Pathophysiology of Heart Failure
Definition of Heart Failure: Systemic perfusion inadequate to meet the oxygen and fuel demands of tissue beds throughout the body secondary to a failing cardiac pump.
Two types of Heart Failure: (1) Systolic: characterized by reduced cardiac contractility. (2) Diastolic: Poor ventricular filling secondary to impaired cardiac relaxation.
Common causes of Heart Failure: 60% of HF patients have left ventricular systolic failure. This is most often due to significant (end-stage) coronary artery disease (CAD). These patients have frequently had myocardial infarctions. Alternatively, many experience more or less chronic under-perfusion of their myocardium. Some patients have both old infarcts and poor cardiac perfusion. Other causes of left ventricular failure are valvular disease, chronic hypertension, congenital heart disease, or cardiomyopathies that may secondary to exposure to heart damaging substances (many drugs, also alcohol) or may be idiopathic. Right sided systolic malfunction is less common and are sometimes seen in high output states such as pregnancy, thyrotoxicosis, A-V fistulas, and severe anemia. Left ventricular diastolic malfunction may also be attributed to chronic myocardial under-perfusion and chronic hypertension. Rarely it may be due to various types of cardiomyopathies (restrictive, hypertrophic or infiltrative.
Risk Factors: Because it is a disease associated with older adults, and because of an aging population, HF incidence is is expected to rise. And while many patients with CAD survive their myocardial infarctions due to modern reperfusion techniques, they are usually left with some residual ventricular dysfunction. About 2% of Americans have primary HF and they account for over a million hospitalizations yearly. In addition, a smaller but still significant number of patients have HF secondary to other diseases and these commonly decompensate and require frequent readmissions to acute care hospitals.
As stated previously the most common causes of HF are hypertension and CAD. However, other significant risk factors for HF include obesity, chronic alcoholism, diabetes mellitus, hypercholesterolemia, and a family history of cardiomyopathy.
Two types of Heart Failure: (1) Systolic: characterized by reduced cardiac contractility. (2) Diastolic: Poor ventricular filling secondary to impaired cardiac relaxation.
Common causes of Heart Failure: 60% of HF patients have left ventricular systolic failure. This is most often due to significant (end-stage) coronary artery disease (CAD). These patients have frequently had myocardial infarctions. Alternatively, many experience more or less chronic under-perfusion of their myocardium. Some patients have both old infarcts and poor cardiac perfusion. Other causes of left ventricular failure are valvular disease, chronic hypertension, congenital heart disease, or cardiomyopathies that may secondary to exposure to heart damaging substances (many drugs, also alcohol) or may be idiopathic. Right sided systolic malfunction is less common and are sometimes seen in high output states such as pregnancy, thyrotoxicosis, A-V fistulas, and severe anemia. Left ventricular diastolic malfunction may also be attributed to chronic myocardial under-perfusion and chronic hypertension. Rarely it may be due to various types of cardiomyopathies (restrictive, hypertrophic or infiltrative.
Risk Factors: Because it is a disease associated with older adults, and because of an aging population, HF incidence is is expected to rise. And while many patients with CAD survive their myocardial infarctions due to modern reperfusion techniques, they are usually left with some residual ventricular dysfunction. About 2% of Americans have primary HF and they account for over a million hospitalizations yearly. In addition, a smaller but still significant number of patients have HF secondary to other diseases and these commonly decompensate and require frequent readmissions to acute care hospitals.
As stated previously the most common causes of HF are hypertension and CAD. However, other significant risk factors for HF include obesity, chronic alcoholism, diabetes mellitus, hypercholesterolemia, and a family history of cardiomyopathy.
In spite of many advancements in the care of patients with heart disease, between 5 and 20% of HF patients will die each year. Not unexpectedly, patients with NYHA Class IV failure are at greatest risk for death. For about half of these, death is sudden. The remaining will die of end-organ hypo-perfusion leading to failure. The most commonly involved organ are kidneys. Renal disease, therefore is an indicator of poor prognosis. Other prognostic signs include cachexia, valvular distortion and dysfunction causing regurgitation, frequent ventricular arrhythmias, reduced ejection fraction (EF). Biomarkers suggesting poor prognosis include elevated B-type natriuretic peptide (BNP) and serum catecholamine levels or severe distension of the left ventricle.
Evolution of Heart Failure: Regardless of the cause, a failing ventricle results in reduced blood volume circulating to all parts of the body. Compensatory mechanisms serve to increase output but, in the long run, make HF progressively worse. Some of these maladaptations are classed as neurohormonal responses. Initially, a decrease in blood flow will result in the activation of the sympathetic nervous system. Release of catecholamines causes peripheral vasoconstriction and "thrashes" the heart causing it to beat faster and harder (increased rate and contratility). Unfortunately, they also drastically increase the amount of oxygen demanded by the myocardium and makes ischemia worse. Increased sympathetic tone also increases arrhythmias and ultimately promote cardiac remodeling. Significantly, catecholamines (and decreased renal perfusion) induce the kidneys to release renin. The RAAS system end-product (Angiotensin II) raises systemic blood pressure increases sodium and water retention, release of aldosterone which further aggravates sodium and water retention. These changes in osmotic conditions (increased sodium and water) and baroreceptor responses cause the hypothalamus to release vasopressin, which influences the distal tubules of the kidneys to retain even more water. Some of these maladaptations are modulated down by the release of BNP from stretched cardiac myocytes themselves. The effects of BNP include, vasodilation throughout the body (systemic and pulmonary), may increase water and sodium excretion, and may directly act counteract the influence of harmful neurohormones.
Over time, neurohormonal effects on the cardiac cells causes them to hypertrophy and elongate. As a result, the heart changes shape (remodels) becoming more dilated and ball-shaped. These changes do result in increased stroke volume (SV) but do not improve EF. The altered shape of the heart is less mechanically efficient (making the heart work harder and demand more oxygen) and the dilation of the ventricles causes increased wall tension. All remodeling makes subendocardial oxygen demand to increase. In the presence of CAD, the body cannot supply more blood to these tissues resulting in myocardial ischemia. The mitral valve that worked perfectly in a normally shaped heart, becomes insufficient in a remodeled and dilated left ventricle. As a result it may regurgitate blood and further increase the work of the heart muscle. The end result of mitral regurgitation is pulmonary congestion.
In diastolic heart failure, as mentioned above, the ventricles are unable to relax and fill during diastole. Though the left atrium works harder to fill the ventricle, pressures build up in the pulmonary capillaries. As this worsens, pulmonary edema develops. These patients are particularly symptomatic with any exertion that increases heart rate. The faster the rate, the briefer the diastolic filling time, the worse the failure. Neurohormonal maladaptations (increased sympathetic tone, RAAS system activation) similarly worsen diastolic dysfunction. Furthermore, these patients are highly susceptible to atrial fibrillation due to the excessive demands on atrial muscle. The loss of atrial "kick" can cause sudden deterioration of ventricular function and consequent pulmonary edema.
Evolution of Heart Failure: Regardless of the cause, a failing ventricle results in reduced blood volume circulating to all parts of the body. Compensatory mechanisms serve to increase output but, in the long run, make HF progressively worse. Some of these maladaptations are classed as neurohormonal responses. Initially, a decrease in blood flow will result in the activation of the sympathetic nervous system. Release of catecholamines causes peripheral vasoconstriction and "thrashes" the heart causing it to beat faster and harder (increased rate and contratility). Unfortunately, they also drastically increase the amount of oxygen demanded by the myocardium and makes ischemia worse. Increased sympathetic tone also increases arrhythmias and ultimately promote cardiac remodeling. Significantly, catecholamines (and decreased renal perfusion) induce the kidneys to release renin. The RAAS system end-product (Angiotensin II) raises systemic blood pressure increases sodium and water retention, release of aldosterone which further aggravates sodium and water retention. These changes in osmotic conditions (increased sodium and water) and baroreceptor responses cause the hypothalamus to release vasopressin, which influences the distal tubules of the kidneys to retain even more water. Some of these maladaptations are modulated down by the release of BNP from stretched cardiac myocytes themselves. The effects of BNP include, vasodilation throughout the body (systemic and pulmonary), may increase water and sodium excretion, and may directly act counteract the influence of harmful neurohormones.
Over time, neurohormonal effects on the cardiac cells causes them to hypertrophy and elongate. As a result, the heart changes shape (remodels) becoming more dilated and ball-shaped. These changes do result in increased stroke volume (SV) but do not improve EF. The altered shape of the heart is less mechanically efficient (making the heart work harder and demand more oxygen) and the dilation of the ventricles causes increased wall tension. All remodeling makes subendocardial oxygen demand to increase. In the presence of CAD, the body cannot supply more blood to these tissues resulting in myocardial ischemia. The mitral valve that worked perfectly in a normally shaped heart, becomes insufficient in a remodeled and dilated left ventricle. As a result it may regurgitate blood and further increase the work of the heart muscle. The end result of mitral regurgitation is pulmonary congestion.
In diastolic heart failure, as mentioned above, the ventricles are unable to relax and fill during diastole. Though the left atrium works harder to fill the ventricle, pressures build up in the pulmonary capillaries. As this worsens, pulmonary edema develops. These patients are particularly symptomatic with any exertion that increases heart rate. The faster the rate, the briefer the diastolic filling time, the worse the failure. Neurohormonal maladaptations (increased sympathetic tone, RAAS system activation) similarly worsen diastolic dysfunction. Furthermore, these patients are highly susceptible to atrial fibrillation due to the excessive demands on atrial muscle. The loss of atrial "kick" can cause sudden deterioration of ventricular function and consequent pulmonary edema.
Heart Failure Complicated by Anemia
Mr. F. is in heart failure. Does he have a "Big O" (oxygenation) problem? You bet! In fact... he has several
Back story: Mr. F is a 58 year old man who has been admitted several times with heart failure. 2 months ago he developed atrial fibrillation and was put on Coumadin (a blood thinner). Unfortunately, no one really took the time to teach him about his medications and he took them improperly. (In addition to his Coumadin, he was taking non-steroidal medications like ibuprophen when he got aches and pains.) Consequently, he began having a slow bleed somewhere in his GI tract and became anemic. The patient states he has gained 6 pounds over the last 2 days.
Assessments:
Vital signs: T = 98.8, P = 115 irregularly irregular, BP = 104/58, R = 28, %sat = 90 on 2L/min
Hematology studies: WBC = 6800, Hct = 22, Hgb = 7.1
Chemistries: Na+ 148, K+ 3.5, Cl- 119, HCO3- 28 BUN 32, Creatinine 2.2 Glucose 115
Observations: Bed is at 45 degree angle, he has jugular vein distention (JVD) and swollen ankles, occasional cough is non-productive,
Physical examination: He has fine crackles in his lung bases that do not clear with cough, he has an extra heart sound (S3), he has few bowel sounds and his stomach is somewhat distended.
Patient reports he "gets whipped" and out of breath if he walks to the bathroom, he has been slightly nauseated (no emesis) and without appetite for the last 5 days, and thinks his last bowel movement was 3 days ago.
And Anemia too?: Depending upon how much pathophysiology you've had, you might recognize that Mr. F has both left and right sided heart failure. For several years he's had a very sick heart which struggles to provide his body with adequate oxygen. But now Mr. F. has become anemic, and his heart is having to work harder (to circulate the reduced amount of hemoglobin) and is getting relatively less oxygen itself. At a pulse rate, of 115 his heart is working harder than it can really afford to. Blood is backing up... into his jugular veins, into the venous system that takes blood from his lower extremities and gut to the inferior vena cava, and back to his heart. Because there is a lot of excess liquid in Mr. F's lungs, his alveoli are filling with fluid, and oxygen is not diffusing readily across the alveolar-capillary membranes. So... let's write a nursing diagnosis (or three) for Mr. F. using proper syntax.
(1) Impaired oxygenation RT impaired diffusion of oxygen across the alveolar capillary membrane AEB 90% sat on 2L/min oxygen, tachycardia, fine basilar rales
(2) Impaired oxygenation RT reduced oxygen carrying capacity of blood AEB Hct of 22 / Hgb of 7.1 and exertional dyspnea, tachycardia at rest.
In the document on the next page(a "Clinical Reasoning Table") note how only the relevant assessment data (a.k.a. "focused assessment") is used to support each of these problem statements
Assessments:
Vital signs: T = 98.8, P = 115 irregularly irregular, BP = 104/58, R = 28, %sat = 90 on 2L/min
Hematology studies: WBC = 6800, Hct = 22, Hgb = 7.1
Chemistries: Na+ 148, K+ 3.5, Cl- 119, HCO3- 28 BUN 32, Creatinine 2.2 Glucose 115
Observations: Bed is at 45 degree angle, he has jugular vein distention (JVD) and swollen ankles, occasional cough is non-productive,
Physical examination: He has fine crackles in his lung bases that do not clear with cough, he has an extra heart sound (S3), he has few bowel sounds and his stomach is somewhat distended.
Patient reports he "gets whipped" and out of breath if he walks to the bathroom, he has been slightly nauseated (no emesis) and without appetite for the last 5 days, and thinks his last bowel movement was 3 days ago.
And Anemia too?: Depending upon how much pathophysiology you've had, you might recognize that Mr. F has both left and right sided heart failure. For several years he's had a very sick heart which struggles to provide his body with adequate oxygen. But now Mr. F. has become anemic, and his heart is having to work harder (to circulate the reduced amount of hemoglobin) and is getting relatively less oxygen itself. At a pulse rate, of 115 his heart is working harder than it can really afford to. Blood is backing up... into his jugular veins, into the venous system that takes blood from his lower extremities and gut to the inferior vena cava, and back to his heart. Because there is a lot of excess liquid in Mr. F's lungs, his alveoli are filling with fluid, and oxygen is not diffusing readily across the alveolar-capillary membranes. So... let's write a nursing diagnosis (or three) for Mr. F. using proper syntax.
(1) Impaired oxygenation RT impaired diffusion of oxygen across the alveolar capillary membrane AEB 90% sat on 2L/min oxygen, tachycardia, fine basilar rales
(2) Impaired oxygenation RT reduced oxygen carrying capacity of blood AEB Hct of 22 / Hgb of 7.1 and exertional dyspnea, tachycardia at rest.
In the document on the next page(a "Clinical Reasoning Table") note how only the relevant assessment data (a.k.a. "focused assessment") is used to support each of these problem statements