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)
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
Goal is to CO via Adrenergic NS ( HR, cont, PVR) RAAS activated via kidney hypoperfusion Neurohormonal Here you go! Mark, can you do the bilateral Posterior Shoulder dislocation trick again.
CHF +++ CHF
Adrenergic NS F-S mech’m Hypertrophy Compensatory mech’m
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 (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 Systolic vs Diastolic
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 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 • 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
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 Hx
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 P/E findings in…
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?
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 evaluationinternational 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
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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.
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