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

• --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

decreased cardiac output -> SNS stimulation -> norepi -> increased HR -> increased CO, vasoconstriction -> increased venous return -> increased ventricular filling/stretch (preload) -> increased contraction -> increased output

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

• 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)

• 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)

• systolic failure: ventricles fail to contract adequately -> decreased EF -> decreased CO
• diastolic failure: heart cannot completely relax -> decreased filling -> decreased SV

• 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

• 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

• 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

• **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

• oxygen - pulm congestion
• **ACE inhibitors**
• beta blockers
• diuretics
• vasodilators
• positive inotropics
• anti-dysrhythmics

• inhibit RAA
• decreased vasoconstriction, decreased aldosterone
• decreased cardiac work, increased cardiac output
• s/e: angioedema, hyperkalemia, cough

• inhibit SNS (beta 1)
• can also inhibit beta 2 -> bronchoconstriction
• use cautiously - reduces force of contraction

• rids excess fluid
• s/e: electrolyte imbalances
• loss of vascular volume can stimulate SNS
• severe HF: Lasix
• moderate HF: thiazide

• 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

• 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

• not usually given d/t depression of left ventricular function
• amiodarone

• low sodium - 1.5 - 2 grams daily
• moderate, progressive exercise program

• intra-aortic balloon pump
• left ventricular assist device

• cardiomyoplasty - lattimus dorsi used to enhance function of heart
• cardiac transplant - immunosuppressants, steroids
• ventricular reduction surgery - removal of part of ventricle to enhance contractility

• fluid volume excess
• activity intolerance
• impaired gas exchange
• decreased cardiac output
• assess for edema, lung sounds, SOB, ascites, nausea
• O2, rest, daily weight

• disease of heart muscle
• affect systolic and diastolic function
• primary or secondary (ischemia, infection, toxins, tissue disorders, metabolic disorders, nutritional deficiencies)

• 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

• 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

• 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