Congestive Heart Failure - Students

8/13/2019 Congestive Heart Failure - Students

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Congestive Heart Failure

Cindy Chan, MD


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Inability of the heart to pump blood

forward sufficiently to meet the

metabolic needs of the body

or the ability to do so only with anabnormally high filling pressure

Heart Failure


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Coronary heart

disease

Hypertension

Valvular disease

Congenitalheart disease

Cardio-

myopathy

CHF


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Epidemiology

5 million in US

500,000 new cases years

75% new cases in pts >65yo


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What do I need to

remember aboutCARDIAC PHYSIOLOGY?


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Cardiac output

Heart rate Stroke volume

Preload Contractility

Afterload+

+


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WHAT IS PRELOAD?

Amount of muscle stretchbefore contraction


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LV End-diastolic VOLUME

STROKEVOLUME


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LV End-diastolic VOLUME

STROKEVOLUME

FRANK - STARLING


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LV End-diastolic VOLUME ~

LV End-diastolic PRESSURE

STROKEVOLUME

FRANK - STARLING


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LV End-diastolic VOLUME ~

LV End-diastolic PRESSURE

STROKEVOLUME

FRANK - STARLING

but the relationship

between volume

and pressureis not linear!


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The LV end-diastolicPRESSURE / VOLUME

relationship

is influenced by theLV chamber compliance


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LV

Pressure

LV Volume

Stiff Normal

Compliance


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EDV

ESV

SV = EDV - ESV


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Baseline

Increase

in EDV(preload)

EDV- ESV = SV


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Baseline

Increase

inContractility

EDV- ESV = SV


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Baseline

Increase

inAfterload

EDV - ESV = SV


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Cardiac output

Heart rate Stroke volume

Preload Contractility Afterload+ +


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Concepts to know

Preload

Afterload

Contractility

Compliance

Ejection fraction


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What are the

clinical manifestationsof CHF?


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Symptoms of CHFDyspnea on exertion (DOE)

Shortness of breath (SOB)

OrthopneaParoxysmal nocturnal dyspnea(PND)

Cardiac Asthma (with chronic cough)Fatigue


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Signs of Left-Sided CHF

Tachycardia

Tachypnea

Pulmonary Rales

Cardiomegaly

S S3 4


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Signs of Right-Sided CHF

Jugular vein distension

Edema

Hepatomegaly


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CHF

A Big Black Box


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CHF

A Big Black Box

Numerous etiologies,

pathophysiologies

and therapies


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Pathophysiology

Low-output HF Left heart failure, right heart failure (LV dysfunction is primary

cause of RV failure)

High-output HF

Normal/supra-normal pump function, but increased metabolic

demands (thyrotoxicosis, severe anemia, arteriovenousshunting, Pagets disease of bone, thiamine deficiency)

Systolic dysfunction

Decreased contractility (ischemia, MI, DCMP, chronic AI/MR)

Increased afterload (HCMP, AS, HTN crisis, coarctation of aorta)

Diastolic dysfunction

Abnormal filling of LV or RV, because of impaired myocardialrelaxation or non-compliant/stiff chamber


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Etiologies of CHF

Coronary Artery Disease

Acute MI

Chronic ischemia

Hypertension

Cardiomyopathy

Dilated

HypertrophicInfiltrative

Valvular Disease

Mitral Regurgitation

Mitral Stenosis

Aortic RegurgitationAortic Stenosis

Pericardial Disease

Tamponade

Constriction

Congenital Disease

High output

Thyrotoxicosis

Beriberi

A-V Fistula

Pagets Disease

Anemia

Right-sidedPulmonary Hypertension

COPD

Pulmonary Embolism

Valvular Disease

Tricuspid RegurgitationTricuspid Stenosis

Pulmonic Regurgitation

Pulmonic Stenosis


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Etiologies of CHF Coronary heart disease

Hypertension

Cardiomyopathy

Dilated

HypertrophicInfiltrative

Valvular heart disease

Pericardial disease (Restrictive)


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Left ventricular

diastolic pressure

COMMON DENOMINATOR of LV FAILURE

Pulmonary capillary pressure

Left atrial pressureBAD

ELEVATED


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20 mmHg

NORMALELEVATEDLV DIASTOLICPRESSURE


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LV End-DiastolicPressure

LV End-Diastolic

Volume

LV End-Diastolic

Stiffness

Mechanism of Heart Failure


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Evaluation

of Systolic Function


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Ejection fraction:

EDV-ESV SV

EDV EDV=


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Evaluation of

Systolic Function

Systolic Function EF

NORMAL > 0.50FAIR 0.30 - 0.50

POOR


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Clinical Evaluation

Heart Failure

Abnormal

Diastolic

Function

Abnormal

Diastolic

Function

Heart failure is predominatelya disease of diastolic function

but systolic function mayvary!


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Clinical Evaluation

Heart Failure

Abnormal

Systolic

Function

Normal

Systolic

Function

70% 30%


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Clinical Evaluation

Heart Failure

AbnormalSystolic

Function

Normal systolic

function withprimary abnormal

Diastolic

Function


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Why does abnormal systolic function

lead to LV diastolic pressure?

Poor contraction leads to:

Use of Frank-Starling mechanism

End-diastolicpressure

Dilated LV


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Why does abnormal diastolic functio

lead to LV diastolic pressure

Poor compliance leads to:

Increase in LV pressure / volume

End-diastolicpressure

Stiff LV


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Dilated Cardiomyopathy


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Hypertrophic myopathy


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Which one has abnormalsystolic function?


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Systolic Dysfunction


Myocardial Infarction End-stage hypertension

Valvular heart disease


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Diastolic Dysfunction

Left Ventricular Hypertrophy

Hypertension

Aortic valve disease

Hypertrophic Cardiomyopathy

Restrictive Cardiomyopathy Constrictive Pericarditis


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Investigations !!


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Labs

Check for anemia, renal failure, thyroid

dysfunction, electrolyte abnormalities

(hyper/hypokalemia, hyponatremia)

BNP (brain natriuretic peptide; expressed

primarily in ventricles and elevated with

high ventricular filling pressures)


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EKG/CXR/Echo

EKGevaluate for underlying arrhythmia,

ischemia; often see low voltage, IV

conduction defects, LV hypertrophy

CXRcardiomegaly, pulmonary venous

congestion, pleural effusions (R-sided or

bilateral)

Echomost useful study


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Normal



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Echocardiogram


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Echocardiogram

Differentiate systolic dysfunction

from diastolic dysfunction

Evaluate presence of:

MI, cardiomyopathy,

Left ventricular hypertrophy (LVH),

Valvular disease, etc.


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CARDIOMYOPATHY


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DILATED HYPERTROPHIC INFILTRATIVE

CARDIOMYOPATHY

Impaired

systolic contraction

Impaired

diastolic relaxation,

vigorous systolic function

Stiff LV

with impaired

diastolic relaxation

CARDIOMYOPATHY


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CARDIOMYOPATHY

Impaired


Impaired



Stiff LV

with impaired


Dilated,

poorly contracting

LVH,

vigorously contracting

speckled

appearance in

infiltrative disease

ECHO:


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Alcohol

Beriberi

Coxsackie , Cocaine

Doxorubicin

F irst Aid


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Lets look at an Echo


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RV

LV

LA

AortaAV

MV


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RV

LV

Posterior

Wall

IV

Septum


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RV

LV Ao

LA

IV Septum

Posterior wall


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LV CAVITY

LV WALL THICKNESS

LV CONTRACLITY

N

N

N

or

or N


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How do we treat a patient? ?with CHF

who has

abnormal

systolic function ?


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Eliminate precipitating

and aggravating factors


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Identify and correct

underlying conditions


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Treat acute symptoms

Improve long-term prognosis


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Drugs for treating CHF

Diuretics

Inotropics Vasodilators

Beta-blockers


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Drugs for treating CHF

Diuretics

Inotropes Vasodilators

Beta-blockers

Diuretic


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Diuretic

Di ti


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Diuretics

Eliminate Na and H O via kidney Decrease intravascular volume

Decrease preload

Decrease pulmonary and peripheral

edema

Decrease symptoms and signs ofCCF

2+

Diuretics


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Diuretics

Side effects Overdiuresis

Electrolyte disturbances

Hypokalemia

Hypomagnesemia

Predispose to

digitalis toxicity

V dil t


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Vasodilators

Venous (Nitrates)

Arteriolar (Hydralazine) Balanced (ACE-I)


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Spironolactone.

Inotropes. Beta blockers.

MERIT-HF


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Gottlieb, S. et al. JAMA 2000;

238:1295-1302.

The Metoprolol Randomized Intervention Trial in


LVEF


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What effect do

these drugs have onthe Frank - Starling curve?


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LV diastolic volumeLV diastolic pressure

normal

STROKEVOLUME

dysfunction

LV EDP


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LV EDP

STROKE

VOLUME

dysfunction

PULMONARY

EDEMA

NORMAL

LOWOUTPUT

NORMAL

OUTPUT

NORMALDIASTOLIC

PRESSURE

normal


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LVEDP

STROKE

VOLUME

normaldysfunction

PULMONARY

EDEMA

LOWOUTPUT

DIURETICS


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LV EDP

STROKE

VOLUME

normaldysfunction

PULMONARY

EDEMA

DIURETICS

LOWOUTPUT


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INOTROPES


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LV EDP

STROKE

VOLUME

normal

dysfunction

PULMONARY

EDEMA

INOTROPES

LOWOUTPUT

BALANCED VASODILATOR


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LVEDP

STROKE

VOLUME

normal

dysfunction

PULMONARY

EDEMA

LOWOUTPUT

BOTH INOTROPES & VASODILATORS


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LVEDP

STROKE

VOLUME

normal

dysfunction

PULMONARY

EDEMA

LOWOUTPUT


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Does the patient have

NORMAL systolic functionor

ABNORMAL systolic function?

L ft H t F il


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Left Heart Failure

SOBOrthopnea

PND

Cardiomegaly

Pulmonary Rales

S3

L ft H t F il


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Left Heart Failure

with abnormalsystolic function

Diuretic

DigoxinACE -I

L ft H t F il

but what if patient has ----


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Left Heart Failure

with normalsystolic function

Diuretic?

Digoxin?ACE -I?

L ft H t F il


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Left Heart Failure

with normalsystolic function

Beta- blocker

NEJM Sept 1999


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Aldosterone Blockade WithSpironolactone Reduces Mortality

From Severe CHF

p

Spironolactone (Aldactone)

Improves

Prolongs

R b


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Improves

symptoms

Prolongs

lifeDiuretics

DigoxinACE-I

Beta-blockers

+ -

+ -+ +

+ +

Spironolactone + +

Remember

Acute treatment


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Acute treatment

O2

MSO4 (increases venous capacitance,

and decreases anxiety)

Diuretic tx

Nitrate tx


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Clinical Presentation of


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CHF

Treatment Algorithm??

Assess LV function


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Assess LV functionby 2-D echo or MUGA

EF > 40%Rx underlying

cause

Diureticsfor congestion

Beta-blockers,

ACE-I

EF < 40%

assess volume status

Signs and symptoms

of fluid retentionNo signs and symptoms

of fluid retention

Diuretic ACE-I

Beta-blocker(low dose)

spironolactone

Hypertension

CHD


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Prognosis of Patients with CHF

Depends on etiology

If non-correctable :

~ 50% mortality in 5 years


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Left ventricularassist device

New heart


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Old

heart


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TransplantationEnd-stage heart disease

Severe limits on daily activity

EF < 0.25

Suitable psychosocial profile

Suitable physiologic age

P t T l t


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Post Transplant

Survival

1 Year 20% 80%

4 Year 55%

Coronary heart

di


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disease

Hypertension

Valvular disease

Congenitalheart disease

Cardio-

myopathy CHF


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Cardiomyopathies


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Dilated

Hypertrophic

Infiltrative


CARDIOMYOPATHY


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CARDIOMYOPATHY


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Impaired


Impaired



Stiff LV

with impaired



CARDIOMYOPATHY


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Impaired


Impaired



Stiff LV

with impaired


Dilated,

poorly contracting

LVH,

vigorously contracting

speckled

appearance in

infiltrative disease

ECHO:



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Global Dilatation

Cross-section.


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Alcohol

Beriberi

Coxsackie , Cocaine

Doxorubicin

F irst Aid



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Etiology Idiopathic, alcoholic, myocarditis, post-

partum, doxorubicin, endocrinopathies,

genetic disease, toxins, viruses S/S

Left or BiVentricular CHF

Cardiomegaly, S3, elevated JVP, crackles



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EKG Sinus tachycardia

ST-Tw changes

Conduction abnormalities

Ventricular ectopy

CXR Enlarged heart

Pulmonary venous congestion

Echo

LV dilation & dysfunction Cardiac catherization

LV dilation & dysfunction, high diastolic pressures, low CO



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Treatment ACE-I

BB

Diuretic

Aldosterone antagonist Dig (2ndline)

Sodium restriction

ETOH cessation

Prognosis 11-13% annual mortality

Takotsubo Cardiomyopathy


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LV apical ballooning following highcatecholamine discharge

LV shape similar to octopus pot (takotsubo

pot)



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Etiology More common in postmenopausal women

Following stressful event (hypoglycemia,

natural disaster, postventricular tachycardia,ETOH withdrawal, post-op, hyperthyroidism,

emotional stress)

S/S

Angina, dyspnea



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EKG ST elevation

Deep, anterior Tw inversion

CXR Normal or with PVC

Echo

LV apical dyskinesia

Cath

LV apical ballooning, normal coronaries



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TreatmentASA

BB

ACE-I Tx until LV function recovers

Prognosis

Recovery expected in weeks to months



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yp p y p y


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yp p y p y

Etiology Hereditary syndrome (autosomal dominant)

Chronic HTN

S/S

Dyspnea, chest pain, syncope Sustained PMI, S4, variable systolic murmur

(increases with Valsalva, decreases with squatting),bisferiens carotid pulse

Afib (from chronically elevated LA pressures),Ventricular arrhtyhmias, sudden death (esp inathletes post-exertion)



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yp p y p y

EKG LVH

Exaggerated septal Qw (may be evidence of MI)

CXR Mild cardiomegaly

Echo LVH, asymmetric septal hypertrophy (1.3-1.5X thickness of

posterior wall), small LV, normal/supranormal fxn, systolicanterior motion of mitral valve, mitral regurg, diastolicdysfunction

Cath Small, hypercontractile LV, dynamic outflow gradient, diastolic

dysfunction



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yp p y p y

Tx BB (slower heart rate assists with diastolic filling of stiff LV) CCB (verapamil)

Disopyramide

Diuretics (2/2 high diastolic pressure and PCWP)

Dual-chamber pacing (to prevent progression of hypertrophy andobstruction)

ETOH septal ablation (injected into septal branches of LCA)

Implantable defibrillator (syncope, family hx of sudden death)

Myotomy-myomectomy (for severe symptoms)

Prognosis variable

Restrictive Cardiomyopathy


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y p y

Amyloidosis of the Heart


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y



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y p y

Etiology Amyloidosis

Hemachromatosis

Sarcoidosis

Connective Tissue disease (scleroderma)

Post-radiation

Post-cardiac surgery

DM

Endomyocardial fibrosis

S/S Dyspnea, fatigue, R-sided CHF

Elevated JVP, Kussmaul sign


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y p y

Tx Little useful tx

Diuretics

BB Cardiac transplantation (for primary cardiac

amyloidosis)

Restrictive Cardiomyopathy vs.

Constrictive Pericarditis


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Constrictive Pericarditis

Restrictive Elevated pulmonary pressure

Constrictive

Ventricular interaction accentuated withrespiration


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Thanks!

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Congestive Heart Failure - Students

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