Transcript CHF - rEMERGs

CHF
(aka 1 whole cardiology fellowship in an hour)
Shawn Dowling, PGY 0.9 or 1.9?
Epidemiology
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Currently, over 500,000 Canadians have HF
50,000 new cases per year
MC reason for A in those >65yoa
Only CVS disease that is  in prevalence
One year MR after Dx ranges from 25-40%,
>50% at 5 years (Framingham Heart Study)
Definitions
• Congestive Heart Failure
– State in which the heart, at normal filling pressures, is
incapable of pumping a sufficient supply of blood to
meet the body’s metabolic demands
• Pulmonary Edema
– is a condition associated with increased loss of fluid
from the pulmonary capillaries into the pulmonary
interstitium and alveoli
– Cardiac vs non-cardiac (i.e. ASA, toxins, sepsis, ARDS, etc)
Just a touch of Physiology
• Cardiac Output = ? X $
• $ = _____ + ____ - _____
• BP = _____ x _____
Just a touch of Physiology
• Cardiac Output = HR X SV
• SV = preload + contractility- afterload
• BP = SVR x CO
• Preload:
– Amt of stretch at ventricle before contraction
– Determined by venous rtn and compliance
– Heart has an optimal preload that allows for
maximal output (fwd flow)
– Either  venous rtn/EDV or  compliance shift
increase preload and thus reduce optimal curve
• Contractility
– Amt of force generated by myocardium for a
given preload/afterload
– Directly related to Ca++
– Certain factors  contr
• Physiologic: O2, CO2, H+, ischemia
• Rx: ß-blocker, anti-dysrhythmic, Ca-antagonists,
barbituates, EtOH
• Afterload:
– Mural tension on
cardiac cells during
ventricular
contraction
– Fx of SVR and
cardiac chamber
size
Optimal Curve
Contractility
Heart Failure
Pressures
HP
COP
Pulmonary Vessels
Putting it together…
• In CHF:
 in LVEDP   Pulm HP (usu >20) 
transudation of fluids into the interstitium (exceeds
the ability of the lymphatics to compensate)  pulmonary congestion
 R heart failure from fluid overload  
forward flow ( CO) and “systemic
congestion”
The prerequisite boring stuff…
MALADAPTIVE over time!!!
Compensatory Mechanisms
•  CO/  in LVEDP triggers a number of
compensatory mechanisms
– Frank-Starling mechanisms ( stretch =  SV)
– Myocardial Hypertrophy ( LVEDP to
maximize F-S mechanisms)
– Neurohormonal changes
It’s actually
quite simple
If you just
remember
RAS/
neurohormonal
fundamentals
Neurohormonal
Here you go!
• Goal is to  CO via
– Adrenergic NS ( HR,
 cont,  PVR)
– RAAS activated via
kidney hypoperfusion
Mark, can you do the
bilateral Posterior
Shoulder dislocation
trick again.
CHF
+++
CHF
Adrenergic NS
F-S mech’m
Hypertrophy
Compensatory mech’m
‘Nuff Physiology
Types of HF
• Systolic vs Diastolic
• High-output vs Low-ouput
– What is it?
• RV –vs- LV –vs- Both (not going to talk
about isolated RV- consult pulmonary)
Systolic vs Diastolic
Systolic (2/3)
(inadequate cont’n)
Diastolic (1/3)
(inadequate relax’n)
Impaired contractility
 LV compliance
Impaired SV +/- EF
 LV filling pressure
Sx of  CO
 Venous congestion
 Afterload
Impaired Contractility
1.MI
2.Chr volume overload
-MR
-AR
3. Dilated CM
1. AS
2. HTN
Systolic Dysfx
L-sided HF
Diastolic Dysfx
Impair’d Vent Relax’n
1.LVH
2.Hypertrophic CM
3.Restrictive CM
Obst to LV Filling
1.MS
2.Pericardial Cons’n
or tamponade
Case 1
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79 yo man
CC: Dyspnea – sats were 83% via EMS
PMHx: ???
Meds: metoprolol, ramipril, nitrates (hasn’t
used in mts), lasix (no  dose), advil,
allopurinol,
• Approach? Dx? Precipitant?
Case 1 (cont)
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ABC’s – IV, O2, monitored bed
Hx, P/E
Investigations?
Reversible causes - i.e. ??
• P/E
– VS: 110/60, HR-90, RR-30, Sats –90% on
NRB, afeb
– JVP???, HS – present – too wheezy to hear
clearly
– Bibasilar crackles, peripheral edema
Hx
• Sx of CHF
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L sided Sx
SOB, SOBOE
PND(?), Orthopnea(?)
Fatigue/confusion
R sided Sx
Peripheral edema
RUQ pain
• ? pointing to etiology
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CP or angina equivalent
Palpitations
Change in Rx/new Rx
Change in diet
Blood loss
P/E findings in…
• What we hear in the ER • What the Cardiologists
claim to find on p/e
–  HR(ANS),  RR
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Diaphoresis (ANS)
Crackles / wheezes
JVD (50% pts)
Peripheral edema (1/3 pts)
Hepatomegaly /
HJR/Kussmaul’s sign (?)
– Peripheral Perfusion
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S3 (25%), +/- S4
Loud P2
Pulsus Alternans
PMI laterally displaced
Investigations
• Labs: CBC, lytes, Cr/BUN, trop, ?miracle
test
• ECG
• CXR
So you think it CHF…
• What’s your DDx
– Structural – think of the components of the heart
(arteries, nerves, myocardium, valves,
pericardium)
– Iatrogenic (Rx (what drug for this guy), diet,
fluids)
– Incompliant with meds
– Infection/Increased metabolic demand: H.O. HF
– Increased Afterload
The son arrives…
• Dad has a Hx of COPD – longtime smoker,
MI yrs ago
• SO is it CHF OR COPD????
• Anyone know of a blood test that may help?
• How should it be used?
Brain Natriuretic Peptide
BNP
• Polypeptide that is synthesized in the
ventricles in response to stretch/pressure
prePro-BNP  Pro-BNP  BNP (active) t1/2 =20 min
nt-BNP (inactive) t1/2 =120 min
• Released in proportion to LV expansion
reflecting the LVEDP
• Will discuss later it’s physiologic role later
What we do know
• N BNP levels are affected by age, renal fx,
drug use (bb & diuretics in particular)
• Correlates with NYHA Class HF
• Likely has a role in Screening, Dx, Tx, Px,
• FP-?chronic CHF
– R heart failure: PE, severe lung disease,
chronic/stable CHF
Should emergency physicians use B-type
natriuretic peptide testing in patients with
unexplained dyspnea?
• CJEM review of 2 articles:
NEJM 2002; 347: 161-167
Circulation 2002; 106:416-422
• Prospective diagnostic test evaluation
international multicentre
• 1586 pts,
• CHF Dx made by two cardiologists
(reviewed charts, blinded to BNP results)
• Treating MD’s* PTP (i.e., pre-BNP) of CHF
– 46.9% fell into the 0%-20% probability group,
– 27.9% fell into the 20%-80% (clinically
uncertain) group,
– 25.4% fell into the 80%-100% probability group
– EP’s or Internists
675
110
346
• BNP study authors concluded that based on
• That the rapid measurement of BNP, using a
cut-off value of greater than 100 pg/cc, will
improve clinicians' ability to differentiate
CHF from non-cardiac dyspnea in the
emergency department.
• Problem:
– Most of the patients (1514/1586) were either in
the CHF unlikely group (0-20% probability) or
in the CHF likely group (80-100%)
– Therefore the CJEM reviewers looked at
indeterminate group
• By setting a binary
cut-off of 100mcg
• Characteristics of the
test are much lower
than what was prev
stated
• Therefore these results
will not really help us
• Sensitivity – 79%
(72–86)
• Specificity - 71%
(66–76)
• PPV - 58% (51–65)
• NPV - 87% (83–91)
• LR+ -2.7 (2.2–3.3)
• LR– - 0.3 (0.2–0.4)
• Based on prior studies – BNP researchers
looked at absolute values and tried to risk
stratify based on these
• PRIDE study looked at proBNP(ntBNP)
• Retrospectively developed an Acute CHF
score (not yet prospectively validated)
Diagnostic Algorithm
• ProBNP <300 = CHF unlikely (NPV = 99%
- don’t mention Sens/Spec)
• ProBNP>10,000 = CHF likely (PPV = 94%
if prior Hx of CHF and 99% if no Hx CHF)
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Elevated proBNP (age cutoffs) – 4 pts
Interstitial edema on CXR – 2 pts
Orthopnea – 2 pts
Absence of fever – 2 pts
Current Loop Diuretic use – 1 pt
Age >75 - 1 pt
Rales on lung exam – 1 pt
Absence of a cough – 1 pt
• Score > 7 high predictive value of CHF
• Sens 90%, Spec - 90%, PPV 83%
aka BASEL study
• RCT, ED setting
• N=452 – BNP (225) or no BNP (227)
• Told treating MD if <100 CHF unlikely,
>500 CHF likely, 100-500 indeterminate
• Endpoints
– LOS and costs
• BNP
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 Time to Tx
 hospitalization,
ICU admissions,
LOS,
costs
CHR
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? Getting it, ? When
$$
Likely getting proBNP (ntBNP)
Run on the same machine as trops therefore
approx approx same wait
BNP in Summary
• Likely coming to the region
• Ongoing research as to how to use it
• Likely will be absolute cut-offs ( ie less than
300 no CHF, >10,000 CHF)
• And some sort of scoring system/further
investigations to assess those in the middle
CHF w/N heart size?
• Is this possible?
• What’s your DDx?
– Cardiac –v- non-cardiac
– Acute
– Chronic
Case #2
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68 y.o. female
CC: Dyspnea – progressive 2-3/7
PMHx: MI, CHF,
Meds: cardio cocktail (ASA, plavix, altace,
metoprolol, lipitor)
• VS: HR-120, RR-40, BP-110/80, sats-78%
Class of CHF - Killip
• Derived retrospectively in the 60’s, post-MI pts
I - No CHF - 5% mortality
II - Mild CHF (bibasilar rales and S3) - 15-25%
mortality
III - Frank pulmonary edema - 40% mortality
IV - Cardiogenic shock - 80% mortality
Killip T 3rd, Kimball JT. Treatment of myocardial infarction in a coronary care unit. A two
year experience with 250 patients. Am J Cardiol. 1967 Oct;20(4):457-64.
NYHA Classification
• Class I: No limitation of physical activity
• Class II: Slight limitation of activity. Dyspnea
and fatigue with moderate activity (>2flights of
stairs)
• Class III: Marked limitation of activity. Dyspnea
and fatigue with minimal activity (i.e. < 2 flights
of stairs
• Class IV: Severe limitation of activity. Sx are
present at rest
Treatment Goals
1. Improve Oxygenation (A&B)
2. Decrease PA pressures while maintaining
adequate cardiac and systemic perfusion
i.e.  congestive state (C) via…
A. Cardiac workload (pre/afterload)
B. Controlling excessive Na/H20 retention
C. Improve cardiac contractility
Treatment Modalities
• TREAT PPT’s (shock ‘em, cath ‘em, dialyze ‘em
or cut ‘em)
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Lasix
Morphine
Nitro
Oxygen
Position pt/+ve pressure vent/Invasive vent
Novel RX (nesiritide, ACE I)
Jessup 2003, NEJM
Lasix?
• The benefits of lasix(esp early) are
primarily from it’s venodilation properties,
not it’s diuretic effects
• But, lasix ramps up the neurohormonal
pathways and can precipitate cardiac
arrhythmias and death
• Dosing: ??
– No absolute dosing regime, dpnt on ?lasix
naïve, kidney function, route of administration
• High dose lasix and low dose nitro has
worse outcomes (MR) than low dose lasix
and high dose nitro
Morphine?
• Acts to  ANS,  agitation,  myocardial
O2 consumption
• Sacchetti et al showed it increased ICU
admissions – odds ratio 3.0
• No evidence for and mounting evidence
against
• Likely some role in extremely anxious
individual
Nitro?
• Increase cGMP and causes vasodilation
Nitrates  nitrites  NO  cGMP  vasc smooth muscle relax’n
• Primarily a venodilator-  preload @ doses
• Can cause arterial dilation -  afterload @  doses
• Shown to be effective in  MR and improving Sx
Nitrates
• Topical: onset in decreasing PCWP at 20 –
30 minutes with peak effect at 120 minutes
• IV: Dose is 10mcg/min and can be titrated
up every 3 – 5 minutes until desired effect
• Sublingual NTG: decreased PCWP by
36%. Onset was 4 min, peak at 9 minutes
• Spray: onset of 1-2 minutes with peak at 5
minutes
Back to the Case…
• 69 yr lady continues trying to die on you
despite maximized medical management
– She’s sating around 88%, ++WOB, RR starting
to fall, become more tired
– Still protecting her airway/secretions, BP = 110
– Is there anything you could do to help with her
respiratory status?
Non-Invasive Ventilation
•  FRC,  oxygenation, WOB, pre/afterload
• CI’s:
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Unstable
Not Breathing
Airway reflexes are absent
Unable to control secretions
Not cooperative & alert enough for NPPV
Unable to fit mask
Recent upper airway or GI surgery
?Ischemic Sounding CP
Evidence for NPPV in CHF
• Meta-analysis
– 3 RCT’s of CPAP, 1 RCT of CPAP vs. BiPAP
• Results:
– CPAP
• dec’s intubation rate RRR 26% (13-38%)
• Trend to dec’d mortality RRR 6.6% (-3 -16%)
– BiPAP vs. CPAP
• No significant differences but higher rate of MI in BiPAP
group ?due to baseline differences & early termination
– CPAP>BiPAP if possible
Pang D et al. The effect of positive pressure airway support on mortality and the
need for intubation in cardiogenic pulmonary edema: a systematic review.
CHEST 1998; 114:1185-1192
Niseritide?
Nesiritide
• Human recombinant BNP
• Throught to be a very sexy new drug for the
mgmnt of CHF in the US
• Like nitro, also  cGMP to cause
vasodilation and therefore  LV filling
pressures
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DB-RCT
Efficacy arm: niseritide –v-placebo
Comparative arm: niseritide –v- std therapy
RESULTS
– Efficacy arm: Niseritide had s.s. PCWP
– Comparative arm: niseritide had similar
improvements in clinical status, dyspnea and
fatigue when compared with std therapy
IV Nesiritide vs Nitroglycerin in the
therapy of decompensated CHF
(VMAC)
• DB-RCT, approx 500 pts
• 1 endpt: PCWP
• 2 endpt: Sx relief @ 3 hrs
• RESULTS
–  PCWP (and improved other cardiac indices)
– No improved Sx relief at 24hrs
– No significant difference in mortality at 18/12 (25% for
nesiritde, 21% Nitro, p=0.32
• Equivalent to Nitro (at best)
• Significant hypotension, bradycardia, renal dysfx
• Trend to higher MR
– JAMA, 2005. Pooled analysis of 860 patients
– MR was 7.2% v 4.0% , p=0.059(niseritide –v- std Tx)
• Nesiritide manufacturer’s sponsored the study
• SUMMARY – No benefit, likely more bad than
good
ACE-Inhibitor?
ACE-I
• Placebo-Controlled, Randomized, Double-Blind Study
of Intravenous Enalaprilat Efficacy and Safety in Acute
Cardiogenic Pulmonary Edema
– DB-RCT, enalaprilat (1mg/2 hours) –v- placebo
– Outcomes (all are hemodynamic parameters)
•  PCWP
•  diastolic and MAP
•  arterial oxygen tension
•  arterial oxygen saturation
ACE-I
• Hamilton et al, Acad Emer Med, 1996;3:205-212.
– DB-RCT, captopril vs placebo + std Tx
– Captopril group had better improvement (43%
vs 25%, p=0.03, less intubation (9 % vs 20%
not s.s.)
• Sacchetti et al showed that it decreased the
admissions to ICU – odds ratio 0.29
Role of ACE-I
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?Consider in sick CHF’ers
Add if other therapies are not working
Formulations in the CHR…
Summary
• BNP has a role, still trying to figure out exactly
what/how it will fit in
• Nitro>lasix
• Morphine – maybe - not a first line Rx
• PPV – yes - very effective
• ACE-I – yes- but for who?
• Niseritide – No
• Pressors – Yes (not discussed here)