Transcript SGD 1: Acute Myocardial Infarction

SGD 1:
Acute Myocardial Infarction
PATHOPHYSIOLOGY
OF SIGNS AND SYMPTOMS
Chest Pain
• An unpleasant sensation in the anterior wall
of the thorax
– actual or potential tissue damage
– mediated by specific nerve fiber to the brain conscious appreciation may be modified by
various factors.
Character of
pain
Location of pain
Pressure
Tightness
Heaviness
Retrosternal,
radiates to the
neck, jaw,
shoulders or
arms
Pulmonary
Sharp
Substernal
Unilateral or
localized
• Pneumonia or pleuritis
• Pulmonary embolism
• Pneumothorax
• Tumor
Gastrointestinal
Burning
Presents
with
abdominal
pain
Retrosternal
Substernal
Epigastric
• Gastroesophageal reflux disease
• Esophageal spasm
• Peptic ulcer disease
• Biliary diseases
• Pancreatitis
Organ System
Cardiovascular
Musculoskeletal
Stabbing
Dull ache
Superficial
Localized
Examples
• Coronary artery disease
• Ischemic heart disease
• Aortic stenosis
• Pericarditis
• Hypertrophic cardiomyopathy
• Cervical disk disease
• Arthritis of the shoulder and spine
• Costochondritis
• Intercostal muscle cramps
Chest Pain Etiology: Cardiac
Condition
Location
Quality
Duration
Aggravating
or Relieving
Factors
Associated
Symptoms
or Signs
Angina
Retrosternal
region;
radiates or
occasionally
isolated to
neck, jaw,
epigastrium,
shoulder or
arms—left
common
Pressure,
burning,
squeezing,
heaviness,
indigestion
<2-10 min
Precipitated by
exercise, cold
weather, or
emotional
stress, relieved
by rest or
nitroglycerin;
atypical
(Prinzmetal’s)
angina may be
unrelated to
activity, often
early morning
S4, or
murmur of
papillary
muscle
dysfunction
during pain
Rest or unstable angina
Same as
angina
Same as
angina but
may be
more severe
Usually <20
min
Same as
angina, with
decreasing
tolerance for
exertion or at
rest
Similar to
stable
angina, but
may be
pronounced.
Transient
cardiac
failure can
occur
Braunwald and Goldman, Primary Cardiology 2nd ed
Chest Pain Etiology: Cardiac
Condition
Location
Quality
Duration
Aggravating or
Relieving
Factors
Associated
Symptoms or
Signs
Myocardial
infarction
Substernal and
may radiate like
angina
Heaviness,
pressure,
burning
Sudden onset,
30 min or
longer
Unrelieved by rest
or nitroglycerin
Shortness of
breath, sweating,
weakness,
nausea, vomiting
Pericarditis
Usually begins
over sternum or
toward cardiac
apex and may
radiate to neck
or left shoulder;
often more
localized than
the pain of
myocardial
ischemia
Sharp, stabbing,
knifelike
Lasts many
hours to days;
may wax and
wane
Aggravated by
deep breathing,
rotating chest, or
supine position;
relieved by sitting
up and leaning
forward
Pericardial
friction rub
Aortic
dissection
Anterior of
chest; may
radiate to back
Excruciating,
tearing, knifelike
Sudden onset,
unrelenting
Usually occurs in
setting of
hypertension or
predisposition
such as Marfan’s
syndrome
Murmur of aortic
insufficiency,
pulse or blood
pressure
asymmetry;
neurologic deficit
Braunwald and Goldman, Primary Cardiology 2nd ed
Chest Pain
(dark red = most typical area, light red = other possible areas)
S1
Influenced by the ff:
– Position of the mitral leaflets at the onset of
ventricular systole
– Rate of rise of the LV pressure pulse
– Presence or absence of structural disease of
the mitral valve
– Amount of tissue, air, or fluid between the
heart and the stethoscope
Soft S1
• Due to poor conduction of sound through
the chest wall
• A slow rise of the LV pressure pulse
• Long PR interval
• Imperfect closure due to reduced valve
substance (e.g. MR)
• Anterior mitral leaflet is immobile due to
rigidity and calcification (e.g. MS)
PATHOPHYSIOLOGY
OF
CORONARY
ATHEROSCLEROSIS
Atherogenesis
• Developmental process of atheromatous
plaques.
Pathogenesis of Atherosclerosis
• Fatty Streak
• Leukocyte
recruitment
• Foam Cell
formation
• Microvessels
• Plaque evolution
Atherothrombosis
• Arterial
Remodelling
(Atherogenesis)
• Rupture of
Fibrous cap
• Arterial Occlusion
• More fibrous
lesion
Plaque Vulnerability
•
•
•
•
Thin fibrous cap (65 um thick)
Atheromatous core size > 30%
Increased macrophage content
Degree of inflammation (systemic or local)
Risk Factors
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Cigarette Smoking
HPN (BP> 140/90 mmHg or on
antihypertensive medication)
Low HDL, Low LDL
DM
Family Hx of premature CHD
– CHD in male first degree
relatives<55y/o
– CHD in female first degree
relatives<65y/o
•
Lifestyle risk factors
– BMI = > 30 kg/m²
– Physical inactivity
– Atherogenic diet
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Age (male>55y/o, female >65y/o)
Sex (Male>Female)
Stress
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•
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Age (55 y/o)
Male
Occupational stress
40 pack years
Heavy alcoholic beverage
drinker
HPN (2003)
Usual BP 130-80
Highest BP 170/100
Nifedipine 30 mg –
irregular intake
Family Hx of DM, HPN,
Premature CAD
CORONARY
ATHEROSCLEROSIS
• Epicardial coronary artery – major site
• Exposure of the plaque in the blood due to
rupture of the fibrous cap, the ff occurs:
– Platelets are activated and aggregate
Coagulation cascade activated
– Deposition of fibrin strands
• Thrombus composed of platelet aggregates
and fibrin stands traps RBC and reduce
coronary blood flow
ISCHEMIC HEART DISEASE
ISHEMIC HEART DISEASE
• Inadequate supply of blood and O2 to the
portion of the myocardium
• Imbalance between myocardial O2 supply
and demand
• Most common cause = Atherosclerotic
disease of the Epicardial Coronary Artery
EFFECTS OF IHD
• Ischemia is transient = Angina Pectoris
• Ischemia is prolonged = Myocardial
necrosis and scarring with or without
clinical picture of AMI
• Reversible - < 20 min for the total
occlusion in the absence of collaterals
• Permanent - > 20 min
ANGINA PECTORIS
Clinical Features of Angina
• Described as heaviness, pressure, squeezing,
smothering, or choking, and only rarely as frank pain.
• Levine’s sign – localization of pain by the pain: placing
his hand (clenched fist) over the sternum to indicate
sqeezing, central, substernal discomfort.
• Crescendo-decrescendo (2-5 min)
• Radiates to either shoulder and to both arms (ulnar
surface of the forearm and hand).
• Also arise in or radiate to the back, interscapular region,
root of the neck, jaw teeth and epigastrium.
Types of Angina Pectoris
Stable angina
• Due to transient myocardial ischemia
• Males 70% ; male >50y/o, female >60y/o
• Chest or arm discomfort that may not be described as
pain but is associated with physical exertion or stess
• Relieved within 5-10 min by rest &/or sublingual
nitroglycerin
• Retrosternal region; radiates to or occasionally isolated
to the neck, jaw, epigastrium, shoulder, or arms – usually
the left
• tight, squeezing, heaviness, indigestion
Types of Angina Pectoris
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2-10 min duration
precipitated by exercise, cold weather or stress
relieved by rest or nitroglycerin
P.E. Usually an S4 is appreciated
No permanent damage
Types of Angina Pectoris
Unstable angina
• It has at least one of these three features:
1. it occurs at rest (or with minimal exertion),
usually lasting >10 min;
2. it is severe and of new onset (i.e., within
the prior 4–6 weeks); and/or
3. it occurs with a crescendo pattern (i.e.,
distinctly more severe, prolonged, or frequent
than previously).
Types of Angina Pectoris
• same location as angina
• same quality as angina but may be more severe
and frequent
• usually < 20 min duration
• same precipitating factor as angina, with
decreasing tolerance for exertion or at rest
• same associated symptoms and signs as
angina, but may be pronounced, transient
cardiac failure can occur.
Prinzmetal (Variant) Angina
• typically consisting of angina (cardiac chest pain) at
rest that occurs in cycles
• caused by vasospasm, a narrowing of the coronary
arteries caused by contraction of the smooth muscle
tissue in the vessel walls rather than directly by
atherosclerosis
• chest pain occurs without the usual precipitating
factors
• associated with ST segment elevation than
depression
Types of Angina Pectoris
• often affects women below 50 yrs. old
• characteristically occurs in the early morning,
awakening patients from sleep
• tends to involve the RCA
• associated with arrythmias or conduction
defects
• NO fixed stenosis
• Ischemia results from coronary vasoconstriction
New York Heart Association
Functional Classification
I.
II.
Px have cardiac disease but without the
resulting limitations of physical activity
does not cause undue fatigue,
palpitation, dyspnea or anginal pain
Px have cardiac disease resulting in
slight limitation of physical activity. They
are comfortable at rest. Ordinary
physical activity results in fatigue,
palpitation, dyspnea, or anginal pain.
New York Heart Association
Functional Classification
III. Px have caridac disease resulting to marked
limitation of physical activity. They are
comfortable at rest. Less than ordinary physical
activity causes fatigue, palpitation, dyspnea, or
anginal pain.
IV. Px have cardiac disease resulting in inability to
carry on any physical activity without discomfort.
Symptoms of cardiac insufficiency or of anginal
syndrome may be present even at rest. If any
physical activity is undertaken, discomfort is
increased.
Canadian Cardiovascular Society
Classification of Angina
I. No angina with ordinary activity. Angina with
strenuous, rapid, or prolonged exertion
II. Slight limitation of ordinary activity; angina when
walking up stairs briskly, or walking on a cold
or windy day
III. Marked limitation; angina when walking at
normal pace up flight of stairs, or walking 1-2
blocks distance
IV. Angina on minimal exertion or at rest
IHD Classification
• Coronary Artery Disease (CAD)
– Stable Angina
• Acute Coronary Syndrome
– AMI with STE
– UA and NSTEMI
WHO Criteria for AMI
Classic WHO Criteria: two (probable) or three (definite) of the
following criteria are satisfied:
• Clinical history of ischemic type chest pain lasting for more than 20
minutes
• Changes in serial ECG tracings
• Rise and fall of serum cardiac biomarkers such as CK-MB fraction
and troponin
Revised (2000)
Cardiac troponin rise accompanied by either typical symptoms,
pathological Q waves, ST elevation or depression or coronary
intervention are diagnostic of MI.
Non-ST Elevation Myocardial
Infarction
• Presents with clinical manifestation of
unstable angina but develops myocardial
necrosis reflected in elevated cardiac
biomarkers
• caused by a reduction in oxygen supply
and/or by an increase in myocardial
oxygen demand (e.g., by tachycardia or
severe anemia) superimposed on a
coronary obstruction
Clinical Presentation
• Chest pain
– typically located in the substernal region or
sometimes in the epigastrium, that frequently
radiates to the neck, left shoulder, and left
arm
PE Findings
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Diaphoresis
Pale cool skin
Sinus tachycardia
Third and/or fourth heart sound
Basilar rales
Sometimes hypotension
Laboratory Findings
• Electrocardiogram
– Transient ST segment elevation (>0.05mv)
– ST-segment depression
– T-wave inversion (0.3 mV)
– New Bundle Branch Block
– Sustained Ventricular Tachycardia
• Cardiac Biomarkers
– Elevated Cardiac-specific troponin T (cTnT)
and cardiac-specific troponin I (cTnI)
Tools for Diagnosis of UA/NSTEMI
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clinical history,
ECG
cardiac markers
stress testing.
Goals in Diagnosing NSTEMI
1.Recognize or exclude MI (using cardiac
markers),
2.Evaluate for rest ischemia (chest pain at
rest, serial or continuous ECGs)
3.Evaluate for significant coronary artery
disease (using provocative stress testing).
Treatment Goals
• To stabilize and “passivate” the acute
coronary lesion
• To treat residual ischemia
• To employ long term secondary prevention
Management
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Admit to monitored bed
Bed rest
Supplemental oxygen
Relief of Chest pain
– Nitrates
– Beta Blockers
– Morphine
• Anti-thrombotic therapy
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–
Aspirin
Clopidogrel
Heparin
GP IIb/IIIa inhibitors
ST Elevation Myocardial Infarction
• occurs when coronary blood flow
decreases abruptly after a thrombotic
occlusion of a coronary artery previously
affected by atherosclerosis
• may be due to coronary artery occlusion
caused by coronary emboli, congenital
abnormalities, coronary spasm, and a
wide variety of systemic disease
particularly inflammatory diseases
Patients at increased risk of
developing STEMI
• Those with:
– multiple coronary risk factors
– unstable angina or Prinzmetal’s variant
angina.
Less common underlying
conditions for developing STEMI
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•
•
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Hypercoagulability
Collagen vascular disease
Cocaine abuse,
Intracardiac thrombi or masses that can
produce coronary emboli.
Clinical Presentation
1. Pain
–
–
–
–
–
–
deep and visceral
described as heavy, squeezing, and crushing
involves the central portion of the chest and/or the
epigastrium, and on occasion it radiates to the arms
accompanied by weakness,sweating, nausea,
vomiting, anxiety, and a sense of impending doom
may commence when the patient is at rest,
If it begins during a period of exertion, it does not
usually subside with cessation of activity
Clinical Presentation
2. Breathlessness
– Sudden in onset
– In elderly patients
– May progress to pulmonary edema
3. Sudden loss of Consciousness (w/ or w/o pain)
4. Confusional state (w/ or w/o Pain)
5. Sensation of profound weakness (w/ or w/o pain)
6. Appearance of an arrhythmia (w/ or w/o pain)
7. Evidence of peripheral embolism (w/ or w/o pain)
8. Unexplained drop in arterial pressure (w/ or w/o
pain)
PE Findings
• Pallor associated with perspiration and coolness
of the extremities
• Combination of substernal chest pain persisting
for 30 min and diaphoresis
• Some patients with anterior infarction have
manifestations of sympathetic nervous system
hyperactivity (tachycardia and/or hypertension)
• Some patients with inferior infarction show
evidence of parasympathetic hyperactivity
(bradycardia and/or hypotension).
PE Findings
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Precordium is usually quiet
Apical impulse may be difficult to palpate
Abnormal systolic pulsation
Ventricular dysfunction:
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fourth (S4) and third (S3) heart sounds,
decreased intensity of S1
Paradoxical splitting of S2
Transient midsystolic or late systolic apical systolic
murmur due to dysfunction of the mitral valve
apparatus
– Pericardial friction rub
– Decreased volume of the Carotid pulse due to
reduced stroke volume.
Laboratory Findings
• Electrocradiogram
– ST-segment elevation
– Q Waves
• Serum Cardiac Biomarkers
– Creatine phosphokinase MB Mass (CKMB
mass)
– Increased Cardiac-specific troponin T (cTnT)
and cardiac-specific troponin I (cTnI) >20
times higher than the upper reference limit
0.05 ng/dl
– Myoglobin in the blood
Management
• Timely reperfusion of infarcted area
– Fibrinolysis
– Percutaneous Catheter Intervention (PCI)
• Primary prevention of vascular events
– Aspirin
– Clopidogrel
• Control of Cardiac pain
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–
–
–
Oxygen
Nitrates
Beta Blockers
Analgesics (Morphine)
• Prevent Ventricular Remodelling
– Reperfusion
– Ace Inhibitors
Complications
• Ventricular Dysfunction
– Ventricular remodeling
• left ventricle begins to dilate from expansion of the
infarct, i.e., slippage of muscle bundles, disruption
of normal myocardial cells, and tissue loss within
the necrotic zone, resulting in disproportionate
thinning and elongation of the infarct zone.
Lengthening of the non-infarcted segments occurs
as well.
Complications
• Cardiogenic Shock
– In patients w/ severe multivessel coronary
artery disease with evidence of “piecemeal”
necrosis extending outward from the original
infarct zone
• Right Ventricular Infarction
• Arrhythmias
– Due to autonomic nervous system imbalance,
electrolyte disturbances, ischemia, and
slowed conduction in zones of ischemic
myocardium
Complications
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•
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•
Recurrent Chest Discomfort
Pericarditis
Thromboembolism
Left Ventricular Aneurysm