Chapter 35 – Heart Failure

 Heart failure
o Complex syndrome
o Is the inability of the heart to provide sufficient blood to meet needs
o Defects
 Either in ventricular filling (Diastolic dysfunction) or ventricular ejection (systolic
dysfunction)
o Ejection fraction
 The amount of blood pumped by the left ventricle with each beat
o Heart failure rates are increasing
 Due to age of population
 Over age 65, HF is the number one reason for hospitalization
 Etiology of Heart failure
o Hypertension and CAD are primary risk factors
o HF is caused by any interference with regulating CO
 Depends on preload, afterload, myocardial contractility, and heart rate
o May be divided into two groups
 Primary causes
 Hypertension
 Coronary artery disease
 Rheumatic heart disease
 Congenital heart defects
 Cardiomyopathy
 Hyperthyroidism
 myocarditis
 Valvular disorders
 Precipitating causes
 Anemia
 Infection
 Pirate talk cirrhosis
 Dysrhythmias
 Obstructive sleep apnea
 Pulmonary embolism
 Paget's disease
 Nutritional deficiencies
 Hypervolemia
 There is also a genetic linkage to HF, but the mechanism is poorly understood
 Pathophysiology
o Left-sided heart failure
 Most common form
 Due to
 Inability of LV to empty during systole
 Inability of LV to fill during diastole
 Systolic failure or Heart failure with Reduced EF
 Inability of the heart to pump blood effectively
o EF of less than 45% (Normal: 55%-60%)
 May be caused by
o Impaired contractily function (MI)
o Increased after load (HTN)
o Cardiomyopathy
 o Mechanical abnormalities (Valvular disease)
 LV loses ability to generate enough pressure
o Dilates and hypertrophies – weakened cannot generate stroke volume
o End diastolic volumes and pressures increase
 Blood backs up into the left atrium
 Fluid accumulates in the lungs
 Hydrostatic pressure causes leakage into alveoli
 Resulting in pulmonary congestion and edema
 Diastolic failure of Heart Failure with preserved EF
 Inability of the ventricles to relax and fill
 HTN is the primary cause
o Female gender, diabetes, and obesity also contribute
 LV becomes stiff and non-compliant
o Decreased filling = decreased stroke volume and CO
 Same manifestations as systolic failure (Pulmonary congestion)
 Diagnosis
o Signs and symptoms of HF
o Normal EF
o Evidence of LV diastolic dysfunction
o Right Sided Heart Failure
 Occurs when the RV fails to pump efficiently
 Fluid backs up into the venous system
o Into tissues and organs
o Manifests as Peripheral edema, abdominal ascites, hepatomegaly,
jugular vein distention
 Most common cause is Left sided heart failure
 As LV fails, fluid backs up into lungs
o RV has to work harder to push blood to pulmonary
o Increased workload weakens RV
 Other causes
 RV infarction, PE, and cor pulmonale (RV dilation and hypertrophy caused by
pulmonary disease)
 Compensatory mechanisms
o HF can be abrupt or subtle
 Heart will try to maintain adequate CO
o Neurohormonal responses to HF
 Renin-angiotensin-aldosterone system (RAAS)
 Role is to promote retention of fluid and sodium
 Vasoconstriction to raise BP
 Pathway
o As CO fails, blood flow to kidneys decreases
 Kidneys release Renin
 Which leads to angiotensin I into II
o Angiotensin II causes
 Activation of the SNS (catecholamines)
 Release of aldosterone
 Increased peripheral vasoconstriction
 Stimulates release of anti-diuretic hormone
o Fluid is retained further in a failing heart
 SNS
  Release of catecholamines (Epinephrine and norepinephrine)
o Increases BP and HR which increase CO
 Positive effect at first, but negative overall in HF
 Overall, SNS and RAAS increase the heart’s workload, cause ventricular
dysfunction and ventricular remodeling
o Remodeling
 Heart hypertrophies
 Abnormal cells are less effective at pumping, and have
increased demand for oxygen
 ACE inhibitors beta blockers, and aldosterone antagonists help
prevent remodeling
o Dilation
 Enlargement of the chambers of the heart
 Occurs when pressures are elevated for prolonged
periods of time
 Muscle fibers become overstretched and CO decreases
 Frank-Starling Law
o Degree of stretch is directly related to the
force of the contraction
o Hypertrophy
 Increase in muscle mass of the heart
 Initial increase of CO
 Over time, develops poor contractility, requires more
o2, and has poorer coronary circulation
o Counterregulatory mechanisms
 Natriuretic peptides
 Hormones produced by the heart
o ANP is released by the atriums
o BNP is released from ventricles in response to increased blood volume
 Have renal, cardiovascular, and hormonal effects
o Renal
 Increased GFR and diuresis
 Excretion of sodium
o Cardiovascular effects
 Vasodilation and decreased BP
o Hormonal
 Inhibition of aldosterone and renin
 Interference with ADH release
 Nitric oxide and prostaglandin
 Released by the vascular endothelium in response to compensatory mechanisms
 Work to relax smooth muscles
o Causes vasodilation and decreased afterload
 Classification of Heart Failure
o Based on American College of Cardiology Foundation or New York heart Association guidelines
 New York – focus is on tolerance to physical activity
 American College – staging is based on disease progression and treatments
o NY patients can change stages
o AHA is a progressive list
 Clinical Manifestations
o Acute decompensated HD (ADHF)
 Sudden onset of signs and symptoms of HF
  May manifest as pulmonary edema
 Life-threatening
o Lung alveoli become filled with serosanguineous fluid
o Most common cause is left sided HF secondary to CAD
 Pulmonary Edema
 Causes patient to show dyspnea and orthopnea
 JVD is often present
 Patient will appear anxious, pale, or cyanotic
o Cold and clammy from vasoconstriction (SNS)
 Breath sounds may show crackles and wheezes
 Fatigue
 One of the earliest symptoms of chronic HF
o Anemia be a cause -due to poor nutrition, renal disease, or drug therapy
 Dyspnea
 Common due to increased pulmonary pressures
 Paroxysmal nocturnal dyspnea
o Occurs when the patient is falling asleep
 Lying flat causes reabsorption of fluids
o Causes a cough that is not relieved by positioning or OTC drugs
 Tachycardia
 Early sign of compensation is increased HR
o Due to SNS activation
 Edema
 Development of dependent edema or sudden weight gain of 2-3 lbs in a day
 Are common signs of ADHF
 Nocturia
 When lying flat, fluid is reabsorbed
 Results in increased perfusion, which leads to diuresis
 Skin changes
 O2 extraction is increased in a person with chronic HF
 Appears dusky
 Low extremities may be shiny and swollen (Minimal hair growth)
 Behavioral changes
 If cerebral circulation is reduced
 Often seen in late stages of HF
 Chest pain
 Due to decreased coronary artery perfusion
 Weight changes
 Renal failure, abdominal fullness, and cardiac cachexia with muscle wasting and
fat loss
o May be masked with edema, so daily weights are important
o Complications of HF
 Pleural effusion
 Fluid builds up in the pleural cavity of the lungs
 Results in increased pressure, which leads to dyspnea, cough, and chest pain
 Dysrhythmias
 Related to enlargement of the heart (Compensatory mechanisms)
o Changes the normal electrical pathways
 Left Ventricular Thrombus
 An enlarged LV and decreased CO increases the risk for thrombi
 Hepatomegaly
  Liver becomes congested with blood
 Impaired function leads to cellular death, fibrosis occurs, and cirrhosis can
develop
 Renal Failure
 Decreased CO means less blood flow to kidneys
 Can lead to failure
 Diagnostic Studies
o Signs and symptoms are not highly specific
o Echocardiogram
 Common diagnostic tool
 Provides information of EF, structure, and function
o Laboratory results
 BNP levels correlate with degree of LV failure
 ADHF care
o Continuous monitor is needed
 If unstable, ICU unit
o Provide supplemental oxygen
 Put in high fowler to decrease venous return
 Helps with breathing
o Ultrafiltration
o Drug Therapy
 Diuretics
 Mainstay to fluid overload
 Reduces preload and allows less volume to return to LV
 In turn this allows the LV to pump more efficiently
 Vasodilators
 Dilate the coronary arteries
o Reduces preload and increases O2 supply to heart
 Morphine
 Reduces preload and afterload
o Dilates both pulmonary and systemic blood vessels
 Positive Inotropes
 Increases myocardial contractility
 Includes beta agonists and digitalis
 Only recommended for short term management
o Goals of therapy
 Treat underlying causes
 Maximize CO
 Reduce symptoms
 Improve ventricular function
 Improve quality of life
 Preserve target organ function
 Reduce mortality and morbidity
 Reduce need for oxygen through adequate rest( Physical and emotional)
o Long term support
 VADs
 Standard of care
 Helps with heart pumping mechanism
 Drug therapy for Chronic HF
o Diuretics
 To reduce edema, pulmonary venous pressure, and preload
 o ACE inhibitors
 Block the RAAS system from completing
 Via blocking angiotensin from creating angiotensin II
 Also helps with decreasing ventricular remodeling
 Use of ARBs is recommend if ACE is not tolerated
 For example, African Americans have high chance of angioedema with ACE
o Aldosterone antagonists
 Block the effects of aldosterone on the heart blood vessels
 Also serve as a potassium-sparing diuretic
o Beta blockers
 Directly block the effects of the SNS on a failing heart
 End in -lol because they are funny
o Vasodilators like Nitrates
 Long term use may cause tolerance
o Positive inotropes like digoxin
 Heart rate needs to be greater than 60 bpm before administration
 Risk for toxicity
 Monitor potassium levels
o Cardiac Sinus Node inhibitors
 New category that inhibits the sinus node
 Reduces HR
 Patient must have HR of 70 before administration
 Nutritional Therapy for HF
o Low sodium diet is recommended
 Less than 2 g a day (Average American eats 7 to 15)
 DASH diet is recommended
o Poor adherence and failure to take prescribed drugs are the two major cause of readmission for HF
patients
o Fluid restrictions only if severe hepatic impairment is present as well
 Nursing management
o Overall goal
 Decrease in symptoms
 A decrease in peripheral edema
 Increase in exercise tolerance
 Adherence with the treatment regimen
 No complications
o Nursing diagnosis
 Impaired gas exchange related to increased preload and alveolar-capillary membrane
changes
 Decreased cardiac output related to altered contractility, altered preload, and altered
stroke volume
 Excess fluid volume related to increase venous pressure and decrease renal perfusion
secondary into heart failure
 Activity and tolerance related to imbalance between oxygen supply and demand
secondary to cardiac insufficiency and pulmonary congestion
 Heart Transplant
o Moving a healthy donor heart into a patient with a diseased heart
o In the united states, approximately 3000 need a transplant
 Only 2000 hearts become available on average
o Criteria for selection include several checks for contraindications
  Age over 70 years, life threatening illness, never mind now it's bad active infection
including HIV , or severe pulmonary disease are all absolute contraindications for
transplant
o Patient must take immunosuppression drugs for life
 Includes corticosteroids, calcineurin, inhibitors, and antiproliferative drugs
 Increases risk for cancer
o To check for rejection of donated organ
 EMB is obtained weekly for a month
 Monthly for the next six months
 Yearly afterwards