Heart Failure Flashcards
associated conditions with heart failure
- CAD + HTN = top offenders
- valve deformities
- cardiomyopathies
- renal disease
- diabetes, alcohol, drugs
- cancer tx
heart failure definition
- heart is unable to maintain adequate CO to meet O2 demand and EOP
- clinical syndrome: dyspnea and fatigue
- manifests as s&s of low CO and/or pulmonary congestion
chronic HF
- progressive
- adequate management
- usually have predictable symptoms, not rapidly changing
- minor tweaks done in outpt setting
- goal for care = slow disease progression, end organ damage, and symptom relief
acute HF
- sudden onset of symptoms
- significant imbalance between S+D
- can be secondary to another acute event or acute deterioration of chronic HF
- requires hospitalization
- goals for care = restoration of S+D balance
acute deterioration of chronic HF is called…
acute decompensated heart failure
acute decompensated HF
- between comp and decomp
- heart is not easily adaptable to minor changes
- any change in S+D can cause decomp
reasons for decompensated HF
- dysrhythmias
- ischemia
- fluid imbalance
- not adhering to sodium restriction
- not being compliant with meds
systolic HF
- HFrEF
- left-sided
- problems with pumping and ventricular emptying
- weak and dilated ventricle
diastolic HF
- HFpEF
- right-sided
- problems with filling
- ventricle is unable to relax, becomes stiff and noncompliant
systolic HF (HFrEF) more facts
- 2/3 HF
- reduced EF <40-45%
- contraction is weak
- Cardiomyocytes become elongated with little or no change in cell diameter.
- Ventricular end-diastolic volumes and pressures increase
- Increase in LV volume.
- Eccentric remodeling, LV diameter is increased but no increase in wall thickness.
- S3
- Poor prognosis, more common in men
systolic HF effects on CO
decreased contractility + increased compliance = increased preload
decreased contractility + increased preload = compensatory increased afterload
decreased contractility + increased preload + increased afterload = decreased CO
diastolic HF (HFpEF) more facts
- preserved EF >40%
- concentric remodeling and hypertrophy of the LV
- Increased wall thickness and/or LV mass.
- Increased ratio of myocardial mass to cavity volume
- Cardiomyocytes increase in diameter, not length.
- S4
- Common contributors: HTN, Hypertrophic CMO, Aortic Stenosis
- Common in women
diastolic HF functional alterations
- Slowed, delayed, and incomplete relaxation of the myocardium.
- Impaired rate and extent of LV filling.
- Increased dependence on LV filling from atrial contraction.
- Increased stiffness and non-distensibility of the LV.
- Reduced ability to augment relaxation during exercise.
- Increased diastolic LV, LA, and pulmonary pressures
LVEDV in relation to preload
left ventricle end diastolic volume = decreased preload
LVEDP
left ventricle end diastolic pressure = increased preload
diastolic effects on CO
contractility - unable to stretch
preload - ventricles are noncompliant, increase in preload can’t be accomodated
contractility (N) + preload (N) + inc afterload = dec CO
comp mechanisms
SNS + RAAS = ventricular remodeling
endothelin
produced by endothelin cells in endothelium of vessels
- potent vasoconstrictor
- effects: vasculature (vasoconstriction), myocardium (inotropic, hypertrophic, proarrythmic), renal (vasoconstriction and Na retention)
what is endothelin release stimulated by?
angiotensin 2 and ADH
why does long term compensation occur?
because neurohormones genetically modify cardiomyocytes
what is the most common cause of right-sided HF signs and symptoms?
issues on the left side
left-sided HF clinical manifestations
- pulm congestion leading to pulm edema
- dyspnea
- orthopnea
- increased WOB
- ABG changes - hypoxemia
- fatigue
- reduced exercise tolerance
- cyanosis (late sign)
right sided heart failure clinical manifestations
- peripheral edema
- liver enlargement
- increased JVD/CVP
what ABG change is noted in pulmonary edema?
respiratory alkalosis in early changes
what V/Q mismatch do you see in pulmonary edema and heart failure?
unable to pump blood forward = decreased CO = dead-space like = decreased gas exchange
fluid in alveoli = shunt-like = decreased compliance and ventilation
what hemodynamic changes do you see in pulm edema?
decreased O2 + increased CO2 and increased WOB + increased HR
pulm edema patho
- unable to pump blood forward
- blood backs up into pulm system
- increased hydrostatic pressure in pulm capillaries
- fluid shifts into alveoli
what dysrhythmias are common in heart failure?
- afib is most common due to high preload/stretch/ interrupt conduction pathways
- vtach and vfib most common cause of death in HF pts
- EF <30% and previous hx of ventricular dysrhythmia are powerful predictors of sudden cardiac death
what is the most important lab value to look at in HF?
BNP
BNP Assays
- secreted by left ventricle in response to over
stretching caused by excessive preload - confirms HF in pts presenting with dyspnea when clinical diagnosis remains uncertain
- BNP levels > 80pg/ml confirms HF
- BNP increases with severity
cardiac enzymes
- trops often elevated in acute HF
- correlates with severity of HF and poorer prognosis
- possibly r/t: ventricular remodeling, CAD, microcirculation abnormalities, reduced coronary reserve, ventricular strain
does an elevated trop in HF mean an MI?
no but it does indicate severity in HF
what do you want to rule out in HF and how do you do this?
ischemia; 12 lead ECG
what is the gold standard imaging for HF?
transthoracic echo (TTE)
- looks at EF, LV diameter, LV mass, and valve structure
EF
- % of blood ejected from LV with each contraction
- normal 60-80%
- <40% = moderate LV dysfunction and systolic HF
- <25% = severe LV dysfunction
LV diameter
- tells us how dilated the L ventricle is, how
enlarged the heart is - Large chamber size increases risk of emboli (d/t pooling), dysrhythmia and mitral regurgitation
LV mass
- measures how much LV hypertrophy and modeling is present
- Hypertrophy is one of the compensatory mechanisms in HF
- One goal of HF therapy is to reduce LV mass towards normal size
valve structure
- Valvular stenosis or regurgitation noted
- Valve disease as cause of HF
- Mitral Regurg occurring in association with HF
valvular disease
- disease of one or more valves of the heart
- problems with mitral and aortic valves are more prevalent
- primary result from aging
- stenosis and regurgitation are the primary abnormalities
stenosis
- narrowing of the valvular opening
- prevents adequate outflow of blood
- results from thickening (calcification) of the leaflets and limits ejection of blood
regurgitation
- Inability of the leaflets to appropriately close at the end of systole
- Blood backflows backwards as leaflets don’t join properly
- Mitral regurgitation is frequently associated with HF
classification of chronic heart failure
NYHA and american heart association/american college of cardiology
new york heart association scale
class 1: no limitation of physical activity
class 2: slight limitation of physical activity, comfortable at rest but ordinary activity causes symptoms
class 3: marked limit of physical activity, comfortable at rest but less than ordinary activity causes symptoms
class 4: severe limitation and discomfort with physical activity
goals of care with HF
- Symptom relief and improve quality of life
- Prevention of End organ damage
- Prevention of disease progression
short term management: meds
- must stabilize acute HF first
- dobutamine, milirone, nitro, lasix
long term management: drug therapy
- used in NYHA class 2 or 3 (symptomatic)
- used in pts who have had an MI
- used in pts with EF <40%
- ACEI + BB TOGETHER SLOW VENTRICULAR REMODELLING AND
PROGRESSION OF HF - If needed- Digoxin, long acting nitrates or hydralazine
- Mineralocorticoid Receptor Antagonist (MRA) -Spironolactone for EF <35%
HF drug therapy
- beta blockers (lols)
- ACE-i (prils)
- ARBs (sartans)
- aldosterone antagonist (spironolactone)
- vasodilator (Isosorbide dinitrate, Hydralazine)
mechanical management for short term acute HF
- post MI- significant HF and myocarditis common
- bipap/mech vent
- IABP/impella/ECMO
implantable cardioverter defibrillators (ICD)
- Sudden cardiac deaths common in pts with chronic HF due to ventricular
arrhythmias - ICDs can pace, overdrive pace, cardiovert and defibrillate
- Indications: EF<30%/ Narrow QRS and/or history of sudden cardiac arrest
- Cons: PTSD
cardiac resynchronization therapy (CRT)
- HF patients often have interventricular conduction delays (BBB)-results in
asynchronous contraction of ventricles - Indication: QRS >0.12 sec for CRT
- Improves LV function and HF symptoms when both ventricles are paced in
synchrony - Has 3 leads: one lead in RV and one in RA but has third lead in LV (lead threaded through the coronary sinus
and paces lateral wall of LV)
LVAD (left ventricular assist device)
- provide cardiac output or “flow” assistance to
HF pts - indications: low EF
- cons: OHS
care of LVAD patient
- generally don’t have a palpable pulse
- use MAP to treat
- assess pt by signs of EOP
cardiac surgery options
- CABG (recruit dormant tissue through reperfusion)
- remodel the heart (remove dysfunctional myocardium)
- stem cells
- valve repair/replacement surgery
- transcatheter valve procedure
- heart transplant
heart transplant complications
- short term: heart is new but rest of the pt is not. chronic issues can damage
the new heart (Sarcoidosis, Amyloidosis, Pulmonary HTN) - Chronic kidney failure exacerbated from surgery cross-clamp time
- Rejection
- Immunosuppressant Therapy
○ Increase cancer risk
○ Infections
○ Kidney injury
○ Gastric issues
long term management
- involves lifestyle changes and life long management to slow disease progression
- underlying cause is irreversible
self-management stratgies
- monitor daily weight
- restrict Na (<2-3g/day)
- fluid restriction
- exercise regularly
*key is to actively listen to pts to understand their capacity to self manage their HF
when to call for help
- > 5 lbs weight gain in a week
- Chest Pain
- Increasing Fatigue
- Increasing SOB
- Increasing orthopnea
- Waking up in the night with SOB
- Increasing edema (tight shoes)
