CHF (aka 1 whole cardiology fellowship in an hour)

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CHF (aka 1 whole cardiology fellowship in an
hour)

• Shawn Dowling, PGY 0.9 or 1.9?

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Epidemiology

• Currently, over 500,000 Canadians have HF
• 50,000 new cases per year
• MC reason for A in those gt65yoa
• Only CVS disease that is ? in prevalence
• One year MR after Dx ranges from 25-40, gt50 at
  5 years (Framingham Heart Study)

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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 bodys 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)

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Just a touch of Physiology

• Cardiac Output ? X
• _____ ____ - _____
• BP _____ x _____

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Just a touch of Physiology

• Cardiac Output HR X SV
• SV preload contractility- afterload
• BP SVR x CO

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• 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

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• 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

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• Afterload
• Mural tension on cardiac cells during ventricular
  contraction
• Fx of SVR and cardiac chamber size

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Optimal Curve
?Contractility
Heart Failure
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Pressures
HP
COP
Pulmonary Vessels
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Putting it together

• In CHF
• ? in LVEDP ? ? Pulm HP (usu gt20) ? 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

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The prerequisite boring stuff
MALADAPTIVE over time!!!
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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

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Its actually quite simple If you just remember
RAS/ neurohormonal fundamentals
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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.
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CHF

CHF
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Adrenergic NS
F-S mechm Hypertrophy
Compensatory mechm
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Nuff Physiology
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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)

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Systolic vs Diastolic

• Systolic (2/3)
• (inadequate contn)
• Impaired contractility
• Impaired SV /- EF
• Sx of ? CO

• Diastolic (1/3)
• (inadequate relaxn)
• ? LV compliance
• LV filling pressure
• Venous congestion

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Impaired Contractility 1.MI 2.Chr volume
overload -MR -AR 3. Dilated CM

• ?? Afterload
• 1. AS
• 2. HTN

Systolic Dysfx
L-sided HF
Diastolic Dysfx
Impaird Vent Relaxn 1.LVH 2.Hypertrophic
CM 3.Restrictive CM
Obst to LV Filling 1.MS 2.Pericardial Consn or
tamponade
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Case 1

• 79 yo man
• CC Dyspnea sats were 83 via EMS
• PMHx ???
• Meds metoprolol, ramipril, nitrates (hasnt
  used in mts), lasix (no ? dose), advil,
  allopurinol,
• Approach? Dx? Precipitant?

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Case 1 (cont)

• ABCs IV, O2, monitored bed
• Hx, P/E
• Investigations?
• Reversible causes - i.e. ??

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• 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

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Hx

• Sx of CHF
• L sided Sx
• SOB, SOBOE
• PND(?), Orthopnea(?)
• Fatigue/confusion
• R sided Sx
• Peripheral edema
• RUQ pain

• ? pointing to etiology
• CP or angina equivalent
• Palpitations
• Change in Rx/new Rx
• Change in diet
• Blood loss

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P/E findings in

• What we hear in the ER
• ? HR(ANS), ? RR
• Diaphoresis (ANS)
• Crackles / wheezes
• JVD (50 pts)
• Peripheral edema (1/3 pts)
• Hepatomegaly / HJR/Kussmauls sign (?)
• Peripheral Perfusion

• What the Cardiologists claim to find on p/e
• S3 (25), /- S4
• Loud P2
• Pulsus Alternans
• PMI laterally displaced

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Investigations

• Labs CBC, lytes, Cr/BUN, trop, ?miracle test
• ECG
• CXR

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So you think it CHF

• Whats 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

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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?

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Brain Natriuretic Peptide
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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 its physiologic role later

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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

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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 106416-422
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• Prospective diagnostic test evaluation
  international multicentre
• 1586 pts,
• CHF Dx made by two cardiologists (reviewed
  charts, blinded to BNP results)

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• Treating MDs 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
• EPs or Internists

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675
346
110
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• 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.

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• 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

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• 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 (7286)
• Specificity - 71 (6676)
• PPV - 58 (5165)
• NPV - 87 (8391)
• LR -2.7 (2.23.3)
• LR - 0.3 (0.20.4)

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• 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)

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Diagnostic Algorithm

• ProBNP lt300 CHF unlikely (NPV 99 - dont
  mention Sens/Spec)
• ProBNPgt10,000 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 gt75 - 1 pt
• Rales on lung exam 1 pt
• Absence of a cough 1 pt

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• Score gt 7 high predictive value of CHF
• Sens 90, Spec - 90, PPV 83

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• RCT, ED setting
• N452 BNP (225) or no BNP (227)
• Told treating MD if lt100 CHF unlikely, gt500 CHF
  likely, 100-500 indeterminate
• Endpoints
• LOS and costs

aka BASEL study
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• BNP
• ? Time to Tx
• ? hospitalization,
• ?ICU admissions,
• ?LOS,
• ?costs

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CHR

• ? Getting it, ? When
• Likely getting proBNP (ntBNP)
• Run on the same machine as trops therefore approx
  approx same wait

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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, gt10,000 CHF)
• And some sort of scoring system/further
  investigations to assess those in the middle

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CHF w/N heart size?

• Is this possible?
• Whats your DDx?
• Cardiac v- non-cardiac
• Acute
• Chronic

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Case 2

• 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

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Class of CHF - Killip

• Derived retrospectively in the 60s, 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
  Oct20(4)457-64.

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NYHA Classification

• Class I No limitation of physical activity
• Class II Slight limitation of activity. Dyspnea
  and fatigue with moderate activity (gt2flights of
  stairs)
• Class III Marked limitation of activity. Dyspnea
  and fatigue with minimal activity (i.e. lt 2
  flights of stairs
• Class IV Severe limitation of activity. Sx are
  present at rest

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Treatment Goals

• Improve Oxygenation (AB)
• Decrease PA pressures while maintaining adequate
  cardiac and systemic perfusion i.e. ? congestive
  state (C) via
• ?Cardiac workload (?pre/afterload)
• Controlling excessive Na/H20 retention
• Improve cardiac contractility

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Treatment Modalities

• TREAT PPTs (shock em, cath em, dialyze em or
  cut em)
• Lasix
• Morphine
• Nitro
• Oxygen
• Position pt/ve pressure vent/Invasive vent
• Novel RX (nesiritide, ACE I)

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Jessup 2003, NEJM
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Lasix?

• The benefits of lasix(esp early) are primarily
  from its venodilation properties, not its
  diuretic effects
• But, lasix ramps up the neurohormonal pathways
  and can precipitate cardiac arrhythmias and death

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• 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

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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

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Nitro?

• Increase cGMP and causes vasodilation
• Nitrates ? nitrites ? NO ? cGMP ? vasc smooth
  muscle relaxn
• Primarily a venodilator- ? preload _at_ ?doses
• Can cause arterial dilation - ? afterload _at_ ?
  doses
• Shown to be effective in ? MR and improving Sx

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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

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Back to the Case

• 69 yr lady continues trying to die on you despite
  maximized medical management
• Shes 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?

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Non-Invasive Ventilation

• ? FRC, ? oxygenation, ?WOB, ?pre/afterload
• CIs
• 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

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Evidence for NPPV in CHF

• Meta-analysis
• 3 RCTs of CPAP, 1 RCT of CPAP vs. BiPAP
• Results
• CPAP
• decs intubation rate RRR 26 (13-38)
• Trend to decd 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
• CPAPgtBiPAP 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 1141185-1192
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Niseritide?
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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

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IV Nesiritide vs Nitroglycerin in the therapy of
decompensated CHF(VMAC)

• DB-RCT, approx 500 pts
• 1? endpt PCWP
• 2? endpt Sx relief _at_ 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, p0.32

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• 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 , p0.059(niseritide v- std
  Tx)
• Nesiritide manufacturers sponsored the study
• SUMMARY No benefit, likely more bad than good

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ACE-Inhibitor?
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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

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ACE-I

• Hamilton et al, Acad Emer Med, 19963205-212.
• DB-RCT, captopril vs placebo std Tx
• Captopril group had better improvement (43 vs
  25, p0.03, less intubation (9 vs 20 not
  s.s.)
• Sacchetti et al showed that it decreased the
  admissions to ICU odds ratio 0.29

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Role of ACE-I

• ???
• ?Consider in sick CHFers
• Add if other therapies are not working
• Formulations in the CHR

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Summary

• BNP has a role, still trying to figure out
  exactly what/how it will fit in
• Nitrogtlasix
• Morphine maybe - not a first line Rx
• PPV yes - very effective
• ACE-I yes- but for who?
• Niseritide No
• Pressors Yes (not discussed here)