THE ABC’S OF ACS

Rapid diagnosis for rapid treatment

 I still find the best way to understand a
hospitalized patient whose care I am taking over is
not by staring at the computer screen but by going
to see the patient; it's only at the bedside that I can
figure out what is important.

Abraham Verghese
ACS DEFINED

Acute Coronary Syndrome encompasses :

 Unstable Angina,
 NSTEMI,

 STEMI

Classification of angina – Canadian Cardiovascular Society classification.

THE MEDIAN DIAGNOSTIC TURN AROUND TIME FROM
PATIENT'S ARRIVAL TO THE REPORTING OF THE
TROPONIN LEVELS RESULT WAS 122 MIN.

Clin Chem Lab Med. 2008;46(7):1030-2. doi: 10.1515/CCLM.2008.185.

Diagnostic, clinical and laboratory turnaround times in troponin T testing.
Ervasti M1, Penttilä K, Siltari S, Delezuch W, Punnonen K.
60 minutes 120 minutes

Troponin I
results
available
The correct diagnosis of ACS in a patient within 30
minutes of arrival to emergency unit is the key in
effective treatment of ACS.
Any delaying factor needs to be measured in a risk
to benefit ratio.

Delaying fibrinolysis to have a confirmation test

done is only advisable when the risk of fibrinolysis
in a specific patient is high.
By remembering we are doctors first – not lab
technicians.

We treat PATIENTS not RESULTS

WHERE DOES EVERY GOOD DOCTOR START
HIS OR HER CONSULTATION?
 HISTORY
What is the PRIMARY symptom patients with ACS
present with?

CHEST PAIN

So an adequate history regarding the PAIN will be

an invaluable clue in diagnosis.
THE HISTORY OF PAIN
TYPE OF PAIN
DULL PRESSURE/CRUSHING PAIN
SHARP/STABBING
DURATION
2-5 MIN, <20 MIN
SECONDSTO HOURS/CONTINUOUS
ONSET
GRADUAL
RAPID
LOCATION/CHEST WALL TENDERNESS
SUBSTERNAL, NOT TENDER TO PALP.
LATERAL CHEST WALL/TENDER TO PALP.
REPRODUCIBALITY
WITH EXERTION/ACTIVITY
WITH BREATHING/MOVING
AUTONOMIC SYMPTOMS
PRESENT USUALLY
ABSENT
PATIENT CONTEXT
RISK STRATIFICATION
EXAMINATION

Remember
your ABC’s
AIRWAY AND BREATHING
Respiratory rate

 The respiratory rate may be increased in

response to pulmonary congestion or anxiety.
CIRCULATION
Heart rate

 The patient's heart rate is often increased (tachycardia

secondary to sympathoadrenal discharge). The pulse may be
irregular because of ventricular ectopy, an accelerated
idioventricular rhythm, ventricular tachycardia, atrial
fibrillation or flutter, or other supraventricular arrhythmias.

 Depressed heart rate may also be present in some cases.

Bradyarrhythmias may be attributable to impaired function of
the sinus node. An atrioventricular (AV) nodal block or
infranodal block may also be present.

 Unequal palpable pulses can be suggestive of the presence of

aortic dissection, which commonly presents with chest pain
radiating to the back, accompanied by a blood pressure
difference of 15 mm Hg or greater between both arms and an
aortic regurgitation murmur.
CIRCULATION
Blood pressure

 In general, the patient's blood pressure is initially

elevated (hypertension because of peripheral arterial
vasoconstriction resulting from an adrenergic
response to pain, anxiety, and ventricular
dysfunction). However, it is not uncommon to have
increased blood pressure as the precipitant of acute
MI.

 Alternatively, hypotension can also be seen. Usually

this indicates either right ventricular MI or severe
left ventricular dysfunction due to a large infarct area
or impaired global cardiac contractility.
 Heart
 On palpation, lateral displacement of the apical impulse, dyskinesis,
a palpable S4 gallop, and a soft S1 sound may be found. These signs
indicate diminished contractility of the compromised left ventricle.

 Paradoxical splitting of S2 may reflect the presence of left bundle-

branch block or prolongation of the pre-ejection period with delayed
closure of the aortic valve, despite decreased stroke volume.

 A new mitral regurgitation murmur (typically holosystolic near the

apex) indicates papillary muscle dysfunction or rupture, or mitral
annular dilatation; it may be audible even when cardiac output is
substantially decreased.

 A holosystolic murmur that radiates to the midsternal border and not

to the back, possibly with a palpable thrill, suggests a ventricular
septal rupture; such a rupture may occur as a complication in some
patients with full-thickness MIs. With resistive flow and an enlarged
pressure difference, the ventricular septal defect murmur becomes
harsher, louder, and higher in pitch than before.

 A pericardial friction rub may be audible as a to-and-fro rasping

sound; it is produced through sliding contact of inflammation-
roughened surfaces.
HEAD TO TOE
Neck veins
 In patients with acute inferior-wall MI with right
ventricular involvement, distention of neck veins
is commonly described as a sign of failure of the
right ventricle. Impaired right ventricular
function also leads to systemic venous
hypertension, edema, and hepatomegaly.
HEAD TO TOE
Extremities
 Peripheral cyanosis, edema, pallor, diminished
pulse volume, delayed rise, and delayed capillary
refill may indicate vasoconstriction, diminished
cardiac output, and right ventricular dysfunction
or failure. Pulse and neck-vein patterns may
reveal other associated abnormalities, as
previously discussed.
PRIMARY INVESTIGATION
GUIDELINES
 Initial 12 lead ECG – goal door to ECG time
10min, read by experienced doctor
 If ECG not diagnostic/high suspicion of ACS –
serial ECGs initially 5 – 10 min intervals
 ANY deviation in serial ECG’s are considered
significant and may be indicative of ACS
 Remember ACS is DYNAMIC an ECG is a
SINGLE point in time meaning just doing ONE
is not prudent medicine.
 Continuous 12 lead ECG monitoring reasonable
alternative to serial ECGs
OTHER CLUES…
 Refractory Pain
 Changes in vitals
BIOCHEMICAL MARKERS
 These are valuable tools in confirmation of an
already suspected diagnosis – a good doctor will
requests tests to confirm a clinical suspicion.
 The role of Trop I has been researched
thoroughly and is part of the AMA
recommendations for the diagnosis of ACS the
key is to use the tests intelligently – remember
TIME is a resource that cannot be replaced.