Cardiac 2

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  1. Hemodynamics effects of vasodilators?
    • 1) dilate resistance vessels (arterioles) decrease cardiac output.
    • 2) dilate veins reduce preload (force which blood is return to the heart)
  2. Therapeutic effects of Vasodilators:
    • Essential hypertension
    • Hypertensive crisis
    • Angina pectoris
    • Heart failure
    • MI
    • PVD --> Peripheral Vascular Disease. diabetes, bloct clots.
  3. Adverse effects of Vasodilators?
    • Orthostatis hypotension
    • reflex tachycardia (pretreat with beta blockers)
    • Expansion of blood volume (treat with diuretics)
  4. Hydralazine (apresoline) effects, mechanism, AE, SE and TU?
    • Dilation of arterioles. Usually combined with beta blockers and diuretics to prevent reflex tachycardia and blood volume increased.
    • Mechanism is unknown
    • AE: Minimal orthostatic hypotension, systemic lupus erythematosus-like syndrome, Other AE of vasodilators. 
    • SE: headache, dizziness, weakness, and fatigue.
    • TU: essential hypertension, hypertensive crisis, heart failure.
  5. Minoxil (loniten) effects, mechanism, AE, SE, and TU?
    • Selective dilates arterioles and the effects and AE are stronger than Hydralazine.
    • TU: use for severe hypertension that is unresponsive to safe drugs. It is safe for pregnant women.
    • AE: like any other vasodilator, and pericardial effusion (rarely).
  6. Diazoxide (hyperstat IV) category? effects? what is the importance of this drug? AE? DI?
    • It is a vasodilator that dilates arterioles.
    • The importance is usage in hypertension emergencies!
    • AE: like all the vasodilators, hyperglycemia, hyperuricemia.
    • DI: diuretics, and anithypertensive drugs.
  7. what is Sodium nitroprusside (nitropress) use as? when? how (administration)? AE>
    • It is used as a vasodilator and it is the fastest-acting agent. Causes both venous and arterioles to dilate.
    • It is used in emergency situation
    • It is administer IV.
    • AE: excessive hypotension.
  8. what is angina pectoris?
    • Sudden pain beneath the sternum, often radiating to left shoulder and arm.
    • Oxygen supply to the heart is insufficient to meet oxygen demand
  9. What are the 2 main goals of angina therapy?
    • Prevention MI and death
    • Prevention of myocardial ischemia and anginal pain. Reducing cardiac workload---reducing workload will relieve pain.
  10. How many types of anginas are there? Describe them.
    • Stable angina: Also called classic, exercise-induced, or effort angina.
    • Vasospastic angina: Also called variant or Prinzmetal’s angina
    • Unstable angina: Also called crescendo or preinfarction angina.
    • Silent ischemia: absence of pain
  11. What is arteriosclerosis?
    • accumulation of fatty deposits  that narrow the lumen of coronary arteries.
    • CAD (coronary artery disease) is associated with atherosclerosis
  12. What are the treatment strategies for an unstable angina medical emergency? What is MONA-B?
    • There are 2 strategies:
    • Maintain oxygen supply
    • Decrease O demand
    • MONA-B: Morphine (pain and vasodilator), Oxygen (hyperoxygenate tissues), Nitrates (pill under the tongue to decrease angina), Aspirin (for pain and platelets and antiplatelets), Beta blockers (decrease HR, Centricule contraction, and BP)
  13. What is organic Nitrates use for? How, name of a drug? AE?
    • - Organic nitrates are used to reduce angina pectoris.
    • - The main drug is Nitroglycerin (Nitrostat, Nitro-bid, Nitro-Dur, etc)
    • - They are vasodilators, and work more in veins than in arterioles.
    • - used for stable and variant angina. In stable angina the nitrate reduces cardiac oxygen demands, in variant angina the nitrate reduces spasms in the coronary arteries increasing oxygen supply.
    • - AE: like any other vasodilator (othostatic hypotension, reflex tachycardia, and  headaches) flushing, etc
    • - Tolerance could happen, pt should be in a 8hr a day free nitrate drug.
  14. What are some drugs that act as Calcium channel blockers (CCB)? what are their effects?
    • "pines" meds except: Verapamil (calan), Diltiazem (cardizem).
    • nifedipine (procardia), amlodipine (norvasc).
    • Vasodilation occrus
    • Reduce myocardial contractibility, and oxygen demand.
    • Greatest impact in the heart and blood vessels.
    • Prevent contractile response.
  15. Verapamil (calan) effects? TU? AE?
    • acts on vascular smooth muscle and the heart reducing O demand.
    • HR decrease and contractility.
    • TU: angina pectoris, essential hypertension, Cardiac dysrhythmia, migraines.
    • AE: Constipation, hypotension dizziness, facial flushing, headaches, etc.
  16. What medications affect the Renin-angiotension-aldosterone-system (RAAS)?
    • Angiotensin-converting enzyme inhibitors (ACE inhibitors)
    • Angiotensin II receptor blockers (ARBs)
    • Aldosterone antagonists.
  17. what are the actions of angiotensin II?
    • Vasoconstriction: it affects the VSM directly, making it a strong vasoconstrictor.
    • Release of aldosterone: Angiotensis II stimulates the adrenal cortex (outside) which increases the synthesis of Aldosterone.
    • Alteration of cardiac and vascular structures: It causes hyperthrohy in the heart, and causes atherosclerosis in the vessels
    • (thickening of the wall)
  18. What are the actions of Aldosterone?
    • Regulation of blood volume: retention of sodium, which causes water to be retained as well, and elimination of potassium and Hydrogen.
    • Pathological cardiovascular effects: like angiotension II, aldosterone could cause remodeling and fibrosis in the heart. Also supress uptake of norepi causing dysrhythmia.
  19. What are ACE inhibitors? Mechanism of action? TU? AE? drug names?
    • Angiotensin-converting enzyme inihibitors
    • MA: reduce levels of angiotensin II, causing vasodilation, lowering blood volume, and prevent for pathological changes in the heart and vessels.
    • TU: hypertension, MI, heart failure, diabetic nepropathy.
    • AE: first dose hypotension, cough, and hyperkalemia.
    • names: "pril" captopril, enalapril, etc.
  20. What are ARBs? MA? TU? AE? drugs names?
    • Angiotensin II Receptor Blockers
    • MA: block angiotensin II, causing Vasodilation, reducing synthesis of aldosterone, preventing pathological changes in the heart and vessels, reducing elimination of potassium, increasing elimination of sodium and water.
    • TU: hypertension, heart failure, MI, etc
    • AE: fetal harm, kideny failure, hypotension, reflex tachycardia, hyperkalemia,
    • names: "sartan" losartan, valsartan, etc
  21. what drug is use to inhibit renin directly? AE? which ppl use this meds?
    • Aliskiren (tuktura)
    • AE: same as all angiotensin II inhibitors: hypotension, reflex tachycardia, hyperkalemia, cough, etc
    • This drug is use for ppl who have resistant HBP.
  22. what are other vasodialators?
    • Adrenergic blocking agents (ganglionic) and beta blockers ("olol)
    • Alpha 1 adrenergic blocking agents ("osin") cause vasodialation.
    • drugs: Doxazosin (cardura), Prazosin (minipress), tamsulosin (flomax)
  23. What are centrally acting agents?
    Methyldopa, and clonidine.
  24. What is preload?
    • Amount of fluid that is in the heart before ejecting.
    • amount of stretching of the ventricule cardiac muscle before contraction.
  25. What is afterload?
    • Resistance against which the heart works.
    • amount of fluid in the heart after ejection.
  26. What does renin do?
    Converts angiotensin I to angiotensin II by ACE.
  27. If we have a rt side problem in the heart, how should it be treated?
    • Positive Chronotrophy (drugs that change the HR by the nerves, or by SA node)
    • Use of diurhetics. (to reduce volume)
    • Beta blockers (to reduce HR)
  28. how to treat problems in the left side of the heart?
    • Vasodilators to relax the vessels and reduce friction (afterload)
    • Diuretics
  29. What is the main goal of CHF treatment? how do drugs relieve symptoms?
    • Reduce preload and afterload to enhance myocardial contraction.
    • Medication relieve symptoms of CHF by: Slowing HR, increasing contractility, reducing cardiac workload.
  30. what is inotropic?
    Modifying the force or speed of contraction of muscles.
  31. what class is Digoxin considered? Does it prolonged life?
    • It is considered as a cardiac glycosides or positive inotropic actions. Its usage is considered as a second-line agent usage today.
    • It does not prolonged life.
  32. Digoxin effect?
    • Increases myocardial contractility and cardiac output.
    • Supresses renin release from the liver (increases urine production)
    • Decreases HR and BP.
  33. Digoxin AE?
    • Dysrhythmia
    • halos around lights
    • heart disease
    • Non-cardiac adverse effects: anorexia, nausea, vomiting, fatigue.
  34. What should be monitored when a pt is in digoxin?
    • Potassium levels must be kept in normal physiological range. Bc potassium competes with digoxin to bing to ATPase receptors.
    • The Therapeutic index is very narrow, so serum should be check constantly to make sure the values are in range.
  35. what is the half life of digoxin? what drugs interact with it?
    • 1.5 days.
    • DI: ACE inhibitors and ARBs, diurhetics, and sympathomimetics.
  36. what is digoxin antidote? and what should be monitored after?
    • Digoxin immune FAB (Digibind) is antidote
    • Monitor BNP levels
  37. Nurse's implications when administering digoxin?
    • Check HR, and BP before giving the drug.
    • stress diet high in potassium.
    • teach patient to monitor pulse
    • assess patient for toxicity
    • weight daily
    • monitor blood levels
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Cardiac 2
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