heart failure

HEART FAILURE

Jorge Garcia, MD

November 22, 2002

CHF: we will talk about:

Part 1. Clinical Syndromes: Left ventricle vs Right Ventricular Failure.

Part 2. Diagnostic Syndromes: Systolic vs. Diastolic Failure.

Part 3. Treatment options.

Part 1. There are 3 clinical “CHF” syndromes:

1. Pure RV failure.2. Pulmonary edema.3. Low output failure. What are the symptoms of these?

What are the symptoms of pure Right Ventricle failure?

Pure Right Ventricle failure:

1. JVD.2. Dependent Pedal

Edema.

What are the symptoms of “CHF” caused by pulmonary edema?

Pulmonary Edema causes Dyspnea: Initially, DOE. then PND. Then dyspnea at rest.

Caused by…?

Pulmonary Edema causes Dyspnea: Initially, DOE. then PND. Then dyspnea at rest.

Caused by…LV failure.

(Why does the patient experience dyspnea?)

(Why does the patient experience dyspnea?) Not hypoxia, but interstitial fluid causing

stiff lungs and increased work of breathing.

Don’t be reassured by a decent O2 sat.

So the first distinction is between pure right ventricular failure and pure left ventricular failure:

RV failure causes pedal edema. LV failure causes pulmonary edema.

Third “CHF” syndrome:

Low cardiac output (pump failure)

What are the symptoms?

Low cardiac output (pump failure) causes:

Dyspnea Swelling of the legs Weakness, fatigue, lethargy,

lightheadedness, and confusion

Low output CHF syndrome is often mixed right and left heart failure.

most common. patients have mix of symptoms.

Do rales=CHF?

?

Rales

Rales present in < 25% of patients with HF, and absence does not rule it out.

When else do you hear rales?

When else do you hear rales?

Rales can be present in other lung conditions, such as pulmonary fibrosis, especially if not basilar, or present in entire respiratory cycle.

What is the more reliable sign of “CHF”?

S3

S3 gallop in adults is considered pathognomonic for heart failure.

S3 in children and adolescents can be normal, and does not imply heart failure.

S4 in elders can be a result of long standing HTN, and not imply heart failure.

What is the best way to hear an S3?

Hearing an S3:

S3 is heard best heard with the bell, with the patient in a left lateral decubitus position.

How do you check for JVD and HJR?

How do you check for JVD and HJR?

Look at the internal jugular.

What is the most common cause of pedal edema?

What is the most common cause of pedal edema? Venous insufficiency.

Another common sign of “CHF” is the new onset of tachycardia. Why do you get sinus tachycardia with CHF?

Sinus Tachycardia.

CO = HR x SV. If SV is reduced and fixed by heart failure, then an increase in CO will require an increase in HR.

Always suspect HF in a patient with unexplained sinus tachycardia.

Part 2: the pathology of “CHF.”The distinction between systolic and diastolic dysfunction.

Systolic dysfunction

Close to what was originally thought of as “CHF.”

After infarction, muscle “scar” is thinner and less contractile. After several MI s one is left with a large flabby heart.

Other causes of dilated cardiomyopathy:

Diastolic dysfunction

May be the more common form of CHF. Thick stiff heart after long history of

HTN.

Systolic dysfunction in more detail... Diffuse dilation of three (if not all four)

heart chambers. Thin ventricular walls, poor global

contractility. Chest x-ray with cardiac enlargement,

pear shaped heart: DDx includes pericardial effusion.

Systolic dysfunction

Most common cause is CAD and infarctions, with remodeling of the ventricular wall.

Cardiomyopathies can also cause systolic dysfunction CHF.

The heart no longer works well in systole: it does not contract well.

Diastolic dysfunction in more detail…What is the pathophysiology of diastolic dysfunction?

Diastolic dysfunction: The ventricle “fights” against

hypertension and against increased afterload by becoming “stronger” and

the heart muscle hypertrophies. Concentric hypertrophy, directed

inwardly, encroaches on the LV cavity. Stiff, fibrotic LV muscle does not relax

in diastole, does not fill enough. Thus, reduced end diastolic volume.

Diastolic dysfunction over time:

Reduced stroke volume, reduced cardiac output.

As it progresses, CAD will often develop and the pathology will overlap with systolic dysfunction.

Diastolic dysfunction:Common, especially in elders with long

standing HTN. Can’t be distinguished on exam from

systolic dysfunction: Chest film: the heart often looks normal. need an echo

Diastolic dysfunction on echo:

Contractility is preserved and ejection fraction is usually normal.

Concentric hypertrophy on echo. Inwardly directed ventricular hypertrophy.

How can diastolic dysfunction lead to atrial fibrillation?

A. Fib.

In the normal heart, left ventricle fills passively, right after the mitral valve opens.

In diastolic dysfunction, the stiff LV does not relax, fills more slowly.

Left atrium “tries” to overcome this by dilating, which increases risk of developing atrial fibrillation.

A. Fib.

The cardiac output becomes increasingly “dependent” on this atrial kick.

When the atrial kick is lost suddenly with A. Fib, your patient may rapidly de-compensate, and develop clinical heart failure that was masked by the atrial kick.

Summary of diastolic vs systolic dysfunction. Diastolic: Cause: HTN. Result: thick LV. Muscle does not

relax. Failure of diastole.

Systolic: Cause: MI Result: thin LV wall. Muscle does not

contract. Failure of systole.

Part 3. Treatment

What is the treatment of systolic dysfunction?

The treatment of systolic dysfunction? ACE-I is the drug of choice: Start Rx

early.

The treatment of systolic dysfunction?

ACE-I is the drug of choice: Start Rx early

Used in the immediate post MI setting, ACE-I will prevent remodeling and thus

prevent CHF. May use an ACE-I alone if no signs of

volume overload.

The treatment of systolic dysfunction? Diuretics only in patients with volume

overload or acute pulmonary edema. Cautious use of beta-blockers.

(Negative inotrope.)

The treatment of systolic dysfunction? What about dig?

Digoxin can be used as a positive inotrope. It also controls ventricular rate in A Fib. Forth line therapy, after ACE-I, beta-

blockers, diuretics. Never proven to decrease mortality.

Avoid in patients in sinus with diastolic dysfunction.

What is the prognosis of patients with systolic dysfunction?

Px of patients with systolic dysfunction terrible: “cardiac cancer.” Progressive deterioration over a few

years, to death.

How do we treat diastolic dysfunction?

Treatment of diastolic dysfunction:

Empiric treatment options only – no decent data.

The problem is not a weak pump, but a stiff, un-relaxing pump.

Making the heart pump harder will make things worse: positive inotropic agents, such as digoxin, are contraindicated.

Treatment of diastolic dysfunction:

ACE-inhibitors are treatment of choice,

because they reverse ventricular hypertrophy.

Treatment of diastolic dysfunction: Negative inotropic agents can help: beta-blockers and Calcium channel

blockers (Verapamil and Diltiazem).

Treatment of diastolic dysfunction:

Nitrates can help, but as in all cases, need to avoid excess lowering of BP.

In addition, maintain your patient in sinus rhythm and keep the atrial kick.

What is the prognosis of diastolic dysfunction?

What is the prognosis of diastolic dysfunction? can be OK, with treated patients

surviving years.

When do you suspect diastolic dysfunction?

When do you suspect diastolic dysfunction?

History of HTN. Intermittent pulmonary edema.

Sudden CHF episodes, with little warning.

“Flash Pulmonary edema.”

When do you suspect diastolic dysfunction?

Worsening failure despite seemingly appropriate therapy with dig and diuretics.

Again, need echo in all new cases of HF. This is the only way to determine if dysfunction is diastolic or systolic.

Summary of treatment of CHF:

Systolic Failure: ACE-I diuretic Beta-blocker dig

Diastolic disfunction: ACE-I beta-blocker Ca Ch. Blocker nitrates.

Which ACE-I should be used?

Which ACE-I should be used?

Look at cost, duration of action, convenience. Otherwise, fairly comparable.

Dosing: usually under used and under dosed. Aim for maximum dose tolerated by BP.

Hey, what about ARBs?

ARBs (Angiotensin-II Receptor Blockers) might work as well, but not yet proven.

They don’t lead to accumulation of bradykinins.

ARBs

Bradykinins are great for decreasing blood pressure and preserving renal function, but also responsible for cough and angioedema of ACE-I.

No mortality study, and only Losartan shown to benefit in HF in a drug company sponsored study.

What are the contraindications to ACE-I?

Contraindications to ACE-I:

Allergy angioedema neutropenia severe skin eruptions – all very rare.

Relative contraindications to ACE-I Hypotension Hyperkalemia – care with K+

supplements or K sparing diuretics. Dysgeusia.

Relative contraindications to ACE-I: CRI CRI: with creatinine 1.5-2.5, use with

caution and monitor creatinine. Avoid with creat > 2.5. Often,

increasing creatinine can be caused by over diuresis and renal hypo-perfusion.

May try to back off on diuretics first.

What about cough with ACE-I?

What is the most common cause of cough in a patient with CHF on ACE-I?

Cough with ACE-I

most common cause of cough in a patient with HF and ACE-I is

pulmonary edema

If ACE-I can not be used?

What can be used instead?

If ACE-I can not be used?

Hydralazine and Nitrates. These have been shown to decrease mortality, but less than ACE-I.

Hydralazine dosed multiple times per day, can cause head aches, palpitations, nasal congestion, reflex tachycardia, tachyphylaxis.

What about diuretics? Can they be used first, and alone in treatment of HF?

??

What about diuretics? Can they be used first, and alone in treatment of HF?

No.

Diuretics and CHF:

Still best for acute symptoms of volume overload.

Not to be used alone long term. Can be counter-productive, in decreasing volume, renal perfusion, activating RAA, promoting tachycardia.

Diuretics and CHF

Used alone, they become increasingly ineffective. Addition of ACE-I can restore effectiveness.

Loop diuretics most potent. Double the dose of Lasix until effective. Single daily does is best. (Lasix is short acting [“Lasts Six – hours”] and not great for BP control, but decent for diuresis.)

Diuretics and CHF

Can often combine types for better effect.

Renal function may dictate type: Creatinine Clearance of > 30 ml/m – may use thiazides. ClCr of 20-30, may use Lozol(indapamide) and Zaroxolyn(metolazone). Lower ClCr may use loops until you need dialysis.

Diuretics and CHF

Spironolactone 25 mg PO qd has been shown to reduce mortality (by 27%, 1600 patients, RALES study NEJM, 1999) but best effect in Class III & IV heart failure. May be useful in other patients. Again, blocks the aldosterone of the RAA system. Can’t use if Creatinine is greater than 2.0.

When can one use Dig?

?

When can one use Dig? Systolic dysfunction, as a positive

inotrope. Reduce HR in A Fib. Forth line therapy, after ACE-I, beta-

blockers, diuretics. Never proven to decrease mortality.

Avoid in patients in sinus with diastolic dysfunction.

When to use beta-blockers?

When to use beta-blockers? Best for patients with diastolic dysfunction,

tachycardia. Use full doses as for HTN. Can be used in systolic dysfunction, with

caution. Start low dose, and titrate slowly, over months. Have been shown to reduce mortality. Mechanism not clear, perhaps restoring body’s sensitivity to catecholamines.

Don’t start during decompensation.

Can we use Calcium Channel Blockers, and if so, which?

?

CCBs in CHF

Think of CCB as two types:

–1. Verapamil and Diltiazem

–2. everything else…(Nifedipine, etc…)

CCBs in CHF

Verapamil: most negative inotropic, not useful in systolic dysfunction, but useful in diastolic dysfunction.

Diltiazem. Less negative than Verapamil, used in the same way.

CCBs in CHF: Everything else...

Dihydropyridines: Nifedipine and all other CCB. Should not be used with HF. Can cause vaso-dilation, and reflex tachycardia. Can cause non-cardiac edema – complicating evaluation.

Amlodipine may be different (Norvasc) but best to group with Nifedipine.

Treatment can save lives: NNT (Number needed to treat) ACE-I: NNT for 4 years to save one live

is 20. Spironolactone: in Class IV only, NNT

for 2 years of treatment to save one life is 9.

Beta-blocker: NNT for 9 months to save one life is ~30.