Heart Failure

olanjones's version from 2016-12-08 03:25

Section 1

Question Answer
Broad strokes HF, what is it?"too pooped to pump" Not enough CO that is sufficient for O2 demand of tissues
Result of HF, broad strokes?heart can't produce enough CO to meet metabolic needs
HF characterized by:vent. dysfunction; ↓exercise intolerance; diminished QOL; shortened life expectancy
HF is a "sydrome" not a disease, what is it associated with?long-standing HTN & C.A.D.; (older population is surviving post MI's)
Tough disease, high morbidity/mortality. % inpatient mortality if admitted 1st time? What's the % if readmitted?1st time= 1 in 20 (4%) will die; if readmitted 10% mortality in 30days & 20-40% in 1 year
Primary risk factors?CAD & Age
Contributing factors?Major→MI (muscle is scar tissue), HTN (long-standing ↑'s x3), DM, smoking, obesity, ↑cholesterol
Precipitating causes (anything that increases workload of heart)anemia, infection, pulm disease, hypervolemia...
Systolic failure hallmark finding↓ in LV ejection fraction (EF)= what % of blood that enters the heart leaves with each beat?
systolic failure aka "inability to pump blood" caused by?impaired contractile function (MI), increased afterload (HTN), cardiomyopathy (decompensated HF, weak heart...this is what happens just before you die), mechanical abnormalities (valve disease)


Question Answer
diastolic failureimpaired ability of ventricles to relax and fill during diastole (decreased SV & CO)
Diagnosis of diastolic failure is based on the presence of what manis?pulm congestion, pulm HTN, ventricular hypertrophy (L&R), normal EF
diastolic failure is caused byLV hypertrophy from chronic HTN, aortic stenosis, hypertrophic cardiomyopathy
R sided V failure onlypulm HTN→ reduced RV emptying→↓LV filing & ↓CO
Mixed systolic/diastolic failureseen in disease states like dilated cardiomyopathy, poor EFs, high pulmonary pressures
Biventricular failureboth ventricles may be dilated & have poor filling & emptying capacity
HF is a good ex of where the feedback & defense mechs start to work against us, how?They increase the workload of the increasingly weaker and weaker heart (interventions work to stop the compensatory mechanisms)
Which compensatory mechanism starts to work first?SNS activation: releases catecholamines (epi/norepi)= ↑HR, ↑myocardial contractility, peripheral vasoconstriction (heart has to push harder)
Compensatory mech: neurohormonal responsekidneys release renin (RAAS) therefore heart must work harder d/t ↑BP
Compensatory mech: neurohormonal response #2Low CO→↓cerebral perfusion→posterior pituitary→releases ADH→increased water reabsorption in the renal tubules→↑water retention & BV= ↑BP
Endothelin compensatory responsearterial vasoconstriction=↑cardiac contractility & hypertrophy
proinflammatory cytokinesreleased by cardiac myocytes in response to cardiac injury→depress cardiac function by causing cardiac hypertrophy, contractile dysfunction & myocyte cell death
HF results over TIME: explain ventricular dilationenlargement occurs when pressure in LV is elevated, initially is an adaptive mech then it becomes inadequate and CO ↓'s
Hypertrophy↑ in muscle mass and cardiac wall thickness in response to chronic dilation; muscle has poor contractility, higher O2 needs, poor coronary artery circulation, prone to ventricular dysrhythmias
Counter-regulatory process ANP & BNPnatriuretic peptides released in response to ↑'s in atrial volume & V pressure; promotes venous/arterial vasodilation to reduce pre and after load→also enhances diuresis to counter RAAS
Counter-reg process Nitric Oxidereleased from vascular endothelium in response to compensatory mechs, Nitric oxide relaxes arterial smooth muscle → vasodilation & ↓afterload

Section 2

Question Answer
cardiac compensationcompensatory mechs are successful in maintaining adequate CO
Left-sided HF etiologiesMI (scarring), HTN (↑ resistance), CAD, cardiomyopathy is the result.
Left-sided HF back up of blood into left atrium & pulm veins= pulm congestion & edema
R sided HF from LHF, what happens with blood if LV failure?backed up into R atrium & venous circulation→pulm congestion→pulm HTN→↑RVafterload→RV hypertrophy→RV failure
Cor Pulmonale can cause RV failureRV hypertrophy secondary to pulm disease can cause RV failure
RV infarct can cause RV failure, manis?JVD, hepatomegaly, splenomegaly, ascites, peripheral edema
HF clinical manis regardless of the causeacute decompensated HF
ADHF usually results in pulmonary edema in the early stages:lungs are told to ↑ RR= ↓O2sats (↑ pulm venous pressure→engorged pulm vascular system→↓ lung compliance → ↑small airway resistance and you find ↑ in RR & paO2 (HgB not circulation to grab O2 & perfuse)
ADHF usually results in pulm edema. IN late stages...if it progresses...lymphatics can't keep up with the draining fluid → interstitial edema → including fluid containing RBC= tachypnea, resp. acidemia → increasingly worse
ADHF physical findings **SATA ??*** *(Think SNS response)orthopnea, dyspnea, tachypnea, use of accessory muscles, cyanosis, cool & clammy skin, frothy/blood-tinged sputum, breath sounds: crackles, wheezes, rhonchi, tachy, hypoTN/hyperTN
Why dependent edema?sudden wt. gain of >3lb in 2D can indicate exacerbation (best long term indicator of fluid retention) *RF can also contribute to this
paroxysmal nocturnal dyspnealegs go up, fluid mobilizes and gets back into circulation...fluid overloaded into heart.
Chronic HF Skin manisdusky, cool DAMP to touch, lower extremities: shiny & swollen (pressure) diminished or absent hair growth
Cough characteristics?persistent dry cough, unrelieved with position change or OTC cough suppressants d/t pressure on alveoli getting tickled
Chronic HF restlessness, confusion & decreased memory, why?hypoxemia
Why chest pain?↓ cardiac perfusion
anorexia, nausea, why?gut has edema also
Complicationspleural effusion, afib **most common dysrhythmia, loss of atrial contraction (kick) can ↓CO by 10-20%
Treatment for afib to help reduce clotscardioversion (get back the atrial kick), antidysrhythmics (stablize rhythm, and/or anticoagulants (prev. clots)
Other complicationsMI, fatal dysrhythmias, hepatomegaly (cirrhosis can develop over time, renal insufficiency or failure, LV thrombus formation-stroke
AHA recommends anticoagulation if:HF + Afib *you need anticoag constantly or if EF is <20%

Section 3

Question Answer
NYHA Functional Classification of Heart DiseaseClass I: no limitation of physical activity. II: slight limit of physical actv. no sx at rest III: marked limitation of physical activity but usu comfortable at rest. IV: can't do physical activity w/o discomfort
AHA stages of HFA: pts. at high risk with HTN, DM, etc. B: structural HD pts. C: pts. with prior or current sx of HF D: pt's with refractory HF (severe sx)
Diagnostic studies primary goalto determine underlying cause which is difficult because many of the s/s are common to other causes
diagnostic studiesH&P, CXR, ECG, labs, hemodynamic assessment, EKG, stress test, cardiac cath, EF
Overall goals of therapy for ADHF & chronic HFsymptomatic relief, won't fix Dx, but minimize Sx: less fluid in lungs, improve LV function, improve QOL, reverse V remodeling
CORE MEASURES in acute mgmt of HF (Joint Commission)D/C: activity, diet, meds, follow up appt., how to take & record daily wt., sx mgmt; LV functioning before/after; If EF <40% then ACE inhibitors; smoking cessation
CC Reduce preload↓ intravascular volume (preload) & ↓ venous return (preload)-reduces amount of volume returned to LV during diastole (high fowler's, IV nitro for vasodilation)
CC reduce afterloadarterial dilation to improve CO & ↓ pulm congestion: IV Na nitroprusside-reduces pre/afterload
sodium nitroprussidedrug of choice for pulm edema-CAUTION watch hypoTN, watch for toxicity (tinnitus, hyperreflexia)
morphine sulfatefor preload and afterload
nesiritidebest at reducing pulm artery wedge pressure, renal perfusion, vasodilator and blocks RAAS
CC improve gas exchange & oxygenationsupplemental O2, morphine sulfate (↓ O2 demand), noninvasive ventilatory support (BiPAP)
CC improve cardiac functiondiuretics, vasodilators, morphine sulfate
Digitalis works where and does whatAV node, makes each beat more efficient and reduces the total # of beats, CHECK PULSE!
CC Reduce anxietyImp. nursing role since anxiety ↑s SNS response which ↑'s O2 demand
Chronic HF main tx goalsTx underlying cause & contributing factors, maximize CO, provide tx to alleviate sx, improve vent. function, improve QOL, preserve target organ function, improve mortality & morbidity
Chronic HF collaborative mgmtO2 administration, physical and emot'l rest, non-pharm therapies (Intra aortic balloon pump, VADs, CRT, cardiac transplant is best
Chronic HF drug therapy-DIURETICS do what??REDUCE PRELOAD auscultate to determine effectiveness; mobilize edema & get it out which will ↓ fluid demand returning & ↑ cardiac function **watch apical pulses
Chronic HF drug therapy-VASODILATORS MOA??reduce afterload & preload: ↑ venous capacity, easier/better contraction, thus reduces dysfunction, ↓ cardiac size: ACE inhibitors *1st line; ARBs; nitrates; BB's
Chronic HF drug therapy-DIGITALISpositive intropic agents increase strength of push; apical pulse; toxicity can kill you; WATCH K!!
Why so important to watch K with digitalis?likelihood of dig toxicity is ↑ in an env't of needs to have K in it.

Section 4

Question Answer
CC Chronic HF nutritional therapylose wt., DASH diet, Na restricted, fluid restriction isn't usu required, daily wts
Chronic HF objective datakeep in mind that regardless of cause, the earliest signs of anything that inhibits O2 which HF does are things like...restless, anxiety, agitation, etc...regardless of a cause you will see this first...the earliest s/s
Nursing mgmt health promotionTx or control of underlying heart disease is key to preventing HF & episodes of ADHF eg. take care of DM
Nursing mgmt health promotion antidysrhythmics, flu & pneumonia vaccines d/t high risk/compromised systems
Chronic HF nursing mgmt meds, diet, exercise regimensexercise training improves sx but often under prescribed, home nursing care
Nursing mgmt acute interventionQOL goals; sx mgmt; restrict salt; conserve energy; support systems are essential for success
Ambulatory & home careexplain physiologic changes that have occurred to the pt.
Nursing mgmt implementationpt. education: meds, taking pulse rate; know when drugs should be withheld & reported to PCP ex. don't take dig with a low pulse
Cardiac transplantation surgeryremove heart except for posterior R/L atrial walls & their venous connections, donor SA node is preserved so sinus rhythm can be achieved post op, immunosuppressive therapy starts in OR room
Cardiac transplant nursing mgmtinfection is primary complication followed by acute rejection in 1st year; after 1 yr. malignancy (esp. lymphoma) & coronary artery vasculopathy are major causes of death

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