Transcript Chief complaint… “Severe chest pain for 2 hours”—first

Chief complaint… “Severe chest pain for 2 hours”—
first thought? Is this an acute coronary syndrome?
• FIRST THINGS FIRST: Any patient with a
suspected acute coronary syndrome should
chew 160-325 mg of ASA; one simple therapy
is associated with a 35-day mortality reduction
exceeding 20%)
• Now, think…what structures are located in the
chest and how should I go about considering
this specific patient with chest pain?
Evaluation of chest pain…
• Cardiac—Acute coronary syndromes, aortic
dissection, pericarditis, myocarditis
• Pulmonary—pulmonary embolism, pleuritis,
pneumothorax
• GI—esophageal spasms, GERD, gall bladder
Evaluation of chest pain…
• Musculoskeletal—costochondritis, muscle
strain, rib fracture
• Neurologic—herpes zoster (“band-like”
burning pain may precede vesicular eruption)
• Psychological—panic disorder, depression
So, use the PQRST + AAA
• Start with the P’s…Pinpoint the pain, what is the
precise location? “show me…”
• LEVINE (pronounced “La Vine” sign…fist held over
sternum is pretty classic for angina or an MI
• Swooping the hand from the back, under the axillary
region and to the front may indicate “shingles”
• Moving the fingers up and down from the bottom of
the sternum to the top may indicate heartburn/GERD
• Severe tearing chest pain radiating to the back – think
aortic dissection (and think it FAST)
• Positional and pleuritic pain with pericarditis
What precipitated the pain?
• Exertion?
• What were you doing when the chest pain
started?
• How long did it take before the chest pain
started? Raking leaves? Shoveling snow?
Cardiac pain usually has a “lag time” to start
• Did the pain start as soon as you picked up
the shovel or the rake?
FYI: Snow-shovel-related medical mishaps
1990-2006
• 195,000+ snow shovel-related injuries treated in
emergency rooms in U.S. between 1990-2006
• 53.9% from acute musculoskeletal exertion
• 20% slip and fall
• 15% hit by a shovel
• 6.7% cardiovascular related
• 4.4% other
• 63% sustained by 18-54 year-olds
• Watson O.S, et al. Amer. J. Emer. Med, 2011
Back to the P’s
• What palliates the pain?
• Stopping the activity? How long did it take before
the chest pain stopped when you ceased the
activity? (cardiac pain—lag time to stop)
• Did you put a little white pill under your tongue?
If so, how many and how long did it take for the
pain to stop?
• Did you take an antacid?
• Does it hurt when you palpate the area? Consider
musculoskeletal pain (Cardiac pain is not
reproduced with palpation)
Quality or Quantity
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What is the Quality of the pain?
Burning? Zoster? GERD? AMI
Squeezing? Angina
Crushing? Vice-like? Acute MI
Tearing? Aortic dissection
Pleuritic w/ dyspnea? pneumothorax
R is for Radiate/Referred
• Where does it Radiate? Is it Referred pain?
• Front, back, side, down arm, up to the jaw,
between the scapula, elbow, jaw only?
The dermatome chart
Dermatomes
• Areas of skin that send their sensory information
into specific spinal cord segments
• Visceral structures share these sensory afferents
with skin areas
• T1-T4—dermatomes shared with the
myocardium, pericardium, aorta, pulmonary
artery, esophagus, and mediastinum
• Maximal intensity of the visceral pain is in the
retrosternal area/precordial area, up the neck,
down the inner arm
Dermatomes
• C3,4, (the phrenic nerves) the center of the
diaphragm and shoulder pain
• The patient with substernal chest pain, left
shoulder pain and intractable nausea—right
coronary artery, “inferior MI”?
• What’s below the center of the diaphragm? The
first part of the duodenum (the “organ of
nausea”…
• The older patient with fever, tachypnea, shoulder
pain and confusion—lobar pneumonia
• A fair, fat, fertile, forty-ish female with flatulence
and right shoulder pain? Gall bladder? AMI
Severity
• What is the severity of the pain…
• On a scale from 1-10, with 1 being the least
and 10 being “outta control”—where do you
rank pain on this scale?
• The classic MI—9 or 10 or greater
Does severity tell you anything special
about outcomes after an acute MI?
• No…in fact, severe chest pain does not herald
worse outcomes.
• Long believed by clinicians that a 9 or 10 on
the scale resulted in worse outcomes
• Severity of chest pain was not significantly
associated with AMI (acute myocardial
infarction) or the composite outcome of death
(Edwards)
Atypical chest pain
• Forty percent of AMI patients older than 85 present
with chest pain vs. 77% of AMI patients younger than
65; Elderly patients more likely to present with
dyspnea, diaphoresis, N & V, syncope
• Women—54% are at risk for misdiagnosis vs. 33% of
men; less likely to present w/ typical chest pain, but
more likely to present with tachycardia and
hypotension; more likely to report pain in the arm,
neck, back and jaw; HA; N & V; dyspnea, cough; chest
pain at rest, with mental stress, or during sleep
Timing or Temporal sequence
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Temporal sequence; Timing
When did it start?
How long did it last?
How often do you experience this type of
pain?
• What’s unique about the time of day and an
acute coronary syndrome?
6 a.m.
• Blood pressure and heart rate begin to rise due to adrenalin
and cortisol—increasing the workload of the heart
• BP is lowest at 4 a.m.
• Sharpest rise of BP at 6:45 a.m.
• Increasing heart rate and BP help you to become upright in
the a.m.
• Increasing blood pressure also means that the vessels are
constricting—risk??
• If on a beta blocker…QD beta blockers (long-acting) should be
taken at night
• Example: Toprol XL (metoprolol)
How about that first morning cigarette
when you first get up?
• vasoconstriction
8 a.m.-10 a.m.
• Risk for AMI
• The liver produces coagulation factors at night and
releases early in a.m.
• The adrenal gland releases cortisol and adrenalin in the
a.m. which increases blood sugar and contributes to
platelet aggregation; BP also rises as does heart rate in
response to adrenalin in a.m.
• Inflammatory mediators are the highest
• Take daily aspirin as soon as you get up to inhibit
platelet “stickiness”;
• ASA stays in the body longer when taken at 7 a.m.
Not only are you at highest risk for an acute coronary
syndrome in the a.m.
• Increased risk of heart irregularities
(arrhythmias)
• Increased risk of sudden cardiac death (usually
due to a ventricular dysrhythmia)
• Increased risk of deaths associated with
congestive heart failure
(August 2005 Journal of Biological Rhythms)
The sure-fired way to avoid cardiovascular
complications in the morning?
• Don’t get up.
PQRST
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Any additional symptoms?
Sweating? Nausea? Fatigue? Impending doom?
Dizziness? Light-headedness
Dyspnea (cardiac or respiratory)?? BNP test (Btype or brain- natriuretic peptide is released in
response to an elevated left ventricular end
diastolic pressure which attempts to decrease
SVR and increase natriuresis—under 100 pg/mL
rules out left ventricular failure; greater than 500
pg/mL rules in CHF)—gray zone between 100 and
500 pg/mL; under 50 pg/mL has a 97% sensivity
How about a 38 yo. woman with chest pain?
• Quick questions to rule OUT a myocardial infarction in a young
woman…what is her risk of having an MI at age 32?
• Diabetes
• Birth control pills? Obesity?
• Autoimmune disease? SLE, RA, vasculitis
• Methamphetamine, cocaine
• Cardiotoxic chemotherapy
• Surgical menopause?
• Family history
The 7 common primary heart diseases
are:
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congenital heart disease
ischemic heart disease (coronary artery disease)
hypertensive heart disease
valvular heart disease – acquired or congenital
pulmonary heart disease (cor pulmonale)
primary disorders of the myocardium (cardiomyopathies,
myocarditis)
• pericardial diseases (pericarditis, tamponade)
Find your lines and your spaces…
• Suprasternal notch
• Clavicle (1st rib is under
the clavicle)
• 2nd rib is the first palpable
rib
• 2nd ICS R and L—base of
heart
• 4th ICS parasternal border
• 5th ICS on L (apical area)
• Epigastric area
• BASE vs. APEX—heart is
upside down
WTF?
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Apex is at the bottom
Base is at the top
No rational explanation
Get over it, but remember it!!
Cardiovascular exam --inspection
• Skin color, nailbeds, capillary refill (4-6
seconds is normal), ankle edema
• 5th L ICS @ MCL for apical impulse
• Left 4th parasternal border for the R
ventricular area—R 4th for tricuspid
• 2nd R ICS—aortic area—heave, pulsation
• 2nd L ICS—pulmonic area—heave pulsation
• Suprasternal notch—pulsation?
• Epigastric area—pulsation?
Palpation…
• The base of the heart…any thrills? Cat
purring…
• A thrill with a murmur means that the
murmur is at least a grade 4 (4/6)
• Think valvular disease—aortic and pulmonic
stenosis in 2nd ICS
• The 5th L ICS at the MCL
The apical area—mitral stenosis
Palpation –palpating hearts and pulses since
1550 B.C. (Egyptians)
• Identify the apical impulse—should be no bigger
than 1-2 cm in size; gentle, brief contraction (only
present in 50% of the population—turn patient on L
side to feel)—if >4 cm (LR 4.7 for a dilated heart)
• Where is it? Outside the MCL (>10 cm from the
MSL)—LR for cardiomegaly is 3.4, depressed ejection
fraction is 10.1, ↑LVEDV is 8.0, and increased PCWP
5.8)
• Is there a pulsation in the epigastric area? Beating up
against the pads of your fingers? Beating against fingertips?
Peripheral arterial disease—a risk
equivalent of CAD
• Have PAD? Most likely have CAD
• Diffuse disease—males, diabetics, smokers,
hypertensive patients
• Check all pulses--Dorsal pedalis? Posterior tibial? If
absent, try femoral and popliteal
• In studies of large numbers of healthy individuals, the
dorsal pedalis pulse is not palpable 3-14% of the time
and the posterior tibial is absent 0-10% of the time.
• Only 0-2% of healthy individuals are missing both
pedal pulses).
• Listen for bruits over femoral arteries; bruits near
umbilicus
Characteristics arguing for the presence of
peripheral arterial disease
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Absence of both pedal pulses (LR 14.9)*
Presence of any limb bruit (LR 7.3)
Presence of wounds or sores on the feet (LR 7.0)
Absence of the femoral pulse (LR 6.1)
Presence of asymmetric coolness of the foot (LR 6.1)
Unhelpful findings—atrophic skin (LR 1.7), hairless lower
limbs (LR 1.7), prolonged capillary refill time (LR 1.9)
•
McGee S. Evidence-Based Physical Diagnosis. WB Saunders, Co. 2001
•
*LR is the Likelihood Ratio
Peripheral arterial disease
• Intermittant claudication—muscular pain, aching,
numbness w/ exercise; relieved by rest
• Ankle/brachial systolic BP—normal is 1-1.2; less
than 0.9 = PAD; claudication 0.5-0.9; rest pain less
than 0.4
• Risk of amputation is 15-40 x higher in the
diabetic
• Tx with cilostazol (Pletal)—reduces time to
claudication and improves exercise capacity
(vasodilators don’t work)
• ACE inhibitors have recently shown to be helpful
Guys, if you’re not getting blood flow to the feet or
the private parts… you are not getting enough blood
to the kidney
Acute mesenteric arterial occlusion
• Severe diffuse abdominal pain—frequently out of
proportion to clinical findings
• Chronic occlusive disease involving the
mesenteric circulation can manifest as abdominal
angina—especially after “exercise”—a meal
• Weight loss, N & V, early satiety
• DON’T forget this as a cause of acute abdominal
pain—especially in patients with CAD, PAD
Acute arterial peripheral occlusion—
medical emergency—6 P’s
• Pulselessness
• Pallor
• Poikilothermia (temperature of the affected
extremity varies with ambient temperature
• Pain
• Paralysis
• Paresthesia
Abdominal aortic aneurysm (AAA)—
usually infrarenal
• Abdominal bruits for abdominal aortic
aneurysm-• Usually silent until complication develops;
abdominal pulsation
• Ultrasound dx—screening for all men age 56-75
who have ever smoked
• risk of rupture increases exponentially with size;
3.0-4.4 cm diameter has a 2%/year risk; 4.5-5.9
cm diameter has a 10%/year risk; > 6 cm = 80%
rupture within 2 years
Triple A--prognosis
• Rupture outside the hospital? 80-90%
mortality; 50% die at scene; 50% who make it
to the hospital die in the OR; 50% of those
who survive the operation die of other comorbid conditions prior to hospital discharge
• When to repair? Aneurysm expansion > 0,5
cm/year; thoracic aortic aneurysm > 6 cm
(Marfan syndrome—other signs?); abdominal
aortic aneurysms > 5.5 cm
Jugular vein distention…
• The absolute best way to check the amount of
volume and pressure on the right side of the heart
• Always check the R jugular vein in everyone but
especially elderly pts
(direct route to heart; L veins cross the mediastinum where the
aorta may compress and falsely elevate).
• If top of neck veins are elevated> 3 cm above sternal
angle check for other signs of heart failure
• Hepatomegaly, peripheral edema, S3 gallop,
pulmonary crackles
Abdominal jugular reflex
• The pressure applied over the abdomen shifts blood
into the thorax and right atrium
• If the right ventricle is unable to handle this
increased load, the result is a sustained increase in
JVP.
• Compression of the liver is unnecessary
• Compression of the periumbilical area will suffice
• Positive with a sustained increase in the JVP greater
than or equal to 4 cm.
• LR ratio of 8 for detecting elevated left diastolic
pressures
Pitting edema…
• Subjective grading 1+-4+
• 1+ slight pitting
• 2+ deeper but no detectable distortion of
tissue
• 3+ noticeably deep, extremity full and
edematous
• 4+ very deep pit (your finger disappears)
dependent extremity is grossly distorted
Peripheral edema…what does it
mean?
• Fluid retention—heart failure
• Unilateral pitting—consider occlusion of major
vein
• Edema without pitting—arterial disease and
occlusion
• Edema as a side effect of drugs that retain
water or that are potent vasodilators—NSAIDS
and Ca+ channel blockers
Now it’s time to listen--Notes on the
stethoscope
• Ear plugs that fit—block out extraneous noise
• Length of tubing no longer than 12”, but 8” is
ideal
• Any stethoscope of a pastel color is worthless
• Do not listen over clothes
• The bell—LOW-pitched sounds; the diaphragm—
HIGH-pitched sounds
• Quiet room—no TV; no visitors; no wives,
husbands, lovers, children; no construction
Heart valves
Position the patient…
• Sitting up and leaning forward—brings base
of heart closer to chest wall
Murmurs of the aortic and pulmonic
valves heard best in this position—highpitched systolic sounds (aortic stenosis)—use
the diaphragm of the stethoscope
• Left lateral recumbent—best position to hear
low-pitched filling sounds during diastole
(mitral stenosis)(use the bell of the
stethoscope—don’t MUSH it on the skin,
hold it lightly!!)
But if you only have a minute…
• …and the patient is NOT a cardiac patient—
you can just listen to the apical or mitral area
If you had two minutes and you know
the following…
• #1 diseased valve of the heart? MITRAL
• #2 diseased valve of the heart? AORTIC
• SO WHERE WOULD YOU LISTEN FOR EACH OF
THE ABOVE?
• L 5th ICS for mitral (apical)
• 2nd R ICS for aortic (base)
Heart sounds—S1, S2
• S1 is the closure of the mitral and tricuspid valves—
the END of diastole or filling of the heart (aortic and
pulmonic valves open signaling the beginning of
systole)
• S2 is the closure of the aortic and pulmonic valves—
the END of systole or ejecting the blood (mitral and
tricuspid valves open signaling the beginning of
diastole)
• Opening and closing valves are silent unless diseased
Listening to heart sounds…
So…when you hear an extra heart
sound…
• First decide if it’s in systole or diastole?
• Extra heart sounds can be murmurs…
• 50% of all murmurs are systolic…therefore,
50% of all murmurs are diastolic. DUH…
Is the murmur after the LUB? Systolic?
Is the murmur after the DUB? Diastolic
The third heard sound
• S3—a diastolic sound
• Gallop…lub dub dub, lub dub dub
• This can be a normal sound under the age of
35
• however, consider the patient’s history before
using this age as a arbitrary number to dismiss
a third heart sound
Characterizing a murmur…
• Timing—systole or diastole
• Duration—early, mid, late, continuous in relation to
S1 and S2
• Pitch—low, medium, high
• Intensity—1 through 6 (4-6 usually assoc. with thrill)
• Quality—descriptive (harsh, blowing, soft)
• Location—where best heard
• Radiation--where does it go
Functional or innocent murmurs…
• Functional or “innocent” murmurs..40-60% of
all kids at some time; best heard with bell,
grade I or II, no radiation, low to medium
pitch, blowing, brief, 2nd L ICS parasternal
border, lying down (may disappear when
sitting or standing)
Characteristics of the 4 most common
heart murmurs—AS, AR, MS, MR
• In general, stenotic valves lead to a state of pressure
overload (aortic stenosis, mitral stenosis)—stenotic
valves develop slowly over time
• In general, regurgitant valves lead to a state of volume
overload; can develop acutely (AMI) or chronically
• Stenotic valves are heart when the valve is normally
OPEN—aortic valve is open during systole (ejection)
therefore aortic stenosis is a systolic murmur; the
mitral valve is open during diastole (filling), hence,
mitral stenosis is a diastolic murmur
Listening to heart sounds…
Characteristics of the 4 most common
heart murmurs
• Regurgitant valves, also known as incompetent
valves, result in a reversal of blood flow—in other
words, the murmur is heard when the valve
should be CLOSED
• Aortic regurgitation—the aortic valve is closed
during the filling of the heart (diastole), hence,
aortic regurgitation is heard during diastole
• Mitral regurgitation—the mitral valve is closed
TIGHT during systole (ejection), therefore, mitral
regurgitation is heard during systole
4 common heart murmurs and the
cardiac cycle
S1 __________S2_______________S1____
•
systole
diastole
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AS, MR
MS, AR
A few more notes…
• Acute aortic or mitral regurgitation can occur
with infective endocarditis (any recent dental
work?)
• Acute mitral regurgitation from an acute MI
(papillary muscle dysfunction)
• No time for compensatory mechanisms to
develop causing an acute elevation in pulmonary
pressure and acute pulmonary edema
• Tricuspid endocarditis is almost exclusively
caused by IV drug abuse
Notes on CHF (HF)
• 500,000 per year; 10% of patients over 70;
diabetes is a high risk; categorized as:
• Hemodynamic state of CV system—
(congestive vs. high output)
• Predominance of ventricle affected
• Predominant form of myocardial dysfunction
(systolic, diastolic)
• Time course (acute or chronic)
Causes of HF
• Betrayed heart – let down by it’s friends –
(hypertension, coronary artery disease, COPD,,
diabetes, thyroid, hemochromatosis)
• Befuddled heart – valvular heart disease
• Broken heart – cardiomyopathy (infiltrative
(amyloid, sarcoid); cocaine; “foam”
cardiomyopathy (due to the cobalt they used to
add to beer to make it foam); thiamine
deficiency; chemotherapy (Herceptin,
adriamycin/doxorubicin); myocarditis (viruses,
expecially Coxsackievirus)
Signs and symptoms of CHF
• Palpitations, skin color (pale, cyanotic), weak
pulses, dyspnea (orthopnea), nocturia, PND, (2-3
hours after falling asleep), cough, wheezing
• “funny things happen in the middle of the night”
• S3 gallop—early soft diastolic sound, best heard
over apex; use bell, lean patient forward;
indicative of abnormal ventricular function in
adults
• One-year mortality rate is higher for those with a
displaced apical impulse (39% vs. 12%) or a 3rd
heart sound (57% vs. 14%)
• The higher the BNP the poorer the prognosis
Treatment of heart failure
• Heart failure— “prils” to decrease preload and
afterload
• REMEMBER: Heart failure is a hyperreninemic state—
triggering the release of more angiotensin 2 and
subsequently her best buddy “AL-dosterone”
• Angiotensin is a potent “REMODELER” of the heart
muscle
• RX? Block “Angie” and “Al” with ACE inhibitors; block
additional “AL” with spironolactone/Aldactone or
eplerenone (Inspra)—improve mortality rates (K+)
• carvedilol (Coreg)—to reduce remodeling (altho’ new
studies at the AHA showed that “PRILS” were better
Treatment of heart failure
• Loop diuretics; may add thiazide diurectics if resistant
to loops
• Sodium restriction
• Fluid restriction
• Monitor daily weights
• Treat acute pulmonary edema with Lasix, morphine,
nitrates, and O2
• Hydralazine and nitrates in combiniation with standard
therapy reduce mortality for African Americans and
class III and IV CHF
• ICDs for ejection fractions < 35%; biventricluar pacing
Diabetes and heart failure
• ARIC study following 15,792 adults recruited
between ages 45 – 64 , living in communities in
NC, MN, MD, MS
• Found that diabetes had the strongest
association and was responsible for the highest
incidence of hospitalization
• A five percent reduction in the incidence of
diabetes in adults over age 45 could reduce the
number of heart failure cases by 30,000
• September 26, 2012 J Am College of Cardiology
Atrial fibrillation
• 3 main treatment concerns—rate control, rhythm
control, prevention of embolic events
• Ventricular response to AF controlled with Beta
blockers, calcium channel blockers, or dig
• Amiodarone may be considered as an alternative
to beta blockers and calcium channel blockers in
patients with low-EF. SIDE EFFECT profile! How
about dronedarone (Multaq)
• Cardioversion
• Anti-coagulants (discussed previously)
Highlights—atrial fibrillation
• New thinking? Why bother with meds?
• Ablation trumps meds for atrial fibrillation treatment
• Usual conservative method—drugs first—effectively stops
AF in 30% of patients
• Catheter ablation is better at 40%
• Surgical ablation is better at 90%
• Only 40% of patients who undergo catheter ablation are
AF-free after 12 months
• Go straight to the surgical ablation
2011 November Annual Meeting of the American Heart Association
Acute coronary syndromes
• Unstable angina (UA), non-STEMI, STEMI
• ST segment elevated MI—ruptured plaque in a
coronary artery results in complete occlusion of
coronary artery with thrombus, leading to
myocardial necrosis of the area supplied Necrosis
may occur throughout the entire thickness of the
myocardium = pathologic Q waves
• Non-ST segment elevated MI—chest pain,
elevated troponin, no ST segment elevations; no
pathologic Q waves; UA is related to non-STEMI
Other causes of AMI
• Demand ischemia
• Coronary artery dissection
• Coronary vasospasm (Prinzmetal’s angina*,
cocaine-induced)
• In situ thrombus formation (with hypercoaguable
disorder – lupus, Factor V Leiden)
• Coronary embolism
• Coronary vasculitis (Kawasaki syndrome)
• Carbon monoxide poisoning
Prinzmetal’s (variant) angina
• 1959 cardiologist Myron Prinzmetal was the first
to identify a variant form of angina, chest pain
caused by a sudden and severe spasm of a
coronary artery that obstructs blood flow
• The spasm is reversible and can occur at any
time, often unprovoked
• Smoking and hyperventilation are triggers
• Slightly more common in women and patients
younger than those with coronary artery disease
• Malfunction of the endothelial cells and the
nerves that stimulate the arterial smooth muscle
Clinical findings
• The usual suspects with atherosclerosis—(PAD-pulses, bruits)
• S3 may be present; S4 (decreased compliance of
an ischemic myocardium)
• Mitral regurgitation (systolic murmur)
• Pulmonary edema
• ECG in the STEMI—increase in amplitude of T
wave (first minutes after vessel occlusion); STsegment elevation (minutes to hours); Q waves
(hours to days); resolution of ST-segment
elevation (hours to days
Chest pain and Electrocardiogram
• Q waves in 2 or more leads: previous MI
• ST depression > 1 mm: ischemia
• ST elevation: AMI or pericarditis (pericarditis often has
involvement of all leads and associated PR depression)
• Left bundle branch block suggests underlying heart
disease (ischemic, hypertensive) (new onset? AMI)
• Right bundle branch block: may be indicative of right
heart strain: pulmonary embolism
• T-wave inversions and nonspecific ST changes: seen in
healthy individuals and in many diseases (not useful)
Troponin
• High sensitivity troponin levels at admission and 3
hours later in the ER can rule in or rule out AMI. If
troponin levels do not rise above the 99th percentile in
3 hours, the chance of an acute MI is nearly zero.
• Conversely, if troponin levels increase by 200% in 3
hours, the likelihood that a patient has had a heart
attack is 96%
• Elevated troponin levels cannot rule out unstable
angina—however patients w/ unstable angina need
aggressive treatment anyway
• (Keller)
Treatment
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O2, ASA (chewed) 162-325 mg
Sublingual NTG (0.4 mg every 5 minutes x 3)
(unless hypotensive) and if NO ED drugs
IV nitrates for persistent pain
IV morphine or fentanyl to reduce pain and decrease
pain-induced sympathetic drive (also lowers cardiac
workload)
• IV beta blocker to control heart rate (with adequate BP
and heart rate) (more contraindications
• Thrombolytic therapy—streptokinase, alteplase,
tenecteplase (single infusion) reteplace
Contraindications to thrombolytic
therapy
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Previous intracranial hemorrhage
Significant closed head injury in past 3 months
Stroke within 1 year
Intracranial neoplasm
Aortic dissection
Active bleeding (excluding menses) 
Percutaneous Coronary Intervention
• Patients with NSTEMI and benefit from glycoprotein Iib/IIIa
inhibitors prior to PCI (abciximab/Reopro;
• PCI –percutaneous coronary intervention for acute MI
(1977)—most frequently performed therapeutic procedure
in medicine; 500,000 per year; within 90 minutse of
presentation
• Drug eluting stent releasing everolimus or zatarolimus
• Followed by dual anti-platelet therapy (pasugrel/Effient and
ticagrelor/Brilinta are more potent than clopidogrel/Plavix)
• CABG for multi-vessel disease and greater complexity
Stefanni G, Holmes R. Drug-Eluting Coronary Artery Stents; N Engl J
Med 2013;368 (3):254-66)
And finally, what can YOU do to
prevent heart disease?
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Stop smoking
Exercise
Lose weight, especially around your belly
Lower your blood sugars
Sleep (sleep apnea also increases the risk)
EAT RIGHT
Say YES to drugs!
Bibliography
• Dornelas EA, Sampson RA, Gray JF, Waters D, Thompson PD. A
randomized controlled trial of smoking cessation counseling after
myocardial infarction. Prev Med.2000;30:261-268.
• Edwards M, et al. Relationship between pain severity and outcomes
in patients presenting with potential ACS Ann Emerg Med 2011
Dec.; 58:501
• Keller T et al. Serial changes I highly sensitive troponin I assay and
early diagnosis of MI. JAMA 2011 Dec 28;306: 2681)
• Levine G. Cardiology Secrets. Mosby. 2010
• McGee S. Evidence-Based Physical Diagnosis. WB Saunders, Co.
2001
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