This document provides an overview of a case of a 70-year-old African American female presenting with acute respiratory distress and signs of a non-ST elevated myocardial infarction (NSTEMI). It discusses her medical history of cardiovascular risk factors and presents her vital signs, physical exam findings, laboratory and imaging results supporting the diagnosis of NSTEMI. The document then outlines her pharmacological management including antiplatelet therapy, anticoagulation, beta-blockers, ACE inhibitors and statins as well as her appropriate treatment options going forward.
2. Provide brief overview of the patients case
Discuss the disease state, presentation and
signs and symptoms
Explain the non-pharmacological and
pharmacological management options
Display the place in therapy of each medications
Provide a synopsis of a major landmark trial
Discuss the patient’s appropriate management
options
2
3. MAGN is a 70 y/o African American female who developed
acute respiratory distress while in the rehab.The patient
was found to be using her abdominal muscle to breath with
slurry speech, tachypnea, and tachycardia. Code 66 was
called after sedating the patient and she was subsequently
intubated.The patient was then sent to the CCU following
intubation due to development of acute respiratory distress
for more close monitoring.
3
4. PMH: HTN, CAD S/P CABG, PVD, DM, right foot
ulcer, osteomyelitis of the 3rd and 5th right toe.
FH: Insignificant
SH: Insignificant
NKDA
VS: Temp: 96 ° F, BP: 193/120 mm Hg, HR: 146 BPM
RR: 22 BPM, O2 Sat: 66%,Pain scale: 0/10
4
5. Physical Findings:
ABW: 165lb (75kg), Height: 5 feet 4.96 inch, IBW: 56.9 kg, AdJBW: 64.14kg.
Mental status: Speech clear, oriented X 3, responds appropriately to
questions
HEENT: No nasal discharge, intubated, no airway obstruction
Lungs: No wheezing, mild rales bilateral middle, mild rhonchi middle chest
CV: Normal rate, normal rhythm, normal S1, normal S2, no murmur no rub
Extremities: Good pulses in all extremities, no swelling/tenderness in the
extremities, pitting edema half way to knees
GI: Normal BS, soft, no abdominal tenderness.
CXR: Persistent infiltration in the right lower lung zone
EKG: Unremarkable
ECHO: Moderate mitral valve regurgitation, Normal LV Ejection fraction,
Mild concentric left ventricular hypertrophy, Mild aortic valve sclerosis
without stenosis. 5
11. Gradual buildup of cholesterol
and fibrous tissues in the
arteries
Most predominant cause of
unstable ACS is due to the
rupture of the plaque
Plaques that occludes up to 70-
90% of the artery are more likely to
rupture
After the plaque ruptures-
formation of a thrombi is seen
on the plaque
Leading to the clotting cascade
Impairment of the blood flow
and if it is long enough
Ischemic cascade begins and
necrosis of the myocardium is seen11
12. 1 per 3 American has an underlying CVD
Estimated that 2/3 of ACS presents as NSTEMI or
unstable angina
NSTEMI accounts for 1.5 million hospital admission
per year
Percentage of patients with diagnosis of NSTEMI is
increasing dramatically
Sensitive assays for MI, available earlier
pharmacotherapy
12
13. Common
Deprivation of oxygen in the myocardium
Adhesion, activation of plateletsPreventing blood
flowresulting in myocardial ischemia
Rare
Progressive atherosclerosis
Recreational drug use
Inflammation of the arteries
Extrinsic cause
13
14. Modifiable Non-Modifiable
Diabetes Age >65 years
Obesity FHx of CAD
PVD History of Angina
Smoking Previous CVD
Hypertension Recent PCI
Dyslipidemia
Anderson JL, Adams CD, Antman EM, et al. ACC/AHA 2007 guidelines for the management of patients with unstable angina/non-ST-elevation myocardial infarction. J Am
Coll Cardiol. 2007;50:1-157
14
15. Factors Characteristics
Chest pain Squeezing, aching,
burning, sharp pain
Prolonged
discomfort ≥ 30
minutes
Radiation to left
arm or neck is very
common
Diaphoresi
s
Classical sign and
symptom of MI
Factors Characteristics
SOB Secondary to
diminished cardiac
output
Anxiety Displayed females,
elderly and DM
Fourth Heart Sound
(S4)
Present in ischemia
Signs of CHF Pulmonary rales
Lower extremity
edema
S3 gallop
Elevated Jugular
Venous Pressure
Sheridan PJ, Crossman DC. Critical review of unstable angina and non-ST elevation myocardial infarction. Postgrad Med J. 2002;78:717-726
Anderson JL, Adams CD, Antman EM, et al. ACC/AHA 2007 guidelines for the management of patients with unstable angina/non-ST-elevation myocardial infarction.
J Am Coll Cardiol. 2007;50:1-157 15
16. KeyTest Characteristics
ECG ST-Wave depression > 0.5 mm
T-Wave Inversion > 2 mm
ECG may be normal
Serial tests 15-30 minute interval
Anderson JL, Adams CD, Antman EM, et al. ACC/AHA 2007 guidelines for the management of patients with unstable angina/non-ST-elevation
myocardial infarction. J Am Coll Cardiol. 2007;50:1-157
Pharmacotherapy-A Pathophysiologic approach-Depiro’s 7th edition 16
17. Key
Tests
Characteristics
CK-MB Sensitivity- 95%
False Positive can occur
Trauma
Surgery
Cardioversion
Troponin Highly Sensitive and
specific
Confirms Diagnosis of MI
Anderson JL, Adams CD, Antman EM, et al. ACC/AHA 2007 guidelines for the management of patients with unstable angina/non-ST-
elevation myocardial infarction. J Am Coll Cardiol. 2007;50:1-157
Pharmacotherapy-A Pathophysiologic approach-Depiro’s 7th edition
17
18. PROGNOSIS
High risk of morbidity and
death from future events
Rate of death is 4-6 times
higher compared to the
general population
Risk of the mortality and
morbidity depends on the
patients risk factor
GOALS OFTREATMENT
Provide early restoration of
blood flow to the infarct-
related artery to prevent
infarct expansion
Relieve ischemia and pain
Prevention of coronary artery
reocclusion
Relief of ischemic chest
discomfort
Prevention of death and other
complications 18
21. Intranasal Oxygen
Oxygen saturation is < 90%
PCI or CABG
Early treatment for high risk
patients
Consider in patients with
moderate risk
Benefit
Results in fewer MI’s
Less hospital readmissions
for a recurrent MI’s
Less need for an additional
revascularization following
hospitalization
Risk (1:1,000 patients)
Bleeding
Infection
Pain at site of insertion
Damage to the blood vessels
Buildup of blood and fluid in
the pericardium
Much higher in patients who
has
▪ Diabetes
▪ CKD
▪ Age > 75
Bavry DA, Kumbhan DJ, Rassi AN, et al. Benefit of early invasive therapy in acute coronary syndromes: A meta-analysis of contemporary,
randomized clinical trials. J Am Coll Cardiol 2006;48:1319–1325 21
22. PCI -feasible and safe to do
so
Straight, quick, and performed at
low risk
Performed for one or stenosed
vessels
Not for multiple stenosed vessels
▪ Greater risk of restenosis
CABG- for multiple-vessel
stenosis
Greater chance of achieving
full revascularization
Choices can be institution
specific
Easier to proceed with PCI
than to wait for an operation
Gunn J et al. Revascularization for AcuteCoronary Sundromes:PCI or CABG? Heart 2003 89: 967-970
http://0.tqn.com/f/p/440/graphics/images/en/19006.jpg 22
24. MOA Irreversibly inhibits COX-1 and 2 decrease formation of
thrombaxaneA2Inhibits platelet aggregation
Important
Pharmacokinetic
Parameter
Hydrolyzed to salicylate via liver (Active)
Half Life
Parent drug (15-20 minutes)
T1/2= 3 hours (300-600 mg)
T1/2= 5-6 hours ( > 1000 mg)
Elimination via Urine
Clcr <10 mL/minute: Avoid use
Drug Interaction NSAID - diminish the cardioprotective effect of Salicylate
Warfarin- enhance anticoagulant effect of warfarin
(additive)
Heparin and Anti-platelets- increase risk of bleeding
Low dose OK
Lexi Comp Online, Lexi-Drugs Online, Hudson, Ohio: Lexi-Comp, Inc.;2007;November 2nd, 2010
24
25. Guideline
Recommendation
Class 1A
Contraindications Hypersensitivity
Active Bleeding
Severe Bleeding Risk
Dose and Duration
of therapy
162–325 mg PO STAT on hospital day 1
75–162 mg PO QD starting day 2 indefinitely
Pt. undergoing PCI- 162–325 mg PO QD for a minimum of
30 days
Monitoring
Parameter
Clinical signs of bleeding- Melena, hematuria, bloody
stool
Upset GI
Baseline CBC and platelet count
CBC platelet count every 6 months
Anderson JL, AdamsCD,Antman EM, et al.ACC/AHA 2007 guidelines for the management of patients with unstable
angina/non-ST-elevation myocardial infarction. J Am Coll Cardiol. 2007;50:1-157
25
26. Clopidogrel (Plavix) Ticlopidine (Ticlid)
MOA Mediate their antiplatelet effects through a
blockade of ADP P2Y12 receptors on platelets
Important
Pharmacokinetic
Parameters
Metabolized
hepatically (CYP2C19)
T1/2= 6 hours
Elimination
Urine-50%
Feces- 46%
Renal Impairment- No
dose adjustment
Hepatic Metabolism
T1/2= 13 hours
Elimination
Urine-60%
Feces- 23%
Preferred Agent? Ticlopidine Neutropenia
Requires frequent monitoring of CBC
Plavix preferred
Lexi Comp Online, Lexi-Drugs Online, Hudson, Ohio: Lexi-Comp, Inc.;2007;November 2nd, 2010
26
27. Reserved for patients allergic toAspirin
Trials shows that the addition of Plavix to Aspirin is
safe and efficacious
CommitTrial
▪ Adding Plavix to Aspirin prevents 10 major vascular events per
1000 treated
Patients scheduled for CABG
Best not to administer Plavix until procedure is complete
If Plavix is already administered
▪ Hold dose for 5-7 days prior to procedure
Anderson JL, AdamsCD,Antman EM, et al.ACC/AHA 2007 guidelines for the management of patients with unstable
angina/non-ST-elevation myocardial infarction. J Am Coll Cardiol. 2007;50:1-157
27
28. Guideline
Recommendation
Class 1A
Dose and Duration
of therapy
300-600 mg PO STAT on hospital day 1
75 mg PO QD starting day 2
Administer for 9 months
Aspirin allergy-Administer Indefinitely
Post-PCI bare-metal stented patients- 1 month
Post-PCI Sirolimus/Paclitaxel stent-12 month
Contraindications Hypersensitivity
Active Bleeding
Severe Bleeding Risk
Adverse Events Bleeding
TTP
Diarrhea
Rash
Anderson JL, AdamsCD,Antman EM, et al.ACC/AHA 2007 guidelines for the management of patients with unstable
angina/non-ST-elevation myocardial infarction. J Am Coll Cardiol. 2007;50:1-157 28
29. Guideline
Recommendation
Class 1A
Drug Interactions Calcium Channel Blockers- Diminish the therapeutic
effect of Plavix
PPI’s- Reduced efficacy of Plavix
Macrolide’s- Diminish the therapeutic effect of Plavix
Warfarin- Enhance the anticoagulant activity of
warfarin
Monitoring
Parameter
Clinical signs of bleeding- Melena, hematuria, bloody
stool
Upset GI
Baseline CBC and platelet count
CBC platelet count every 6 months
Anderson JL, AdamsCD,Antman EM, et al.ACC/AHA 2007 guidelines for the management of patients with unstable
angina/non-ST-elevation myocardial infarction. J Am Coll Cardiol. 2007;50:1-157
Lexi Comp Online, Lexi-Drugs Online, Hudson, Ohio: Lexi-Comp, Inc.;2007;November 2nd, 2010
29
30. Recommended for HIGH
risk patients
Patient undergoing PCI
Continued or recurrent
ischemia despite
treatment
▪ Aspirin
▪ Plavix
▪ Anticoagulant
Pharmacotherapy-A Pathophysiologic approach-Depiro’s
7th edition
30
32. Guideline
Recommendation
Class I- for patients who are undergoing PCI
Class Iib-without high-risk features or who are not
undergoing PCI
Contraindications Thrombocytopenia
Active Bleeding
Prior stroke
Monitoring
Parameter
Clinical signs of bleeding
A baseline CBC and platelet count
Daily CBC
Platelet count at 4
hours after initiation then daily
Anderson JL, AdamsCD,Antman EM, et al.ACC/AHA 2007 guidelines for the management of patients with unstable angina/non-ST-elevation
myocardial infarction. J Am Coll Cardiol. 2007;50:1-157
32
33. Invasive strategy is
selected
Enoxaparin, UFH,
Bivalirudin, and
fondaparinux
If heparin continue dose
for 48 hours
Enoxaparin or
Fondaparinux
Administer dose for a
maximum of eight days
Conservative strategy
Preferred: Lovenox or
Fondaparinux
Fondaparinux if increase risk
of bleeding
If CABG planned
Fondaparinux
33
37. Indicated for patients with persistent ischemia,
hypertension, and symptoms of acute heart failure
Produce venous and arterial vasodilation
SL followed by IV after 3 doses
NTG in all patients w/o contraindications
SBP <90 mm Hg
HR <50 beats/min
Right ventricular infarction
Sildenafil or vardenafil within 24 hours
Tadalafil within 48 hours
37
38. Nitroglycerin
MOA Primarily reduces cardiac oxygen demand by decreasing preload or
the left ventricular end-diastolic pressure
Pharmacokinetics T1/2= 1-4 minutes
Metabolized via the liver
Drug Interactions Heparin - diminish the anticoagulant effect of Heparin
Phosphodiesterase 5 Inhibitors - enhance the vasodilatory effect
of Nitroglycerin
ADR Tachycardia, Flushing, Hypotension
Monitoring Parameters BP and HR every 2 hours
38
39. Guideline Recommendation Dose
Nitroglycerin Class 1 0.4 mg SL, repeated every 5
minutes × 3 doses
5–10 mcg/min IV infusion
titrated
Continue IV infusion for 24–
48 hours
up to 200 mcg/min until
relief of symptoms or limiting
side-effects
headache
SBP <90 mm Hg
Discontinue if SBP drops
>30 mm Hg below baseline
SBP
39
40. Morphine- Class IIa recommendation
If Nitroglycerin is not sufficient
Produce vasodilation and reduces the heart rate and
your systolic BP to further reduce Myocardial oxygen
demand
Alternative to nitroglycerin when nitroglycerin is
contraindicated
40
41. MOA Produce vasodilation and reductions in HR through
increased vagal tone and systolic BP to further reduce
myocardial oxygen demand
Pharmacokinetic Hepatic metabolism
F= 17-33% PO
T1/2= 2-4 hours
Excretion
Urine- 2 to 12%
Feces- 10%
CrCl 10-50 mL/min- Administer 75% of the normal dose
CrCl< 10 mL/min- Administer 50% of the normal dose
Drug Interactions Alcohol- enhance CNS depression of alcohol
Thiazide diuretics- Enhance the effect of orthostatic HOTN
Succinylcholine- increase bradycardic effect of morphine
41
42. Dose 2-5 mg IV bolus dose
Can be repeated every 5-30 minutes PRN
Contraindications Hypotension
Respiratory Depression
Confusion
ADE Hypotension
Respiratory Depression
Monitoring
Parameters
Blood pressure and respiratory rate 5 minutes
after each bolus dose
42
43. Reduces the risk of recurrent ischemia, infarct size, risk of
reinfarction in the hours and days following MI
Selective Beta-Blockers
Continue indefinitely
Do not use in patients who are hemodynamically unstable
IV route preferred over PO
Persistent Ischemia
Hypertension
Tachycardia
Goal of resting heart rate= 50-60 BPM
43
44. Metoprolol Propranolol Atenolol
MOA Selectively inhibits B1- receptorReduces heart rate,
myocardial contractility and BP Decreasing oxygen demand
Pharmacokinetics Extensively
metabolized via the
liver
F=50% Oral
T1/2=3-8 hours
Renal or hepatic
failure- No dose
adjust
Hepatic via
CYP2D6, and
CYP1A2
T1/2
Immediate
release-3-6 hours
Extended
Release-8-10 hours
Hepatically
metabolized
T1/2 Adults=6-7
hrs
Elimination
50% urine
40% urine
Adults w/ ESRD
T1/2=15-35 hrs
CrCl <15-35= Max
50mg/day
CrCl <15mL/min=
Max 50mg QOD 44
46. Metoprolol Propranolol Atenolol
ADR Hypotension
Bradycardia
Heart block
Monitoring
Parameters
BP, RR, HR
12-lead ECG
Clinical signs of heart failure every 5 minutes during
bolus intravenous dosing
Every shift during oral administration during
Hospitalization, then BP and HR every 6 months
following hospital discharge
46
47. Indication for use
Patients with continuing or recurrent ischemic symptoms despite Nitrate and
Beta-Blocker therapy
Contraindication to Beta-Blocker’s
Preferred over Beta-Blocker
cocaine induced ACS
Prinzmetal angina
Reduces coronary spasm by relaxing the smooth muscle in the arteries
DHP’s not so much favored
No effect on AV node No effect on heart rate
Can increase myocardial ischemia
Non-DHP’s Preferred
Holds anti-ischemic effect by reducing contractility and the conduction AV
node decrease heart rate
47
48. Diltiazem Verapamil
MOA Prevent the entry of Ca2+ into the vascular smooth
muscle and the myocardium Relaxing the vascular
smooth muscle and increase O2 delivery
Pharmacokinetics Hepatic Metabolism
First Pass effect
F= 40 % PO
T1/2
IR= 3-4.5 hours
XR= 6-9 hours
Renal Impairment= No
Dose adjustment
necessary
Hepatic Metabolism
First Pass effect
F= 35 % PO
T1/2= 3-7 hours
Hepatic
Impairment= 14-16 hours
Elimination= 70% Urine;
20% Feces.
Renal Impairment= Use
low dose
Hepatic Impairment=
Decrease dose by 70%
48
49. Diltiazem Verapamil
Drug Interactions Antifungal= Decrease metabolism of CCB
Atorvastatin= Increase serum level of both
Atorvastatin and CCB
Calcium Salts= Diminish the therapeutic effect of CCB
ADR Hypotension
Bradycardia
Heart Block
Heart Failure
Gingival Hyperplasia
Contraindications Pulmonary Edema
SBP < 100 mm HG
PR interval >0.25 sec on ECG
2nd or 3rd degree AV block
HR <60 BPM 49
50. Diltiazem Verapamil
Recommended dose 120-360 mg SR QD 180-480 mg SR QD
Monitoring
parameters
BP and HR
Signs of heart failure on every shift
during hospitalization
Then assess every 6 months for similar
signs following discharge
Dental exam and cleaning teeth every 6
month
50
51. Should be used in all
patients with
Left ventricular systolic
dysfunction
▪ EF <40%
Heart Failure
HTN
Cardiogenic Shock
Started w/in 24 hours
following post-stabilization
Shown to reduce
▪ Mortality
▪ Decrease reinfarction
▪ Prevent development of
heart failure
Benefit: Ability to prevent
cardiac remodeling
BP Optimal Goal: 125/75 mm
Hg
Ideally < 130/85 mm Hg 51
53. Data portrays the benefit of Statin in CAD
Low Mortality
Less incidence of stroke
Use statin in all patients withACS, regardless of
LDL cholesterol levels
Goal LDL < 100 mg/dL
Preferred <70 mg/dL
53
55. Cardiac Rehabillation
Increase functional capacity
Aerobic and weight-bearing
exercise 4 to 5 times per
week for >30 minutes
PLUS
Continue Antiplatelet
therapy
▪ Indefinitely
▪ 1° option-Aspirin PLUS Plavix
▪ 2° option-Clopidogrel alone
PLUS
Continue Beta-Blockers
▪ Indefinitely
▪ Metoprolol,Atenolol,
Propranolol
PLUS
Statins
▪ Indefinitely
Adjunct
ACE/ARB
▪ Patients who has EF <40%
▪ Heart Failure
▪ Ongoing Ischemia
55
56. Inpatient follow up with in 1-2 weeks of
discharge
Monitor Lipids at least every 6 months
LDL < 70mg/dL
Control and monitor HTN
<130/80 mm Hg
56
57. Purpose: To evaluate the efficacy and safety of clopidogrel when used along with
aspirin in patients without ST-segment elevation, because it was seen that these
patient has a very high rates of major vascular events
Study Design: Randomized, Double blind, Placebo-Controlled trial.
Methods:
12,562 patients were randomized
6,259 patients received clopidogrel 300 mg followed by 75 mg PLUS
aspirin post 24 hour onset of symptoms
6,303 patients received a placebo PLUS aspirin post 24 hour onset of
symptoms
57
58. Primary endpoint: Assess the
composite of death that
occurred from cardiovascular
causes, nonfatal myocardial
infarction, or stroke
Conclusion: Clopidogrel has
beneficial effects in patients
with acute coronary syndromes
without ST-segment elevation,
in addition also has a risk of
major bleeding among patients
treated with clopidogrel
Result
58
59. Fish Oil
ω- 3 Fatty Acids
▪ EPA and DHA-Abundant in fish
Diet high in EPA & DHA or supplementation of fish oil
▪ Reduces the risk of CV mortality,
▪ Reinfarction
▪ Stroke
Three 1 gram fish oil capsule should be consumed per
daywill provide 1 gram of ω- 3 Fatty Acid
Grupo Italiano per lo Studio dela Sopravvivenza nell’infarcto miocardio.Dietary Supplementation with n-3 fatty acids and
Vitamin E after myocardial infarction: Results of GISSI- Prevenzione trial. Lancet 1999;354:447-455
59
60. Mainstays of therapy include risk stratification, and early
angiography and revascularization with either PCI or
CABG for patients with NSTE ACS at high risk for MI and
death
Pharmacotherapy for acute treatment includes SL NTG,
antiplatelets, anticoagulants and B-blockers
Ensuring selection of evidence-based therapies in all
patients without contraindications results in lower
mortality
Pharmacists have an important role in encouraging
patient adherence and persistence to pharmacotherapy
60
61. Severe respiratory distress
Slurry speech and was wheezing
Low O2 saturation (66%)
Tachypneic and tachycardia (HR= 146 BPM)
Elevated blood pressure (193/120 mm Hg)
Lower extremity edema
Troponin level: 5.5 ng/mL
CK-MB: 43.5 U/L
Low Hgb (9.3 g/dL) and Hct (28%)
61
62. Previous history of CABG
It is possible that thrombi formed, occluding the
coronary blood flow and resulting in myocardial
ischemia
Other significant risk hypertension, diabetes
mellitus and being elderly
62
63. Administer oxygen
TIMI RISK: 5-Moderate
Patient is greater than 65 years
old (71)
She has as known history of
CAD
The patient has been taking
aspirin for the last 7 days
ECG revealed ST- segment
depression
The patient has positive
biochemical markers of
infarction as seen by the
troponin level and the CK-MB
level
Does not need to go for any sort
of early coronary angiography
and revascularization
ECHO revealed no stenosis
63
64. Aspirin 325 mg as a single dose
followed by aspirin 81 mg
indefinitely
Clopidogrel (Plavix) 300-600mg via
NG-Tube as a loading dose on day 1
followed by 75 mg via NG-Tube once
daily
atorvastatin (Lipitor) 10-80 mg/day
orally
Metoprolol (Lopressor) 5 mg slow IV
push (Over 1-2 minutes), repeated
every five minutes for a total of 15
mg followed in 15-30 minutes by 25-
30 mg by mouth Q6H
64
65. Bavry DA, Kumbhan DJ, RassiAN, et al. Benefit of early invasive therapy in acute
coronary syndromes: A meta-analysis of contemporary, randomized clinical trials.
Am Coll Cardiol 2006;48:1319–1325
Pharmacotherapy-A Pathophysiologic approach-Depiro’s 7th edition
Anderson JL,Adams CD,Antman EM, et al.ACC/AHA 2007 guidelines for the
management of patients with unstable angina/non-ST-elevation myocardial
infarction. J Am Coll Cardiol. 2007;50:1-157
Lexi Comp Online, Lexi-Drugs Online, Hudson, Ohio: Lexi-Comp, Inc.;2007;October
2010.
65
parts of the spectrum of clinical manifestations of acute coronary syndrome (ACS)
NSTE MI differs from unstable angina in that ischemia is severe
enough to produce myocardial necrosis, resulting in the release of a
detectable amount of biochemical markersIschemia produces myocardial necrosis
Release large amount of biochemical markers into the blood stream
Troponin I or T
CK-MB
, mainly troponin I or T,
and creatine kinase myocardial band (CK MB) from the necrotic
myocytes into the bloodstream
IN STEMI you have complete occlusion of the artery.
End with “Leading to an imbalance in the myocardial oxygen demand and supply”
The red are the key risk factors and diagnostic factors when performing H/P
CBC
Measure Hgb and Hct
Secondary cause of NSTEMI
Acute blood loss
Anemia
Assess thrombocytopenia
estimate bleeding risk
BUN and Scr
Dose renally adjusted drugs
LFTs
For drugs that undergo hepatic metabolism
CXR
R/O pneumonia, pneumothorax, and esophageal rupture
Can mimic cardiac ischemia
P2Y12= Purinergic receptor subtype 12
The ACC/AHA guidelines give no preference for the use of UFH, enoxaparin, fondaparinux, or bivalirudin in patients in when an invasive strategy is selected, but state that the evidence for the use of the first two is stronger
NTG= Nitroglycerin
NO Monitoring parameter noted
The exception of alpha 2 agonist interaction are: Apraclonodine,Brimonidine
Secondary endpoint: Severe ischemia, heart failure, and the need for revascularization