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PSL-3 TOSCE 2017

Hypertension

BP = CO x PR

Why do we want to lower blood pressure? To decrease risk of complications from HTN (stroke,
heart attack, etc.)

HTN is a risk factor for:


-CV disease
-Coronary artery disease
-Congestive heart failure
-Renal failure
-Peripheral vascular disease
-Dementia
-Atrial fibrillation
-Erectile dysfunction

What are risk factors for HTN:


-smoking
-diabetes
-sedentary lifestyle
-unhealthy diet high in saturated/trans fats

Targets for HTN:


Normal 140/90
Diabetic 140/90
Elderly >80 yo 150/80

**Anti-hypertensive drugs used in mild hypertension (140-159/90-99) have not been shown to
reduce mortality or morbidity! Low risk = low benefit
Drugs that increase BP:
-NSAIDs (vasoconstriction)
-Decongestants (vasoconstriction)
-Alcohol
-Estrogen
4 things to consider when picking an anti-hypertensive:
-Efficacy – similar efficacy
-ADR - see table
-Convenience – all once daily or BID dosing
-Cost – similar, perindopril is $$, thiazides are cheap
Class ADR’s Cautions Comments
Thiazides -dizziness -Hx gout, diabetes, Biochemical
-increased urination hypokalemia, abnormalities are
1st line in (generally short lived hyponatremia less with lower doses
uncomplicated HTN, 2-4 weeks)
isolated systolic -increasing sun-
HTN, elderly, black sensitivity -Elderly
-hypokalemia, -Black
hyponatremia,
increased lipids, *thiazides increase
increased uric acid, uric acid and glucose
increased glucose levels
-muscle cramps
ACEi -DRY COUGH -Hx bilateral renal
-increase K+, artery stenosis,
1st line in diabetes in increased serum NSAID use
kidney disease creatinine (if it goes
higher than 40%
increase, stop ACEi
ARB -increase K+, -Hx bilateral renal
increased serum artery stenosis,
creatinine (if it goes NSAID use
higher than 40%
increase, stop ACEi
BB -cold extremities Hx asthma, severe **Not generally used
-fatigue PAD, heart block, age for lone HTN.
-decrease HR over 60
-decrease exercise Only used as first line
tolerance if CHF or angina or as
-vivid dreams option for A. fib
-impotence
CCB -DHP: flushing ankle Hx heart failure (for
edema, headache non-DHP)
*1st line for ppl who
don’t want to do lab -non-DHP: flushing -Add-on therapy
tests ankle edema,
headache, decrease
HR, heart block,
worsened HF,
constipation
(verapamil,
diltiazem)
Monitoring:
Thiazides -Check Na+ and K+ levels
-In about 2 weeks
-For SE (dizziness)
ACEi -Check kidney function
-Check K+ and SCr levels
-Check these in a couple of weeks
-Warn about dry cough
ARB -Check kidney function
-Check K+ and SCr levels
-Check these in a couple of weeks
BB -No labs
-Monitor for hypotension, decreased HR,
fatigue, insomnia, dizziness
-Affects lipids and glucose
CCB -No labs
-Monitor for flushing, headache, edema

*For those without kidney disease, ACEi and ARB reduce likelihood of developing
microalbuminuria, but not doubling of SCr or ESRD.
*For those with diabetic kidney disease, ACEi and ARB both delay progression of nephropathy
to ESRD

Should we increase the dose or add another drug?


-Increasing the dose does not benefit much, only increases side effects

Use of  1 antihypertensive drug at bedtime reduced CV events more than use of all drugs in
the morning in CKD.

Combination Therapy Take Home:


-Using two drugs to start is generally not a rational approach for drug therapy
-Smaller doses often do almost as good of a job at BP reduction as larger doses
-Adding an agent is additive for BP reduction, but less than additive for adverse events
-Important exception for comorbid diseases (ex. CHF, post-MI)
-If we have large trial evidence of target drug doses showing hard outcomes, we should
aim for those doses
-Taking  1 antihypertensive HS may be beneficial

Treating HTN in the elderly:


-Elderly are more sensitive to sympathetic inhibition and volume depletion
-Increases orthostatic HTN
-Increases morbidity, increase risk of falls
-Low BP may be associated with dementia, cancer, HF, and MI
-Isolated systolic HTN (ISH) and wide pulse pressures increase risk of MI, stroke, renal failure,
etc.
**Dropping BP in elderly can harm them but if we don’t treat it we cause strokes, heart attacks,
and renal failure

HTN in Elderly Take Home:


-BP reduction target = < 150/80 (likely not applicable to frail elderly)
-Outcome benefits apparent within first year
-Class effect vs BP lowering effect (either way, a thiazide is a good first line option)
-With up to 2 agents – 50% will reach target BP

Anti-hypertensives that can help control his rapid heart rate:


-BB and non-DHP CCB
Hypertension TOSCE Outline

1) Intro: “Hi, my name’s Sam, I’m the pharmacist on duty, did you want to have a seat and we
can discuss this further? Just so you know everything here is private and confidential.”

2) MAPPL
-Medical conditions and how long they’ve had them
-Allergies & Type of reaction
-Prescription Meds, Herbals, OTC/Vitamins
-Pregnant/Breastfeeding
-Lifestyle

3) SCHOLAR
-Symptoms
-Characteristics
-History
-Onset
-Location
-Aggravating factors
-Relieving factors

4) Hypertension Lifestyle Questions:


-Diet
-Exercise
-Smoker
-Alcohol
-Stress
-Caffeine
-Illicit drugs
-Family history
-Decongestants, NSAIDs
-Ask where they took their BP readings and what are the most recent BP readings

5) Other questions:
-Seen a Doctor, Diagnosed?
-Tried anything yet?
-Patient preferences ?

6) STATE THE FRIGGIN DTP & TREATMENT/PROBLEM RESOLUTION

7) Non-pharms: Allow 3-6 months of lifestyle modification before considering medication!


-Exercise (get up to 150 mins of mod-vig exercise/week)
-Decrease salt intake to 2000mg/day (most people consume 3000-3500mg/day)
-Weight reduction
-Caffeine reduction
-Stress management
-Decrease alcohol (no more than 2 drinks/day not exceeding 14/week for men and 9/week for
women

8) Monitoring:
-BP within target
-Side effects

9) Follow-up
-In a week for side effects
-Should start seeing a consistent effect within 1 month of BP meds

Special Populations Preferred Agent


Pregnancy Methyldopa, Labetolol
Black patients Thiazides
Elderly Thiazides
Kidney failure ACEi
Diabetes ACEi
Dyslipidemia

Healthy values:
TChol < 5.2 mmol/L
LDL < 3.4 mmol/L
HDL > 1.0 (men)
HDL > 1.3 (women)
TG < 1.7 mmol/L

Positively affect lipid profile & decrease risk of CV events:


1) Stop smoking
2) Physical activity (Target 150 mins/week)
3) Diet (Mediterranean diet or DASH diet) – low in salt and saturated and trans fats (eat
lots of fruit and vegetables)
4) Limit alcohol use to 2 drinks/week

Reducing cholesterol is good because:


-reduces risk of developing heart disease
-reduces risk of heart attack and stroke
-reduces risk of vascular disease

LDL > 5 mmol/L = go on a statin


If you have diabetes, should be on a statin if you have > 10% risk of CVD in the next 10 years

Relative Risk Reduction of CV events: 25-30%


10% get muscle aches

When choosing a statin:


Efficacy – all the same
Harm – all the same
Cost – similar
Drug interactions – Simvastatin & Lovastatin > Atorvastatin > Pravastatin & Rosuvastatin

Statin-induced myopathy treatment:


-Obtain CK level
+/- Hold statin
-Continue for 1-2 weeks with monitoring
-Reassess risk vs. benefit of restarting Statin

Myositis:
-CK levels > 2-4x ULN but < 10 x ULN
-D/C Statin
Rhabdomyolysis:
-Severe muscle pain and weakness
-CK > 3-10x ULN and marked SCr
-D/C statin & hospitalization for supportive treatment
-May later re-challenge w low dose of different statin

Other Dyslipidemia Meds:


-Ezetimibe
-Fenofibrates – not effective

Drug Interactions with statins:


-Grapefruit inhibits CYP3A4, increasing concentrations, increasing risk for myalgias
-Azole antifungals
-St. John’s wort
-Macrolide antibiotics
-Diltiazem
-Verapamil
-HIV protease inhibitors

Only thing we can combine with Statin: Ezetimibe


Dyslipidemia TOSCE Outline

1) Intro: “Hi, my name’s Sam, I’m the pharmacist on duty, did you want to have a seat and we
can discuss this further? Just so you know everything here is private and confidential.”

2) MAPPL
-Medical conditions and how long they’ve had them
-Allergies & Type of reaction
-Prescription Meds, Herbals (st. john’s wort), OTC/Vitamins
-Pregnant/Breastfeeding
-Lifestyle

3) SCHOLAR
-Symptoms
-Characteristics
-History
-Onset
-Location
-Aggravating factors
-Relieving factors

4) Dyslipidemia Lifestyle Questions:


-smoker
-alcohol use
-weight/BMI
-family history
-stress

5) Other questions:
-Seen a Doctor?
-Tried anything yet?
-Patient preferences ?
Statin-induced myopathy questions:
-Bilateral or unilateral ? If bilateral, more likely statin-induced
-Brought on by exercise ?
-Worsened with exercise ?
-Has this happened before?
-When did it start ?
-Which muscles are affected? (starts in larger muscles)
-Anything that makes it better or worse ?
-Any change in urine color ? (if yes, sign of rhabdomyolysis)

6) STATE THE FRIGGIN DTP & TREATMENT/PROBLEM RESOLUTION


7) Non-pharms: Allow 3-6 months of lifestyle modification before considering medication!
-Exercise (get up to 150 mins of mod-vig exercise/week)
-Decrease salt intake to 2000mg/day (most people consume 3000-3500mg/day)
-Weight reduction
-Stress management
-Decrease alcohol (no more than 2 drinks/day not exceeding 14/week for men and 9/week for
women

8) Monitoring:
-LDL levels (below 2 mmol/L or 50% reduction)
-Monitor Lipid Levels, CK, and LFTs: Baseline, 6-8 weeks after initiation, then every 6 months
Side effects:
-Muscle pains (10%)
-GI upset
-sleep disturbances (less than 1%)
-dark urine, ab pain, yellowing of eyes or skin (indicative of liver damage) (less than 1%)

9) Follow-up

In 1 week to ask about side effects.


Diabetes

Using an insulin pen:


-4 sites (back of arm, outside of thigh, top of butt, stomach)
-rotate sites
-prime pen every time to ensure air is all out of the pen
-goes up by 2 units
-leave pen inside for 10 seconds to ensure entire dose was administered
-dispose of needles in a sharp’s container
-store @ room temp (for up to 28 days) – store the other ones in the fridge

Picking the right needle: ___________________________________

Hypoglycemia:
Early Signs: Sweating, hunger, shakiness, palpitations
-If untreated, may progress to: Blurred vision, confusion, slurred speech, convulsion, coma,
death
-Can be brought on by vigorous exercise, skipping meals, overdose of antihyperglycemics
Treatment: 15, 15, 15 Rule
-Take 15 grams of carbs
-Wait 15 minutes and test BG again
-If still under 4 mmol/L, ingest another 15g of carbs
-Make sure BG rises above 4 mmol/L
-If next meal is over an hour away, have a snack.

ASK patient about their glycemic levels:


-A1C
-FPG
-2hr after meal levels

Targets for adults:


A1C  7%
Premeal/FPG = 4-7 mmol/L
2 hr after meals = 5-10 mmol/L or 5-8 (if A1C target not met)
*Want to reach targets within 3-6 months of diagnosis !!!

Prediabetes: A1C = 6.0-6.4%


Examples Onset Duration
Bolus Rapid-acting -Insulin Aspart 10-15 min 3-5 hours
-Insulin Glulisine
-Insulin Lispro
Short-acting -Humulin-R 30 min 6.5 hours
-Novolin ge Toronto
Basal Intermediate-acting -Humulin-N 1-3 hours Up to 18
-Novolin ge NPH hours
Long-acting -Insulin detemir 90 mins Up to 24
-Insulin glargine hours

Diabetic Ketoacidosis:
-HYPERglycemia puts patients at risk for DKA.
-This condition develops when your body can’t produce enough insulin.
-Without insulin, your body starts to break down fat as a fuel bc it can’t break down sugar.
-When fat breaks down, ketones can be present in urine and blood.
-Treatment: Insulin

Type 1 Diabetes:
Initial dosing:
-0.5-1 units/kg per day
-50% basal
-50% rapid acting

For Hyperglycemia:
In most cases, insulin adjustments should approximate a 10% increase to the insulin (long-
acting) causing the effect. If it’s short or rapid acting, you can use the correlation factor.

For Hypoglycemia:
The insulin causing the low level should be typically decreased by 10%

Correlation Factor or Insulin Sensitivity Factor:


For rapid-acting insulin:
100/TDD (total daily dose) = the reduction in BG for 1 unit of rapid-acting insulin
For short-acting insulin:
85/TDD (total daily dose) = the reduction in BG for 1 unit of short-acting insulin

-Used for hyperglycemia to determine how much insulin to increase in order to reduce BG

Insulin to carbohydrate ratio (ICR) using the “Rule of 500”:


-500/TDD = how many grams of carbs used for 1 unit of insulin
**OR use the exact amount of carbs per day if they know that

-Used for figuring out how much insulin to inject for extra carbs
Type 2 Diabetes:

Sick days & Diabetes:


-The objective of sick day management in insulin-managed diabetes is to minimize metabolic
imbalance, avoid severe hypoglycemia, and prevent hyperglycemia and ketosis leading to the
development of diabetic ketoacidosis (DKA)
-Illness and infection allow the body to release counter regulatory hormones that oppose the
action of insulin. This allows the circulating levels of glucose to rise quickly along with an
increase in circulating fat cells. With lower insulin levels, higher glucose levels and increasing
fat cells the blood becomes more acidic and ketone bodies increase.
-Ketone testing is recommended for all ppl with T1DM during periods of acute illness
accompanied by elevated BG; when preprandial BG levels remain elevated (>14 mmol/L) or
when symptoms of DKA such as nausea, vomiting or ab pain are present. (also for T2DM)
-Insulin should never be omitted during sick days
-Continue usual dose of intermediate and long-acting in most cases
-Rapid or short acting insulin may be needed for hyperglycemia and ketosis.
-In general, ketones are markers of insulin deficiency and indicate the need for supplemental
insulin. However, if BG remains elevated – with or without ketones – additional doses of insulin
should be given.
-Supplemental rapid or short acting insulin can be safely given every 3-4 hours, without
discussion with a physician
-Usually, additional rapid or short acting insulin is required, however in the face of
hypoglycemia, a reduction in dose may be advised
-BG and ketones should be monitored every 2-4 hours around the clock (including usual SMBG
times, ac meals, and bedtime snack, even if not eating) as long as significant hyperglycemia
and/or ketonuria/ketonemia persist.
Targets: BG < 14, urinary ketones negative, blood ketone 0.6 or less
-If a client has difficulty eating solids during illness, 10-15 grams of CHO should be taken every
1-2 hours
-Extra fluids (sugar-free) should be taken to prevent dehydration and facilitate excretion of
ketones in the urine. The body needs at least 2200mL (9 cups) of fluid daily to prevent
dehydration. As a rule of thumb, 1 cup an hour while awake can be recommended during times
of illness.
Hold SAD MANS: sulfonylurea, ACEi, diuretics, direct renin inhibitors, metformin, ARB,
NSAIDs, SGLT2 bc at risk of declining kidney function
Questions to ask:
-Are they able to keep food down?
-Are they still getting enough fluids?
-Nausea, vomiting or ab pain, fever?
-How often are the vomiting?
-How often are they having loose stools (diarrhea) ?

Gestational Diabetes:
Exercise & Diabetes:
-SMBG should be done before, during & after exercise to determine how individual’s BG varies
in response to exercise
-Exercise should be avoided if BG is below target OR > 14 mmol/L and ketones in urine or
ketones > 0.5 mmol/L in blood
-Young children often need extra food bc activities are unplanned
-As activity becomes planned, adjusting insulin is preferred
-Hypoglycemia can be prevented by decreasing insulin dose or adding food
-Always carry a source of fast-acting glucose when exercising
-Hypoglycemia can occur during or after exercise (Up to 36 hours post exercise)

Insulin adjustments for Planned Activity:


Type of Activity Duration Insulin Reduction (Peaking
Insulin)
Low intensity (walking, If less than 30 mins No adjustment may be
bowling) necessary
If greater than 30 mins 10% reduction
Moderate intensity (tennis, 20% reduction
swimming, biking)
High intensity (running, 30-50% reduction
soccer, hockey)
Prolonged intensity Lasting throughout the day 50% or greater reduction

Extra Carbs Required for Unplanned Activity:


Type of Activity Duration Extra CHO
Low intensity If less than 30 mins No extra CHO required
If greater than 30 mins 10-15 grams/hr of exercise
Moderate intensity 1g CHO/kg/hr (ideally given
every 20 minutes during the
hour)
High intensity 1.5g CHO/kg/hr of exercise
(ideally given every 20
minutes during the hour)

4 important things for exercising with diabetes:


-Drink lots of sugar-free fluids
-Have a fast-acting glucose source on hand
-Have a snack on hand
-Monitor blood glucose before, during, and after (delayed hypoglycemia can happen up to 36h
post-exercise)
Diabetes TOSCE Outline

1) Intro: “Hi, my name’s Sam, I’m the pharmacist on duty, did you want to have a seat and we
can discuss this further? Just so you know everything here is private and confidential.”

2) MAPPL
-Medical conditions and how long they’ve had them – Ask if it’s Type 1 or 2, and ask about
kidney function
-Allergies & Type of reaction
-Prescription Meds, Herbals, OTC/Vitamins
-Pregnant/Breastfeeding
-Lifestyle

3) SCHOLAR
-Symptoms
-Characteristics
-History
-Onset
-Location
-Aggravating factors
-Relieving factors

4) Diabetes Lifestyle Questions:


-smoker?
-alcohol?
-exercise?
-diet?
-family history?
-weight?
-ASK ABOUT TARGETS (A1C, FPG, and 2hr after meal levels)

Targets:
Age A1C (%) FPG (mmol/L) 2hr after meal Comments
(mmol/L)
<6 <8 6-10
6-12 <7.5 4-10
13-18 <7 4-7 5-10
(5-8 if A1C not
met)
Elderly <8.5 5-12

Pregnancy
5) Other questions:
For insulin adjustments for exercise:
-What type of exercise
-How long they will exercise for and how often
-You are going to be reducing insulin dose for exercise!

6) STATE THE FRIGGIN DTP & TREATMENT/PROBLEM RESOLUTION

7) Non-pharms:
1) Weight management
-BMI 18.5-25
-Waist circumference (<100 cm males & <90 cm in females)
-Goal of 5-10% weight reduction

2) Physical exercise
-individualized according to patients’ current exercise status
-Goal 30-60 min of moderate activity/day

3) Counsel on hypoglycemia
4) Counsel on how to use insulin pens and storage
5) Counsel on ketone testing if they’re nausea, vomiting, ab pain or if FPG > 14 mmol/L

8) Monitoring:
-Monitor that BG is within targets (see above)
-Hypoglycemic symptoms

9) Follow-up
ACS – NSTEMI or STEMI (not angina)

3 types of ACS:
-UA – unstable plaque, plaque disruption and platelet aggregation
-NSTEMI – mostly platelets, partial occlusion
-STEMI – a lot of fibrin, complete occlusion

UA NSTEMI STEMI
Troponin - + +
ST elevation - - +

*Troponin and CK-MB is released well cardiac cells die.

CK-MB:
-Detectable in serum within 3-6 hours after MI, peaks in 12-24 hours, stays elevated for 2-3
days

Troponin:
-Detectable in serum within 4-12 hours after MI onset, peaks in 12-48 hours, and stays elevated
for 7-10 days

*Biomarker assays should be done STAT on presentation, then repeated q4-6 hours for the first
12-24 hours, then periodically
*For diagnosis of STEMI or NSTEMI, at least 2 elevated CK-MB or 1 TnT exceeding the upper
reference range is needed (usually 2 successive blood samples)

-12-lead ECG should be done within 10 mins on presentation to ED


-ECG an important tool in distinguishing STEMI from NSTEMI and informs location of myocardial
damage (anterior, lateral, inferior, posterior); affects decision pathway and management
ECG diagnostic criteria:
-ST segment elevation in > 2 contiguous leads, exceeding 0.2 mV in leads V1, V2, V3 or 0.1 mV
or greater in other leads, or new left bundle branch block (LBBB)
-A pathologic Q wave is more indicative of an old infarct and may not be present in the
immediate onset of a STEMI
STEMI
-Most severe type of ischemia in the pathophysiologic continuum of acute coronary syndrome
-Caused by complete occlusion of the coronary artery by clot (rupture of atherosclerotic
plaque)
-STEMI comprises approximately 25-40% of MI presentations

Diagnosis of STEMI:
-signs and symptoms
-ECGs
-cardiac biomarkers of cell death (CK-MB and TnT)

Symptoms:
-central chest pain (typically radiating to shoulder, down the left arm, to the back or jaw)
-shortness of breath
-nausea or vomiting
-diaphoresis (sweating)
-CAN BE SILENT TYPE (NO SYMPTOMS)

Elderly, diabetic and women are less likely to have classic symptoms.
On average, women experience longer time interval than men between symptom onset and
Emergency Department (ED) Care.

Signs:
-syncope
-bradycardia (inferior infarction), tachycardia (increased sympathetic activity, decreased cardiac
output), other arrhythmias
-elevated or low BP
-diffuse rales, wheezing or respiratory distress usually indicate pulmonary edema and CHF
-jugular venous distention indicates right atrial hypertension, usually from RV infarction or
elevated LV filling pressure

Initial Management: MONA


-Morphine 2-5 mg IV q5-30 min prn (could use other analgesics such as fentanyl) – if pain not
relieved by nitro
-Oxygen at 4L/min by nasal prong to maintain O2 saturation > 90% (preferably > 95%)
-Nitroglycerin SL or IV (give nitro first before morphine)
-ASA 162-325 mg PO chew/swallow (if not already given by EMS)

Reperfusion:
-Time is muscle in STEMI
-Priority is to re-establish blood flow to the occluded artery as quickly as possible
-2 types of reperfusion strategies in STEMI:
1) Primary percutaneous coronary intervention (PCI)
2) Fibrinolytics
Choice of reperfusion strategies dependent on geographical location, availability of PCI-capable
facilities, onset of symptoms.

Reperfusion Goals of therapy:


-Decrease mortality and complications
-Reduce or contain infarct size
-Salvage functioning myocardium and prevent remodelling
-Re-establish patency of the infarct-related artery

Reperfusion Current Recommendations:


-Reperfusion therapy should be administered to all eligible patients with symptom onset within
the prior 12 hours.
-Primary PCI is the recommended method of reperfusion when it can be performed in a timely
fashion by experienced operators
-Ideal door-to-balloon (medical contact to device) time of < 90 mins should be targeted for
primary PCI
-If a STEMI initially presents to a non-PCI capable hospital, Immediate transfer to a PCI capable
hospital for primary PCI should be considered if a medical contact-to-device time of < 120 min
can be achieved.
-When fibrinolytic therapy is indicated or chosen as the primary reperfusion strategy, it should
be administered within 30 min of hospital arrival.

Primary PCI:
-Diagnostic catheter is placed and advanced through the femoral artery to the aorta and the
coronary arteries
-Contrast dye is injected once the catheter is in place. X-rays are taken to locate the exact
location of coronary occlusion.
-A balloon catheter (with or without a stent mounted) is advanced to the blockage site. Once at
the site, the balloon is inflated for a few seconds to open the blocked coronary artery.
-The stents are left in place to keep the coronary vessel open.
-Once the balloon has deflated, or when stent is in place, repeat x-rays are taken with contrast
dye to ensure optimal coronary blood flow has been achieved:
TIMI grade flow: adopted scoring system of 0-3 referring to the level of coronary blood
flow assessed during PCI
Want to achieve TIMI 3 flow (complete perfusion)
-Angioplasty without stenting is rarely used in the setting of ACS now
-PCI procedures will almost always involve a bare metal stent (BMS) or drug eluting stent (DES)
-Drug eluting stent have Antiproliferative drugs coated on the stent scaffold, which is released
slowly over time to prevent restenosis.
-DES have been shown to reduce restenosis rates compared to BMS and is commonly used in
NSTEMI/STEMI patients undergoing PCI
-Patients who received DES will require dual-antiplatelet therapy for a minimum of 1 year

Fibrinolytics:
-Benefit of fibrinolytics is directly related to the time from MI onset
-Greatest mortality reduction is achieved when fibrinolytics is given within 0-2 hours.
-Target 30 mins within arrival
**Fibrinolytics not administered to NSTEMI/UA patients bc there is not much fibrin, mostly
made up of platelets
-Tenecteplase (TNK) is the fibrinolytic of choice
-5 second single bolus
-Weight-tired dosing
-Major concern of fibrinolytic therapy is bleeding complications
-CI’s to fibrinolytic use must be evaluated to minimize major bleeding risk

Antithrombotics:
-Antithrombotics (antiplatelets, anticoagulants) are the cornerstone therapy in STEMI
management

For STEMI patients undergoing primary PCI:


Loading dose:
-ASA 162-325 mg PO should be given before PCI
PLUS
-A loading dose of a P2Y12 receptor inhibitor as early as possible before PCI
-Clopidogrel 600mg
-Prasugrel 60mg
-Ticagrelor 180mg

Maintenance dose:
-ASA 81-162 mg PO daily
PLUS
-P2Y12 receptor inhibitor at maintenance dose should be continued
-Clopidogrel 75mg daily
-Prasugrel 10mg daily
-Ticagrelor 90mg BID

-LMWH or UFH is usually initiated on presentation and discontinued after PCI

For STEMI patients receiving fibrinolytics:


-ASA 162-325 mg PO should be given on presentation
PLUS
-Clopidogrel 300mg LD in patients < 75 or Clopidogrel 75mg LD in patients > 75
PLUS
-Clopidogrel 75mg daily should be continued for 14 days unless pt undergoes subsequent PCI
-LMWH or UFH should be initiated at time of fibrinolysis and continued for a minimum of 48
hours and up to 8 days (or until revascularization with PCI)
-DAPT for 1 year (ASA + P2Y12 inhibitor) after PCI
Enoxaparin in STEMI:
In STEMI patients < 75 yo:
-Give enoxaparin 30 mg IV bolus before TNK
-Continue enoxaparin 1 mg/kg SC q12h after TNK
-Maximum dose enoxaparin 140mg SC q12h after the first 24 hours

In STEMI patients > 75 yo


-Do not give enoxaparin IV bolus
-Enoxaparin 0.75 mg/kg SC q12h after TNK
-Maximum dose enoxaparin 100mg SC q12h after the first 24 hours

Heparin:
-Use in patients > 149 kg (little evidence to support LMWH in these patients)
-For those with renal impariemtn, CrCl < 30
-Use UFH 60 units/kg IV load, followed by 12 units/kg/hr IV infusion
-Target aPTT 49-65 seconds

Antiplatelets in STEMI:
-ASA 162-325 mg PO x 1 for all STEMI patients (unless CI)
-ASA + Clopidogrel was the conventional DAPT regimen for patients undergoing PCI in ACS
-New P2Y12 antagonists emerged 5 years ago (prasugrel and ticagrelor)
-Both drugs are more favorable than clopidogrel in terms of pharmacokinetics and
pharmacodynamics properties
-Clinical trials suggest better efficacy profile with ASA+prasugrel or ASA+ticagrelor compared to
ASA+clopidogrel in patients with STMEI undergoing primary PCI
-Prasugrel should not be used in patients with history of stroke or TIA due to higher rates of
major bleeding in these population

Triple therapy (DAPT + Warfarin) may be indicated in STEMI patients with low ejection fraction
or has concurrent AF

STEMI Complications:
1) Heart Failure
-LV myocardium may be ischemic, stunned, hibernating or irrevocably injured after MI
-ECG is warranted to assess LVEF (want it >40%)
-Medical therapy with diuretics, vasodilators and inotropic may be required based on
symptoms and echo results

2) Cardiogenic shock
-Decreased CO & evidence of tissue hypoxia in presence of adequate intravascular
volume
-Often due to extensive LV infarction
-Can be due to systolic, diastolic, or valvular dysfunction

3) Arrhythmias
-may arise post MI due to ischemia and severe HF
-ventricular arrhythmias more probable in the peri-infarction period; leading cause of
sudden cardiac death in the setting of STEMI
-implantable cardioverter-defibrillator (ICD) is indicated before discharge in patietns
who develop sustained VT/VF more than 48 hours after STEMI
-Atrial Fibrillation or other conduction defects also possible
4) Pericarditis
-Uncommon and usually presents within 72 hours post MI
-Symptoms usually resolve within 3-4 days
-Tx with ASA 650 mg po QID or NSAIDs

Goals of Adjunct Therapy:


-Reduce the risk of short term and long term complications associated with STEMI
-Slow progression of coronary heart disease and minimize the risk of future CV events and
other morbidities
-Improve mortality and restore QOL
MOA Initiated CI Dose Examples Monitoring
when?
B-Blockers -Increase -Within Hypotension -Start at Metoprolol -BP
myocardial 24 hours Bradycardia low dose Atenolol -HR
salvage in the after Acute HF and Carvedilol -Signs &
infarct area onset of Cardiogenic titrate to symptoms of HF
-Prevent MI shock maintain
extension of unless CI Asthma resting HR
infarction by 2nd or 3rd of 55-60
reducing oxygen degree AV bpm
consumption/de block
mand
ACEi -Minimize -Within Caution in Titrate to Ramipril -SCr
ventricular 24 hours those with evidence Enalapril -Electrolytes
remodelling of MI renal based Lisinopril -Watch for
-Reduce O2 once BP impairment doses Captopril hyperkalemia
demand has been and
-Reduce stabilized hyperkalemia
myocardial wall unless CI
stress by
reducing preload
and afterload
ARBs -Same as ACEi -Within Caution in Titrate to Candesartan -SCr
-Indicated for 24 hours those with evidence Telmisartan -Electrolytes
ACEi intolerant of MI renal based Valsartan -Watch for
patients once BP impairment doses hyperkalemia
has been and
stabilized hyperkalemia
unless CI
Statins -Decrease LDL -If not at Atorvastatin -Lipid panel
-Pleiotropic max dose Rosuvastatin -LFTs
benefits of already, Simvastatin -CK
statins extend titrate to -signs and
beyond lipid achieve symptoms of
lowering effect 50-60% myopathy and
reduction rhabdomyolysis
in LDL (dark urine)
Aldosterone -For -Caution in Low dose, Spironolacto -Check K+ at
Antagonist consideration in patients with titrate ne baseline and
patients with CrCl < 30 and Eplerenone within 1 week of
LVEF < 40% K > 5 mEq initiation

DAPT ASA 81 mg daily x life + Clopidogrel 75 mg daily x 1 year


NSTEMI

Risk Stratification:
TIMI Risk Score All-cause mortality, new or recurrent MI, or
severe recurrent ischemia requiring urgent
revascularization through 14 d, %
0-1 4.7
2 8.3
3 13.2
4 19.9
5 25.2
6-7 40.9
1 point is given for each of the following: >65, >3 risk factors for CAD (ex. HTN, DM, smoker),
prior coronary stenosis > 50%, ST deviation on ECG, >2 anginal events in prior 24h, use of
aspirin in prior 7 days, elevated cardiac biomarkers

Initial Treatment Strategy for NSTEMI:


1) Early invasive strategy (sending them for PCI)
-Angiography +/- revascularization (PCI) within 24 hours
-Indicated for high risk patients (TIMI risk score  2, or presence of other high risk
characteristics)

2) Ischemia-guided strategy (medical management)


-Patients with low risk features
-May be referred for revascularization if ischemia worsens, or if new high risk features
occurs

3) CABG
-High risk patients with multivessel disease may be referred for CABG (hold DAPT 5-7 `
days prior to surgery if possible)

Antiplatelets:
Loading Dose Maintenance Dose
ASA 160-325 mg STAT (chewed) 80-325 mg daily
Ticagrelor 180 mg 90mg BID
Clopidogrel 150-300 mg 75 mg
Prasugrel 60 mg 10 mg

DAPT:
-UA/NSTEMI patients who underwent early invasive strategy with PCI should receive DAPT as
outlined for STEMI patients
-For patients with ischemia-guided strategy (medical management), current guidelines
recommend DAPT with ASA plus ticagrelor or clopidogrel
-DAPT x 1 year for all ACS patients

GP 2b/3a receptor antagonists:


-potent antiplatelet agents
-block binding of fibrinogen to GP 2b/3a receptor on platelet surface, therefore inhibit platelet
aggregation
-Abciximab, eptifibatide, tirofiban
-Given IV in combo with anticoagulant and DAPT
-Demonstrating benefit in reducing death/MI in patients with UA/ACS who undergo PCI
-Not generally used in patients receiving medical management due to questionable benefit
Anticoagulants:
-Prevent progression to MI and death

LMWH – standard
-Enoxaparin 1mg/kg SC q12h (max 100mg) until PCI or hospital discharge shown to decrease
risk of death, MI and stroke
-Advantage: easier to give, no monitoring, lower incidence of HIT (heparin induced
thrombocytopenia)
-Disadvantage: long acting, renal elimination

UFH – for obese or chronic kidney failure


-60 units/kg load, then 12 units/kg/hr infusion
-Titrate to aPTT 1.5-2x control
-Until PCI or 48 hours

Monitor: signs of bleeding, Hbg, platelets

Fondaparinux
-Indirect-acting factor Xa inhibitor
-2.5mg SC once daily (until PCI or hospital discharge)
-Non-inferior to enoxaparin
-Lower rate of major bleeding
-Increased risk of thrombus formation post-PCI
-Give UFH bolus during PCI
-May be preferable in patients at higher risk of bleeding

Goals of adjunct therapy:


-Reduce the risk of short term and long term complications associated with ACS
-Slow progression of coronary heart disease and minimize the risk of future CV events and
other morbidities
-Improve mortality and restore QOL

Complications are the same as STEMI


Meds are the same as STEMI

Only initial therapy/treatment is different !!!


Other Issues to Consider Post-MI
-Hormone therapy not indicated in postmenopausal women – may increase CV risk
-Avoid NSAIDs, including selective COX2 inhibitors (celecoxib) if possible
-For active, ongoing users of cocaine and methamphetamine, BB should be avoided due to risk
of potentiating coronary spasm
ACS TOSCE Outline

1) Intro: “Hi, my name’s Sam, I’m the pharmacist on duty, did you want to have a seat and we
can discuss this further? Just so you know everything here is private and confidential.”

2) MAPPL
-Medical conditions and how long they’ve had them
-Allergies & Type of reaction
-Prescription Meds, Herbals, OTC/Vitamins
-Pregnant/Breastfeeding
-Lifestyle

3) SCHOLAR
-Symptoms
-Characteristics
-History
-Onset
-Location
-Aggravating factors
-Relieving factors

4) ACS Lifestyle Questions:


-smoker?
-alcohol?
-exercise?
-diet?
-family history?

5) Other questions:
-Is this your first heart attack?

6) STATE THE FRIGGIN DTP & TREATMENT/PROBLEM RESOLUTION

7) Non-pharms:
1) Weight management
-BMI 18.5-25
-Waist circumference (<100 cm males & <90 cm in females)
-Goal of 5-10% weight reduction

2) Physical exercise
-individualized according to patients’ current exercise status
-Goal 30-60 min of moderate activity
3) ICD – Implantable Cardioverter/defibrillator assessment for patients with ongoing LV
dysfunction

4) Address potential psychosocial issues


-Stress management
-Depression screening

5) Risk factor modification:


-Smoking cessation
-Hypertension
-Dyslipidemia
-Obesity
-Sedentary lifestyle
-Stress

8) Monitoring:
1) Efficacy
-Signs and symptoms of ongoing chest pain, ECG changes, serial monitoring of
biomarkers
-Stent thrombosis
-Complications: arrhythmias, HF, pericarditis
2) Safety
-Major and minor bleeding complications, Hbg, platelets
-Clinical signs of bleeding including bloody stools, melena, hematuria, hematemesis,
bruising, and oozing from arterial or venous puncture sites

9) Follow-up

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