CHF (aka 1 whole cardiology fellowship in an hour)

Shawn Dowling, PGY 0.9 or 1.9?

Epidemiology

• 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)

• Cardiac Output = ? X $

• $ = _____ + ____ - _____

• BP = _____ x _____

Just a touch of Physiology

• Cardiac Output = HR X SV

• SV = preload + contractility- afterload

• BP = SVR x CO

Just a touch of Physiology

• 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

Contractility

Heart Failure

Optimal Curve

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 simpleIf you just remember RAS/neurohormonal fundamentals

Neurohormonal

• 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.

Here you go!

CHF CHF+++

F-S mech’mHypertrophy

Adrenergic NS

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)

Impaired contractility

Impaired SV +/- EF

Sx of CO

Diastolic (1/3)

(inadequate relax’n)

LV compliance

LV filling pressure

Venous congestion

L-sided HF

Impaired Contractility1.MI2.Chr volume overload

-MR-AR

3. Dilated CM

Afterload

1. AS2. HTN

Systolic Dysfx

Impair’d Vent Relax’n1.LVH2.Hypertrophic CM3.Restrictive CM

Obst to LV Filling1.MS2.Pericardial Cons’n or tamponade

Diastolic Dysfx

Case 1

• 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)

• 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– 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

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/Kussmaul’s sign (?)

– Peripheral Perfusion

• What the Cardiologists claim to find on p/e– 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:

Circulation 2002; 106:416-422

NEJM 2002; 347: 161-167

• 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

110 346

675

• 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)

• 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%

• 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

aka BASEL study

• BNP Time to Tx hospitalization, ICU admissions, LOS, costs

CHR

• ? 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

• 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 ptsI - No CHF - 5% mortalityII - Mild CHF (bibasilar rales and S3) - 15-25%

mortalityIII - Frank pulmonary edema - 40% mortalityIV - 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)

• 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:

– 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 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. need for intubation in cardiogenic pulmonary edema: a systematic review. CHEST 1998; 114:1185-1192CHEST 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

• 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

• ???

• ?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)