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Heart Failure

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Heart Failure

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Heart failure is increasingly common due to an aging population and high prevalence of contributing risk factors.

Heart failure = A clinical syndrome in which the heart's ventricles cannot pump enough blood to meet the body's needs (insufficient cardiac output).

Reduced cardiac-output (CO) is due to reduced stroke volume.
Reduced stroke volume can be due to:
Systolic dysfunction, i.e., impaired contraction
Diastolic dysfunction, i.e., impaired compliance

Both scenarios can ultimately lead to increased left ventricular end diastolic pressure, which, as we'll see, can lead to pulmonary congestion.

As a clinical syndrome, heart failure is the culmination of other cardiovascular diseases, which may co-exist.
Common culprits include: ischemic heart disease, hypertension, cardiomyopathies, diabetes mellitus, metabolic syndrome, atherosclerosis, and myocardial infarctions.

Diagnosis can rely on echocardiography, ECG, cardiac MRI, and measurement of serum B-type natriuretic peptide (BNP) levels.

S3 or S4 sounds may be heard (be aware of intertextual variation on the importance of S4 sounds and heart failure); pulmonary crackles may audible when pulmonary edema sets in.

Treatments vary, and include life-style changes and, where appropriate, addressing the causative disease(s).

Treatments to reduce symptoms include: diuretics, digoxin, and nitrates.

Long-term treatments tend to focus on lowering ventricular pressures, and include: ACE-inhibitors, angiotensin II receptor blockers (ARBs), Beta-blockers, and Aldosterone antagonists.

Device therapies include implantable cardiac defibrillators, cardiac resynchronization therapy, biventricular pacemakers, and left ventricular assist devices.

Left Heart Failure

We draw a very generalized illustration of left heart failure; bear in mind that this is only representative, due to the varied causes of heart failure.

Pathophysiology:
LHF is the result of reduced stroke volume, which reduces systemic perfusion.
Reduced stroke volume also leads to increased left ventricular end diastolic pressure (LVEDP); be aware that this can be the result of a variety of mechanisms, which we'll address, soon.

Increased left ventricular end diastolic pressure leads to an increase in left atrial pressure, which, ultimately, raises pulmonary pressures.

Increased pressures in the pulmonary vascular system "push" fluids out of vessels and into the surrounding tissues.
Pulmonary edema occurs when this fluid enters the alveolar sacs and lung spaces.
Pleural effusions occur when the fluid accumulates between the pleural space.

Symptoms of LHF:
Dyspnea upon exertion is a common early sign; it occurs because the heart cannot increase cardiac output despite increased metabolic demands.
Orthopnea is characterized by dyspnea that occurs when lying flat, but is quickly relieved by sitting upright or standing; orthopnea occurs because the heart is unable to adjust to the redistribution of body fluids that occurs when lying flat.
Paroxysmal nocturnal dyspnea, as its name suggests, is characterized by sudden episodes of dyspnea that awaken a person after 1-2 hours of sleep, usually at night.
Sleep-disordered breathing includes obstructive sleep apnea and Cheyne Stokes Respiration; show that Cheyne Stokes Respiration is characterized by cycling periods of tachypnea or hyperpnea alternating with periods of apnea.

Other symptoms may also be present, often reflecting reduced cardiac performance; for example, patients may experience cognitive impairments, arrhythmias, cyanosis, or thrombi formation in the heart chambers.

Heart Failure with Reduced Ejection Fraction

The ejection fraction measures how much of the blood in the ventricle was pumped out (ejected) during a contraction.
For reference, a "normal" ejection fraction is between 50% and 70%.

In Heart Failure with Reduced Ejection Fraction, the left ventricle ejection fraction is 40% or less.
The lower ejection fraction is the result of reduced contractility of the myocardium, and is associated with systolic dysfunction (since the left ventricle contracts during systole).

Be aware that systolic and diastolic dysfunctions may co-exist, which is why clinical focus has shifted somewhat from systolic vs. diastolic dysfunction to the ejection fraction.

Heart failure with reduced ejection fraction is particularly associated with dilated cardiomyopathies, valvular heart diseases, and myocardial infarctions.

Pathophysiology - we use dilated cardiomyopathy as an example:
Contractility is impaired, so the ejection fraction is reduced, and, via a variety of mechanisms, the left ventricular end diastolic pressure increases.

Compensatory mechanisms in HFrEF:
Several mechanisms raise blood volume and vascular resistance in attempt to increase preload and, as a result, stroke volume and tissue perfusion.

Cardiac remodeling leads to dilation and myocyte hypertrophy. These changes can ultimately lead to increased stiffness and further impair cardiac performance, and even facilitate mitral valve regurgitation.

Reduced systemic perfusion triggers systemic and renal responses that increase blood volume and vascular resistance – recall that the renin-angiotensin-aldosterone system, the sympathetic nervous system, and the vessels themselves dynamically regulate changes in blood flow.

However, these effects also exacerbate pulmonary hypertension and congestion in a positive feedback loop.

Thus, some long-term treatments for heart failure with reduced ejection fraction specifically target these responses (for example, ACE-inhibitors that inhibit the effects of the RAAS response).

Heart Failure with Preserved Ejection Fraction

Characterized by Left Ventricular Ejection fractions equal to or above 50%.
It is caused by impaired relaxation and/or compliance of the myocardium, which produces diastolic dysfunction.

It is especially common in elderly people and women, and is associated with hypertrophic and restrictive cardiomyopathies, hypertension, and renal diseases.

Pathophysiology - we use a hypertrophic heart as an example:
Compliance is reduced, diastolic filling is impaired, and left ventricular end diastolic pressure is increased.
Impaired filling can lead to reduced stroke volume and cardiac output.

Prognosis
This type of heart failure often has a worse prognosis than heart failure with reduced ejection fraction, especially because it is less responsive to current treatments.

Right Heart Failure

RHF is often the result of left heart failure.

Cor pulmonale: when right heart failure is isolated, it is typically due to pulmonary issues, and, therefore, is referred to as cor pulmonale.

Pathophysiology:
Right ventricular end diastolic pressure is elevated, which leads to increased pressures in the right atrium. As a result, the blood becomes "backed up" and raises systemic venous pressures.

Signs and Symptoms: RHF elevates systemic venous pressure and hepatic congestion.

Elevated systemic venous pressure and congestion leads to peripheral edema.

Elevated SVP often produces so-called "pitting edema" in the lower extremities, and congestion in the abdominal organs, especially the liver.

Hepatic portal congestion gives the liver a "speckled" or "mottled" appearance, often referred to as "nutmeg liver;" note that hepatoportal congestion exacerbates edema.

Hepatojubular reflux is a sign of right heart failure; it is characterized by distension of the jugular veins in the neck when pressure is applied to the right abdominal quadrant (over the liver).
Pericardial and peritoneal effusions (ascites) may occur.

Clinical Cases

Case 1: Laboratory Testing in Heart Failure

A 65-year-old female presents to the emergency department with a primary complaint of dyspnea. She reports her symptoms have progressed over the past 24 hours. Additionally, she reports fatigue and swelling in her legs and ankles for the past week. The patient denies any chest pain or other associated symptoms. Her past medical history is significant for diabetes, hypertension, rheumatoid arthritis, and hyperlipidemia.

On physical examination, she is afebrile, weighs 75 kg (165 lb), her blood pressure is 170/100 mm Hg, heart rate 90/min, respiratory rate 20/min, and oxygen saturation is 94 percent on 2L of oxygen via nasal cannula. Evaluation of her neck reveals jugular venous distention. Assessment of her chest demonstrates a laterally displaced apex beat and a third heart sound audible on auscultation. Otherwise, her lungs are clear. She also has 2 plus pitting edema bilaterally up to her knees. You order a chest x-ray and electrocardiogram.

What blood test is most likely elevated in this patient secondary to her diagnosis?

Answer

  • B-Type Natriuretic Peptide

Explanation

The patient in this scenario presents with signs and symptoms consistent with congestive heart failure. This is supported by her history and physical findings of jugular venous distention, laterally displaced apex beat and third heart sound (S3), and bilateral lower extremity edema.

An elevation in her plasma level of B-type natriuretic peptide (BNP) would be expected in this case. BNP is a hormone secreted from cardiac cells (ventricular myocytes) in response to myocardial stretch and stress. A normal BNP level in a healthy individual is less than 100 pg/ml.

Measurement of a BNP level is used to distinguish between cardiogenic and noncardiogenic causes of shortness of breath (dyspnea). Comparisons of levels among different patients is less useful than tracking an individual patient's levels over time (trajectory).

The overall sensitivity of BNP in detecting heart failure is 97 percent. A normal BNP level (less than 100 pg/ml) essentially excludes heart failure as the cause of a patient's dyspnea. It should be noted that baseline levels are often higher in patients with diabetes, renal failure, and acute coronary syndrome (ACS), as well as in obese patients.

References

  • Francis GS, Felker GM, Tang WH. A Test in Context: Critical Evaluation of Natriuretic Peptide Testing in Heart Failure. J Am Coll Cardiol. 2016 Jan 26;67(3):330-7.
  • Koratala A, Kazory A. Natriuretic Peptides as Biomarkers for Congestive States: The Cardiorenal Divergence. Dis Markers. 2017;2017:1454986.

Exercise 2: Management of Decompensated Heart Failure

A 58-year-old male presents to the ER with compliant of dyspnea that started 5 days ago. He reports that it wakes him up and night and prevents him from falling back asleep. This is the first time the patient has experienced such symptoms. His past medical includes hypertension, which has not been controlled due to noncompliance. The patient was treated with anticoagulants for 6 months 6 years ago for a DVT that developed after surgery following a motor vehicle accident. The patient has been using tobacco since the his early 20s as well but denies the use of alcohol.

Upon examination, the patient's blood pressure is 180/110 mmHg, pulse is 112, and SaO2= 90% on room air. Pulmonary auscultation reveals audible crackles in both lung bases in addition to scattered wheezing.

What would be the next step in managing this patient?

Answer

  • Furosemide administration

Explanation

This patient is experiencing symptoms of dyspnea, paroxysmal nocturnal dyspnea, and orthopnea, which are secondary to volume overload, consistent with a diagnosis of acute decompensated heart failure. Bibasilar crackles, wheezing and hypoxemia may or may not be present; in this case, they are present. Furosemide is a loop diuretic that acts on the kidneys to increase water loss, which will treat this patient's volume overload.

Note that using beta blockers in acute management may worsen the patient's condition.

References

  • Muñoz, D., & Felker, G. M. (2013). Approaches to decongestion in patients with acute decompensated heart failure. Current cardiology reports, 15(2), 1-6.
  • Heart Failure Society of America, Lindenfeld, J., Albert, N. M., Boehmer, J. P., Collins, S. P., Ezekowitz, J. A., Givertz, M. M., Katz, S. D., Klapholz, M., Moser, D. K., Rogers, J. G., Starling, R. C., Stevenson, W. G., Tang, W. H., Teerlink, J. R., & Walsh, M. N. (2010). HFSA 2010 Comprehensive Heart Failure Practice Guideline. Journal of cardiac failure, 16(6), e1–e194. https://doi.org/10.1016/j.cardfail.2010.04.004

Board Review

Heart Failure

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References

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  • "CV Physiology | Heart Failure - Introduction." Accessed June 21, 2019. https://www.cvphysiology.com/Heart%20Failure/HF002#What%20are%20the%20causes.
  • Gazewood, John D., and Patrick L. Turner. "Heart Failure with Preserved Ejection Fraction: Diagnosis and Management." American Family Physician 96, no. 9 (November 1, 2017): 582–88.
  • Havakuk, Ofer, Kevin S. King, Luanda Grazette, Andrew J. Yoon, Michael Fong, Noa Bregman, Uri Elkayam, and Robert A. Kloner. "Heart Failure-Induced Brain Injury." Journal of the American College of Cardiology 69, no. 12 (March 2017): 1609–16. https://doi.org/10.1016/j.jacc.2017.01.022.
  • Hawkins, Nathaniel Mark, Mark C. Petrie, Pardeep S. Jhund, George W. Chalmers, Francis G. Dunn, and John J.V. McMurray. "Heart Failure and Chronic Obstructive Pulmonary Disease: Diagnostic Pitfalls and Epidemiology." European Journal of Heart Failure 11, no. 2 (February 2009): 130–39. https://doi.org/10.1093/eurjhf/hfn013.
  • "Heart Disease and Stroke Statistics—2019 Update: A Report From the American Heart Association | Circulation." Accessed June 25, 2019. https://www.ahajournals.org/doi/full/10.1161/CIR.0000000000000659.
  • "Heart Failure (HF) - Cardiovascular Disorders." Merck Manuals Professional Edition. Accessed June 21, 2019. https://www.merckmanuals.com/professional/cardiovascular-disorders/heart-failure/heart-failure-hf.
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  • Mukerji, Vaskar. "Dyspnea, Orthopnea, and Paroxysmal Nocturnal Dyspnea." In Clinical Methods: The History, Physical, and Laboratory Examinations, edited by H. Kenneth Walker,
  • W. Dallas Hall, and J. Willis Hurst, 3rd ed. Boston: Butterworths, 1990. http://www.ncbi.nlm.nih.gov/books/NBK213/.
  • Ware, Lorraine B., and Michael A. Matthay. "Acute Pulmonary Edema." New England Journal of Medicine 353, no. 26 (December 29, 2005): 2788–96. https://doi.org/10.1056/NEJMcp052699.
  • Yancy, Clyde W., Mariell Jessup, Biykem Bozkurt, Javed Butler, Donald E. Casey, Monica M. Colvin, Mark H. Drazner, et al. "2016 ACC/AHA/HFSA Focused Update on New Pharmacological Therapy for Heart Failure: An Update of the 2013 ACCF/AHA Guideline for the Management of Heart Failure." Journal of the American College of Cardiology 68, no. 13 (September 2016): 1476–88. https://doi.org/10.1016/j.jacc.2016.05.011.
  • "2017 ACC/AHA/HFSA Focused Update of the 2013 ACCF/AHA Guideline for the Management of Heart Failure." Journal of the American College of Cardiology 70, no. 6 (August 2017): 776–803. https://doi.org/10.1016/j.jacc.2017.04.025.
  • Yancy, Clyde W., Mariell Jessup, Biykem Bozkurt, Javed Butler, Donald E. Casey, Mark H. Drazner, Gregg C. Fonarow, et al. "2013 ACCF/AHA Guideline for the Management of Heart Failure." Journal of the American College of Cardiology 62, no. 16 (October 2013): e147–239. https://doi.org/10.1016/j.jacc.2013.05.019.
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