Heart Failure Flashcards
1
Q
what is heart failure?
A
a complex clinical syndrome that results from any structural or functional cardiac impairment of ventricle filling or ejecting blood. The heart is unable to pump sufficiently to maintain the blood flow to meet the body’s needs
2
Q
heart failure is most common in what patient populations?
A
males and the elderly
3
Q
HF is responsible for more hospitalizations than all ____ combined
A
cancers
4
Q
HF is the leading cause of hospitalization in patients older than _____
A
65
5
Q
50% of patients diagnosed with HF will die within __ years
A
5
6
Q
what are some conditions that increase risk for heart failure?
A
MI, HTN, myocarditis, anemia, COPD etc.
7
Q
what are some drugs that increase risk for heart failure?
A
NSAIDs, corticosteroids, chemotherapies, biologic DMARDs
8
Q
what are some social hx/diet factors that increase risk for HF?
A
excessive fluids, salt, alcohol intake, use of illicit drugs like cocaine, emthamphetamine, and ecstast (MDMA)
9
Q
decreased CO caused by HF results in activation of which nervous system? what is the consequence of activating this nervous system?
A
sympathetic; causes the release of cathecholamines to increase HR, contractility and vasoconstriction
10
Q
activation of the SNS by decreased CO causes what changes in pre-load and after load?
A
increases both (increasing preload is good, increasing after load is bad)
11
Q
what is the eventual effect of SNS activation on CO?
A
will initially increase, but the cardiac O2 demand and work will also increase and eventually lead to decreased CO
12
Q
what is teh effect of SNS activation on cell death?
A
increases
13
Q
decreased cardiac output causes ____(activation or deactivation) of the RAAS system. What is the effect of this?
A
activation: decreased renal perfusion, renin release, increased angiotensin 2, increased aldosterone levels
14
Q
how is activating the RAAS system crucial to CO?
A
maintains effective circulating volume (preload) mediated by aldosterone secretion and Na and water retention to increase CO
15
Q
what is the “negative” of decreased CO causing activation of the RAAS system?
A
increased vasoconstriction leads to increased afterload, increased myocardial energy use, cell hypertrophy, fluid retention and edema
16
Q
decreased CO causes a ______(increase or decrease) in ADH, what is the effect of this?
A
increase: increases the circulating volume which increases the preload but also may cause pulmonary edema
17
Q
what 3 things affect stroke volume?
A
preload, afterload and contractility
18
Q
what 2 things affect CO?
A
stroke volume and heart rate
19
Q
what 2 (physiological) things affect BP?
A
cardiac output and systemic vascular output
20
Q
describe NYHA class 1
A
physical activity not limited. Ordinary physical activity does not cause undue fatigue, heart palpatation, SOB or chest pain
21
Q
describe NYHA class 2
A
some limitation on physical activity. comforatble at rest, but ordinary physical activity causes fatigue, heart palpatations, SOB, or chest pain
22
Q
describe NYHA class 3
A
marked limitation on physical activity. Comfortable at rest, but less-than ordinary physical activity causes fatigue, heart palpitations, SOB or chest pain
23
Q
describe NYHA class IV
A
Unable to carry on any physical activity w/o discomfort, may even have sx at rest and if any physcial activity is done, discomfort increses
24
Q
what are the A-D classification of HF?
A
A: high risk (has HTN, CAD, diabtes, family hx etc.)
B: has asymptomatic LVD (past MI, systolic dx etc.)
C: symptomatic HF: known structural heart dx, has sx
D: refractory end-stage HF (marked sx at rest)
25
what is systolic dysfunction?
hypofunctioning ventricle (decreased contractility)
26
what is diastolic dysfunction?
stiff ventricle, imparied ventricle relaxation
27
what is the most common type of ventricular dysfunction?
left ventricular
28
when is right ventricular dysfunction typically seen?
in combo with LVD and can occur alone in pulmonary HTN
29
what is biventricular dysfunction?
combo of RV and LV dysfunction
30
what is ejection fraction?
amount of blood pumped out of the ventricle per heart beat
31
ejection fraction is typically referring to which ventricle?
left, as it is teh main pumping ventricle of teh heart
32
what is the normal EF%?
55-70%
33
explain in words what an EF% means
means that % of the total blood in the left ventricle is pumped out with each heart beat
34
in HFpEF, what is the LVEF?
50 or greater
35
in mid-range HF, what is the LVEF?
41-49%
36
in HFrEF, what is the LVEF?
40% or less
37
t/f patients can move back and forth between HFrEF and HFpEF depending on if they improve or worsen
true (if they improve goes to HFpEF and worsen goes to HFrEF)
38
what are the main sx of HF? what are the secondary sx?
Main: fatigue, SOB, peripheral edema
secondary: weakness, exercise intolerance, weight gain, paroxysmal nocturnal SOB, orthopnea, nocturia
39
what changes in vital signs would you expect in a HF patient?
BP may be up or down, increased HR and RR, decreased O2 sat
40
what respiratory findings would you expect in a HF patient?
normal or decreased air bilaterally, crackles (rales) at the base
41
what CV findings would you expect in a HF patient?
increased JVP, S3 sounds, hepatojugular reflux
42
what GI findigs might you see in HF?
abdominal distention, anorexia
43
what genito/urinary findings might you expect in a HF patient?
scrotal edema, may have decreased urine output
44
what MSK findings might you expect in a HF patient?
cool extremities, sacral edema, peripheral edema
45
what would expect the Na to be in a HF patient?
can be normal or low (due to high volume of fluid --> hypervolumic hyponaturemia)
46
what would expect of Scr and urea in a HF patient?
can be increased due to decreased renal perfusion
47
what would you expect of troponin in a HF patient?
can be slightly elevated from cardiac strian
48
what would you expect of BNP or NT-proBNP in HF patient?
often increased, there are cutoffs depending on age and clinical setting
49
what would you expect of chest XR in HF patient?
cardiomegaly, pulmonary edema, pleural effusions
50
what physical findings would you expect to find on ECG of HF patient?
LV hypertrophy
51
what is the gold standard for assessing teh function of teh heart in HF?
echo (gives us the most information about heart function)
52
volume or pressure overload causes the release of _____(natriuretic peptide) mainly from the ventricular myocardium
proBNP
53
proBNP is cleaved into ___ and ____
active BNP and inactive NT-proBNP
54
the action of BNP causes what effects?
natriuresis, vasodilation, decreased afterload, inhibits RAAS, reduces fibrosis
55
natriuretic peptides are used as diagnostic and prognostic tools (T/f)
true
56
HF is very likely of BNP is >___ and it is unlikely of BNP in
400pg/mL; 100pg/mL
57
for people aged less than 50, what NT-proBNP shows unlikely and very likely HF?
unlikely <300pg/mL, very likely>450pg/ML
58
for someone aged 50-75, what NTpronBNP is unlikley for HF and very likely for HF?
unlikely: <300pg/ml, very likely: >900pg/mL
59
for patients aged >75, what NT-proBNP is unlikely for HF and very likely for HF?
unlikely: <300pg/mL, very likely: >1800pg/mL
60
what are lifestyle modifications that can decrease risk and progression of HF?
1. improving CV risk (managing lipids, BP, diabetes, alcohol and tobacco use)
2. diet (lowering fluid and salt intake)
3. moderate exercise
4. keeping up to date on immuniazations (flu and pneumona0
61
what are the CCS recommendations around exercise in HF?
regular exercise to improve exercise capacity, sx, QOL and decrease hospital admissions in all HF patients
62
what should sodium be restricted to in HF patients?
2-3g/day
63
how should body fluid be managed?
diuretics, daily weights, limiting intake of liquid to 2L/day
64
what are the 4 classes of drugs in goal directed medical therapy (GDMT)?
1. ACE/ARB/ARNI
2. BB
3. MRA
4. SGLT2-i
65
GDMT is recommended in what HF population?
HfrEF (40% or less) and have symptoms
66
if a patient has been optimized on GDMT, and has HR >70bpm and sinus rhythm, what is an additional drug option?
ivabradine
67
if a patient has been optimized on GDMT, and has been hospitalized in the past 12 months, what is an additional drug option?
vericigaut
68
if a black patient has been optimized on GDMT or is unable to tolerate ACE/ARB/ARNI and requires additional therapy, what is an option?
combo hydralazine-nitrates
69
if a patient has AF and if having inadequate rate control or persistent symptoms despite optimized GDMT, what is a drug option?
digoxin
70
when starting new therapies, they should typically be titrated every ____weeks, and want to reach target doses by ___months
2-4 weeks; 3-6 months
71
what drugs are recommended in HFrEF patients who are asymptomatic?
beta blockers for all LVEF <40% and ACE for all with EF<35% (both)
72
what are the 2 ways to titrate medications? Is one way better than another?
1. in-parallel: do all of them at once
2. strict sequential: fully titrate 1, then start the next
Neither has been proved to be better, but should consider pt factors like hemodynamics, renal fx, medication access, adherance, tolerability and preferences
73
what was found by the HOPE trial?
ramipril more effective than placebo in HF
74
what was found in the SOLVD trial?
enalapril decreased HF death compared to placebo
75
in the CONSENSUS and SOLVD trials, what other drugs were patients takign other than the ACE?
most were on diuretic and digoxin, <10% were on a BB
76
the SAVE, AIRE, and TRACE trials enrolled patients within a week of ___
acute MI
77
what was found by the SAVE, AIRE and TRACE trials?
ACE decreased mortalilty and readmission comaped to palcebo
78
what should be monitired in ACE use for HF?
1. lying and standing BP
| 2. SCr and K at baseline, 3-7 days later, then 1 month, then q 3months
79
in ACE/ARB/ARNI use, it is not uncommon for the SCr to up by __%
30
80
all RAAS inhibitin agents should be held if serum K is above ___mmol/L
5.9
81
what can be done to manage sympotomatic hypotension while on ACE/ARB/ARNI?
seperate dose timings, lower the dose of diuretic if patient is stable, reassess their need for other vasodilators like nitrates and CCB for HTN
82
what was found by the CHARM study?
looked at pts who were taking candesartan bc they were intolerant to ACE and found that it decreased CV death and hospital admission for HF
83
what was found by the Val-HeFT trial?
increased survival with valsartan compared to placebo, also found that patients previously taking both ACE and BB had increased mortality
84
what was found in the CHARM-Added trial?
looked at combo candesartan with ptaients already on ACE and found that there was increased hypotension, hyperkalemia, and increased SCr
85
what does ARNI stand for?
angiotensin receptor neprilysisn inhibitor
86
what is the MOA of ARNI?
inhibit neprilysin which breaks down natriuretic peptides and other vasoactive peptides. By inhibiting this, those peptides like bradykinin and BNP can lower BP and promote Na excretion
87
inhibiting neprilysin causes an increase in ____, so a neprilysin inhibitor must be combined with a ___ drug
angiotensin 2; RAAS blocking
88
give an example of ARNI
entresto (sacubitril and valsartan)
89
what was found in the PARADIGM-HF trial?
sucubitril/valsartan had less cough, less increased Scr, less hyperkalemia and more symptomatic hypotension than enalapril 10mg BID and entresto showed lower death and hospitalization
90
when does the CCS recommend ARNI?
1. in place of ACE/ARB in HFrEF patients who remain symptomatic despite optimal GDMT to decrease hosptialization, death and symptoms
2. for patients admitted for acute decompensated HFrEF switch to ARNI from ACE or ARB when stabilized and before discharge
91
what is an ARNI suggestion from CCS?
suggest giving ARNI as first line as an alternative to ACE/ARB with new diagnosis for HFrEf and admitted to hospital
92
when should ARNI use be avoided?
eGFR <30mL/min, K>5.2, symptomatic hypotension + SBP <100, hx of angioedema
93
when switching from ACE to ARNI, you need a __hr washout period
36
94
what should be monitored with ARNI?
1. SCr and K at baseline, w/i 1 week, 1 month, q3 months (more frequent if dehydrating illness)
2. lying and standing BP (llok out for orthostatic hypotension)
3. can monitor NT-proBNP, but BNP will be elevated due to the MOA
95
if the patient was on a low dose of ACE (<50% of target dose), what starting dose of entresto do you give?
50mg BID
96
if patient had been on a high dose ACE/ARB (>50% of target), what starting dose of entresto should you give?
100mg BID
97
entresto should be titrated every __weeks to a target dose of ___
3-6; 200mg BID
98
50mg entresto contains __mg sacubitril and __mg valsartan
24.3, 25.7
99
100mg entresto contains __mg sacubitril and __mg valsartan
48.6, 51.4
100
200mg entresto contains __mg sacubitril and __mg valsartan
97.2, 102.8
101
103 mg of valsartan in Entresto is equal to ___mg of valsartan in Diovan
160
102
what are the exception status qualifications for entresto?
LVEF <40%, NYHA 2-3 despite 4 weeks of stable doses of: ACE/ARB, BB,and other recommended therapies like MRA
103
patients should be ___ before starting BB if they are NYHA class IV
stable
104
BB are clinically proven in patients with LVEF ___% or less
40
105
which BB trials showed decreased HF hosptalizations?
CIBIS 2 (bisoprolol) and COPERNICUS (carvedilol)
106
what was found in the COMET trial? why is it controversial?
1. compared carvedilol and metoprolol tartrate and found carvedilol had lower deaths.
2. controversial over whether tartrate was the best formulation compared to succinate
107
significant improvement in LV function from BB may take ___months
6-12
108
patients may notice that their HF symptoms may get worse for ___(length of time)while on BB before it gets better
days to weeks
109
if reactive airways are present, what BB should be used?
bisoprolol
110
if a patient is hypotensive while in a BB, what should be done?
consider decreasing the dose of other medications or change the timing and spacing of doses
111
if a patients has bradycardia while on BB or AV block is present, decrease or stop what other medications?
digoxin or amiodarone if appropriate
112
BB should not be abruptly stopped unless patient is experiencing ___
cardiogenic shock
113
when a patient presents with new HF, should we start a BB or ACE first?
CIBIS 3 found that there is no significant difference in what one you start
114
MRAs are recommended for HFrEF when symptoms are of what level?
moderate to severe
115
what was found by the RALES trial?
spironolactone 25mg daily vs placebo (both also taking ACE and LVEF <35%) found increased survival and decreased HF hospitalization in spironolactone group
116
a trend was seen where spironolactone Rx increased after the rales trials, but what also increased?
death from hyperkalemia
117
what was found in the EMPHASIS-HF trial?
patients on ACE/ARB randomized to eplenerone 50mg vs placebo and found that drug decreased death and HF hospitalization, did find more K abnormalities
118
when should MRA be avoided?
CrCl<30ml?min, K>5, on other K sparing diuretics
119
what drugs should be avoided in MRA to avoid hyperkalemia?
NSAIDs and sulfamethoxazole/trimethoprim
120
start spironolactone at ___ and titrate to ___
12.5mg, 25-50mg daily
121
start eplenerone at ___mg and titrate to ___
25mg, 50mg daily
122
what should be monitored on MRA?
K at baseline, 1 week, 1 month, every 3 months and increase frequency when acute dehydrating illness
123
supplemental K is not recommended unless K is < ____
4 mmol/L
124
why is eplenerone associated with less gynecomastia than spironolactone?
it has better affinity for teh mineralocorticoid receptors and less affinity for hormone receptors
125
what were the findings of the DAPA-HF trial?
dapagliflozins 10mg UID vs palcebo (patients already on standard GDMT), found decreased hospitalizations and death and it did not matter if they had DM or not
126
what was found in the EMPEROR-reduced trial?
emapgliflozin 10mg UID (basically the same as dapagliflozin)
127
which NYHA classes were found to be most likely to benefit form SGLT2?
2 more than 3-4
128
what is the CCS recommendation for SGLT2?
for those with mild to moderate HfrEF to improve symptoms, QOL, and reduce risk of HF hospitalizations and or CV death
129
what is the coverage issue with SGLT2?
only covered if they have T2DM
130
what is the most common ADR of SGLT2-i?
genital mycotic infections
131
SGLT2-i may temporarily decrease eGFR by ___% and this typically takes how long to resolve?
15-20%, 1-3 months
132
should SGLT2 be held on sick days
yes
133
there is a rare risk of DKA with normal glucose levels in SGLT2, what can be monitored if it is suspected?
serum ketones
134
SGLT2-i can contribute to diuresis, so you should keep an eye on volume status and possibly decrease loop diuretic dose by ___%
30-50
135
what are the ionotropic effects of digoxin?
increased ventricular force of contraction, increased contractility
136
what are the chronotropic effects of digoxin?
increased parasympathetic tone, lowered HR
137
how does digoxin increase ionotropy?
inhibit Na/K exchange, which causes more Ca to be released, which increases contractility
138
how does digoxin decrease chronotropy?
increase parasympathetic activity of AV node, slowing AV conduction to decrease HR
139
of ionotropic and chronotropic activity, which does digoxin increase and which does it decrease?
increase ionotropic and decrease chronotropic
140
what was found by the DIG trial?
digoxin reduced HF hospitalization compared to placebo
141
what is the main goal with digoxin therapy?
improving symptoms, QOL and exercise tolerance
142
what is the typical dose of digoxin? wha does it depend on?
0.0625mg - 0.25mg; depends on age and renal fx
143
there is no reason to monitor digoxin levels unless toxicity is suspected, but if you are going to take it, you should draw when its at ___level or at least __hrs post dose. Why?
trough level or 6-8 hrs after dosing to allow for distribution
144
what is teh target concentration for digoxin in HF?
<1.3nmol/L
145
tell me everything you know about the Vd of digoxin
4-7L/kg due to extensive tissue binding and is not affected by obesity bc it is not very lipophillic and dosing should be based on ideal body weight
146
tell me everything you know about the elimination of digoxin?
renal 60-80%, excreted unchanged in teh urine, teh otehr 1/3 is excreted by teh hepatobiliary route
147
what is the T1/2 of digoxin?
30-40 hours
148
how long does it take digoxin to reach steady state?
6-8 days
149
digoxin is a substrate and inhibitor of ___ and this causes many drug interactions
PgP
150
how should the interaction between digoxin nad amiodarone or verapamil be managed?
reduce digoxin by 50%
151
aside from amiodarone and verapamil, what otehr drugs interact with digoxin? How should these interactions be managed?
clarithromycin, cyclosporine, diltiazem, erythromycin, itraconazole, ketoconazole, propafenone: adjust, monitor serum digoxin levels and adjust accordingly, consider empiric dose reduction
152
drugs and diseases that alter electrolytes affect digoxin levels. What is the effect of hypokalemia on digoxin?
increased digoxin toxicity
153
what is the effect of hypothyroidism, old age and renal dysfunction on digoxin levels?
increased digoxin levels and decreased Vd
154
other than toxicity, when might you get a digoxin level?
when starting or stopping interacting drugs
155
t/f the ADRs and toxicity of digoxin are dose-related
t
156
what are the CNS ADRs / signs of toxicity of digoxin?
disorientation, confusion, depression
157
what are the visual disturbances / signs of toxicity in digoxin?
blurriness, yellow/green vision, dark or movinf spots, photophobia, halos
158
t/f digoxin can cause arrhythmias
t
159
what are some of the GI ADRs / signs of toxicity of digoxin?
anorexia, nausea, vomiting, diarrhea
160
what is the antidote for digoxin?
DigiFAB, an antibody fragment that binds to digoxin
161
when is digiFAB indicated?
life-threatening toxicity
162
According to teh IWK, when is digiFAB indicted?
when digoxin toxicity causes: tachy or brady-arrhythmias, hypotension, hyperkalemia (greater than 5 mEq/L) and/or a digoxin serum level of greater than 12.8 nmol/L (greater than 10 ng/mL).
163
what are suggestions for digoxin use from teh CCS?
1. if patients with HFrEF in sinus rhythm who continue to have moderate to severe symptoms despite optimal GDMT
2. in patients with HFrEF and AF with poor rate control or persistent symptoms despite optimal BB or if BB not tolerated
164
what is the MOA of nitrates in HF?
venous dilation, reduces preload
165
what is the MOA of hydralazine in HF?
aterial dilation and reduces after load
166
what is the combined role of nitrates/hydralazine for HF?
relive Sx of HF and increase exercise tolerance
167
what are the ADR of nitrates/hydralazine?
hypotension, headache, dizziness
168
what should be monitored when on nitrates/hydralazine?
BP and HR
169
what were the findings of the V-HeFT trial?
looked at hydralazine/ISDN in patients already taking digoxin and loop diuretic and found that this combo had lower mortality and prazosin had no benefit
170
what were the findings of the V-HeFT trial?
looked at hydralazine + ISDN vs enalapril and found that enalapril was superior
171
what are the CCS recommendations for nitrate+hydralazine use?
1. patients with HFrEF unable to tolerate ACE, ARB, or ARNI due to hyperkalemia or renal dysfunction
2. in black patients in addition to regular GDMT with advanced sx
172
what is the MOA of Ivabradine?
selectively inhibits the depolarizing If current in the SA node
173
what were the findings of the SHIFT trial?
looked at NYHA 2-4 with normal sinus rhythm, resting HR >70, LVEF 35% and HF admission in past 12 months and found that ivabradine in addition to GDMT decreases CV death and HF admission
174
Ivabradine can be considered for what patients?
symptomatic depsite adequeate GDMT, resting HR >70, sinus rhythm, hospitalization in past 12 months
175
what is the dose and titration for ivabradine?
2.5-5mg PO BID with food; titrate q2-4 weeks to max of 7.5mg PO BID with food
176
dose ivabradine to target a HR of ___
50-60 BPM
177
t/f ivabradine is typically initiated by a specialist
t
178
what are the drug interactions with ivabradine?
CYP3A4 inhibitors
179
ivabradine is C/i when taking what other medications?
amiodarone, digoxin, simvastatin
180
what are the ADRs of ivabradine?
bradycardia, AF, flashes of light
181
will ivabradine lower BP?
it should not, as it is meant to be specific to the SA node
182
drug coverage for ivabradine
exception status
183
what is the role for diuretics in HF?
relieve signs/sx of Hf such as edema, congestion, SOB, weight gain
184
what is the goal of diuretic therapy in HF?
achieve dry weight wile avoiding dehydration, hypotension, and renal dfx
185
which type of diuretic is recommended for most patients with congestive symptoms (volume overload)?
loop diuretics like furosemide
186
loop diuretics have more intense diuresis and natriuresis than ____ diuretic s
thiazide
187
thiazides are not commonly used for HF with the exception of ___, which is ADDED to loop diuretics if there is diuretic resistance
metalozone
188
t/f the lowest effective dose of loop diuretics should be used
t
189
what should be monitored on furosemide??
electrolytes (Na, K, Ca), SCr, urea, lying and standing BP and daily weights
190
what is the typical PO dosing for furosemide?
20-40mg PO BID with increased dose for renal impairment
191
t/f some patients may take furosemide on a sliding scale based on weight gain
t
192
what are the 3 loop diuretics?
1. furosemide
2. bumetanide
3. ethracrynic acid
193
tell me what you know about bumetanide
it is a daily loop diuretic and it is very rarely used
194
if someone has a true allergy to furosemide, what drug are they given>
ethacrynic acid
195
is ethacrynic acid daily or BID dosing?
BID
196
HFpEF is also known as ____ heart failure
diastolic
197
__% of patients with heart failure have HFpEF
50
198
HFpEF is most common in what [atient population?
elderly women, longstanding HTN
199
t/f the morbidity (i.e. hospitalizations) are similar in HFpEF to those of HFrEF
t
200
explain the pathophysiololgy of HFpEF
there are abnormalities in diastolic function (relaxation and or stiffness), the ventricle cannot accept adequate blood volume during diastole and the volumes are not enough to maintain appropriate stroke volume
201
what are the 4 principles of HFpEF?
1. identify and treat underlying things that may have caused them to develop HFpEF
2. identify and treat comorbid conditions that might worsen HF
3. control their symptoms
4. realization of clincally relavant CV end points like hospitalization and mortality
202
the CCS suggests which ARB could be considered for patients with HFpEF?
candesartan
203
for HFpEF, the CCS recommens that ____ be controlled
HTN (strong recommendation)
204
for HFpEF, the CCS recommends the use of ____ to control symptoms of congestion and peripheral edema
loop diuretics
205
for HFpEF patients with serum K <5.0mmol/L and eGFR >30mL/min, the CCS suggests the use of _______ with close SCr and K monitoring
MRA like spironolactone
206
what were the findings of the CHARM-preserved trial?
looked at candesartan 32mg for EF>40% and found no difference in cardiac death or HF hospitalization unless it was their first HF hospitalization
207
what was found in the i-preserved study?
looked at irbesartan 300mg daily vs placebo for EF>45% and found no difference
208
what was found in the PEP-CHF trial?
looked at perindopril 4mg daily vs placebo for EF>40% and found no difference in death or unplanned hospitalization (but also may decrease hospitalization?)
209
what was found about BB for use in HFpEF from observational studies?
BB statistically benefit all-cause mortality with no benefit in terms of HF hospitilization
210
what was found about BB for use in HFpEF from 2 RCTs?
that BB had no significant decrease in all-cause mortality or HF hospitalization
211
what was found from the TOPCAT trial?
spironolactone 15-45mg po daily NYHA EF>45% and found spironolactone vs placebo had no significant effect on death, but did decrease HF hospitalization (however, there was higher K and SCr )
212
what was found from the PARAGON HF trial?
looked at ARNI (entresto 97/103mg BID) for HFpEF and found no significant difference in HF hospitalizations of death. They were more likely to have hypotension and angioedema but less likely to have hyperkalemia
213
what is acute decompensated HF?
term used to describe worsening signs & symptoms of HF usually caused by volume overload or hypoperfusion that leadds to additional medical care like ER visits and hospitalizations
214
what are 4 common etiologies of acute decompensated HF?
1. diet, Rx and non-Rx medications
2. non-adherence
3. concurrent illness like infection
4. cardiac event like MI, arrhythmia, HTN, valvular insufficiency
215
what are the goals of therapy for acute decompensated HF?
reduce mortality, address underlying causes and triggers, get volume back to normal, treat congestive sx, treat sx of low CO, prevent readmissions, optimize QOL
216
give a simple explanation of how acute decompensated HF is treated
1. determine if its wet or dry (if wet, give IV diuretics like furosemide +/- nitrates like IV NTG or topical nitrates), if its dry, may require careful fluid resuscitation
2. determine if cold or warm (cold means poor perfusion to the periphery due to low CO)
217
what is the most common type of acute decompensated HF?
wet with cold
218
what is cardiogenic shock?
acute decompensated HF with critically low optput resultsing in organ system dysfunction
219
what is used to treat cardiogenic shock?
ionotropes and or vasopressors as IV infusions to increase CO and or maintain sufficient BP in acute care setting
220
what are 2 ionotropes that are used for treatment of cardiogenic shock?
dobutamine and milronone
221
give 2 examples of vasopressors used for the treatment of cardiogenic shock2
NE and epi
