Cardiovascular Flashcards
- What is stable/classic angina
2.What is unstable angina?
3.What is variant angina?
The term “pectoris” is derived from Latin, meaning “of the chest.”
In “angina pectoris,” it specifically refers to chest pain caused by reduced blood flow and oxygen supply to the heart muscle (myocardial ischemia). The full phrase emphasizes that this type of angina is associated with discomfort or pain in the chest area.
1. Classic (Stable) Angina occurs during physical activity or emotional stress due to artery narrowing or partial occlusion, which reduces blood flow to the heart. The chest pain typically resolves within 15 minutes and is relieved by rest or nitroglycerin.
= Effort Angina:
It’s called “Effort Angina” because it’s triggered by physical activity or stress when the heart needs more oxygen.
2.Unstable Angina occurs when chest pain becomes unpredictable, often unrelated to activity. It is more severe, frequent, and prolonged compared to stable angina. This condition is caused by artery narrowing or partial occlusion, usually due to unstable plaque or blood clot(thrombus). It is a critical warning sign of a potential heart attack and requires urgent medical attention.
Pay attention to Blood Clot and unrelated to activity!!!
Unstable Angina = Crescendo Angina:
The term “Crescendo” comes from music and means “getting louder or stronger.” It reflects how the symptoms of unstable angina become more frequent, severe, or last longer over time.
(Thrombus usually refers to a blood clot that forms inside a blood vessel or the heart and remains in place, potentially causing issues like reduced blood flow or blockage.)
- Variant Angina occurs during rest and is caused by vasospasm of the coronary arteries.
Variant Angina = Prinzmetal Angina:
This is named after Dr. Prinzmetal, who discovered it. It’s also called “Variant” because it’s caused by coronary artery spasms, not blockages.
Angina 的词源及含义
词源: Angina 来自拉丁文,意思是 “紧缩” 或 “压迫”,通常用于描述一种疼痛或不适的感觉。
医学定义: 在没有修饰词(如 pectoris 或其他)的情况下,angina 通常是泛指一种疼痛或不适的症状,但它并不特指某一部位。
Artery vs Coronary artery?
When we talk about arteries, we’re referring to all the blood vessels in the body that carry oxygen-rich blood from the heart to other parts of the body. It’s a general term. For example, atherosclerosis can happen in any artery—like the ones in your legs, arms, or even your brain.
Now, coronary arteries are a specific type of artery that supply blood to the heart itself. They’re essential for keeping the heart muscle healthy and functioning properly. If there’s narrowing or blockage in the coronary arteries, it directly affects the heart’s ability to get oxygen, which can lead to conditions like stable angina, unstable angina, or even a heart attack.
So, the key difference is: if we’re talking about a general blood vessel issue anywhere in the body, we just say “artery.” But if it’s a heart-specific problem, like angina or coronary artery disease, we say “coronary artery” to be precise.
Preload vs Afterload
Preload refers to the volume of blood in the right ventricle (RV), at the end of diastole. It represents the degree of ventricular filling before contraction. Preload increases in conditions such as hypervolemia (excess blood volume), regurgitation of cardiac valves (backflow of blood into the ventricles), and heart failure (impaired pumping ability of the heart). Elevated preload places additional strain on the heart by increasing the workload and oxygen demand of the myocardium.
Afterload, on the other hand, is the resistance the left ventricle must overcome to eject blood into the systemic circulation. It rises in cases of hypertension (increased blood pressure) and vasoconstriction (narrowing of blood vessels), further increasing the heart’s workload and oxygen consumption.
The Relationship Between the Heart, Myocardium, and Coronary Arteries: Understanding Angina and Nitroglycerin’s Role
The heart pumps blood to the entire body, but it relies on the myocardium (heart muscle) to provide the force for this function. The myocardium, as the engine of the heart, needs a continuous supply of oxygen and nutrients, which comes exclusively from the coronary arteries. When these arteries are narrowed by plaque (as in Stable Angina) or blocked by a blood clot (as in Unstable Angina), or when they constrict suddenly (as in Variant Angina), the myocardium doesn’t get enough oxygen, leading to myocardial ischemia and chest pain (angina).
In Stable Angina, the plaque buildup is stable and symptoms occur predictably during exertion when oxygen demand exceeds supply. In Unstable Angina, the plaques are unstable, prone to rupture, and can form blood clots, causing more severe and unpredictable symptoms even at rest. Nitroglycerin helps relieve angina by reducing the workload of the myocardium (lowering oxygen demand) and improving coronary blood flow (increasing oxygen supply). It is highly effective for Variant Angina, moderately effective for Stable Angina, and less effective for Unstable Angina, as it cannot stabilize ruptured plaques or remove blood clots.
Nitroglycerin alleviates angina symptoms by dilating blood vessels, targeting both veins and coronary arteries.
In Classic (Stable) Angina, it works by dilating veins to reduce preload, which decreases the volume of blood returning to the heart, ultimately lowering the heart’s oxygen demand.
[How it works: Nitroglycerin relaxes and dilates veins. This leads to pooling of blood in the peripheral veins, reducing the amount of blood returning to the heart (venous return).]
Result: This decreases preload (the volume of blood in the heart before contraction), reducing the heart’s workload and oxygen demand.
For Variant (Vasospastic) Angina, it relaxes the coronary arteries, resolving vasospasms and improving oxygen supply to the myocardium. Additionally, nitroglycerin causes generalized vascular and coronary vasodilation, which increases blood flow to the myocardium, helping to reduce myocardial ischemia. However, this vasodilation can also lead to a drop in blood pressure as a side effect.
PVR=Peripheral Vascular Resistance
Peripheral vascular: Refers to the blood vessels outside of the heart and brain, primarily those supplying blood to the body’s extremities.
Peripheral vascular resistance (PVR) refers to the resistance to blood flow within the peripheral blood vessels, which are the smaller arteries, arterioles, and capillaries located away from the heart, such as in the arms, legs, and other extremities.
Nitroglycerin reduces PVR by vasodilating peripheral blood vessels, which lowers afterload, meaning the heart doesn’t have to work as hard to pump blood out to the body.
smooth muscle cells
Smooth muscle cells are like the “faucets” of blood vessels, regulating the flow of blood by vasoconstriction and vasodilation and while they are present in all blood vessels, they are most abundant in arteries. The function is consistent throughout the entire vascular system.
What are the different methods of using nitroglycerin?
Nitroglycerin is available in various dosages and can be administered either orally (PO) or sublingually (SL). Among these, the sublingual (SL) route is the most commonly used due to its rapid absorption and quick onset of action, typically within 1-3 minutes, with effects lasting approximately 10 minutes. SL tablets are sensitive to environmental factors, decomposing when exposed to heat and light, so they must be stored in their original containers to maintain effectiveness.
Translingual Spray
Nitroglycerin can be administered as a translingual spray, which is applied directly on or under the tongue. This method allows the medication to be rapidly absorbed through the oral mucosa into the bloodstream, providing fast relief of acute angina symptoms. Typically, 1-2 sprays are recommended during an episode, and the spray is particularly effective for emergencies due to its rapid onset of action.
IV (Intravenous)
Nitroglycerin can be administered intravenously (IV) to provide rapid relief of angina or to manage acute exacerbations of heart failure (HF). The dosage is titrated, meaning it is adjusted gradually based on the patient’s condition and response to the medication. IV nitroglycerin is stored in glass containers and requires special tubing because the drug can bind to plastic, reducing its effectiveness. Using glass and appropriate tubing ensures the stability and proper delivery of the medication.
Topical (Ointment and Transdermal Patch)
Nitroglycerin can also be applied topically as an ointment or a transdermal patch. Ointments are spread directly on the skin, where the drug is absorbed slowly into the bloodstream for long-term symptom control. Transdermal patches contain pre-measured doses, ensuring accurate and convenient application. These patches are typically applied to the chest or thigh, where absorption is most efficient. Healthcare providers, such as nurses, must wear gloves when handling transdermal patches to avoid accidental absorption of the drug. Both ointments and patches must be removed after 12 hours, often at bedtime, to provide an 8-12 hour nitrate-free interval. This interval helps prevent tolerance, a condition where the medication’s effectiveness diminishes with prolonged use.
PO (Oral)
Nitroglycerin is also available in oral formulations such as extended-release capsules or tablets. These are designed for chronic management rather than acute symptom relief. The extended-release feature ensures a slow and steady release of the medication into the bloodstream, maintaining stable blood levels over time.
Nitroglycerin’s side effect
Most Common Side Effects/Adverse Reactions:
Headache (acetaminophen PRN):
Nitroglycerin’s primary mechanism of action, vasodilation, can lead to several common side effects. The dilation of blood vessels increases blood flow to the brain, often causing headaches, which are among the most frequently reported side effects. These headaches can usually be relieved with acetaminophen (PRN, as needed). Additionally, vasodilation lowers blood pressure (↓ BP), which may result in dizziness or lightheadedness, particularly when standing up quickly, due to reduced blood flow to the brain.
Rebound effect of myocardial ischemia if ointment or transdermal patch not tapered over several weeks:
Abruptly discontinuing nitroglycerin ointment or patches can lead to a rebound effect, where myocardial ischemia (and angina symptoms) worsens.
Gradually reducing the dosage (tapering) over several weeks is necessary to prevent this effect and allow the body to adjust to the absence of the medication.
Reflex tachycardia if given too rapidly:
Administering nitroglycerin too quickly can cause reflex tachycardia, a compensatory increase in heart rate triggered by a rapid drop in blood pressure.
In extreme cases, nitroglycerin can cause severe hypotension due to excessive vasodilation, resulting in circulatory collapse, a life-threatening condition.
Combining nitroglycerin with beta blockers, calcium channel blockers, antihypertensive drugs, or alcohol can amplify the blood pressure-lowering (hypotensive) effect, increasing the risk of dangerously low blood pressure.
IV Nitro May Decrease Effects of Heparin:
Intravenous nitroglycerin may reduce the anticoagulant effects of heparin, potentially requiring an adjustment in the heparin dosage to maintain its efficacy.
Nitroglycerin is contraindicated if the patient has taken PDE5 inhibitors (such as sildenafil, marketed as Viagra) in the past 24-48 hours.
Reason: Using these drugs together can cause a dramatic drop in blood pressure, leading to severe hypotension or cardiovascular collapse.
PDE5 stands for phosphodiesterase type 5, which is an enzyme found in the smooth muscle cells of blood vessels, especially in the lungs and the penis. Its main role is to break down a molecule called cGMP (cyclic guanosine monophosphate), which is involved in relaxing smooth muscle and dilating blood vessels.
Inhibitors like sildenafil (Viagra): By blocking PDE5, these drugs increase levels of cGMP, leading to better relaxation of blood vessels, improved blood flow, and their use in conditions like erectile dysfunction and pulmonary hypertension.
Antihypertensives, Antidysrhythmic Class II: Beta Blockers
What is the mechanism of action of beta blockers?
Beta blockers function by inhibiting beta₁ and beta₂ receptor sites, which are part of the sympathetic nervous system. These receptors are normally activated by catecholamines such as epinephrine (adrenaline) and norepinephrine, which increase heart rate, contractility, and overall cardiac workload. By blocking these receptors, beta blockers reduce the effects of the sympathetic nervous system, leading to a decrease in heart rate and blood pressure. This action helps to alleviate stress on the heart and reduce its oxygen demand, making beta blockers effective in managing various cardiovascular conditions.
What are the main uses of beta blockers?
Beta blockers are used to manage several cardiovascular conditions due to their diverse effects. As antianginal agents, they reduce oxygen demand/consumption and help relieve symptoms of angina. As antidysrhythmic agents, they stabilize the heart’s electrical activity, making them effective for managing abnormal heart rhythms. Additionally, as antihypertensives, they lower blood pressure by reducing the effects of the sympathetic nervous system on the heart and peripheral blood vessels.
Can you name some common examples of beta blockers?
Common examples of beta blockers include metoprolol, atenolol, and propranolol. Metoprolol is frequently prescribed for conditions such as hypertension and heart failure due to its cardio-selective properties. Atenolol is another selective beta blocker commonly used to manage angina and high blood pressure. Propranolol, a non-selective beta blocker, is used for various conditions, including arrhythmias and anxiety, as it affects both beta₁ and beta₂ receptors.
Why are beta blockers effective for treating angina?
Beta blockers are particularly effective for treating classic (stable) angina pectoris. They reduce the heart’s workload by decreasing heart rate and BP, which in turn lowers oxygen consumption. By addressing the imbalance between oxygen supply and demand, beta blockers alleviate myocardial ischemia and reduce the pain associated with angina. This mechanism makes them a reliable choice for managing chronic stable angina symptoms.
Nitroglycerin: Primarily reduces preload by dilating veins, reducing the amount of blood returning to the heart.(However, the dilation of coronary arteries plays a significant role, especially in conditions like variant (Prinzmetal’s) angina, where coronary artery spasm is the main problem.)
Beta blockers: Primarily reduce afterload through HR and myocardial contractility, with a secondary, less significant effect on preload.
What are non selective Beta Blockers?
Nonselective beta blockers block both β₁ and β₂ receptors on both heart and lung. A common prototype is propranolol, which reduces heart rate (HR) and blood pressure (BP) as antihypertensives. They can be also used for anxiety. However, blocking β₂ receptors in the lungs can cause adverse effects such as bronchoconstriction, making these drugs risky for patients with asthma or chronic obstructive pulmonary disease (COPD). Other adverse effects include impotence in some patients. During treatment, vital signs should be monitored closely, especially early on, to assess the drug’s impact on HR and BP. It is also important to monitor lung function because these drugs can trigger bronchospasm.
What are selective beta blockers?
Selective beta blockers primarily block β₁ receptors, focusing their effects on the heart. The prototype for this class is metoprolol, which lowers HR and BP, reducing cardiac workload and oxygen demand. These drugs are safer for patients with respiratory conditions because they have minimal effects on β₂ receptors in the lungs. Vital signs, including HR and BP, should still be closely monitored early in treatment to ensure the patient has no side effects like bradycardia, hypotension, and 1st AV block.
As antidysrhythmic Class II, it blocks beta-adrenergic receptors causing depression of phase 4 of the action potential. Slow the recovery of the cells, leading to slowing of conduction and automaticity. It lowers ventricular rate/conduction in atrial dysrhythmias. The adverse reactions include broncospasm(non-selective), dyspnea, bradycardia, hypotension.
What are important Considerations for Beta Blocker Use?
Beta blockers should not be discontinued abruptly. Stopping these drugs suddenly can cause rebound tachycardia or a recurrence of angina symptoms due to heightened sympathetic activity. Instead, the dosage should be tapered over several days. Beta blockers are usually avoided in patients with low HR (<60 bpm) or low BP (<100/60 mmHg), as they may exacerbate bradycardia or hypotension.
A significant caution is the potential for hypoglycemia unawareness, where beta blockers can mask symptoms like increased heart rate, making it difficult for diabetic patients to recognize low blood sugar levels. Additionally, beta blockers should not be stopped during the perioperative period, even if the patient is NPO (nothing by mouth), because sudden withdrawal can lead to severe cardiac events under stress. Beta blockers are contraindicated in patients with second- or third-degree AV block, as they can worsen conduction disturbances which potentially lead to fatal outcomes.
Why Beta Blockers May Cause Hypoglycemia Unawareness?
Beta blockers can mask the symptoms of hypoglycemia, such as increased heart rate, palpitations, or shakiness, which are typically mediated by the sympathetic nervous system. These symptoms act as early warning signs for low blood sugar. Since beta blockers inhibit the sympathetic response by blocking beta₁ and beta₂ receptors, patients, particularly those with diabetes, may not recognize the onset of hypoglycemia, leading to unawareness and delayed treatment.
Why Beta Blockers Should Not Be Stopped During the Perioperative Period?(Even if NPO)
Stopping beta blockers abruptly during the perioperative period can cause a rebound effect, such as severe tachycardia, hypertension, or even myocardial ischemia, due to heightened sympathetic activity. Stress from surgery or anesthesia can further exacerbate the cardiac workload if beta blockers are discontinued. Continuing beta blockers ensures cardiovascular stability, even if the patient is NPO (nothing by mouth), to prevent potential complications during surgery. They can often be administered intravenously if oral intake is restricted.
Antidysrhythmic : Class III
Amiodarone is a Class III antidysrhythmic drug primarily used to treat ventricular tachycardia and ventricular fibrillation. It works as a potassium channel blocker, prolonging repolarization and slowing down heart conduction. Although its exact mechanism is not fully understood, it effectively stabilizes heart rhythms, making it useful in life-threatening arrhythmias.
While amiodarone is effective, it comes with several serious side effects. Common adverse reactions include hypotension, bradycardia, and heart blocks. Long-term use can affect the thyroid, leading to either hypothyroidism or hyperthyroidism, as well as hepatic dysfunction. It may also cause peripheral neuropathy and blue-gray skin discoloration, especially in sun-exposed areas.
Patients taking amiodarone should avoid grapefruit juice, as it inhibits the metabolism of the drug, increasing the risk of toxicity. Amiodarone also interacts with other medications, such as quinidine, digoxin, and warfarin, raising blood levels and increasing the risk of bleeding or arrhythmias. Additionally, when taken with certain antibiotics like azithromycin, it can prolong the QT interval with certain antibiotics like azithromycin, increasing the risk of dangerous heart rhythms like torsades de pointes.
When administering IV amiodarone, it is essential to monitor the IV site frequently, as the drug can cause irritation and phlebitis. Patients should be taught to check their pulse regularly and monitor vital signs, as bradycardia and hypotension are common side effects.
Long-term use of amiodarone requires monitoring for neurotoxicity, thyroid function, and eye health, as the drug can cause neuropathy, hypothyroidism or hyperthyroidism, and visual disturbances. Patients should be informed that food increases the absorption rate of amiodarone, which may impact dosing and effectiveness.
Continuous ECG monitoring is necessary, especially during IV administration or when initiating oral (PO) therapy, to detect potential QT prolongation or arrhythmias. Additionally, since amiodarone carries a risk of pulmonary toxicity, patients should be assessed for shortness of breath (SOB), cough, or lung complications, which may indicate pulmonary fibrosis.
Proper patient education and routine monitoring help reduce complications and ensure the safe and effective use of amiodarone.
Antihypertensive, Antianginal, and Antidysrhythmic drugs
How do Calcium Channel Blockers work?
Calcium channel blockers (CCBs) work by inhibiting the influx of calcium ions (Ca²⁺) through calcium channels located in vascular smooth muscle and myocardial cells. Since calcium is essential for muscle contraction, blocking its entry reduces the contraction of blood vessels and the heart muscle. This results in relaxation of vascular smooth muscle and a decrease in myocardial contractility.
Calcium channel blockers (CCBs) are widely used medications that are labeled as antihypertensive, antianginal, and antidysrhythmic drugs, meaning they have multiple important uses. They work by blocking calcium from entering the smooth muscle of blood vessels and myocardium during depolarization, which leads to relaxed coronary arteries, improved myocardial oxygen delivery in patients with vasospastic angina, and lower vascular resistance. There are two main types: non-dihydropyridines (like diltiazem), which are mainly used for heart rhythm issues (dysrhythmias), and dihydropyridines (like nifedipine), which are primarily used for high blood pressure (HTN).
What are effects of Calcium Channel Blockers?
Workload?
Calcium channel blockers decrease cardiac contractility through a negative inotropic effect by reducing calcium entry into myocardial cells. This lowers the force of contraction, decreasing the heart’s workload. Additionally, CCBs cause relaxation of vascular smooth muscle, leading to dilation of coronary arteries, which improves oxygen supply to the heart, and peripheral arteries, which reduces afterload. These effects together result in decreased workload, myocardial oxygen demand, afterload, and peripheral vascular resistance, ultimately lowering blood pressure.
Definition: The overall effort or energy the heart needs to pump blood, which includes both the force needed to eject blood and the oxygen consumption of the heart muscle.
Components of workload:
Preload: More blood returning to the heart increases workload because the heart has to handle a larger volume.
Afterload: The resistance the heart has to overcome to pump blood out of the ventricles.
Heart rate: A faster heart rate increases workload because the heart is working more frequently.
Contractility: Stronger contractions require more energy and oxygen.
How do CCBs treat angina?
CCBs are effective in treating both classic (stable) and variant (vasospastic) angina. For classic angina, they reduce oxygen demand by relaxing peripheral arterioles, which lowers blood pressure and afterload, helping to balance oxygen supply and demand during physical exertion. For variant angina, CCBs relax coronary arteries to relieve arterial spasms and restore blood flow to the myocardium.
In addition to treating angina, CCBs are used to manage dysrhythmias, such as supraventricular tachycardia (SVT), by slowing conduction through the heart’s electrical system and stabilizing abnormal rhythms. They are also effective for managing hypertension by lowering blood pressure through arterial dilation, which reduces peripheral vascular resistance.
How do CCBs treat dysrhythmia?
It blocks calcium channel in the heart muscle cellls, leading to prolongation of repolarization period, slowing conduction through AV node.
It is used to treat atrial flutter/fibrillation, SVT
Adverse reactions include bradycardia, hypotension, prolonged QT
What are CCBs prototype drugs?
Diltiazem, a non-dihydropyridine calcium channel blocker, has a greater impact on heart function than on vasodilation. It reduces heart rate and myocardial contractility, making it effective for managing dysrhythmias such as atrial fibrillation or supraventricular tachycardia (SVT). This type of calcium channel blocker is often used in in-patient settings where precise control of heart rate is required. In contrast, nifedipine, a dihydropyridine calcium channel blocker, primarily causes vasodilation, particularly in peripheral blood vessels, with less effect on heart rate or contractility. It lowers blood pressure by relaxing arterial smooth muscle and reducing afterload, making it a common choice for treating hypertension in outpatient settings.