Flashcards in Heart Failure Deck (48):
Define heart failure.
What are the 3 "cardinal manifestations"?
Structural or functional cardiac defect that impairs the hearts ability to fill with or eject a sufficient amount of blood to supply the body or to do so only with elevated filling pressures.
1. dyspnea- shortness of breath
2. fatigue due to low CO
3. volume overload (pulmonary or systemic edema)
In the majority of patients with HF, symptoms are due to ___________dysfunction.
Heart failure is ALWAYS due to some underlying cardiac pathology. Defining this is important for management and treatment.
What "underlying pathology" accounts for 2/3 of patients with heart failure due to systolic dysfunction.?
What are the 7 etiologies of heart failure?
1. coronary artery disease
3. primary cardiomyopathy (restrictive, hypertrophic, dilated)
4. valvular disease
5. pericardial disease
6. toxins (alcohol, chemo, radiation)
7. inflammation (post-partum/ viral)
What is the primary inciting factor for patients with systolic dysfunction?
injury or stress to the myocyte
Acute stess - MI
Chronic stress - hypertension, adverse remodeling, hemodynamic stress due to valve disease)
What is remodeling?
What are the effects of remodeling on preload, afterload and CO?
Progressive changes in the ventricle in response to injury or stress (MI, hypertension, valvular defect, shunting)
3. more spherical shape
Enlargement of the ventricle will increase preload (which is initially helpful to maintain CO due to frank-starling forces)
Remodelling increases afterload negatively effecting ventricle performance.
CO is maintained at first but then starts to decline
In addition to changing the shape of the heart and eventually decreasing LV function and SV, what else can result from adverse ventricular remodeling?
What are the short term and long term effects?
It can activate endogenous neurohumoral systems like SNS and RAAS.
SNS- vasoconstriction and stimulation of myocardial growth (hypertrophy). This increases contractility in the short term, but in the long term has high O2 expenditure leading to more cell death.
RAAS- salt and water retention and increased PVR which in short term increases preload but long term increases myocardial energy expenditure--> cell death
Describe the neurohumoral activation of HF.
1. myocardial injury
2. decreased LV performance, increased wall stress
3. activation of SNS and RAAS
4. cell alterations lead to hypertrophy, fibrosis, apoptosis
5. MORE remodeling- decrease LV function-> pump failure and arrhythmia
6. Vasoconstriction and hemodynamic alterations lead to fatigue, DOE, pulm congestion, edema
What assessment is critical to establish the diagnosis of systolic or diastolic cardiac dysfunction?
LVEF= LVEDV-LVESV / LVEDV and it should be around 55%.
With systolic dysfunction, cardiac chambers are dilated and contraction is abnormal so you will see a LVEF less than 40%
With diastolic dysfunction, cardiac chambers have normal dimension and normal contraction, but decreased filling
With systolic dysfunction, what happens to the cardiac chambers and contraction?
They are dilated and contraction is abnormal. LVEF is less than 40%
With diastolic dysfunction, what happens to the cardiac chambers and contraction?
The cardiac chambers have relatively normal dimensions and normal contractile function but have stiff and noncompliant walls so there is increased filling pressure (LVEDP is increased)
What are the 3 most common causes of diastolic heart failure?
2. ischemic heart disease
3. hypertrophic cardiomyopathy
Both systolic and diastolic dysfunction show a decrease in ____________ leading to _________________.
Stroke volume - this leads to activation of SNS
How do systolic and diastolic dysfunction in HF differ in:
2. Heart size
3. common etiology
3. hypertension, ischemic heart disease, hypertrophic cardiomyopathy
The most effective therapies for treatment of heart failure are those that ______________.
Interrupt the adverse neurohumoral activation
What are the AMA stages of heart failure?
A- high risk, but no structural/functional heart changes or symptoms
B- structural heart disease without symptoms
C- structural heart disease with prior or current symptoms
D- refractory HF requiring specialized intervention
What is the therapy for someone with Stage A heart failure?
1. Lifestyle modification- smoking cessation, treat lipid disorder, regular exercise, diet modification, reduce alcohol/drugs
2. ACEI in diabetics
What is therapy for someone with Stage B HF?
They have structural/functional changes but no symptoms.
2. ACEI in diabetics
3. BB in CAD/angina
What is therapy for someone with stage C HF?
Structural/functional heart changes with prior or current symptoms.
2. ACEI or ARB
4. Device therapy if at risk for arrhythmia
What is therapy for someone with stage D HF?
structural/functional heart defects requiring special intervention.
1. All stage A B C measures
2. mechanical assist
3. heart transplant
4. continuous IV ionotropes for palliative care
A patient comes to you with:
1. previous MI
2. LV systolic dysfunction
3. asymptomatic valvular disease
What ACC/AHA stage are they in?
A patient comes to you with:
1. structural heart defects
2. shortness of breath and fatigue
3. reduced exercise tolerance
What stage of AHA HF are they in?
What are the three "giveaway" symptoms that a person has decreased CO?
Elevated left side filling pressures result in _______ and ________ while right side filling pressure increase results in ________, ___________, and ____________.
dyspnea and othopnea due to increased LV pressure-> increased LA pressure-> increased pulmonary venous pressure
peripheral edema, JVD, abdominal pain, weight gain due to blood backing up in systemic venous circulation.
What physical exam finding is specific for ACUTE forms of LHF? (it is absent in chronic)
Rales- they are present in acute and absent in chronic due to increased lymphatic circulation
What are the physical exam/auscultation signs of LHF?
1. Rales (in acute)
2. S3, S4
4. pleural effusion
What are the physical exam/auscultation signs of RHF?
4. right sided S3, S4
What are the three most important exam findings of low output state?
2. cold extremities
3. Low BP
What are the 4 classes of NYHA classification of HF?
All four classes of NYHA fall into what 2 stages of the AHA assessment of HF?
Class I- symptoms with extensive effort
Class II- symptoms with ordinary exertion, none at rest
Class III- less than ordinary exertion
Class IV- symptoms at rest
All four are in stages C and D
What is the annual mortality for someone with:
1. asymptomatic LV dysfunction
2. NHYA classI
3. NHYA class II
4. NHYA class III
5. NHYA class IV
What are over 50% of deaths contributed to?
Over 1/2 of the deaths are due to sudden cardiac death (V fib, high-grade AV block, cardiac standstill)
What are the 3 major diagnostic evaluations that need to be done to identify causes of HF?
1. Blood work (CBC, LFT, TFT, electrolytes, CkT, BNP levels)
2. CXR, EKG
3. assess cardiac function (echo, cath)
What is BNP?
What is it directly proportional to?
What do the levels vary with?
Brain natriuretic peptide- a polypeptide stored in ventricles with diuretic, natriuretic and smooth muscle vasodilating properties.
Release of BNP is DIRECTLY proportional to volume and pressure overload of the ventricle
BNP levels rise with age and vary btw genders but if there is BNP >100mg/dl, there is 95% sensitivity and 98% specificity for differentiating HF from pulmonary causes of dyspnea/orthopnea.
You have a patient with cloudy lungs. You want to decide if it is a pulmonary problem or a cardiac problem. What test do you order?
Blood workup to check BNP levels. If the level is above 100 it is nearly certain that this is a problem of CHF.
BNP cannot reliable distinguish between HF due to __________ versus _________.
systolic vs. diastolic dysfunction
What does the CXR show for heart failure (systolic)?
1. enlarged heart
2. pulmonary vascular congestion
3. pulmonary vascular redistribution (due to increased pressure in the vasculature)
4. leakage into alveolar spaces (butterfly infiltrate)
What does the ECG show for heart failure?
1. chamber enlargement
2. Q waves from prior infarction
HUGE CLUSTER FUCK
Why is echo useful in assessing heart failure?
It shows structure and FUNCTION of the heart. You can assess:
1. chamber size
2. wall thickness
3. valve structure/function
1. Doppler can assess velocity of RBC and myocardial tissue to see if systolic and diastolic function are proper.
In the acute setting of heart failure, what is treatment directed to do?
What is used?
Decrease pulmonary and systemic congestion.
Diuretics are used
What are the drugs that predominantly dilate arterial circulation? Venous?
2. nitroprusside (Both)
What is the effect of vasodilation on:
1. patients with decompensated HF with increased filling pressures
2. patients with compensated HF and normal filling pressures
1. There is a decrease in LVEDP and an increased CO
2. There is a decreased LVEDP and a decreased CO
What is the most important medical therapy for patients with HF?
1. ACEI, ARB
3. aldosterone antagonists (spironolactone)
Which neurohumoral antagonist was shown to have a favorable effect on ventricular remodeling, thus improving LV function?
BB should not be started in patients with HF until they are ________. They should be started at _________ and titrated up.
Start at low doses
What 2 drugs are in BiDil? Who does this combination improve survival in?
2. isosorbide dinitrate
It is effective in lowering mortality risk in AA males and in patients who have contraindications with ACEI/ARBs (like those in kidney failure or those with abnormally high K)
Which drugs is shown to decrease mortality in patients with advanced heart failure (class III/IV)
What is the only + ionotropic agent recommended for routine management of patients with moderate to severe heart failure?
What's the drawback?
Digoxin- it has a narrow therapeutic window so toxicity risk is high
What 2 drugs are used as IV ionotropic agents for patients with advanced HF that are refractory to other therapy and are awaiting heart transplant?