Heart Failure Flashcards
What is hemodynamics ?
the force or mechanisms involved in circulation
- arteries=higher pressure & veins=lower pressure
- arteries carry less volume
What are the primary causes of HF ?
- CAD
- HTN
- ACS
- cardiomyopathy
- congenital heart defects
What is ejection fraction ?
percentage of total blood volume in the Lt ventricle at the end of diastole that is pumped out of the Lt ventricle
What is heart failure with reduced ejection fraction (HFrEF) ?
impaired ventricular systolic function
- problem is with squeezing fluid out
What is heart failure with preserved ejection fraction (HFpEF) ?
impaired ventricular diastolic function
- problem is with filling of ventricles
What are S&S of Lt sided HF ?
RESPIRATORY
- dyspnea (RR=30-40)
- shallow respiration
- crackles & cyanosis
- pink frothy sputum
- paroxysmal nocturnal dyspnea (PND)
- tachycardia
- S3 & S4
- restlessness, confusion, weakness/fatigue)
What causes Rt sided HF ?
usually caused by Lt HF
- LV fails and fluids back up into the lungs
- increased pressure in lungs causes the RV to work harder to push blood into the lungs
- increases workload which weakens the RV and fluid backs up into venous
What are some S&S of Rt sided HF ?
everywhere else
- weight gain
- dependent edema
- murmurs
- JVD
- ascites
- hepatomegaly
- splenomegaly
- anxiety/depression, fatigue
What is remodeling ?
when the heart enlarges overtime to cope with the increased volume (from edema)
- the heart muscle will also enlarge
- causes large and irregularly shaped ventricular walls (can decrease filling volumes)
What is the compensatory mechanism for neuro-hormonal response ?
as CO decreases the blood flow to the kidney decreases
- activation of RAAS system in kidneys
- sodium and water retention
- causing edema
What is the SNS response when trying to compensate ?
increase HR and vasoconstriction (increase BP)
What is the steps to the compensatory mechanisms to HF ?
- Sympathetic NS activation
- neuro-hormonal response
- dilation (remodeling)
- hypertrophy
What is BNP ?
hormones released from the heart when increased blood volume and cardiac wall stretching
- normal is <100
What happens in stage A of HF ?
pt’s are at high risk for developing HF (HTN, CAD, DM, metabolic syndrome)
- no structural or functional disorders of the heart
- no S&S
- Meds: BP meds, atorvastatin, diabetes meds
What happens in stage B of HF ?
pt’s with structural disorder of the heart (Hx of MI, valve disease)
- no S&S of HF
- Meds: BP meds, atorvastatin, diabetes meds
What happens in stage C of HF ?
pt’s with current or prior symptoms of HF associated with underlying structural heart disease
- Meds: diuretics
What happens in stage D in HF ?
pt’s with advanced structural heart disease
- marked symptoms of HF at rest despite maximal therapy who require specialized interventions
- end stage disease who require mechanical circulatory support, continuous inotropic infusions, transplantation or hospice care
- interferes with ADLs
- Meds: positive inotropes
What happens in class 1 of functionality ?
no limits on physical activity
- ordinary activity doesn’t cause fatigue, palpations, or angina
What happens in class 2 of functional classifications ?
slight limits on physical activity
- no symptoms at rest
- ordinary physical activity causes fatigue, dyspnea, palpations or angina
What happens in class 3 of functional classifications ?
marked limitation of physical activity
- comfortable at rest but less than ordinary activity causes fatigue, palpations, or dyspnea, or angina
What happens in class 4 of functional classifications ?
inability to carry on any physical activity without discomfort
- symptoms of cardiac insufficiency or of angina may be present even at rest
- any physical activity is undertaken discomfort is increased
What is acute decompensated (exacerbation) heart failure
deteriorating heart function = lack of CO = imminent danger of life
- kidneys try to compensate by activating RAAS, leads to fluid retention
- worsening edema, dyspnea, fatigue
- BNP very high: >500
- usually requires hospital admission (volume overload & pulmonary edema causes acute respiratory impairment)
What are some S&S of fluid overload ?
- significant edema in dependent areas: extremities, scrotum (HIGH RISK FOR SKIN BREAKDOWN)
- JVD
- ascites
- hepatomegaly
What are some S&S of pulmonary edema ?
- dyspnea (RR>30)
- low SpO2 (<92)
- orthopnea
- cyanotic/pale
- crackles in bilateral lungs
- blood tinged frothy sputum
- anxious
- JVD
What are some nursing interventions for pulmonary edema ?
- O2 support: high-flow O2, non-rebreather, bi-pap, vent
- high fowlers position” oxygenate, reduce preload of the heart
What are some characteristics of Furosemide (Lasix) ?
main med given in overload and in pulmonary edema
- can be given in high doses IVP or IV continuous infusion
- watch K+ and Mg closely
- watch kidney function close to ensure not over-diuresing
What are some characteristics of Nesiritide ?
a vasodilator used to decrease the circulation blood volume
- nesiritide is given IV to reduce arterial and venous pressures
- closely monitor pressure when beginning this med
What are some characteristics of positive inotropes ?
will increase the cardiac contractility and short-term use for pt’s unresponsive to diuretics and vasodilators (not long term because it’s bad for the heart)
- dopamine, dobutamine, & norepi
- milrinone (phosphodiesterase inhibitors) also vasodilator
- digoxin: short-term because it can cause life-threatening dysthymias
What is a Intra-Aortic balloon pump (IABP) ?
for left ventricular heart failure with shock
- pump remains in the aorta until cardiac function maximized
- decreases SVR and PAP leading to increase CO
What is a left ventricular assist devices ?
implanted device that helps pump blood from the LV to the rest of the body (controller until outside of body)
- LVAD may be implanted than pt may go home
- must be highly compliant with care
- may be used as bridge to transplant
What are the goals for chronic HF ?
slow the progression & decrease exacerbations
What are the key teaching points for a pt with chronic HF ?
- Diet: low sodium (<2g everyday), use salt substitute’s sparingly, label reading, frequent small meals
- daily weights: accurate assessment for fluid retention, weigh at same time daily
- weight gain of 3lbs in 2 days or 3-5 lbs in a week should be reported
- activity: increase walking gradually, consider cardiac rehab, monitor BP and HR with activity, rest-balance and activity, plan days to avoid overexertion
- ongoing monitoring: pt need to report immediately difficulty breathing, waking up at night SOB (PND), increased swelling in feet, or increased abdominal girth. dizziness or fainting (many times this is from meds)
What is the treatment for digoxin toxicity ?
digiband
- S&S of toxicity: nausea, vomiting, auras
What lab values have to be monitored while on Digoxin ?
- digoxin levels have to be <2 mg/dL
- potassium levels must be >4
What are the meds used for acute HF ?
- furosemide
- nesiritide
- positive inotropes: dopamine, dobutamine, and norepi, milrinone, digoxin
- morphine
What are some RN interventions for acute HF ?
- cardiac/SpO2 monitoring
- strict I/Os
- daily weights
- labs: CMP daily (electrolytes, kidney function, liver function)
- edema/skin control: elevate dependent body areas, protect skin and leg wrap is severe
What meds are used for chronic HF ?
- diuretics: furosemide & spironolactone (works best with furosemide)
- vasodilators: nitros, isosorbide dinitrate & mononitrate
- positive inotropes: digoxin
How do beta blockers help with chronic HF ?
- slows HR
- better filling times
- prevents remodeling
(metoprolol)
How do alpha beta blockers help with chronic HF ?
also slows the HR and vasodilate
(carvedilol)
How do antihypertensives help with chronic HF ?
after-load reducers, makes it easier for the heart to eject the blood
- ACE inhibitors
- ARBs
