Chapter 34 Heart Failure

Question 1

Cultural and Ethnic Health Disparities

Heart Failure

Answer 1

• African Americans have a higher incidence of HF, develop HF at an earlier age, and experience higher mortality rates related to HF than whites.
• African Americans may experience more ACE inhibitor–related angioedema than whites.
• Isosorbide dinitrate/hydralazine (BiDil) is used for the treatment of HF in African Americans. This combination drug is approved for use only in this ethnic group.
• Asians have an extremely high risk (15%-50%) for ACE inhibitor–related cough.
ACE, Angiotensin-converting enzyme; HF, heart failure

Question 2

complex clinical syndrome that results in the inability of the heart to provide sufficient blood to meet the O2 needs of tissues and organs

Answer 2

Heart failure (HF)

Question 3

key manifestations of HF

Answer 3

A defect in either ventricular filling (diastolic dysfunction) or ventricular ejection (systolic dysfunction)

Question 4

The amount of blood pumped by the left ventricle with each heart beat is called the ejection fraction (EF). The American Academy of Cardiology Foundation (ACCF) has adopted the terms?

Answer 4

heart failure with reduced EF (HFrEF) and heart failure with preserved EF (HFpEF) to describe systolic and diastolic HF

Question 5

primary risk factors for HF

Answer 5

Hypertension and CAD
- Hypertension is a modifiable risk factor that should be aggressively treated and managed. Long-term treatment of hypertension reduces the incidence of HF by 50%.1 Other co-morbidities, such as diabetes, metabolic syndrome, advanced age, tobacco use, and vascular disease, also contribute to the development of HF.

Question 6

Primary Causes of Heart Failure

Answer 6

• Hypertension, including hypertensive crisis
• Coronary artery disease, including myocardial infarction
• Rheumatic heart disease
• Congenital heart defects (e.g., ventricular septal defect)
• Pulmonary hypertension
• Cardiomyopathy (e.g., viral, postpartum, substance abuse)
• Hyperthyroidism
• Valvular disorders (e.g., mitral stenosis)
• Myocarditis

Question 7

Pathophysiology
Left-Sided Heart Failure.
The most common form of HF is left-sided HF. Left-sided HF results either from the inability of the left ventricle (LV) to?

Answer 7

(1) empty adequately during systole or (2) fill adequately during diastole. Left-sided HF can be further classified as systolic, diastolic, or mixed systolic and diastolic failure.

Question 8

Systolic Failure or Heart Failure with Reduced EF.
Systolic failure, also known as HFrEF, results from an inability of the heart to pump blood effectively.
1) The hallmark of systolic failure is?
2) Normal EF is 55% to 60%. Patients with HFrEF generally have?
3) HFrEF is caused by?

Answer 8

1) a decrease in the EF.
2) EF less than 45%. It can be as low as 5% to 10%.
3) impaired contractile function (e.g., MI), increased afterload (e.g., hypertension), cardiomyopathy, and mechanical abnormalities (e.g., valvular heart disease).

Question 9

Systolic Failure or Heart Failure with Reduced EF

• The LV in systolic failure loses its ability to generate enough pressure to eject blood forward through the aorta.
  1) Over time, the LV becomes?
  2) The weakened heart muscle cannot generate adequate stroke volume, which affects CO. Because the LV cannot effectively push blood forward, what happens?
  3) When the LV fails, blood backs up into the?

Answer 9

1) LV becomes dilated and hypertrophied.
2) end diastolic volumes and pressures in the LV increase. 3) left atrium. This causes fluid accumulation in the lungs. The increased pulmonary hydrostatic pressure causes fluid leakage from the pulmonary capillary bed into the interstitium and then the alveoli. This results in pulmonary congestion and edema

Question 10

Systolic HF main points

Answer 10

• Weak pump
• Dilated, hypertrophied
• Decreased ejection fraction
• Impaired contractility
• Increased afterload

Question 11

Diastole HF main points

Answer 11

• Impaired filling
• Stiff ventricle
• Decreased stroke volume
• Normal ejection fraction
• Left ventricular hypertrophy

Question 12

Heart Failure Facts

Answer 12

• Heart unable to pump enough blood to other organs and tissues.
• Vasoconstriction (SVR)/Fluid Retention(Preload)
• CAD, advancing age, hypertension, diabetes, cigarette smoking, obesity, high cholesterol.
• Heart failure is associated with numerous CV diseases, particularly long standing HTN, CAD and MI.
• This is primarily a disease of older adults.
• Same incidence in men and women.
• Smoking, diabetes, high cholesterol and obesity of course lead to this.

Question 13

Systolic vs Diastolic Heart Failure

Answer 13

1) Systolic:
- Weak pump
- Dilated, hypertrophied
- Decreased ejection fraction
- Impaired contractility
- Increased afterload

2) Diastolic:
- Impaired filling
- Stiff ventricle
- Decreased stroke volume
- Normal ejection fraction
- Left ventricular hypertrophy

• Systolic
• Innability of the heart to pump effectively
• Hallmark is a decrease in EF – What is EF? Ejection Fraction – Normal is 55% to 60% – pt with Systolic HF generally have an EF less than 45% and can be as low as 5% to 10%.
• So systolic heart failure is caused by impaired contractile function (e.g. MI), increased afterload (e.g. HTN).
• Diastolic failure
• Inability of the ventricles to relax and fill during diastole.
• HTN is the most important cause.
• Old age, female, diabetes and obesity are risk factors
• The left vent is generally stiff and non compliant.
• High filling pressures because of the stiff ventricles.
• Decreased filling results in decreased stroke volume and cardiac output.

Question 14

Diastolic Failure or Heart Failure With Preserved EF.

1) Diastolic failure, or HFpEF, is the?
2) Approximately 50% of patients with HF have HFpEF. What is the most important cause of diastolic failure?
3) Other risk factors include?
4) In diastolic failure, the?
5) Diastolic failure is characterized by?
6) The end result of diastolic failure is?
7) HFpEF is diagnosed by the following criteria:
8) Therapies for HFpEF are targeted at?

Answer 14

1) inability of the ventricles to relax and fill during diastole. 2) Hypertension is the most important cause of diastolic failure
3) older age, female gender, diabetes, and obesity
4) LV is generally stiff and noncompliant.
5) high filling pressures because of stiff ventricles. Decreased filling of the ventricles results in decreased stroke volume and CO.
6) the same as systolic failure (e.g., pulmonary congestion).
7) (1) signs and symptoms of HF
(2) normal EF
(3) evidence of LV diastolic dysfunction by echocardiography or cardiac catheterization.
8) reducing underlying risk factors and treating co-morbidities.

Question 15

Heart Failure

• Men
• Women

Answer 15

• Men
  • Men experience systolic failure more frequently than women.
  • Men with asymptomatic systolic failure experience greater mortality benefit from ACE inhibitor therapy than women.
• Women
  • Women experience diastolic failure more frequently than men.
  • Women have a higher risk of ACE inhibitor–related cough than men.
  • Women experience more digitalis-related death than men.
  • Women with diabetes are more predisposed to HF than men.
  ACE, Angiotensin-converting enzyme; HF, heart failure.

Question 16

Right vs Left Heart Failure

Answer 16

1) Right
- Backup to right atrium and venous circulation.
- JVD
- Hepatomegaly
- Splenomegaly
- Peripheral edema, weight gain,
- Fatigue, anorexia, GI Bloating
- Right side HF happens when the right ventricle (RV) fails to pump effectively, When this happens, fluid backs up into the venous system. Causing movement of fluid into the tissues and organs (e.g. peripheral edema, abdominal ascites, JVD). This also means a decrease of blood flow to the lungs. Most common cause of right side HF is left side HF.
Think about how the heart has to work — all this fluid is backed up… JVD, edema
2) Left
- Most common
- Backup to left atrium and pulmonary veins.
- Fluid backup to pulmonary capillary bed.
- Interstitium
- Alveoli, Weak, anxious, Shallow rapid breathing.
- Results from inability of LV to empty adequately during systole or fill adequately during diastole.
- Its job is to squeeze the blood out through aortic valve
- decrease amount of oxygenated blood out the body.
- The heart is not pumping so blood backs into the lungs - will hear crackles, have dyspnea,
- Will feel fatigued, decrease pulses.

Question 17

Pathophysiology of heart failure.

Answer 17

• Elevated systemic vascular resistance results in left-sided heart failure that leads to right-sided heart failure.
• Systemic vascular resistance and preload are exacerbated by the renin-angiotensin-aldosterone system.

Question 18

Right-sided HF occurs when?

Answer 18

the right ventricle (RV) fails to pump effectively. When the RV fails, fluid backs up into the venous system. This causes move­ment of fluid into the tissues and organs (e.g., periph­eral edema, abdominal ascites, hepatomegaly, jugular venous distention).

Question 19

1) The most common cause of right-sided HF is?

2) Other causes of right-sided HF (independent of the function of the LV) include?

Answer 19

1) left-sided HF. As the LV fails, fluid backs up into the pulmonary system, causing increased pressures in the lungs. The RV has to work harder to push blood to the pulmonary system. Over time, this increased workload weakens the RV and gradually it fails.
2) RV infarction, pulmonary embolism, and cor pulmonale (RV dilation and hypertrophy caused by pulmonary disease)

Question 20

Left sided HF

Answer 20

• Paroxysmal nocturnal dyspnea (sensation of shortness of breath that awakens the patient)
• Elevated pulmonary capillary wedge pressure
• Pulmonary congestion: cough, crackles, wheezes, blood tinged sputum, tachypnea
• Restlessness
• Confusion
• Orthopnea (sensation of breathlessness in the recumbent position, relieved by sitting or standing)
• Tachycardia
• Exertional Dyspnea
• Fatigue
• Cyanosis

Question 21

Right Sided HF

Answer 21

• Fatigue
• Increased peripheral venous pressure
• Ascites
• Enlarged liver and spleen (Hepatosplenomegaly)
• May be secondary to chronic pulmonary problems (COPD)
• DJV
• Anorexia and complaints of GI distress
• Weight gain
• Dependent edema

Question 22

Compensatory Mechanisms.
HF can have an abrupt onset as with acute MI, or it can be a subtle process resulting from slow, progressive changes. The overloaded heart uses com­pensatory mechanisms to try to maintain adequate CO. The main compensatory mechanisms include

Answer 22

(1) neurohormonal responses: renin-angiotensin-aldosterone system (RAAS) and the sympathetic nervous system (SNS)
(2) ventricular dilation
(3) ventricular hypertrophy

Question 23

HF Vicious Cycle

• Abrupt or?
• Progressive
• Compensatory mechanisms

Answer 23

• Abrupt or insidious
• Progressive
• Compensatory mechanisms
• Sympathetic nervous system
• Neurohormonal mechanisms
• Ventricular dilation
• Ventricular hypertrophy

Question 24

Sympathetic nervous system.
In response to an inadequate stroke volume and CO, the SNS is activated, resulting in the release of catecholamines (epinephrine and norepinephrine).
1) The circulating catecholamines enhance?
2) Initially, the compensatory mechanisms are beneficial with a result of increased CO. However, over time these factors become?

Answer 24

1) peripheral vasoconstriction and cause an increase in the HR (chronotropy) and myocardial contractility (inotropy).
2) harmful and counterproductive, as they increase the workload, preload (volume), and O2 requirement in an already failing heart.

Question 25

Sympathetic nervous system 1) In HF, continuous activation of the neurohormonal responses (RAAS and SNS) leads to elevated levels of? 2) Together, these factors result in an increase in the? 3) Remodeling involves? 4) Although the ventricles become larger, they become less effective pumps. Ventricular remodeling is a risk factor for? 5) Drug therapies to prevent or reverse remodeling and decrease mortality are recommended. These include?

Answer 25

1) norepinephrine, angiotensin II, aldosterone, ADH, endothelin, and proinflammatory cytokines. 2) heart's workload, ventricular dysfunction, and ventricular remodeling. 3) hypertrophy of the ventricular myocytes. This results in large, abnormally shaped contractile cells. This altered shape of the ventricles eventually leads to increased ventricular mass, increased wall tension, increased O2 consumption, and impaired contractility. 4) life-threatening dysrhythmias and sudden cardiac death (SCD). 5) ACE inhibitors, β-adrenergic blockers (β-blockers), and aldosterone antagonists.

Question 26

Sympathetic Nervous System Main Points

Answer 26

- Low cardiac output - Release of epinephrine and norepinephrine - Increased heart rate, contractility and peripheral vasoconstriction - Increased myocardial oxygen need. - Compensating mechanisms increase problems for the heart. * This is a response to an inadequate stroke volume and cardiac output. Results in the release of catecholamines. When circulated it enhances the peripheral vaso- constriction and caused an increase in HR and contractility. At first this is great but over time this becomes harmful and counterproductive as they increase the workload of the already failing heart.

Question 27

Neurohormonal Response Main Points

Answer 27

- Decreased cardiac output- decreased perfusion of the kidneys - Decrease in cerebral perfusion pressure * Posterior pituitary- release of ADH - Release of renin * Angiotensin II * Adrenal cortex- release of aldosterone * Peripheral vasoconstriction - The RAAS works to maintain normal hemostasis. The activation results in BP, fluid and electrolyte control. As the cardiac output falls, blood flow to the kidneys decreases – this is sensed by the juxtaglomerular apparatus in the kidneys as a decreased volume problem. In response the kidneys release renin which circulates around until it reaches the liver and converts angiotensin to angiotensin I --- angiotensin I is converted to angiotensin II in the lungs --- this causes the activation of the SNS to increase BP, HR --- the adrenal cortex releases aldosterone which then results in retention of sodium and water, this increases peripheral vasocontraction Basically what you should know is that this results in further vasoconstriction and an increase in cardiac contractility and hypertrophy to a sick heart.

Question 28

Neurohormonal Response Renin-angiotensin-aldosterone system. The RAAS is a regulatory system that works to maintain normal homeostasis. 1) The activation of the RAAS results in? 2) In response to stress, the role of the RAAS is to promote?

Answer 28

1) BP control and fluid and electrolyte balance. 2) retention of fluid and sodium and cause vasoconstriction to raise BP. However, recurrent activation of the RAAS in HF is what is responsible for the signs and symptoms that develop.

Question 29

Neurohormonal Response Renin-angiotensin-aldosterone system. 1) As CO falls, blood flow to the kidneys decreases. This is sensed by the juxtaglomerular apparatus in the kidneys as decreased volume. In response, the kidneys release? 2) Angiotensin I is next converted to angiotensin II by a converting enzyme made in the lungs. Angiotensin II causes? 3) The outcome of the cascade results in further water and sodium retention in an?

Answer 29

1) renin, which converts angiotensinogen to angiotensin I. 2) (1) activation of the SNS to increase BP and HR (2) release of aldosterone from the adrenal cortex, which results in sodium and water retention (3) increased peripheral vasoconstriction, which increases BP (4) stimulation of the pituitary gland, which releases antidiuretic hormone (ADH), which results in water reabsorption. 3) already overloaded state and increased workload of the failing heart.

Question 30

Neurohormonal Response Renin-angiotensin-aldosterone system. Other factors also contribute to the development of HF. 1) The production of endothelin, a potent vasoconstrictor produced by the vascular endothelial cells, is stimulated by?

Answer 30

ADH, angiotensin II, and catecholamines. This results in further arterial vasoconstriction and an increase in cardiac contractility and hypertrophy.

Question 31

Neurohormonal Response Renin-angiotensin-aldosterone system. 1) Locally, proinflammatory cytokines are released by heart cells in response to? 2) Two cytokines, tumor necrosis factor (TNF) and interleukin-1 (IL-1), further depress heart function by causing?

Answer 31

1) various forms of heart injury (e.g., MI). | 2) hypertrophy, contractile dysfunction, and cell death. Over time, a systemic inflammatory response also occurs.

Question 32

Dilation Main Points

Answer 32

- Chamber enlarges in response to increased pressure. - Muscle fibers stretch - Remember Frank Starling law. - Overstretch * The Frank–Starling law of the heart (also known as Starling's law or the Frank–Starling mechanism or Maestrini heart's law) states that the stroke volume of the heart increases in response to an increase in the volume of blood filling the heart (the end diastolic volume) when all other factors remain constant.

Question 33

- Backup to left atrium and pulmonary veins. - Fluid backup to pulmonary capillary bed. - Alveoli, Weak, anxious, Shallow rapid breathing

Answer 33

Left sided HF

Question 34

Remember, the blood cant pump on the right side, so then there is a backup in the body.

Answer 34

Right sided HF

Question 35

HF can have an abrupt onset when someone has an MI or it can be slow resulting from slow progressive changes. The overloaded heart uses compensatory mechanisms to try to maintain CO. This includes?

Answer 35

RAAS – renin angiotensin aldosterone system and the SNS system. Ventricular dilation and hypertrophy.

Question 36

Dilation is an enlargement of the chambers of the heart. It occurs when pressure in the heart chambers (usually the LV) is elevated over time. 1) The heart muscle fibers stretch in response to the? 2) The degree of stretch is directly related to the? 3) This increased contraction initially leads to increased CO and maintenance of BP and perfusion. Dila­tion starts as an adaptive mechanism to cope with increasing blood volume. Eventually this mechanism becomes?

Answer 36

1) volume of blood in the heart at the end of diastole. 2) force of the contraction (systole) (this is the Frank-Starling law). 3) inadequate, because the elastic elements of the muscle fibers are overstretched and can no longer contract effectively, thereby decreasing the CO.

Question 37

Hypertrophy Main Points

Answer 37

- Increase in muscle mass and cardiac wall thickness. - Poor contractility and requires more oxygen - Prone dysrhythmias

Question 38

Hypertrophy is an increase in the muscle mass and heart wall thickness in response to overwork and strain. It occurs slowly because it takes time for this increased muscle tissue to develop. Initially, the increased contractile power of the muscle fibers leads to an increase in CO and maintenance of tissue perfusion. Over time, hypertrophic heart muscle has?

Answer 38

poor contractility, requires more O2 to perform work, has poor coronary artery circulation (tissue becomes ischemic more easily), and is prone to dysrhythmias.

Question 39

Natriuretic Peptides Main Points

Answer 39

- BNP - Enhance diuresis- increases glomerular filtration rates. - Venous and arterial dilation - Inhibit the development of hypertrophy - Triggered by increased pressure * In the bodies attempt to maintain balance they have several conterregulatory processes One is the BNP – brain natriuretic peptide – produced by the heart muscle. This is released by the ventrical – this the hearts way of “waving the white flag” Cry for help – Im drowning. BNP levels go up when the heart cannot pump the way it should. A result greater than 100 pg/ml is abnormal. The higher the number, the more likely heart failure is present and the more severe it is.

Question 40

The body's attempts to maintain balance are demonstrated by several counterregulatory processes. Natriuretic peptides (atrial natriuretic peptide [ANP] and brain [b-type] natriuretic peptide [BNP]) are?

Answer 40

hormones produced by the heart muscle. ANP is released from the atria, and BNP is released from the ventricles in response to increased blood volume in the heart.

Question 41

The natriuretic peptides have renal, cardiovascular, and hormonal effects. 1) Renal effects include? 2) Cardiovascular effects include? 3) Hormonal effects include? 4) The combined effects of ANP and BNP help to?

Answer 41

1) Renal effects include (1) increased glomeru­lar filtration rate and diuresis and (2) excretion of sodium (natriuresis). 2) Cardiovascular= vasodilation and decreased BP. 3) Hormonal= (1) inhibition of aldosterone and renin secretion and (2) interference with ADH release. 4) counter the adverse effects of the SNS and RAAS in patients with HF.

Question 42

Acute HF Main Points

Answer 42

- Pulmonary Edema - Left ventricular failure secondary to CAD - Increased pulmonary vascular pressure - Tachypnea, dyspnea, cough - Decreased O2, Increased CO2 - Anxious, pale, clammy - Orthopnea, wheezing, coughing - Crackles, wheezes, rhonchi * Acute heart failure is defined as the sudden onset of signs and symptoms of HR, requiring urgent medical care. Pulmonary and systemic congestion due to elevated left side and right side filling pressures. Signs and symptoms to look for are listed