Lecture 6: HF Flashcards
pts diagnosed w HF have a ____________ _____________ mortality rate after their 1st hospital admission
50% 5-year
one in every 2 pts diagnosed will die at 5 yrs, this increases w each hospitalization, and profoundly after the 3rd
common misconceptions around HF
It is a chronic condition, can come on suddenly
Long term condition
Your heart does not stop beating - it just beats ineffectively
This is NOT normal for aging, comes from damage to the heart muscle
More exacerbations the more compromises the patient will have
what is HF
- characterized by inability of myocardium to pump enough blood to meet body needs
- abnormal clinical syndrome involving impaired cardiac pumping or filling, or both
- response to cardiac dysfunction
what is the most common cause of HF
Most common cause of heart failure: HTN (because heart is pumping against pressure, and if it can’t pump effectively it decreases C/O)
Maintain our hypertension
what can high cholesterol lead to
High cholesterol -> coronary artery disease -> heart attack and stroke
what can hypertrophy of the heart cause
Hypertrophy heart -> you wont have the same filling as you would if your heart could relax causing decreased C/O.
why is increased HR bad
Increased HR - decreasing filling time - don’t get perfusion from arteries to heart - so overall less effective
what is valvular disease
Valvular disease -> when valves don’t open and shut properly. If your valves aren’t shutting properly, we won’t have that closed system and will have leakage. If we have stenosis - this will be pushing against higher pressure, so takes more energy.
R sided HF
R sides HF - having trouble pulmonary system (PE, pulmonary HTN - will increase pressure in this system)
L sided HF
L side - having trouble pumping to systemic system
top 3 most common HF causes
- CAD -> MI
- hypertension
- valvular disease -> rheumatic disease
most common causes of HF overall (a lot)
- CAD, MI
- HTN
- valvular disease
- CHD
- pulm HTN (r sided), PE
- infiltrative disorders
- pericardial disease
- inflammatory (myocarditis)
- cardiomyopathy
- dysrhythmias
- meds non-compliance
review norm circulation
what are 3 major sys that are recruited when myocardial injury occurs
- SNS
- RAAS
- Natriuretic peptide sys
explain how the 3 major sys that are recruited when myocardial injury occurs (i am sorry this is so long fix this slide)
Myocardial dysfunction
- Decreased CO, systemic bp, and perfusion to kidneys
So this stim SNS sys - what can we do to increase output?
Can increase bp, and HR to help perfusion.
Vasoconstriction - increased BP and HR
Good ideas except, heart is not pumping enough out bc its failing, so makes it difficult to do its job. So this isn’t very helpful. Lessens our perfusion, increase stuff on the heart. Not great if someone has HF.
Our HF pts are on beta blockers bc it interferes w SNS.
Will also activate our RAAS sys -> causes vasoconstriction - increasing bp, stim release of aldosterone, also increase pressure, further cause vasoconstriction, increase pertrophy?, overtime these are not helpful not good longterm. -> so to stop our RAAS sys = we use ACE inhibitors + ARBs if they cant tolerate ACE.
Natriuretic peptide sys - in our atria and ventricles, increased stretch our heart releases these peptides, increased stretch = increased volume, which we know in HF we are not pumping out well, if RAAS sys is instigated and retaining fluid - this puts up our volume. Our pituitary gland - antidiuretic hormone - works on distal tubules to increase volume - and then we have stretch - our heart releases our naturetic peptides, and they do a few things. They interfere w RAAS sys, cause vasodilation, increase excretion of Na and H2o, we like this sys so we do things to keep making this system work.
how does SNS elevation try to compensate for HF
- increases HR and contractility
how does neural-hormonal response try to compensate for HF
- increase in Na and H2O retention (RAAS)
- posterior pituitary gland secretes ADH
- production of endothelin - potent vasoconstrictor
- proinflammatory cytokines are released by heart - causing hypertrophy, contractile dysfunction, and cell death
how does the frank starling mechanism try to compensate for HF
- dilation of ventricle
- increased pressures result in increased volume at end of diastole
- increased stretch initially adaptive - eventual overstretch results in ineffective contraction
how does ventricular hypertrophy try to compensate for HF
- increase in muscle mass and cardiac wall thickness in response to overwork and strain
- develops overtime, generally following persistent or chronic dilation
what do HF hearts look like + why is hypertrophy not great
HF can have big stretchy hearts.
Initially more heart muscle is good, but overall not sustainable.
what does the natriuretic peptide system impact + what are the 2 natriuretic peptides
- impacts salt and water handling, pressure regulation, and may influence myocardial structure and function
- BNP (brain natriuretic peptide)
- ANP (atrial natriuretic peptide)
BNP (brain natriuretic peptide)
a natriuretic hormone primarily released from the heart - particularly the ventricles
ANP (atrial natriuretic peptide)
a hormone released by the myocardial cells in the atria
what similarities does the 2 natriuretic peptides have
- both are released in response to increased wall stress and volume expansion
- both have diuretic, natriuretic, and hypotensive effects
- both inhibit RAAS and impair systemic and renal sympathetic activity
in comparison to other compensatory mechanisms - which one is actually a good thing
The natriuretic peptide system is a good thing - the others not so much so we try and help the peptide system.
what 3 sys kick in to regular the issue w HF
SNS + RAAS + NP
over time the compensatory mechanisms become maladaptive… why is this (4)
- elevation of diastolic pressures transmitted to atrial/pulmonary/systemic venous circulations promotes congestion and edema
- increase in LV afterload (vasoconstriction) can both directly depress cardiac function and enhance the rate of deterioration of myocardial function
- increases contractility, HR, LV afterload can worsen or provoke coronary ischemia
- catecholamines, angiotensin 2, aldosterone promote the loss of myocytes through apoptosis, and cause myocardial hypertrophy and fibrosis
describe acute HF
often related to a significant event like a MI. can progress over days or hours.
sudden onset, w no compensatory mechanisms
describe chronic HF + s/s
CAD, HTN, valvular disease. They can also have acute on chronic event
- ongoing process mo to yrs
- progressive worsening of ventricular function
- chronic neuro-hormonal activation that results in ventricular remodelling
- fatigue, dyspnea, tachycardia, edema, nocturia, depression chest pain, wt changes
describe L sided HF
- left ventricular dysfunction
- disturbance of contractile function of L ventricle, resulting in low c/o state
describe R sided HF
- ineffective R ventricular contractile function
- backwards flow
what kind of HF do most ppl have…
Where does blood come from to L side of heart - backing up into lungs - so if we increase pressure bc L side of heart is failure, puts pressure on the R side. Most ppl have this bc L ventricle is compromised.
systolic HF
- abnormality of heart muscle that markedly decreases contractility during systole (ejection) and lessens the quantity of blood that can be pumped out of the heart
diastolic HF
- describes abnormality of heart muscle that makes it unable to relax, stretch, or fill during diastole, EF can be normal
if your heart is having a pumping problem…
Pumping problem - systolic problem
if your heart is having a filling problem…
Or filling problem - heart is resting diastolic
describe ejection fraction
calculated doing a ultrasound and look at the V in the L ventricle, and then they calculate how much blood is pumped out. If L ventricle held 100 mLs pumps out 50, your % would be 50%.
CO is V that is being pumped out.
if you have a problem w filling… and you only have 50 mLs ad you pump out 25mLs what % is this…
50%
diastolic problem
their ejection fraction is rly good, but their volume being pumped out is bad.
describe heart failure reduced ejection fraction (HFrEF)
- formally called systolic dysfunction - inability to pump
- LVEF <40%
- aggressively treated w medical therapy and cause for etiology determined ASAP
Ejection fraction less than 40%, rly bad at pumping the volume out. Treat w beta blockers, ACE inhibitors.
describe heart failure preserved ejection fraction (HFpEF)
- formally called diastolic dysfunction - inability to relax
- LVEF >50%
- treatment of symptoms
Heart doesn’t fill very well - decreased CO. treat sympt.
describe heart failure midrange ejection fraction (HFmEF)
- “new” classification of pts
- LVEF 40-49%
- treatment pathway still under review, may be individualized
Mix of both the above for treatment. bit of a pump and fill problem. Decreased CO.
what are 5 complications of HF
- pleural effusions
- dysrhythmias
- L ventricular thrombus
- hepatomegaly
- renal failure
what is a pleural effusion
backing fluid into our lungs increases pressure. Movement of fluid outside capillaries. Build of of pressure and fluid.
what causes dysrhythmias
enlarged chambers, electrolyte imbalances, etc.
what is L ventricular thrombus
blood stagnant in atria, pt at risk for clot. Ventricle not pumping well can also cause clotting. Want to treat this so a clot is not pumped out.
what is hepatomegaly
increase in fluid in liver sys
what is renal failure
ex of prerenal because we are not perfusing them
R sided HF s/s
- fatigue, weakness
- hypotension: reflects severe disease
- fluid overload
- wt gain
- anorexia
- peripheral edema, +/- JVP
- decreased SaO2
- murmurs
- ascites/anasarca (massive, generalized body edema)
- hepatomegaly
- R heaves
- renal impairment
- tachypnea
- tachycardia
L sided HF s/s
- fatigue, weakness
- HTN
- hypotension - reflects severe disease
- fluid overload
- wt gain
- pulmonary edema (crackles)
- decreased SaO2
- extra heart sounds (S3 and S4)
- peripheral edema
- L heaves
- renal impairment
- tachypnea
- tachycardia
- nocturia
- dyspnea
- orthopnea
w R sided HF what do u get
- congestion of peripheral tissues
- dependent edema and ascites
- GI tract congestion
- liver congestion
w L sided HF what do you get
- decreased c/o
- pulmonary congestion
- impaired gas exchange
cyanosis and signs of hypoxia
- pulmonary edema
cough with frothy sputum, orthopnea, paroxysmal nocturnal dyspnea
SOBOE (on exertion) is a early symptom of HF from…
pulmonary congestion
described what would be diff on assessment w HF from normal
- severely decompensated HF including hypotension, worsening renal function, or altered mentation
- dyspnea at rest
- worsened congestion, even if w/o dyspnea at rest
- s.s of pulmonary or systemic congestion even in absence of wt gain
- major electrolyte disturbance
- associated comorbid conditions such as pneumonia, pulmonary embolus, DKA, ACS, or stroke symptoms
- repeated implantable cardioverter defibril firings
- previously undiagnosed HF w s/s of systemic or pulm congestion
- hemodynamically significant arrhythmia including new onset of atrial fibrillation w rapid ventricular response
early abnorm heart sound
s3
late abnorm heart sound
s4
what are S3 S4
3rd and 4th heart sounds are resistance to filling
S3 and s4 can’t fill properly
At risk for HF
describe murmurs
not going to get tested on thank god but murmurs are turbulent blood flow + usually indicative of abnormal blood flow, or something is impeding it
grade 1 class for ejection fraction
normal
>50%
Rarely eject greater than 80%
Greater than 50% is chill (50-80)
grade 2 class for ejection fraction
mild
41-49%
41-49 is compromised (mixed HF - combo of pumping and filling)
grade 3 class for ejection fraction
moderate
30-41%
Less than 40 - Pt w reduced ejection fraction
grade 4 class for ejection fraction
severe
<30%
Less then 30% this is quite severe - “cardiac cripples”
what lab work do we do for HF
- BNP (brain natriuretic peptide)
- renal function
- glucose
- CBC
- liver function/hepatic congestion
- thyroid function
- electrolytes - Na+,K+
- troponin, CK
- blood gases
what are u at risk for slow rhythm if u have
hypothyroidism
tell me about BNP lab work readings
- can be elevated in pts w renal failure (products cleared by kidneys)
- also elevated in CAD, valvular heart disease, pulmonary hypertension, sepsis
diagnostics for HF
- ECG
- Chest radiograph
- Echo
- Exercise Testing
- Stress Test
- MRI - cardiac
- Cardiac Catheterization
in HF what do we look at with ECG’s
for evidence of ischemia, infarction, arrhythmia (ex: afib)
what does chest radiograph in HF look at
- assess for signs of pulm edema, cardiomegaly, alternative diagnoses (ex: pneumonia)
- norm radiograph does not rule out HF
what does an Echo look at for HF
- ejection fraction
- if cardiac or valvular function is not known
- f/u to compare to previous
what is NYHA class
new york heart association classification
NYHA Class 1
- no symptoms
- can perform ordinary activities w/o any limitations
NYHA Class 2
- mild symptoms
- occasional swelling
- somewhat limited in ability to exercise or do other strenuous activities
- no symptoms at rest
NYHA Class 3
- noticeable limitations in ability to exercise or participate in mildly strenuous activities
- comfortable only at rest
NYHA Class 4
- unable to do any physical activity without discomfort
- symptoms at rest
what vastly improves outcomes for HF
med management
nutrition wise for HF what do we do for sodium
restrict
<2-3 g /day
1.5 g/day - severe HR
nutrition wise for HF what do we do for fluid restriction
1.5-2 L/day
- daily wts
- 1-1.5 kg (2-3lb) per day or 2.5 kg (5lbs) over 5-7 days
what are 3 things to note about pharma for HF
- start low, go slow
- one med at a time
- re-evaluate symptoms, status, v/s, adverse events, lab values
sinus rhythm is the goal. if not 2nd goal is HR less than 70.
all efforts treating HF pts should be 2 fold… what are the 2 things
- reduce HR to < 70 BPM
- restore NSR if not already
how do we know what agent to start first for HF meds
- usually afterload reduction (ACE/ARB( first, however this is not always a rule - it is a clinical decision.
(are they hypotensive, tachycardiac, volume overloaded??) - meds are often held, interrupted, discontinued for inappropriate reasons.
what’s common pharma for afib
beta blocker, CCB
pharma management of MI
beta blocker, nitrates
when are diuretics used
fluid overload
meds for HF preserved Ejection Fraction
- treatment targets associated conditions (HTN and edema)
- AFib common - bb or CCB
- MI - BB, nitrates
- diuretics - volume overload
HF reduced ejection fraction pharma management
- ACE-I/ARB
- B-Blocker
- MRA
describe ACE-I/ARB
- inhibit the RAAS sys
- block conversion of ATI to ATII lowering arteriolar resistance
- also prevents release of aldosterone (opposes natriuresis)
- afterload reduction
describe b-blocker
- competitive antagonists that block receptors of catecholamines of SNS
- some are cardioselective (B1)
- reduce HR, sllow for prolonged diastolic filling time
describe MRA
- mineralocorticoid receptor antagonist (receptor for aldosterone)
- regulates Na reabsorption and fluid balance
describe the new drug neprilysin inhibitor + example
ex: sacubitril
- decrease BP, sympathetic tone
- decrease aldosterone levels
- decrease myocardial fibrosis and hypertrophy
- increases natriuresis and diuresis
breaks down BMP ( so we don’t like this)
describe the new drug angiotensin receptor neprilysin inhibitor + examples
ex: sacubitril/valsartan - entresto
- decreased Na and H2O retention
- decreased vasoconstriction, increased vasodilation
- decreased hypertrophy
- decreased fibrosis
- increases natriuresis and diuresis
- increased aldosterone suppression
describe the new drug ivabradine-lancora + examples
- acts on the l(subscript)f channel which is highly expressed in the sinoatrial node
- reduces pacemaker rate selectively and allows more time for relaxation/end diastole
- there is reduced HR w/o loss of contractility
- NO BP lowering effects
- therapy is added in addition to routine therapy (beta-blockers)
describe the new drug glucose cotransporter 2 (SGLT2) inhibitor - dapalgliflozin + examples
- may be used in persistently symptomatic pts who are alr optimized on other therapies
- reduces reabsorption of filtered glucose from the tubular lumen and lowers the renal threshold for glucose (RT subscript G) result in increased urinary excretion of glucose, thereby reducing plasma glucose concentrations
- reduces sodium reabsorption and increased sodium delivery to the distal tubule, which may decrease cardiac preload/afterload
- improves myocardial metabolism and thus improve cardiac efficiency
- may also have vascular effects (including improving endothelial function) that promote vasodilation and thus may also reduce afterload
describe diuretics
1. thiazide
2. loop
- thiazide diuretics
- inhibits Na reabsorption in distal tubule - loop diuretics - promotes Na, Cl and H2O excretion in ascending loop of Henle
- consider onset and duration of action
- set targets - wt loss, FiO2 concentration, symptom resolution
- is pt already taking lasix?
- pt should be on PO lasix w stable symptoms/wt for 24 hrs prior to leaving the hospital
describe vasodilators
1. nitroglycerin
2. renal impairment
- vasodilation, reduction of preload and afterload
- consider hydralazine and nitrates
describe digoxin
- acts by inhibiting the Na-K-ATPase pump
- decreases HR (assess HR prior to administration)
- increased myocyte contractile performance (increased shortening velocity) and improved overall LV systolic function
how do we manage venous thromboembolism prophylaxis
- anticoagulation
- low dose unfractionated heparin or LMWH (for pts who are not alr anticoagulated and have no contraindications to anticoagulation)
- not used for all pt’s w HF
- HX of afib
- EF <35%
surgical interventions for HF
- heart transplant
- valvular replacement
- coronary revascularization procedures (CABG, PCI)
how long do HF pts usually have a change in symptoms b4 ER visit
2-3 days
for HF exacerbations how do we recognize a change
- increase in wt >2-3 lbs above baseline overnight or 5 lbs in a week
- increase in orthopnea, PND
- worsening dyspnea, edema
can pts recover from HF
nah its progressive
