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Acute Coronary Syndromes



Rajesh Rajani and Farhad N. Kapadia


A previously healthy smoker presented with severe chest pain to the emergency department. On arrival he was clinically stable. The ECG showed ST-segment elevation in the anterior leads and blood test showed elevated troponin T and CK-MB. The echocardiograph showed hypokinesia in the anteroseptal region. In the emergency department, his symptoms progressively worsened with ongoing intense chest pain, and he became increasingly restless and breathless.

Acute coronary syndrome (ACS) is a common diagnosis in patients presenting to the emergency department with acute onset chest pain. Timely and appropriate management in a protocolized manner is mandatory to salvage patients from this life-threatening syndrome.

Step 1: Initiate resuscitation

Patients with acute chest pain should have immediate intravenous access as they may deteriorate suddenly.

A continuous ECG monitor and pulse oximeter should be placed. Give oxygen and assist breathing if needed.

In the case of cardiac arrest, follow ACLS (advanced cardiac life support) protocol (see Chap. 19).

Cardiovert immediately if ventricular or atrial tachyarrhythmia is detected and patient is hemodynamically unstable (shock or pulmonary edema).

R. Rajani, M.D., D.M. (*)

P.D. Hinduja Hospital and Medical Research Centre, Mumbai, India e-mail: rrajani20@gmail.com

F.N. Kapadia, M.D., F.R.C.P.

P.D. Hinduja National Hospital and Medical Research Centre,

Mumbai, India

R. Chawla and S. Todi (eds.), ICU Protocols: A stepwise approach,


DOI 10.1007/978-81-322-0535-7_23, © Springer India 2012



R. Rajani and F.N. Kapadia



Urgent transcutaneous or temporary intravenous pacing is required if severe symptomatic bradycardia is not responding to intravenous atropine.

Step 2: Take focused history and perform physical examination

Elaborate the symptom of chest pain—site, type, severity, relation to exertion


Cardiorespiratory symptoms

Symptoms of low output state such as fatigue, dizziness, and syncope

Risk factors for ischemic heart disease—hypertension, diabetes, hyperlipidemia, smoking, positive family history

History of bleeding diathesis or recent blood loss

BP in both arms

Palpate all peripheral and central pulses

Auscultate the heart for gallop or murmurs

Auscultate the chest for basal crepitations

Step 3: Perform basic investigation

12-lead ECG

Look for features of new ST elevation acute myocardial infarction (STEMI)

New ST elevation in two or more contiguous leads (inferior or anterior) Threshold values for new ST-segment elevation consistent with STEMI are:

J-point elevation 0.2 mV (2 mm) in leads V2 and V3 and 0.1 mV (1 mm) in all other leads (men more than 40 years old)

– J-point elevation 0.25 mV (2.5 mm) in leads V2 and V3 and

0.1 mV(1 mm) in all other leads (men less than 40 years old)

J-point elevation 0.15 mV (1.5 mm) in leads V2 and V3 and 0.1 mV (1 mm) in all other leads (women)

New LBBB (left bundle branch block)

ST elevation in right precordial leads V4r for right ventricular myocardial infarction (MI)

ST depression in precordial leads (V1–V3) for posterior MI

Pathological “Q” waves


Regional wall motion abnormality

Poor ejection fraction

Mechanical complication–papillary muscle rupture, VSD

Chest X-ray


Pulmonary congestion

Cardiac enzymes

Raised troponins, CPK-MB

A complete blood count

Leukocytosis in MI

Platelet count, prothrombin time, activated partial thromboplastin time (APTT)

Liver and renal function test


Look for hypokalemia, hypomagnesemia

23 Acute Coronary Syndromes




Table 23.1 Causes of acute

Life-threatening causes

chest pain

ACS (unstable angina, NSTEMI, STEMI)



Pulmonary embolus (may be associated with ↑ troponin)


Aortic dissection (may be overlooked due to associated MI)


“Benign” causes


Pericarditis (both ↑ troponin and ST elevation may occur)


Gastrointestinal (esophageal reflux, spasm)


Musculoskeletal (e.g., costochondritis)


Neurologic (cervical radiculopathy, herpes zoster)

Table 23.2 Causes of raised troponin

ACS (unstable angina, NSTEMI, STEMI)

Pulmonary embolism

Chronic renal insufficiency

Intracranial hemorrhage

Ingestion of sympathomimetic agents

Cardiac contusion

DC cardioversion

Cardiac infiltrative disorder



Cardiac transplantation

Step 4: Confirm diagnosis of ACS

Typical chest pain in patients at risk of myocardial ischemia with classical ECG changes and raised cardiac enzymes establishes diagnosis in many cases.

Consider other causes of chest pain (Table 23.1).

Consider other causes of raised troponin (Table 23.2).

Occasional patients have typical chest pain without ECG abnormalities or atypical chest pain (diabetics, female, elderly) and nonspecific changes on ECG. In these situations, perform serial monitoring of ECG and cardiac enzymes. An early echo is useful to look for regional wall motion abnormalities.

Step 5: Give pain relief

Sublingual nitroglycerine (0.3–0.6 mg) may be repeated twice or thrice or as an intravenous infusion (5–200 mcg/min) or as a transdermal patch.

Avoid nitrates in the following situations:

Hypotension (systolic <90 mmHg) or fall of more than 30 mmHg from baseline

Bradycardia (<50/min)

Intake of phosphodiesterase inhibitors like sildenafil for erectile dysfunction in the previous 24–48 h

In patients with inferior wall MI and suspected right ventricular (RV) involvement because these patients require adequate RV preload


R. Rajani and F.N. Kapadia



Morphine sulfate (2–4 mg IV) with increments of 2 mg IV should be repeated at 5–15 min for persistent chest pain unresponsive to nitroglycerine.

Avoid nonsteroidal anti-inflammatory drugs (except aspirin) due to increased risk of mortality, reinfarction, hypertension, and heart failure, and myocardial rupture has been associated with their use.

Step 6: Give antiplatelets

A combination of uncoated aspirin (160–325 mg orally or chewed) and clopidogrel (300–600 mg orally) should be given as a loading dose.

This should be followed by aspirin (150 mg/day) indefinitely and clopidogrel (150 mg/day) for 7 days, then 75 mg/day for at least 1 year.

Prasugrel (60 mg) can be used as an alternative to clopidogrel.

Due precautions should be taken regarding complications such as known allergies and gastric intolerance.

Proton pump inhibitors are often used concurrently to prevent gastric complications. These should be spaced out (mainly omeprazole) for 12 h after clopidogrel to prevent potential drug interaction.

Clopidogrel may need to be withheld if the need for early surgery is anticipated in the following:



Known multivessel disease

Cardiogenic shock

Mechanical complications

Step 7: Stratify and document risk category

The categorization of the type and extent of the myocardial infarction is primarily determined by the presence or absence of ST elevation and cardiac biomarkers of tissue injury.

Based on this, the management should proceed for a STEMI (with or without Q waves) or non-ST elevation myocardial infarction (NSTEMI) (positive troponin) or unstable angina (negative troponins).

Patients with unstable angina or NSTEMI should be risk stratified to conservative or invasive strategies (Table 23.3).

Proper documentation of findings, ECG interpretation, medications given, and plan of action should be made in patient’s case notes (Table 23.4).

Proper coordination among all disciplines concerned with patient care should be organized in a timely fashion.

Step 8: Consider reperfusion therapy (Table 23.5)

This can be accomplished by pharmacological (fibrinolysis) or catheter-based (primary percutaneous coronary intervention [PCI]) approaches or by emergency coronary artery bypass grafting (CABG).

23 Acute Coronary Syndromes




Table 23.3 Selection of initial treatment strategy for patients with non-ST elevation ACS: invasive versus conservative strategy

Preferred strategy

Patient characteristics


Recurrent angina or ischemia at rest or with low-level activities despite


intensive medical therapy


Elevated cardiac biomarkers (TnT or TnI)


New or presumably new ST-segment depression


Signs or symptoms of heart failure or new or worsening mitral regurgitation


High-risk findings from noninvasive testing


Hemodynamic instability


Sustained ventricular tachycardia


PCI within 6 months


Prior CABG


High-risk score (e.g., TIMI [thrombolysis in myocardial infarction])


Reduced LV function (left ventricular ejection fraction [LVEF] < 40%)


Low-risk score (e.g., TIMI)


The patient or physician preference in absence of high-risk features

Table 23.4 ACS: drug orders (for the initial 24 h)

Time of the onset of chest pain:

ECG taken at:

ECG diagnosis: ACS-ST elevation/non-ST elevation

Is the patient a candidate for primary angioplasty (PAMI)? Y/N

Drug class


Prescribed? (Y/N) Dose Time given Given by







Thrombolytic therapy

Contraindications to thrombolytic therapy? (Y/N)

Hemorrhagic stroke at any time, ischemic stroke within 1 year, intracranial neoplasm, active internal bleeding, suspected aortic dissection, major surgery (<3 weeks), major trauma (2–4 weeks), uncontrolled hypertension >180/110 mmHg

Heparin/low-molecular- weight heparin








Implementation of these strategies varies on the basis of capabilities at the treating facility and transport time to advanced facility.


R. Rajani and F.N. Kapadia



Table 23.5 Initial documentation, choice of reperfusion strategy, and medication: assessment of reperfusion options for STEMI patients

Step 1: Assess time and risk

Time since the onset of symptoms

Risk of STEMI

Risk of fibrinolysis

Time required for transport to a skilled PCI laboratory

Step 2: Determine if fibrinolysis or invasive strategy is preferred

If presentation is <3 h and there is no delay to an invasive strategy, there is no preference for either strategy

Step 3: Fibrinolysis is generally preferred if

Early present (£3 h from symptom onset and delay to invasive strategy)

Invasive strategy is not an option

Catheterization laboratory occupied or not available:

Vascular access difficulties

Lack of access to a skilled PCI laboratory

Delay to invasive strategy

Prolonged transport

Door-to-balloon time more than 1 h

Medical contact-to-balloon or door-to-balloon more than 90 min

Step 4: An invasive strategy is generally preferred if

Skilled cardiac catheterization laboratory is available with surgical backup Medical contact-to-balloon or door-to-balloon less than 90 min

High-risk score (TIMI) Cardiogenic shock Killip class ³3

Contraindications to fibrinolysis including increased risk of bleeding and intracranial hypertension

Late presentation

Symptom onset was more than 3 h ago Diagnosis of STEMI is in doubt

Step 9: Consider primary angioplasty as the preferred mode of treatment for all suitable STEMI patients

Coronary angioplasty with or without stent placement is the treatment of choice for the management of STEMI when it is performed effectively with a door-to- balloon time (<90 min) by a skilled provider, at a skilled PCI facility.

Documented outcome benefits of PAMI (primary angioplasty in myocardial infarction) included a trend for a reduction of in-hospital mortality, reduction in combined end point of death or reinfarction, and intracranial hemorrhage.

Treatment with primary angioplasty appears to reduce infarct rupture and has been associated with a significant reduction in acute mitral regurgitation, ventricular septal rupture, and a lower risk of free wall rupture.

PAMI was also beneficial when comparing surrogate markers such as ST-segment resolution and the tissue myocardial perfusion.

23 Acute Coronary Syndromes







Table 23.6 Comparison of approved fibrinolytic agents














1.5 MU in

Up to 100 mg in

10 U × 2 (30 min

30–50 mg based


30–60 min

90 min (based

apart) each over

on weight



on weight)

2 min

















Allergic reactions





(hypotension most










Systemic fibrinogen










The degree of benefit depends on the severity of the disease, age, and delay in instituting therapy. “Door-to-balloon” time should be kept as short as possible and should be regularly audited.

The contraindications to primary angioplasty are limited to patients who cannot receive heparin, aspirin, or thienopyridines (clopidogrel), documented lifethreatening contrast allergy, or lack of vascular access.

High-risk patients who receive fibrinolysis in a non-PCI center should be transferred to a PCI center within 6 h of presentation to receive early PCI if indicated.

Step 10: Consider fibrinolysis in selected patients (Table 23.6)

Fibrinolysis is restricted to patients with STEMI.

This modality of reperfusion is best suited for patients presenting early (<3 h) and at low risk of bleeding.

At centers without PCI facility, fibrinolysis can be given as a definitive treatment or as a bridging therapy prior to triaging to the higher center for PCI.

STEMI patients best suited for are those presenting early after symptom onset with low bleeding risk.

The benefit of fibrinolytic therapy appears to be greatest when agents are administered as early as possible, with best results when the drug is given less than 2 h after symptoms begin. “Door-to-needle” time should be kept as short as possible and should be regularly audited.

Mortality reduction may still be observed in patients treated with thrombolytic agents between 6 and 12 h from the onset of ischemic symptoms, especially if there is an ongoing chest pain.

Tenecteplase (TNK-t-PA) given as a 30–50-mg bolus is associated with the least bleeding complications and is generally seen as the preferred agent.

The accelerated dose regimen of t-PA over 90 min produces more rapid thrombolysis than the standard 3-h infusion of t-PA.


R. Rajani and F.N. Kapadia



The recommended dosage regimen for t-PA is a 15-mg intravenous bolus followed by an infusion of 0.75 mg/Kg (maximum 50 mg) over 30 min, followed by an infusion of 0.5 mg/Kg (maximum 35 mg) over 60 min.

It is associated with lower mortality and slight increase in incidence of intracranial hemorrhage but with a better overall composite outcome of death and disabling stroke.

Contraindications for thrombolysis should be considered prior to using lytic agents (see Chap. 9).

Intracranial hemorrhage may be fatal in half to two-thirds of patients and remains a devastating peril of thrombolytic therapy.

In a comparative analysis, the risk of intracranial hemorrhage was found to be 1% with thrombolysis and 0.05% with PCI.

Bleeding can also occur in sites like the gut or other sites including those of recent trauma or surgery.

Other complications are reperfusion arrhythmias and allergic reactions.

Step 11: Consider adjunctive therapies


Nitrates have a limited role in ACS.

The indication in the setting of an ACS is limited to ongoing chest pain or ischemia, hypertension, or as a vasodilator in the management of pulmonary edema secondary to left ventricular (LV) failure.

Route and dose of nitrate should be individualized.

Due precaution should be taken while using nitrates (see Step 5).


Oral b-blockers should be used within the first 24 h in those without evidence of heart failure, low cardiac output, shock, bradyarrhythmias, or conduction blocks and other conventional contraindication like asthma.

Cardioselective agents without intrinsic sympathomimetic activity are preferred. Metoprolol (50–200 mg/day) is the most commonly used agent.

Intravenous b-blocker is used (metoprolol 5 mg IV thrice a day) titrated to patient response, heart rate (avoid if <50/min), and blood pressure (avoid if less than 100 mmHg systolic).

Its use is best limited to situations with ongoing chest pain or uncontrolled tachycardia or hypertension.

Calcium channel blocking agents (diltiazem) may be used as alternative therapy in patients with contraindication to b-blockers but should be avoided in patients with poor left ventricular function and pulmonary congestion.

Anticoagulants: Indications

Low-molecular-weight heparins (enoxaparin 1 mg/Kg 12-hourly SC or dalteparin 120 U/Kg 12-hourly SC), or fondaparinux 2.5 mg SC once daily, are commonly used agents.

Bivalirudin (0.1 mg/Kg bolus followed by 0.25 mg/Kg/h infusion) may be considered as an alternative agent.

Appropriate dosing adjustments need to be done for renal dysfunction.

23 Acute Coronary Syndromes




As with antiplatelets, active bleeding and other contraindications need to be excluded, and the regime should be timed in consultation with cardiologist for patients requiring intervention.

Conventional unfractionated heparin is preferable if rapid reversal prior to surgery (CABG) is anticipated.

It should be given as a bolus of 60 U/Kg (maximum 4,000 units), then 14 U/Kg/h (maximum 1,000 U/h)—titrate to APTT 2.5 times control (see in Chap. 9).

A weight-based nomogram may be followed for heparin titration.

If intervention is not done, the duration for continuing anticoagulation is usually 5–10 days.

GP IIb/IIIa inhibitors

Abciximab 0.25 mg/Kg IV bolus and then 0.125 mcg/Kg/min (maximum 10 mcg/ min) may be given “upstream” prior to primary PCI in the catheterization laboratory.

Eptifibatide 180 mcg/Kg bolus, then 2 mcg/Kg/min infusion or tirofiban 0.4 mcg/Kg/min for 30 min, and then 0.1 mcg/Kg/min infusion should be started as a part of early intervention strategy in high-risk patients with non-STEMI.

Angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers

These drugs should be used within the first 24 h of ACS in patients without hypotension.

They are most beneficial in patients with pulmonary congestion and depressed LV systolic function.


The primary role of these agents is in long-term secondary prevention by lipid control.

They may have some additional advantage in the early phase of ACS. An agent like atorvastatin is initially used in a relatively high dose (40–80 mg), and the dose can later be decreased to achieve the target lipids (LDL < 70–100 mg/dL).

Patients who are already on statin should be continued on it.

Step 12: Manage arrhythmic complication

Primary ventricular fibrillation (VF) accounts for the majority of early deaths during AMI. The incidence of primary VF is highest during the first 4 h after the onset of symptoms but remains an important contributor to mortality during the first 24 h.

Secondary VF occurring in the setting of congestive heart failure or cardiogenic shock can also contribute to death from AMI.

Prompt defibrillation and appropriate pharmacotherapy should be instituted (see Chap. 19).

Maintain serum potassium more than 4 mEq/L and magnesium more than 2 mEq/L.

Prophylactic antiarrhythmics are not recommended.

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