CHF is a progressive clinical syndrome that occurs when the hearts ability to pump effectively slows dwon and the heart can’t supply sufficient quantities of blood and O2 to meet the metabolic needs of the body’s tissues. It begins with injury to the myocardium that impairs the ventricles to fill or eject blood. Yielding hypertrophy of 1 or both ventricles (makes heart work harder)
A decreased outputoccurs d/t the increased preload(amount of fluid in the ventricles) at the end of diastole (filling phase/relaxed muscle). As CO drops the BP often falls as well.This process leads to increased heart work load. As the process continnues filling ans stretching worsen. The BP remains below normal. Despite the increased effort on the hearts part the the low BP is a direct result of the hearts inablilty to pump strong enough to mainatin the C.O. The Tx of CHF is focused on STOPPING this cycle.
When there is a decrease in CO the sympathetic nervous system is stimulated and compensatory changes begin(increased HR, vasoconstriction.)The kidney also attempts to compensate. (the decreased perfusion from the low CO activates the renin-angio-tensin-aldosterone system. Angiotensin II and aldosterone are released which lead to NA+ retention and vasoconstriction. This in turn activates the increased anti-diuretic hormone (ADH) the ADH causes the kidney to reabsorb more h20The combination of retained Na+ and H2o leads to further increased preloadIn Acute and Chronic CHF these initial compensatory mechanism eventually become counterproductive and maladaptive.
Example: Diastolic HF may be caused by increased resistance to ventricular inflow and reduced ventricular diastolic capisty (clues to cause live HTN or MI)NYHA: class I- clients without physical limitations thru class IV Clients who are symptomatic with rest or activity
Left Sided HF is the most common and right often results from left sided HF.When the R or L ventricle lose the ability to handle the extra or increased preload;there is a back up of fluid. If the L ventricle is involved then the fluid backs up into the lungs, is the right ventricle is invovled fluid backs up into the systemic circulation.
ACE (angiotensin converting enz) produce vasodilatation, block angiotensin-aldosterone compensatory mechanism. Result is decreased preload and L ventricle filling pressure which increases CODiuretics :reduce and eliminate excess fluid or symptom relief of clientBeta blockers, improve left ventricular fxn and increase force of contractions. Start low and go slow.The best chance of cardiac recovery comes with higher doses that reduce the workload of the heart. (MS reduces hemodynamic workload by reducing pain /anxiety, NTG to vasodialate and decrease cardiac oxygen demand, prelaod and afterload while decreasing CO, dopamine to perfuse the kidney increase BP ad CO
Despite the advances in Medical surgical management of clients with HF, mortality remains high.
Nursing care for CHF
Nursing Care for Clients living with CHF <br />Lisa Barrett MSN RN<br />
Learning objectives<br />Describe the pathophysiologicchanges seen with congestive heart failure (CHF)<br />Pharmacological management of heart failure<br />Apply the nursing process in the management of a client with CHF<br />
Heart Failure<br />Progressive<br />Inability of heart to pump enough blood to meet demands<br />Stems from injury to the myocardium<br />
Causes of HF (Types of injury)<br />Aortic stenosis or regurgitation<br />CAD(coronary artery disease)<br />Disrhythmias (A-fib)<br />HTN<br />Medications<br />MI<br />
It is important that the nurse is knowledgeable about cardiac output in order to:<br />a. Determine electrical activity of the myocardium<br />b. Evaluate blood flow to the peripheral tissues<br />c. Provide information on the immediate need for oxygen<br />d. Implement nutritional changes<br />
b. Evaluate blood flow to the peripheral tissues<br />Rationale: Blood flow to the tissues is measured as C.O. and assists to predict tissue perfusion. Electrical activity is evaluated by ECG. While it is important for perfusion and oxygenation, the O2 sat would provide more valuable information. Nutritional changes would be targeted to Na and would depend on the symptoms of the disease. <br />
Classifications<br />Systolic or Diastolic <br />New York Heart Association “functional” class for patients<br />Right sided or Left sided<br />Others<br />
A nurse administering IV furosemide (lasix) to a patient admitted with CHF,after the infusion,which of the following symptoms is NOT expected:<br />Increased urinary output<br />Decreased edema<br />Decreased pain<br />Decreased BP <br />
Measure degree of JVD (kussmaul’s sign)<br />Assess Edema<br />
Interventions<br />Assess ascites<br />Monitor vitals/postural hypotension/<br />Monitor for changes in LOC<br />Monitor O2 saturation<br />Palpate the liver<br />Rate discomfort r/t DOE<br />Teaching (S/Sx,FR, Low NA diet etc)<br />
An elderly client is being monitored for evidence of CHF. To detect early signs of heart failure, the nurse would instruct the Nursing Assistant to do which of the following during care of the Patient?<br />Observe ECG readings and report deviations <br />Assist the client to ambulate 3x/shift<br />Monitor VS q 15mis and report each reading to the nurse<br />Accurately weigh the client and report and record the readings<br />
d. Accurately weigh the client and report and record the readings<br />Rationale: Due to fluid accumulation, an expanded blood volume can result when the heart fails. Body weight is a sensitive indicator of water and sodium retention, which will manifest itself with edema and dyspnea. It is not with in the role of a NA to monitor ECG readings and ambulation is not an assessment. VS every 15 minutes are not necessary for this level of patient care.<br />