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Questions and Answers
What is the main effect of nitroglycerin in peripheral vascular beds?
What is the main effect of nitroglycerin in peripheral vascular beds?
- Increases cardiac output
- Causes vasodilation (correct)
- Decreases heart rate
- Increases blood pressure
Which is an appropriate response if a patient experiences hypotension while using morphine?
Which is an appropriate response if a patient experiences hypotension while using morphine?
- Discontinue all medications immediately
- Elevate the patient's legs and give IV fluids (correct)
- Provide the patient with oxygen
- Administer an additional dose of morphine
What is a contraindication for administering nitroglycerin?
What is a contraindication for administering nitroglycerin?
- Patient with chest pain
- History of myocardial infarction
- Use of antihypertensive drugs
- Systolic blood pressure less than 90 mm/Hg (correct)
Which type of drug class do beta blockers belong to?
Which type of drug class do beta blockers belong to?
What is a common side effect of morphine's action as a venodilator?
What is a common side effect of morphine's action as a venodilator?
What acronym is often used to remember the initial treatment options for a patient with acute coronary syndrome?
What acronym is often used to remember the initial treatment options for a patient with acute coronary syndrome?
Which of the following treatments is administered first in the case of acute coronary syndrome if O2 saturation is below 94%?
Which of the following treatments is administered first in the case of acute coronary syndrome if O2 saturation is below 94%?
What is the standard recommended dosage of aspirin for treating acute coronary syndrome?
What is the standard recommended dosage of aspirin for treating acute coronary syndrome?
How often can nitroglycerin be repeated if the patient does not experience relief from chest pain?
How often can nitroglycerin be repeated if the patient does not experience relief from chest pain?
What is the primary role of aspirin in the management of acute coronary syndrome?
What is the primary role of aspirin in the management of acute coronary syndrome?
What is the mechanism of action of nitroglycerin in treating chest pain during acute coronary syndrome?
What is the mechanism of action of nitroglycerin in treating chest pain during acute coronary syndrome?
What happens to blood flow to cardiac muscle when a plaque in a coronary artery ruptures?
What happens to blood flow to cardiac muscle when a plaque in a coronary artery ruptures?
What condition is described by acute coronary syndrome?
What condition is described by acute coronary syndrome?
What is the primary use of Angiotensin II Receptor Blockers (ARBs)?
What is the primary use of Angiotensin II Receptor Blockers (ARBs)?
What is the main mechanism by which diuretics help patients with heart failure?
What is the main mechanism by which diuretics help patients with heart failure?
Which of the following best describes the role of statins in managing cholesterol?
Which of the following best describes the role of statins in managing cholesterol?
Which medication is categorized as both an antiplatelet and anticoagulant?
Which medication is categorized as both an antiplatelet and anticoagulant?
Why are diuretics sometimes prescribed to manage heart failure symptoms?
Why are diuretics sometimes prescribed to manage heart failure symptoms?
What is the role of antidiabetic drugs in relation to cardiovascular health?
What is the role of antidiabetic drugs in relation to cardiovascular health?
Which of the following is NOT a typical indication for using statins?
Which of the following is NOT a typical indication for using statins?
What is the primary action of aspirin in the context of acute coronary syndrome (ACS)?
What is the primary action of aspirin in the context of acute coronary syndrome (ACS)?
What is the primary action of clopidogrel on platelets?
What is the primary action of clopidogrel on platelets?
Which class of medications is known for inhibiting the glycoprotein IIb/IIIa receptor?
Which class of medications is known for inhibiting the glycoprotein IIb/IIIa receptor?
What is a notable feature of low-molecular-weight heparin (LMWH) in comparison to unfractionated heparin?
What is a notable feature of low-molecular-weight heparin (LMWH) in comparison to unfractionated heparin?
Which of the following is an example of a fibrinolytic medication?
Which of the following is an example of a fibrinolytic medication?
What potential benefit do glycoprotein IIb/IIIa inhibitors provide in cardiovascular treatment?
What potential benefit do glycoprotein IIb/IIIa inhibitors provide in cardiovascular treatment?
Why might low-molecular-weight heparin (LMWH) be preferred in clinical settings?
Why might low-molecular-weight heparin (LMWH) be preferred in clinical settings?
What is the mechanism of action for anticoagulants such as heparin?
What is the mechanism of action for anticoagulants such as heparin?
In the context of treatment for STEMI, what is the gold standard for reperfusion therapy?
In the context of treatment for STEMI, what is the gold standard for reperfusion therapy?
Flashcards
What is Acute Coronary Syndrome (ACS)?
What is Acute Coronary Syndrome (ACS)?
Acute coronary syndrome (ACS) refers to a range of heart conditions that involve a sudden blockage of a coronary artery, leading to damage or death of heart muscle. This includes unstable angina, non-ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI).
What's the cause of ACS?
What's the cause of ACS?
A plaque, a fatty deposit, breaks or erodes in a coronary artery, leading to a cascade of clotting events. This creates a blood clot, blocking the artery and stopping blood and oxygen flow to the heart muscle.
What is MONA?
What is MONA?
A mnemonic acronym used to remember the initial medical treatment options for a patient with ACS: Morphine, Oxygen, Nitroglycerin, Aspirin. However, the drugs aren't administered in this order, but in the order of OANM.
Why give Oxygen (O) in ACS?
Why give Oxygen (O) in ACS?
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Why give Aspirin (A) in ACS?
Why give Aspirin (A) in ACS?
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Why give Nitroglycerin (N) in ACS?
Why give Nitroglycerin (N) in ACS?
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How does Nitroglycerin work?
How does Nitroglycerin work?
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Why give Morphine (M) in ACS?
Why give Morphine (M) in ACS?
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Nitroglycerin: What is it and what does it do?
Nitroglycerin: What is it and what does it do?
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Morphine: Why is it used for chest pain?
Morphine: Why is it used for chest pain?
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Alpha-1 Blockers: What do they do?
Alpha-1 Blockers: What do they do?
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ACE Inhibitors: What makes them effective?
ACE Inhibitors: What makes them effective?
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Angiotensin Receptor Blockers (ARBs): What are they?
Angiotensin Receptor Blockers (ARBs): What are they?
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When to use ARBs?
When to use ARBs?
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How do diuretics work?
How do diuretics work?
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What is the goal of antihyperlipidemic drugs?
What is the goal of antihyperlipidemic drugs?
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How antiplatelets protect the heart?
How antiplatelets protect the heart?
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What is the mechanism of action of Angiotensin II Receptor Blockers (ARBs)?
What is the mechanism of action of Angiotensin II Receptor Blockers (ARBs)?
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How do diuretics help manage heart failure?
How do diuretics help manage heart failure?
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What is the role of antihyperlipidemic drugs in cardiovascular disease?
What is the role of antihyperlipidemic drugs in cardiovascular disease?
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How do antiplatelet medications work in the context of ACS?
How do antiplatelet medications work in the context of ACS?
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What are Glycoprotein IIb/IIIa Inhibitors?
What are Glycoprotein IIb/IIIa Inhibitors?
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How does Clopidogrel work?
How does Clopidogrel work?
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How do Heparin and LMWH work?
How do Heparin and LMWH work?
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What are Fibrinolytics?
What are Fibrinolytics?
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What is PCI?
What is PCI?
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What are the two main methods for reperfusion in STEMI?
What are the two main methods for reperfusion in STEMI?
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What is the gold standard treatment for STEMI?
What is the gold standard treatment for STEMI?
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What are the benefits of using Glycoprotein IIb/IIIa inhibitors?
What are the benefits of using Glycoprotein IIb/IIIa inhibitors?
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Study Notes
Cardiovascular Drugs - Module 7
- Heart medications manage arrhythmias, angina (chest pain), blood pressure, cholesterol, and blood clots.
Acute Coronary Syndrome (ACS)
- ACS refers to a spectrum of clinical manifestations associated with acute myocardial infarction (NSTEMI & STEMI) and angina (stable & unstable [UA]).
- A plaque in a coronary artery ruptures or becomes eroded, triggering the clotting cascade.
- A blood clot forms, occluding the artery and interrupting blood and oxygen flow to cardiac muscle.
Plaque Formation
- Plaque forms within the artery.
- The plaque consists of an atherosclerotic plaque.
- The plaque is within the endothelium (lining of the artery).
- The plaque is within the artery wall.
Lipid Deposition
- Lipid deposition occurs at the site of endothelial injury.
Thrombus Formation
- A thrombus forms due to a fissure and rupture of a plaque.
Platelet Adhesion
- Platelets adhere to the site of injury in the artery.
Embolus Formation
- A thrombus can detach and become an embolus.
Occlusion Causes Infarction
- A thrombus can occlude an artery, causing infarction.
ACS Drug Treatment
- Initial treatment includes ABCs, O2, IV, monitor; vital signs, pulse oximeter, blood pressure; assess discomfort.
- Obtain a 12-lead ECG.
- Administer aspirin, nitroglycerin, and morphine as indicated (if no contraindications).
- Evaluate 12-lead ECG and reperfusion checklist.
- Obtain baseline cardiac biomarker levels, electrolytes, coagulation studies, and chest x-ray.
Medical Treatment Options (MONA)
- Morphine
- Oxygen
- Nitroglycerin
- Aspirin.
- Drugs are not given in alphabetical order but in order of OANM.
Oxygen Administration
- Oxygen (O2) is given if the patient's O2 saturation level is below 94%.
Aspirin
- 160-325 mg of chewable aspirin to speed absorption.
- Lowers the risk of further occlusion or re-occlusion and recurrent ischemic events.
Nitroglycerin
- 0.4mg is given sublingually (spray or dissolving tablet).
- If the first dose does not improve chest pain, the dose may be repeated every 5 minutes.
- No maximum dose.
- A potent vasodilator that relaxes vascular smooth muscle beds, thus improving blood flow to ischemic areas.
- Decreases myocardial oxygen consumption, enabling the heart to function with lower oxygen demand.
Morphine
- 2.5mg may be repeated every 5 mins via IV push if chest pain does not resolve with sublingual or IV nitroglycerin.
- Maximum dose is 10mg.
- An opioid that acts primarily on pain receptors, as well as a venodilator, decreasing ventricular preload and cardiac oxygen requirements.
Antihypertensive (Blood Pressure) Drugs
- Alpha1-blockers (doxazosin, prazosin, terazosin)
- Beta-blockers (propranolol, acebutolol, esmolol)
- ACE inhibitors (captopril, enalapril, lisinopril, quinapril, ramipril, benazepril, fosinopril)
- Angiotensin receptor blockers (ARBs)
- Calcium channel blockers (CCBs) (verapamil, diltiazem, nifedipine)
- Diuretics (chlorothiazide, hydrochlorothiazide, furosemide and bumetanide)
- Vasodilators (hydralazine, sodium nitroprusside)
Antihyperlipidemic Drugs
- These medications manage cholesterol and prevent fatty plaques.
- Cholesterol medicines stabilize fatty plaques, stopping them from breaking up.
- HMG-CoA Reductase Inhibitors (Statins): reduce re-infarction, recurrent angina, re-hospitalization, and stroke.
- These are used in combination with a prehospital and UA/NSTEMI AHA algorithm.
Cholesterol Metabolism
- Cholesterol is a component in cell membranes and hormone production.
- Synthesized in the liver, dependent on HMG CoA reductase.
- Stored in tissues for later use, not soluble in plasma and needs transport mechanisms.
Lipoproteins
- Lipids are surrounded by a protein coat to hide hydrophobic fatty core.
- Described by density: VLDL, LDL, IDL, HDL, VHDL.
- LDLs transport liver cholesterol to tissues and are considered "bad."
- HDLs move cholesterol back to the liver and are considered "good."
Why Fear Cholesterol?
- Risk of CAD (Coronary Artery Disease) is linked to LDL.
- LDLs deposited under endothelial surface, oxidized.
- Oxidized LDL attracts macrophages, forming foam cells.
- Foam cells protrude against intimal lining, forming tough cap, decreasing vascular diameter and blood flow.
Plaque Cap Rupture
- Plaque cap ruptures.
- Collagen is exposed.
- Clotting cascade triggered.
- Platelet adhesion occurs.
- Thrombus and embolus formation is possible.
- Occlusion causes ischemia.
Antiplatelet Agents
-
Goal: Decrease LDL, inhibit LDL synthesis and receptors increase in the liver, target LDL < 200 mg/dL
-
Includes Statins, HMG-CoA reductase inhibitors
-
Includes; Aspirin, Clopidogrel (Plavix)
-
Aspirin inhibits aggregation; Plavix inhibits binding to other platelets, lasting for the entire lifespan of the platelet, making it an anticoagulant
-
These are often used in conjunction with other anticoagulants.
-
Platelet Inhibitors: inhibit aggregation for progressive MI or CVA
Glycoprotein IIb/IIIa Inhibitors
- Inhibit platelet aggregation by inhibiting glycoprotein IIb/IIIa receptor pathways.
- Very potent platelet inhibitors (Abciximab, Eptifibatide, Tirofiban)
Anticoagulants
- Low molecular weight Heparin (LMWH) inhibits thrombin and prevents fibrin formation and platelet activation.
- Include; unfractionated heparin, enoxaparin (Lovenox)
- MOA: acts at multiple sites in the normal coagulation system to interrupt clotting cascade.
- Heparin negatively charged; protamine positively charged (antidote)
Fibrinolytics
- Reperfusion therapy—dissolving blood clots in arteries or veins, e.g., Activase.
- These include an example of meds like streptokinase, alteplase, anistreplase, reteplase, and tenecteplase—used to dissolve clots.
Occlusion Mechanism
- A thrombus occludes (blocks) the artery.
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