Heart Failure Flashcards
What kind of conditions cause HF
conditions that directly damage the heart
What disorders directly damage the heart
HTN, CAD (MI), inflammatory heart conditions, congenital defects, cardiomyopathy, postpartum, substance abuse, hypertrophic
What kind of conditions are secondary causes for HF
any condition that increase the workload of the heart
what conditions increase the workload of the heart
sepsis, thyrotoxins, dysrhythmias (a fib or Vtach), obstructive sleep apnea, pulmonary embolism, hypervolemia
how does cardiac cachexia progress
early saiety which causes NV which causes anorexia which causes cardiac cachexia
what are some diagnostic tests you could do to get more info on HF
Echocardiogram, 12 lead ECG, chest xray, 6 min walk test, cardiopulmonary stress test, heart cath, endomyocardial biopsy
what does echocardiogram test show you
gives info on ejection fraction, shows heart chambers to differentiate between systolic and diastolic HF
what are some ss you would expect to find in someone with HF
fatigue, dyspnea, orthopnea, tachycardia, noctura, early satiety,
what does FACES stand for when describing HF ss
fatigue, activity limitation, chest congestion/cough, edema, shortness of breath
what are some objective data you will collect when evaluating someone for HF
of pillows used, paroxysmal noctural dyspnea, insomnia, chest pain, RUQ pain, abdominal discomfort (from congested liver), behavioral changes, vision changes
what are some subjective data you will collect when evaluating someone for HF
skin color, temp changes, edema, RR, lung sounds, frothy blood tinged sputum, HR, abdominal distention, LOC changes, I/O
do you want a positive or negative I/O
negative so you know fluid is coming off
what happens to BNP and NT-ProBNP levels with worsening HF
increase
what are some ss of pleural effusion
dyspnea, cough, chest pain
what kind of dysrhythmias could be caused by HF
Afib Vtach
how could HF cause LV thrombus
from decrease ejection fraction — risk for stroke
how could HF cause hepatomegaly
RV failure = congested liver = decrease liver function= liver cells die = fibrosis and cirrhosis
how could HF cause Renal failure
decrease perfusion can lead to insufficiency or failure
what are the goals for treating HF
treat the underlying cause, maxamize CO, decrease symptoms, improve ventricular function, preserve target organs
how does ultrafiltration work
advanced treatment that works as a form of dialysis for fluid volume overload and resistance to diuretics
if you couldn’t use ultrafiltration what is another advanced treatment option
circulatory assistance devices
how do cardiomems work
device to help monitor pulmonary pressure remotely (aka at home) via implanting the device in the distal pulmonary artery then at home the patient can lay on a special pillow that will send the info straight to the doctor
how does left ventricular device work
assist the failing LV by continuous flow - the heart is pumped via a driveline that exits the abdominal wall and is attached to a system controller with patient specific settings
what must a patient still get for a left ventricular device
electrical conduction like ICD/PM
what are the patient risks for a left ventricular device
infection, stroke, bleeding (warfarin),
what is the intervention of choice for HF
Bi-pap + diuretic + nitro
how does cardiac resynchronizing work
an extra lead is placed in the LV and RV to aide in contractions to increase LV function and CO
why would someone need cardiac resynchronizing
because of remodeling causing dysrhythmias in LV and RV which can cause wide bundle branch block
how does a extracorporeal membrane oxygenation (ECMO) work
providing prolonged cardiac and respiratory support to a person whose heart and lungs are unstable to give adequate amount gas exchange or perfusion to sustain life
what are the risks for the patient receiving ECMO treatment
bleeding, stroke, infection, pressure, ulcer
how long can a patient be on ECMO
only temporary support
what kind of nutrition teaching would you give for someone with HF
smaller meals, low sodium (2g daily), fluid restriction (1.5-2L a day),
What should someone consider when evaluating weight of a person with HF
daily weight (gain of 3lbs over 2 days or 3-5 over a week should be reported to doc)
whos treatment of choice is heart transplant
refractory end stage HF, inoperable CAD, cardiomyopathy,
what are some immunosuppresants someone with a heart transplant would take
predisone, cyclosporine/tacrolimus, myophenolate mofetil
how often is a endomyocradial biopsy taken after transplant
from RV weekly for first month, then monthly for next 6 months then yearly
why is endomyocradial biopsy taken after transplant
to detect rejection
what kind of evaluation is done from someone trying to get a new heart
physical, diagnostic, and psychological
when could acute rejection of a heart transplant happen
within a year
why is malignancy a complication of heart transplant
because of the immunosuppresants
how can you determine cardiogenic shock via BP
systolic BP less then 90 for 30 min or more with tachycardia
what are the ss of cardiogenic shock
poor tissue perfusion (oliguria, cyanosis, cool extremities, altered mental status)
what would lactate levels look like in cardiogenic shock
Increased levels - tell tissue death
what would pulmonary capillary wedge pressure levels look like in cardiogenic shock
greater then 15
what would cardiac index levels look like in cardiogenic shock
less then 2.2 = wet and cold
what kind of drugs would be used in patients with inadequate tissue perfusion and adequate intravascular volume
inotropic and or vasopressors to maintain MAP at 60-65, to decrease plasma volume and peripheral edema
what is the focuses of treatment for cardiogenic shock
fluid resuscitation (brings BP and volume up), restoration of coronary blood flow, correction of electrolytes and acid base balance (low K and Magnesium and acidosis), place central line (to monitor central venous pressure), arterial line (continuous BP monitoring)
who would you not want to give fluid resuscitation to
someone with pulmonary edema
how does renin-angiotensin- aldosterone compensate for heart overload
the decrease on CO cause a decrease blood flow to the kidneys (decrease volume) so the RAAS system holds fluid and salt which causes vasoconstriction which will increase BP
how does ventricular remodeling compensate for heart overload
hypertrophy and dilation of ventricles
what can ventricular remodeling negatively cause
Dysrhythmias and sudden cardiac death
what beta blockers are used to help in heart overload
metoprolol and carvedlol
what 2 meds are more effective in treating heart overload in African Americans
hydralazine and isosorbine
what diuretics are used for heart overload
lasix, bumex,
when taking lasix and bumex what should you monitor for
hyperkalemia
what are the outcomes you want for taking bumex and lasix for heart overload
decrease edema, water/sodium secretion
what are the ss of digoxin toxicity
N/V/D, lethargic, visual halo, decrease HR
how does the SNS compensate for heart overload
releases catecholamine (norepinephrine and epinephrine) to increase HR and increase myocardial contractility, and peripheral constriction to increase BP
what meds inhibit RAAS system
ACE, ARBs, aldosterone antagonist or entrestochew (in place of ACE or ARB)
what should you monitor in someone taking an ACE
hypotension, cough, hyperkalemia, angioedema, and renal insufficiency
what does ACEs end in
pril
what should you monitor for in someone taking an ARB
hypotension, hyperkalemia, and renal insufficiency
what do ARBs end in
sartan
who shouldn’t take entrestochew
if history of angioedema
what should you monitor for when someone is taking aldosterone antagonist
hyperkalemia
what are some positive inotropic agents
digoxin or malirione
when should you not give digoxin
narrow therapeutic window so hold if HR less then 60 and never redose
when is malirione used
as a last resort because it requires continuous infusion via PICC
what happens to ejection fraction for systolic heart failure
reduced ejection fraction less then 40% can be as low as 5-10%
what is normal ejection fraction of the heart
55-60%
what could be some causes of systolic heart failure
impaired contractile fraction (MI), increased afterload (HTN), cardiomyopathy, mechanical abnormalities (valve issues)
what happens to the heart for diastolic heart failure
ejection fraction is good but the ventricles arent filling up enough
how could you diagnosis diastolic HF
looks like the muscle is too thick
what type of med could you give to improve diastolic HF
decrease HR to allow the ventricles to fill more
what could cause diastolic hf
LV hypertrophy from HTN, older age, DM, Obesity
what is the most common cause of left sided heart failure
HTN and CAD = LV dysfunction
what are some ss of left sided HF
paroxysmal noctural dyspnea, increased pulmonary wedge pressure, restlessness, increased HR, cyanosis, pulmonary congestion (cough, crackles, blood-tinged sputum)confusion, external dyspnea
what implantation is recommended in LV dysfunction
cardioverted defib because they are more at risk for sudden cardiac death
what happens in the heart for left sided HF
blood backs up into the LA and pulmonary veins which increase pulmonary pressure causes leaks = pulmonary congestion
what causes right sided HF
most common is left sided HF, other causes could be RV infarction, pulmonary embolism, pulmonary hypertension
what are the ss of right sided HF
fatigue, increase peripheral venous pressure, ascites, enlarged liver/spleen, distended jugular vein, weight gain, dependent edema
what happens in the heart in right sided HF
fluid backs up in venous system by fluid moving into tissue and organs
what does dry - warm mean for acute decompensated HF
dry lungs, good perfusion
what does dry- cold mean for acute decompensated HF
dry lungs, poor perfusion
what does wet - warm mean for acute decompensated HF
wet lungs, good perfusion
what does wet-cold mean for acute decompensated HF
wet lungs, poor perfusion
what is the early progression of acute decompensated HF
increased pulmonary venous pressure (increased HR, decreased PaO2)
when do you need to intervene for someone PaO2 levels
lower then 60 with bi-pap
what is the later progression of acute decompensated HF
Interstitial edema (tachypnea)
what is the final progression of acute decompensated HF
Alveolar edema (respiratory academia = decreased PaO2 and increased Co2) leads to cariogenic shock
what is normal PaO2
60-80
why are diuretics used in acute decompensated HF
to decrease volume overload (preload)
why are vasodilators used in acute decompensated HF
to decrease afterload and improve coronary artery circulation
when titrating nitroglycerin (vasodilator) what do you need to do
monitor every 5-10min for decreased BP
why is morphine used for acute decompensated HF
to decrease preload and afterload, relieve dyspnea/anxiety
why are positive inotropes used for acute decompensated HF
increase myocardial contractility
what meds should you stop if they have acute decompensated HF
beta blockers
what are some positive inotropes
milrione, digitails, and b-agonists (beta blockers)
what are some ss of acute decompensated HF
sudden onset of HF ss, most common is pulmonary edema from pulmonary and systemic congestion due to increase left and right sided filling pressure
what is normal Co2
35-45
what should you monitor for acute decompensated HF
Continuous VS,O2, UOP, hemodynamic monitoring (BP), pulmonary artery cath to evaluate CO and pulmonary artery wedge pressure
how is therapy titrated for acute decompensated HF
to maximize CO and pulmonary artery wedge pressure, so using supplemental O2, Bipap (mech vent if unstable), and high fowlers
what is normal pulmonary artery wedge pressure
8-12
what is the pulmonary artery wedge pressure in someone with acute decompensated HF
over 15 can be as high as 30
what are some ss of pulmonary edema
anxious, pale, cyanotic, cool, clammy skin, dyspnea, orthopnea, increased RR (over 30), cough with frothy sputum, crackles, wheezes, increased HR, decreased BP
