67. Heart Failure Flashcards
Heart failure: 3 components involved
structural or functional abnormalities of CV
elevated Intracardiac pressures or depressed CO
clinically recognizatble s or s due to elevated IC pressures or depressed output
HF with reduced EF defn
<40%
HF midrange Ef
40-50%
HF preserved EF
> 50%
Risk factors for HF
age
obesity
htn
dm
tobacco smoking
dld
low ses
ischemic heart disease
CO equation
CO = heart rate x edv x ef
which really means chrontropy (speed) x lusitropy (rate of myocardial relaxation) x inotrophy (squeeze amount)
What does the Frank Starling mechanism do?
talk about relationship between stroke volume (squeeze amount each beat) and EDV (heart ability to relax to fill)
Frank Starling: in an ideal scenario how do sv and edv work together?
EDV increasing leads to increasing SV because of the stretch, allows for greater contraction
ie preload under ideal conditions
Repeated exposures to increased LVEDV (and resultant LVEDP) cause fibrosis and myocardial hypertrophy that ultimately lead to a what kind of ventricle?
stiff
noncompliant
ultimately diastolic dysfunction
What other organ systems and processes can influence HF - ie decreased cardiac output and incr filling pressures?
- Vascular: incr systemic artery tone, loss of laminar flow and impaired ventricular vascular coupling
Microvascular and coronary dysfunction, ischemia - Volume distribution or retension can lead to reduced capacitance of venous reservoirs
- Neurochem/autonomic activity at the brain
- Endocrine responses to stress
- Pulmonary: resp failure, decreased endc organ o2 delivery, impaired RV/PA coupling
- Renal dysfunction and diuretic R
- Coagulaopthy - abnormal RBC mass
What ventricular changes may ensue specifically from diastolic dysfunction? (specific to other heart functions)
decreased myocardial oxygen reserve, abnormalities in nitric oxide signaling, decreased aortic and pulmonary artery compliance, decreased ventricular volume, right ventricular dysfunction, and worsening interventricular and ventricular-circulatory coupling, resulting in depressed tolerance of increased preload and afterload
How does the heart compensate for its diastolic dysfunction (change in EDV) - effects what other CO parameter?
HR - to a degree
hence at certain point even further tachy is detrimental because the heart cannot go any further
Natriuretic peptides are upregulate in heart failure - why?
due to changes in FS curve so that they induce natriuresis and diuresis, vasodilation and antifibrotic effects to remodel to heart
How do the major classes of therapies for Acute HF work?
either by moving the Starling curve left- ward with diuretics or venodilators (decr preload), moving the curve upward to a higher level of efficiency for a given EDV with inotropes or arterial vasodilators (SV), or both
Simple but useful hemodynamic classifcation of hF in the ED - is it a c__ problem or a v___ problem
cardiac (ie, primary pump failure predominates) and vascular (ie, acutely increased preload or afterload predominates) phenotypes of AHF
Central congestion defn Ac HF
true vol overload with excessive intake effecting vena cava/great arteries or proximal organs vs retension - typically via poor pump)
What is one of the largest critical venous reservoirs?
splanchnic circulation
What 3 endocrine/systems may cause the splanchnic circulation to dilate/contract?
central circulation baroreceptors
sympathetic tone
Renin angiotensin aldosterone system
What, under normal circumstances, can act like a buffer to maintain central volume in the splanchnic circulation?
hepatic veins
Hepatic veins, under normal circumstances, can act like a buffer to maintain central volume in the splanchnic circulation - how does this change in HF?
neurohormonal mediators are chronically activated, leading to basal splancnic vasoconstriction and a reduction in the buffer capacity – so fluid shifts can happen more acutely with a “lesser” stress than normal
Afterload: what is this?
pressure at which ventricle must contract to eject blood
ie aortic and pulmonary a pressure for LV and RV respectively
Afterload: What ventricle is more sn to presure and volume tolerant?
RV
Afterload: as this rises, what happens to SV?
declines until extreme pressure reached, then worsening function as ventricle cannot overcome
What is ventricular vascular decoupling?
ratio of o2 consumption to stroke work increases as afterload rises
heart already diminished o2 at baseline, now has less
In flash pulmonary edema, what is happening at the level of the heart?
severe afterloador hypertensive form of acute heart failure
Heart failure - can also have asynchrony of contracting parts play a role - why might this happen?
fixed - ie MI scar
vs
transient: localized demand ischemia
What treatments of heart failure help with synchronicity of the heart?
nippv
diuresis and vasodilation
Acute heart failure triggers: FAILURE
Failures:
forgot meds
arrh/anemia/AS/aorta
ischemia/hypoxemia/infxn/infarction
lifestyle (salt)
upreg: infxn, anemia, thyroid, pregnant
renal failure
emboli
Most sn symptom and sign?
dyspnea
peripheral edema
Investigations for HF
ecg
trop if ischemia
cbc and chem7 if anemia, hypona
cxr- cardiomegaly best
BNP is no better than erp gestalt (>1500 yes, <300 no, between hard)
POCUS!! - B lines +
PPV HAVoc HF tx
PPV or HFNC
Hypotnesion
afterload reduction with NTG
vol status - diureiss if + hypervolemic
cause - fix it
Time to diuresis matters for ICU, mortality - in HF
diuresis within 1 hour
SCAPE tx
will have high BP - target sbp 140
bipap
oxygen
nitro bolus 1000mcg x3 SL vs IV OR
NTG infsuion start @ 100mcg/min with rapid titration 100 to 200 to 400 to 800
if refractory to NTG - 800mcg/min consider nicardinpine, captoprik, enalaprilat
Cardiac phenotype: clinically -
normotensive
peripheral overload
Cardiac phenotype: HF tx
diuresis - home dose of 40 if naiive vs 1-2.5x home dose –> consider ckd/hrs if resistant
NIPPV
NTG
if R - acetazolamide 250-500mg
3rd type of HF:
cardiogenic shock
(vs vascular problem or cardiac pump problem)
HF: tx of pulmonary edema and hypotension?
PPV
vasopressors
HF tx of afterload if hypertensive?
ntg
diuresis
HF: optimize vol status: 2 ways to do that?
diuresis
iv vol repletion
shock index calculation
HR/SBP >0.8
has to be sinus rhythm and no chronotropes
Signs of end organ perfusion issues from cardiogenic shock
oliguria
aki
shock liver
lactic acidosis
aloc
shock index >0.8
skin delayed cap refill
Narrow pulse pressure <25% sbp suggest poor CO
Forrester classifications:
class I - IV
warm and dry
warm and wet
dry and warm
dry and cold
SCAI shock classification
A-E
At risk, beginning, classic, deteriorating, e
looks at PE, biochemical markers, HD
POCUS in cardiogenic shock: look at:
b line >15cm down
global lb function
vol status
RV dysfunction: signficant predictors of RVD
missed antiHTN meds within 7d
ED PPV
copd hx
LVEF
lung u/s congetion severity
RV systolic pressure
Acute myocardial infarction KEY two things for defn
cTn elevation is above 99th % for a given assay
clinical suspicion for ischemia
Cardiorenal syndrome defn
worsening renal function due to acute heart failure
How much CO do kidneys receive at given point?
25%
Even a slight elevation in CVP therefore causes renal venous hypertension which can lead to …
central congestion
and aki
Management of AS in HF
phenlyephrine
tachy down as much as possible
need some volume avoid NTG
Type 1 MI as cause of AHF - tx
pci
Type II MI as cause of AHF - tx
optimize o2 mismatch demand with tx cause
directed therapy to optimize preload, afterload, diuresis, NIPPV, vasodilation
MC rhythm causing AHF
afib
Name 5 precipitate of HF
Ischemia
Infection
Arrhythmias
Med no adherence
CRS
Two main mechanisms behind CRS
- Venous hypertension from central circulation congestion
- Peripheral vasoconstriction limiting arterial flow to kidneys
HF signs on CXR
Pulmonary edema
Capitalization
Kerley B lines
- can have n cxr
Name 8 ddx for acute heart failure
Pneumonia
COPD/astham exacerbatuon
ACS
Unstable tachy or Brady arrhythmia
ARDS
Anemia
CRS
severe metabolic acidosis or tox phenomenon
No cardiac causes of pulmonary edema - cirrhosis, amlodipine. PVD, nephrotic syndrome, venous thrombosis
PE
PTX
COVID
Best + LR HF
Hx ckd
Hx hf
Orthopnea
JVD
ISCHEMIC change ecg
Kerley B lines cxr
Interstitial edema
BNP > 450 if age <50 / BNP > 500 all comers
Best - LR HF
Exertional dyspnea
Any pulmonary edema on cxr
BNP > 100, pro bnp > 450 in <50y
POCUS 6-8 point B lines
Lab tests for hf
CBC
Lytes
Trop
Bnp
Chem 7
TSH
What bnp basically rules out hf
< 100
What effects natriueritc peptide and how?
Obesity - decreases concentration
CKD-incr
What is an 8 point lung exam?
Two anterior and two lateral pics in each hemothorax - positive if 3 or more B lines are present in at least one ICS on each side
Cardiogenic shock findings in HF
AMS
elevated serum lactate
oLiguria
Cold extremities
SBP <90 after adequate fluid resuscitation
Breathing support in HF
BIPAP/cpap (NIPPV)
Then if CI
HFNC
3 main phenotypes of HF
CS
Cardiac - SBP 90-140; slow progression more edema = diuresis
Vascular - >140 - dyspnea dramatic onset +- peripheral edema
= Ntg 0.4mg SL .lx1-5
If persistent high - ntg 1-2mg iv push or possible infusion 0.3-0.5 micro gram per kg per min
+/- furosemide diuresis
Tx of CS
Small bolus 250-500
Norepi
Once bp supported —> inotrope (dob vs mili)
Not stabilized - perc ventricular assist device or IABP or VA ecmo
Complications into cardiogenic shock of a HF pt?
Stemi
Mechanical - pap m rupture, septal rupture, free wall rupture
Hx of end stage HF, valvular disease or LVAR = mech support
Why does nitroglycerin work for vascular HF?
Reduces pre and after load
First dose loop diuretic in cardiac phenotype HF patients
40-80mg IV if naiivr
If at home, take PO dose and do IV
What decrease in urine output do I worry someone with HF has diuretic resistance
<140ml u/o per 40mg of IV furosemide in first 3 hours of presentation
If someone shows diuretic resistance in first 3 hours, what can you consider doing?
Repeat lasix at hour dose
Metolazone 5-10mg (non loop diuretic)
RF for loop diuretic R
CKD
Low albumin
Past hx R
Extremely low CO
more severe HF
High home dose lasix
Total urine sodium 1st hour after loop diuretic <480ml
Total yrine sodium in 1st hour post diuretic <35.4mmol
Diuretic efficacy at 3 hours <3.5ml urine/ng iv furosemide
If I am worried about the following scenarios in loop diuretics R, what should I use?
A. Unable to tolerate PO but want thiazide type diuretic
B. Metabolic alkalosis by chronic loop diuretic use
-. Chlorothiazide 0.5-1g IV
- acetazolamide 250-500mg Po
High risk features that may indicate admission of HF patient to ICU
Cardiogenic shock
Resp failure
HD unstable arrhythmias
ACS
Moderate RF of HF for admission to general unit?
Required IV vasodilator
Fluid overload requiring multiple diuretic doses
Comorbid complexity
New arrhythmia
New hepatic or renal dysfunction
Elevated trop with it ACS
RV dysfunction
PHTN
Hyponatremia
Worsening functional status
Low risk features of HF to d/c someone home
SBP > 160 without HTN emergency
Few comorbidities
Normal trop
Renal and hepatic function unchanged from BL
High diuretic efficiency in ED
List 5 meds involved in GDMT OF HFrEF
Beta blockers
Acei or arb or arni
Aldosterone antagonist if Lvef <=40% and eGFR > 30
Hydralazine isosorbide dinitrate if NYHA CLASS iii-iv
Loop diuretic if sign and sx congestikn
List 3 main ways to manage HFpEF
Med management htn and afib
Loop diuretic if sx and signs congestion
Clinical decision rules for Ed risk stratification of AHF
EHMRG
STRATIFY
RF for increased 7d mortality after discharge from ED for HF pt
Age > 80
Outpatient f/u within week decreases risk
SBP <100
Tachycardia
Bradycardia
Hypoxia on Ed arrival
Hyperkalemia
