Heart Failure

last authored: Aug 2009, David LaPierre
last reviewed:

 

 

Introduction

Heart Failure (HF), an extremely common and serious outcome of cardiovascular disease, is the inability of the heart to provide enough blood to meet the needs of the body. It is the most common cause of hospitalization in patients over 65 and is responsible for 9% of deaths. There is an approximate 30% readmission rate within 3 months.

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The Case of Mr. RT

Mr RT is a 56 year-old man with longstanding, poorly controlled hypertension. He comes to his family physican with increasing fatigue, shortness of breath, and swelling in his legs. His family doctor is concerned this might be heart failure.

 

 

Causes and Risk Factors

HF can be caused by a variety of underlying conditions and diseases, either systolic or diastolic, and is the common end point for many cardiovascular diseases. The end cause is venous congestion in the lungs and/or rest of the body.

 

It is important to rule out treatable causes.

In someone with underlying disease, exacerbations can follow times of increased salt or fluid intake,such as can occur around holidays.

Left-sided heart failure is commonly caused by:

Right-sided heart failure is commonly caused by:

 

Other causes of heart failure:

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Pathophysiology

In many cases, heart failure is preceded by cardiac hypertrophy in an attempt to maintain cardiac output. Progression of anatomical, cellular, and molecular changes leads to left ventricular remodeling.

 

At the same time, neurohormonal activation of epinephrine/norepinephrine, atrial natriuretic peptide, and the renin-angiotensin-aldosterone system become important drivers of continued heart dysfunction.

 

The heart is unusally heavy, perhaps 2-3x normal, and is large and flabby. Dilation of all four chambers occurs. Wall can be less than, equal to, or greater than normal. Mural thrombi are common.

 

Cardiac hypertrophy

main article: heart as a pump

The heart is generally believed to be incapable of cell division in adulthood, leaving hypertrophy as the principle means of increasing heart contractility. The Frank-Starling mechanism, along with neurohormonal trophic factors, can increase protein and organelle synthesis, leading to length and size of cardiomyocytes.

 

Pressure overload tends to result in concentric hypertrophy, with increased wall thickness. Volume overload hypertrophy is characterized by dilation, with increased ventricular diameter but not necessarily increased wall thickness. Decreased capillary density and intercapillary distance, along with increased fibrosis occurs in the face opf increased oxygen demand. This tonic ischemic environment often evolves into cardiac failure.

 

Changes is calcium handling, in adrenergic receptors, contractile proteins, apoptosis, connective tissues.

 

Numerous transcriptional and morphologic changes occur. Early mediators include c-jun, c-fos, and c-myc and are followed by fetal gene programs. Molecular changes which act to enhance contraction may be less functional or normal, however, and, together with apoptosis, can actually do more harm than good.

 

CHF also leads to systemic hypoxia and congestion, both which have effects on involved tissues. Liver congestion can lead to hepatomegaly, with centrilobular necrosis or sclerosis possible. Edema of the spleen or large bowel are also possible.

 

Systolic Heart Failure represents problems with ejection. The heart hypertrophies, and ejection fraction falls below 40%.

 

Diastolic Heart Failure is difficulty is more with heart filling than ejecting. Less hypertrophy and less mortality, but same hospitalization rates.

 

Mechanisms designed to increase cardiac output can lead to SNS activity and activation of RAAS, increasing peripheral resistance. EDV and preload increase.

 

Damage can be done in many ways (make chart)

Alcohol toxicity is strongly associated with development of dilated cardiomopathy in some people, either through direct toxic effects or secondary nutritional deficiencies.

 

The heart is unusally heavy, perhaps 2-3x normal, and is large and flabby. Dilation of all four chambers occurs. Wall can be less than, equal to, or greater than normal. Mural thrombi are common.

 

Edema comes from capillary leak, which is usually dealt with by lymphatics.

 

With hemodynamic pulmonary edema, pulmonary congestion results in heavy, wet lungs. Fluid accumulates initially in the lower lobes because of increased hydrostatic pressure. Alveolar capillaries become engorged. Alveolar microhemorrhages and hemosiderin-laden macrophages may be present. Chronic edema leads to interstitial fibrosis, leading to brown induration. Infection is more likely.

 

If edema results from damage to capillaries, fluid leaks first into the interstitial space and in more severe cases into the alveoli. If caused by a localized pneumonia edema is secondary in concern, but if widespread, can be an important contributor to acute respiratory distress syndrome.

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Signs and Symptoms

CHF can only be diagnosed clinically, not simply by echocardiogram, CT, catheter, or other modilities.

  • history
  • physical exam
  • lab investigations
  • diagnostic imaging
  • infants and children

History

DCM presents with slowly progressing signs and symptoms of congestive heart failure, including shortness of breath, easy fatigue, and poor exercise tolerance.

 

Congestive heart failure can have a profound impact on the way people feel and function, causing:

  • easy fatigue
  • shortness of breath and tachypnea
  • poor exercise capacity
  • diaphoresis and pallor (a serious sign - SNS activated to increase cardiac output. Beta-block.)

Left heart failure can lead to pulmonary congestion:

  • cough, crackles, pleural effusion
  • orthopnea
  • paroxysmal nocturnal dyspnea

 

  • weight gain
  • poor appetite

Advanced CHF can lead to hypoxic encephalopathy, with irritability, restlessness, and loss of attention span, potentially progressing into stupor and coma.

 

 

NYHA Classifications

  • Class I - no symptoms with ordinary physical activity
  • Class II - slight limitation. Comfortable at rest, but ordinary exertion results in palpitations, fatigue, dyspnea, or angina.
  • Class III - Comfortable at rest, but marked limitiations otherwise; can't get up one flight of stairs. Likely can't work for a living because of fatigue.
  • Class IV - symptoms of cardiac insufficiency at rest or with minimal activity. likely needs institutionalization. Symptoms of cardiac insufficiancy at rest.

 

Frail elderly present atypically

 

 

Physical Exam

Clinical accuracy rate is 75-80% in cases of acute decompensation.

 

Cardiovascular

  • tachycardia (100-120 is common)
  • soft heart sounds (in systolic CHF)
  • S3

 

Right heart failure can lead to systemic congestion and its symptoms:

  • edema (ascites more in older folks, pitting edema in younger)
  • weight gain
  • elevated jugular venous pressure
  • hepatomegaly
  • pleural effusions

Lab Investigations

 

  • low O2 sats
  • low Na+ (poor prognosticator)
  • azotemia (renal hypoperfusion)

 

 

BNP - B-type natriuretic peptide

  • increases with age
  • <100 means CHF is unlikely; >400 pg/ml strongly suggests it
  • secreted by ventricles of heart in response to stress or excessive stretching by myocytes
  • I heard it causes vasoconstriction and diuresis
  • elevated levels in blood can be helpful, but there are false +ves
  • pricey
  • over 90% when combining clinical impression with BNP
  • if its obvious, don't use it. Use in cases of uncertainty

 

RVSP is normally ~35 mmHg. Part of this is pulmonary wedge pressure. If RVSP is elevated, it may be left-sided heart failure. Assess this before diagnosing pulmonary hypertension.

Diagnostic Imaging

 

ECG

 

Chest X Ray

Extracardiac effects of left-sided failure are most prominent in the lungs. Increased pressure backs up into pulmonary capillaries and arteries, resulting in pulmonary edema. Perivascular and interstitial transudate forms, particularly in the interlobular septa. This is responsible for Kerley's B lines, or septal lines. Progressive widening of alveolar septa eveltually leads to accumulation of fluid in the alveolar air spaces themselves.

Peribronchial cuffing - fluid extravasation around bronchi (online image)

Vascular redistribution (cephalization of flow) - increased flow to the apices of the lung as a result of increased pulmonary venous pressure.

 

 

Echocardiography

Ejection fraction is a useful feature.

 

 

MUGA Scan

More specific

Infants and Children

cardinal findings

  • tachypnea
  • tachcardia
  • cardiomegaly

other findings

  • hepatomegaly
  • failure to thrive
  • cyanosis, especially during feeding or exertion

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Differential Diagnosis

CHF may be confused with other cardiovascular or respiratory conditions, including:

 

 

 

 

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Comorbid Conditions

Virtually all older patients will have at least one morbidity, and the majority will have more. These include:

 

 

 

Management of Heart Failure

Treatments are designed to unload the heart, increase the strength of contraction, and block the SNS effects.

 

Treatments for DCM are similar to those for other types of CHF. However, given the young age of patients, and high rates of mortality, cardiac transplantation is frequently recommended.

 

Cause of readmission include volume overload, noncompliance, arrhythmia, ischemia, and others.

  • medication

  • lifestyle

  • exercise

  • education

  • implantable
    devices
  • pediatric
    treatments
  • frail
    elderly
  • acute
    decompensation

Medication

Treatments improving mortality target neurohormonal mediators of heart function. Treatment protocol depends on functional class, ability to come for blood testing, and other reasons.

Medications are used to stabilize cellular changes; recovery is rare.

 

Diuretics

Dieuretics are used to reduce fluid overload and reduce the load on the heart.

  • furosemide (PO/IV) BID recommended for congestive symptoms. Once acute congestion is dealt with, use lowest dose
  • in pts with refractory failure, a 2nd diuretic (thiazides or low-dose metozalone) can be added cautiously
  • if decompensated, edema is substantial in gut and absorption drops; Use IV at first.

 

Aldosterone Antagonists

triamterine and amiloride: acts on distal tubules to increase K uptake

spironolactone

  • reserve for pts who have failed other treatments

minimal impact on BP, but major effect on creatinine and potassium

hydralazine, together with nitrates, may be better in the black population.

metolazone

 

 

ACE inhibitors and Angeiotensin Receptor Blockers

  • together with beta blockers, are standard therapy
  • provide ~20-25% improvement in many regards - hypertrophy, hospitalizations, stroke
  • contra: hypokalemia, severe renal insufficiency, severe hypotension
  • long term mortality benefit - up to 12 years
  • reduce TPR and therefore preload and afterload
  • decrease aldosterone leading to lowered preload
  • decreased NE release
  • decreased bradykinin breakdown
  • decreased ventricular remodeling

ARBs can be considered as an alternative in patients with AMI with acute HF or LVEF <40%. They are commonly used if side effects arise with ACEi, such as cough or angioedema.

    • can be used in addition to ACEIs and further drops in negative outcomes
    • additional cost, effort, side effects

 

Beta blockers

beta blockers block SNS activity

  • metoprolol XL blocks signs and symptoms of CHF; decreases HR
  • carvedilol (a nonselective SNS antagonist) reduces signs and symptoms, slows progression, and decreases
  • bisoprolol
  • mortality
    • β1 antagonism decreases HR
    • α1 antagonism blocks vasoconstriction and decreases afterload
    • perhaps bb's lower concentration of recpetors
    • airplane headphones analogy
  • side effects: hypotension, fluid retention, braducardia/heart block

as bb's reduce HR and contractility, too much too soon can decrease EF and make them very sick. Therefore, titrate slowly upwards to avoid initial deterioiration and to then build clincial beenfits.

 

reduce mortality by 30-40%, most pronounced in sickest patients.

We think it antagonizes toxic neurohormonal effects, but we don't know.

 

 

cardiac glycosides - digoxin

improves exercise, symptoms, hospitalizations, though no impact on mortality.

  • increased contractility, leading to increased CO
  • anti-arrhythmic
  • Na/H exchange inhibitor
  • reserved for pts with many symptoms

 

 

Avoid antiarrhythmic medications other than amiodarone in CHF, as they are negative inotropes and increase the risk of sudden death.

 

 

 

vasodilators, ie nitroglycerin, used acutely.

  • nitroglycerin
  • nitroprusside
  • nesiritide

 

ionotropic agents, ie dobutamine, used acutely.

 

low dose dopamine: vasodilator in renal beds, allowing diuretics to penetrate

 

 

isosorbide dinitrates + hydralazine

  • used together
  • strict vasodilator
  • use in in people unable to tolerate ACEis and ARBs
  • appear particulary useful in black folks

 

anticoagulation

  • only use in ppl with arrhythmias or people with clots

 

Avoid:

  • Ca2+ channel blockers, other than amlodipine, can be dangerous
  • NSAIDs (may cause fluid retention)
  • some antipsychotics
  • corticosteroids

Nutrition

Sodium intake should be limited to 2000 mg daily.

For patients in whom fluid levels are difficult to control with medication, fluid restriction should be implemented at 1.5-2L daily.

Daily weights should be used to assess this, and should be kept within +/- 2lb.

 

 

Exercise

Regular mild exercise promotes efficient blood flow. A stress test is recommended.

Exercise

 

 

Education

people with heart failure often have complex comorbidities and can't learn well.

5% of pts with CHF can explain what CHF is (get ref for this!)

Many therapies aren't taken.

  • aggressive risk factor reduction
  • lifestyle
  • fluid/salt vigilance

Implantable Devices

Devices include resynchronization or biventricular pacing.

They can lead to symptom improvement in 70%

Indications include:

  • 1
  • 2
  • 3

Impantable cardiac defirillators (ICDs) are very effective, and cost-effective, in preventing sudden cardiac arrest.

 

Pediatric Treatments

fix underlying cause

medication

  • reduce preload: diuretics
  • inotropics: digoxin, dopamine, dobutamine
  • reduce afterload: ACE inhibitors

nutrition

anemia

measure success by growth

Frail Elderly

 

CCS 2006 recommendations for elderly HF patients, with the focus on symptoms and quality of life, rather than

ACE inhibitors (monitor renal function and electrolytes) and beta-blockers are first line recommendations

beta blocker uptitration is less frequently successful due to postural hypotension

Assess for relevant co-morbidities: depression, dementia

Acute Decompensation

Acute decomensation may be treated as effectively in home as in hospital, providing adequate care is delivered, and at less cost (Tibaldi et al, 2009).

 

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Consequences and Course

Mortality depends on symptoms and LV function. The annual mortality rate is 5% for mild symptoms, and up to 30% for patients with severe symptoms.

 

Increased heart mass predisposes to sudden death.

 

Complications

 

Avg age for admission is 75

Within 1 year 10-20% mortality rate (50% sudden).

25-40% total hospitalization rate

lost days

9.5 dealths/100 hosp pts over 65

readmissions are over 30% within 1 year

 

People with DCM can quickly fall into a decompensated function state. In the end stage, ejection fractions are often less than 25%.

Secondary mitral regurgitation, arrhythmias, and emboli are common.

Mortality is high, with only 25-50% of people alive after 5 years.

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Additional Resources

Jaarsma T. 2005. Interprofessional team approach to patients with heart failure. Heart. 91:832-838.

 

Tibaldi V et al. 2009. Hospital at Home for Elderly Patients With Acute Decompensation of Chronic Heart Failure. Archives of Internal Medicine. 169(17):1569-1575.

 

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Topic Development

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