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CHF study guide

Unit A Congestive Heart Failure Study Notes

QuestionAnswer
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