Angina pathophysiology

pathophysiology of angina pectoris

2. INTRODUCTION:
 Angina pectoris – chest pain due
to ischemia of the heart muscle, due in general
obstruction or spasm of the coronary arteries. 
 Generally heavy or gripping sensation of pain
radiated to left arm or neck.
 The main cause of angina pectoris is improper
contractility of the heart muscle, coronary
artery disease, atherosclerosis of the arteries.
 The term derives from the Greek  ankhone -
strangling, and pectus - chest, so, a strangling feeling
in the chest.
 In some cases, angina can be extremely serious
and has been known to cause death before the
age of 55.
 There is a relationship between severity
of pain and degree of oxygen deprivation in the
heart muscle – Angina.
 Sometimes angina can occur without pain.

3. CLASSIFICATION
OF ANGINA:

4. Stable angina
 Also known as Effort angina, is more common
form of angina related to myocardial ischemia.
 Chest discomfort and associated symptoms
precipitated by some activity (running, walking,
etc.).
 Symptoms typically abate several minutes
following cessation of precipitating activities and
recur when activity resumes.
Microvascular angina/ Variant angina:
 Microvascular Angina or Angina Syndrome X is
characterized by angina-like chest pain, but the
cause is unknown.
 It appears to be the result of spasm in the
tiny blood vessels of the heart, arms, and legs.
 Since Microvascular angina is not
characterized by arterial blockages, it is harder
to recognize and diagnose.

5. Unstable angina:
 Unstable angina is a form of acute coronary
syndrome.
 Worsening ("crescendo") angina attacks.
 Sudden-onset angina at rest, lasting more than
15 minutes are symptoms of unstable angina.
 UA may occur unpredictably at rest, which may
be a serious indicator of an impending heart
attack.
 64% of all unstable anginas occur between 10
PM and 8 AM when patients are at rest.

9. CHEST DISCOMFORT:
Pressure,
 Retrosternal pain
 Heaviness,
 Tightness,
 Squeezing,
 Burning sensation
 Arrhythmia
OTHER DISCOMFORTS:
Dyspnea
 Anorexia
Diaphoresis
 Increased Pulse rate
 Increased Blood pressure
AUTONOMIC SYMPTOMS:
 Nausea,
Vomiting,
SYMPTOMS:

10. DURATION OF PAIN:
• typically 1-5 minutes
• range 15sec-15min
RISK FACTORS:
• Smoking
• Hyperlipidemia
• Diabetes
• Obesity
• Sedentary lifestyle
• Family history
• Male gender

11. PATHOPHYSIOLOGY
 Oxygen is delivered to the heart by larger arteries,
arterioles and capillaries.
 In a healthy heart, there is little resistance to
blood flow in the epicardial vessels.
 When atherosclerotic plaques are present, blood
flow is increased by autoregulation process, which
dilate myocardial vessels in response to decreased
oxygen delivery and higher demand.
 The most important mediators involved in
myocardial perfusion are adenosine (a potent
vasoconstrictor), other nucleotides, nitric oxide,
prostaglandins, carbon dioxide, and hydrogen ions.

12.  The process starts with atherosclerosis,
and when inflamed leads to an active plaque,
which undergoes thrombosis and results in
acute ischemia, which finally results in cell
necrosis after calcium entry.
 Symptoms are results of myocardial
ischemia due to insufficient blood flow
through atherosclerotically changed coronary
vessels.
 In stable angina , the
developing atheroma is protected with
atherosclerotic plaque.
The unstable angina, atherosclerotic plaque
may rupture, leads to reduction of coronary
flow due to platelet aggregation, coronary
artery spasms thrombosis.


This explains why an unstable angina
appears to be independent of activity.

13. PATHOPHYSIOLOGY:
O2 SUPPLY
O2 DEMAND

14. DIAGNOSIS:
Laboratory tests (leukocytes, hemoglobin,
thyroid hormones, troponin I)
Resting ECG
Excercise ECG
Cardiac scintigraphy
Echocardiography
Coronary angiography

15. TREATMENT
 Prognostic therapy: Aspirin, lipid-lowering
therapy
 Symptomatic treatment: Beta-blockers,
long-acting nitrates, calcium-channel
blockers, ACEI.
 Percutaneous coronary intervention,
coronary artery bypass grafting