L8 - Anti - Anginals Flashcards
What is angina?
Angina is chest pain or discomfort caused by an insufficient blood supply (lack of oxygen-rich blood) to the myocardium (heart muscle). It is often associated with coronary artery disease, though not always.
What is the main cause of angina?
The primary cause of angina is a “supply and demand” issue, where the heart muscle requires more oxygen than the coronary arteries can supply, often due to blockages or narrowing (atherosclerosis) of the coronary arteries.
How does coronary artery disease lead to angina?
In coronary artery disease, atherosclerotic plaques narrow or block the coronary arteries, reducing blood flow to the myocardium. This results in insufficient oxygen delivery, causing chest pain (angina), especially during physical exertion or stress when the heart’s oxygen demand increases.
Is angina always caused by coronary artery disease?
No, while angina is often caused by coronary artery disease, it can also occur due to other factors, such as coronary spasm, anemia, or increased heart rate, that lead to reduced oxygen supply to the heart.
How do stable, variant, and unstable angina differ?
Stable Angina: Triggered by exertion or stress, caused by atherosclerosis narrowing coronary arteries, leading to insufficient oxygen supply during increased heart demand. Symptoms are predictable and relieved by rest or medication.
Variant Angina (Prinzmetal’s): Caused by coronary artery spasm, occurring at rest or during sleep, not related to physical exertion. It results in temporary narrowing of the arteries and reduced blood flow.
Unstable Angina: Occurs unpredictably, at rest or minimal exertion, and can last longer. It suggests a high risk of a heart attack and requires urgent medical attention.
What is the cause of stable angina?
Stable angina is caused by atherosclerotic plaques narrowing coronary arteries, leading to insufficient oxygen supply during increased heart demand, typically triggered by exertion or stress.
What causes variant angina?
Variant angina is caused by a spasm in a coronary artery, leading to temporary narrowing and reduced blood flow, often occurring at rest or during sleep.
Why is unstable angina more dangerous?
Unstable angina is more dangerous because it occurs unpredictably, can last longer, and may indicate an impending heart attack, requiring immediate medical intervention.
What is the first line of management for stable angina?
The first line of management for stable angina involves lifestyle modifications, including stopping smoking, adopting a cardioprotective diet, achieving and maintaining a healthy weight, increasing physical activity within individual limits, and limiting alcohol consumption to recommended levels.
How does smoking cessation impact the management of stable angina?
Stopping smoking helps reduce the risk of atherosclerosis, improves blood vessel function, and lowers the chances of worsening coronary artery disease, thereby alleviating angina symptoms and improving overall heart health.
What dietary changes are recommended for managing stable angina?
: A cardioprotective diet is encouraged, which includes reducing intake of saturated fats, trans fats, and cholesterol while increasing the consumption of fruits, vegetables, whole grains, and healthy fats (e.g., omega-3 fatty acids) to improve heart health and reduce the risk of further plaque build-up in coronary arteries.
How does maintaining a healthy weight help manage stable angina?
Achieving and maintaining a healthy weight reduces the heart’s workload, lowers blood pressure, and improves cholesterol levels, all of which help manage angina and prevent the progression of coronary artery disease.
What role does physical activity play in managing stable angina?
ncreasing physical activity levels, within individual tolerance limits, improves cardiovascular fitness, helps control weight, and reduces risk factors such as hypertension and diabetes, which can improve angina symptoms and overall heart function.
Why is alcohol consumption limited in the management of stable angina?
Limiting alcohol consumption helps reduce the risk of high blood pressure, arrhythmias, and weight gain, all of which can worsen the symptoms of stable angina and contribute to the progression of coronary artery disease.
What are β blockers and how do they work?
β blockers (β adrenergic receptor antagonists) are drugs that block β-adrenergic receptors, reducing the effects of adrenaline (epinephrine) and noradrenaline on the heart and blood vessels.
How do β blockers affect heart rate and stroke volume?
β blockers decrease heart rate (HR) by blocking β1 receptors in the heart, leading to slower electrical conduction and reduced contractility. This also reduces stroke volume (SV) and overall cardiac output (CO), lowering the heart’s demand for oxygen.
What is the effect of β blockers on blood pressure (BP)?
β blockers lower blood pressure by reducing cardiac output (CO) through decreased heart rate and stroke volume. They also inhibit renin release from the kidneys, reducing the activity of the renin-angiotensin-aldosterone system (RAAS), which helps to lower BP.
How do β blockers influence the renin-angiotensin-aldosterone system (RAAS)?
β blockers reduce the release of renin from juxtaglomerular (JG) cells in the kidneys, leading to decreased production of angiotensin II, which in turn lowers aldosterone levels. This results in reduced vasoconstriction and fluid retention, contributing to lower blood pressure.
What are the effects of β1 receptor stimulation?
Stimulation of β1 receptors results in positive cardiac chronotropy (increased heart rate) and inotropy (increased cardiac contractility). It also stimulates renin release in the kidneys, activating the renin-angiotensin-aldosterone system (RAAS), which contributes to blood pressure regulation.
What happens when β2 receptors are stimulated?
β2 receptor stimulation induces smooth muscle relaxation (e.g., in the lungs, causing bronchodilation), tremor in skeletal muscle, and increased glycogenolysis in the liver and skeletal muscles, providing more glucose for energy.
What are the effects of β3 receptor stimulation?
β3 receptor stimulation promotes lipolysis, leading to the release of free fatty acids from adipose tissue, which can be used as an energy source by the body.
What are the main effects of β blockers on the heart?
The main effects of β blockers on the heart are a decrease in cardiac output (CO) and blood pressure (BP). This occurs through a reduction in heart rate (HR) and stroke volume (SV), which lowers cardiac output. The equation for cardiac output is:
Cardiac Output = Stroke volume (End Diastolic Volume – End Systolic Volume) x Heart Rate.
For blood pressure, the equation is:
Blood Pressure = Cardiac Output x Resistance.
By reducing cardiac output, β blockers lower blood pressure, particularly in acute settings.
How do β blockers affect renin and the renin-angiotensin-aldosterone system (RAAS)?
β blockers decrease renin release from the kidneys, which leads to lower production of angiotensin II and aldosterone. This results in increased renal loss of sodium and water, contributing to a long-term decrease in arterial pressure (chronic effect).
How do β blockers have an anti-anxiety effect?
β blockers have an anti-anxiety effect by blocking β receptors, particularly in the heart and central nervous system, which reduces the physical symptoms of anxiety such as tachycardia (increased heart rate) and tremors, helping to calm the body’s stress response.
What is the danger of β2 receptor stimulation in the bronchial tree?
Stimulation of β2 receptors in the bronchial tree leads to smooth muscle relaxation, which is generally beneficial for bronchodilation. However, in certain situations (e.g., in patients with asthma or chronic obstructive pulmonary disease), the use of β blockers, especially non-selective ones, can block β2 receptors, leading to bronchoconstriction. This may worsen breathing difficulties and potentially trigger bronchospasms.
Why are non-selective β blockers dangerous in patients with respiratory conditions?
Non-selective β blockers block both β1 and β2 receptors. Blocking β2 receptors in the lungs can result in bronchoconstriction and worsen conditions like asthma or chronic obstructive pulmonary disease (COPD), leading to increased difficulty in breathing.
Q: What are the cardiovascular uses of β-blockers (pre-2006)?
Hypertension: β-blockers reduce heart rate and cardiac output, lowering blood pressure.
Arrhythmias: They help manage arrhythmias by reducing heart rate and stabilising electrical conduction.
Angina: β-blockers reduce myocardial oxygen demand by decreasing heart rate and contractility, easing angina symptoms.
Hypertrophic Cardiomyopathy: They improve symptoms by reducing heart rate and decreasing myocardial contractility.
Phaeochromocytoma: β-blockers are used to control hypertension in phaeochromocytoma, often alongside α-blockers.
Secondary Prevention: After a myocardial infarction, β-blockers reduce the risk of further cardiac events by decreasing workload and improving heart function.
Cardiovascular
uses of β-blockers
(post-2006)
Cardiac Arrhythmias
Angina
Hypertension
Hypertrophic Cardiomyopathy
Phaeochromocytoma
Secondary Prevention
How does cardiac muscle contraction occur through β-adrenergic receptors?
Norepinephrine (NE) is released from sympathetic nerve terminals and binds to β1 or β2 adrenergic receptors on cardiac muscle cells.
This binding activates the Gs protein (stimulatory G protein).
Gs activates adenylyl cyclase, which increases cAMP levels.
cAMP activates protein kinase A (PKA), which phosphorylates key proteins involved in muscle contraction, such as L-type calcium channels and proteins of the contractile apparatus.
This results in an increase in intracellular calcium levels, leading to cardiac muscle contraction (positive inotropy).
What is the role of β1 and β2 receptors in cardiac muscle contraction?
β1 receptors are predominantly responsible for increasing heart rate and contractility in the heart.
β2 receptors also contribute to relaxation and vasodilation but play a lesser role in cardiac muscle contraction compared to β1 receptors.
How does adrenergic stimulation lead to vascular smooth muscle relaxation?
A:
Adrenergic neurotransmitters (e.g., adrenaline (Adr) or noradrenaline (NA)) bind to β2 adrenergic receptors on vascular smooth muscle cells.
This activates the Gs protein, which increases cAMP levels.
cAMP activates protein kinase A (PKA), which inhibits myosin light chain kinase (MLCK).
The inhibition of MLCK reduces phosphorylation of the myosin light chain, leading to decreased interaction between actin and myosin filaments.
This results in smooth muscle relaxation, leading to vasodilation and a decrease in vascular resistance.
What is the mechanism of action of Carvedilol as a vasodilatory agent?
Carvedilol is a non-selective β-adrenergic receptor blocker (β1, β2) and an α1 adrenergic receptor blocker. By blocking β1 receptors, it reduces heart rate and ventricular contractility, decreasing myocardial oxygen demand. The α1 blockade causes vasodilation, further reducing the workload of the heart and lowering blood pressure.
