Heart failure Flashcards
Frank starling
More blood (EDV) = more stretching (more preload) = greater contraction (more SV)
Describes the relationship between preload & cardiac performance
Normal systolic contractile performance (SV or CO) is proportional to preload within the normal physiologic range
Contractility is reasonably reflected by EF (percentage of end diastolic volume ejected with each contraction (SV)
Cardiac reserve is the
ability of the heart to increase its performance above resting levels in response to stress or need for increase oxygen consumption
cardiac reserve does what? (think sympathetic) and helps with what in HF?
Increase in HR
Increase in systolic /diastolic volumes
Increase in tissue extraction of oxygen
This compensatory mechanism helps with decreased blood flow in HF
Heart failure - is it the ventricles or the atria?
A clinical syndrome resulting from structural or functional cardiac disorders that impair the ability of the ventricles to fill or eject blood It is a syndrome of ventricular dysfunction.
Left ventricle fails and causes what symptoms? (just 2) (Levi - the one you forget)
shortness of breath and fatigue
Right ventricle fails and causes
peripheral and abdominal fluid accumulations
HF is a clinical syndrome characterized by signs and symptoms of (HF is fluid)
fluid overload or inadequate tissue perfusion.
HF is a complication that results from problems such as (brad, tjan, and val cause HF)
cardiomyopathy, valvular heart disease, endocarditis
HF - gender (HF does not discriminate)
equal between men and women
HF more common at what age? (same as always)
among 65 +, overweight, and african american
death from HF is dropping, but
readmissions are high
The term heart failure indicates myocardial disease, in which there is a problem with the
contraction of the heart (systolic failure) or filling of the heart (diastolic failure)
HF - permanent or reversible?
Some cases are reversible depending on the cause
HF develops fast or slow?
Develops slowly and gradually, as the heart loses the ability to work and pump blood efficiently, d/t a change in normal mechanisms of circulation and cardiac output
Most HF is a chronic,
progressive condition managed with lifestyle changes and medications
In the past, HF was often referred to as
congestive heart failure (CHF), because many patients experience pulmonary or peripheral congestion with edema.
HF - Heart does not provide tissues with adequate
blood for metabolic needs
HF - elevation of pulmonary or systemic venous pressures may result in (pressure on the freeway turns into congestion)
organ congestion
HF Causes abnormalities in systolic or diastolic?
one or the other or both
Structural defects can also cause HF - ex - and what about thyroid?
Congenital defects, valvular disorders, rhythm abnormalities, high metabolic demands (thyrotoxicosis)
HF - collagen
thickens
types of HF
Heart failure with reduced ejection fraction (HFrEF) or systolic HF
Heart failure with preserved ejection fraction (HFpEF) or diastolic HF
Left ventricular failure
Right ventricular failure
what determines HF? (HF is just CO and EF)
Cardiac output
Ejection fraction
HF factors
Factors
HR, SV, preload, afterload, contractility
HF Key
Recognize and assist compensation (BNP and RAAS system)
HF goal
Restore C.O. and gas exchange
HF is determined by just one thing - what is it?
ejection fraction, the percentage
HFrEF (HF with reduced ejection fraction) - caused by what? (the lefties reducies)
Caused by global LV systolic dysfunction
LV contracts poorly, empties inadequately
HFpEF (HF with preserved ejection fraction) (preserve is not preserving the filling)
LV filling is impaired (not necessarily the contraction part)
HFpEF - causes (wizard door)
Age related changes, diabetes, obesity, CKD and/ or causes of systemic inflammation
HFpEF goals - (preserve my BP and DM)
BP control
DM management
LV failure (what about lymph nodes)
Due to LV dysfunction
CO decreases and pulmonary venous pressure increases
When pulmonary capillary pressure exceeds oncotic pressure of plasma proteins, fluid leaks from capillaries to interstitial space and alveoli
Pulmonary compliance is decreased, and work of breathing is increased
Lymphatic drainage increases to compensate but cannot meet demands
Pulmonary edema occurs
Pulmonary effusions develop leading to more dyspnea
MV increases (PaCo2 decreases, pH increases leading to respiratory alkalosis)
Interstitial edema worsens and interferes with ventilation and leads to increase CO2 and respiratory failure
RV failure - what about aldosterone? And anemia? (Alden has anemia in the RV)
Systemic venous pressure increases
Fluid leaks and causes edema (dependent)
Feet, ankles, abdominal viscera
Organs most affected are the liver, stomach, intestines, peritoneal cavity (ascites)
Causes hepatic dysfunction (increase bilirubin, PT, alkaline phosphatase, GGT) and the damaged liver breaks down less aldosterone which then leads to more fluid accumulation
Anorexia, malabsorption, hypoalbunemia, diarrhea, anemia (chronic GI blood loss), ischemic bowel
HF - hemodynamics - Effects of decreased CO (and what about potassium?)
lower BP, decreased oxygen delivery, parasympathetic tone (arterial baroreceptors), renal perfusion, coronary perfusion, potassium excretion
HF - renal system (what happens to sodium and water?) think edema
Renal venous congestion, decreased renal blood flow, filtration and reabsorption and GFR leading to sodium and water retention (RAAS, ADH)
HF - neurohormonal - TNF?
Maintain a normal balance between vasoconstriction, stimulating and dilation, relating of the myocardium
Norepinephrine, RAAS, aldosterone, vasopressin, BNP
TNF (tumor necrosis factor is produced from a failing heart
HF diagonsis - using what? (cath can find HF)
Pulmonary Artery Catheter (Swan-Ganz)
HF diagnosis using an arterial line - which one? (Art can diagnose HF with a radio)
Radial artery, continuous BP measurement
Allen’s test & the 5 P’s for pulses (pain, pallor, pulse, paresthesia, paralysis)
HF - BNP: B-type natriuretic peptide (Bumpin 100 to a 1000)
BNP: B-type natriuretic peptide (ventricular stretch)
> 100pg/mL = heart failure
> 1000 your patient is REALLY sick
HF diagnosis - CXR - xray - (xray my large, fat heart)
Enlarged heart, pulmonary edema
HF diagnosis - ECG measures what? (E for ECG, E for EF)
Echocardiogram
EF, pumping action
HF - New York Heart Association Functional Classification (just 1-4)
1-4 (4 being the worst)
manifestations of right sided failure
Viscera and peripheral congestion
Jugular venous distention (JVD)
Dependent edema
Ascites
Weight gain
Enlarged organs
Hepatomegaly
manifestations of left sided failure - and cough?
Pulmonary congestion, crackles
Dyspnea on exertion (DOE), dyspnea
Low O2 sat
Dry, nonproductive cough initially
Blood-tinged frothy sputum
signs of HF in general (OVERLOAD)
O orthopnea
V ventricular failure
E enlarged heart
R reported weight gain
L lungs congested
O output decreased
A apprehension
D dependent edema
HF gerontologic - signs (really the same ones)
May present with atypical signs and symptoms such as fatigue, weakness, and somnolence
HF and aging - these are all normal parts of aging, but they lower the threshold - left ventricle diastole? (left ventricle got collagen in its old age)
Lowers the threshold for HF
Decline in left ventricular diastolic function due to increase of myocardial collagen, myocardial stiffening and prolonged myocardial relaxation
HF management
Drug therapy
Nutritional therapy
Fluid restriction
Weight monitoring
Research therapies
Transplantation
LVAD (left ventricular heart device) **THESE ppl will not have a BP, just a mean arterial
drugs that decrease afterload (the As decrease A-afterload)
ACE, (end in captopril) ARBs
decrease afterload and preload (Arby’s before and after)
ARB (valsartan)
vasodilators decrease preload or afterload? (dilate when it’s too late)
decrease afterload (hydro and nitro)
diruetics decrease
preload
digotoxin does what? (digs for a deeper contraction)
increases contractility
HF nursing management
provide symptom relieve and education, improve ventilation (RR, O2, position, monitor lungs), energy management (prevent fatigue, monitor activity, encourage activity), hemodynamic regulation (HR, preload, afterload, contractility, electrolytes, fluids, meds, I&O, weights)
ACE inhibitors - monitor for (hyper kalema plays with aces)
ACE inhibitors block aldosterone, which increases sodium. hypotension, hyperkalemia, and altered renal function; cough
beta blockers - how long to start working?
prescribed in addition to ACE inhibitors; may be several weeks before effects seen; use with caution in patients with asthma
dig - monitor for
monitor for digitalis toxicity especially if patient is hypokalemic
IV medications - which one for LV failure?
indicated for hospitalized patients admitted for acute decompensated HF
Milrinone: decreases preload and afterload; causes hypotension and increased risk of dysrhythmias
Dobutamine: used for patients with left ventricular dysfunction; increases cardiac contractility and renal perfusion
Ivabradine (Corlanor) – (Ivan blocks and slows down my heart)
Ivabradine (Corlanor) – blocks SA node channel and decreases HR.
Goal is HR <70 since there is a 30% > risk of death with a HR >70
Take with food
Increases risk for atrial fibrillation
Sacubitril/ Valsartan (Entresto) - neprilysin
Sacubitril/ Valsartan (Entresto) - neprilysin inhibitor sacubitril and the angiotensin receptor blocker valsartan
Used for HF and HFrEF
Relaxes blood vessels, improves blood flow (kidneys), decreases stress on the heart
Monitor for hypotension, hyperkalemia, and changes in renal function
Twice daily dosing
ABCDE
ACE, ARBS, Aldactone, ARNI
Beta blockers
Cessation of cigarettes, Corlanor (ivabradine)
Digoxin, diuretics, diet
Education, exercise, Entresto
chronic HF -more common with what age? (close)
The incidence of HF increases with age
Most common in people older than 75 years
Most common reason for hospitalization of people older than 65 years and is the second most common reason for visits to a physician’s office
Approximately 25% of patients discharged after treatment for HF are readmitted to the hospital within 30 days
The cost to the healthcare system in the US is about 32 billion a year
Affects about 6.5 million people in the US with > 950.000 new cases each year.
About 26 million people are affected worldwide.
COPD
advanced HF monitoring (tele savalis is advanced)
Self monitoring of symptoms
Labs (can do this at home)
Telemonitoring
Arrhythmia monitoring
advanced therapy - when all else fails
When all else fails – maximum symptos at rest despite optimal therapy:
Mechanical circulatory support - bridge to transplant or destination therapy
ECMO (blood oxygenated outside of body and then put back in)
LVAD – decreases LV filling pressure; LV size; PA pressure; wall size and stress and HF symptoms; increases LV output
heart transplant
Transplant –survival is about 88% 1 year; 75% at 5 years & 62% at 10 years
3500 listed
320 die waiting
49% wait more than a year
3100/day on the waitlist
LVAD patient education - alerts (Vladamir is less than 65, so can’t have CPR)
DONT DO CPR. if SV < 65mL/beat
CO (flow rate < 3.5L/min) if it’s low, it’s usually a battery problem
cardiomyopathy
Abnormal heart muscle that is enlarged, thickened, or stiffened
Impairs ventricular function and leads to decreased CO
types of cardiomyopathy
dilated, hypertrophic, and restrictive
dilated cardiomyopathy
Thick/enlarged ventricular walls
Dilation of chambers
Impairs systolic function (pumping)
hypertrophic cardiomyopathy (no more filling for hypertrophy, already too much)
Ventricles enlarge and ventricular cavities reduce in size therefore filling (diastolic function) is decreased
DIALATED is only one that is systolic
restrictive cardiomyopathy (restriction may di)
Ventricles become rigid and fibrotic and filling(diastolic function) is reduced
cardiomyopathy - causes
Idiopathic, HTN, viral infections, post MI
cardiomyopathy symptoms
Manifestations of decreased CO
Left sided HF symptoms – activity intolerance, weakness, narrow pulse pressure, decreased peripheral pulse strength, pre/syncope, angina, dyspnea, orthopnea, pulmonary congestion, dysrhythmias (PVCs, VT), murmurs, S3 & S4
Right sided HF symptoms – JVD, peripheral edema, atrial dysrhythmias (AF, PACs), orthopnea, PND, nocturia, hepatomegaly, splenomegaly, abdominal distension, anorexia, nausea
Bradycardia in restrictive due to heart blocks, conduction dysfunction
cardiomyopathy treatment
No cure, treat underlying cause
Treatment palliative (symptom management) or surgical (heart transplant, muscle resection, valve replacement)
Manage heart failure
Maximize CO, maintain gas exchange, modify activity to tolerance
Medications
ACE inhibitors, afterload reducers, inotropes, calcium channel blockers, beta blockers, diuretics
Biventricular pacemaker
ICD
transplant - indications
End stage HF refractory for medical care; inoperable/decompensated valvular disease; recurrent life-threatening arrhythmias not responsive to maximal interventions
all immunosuppressants increase the risk of..and will accelerate what?
cancer, esp lymphoma, and will accelerate CAD
pulmonary edema - Is it venous or artery pressure? And fluid moves from where to where?
Acute LV failure with pulmonary venous HTN and alveolar flooding
When LV pressure increases suddenly, plasma moves from pulmonary capillaries into interstitial spaces and alveoli.
causes of pulmonary edema - Cardiogenic
Cardiogenic
CAD-leading to coronary ischemia
Cardiomyopathy
Arrhythmia
Valvular disease
HTN-leads to HF with preserved EF
causes of pulmonary edema - Noncardiogenic (without cardiac disease) (think non-heart lung issues) (infections, smoke, altitude)
Lung infections
ARDS
HAPE (high altitude)
Toxic exposures
Smoke
Renal disease
hypoxia =
restlessness, anxiety, agitation, etc.
pulmonary edema - symptoms (wheezy has a fat lung)
Common findings are severe dyspnea, wheezing (cardiac asthma) , sometimes a cough with pink or blood- tinged frothy sputum
JVD will be which sided-failure?
right
pulmonary edema diagnosis (fat lung is bumpin and needs an xray)
Assessment findings of severe dyspnea and pulmonary crackles
CXR –assessment of interstitial edema
BNP (brain naturetic peptide) or NT-pro-BNP (N-terminal-pro-BNP)
pulmonary edema treatment (fat lung like angina, it’s da bute)
Oxygen
IV diuretic
Nitrates (SL then IV 10-20 mcgs/min titrate up to max of 300 mcgs/min if SBP >100 mmHg) in the critical care unit
IV inotropes (dobutamine) in the critical care unit
Morphine
Ventilatory assistance in the critical care unit
Position upright with legs down
Monitor daily weight
Medications
pulmonary edema treatment - AMI or other ACS (acute cardiac syndrome) (fat lung needs a stent)
Specific additional treatment depends on etiology
AMI or other ACS (acute cardiac syndrome)-thrombolysis or PCA with/out stent
pulmonary edema MOSTDAMP
M medications
O oxygen
S sit up
T tourniquet to decrease preload
D diuretics
A assess anxiety
M monitor
P positive pressure
which sided failure is more common?
left
The nurse is obtaining data on an older adult client. What finding may indicate to the nurse the early symptom of heart failure? (HF can’t exercise early in the morning)
Dyspnea on exertion
late signs of HF (have fun late with hypo and tachy)
hypotension and tachycardia
HF left side (the neas)
dyspnea, orthopnea, crackles, pink frothy
HF right side (right side rocks the body with fluid)
JVD, edema, ascities, hepatomeglia, spleenomeglia
main cause of HF
HTN
sleep apnea - right or left sided failure?
right
HF causes changes in collagen how?
Cardiac myocyte function
Collagen turnover
HF - what causes left-sided failure? (usually ventricle, that’s all)
Left most commonly d/t LV dysfunction
HF - right side
Right ventricle is thinner and more compliant and accepts blood @ low pressures and ejects against lower vascular resistance.
HFrEF - does diastolic increase or decrease? (reduce is opposite)
increased diastolic volume and pressure (preload) and decreased EF
HfPef - LV end-diastolic pressure is increased when? (di is always under pressure, preserve it)
rest and during exertion
HfpEF - contractility (contracts and EFs are preserved and normal)
Contractility and EF remain normal & end-diastolic volume is normal (in most patients)
HfpEF - Diastolic dysfunction results from (preserve the dying bc they’re stiff and can’t relax)
impaired ventricular relaxation, increased ventricular stiffness
HF results from (MI hypertension, diabetes, and smoking is causing HF)
acute MI, and hypertension, diabetes, salt, smoking
HfPEF - causes (preserving the endothelium is secondary)
endothelial dysfunction, cardiac microvascular dysfunction or secondary myocardial injury
HfPEF - goals (preserve spiro for sleep apnea)
Aldosterone blockage treatment (controversial-use of spironolactone and eplerenone results in reduced vascular stiffness and diuresis, causing a decrease in BP)
OSA (sleep apnea) treatment
HfPEF goals - meds? (preserve the diuretics and statins)
CAD treatment
AF treatment (rate & rhythm)
Diuretics
statins
anorexia, diahrrea, anemia -right or left side? (anorexia is not right)
right
HF - hemodynamics
Effects of increased sympathetic tone (arterial baroreceptors), HR, sodium and water retention, preload, afterload, cardiac workload, congestion
Pulmonary Artery Catheter (Swan-Ganz) does what? (cath measures the pressure)
Measures pressures inside the heart
Helps determine the cause of decreased CO
what heart sound with left-sided failure? (gallop to the left 3 times)
S3 or “ventricular gallop”
left side - pee, or no? (olga on the left)
Oliguria
left side - slow or fast HR?
Restlessness
Tachycardia
left side - big one - what about lying down and breathing? and nighttime breathing?
Orthopnea
Nocturnal dyspnea
HF - older adults and renal function - what to watch out for
Decreased renal function can make older patients resistant to diuretics and more sensitive to changes in volume
HF - older adults - kidney stuff
Administration of diuretics to older men requires nursing surveillance for bladder distention caused by urethral obstruction from an enlarged prostate gland; monitor older persons for incontinence, retention, UTI, presyncope/syncope, dehydration, electrolytes
be aware of BPH in men - this could cause kidney failure
HF - older adults - normal changes (the left side goes down with age)
Modest decline in LV systolic function
Decline in ability to respond to increased work demands (beta adrenergic stimulation)
Response to exercise and stressors decreases
HF older adults
Hypoxia, infections (PNA), fluid overload, renal failure, non-adherence to drugs regimens or diets (low sodium)
LVAD (left ventricular heart device) **THESE ppl will not have a (vlad has no blood pressure)
BP, just a mean arterial
restrictive cardiomyopathy - causes (amy and radiation restrict brad)
d/t amyloidosis, XRT (radiation)
cardiomyopathy - causes
, thyroid disease, diabetes, peripartum, alcoholism, anabolic steroid use, chemotherapy, XRT, connective tissue disorders
pulmonary edema - most cases result from what? (I FFAV my fat lung)
½ of all cases worldwide result from acute coronary ischemia followed by heart failure, arrhythmia, acute valvular disorder and acute volume overload due to IV fluids.
Drug or dietary non-adherence is often involved.
pulmonary edema - how do pts act?
Patients usually present with restlessness and anxiety with a sense of suffocation
pulmonary edema - pt appearance?
Patients appear pale, cyanotic and have marked diaphoresis; some froth at the mouth
pulmonary edema - how is the pulse? and lung sounds?
Pulse is rapid and weak, BP is variable
Upon auscultation there are fine pulmonary crackles in both lung fields either widely dispersed or dependent.
pulmonary edema - heart sounds (galloping into edema)
Heart sounds include a summation gallop (merge of S3 & S4)
Signs of right ventricular failure may be present (JVD, peripheral edema)
pulmonary edema - does COPD seem like it?
COPD exacerbation can mimic pulmonary edema. The BNP will be normal in COPD patients without pulmonary edema)
tests to identify pulmonary edema (fat eats the bun, it’s the abcs)
ECG, cardiac markers and other tests to identify etiology (cardiac echo)
ABGs, BUN/Cr, electrolytes, pulse oximetery
HfRef Causes defects in (reduced energy zaps my electricity and contractility)
Causes defects in energy utilization, supply, electrophysiolgic function and contractility (intracellular calcium & cAMP production)
common causes of LVF (mei and brad flew left through the vents and failed)
LV failure often leads to RV failure
Common causes are AMI, myocarditis, dilated cardiomyopathy
1st treatment for pt with confirmed MI (angie comes first with MI)
PCI (percutaneous coronary intervention) angioplasty
HF older adults - causes (old man corner)
hyperthyroidism, anemia, HTN, myocardial ischemia
pulmonary edema - ½ of all cases worldwide result from - but what type?
acute coronary ischemia
HF older adults - causes
LVAD (left ventricular heart device) use of NSAIDs
is HF a problem with the ventricles or atria?
VENTRICLES
pulmonary edema treatment - diet?
Low sodium diet, fluid restrictions
Prevent when possible, by checking lung sounds, daily weight, avoid FVE
pulmonary edema - treatment - Severe HTN
Severe HTN- IV vasodilator
pulmonary edema treatment - SVT, VT
SVT, VT –cardioversion
pulmonary edema treatment - AF with rapid ventricular response
Cardioversion or IB beta blocker, digoxin or calcium channel blocker (CAUTION)
pulmonary edema treatment - patients with decompensated HF or shock (da bute decomensates)
IV dobutamine or IABP for SBP <100 mmHg
HfpEF diastolic dysfunction (preserve the dying w/ valves, peri and amy)
Valvular disease (aortic stenosis, MVP/MVR), constrictive pericarditis or amiloid infiltration of the myocardium
HfpEF diastolic dysfunction (preserve the dying for ischemia and hypertrophy)
Acute myocardial ischemia
Hypertrophic cardiomyopathy
HFrEF - causes (MI, Mei, and Brad cause the ref to lose)
AMI, myocarditis, dilated cardiomyopathy
HFpEF happens when (the preserved are stiff)
ventricles can’t relax due to stiffness from anything that causes stiffness
which cardiomyopathy for HFrEF?
dilated
which cardiomyopathy for HFpEF? (the stiff one)
hypertrophic
which HF is apnea?
preserved - the stiff one
decompensated HF meds
mili and da bute
brad’s left side symptoms
decreased pulse
too old for transplant?
70, or 65 physical age
normal digoxin levels (dig, give me high 5 at 2)
0.5 to 1.9 nanograms per milliliter of blood
pumonary edema - what sounds?
fine crackles in BOTH lungs
