Transcript Document

Acute Coronary
Syndromes
By: Dr azimian
The motion of the
heart is best
understood by God
alone.
- Harvey
Time lost life lost
Definitions
• Acute coronary syndrome is
defined as myocardial ischemia
due to myocardial infarction
(NSTEMI or STEMI) or
unstable angina or Sudden
cardiac death
•
23.8% of admissions to resus. unit for chest
pain/acs related (stats 1Jan 2009 – 28 Feb
2009) 150/628 entries.
• In US – 1.56 million admissions for ACS –
669 000 for unstable angina, 896 000 for MI
• Higher prevelance for NSTEMI.
• CAD is a continuum of disease….
• Angina -> unstable angina -> AMI -> sudden cardiac death
• Acute coronary syndrome encompasses unstable angina,
NSTEMI, STEMI
• Stable angina – transient episodic chest pain d/t myocardial
ischaemia, reproducible, frequency constant over
time.usually relieved with rest/NTG.
• Classification of angina – Canadian Cardiovascular
Society classification.
Canadian Cardiovascular Association Classification of Angina
CLASS 1
NO PAIN WITH ORDINARY PHYSICAL ACTIVITY
CLASS 2
SLIGHT LIMITATION OF PHYSICAL ACTIVITY –
PAIN OCCURS WITH WALKING, CLIMBING
STAIRS,STRESS
CLASS 3
SEVERE LIMITATION OF DAILY ACTIVITY – PAIN
OCCURS ON MINIMAL EXERTION
CLASS 4
UNABLE TO CONDUCT ANY ACTIVITY WITHOUT
PAIN, PAIN AT REST
• WHY IS IT IMPORTANT TO
RECOGNISE PATIENTS WITH
UNSTABLE ANGINA??
• 5 -17% suffer an MI within a week
after admission.
• 3 -15% die within a year.
• UNSTABLE ANGINA –
• Pain occurring at rest – duration > 20min, within
one week of first visit
• New onset angina – ~ Class 2 severity, onset with
last 2 months
• Worsening of chest pain – increase by at least 1
class, increases in frequency, duration
• Angina becoming resistance to drugs that
previously gave good control.
• NB! ECG – normal, ST depression(>0.5mm), T
wave changes
Pathophysiology of ACS
• Plaque rupture and subsequent formation of
thrombus – this can be either occlusive or nonocclusive (STEMI, NSTEMI, USA)
• Vasospasm such as that seen in Prinzmetal’s
angina, cocaine use (STEMI, NSTEMI, USA)
• Progression of obstructive coronary
atherosclerotic disease (USA)
• In-stent thrombosis (early post PCI)
• In-stent restenosis (late post PCI
• Poor surgical technique (post CABG)
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ATHEROSCLEROSIS
START
END
Pathophysiology of ACS
• Acute coronary syndromes can also be due
to secondary causes
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Thyrotoxicosis
Anemia
Tachycardia
Hypotension
Hypoxemia
Aterial inflammation (infection, arteritis)
‫تاکی کاردی‬
‫هیپرتانسیون‬
‫سیگار‬
‫عفونت‬
‫تب‬
‫استرس‬
‫فعالیت‬
‫یبوست‬
‫پرخوری‬
‫درد‬
‫هیپوولمیا‬
‫گشادی عروق‬
‫تنگ کننده های عروق‬
‫‪Supply‬‬
‫‪Demand‬‬
‫‪O2‬‬
Assesment
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1.
2.
3.
4.
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6.
Hx
Physical Exam
EKG
Exercise EKG
Thallium Scan
Coronary Angiography
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7.
Cardiac Enzymes
Diagnosis
• Dx of acute coronary syndrome is based on
history, physical exam, ECG, cardiac enzymes
• Patients can then be divided into several groups
– Non-cardiac chest pain (i.e., Gastrointestinal,
musculoskeletal, pulmonary embolus)
– Stable angina
– Unstable angina
– Myocardial infarction (STEMI or NSTEMI)
– Other cardiac causes of chest pain (i.e., aortic
dissection, pericarditis)
ECG for acute chest pain
• Not a perfect diagnostic tool (specificity-sensitivity)
– 10% of new ST-elevations are not caused by MI
– Up to 50% of MI patients present with normal or
inconclusive ECG (e.g. previous MI, LV hypertrophy)
– 2% of patients with normal ECG will develop MI
• 15-lead ECG for right ventricular or posterior MI
• Request previous ECG for comparison
• Serial ECGs (and continuous ST-monitoring?) improve
sensitivity
Ischemia ,Acute Injury, Infarction
Ischemia
•T wave inversion, ST segment depression
•Acute injury: ST segment elevation
•Dead tissue: Q wave
Gender Differences in MI
Females, when compared to males:
-present with MI later in life
-have poorer prognosis and high morbidity
-are 2x as likely to die in the first weeks
-are more likely to die from the first MI
-have higher rates of unrecognized MI
-NSTEMI MI vs STEMI
The perfect marker
• Marker for myocardial necrosis, and also for cardiac
ischemia
• Linear relationship between blood levels and extent of
myocardial injury (and prognosis)
• 100% sensitive
• 100% specific
• Immediate increase (+ constant blood level for hours to
days)
• Test kits : reliable, rapid, universally available and
inexpensive
What about troponin T and I ?
• Very high sensitivity for myocardial necrosis
• Related to prognosis
BUT
• Not 100% specific for atherosclerotic coronary
artery disease
– (myocarditis, cardiomyopathy, myocardial
contusion, renal failure, auto-immune diseases, ...)
• Up to 6 hours before raised blood levels
no early MI diagnosis possible
• Raised blood levels for many days
troublesome diagnosis of re-infarction
TROPONINS T/I
• Troponin T vs I –
• both equivalent in diagnostic and prognostic abilities (
except in renal failure – Trop T less sensitive)
• Elevation ~ 2hrs to 12hrs
• ~30 – 40% of ACS patients without ST elevation – had
normal CKMB but elevated troponins on presentation
• Meta-analysis (Heindereich et al) – odds of death
increased 3 to 8 fold with positive troponin
Role for myoglobin ?
• Initial elevation : 1 to 4h after onset
better early marker than troponins
BUT : early myoglobin is less sensitive and
less specific (due to skeletal muscle
trauma) than late troponin
decisions mainly based on clinical
skills, ECG and late troponin (except
rarely for reperfusion therapy)
• Duration of elevation : 24 – 48h
useful for re-infarction diagnosis
Role for CK-MB ?
• Initial elevation comparable with troponins
• Less sensitive than troponins
• High specificity (comparable with troponins)
• Rapid rise and fall (instead of gradual fall for
troponins) allowing more accurate estimation
of MI extent
MYOGLOBIN
• Rapid release within 2 hours
• Not cardiac specific
• Rule out for NSTEMI rather than rule in.
CKMB
Used in conjunction with troponins
Useful in diagnosing re-infarction
Pre-test Probability
• In the absence of abnormal findings on physical
exam, ECG, or enzymes, the pre-test probability
of acute coronary syndrome must be determined
by the clinician
• A good history is crucial (is the chest pain typical
or atypical; what are the associated symptoms)
• Determination of risk factors is also crucial (male,
age >55, smoking, DM, HTN, FamHx,
hyperlipidemia, known CAD)
Angiogram pre/post PTCA
‫در اكوكارديوگرافي تجمع مايع در حفره‬
‫پريكارد مشاهده مي شود ‪.‬‬
imaging
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Treatment of ACS; Aspirin
• Aspirin is an antiplatelet agent that initiates
the irreversible inhibition of cyclooxygenase,
thereby preventing platelet production of
thromboxane A2 and decreasing platelet
aggregation
• Administration of ASA in ACS reduces
cardiac endpoints
ACC/AHA Guidelines for
Aspirin Therapy
• Aspirin should be given in a dose of 75-325
mg/day to all patients with ACS unless
there is a contraindication (in which case,
clopidogrel should be given)
• Newest guidline: clopidogrel+ asprin
Treatment of ACS; Nitrates
• Nitroglycerin is considered a cornerstone of antianginal therapy, despite little objective evidence
for its benefit
• Benefit is thought to occur via reduction in
myocardial O2 demand secondary to venodilation
induced reduction in preload as well as coronary
vasodilation and afterload reduction
• Titrate to relief of chest pain; chest pain = death
of myocardial cells
• No documented mortality benefit
Side/Adverse Effects
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Vascular HA (may be severe)
Hypotension (may be marked)
Tachycardia
Palpitations
Treatment of ACS; Beta Blockers
• Beta Blockers reduce myocardial oxygen
demand by reducing heart rate, contractility,
and ventricular wall tension
• Administration of beta blockers in ACS
reduces cardiac endpoints
Beta Blocker Trials
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HINT (metoprolol)
Beta Blocker Heart Attack Trial (propranolol)
Esmolol vs. placebo
Carvedilol vs. placebo
Propranolol vs. placebo
Overall, treatment with beta blockers reduces
primary endpoints when compared to placebo
AHA/ACC Guidelines for Beta
Blocker Therapy
• Intravenous beta blockers should be used
initially in all patients (without
contraindication) followed by oral beta
blockers with the goal being decrease in
heart rate to 60 beats per minute
• A combination of beta blockers and nitrates
can be viewed as first line therapy in all
patients with ACS
Treatment of ACS; Heparin
• Heparin (unfractionated heparin or UFH)
has traditionally been the mainstay of
therapy in acute coronary syndromes as its
efficacy has been documented in several
large, randomized trials
Heparin Trials
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Heparin/Atenolol Trial
The Canadian Heparin/Aspirin Trial
The RISC Trial
Overall, UFH therapy generally results in an
important clinical benefit when compared to
placebo. It is more effective when given in
continuous infusion rather than intermittent
boluses
Treatment of ACS; LMWH
• More recent studies indicate that low
molecular weight heparin is also effective in
the reduction of end points such as
myocardial infarction or death
• Some studies report that LMWH, when
used in combination with ASA, may be
superior to continuous infusion of Heparin
ACC/AHA Guidelines for
Heparin Therapy
• All patients with acute coronary syndromes
should be treated with a combination of
ASA (325 mg/day) and heparin (bolus
followed by continuous infusion with goal
of PTT 1-2.5X control) or ASA and low
molecular weight heparin unless one of the
drugs is contraindicated
Treatment of ACS; ACE-I
• The best documented mechanism by which
these agents act is to reduce ventricular
remodeling over days to weeks after
myocardial damage. However, there is data
that a mortality benefit exists when these
agents are used early in the course of ACS
• Administration of ACE-I in ACS reduces
cardiac endpoints
AHA/ACC Guidelines for ACE-I
Therapy
• ACE-I should be administered to all
patients in the first 24 hours of ACS
provided hypotension and other clear cut
contraindications are absent
Treatment of ACS; Statins
• Statins may be of benefit in ACS
• Possible mechanisms include plaque
stabilization, reversal of endothelial
dysfunction, decreased thrombogenicity,
and reduction of inflammation
TIMI Risk Score
Thrombolysis In Myocardial Infarction',
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Age >65 yrs
Daily ASA Therapy (>7 days prior to event)
Symptoms of Unstable Angina
Documented CAD (stenosis > 50%)
3 or more traditional cardiac risk factors
Elevated cardiac enzymes
ECG changes
TIMI Risk Score
• Score of 3 or less = low risk
• Score of 4-5 = intermediate risk
• Score of 6-7 = high risk
Treatment of ACS; Clopidogrel
• Clopidogrel is a potent antiplatelet agent
• It should be administered to all patients who
cannot take ASA
• The CURE trial suggests a benefit to adding
Clopidogrel to ASA/Heparin in patients
going for PCI
• Give 300 mg loading dose followed by 75
mg/day
AHA/ACC Guidelines for
Clopidogrel
• Clopidogrel should be administered to patients
who cannot take ASA because of hypersensitivity
or gastrointestinal intolerance
• In hospitalized patients in whom an early,
noninterventional approach is planned,
clopidogrel should be added to ASA as soon as
possible on admission and administered for at
least 1 month and up to 9 months. Do not use
clopidogrel if there is any possibility patient
may be candidate for CABG
Treatment of ACS; Emergent
Revascularization
• In the setting of STEMI primary PCI is
associated with better outcomes than
thrombolysis
• Emergent PCI is also indicated in the setting
of a new LBBB
AHA/ACC Guidelines for
Primary PCI
• Primary PCI is indicated as an alternative to
thrombolysis when the following criteria are met:
– STEMI or new LBBB
– Can undergo PCI within 12 hours of the onset of
symptoms
– The MD doing the intervention does more than 75
PCI’s/yr
– The procedure is done in a center that does more than
200 PCI’s/yr and has surgical backup
Conclusions; Approach to Chest
Discomfort
• Good History and Physical (note time and
duration of symptoms)
• Careful evaluation of ECG (compare to
previous when possible)
• Check Cardiac Enzymes
• Monitor on Telemetry
• Oxygen
Acute Angina Treatment
Goal: Enhance 02 supply to myocardium:
M- Morphine for pain
O- Oxygen 4-6L as ordered
N- NTG sublingual, repeat q5 minutes x3
A- Aspirin to prevent platelet aggregation
Patient education
Lifestyle modifications for controllable risk
factors. Support groups are helpful,
Example: Weight watchers,
Smoke-enders, stress workshops, cardiac
rehabilitation. Supply patients with
information, name of contact person and
phone numbers
Identify precipitating factors for Anginal pain
Medication compliance
Nursing Interventions
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Obtain EKGs
Monitor mentation
Assess heart sounds
Assess lungs
Assess peripheral circulation/skin
Assess urinary output
Assess GI function
Assess pain
Nursing Interventions
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Activity
Safety
Reduce anxiety
Patient Education
Nutrition
‫زندگی چون گل سرخیست‬
‫پرازخارو پراز برگ وپراز عطر لطیف‬
‫یادمان باشد اگر گل چیدیم‬
‫عطروبرگ وگل وخار‬
‫همه همسایه دیوار به دیوار همند‬
‫دکترعلی شریعتی‬