dietary instruction (green leafy veggies - eat in moderation, be consistent with number of servings per week, no abrupt changes, avoid acute alcohol binging and no more than 2 drinks per day) (warfarin) 4. Need for strict compliance with meds 5. Anticipated duration of therapy 6. Side effects (what signs of bleeding to look for, what to do about a bleed, how to prevent bleeding - brush teeth carefully, use electric razor instead of manual razor, if severe bleed - go to ER, go to ER if bump head) 7. Drug interactions (ask before start OTCs, inform other doctors of OAC therapy) 8. Signs of VTE/stroke: leg swelling, chest pain, SOB, vision changes, numbness 9. Wear a MedAlert bracelet/necklace 10. Avoid contact sports, such as football, wrestling, etc. 11. Safety issues - be careful with loose rugs, icy steps, etc. 12. Avoid pregnancy 13. How to prevent VTE with prolonged travelHeart valve replacementsA. Prosthetic: Mechanical, Bioprosthetic (tissue) B. Need OAC to prevent blood clot in heart (which can travel to brain and cause a stroke) C. Warfarin, not DOAC D. Mechanical: mitral - warfarin (INR 2.5-3.5), aortic - warfarin (INR 2-3 or 2.5-3.5) lifelong E. Bioprosthetic: mitral - warfarin (INR 2-3), aortic - warfarin (INR 2-3) or aspirin 81mg daily X3 months F. Bridge with treatment dose of heparin product for procedures G. Add aspirin 81mg if TE despite adequate anticoagulation - Mechanical heart valve need anticoagulation for lifeVTE prophylaxis- prevention of VTE in hospitals - this isn't somebody who has a Dvt (they probably came to the hospital for something else like diabetes or HF) 1. Non-pharmacological (We do this for surgical patients, in addition to the pharmacological one. Also are done if the patient has a bleed, and we don't want to give a pharmacological DVT treatment.) 1. Intermittent pneumatic compression devices (IPCDs) 2. Elastic stockings (ES) 2. Pharmacological a. Low dose unfractionated heparin (LDUH): 5,000 units SQ Q12 hours i. BMI>40: Q8 hours b. Low molecular weight heparin (LMWH): enoxaparin 40mg SQ daily i. CrCl <30ml/min: 30mg SQ daily ii. BMI>40: 40mg SQ twice daily c. Warfarin, DOAC (if outpatient medication)Nebulized epinephrine (vasoconstrictor from alpha adrenergic effect) can be used ifthere is post-extubation "stridor" - a type of inflammation that is usually associated with irritation from either the endotracheal tube or a disease (croup, aspiration) - Corticosteroids can also be used, but you would need to predict that it will be a problem because they take hours (4-6h) to start working.If there is no cuff-leak when the patient is getting close to time for extubation, it may be that there isswelling around the ET tube. That is an indication to give some systemic corticosteroids before the extubation attempt (different regimens, but best to start at least 4-6hrs prior to pulling the tube)