Angina pectoris
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Angina pectoris
Cardiovascular system
Cardiac arrhythmias
Atrioventricular block
Bundle branch block
Pulseless electrical activity
Atrial fibrillation
Atrial flutter
Atrioventricular nodal reentrant tachycardia (AVNRT)
Premature atrial contraction
Wolff-Parkinson-White syndrome
Brugada syndrome
Long QT syndrome and Torsade de pointes
Premature ventricular contraction
Ventricular fibrillation
Ventricular tachycardia
Cardiac tumors
Cardiac tumors
Shock
Shock
Vascular disorders
Arterial disease
Aneurysms
Aortic dissection
Angina pectoris
Coronary steal syndrome
Myocardial infarction
Prinzmetal angina
Stable angina
Unstable angina
Abetalipoproteinemia
Familial hypercholesterolemia
Hyperlipidemia
Hypertriglyceridemia
Coarctation of the aorta
Conn syndrome
Cushing syndrome
Hypertension
Hypertensive emergency
Pheochromocytoma
Polycystic kidney disease
Renal artery stenosis
Hypotension
Orthostatic hypotension
Lymphangioma
Lymphedema
Peripheral artery disease
Subclavian steal syndrome
Nutcracker syndrome
Superior mesenteric artery syndrome
Angiosarcomas
Human herpesvirus 8 (Kaposi sarcoma)
Vascular tumors
Behcet's disease
Kawasaki disease
Vasculitis
Chronic venous insufficiency
Deep vein thrombosis
Thrombophlebitis
Cardiovascular system pathology review
Acyanotic congenital heart defects: Pathology review
Aortic dissections and aneurysms: Pathology review
Atherosclerosis and arteriosclerosis: Pathology review
Cardiac and vascular tumors: Pathology review
Cardiomyopathies: Pathology review
Coronary artery disease: Pathology review
Cyanotic congenital heart defects: Pathology review
Dyslipidemias: Pathology review
Endocarditis: Pathology review
Heart blocks: Pathology review
Heart failure: Pathology review
Hypertension: Pathology review
Pericardial disease: Pathology review
Peripheral artery disease: Pathology review
Shock: Pathology review
Supraventricular arrhythmias: Pathology review
Valvular heart disease: Pathology review
Vasculitis: Pathology review
Ventricular arrhythmias: Pathology review
Assessments
Angina pectoris
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External References
First Aid
2022
2021
2020
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2018
Acebutolol p. 246
angina and p. 326
Angina
aortic stenosis p. 298
atherosclerosis p. 308
cilostazol/dipyridamole for p. 445
cocaine causing p. 594
contraindicated drugs p. 326, 329
drug therapy for p. 325, 326, 363
glycoprotein IIb/IIa inhibitors for p. 445
ischemic disease and p. 310
presentation p. 716
unstable/NSTEMI treatment p. 316
Intestinal angina p. 395
Angina pectoris
β -blockers for p. 247
Atherosclerosis p. 308
stable angina with p. 310
β -blockers p. 247
angina p. 326
Calcium channel blockers p. 325
angina p. 325
“Intestinal angina p. 395
myocardial O2 consumption/demand p. 292
angina treatment p. 326
Nitroglycerin p. 325
angina p. 310
Stable angina p. 310
Triptans p. 567
angina and p. 310
Variant angina p. 310
Transcript
Content Reviewers
Contributors
Angina comes from the latin angere, which means to strangle, and pectoris comes from pectus, meaning chest—so angina pectoris loosely translates to “strangling of the chest”, which actually makes a lot of sense, because angina pectoris is caused by reduced blood flow which causes ischemia to the heart muscle, or lack of oxygen to the heart, almost like the heart’s being strangled which causes terrible chest pain.
Stable angina or chronic angina is the most common type of angina and it usually happens when the patient has greater than or equal to 70% stenosis, meaning 70% of the artery is blocked by plaque buildup.
This small opening that blood flows through might be enough to supply the heart during rest, but if the body demands more blood and oxygen, like during exercise or stressful situations, the heart has to work harder, and therefore needs more blood and oxygen itself.
It’s during these time of exertion or emotional stress that people with stable angina have chest pain, since the blood flow isn’t meeting the metabolic demands of the heart muscle, or myocardium.
But the pain usually goes away with rest.
In the majority of cases, the underlying cause of stable angina is atherosclerosis of one or more the coronary arteries—arteries supplying blood to the heart muscles.
Other heart conditions that might lead to stable angina are ones that cause a thickened heart muscle wall, which would require more oxygen.
This increase in muscle size can be due to hypertrophic cardiomyopathy from a genetic cause, or as a result from the heart having to pump against higher pressures, as is the case in aortic stenosis, which is a narrowing of the aortic valve, or hypertension.
Sources
- "Robbins Basic Pathology" Elsevier (2017)
- "Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)
- "Pathophysiology of Disease: An Introduction to Clinical Medicine 8E" McGraw-Hill Education / Medical (2018)
- "Pathogenesis of angina pectoris" undefined (1982)
- "Unstable angina pectoris: Pathogenesis and management" Current Problems in Cardiology (1989)
- "Management of Chronic Stable Angina" Critical Care Nursing Clinics of North America (2017)
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