ACUTE CORONARY

SYNDROME
BY:
JOBELYN DELENA TUNAY, RN
ACUTE CORONARY SYNDROME (ACS):

• IS A SET OF SIGNS AND SYMPTOMS SUGGESTIVE

OF SUDDEN CARDIAC ISCHEMIA.

• USUALLY CAUSED BY DISRUPTION OF

ATHEROSCLEROTIC PLAQUE IN AN EPICARDIAL
CORONARY ARTERY.
INCLUDE:
• UNSTABLE ANGINA (UA)
• NON-ST SEGMENT ELEVATION MYOCARDIAL
INFARCTION (NSTEMI),
&
• ST SEGMENT ELEVATION MYOCARDIAL INFARCTION
(STEMI), COMMONLY REFERRED TO AS A HEART
ATTACK.
SPECTRUM OF ACUTE CORONARY SYNDROME
＋ : positive Cardiac
Presentation Ischemic Discomfort
Biomarker
at Rest

No ST-Segment ST-Segment
Emergency Elevation Elevation
Department

＋ ＋ ＋

Unstable Non Q-Wave

Q Wave MI
Angina MI
In-Hospital
• New Terminology in ACS
Plaque
Rupture

Stable Unstable Non– Q-wave

Old Term Angina Angina Q-wave MI MI

New Term Atherothrombosis UA/NSTEMI STEMI

Days- Minutes-
weeks hours

Antithrombotic Thrombolysis
Therapy Primary PCI
 ACS STABLE ANGINA
UNSTABLE
ANGINA
•
 UNSTABLE ANGINA

•
•

•
 NSTEMI

RELEASE OF
CARDIAC ENZYMES
 CAUSES:
•Coronary Atherosclerotic Heart Disease Pathophysiology of
•Coronary Thrombosis/Embolism
•Decreased Blood Flow w/ Shock &/or Hemorrhage
Myocardial Infarction

Myocardial Oxygen
Myocardial Ischemia Supply Cellular Hypoxia

Cardiac Output Myocardial Altered Cell

Contractility Membrane Int.

Arterial Pressure Stimulation of Stimulation of

Baroreceptors Sympathetic Receptors

Peripheral Afterload
Vasoconstriction
Decreased
Myocardial Diastolic Myocardial Tissue
Heart Rate Filling Per.
Contractility

Myocardial
Oxygen Demand
 SIGN AND SYMPTOMS
S – site of pain;
O – onset of pain;
C – character of the pain;
R – any radiation;
A – associated factors;
T – timing of the pain;
E – exacerbating/alleviating factors; for example, position or
inspiration;
S – severity of the pain using a rating scale of 1-10 (10 being the
worst pain).
 SIGND AND SYMPTOMS
Chest pain
Nausea or vomiting
Shortness of breath (dyspnea
PATHOLOGICAL MECHANISM
Angina pectoris is the result of
myocardial ischemia caused by an
imbalance between myocardial
blood supply and oxygen demand.
It is a common presenting symptom
(typically, chest pain) among
patients with coronary artery disease
Nausea and vomiting occurring
during myocardial ischemia is
believed to be associated with
inferior wall infarction.
Patients with cardiac insufficiency
often have pulmonary edema that
impairs gas exchange as well as
increasing the work of breathing,
both of which add to the feeling of
shortness of breath.
 SIGND AND SYMPTOMS
Sudden, heavy sweating (diaphoresis)
Lightheadedness, dizziness or fainting
Unusual or unexplained fatigue
PATHOLOGICAL MECHANISM
Excess stimulation of the sympathetic
nervous system (or more technically,
neurohumoral mechanisms) in an attempt
to compensate, which by its effects on
heart contractility and rate increases the
amount of pumped blood to match the
need. This sympathetic outflow also causes
increased sweating, nervousness, dry
mouth etc. Sweating, nervousness are
cardinal signs of acute MI.
Feeling faint, light-headed or dizzy may be
due to a reduction of blood flow to the
brain. Sudden loss of consciousness usually
means that the blood supply to the brain is
seriously reduced.
Fatigue is a particularly concerning
symptom because it is reported by up to
70% of patients diagnosed with AMI
 SIGND AND SYMPTOMS PATHOLOGICAL MECHANISM

Feeling restless or apprehensive Observational studies have found

repeatedly that patients report
excessive anger, anxiety, sadness,
grief, or acute stress immediately prior
to onset of MI
•ON EXAMINATION

•25% with anterior infarction—sympathetic sysrem hyperactivity (tachycardia)

•50% of inferior infarction– parasympathetic hyperactivity(bradycardia

&/hypotension)

•Raise in temp upto 38°C

•Arterial press:-variable

•PRECORDIUM-quite..

•Apical impulse-difficult to palpate

•S1-decreasing in intensity, S2-paradoxical splitting, audible S3 &S4.

•Trasient midsystolic/late systolic murmur in apical

area (dysfunction of mitral valve apparatus)
 LABORATORY FINDINGS
Electocardiogram:
•ST segment elevation-in 2 or more contiguous leads
(corresponding to wall supplied by epicardial artery)
•75%- presence of Q waves
•Gradually ST segment elevation decrease & T wave inversion develops
•T wave inversion-persist 4 wks to months.
•Q waves-persist 4 months to years, sometimes lifelong

Cardiac markers:
•CK-rises within 4-8hrs,returns to normal by 48-72hrs (lacks specificity for
STEMI)
•CK-MB (more specific)-rises 6-10hrs aft onset of infarction,
(in absence of reperfusion/thrombolysis), peaks-24hrs, & returns to
normal- 36-72hrs
•Troponins(cTnT & cTnI)-rises 3-6hrs & peak-24hrs,remain elevated
for 7-10 days
•Myoglobin: for rapid diagnosis

BIOCHEMICAL MARKERS
 BIOCHEMICAL MARKERS

Protein Molecular First Duration of Sensitivity Specificity

mass (kD) detection detection
Myoglobin 16 1.5–2 8–12 hours +++ +
hours
CK-MB 83 2–3 1–2 days +++ +++
hours
Troponin I 33 3–4 7–10 days ++++ ++++
hours
Troponin B 38 3–4 7–14 days ++++ ++++
hours
 NON MI CAUSES OF
TROPONIN ELEVATION
•Tachycardia

•PE w/ Right Vent: infarct

•Cardiac failure w/ myonecrosis

•Cardiac surgery

•Myocarditis

•Renal failure
 CORONARY ANGIOGRAM
•Observer variability

•Discordance between severity of lesion

and physiologic effects

–Greater stenosis vs more unstable plaques?

•2-D picture of a 3-D problem

–Diffuse disease may limit estimation of

“abnormal segments”

•Missed lesions
 THERAPEUTIC GOALS
•
•
•

MEDICAL MANAGEMENT
•
 CURRENT MEDICAL MANAGEMENT
OF UNSTABLE ANGINA AND NSTEMI*
ACUTE THERAPY MAINTENANCE THERAPY

•ANTI-PLATELET THERAPY

• BETA-BLOCKERS
• CALCIUM CHANNEL BLOCKERS
• LIPID LOWERING AGENTS
• ACE INHIBITORS
Anti-Ischemic Therapy
- nitrates, beta-blockers, calcium
antagonist

Anti-thrombotic Therapy

•Anti-platelet Therapy
- aspirin, ticlopidine, clopidogrel,
GP IIb/ IIIa inhibitors

•Anticoagulant Therapy
- heparin, low molecular weight
heparin (LMWH), warfarin,
hirudin, hirulog
 ANTI-ISCHEMIC THERAPY
•restrict activities
•morphine
•oxygen
•nitroglycerine
–pain relief, prevent silent ischemia, control hypertension,
improve ventricular dysfunction
–nitrate free period recommended after the first 24-48 hours
•beta-blockers
- lowering angina threshold
- prevent ischemia and death after MI
- particularly useful during high sympathetic tone
•calcium antagonists
- particularly the rate-limiting agents
- nifedipine is not recommended without concomitant ß-
blockade
 ANTI-PLATELET THERAPY
•Aspirin is the “gold standard”
–irreversible inhibition of the cyclooxygenase pathway in platelets,
blocking formation of thromboxane A₂, and platelet aggregation.
–in UA, ASPRIN reduced the risk of fatal or nonfatal MI by 71%
during the acute phase, 60% at 3 months, and 52% at 2 years
–bolus dose of 160-325 mg, followed by maintenance dose of 80-160
mg/d

•Thienopyridines
-- Ticlopidine (Ticlid )
-- clopidogrel (Plavix )

( block platelet aggregation induced by ADP and the transformation of

GP IIb/IIIa into its high affinity state )
• GP IIb/IIIa inhibitor
–abciximab (monoclonal antibody)
–eptifibatide (peptidic inhibitor)
–lamifiban and tirofiban (non-peptides)

( direct occupancy of the GP IIb/IIIa receptor by a monoclonal antibody

or by synthetic compounds mimicking the RGD sequence for fibrinogen
binding prevents platelet aggregation )
 ANTI-COAGULANT THERAPY
•Heparin

- trials showed a 33% risk reduction in MI and death, but with a two
fold
increase in major bleeding
- titrate PTT to 2x the upper limits of normal

•Low-molecular-weight heparin

--advantages over heparin:

-- better bio-availability
-- higher ratio (3:1) of anti-Xa to anti-IIa activity
-- longer anti-Xa activity, avoid rebound
-- induces less platelet activation
-- ease of use (subcutaneous - qd or bid)
-- no need for monitoring
 CORONARY INTERVENTIONS
• early intervention vs conservative strategy
(coronary angiography within 24-48 hrs,
followed by angioplasty {PCI} or bypass surgery
{CABG} )

LONG TERM MANAGEMENT

Risk factor modification, optimal wt :, diet
Cessation of smokeing, daily exercise, BP control, tight
control of hyperglycemia
Lipid management
Drugs ( B-blockers, statins, ACE inhibitors etc )
 STEMI
Acute, evolving or recent MI

Requires 1 of 2:
1.Typical rise and gradual fall (troponin) or more rapid rise
and fall (CK- MB) of markers of myocardial necrosis with >= 1 of:
-Symptoms
-Q waves
-ECG c/w ischemia
-S/p coronary artery intervention

2.Pathologic findings of AMI

•Chest, epigastric, arm, wrist, jaw pain or

discomfort w/ exertion or at rest
•Pain-is deep & visceral (heavy, squeezing & crushing,
stabbing or burning) IIar in charcteristic of angina pectoris; but more
severe & lasts longer.

•Associated sx
: dsypnea, diaphoresis, nausea, vomiting, light
headedness,anxiety,weakness & sense of impending doom.

•Other presentation
-sudden loss of consciousness
confusional state.

•Substernal pain(>30min)+diaphoresis– strongly suggests STEMI

 PREHOSPITAL CHEST PAIN
EVALUATION AND TREATMENT
•Prehospital EMS providers should administer 162 to 325 mg of

aspirin (chewed) to chest pain patients suspected of having STEMI

unless contraindicated or already taken by the patient. Although

some trials have used enteric-coated aspirin for initial dosing, more

rapid buccal absorption occurs with non–enteric-coated

formulations.
 ELECTROCARDIOGRAM
If the initial ECG is not diagnostic of STEMI, serial ECGs or

continuous ST-segment monitoring should be performed

in the patient who remains symptomatic or if there is high

clinical suspicion for STEMI.

LABORATORY EXAMINATIONS
• Laboratory examinations should be performed as part of
the management of STEMI patients, but should not delay the
implementation of reperfusion therapy.
Serum biomarkers for cardiac damage
Complete blood count (CBC) with platelets
International normalized ratio (INR)
Activated partial thromboplastin time (aPTT)
Electrolytes and magnesium
Blood urea nitrogen (BUN)
Creatinine
Glucose
Complete lipid profile
 BIOMARKERS OF CARDIAC
DAMAGE
Cardiac-specific troponins should be used as the

optimum biomarkers for the evaluation of patients

with STEMI who have coexistent skeletal muscle injury.

For patients with ST elevation on the 12-lead ECG

and symptoms of STEMI, reperfusion therapy

should be initiated as soon as possible and is not

contingent on a biomarker assay.

 IMAGING
Patients with STEMI should have a portable chest X-ray, but this
should not delay implementation of reperfusion therapy (unless a
potential contraindication is suspected, such as aortic dissection).

Imaging studies such as a high quality portable chest X-ray,

transthoracic and/or transesophageal echocardiography, and a
contrast chest CT scan or an MRI scan should be used for
differentiating STEMI from aortic dissection in patients for whom
this distinction is initially unclear.
 OXYGEN
Supplemental oxygen should be administered to patients

with arterial oxygen desaturation (SaO₂ < 90%).

It is reasonable to administer supplemental oxygen to all

patients with uncomplicated STEMI during the first 6 hours.

 NITROGLYCERIN
Patients with ongoing ischemic discomfort should receive
sublingual NTG (0.4 mg) every 5 minutes for a total of 3 doses,
after which an assessment should be made about the need for
intravenous NTG.

Intravenous NTG is indicated for relief of ongoing

ischemic discomfort that responds to nitrate therapy,
control of hypertension, or management of pulmonary
congestion.
 NITROGLYCERIN
Nitrates should not be administered to patients with:
systolic pressure < 90 mm Hg or ≥ to 30 mm
Hg below baseline
severe bradycardia (< 50 bpm)
tachycardia (> 100 bpm) or
suspected RV infarction

Nitrates should not be administered to patients who have received

a phosphodiesterase inhibitor for erectile dysfunction within the last
24 hours (48 hours for tadalafil).
 NITROGLYCERIN
Mechanism of Action:

The principal pharmacological action of nitroglycerin is relaxation of

vascular smooth muscle. Although venous effects predominate,
nitroglycerin produces, in a dose-related manner, dilation of both arterial
and venous beds.

Patient Teaching:

Patient instructed on Nitroglycerin sublingual tablets usually give relief in 1 to

5 minutes. If the pain is not relieved, you may use a second tablet 5 minutes
after you take the first tablet. If the pain continues for another 5 minutes, a
third tablet may be used. If you still have chest pain after a total of 3 tablets,
contact your doctor or go to a hospital emergency room right away. Do not
drive yourself and call Emergency Response if necessary.
 ANALGESIA
Morphine sulfate (2 to 4 mg intravenously with increments of 2 to 8
mg intravenously repeated at 5 to 15 minute intervals) is the
analgesic of choice for management of pain associated with
STEMI.
Mechanism of Action:

• Morohine and other opiods exert their major effects by interacting with opiod receptors in
the CNS and other structures, such as the gastrointestinal (GI) tract and the urinary bladder

• Morphine also acts at K receptors in the spinal cord. It decreases the release of substance
P, which cause pain perception in the spinal cord

• Morphine also inhibit the release of many excitatory transmitters from nerve terminals
carrying nociceptive (painful) stimuli
 ANALGESIA
Patient Teaching:

This is can slow or stop your breathing, especially when you start using this
medicine or whenever you dose is changed. Never take morphine in larger
amounts, or for longer than prescribed. Tell your doctor if the medicine seems
to stop working as well in relieving your pain. Get emergency medical help if
you have signs of an allergic reaction to morphine: hives; difficult breathing,
swelling of your face, lips, tongue, or throat. Call your doctor at once if you
have: slow heart rate, sighing, weak or shallow breathing, chest pain, fast or
pounding heartbeats, extreme drowsiness, feeling like you might pass out.
Morphine is more likely to cause breathing problems in older adults and
people who are severely ill, malnourished, or otherwise debilitated. Common
morphine side effects may include: drowsiness, dizziness; constipation,
stomach pain, nausea, vomiting, headache, tired feeling, anxiety or mild
itching.
 ASPIRIN
Aspirin should be chewed by patients who have not taken aspirin before
presentation with STEMI. The initial dose should be 162 mg to 325 mg

Although some trials have used enteric-coated aspirin for initial dosing, more rapid
buccal absorption occurs with non–enteric-coated formulations.

Patient Teaching:

Instructed patient/caregiver on general precautions while taking aspirin: take

with food, milk, or large glass of water to decrease gastric symptoms. (Enteric
coated or buffered may be better tolerated.); avoid alcohol due to possible
internal bleeding; only take the recommended amount; use cautiously with
Asthma; observe and report s/s of bleeding (easy bruising, bleeding gums, black
stools); discard medications if vinegar odor is present; do not take antacids due
to decreased effectiveness; avoid chewing or crushing enteric coated.
 ASPIRIN
Mechanism of Action:
Anticoagulants such as heparin or warfarin (also called
Coumadin) slow down your body's process of making clots.
Antiplatelet drugs, such as aspirin, prevent blood cells called
platelets from clumping together to form a clot.

Aspirin and other non-steroid anti-inflammatory drugs (NSAIDs)

inhibit the activity of the enzyme now called cyclooxygenase
(COX) which leads to the formation of prostaglandins (PGs) that
cause inflammation, swelling, pain and fever.
 BETA-BLOCKERS
Oral beta-blocker therapy should be administeredpromptly to those patients
without a contraindication, irrespective of concomitant fibrinolytic therapy or
performance of primary PCI.

It is reasonable to administer intravenous beta-blockers promptly to STEMI patients

withoutcontraindications, especially if a tachyarrhythmia or hypertension is present.

Mechanism of Action:

Beta blockers, also known as beta-adrenergic blocking agents, are medications that
reduce your blood pressure. Beta blockers work by blocking the effects of the
hormone epinephrine, also known as adrenaline. When you take beta blockers, your
heart beats more slowly and with less force, thereby reducing blood pressure.
 BETA-BLOCKERS
Patient Teaching:

Before administering beta-blockers:

•Check for allergies

•Know what other drugs the patient is receiving including over the counter
(OTC) and herbs. Do •any of them have the same “effect” as the beta-
blocker?
•Know why the patient is receiving the drug
•Obtain current BP and apical pulse rate; if below 90 systolic or 60 beats
per minute(BPM) hold •the drug and notify the health care provider (HCP).
Check your institution’s policy, some say hold below 50 BPM
 BETA-BLOCKERS
After administering beta-blockers:

• Observe for intended effect

• Monitor for side effects, especially orthostatic hypotension
• Monitor older pts for mental confusion or changes in LOC which may indicate an
overdose
• Diabetics are not usually given beta-blockers because they can effect the blood
glucose level and because the drugs will mask the cardiovascular effects of
hypoglycemia such as tachycardia, mild tremors and diaphoresis. If your pt is a
diabetic and on a beta-blocker monitor closely for signs of hypoglycemia unique
to the pt and monitor blood glucose frequently
• Patients with COPD (including asthma) should be monitored closely for respiratory
issues such as wheezing and difficulty breathing (remember what beta blockers
BLOCK – bronchodilation) They should not be given nonselective beta-blockers.
 BETA-BLOCKERS
Teaching:

• Safety measures to prevent orthostatic hypotension such as changing positions

slowly, hold onto railings when using stairs
• To check pulse rate and when to call HCP
• Common side effects as well as potential long term effects such as sexual
dysfunction and depression. If any issues arise, discuss with HCP.
• DO NOT STOP TAKING DRUG SUDDENLY. Doing so may cause tachycardia,
dysrythmias, elevated BP, angina and MI.
• ALWAYS inform HCP before surgery or dental work they are on a beta-blocker
• Any chest pain experienced during activity should be discussed with the HCP so
that safe activity levels can be discussed. (If they exercise regularly, their target
heart rate may need to be lowered)
• Extended release forms of the drug should never be crushed and taken.
 NON-PHARMACOLOGIC
MANAGEMENT
Diet and Nutrition
•Controlling the amount of salt in the diet (<2,000mg) is relevant in patients with
advanced HF and a fluid restriction of 1,500-2,000ml should be advised to advanced
HF patients.

•It should also be advised that salt substitutes must be used with caution, as they
may contain potassium. In large quantities, in combination with an angiotensin-
converting enzyme (ACE) inhibitor, they may lead to hyperkalaemia.

•Alcohol consumption must be prohibited in suspected cases of alcoholic

cardiomyopathy, but otherwise moderate alcohol intake is permitted. Other
nutritional advice includes weight reduction in the overweight or obese (body mass
index (BMI) >25) and prevention of malnutrition and cardiac cachexia.
Rest and Exercise

Traditionally, patients with HF have been instructed not to exercise in

order to avoid deterioration. More recently, physical rest is only advised
in acute HF or destabilisation of chronic HF.4 If in a stable condition, the
patient should be encouraged to, and advised how to, carry out daily
physical and leisure-time activities that do not induce symptoms, in order
to prevent muscle de-conditioning. In earlier days HF was described as a
contraindication for exercise training.
Improve Symptom Recognition and Related Self-care Behaviour:

In order to make patients recognise deterioration and take relevant

action in case of exacerbation, patients and partners need information
on HF symptoms. Patients are advised to weigh on a regular basis
(once a day to twice a week) and, in case of a sudden unexpected
weight gain of more than 2kg in three days, to take appropriate
action. Patients are also encouraged to monitor other HF symptoms or
note unexpected changes in the health status. They need to be aware
how serious these symptoms can be and what appropriate actions are.

More recently, a flexible diuretic regimen has been suggested as an

option in relation to increasing HF symptoms. Based on changes in
symptoms, daily weight and fluid balance, patients are advised to
increase or decrease their diuretics within pre-specified and
individualised limits.
Other Lifestyle Changes and Other Therapies:

• Smoking should always be discouraged.

• Pneumococcal and influenza immunisation may reduce the
incidence of respiratory infections that may worsen HF.
• Continuous positive airway pressure (CPAP) to improve daily
functional capacity and quality of life may be used in patients with
HF and obstructive sleep apnea.
• Non-pharmacologic techniques for stress reduction may be
considered as a useful adjunct for reducing anxiety in patients with
HF.
Drug Counselling:
On average, HF patients are prescribed 7.5 different drugs, with various advice, such
as at what time of day to take them. In addition to this complex regimen, patients
sometimes suffer from side effects of HF medication. To optimise compliance, patient
education is vital. Topics to address are:

• reason for prescription and the relationship of the drug with HF;
• nature of each drug, dosing, desired effects and side effects of all drugs;
• need for refills of the prescribed medication;
in some drugs, improvement may be gradual and only complete after several
weeks, and with some drugs months, of treatment;
• Some medications (ACE inhibitors and beta-blocking drugs) will be gradually up-
titrated to desired dosage levels, which will not directly improve the patient signs and
symptoms.
• how to cope with a complicated regimen (e.g. using medication organisers);
• what to do in case of skipped doses;
• what to do if dehydration occurs;
• how to act if symptomatic hypotension occurs; and
• which drugs to avoid (e.g. non-steroidal anti-inflammatory drugs (NSAIDS)
Improve Compliance with Medication and Other Lifestyle Changes:

Compliance with the long-term medical regimen of patients with HF is poor, with
overall non-compliance rates ranging from 42% to 64%. In a study of elderly patients
with HF, only 55% of the patients could correctly name which medication had been
prescribed, 50% were unable to state the prescribed doses and 64% could not
account for the medication that was to be taken, i.e. at what time of day and
when in relation to meals the medication was to be taken. Noncompliance extends
to other aspects of the treatment regimen like daily weighing, keeping a salt-
restricted diet, restricting fluid and alcohol intake, and exercise.

Adequate Disease Management and Follow-up:

Recently, several meta-analyses described that comprehensive discharge planning

plus post-discharge support for older patients with HF significantly reduce
readmission rates and may improve health outcomes such as survival and quality of
life without increasing costs. Various models have been tested (HF clinics, nurse-led
home visits and/or telephone follow-up, multidisciplinary care, extended home care
services) but it is not clear which model is superior.
 Initial Treatment of ACS

STEMI NSTEMI

Anti-platelet, Anti-ischemic Anti-platelet, Anti-ischemic

or Anticoagulant Therapy or Anticoagulant Therapy

Thrombolytics PCI or CABG PCI or CABG

Long Term Medical Management

 Management of ACS
A thorough clinical history and physical examination should be undertaken and
supported by an ECG. This helps delineate the treatment pathway and, in cases of
STEMI, decide whether the patient needs urgent reperfusion. If ACS is suspected, the
emergency services should be called and, on arrival, paramedics should perform an
immediate ECG. Many paramedics are trained to recognise ECG changes seen in
STEMI, which include ST elevation of ≥1mm height in two adjacent chest leads, ST
elevation of ≥2mm in two adjacent limb leads, and new left bundle branch block.

If STEMI is suspected, paramedics will aim to take patients directly to a ‘heart attack
centre’ that offers primary percutaneous coronary intervention (PCI). Often they will
communicate with the cardiology team before arrival, which will facilitate urgent
coronary reperfusion strategies (coronary angioplasty with/without stents placed in
the affected coronary artery) once the patient has arrived in hospital.
 MANAGEMENT OF ACS
Primary PCI has become the first-line treatment in patients with STEMI
presenting within 12 hours of onset of symptoms, provided it can be given
within 120 minutes of the time in which thrombolysis could be given (NICE,
2013a). If primary PCI is not available or there is a delay, thrombolysis may
be performed (using drugs such as alteplase and reteplase) after
discussion with the on-call cardiologist – if there are no major
contraindications.

If the ECG does not reveal an MI but cardiac ischaemia is suspected,

patients should be admitted and have serial 12-lead ECGs to assess any
dynamic changes. If there is myocardial damage, cardiac enzymes
(typically troponins T and I) are raised, which can help confirm the
diagnosis. NICE (2013b) advises that troponin be included in the initial
assessment on admission and a second sample be taken 10-12 hours after
symptoms began.
 MANAGEMENT OF ACS
Increases or decreases of troponin above or below the normal limit on the repeat
test can confirm NSTEMI. A negative troponin and no ECG changes can support a
decision to discharge patients who may have unstable angina. These patients
should receive follow-up in a rapid chest pain clinic or in cardiology; their risk of
adverse cardiac events is 0.2% (Weinstock et al, 2015).

Adults with NSTEMI or unstable angina should be assessed for their risk of future
adverse cardiovascular events using an established risk scoring system that predicts
six-month mortality (NICE, 2013b). This helps to plan clinical management and
decide on the best place of care (for example, coronary care or a medical
assessment unit). Several tools are available to stratify mortality risk in ACS, including:
•Global Registry of Acute Coronary Events score (GRACE) (Granger et al, 2003);
• Thrombolysis in Myocardial Infarction (TIMI) score (Antman et al, 2000).
 REPERFUSION
-is a medical treatment to restore blood flow, either through or around,
blocked arteries, typically after a heart attack (myocardial infarction (MI)).
Reperfusion therapy includes drugs and surgery. The drugs are thrombolytics
and fibrinolytics used in a process called thrombolysis.

•Given the current literature, it is not possible to say definitively that a

particular reperfusion approach is superior for all pts, in all clinical settings, at
all times of day
•The main point is that some type of reperfusion therapy should be selected
for all appropriate pts with suspected STEMI
•The appropriate & timely use of some reperfusion therapy is likely more
important than the choice of therapy
 Assessment Diagnosis Inference Planning Intervention Rationale Evaluation
SUBJECTIVE: Pain r/t tissue Occlusion of After 8 hours of Independent:
"Sumasakit ang ischemia coronary nursing Goal met,
dibdib ko" (I've (coronary artery intervention the ° Obtain full ° Pain s a subjective patient has
been artery patient will description of pain experience and verbalized
experiencing occlusion) verbalize relief/ from patient must be described relief/ control
chest pains) as Decreased control of chest including location, by patient. of chest pain
verbalized by the blood flow to pain within intensity (0-10), within
paient the appropriate time duration, appropriate
myocardium frame for characteristics time frame for
administered (dull/crushing), and administered
OBJECTIVE: medications. radiation. Assist medications.
° restlessness Decreased patient to quantify
° facial grimace oxygen supply pain by comparing
° pain scale of 9 (ischemia) it to other
out of 10 experiences
° v/s taken as
follows °Instruct patient to ° Delay in reporting
T: 37.6 Anaerobic report pain pain hinders pain
P: 112 metabolism immediately relief/ may require
R: 27 increased dosage of
BP: 140/100 maedication to
Lactic ascid achieve relief
formation

°Provide quiet ° Decreases external

environment, calm stimuli, which may
Pain activities, and aggravate anxiety
comfort measures and cardiac strain,
Assessment Diagnosis Inference Planning Intervention Rationale Evaluation
limit coping abilities
and adjustment to
current situation

° Assist/instruct in ° Helpful in
relaxation techniques, decreasing
e.g., dep/slow perception
breathing, distraction of/response to pain.
behaviors, Provides a sense of
visualization, guided having some control
imagery over the situation,
increase in positive
attitude.

Administer ° Increases amount

medications as of oxygen available
indicated: for myocardial
• Antianginals e.g., uptake and thereby
nitroglycerin, may relieve
isosorbide dinitrate discomfort
(Isodril) associated with
tissue ischemia

• Beta-blockers, e.g, • Nitrates are useful

atenolol, propanolol, for pain control by
metoprolol coronary vasdilating
effects, which
increase coronary
Assessment Diagnosis Inference Planning Intervention Rationale Evaluation
blood flow and
myocardial perfusion

° Analgesics e.g, ° Important 2nd line

morphine, agents for pain
meperidine control through
effect of blocking
sympathetic
stimulation, thereby
reducing heart rate,
systolic BP and
myocardial oxygen
demand

°Although IV
morphine is the usual
drug of choice, other
injectable narcotics
maybe used in acute
phase/ recurrent
chest pain unrelived
by nitroglycerin to
reduce severe pain,
provide sedation and
decrease myocardial
workload
 Assessment Diagnosis Inference Planning Intervention Rationale Evaluation
SUBJECTIVE: Activity Weakness & STG: INDEPENDENT: STG:
intolerance r/t Fatigue °Within 3 days of Within 3 days of
“Nanghihina ang cardiac nursing 1. monitor heart 1.changes in VS nursing
katawan ko” dysfunction, interventions, the rate, assist with interventions,
(I'm experiencing changes in client will be able rhythm, monitoring the client
body weakness) as oxygen supply Decreased to tolerate activity respirations and physiologic tolerated
verbalized by the and oxygen without excessive blood pressure responses to activity without
patient. consumption os dyspnea and will for increase in excessive
evidenced by be able to utilize abnormalities. activity. dyspnea and
shortness of breathing Notify had been able
OBJECTIVE: breath. Increased CO₂ techniques & physician of to utilize
levels eergy significant breathing
- Discomfort DEFINITION: conservation changes in VS. techniques
Insufficient techniques and energy
-Increased blood physiological effectively. 2. Identify 2. Alleviation of conservation
pressure energy to Decreased causative factors that are techniques
BP=(140/100) endure or blood pH LTG: factors known to create effectively.
complete ° Within 5 days of leading to intolerance can
-RR= 27 required or nursing intolerance of assist LTG:
desired daily interventios, activity. with Within 5 days of
-Dyspnea with activities Deep & laored the client will be development of nursing
exertion breathing able to increase & an activity level interventions,
achieve desired program. the client
-Fatigue & activity level, increased and
weakness progressively, with 3. encourage 3. to help give achieved desired
no intolerance patient to assist the patient a activity
STRENGTHS: able to symptoms noted, with planning feeling of level,
comply w/ meds such as repiratory progressively,
compromise
Assessment Diagnosis Inference Planning Intervention Rationale Evaluation

activities, with self-worth and with

rest periods as well-being. no intolerance
necessary. symptoms noted,
such
4. instruct patient in 4. to decrease as respiratory
energy energy compromise.
conservation expenditure and Goal was met
techniques. fatigue.

5. turn patient at 5. to maintain joint

least every mobility and
2 hours, and prn. muscle tone.

6. instruct patient in 6. to improve

isometric and breathing and to
breathing increase activity
exercises. level.
Goal was met.
 Assessment Diagnosis Inference Planning Intervention Rationale Evaluation
SUBJECTIVE: Deficient STG: INDEPENDENT: STG:
The client Knowledge r/t The client will 1. monitor patient’s 1. to promote The client
verbalizes new diagnosis be able to readiness to learn optimal verbalized and
questions and lack of verbalize and and learning demonstrated
regarding understanding demonstrate determine best environment understanding
problems and of medical understanding methods when patient of
misconceptions condition. of information to use for teaching. show information
about his given regarding willingness to given
condition. condition, learn. regarding
medications, 2. provide time for condition,
OBJECTIVE: and treatment individual 2. to establish trust. medications,
•Lack of regimen within interaction with and
improvement 3 days of patient. treatment
of previous nursing regimen
regimen interventions. 3. instruct patient on within 3 days of
procedures that 3. to provide nursing
•Inadequate LTG: may be information interventions.
follow-up The client will performed. to manage Goal was met.
on able to correctly Instruct patient on medication LTG:
instructions perform all medications, dose, regimen and to The client had
given. tasks prior to effects, side effects, ensure been able to
discharge contraindications, compliance correctly
•Anxiety and perform all
signs/symptoms to tasks prior to
•Lack of report discharge.
understaning to physician. Goal was met
Assessment Diagnosis Inference Planning Intervention Rationale Evaluation

4. instruct in dietary 4. client may need to

needs and restrictions, increase dietary
such as limiting sodium potassium if placed on
or increasing potassium. diuretics; sodium should
be limited because of
5. provide printed the potential for fluid
materials when possible retention.
for patient/family to
reviews. 5. to provide reference
for the patient and
6. have patient family to refer.
demonstrate all skills
that 6. to frovide information
will be necessary for that patient has gained
postdischarge. a full understanding of
instruction.
7. instruct exercises to
be 7. these are helpful in
performed, and to improving cardiac
avoid function.
overtaxing activities.

DEPENDENT:
1. refer patient to 1. to provide further
cardiac improvement and
rehabilitation as rehabilitation
ordered postdischarge