Term
| Trace the path of a drop of blood through the body, starting in the right atrium: |
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Definition
“Starts in the right atrium goes to r ventricle out through the pulmonary artery to the lungs. Back through the pulmonary veins into the left atrium down to the L ventricle out through the aorta and out to the rest of our body.” -Sivadon
“Right atrium to the right ventricle via the tricuspid valve.
The right ventricle pumps blood through the pulmonic valve into the pulmonary artery and to the lungs.
Oxygenated blood flows from the lungs to the left atrium via the pulmonary veins. It then passes through the mitral valve and into the left ventricle. As the heart contracts, blood is ejected through the aortic valve into the aorta and thus enters systemic circulation.” –Lewis text |
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Term
| The coronary arteries supply the |
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Definition
| myocardium (heart muscle) with oxygenated blood. |
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Term
| List the major coronary arteries: |
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Definition
• Left (coronary) main artery “widow maker” which divides into the:
a. Left Anterior Descending “feeds front part of heart” (Anterior apex)
b. Left circumflex artery “goes underneath armpit” (Lateral part of heart)
• Right coronary artery “feeds backside and bottom part of the heart.” |
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Term
| Trace a normal electrical impulse through the heart: |
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Definition
Originates in the sinoatrial (SA) node (aka: pacemaker) travels down the intra nodal pathway
through the atrial ventricular (AV) node (aka: gate keeper/tollbooth) into the Bundle of His and divides into the
right bundle branch (goes to right ventrical) and left bundle branch (goes to left ventrical) and finishes in the Purkinje fibers. |
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Term
| Depolarization (cellular polarization) |
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Definition
| begins the contraction of the myocardium |
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Term
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Definition
| is the contraction of the myocardium |
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Term
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Definition
| is the relaxation of the myocardium (ventricles fill back up with blood). |
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Term
| Define cardiac output: “key term to know” |
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Definition
| Amount of blood pumped each ventricle in one minute (one minute worth of blood) |
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Term
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Definition
| Amount of blood “per squeeze” ejected from the ventricle with each heartbeat. |
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Term
| How is cardiac output calculated? |
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Definition
| CO= Stroke volume x heart rate |
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Term
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Definition
| After the heart beats, preload is the amount of blood left over in the ventricle. It’s the “pre” for the next cycle. After the contracton, before the heart fills back up. It is based on the pressure placed on the myocardial fibers. |
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Term
| What medications effect preload? |
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Definition
| Vasodilators “nitrates,” which increase preload by dilating everything out, so more can be “pushed out” which can increase the SV (stroke volume). |
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Term
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Definition
| The resistance that the blood has to push against whenever the heart contracts, which is affected by size of ventricle, wall tension, and arterial blood pressure. |
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Term
| What medications effect afterload? |
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Definition
| Anti-hypertensives because “we decrease that pressure that we need to push against and also decrease that systemic blood volume—so not as much has to be pushed against it.” |
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Term
| Define ejection fraction (EF): “term you want to know” |
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Definition
| EF is seen in all cardiac patients, “that’s going to be something that will tell you a lot about the patient’s condition such as the diagnosis, prognosis.” So, like we said, when the heart contracts it doesn’t empty it out dry, right? There is blood left over. Well, the ejection fraction is just what it says. It’s the ejection of blood that’s ejected on each heartbeat. |
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Term
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Definition
| You will never see anything that is 100%, because we won’t be “dry,” right? So, a normal EF is anything greater than 50%. You will hear different numbers. You may hear 55% or 60%, but as far as what the American Cardiac Association considers normal is anything greater than 50%. |
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Term
| What is the leading cause of death for people > 85 years old? |
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Definition
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Term
| What is the most common cause of hospitalization for adults < 85 years old? |
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Definition
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Term
| What is the 2nd leading cause of death for adults < 85 years old? |
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Definition
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Term
| List the major changes that occur in the aging cardiovascular system: |
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Definition
The valves get calcified;
The arteries get stiff as we age—a normal process;
A decreased heart response to stress “like when you go to get up and walk, our heart doesn’t keep up with us as much, or you get stressed out.”;
Increased O2 demand;
Decreased cardiac output (CO) because the muscle “gets sluggish, it doesn’t work quite as well”;
Decreased stroke volume (SV);
Decreased contractility. |
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Term
| History and physical (H&P) is the most helpful in assessing a cardiac patient |
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Definition
| History when talking to a cardiac patient cant be “what happened in the last 24 hours?” “Tell me about it” When they start saying, “well you know, I was out shoveling snow and I got about halfway down the sidewalk, I just started having this burning sensation”—this is considered part of the history, even though it was in the last 12-24 hours—it is still the history. The history entails the “whole picture” how they describe their pain, how it started, when they sit down did it go away? |
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Term
| List the common sites for palpating pulses: |
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Definition
| Carotid, Brachial, Radial, Ulnar, Femoral, Popliteal, Posterior tibial, and dorsalis pedis—the main places. The further away that you can feel a pulse, the higher the blood pressure is. “if you can feel a carotid, you know their pressure is at least 40.” “If you can feel the brachial, femoral, as it moves down the further away from the heart—the higher the blood pressure has to be.” |
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Term
| Identify the most common cardiac markers: Creatine kinase “CK-MB” |
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Definition
| “that used to be the classic” The CK is an enzyme released after injury, it’s skeletal tissue, cardiac tissue is skeletal tissue. So, you will still see CK-MB’s with any kind of muscle injury—if someone hits a steering wheel, you will see that released. The hard thing about CK-MB’s is that the start to rise after about 6 hours, peak in 18 hours, and after 24-36 hours they are back to baseline. So if someone is having chest pain, and they put it off and put it off, so it’s two days later and they’ve had an MI it may not show. So when these people come to the hospital you draw it, wait 4 hours, draw it, draw another one and wait 4 more hours, so we can see if they were going up or coming down. It can tell us the pace of it. Used to Dx heart attacks. |
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Term
| Identify the most common cardiac markers: Troponin |
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Definition
| discovered in about 2000 and it is much more cardiac specific and it is actually a protein, so it stays in our blood system. But the amount in our blood system is so low that just the slightest cardiac injury will show up in that. A normal troponin is below 0.2. So anything that bumps up above that is cardiac issues. Troponin starts to show up in about 4-6 hours, and peaks at about 10-24 hours, but it will stay in the system for up to 2 weeks. So the patient that waits for a couple of days, their troponin will still be elevated. Used to Dx heart attacks. |
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Term
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Definition
| Used to Dx heart failure. B-type naturitic peptide. It is released from the venticles into the blood stream. |
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Term
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Definition
| Main storage of lipids—95% fat tissue. Increased by sugar which can lead to DM, alcohol intake because of sugar content will increase it, needs to be < 150. |
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Term
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Definition
| Cholesterol: Absorbed from GI tract, and we get it from food. Synthesized in the liver. Like it to be < 200. |
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Term
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Definition
| Phospholipids: Lipoproteins that are synthesized in the liver. |
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Term
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Definition
| (mostly cholesterol) Like for them to be < 130, but if the patient has a Hx of Coronary artery disease (CAD) we want the LDL to be < 100. LDL is “low.” The lower the better. |
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Term
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Definition
| need to be > 40. HDL is “high” The higher the better. |
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Term
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Definition
| Looks at the silhouette of the heart, can show if heart is enlarged, if the heart is in their “backwards,” any fluid around the pericardium, any interstitial fluid whatsoever. |
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Term
| :Electrocardiogram (ECG or EKG) |
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Definition
Electrocardiogram (ECG or EKG)-
Shows electrical activity of the heart. ST segment can dx an MI, the ischemia in the heart, whether the heart can be used for heart blocks, any electrical problems, any dysthymias. |
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Term
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Definition
| Is an ultrasound of the heart. Looks at blood flow through the valves, chambers, mostly used for structural things. One of the main tools to get an ejection fraction “EF.” How the ventricles are pumping, if they’re pumping appropriately, if there is any valve regurgitation or valve stenosis. |
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Term
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Definition
| will hook the patient up to an EKG and put them on a treadmill. Will show any EKG changes while the patient is exercising, which could indicate ischemia to the heart muscle. |
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Term
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Definition
| will inject a radioactive isotope, exercise, and scan again. Will show if there is any ischemia that is reversible. |
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Term
| Depending on the patient’s Hx, they will do either a regular stress test, and the results are remarkable, then they will do a nuclear stress test, if that is remarkable—they may go to an angiogram. |
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Definition
| Depending on the patient’s Hx, they will do either a regular stress test, and the results are remarkable, then they will do a nuclear stress test, if that is remarkable—they may go to an angiogram. |
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Term
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Definition
| Shows the blood flow in the heart muscle through the coronary arteries. Cardiac catheterization is THE most definitive way to find out if a patient has any blockages in their artery—because you are actually looking at the arteries, looking at blood flow because we inject a dye, any blockage will be shown. Doing the angiogram is more risky, because you are going through the femoral artery, inserting a catheter. There can be nerve damage or clots from this. So unless the patient comes in with chest pain and the EKG and all of the signs point toward it—they will do non-invasive first, less risky. Then move toward more invasive. |
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Term
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Definition
| When a patient has a dysrhythmia, like a. fib. A. flutter, tachycardias. They will take the patient in and hook electrodes in the heart and can observe the entire electrical system from the inside out. They can find out where there are electrical issues, can put a catheter in and can apply heat “ablation” to the tissue on the inside of the heart, and it scars it. So electrical activity can’t pass the scar and can be redirected. This is done in the cath lab. |
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Term
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Definition
| Hardening of arteries. As plaques build up and bursts, it is called a ruptured plaque. When it opens up and blood is going by it, coagulation can occur. That is what makes a clot and can block an artery. Over time if they don’t build up and rupture, the fat hardens like “lard or Crisco,” as we age Calcium joins the lipids and it ends up becoming very stiff. Instead of having a piece of rubber tubing, like the inner tubing of a bike, you have more like a water hose because it is stiffer. Putting water in the hose won’t allow for expansion. This is what causes HTN, the arteries get stiff and as the blood pumps through there it has more resistance. This is the major cause of coronary artery disease (CAD). It either builds up and ruptures are plaque, or it builds up and gets lumpy the RBC’s start building up on it and cause a clot and ruptures—when it ruptures it can even push a piece of skin off (kind of like a blister) and it can shut off the blood flow. It can be acute (like the plaque rupturing) or it can just get larger and gradually make the space smaller. |
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Term
| Define collateral circulation: |
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Definition
| Kind of like when trees fall into a river—the river floods around trees and the “trees” work harder and harder. This builds up over time. This is something that increases a little bit at a time as the heart muscle works more, the blood gradually works around it. The longer that this is happening, the better collateral circulation gets—the vessels work harder. |
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Term
| Identify risk factors for coronary artery disease (CAD) and note if they are modifiable or non-modifiable: |
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Definition
Nonmodifiable: HTN, age, gender, ethnicity, family history, hyperlipidemia, high cholesterols. The family hx also is considered (mainly parents and siblings) if they have heart disease earlier than 50-55 this is considered pertinent.
Modifiable: lipids, exercise, TOBACCO USE—not just smoking, even people who dip, it is the nicotine that causes vascular disease, heart disease. Quitting smoking and chewing nicotine gum forever will still put you at risk. Overweight or smoke. HTN is the second major risk factor for CAD, because of elasticity of the arteries. HTN is > 140/90. If you have DM it should be < 130/80. DM is a big risk factor for CAD—it is kind of a contributing factor. Symptoms show up differently with diabetics. The diabetes can kind of disguise the symptoms. Psychological state: stress, anxiety, depression increase the risk for CAD. Substance abuse: cocaine, meth, any kind of stimulants also increases the risk for CAD. Coronary spasm is seen with meth and cocaine. Even some herbals—anything that has ephedra in it—it’s a stimulant. Type A personalities. White middle aged men > women until age 65, then it is more =. |
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Term
| List strategies that can help prevent CAD: |
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Definition
| Therapeutic lifestyles, increase physical activity, control BP, diet/exercise. Drugs for high cholesterol= -statins. Something to know, we are seeing a lot of people on –statins these days. Some people can take niacin, some people can’t take it because of the hot flushing side effects. What –statins and niacin do is vasodilation. This is why exercise is so important, vasodilation occurs. The statins kind of do the same thing with vasodilation. Stop smoking is the biggest thing you can teach. Control diabetes, have a healthy diet (DASH)—2400 sodium, low fat, increase fatty omega 3’s tuna, salmon, cold water fish. Walnuts, avocados, almonds are all good fats. Any man over 40 should take a baby ASA a day. Women it hasn’t been shown to be effective unless she has already had a cardiac event. Anybody who has had a cardiac event should take a baby aspirin a day. |
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Term
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Definition
| Chest pain. How we assess and treat it. Women have atypical S/S: which is why death is increased. |
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Term
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Definition
| This is irreversible ischemia—it can’t be fixed. Can also be irritated by exertion. A chronic situation. Usually will have known coronary disease and possible damage. Nitro will treat this. If the nitro isn’t treating it, pt needs to go to the hospital. Will not happen at rest, only with exertion. |
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Term
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Definition
| It is unpredictable, usually with exertion but not always-- like shoveling the snow, the heart muscle demands more O2. If you have an artery that is partially blocked, when you exercise more demand is put on the artery. The BP increased, which kind of restricts a little more. As you are pumping it, the heart muscle needs a little more because it can’t push any more blood. The O2 demand in the heart is greater than what can be produced. Stop. Sit down, the O2 demand will decrease and the pain will go away. Will lead to a pt coming to the hospital. It will increase with intensity, episodes. Nitro will not relieve it. This is reversible ischemia—it can be fixed. This will lead to an acute event. |
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Term
| List the steps in assessing a patient-experiencing angina: |
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Definition
P
Precipitating events
What events or activities precipitated the pain (e.g., argument, exercise, resting)?
Q
Quality of pain
What does the pain feel like (e.g., pressure, dull, aching, tight, squeezing, heaviness)?
R
Radiation of pain
Where is the pain located? Does the pain radiate to other areas (e.g., back, neck, arms, jaw, shoulder, elbow)?
S
Severity of pain
On a scale of 0 to 10 with 0 indicating no pain and 10 being the most severe pain you could imagine, what number would you give the pain?
T
Timing
When did the pain begin? Has the pain changed since this time? Have you had pain like this before? |
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Term
| Define acute coronary syndrome (ACS): |
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Definition
| Umbrella for an unstable angina that leads to an MI. An unstable angina that is not treated WILL lead to an MI. When patient’s have unstable angina, it can be in all areas of the chest. Typical: upper chest, sometimes epigastric, sometimes it will radiate to the jaw, down the left arm. Seldom does it radiate down the right arm—through the back. |
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Term
| Define myocardial infarction (MI): |
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Definition
| Death of the heart muscle due to ischemia. Is it anterior? Posterior? Lateral? Inferior? Will have pain. N/V. Increased BP. Anxiety, diaphoresis, ashen color, clammy. Dx with an EKG, and angiography is definitive. |
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Term
| What is the difference in a STEMI and a NSTEMI |
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Definition
STEMI- in an elevated ST segment of EKG. There is no blood flow leading to the artery—totally occluded.
NSTEMI- non-ST-elevated MI. Partially occluded artery. |
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Term
| Identify complications associated with a MI: |
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Definition
| Death of myocardial tissue. Decreases the pumping function, which decreases cardiac output (CO)—this will lead to a decreased EF, which can lead to heart failure. Also, arrhythmias: ventricular fibrillation, atrial fibrillation. Blood vessels (like the SA node) has to have blood flow. So if the artery that is being affected is the right coronary artery—so with the SA node not having blood flow there will not be regulation of the cardiac rhythm. |
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Term
| What is the goal of treatment of a MI? |
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Definition
| Revascularization. Meaning, we want to get vascular blood flow to the part of the heart that is affected. The most prominent way that we do that is with stenting—coronary balloons that pushes the plaque out and the stent keeps the arterial wall open. After a pt. receives a stent, they often go on Plavix, because we want to anticoagulant the foreign object. Aspirin also. Some stents are also coated with antibiotics—they are called drug-coated stents, the medicine helps the tissue heal better. |
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Term
| What are the three most effective modes of treatment of a MI? |
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Definition
The most prominent way that we do that is with stenting—coronary balloons that pushes the plaque out and the stent keeps the arterial wall open. After a pt. receives a stent, they often go on Plavix, because we want to anticoagulant the foreign object. Aspirin also. Some stents are also coated with antibiotics—they are called drug-coated stents, the medicine helps the tissue heal better.
Fibrinolytics, clot-busting drugs, TPA—unusual unless it is in a remote area and there is not access to a cath lab. This thins out everything—the whole body.
CABG can also revascularize but it has to be > 70% blocked before it is treated with angioplasty. < 70% blocked—studies show that it doesn’t really help. (With non-stemi MI’s—because a STEMI is 100% occluded). When all 3 arteries, the left ascending, circumflex, and right coronary blocked it is more practical to have a CABG. |
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Term
| List most common medications used in treating CAD and MI: |
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Definition
| List most common medications used in treating CAD and MI: |
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Term
List most common medications used in treating CAD and MI:
O2: |
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Definition
| The first thing—put the patient on oxygen because that is why they are having chest pain. Their heart needs more oxygen then what it is getting from the blood vessels. |
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Term
List most common medications used in treating CAD and MI:
Nitroglycerin |
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Definition
| q 5 minutes up to 3x until relieved. Check the blood pressure between giving nitro, we do not give nitro if their blood pressure is less than 100. Because nitro drops the blood pressure due to the vasodilation—makes the hole bigger and the blood pressure decreases. |
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Term
List most common medications used in treating CAD and MI:
Morphine |
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Definition
| (if the nitro doesn’t get rid of the pain) |
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Term
List most common medications used in treating CAD and MI:
ASA |
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Definition
| Chew 4 baby ASA somewhere in there. May not be the first thing you do, it may be the second—or when convenient. Maybe have them chew the baby ASA on the way to the hospital. |
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Term
List most common medications used in treating CAD and MI:
B-Blockers |
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Definition
| increase the myocardial O2 demand—slow down the HR; decrease BP, classic to use them within the first 24 hours of an MI. When someone has an MI, the pt will be on B-Blockers for the rest of their life unless it is contraindicated for some reason. One of the core measures. |
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Term
List most common medications used in treating CAD and MI:
ACE inhibitors- |
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Definition
| if a patient has a STEMI and an EF < 40% then they will be started on the ACE inhibitor. Only as indicated. |
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Term
|
Definition
|
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Term
| -statins (another core measure) Amcor, Zocor— |
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Definition
| a big problem with –statins is why most people quit taking them: muscle fatigue can also cause hepatic problems. If one causes muscle fatigue, the patient can change and try another one. Teach the patient not to just stop taking it, talk to the doctor and work through it. |
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Term
| List nursing diagnosis for patients with CAD and MI: |
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Definition
Decreased cardiac output
Impaired tissue perfusion
Acute pain
Anxiety
Activity intolerance
Knowledge deficit |
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Term
| What are important teaching points for cardiac patients? |
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Definition
| S/S, diet, exercise regularly, medication compliance (especially for HTN, cholesterol) because the patient can’t see immediate response, |
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Term
| Define sudden cardiac death (SCD): |
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Definition
| This is also known as cardiac arrest. |
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Term
| What is heart failure (HF)? Distinguish between systolic and diastolic failure. |
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Definition
| Dysfunction of the ventricles—either the pumping part or the filling part. It is all about the function of the ventricles. |
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Term
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Definition
| inability of the heart to pump blood effectively. Systolic is when the heart is contracting. Caused by impaired contractility, increased afterload (big deal about after load: hypertension), cardiomyopathy and valve disease are causes. |
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Term
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Definition
| Inability of the ventricles to fill. Which can lead to a decreased stroke volume, which decreased the cardiac output which causes pulmonary congestion. It also can lead to hypertrophy and you may also see normal blood pressures? |
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Term
| List the primary risk factors for HF: |
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Definition
| Age and CAD—primary. Contributing: HTN, obesity, DM, drug use, high cholesterol—everything that goes along with CAD. |
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Term
| Identify the primary causes of HF: |
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Definition
| Chronic HTN, CAD, MI. With MI the myocardium is necrotic and can’t pump. |
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Term
| Define left-sided failure and its symptoms. |
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Definition
| Most common kind of HF. Left ventricle is screwed up—backs up into the left atrium and pulmonary veins causing pulmonary congestion, pulmonary edema. |
|
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Term
| Define right-sided failure and its symptoms. |
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Definition
Dysfunction of the right ventricle—back up of blood through the right atrium, and to the peripheral system. See jugular vein distension, peripheral edema because the body is not taking the fluid back in.
Can be a result of left-sided failure, because the left side is backing up into the lungs—and if you can’t pump out from the left side to the lungs, everything backs up. Right and left sided failure is possible. |
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Term
| What is pulmonary edema? Signs and symptoms? |
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Definition
| Classic sign: pink, frothy sputum. An acute “oh my God” situation. Life threatening. Most common cause is acute left sided heart failure caused by CAD. Pt. SOB, will feel smothered and drowning, pt will be anxious, want to sit up, will have tachypnea, Classic Tx: Lasix and morphine. Massive IV lasix pulls fluid out, morphine will decrease the O2 demand and provide some relaxation. Call a rapid response, hopefully before it gets to this point. Or in ICU, call the physician. Big Nsg Dx: impaired gas exchange. |
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Term
| Identify complications of chronic HF. |
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Definition
Hypertrophy—if the ventricles are small, there isn’t as much to push out
With dilated ventricles—there isn’t as much contractility, too much force to push against |
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Term
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Definition
| pt comes in with a huge infarction and the ventricles aren’t pumping—you’re going to have an acute episode of HF. Once the pt is revascularized, on medication, they may not have any other problems. |
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Term
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Definition
| They have a huge infarc and a lot of muscle dies, and they don’t get it back. But a lot of time when a pt has an MI and they get tx’d quick enough they will be able to get some function back. The cardiac muscles don’t regenerate themselves but it may just be injured for a little while. Prolonged ischemia, function will not come back. People who are chronic kind of battle this every day. Could be from an MI, drug use, rheumatic fever as a child, atrial fibrillation—an arrhythmia where instead of one impulse coming from the atrium, a lot of impulses occur. A. fib patients will be put on Coumadin to prevent a CVA. It is very classic to see these patients have HF, especially the longer they have it. |
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Term
|
Definition
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Term
| How is HF diagnosed? "The big one" |
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Definition
| BNP is the big one > 100 is considered heart failure. (Can review other classes, but it’s a nice to know). Pt presents with a BNP of 150, you may know this is just an onset of it. Some of these chronic patients that ends up having acute episodes. Like someone with chronic heart failure—it’s thanksgiving: they eat the ham and retain the fluid. So if the heart is already having trouble pumping the fluid out, now they have all the Na in the body—these people will present with acute episodes because their heart was already having problems before—then they will have an acute event. Maybe they are non-compliant with medications, or their diet will retain fluid. So yes, chronic can lead to acute. Acute usually leads to chronic though. You will see HF gradually deteriorate and the patient will have more acute episodes. Sometimes the patient with acute episode and pulmonary edema will present with a BNP in the thousands. 600 may even be the best they get from them—you can even ask patients; they are usually tuned into that thing. If they’re in chronic heart failure, they probably know where their BNP is. “You’re BNP is 850!” –“Well, it is usually 800.” Kind of like DM—the patients can really teach you about these disease processes. |
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Term
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Definition
| you will see their EF. Definition of heart failure: dysfunction of the ventricles, so an echo will tell us about the function of the ventricles. |
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Term
|
Definition
| Sometimes a chest x-ray will pick up on congestion, but not always—like with right hearted failure you know they won’t always have the congestion. |
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Term
|
Definition
| CHF and decreased CO go hand-in-hand. They get tired and don’t have enough “get up and go,” not enough blood pumping to the rest of the body to get them going. You will SOB, with left sided failure—we will start seeing that buildup in the lungs so they will be SOB. Sometimes they’ll cough, you’ll see edema in the lungs or peripherally. You will see dysrhythmias. Because once you start seeing heart muscle relocated—we have this conduction system meant to go “here, here, here.” Well, as we age and these ventricles change the muscle gets stretched out—so the paths kind of change a little bit. So the electrical changes occur and we can see dysrhythmias (can be atrial and/or ventricular arrhythmias. Because the patient has an ejection factor of < 30%-- they will put in a defibrillator because of the ventricular arrhythmias are known to cause sudden cardiac death. Can have biventricular heart failure, and they get out of synch with each other. Once they get out of synch with each other—everything is screwed up and out of synch, these patients will rec’v a biventricular pace maker. They will insert a pace lead on the right and left side of the heart—so they can send the signal at the same time. On an echo, we look at the pumping of the ventricles. With these new devices, you can time when you want the impulse to go. So they will look at the echo and see how the ventricles are pumping, they can change: when the left sided wire triggers and when the right sided wire triggers so they can make them synchronized again. This is called resynchronization therapy. (Next to know) |
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|
Term
List medications commonly used in the treatment of HF.
Diuretics |
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Definition
| Diuretics are one of the big ones, because we want to be able to keep that fluid volume appropriate—want to keep it down. |
|
|
Term
List medications commonly used in the treatment of HF.
Vasodilators |
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Definition
| Vasodilators with patients, depending on what type of HF, we may need to give them vasodilators. What decreased with dilators? Decreases afterload. Because of systemic resistance. These are the patiens who are more chronic. |
|
|
Term
List medications commonly used in the treatment of HF.
Morphine |
|
Definition
| Morphine will be used to Tx in a very acute episode. You see pulmonary edema, what do we Tx them with? Morphine and Lasix. But you won’t really Tx chronic patients with this – you won’t send them home on morphine. |
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|
Term
List medications commonly used in the treatment of HF.
Dixoxin |
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Definition
| - the number ONE drug that you will see patients with HF. Know how dig affects it—how it works. It can be used with acute too. Because if they are not only on it, you put them on it IV. But the chronic will probably be on it. Works by burning up the heart, gives the heart more kick—makes it have a harder kick, increases CO, but it also help slow down a. fib. Don’t give Dig with a HR < 60—but if you have a pt who has CAD, and they have HF—they are on B-Blockers to decrease HR, they’re on Dig—which lowers the HR, so you will see patients all of the time who live with a heart rate of 54. It is kind of what we want. As a nurse, be smart about it and always check the HR—some physicians will even write an order to NOT hold Dig if HR is < 60—but he took responsibility of it—just remember: everything is not black and white and end-all be-all. The reason we are Tx-ing this pt is because we want them to have a lower HR. |
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Term
List another medications commonly used in the treatment of HF.
"Core measure" |
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Definition
B-Blockers are common.
Another big one is carbetolol—a big one that is given to patients a lot |
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Term
| List nursing diagnoses for HF patients |
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Definition
Excessive fluid volume
Activity intolerance
Impaired gas exchange
Decreased CO
Knowledge deficit
In acute episdoes: can cause anxiety. That respiratory is a huge one—that anxiety from the feeling of drowning when they get a rapid HR, can’t breather, and get more anxious because they can’t breather, the more anxious they get the faster the HR goes, and they can’t breathe. It becomes a vicious cycle. |
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Term
| Identify treatment options for HF patients. |
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Definition
Medication regimen : HF patients are those that you will try and get them to the best that they can be. It may be mostly palliative care, but you want to optimize them and get them to the best they can be. Sometimes it is just constant: changing their meds, ensuring they’re taking their medications.
Biventricular tracing is a Tx-ment for HF—to help improve.
In extreme cases: transplant—it kind of depends on what is going on—some of these patients who get to these points have multiple issues. Like if you’re already a diabetic with other issues, transplant lists are full—and they have criteria. It will be main for the pt who has 15% EF. |
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Term
| What are teaching points for HF patients? |
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Definition
| Diet, exercise, teach to control anxiety, medication compliance—same stuff for the heart. S/S: main thing we teach pt’s with HF—it’s all about moving the fluid. Monitor with daily weights—it depends on the doctor. If you gain more than 3 pounds in two-three days and 3-5 in a week. |
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