WVU NSG 312 Exam 2 Complications of Heart Disease Content

What are specific pharmacological actions we can provide for HF?

*ACE Inhibitors* -decrease BP -decrease afterload *Angiotensin Receptor Blockers* -decrease BP -decrease afterload *Beta Blockers* -dilates blood vessels and decreases afterload -improves exercise capacity *Diuretics* -decrease fluid volume overload *Digitalis* -improve contractility *Ca++ Channel Blockers* -vasodilation and decrease SVR

How do we treat pulmonary edema?

*Diuretics* -ex. Lasix -we want to get that fluid out of there *CPAP and BiPAP* -this squishes the fluid into the tissue and out of the lungs, thus improving gas exchange

How do we manage heart failure?

*Eliminate Cause or Contributing Factors* -ex. A-fib, HTN, Obesity *Pharmacology* -inotropes like digoxin ^muscle needs to stretch for better rebound -beta blockers: vasodilator the vessels (makes the LV work less) and decreases HR (slowing down so the LV has time to stretch and fill) *Reduce Workload of the Heart by Reducing Preload and Afterload* -LVAD: left ventricular assistive device -it takes the fluid that's backing up in the left ventricle and brings it back to the right atrium *Teaching* -promote healthy lifestyle -prevent exacerbations of decompensation

View Cardiac Dysfunction Chart!

*Explanation/Pathophysiology* "Systolic heart failure results in decreased blood ejected from the ventricle. The decreased blood flow is sensed by baroreceptors in the aortic and carotid bodies. The sympathetic nervous system is then stimulated to release epinephrine and norepinephrine. The purpose of this initial response is to increase heart rate and contractility and support the failing myocardium, but the continued response has multiple negative effects. Sympathetic stimulation causes vasoconstriction in the skin, GI tract, and kidneys. A decrease in renal perfusion due to low CO and vasoconstriction then causes the release of renin by the kidneys. Renin converts the plasma protein angiotensin to angiotensin I, which then circulates to the lungs. Angiotensin-converting-enzyme (ACE) in the lumen of the pulmonary blood vessels converts angiotensin I to angiotensin II, a potent vasoconstrictor, which then increases the blood pressure and afterload. These mechanisms lead to fluid volume overload commonly seen in HF. Angiotensin, aldosterone, and other neurohormones lead to an increase in preload and afterload, which increases stress on the ventricular wall, causing an increase in cardiac workload. A counter-regulatory mechanism is attempted through the release of natriuretic peptides. ANP and BNP are released from the overdistended cardiac chambers. These substances promote vasodilation and diuresis. However, their effect is usually not strong enough to overcome the negative effects of the other mechanisms. As the heart's workload increases, contractility of the myocardial muscle fibers decreases. Decreased contractility results in an increase in end-diastolic blood volume in the ventricle, stretching the myocardial muscle fibers and increasing the size of the ventricle. One way the heart compensates for the increased workload is to increase the thickness of the heart muscle (ventricular hypertrophy). However, hypertrophy results in abnormal changes in structure and function of myocardial cells, a process known as ventricular remodeling. Under the influence of neurohormones, enlarged myocardial cells become dysfunctional and die early, leaving the other myocardial cells struggling to maintain cardiac output. As cardiac cells die and the heart muscle becomes fibrotic, diastolic HF can develop, leading to further dysfunction. A stiff ventricle resists filling, and less blood in the ventricles causes a further decrease in CO. All of these compensatory mechanisms that make the heart work harder, worsening heart failure." (Hinkle & Cheever, pp. 820)

What patient teaching needs to occur with HF?

*Tell your doctor right away if you...* -gain 3 or more lbs in a day or so -see swelling in the feet, ankles, or other parts of the body -have trouble breathing -can't perform ADLs -feel like you have the flu -have a fever -have chest pain *Other ways your heart might not be working right is...* -coughing up pinkish, blood-tinged mucus -confusion, difficulty thinking, dizziness or lightheadedness -changes in your eating habits and appetite *What should I do?* -visit the doctor and follow his/her advice -read food labels and avoid foods high in sodium -start an aerobic exercise plan, per MD order

What are the signs and symptoms of right sided heart failure?

-fatigue -increased peripheral venous pressure -ascites -enlarged liver and spleen -JVD -anorexia and complaints of GI distress -weight gain -dependent edema

What occurs during pulmonary edema?

-fluid accumulates in the interstitium of the lung and diffuses into the alveoli -this causes *hypoxia*

What is Left Sided Heart Failure?

-inability to pump blood out of the heart and into the system -if CO is decreased, it can cause back flow into the left atrium, which then flows back into the lungs ^this causes *pulmonary edema* -can get arrhythmia because the dead tissue cannot carry proper messages to the left ventricle

What is Right Sided Heart Failure?

-inability to pump into the pulmonary system or accommodate venous return due to pulmonary congestion or pressure (ex. COPD) -typically referred to as Cor Pulmonae -the right ventricle is not as strong as the left ventricle, so when opposing pressure pushes on the right ventricle, it can't battle it -when the blood can be pushed out of the right ventricle, it backs up into the right atrium, and then to the rest of the body

What are the signs and symptoms of left sided heart failure?

-paroxysmal nocturnal dyspnea -elevated pulmonary capillary wedge pressure -restlessness -confusion -orthopnea -tachycardia -exertional dyspnea -fatigue -cyanosis -anxious *Pulmonary Congestion* -cough -rales -may hear wheezing -frothy, pink secretions -tachypnea

What is an IABP?

-this device reduces the systolic blood pressure to reduce afterload and thus decrease the cardiac workload and enhance the aortic diastolic pressure to improve coronary arterial blood flow -for HF patients, it works primarily as a bridge-to-transplant while they are hospitalized and waiting for an appropriate organ to be available -a balloon is percutaneously inserted through the femoral artery into the thoracic aorta -the pump provides counterpulsation (opposite to the ventricular contractions) that causes the balloon to deflate and inflate, causing a rise in diastolic arterial pressure that improves coronary blood flow to the myocardium -only for *ICU*