Ch 35: Heart Failure

Question 1

Abnormal cardiac function involving impaired cardiac pumping and/or filling. Associated with HTN, CAD, and MI. Primarily affects older adults. High morbidity and mortality. Unable to provide sufficient blood to meet the O2 needs of tissues.

Answer 1

Heart failure

Question 2

Risk factors of heart failure

Answer 2

CAD, age, HTN- primary factors.
Diabetes, smoking, obesity, high cholesterol. African americans have a higher incidence, develop it at an earlier age, have higher mortality rates (BP and heart disease big in this population).

Question 3

___ failure results from an inability of the heart to pump blood effectively. It is caused by impaired contractile function (MI), increased after load (HTN), cardiomyopathy, and mechanical abnormalities (valvular heart disease). The LV loses its ability to generate enough pressure to eject blood forward through the aorta. Over time, the LV becomes dilated and hypertrophied. Hallmark is a decrease in LV ejection fraction.
S/S: LV hypertrophy, decreased EF

Answer 3

Systolic failure leading to heart failure. Problem with pumping.

Question 4

The enablity of the ventricles to relax and fill during diastole. Often referred to as HF with normal ejection fraction. Decreased filling of the ventricle results in decreased SV and CO. Characterized by high filling pressures because of stiff ventricles. This results in venous engorgement in both the pulmonary and systemic vascular systems. Usually the result of LV hypertrophy from HTN, myocardial ischemia, valve disease, or cardiomyopathy. Dc made based on the presence of HF symptoms with a normal EF. Occurs more frequently in older adults, women, and people who are obese.
S/S: pulmonary congestion, pulmonary HTN, ventricular hypertrophy, normal EF.

Answer 4

Diastolic failure leading to heart failure. Problem with filling.

Question 5

Often the first mechanism triggered in low-CO states. Least effective compensatory mechanism. Release of actecholamines=increase HR, increased myocardial contractility, and peripheral vasoconstriction. Over time these factors are harmful, since they increase the already failing heart’s workload and need for O2.

Answer 5

SNS activation as compensatory mechanism

Question 6

As CO falls, blood flow to kidneys decreases=sensed by juxtaglomerular apprartus as decreased volume=renin release, which converts angiotensinogen to angiotensin I. AI to AII in lungs. AII causes adrenal cortex to release aldosterone, which results in Na+ and H2O retention, increased vasoconstriction=increased BP. ADH also secreted from pituitary d/t decrease in CO leading to decrease is cerebral perfusion pressures. Increases H20 resorption=water rentention=increased blood volume in person already volume overloaded. Endothelin-potent vasoconstrictor produced by vascular endothelial cells; results in further arterial vasoconstriction and increase in cardiac contractility and hypertrophy.

Answer 6

Neurohormonal response as compensatory mechanism

Question 7

Occurs when pressure in the heart chambers (usu. the LV) is elevated over time. The heart muscle fibers stretch in response to the volume of blood in the heart at the end of diastole. Increased stretch–> increased force of contraction–> increased CO (initially). Eventually this mechanism becomes inadequate b/c the elastic elements of the muscle fibers are overstretched and can no longer contract effectively, thereby decreasing the CO

Answer 7

Ventricular dilation as compensatory mechanism for HF

Question 8

Increase in the muscle mass and cardiac wall thickness in response to overwork and strain. Occurs slowly b/c it takes time for this increase muscle tissue to develop. Over time leads to poor contractility, requires more O2 to perform work, has poor coronary circulation (tissue becomes ischemic more easily) and is prone to dysrhythmias.

Answer 8

ventricular hypertrophy as compensatory mechanism for HF

Question 9

Counterregulatory mechanisms

Answer 9

Production of ANP, BNP, and NO. Causes vasodilation and diuresis. Blocks the effects of RAAS. Inhibits the development of hypertrophy.

Question 10

Most common form of HF. Results from LV dysfunction. This prevents normal, forward blood flow and causes blood to back up into the LA and pulmonary veins. The increased pulmonary pressure causes fluid leakage from the pulmonary capillary bed into the interstitium and then the alveoli. This manifests as pulmonary congestion and edema

Answer 10

Left sided heart failure

Question 11

Occurs when the RV fails to contract effectively. Causes a backup of blood into the RA and venous circulation. Venous congestion in the systemic circulation results in JVD, hepatomegaly, splenomegaly, vascular congestion of the GI tract, and peripheral edema. May results from an acute condition (RV infarction, PE). For pulmonale (RV dilation and hypertrophy cause by pulmonary disease) can also be a cause. Primary cause is left-sided HF- results in pulmonary congestion and increased pressure in the blood vessels of the lung (pulm. HTN). Eventually, chronic pulm HTN (increased RV after load) results in right-sided hypertrophy.

Answer 11

Right-sided heart failure

Question 12

Acute decompensated heart failure (ADHF)

Answer 12

An increase in the pulmonary venous pressure is caused by failure of the LV. This results in engorgement of the pulmonary vascular system. As a result, the lungs become less complicant and there is increased resistance in the small airways. The lymphatic system increases its flow to help maintain a constant volume of the pulmonary extravascular fluid. This early stage is assoc. with a mild increase in the respiratory rate and a decrease in the partial pressure of oxygen in the arterial blood (PaO2).

Question 13

Pulmonary edema

Answer 13

Acute, life-threatening situation in which the lung alveoli become filled with serosanguineous fluid Most common cause is left-sided HF 2* to CAD.
S/S: Anxious, pale, possible cyanotic. Cold and clammy skin from vasoconstriction caused by sim. of SNS. Dyspnea and orthopnea. RR >30 breaths/min, use of accessory muscles. Wheezing and coughing with the production of frothy, blood-tinged sputum. Crackles, wheezes, rhonchi. Increased HR and potential increased BP.

Question 14

S/S of chronic HF

Answer 14

Fatigue; activity limitation. Cough (dry, non-productive, may be 1st clinical sx). Edema. SOB, orthopnea, PND. Tachycardia. Nocturia, weight gain.

Question 15

S/S right-sided failure

Answer 15

Murmurs. Heaves. JVD. Edema. Weight gain. Ascites. Hepatomegaly. Fatigue. Nausea. Anorexia/GI bloating.

Question 16

S/S left-sided heart failure.

Answer 16

S3, S4. Heaves. PMI displaced. Hypoxia. Crackles, pleural effusion. Dyspnea. Restlessness. Confusion. Fatigue. PND, orthopnea. Cough. Frothy, pink-tinged sputum.

Question 17

Results from increasing pressure in the pleural capillaries. Can cause lung collapse if significant enough.

Answer 17

Pleural effusion. Cx of HF

Question 18

Chronic HF causes enlargement of the chambers of the heart. This enlargement can cause changes in the normal electrical pathways.

Answer 18

Dysrhythmias. When numerous spots in the atria fire spontaneously and rapidly (atrial fibrillation), the organized atrial depolarization (contraction) no longer occurs. A-fib may promote thrombus formation within the atria. Thrombi may break loose and form emboli. Places pts at risk for stroke. They require tx with antidysrhythmics and/or anticoagulants

Question 19

With ADHF or chronic HF, the enlarged LV and decreased CO combine to increase the change of thrombus formation in the ____. Once a thrombus has formed, it may also decrease LV contractility, decrease CO and worsen the pt’s perfusion. It places the pt at risk for a stroke

Answer 19

Left ventricular thrombus

Question 20

The liver becomes congested with venous blood. The hepatic congestion leads to impaired liver function. Eventually, liver cells dies, fibrosis occurs, and cirrhosis can develop.

Answer 20

Hepatomegaly

Question 21

Decrease CO that accompanies chronic HF can result in decreased perfusion the the kidneys

Answer 21

renal failure

Question 22

Diagnostic studies for HF

Answer 22

Goal is to determine the cause. EF (ejection fraction) distinguishes between systolic and diastolic HF- through echo or MUGA. BNP differentiates if dyspnea is from HF.

Question 23

Tx of ADHF

Answer 23

Need continuous monitoring and assessment (may be done in ICU if pt is unstable). High Fowler’s position (if dyspneic) with feet horizontal or dangling to help decrease venous return and increases thoracic cavity to improve breating. Oxygen. ECG, O2 sat monitoring. VS, urine output hourly. Hemodynamic monitoring. Ultrafiltration for volume overload. Circulatory assist devices. Treat depression.

Question 24

Drug tx for ADHF.

Answer 24

Morphine: reduces preload and afterload. Dilates both the pulmonary and systemic blood vessels. Relief of dyspnea. Give first to decrease dyspnea and anxiety associated with it.
Diuretics: Furosemide (Lasix). Decrease Na+ reabsorption–> enhanced Na+ and H20 loss. Decreases preload and subsequently the volume returning the the LV (allows LV to contract more effectively). CO increased, gas exchange improved.
Vasodilators: IV nitroglycerine (reduces circulating blood volume), sodium nitroprusside (NIpride), nesiritide (Natrecor). Reduces preload.
Positive inotropes: Digitalis, dopamine, dobutamine, epinephrine, norepinephrine. Increases contractility. Short-term management who have not responded to other therapy.

Question 25

Chronic HF tx

Answer 25

Oxygen. Physical/emotional rest (cardiac rehab). Biventricular pacing or cardiac resynchronization therapy. May also have implanted cardrioverter-defibrillator (ICD; telehealth monitoring). Circulation assist devices

Question 26

Chronic HF drug tx

Answer 26

Diuretics (thiazide are first choice). ACE inhibitors or ARBs. Aldosterone antagonists (spironolactone). BiDIl- only for african americans. Use cautiously: beta blockers (Carvedilol/Coreg), positive inotropes (Digoxin/Lanoxin).

Question 27

Nutrition for HF

Answer 27

Always do an assessment (3 day diary). Sodium restriction (If alb over 2 days)

Question 28

Nursing interventions

Answer 28

Health promotion: Aggressively identify and treat risk factors. Flu and pneumonia vaccination. Education about diet, meds, exercise.
Acute: Conserve energy, decrease anxiety. May need salt and fluid restriction. Need support systems.
Ambulatory/Home care: Must take meds even when feeling well. Treat anxiety and depression. Teach to take pulse rate with digitalis and beta blockers. Energy-conserving behaviors. Know s/s of worsening HF. Know what to call the doctor for.

Question 29

When to call the doctor

Answer 29

Fatigue, weakness, dizziness, fainting. 
Activities needing to be limited. 
Chest congestion/cough
Edema (swelling of the ankles, feet, abdomen, weight gain of 3# in 2 days or 3-5# in week) 
SOB 
Swelling of face or difficulty breathing