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IT 2 Exam 2 Info.docx

IT 2 Exam 2 Information

Venous Thromboembolism I & II

Identify the physiologic risk factors for developing VTEs.

  • Venous thromboembolism (VTE) can develop into deep vein thrombosis (DVT) or pulmonary embolism (PE)
    • blood clot in distal location (CVT) → travels up the deep vein of the thigh → into inferior vena cava → goes into lungs (PE)
  • VTE is the leading cause of death and disability worldwide

Based on variables, select an appropriate pharmacologic regimen to prevent VTE and treat VTE.

  • prophylaxis options
    • remember: subq heparin is for prophylaxis

risk level

characteristics

therapeutic options

low

pt w/o risk for VTE

-pharmacologic prophylaxis not needed.
-ambulation (walking)

moderate

most hospitalized pt w/ medical illness plus risk factors


CI: pt has a bleeding risk

pharm options
-UFH 5000u SQ q12 (or q8 obese)

-LMWH (enoxaparin) SQ 40 mg QD (or 30 mg BID for obese)

OR

Nonpharm options

-intermittent pneumatic compression

-sequential compression device (SCD)

high

most hospitalized pt w/

-cancer

-critical illness

-stroke

-obese

do both and give a higher dose of heparin

  • risk assessment for VTE prophylaxis
    • bleeding risk
      • platelet count < 50,00 uL
      • bleeding within 3 months
      • active GI ulcer
    • thromboembolic risk
      • age> 60 years*
      • recent VTE*
    • hypercoagulable state
      • malignancy (cancer)
      • pregnancy
      • oral contraceptives/hormones
      • thrombophilia (increased risk of thrombosis)
      • circulatory stasis (period of low blood movement)
        • ICU stay
        • immobility - paralysis, sitting or sleeping for a whole
          • prolonged immobility > 3 days
        • polycythemia vera (production of too many blood cells)
        • obesity
      • vascular wall injury
        • atherosclerosis
      • conditions like DM, sepsis, HF, COPD

Identify variables that impact the safety and efficacy of anticoagulation therapy.

  • s/s of vte
    • DVT
      • unilateral swelling
      • pain
      • erythema
    • PE
      • chest pain
      • SOB
  • Revised Geneva Score or Wells Score for PE*
    • these give the Pre-Test Probability for PE (PTP)
    • High PTP ≥ 50%
  • Diagnostic Testing
    • Lower Extremeties Dopplers or Ultrasound
    • V/Q Scan - looking for a mismatch of perfusion between left and right heart
    • CT Scan (CTPA or chest CT with contrast)*
      • this is the cold standard to diagnose PE
    • D-Dimer - this test is used to rule out VTE, <500
  • Severity: PE > Proximal DVT > Distant DVT > Superficial VTE
    • hemodynamic instability and AKG changes indicate a severe VTE
    • cardiac arrest indicates very severe VTE
  • CHEST guidelines are considered the Gold Standard for anticoagulation management
    • American Society of Hematology is the newer guideline with a first author being a pharmacist

Given subjective and objective patient information, select an initial pharmacologic regimen to maximize therapeutic efficacy and minimize potential toxicity.

  • How to choose a treatment?
    • DOACs are preferred bc oral and greater safety
    • cancer - doac
    • pregnancy - heparins
    • heparin induced thrombocytopenia - warfarin/doac
    • use warfarin for lupus, antiphospholipid syndrome, clot in “strange places”
  • UFH
    • onset: IV is immediate. “quick on quick off”
    • elimination: half life is short. non-renal so good for PT w/ kidney impairment
    • monitoring: anti-Xa and aPPT
    • reversal: protamine
    • dosing is actual body weight based
    • no drug interactions
    • great for patients that are hemodynamically unstable
  • LMWH (enoxaparin (lovenox))
    • onset: longer than UFH
    • elimination: longer half life than UFH. renally excreted.
    • monitoring: Anti-Xa
    • reversal: protamine
    • dosing is actual body weight based
    • dosing is 1 mg/kg q12 or 1.5 mg/kg q24

exceptions to monitoring tests:

(1)baseline prolonged aPTT due to lupus anticoagulant require alternative testing

(2)anti-Xa assay is not viable in patients who take doacs

  • Warfarin
    • onset: 2-3 days
    • elimination: cyp2C9 and 3A4
    • monitoring: INR
      • 1.5 - 2.0 for mechanical heart valve
      • 2.0 - 3.0 for stroke prevention in afib and VTE treatment
      • 2.5 - 3.5 for mechanical aortic valve w/ 1 risk factor and mechanical mitral valve
    • reversal: vitamin k
    • moa: vit k epoxidase inhibitor which inhibits factor SNOT (7, 9, 10, 2) and protein C and protein S (the natural anti-coag proteins)
    • CI: pregnancy, current bleed
    • strength and colors of warfarin
      • Please - 1mg Pink
      • Let - 2mg Lavender
      • Granny - 2.5mg Green
      • Brown - 3mg Brown
      • Bring - 4mg Blue
      • Peaches - 5mg Peach
      • To - 6mg Teal
      • Your - 7.5mg Yellow
      • Wedding - 10mg White
    • assessing for warfarin sensitivity - pt w/ multiple risk factors should receive lower dose warfarin (2.5 mg green)
      • baseline INR ≥ 1.5
      • age>65
      • abw<45kg or abw<ibw
      • current antiplatelet therapy
      • lower INR goal should start on lower dose
      • check CBC before starting (low platelet means higher bleed risk)
    • factors that increase INR
      • drug interactions with inhibitors should start on lower dose
      • malnourished
      • foods high in vit K (leafy green vegetables, basil in pesto)
      • excessive alcohol consumption
      • illness like diarrhea
    • initiating warfaring:
      • warfarin must be bridged with IV heparin for 5 days until INR is at goal
        • during the first 5 days, patient is hypercoagulable bc warfarin depletes protein C and S
    • drug interactions (slides 53 and 54)
      • PD have additive effects with antiplatelets (aspirin, clopidogrel) and NSAIDs
      • PK inhibitors (GPACMAN) increase INR while inducers reduce INR
      • in general increase or decrease warfarin dose by 25%
        • for amiodarone, decrease warfarin dose by 50% after 2 weeks of dual therapy
        • for rifampin increase warfarin dose by 50% after 2 weeks of dual therapy
  • Subq Factor Xa inhibitors (fondaparinux)
    • good for pt allergic to heparin
    • CI: CrCl<30
      • prophylaxis is contraindicated when wt<50kg
    • dosing is only subq
      • DVT prophylaxis - wt>50kg: 2.5mg subq QD
      • VTE treatment -
        • wt<50kg: 5mg subq QD
        • wt 50kg-100kg: 7.5 mg subq QD
        • wt >100kg: 10 mg subq QD
  • DOACs
    • onset: 2-4 hours
    • elimination: half life is 12 hours
    • monitoring: none!
    • reversal: Andexanet (factor Xa antidote) and Praxbind (dabigatrin)
    • these drugs have better efficacy/safety when compared to warfarin
    • absorption is mediated by P-gp, do not use w/ carbamazepine, phenytoin, barbiturates
    • dabigatran (pradaxa) - direct thrombin inhibitor
      • indication/dosing:
        • stroke prevention (nonvalvular afib(NVAF)) - 150 mg BID
        • VTE - start 5 days heparin bridging then 150 mg BID
      • CI: CrCl<30
      • AE: GI bleed (GI ulcers, Chron’s disease)
      • Pgp inhibitors increase dabigatran lvls
    • apixaban (eliquis)
      • indication/dosing:
        • prophylaxis in NVAF - 5 mg BID or 2.5 mg if (1) ≥80yo (2)≤60kg (3)SCr≥1.5
        • VTE - 10 mg BID for 7 days then 5 mg BID
    • rivaroxaban (xarelto)
      • good for patients who want a QD dosing
      • indication/dosing:
        • prophylaxis NVAF - 20 mg QD w/ dinner
        • VTE - 15 mg BID for 21 days then 20 mg QD w/ dinner
    • edoxaban
      • if you see this drug calculate creatinine clearance
      • CI: CrCl > 95
  • inferior vena cava filter (IVC)
    • used for pt CI to anticoag meds
    • long term risk of DVT bc accumulation of thrombus on the filter

Given a therapeutic regimen for treating VTE, recommend a monitoring plan which includes duration of treatment, therapeutic efficacy, and toxicity.

  • treatment duration: based on factors + risk of bleeding
    • phases of treatment:
      • initial management → primary treatment → secondary prevention
      • initial management: 5-21 days of loading or co-dose
      • primary treatment: 3-6 months of anticoag treatment
      • secondary prevention: indefinite duration, decision based on risk factors
    • always have an initial 3 months of anticoag therapy
      • do not stop anticoag in these 3 months
    • d/c if the VTE is provoked and risk factors are reversible
    • continue if VTE is (1)unprovoked (2)risk factors are chronic or (3)pt cancer
    • HAS-BLED Assessment Score for bleeding - the more risk factors the more like the patient will bleed
      • treat risk factors for bleeding
  • toxicity
    • bleeding - s/s of internal bleed are gum bleeding, blood in pee (pink or red blood), large bruises, black or red poop
    • heparin induced thrombocytopenia (HIT) - a drop platelet count
  • inactivated prothrombin concentrates (PCCs) - Kcentra, which is factor II, VII, IX, and X in inactive form

Given a clinical scenario, (1)recommend therapeutic agents to reverse the effect of anticoagulation. (2)recommend therapeutic intervention to manage warfarin anticoagulation. (3)recommend bridging/switching strategies and monitoring plans.

  • transition from heparin to warfarin: initiate warfarin while still on heparin until INR is therapeutic for 1-2 consecutive days
  • transition from heparin to doac: start doac w/in 12 hours of second BID dose (lmwh) or when infusion is stopped (ufh)
  • transition from doac to warfarin: overlap doac and warfarin until INR is therapeutic. titrate warfarin
  • transition from warfarin to doac: start doac when INR is therapeutic (~2)

Chronic coronary disease (formerly known ischemic heart diseases) aka angina

about chronic coronary disease

  • definition
    • group of conditions that includes obstructive and nonobstructive CAD with or without previous myocardial infarction (MI) or revascularization
  • prevalence
    • leading cause of death for men, women, and people of most racial and ethnic groups
    • One person dies every 33 seconds from cardiovascular disease
  • diagnosed only by
    • noninvasive testing
    • angina symptoms
  • s/s
    • angina*
    • cold sweats
    • dizziness
    • women are more likely to complain about
      • dizziness
      • nausea
      • no symptoms at all
  • goal of treatment
    • minimize the likelihood of death (reduce premature CV death, prevent MI and HF)
    • maximize health and function (eliminate symptoms, restore satisfactory level of activity)
  • risk factors of major adverse CV events in pt with chronic coronary disease
    • high troponin (sign of heart inury)
    • b-type natriuretic peptide (sign of HF)
    • smoking status
    • high lipoproteins
    • high cholesterol
    • high blood pressure
    • high A1c

treatment options

  • risk factor modification
    • lifestyle modification
      • diet low in saturated fat and cholesterol reduce LDL and cholesterol
        • DASH (dietary approach to stopping hypertension) diet with more fruits, vegetables, whole grains, and low-fat dairy products
      • 10 lb weight loss reduce LDL and cholesterol
      • physical activity
        • aerobic or dynamic 90-150 min/wk
      • alcohol consumption - reduce consumption to men≤2 drinks and female≤1 drink
    • lipid management
      • goal: lower LDL by ≥50%
      • high risk should have high intensity statin on highest dose they can tolerate
      • not high risk use high intensity statin → if not tolerated (or pt is >75) use moderate intensity statin
      • ezetimibe can be added if LDL ≥70 mg/dL
        • then PCSK-9 inhibitors can be added after
        • if statins are not tolerated, use bile acid sequestrants, niacin or both
      • how to assess risk
        • very high risk -
          • history of multiple major ASCVD events
          • OR
          • one major ASCVD event and >2 high risk conditions
        • major ASCVD events include
          • recent (w/in a year) ACS (unstable angina, STEMI, and NSTEMI)
          • history of stroke
          • symptomatic PAD
        • high risk conditions include
          • age>65
          • smoker
          • genetics (familial hypercholesterolemia)
          • history of CABG (ACS) or PCI (first line for STEMI)
          • diabetes, htn, CKD, persistent hyperlipidemia, CHF
      • statins
        • High intensity: atorvastatin 40-80mg, rosuvastatin 20-40mg
        • Moderate intensity: atorvastatin 10-20mg, rosuvastatin 5-10mg, simvastatin 20-40mg, lovastatin 40 mg
        • Monitoring: after 4 weeks to three months, do repeat labs
          • if someone is stable, check in 6 months to a year
        • CI: pregnancy, nursing mothers, liver disease
      • PCSK9
        • praluent (alirocumab) and repatha (evolocumab)
        • these are brand name only, monoclonal antibody therapies, injection therapy
    • blood pressure management
      • choice in therapy is guided by indications for each class of antihypertensive drug
      • pt may require combo therapy
      • slide 29 for chart
    • diabetes mellitus management
      • goal: <6.5%
        • goal is 7-8% in pt with history of severe hypoglycemia, hypoglycemia unawareness, limited life expectancy, and renal disease
      • rosiglitazone is CI in pt with SIHD
    • antiplatelet
      • aspirin 81 mg should be started indefinitely
        • use clopidogrel if aspirin is CI
      • there is a risk of bleeding with use of both
      • dual antiplatelet therapy (DAPT) is prescribed post MI or after stent placement
    • smoking cessation
    • getting vaccines (specifically flu, covid-19, and RSV vaccines)
    • decrease stress
  • symptomatic relief
    • symptomatic CCD is defined as angina
    • beta blockers are the first line to CCD
      • lopressor metoprolol tartrate
      • toprol xl metoprolol succinate
      • tenormin atenolol
      • inderal propranolol hcl
    • CCB and/or long acting nitrates are used when beta blockers are CI
      • these two are added when beta blockers are unsuccessful in relieving symptoms
        • CCB names:
        • cardizem dilt
        • tiazac dilt
        • calan verapamil
        • norvasc amlodipine
        • procardia nifedipine
    • sublingual or spray nitroglycerin is recommended for immediate relief of angina
      • keep in the original container
      • do not store in a container with child-resistant safety cap
      • do no store in bathroom bc humidity may degrade
      • the sublingual tablet should NOT be chewed or swallow. both dosage forms should be place under tongue and let it dissolve
      • after administration, patient should sit down bc this drug can cause headache and lightheadedness
      • tablet should be refilled every 6 months and spray every 3 years
      • can be taken 30 minutes in advance of physical exertion
      • after 3 doses given every 5 minutes (15 minutes total), seek medical attention immediately
    • long acting nitrates require a nitrate free period bc of tolerance build up. pt should have 10-14 hour nitrate free period every day
      • for nitroglycerin patch (1)wear for 12-14 hr then remove (2)rotate sites on chest
    • ranolazine ER (ranexa)
      • moa: antiischemic and antianginal effect, doesnt effect HR or BP
      • this drug is a CYP3A4 substrate
      • interacts with Simvastatin (use 20 mg simvastatin), and NTI drugs like cyclosporine, tacrolimus, and sirolumus

Acute Coronary Syndrome I & II

Describe the etiology and pathophysiology of acute coronary syndrome (ACS)

    • ACS is an occlusion of the coronary artery
    • types of MI - Universal Classification of MI
      • Type 1 - spontaneous MI
      • Type 2 - MI secondary to ischemic imbalance (supply demand mismatch, drug use, increase sympathetic stimulation. no blockage)
      • Type 3 - MI resulting in death w/o biomarkers or ekg
      • Type 4a - MI related to percutaneous coronary intervention (PCI)
      • Type 4b - MI related to stent thrombosis
      • Type 5 - MI related to coronary artery bypass grafting (CABG)

List the signs and symptoms of myocardial infarction (MI)

    • cardiac troponin levels have to be elevated to be considered myocardial injury
      • acute myocardial injury is when there is a rise and fall of troponin values
    • myocardial infarction is elevated troponin (injury) + evidence of ischemia
    • signs of ischemia
      • ECG/AKG changes
      • symptoms of MI
      • imaging of heart
    • symptoms and clinical presentation
      • typical presentation: a crushing or pressure-like feeling radiating to the jaw or left arm
      • atypical: sweating, difficulty breathing, nausea, isolated jaw or left arm pain
        • typically females and older patients experience atypical presentations of MI
      • chest pain can be (1)cardiac, (2)possibly cardiac, (3)noncardiac
        • right sided is likely not ischemia
        • central, pressure, squeezing, and left side is more likely ischemia

Differentiate between NSTEMI, STEMI and unstable angina (UA)

    • types of ACS
      • unstable angina
        • chest pain
        • normal troponin
        • lack of ST elevation
      • NSTEMI
        • chest pain
        • high troponin
        • lack of ST elevation
      • STEMI
        • chest pain
        • high troponin
        • ST elevation
    • calculate TIMI (or GRACE) score for NSTEMI and UA patients - this guides treatment
      • 0-2 low risk
      • 3 intermediate
      • ≥4 high risk
    • do NOT calculate TIMI for STEMI
    • initial evaluation:
      • get an EKG/ECG
      • check cardiac troponin levels (I or T)
      • look at their symptoms and PMH

Recommend pharmacologic therapy for patients with STEMI and NSTE-ACS

  • all patients with ACS should receive
    • MONA-B (unless CI)
      • M - morphine or other opioids
        • typically fentanyl is given instead of morphine if MONA-B is desired
        • second option for chest pain
      • O - oxygen
        • only for patients with SaO2<90%
      • N - nitroglycerin
        • everyone will likely receive
        • for chest pain
        • 0.3-0.4 mg spray or sublingual tablet q5min for up to 3 doses
        • then give IV continuous infusion after 3 doses
        • CI: pde-5 inhibitor, HR<50, SBP<90
        • never use oral for acute management
      • A - aspirin
        • everyone will likely receive
        • use chewable and non-enteric coated tablet
        • give 1 dose is 162-325 mg
        • then baby aspirin 81 mg
        • use clopidergril for pt that cannot have aspirin
      • B - beta blocker
        • everyone will likely receive
        • start oral beta-blocker within 24 hours
        • CI: cardiogenic shock, bradycardia
        • use non-DHP CCB is beta-blocker is CI
    • Antiplatelet
      • every pt with ACS needed dual antiplatelet therapy (DAPT)
      • for all ACS pt use Aspirin +
        • (1st choice) prasugrel
          • not used with NSTEMI treated with medical management
        • (2nd choice) ticagrelor
        • (3rd choice) clopidogrel
          • becomes #1 among

elderly

high bleed risk

if STEMI was treated with fibrinolytics (”-plase” drugs)

      • continue dual therapy for at least 1 year/12 months
      • all antiplatelet therapy requires a loading dose
      • aspirin
        • LD: 162-325 mg
        • MD: 81 mg QD
      • oral P2Y12 inhibitor
        • clopidogrel (prodrug)
          • LD: 300-600 mg
          • MD: 75 mg
          • becomes #1 among

elderly

high bleed risk

if STEMI was treated with fibrinolytics (”-plase” drugs)

        • prasugrel (prodrug)
          • LD: 60 mg
          • MD: 10 mg QD or

5 mg QD in pt <60kg or ≥75yo

          • CI: stroke or TIA
        • ticagrelor
          • LD: 180 mg QD
          • MD: 90 mg BID
          • efficacy decreases in aspirin doses greater than 300 mg QD
        • cangrelor is an IV options
    • Anticoagulant
      • options are
        • bivalirudin
        • fondaparinux
          • cannot be used for sole anticoag when pt is getting PCI
        • enoxaparin
        • UFH
      • how to treat
        • STEMI w/ fibrinolytics - enoxaparin
        • STEMI - UFH, bivalirudin, fondaparinux
        • NSTEMI w/ PCI - UFH, bivalirudin, fondaparinux
        • NSTEMI w/medical management - UFH, enoxaparin, fondaparinux
      • anticoag treatment for the duration of
        • invasive procedure (PCI and CABG) then d/c once procedure is done
        • hospital stay (up to 8 days) for pt treated with fibrinolysis
      • UFH
        • given bolus and maintainence IV
        • LD: 60u/kg (max 4000 u)
        • MD: 12u/kg/hr (max 1000u/hr)
        • goal aPTT: 50-70
      • enoxaparin
        • given subq
        • does not require monitoring
        • dosing is kidney function dependent
          • usually BID
          • if CrCl<30, give QD
      • fondaparinux
        • given subq
        • no monitoring
        • CI: CrCl<30
      • bivalirudin (think UFH)
        • goal aPTT: 50-70 (same as UFH)
        • dosing is kidney function dependent
          • if CrCl<30, reduce the infusion
  • STEMI
    • reperfusion is the goal for treating STEMI
    • the FMC (first medical contact) starts when the medical professionals encounters pt (emt) or pt gets to ED
    • PCI is the first line for treating STEMI
      • should happen within 90 min of first medical contact (FMC)
      • when at hospitals w/o PCI capability, increase time to 120 min
      • should be done <12 hours of symptoms in pt w/ CI to fibrinolytic therapy
    • if PCI is contraindicated, use fibrinolytic therapy
      • alteplase
      • reteplase
      • tenecteplase
      • “-plase” drugs
      • should happen within 30 minutes of arrival at hospital
      • alteplase dose:
        • accelerated infusion (hour and 30 infusion)
          • *>67kg: 15mg IVP over 1-2min → 50mg over 30 min → 35 mg over 1 hr

most common

          • ≤67kg: 15mg IVP over 1-2 min → 0.75mg/kg IV over 30 → 0.5 mg/kg over 1 hr
        • 3 hour infusion
          • ≥67kg: 10mg IVP → 50mg IV over 1hr → 20mg over 1hr → 20 mg over 1 hr
      • absolute CI:
        • hemorrhagic stroke
        • ischemic stroke w/in 3 months
        • active internal bleed
        • aortic dissection
        • BP>180/110 and unresponsive to therapy
      • relative CI:
        • BP>180/110, you have to lower the BP first
    • CABG
      • recommended in left main disease or triple vessel disease
      • hold antiplatelets and anticoag before CABG (memorize slide 66)
        • antiplatelets
          • aspirin: do not hold
          • clopidogrel ticagrelor: 5 days
          • prasugrel: 7 days
        • anticoagulants
          • bivalirudin: 1-3 hrs
          • UFH: 1-4 hour
          • enoxaparin: 12 hrs
          • fondaparinux: 3-5 days
  • NSTEMI and UA
    • get the grace and TIMI score
      • low risk: use ischemia-guided management plan
      • intermediate or high risk: early invasive approach
    • ischemia-guided therapy (medication therapy without any procedures)
      • low risk GRACE or TIMI score
      • low life expectancy
      • pt or clinician expectancy (did I mean preference?)
      • this is using medication to treat
        • CCD/ISHD is for patients who had these things (ACS) in the past and now continue to
    • early invasive strategy (use of PCI and CABG)
      • high risk GRACE or TIMI score
      • cardiogenic shock
      • life threatening arrhythmias, like Vfib
      • prior CABG
      • PCI w/in the past 6 months

Secondary Prevention

  • DAPT
    • continue for 12 months unless there is a high /risk of bleed
    • aspirin should be continued indefinitely
  • lipid lowering
    • all pt should receive high intensity statin post-ACS (preferably before revascularization)
    • goal: 70 mg/dL or less
  • beta blockers
    • for all pt
    • continue for at least 3 years (unless there is an indication)
  • ACEi/ARB
    • for pt who just had STEMI/NSTEMI + HFrEF, HTN, CKD or DM
    • ARNI is only indicated for HF
  • MRA
    • for pt who just had STEMI/NSTEMI + already on ACE and beta blocker + HFrEF
    • unless CI (CrCl<30, K>5, etc.)

ACLS

Describe the prevalence and causes of cardiac arrests

  • causes of cardiac arrest can be categorized as the H’s and the T’s

H

T

-Hypovolemia (low blood or H2O volulme)

-Tablets (drugs OD)

-Hypoxia (low oxygen)

-Tamponade (increased pressure around the heart)

-hydrogen (acidosis)

-Thrombosis in the heart (ACS, clot inside the heart)

-Hyper/hypokalemia (potassium imbalance)

-Thrombosis in the lung (PE, clot inside the lung)

-Hypothermia

-Trauma (a penetrating injury in the heart)

-Hypoglycemia

  • types of rhythms during cardiac arrest
    • VF - ventricular fibrillation
    • VT - ventricular tachycardia
    • asystole
    • PEA - pulseless electrical activity

Understand the role of a pharmacist in ACLS

  • role of pharmacist
    • we verify the appropriateness of treatment
    • calculate appropriate doses
    • obtain and prepare medication
    • ensure proper administration of medication
  • goal of treatment
    • rapid recognition
    • prompt CPR
    • defibrillation
    • timely administration of meds to treat underlying causes

Identify the agents encountered during different types of emergency responses

  • protocol to achieve Return of Spontaneous Circulation (ROSC)
    • Always (1)start CPR [1]
    • (2)Give oxygen and
    • (3)Attach monitor/defibrillator
      • if rhythm is shockable (pulse is VF or pVT) →
        • give a shock [1]
        • CPR [2] (30 compressions + 2 rescue breaths)
          • +treat underlying issues with IV therapy
        • shock [2]
        • CPR [3]

give epinephrine every 3-5 minutes

          • up to 5 doses of epinephrine
        • shock [3]
        • CPR [4]
          • +amiodarone (after 5 doses of epinephrine)
          • +lidocaine (after dose of amiodarone)
      • if rhythm is NOT shockable (pulse is asystole or PEA)
        • administer epinephrine ASAP
          • give epinephrine every 3-5 minutes
          • up to 5 doses of epinephrine
        • CPR [2]
          • if rhythm becomes shockable, switch to that protocol
        • CPR [3]
          • +treat underlying issues with IV therapy
  • agents during emergency response
    • Cardiopulmonary resuscitation (CPR)
      • 30 chest compressions (allow chest to return to normal position after each compression)
      • 2 breaths
      • 2in depth
      • 100-120 BPM
    • epinephrine
      • for ALL types of rhythms
      • dosing: 1 mg q3-5min IVP
    • amiodarone
      • only for shockable rhythms (Vfib/VT)
      • dosing: 300mg IV 1x → (if vfib/pVT continues) 150mg IV over 1-2min 1x → (if more required) start infusion
    • lidocaine
      • only for shockable rhythms (Vfib/VT)
      • dosing: 1-1.5 mg/kg over 1-4min (bolus dose, max 25mg/min in pt w/ pulse) → 1-4 mg/min
      • monitoring: serum level 1-5 mcg/mL
  • secondary agents during emergency response
    • only used as an adjunct/add on NOT a replacement
    • sodium bicarbonate
      • only for hyperkalemia
      • dosing: 50 mEq over 5 minutes
    • calcium
      • only for hyperkalemia or CCB overdose
    • magnesium sulfate
      • only for QT prolongation (torsades de pointes)
      • dose: 1-2g
    • alteplase
      • ECHO should be done during CPR to rule out PE
      • dose: 50-100mg as bolus
        • recommended is 50mg IV push → 50mg in 10-15 minutes
        • no more than two doses
JK

IT 2 Exam 2 Info.docx

IT 2 Exam 2 Information

Venous Thromboembolism I & II

Identify the physiologic risk factors for developing VTEs.

  • Venous thromboembolism (VTE) can develop into deep vein thrombosis (DVT) or pulmonary embolism (PE)
    • blood clot in distal location (CVT) → travels up the deep vein of the thigh → into inferior vena cava → goes into lungs (PE)
  • VTE is the leading cause of death and disability worldwide

Based on variables, select an appropriate pharmacologic regimen to prevent VTE and treat VTE.

  • prophylaxis options
    • remember: subq heparin is for prophylaxis

risk level

characteristics

therapeutic options

low

pt w/o risk for VTE

-pharmacologic prophylaxis not needed.
-ambulation (walking)

moderate

most hospitalized pt w/ medical illness plus risk factors


CI: pt has a bleeding risk

pharm options
-UFH 5000u SQ q12 (or q8 obese)

-LMWH (enoxaparin) SQ 40 mg QD (or 30 mg BID for obese)

OR

Nonpharm options

-intermittent pneumatic compression

-sequential compression device (SCD)

high

most hospitalized pt w/

-cancer

-critical illness

-stroke

-obese

do both and give a higher dose of heparin

  • risk assessment for VTE prophylaxis
    • bleeding risk
      • platelet count < 50,00 uL
      • bleeding within 3 months
      • active GI ulcer
    • thromboembolic risk
      • age> 60 years*
      • recent VTE*
    • hypercoagulable state
      • malignancy (cancer)
      • pregnancy
      • oral contraceptives/hormones
      • thrombophilia (increased risk of thrombosis)
      • circulatory stasis (period of low blood movement)
        • ICU stay
        • immobility - paralysis, sitting or sleeping for a whole
          • prolonged immobility > 3 days
        • polycythemia vera (production of too many blood cells)
        • obesity
      • vascular wall injury
        • atherosclerosis
      • conditions like DM, sepsis, HF, COPD

Identify variables that impact the safety and efficacy of anticoagulation therapy.

  • s/s of vte
    • DVT
      • unilateral swelling
      • pain
      • erythema
    • PE
      • chest pain
      • SOB
  • Revised Geneva Score or Wells Score for PE*
    • these give the Pre-Test Probability for PE (PTP)
    • High PTP ≥ 50%
  • Diagnostic Testing
    • Lower Extremeties Dopplers or Ultrasound
    • V/Q Scan - looking for a mismatch of perfusion between left and right heart
    • CT Scan (CTPA or chest CT with contrast)*
      • this is the cold standard to diagnose PE
    • D-Dimer - this test is used to rule out VTE, <500
  • Severity: PE > Proximal DVT > Distant DVT > Superficial VTE
    • hemodynamic instability and AKG changes indicate a severe VTE
    • cardiac arrest indicates very severe VTE
  • CHEST guidelines are considered the Gold Standard for anticoagulation management
    • American Society of Hematology is the newer guideline with a first author being a pharmacist

Given subjective and objective patient information, select an initial pharmacologic regimen to maximize therapeutic efficacy and minimize potential toxicity.

  • How to choose a treatment?
    • DOACs are preferred bc oral and greater safety
    • cancer - doac
    • pregnancy - heparins
    • heparin induced thrombocytopenia - warfarin/doac
    • use warfarin for lupus, antiphospholipid syndrome, clot in “strange places”
  • UFH
    • onset: IV is immediate. “quick on quick off”
    • elimination: half life is short. non-renal so good for PT w/ kidney impairment
    • monitoring: anti-Xa and aPPT
    • reversal: protamine
    • dosing is actual body weight based
    • no drug interactions
    • great for patients that are hemodynamically unstable
  • LMWH (enoxaparin (lovenox))
    • onset: longer than UFH
    • elimination: longer half life than UFH. renally excreted.
    • monitoring: Anti-Xa
    • reversal: protamine
    • dosing is actual body weight based
    • dosing is 1 mg/kg q12 or 1.5 mg/kg q24

exceptions to monitoring tests:

(1)baseline prolonged aPTT due to lupus anticoagulant require alternative testing

(2)anti-Xa assay is not viable in patients who take doacs

  • Warfarin
    • onset: 2-3 days
    • elimination: cyp2C9 and 3A4
    • monitoring: INR
      • 1.5 - 2.0 for mechanical heart valve
      • 2.0 - 3.0 for stroke prevention in afib and VTE treatment
      • 2.5 - 3.5 for mechanical aortic valve w/ 1 risk factor and mechanical mitral valve
    • reversal: vitamin k
    • moa: vit k epoxidase inhibitor which inhibits factor SNOT (7, 9, 10, 2) and protein C and protein S (the natural anti-coag proteins)
    • CI: pregnancy, current bleed
    • strength and colors of warfarin
      • Please - 1mg Pink
      • Let - 2mg Lavender
      • Granny - 2.5mg Green
      • Brown - 3mg Brown
      • Bring - 4mg Blue
      • Peaches - 5mg Peach
      • To - 6mg Teal
      • Your - 7.5mg Yellow
      • Wedding - 10mg White
    • assessing for warfarin sensitivity - pt w/ multiple risk factors should receive lower dose warfarin (2.5 mg green)
      • baseline INR ≥ 1.5
      • age>65
      • abw<45kg or abw<ibw
      • current antiplatelet therapy
      • lower INR goal should start on lower dose
      • check CBC before starting (low platelet means higher bleed risk)
    • factors that increase INR
      • drug interactions with inhibitors should start on lower dose
      • malnourished
      • foods high in vit K (leafy green vegetables, basil in pesto)
      • excessive alcohol consumption
      • illness like diarrhea
    • initiating warfaring:
      • warfarin must be bridged with IV heparin for 5 days until INR is at goal
        • during the first 5 days, patient is hypercoagulable bc warfarin depletes protein C and S
    • drug interactions (slides 53 and 54)
      • PD have additive effects with antiplatelets (aspirin, clopidogrel) and NSAIDs
      • PK inhibitors (GPACMAN) increase INR while inducers reduce INR
      • in general increase or decrease warfarin dose by 25%
        • for amiodarone, decrease warfarin dose by 50% after 2 weeks of dual therapy
        • for rifampin increase warfarin dose by 50% after 2 weeks of dual therapy
  • Subq Factor Xa inhibitors (fondaparinux)
    • good for pt allergic to heparin
    • CI: CrCl<30
      • prophylaxis is contraindicated when wt<50kg
    • dosing is only subq
      • DVT prophylaxis - wt>50kg: 2.5mg subq QD
      • VTE treatment -
        • wt<50kg: 5mg subq QD
        • wt 50kg-100kg: 7.5 mg subq QD
        • wt >100kg: 10 mg subq QD
  • DOACs
    • onset: 2-4 hours
    • elimination: half life is 12 hours
    • monitoring: none!
    • reversal: Andexanet (factor Xa antidote) and Praxbind (dabigatrin)
    • these drugs have better efficacy/safety when compared to warfarin
    • absorption is mediated by P-gp, do not use w/ carbamazepine, phenytoin, barbiturates
    • dabigatran (pradaxa) - direct thrombin inhibitor
      • indication/dosing:
        • stroke prevention (nonvalvular afib(NVAF)) - 150 mg BID
        • VTE - start 5 days heparin bridging then 150 mg BID
      • CI: CrCl<30
      • AE: GI bleed (GI ulcers, Chron’s disease)
      • Pgp inhibitors increase dabigatran lvls
    • apixaban (eliquis)
      • indication/dosing:
        • prophylaxis in NVAF - 5 mg BID or 2.5 mg if (1) ≥80yo (2)≤60kg (3)SCr≥1.5
        • VTE - 10 mg BID for 7 days then 5 mg BID
    • rivaroxaban (xarelto)
      • good for patients who want a QD dosing
      • indication/dosing:
        • prophylaxis NVAF - 20 mg QD w/ dinner
        • VTE - 15 mg BID for 21 days then 20 mg QD w/ dinner
    • edoxaban
      • if you see this drug calculate creatinine clearance
      • CI: CrCl > 95
  • inferior vena cava filter (IVC)
    • used for pt CI to anticoag meds
    • long term risk of DVT bc accumulation of thrombus on the filter

Given a therapeutic regimen for treating VTE, recommend a monitoring plan which includes duration of treatment, therapeutic efficacy, and toxicity.

  • treatment duration: based on factors + risk of bleeding
    • phases of treatment:
      • initial management → primary treatment → secondary prevention
      • initial management: 5-21 days of loading or co-dose
      • primary treatment: 3-6 months of anticoag treatment
      • secondary prevention: indefinite duration, decision based on risk factors
    • always have an initial 3 months of anticoag therapy
      • do not stop anticoag in these 3 months
    • d/c if the VTE is provoked and risk factors are reversible
    • continue if VTE is (1)unprovoked (2)risk factors are chronic or (3)pt cancer
    • HAS-BLED Assessment Score for bleeding - the more risk factors the more like the patient will bleed
      • treat risk factors for bleeding
  • toxicity
    • bleeding - s/s of internal bleed are gum bleeding, blood in pee (pink or red blood), large bruises, black or red poop
    • heparin induced thrombocytopenia (HIT) - a drop platelet count
  • inactivated prothrombin concentrates (PCCs) - Kcentra, which is factor II, VII, IX, and X in inactive form

Given a clinical scenario, (1)recommend therapeutic agents to reverse the effect of anticoagulation. (2)recommend therapeutic intervention to manage warfarin anticoagulation. (3)recommend bridging/switching strategies and monitoring plans.

  • transition from heparin to warfarin: initiate warfarin while still on heparin until INR is therapeutic for 1-2 consecutive days
  • transition from heparin to doac: start doac w/in 12 hours of second BID dose (lmwh) or when infusion is stopped (ufh)
  • transition from doac to warfarin: overlap doac and warfarin until INR is therapeutic. titrate warfarin
  • transition from warfarin to doac: start doac when INR is therapeutic (~2)

Chronic coronary disease (formerly known ischemic heart diseases) aka angina

about chronic coronary disease

  • definition
    • group of conditions that includes obstructive and nonobstructive CAD with or without previous myocardial infarction (MI) or revascularization
  • prevalence
    • leading cause of death for men, women, and people of most racial and ethnic groups
    • One person dies every 33 seconds from cardiovascular disease
  • diagnosed only by
    • noninvasive testing
    • angina symptoms
  • s/s
    • angina*
    • cold sweats
    • dizziness
    • women are more likely to complain about
      • dizziness
      • nausea
      • no symptoms at all
  • goal of treatment
    • minimize the likelihood of death (reduce premature CV death, prevent MI and HF)
    • maximize health and function (eliminate symptoms, restore satisfactory level of activity)
  • risk factors of major adverse CV events in pt with chronic coronary disease
    • high troponin (sign of heart inury)
    • b-type natriuretic peptide (sign of HF)
    • smoking status
    • high lipoproteins
    • high cholesterol
    • high blood pressure
    • high A1c

treatment options

  • risk factor modification
    • lifestyle modification
      • diet low in saturated fat and cholesterol reduce LDL and cholesterol
        • DASH (dietary approach to stopping hypertension) diet with more fruits, vegetables, whole grains, and low-fat dairy products
      • 10 lb weight loss reduce LDL and cholesterol
      • physical activity
        • aerobic or dynamic 90-150 min/wk
      • alcohol consumption - reduce consumption to men≤2 drinks and female≤1 drink
    • lipid management
      • goal: lower LDL by ≥50%
      • high risk should have high intensity statin on highest dose they can tolerate
      • not high risk use high intensity statin → if not tolerated (or pt is >75) use moderate intensity statin
      • ezetimibe can be added if LDL ≥70 mg/dL
        • then PCSK-9 inhibitors can be added after
        • if statins are not tolerated, use bile acid sequestrants, niacin or both
      • how to assess risk
        • very high risk -
          • history of multiple major ASCVD events
          • OR
          • one major ASCVD event and >2 high risk conditions
        • major ASCVD events include
          • recent (w/in a year) ACS (unstable angina, STEMI, and NSTEMI)
          • history of stroke
          • symptomatic PAD
        • high risk conditions include
          • age>65
          • smoker
          • genetics (familial hypercholesterolemia)
          • history of CABG (ACS) or PCI (first line for STEMI)
          • diabetes, htn, CKD, persistent hyperlipidemia, CHF
      • statins
        • High intensity: atorvastatin 40-80mg, rosuvastatin 20-40mg
        • Moderate intensity: atorvastatin 10-20mg, rosuvastatin 5-10mg, simvastatin 20-40mg, lovastatin 40 mg
        • Monitoring: after 4 weeks to three months, do repeat labs
          • if someone is stable, check in 6 months to a year
        • CI: pregnancy, nursing mothers, liver disease
      • PCSK9
        • praluent (alirocumab) and repatha (evolocumab)
        • these are brand name only, monoclonal antibody therapies, injection therapy
    • blood pressure management
      • choice in therapy is guided by indications for each class of antihypertensive drug
      • pt may require combo therapy
      • slide 29 for chart
    • diabetes mellitus management
      • goal: <6.5%
        • goal is 7-8% in pt with history of severe hypoglycemia, hypoglycemia unawareness, limited life expectancy, and renal disease
      • rosiglitazone is CI in pt with SIHD
    • antiplatelet
      • aspirin 81 mg should be started indefinitely
        • use clopidogrel if aspirin is CI
      • there is a risk of bleeding with use of both
      • dual antiplatelet therapy (DAPT) is prescribed post MI or after stent placement
    • smoking cessation
    • getting vaccines (specifically flu, covid-19, and RSV vaccines)
    • decrease stress
  • symptomatic relief
    • symptomatic CCD is defined as angina
    • beta blockers are the first line to CCD
      • lopressor metoprolol tartrate
      • toprol xl metoprolol succinate
      • tenormin atenolol
      • inderal propranolol hcl
    • CCB and/or long acting nitrates are used when beta blockers are CI
      • these two are added when beta blockers are unsuccessful in relieving symptoms
        • CCB names:
        • cardizem dilt
        • tiazac dilt
        • calan verapamil
        • norvasc amlodipine
        • procardia nifedipine
    • sublingual or spray nitroglycerin is recommended for immediate relief of angina
      • keep in the original container
      • do not store in a container with child-resistant safety cap
      • do no store in bathroom bc humidity may degrade
      • the sublingual tablet should NOT be chewed or swallow. both dosage forms should be place under tongue and let it dissolve
      • after administration, patient should sit down bc this drug can cause headache and lightheadedness
      • tablet should be refilled every 6 months and spray every 3 years
      • can be taken 30 minutes in advance of physical exertion
      • after 3 doses given every 5 minutes (15 minutes total), seek medical attention immediately
    • long acting nitrates require a nitrate free period bc of tolerance build up. pt should have 10-14 hour nitrate free period every day
      • for nitroglycerin patch (1)wear for 12-14 hr then remove (2)rotate sites on chest
    • ranolazine ER (ranexa)
      • moa: antiischemic and antianginal effect, doesnt effect HR or BP
      • this drug is a CYP3A4 substrate
      • interacts with Simvastatin (use 20 mg simvastatin), and NTI drugs like cyclosporine, tacrolimus, and sirolumus

Acute Coronary Syndrome I & II

Describe the etiology and pathophysiology of acute coronary syndrome (ACS)

    • ACS is an occlusion of the coronary artery
    • types of MI - Universal Classification of MI
      • Type 1 - spontaneous MI
      • Type 2 - MI secondary to ischemic imbalance (supply demand mismatch, drug use, increase sympathetic stimulation. no blockage)
      • Type 3 - MI resulting in death w/o biomarkers or ekg
      • Type 4a - MI related to percutaneous coronary intervention (PCI)
      • Type 4b - MI related to stent thrombosis
      • Type 5 - MI related to coronary artery bypass grafting (CABG)

List the signs and symptoms of myocardial infarction (MI)

    • cardiac troponin levels have to be elevated to be considered myocardial injury
      • acute myocardial injury is when there is a rise and fall of troponin values
    • myocardial infarction is elevated troponin (injury) + evidence of ischemia
    • signs of ischemia
      • ECG/AKG changes
      • symptoms of MI
      • imaging of heart
    • symptoms and clinical presentation
      • typical presentation: a crushing or pressure-like feeling radiating to the jaw or left arm
      • atypical: sweating, difficulty breathing, nausea, isolated jaw or left arm pain
        • typically females and older patients experience atypical presentations of MI
      • chest pain can be (1)cardiac, (2)possibly cardiac, (3)noncardiac
        • right sided is likely not ischemia
        • central, pressure, squeezing, and left side is more likely ischemia

Differentiate between NSTEMI, STEMI and unstable angina (UA)

    • types of ACS
      • unstable angina
        • chest pain
        • normal troponin
        • lack of ST elevation
      • NSTEMI
        • chest pain
        • high troponin
        • lack of ST elevation
      • STEMI
        • chest pain
        • high troponin
        • ST elevation
    • calculate TIMI (or GRACE) score for NSTEMI and UA patients - this guides treatment
      • 0-2 low risk
      • 3 intermediate
      • ≥4 high risk
    • do NOT calculate TIMI for STEMI
    • initial evaluation:
      • get an EKG/ECG
      • check cardiac troponin levels (I or T)
      • look at their symptoms and PMH

Recommend pharmacologic therapy for patients with STEMI and NSTE-ACS

  • all patients with ACS should receive
    • MONA-B (unless CI)
      • M - morphine or other opioids
        • typically fentanyl is given instead of morphine if MONA-B is desired
        • second option for chest pain
      • O - oxygen
        • only for patients with SaO2<90%
      • N - nitroglycerin
        • everyone will likely receive
        • for chest pain
        • 0.3-0.4 mg spray or sublingual tablet q5min for up to 3 doses
        • then give IV continuous infusion after 3 doses
        • CI: pde-5 inhibitor, HR<50, SBP<90
        • never use oral for acute management
      • A - aspirin
        • everyone will likely receive
        • use chewable and non-enteric coated tablet
        • give 1 dose is 162-325 mg
        • then baby aspirin 81 mg
        • use clopidergril for pt that cannot have aspirin
      • B - beta blocker
        • everyone will likely receive
        • start oral beta-blocker within 24 hours
        • CI: cardiogenic shock, bradycardia
        • use non-DHP CCB is beta-blocker is CI
    • Antiplatelet
      • every pt with ACS needed dual antiplatelet therapy (DAPT)
      • for all ACS pt use Aspirin +
        • (1st choice) prasugrel
          • not used with NSTEMI treated with medical management
        • (2nd choice) ticagrelor
        • (3rd choice) clopidogrel
          • becomes #1 among

elderly

high bleed risk

if STEMI was treated with fibrinolytics (”-plase” drugs)

      • continue dual therapy for at least 1 year/12 months
      • all antiplatelet therapy requires a loading dose
      • aspirin
        • LD: 162-325 mg
        • MD: 81 mg QD
      • oral P2Y12 inhibitor
        • clopidogrel (prodrug)
          • LD: 300-600 mg
          • MD: 75 mg
          • becomes #1 among

elderly

high bleed risk

if STEMI was treated with fibrinolytics (”-plase” drugs)

        • prasugrel (prodrug)
          • LD: 60 mg
          • MD: 10 mg QD or

5 mg QD in pt <60kg or ≥75yo

          • CI: stroke or TIA
        • ticagrelor
          • LD: 180 mg QD
          • MD: 90 mg BID
          • efficacy decreases in aspirin doses greater than 300 mg QD
        • cangrelor is an IV options
    • Anticoagulant
      • options are
        • bivalirudin
        • fondaparinux
          • cannot be used for sole anticoag when pt is getting PCI
        • enoxaparin
        • UFH
      • how to treat
        • STEMI w/ fibrinolytics - enoxaparin
        • STEMI - UFH, bivalirudin, fondaparinux
        • NSTEMI w/ PCI - UFH, bivalirudin, fondaparinux
        • NSTEMI w/medical management - UFH, enoxaparin, fondaparinux
      • anticoag treatment for the duration of
        • invasive procedure (PCI and CABG) then d/c once procedure is done
        • hospital stay (up to 8 days) for pt treated with fibrinolysis
      • UFH
        • given bolus and maintainence IV
        • LD: 60u/kg (max 4000 u)
        • MD: 12u/kg/hr (max 1000u/hr)
        • goal aPTT: 50-70
      • enoxaparin
        • given subq
        • does not require monitoring
        • dosing is kidney function dependent
          • usually BID
          • if CrCl<30, give QD
      • fondaparinux
        • given subq
        • no monitoring
        • CI: CrCl<30
      • bivalirudin (think UFH)
        • goal aPTT: 50-70 (same as UFH)
        • dosing is kidney function dependent
          • if CrCl<30, reduce the infusion
  • STEMI
    • reperfusion is the goal for treating STEMI
    • the FMC (first medical contact) starts when the medical professionals encounters pt (emt) or pt gets to ED
    • PCI is the first line for treating STEMI
      • should happen within 90 min of first medical contact (FMC)
      • when at hospitals w/o PCI capability, increase time to 120 min
      • should be done <12 hours of symptoms in pt w/ CI to fibrinolytic therapy
    • if PCI is contraindicated, use fibrinolytic therapy
      • alteplase
      • reteplase
      • tenecteplase
      • “-plase” drugs
      • should happen within 30 minutes of arrival at hospital
      • alteplase dose:
        • accelerated infusion (hour and 30 infusion)
          • *>67kg: 15mg IVP over 1-2min → 50mg over 30 min → 35 mg over 1 hr

most common

          • ≤67kg: 15mg IVP over 1-2 min → 0.75mg/kg IV over 30 → 0.5 mg/kg over 1 hr
        • 3 hour infusion
          • ≥67kg: 10mg IVP → 50mg IV over 1hr → 20mg over 1hr → 20 mg over 1 hr
      • absolute CI:
        • hemorrhagic stroke
        • ischemic stroke w/in 3 months
        • active internal bleed
        • aortic dissection
        • BP>180/110 and unresponsive to therapy
      • relative CI:
        • BP>180/110, you have to lower the BP first
    • CABG
      • recommended in left main disease or triple vessel disease
      • hold antiplatelets and anticoag before CABG (memorize slide 66)
        • antiplatelets
          • aspirin: do not hold
          • clopidogrel ticagrelor: 5 days
          • prasugrel: 7 days
        • anticoagulants
          • bivalirudin: 1-3 hrs
          • UFH: 1-4 hour
          • enoxaparin: 12 hrs
          • fondaparinux: 3-5 days
  • NSTEMI and UA
    • get the grace and TIMI score
      • low risk: use ischemia-guided management plan
      • intermediate or high risk: early invasive approach
    • ischemia-guided therapy (medication therapy without any procedures)
      • low risk GRACE or TIMI score
      • low life expectancy
      • pt or clinician expectancy (did I mean preference?)
      • this is using medication to treat
        • CCD/ISHD is for patients who had these things (ACS) in the past and now continue to
    • early invasive strategy (use of PCI and CABG)
      • high risk GRACE or TIMI score
      • cardiogenic shock
      • life threatening arrhythmias, like Vfib
      • prior CABG
      • PCI w/in the past 6 months

Secondary Prevention

  • DAPT
    • continue for 12 months unless there is a high /risk of bleed
    • aspirin should be continued indefinitely
  • lipid lowering
    • all pt should receive high intensity statin post-ACS (preferably before revascularization)
    • goal: 70 mg/dL or less
  • beta blockers
    • for all pt
    • continue for at least 3 years (unless there is an indication)
  • ACEi/ARB
    • for pt who just had STEMI/NSTEMI + HFrEF, HTN, CKD or DM
    • ARNI is only indicated for HF
  • MRA
    • for pt who just had STEMI/NSTEMI + already on ACE and beta blocker + HFrEF
    • unless CI (CrCl<30, K>5, etc.)

ACLS

Describe the prevalence and causes of cardiac arrests

  • causes of cardiac arrest can be categorized as the H’s and the T’s

H

T

-Hypovolemia (low blood or H2O volulme)

-Tablets (drugs OD)

-Hypoxia (low oxygen)

-Tamponade (increased pressure around the heart)

-hydrogen (acidosis)

-Thrombosis in the heart (ACS, clot inside the heart)

-Hyper/hypokalemia (potassium imbalance)

-Thrombosis in the lung (PE, clot inside the lung)

-Hypothermia

-Trauma (a penetrating injury in the heart)

-Hypoglycemia

  • types of rhythms during cardiac arrest
    • VF - ventricular fibrillation
    • VT - ventricular tachycardia
    • asystole
    • PEA - pulseless electrical activity

Understand the role of a pharmacist in ACLS

  • role of pharmacist
    • we verify the appropriateness of treatment
    • calculate appropriate doses
    • obtain and prepare medication
    • ensure proper administration of medication
  • goal of treatment
    • rapid recognition
    • prompt CPR
    • defibrillation
    • timely administration of meds to treat underlying causes

Identify the agents encountered during different types of emergency responses

  • protocol to achieve Return of Spontaneous Circulation (ROSC)
    • Always (1)start CPR [1]
    • (2)Give oxygen and
    • (3)Attach monitor/defibrillator
      • if rhythm is shockable (pulse is VF or pVT) →
        • give a shock [1]
        • CPR [2] (30 compressions + 2 rescue breaths)
          • +treat underlying issues with IV therapy
        • shock [2]
        • CPR [3]

give epinephrine every 3-5 minutes

          • up to 5 doses of epinephrine
        • shock [3]
        • CPR [4]
          • +amiodarone (after 5 doses of epinephrine)
          • +lidocaine (after dose of amiodarone)
      • if rhythm is NOT shockable (pulse is asystole or PEA)
        • administer epinephrine ASAP
          • give epinephrine every 3-5 minutes
          • up to 5 doses of epinephrine
        • CPR [2]
          • if rhythm becomes shockable, switch to that protocol
        • CPR [3]
          • +treat underlying issues with IV therapy
  • agents during emergency response
    • Cardiopulmonary resuscitation (CPR)
      • 30 chest compressions (allow chest to return to normal position after each compression)
      • 2 breaths
      • 2in depth
      • 100-120 BPM
    • epinephrine
      • for ALL types of rhythms
      • dosing: 1 mg q3-5min IVP
    • amiodarone
      • only for shockable rhythms (Vfib/VT)
      • dosing: 300mg IV 1x → (if vfib/pVT continues) 150mg IV over 1-2min 1x → (if more required) start infusion
    • lidocaine
      • only for shockable rhythms (Vfib/VT)
      • dosing: 1-1.5 mg/kg over 1-4min (bolus dose, max 25mg/min in pt w/ pulse) → 1-4 mg/min
      • monitoring: serum level 1-5 mcg/mL
  • secondary agents during emergency response
    • only used as an adjunct/add on NOT a replacement
    • sodium bicarbonate
      • only for hyperkalemia
      • dosing: 50 mEq over 5 minutes
    • calcium
      • only for hyperkalemia or CCB overdose
    • magnesium sulfate
      • only for QT prolongation (torsades de pointes)
      • dose: 1-2g
    • alteplase
      • ECHO should be done during CPR to rule out PE
      • dose: 50-100mg as bolus
        • recommended is 50mg IV push → 50mg in 10-15 minutes
        • no more than two doses
robot