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67. Heart Failure Flashcards

1
Q

Heart failure: 3 components involved

A

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

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2
Q

HF with reduced EF defn

A

<40%

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3
Q

HF midrange Ef

A

40-50%

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4
Q

HF preserved EF

A

> 50%

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5
Q

Risk factors for HF

A

age
obesity
htn
dm
tobacco smoking
dld
low ses
ischemic heart disease

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6
Q

CO equation

A

CO = heart rate x edv x ef

which really means chrontropy (speed) x lusitropy (rate of myocardial relaxation) x inotrophy (squeeze amount)

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7
Q

What does the Frank Starling mechanism do?

A

talk about relationship between stroke volume (squeeze amount each beat) and EDV (heart ability to relax to fill)

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8
Q

Frank Starling: in an ideal scenario how do sv and edv work together?

A

EDV increasing leads to increasing SV because of the stretch, allows for greater contraction

ie preload under ideal conditions

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9
Q

Repeated exposures to increased LVEDV (and resultant LVEDP) cause fibrosis and myocardial hypertrophy that ultimately lead to a what kind of ventricle?

A

stiff
noncompliant

ultimately diastolic dysfunction

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10
Q

What other organ systems and processes can influence HF - ie decreased cardiac output and incr filling pressures?

A
  1. Vascular: incr systemic artery tone, loss of laminar flow and impaired ventricular vascular coupling
    Microvascular and coronary dysfunction, ischemia
  2. Volume distribution or retension can lead to reduced capacitance of venous reservoirs
  3. Neurochem/autonomic activity at the brain
  4. Endocrine responses to stress
  5. Pulmonary: resp failure, decreased endc organ o2 delivery, impaired RV/PA coupling
  6. Renal dysfunction and diuretic R
  7. Coagulaopthy - abnormal RBC mass
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11
Q

What ventricular changes may ensue specifically from diastolic dysfunction? (specific to other heart functions)

A

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

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12
Q

How does the heart compensate for its diastolic dysfunction (change in EDV) - effects what other CO parameter?

A

HR - to a degree

hence at certain point even further tachy is detrimental because the heart cannot go any further

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13
Q

Natriuretic peptides are upregulate in heart failure - why?

A

due to changes in FS curve so that they induce natriuresis and diuresis, vasodilation and antifibrotic effects to remodel to heart

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14
Q

How do the major classes of therapies for Acute HF work?

A

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

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15
Q

Simple but useful hemodynamic classifcation of hF in the ED - is it a c__ problem or a v___ problem

A

cardiac (ie, primary pump failure predominates) and vascular (ie, acutely increased preload or afterload predominates) phenotypes of AHF

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16
Q

Central congestion defn Ac HF

A

true vol overload with excessive intake effecting vena cava/great arteries or proximal organs vs retension - typically via poor pump)

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17
Q

What is one of the largest critical venous reservoirs?

A

splanchnic circulation

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18
Q

What 3 endocrine/systems may cause the splanchnic circulation to dilate/contract?

A

central circulation baroreceptors

sympathetic tone

Renin angiotensin aldosterone system

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19
Q

What, under normal circumstances, can act like a buffer to maintain central volume in the splanchnic circulation?

A

hepatic veins

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20
Q

Hepatic veins, under normal circumstances, can act like a buffer to maintain central volume in the splanchnic circulation - how does this change in HF?

A

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

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21
Q

Afterload: what is this?

A

pressure at which ventricle must contract to eject blood

ie aortic and pulmonary a pressure for LV and RV respectively

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22
Q

Afterload: What ventricle is more sn to presure and volume tolerant?

A

RV

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23
Q

Afterload: as this rises, what happens to SV?

A

declines until extreme pressure reached, then worsening function as ventricle cannot overcome

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24
Q

What is ventricular vascular decoupling?

A

ratio of o2 consumption to stroke work increases as afterload rises

heart already diminished o2 at baseline, now has less

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25
In flash pulmonary edema, what is happening at the level of the heart?
severe afterloador hypertensive form of acute heart failure
26
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
27
What treatments of heart failure help with synchronicity of the heart?
nippv diuresis and vasodilation
28
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
29
Most sn symptom and sign?
dyspnea peripheral edema
30
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 +
31
PPV HAVoc HF tx
PPV or HFNC Hypotnesion afterload reduction with NTG vol status - diureiss if + hypervolemic cause - fix it
32
Time to diuresis matters for ICU, mortality - in HF
diuresis within 1 hour
33
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
34
Cardiac phenotype: clinically -
normotensive peripheral overload
35
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
36
3rd type of HF:
cardiogenic shock (vs vascular problem or cardiac pump problem)
37
HF: tx of pulmonary edema and hypotension?
PPV vasopressors
38
HF tx of afterload if hypertensive?
ntg diuresis
39
HF: optimize vol status: 2 ways to do that?
diuresis iv vol repletion
40
shock index calculation
HR/SBP >0.8 has to be sinus rhythm and no chronotropes
41
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
42
Forrester classifications: class I - IV
warm and dry warm and wet dry and warm dry and cold
43
SCAI shock classification
A-E At risk, beginning, classic, deteriorating, e looks at PE, biochemical markers, HD
44
POCUS in cardiogenic shock: look at:
b line >15cm down global lb function vol status
45
RV dysfunction: signficant predictors of RVD
missed antiHTN meds within 7d ED PPV copd hx LVEF lung u/s congetion severity RV systolic pressure
46
Acute myocardial infarction KEY two things for defn
cTn elevation is above 99th % for a given assay clinical suspicion for ischemia
47
Cardiorenal syndrome defn
worsening renal function due to acute heart failure
48
How much CO do kidneys receive at given point?
25%
49
Even a slight elevation in CVP therefore causes renal venous hypertension which can lead to ...
central congestion and aki
50
Management of AS in HF
phenlyephrine tachy down as much as possible need some volume avoid NTG
51
Type 1 MI as cause of AHF - tx
pci
52
Type II MI as cause of AHF - tx
optimize o2 mismatch demand with tx cause directed therapy to optimize preload, afterload, diuresis, NIPPV, vasodilation
53
MC rhythm causing AHF
afib
54
Name 5 precipitate of HF
Ischemia Infection Arrhythmias Med no adherence CRS
55
Two main mechanisms behind CRS
1. Venous hypertension from central circulation congestion 2. Peripheral vasoconstriction limiting arterial flow to kidneys
56
HF signs on CXR
Pulmonary edema Capitalization Kerley B lines * can have n cxr
57
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
58
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
59
Best - LR HF
Exertional dyspnea Any pulmonary edema on cxr BNP > 100, pro bnp > 450 in <50y POCUS 6-8 point B lines
60
Lab tests for hf
CBC Lytes Trop Bnp Chem 7 TSH
61
What bnp basically rules out hf
< 100
62
What effects natriueritc peptide and how?
Obesity - decreases concentration CKD-incr
63
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
64
Cardiogenic shock findings in HF
AMS elevated serum lactate oLiguria Cold extremities SBP <90 after adequate fluid resuscitation
65
Breathing support in HF
BIPAP/cpap (NIPPV) Then if CI HFNC
66
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
67
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
68
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
69
Why does nitroglycerin work for vascular HF?
Reduces pre and after load
70
First dose loop diuretic in cardiac phenotype HF patients
40-80mg IV if naiivr If at home, take PO dose and do IV
71
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
72
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)
73
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
74
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
75
High risk features that may indicate admission of HF patient to ICU
Cardiogenic shock Resp failure HD unstable arrhythmias ACS
76
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
77
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
78
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
79
List 3 main ways to manage HFpEF
Med management htn and afib Loop diuretic if sx and signs congestion
80
Clinical decision rules for Ed risk stratification of AHF
EHMRG STRATIFY
81
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

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