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Angina Pectoris Pathophysiology

This document discusses angina pectoris and the factors that can lead to it. Angina is caused by a lack of oxygenated blood flow to the heart muscle, typically due to blockages in the coronary arteries from atherosclerosis. It summarizes both modifiable factors like diet, obesity, and smoking and non-modifiable factors like age, gender, and family history that can increase the risk of angina. The document then outlines the physiological process where exertion increases oxygen demand on the heart but reduced blood flow cannot meet this demand, causing chest pain. If compensatory mechanisms in the body fail to address this imbalance, it can lead to a myocardial infarction.

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dana
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5K views2 pages

Angina Pectoris Pathophysiology

This document discusses angina pectoris and the factors that can lead to it. Angina is caused by a lack of oxygenated blood flow to the heart muscle, typically due to blockages in the coronary arteries from atherosclerosis. It summarizes both modifiable factors like diet, obesity, and smoking and non-modifiable factors like age, gender, and family history that can increase the risk of angina. The document then outlines the physiological process where exertion increases oxygen demand on the heart but reduced blood flow cannot meet this demand, causing chest pain. If compensatory mechanisms in the body fail to address this imbalance, it can lead to a myocardial infarction.

Uploaded by

dana
Copyright
© Attribution Non-Commercial (BY-NC)
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as DOCX, PDF, TXT or read online on Scribd
  • Angina Pectoris Pathophysiology
  • Progression of Angina Pectoris

Angina Pectoris

MODIFIABLE FACTORS NON MODIFIABLE FACTORS


 High cholesterol diet  Age
 Obesity  Gender
 Cigarette smoking  Family history
 Sedentary lifestyle

Formation of thrombus

Presence of atherosclerosis

Eating heavy meals Exposure to cold, Physical


emotional stress, exertion
smoking
 Blood flow in the
mesenteric region  Myocardial 02
Vasoconstriction
demand

Reduced coronary tissue perfusion

↓myocardial oxygenation

 O2 demand
Aerobic metabolism

HR accelerates
 Lactic acid ↓ ATP

↓ Cardiac contraction Myocardium Vent. filling


Lactic acidosis becomes ischemic time
strength

Chest pain
Depression of Vent. perform ↓SV
vent. function deteriorates
Auto regulation of
blood flow or LV diastole
compensation ↓SV pressure rise

 In diameter of blood Change in systemic BP Pulmonary


vessels and arteries congestion dyspnea
Angina Pectoris

If compensatory
mechanism fails

Prolonged ischemia and


myocardium

Myocardial infarction

↓ myocardial ↓SV ↓ ejection Altered vent.


contractility traction Compliance

Decreased cardiac output

Decreased perfusion

Stimulate the renin angiotensin aldosterone


system

Stimulation of CNS

Release of epinephrine and norepinephrine

 Heart rate

If compensatory mechanism fails

Complications such as:

 Dysrithmia
 Cardiogenic shock

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