Pathophysiology of Atherosclerosis Flashcards
What affects myocardial oxygen demand?
All factors that affect cardiac output (CO) also affect myocardial oxygen demand.
What is cardiac output (CO) dependent on?
Cardiac output depends on Stroke Volume (SV) and Heart Rate (HR).
How does activation of beta 1 adrenergic receptors affect heart rate?
Activation of beta 1 adrenergic receptors increases heart rate (HR).
What effect does the parasympathetic nervous system (PANS) have on heart rate?
The parasympathetic nervous system (PANS) decreases heart rate (HR) through M2 muscarinic receptors.
What factors influence preload?
Preload is influenced by venous return and regulated by alpha1 adrenergic receptors on veins, as well as the total volume of blood in the body regulated by the Renin-Angiotensin-Aldosterone System (RAAS) via the kidneys.
What is afterload in the context of cardiac function?
Afterload refers to all the forces opposing the movement of blood from the heart into the circulation, typically including systemic resistance and factors such as aortic valve stenosis and arterial stiffness.
What is contractility, and how does it affect cardiac output?
Contractility represents the strength of cardiac muscle contraction. The stronger the contraction (regulated mostly by beta1 adrenergic receptors on the heart), the more blood is ejected, impacting stroke volume and cardiac output.
What is the process of matching oxygen delivery to oxygen demand in the heart muscle known as?
It’s called “Matching O2 delivery to O2 demand in heart muscle.”
What are the determinants of cardiac oxygen demand?
The determinants of cardiac oxygen demand include heart rate, contractility, and afterload
What is the primary factor that regulates Cardiac Output (CO)?
Cardiac Output (CO) is primarily regulated by stroke volume (SV) and heart rate (HR).
How would you define atherosclerosis, and what is its development process?
Atherosclerosis is a condition characterized by the buildup of fatty plaques in the walls of arteries. It develops as cholesterol and other substances accumulate in arterial walls, leading to the formation of plaques.
What are the main types or classifications of atherosclerosis?
Atherosclerosis can be classified into various types, including coronary artery disease, carotid artery disease, and peripheral artery disease, depending on the location of the affected arteries.
What are some clinical signs and consequences of atherosclerosis?
Clinical signs and consequences of atherosclerosis can include chest pain (angina), heart attacks, stroke, peripheral artery disease, and other complications related to reduced blood flow due to narrowed or blocked arteries.
What is the relationship between cardiac output (CO) and the oxygen needs of the heart muscle?
Cardiac output must match the oxygen demand of the heart muscle to ensure it receives enough oxygen.
How is cardiac output (CO) regulated?
Cardiac output is regulated by factors like stroke volume (SV), heart rate (HR), peripheral vascular resistance, and venous return.
How does arterial plaque form in atherosclerosis?
Arterial plaque forms when cholesterol, fatty substances, cellular debris, and calcium accumulate in arterial walls following endothelial cell damage.
What role does inflammation play in atherosclerotic plaque formation and stability?
Inflammation involves the invasion of inflammatory cells, such as macrophages, and the formation of foam cells, contributing to plaque development and its stability.
What is the natural progression of atherosclerotic disease?
Atherosclerotic disease progresses as plaques gradually accumulate in arteries over time, potentially reducing blood flow and increasing the risk of complications.
What are the key differences between stable angina and acute coronary syndrome (ACS)?
Stable angina is typically triggered by exertion, relieved by rest or nitroglycerin, and follows a predictable pattern. ACS includes unstable angina and heart attacks, often featuring unpredictable chest pain, which may not be relieved by rest or nitroglycerin.
How can you identify a patient with acute coronary syndrome (ACS)?
ACS is characterized by symptoms like severe chest pain, shortness of breath, sweating, nausea, and radiating pain. Diagnosis is confirmed through ECG changes and cardiac biomarker elevation.
What are some conditions that increase the risk of atherosclerosis?
Conditions that increase risk include high blood pressure, high cholesterol, smoking, diabetes, obesity, and a family history of heart disease.
How do these conditions contribute to atherosclerosis?
They contribute through mechanisms like endothelial dysfunction, inflammation, oxidative stress, and the formation of arterial plaque. High blood pressure, for example, damages artery linings, and high cholesterol accumulates as fatty deposits in arterial walls.
Why is it crucial for all working tissues to receive an adequate supply of oxygen and energy?
All working tissues require oxygen and energy to function normally, and if the supply doesn’t match the demand, tissue damage can occur, potentially leading to tissue death.
How is the oxygen demand of the heart determined?
In the heart, oxygen demand is primarily determined by the work of the heart. While internal work (maintenance of tissue integrity) is constant, the external work of the heart, represented by the blood flow generated during cardiac contraction, changes.
What dictates the cardiac oxygen demand in the heart?
Cardiac output (CO) dictates the cardiac oxygen demand in the heart. The amount of blood flow generated by cardiac contraction influences the oxygen demand of the heart.
What is the relationship between preload and heart muscle oxygen demand?
An increase in preload will lead to an increase in heart oxygen demand.
What does preload refer to in the context of cardiac function?
Preload represents the volume of blood in the heart before contraction.
What factors influence preload?
Preload depends on venous return and is regulated by the alpha1 adrenergic receptor on veins. It also depends on the total volume of blood in the body, which can be regulated by the Renin-Angiotensin-Aldosterone System (RAAS) via the kidneys.
How does the activation of the alpha1 adrenergic receptor in veins affect blood flow?
Activation of the alpha1 adrenergic receptor in veins leads to increased intracellular calcium, causing venous smooth muscle contraction. This, in turn, increases venous pressure and facilitates the flow of blood to the right atrium, where the pressure is lower.
What does “afterload” refer to in the context of cardiac function?
Afterload refers to all the forces opposing the movement of blood from the heart into the circulation.
What is the primary physiological factor that contributes to afterload, and how does it affect blood flow and cardiac output?
Physiologically, afterload is primarily determined by arterial resistance, which opposes blood flow and cardiac output (CO).
How is arterial resistance regulated, and what effect does it have on smooth muscle in arteries and arterioles?
Arterial resistance is regulated by alpha1 adrenergic receptors on systemic arteries and arterioles. Activation of these receptors in smooth muscle increases intracellular free cytoplasmic calcium, leading to smooth muscle contraction.
