Heart Day [with Deb]
Will test questions be patho questions like in 205 last semester? No, they will be scenarios w/ clients
Called “Heart failure”: No longer called “CHF” which is still overused.
Mr. Ames age 59, has been on your floor since yesterday am. He was admitted with right sided heart failure following an MI 3 months ago. He has an IV of NS at 200 ml/hr, a F/C draining cloudy amber urine and has had no energy or appetite since admission.
What causes R side heart failure (which is uncommon)? Rt side failure either means respiratory stuff or rt ventricular MI. Usually caused by respiratory problems: “increased pressures in the pulm vasculature,” such as pulm fibrosis, COPD. An MI causes failure b/c the tissue dies. COPD + Rt Heart failure is called: Cor Pulmonale
Rt side heart failure causes edema to the periphery, esp the sacrum. Also splenomegaly, hepatomegaly. You won’t hear crackles or wheezes, b/c the blood backs up into the systemic circuit, [instead of the lungs, as in left sided heart failure.]
Heart failure of any type can also be caused by issues of preload: putting blood into the atria and preparing to eject it. If you don’t have good volume, you can’t pump it out well—too much volume means the heart gets stretched out over too much time [Starling’s Law: cardiomegaly/pooped out rubberband theory]
When talking about Heart failure, we care about:
Preload [gets blood into heart]: “In cardiac physiology, preload is the pressure stretching the ventricle of the heart, after passive filling and atrial contraction. Preload is theoretically most accurately described as the initial stretching of a single cardiac myocyte prior to contraction.” (wikipedia)
Contractility [how well the heart pumps the volume]: “Myocardial Contractility is a term used in physiology to describe the performance of cardiac muscle. Contractility is often defined as the intrinsic ability of a cardiac muscle fibre to contract at a given fibre length.” (wikipedia
And afterload [the resistance that you have to pump against.]: In cardiac physiology, afterload is used to mean the tension produced by a chamber of the heart in order to contract. In the clinic, the term end-systolic pressure is usually more appropriate, although not equivalent. Afterload can also be described as the pressure that the chamber of the heart has to generate in order to eject blood out of the chamber. Everything else held equal, as afterload increases, cardiac output decreases. In the case of the left ventricle, the afterload is a consequence of the blood pressure, since the pressure in the ventricle must be greater than the peripheral blood pressure in order to open the aortic valve.
What matters is how much you get in [preload], how hard the pumping is [contractility], and how hard you have to push against to get it out of the heart. [afterload]
Effects on the heart, compensatory mechanisms:
Dehydration= low blood volume. Overhydration=too much volume
Contractility: if you have cardiomegaly, you get too much volume in the heart, but it doesn’t pump enough blood out.
Tach: the body compensates for the lack of blood making its way out of the heart by kicking up the heart rate. Also increased BP and contractility.
Pumping against tough pipes: afterload is effected by how hard your pipes are: your pipes are hardened by plaque [atherosclerosis.]
kidneys aren’t getting enough fluid, they respond by saving salt, and therefore secrete Aldosterone—which causes higher vascular volume, and the preload and afterload increase.
ANP and BNP [atrial and Brain Natriuretic [sodium wasting via urine] Peptides are released, which causes vasodilation.
Ventricular remodeling: initially makes more productive contractions, the ventricles dilate to allow the excess blood volume of the body. Ultimately, this turns into ventricular hypertrophy and the O2 needs of the heart increase, and pooped-out-rubberband disorder.
What do we want to know from report?
UTI? Meds?
Test/check renal function [BUN, serum Creatinine]. The body will defend the kidneys last, and protect the heart and brain. The kidneys will shut down, so renal failure and acidosis are next up. Hepatomegaly/increased pressure on liver can cause it damage.
What are pt VS? Chest pain, peripheral edema, lung assessment, O2 sats. SOB? Tach? This client should be on tele; and those sinus rhythms should be reported. Why no appetite? [easy: he feels like crap.] His blood is gorged in his spleen and liver. IV is too fast. Does he really need isotonic solution? NS may cause him to retain. He should probably be on fluid restriction.
We’re looking up recent labs. What do you want: CBC: look for infections [b/c he is highly at risk], weight, electrolytes [esp sodium, and K.] This guy might not need blood gases taken.
What’s the first thing we do when we go in the room? Vitals. Sacral and peripheral edema. Sacral edema is “dependent edema.” You want to check the F/C, the IV, the lungs—which should not be affected unless the L side of the heart is now involved. Does he have pink frothy sputum [indicating pulmonary edema].
Things that look bad: Weight: a few pounds of weight gained is a big problem—daily weight is critical, control for every piece of clothing, use the same scale, etc.
LABS: Diagnosed w/ ANP and BNP labs-- Atrial and Brain Natriuretic [sodium wasting]. BNP lab: Human natriuretic peptides. Released as heart muscle stretches-- Peptides are released, which causes vasodilation.. They classify HF based on this lab. 100+ is ‘mild.’ 300-600=mod. 600-900= severe.
Serum electrolytes: measure to detect fluid rentention
Kidney and liver function tests
Thyroid tests to see if thyroid is the source [hypo or hyper]
Chest x ray shows pulm congestion and cardio megaly
HF is usually side effect of something else:
Meds: What do we want meds to do? Effect those 3 things: preload, contractility, afterload.
- Preload: it’s about volume—effected by diuretics. Why to HF pts take diuretics? Why do we like Lasix? It’s cheap. Why is it bad: it’s not potassium sparing, and if you’re on Dig too, you’ll become Dig toxic. We like potassium sparing diuretics. These get rid of both sodium and water. So never give diuretics at nighttime, or past
- What takes care of contractility? Dig. Lowers HR, increases contractility; stronger and slower [pos ionotrope.] Therefore increased volume due to slower HR, and better afterload b/c of contractility. Also works as a diuretic b/c the blood makes it to the kidneys better.
- How do I know dig tox: Bradycardia, seeing halos/auras.
- Afterload: what causes vasodilation? Pick a beta blocker. HR slow, vasodilation. ACE inhibitors, ARB’s.
Once you have perfusion finally, people have some negative side effects: headaches b/c you finally have blood getting to the brain. The baroreceptors freak out and try to get the BP down quickly to counter the new perfusion that is ‘normal’ but seems ‘too high’ to the baroreceptors.
Teaching; pt takes their pulse at home for 60 sec. This is trickier than it looks. Tell them to hold Dig if HR is less than 60, AND call their doc.
If they are on lasix, they should be getting K+ supplement. The lower your K is this happier your dig is, and out you go in to bradycardia land. How to eat K pills: dissolve them, cut them in half, etc. Daily weight: ½ lb or more means call the doc. Low Na+ diet.
How do I know they are better: pale urine, no edema, pink skin, appetite,
Getting worse: weight gain, cyanotic, low BP, ascites [fluid in abd], splenomegaly or hepatomegaly. VS going south. I/O: a lot in, nothing out means bad.
Do daily weight for HF clients. You don’t need an MD order. Give people their meds, make sure they are on the right meds.
Prognosis of HF: always fatal. Terminal disease when treated. When this guy goes home, he’s not cured, it’s not reversible. He has 5-8 years. What about transplant? Yes it happened for lots of pts. Most pts are older and have complex Hx. And, if you’ve got the cash, you can have a new heart. DM pts have a lot of HF.
Ryan Sanchez age 20 has been admitted to your unit with a diagnosis of chest pain and heart failure. Four weeks ago he had a “cold” with a very sore throat. It was busy at his work and he was unable to take time off. During his cold he had a high fever, red rash on his chest and swelling of his knees. Currently he is scheduled for an echo, VS stable except for a murmur. The night nurse is not sure what kind because she is “not very good at hearing heart murmurs.”
Rheumatic Fever: Sequelae. This is why you treat strep every time without fail.
One sequelae: when the antibodies of the immune system bind to the bacteria, they create ‘immune complexes’ These can attack the renal system [glomerular nephritis], and the mitral/bicuspid valve [on the left side of the heart.] This creates vegetations on the edges of the AV valves, especially the mitral valve, called “aschoff bodies.” Aschcoff Bodies are necrotic tissue surrounded by immune cells. The pt had strep and is now being treated for rheumatic fever. Pt thought he had a cold: but he had redness on his chest, swelling of knees. Now in hosp for HF/rheumatic fever.
What else do I want to know: what kind of murmur? He has a ‘grade 2 systolic murmur.’ We expect to hear murmur at the “money/mitral” position. Grading of murmurs means how loud: the grade 2 is pretty obvious, grade 4 you can hear at Bedside w/o stethoscope. Grade 2 is a trademark of rheumatic fever.
Labs to confirm rheumatic fever:
an ASO titer [antistreptolysin]—shows body reactivity to strep,
These say you have an infection: A SED rate [erythro sedification rate] and positive ‘C reactive protein’; these lab values just check for inflammation.
There is no reason to do a rapid strep test, b/c that infection is over, but it will ikely show Group A strep.
Cardiac enzymes elevated in severe carditis
So why does this guy have HF at 20?
Rheumatic fever hit a lot of people when we didn’t have PCN, and they would have valve replacements.
Things we want to know: What kind of heart failure? What’s his Hx of chest pain: is it resting or during activity, how new is the symptom? I/O, VS, his weight. How long has he been so sick, his diet, general health status, where does he work?
First thing I do in the room: vitals, if he’s experiencing chest pain. Right now.
Never take chest pain lightly.
How to rule out the heart in chest pain: give them Maalox to r/o GI, take deep breaths b/c pain on inhalation might be more lung than heart, etc.
Mitral valve means L side, water backing up into lungs.
He’ll come back from echo w/ positive for Ashcoff’s bodies: and he’ll get a valve replacement. Pretty much the only treatment.
Risks of replacement: endocarditis, infection/rejection [prophylactic antibiotics], etc. Clot formation: so coumadin, etc.
Meds: 10 day course of PCN to drop the strep, plus IM injection of PCN prophylaxis over several years. Pain meds/ anti inflamatories.
Nursie does: teaching about sequelae, how to prevent strep. How to handle carditis [surgery.] Interventions, teaching for pain and activity intolerance for the meantime.
Mrs. Wayans arrives to the outpatient surgery center for her second cataract surgery. While starting her IV she complains of chest pain. She tells you she has a history of angina. What are your first assessments? Interventions?
Questions to ask: what quality of pain, when, 0/10. “Do you take nitro, do you have it with you?” If yes, tell her to eat one. Also give her oxygen. Oxygen is mainstay of treatment for chest pain. I care about her vital signs, b/c the NTG opens all her arteries, and her BP drops.
Angina: caused by too much schmoo in the he-arteries, or heart spasms. The pain is caused by tissue crying out for O2, and there’s not enough blood coming thru the heart-eries.
Call primary care: let them know what’s up.
There is a fine line that says you cannot prompt her to eat her PRN med—b/c that’s not our med to serve her—it’s not a med that the outpatient center has orders for.
Question is: can she have her surgery today? We won’t. She’s not worried about the pain, but we are.
We need to be sure that at home, she is having good results w/ her NTG.
People w/ stable angina can take up to 3 NTG, but first they have to sit down. If they have oxygen at home, they need to put it on. You need to decrease O2 demand of the heart by resting, and supplement O2. beta blockers and calcium channel blockers [vasodilators, HR slow] can help mellow the heart’s demands as well. Then they take a Nitro, wait 15 mins, take another PRN, wait another 15, take a 3rd, if that doesn’t work, CALL. Anyone else w/ chest pain that isn’t stable angina should get to the ED.
We send her home, but she is still at risk for MI. So you still want to remind/teach her the S&S of MI, and how to decrease O2 demands at home.
Does diet matter? Yes: we don’t need any more schmoo in the arteries. Mild exercise.
Beta blockers lead to impotence. Sex is still important to grampa and grama, so it needs to be talked about. Ca+ channel blockers don’t cause impotence.
1 comment:
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