Download coronary artery disease

Acute Coronary Syndrome
The usual cause of an acute coronary syndrome
is the rupture of an atherosclerotic plaque
(Phalen and Aehlert, 2006, p. 61)
Plaque Rupture
Classifications
1.ST-Segment Elevation Myocardial Infarction
2. Unstable Angina and Non–ST Elevation
Myocardial Infarction
3. Stable Ischemic Heart Disease
Acute Coronary Syndrome
Unstable Angina
Cause:
Thrombus partially or intermittently occludes
the coronary artery
Diagnostic Findings:
ST-segment depression or T-wave inversion
Normal Cardiac Markers
(Overbaugh, 2009, p. 46)
NSTEMI
Cause:
Thrombus partially or intermittently the
occludes coronary artery
Diagnostic Findings:
ST-segment depression or T-wave inversion
Elevated Cardiac biomarkers
(Overbaugh, 2009, p. 46)
Clinical Indicators of Increased Risk in
UA/NSTEMI
Approach to the Patient with Chest
Pain
• CAUSES OF ACUTE CHEST PAIN
• DIAGNOSTIC CONSIDERATIONS
• IMMEDIATE MANAGEMENT
ACUTE CHEST PAIN
• Acute chest pain is one of the most common
reasons for presentation to the emergency
department
• 15% to 25% of patients with acute chest pain
actually have ACS
• The diagnosis of ACS is missed in approximately
2% of patients
• Mortality for patients with acute myocardial
infarction (MI) who are mistakenly discharged
from the ED increases twofold
CAUSES OF ACUTE CHEST PAIN
• Myocardial Ischemia or Infarction,
• Pericardial Disease,
• Vascular Disease,
• Pulmonary Conditions,
• Gastrointestinal Conditions,
• Musculoskeletal and Other Causes,
Ischemia
May occur as a result of either or both of the following:
Demand Ischemia: Increased myocardial O2 demand
(Anemia, hypoxemia, coronary artery narrowing due to a
thrombus, vasospasm, or rapid progression of atherosclerosis)
Supply Ischemia: Reduced myocardial O2 supply
(Exercise, smoking, heavy meals, fever, HF, tachydysrhythmias,
OCM, cocaine, amphetamines, emotional stress, hypertension,
cold weather, aortic stenosis, pheochromocytoma,
thyrotoxicosis)
Injury
Ischemia prolonged more than just a few minutes
results in myocardial injury.
Injured myocardial cells are still alive but will infarct if
the ischemia is not quickly corrected
ECG Changes: ST-segment elevation
(Injured myocardial cells do not depolarize
completely, remaining electrically more positive
than the uninjured areas surrounding them)
Infarction
A myocardial infarction occurs when blood flow to the
heart muscle stops or is suddenly decreased long
enough to cause cell death
Infarcted cells are without function and cannot respond
to electrical stimulus or provide any mechanical
function
(Thalen and Aehlert, 2006, p, 67)
ECG Changes: ST-segment elevation,
T-wave inversion, abnormal Q waves
Initial Assessment
• Evaluation of the patient with acute
chest pain
• Hemodynamic instability
• A 12-lead electrocardiogram (ECG)
Initial Assessment
• History
• Physical Examination
• Electrocardiography
• Chest Radiography
• Biomarkers
Physical Examination
• Vital signs,
• Examination of the peripheral vessels
– Bruits or absent pulses
• Identify potential precipitating causes
– Uncontrolled hypertension, anemia, hyperthriodism
• Important comorbid conditions
– Chronic obstructive pulmonary disease
• Evidence of hemodynamic complications
– Congestive heart failure,
– New mitral regurgitation, hypotension
Electrocardiography
• 10 minutes after
presentation
• New persistent or transient
ST-segment abnormalities
(≥0.1 mV) and T inversion
(≥0.2 mV)
• During a symptomatic
episode at rest and resolve
Chest Radiography
• Usually non-diagnostic
• Pulmonary edema (ischemia-induced
diastolic or systolic dysfunction)
• Pneumothorax, Pneumonia
Biomarkers
• A cardiac troponins (T or I; cTnT or
cTnI)
• Creatine kinase MB isoenzyme (CKMB, less sensitive)
Biomarkers for Evaluation of Patients with STEMI
Troponins_True myocardial damage
• Myocarditis,
• Myocardial contusion,
• Cardioversion or defibrillation,
• Left ventricular strain from congestive heart
failure
• Hypertensive crisis,
• Extreme exercise,
• Right ventricular strain from pulmonary embolus,
• Other causes of acute pulmonary hypertension
Troponins_mechanism remains unclear
• Patients with renal disease
• Severe sepsis
Troponins
• Blood should be obtained for testing at hospital
presentation, and at 6 to 9 hours
• A normal reference values 0.01 to 0.07 ng/ml
• Ultrasensitive assays <0.001 ng/ml or <1 pg/ml
• Serial sampling up to 12 hours after presentation
%90 to %95
• 3 hours of the onset of chest pain 80% to 85%
Creatine Kinase MB Isoenzyme
lack of specificity
•
Found in
–
–
–
–
Skeletal muscle,
Tongue,
Diaphragm,
Small intestine, uterus, and prostate
–
–
–
–
Muscular dystrophy
High-performance athletics
Rhabdomyolysis
Alcohol abuse or trauma vs
• Eleveted
• Shorter half-life
– Useful for gauging the timing of an MI
– Diagnosing reinfarction
Other Markers
•
•
•
•
•
•
•
•
Serum myoglobin
heart-type fatty acid binding protein
C-reactive protein
serum amyloid A,
myeloperoxidase
interleukin-6
D-dimer
B-type natriuretic peptides
Acute Coronary Syndrome
Likelihood That Signs and Symptoms
ST Elevation Myocardial
Infarction
Assessment of Reperfusion Options
for STEMI Patients
Step 1: Assess time and risk.
• Time since onset of symptoms
• Risk of STEMI
• Risk of fibrinolysis
• Time required for transport to a skilled
PCI laboratory
A
C
B
D
An invasive strategy is generally preferred if
• Skilled PCI laboratory is available with surgical backup
– Skilled PCI laboratory is available, defined by
– Medical contact-to-balloon or door-to-balloon less than
90 min
• High risk from STEMI
– Cardiogenic shock
– Killip class ≥ 3
•
Contraindications to fibrinolysis,
•
Late presentation
– Symptom onset was more than 3 hr ago
Hemodynamic Classifications of Patients with
Acute Myocardial Infarction
• Based on Clinical Examination
I. Rales and S3 absent
II. Crackles, S3 gallop, elevated jugular
venous pressure
III. Frank pulmonary edema
IV. Shock
Modified from Killip T, Kimball J: Treatment of myocardial infarction in a
coronary care unit. A two year experience with 250 patients. Am J Cardiol
20:457, 1967
Hemodynamic Classifications of Patients with
Acute Myocardial Infarction
• Based on Invasive Monitoring
I.
Normal hemodynamics; PCWP < 18 mm Hg, CI > 2.2
II.
Pulmonary congestion; PCWP > 18 mm Hg, CI > 2.2
III. Peripheral hypoperfusion; PCWP < 18 mm Hg, CI < 2.2
IV. Pulmonary congestion and peripheral hypoperfusion;
PCWP > 18 mm Hg, CI < 2.2
Modified from Forrester J, Diamond G, Chatterjee K, et al: Medical therapy of
acute myocardial infarction by the application of hemodynamic subsets. N Engl J
Med 295:1356, 1976.
Fibrinolysis is generally preferred if
• Delay to invasive strategy:
– Prolonged transport
– Medical contact-to-balloon or door-to-balloon more
than 90 min
• Early presentation (≤3 hr from symptom onset and
delay to invasive strategy; see below)
•
Invasive strategy is not an option:
– Catheterization laboratory occupied or not available
– Vascular access difficulties
– Lack of access to a skilled PCI laboratory
Approved Fibrinolytic Agents
Reperfusion Options for STEMI Patients
Post Myocardial
Infarction
Complications
Post MI Complications
Arrhythmias
Heart Failure
Cardiac Arrest
Mitral Insufficiencies
Cardiac Muscle
Dysfunction
Pericarditis
Cardiogenic Shock
Thromboembolism
GI Complaints
(Haworth and Pratowski, 2000 p. 90)
Post MI: Common Arrhythmias
Atrial Fibrillation
Premature Ventricular Contractions
Ventricular Tachycardia
Accelerated Idioventricular Rhythm
Ventricular Fibrillation
Atrioventricular Block
(Haworth and Pratowski, 2000 p. 91)
Unstable Angina and
Non–ST Elevation Myocardial
Infarction
Unstable Angina
Cause:
Thrombus partially or intermittently occludes
the coronary artery
Diagnostic Findings:
ST-segment depression or T-wave inversion
Normal Cardiac Markers
(Overbaugh, 2009, p. 46)
NSTEMI
Cause:
Thrombus partially or intermittently the
occludes coronary artery
Diagnostic Findings:
ST-segment depression or T-wave inversion
Elevated Cardiac biomarkers
(Overbaugh, 2009, p. 46)
Clinical Indicators of Increased Risk in
UA/NSTEMI
Treatment
UA
• Oxygen to
maintain O2 sat
> 90%
• NTG or MSO4
to control pain
• BB’s, CCB’s,
ACEI’s, statins,
clopidogrel,
unfractionated
heparin or
LMWH,
glycoprotein
IIb/IIIa
inhibitors
NSTEMI
Same as UA plus:
 Cardiac cath &
possible PCI for
patients with
ongoing CP,
hemodynamic
instability, or
increased risk of
worsening clinical
condition
General Treatment Measures
• Antiplatelet Therapy
• Anticoagulant Therapy
• Control of Cardiac Pain
–
–
–
–
Analgesics
Nitrates
Beta Blockers
Oxygen
• Limitation of Infarct Size
– Early reperfusion
– Reduction of myocardial energy demand
Antiplatelet Therapy
• Aspirin
– 162-325 mg, nonenteric-coated ASA to
be chew
– maintenance of 75-162 mg daily
Antiplatelet Therapy
• Clopidogrel 300600 mg loading
75 mg/day
• Prasugrel oral
loading dose of
60 mg and 10 mg
orally daily
• Ticagrelor a loading
dose of 180 mg and
90 mg twice daily
Anticoagulant Therapy
• Heparin activated
partial
thromboplastin time
(aPTT) target of 1.5
to 2 times that of
control
• Low-Molecular-
Weight Heparins
• Bivalirudin (STMI)
Control of Cardiac Pain
– Analgesics
• meperidine, pentazocine, and morphine
• Morphine 2 to 8 mg/ 5 to 15 minutes --until the
pain is relieved or there is evident toxicity
– Nitrates
• sublingual nitrates, intravenous nitroglycerin
• systolic pressure <90 mm Hg
• right ventricular infarction
Control of Cardiac Pain
– Beta Blockers
• Killip class II or higher (precipitating
cardiogenic shock)
• Patients with heart failure (rales > 10 cm up from diaphragm),
•
hypotension (blood pressure < 90 mm Hg),
•
bradycardia (heart rate < 60 beats/min),
Control of Cardiac Pain
• Oxygen
– pulse oximetry
– Sao2 < 90%
– 2 to 4 liters/min of 100% oxygen
– 6 to 12 hours
Limitation of Infarct Size
• Early reperfusion
• Routine Measures for Infarct Size
Limitation
– Beta blocker (HR 50-70)
– Inhibitors of the renin-angiotensinaldosterone system (RAAS)
– Arterial oxygenation
Limitation of Infarct Size
•
Angiotensin-converting enzyme (ACE) inhibitor
– Start ACE inhibitor orally in patients with pulmonary
congestion or LVEF <40%
– if the following are absent: hypotension (SBP
<100 mm Hg or <30 mm Hg below baseline) or known
contraindications to this class of medications.
•
Angiotensin receptor blocker (ARB)
– Start ARB orally in patients who are intolerant of ACE
inhibitors and with either clinical or radiologic signs of
heart failure or LVEF <40%
Long term therapies
•
Risk factor control, particularly smoking, must be stringent.
•
Antiplatelet therapy is indicated indefinitely.
•
Dual antiplatelet therapy is indicated up to 12 months.
•
Oral treatment with beta-blockers is indicated in patients with
heart failure or left ventricular dysfunction.
•
A fasting lipid profile must be obtained in all patients.
•
A high-dose statin should be initiated or continued early after
admission in all patients without contraindication or history of
intolerance.
•
ACE inhibitors are indicated in patients with heart failure, LV
systolic dysfunction diabetes or an anterior infarct.
•
An ARB is an alternative to ACE inhibitors.
•
Aldosterone antagonists are indicated if EF ≤40% or heart failure
or diabetes, provided there is no renal failure or hyperkalaemia.