14. ACUTE CORONARY SYNDROME
Acute coronary syndrome is a term that encompasses
both unstable angina and myocardial infarction (MI).
It is characterised by new-onset or rapidly worsening
angina (crescendo angina), angina on minimal exertion or
angina at rest in the absence of myocardial damage.
In contrast, MI occurs when symptoms occur at rest and
there is evidence of myocardial necrosis, as
demonstrated by an elevation in cardiac troponin or
15. Introduction
Two steps to develop ACS: 1) developing
atherosclerosis plaque —> 2) ruptured AT plaque.
Development of at plaque in the coronary artery cause
stable angina which called myocardial ischemia.
Ischemia is an inadequate blood supply to the organ
that results subsequently in infarction, which is
localized area of necrosis.
16. The common mechanism to all ACS is rupture or erosion of
the fibrous cap of a coronary artery plaque.
This leads to platelet aggregation and adhesion, localized
thrombosis, vasoconstriction and distal thrombus
embolization.
The presence of a rich lipid pool within the plaque and a
thin fibrous cap are associated with an increased risk of
rupture.
Thrombus formation and the vasoconstriction produced by
17. Most important risk factors
Modifiable
Serum lipid levels
Hypertension
Smoking/tobacco use
Sedentary lifestyle
Obesity
Diabetes mellitus
Diet
Non modifiable
Age
Gender
Ethnicity
Family history
Genetics
Menopause
22. HOW TO APPROACH TO CHEST
PAIN?
Clinical presentation
Patients with an ACS may complain of a new onset of
chest pain, chest pain at rest, or a deterioration of pre-
existing angina.
However, some patients present with atypical features
including indigestion, pleuritic chest pain or dyspnoea.
23. Physical examination can detect alternative diagnoses
such as aortic dissection, pulmonary embolism or
peptic ulceration.
In addition it can also detect adverse clinical signs such
as hypotension, basal crackles, fourth heart sounds
and cardiac murmurs.
24. Site & onset: substernal, severe & persistent pain.
Character: dull, heavy and pressure-like pain.
Radiation: shoulders, arms, and jaws.
Associated symptoms:
○ sympathetic effect: diaphoresis, cool and clammy skin,
palpitation and syncope.
○ Parasympathetic effect: nausea, vomiting & weakness
SIGNS & SYMPTOMS
25. ○ Inflammatory response: Mild fever
Cardiac findings:
○ S4 (and S3 if systolic dysfunction present) gallop.
○ Systolic murmur (if mitral regurgitation or VSD).
Other: ○ Pulmonary rale (id heart failure present)
○ Jugular venous distention (if heart failure
or right vent. MI)
26. What Are the Differential Diagnosis of Chest Pain?
Non-ischaemic causes of chest pain
27. ECG
Electrocardiogram is usually done to monitor the ST segment.
➢ ST segment elevation is seen with STEMI due to transmural
ischaemia.
New ST Elevation at the J point in V2-3 of at least two contiguous
leads; ≥2mm in men and ≥1.5mm in women
New ST Elevation in the J point of at least 1mm in two contiguous
leads (except for V2-3)
➢ A T-wave inversion and Q wave (not present normally) are highly
suggestive for ACS. They may not appear during the first day of
onset, so your diagnosis can’t be based upon them.
28. ➢ Note that normal ECG does not exclude the possibility of ACS.
50% of patients with NSTE-ACS have normal ECG
➢ ECG must be performed as soon as the patient presents to the
ER. In fact ECG must be performed upon anyone who presents with
chest pain of any cause.
29.
30.
31.
32.
33. CARDIAC BIOMARKERS
● Elevated ck-mb and troponin-i indicate STEMI or
NSTEMI. (Because there is necrosis) ● normal ck-mb and
troponin-i indicates unstable angina.
● Ck-mb is used to detect reinfarction (because it returns
to normal before troponins).
34. Troponin - Cardio-specific proteins. - Troponin I, and T are the most
sensitive & specific markers for myonecrosis. - Released with 4-6hrs, but
can last upto 2 week
Creatine Kinase (CK) - Creatine Kinase (CK) is released from multiple
organs such as the myocardium, skeletal muscles, and the brain. - The Iso-
form CK-MB, is cardio-specific. (Not that much specific) - Starts to rise 4-6
hrs after onset of ischemia, then falls within 48-72 hrs.
35.
36. TIMI Risk score (Predict 30d and 1yr mortality in UA/NSTEMI)
1. Age >= 65 yo
2. Markers (Elevated cardiac biomarkers)
3. ECG (ST segment deviation (>=0,5 mm)
4. Risk factors (3 or more CAD)
5. Ischemic chest pain (at least 2 or more anginal events in < 24 hours.
6. Coronary stenosis (prior stenosis of 50% or more)
7. Aspirin usage in past 7 days.
39. Nursing Management of ACS
The aim of the therapy is to:
1. Open Artery and Improve oxygen supply:
a. Supplemental O2 (ONLY if O2 Sat < 95%
b. Coronary vasodilators (Nitroglycerine) (increase supply and
dilates systemic veins (decrease preload and thus O2 demand)
c. Antiplatelet agents
d. Reperfusion therapy by 2 ways:
i. Fibrinolytic therapy
ii. Primary Percutaneous coronary intervention (PCI)
e. Antithrombotic agents.
40. 2. Reduce O2 demand:
a. Beta blockers (Block the stimulation of heart
contractility and therefore reduce o2 demand)
b. b. Analgesics (Morphine) (analgesic as well as
vasodilator)
3. Other medications:
a. ACE inhibitors. (acts as a vasodilator)
b. b. Statin therapy. (Pleiotropic effect) (reduction in
the plaque lipids which will make the plaque
more stable)
41.
42. Anti-ischemic Therapy
● BB - COMMIT-CCS trial Day 2-15
○ Reduced the endpoint of death/ MI/ cardiac arrest
○ 1 month up to 3 year for normal LVEF
● ACEI - ISIS-4 6 weeks, PEACE no benefit
● Statin - Superior stabilization of vulnerable plaque
● NTG
● PPI
● Regular activities - 1 week if revascularized/ 1 month for sports
43. Antiplatelets
1. Aspirin (ASA): Aspirin will inhibit cox-1 enzyme which lead to inhibition
of platelet aggregation . Chewable 160 to 325 mg at presentation, then
75 to 325 mg daily.
2. P2Y12 inhibitors (G-inhibitory-protein receptor in the platelet
membrane): (can be used for patients with aspirin allergy) More potent
than ASA and is combined with ASA and both agents are powerful
adjuncts to reperfusion therapy. Examples: Clopidogrel, Ticagrelor and
Prasugrel.
44. Reperfusion therapy:
1- Fibrinolytics (Thrombolytics): (door to needle time < 30 min)
● ONLY USED FOR STEMI (NOT NSTEMI).
● Reduces short and long term mortality following MI.
● Should be given during a 12hr window, and given As soon as possible.
There is no benefit if you give it after 12 hrs. Because after 12hrs the
damage that has been done to the heart is irreversible so reperfusion by
fibrinolytic won't be useful
● If Fibrinolytics fails after 30-60 minutes, refer to PCI.
45. There are 2 types of fibrinolytics:
1. Non Fibrin specific: Streptokinase.
2. Fibrin specific: Tenecteplase (TNK) - Alteplase (first
choice) - Reteplase.
46. Absolute Contraindications to thrombolytic therapy
➔ Any prior intracranial haemorrhage.
➔ Know cerebral vascular lesion.
➔ Known intracranial neoplasm.
➔ Ischaemic stroke within past 3 months.
➔ Recent major trauma/surgery/head injury (within 3 months)
➔ Active bleeding or Known bleeding disorder ( excluding
menstruation)
➔ Suspected Aortic dissection.
47. Relative Contraindications to thrombolytic therapy
➔ Oral anticoagulant therapy (example: Warfarin)
➔ Pregnancy or within 1 week postpartum.
➔ Noncompressible vascular punctures
➔ Traumatic resuscitation
➔ Poor controlled Refractory hypertension (systolic blood pressure
>180 mmHg)
➔ Internal bleeding, e.g. active peptic ulcer
➔ Dementia.
48. 2- Revascularization (surgical):
An angiography must be done first.
PCI (Percutaneous coronary intervention)
The procedure only aims to remove the clot, but a stent 3 could be placed in
the artery to improve the outcome. Preferred treatment for STEMI, as long
as it’s performed within 90 minutes from patient’s admission. (door to
balloon time < 90 mins)
CABG (Coronary Artery Bypass Graft)
49.
50. CHRONIC CORONARY SYNDROME
Chronic coronary syndromes, also called stable coronary artery
disease (CAD), stable ischemic heart disease (SIHD), chronic
stable angina or stable angina pectoris, is a clinical syndrome
characterized by squeezing, heaviness or pressure discomfort in the
chest, neck, jaw, shoulder, back, or arms which is usually precipitated
by exertion and/or emotional stress and relieved by rest and/or
Nitroglycerin.
51. It is caused by myocardial ischemia that is commonly associated
with narrowing of the coronary arteries.
•Obstructive CAD has ≥50% stenosis while nonobstructive CAD has
<50% stenosis
Angina is stable when it is not a new symptom and when there is no
deterioration in frequency, duration or severity of episodes
52. CAD indicates coronary artery disease; INOCA, ischemia and no obstructive coronary artery
disease; MINOCA, myocardial infarction and no obstructive coronary artery disease; NSTEMI,
non–ST-segment–elevation myocardial infarction; STEMI, ST-segment–elevation myocardial
infarction; and UA, unstable angina. (AHA)
53. Epidemiology
•Leading cause of death worldwide
•Global prevalence of ischemic heart disease in 2020 is 138/100,000 in
males and 90/100,000 in females
•Prevalence in 2020 ranges from 1556-<3345/100,000 in Southeast
Asia
Pathophysiology
•Due to inadequate blood supply to the myocardium as a result of
obstruction of the epicardial coronary arteries usually resulting from
atherosclerosis
54. Signs and Symptoms
•Quality of chest pain
• Described as squeezing, grip-like, suffocating and heavy pain but rarely
sharp or stabbing and typically does not vary with position or
respiration
• Occasionally, the patient may demonstrate a Levine’s sign in which a
clenched fist is placed over the precordium to describe the pain
• Many patients do not describe angina as frank pain but as tightness,
pressure or discomfort
55. •Other patients, particularly women and elderly, can manifest with atypical
symptoms such as nausea, vomiting, midepigastric discomfort or sharp
(atypical) chest pain
•Location of pain or discomfort
• Usually substernal and pain can radiate to the neck, jaw, epigastrium,
shoulders, back or arms
• Pain above the mandible, localized to a small area over the left lateral
chest wall or below the epigastrium is rarely anginal
•Duration of pain
• Lasts for minutes, usually not >20 minutes
59. Rule Out Unstable Angina
•Unstable angina is defined as angina of new onset, increases in
frequency, intensity or duration, or occurs at rest
•Presence of unstable angina predicts a higher short-term risk of acute
coronary event
•Moderate- to high-risk patients should be promptly evaluated and
treated in the emergency department because of higher risk of
coronary artery plaque rupture and death
•Low-risk patients are comparable to those patients with stable angina
and their evaluation can be performed safely and expeditiously in an
outpatient setting
60. Clinical Classification of Chest Pain
Typical angina (definite or stable) has (1) substernal chest discomfort
with a characteristic quality and duration provoked by exertion and/or
emotional stress and (2) relieved by rest and/or Nitroglycerin within
minutes
Atypical angina (probable) has two of the characteristics of typical angina
Noncardiac/anginal chest pain only has one or none of the characteristics
of typical angina
61. Physical Examination
•It is usually normal or nonspecific in stable angina patients
•Exam during or immediately after an episode of pain may be beneficial
since S4 or S3 heart sound or gallop, mitral regurgitation murmur,
paradoxically split S2, basilar rales or chest wall heave that dissipates when
pain decreases are all predictive of IHD
•Careful CV exam may reveal other related conditions such as heart failure,
valvular heart disease or hypertrophic cardiomyopathy
•Audible rub suggests pericardial or pleural disease
62. •Presence of carotid bruit, renal artery bruit, diminished pedal pulse or
palpable abdominal aneurysm are evidences of vascular disease
•Elevated blood pressure (BP), xanthomas and retinal exudates are signs
which suggest the presence of IHD risk factors
•Chest pain elicited by pressure on the chest wall can be caused by
musculoskeletal syndromes but does not eliminate the possibility of angina
due to IHD
•Body mass index (BMI), waist circumference and waist-to-hip ratio should
also be taken to determine possible metabolic syndrome, non-coronary
vascular disease and other signs of comorbid conditions
63. Laboratory Tests
•Fasting lipid profile
•Fasting blood glucose and glycated hemoglobin (HbA1c)
• Complete blood count (CBC)
• Serum creatinine
• Cardiac enzymes (troponins, creatine kinase)
• Liver function tests
• Thyroid function test
Imaging
• Chest X-ray
64. Non-invasive Cardiac Investigations
Resting Electrocardiogram (ECG)
Resting Echocardiography
Exercise ECG or ECG Stress Test
Stress Testing in Combination with Imaging
Computed Tomography (CT)
Cardiac Magnetic Resonance Imaging (CMR)
Ambulatory Electrocardiogram (Holter) Monitoring
Coronary Computed Tomography Angiography (CCTA)
Invasive Cardiac Investigation
Invasive Coronary Angiography (ICA)
67. Prevention
Influenza Vaccination especially for the elderly
Coronavirus Disease 2019 (COVID-19) Vaccine
Pneumococcal Vaccine
Follow-up and Monitoring
Patient Education
Lifestyle Modification
68. Nursing Care Plan for Acute Coronary Syndrome
Immediately assess the patient to identify whether the symptoms are chest
pain (angina) or myocardial infarction (MI).
Obtain ECG during chest pain symptoms
MI is require immediate intervention to save cardiac tissue.
As soon as an acute mi patient is brought to the emergency room, steps are
taken to reduce ischemia, relieve pain, and stop progressive circulatory
collapse and shock.
The MONA regimen is started (morphine, oxygen, nitrates, and aspirin).
69. The patient is placed on a cardiac monitor.
Iv access is established for the administration of fluids and emergency
medications.
Additional tests and procedures, such as cardiac catheterization or
CABG, may be required.
The nurse encourages and educates the patient on medication
adherence, diet and weight management, and risk factor modification
after mi.
Cardiac rehabilitation programs may be advised after discharge for
ongoing recovery.
70. Administer thrombolytic therapy as ordered.
Administer beta blockers as ordered.
Establish IV access for the immediate administration of medication, IV
fluids, and blood products.
Encourage bed rest and activity restrictions.
Bed rest lessens the workload, preventing inadequate perfusion and
potential harm to the heart.
Following a cardiac catheterization, the patient should be advised not to lift
over 10 lbs or partake in strenuous activity.
AC, atrial circumflex branch;
AM, acute marginal branch;
AV, atrioventricular node;
CB, conus branch;
D1, first diagonal branch;
D2, second diagonal branch;
LAD, left anterior descending coronary artery;
LCA, left coronary artery;
LCX, left circumflex coronary artery;
OM, obtuse marginal branch;
PD, posterior descending branch;
PL, posterolateral branch;
RCA, right coronary artery;
RPD, right posterior descending branch;
RV, right ventricle;
SN, sinus node.
Age: CAD prevalence increases after 35 years of age in both men and women. The lifetime risk of developing CAD in men and women after 40 years of age is 49% and 32%, respectively.
Gender: Men are at increased risk compared to women.
Ethnicity: Blacks, Hispanics, Latinos, and Southeast Asians, are ethnic groups with an increased risk of CAD morbidity and mortality.
Family history: Family history is also a significant risk factor. Patients with a family history of premature cardiac disease younger than 50 years of age have an increased CAD mortality risk. A separate article indicated that a father or brother diagnosed with CAD before 55 years of age, and a mother or sister diagnosed before 65 years of age are considered risk factors.
Remember: you have to ask the patient about the onset (sudden or gradual), the duration, aggravators & relievers and severity (using scale from 1 - 10 or other methods). ○ We have to differentiate between stable and unstable angina by asking about if the chest pain is even at rest or only with exertion.
