Congestive Heart Failure and Cardiomyopathy

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Transcript Congestive Heart Failure and Cardiomyopathy

Shot Through the Heart &
You’re to Blame,You Give
Love a Bad Name: CHF &
Cardiomyopathy
Resident Rounds
Nov 28/02
A.F. Chad, MD, CCFP
Heartbreak Hotel
• Failure to maintain adequate
circulation of blood
• Left versus Right sided CHF
• Systolic versus Diastolic CHF
• High versus Low Output CHF
What is Love, if not
Neurohormonal
Mechanism
• 1. Sympathetic system activation
• 2. Activation of the ReninAngiotensin Aldosterone system
(RAAS)
• 3. Increased naturetic peptides
• 4. Increased Antidiuretic hormone
• 5. Increased Endothelins
Getting in the Mood:
Sympathetic Activation
• Causes increased cardiac output,
increased heart rate, and peripheral
vasoconstriction
• If sustained activates the RAAS which
increases both preload and afterload
• Stimulation of alpha and beta receptors
leads to myocardial hypertrophy and
fibroblast hyperplasia which lead to
decreased compliance
• Increased norepinephrine levels lead to
myocardial cell death and areas of focal
necrosis further impairing LV function
Feeling “RAAS”NDY
Yeah Baby!
• Stimulation leads to increased
Angiotensin II which leads to :
• 1. Increased aldosterone
• 2. Increased norepinephrine
• 3.Inhibition of vagal tone
The Male Love Hormone
(Kind of): Aldosterone
• Shown to be elevated up to 20 times in
patients with CHF
• Causes growth promoting activity in
nonepithelial cells
• Stimulates fibroblasts which leads to
interstitial and perivascular fibrosis which
increases LV stiffness
• Produced in nonrenal sites such as the
vessels and heart
• Up to 40% of patients will have elevated
levels despite being on ACE inhibitors
Some like it hot & wet:
Antidiuretic Hormone
• Is elevated in severe heart
failure
• Higher levels have been
reported in patients on diuretics
• Can lead to hyponatremia
More than an Endothelin
• Secreted by vascular endothelial
cells
• Potent vasoconstrictor peptide which
leads to sodium retention
• Increases in proportion to the
hemodynamic severity of heart
failure
• Interest in developing endothelin
receptor antagonists
Naturetic Peptides by
Nature
• 3 types
• 1. Atrial Naturetic Peptide (ANP) – released
from the atria in response to stretch. Is
very sensitive and will be released even
with exercise. Causes naturesis and
vasodilatation
• 2. Brain Naturetic Peptide (BNP) – release
from the venticles in response to elevated
LVEDP. Has the same effect as ANP
Naturetic Peptides by
Nature cont’d
• 3. C-type naturetic peptide –
limited to the vascular
endothelium and has limited
effects on naturesis and
vasodilatation
From the Bottom of my
heart (filling my lungs)
• Capillary pressure (12-15mmHg)
• Plasma oncotic pressure (25mmHg)
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Cardiac (Hi PCWP)
ARDS
Low oncotic P
Negative P
Lymphatic insufficiency
Other
Where does my heart go
now?
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3.2 million in USA
400,000 new per year
1-2% prevalence
High 5-yr mortality: 60% M, 45% W
Median survival: 3.2 yr M, 5.4 yr W
Progressive CHF vs sudden death
Why you Wanna Break
My Heart?
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ISCHEMIA!!!!!!
Non-compliance
Valvular
HTN
CM
Infectious
Thyrotoxicosis, anemia
To Find My Heart
• Exertional Dyspnea: most sensitive
(Spec<60%)
• PND / Othopnea (sens<30%)
• Cough
• Edema
• Anxiety
• Non-specific stuff
Piece of My Heart?
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COPD
Asthma
PE
Tamponade
Pneumonia
ARDS
Heart and Soul: CCS
• I - ordinary activity = no angina, +++
activity = angina
• II - slight limitations, angina >2 blocks
level (+/- stress)
• III - marked limitations, angina <2 blocks
level
• IV - no activity w/o discomfort +/- angina at
rest
• 59% Validity, 73% reproducible
Heart and Soul: NYHA
• I - ordinary activity = no Sx
• II - slight limitations, ok at rest,
ordinary activity = S
• III - marked limitations, less than
ordinary activity = Sx
• IV - no activity w/o discomfort, Sx at
rest
• 51% Validity, 56% reproducible
Sea of Love
• Physical exam
–90% specific
–20-30% sensitive
Love Shack . . . Left’s
where it’s at!!!
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Tachypnea / tachycardia
S3, gallup
Diaphoresis
Crackles / wheezes
Pulsus Alternans
PMI laterally displaced
Love Shack . . . Right’s
where it’s at!!!
• JVD
• Edema
• Hepatomegaly / HJR
Heart and Soul: Killip
• 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
Find My Heart
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CBC
Lytes
Creatinine
LFT’s
TNT?
TSH?
BNP?
You Down with BNP?
Yeah, you know me!
• New polypeptide that is produced in the
ventricles
• Released in proportion to LV expansion
reflecting the LVEDP
• Levels rise with age (due to increased LV
stiffness)
• Levels are elevated with pulmonary disease
(due to increased RVEDP)
• Levels are elevated in end-stage renal
disease reflecting decreased excretion
You Down with BNP?
Yeah, you know me!
• There is a bedside test that is FDA
approved, but it costs $25 - $40 per test.
• Cut off has been determined
retrospectively in studies
• Levels below 75 – 100 pg/ml correlate with
fairly normal LV function
• The higher the level the worse the LV
function
• If a patient presented with acute
worsening, one would expect a level > 300
pg/ml
You Down with BNP?
Yeah, you know me!
• This test will probably be used to also
follow therapy for patients. Studies have
shown that better optimization of ACE
therapy can be instituted.
• It may reduce the need for repeat ECHO’s
• Levels rise acutely and decline with
effective treatment within hours – the ½
life is 22 minutes in patients without renal
disease
You Down with BNP?
Yeah, you know me!
• The best use is in patients with multiple
medical problems who present with
increased dyspnea.
• If patients have COPD, are at risk for PE
and have a history of CHF then BNP can
help separate cardiac from other causes of
dyspnea
– Maisel AS, Krishnaswamy P, Nowak RM, McCord J,
Hollander JE, Duc P, Omland T, Storrow AB, Abraham
WT, Wu AH, Clopton P, Steg PG, Westheim A, Knudsen
CW, Perez A, Kazanegra R, Herrmann HC, McCullough
PA.
Rapid measurement of B-type natriuretic
peptide in the emergency diagnosis of heart failure. N
Engl J Med. 2002 Jul 18;347(3):161-7.
Find My Heart
• ECG
– Ischemia
– Hypertrophy
– Dysrhythmias
• CXR
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Cardiomegaly (lots of love)
Redistribution (PCWP12-18mmHg)
Kerley B lines(PCWP 25mmHg)
Pulmonary edema (PCWP >25mmHg)
Find My Heart,
Find My Heart
• ECHO
– WMA
– EF
– Cardiac FNC
– Valves
– Tamponade
– Size
– Dimensions
Find My Heart
• Cath?
– ?definitive Rx
• MUGA?
– ?echo good enough
• Swan?
– No benefit with mortality
– ?helpful clinically
How do You mend a
Broken Heart?
• Acute emergency therapy
• Chronic maintenance therapy
How do You mend a
Broken Heart?
• ABCD!!!!
• O2, IV’s, Monitors
• CPAP / BiPAP for Edema (more MI
with BiPAP)
– Sacchetti A. Effectiveness of BiPAP for
congestive heart failure. J Am Coll
Cardiol. 2001 May;37(6):1754-5.
• Elevate head & Lower legs
• Cheesy Poetry
How do You mend a
Broken Heart?
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What is the cause?
TREAT THE CAUSE!!!!!
Nitrates
ACE
Diuretics
Morphine
hBNP
Inotropes
Sex Bomb: Nitrates
• Decreases preload and afterload
(slightly)
• Shown to be effective in reducing
mortality and improving symptoms
• Can be given sublingual, IV, or as a
patch
• Dose is 10mcg/min and can be
titrated up every 3 – 5 minutes until
desired effect.
• Can cause hypotension
Sex Bomb: Nitrates
• Can switch to a patch from IV
nitrates, however this switch worked
only when patients were on lower
doses (< 50 mcg/ml)
• Topical patches have an onset in
decreasing PCWP at 20 – 30 minutes
with peak effect at 120 minutes.
Therefore, their use in an acute
severe decompensation is not
warranted as first line therapy
Sex Bomb: Nitrates
• Sublingual NTG tabs decreased
PCWP by 36%. Onset was 4
minutes with peak effect at 9
minutes
• The spray had an onset of 1-2
minutes with peak effect at 5
minutes
Ace of the Heart
• Haude M, Steffen W, Erbel R, Meyer J.
Sublingual administration of
captopril versus nitroglycerin in
patients with severe congestive
heart failure. Int J Cardiol. 1990
Jun;27(3):351-9
Ace of the Heart
• Captopril sublingually decreased
PCWP after 10 minutes with a peak
effect seen at 30 minutes.
– Sacchetti et al showed that it decreased
the admissions to ICU – odds ration 0.29
– Haude M, Steffen W, Erbel R, Tschollar W,
Belz GG, Meyer J. [Hemodynamics after
sublingual administration of captopril in
severe heart failure. A pilot study] Dtsch
Med Wochenschr. 1989 Jul 14;114(2829):1095-100.
IV Ace of the Heart
• Annane D, Bellissant E, Pussard E,
Asmar R, Lacombe F, Lanata E,
Madonna O, Safar M, Giudicelli JF,
Gajdos P. Placebo-controlled,
randomized, double-blind study of
intravenous enalaprilat efficacy and
safety in acute cardiogenic
pulmonary edema. Circulation. 1996
Sep 15;94(6):1316-24
Hot &Wet: Diuretics
• Have venodilatory properties as well as
decreasing intravascular volume through
diuresis.
• Causes increased plasma renin and
Norepinephrine levels leading to Increased
SVR
• A study comparing high dose NTG and low
dose diuretics showed lower mortality than
high dose diuretic and low dose NTG
Fool for Love: Morphine
• Causes venodilation through
histamine release (lasts around 10
minutes)
• Causes sedation and respiratory
depression
• Sacchetti et al showed it increased
ICU admissions – odds ratio 3.0
Nesiritide (human
recombinant BNP): New Love
• Increases cyclic GMP->second messenger >dilate veins and arteries
• Decreases PCWP & Dyspnea
• 2 mcg/kg IV bolus over 60 s; follow by 0.01
mcg/kg/min continuous infusion
– Elkayam U, Akhter MW, Tummala P, Khan S, Singh
H. Nesiritide: a new drug for the treatment of
decompensated heart failure. J Cardiovasc
Pharmacol Ther. 2002 Jul;7(3):181-94.
Acute treatment –
conclusions
• 1. Nitrates are first line therapy and
should be given intravenously if the
patient is sick
• 2. Ace inhibitors are beneficial in
acute CHF
• 3. Diuretics should be used in
moderation
• 4. Morphine should be used with
extreme caution
Chronic Therapy
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Ace Inhibitors/ ARB’s
Betablockers Spironolactone
Diuretics
Digoxin
Ace of the Heart
• Considered first line therapy for CHF.
• Recommended for all stages of CHF
• Absolute mortality reduction is around 15%
at one year for class III/IV patients with a
NTT of 6 (relative risk reduction is 30 –
35%)
• The effect on mortality was dose related
and the higher the dose till the target range
was reached ;the lower the mortality
Ace of the Heart
• These results were based on the
CONSENSUS I/II, SOLVD, AND
SAVE trials
• Note the effect of ace inhibitors
is reduced on patients who are
on NSAIDS as well as ASA
Angiotensin Receptor
Blockers (of love)
• Were thought to be better because
angiotensin II was still produced in
patients on Ace inhibitors.
• These drugs block the Angiotensin II
receptor.
• Also they do not produce Bradykinens
which Ace inhibitors do. These
Bradykinens lead to S/E such as cough and
angioedema
ARB’s of love
• Elite II – showed that there was no
difference between ARB’s and Ace
inhibitors. Mortality was 17.7% and 15.9%
respectively
• ARB’s were better tolerated
• They are recommended for patients who
can’t tolerate Ace inhibitors
• The current research is to see whether
combined therapy will reduce mortality
Lip Lockers,
Betablockers
• Recommended for all patients
with CHF
• Shown to increase LVEF by 30%
• Decreases mortality by 4 – 5 %
with NNT of 23
– MERIT-HF
Spare my Heart:
Spironolactone
• RALES - showed 25 mg of
spironolactone had a 30% relative
risk reduction and an absolute risk
reduction of 11% with a NNT of 9
• Recommended for patients with
class III/IV CHF
• Note side effects were < 5% at this
low dose
Hot & Wet: Diuretics
• Help control symptoms
• No effect on mortality
Love is a rose, or a
foxglove: Digoxin
• No effect on mortality
• Reduced hospitalizations by 11% with a
NNT of 9 to prevent 1 hospitalization per
year
• Used as 4th line agent after ace inhibitors,
beta blockers, spironolactone.
– Jaeschke R, Oxman AD, Guyatt GH: To what
extent do congestive heart failure patients in
sinus rhythm benefit from digoxin therapy? A
systematic overview and meta-analysis. Am J
Med 1990 Mar; 88(3): 279-86
Broken Heart
• Steroids?
– Increase mortality
• CCB?
– Dyhidropyridines BAD
– ?Central acting in diastolic dysfnc
Greatest Love of All:
Dilated CM
• Most common CM
• Difficult to find #’s as similar Rx
I’ll Make Love to You:
Dilated CM
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30% idiopathic
X-linked (dystrophin gene)
Booze
Heavy Metal
Drugs
Infectious (viral, Chagas)
Post partum
Collagen vascular disease
Glycogen storage disease
Thiamine, PO4, zinc deficiency
Amyloidosis
Neuromuscular disorders
Stop Dragging My Heart
Around: Dilated CM
• Biopsy helpful for etiology
• Rx same as other CHF
• MDC (Metoprolol in Dilated CM)
– 34% reduction in primary endpoints
(death, Tx)
• Multicenter Myocarditis Treatment
Trial:
– no benefit of corticosteroids and
azathioprine for Rx of biopsy-proven
inflammation in dilated CM
Endless Love:
HCM
• Inappropriate hypertrophy w/o
stimulus
• Usually asymmetric
• IVS usually affected
• 4% mortality per year (sudden death)
Quit Playin’ Games With
My Heart: HCM
• 50% familial (AD, 6 genes, 4
chromosomes)
• Abn Ca++ kinetics
• Abn sympathetic stim
• Abn Coronaries
• Subendocardial ischemia
• Structural abn
Tearin’ Up my Heart:
HCM
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0.05% of outpt echo
25% 1st relatives of HCM
Usually 3rd decade, but anytime
M>F
HOCM vs HCM
– SAM
Sunshine of my Love:
HCM
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Sudden Death
Dysrhythmia
CHF
Presyncope / Syncope
Angina
Why Can’t This be
Love?:
HCM
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CHF Sx
JVD - big “a” wave
Double impulse pulse
PMI increased & lateral
SEM / HSM
Split S2
Love in an Elevator :
HCM
• Genetic Studies
• ECG
• Doppler Echo
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LV outflow gradient >50mmHg
Diastolic dysfnc
Ground glass
HOCM: septum >1.4:1 ratio to post wall
This Year’s Love:
HCM
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ABCD
Normal CHF / CAD Rx
Myomectomy
Catheter septal ablation
MV replacement
ICD
B-blockade
CCB
Anti-arrhythmias
My Love is Restricted to
You
• Least common CM
• ? Incidence ?
• Important (but DIFFICULT) to
differentiate from constrictive
pericarditis as different Rx and
prognosis
• Poor prognosis
Why My Love is
Restricted to You
• Idiopathic restrictive cardiomyopathy
– EMF
– Loeffler eosinophilic endomyocardial
disease
• 2ndary restrictive cardiomyopathy
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Hemochromatosis
Amyloidosis
Scleroderma
Carcinoid heart disease
Glycogen storage disease of the heart
Looking For Love
• Chest x-ray
– Absence of cardiomegaly, normal
cardiac silhouette
– CHF
• Electrocardiogram
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LBBB common, RBBB possible
Low voltage
Nonspecific ST-T changes
Various arrhythmias
Chamber enlargement
Radar Love
• Echocardiography
– Normal to symmetrically thickened
walls
– Rapid early-diastolic filling, slow
late-diastolic filling
– Normal or slightly reduced
ventricular volume and systolic
function
Pain is Love
• Cardiac catheterization
– Elevated ventricular end-diastolic
pressure
– Dip and plateau configuration of the
diastolic portion of the ventricular
pressure pulse
– Normal to slightly decreased ejection
fraction
– Prominent x and y descent
Gangsta of Love
• Endomyocardial biopsy
– May detect typical eosinophil infiltration
in the inflammatory stage
– May detect myocardial fibrosis in laterstage cases
– Negative findings do not exclude
diagnosis
Love Spreads
• Treat underlying cause if possible
• Therapy similar for other causes of
CHF
• Consider anticoagulation as prone to
thromboembolism
All You Need is Love
• Thanks to Dr Arun Abbi for
“lending” many of these slides