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CHF study guide
Unit A Congestive Heart Failure Study Notes
| Question | Answer |
|---|---|
| Classifications of CHF | low output high output, systolic vs. diastole, right vs. left, acute vs. chronic |
| a state in which the heart is no longer able to pump sufficient blood to meet all metabolic needs of the body systems. | CHF |
| Typically left/right heart failure | low output HF |
| cardiac output remains above normal or normal; caused by increased metabolic needs or hyperkinetic conditions- septicemia, anemia, hyperthyroidism | high output |
| heart unable to contract forcefully enough during systole to eject adequate amounts of bld into circulation. | systolic HF |
| increase preload with decrease contractility, increase afterload as a result of increase peripheral resistance. | systolic HF |
| The percentage of blood ejected from the heart during systole. | ejection fraction |
| decreased ejection fraction leads to what? | decreased tissue perfusion, and increase blood accumulation in pulmonary vessels |
| Left ventricle is unable to relax adequately during diastole. Represent 20-40% of all heart failures. | diastolic HF |
| Inadequate relaxtion equals what to the heart? | "stiffening", prevents ventricle from filling w/ sufficient bld to ensure an adequate output. |
| What is the regular ejection fraction of the heart? | 60-70% |
| class I (ny heart assoc. classification of heart failure) | ejection fraction less than 45%, no symptoms, only dx with echo, cardiac cath, cardiac test. |
| Class II | symptoms of heart failure occur with maximal exertion. |
| Class III | symptoms of heart failure with no exertion |
| Class IV | symptoms at rest. |
| What is the most common cause of acute onset of CHF? | Acute MI |
| How does dysrhythmias cause acute onset of heart failure? | decrease filling of ventricles, decrease stroke volume, and increase oxygen demand. |
| thyroid disorders cause heart failure how? | due to xtreme tachycardia and increase o2 demand |
| hypertensive crisis | end organ damage of the heart |
| Rupture of the papillary muscles affects the heart how? | Affects the valves of the heart muscles to where there is no control of bld flow. |
| ventricular septal defect | hole between 2 ventricles |
| what are the acute onset of CHF | MI, Dysrhythmias, pulmonary emboli, thyroid disorders, HtN crisis, rupture of the papillary muscle, ventricular septal defect, infection, stress, hypervolemia. |
| Chronic onset of heart failure | CAD, rheumatic heart disease, congenital heart disease, pulmonary disease, anemia- d/t acute hypoxia of cardiac tissues, bacterial endocarditis, cessation of meds. |
| Risk factors of heart failure | men, elderly, htn, cad, smokers, dm, hyperlipidemia. women after menopause. |
| The amount of bld ejected with each ventricular contraction; normal 70ml/contraction | stroke volume |
| what is stroke volume dependent on | preload, contractility, afterload |
| the degree of fiber stretch at the end of diastole, heart is relaxed; corresponds to end diastolic volume and pressure | preload |
| the ability of the heart muscle to contract | contractility |
| the pressure that the ventricles must pump against to empty the chamber effectively;systemic bld pressure | afterload |
| Preload depends on what in order to work properly? | valves, bld volume, ventricular wall compliance, venous tone, starlings law. |
| the ability of the cardiac fibers to stretch and snap back appropriately(fibers lengthen and shorten in response to need) | starling's law |
| changes in force of contraction occur with what? | increased SNS stimulation, positive inotropes, decreased with hypoxemia, decreased negative inotropes. increased preload = increased contractility |
| afterload depends on: | tone of systemic arterioles, systemic vascular resistance, bld viscosity |
| What happens when the heart has increased afterload? | myocardial oxygen demand increases. |
| _________ in aorta and carotid responds to increase CO2 and sends impulses to basomotor center in the medulla which stimulate nervous system to respond. | Chemoreceptor |
| Increased afterload leads to what and why? | decreased stoke volume because with increased afterload, the left ventricle requires more energy to eject its contents. |
| Apoptosis | disintergration of cells into membrane-bound particles that are eliminated by phagocytosis or shedding. (programmed cell death.) |
| name the neurohormones that are released in heart failure | epinephrine, norepinephrine, aldosterone, angiotensinII, BNP |
| What is hBNP? | hormone produced and released by the ventricles, increased to counterbalance the RAS, thus decreasing preload. Determines the degree of HF. |
| RAS? And how is RAS activated in HF clients? | renin-angiotensin system. Occurs when there is a reduced blood flow to the kidneys, d/t low-output states. |
| What occurs in the body when RAS is activated? | Vasoconstriction becomes more pronounced in response to angiotensin 2 and aldosterone secretion causes h2o and nacl retention. Preload and afterload increase. |
| which hormone from the RAS system contributes to ventricular remodeling? | angiotensin II |
| What happens to the heart once it begins the ventricular remodeling process? | contractile dysfunction. |
| When the heart fails and CO is no longer meeting metabolic needs, 3 mechanisms occur to maintain what? | Adequate perfusion, pressure, and cardiac output. |
| Compensatory Mechanisms: Adrenergic | Increased SNS= beta 1, beta 2 stimulation; increased peripheral vasoconstriction, RAS activated |
| Neurohormonal control- compensatory mechanisms | is not meant to be longterm control |
| First mechanism utilized by the heart | beta 1: Tachycardia |
| Tachycardia does what to compensate for CO loss? | increase heart rate to increase cardiac output. |
| What happens when tachycardia does not work anymore? | the heart rate will be so rapid that the filling time of the ventricles will decrease. |
| Ventricular Dilation | 2nd mechanism, increase stroke volume |
| Describe ventricular dilation. | Muscle fibers begin to lengthen, increase vol. in the ventricles, stretched muscle fibers contracts more forcefully, heart requires more o2, less bld flow, and compensate more than tachycardia. |
| What eventually happens to the heart muscle during ventricular dilation. | the heart loses its elasticity after it stretches beyond the natural stretch, muscle walls get thicker. |
| Third and final mechanisms, initially increases the force of contraction and enlarges the heart and increase oxygen demand. | Ventricular Hypertrophy |
| Describe the events of the heart during ventricular hypertrophy | the heart muscles enlarges, begins to cause ventricular remodeling- increase force of contraction, afterload, O2 demand, and wall thickness. |
| What happens to the heart as the heart enlarges and the wall thickens? | May result in hypoxia and decreased contractility, stroke volume, and cardiac output. |
| During compensatory mechanism, clients of CHF are usually _______. | asymptomatic. |
| Once all compensatory mechanism of the heart have failed the client will show what______? | Signs/symptoms of CHF. |
| Normal BNP levels? | 0-100 |
| BNP levels of 100-400 | excludes the symptoms of dyspnea- an increase BNP best differentiates between the dyspnea of HF and that associated with lung dysfunction. |
| BNP > 400 | = Heart failure. |
| Usually the first to fail; the ventricle is unable to pump the sufficient blood in a forward direction. | Left Ventricular Heart Failure. |
| Blood build up in left ventricle causes: | decreased CO, tissue perfusion. |
| What happens to blood flow in left sided HF? | bld flow back in to LA, then to lungs causing SOB, and crackles. |
| Early clinical manifestations of Left HF: | Fatigue, dry cough- due to irritation, and vascular engorgement, dypnea, exertional dyspnea (early), and dyspnea at rest (later). |
| Pulmonary clinical manifestation in Lf HF include: | Crackles- d/t leaking of plasma into lungs and pulmonary artery engorgement; orthopnea, PND, cheyne-stokes respirations, cardiac asthma |
| The inability to lay flat with comfortable breathing. | orthopnea |
| Wake up with shortness of breath. | PND- Paroxysmal Nocturnal Dyspnea |
| irregular breathing pattern- apnea/tachypnea breathing | Cheye-stokes respirations. |
| Wheezing associated with cardiac cause | Cardiac asthma. |
| Heart sounds associated with left heart failure. | S3 and S4 |
| decreased tissue perfusion to the brain causes these symptoms in client with left HF | anxiety, irritability, confusion, memory loss. |
| Renal symptoms in heart failure include: | Nocturia-urinate at night, early sign. And oliguria- decrease urine output, in late stage. |
| Why does nocturia happens at night? | lying down promote kidney perfusion at night. |
| During the late state of HF, oliguria occurs, why? | due to decreased cardiac output= to decreased kidney perfusion= decreased kidney output |
| One of the cardiac clinical manifestations include laterally displaced PMI, why? | the heart is larger which moves the PMI |
| Decreased bld flow causes what to the peripheral pulses | become diminished or weak |
| Pulsus alternans | occurs when the proportional pulse pressure is less than 25%, and is described as weak and strong pulses alternates. |
| Left sided HF is the most common cause of this type of heart failure. | Right ventricular heart failure. |
| How does left sided heart failure cause right sided heart failure? | Lt side HF increase workload of rt ventricles, rt ventricles are working against congested lungs. |
| Describe the events that occur during rt sided hf. | Large amt of blood build up in rt ventricles, unable to pump bld forward into lungs due to decreased CO; bld back up to rt. atria-then to vena cavas- into peripheral vessels |
| In rt ventricular heart failure, peripheral congestion in venous system causes what to the body? | Edema to dependent areas. |
| Which organs are mostly affected by Rt. sided HF? | Liver and spleen become congested and large. (hepato/spleno- megaly) |
| Clincial manifestations of right ventricular heart failure. | Weakness, JVD, anorexia, nausea and bloating, hepatomegaly, dependent edema, cyanosis of nailbeds. |
| In rt sided heart failure, bld backed up into peripheral circulation causes what to the vein in the neck? | sticks out. Jugular venous distention JVD |
| Rt sided heart failure causes venous congestion of the GI, symptoms include? | nausea, anorexia, bloating. |
| Client with RHF c/o abdominal pain, and have jaundice, due to? | enlargement of the liver (hepatomegaly), which leads to cardiac cirrhosis and jaundice. |
| This symptom is common in Rt sided heart failure and is most prominent at the end of the day. | dependent edema, pitting edema. |
| while assess the client with rt sided heart failure you noticed the nailbeds are cyanotic and capillary refills >3, in analyzing these symptoms, you realized these symptoms are due to: | venous congestion and compromised perfusion. |
Created by:
edturner75
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