Case Study – Unstable Angina

Name: A70334
Residence: DOB:

Admission Notes

Presenting Complaint(s) (PC)

Admitting this x year old I-Taukei female with the k/c/o unstable angina with

 Chest pain or pressure

 Pain or pressure in the back, neck, jaw, abdomen, shoulders or arms
 Sweating (diaphoresis) × 2/7
 Dyspnoea
 Nausea, vomiting
 Dizziness or sudden weakness
 Fatigue
 Notes

 Unstable angina belongs to the spectrum of clinical presentations referred to collectively as

acute coronary syndromes (ACSs), which range from ST-segment elevation myocardial
infarction (STEMI) to non-STEMI (NSTEMI).
 Unstable angina is considered to be an ACS in which there is myocardial ischemia
without detectable myocardial necrosis (i.e., cardiac biomarkers of myocardial necrosis—
such as creatine kinase MB isozyme, troponin, myoglobin—are not released into the
circulation).
 Patients with this condition have also been categorized by presentation, diagnostic test
results, or course over time; these categories include new-onset angina, accelerating angina,
rest angina, early post infarct angina, and early post revascularization angina.
 Atherosclerotic plaque and overlaid thrombi is present in many cases of unstable angina,
with consequent hemodynamic deficit or microembolization. Thus, the condition is distinct
from stable angina, in which the typical underlying cause is a fixed coronary stenosis with
compromised blood flow and slow, progressive plaque growth that allows potential
development of collateral vessels.
 Other causes of angina, such as hypertrophic obstructive cardiomyopathy (HOCM) or micro
vascular disease (syndrome X), causes ischemia.

Pathophysiology

Factors involved

Supply-demand mismatch
 Excessive demand or inadequate supply of
oxygen, glucose, and free fatty acids
 Increased myocardial oxygen demand may
be caused by the following:
- Fever, AFib/Flut, Thyrotoxicosis, drug use,
Aortic stenosis and (CHF).
 Decreased oxygen supply may be caused by
the following:
- Anaemia, Hypoxemia, Polycythemia &
Hypotension.
Case
Pt. having chronic GI bleeds with CAD – Don’t=-
give anticoagulants or antiplatelets.
Plaque disruption
 Accumulation of lipid-laden macrophages and smooth
muscle cells, so-called foam cells, occurs within
atherosclerotic plaques.
 The oxidized low-density lipoprotein cholesterol (LDL-C) in
foam cells is cytotoxic, procoagulant, and chemotactic. As
the atherosclerotic plaque grows, production of
macrophage proteases and neutrophil elastases within the
plaque can cause thinning of the fibromuscular cap that
covers the lipid core.
Vasoconstriction and thrombosis
 Most patients with ACS have recurrent transient reduction
in coronary blood supply because of vasoconstriction and
thrombus formation at the site of atherosclerotic plaque
rupture.
 These events occur as consequences of episodic platelet
aggregation and complex interactions among the vascular
wall, leukocytes, platelets, and atherogenic lipoproteins.
 Can have genetic causes
 History Taking

See if evidence of angina is present

Aim to identify whether it is stable or unstable

Unstable Angina

 Discomfort is usually more intense and easily provoked, and ST-

segment depression or elevation on ECG may occur.
 symptoms may (1) occur at rest; (2) become more frequent, severe,
or prolonged than the usual pattern of angina; (3) change from the
usual pattern of angina; or (4) not respond to rest or nitroglycerin.

Ask for any associated discomfort and its frequency, location, radiation pattern, and precipitating
and alleviating factors.

Ischemic pain can manifest as heaviness, tightness, aching, fullness, or burning of the chest,
epigastrium, or arm or forearm (usually the left). These sensations less typically involve the back,
lower jaw, neck, shoulders, or arms.

Physical Examination

 Vital signs, and perform a cardiac examination.

 Clearly considered are the following:
- Aortic dissection
- Leaking or ruptured thoracic aneurysm
- Pericarditis with tamponade
- Pulmonary embolism
- Pneumothorax
- Peptic ulcer disease