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heart failure
- heart is unable to pump sufficient blood to meet metabolic demands of the body
- decreased cardiac output -> decreased tissue perfusion
- compensatory mechanisms activated -> vascular congestion
- develops 2/2 HTN, CAD, COPD
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CHF etiology
- --impaired myocardial contraction r/t damaged muscle s/t MI, inflammation
- --long standing excessive workload r/t HTN, valve disorders
- --acute excess demands r/t fluid volume overload, thyroid storm, PE
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SNS compensation
decreased cardiac output -> SNS stimulation -> norepi -> increased HR -> increased CO, vasoconstriction -> increased venous return -> increased ventricular filling/stretch (preload) -> increased contraction -> increased output
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RAA compensation
RAA: decreased cardiac output -> decreased blood flow to kidneys -> renin -> vasoconstriction, aldosterone, ADH -> Na, H20 retention, more vasoconstriction -> increased blood volume -> increased venous return -> increased ventricular filling/stretch (preload) -> increased contraction -> increased output
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other compensation
- atrial/ventricular stretch causes release of ANP/BNP -> excrete Na, H20, inhibit norepi, renin, ADH
- ventricular remodeling (heart adapts to excess volume) -> ventricular hypertrophy (increased contractility)
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CHF decompensation
- rapid HR -> decreased filling time -> decrease coronary artery perfusion -> increased O2 demand -> ischemia -> impaired output
- beta receptors less sensitive to continued SNS stimulation -> decreased HR and contractility
- alpha receptors (peripheral) more sensitive -> increased vasoconstriction -> increased afterload -> increased workload
- chronic ventricular overfilling -> degenerated ventricle wall -> reduced force of contraction (Frank-Starling fails)
- chronic distention depletes ANP/BNP -> no inhibition of norepi, renin, ADH -> Na, H20 retention, vasoconstriction -> increased preload and afterload
- little to no cardiac reserve (ability to quickly adjust to demands)
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CHF classifications
- systolic failure: ventricles fail to contract adequately -> decreased EF -> decreased CO
- diastolic failure: heart cannot completely relax -> decreased filling -> decreased SV
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L-sided failure
- caused by CAD, HTN
- can lead to R-sided failure (pulm vascular pressure increases -> R-side workload increases)
- increased pressure in left chambers -> impaired filling
- backward -> increased pulmonary congestion -> dyspnea, SOB, cough, orthopnea, cyanosis, crackles, wheezes, S3
- forward -> decreased cardiac output
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R-sided failure
- caused by L-sided heart failure or acute/chronic pulmonary disease (COPD)
- increases L-ventricular preload
- increased pressure in pulmonary vasculature or R ventricle damage -> ineffective pumping
- backward -> increased systemic congestion -> peripheral edema, anorexia, nausea (GI congestion), enlarged liver, JVD
- forward -> decreased cardiac output
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CHF complications
- hepatomegaly/splenomegaly r/t engorgement of portal venous system -> increased abd pressure, ascites, GI problems
- dysrhythmias
- pleural effusion
- cardiogenic shock
- acute pulmonary edema
- LV thrombus/emboli r/t increased blood stasis s/t decreased EF
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CHF dx
- **ANP/BNP** - hormones released by heart in response to change in blood volume - increased in HF (normal < 100)
- electrolytes - low serum osmolality r/t fluid retention
- UA, BUN, creat - kidney function
- LFTs - monitor liver function
- thyroid panel - r/o thyroid disorders
- ABGs - gas exchange (acute HF)
- CXR - pulmonary vascular congestion, cardiomegaly
- echo - evaluate structure and function of heart
- EKG - dysrhythmias, myocardial ischemia and infarction
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CHF meds
- oxygen - pulm congestion
- **ACE inhibitors**
- beta blockers
- diuretics
- vasodilators
- positive inotropics
- anti-dysrhythmics
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ACE inhibitors
- inhibit RAA
- decreased vasoconstriction, decreased aldosterone
- decreased cardiac work, increased cardiac output
- s/e: angioedema, hyperkalemia, cough
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beta blockers
- inhibit SNS (beta 1)
- can also inhibit beta 2 -> bronchoconstriction
- use cautiously - reduces force of contraction
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diuretics
- rids excess fluid
- s/e: electrolyte imbalances
- loss of vascular volume can stimulate SNS
- severe HF: Lasix
- moderate HF: thiazide
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vasodilators
- arterial dilation -> reduces peripheral vascular resistance/afterload
- venous dilation -> reduces venous return/preload
- pulmonary dilation -> reduces pressure, allows for reabsorption of extra fluid in lungs
- nitrates, hydralazine
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positive inotropic agents
- digitalis
- increases strength of heart contractions by increasing calcium concentration
- slows conduction through SA node -> increases ventricular filling time
- monitor dig level - s/s of tox: anorexia, nausea, vomiting, HA, halos
- low K, low mag, high Ca increase risk of dig tox
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antidysrhythmics
- not usually given d/t depression of left ventricular function
- amiodarone
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diet
- low sodium - 1.5 - 2 grams daily
- moderate, progressive exercise program
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mechanical assist devices
- intra-aortic balloon pump
- left ventricular assist device
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CHF surgery
- cardiomyoplasty - lattimus dorsi used to enhance function of heart
- cardiac transplant - immunosuppressants, steroids
- ventricular reduction surgery - removal of part of ventricle to enhance contractility
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CHF nursing
- fluid volume excess
- activity intolerance
- impaired gas exchange
- decreased cardiac output
- assess for edema, lung sounds, SOB, ascites, nausea
- O2, rest, daily weight
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cardiomyopathy
- disease of heart muscle
- affect systolic and diastolic function
- primary or secondary (ischemia, infection, toxins, tissue disorders, metabolic disorders, nutritional deficiencies)
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dilated cardiomyopathy
- most common (87%)
- r/t CAD, ETOH, pregnancy
- dilated heart chambers, impaired ventricular contraction
- reduced EF (10-20%) -> reduced cardiac output
- treated like CHF (R and L)
- 50% mortality/75% after 10 years
- tx: heart transplant, ACE inhibitors, vasodilators, digoxin
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hypertrophic cardiomyopathy
- decreased chamber size r/t hypertrophy of ventricle
- decreased ventricular filling -> low cardiac output
- genetic
- sudden cardiac death (young athletes) r/t dysrhythmias
- s/s: dyspnea, angina, syncope, systolic murmur
- tx: beta blockers, decreased activity, remove muscle, heart transplant
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cardiomyopathy dx
- echo - chamber size and thickness, ventricular wall motion, valve function, systolic/diastolic function
- EKG - dysrhythmias
- CXR - size of heart
- hemodynamics - cardiac output, pressures
- radionuclear scans - changes in ventricular volume and mass
- cardiac cath - eval perfusion
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