ICL 5.2: Clinical CHF Syndromes Flashcards
how have CHF rates changed?
overall reduction
probably due to stunting and early detection of CAD
but reduced CHF is starting to go up in women a bit
does preserved or reduced CHF have lower risk for CV death?
risk for CV death was lower for HFpEF
but they have the same risk for non-CV death
what are the stages of CHF?
A: high risk for CHF like HTN, CAD, DM, family history of cardiomyopathy
B: asymptomatic LV dysfunction – previous MI, LV systolic dysfunction, asymptomatic valvular disease, low EF, LV hypertrophy
C: symptomatic HF – structural heart disease,e DOB, fatigue, reduced exercise tolerance
D: end stage HF – symptoms at rest despite maximal medical therapy
what are the goals and treatment for stage A CHF?
- treat BP
- smoking cessation
- regular exercise
- reduce alcohol/drug use
- treat HTN, DM, dyslipidemia or atherosclerosis if needed
treat with ACEI or ARBs for vascular disease/DM
what are the goals and treatment for stage B CHF?
- treat BP
- smoking cessation
- regular exercise
- reduce alcohol/drug use
treat with ACEI or ARB and B blockers
B blockers because they have a structural problem and B blockade can help reestablish B receptor ratio and get the heart to positively remodel
how does treating HTN help prevent CHF?
by aggressively controlling BP, you decrease the risk of new HF by 50% and by 56% in DM2 population
if you control it in patient with prior MI, you decrease the risk of new HF by 80%
which medications do you use to treat stage A CHF?
- ACEI
especially in patients with CAD, peripheral vascular disease, stroke or DM
- ACEI and B blockers are recommended for all patients with a prior MI
how do you diagnose stage B HF?
they’re asymptomatic so they’ll have a negative HPI, ROS and PE
they’ll have an abnormal surveillance testing found coincidentally during an EKG or CXR that then necessitates an echo
then once they do the echo they’ll see the abnormal structure
how do you treat stage B HF?
- ACEI
- ARBs
- B blockers
especially in people who have a history of silent MI and EF <40%
this decrease hospitalizations and mortality even if they don’t have symptoms but they’re post MI or LVEF <40%
what are the 2 classes of HF?
- systolic
2. diastolic
what is heart failure with reduced ejection fraction?
HF with EF <40%
aka systolic HF
what is heart failure with preserved ejection fraction?
EF >50%
aka diastolic HF
60-90% of HFpEF patients have HTN so treating HTN leads to less episodes of HF
we really don’t know much about HFpEF
what is borderline heart failure with preserved ejection fraction?
EF 41-49%
characteristics and outcomes appear similar to those of patients with HFpEF so treat similarly
what is improved heart failure with preserved ejection fraction?
if they had previous reduced HF but now they have preserved EF and an EF >40%
we really don’t know what to do with these patients we need more studies
what conditions cause HFrEF? how do you diagnose it?
- CAD/MI
- PAD
- HTN
- obesity and insulin resistance/DM
EF<40%
get an echo to see wall motion or a nuclear test to test blood flow
what conditions cause HFpEF? how do you diagnose it?
- HTN
- CAD
- arrhythmias
- morbid obesity
- hyperlipidemia
use echo to diagnose
what is class I HF?
no limitations
ordinary physical exercise doesn’t cause fatigue, dyspnea or palpitations
what is class II HF?
slight limitations
comfortable at rest but ordinary activity results in fatigue, dyspnea or palpitations
what is class III HF?
marked limitations
comfortable at rest but less than ordinary activity results in symptoms
what is class IV HF?
unable to carry out any physical activity without discomfort
symptoms of HF are present even at rest with increased discomfort with any activity
what are the signs of decreased perfusion?
systolic dysfunction = lower CO = poor perfusion
- cool extremities
- altered mental status
- fatigue
- low urine output
- inadequate response to IV diuretic
- kidney dysfunction
- palpations/tachycardia
what are the signs of congestion?
- SOB
- orthopnea = can’t lay flat
- PND
- increased jugular venous distention
- increased hepatojugular reflex
- peripheral edema
- S3
- splanchnic congestion
how do you classify acute heart failure?
are they having perfusion or congestion symptoms or both?
what are the clinical signs of stage C or D HF?
- tachycardia
- HTN (in HFpEF)
- orthostasis
- hypotensive (in HFrEF)
- increased respiratory rate
- decreased breath sounds/crackles/rales/wheezing
- abdominal swelling, ascites, hepatomegaly, peripheral edema
- JVD*
- murmur usually MR or TR
what is JVD? how is it related to HF?
JVD = jugular venous distention
put the patient at HOB 45 degrees and measure from the chest wall to the clavicle (5 cm) then add how many cm above that you can see the JV
in a normal patient you should’ve be able to see it over the clavicle so their JVP will be 5
JVD is the most specific sign for CHF – it’s a short term and long term independent predictor of mortality
what do you do during a basic evaluation for HF?
- PE
- CXR
- EKG
- Labs = CBC, electrolytes, BUN, creatine, LFTs, BNP, T4, lipids, A1C, urinalysis
what do you do during further evaluation for etiology, prognosis and plan of HF?
- echo with doppler
- nuclear imagining for ischemia
- myocardial viability when all scar on nuclear
- catheterization increasing right heart pressures
- exercise test to look at maximal oxygen uptake
- MUGA to asses EF of ventricles
what lab values are associated with an increased risk for in hospital mortality in acute HF?
- BUN>43
- creatinine >2.75 mg/dL
- hypotension SBP <115 mmHg
these are poor prognostic signs in acute HF patients
what conditions can cause increased BNP?
- myocarditis, pericardial disease, atrial fib
- age
- anemia
- renal failure
- pulmonary problems
what are some conditions that can cause stage C and D acute HF?
- ACS
- uncontrolled HTN, accelerated HTN, hypertensive emergency
- right HF
- arrhythmias
- PE
- aortic dissection
what are some common causes of stage C and D acute HF?
- nonadherence with medication regimen, sodium and/or fluid restriction
- recent addition of negative inotropic drugs (eg, verapamil, nifedipine, diltiazem, beta blockers)
- initiation of drugs that increase salt retention (eg, steroids, thiazolidinediones, NSAIDs)
- excessive alcohol or illicit drug use
- endocrine abnormalities (eg, diabetes mellitus, hyperthyroidism, hypothyroidism)
- concurrent infections (eg, pneumonia, viral illnesses)
- additional acute cardiovascular disorders (valve diseases, endocarditis, myopericarditis)
how do you treat stage C and D acute HF with preserved EF?
- control HTN
- DVT prophylaxis
- IV loop diuretics
- ACEI/ARB of BB AFTER IV HF meds are given
- low dose dopamine
- hemodialysis to reduce blood volume
- IV nitroglycerine
how do we treat HFpEF?
we only know that we need to control HTN by using diuretics
make sure they don’t have CVD
manage Afib if they have it
what pharmacological treatment do you use for stage C HFrEF?
ACEI/ARB with a BB
for classes I-IV
if the patient has volume overload, add a diuretic (loop like bumetanide, furosemide or torsemide)
if the patient has symptoms on the ACEI/BB and get SOB, cool extremities etc. and they’re african american, add nitrate = venous and arterial vasodilator and hydralazine = pure arterial vasodilator
for class III and IV and have functional kidneys, add mineralocorticoid aldosterone inhibitor
which drugs are ACE inhibitors?
“pril”
- lisinopril
- quinapril
- captopril
which drugs are ARBs?
“sartan”
- candesartan
- losartan
- valsartan
after decompensation of HF but before DC from hospital, at medications should patients be on?
BB therapy and stop IV medications
BB = bisoprolol, carvedilol, metoprolol
which drugs are aldosterone antagonists?
- spironolactone
- eplerenone
mineralocorticoids
if you have significant kidney dysfunction don’t use these
what are the effects of neprilysin inhibitors?
- increased BNP and ANP
- increased bradykinin
- decreased neurohormonal activation, vascular tone, cardiac fibrosis, hypertrophy and sodium retention
what is entresto?
combination of neprilysin inhibitor sacubitril and ARB valsartan
stop previous ACE inhibitors for 36 hours before starting
don’t use in patients with angioedema
start with low dose and go up slowly so the vasodilation effect doesnt drop the BP too much
what is ivadradine?
use when beta blocker therapy isn’t enough
it inhibits funny channels so it slows HR in the SA node different than the MOA of BB and it’s good for HF
this lets you use less energy which is great in HF
don’t use in 3rd degree heart block because it effects funny channels
who qualifies for a ventricular defibrillator?
HFrEF stage patients who still have ischemic cardiomyopathy 40 days pots MI with an EF < 35%
they’re also used in non-ischemic cardiomyopathy and dilated cardiomyopathy if meds don’t work
they have to have a life expectancy of at least 1 year so no cancer
what is cariogenic shock?
loss of CO with hypotension and loss of adequate organ/tissue perfusion
SVR will be high to try and compensate for loss of CO (MAP = CO x SVR)
increased preload and after load but decreased CO
you’re at risk for cardiac myocyte death/injury
can happen with MI, drugs, toxins, viruses, arrhythmias
what is hypovolemic shock?
decreased preload, increased after load from increased SVC so ultimately decreased CO
how do you treat cariogenic shock?
positive inotropes = dobutamine
make the heart pump harder
how do you treat hypovolemic shock?
fluid repletion = IV bolus or blood transfusion
