Pathophysiology of Congestive Heart Failure

PATHOPHYSIOLOGY

Medical Diagnosis: Congestive Heart Failure

Definition: Congestive Heart Failure is the weakening and dysfunction of the heart in which it is unable to produce enough cardiac output to meet the tissue’s demand (Nowak & Handford, 2014).

Cellular Description:

          Congestive heart failure (CHF) is the inability of the heart to 1) properly fill the ventricles (diastolic dysfunction) and 2) effectively pump blood out of the heart (systolic dysfunction) (Colucci & Cohn, 2019).  Heart failure can be limited to one side of the heart or affect both the left and right ventricle.  It can also be acute or chronic depending on the onset and duration.  There are typically two classifications of CHF: heart failure with preserved ejection fraction (HFpEF) and heart failure with reduced ejection fraction (HFrEF).  In HFpEF, the ventricle is stiff and thickened due to increased volume of myofibrils and cardiomyocyte diameter.  In HFrEEF, the ventricle is dilated and stretched.  There are a variety of ways to categorize the stages of heart failure, but most systems differentiate the risk for HF, the presence of HF without symptoms, the presence of HF with symptoms, and HF with significant symptoms and required interventions.  Regardless of the classification, the prevalence of heart failure demonstrates dysfunction of the heart with a resulting decrease in cardiac output (CO) and thus insufficient perfusion of blood to the oxygen demanding tissues (Inamdar & Inamdar, 2016). 

          The causes of the heart’s failure are extensive.  One such cause is myocardial ischemia. Atherosclerosis and thrombosis can decrease the blood flow to the heart and disrupt the vital delivery of oxygen by the coronary arteries.  Without oxygen, the myocardium is damaged and progressively become necrotic.  As the tissues undergo more and more damage, fibrous connective is deposited.  Fibrosis stiffens the myocardium and decreases its compliance and ability to expand during diastole.  Consequently, the stiffening inhibits the ventricles from filling appropriately and pushes the blood back up into the atria.  The fibrosis and necrosis also weaken the muscle’s ability to contract and eject blood yielding decreased cardiac output (Nowak & Handford, 2014).

          Other causes of congestive heart failure include myocarditis and cardiomyopathies.  These conditions directly damage the heart.  Cardiac valve abnormalities or malfunction may decrease the heart’s ability to cope with the preload and effectively manage the blood within the chambers.  Incompetent valves allow back flow of blood when they are unable to close tightly.  Valves that cannot open fully reduce blood flow through the heart.  Physical obstructions within the heart can also impede cardiac flow.  Obstructions could be a congenital malformation, a mass, thrombus, or a tumor (also known as a myxoma), all of which restrict normal movement of blood through the heart.  Direct damage to the heart’s pericardium, such as adhesions or fibrosis, can affect the heart’s pumping efficacy.  Cardiac tamponade, accumulation of fluid in the pericardium, can place excessive pressure on the heart making it work harder (Nowak & Handford, 2014).

          Yet, there are still more potential causes of CHF.  Alteration of the heart’s electrical conduction, or cardiac dysrhythmias, can compromise CO since they alter the rate and rhythm of the heart.  Hypertension makes the heart work harder to maintain proper CO.  The left ventricle in particular must work harder to overcome the increased resistance and afterload.  Diseases such as chronic anemia and thyrotoxicosis place a high demand on the heart to provide enough blood supply to the body’s tissues.  Whatever the cause of heart failure, there is a consistent characteristic of a dysfunctional heart and decreased cardiac output (Nowak & Handford, 2014).

         In response to these insults on the heart, numerous physical responses are noted.  A process of cardiac remodeling takes place, specifically “structural, functional, cellular, and molecular changes involving the cardiac myocytes and the interstitial collagen matrix” (Colucci & Cohn, 2019).   Hemodynamics, blood pressure, neurohormonal activation, and cytokines contribute to the alterations within the heart.  In CHF, the pathologic alterations typically seen include concentric hypertrophy or thickening of the ventricular wall(s), eccentric hypertrophy or dilation of the ventricular chamber(s), and/or potentially distortion of the entire heart shape from elliptical to spherical.  Intense stress on the ventricle walls from increased preload yields the synthesis of new contractile proteins and new sarcomeres.  Insults to the heart kill cardiomyocytes and cause others to undergo apoptosis.  In response to decreased numbers, the surviving myocytes elongate or grow in diameter as a compensatory mechanism to maintain stroke volume, hence the manifestation of cardiomegaly.  The enlargement of the heart is in good intentions, but it only adds to the stress and demand on the heart as it itself requires more blood supply and oxygen.  The degree to which these alterations change the heart is often directly correlated to the prognosis and pathogenesis of heart failure (Colucci & Cohn, 2019).

          In addition to these physiological and pathological alterations within the heart, there are other systems within the body that seek to help compensate.  The sympathetic nervous system (SNS) increases stimulation to the SA node to increase the heart rate.  The SNS also causes a positive inotropic effect on the heart to strengthen its contractions.  These mechanisms improve cardiac output, but also increase vasoconstriction and blood pressure, which as discussed earlier, is a contributor to the pathogenesis of CHF.  The purpose of vasoconstriction, however, is to ensure blood supply to the major organs.  So, the SNS compensatory mechanisms are both beneficial but also potentially deleterious.

          The kidneys also seek to provide assistance to the dysfunctional heart.  The kidneys are excellent detectors of decreased cardiac output by the heart.  In response, the kidneys release renin to foster the initiation of the renin-angiotensin-aldosterone system.  Essentially, this increases plasma fluid volume to increase blood pressure.  The system has good intentions to improve cardiac output, but more often, the excess fluid only contributes to the major problem of edema seen in CHF.    

          Ultimately, congestive heart failure is a chronically progressive disease.  The body puts in a good effort to try and compensate for the dysfunctional, damaged heart but in most cases, the use of therapeutic interventions is the best route (Nowak & Handford, 2014).

Epidemiology:

• Affects 2-3% of Americans. Within this, 10% are males and 8% are females.
• Recognized as a disease that primarily affects the elderly above age 60.
• There are >3 million doctor visits each year for patients with HF.
• In 2013, there were 5.1 million HF patients in the US.
• In 2013, costs associated with HF was $32 billion. This cost is predicted to increase by three-fold by 2030.
• In 2011, it was estimated that HF costed $110,00/year for one individual patient.
• Approximately 50% of HF patients have a five-year mortality rate.
• Acute decompensated HF accounts for 80% of hospitalizations r/t HF.

(Inamdar & Inamdar, 2016). 

• Mortality of HFpEF is 30% lower than HFrEF.
• In a four-decade study, coronary disease as a cause of HF increased by 41% per calendar decade in men and by 25% in women.
• In a four-decade study, diabetes as a cause of HF increased by. 20% peer decade.
• There are approximately 23 million people worldwide with HF.

(Vasan & Wilson, 2019). 

Risk Factors:

• High BMI
• Metabolic syndrome
• Elevated apolipoprotein B/apolipoprotein A ratio
• Cigarette smoking
• Alcohol abuse
• Acute coronary syndrome/ischemia
• Myocardial infarction
• Thyroid conditions- hyper or hypothyroidism
• Diabetes mellitus
• Anemia
• Depression
• Atherosclerotic disease
• Valvular heart disease
• Congenital abnormalities
• Cardiomyopathy
• Hypertension

(Inamdar & Inamdar, 2016). 

Signs & Symptoms  (Differentiate between Early vs. Late signs/symptoms)

Treatment

Medications(drug classification and a brief description of how the med works),, Diet,  Lifestyle, Surgery,  Activity

Symptoms of HF typically take time to manifest as the heart progressively weakens and efficacy declines. Early stages are often asymptomatic.

• Weakness
• Fatigue
• Lethargy
• Pulmonary congestion
• Edema (dependent)
• Tachycardia
• Cool, clammy skin
• Dyspnea
• Paroxysmal nocturnal dyspnea
• Orthopnea
• Cyanosis
• Cardiomegaly
• Atrial and/or ventricular hypertrophy
• Hypoxia
• Systemic congestion and edema
• Hepatomegaly
• Nutmeg liver
• Splenomegaly
• Distended jugular veins

(Nowak & Handford, 2014).

• Abdominal distention
• Right hypochondrial pain
• Increased jugular vein distention
• Adventitious lung sounds
• Ascites

(Inamdar & Inamdar, 2016). 

• Exercise intolerance
• Unintentional weight loss
• Hypotension
• Low pulse pressure
• Poor or worsening renal function
• Hypoalbuminemia
• Hyponatremia
• Elevated serum natriuretic peptide levels

(Colucci & Dunlay, 2019).

Pts with HFrEF typically respond better to pharmacological treatments and have a better prognosis than pts with HRpEF.

The goal for treatment of HF is to improve the prognosis, reduce mortality, and alleviate symptoms.

Pharmacological methods:

• Diuretics (ex. Thiazides, loop diuretics, potassium sparing)- reduce edema.
• Angiotensin-converting enzyme inhibitors (ex. Enalapril), Angiotensin receptor blockers (ex. Valsartan), Nitrates, Hydralazine- vasodilation and improve left ventricle ejection fraction.
• Beta adrenergic blockers (ex. bisoprolol)
• Aldosterone antagonists (ex. Spironolactone)
• Digoxin- increase cardiac output
• Anticoagulants- decrease risk for thromboembolism.
• Inotropic agents- increase contraction of heart.

• CardioMEMS Sensor- implanted devisee that monitors hemodynamics
• Coronary by-pass surgery
• Angioplasty

Non-pharmacological methods:

• Healthy lifestyle changes
• High fiber diet w/ vegetables
• Regular exercise
• Smoking cessation
• Limited alcohol use
• Improve treatment management and adherence
• Weight monitoring

(Inamdar & Inamdar, 2016). 

Diagnostics (Labs, Radiology, Biopsy, others)

Tests:  List all diagnostic tests that you would expect to be completed with this diagnosis. Give expected values and/or descriptions of each test.

• Physical examination to asses for signs/symptoms (listed above).
• Complete blood count.
• Systolic blood pressure <115 mmHG
• Left ventricular ejection fraction <45%.
• Urinalysis
• Complete metabolic profile for levels of serum electrolytes. Hyponatremia and hypoalbuminemia are seen in HF.
• Blood urea nitrogen
• Serum creatinine > 2.72 mg/dL
• Serum urea >15 mmol/L
• Blood glucose. Normal= 70-99 mg/dL.
• Liver function tests
• Electrocardiogram- abnormal Q, ST, and T waves may be seen.
• Thyroid stimulating hormone
• Chest X-ray to evaluate heart size, pulmonary congestion, and to detect cardio-pulmonary diseases that could cause/contribute to HF.
• Transthoracic echocardiography assesses ventricular function, size, thickness, motion, valve function, and ejection fraction.
• Computerized tomography scans
• Magnetic resonance imaging assesses left ventricle volume and ejection fraction, myocardial perfusion, viability, fibrosis, and heart structures.
• Cardiac CT assess cardiac structure and function.
• Brain natriuretic peptide (BNP) and N-terminal pro-brain natriuretic peptide (NTproBNP). BNP levels less than or equal to 100pg/ml and NTproBNP less than or equal to 300 pg/ml rule out HF. NTproBNP >986 pg/ml increased mortality of HF. 

(Inamdar & Inamdar, 2016). 

• Exercise test to assess cardiopulmonary capability. HF diagnosis if 6 minute walk test distance is less than or equal to 300m, people Vo2 is less than or equal to 12 kg/min.
• Low cardiac index less than or equal to 2.2 L/min/m^2.
• Right atrial pressure greater than or equal to 12 mmHg.
• Mean pulmonary capillary wedge pressure >20 mmHg.
• Right heart catheterization

(Colucci & Dunlay, 2019).

References (APA format)

• Colucci, W. S. & Cohn, J. N. (2019). Pathophysiology of heart failure with reduced ejection fraction: hemodynamic alterations and remodeling. In UpToDate. Retrieved on November 22, 2019 https://www-uptodate-com.ezproxy.coloradomesa.edu/contents/pathophysiology-of-heart-failure-with-reduced-ejection-fraction-hemodynamic-alterations-and-remodeling?search=congestive%20heart%20failure%20cellular&source=search_result&selectedTitle=7~150&usage_type=default&display_rank=4#H1683611.
• Colucci, W. S. & Dunlay, S. M. (2019). Clinical manifestations and diagnosis of advanced heart failure. In UpToDate. Retrieved on November 23, 2019 from https://www-uptodate-com.ezproxy.coloradomesa.edu/contents/clinical-manifestations-and-diagnosis-of-advanced-heart-failure?search=Molecular%20and%20Cellular%20Mechanisms%20in%20Heart%20Failure&source=search_result&selectedTitle=7~150&usage_type=default&display_rank=6.
• Inamdar, A. A. & Inamdar, A. C. (2016). Heart failure: diagnosis, management, and utilization.  In Journal of clinical medicine. Retrieved on November 23, 2019 from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4961993/.
• Nowak, T. J., Handford, A. G. (2014). Pathophysiology: concepts and applications for health care professionals (pp. 269-277). (3rd Ed). United States: The McGraw-Hill Companies.             
• Vasan, R. S. & Wilson, P. W.F. (2019). Epidemiology and cause of heart failure. In UpToDate. Retrieved on November 23, 2019 from https://www-uptodate-com.ezproxy.coloradomesa.edu/contents/epidemiology-and-causes-of-heart-   failure?search=congestive%20heart%20failure&source=search_result&selectedTitle=4~150&usage_type=default&display_rank=4.