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ACS Management
Cary Bybee MD
ER Management
 History
of presentation
 Physical exam
 Differential diagnosis
 Workup
 Treatments
History of Presentation
 Present
History
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Type of pain (dull, crushing)
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Quality of pain (intermittent, constant)
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Quantity of pain ( 10:10 for 15 min)
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Location and radiation (substernal, left arm, jaw)
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Timing of pain (at rest, with exertion)
History of Presentation
 Continued
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Nausea
Diaphoresis
Sense of dying
Short of breath, palpations
Syncopy, dizzy, light headed
Back pain, flank pain, bladder pain
Fever, chills
Past Medical History
History of heart disease and arrhythmia include
family
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Previous angina symptoms
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CAD, PAD, claudication
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Diabetes
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Hypertension
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Hyperlipidemia
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Other diseases including anemia
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Obesity, smoking, drinking, drug use
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GI disease and/or symptoms
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Surgeries, medications, pace maker
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Physical Exam
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EKG in first 5 to 10 min of admit
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SPO2 on room air and with supplemental oxygen
Skin cool, clammy, diaphoretic
Hypotension or hypertension
JVD >3cm @ 30 degrees (Kussmaul’s sign)
Peripheral pulses (weak, strong, absent)
Pulsus paradoxus > 10mmHg with inspiration
Pulsus tardus et parvus (weak and late)
Apical Impulse (See PMI slide)
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Physical Exam
 Continued
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Mental status (altered, foreboding, anxious)
Extremity edema, pulmonary edema
Chest wall tenderness or pain with inspiration
Positional pain
Abdominal or bladder tenderness, hepatomegaly
Abnormal auscultations (murmur, S3, S4)
Chest Pain Assessment
Palpable chest pain or pain with inspiration
is non-cardiac pain.
PMI Interpretation
Observation of the PMI
Prior to observation, have your subject lay flat, you should observe the pulsations from the PMI from the side of the
subject.
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Exam findings
 Normal
 The normal PMI is usually located inside the mid clavicular point at intercostal space 5 (see figure
below)
 Observe a single outward impulse, representing the systolic contraction of the left ventricle ("E" wave in
figure below)
 Abnormal
 Double impulse: visible over the apical region seen in hypertrophic cardiomyopathy . This is caused by
a second impulse after the first one from filling of the enlarged ventricle during diastole ,('a' wave in
figure below)
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Lateral displacement of the PMI (to left): usually seen in an enlarged heart (also seen in right large
pleural effusion, right tension pneumothorax and left-sided pulmonary fibrosis)
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Epigastric & subxiphoid movements: usually seen in right ventricular hypertrophy, right ventricular
dilation or an abdominal aortic aneurysm
 Can also be normally seen with emphysema, children, or a scaphoid abdomen, and the very thin
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Right 2nd intercostal pulsation: may indicate an aneurysm of ascending aorta
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Left 2nd (or 3rd) intercostal pulsation: less common, can be seen with a dilated pulmonary artery
Retraction of chest wall: seen in biventricular hypertrophy or constrictive pericarditis
Apex Cardiogram
Auscultation Location
Volume Curve
Heart Sounds
S3 and S4 Heart Sounds
S3 at apex= slosh S1 ing S2 in S3= heart
failure (CHF)
S4 at LSB= a S4 stiff S1 wall S2= HLV
Assessing Murmurs
Differential Diagnosis
 If EKG is equivocal
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Acute pericarditis, endocarditis
Panic attack
Aortic stenosis
Asthma, bronchitis, pneumonia, PE
Gerd
Pancreatitis
Esophagitis, Mallory Weiss
Work Up
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Serial EKG’s
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Serial cardiac markers
CBC with diff
CMP
UA with C&S
UDS (cocaine, tricyclics, lithium)
CXR (wide mediastinum, pneumonia)
Lipid panel
PT, aPTT, and INR
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Work Up
 Continued
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Possible echo (endocarditis-electrical alternans)
Possible D-Dimer (suspect PE)
CT chest (suspect PE or aortic aneurysm)
Possible carotid Doppler (A-fib and suspect stroke)
Venous Doppler (suspect DVT)
Cardiac Marker Interpretation
Cardiac Marker sensitivity
Electrolite Abnormalities
Hyperkalemia (see slides)
 Hypokalemia (see slides)
 Hypocalcemia (prolonged QTc, prolonged ST)
 Hypercalemia (short QT and J waves)
 Hypomagnesia (prolonged QTc)
 Uremia (pericarditis and tamponade)
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Hyperkalemia
 Peak T waves early
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PR widened, flatten, then disappear
Wide QRS, AV block with sinus brady
Asystole, PEA,VF
Hypokalemia
Increased amplitude and width of the P wave
 Prolongation of the PR interval
 T wave flattening and inversion
 ST depression
 Prominent U waves (best seen in the precordial leads)
 SVT,VT, VF and Torsades de Pointes
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Drug Induced Cardiac
Symptoms
 Cocaine, amphetamine
Tricyclics
 SSRI’s
 Beta blockers
 Digoxin
 Lithium
 Alcohol
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EKG Interpretation
NSTEMI
STEMI
Major Acute Coronary Event Risk
Assessment
ACS Initial Treatments
Not in order of importance
 ASA 325 chewable, or Clopidogril if allergic
 Oxygen only if SPO2 <90%
 Nitro .4mg SL if no signs of right HF
 Morphine if no signs of right HF
 P2Y12 drug
 LMWH
 GPI drugs
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UA/NSTEMI
STEMI Guidelines
Post Diagnosis Drug Management
ABCDE’s
 Antiplatelets and antiangina
 Beta blockers and BP control
 Cholesterol lowering, Cigarette stop
 Diabetes control and Diet
 Education and Exercise
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Congestive Heart Failure
 Causes
Idiopathic dilated/hypertrophic
 CAD
 HTN/renal disease
 Drugs/chemo
 PHT/COPD
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CHF Types
Systolic: poor contraction
 Diastolic: poor relaxation
 Subtypes
 Dilated: Chagas, cocaine, ETOH
 Hypertrophic S4: HTN, valve, MI
 Restrictive low voltage: inflammation, amyloids, iron
 Constrictive low voltage: surgery, radiation, tb, viral
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Clinical Symptoms
 Low Spo2, sob, wheezing, cough
Pitting edema
 Weakness, fatigue, dizzy
 Hyper/hypotension
 Tachycardia, A-fib
 AMS
 JVD
 S3 w/ gallop
 Rales
 Orthopenia, paroxysmal nocturnal dyspnea
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Diagnostics
 CO low, SVR high, Wedge high, RA pressure high
EKG: tachycardia, A-fib, arrhythmia
 CXR: pleural effusions and congestion
 Echo w/ EF- if below 35% needs bivent ICD
 CBC, CMP, TSH, Lipids, BNP
 Medication evaluation
 Glucose level
 BP
 SpO2
 ABG
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LHF and DCM Treatment
 O2
Telemetry
 Nitro and morphine acutely
 ACE/ARB to turn off renin/angiotensin
 Lasix, Bumex, metolazone
 Spironolactone
 Statin
 Coreg, Lopressor
 Anti-arrhthymics
 Inotropics
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RHF and HCM Treatment
 O2
Telemetry
 ACE/ARB may be acceptable
 Lasix, Bumex, Metolazone
 Statin
 Coreg, Lopressor
 Anti-arrhythmics
 DO NOT give digoxin, spironolactone, careful with
nitro and diuretics
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Restrictive/Constrictive HF
 Restrictive
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Low voltage EKG, JVD w/ inhalation, SOB
Treat w/ diuretics and correct cause
Constrictive
RHF
Edema
Acites
Hepatomegaly w/ JVD w/ inhalation or liver pressure
Paricardial knock
Low voltage EKG
CXR w/ calcifications
Treat w/ diuretics and surgery
Inotropic Drugs for CHF
 Dobutamine: increase contractility and reduce
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afterload but lower BP
Milrinone: phosphodiesterase inhibitor increases
contractility and reduce afterload
Dopamine: increases contractility but increases
afterload and BP.
Digoxin has some inotropic actions, but is primarily a
rate control drug for A-fib. Never use for acute CHF w/
pulmonary edema.