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
- 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
- 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
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)
5 mg QD in pt <60kg or ≥75yo
- 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