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Flashcards in Cardio Drugs pt.2 Deck (66):

Coronary Artery Disease is also known as atherosclerosis. What are some risk factors?

Lifestyle - sedentary, stress, obesity


____ deposits build up in blood vessel walls and narrow the passageway for movement of blood. This will eventually lead to blockage of the coronary arteries and a "heart attack."



What are the clinical manifestations of CAD (Coronary Artery Disease)?

Early stages are asymptomatic

Excessively fatigue
chest pain
palpitations (a noticeably rapid, strong, or irregular heartbeat due to agitation, exertion, or illness.)
ECG change


How do we treat CAD?

Statins (Lipitor/Zocor)
ACE inhibitors
Antiplatelet agents (aspirin)
Calcium channel blocker
Surgical - angioplasty


Which cholesterol is the "good" one? HDL or LDL?


H for helper


What do we want to see in cholesterol?

Reduction in LDL and triglycerides

Improved HDL

Improved HDL to LDL ratio


What types of medication can we use to lower lipids

Bile Acid Sequestrants such as Cholestyramine (QUestran)
*This medication is like metamucil. You stir it into water and it becomes thick and sludgy. When you drink it, it binds to bile acids (which contain cholesterol) and carries them out in feces, thereby reducing cholesterol. Reduces plasma cholesterol levels. The liver then uses the remaining serum cholesterol in the body to produce bile.

HMG - CoA reductase inhibitors (Statins) such as atorvastatin (Lipitor/Crestor).
*HMG-CoA reductase is used in synthesis of cholesterol. If we inhibit this enzyme, less cholesterol is synthesized. Serum levels will decrease because existing LDLs will be absorbed for processing into cholesterol (HDL levels will increase slightly).

Cholesterol Absorption Inhbitor such as ezetimibe (Zetia).
*This medication prevents absorption of cholesterol in the small intestine. This means less cholesterol makes it to the liver, therefore, the liver will use serum cholesterol and the overall cholesterol level will drop.

Other antihyperlipidemic Agents
*Niacin (Vitamin B3) - inhibits the release of free fatty acids from adipose tissue, increases the rate o triglyceride removal from plasma and reduces LDL, Trigylcerides while increasing HDL levels.
*Fenofibrates - includes fenofibrate/TriCor and gemfibrozil (Lopid). Stimulate breakdown of lipoprotein from the tissues and their removal from the plasma. Leads to decrease i lipoprotein and triglyceride synthesis and secretion


Why would a patient be given crestor over lipitor?

Lipitor can cause pain in muscles due to breakdown of muscle. Can lead to kidney damage when putting out so much creatinine. Crestor does not.


QUestran is not seen often. Why?

GI issues.
Causes loss of fat soluble vitamins (A & E especially)
Increases bleeding time
Taken with medications prevents absorption of medications MUST TAKE SEPARATELY


What is rhabdomyolysis?

the destruction of striated muscle cells


When taking atorvastatin (Lipitor ), a lipid lowering agent (HMG-CoA Inhibitor), what must the patient be taught to report? To avoid?


Report muscle pain (causes rhabdomyolysis)
Take the medication in the evening (lipids are produced at night)

Avoid grapefruit juice and alcohol


ezetimibe (Zetia prevents absorption of cholesterol in the small intestine. Just like other lipid lowering agents it can cause what adverse effects?

abdominal pain, headache, dizziness.


Niacin (Niaspan) is also known as Vitamin B3 and inhibits the release of free fatty acids from adipose tissue. What is the biggest issue with this drug?

How you take it because it causes severe flushing (skin feels like it is falling off/burning). You must increase it slowly!

Steps to take it:
1. You take an aspirin or an advil and wait twenty minutes
2. eat low fat snack and wait
3. take niacin then go to bed
4. skin feels like its falling off or burning
5. Patient either calls Dr or goes to ER because they think something is wrong.

Over time it becomes more tolerable.

DO NOT TAKE WITH Niacin (Vitamin B3) because it is essentially the same thing.


What is angina?


a condition marked by severe pain in the chest, often also spreading to the shoulders, arms, and neck, caused by an inadequate blood supply to the heart.

Caused by insufficient blood flow to the heart. Results from temporary myocardial ischemia

Angina Pectoris is translated as suffocation of the chest


If the heart does not have pain fibers, how does it feel pain? Why is this important?

The body's response to lack of oxygen in heart muscles is to release substance P which reacts with pain receptors elsewhere. This is why patients with angina pectoris complain of chest or left arm pain, while other have pain in the jaw or teeth. Most people react to this pain by stopping whatever one is doing. Once they rest long enough, oxygen is able to catch up to meet demands and the pain is gone.

THis is called STABLE ANGINA because no damage to muscles takes place and blood is restored. It can be a chronic problem.


What is unstable angina?

After administering med and resting no relief? Unstable Angina.

Narrowing of arteries becomes more pronounced and patient experiences ischemia** even at rest. THis is called unstable angina. Although heart muscle may not be damaged, the patient is at increased risk of complete blockage of blood supply to the heart muscles IF the heart needs to work harder or he oxygen demand increases.


an inadequate blood supply to an organ or part of the body, especially the heart muscles.


What is an uncommon form of angina? What causes it?

prinzmetal angina, caused by spasm of the blood vessels. Even at rest this person may feel the pain. We would see an ECG change.


What group of meds relieve angina pectoris?

Nitrates (nitroglycerin - Nitrostat)
Beta Blockers (metoprolol - Toprol)
Calcium Channel Blockers (do;toaze, (Cardizem)
Antiplatelet agents (aspirin)

Remember that slowing the heart down can also decrease angina. That is why Beta Blockers, Calcium Channel Blockers, Antiplatelet agents work.


How do we diagnose?

EKG during an attack
Coronary angiograph/angiogram


________ relieve angina by dilating veins and coronary arteries. It acts on smooth muscle to promote relaxation. Give them three time with a five minute delay between each dose.

nitroglycerin (Nitrostat)

*Make sure you rinse the mouth before administering
*Keep in dark container


Why do we give nitrates sublingually?

Faster absorption

Can also be given:

Translingual spray
Transmucosal tablet
Oral, SR tablet
Transdermal (patch) - remove old, change location, sign&date


What is the main contraindication for Nitrate? Cautions? Adverse Effects?

severe anemia.

do not take with conditions that limit cardiac output (remember we are going to slow the HR down and reduce cardiac output. Therefore, slowing further could be devastating).

Causes an instant headache. It causes vasodilation which leads to a headache.


What is the best antianginal agent to use for long term management of angina? How do they work?

beta-adrenergic blockers (metoprolol Toprol or propranolol Inderal) relieve angina by decreasing the oxygen demands on the heart. SLOWS THE HR!

ALWAYS REMEMBER: caution in diabetes - may lead to hyperglycemia; hides hypoglycemic symptoms


What is the best antianginal agent to use for Prinzmetal's angina (remember it is caused by spasm)?

Calcium Channel Blocker (diltiazem - ardizem) because it blocks contraction.


What are non drug treatments for angina?

Angioplasty - surgical repair or unblocking of a blood vessel, especially a coronary artery

Stents - a tubular support placed inside a blood vessel, canal, or duct to aid healing or relieve an obstruction.

Intraaortic balloon pump - The Intra-aortic balloon pump (IABP) is a mechanical device that increases myocardial oxygen perfusion while at the same time increasing cardiac output. Increasing cardiac output increases coronary blood flow and therefore myocardial oxygen delivery.


T or F: MI is major cause of death caused by CAD.


Men and women have varying symptoms.

*Symptoms include acute, crushing/squeezing chest pain that is unrelieved by rest or nitroglycerin (>15 min).
*Pain radiates to left arm or up to jaw.
*Cool/clammy and/or pallor skin
*Confusion, dizziness, fainting


How do we test if a person had a heart attack (MI)?

release of cardiac anzymes.

Troponins (rise earlier than CK-MB)
Cardiac cath/Angiography
Lipid profile


How do we treat MI?

MONA - morphine, oxygen, nitrates, antiplatelet

Morphine - relieves pain and anxiety

OXYGEN - if trouble breathing, give oxygen (ask for forgiveness not permission with this one).

Nitroglycerin - vasodilator relieves angina

Antiplatelet - aspirin

Eventally, after finding out for certain it is in fact a heart attack, administer:

Anticoagulants - heparin
Thrombolytic agents - makes thrombus break apart.
Anti-dysrhythmia (ACEi/Beta)


What is heart failure?

a syndrome that involves dysfunction of cardiac muscle.

WIthin the muscle sarcomeres are the main component. Sarcomeres contain myosin and actin which react to create muscle contraction. Troponin keeps them from causing a contraction. When calcium enters the picture, it deactivates troponin allowing the sarcomere to contract again.

HF causes dysfunction of this mechanism. The end result is that the heart cannot pump blood efficiently, leading to CHF

The body has compensatory mechanisms. The body will attempt to solve the problem FIRST by increasing HR, BP and rate and deptth of respiration as well as positive inotropic effect (increased for of contraction) and increase in blood volume (thru aldosterone). The trouble is that these mechanisms can increase the workload of the heart, leading to further development of HF.

Eventually the heart OVER stretches (hypertrophy - called cardiomegaly). The pumping becomes even more inefficient (myosin and actin won't be close enough to each other to react causing a contraction).


What causes left and/or right sided heart failure?



What is cardiogenic shock?

Cardiogenic shock is a condition in which your heart suddenly can't pump enough blood to meet your body's needs. The condition is most often caused by a severe heart attack. LEADS TO ORGAN FAILURE (kidney, renal, respiratory)

Complication of CHF!!!


Why should a person weight themselves everyday once they have CHF?

2 lbs increase or loss = fluid gain or loss.

Gain needs lasix (up to 240mg).


What does typical CHF look like (steps of blood back up)? What are common causes of CHF?

1. Left ventricle backs up (cannot push blood through aorta)

2. Blood backs up to left atrium (LEFT SIDED HEART FAILURE AT THIS POINT)

3. Blood backs up to lungs (!!!!!!leading to pulmonary congestion and edema!!!!!!)

4. Blood back up to right ventricle (causing rt side heart failure)

5. Blood backs up to right atrium

6. Blood backs up to extremities (edema) and abdomen (ascites).

Common causes are HTN and CAD


Treatments and care for CHF (non medicinal)?

Since fluid build up is the name of the game, we need to limit intake of fluids. Monitor I&O. Daily weight.

Limit activity (keep the heart calm)


Drug treatment for CHF?

OXYGEN - if trouble breathing, give oxygen (ask for forgiveness not permission with this one).

ACEi (RESTRUCTURES THE HEART, decrease cardiac workload, relaxes vascular smooth muscle to DECREASES AFTERLOAD and allow pooling in veins which DECREASES PRELOAD of the heart.)

Beta blockers - carvedilol long term because it lengthens life of people with CHF due to alpha property.

Beta agonists per book... here is how it works: stimulates SNS-->increases calcium flow into heart cells-->increases contraction (positive inotropic effect.

Nitrates (decrease cardiac workload, relaxes vacular smooth muscle to DECREASES AFTERLOAD and allow pooling in veins which DECREASES PRELOAD of the heart.)

Calcium channel blockers - rarely used for CHF, use only for specific CHF cases.

Diuretics - decrease bloos volume, which decreases venous retun and BP resulting in DECREASED AFTERLOAD, PRELOAD and cardiac workload. Lasic and spironolactone.

Digitalis (Digoxin) - heart works harder and pumps better, does not extend life (0.5-2.0 ng/ml therapeutic range).


How do cardiotonic agents work?

They affect intracellular calcium levels in the heart muscle, leading to increased contractility, whihc leads to increase cardiac output/renal blood flow/urine production.

Digoxin (Lanoxin), inamrinone (Inocor)(


Digoxin ______ the force of myocardial contraction & ____ the heart rate by ______ intracellular calcium.

increases force

slow heart rate

increasing intracellular calcium

Side note:
Digoxin increases cardiac output and renal perfusion while decreasing renin (No angiotensin system going bananas, no aldosterone release saying hold onto salt and water!).

Has a diuretic effect which:
1. helps lower blood volume (DO NOT GIVE without solid kidney function for this reason)
2. Is why we need to watch potassium


What must we ALWAYS do before administering Digoxin?

Watch for toxicity! Check for Sever bradycardia (


What is the Digoxin reversing agent?


Binds to dig.


What herbs potentiate (increase the effect of) Digoxin?



What are the reversal agents for each of these?


Heparin - Protamine sulphate

Coumadin - Vitamin K

Digoxin - Digibind


Inotropic means the same thing as ...



Inamrinone (Inocor) is approved for use in CHF that has not responded to?

digoxin, diuretics, and vasodilators.

It's usually seen in ICU. Not tested on it but should know it. Allows more calcium to enter the cell.


Why do you lift the legs when someone is in shock?

shock is characterized by the inability of cardiovascular system to pump enough blood to meet metabolic needs of the tissues. Legs up, blood returns back.


T or F: Normal clotting takes about 3 minutes. Fibrin is the final product that stops blood loss.


Yes Fibrin is Final, but it takes up to 6 minutes for normal blood clotting.

Why is this important? We watch clotting times to adjust meds. We will see this shortly


The transformation of fluid blood into a solid state to seal breaks in the vascular system is known as ______



The ______ process involves vasoconstriction, platelet aggregation to form a plug, and intrinsic & extrinisc clot formation initiated by hageman factor to plug breaks in the system



What does plasminogen do?

dissolves clot


The conversion of _______ to thrombin results in insoluble fibrin threads and is the final step of clot formation.

prothrombin - It is converted by prothrombin activator (also known as tissue plasminogen activator TPA) or prothrombinase

Thrombin converts fibrinogen to fibrin (framework for clot)


_____ is the process of clot removal

fibrinolysis (starts 24-48 hours after clot formation)

read the steps but don't memorize


CVA's can be _____ or ______

ischemic (clot blocks blood flow to brain) or hemmorhagic (bleed inside skull, compresses brain leads to tissue death)

You get 3-6 hours before permanent tissue death


_______ when given quickly after the onset of a stroke, can restore some or all of the previous brain function.

The prototype is urokinase (but we usually use TPA in the hospital).


(thrombus = clot; lytic...lysis....)

Since it destroys clots, the time you would NOT want to give this ? When someone is actively bleeding.

Look at PTT - Use Amicar to reverse


We would treat _______, _____ _____ and _____ _____ ______ with clotting factors.


liver disease

bone marrow disorders


We use antihemophilic factor to treat?

hemophilia - replaces clotting factors. Trade name is BIOCLATE (bio - clate clot)


Systemic hemostatic agents stop the natural plasminogen by blocking its activation.

What does plasminogen do?


plasminogen dissolves clots. We stop the dissolution of clots with this drug (Amicar).


What is disseminated Intravascular coagulation?

a lot of bleeding and a lot of clotting


Thrombolytics also dissolve clots. Aminocaproic acid (________ ) is used to reverse thrombolytics by stopping them from dissolving clots and stops plasminogen (clot dissolver) by preventing it from being formed.

Since it keeps blood liquid, we have to watch out for edema.

Do not give with anticoagulant. works against each other.


Since it keeps blood liquid, we have to watch out for edema.

Do not give with anticoagulant with this med because they work against each other.


Blood is made of _____ and ____ _____

plasma and formed elements (rbc, wbc. hemoglobin, etc)


What is the purpose of iron?

to form hemoglobin rings to carry the oxygen.

We also need folic acid and vitamin B12.


Anemia results from alteration in erythropoiesis (part of RBC production). The rate of RBC production is controlled by erythropoietin (which is released by the kidneys due to decreased oxygen or blood flow).

Anemia can occur if ertyhropoeitin levels are low or when we are missing pieces for the building of RBC. What two suggestion for this problem can you come up with?

1. Renal failure (kidney cannot produce eryhthropoetin)

2. Insufficient amount of iron (iron deficiency anemia), B12 and folic acid (megaloblastic anemia...remember Blast is the cell that Builds....if you are missing pieces to BUILD, it is related to BLAST)


___________ anemia is when there is insufficient folic acid or B12 to create structures for RBC.

______ ______ anemia is when a negative iron balance occurs

______ anemia is when the gastric mucosa cannot produce intrinsic factor, and B12 cannot be absorbed.

megaloblastic (causes of Folate deficiency include absorption problems, drugs, malnutrition and alcoholism. B12 deficiency caused by poor diet, increased demands and lack of intrinsic factor in stomach).

iron deficiency



If a person lacks red blood cells, what can we give them to assist with increasing their numbers?

epoetin alpha (Epogen)

treats anemia associated with renal failure; no need for blood transfusions.

acts like natarul erythropoetin to stimulate production of RBCs

darbepoetin/ Aranesp is another edition


Who is at risk for iron deficiency?

1. menstruating women
2. pregnant and nursing women
3. rapid growing adolescents
4. Persons with GI bleeding


WHat are we looking for in labs to diagnose iron deficiency?


lack of Hgb, should be 14-42

All Iron drugs have FE as first two letters in their name (Ferrous fumarate (Feostat)


What vitamin should you take with Iron?

Vitamin C; helps absorption


What is the most common side effects for Iron?

1. constipation
2. black tarry stool