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.
Side effects of CCBs
Why should the patient on CCB not take grapefruit juice or eat grapefruit?
Calcium channel blockers are associated with several side effects due to their vasodilatory and cardiovascular effects. Common side effects include headache, which results from increased blood flow to the brain, and hypotension, more frequently observed with dihydropyridines like nifedipine and less common with non-dihydropyridines like diltiazem. Other effects include dizziness, flushing of the skin, and reflex tachycardia, which occurs as a compensatory response to the drop in blood pressure. Additionally, peripheral edema may occur due to fluid retention in the lower extremities caused by vasodilation.
Because of their broad applications, CCBs are commonly used to treat hypertension, chest pain (angina), and heart rhythm disorders, but they do come with some side effects. Common ones include headaches, dizziness, low blood pressure, skin flushing, and leg swelling (peripheral edema). One thing to watch out for with dihydropyridines like nifedipine is reflex tachycardia, where the heart speeds up in response to the drop in blood pressure. Also, patients should avoid grapefruit, as it can interfere with drug metabolism and lead to stronger effects than intended.
(Grapefruit (juice, fruit) has flavanoid and nonflavanoid (furanocoumarins) components that interferes with enterocyte cytochrome P450 3A4 (CYP3A4 for short) activity. CYP3A4 is involved in the bioinactivation of CCB). CYP3A4 is located in epithelial cells (enterocytes) lining the small intestines and colon, and in the parenchymal cells of the liver (hepatocytes). Consuming grapefruit (Seville oranges, limes and pomelos/ˈpɑː.mə.loʊz/ too) can significantly increase the amount of oral CCB in the serum, increasing its effect, leading to potential toxicity. Similar effect is seen in taking grapefruit with statins, amiodarone, warfarin, and many others.)
Patient Teaching for Antianginals
When using nitroglycerin, patients should take one tablet at the onset of chest pain. If the pain persists or worsens after five minutes, they must call 911 immediately. They can take up to three doses, each spaced five minutes apart, but only if medical help has been contacted. To maintain the medication’s effectiveness, nitroglycerin pills should be stored away from direct sunlight, which can degrade the drug. For beta blockers and calcium channel blockers, patients should be taught how to monitor their own pulse and be aware of side effects like dizziness or faintness, which could indicate low blood pressure (hypotension). It is critical to notify the healthcare provider if these symptoms occur. Additionally, patients should never stop taking any antianginal medication without first consulting their provider to avoid potential complications or worsening of their condition.
Antidysrhythmic: Pharmacodynamics
Antidysrhythmic: Nursing Intervention
Block adrenergic stimulation of heart
depress myocardial excitability and contractility
decrease conduction velocity in cardiac tissue
increase myocardial recovery time(repolarization)
suppress automaticity(spontaneous depolarization to initiate beats)
Most antidysrhythmics are also proarrhythmic and vasodilator
Give medications as schedule
Monitor HR and BP
Monitor ECG(prolonged QT), liver(AST/ALT) and renal function(creat.)
monitor drug levels of procainamide for s/s of toxicity like seizure
avoid alcohol, caffeine, tobacco,
monitor for orthostatic hypotension
Aspirin as antiplatelet
Aspirin is an antiplatelet medication that works by inhibiting platelet aggregation. Its mechanism of action involves blocking the enzyme cyclooxygenase (COX), which is essential for the synthesis of thromboxane A2 (TxA2), a chemical required for platelet activation and clot formation. Aspirin is used in various conditions to reduce the risk of clot-related complications. In acute myocardial infarction (MI), patients are advised to bite and chew aspirin to ensure rapid absorption and effect. It is also used for both treatment and prophylaxis of cerebrovascular accidents (CVA), especially within 24-48 hours of a stroke, and for coronary artery disease (CAD) prophylaxis. Aspirin can also be administered as a suppository in situations where oral intake is not feasible, such as when the patient is vomiting or unconscious.
Common side effects include tinnitus (ringing in the ears) and an increased risk of bleeding, particularly in those prone to gastrointestinal bleeding. It is not recommended for children with viral infections due to its association with Reye’s syndrome, a rare but serious condition. Adverse reactions can include nausea, dyspepsia, heartburn, gastrointestinal bleeding, toxicity, hypersensitivity reactions, and anaphylactoid reactions.
Aspirin has no specific antidote, and its effects cannot be reversed immediately. To reduce bleeding risks, it should be discontinued one week before surgery. Despite its short half-life of 20 minutes, aspirin has long-lasting effects on platelets. It is rapidly absorbed in the gastrointestinal tract, with an onset of action within 5-30 minutes, reaching peak antiplatelet activity within 25 minutes to 2 hours and lasting for 3-6 hours. Precautions include avoiding concurrent use with NSAIDs, as this combination increases the risk of bleeding. Additionally, aspirin should be used cautiously in patients over 70 years old (as per Beers Criteria) due to heightened bleeding risks and uncertain benefits for primary prevention of cardiovascular events.
Heparin
Heparin is derived from pork and should not be administered to clients who are allergic to pork products.
Intravenous heparin dosing is based on weight and institution-specific protocols.
What Happens When the Sympathetic Nervous System (SNS) Kicks In?
When the SNS is activated, your heart rate (HR) and stroke volume (SV) go up, pumping more blood to keep up with the body’s energy demands. Your bronchioles expand, making it easier to breathe, and blood flow to your muscles and heart increases (β₂-mediated vasodilation) so you’re ready to run or fight. At the same time, blood vessels in your skin, digestive tract, and kidneys tighten up (α₁-mediated vasoconstriction) to redirect blood to where it’s needed most. Even your spleen squeezes out extra blood, giving your circulation a boost.
Your eyes adjust too—your upper eyelids lift, your pupils widen, and your eyeballs slightly protrude to sharpen your vision and expand your field of view. To fuel this high-energy state, your liver pumps out more glucose (from glycogenolysis and gluconeogenesis), making sure your brain and muscles have quick access to energy. Meanwhile, your digestive system slows down, your GI walls relax, and your sphincters tighten up, putting digestion on hold. The same thing happens to your bladder—the bladder wall relaxes, but the internal sphincter contracts, preventing any inconvenient pit stops.
To supercharge this whole response, your adrenal medulla releases epinephrine (Epi) and norepinephrine (NE), flooding your bloodstream with even more of these powerful messengers. On top of that, your kidneys release renin, triggering the RAAS system, which leads to aldosterone secretion—helping your body hold onto sodium (Na⁺) and water to keep blood pressure up. Almost all blood vessels constrict (α₁ effect), except for the ones going to your heart and skeletal muscles (β₂ effect), which widen to make sure they get plenty of oxygen and nutrients.
In short, your body goes into high-performance mode, pushing oxygen, blood, and energy toward the heart, muscles, and brain, while putting digestion and urine production on the back burner until the danger has passed.
Norepinephrine vs epinephrine?
Norepinephrine (NE) is primarily released from sympathetic nerve endings and works locally to increase blood pressure by constricting blood vessels and raising heart rate. A small amount of NE is also released from the adrenal medulla, but its main role is as a neurotransmitter in the sympathetic nervous system. Epinephrine (E), on the other hand, is mainly secreted by the adrenal medulla and enters the bloodstream, affecting the whole body. It increases heart rate and blood pressure but has an additional effect—it relaxes the airways (bronchodilation), making breathing easier. This is why norepinephrine is mainly used to treat low blood pressure (shock), while epinephrine is used for severe allergic reactions (anaphylaxis) to open up the airways.
Epinephrine acts on β₂ receptors, leading to bronchodilation, which improves oxygen delivery. At the same time, it also stimulates β₁ receptors, increasing heart rate and cardiac output (CO).
Norepinephrine primarily acts on α₁ receptors, causing vasoconstriction, which raises blood pressure (BP). This makes it especially useful for treating hypotensive shock.
The adrenal medulla secretes epinephrine and norepinephrine, while the adrenal cortex secretes aldosterone, cortisol, and androgens.
Renin-Angiotensin-Aldosterone System (RAAS)
The Renin-Angiotensin-Aldosterone System (RAAS) is the body’s way of regulating blood pressure and fluid balance. It all starts when there’s a drop in blood pressure or blood volume—this can happen due to dehydration, blood loss, or even heart failure. When the body senses this drop, the Juxtaglomerular cells release renin, an enzyme that kicks off the RAAS cascade.
Renin then acts on angiotensinogen, a protein made by the liver, converting it into angiotensin I. But angiotensin I itself isn’t very active—it needs to be converted into something more powerful. That’s where ACE (angiotensin-converting enzyme) comes in. ACE is mainly found in the lungs, and its job is to convert angiotensin I into angiotensin II, which is the real player in blood pressure control.
Angiotensin II has three major effects:
✅ Vasoconstriction – It makes blood vessels narrow, which increases blood pressure. This helps maintain circulation when blood volume is low.
✅ Direct Action on Renal Tubules – Angiotensin II directly stimulates the proximal tubules in the kidney to reabsorb sodium (Na⁺) and water (H₂O), helping to increase blood volume and blood pressure even before aldosterone is involved.
✅ Aldosterone Release – Angiotensin II acts on the adrenal cortex, telling them to release aldosterone. Aldosterone then signals the distal tubules and collecting duct to retain sodium (Na⁺) and water (H₂O), while excreting potassium (K⁺). By holding on to more fluid, blood volume increases, and blood pressure goes up.
So, in simple terms, the RAAS system is designed to keep blood pressure stable by tightening blood vessels and increasing fluid retention. However, when overactivated—like in chronic hypertension—it can actually lead to high blood pressure, fluid overload, and even heart failure. That’s why medications like ACE inhibitors, ARBs, and direct renin inhibitors are used to block different parts of the RAAS system and lower blood pressure.
Ace Inhibitors’ Mechanism of Action & Indications
ACE inhibitors, like lisinopril, work by blocking the angiotensin-converting enzyme (ACE), which is mainly found in the lungs. Normally, ACE converts angiotensin I into angiotensin II, a powerful vasoconstrictor. Angiotensin II also acts on the adrenal glands to stimulate aldosterone release, which causes sodium and water retention. By blocking ACE, these drugs lower blood pressure and reduce fluid overload, making them useful for hypertension (HTN) and heart failure (HF). One key thing to remember is that ACE inhibitors do not affect heart rate, so they are not antiarrhythmic drugs.
Ace Inhibitors’ Side Effects
Now, let’s talk about side effects. One of the most serious is angioedema, which causes deep tissue swelling, often in the face, lips, and throat. The biggest danger? Airway obstruction. If the swelling blocks the airway, the patient could have trouble breathing, which is a medical emergency. Another classic side effect is the dry cough, caused by bradykinin buildup in the lungs—since ACE normally helps break bradykinin down, blocking it leads to irritation. Other side effects include hyperkalemia (too much potassium, which can affect the heart). This happens because ACE inhibitors reduce aldosterone levels, and aldosterone normally acts on the kidneys to increase sodium (Na⁺) reabsorption and potassium (K⁺) excretion. Without enough aldosterone, the body retains more potassium instead of excreting it through urine, leading to higher potassium levels in the blood. Lastly, ACE inhibitors can also cause agranulocytosis/neutropenia, meaning fewer white blood cells and a higher risk of infection.
Ace Inhibitors’ Considerations for Use
When prescribing ACE inhibitors, there are a few key things to keep in mind. They should never be used in pregnancy, as they can cause serious harm to the baby, especially in pregnancy-induced hypertension. Also, elderly patients don’t respond well to ACE inhibitors alone, so they’re usually given with other antihypertensives. Lastly, that bradykinin buildup I mentioned doesn’t just cause a cough—it can also trigger an anaphylaxis-like reaction, leading to severe inflammation and swelling. If a patient develops significant swelling or breathing issues, we need to stop the drug immediately and treat the reaction.
The nurse should prepare patients for CBC, pregnancy test and Comprehensive metabolic panel test to assess electrolyte levels.
ARBs‘ Mechanism of Action & Indications
ARBs, or Angiotensin II Receptor Blockers, like losartan, work by blocking angiotensin II from binding to its receptors. Normally, angiotensin II causes blood vessels to tighten and triggers aldosterone release, which makes the body hold on to sodium and water, raising blood pressure. But when we block those receptors, blood vessels stay relaxed, and less aldosterone is released, which helps lower blood pressure. That’s why ARBs are mainly used to treat hypertension (HTN).
ARBs’ side effects
Now, let’s talk about side effects. The most common ones with ARBs are dizziness, diarrhea, and insomnia. But one big advantage of ARBs over ACE inhibitors is that they don’t cause that annoying dry cough. That’s because ACE inhibitors mess with bradykinin, which leads to the cough, but ARBs work differently—they just block angiotensin II from acting, without affecting bradykinin. So, if a patient can’t tolerate ACE inhibitors because of the cough, ARBs are a good alternative.
ARBs‘ Considerations for Use
When we prescribe ARBs, there are a few things to keep in mind. They’re generally better tolerated than ACE inhibitors, especially for people who get that persistent cough with ACE-Is. That being said, some patients may feel dizzy or have trouble sleeping, so it’s something to watch for. Since ARBs block angiotensin II at the receptor level, they’re a great option for lowering blood pressure while avoiding some of the side effects that come with ACE inhibitors.
Direct renin inhibitors’ Mechanism of Action & Indications
Direct renin inhibitors, like aliskiren, work at the very beginning of the RAAS (Renin-Angiotensin-Aldosterone System) cascade. Normally, the kidneys release renin, which acts on angiotensinogen from the liver to form angiotensin I. Then, ACE converts it into angiotensin II, which causes vasoconstriction and stimulates aldosterone release. But when we block renin, we stop this whole chain reaction—less angiotensin I, less angiotensin II, and less aldosterone. This leads to lower blood pressure, which is why these drugs are used for mild to moderate hypertension (HTN).
Direct renin inhibitors’ side effects
Now, when it comes to side effects, hypotension is a big one because these drugs lower blood pressure. Some patients may also get peripheral edema (swelling in the legs), diarrhea, or hyperkalemia—which happens because less aldosterone means the kidneys don’t get rid of potassium as efficiently. Another major concern is heart failure (HF) in some cases. And one of the most serious but rare side effects is Stevens-Johnson syndrome (SJS).
Stevens-Johnson syndrome usually starts off like the flu—fever, body aches, maybe a sore throat. But then, the skin reaction kicks in: painful blisters, peeling skin, and raw, exposed areas, especially on the mucous membranes. It gets so bad that some patients end up in burn units or ICUs because of how much skin they lose. Since it affects the mouth and throat, it hurts to eat and drink, which can lead to malnutrition and dehydration. If caught early and treated properly, patients can start recovering in about 2 to 3 weeks.
Direct-Acting Arteriolar Vasodilators
Hydralazine is a direct-acting vasodilator that works by relaxing the smooth muscles of arteries, leading to vasodilation and lowering blood pressure. It is mainly used for severe hypertension or hypertensive emergencies when immediate blood pressure control is needed.
However, because it directly dilates arteries, the body may try to compensate by increasing heart rate, leading to tachycardia and palpitations. Other side effects include headache, dizziness, edema, nasal congestion, GI bleeding, and even excessive hair growth. A key adverse reaction to watch for is lupus-like symptoms, which can cause muscle and joint pain, fever, and rash.
Because of its strong vasodilatory effects, hydralazine is usually given with a beta-blocker to control the reflex tachycardia. It’s an effective drug for short-term blood pressure management, but long-term use requires monitoring for side effects.
(Lupus-like symptoms refer to drug-induced lupus (DIL), which happens when certain medications—like hydralazine, procainamide, and isoniazid—cause lupus-like reactions. Unlike systemic lupus erythematosus (SLE), DIL is not an autoimmune disease and usually goes away after stopping the drug. Symptoms include swollen joint, swollen lymph node, chest pain and fatigue. Blood tests show positive ANA but usually negative dsDNA, which helps differentiate it from real lupus. Treatment is simple—stop the drug, and symptoms typically resolve within weeks to months. NSAIDs can help with joint pain, and steroids are rarely needed)
One key difference between hydralazine and nitroglycerin is where they work. Hydralazine primarily acts on peripheral arteries, reducing afterload, making it useful for hypertension. In contrast, nitroglycerin mainly works on peripheral veins and coronary arteries, reducing preload, which makes it more effective for conditions like angina and heart failure.
What are adrenergic receptors?
Adrenergic receptors, also known as adrenoreceptors, are named because they respond to adrenaline (epinephrine) and noradrenaline (norepinephrine), which are released by the adrenal gland and the sympathetic nervous system. These receptors play a key role in regulating blood pressure, heart rate, and airway function as part of the body’s “fight or flight” response. There are four main types of adrenergic receptors: α₁, α₂, β₁, and β₂.
Adrenergic receptors play a key role in regulating blood pressure, heart rate, and airway function. There are four main types: α₁, α₂, β₁, and β₂, each with distinct effects.
α₁ receptors are found in peripheral blood vessels, causing vasoconstriction, leading to an increase in blood pressure (↑BP). Drugs like norepinephrine and phenylephrine activate α₁ receptors to raise blood pressure in hypotensive states.
α₂ receptors are mainly located in the central nervous system (CNS) and work by inhibiting the sympathetic nervous system, which results in vasodilation and lower blood pressure (↓BP). A common α₂ agonist is clonidine, which is used to treat hypertension.
β₁ receptors are primarily found in the heart and are responsible for increasing heart rate and contractility, improving cardiac output. Drugs like dopamine and dobutamine target β₁ receptors to enhance heart function in conditions like heart failure.
β₂ receptors are located in the lungs and blood vessels, where they promote bronchodilation and vasodilation, making breathing easier. Albuterol, a β₂ agonist, is commonly used to treat asthma by opening up the airways.
Antihypertensives: Alpha-2 Agonists
Clonidine is an alpha-2 agonist that works by reducing sympathetic activity in the central nervous system. This leads to a decrease in heart rate (HR) and blood pressure (BP), lowering cardiac output (CO). It also reduces levels of epinephrine, norepinephrine, and renin, causing vasodilation and lowering peripheral vascular resistance (PVR).
Since clonidine affects fluid balance and heart function, it has some notable adverse reactions. Peripheral edema can occur due to sodium and water retention. It may also cause bradycardia, dizziness, and even heart block, especially when used with digoxin, calcium channel blockers (CCBs), or beta-blockers. A serious concern is rebound hypertensive crisis if the drug is abruptly discontinued, so it must be tapered off gradually.
One major consideration is that clonidine should never be given with beta-blockers, as this can intensify bradycardia and lead to dangerous drops in heart rate. Additionally, liver enzymes should be monitored in patients on long-term therapy.
Antihypertensive: Alpha1Blockers
Prazosin is an alpha₁ blocker that works by blocking alpha₁-adrenergic receptors, leading to vasodilation and a decrease in blood pressure (BP). It is primarily used to treat hypertension (HTN) but is also effective for benign prostatic hyperplasia (BPH) because it relaxes the bladder sphincter, allowing for improved urine flow.
While it is beneficial in lowering BP and easing urinary symptoms, it comes with some side effects, including orthostatic hypotension, dizziness, syncope (sudden loss of consciousness), and impotence. Because of the risk of a sudden drop in BP, nurses should always check the patient’s blood pressure before administering the medication. Patients should also be monitored for orthostatic hypotension, especially when changing positions, to prevent dizziness and falls.
If the drug is being used for BPH, the nurse should also assess the patient’s urinary symptoms to ensure improved urine flow and relief from urinary retention. Since alpha₁ blockers cause vasodilation, careful monitoring is needed to prevent excessive hypotension and related complications.
Benign Prostatic Hyperplasia (BPH) is a non-cancerous enlargement of the prostate gland, which commonly happens in older men. As the prostate grows, it can press against the urethra, making it harder for urine to pass.
Symptoms include：
Difficulty starting urination (hesitancy)
Weak urine stream
Frequent urination, especially at night (nocturia)
Feeling like the bladder is not completely empty
Urgency to urinate
Antihypertensives: Alpha 1 and Beta Blockers
Carvedilol is a combined alpha₁ and non-selective beta blocker, meaning it blocks both alpha₁ and beta receptors to lower blood pressure. By blocking alpha₁ receptors, it causes vasodilation, which helps reduce blood pressure. At the same time, beta blockade slows the heart rate and decreases cardiac output, reducing the workload on the heart. Because of this dual action, carvedilol can be used alone or in combination with other antihypertensive agents, such as thiazide or loop diuretics, to improve blood pressure control.
However, because it lowers both blood pressure and heart rate, common side effects include hypotension and bradycardia. More serious contraindications include heart failure, heart block, cardiogenic shock, and severe bradycardia, as excessive suppression of heart function can be dangerous. A major concern with beta blockers, including carvedilol, is their effect on the lungs. Even cardioselective beta blockers should not be used in patients with a history of obstructive airway diseases, such as asthma or COPD, because blocking β₂ receptors can lead to bronchoconstriction, making it harder to breathe. Since carvedilol is a non-selective beta blocker, it poses an even higher risk for respiratory complications in these patients.
Patient Education for Antihypertensives
Patients taking antihypertensive medications should be educated on proper use and potential risks. It is important to take the medication at the same time every day to maintain stable blood pressure control. Stopping the medication abruptly can lead to rebound hypertension, which can be dangerous. This is especially true for beta blockers, which should never be stopped before surgery, even if the patient is NPO, to prevent sudden blood pressure spikes and heart complications.
Patients should be taught how to check their blood pressure (BP) and pulse daily and to change positions slowly to avoid dizziness from orthostatic hypotension. Any side effects should be reported, and regular follow-ups, including lab tests and eye exams, should be scheduled to monitor for any long-term effects.
Certain over-the-counter cold and cough medications should be avoided, as they can raise blood pressure or interfere with antihypertensive drugs. Reducing alcohol intake is also recommended, as alcohol can worsen hypotension. Patients should be aware that some antihypertensive medications may cause sexual side effects, such as impotence in men. Finally, stress management is crucial, as stress can contribute to high blood pressure and reduce the effectiveness of treatment.
No extra salt
lose weight
avoid tobacco
Drugs that we use to treat Heart Failure
Inotropes/ˈaɪ.nəˌtroʊps/ are medications that increase the force of heart contractions, making them useful in the management of heart failure and shock. Two commonly used inotropes are dopamine and dobutamine, both of which act on beta-adrenergic receptors to improve heart function. Dopamine is a beta-adrenergic agonist that increases both heart rate and blood pressure, making it particularly useful in hypotension and shock. Dobutamine, on the other hand, is a sympathomimetic drug with beta-adrenergic activity, meaning it enhances the force of myocardial contraction (positive inotropic effect) and increases heart rate (positive chronotropic effect), helping to improve cardiac output.
These medications are primarily used in conditions such as heart failure, hypotension, and shock states to improve perfusion and maintain blood pressure. However, when used in shock, it is essential to administer fluids first to ensure adequate blood volume before giving inotropes, as these medications work best when there is enough circulating fluid to support increased cardiac output. Common side effects of inotropes include tachycardia, premature ventricular contractions (PVCs), angina, nausea, vomiting, piloerection and hypertension. More serious adverse reactions include ventricular tachycardia (V-tach), ventricular fibrillation (V-fib), and myocardial infarction (MI), so patients receiving these medications must be closely monitored for dysrhythmias and cardiac complications.
Piloerection is the medical term for “goosebumps” or “gooseflesh”—when the tiny muscles at the base of hair follicles contract, causing the hairs on your skin to stand up.
