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What is Heart failure

  • occurs when the heart cannot pump enough blood fasst enough to meet the metabolic needs of the body
  • no longer use the term "congestive" because all heart failure does not result in clinically apparent volume overload

Fast Facts:

  • Leading diagnosis for group over 65
  • median survival is 3.2 years for men and 5.4 years for women
  • most common cause of death is progressive HF, but sudden death may account for up to 45% of all deaths
  • Patients with coexisting IDDM have a significantly higher mortality rate



  • the amount of blood the heart must pump with each beat
  • determined by: venous return to heart and strength of muscle fibers
  • increasing preload-->increased stroke volume in normal heart
  • increasing preload-->impaired heart-->decreased SV.  Blood is trapped-->chamber becomes enlarged



  • the pressure that must be overcome for the heart to pump blood into the arterial system
  • dependent on the systemic vascular resistance
  • with increased afterload the heart muscles must work harder to overcome the constricted vascular bed-->chamber enlargement
  • increasing the afterload will eventually decrease the cardiac output


dilated congestive cardiomyopathy

heart muscle disorders in which the ventricles enlarge but are not able to pump enough blood for the body's needs, resulting in HG (example: CAD, myocarditis, etoh, HIV)


hypertrophic cardiomyopathy

heart disorders in which the walls of the ventricles thicken and become stiff, even though the worklaod of the heart is not increased.  Ex: congenital HCM, or acquired


restrictive (infiltrative) cardiomyopathy

heart disorders in which the walls of the ventricles become stiff but not necessarily thickened and resist normal filling with blood between heartbeats.  EX: ratiation, amyloidosis


adaptive mechanisms of the heart to increase load

  • frank sterlin mechanism
  • ventricular hypertrophy : increased mass of contractile elemts cuases increased strength of contraction
  • increased sympathetic adrenergic activity: increased HR, increased contractility
  • increased activity of R-A-A system


systolic cardiac heart dysfunction (systolic HF)

when the heart muscle doesn't contract with enough force so there is not enough oxygen rich blood to be pumped throughout the body


diastolic cardiac dysfunction (or diastolic HF)

when the heart contracts normally, but the ventricle doesn't relax properly so less blood can enter the heart


Stages of HF


  • A: risk factors but no symptoms
  • B: structural changes but no symptoms
  • C: patients with structural change symptoms, but they're treatable with medication
  • D: refractory.  Structural changes, symptoms, not responsive to medication

New york heart association: class 1, 2, 3, and 4

  • Class 1: no obvious symptoms, no limitations on patient physical activity (35% EF or higher)
  • Class 2: some symptoms during or after normal activity, mild physical activity limitations (35 %)
  • Class 3: symptoms with mild exerction, moderate to significant physical activity limitations (25%)
  • Class 4: Significant symptoms at rest, severe to total physical activity limitations (5%)


Cuases of HF

  • CAD
  • problems with the heart muscle itself (known as cardiomyopathy, myocarditis, et)
  • HTN
  • problems with any of the heart valves
  • abnormal heart rhythms (also called arrhythmias)
  • toxic substances (EtOH, cocain)
  • Congenital heart disease
  • diabetes
  • thyroid problems
  • HIV


DIastolic HF

  • Diastolic HF is defined as a condition caused by increased resistance to the filling of one or both ventricles, this leads to symptoms of congestion from the inappropriate upward shift of the diastolic pressure-volume relation
  • 40% patients
  • increasing age
  • more common in women
  • HTN and cardiac ischemia are most common causes
  • alterations involve relaxation and or filing and or distensibility
  • arterial HTN associated to LV concentric remodeling is the main determinant of DD but several other cardiac diseases, including myocardial ischemia, and extra-cardiac pathologies also possible


Patient differences with HF

  • a hemodynamic disorder but there is poor relationship between measures of cardiac performance and patient symptoms
  • for ex: pts with very low EF may be asymptomatic while someone with preserved EF may be severely disabled with symptoms


body compensatory mechanisms of HF

  • epi and norepi releases which increases HR and contractility which increases myocardial work load
  • decrease in salt and water excretion from kidneys which helps maintain BP by increased BV, this leads to stretching of heart's chambers which can impair ability to contract
  • hypertophy and thickening of heart muscle which initially increases contractility but over time leads to stiff chambers
  • HF pts have higher levels of epi, norepi, aldosterone, angiotensin 2, enothelin, inflammatory cytokines, and vasopressin which contributes to heart remodeling, progression of HF, and higher levels are associated wiht increased mortality


neurohormonal with HF

  • Stimulated by decreased perfusion leadin gto secretion of hormones
  • Epi: increases contractility, increases rate and pressure, vasoconstriction leads to SVR
  • Vasopressin: pituitary gland, mild vasoconstriction, renal water retention


renin angiotensin mechanism in HF

  • Decreased renal blood flow secondary to low cardiac output triggers renin secretion by thte kidneys
  • aldosterone is released--> increased sodium retention and water retention
  • preload increases
  • worsening failure


ventricular hypertophy

  • long term compensatory mechanism
  • increases size due to increase in work load ie skeletal muscle

potential reasons

  • alternation in ventricular distensibility
  • valvular regurgitation
  • pericardial restrain
  • cardiac rhythm
  • conduction abnormalities
  • rv function
  • also several non-cardiac factors including peripheral vascula fxn, reflex autonomic activity, renal sodium handling, etc


HF risk factors history

  • smoking
  • etoh use
  • SM HTN
  • dyslipidemia
  • thyroid disorder
  • chemo
  • radiation
  • cardiotoxic drugs
  • fam HX of sudden death, CAD, conduction problems, HCM
  • HIV status


Cardiovascular medical HX

  • Hx heart failure
  • angina
  • mi
  • cabg
  • pci
  • pacemaker/icd
  • embolic events
  • arrhythmias
  • cva
  • pvd
  • rheumatic dx
  • other valvular hx
  • congenital


sign and symptoms of HF

  • dyspnea
  • pnd
  • orthopnea
  • cough
  • exercise intolerance
  • edema
  • fatigue
  • nausea
  • abdominal fullness
  • rales (usally starts at bases)
  • s3 (position patient left lateral to hear)
  • pulmonary edema
  • jvd
  • tachycardia
  • cardiomegaly
  • hepatojugular reflex (apply pressure, see distention, let go it stays pretty long)
  • peripheral edema
  • hepatomegaly


physical exam of HF: signs that suggest HF include

  • tachycardia
  • third heart sound (listen LL recumbent)
  • increased jugular venous pressure
  • positive hepatojugular reflux
  • bilateral rales (not always present, only in L sided HF)
  • peripheral edema not due to venous insufficiency
  • laterally displaced apical impulse (from midclavicular (normal) to mid-axillary)
  • weight gain


HF diagnosis and assessment

  • primarily a clinical dx, but additional infor via other diagnostic can be beneficial
  • look at CXR, BNP, EKG
  • evaluation depends on if this is first presentation, change in clinical symptoms certainty of dx, etc


what we should know about the individual patient's HF

  1. identify the patients with HF
  2. assess for S/S and risk factors for HF
  3. Initial workup should have been included work up for reversible causes if appropriate (TSH, HIV)
  4. echocardiogram to determine systolic and diatstolic LV performance, cardiac output (EF) and pulmonary artery and ventricular filling pressures


Elevated BNP levels have been associated with?

reduced LVEF, LVH, and elevated LV filling pressure, and acute MI

evidence supports getting baseline BNP


chest xrays in hf help to identify?

  • identify cascular congestion, infiltrates, effusions
  • evaluation and classification of severity of heart failure
  • nuclear imaging for assessment of ej or areas of ischemia


clinical use of BNP

  • levels below 100 may indicate no heart failure
  • levels 100-300 suggest heart failure is present
  • levels above 300 indicate mild heart failure
  • levels above 600 indicate moderate hf
  • levels above 900 indicate severe HF


left ventricular hf

  • occurs when the left ventricle fails as an effective forward pump
  • back pressure of blood into the pulm circulation
  • results in pulmonary edema
  • cannot eject all of the blood delivered from the right heart
  • left atrial pressures rise causing increased pressure in the pulm veins and capillaries
  • when pressure becomes to high, the fluid portion of the blood is forced intot he alveoli
  • leads to decreased o2 capacity of the lungs
  • ami common with lvf suspec


clinical presentations of LVHF

  • Severe resp distress evidenced by orthopnea, dyspnea, hx of parozsymal nocturnal dyspnea
  • severe apprehension, agitation, confusion, resulting from hypoxia, feels like he is smothering
  • cyanosis
  • diaphoresi results from sympathetic stimulation
  • pulmonary congestion: rales, rhonchi, wheezes
  • JVD from backed up pressure
  • vital signs: BP elevated, pulse elevated, resp rapid and labored
  • LOC may vary, depends on level of hypoxia
  • chest pain may be present, masked by the RDs


right sided HF

  • acute mi (inferior)
  • pulmonary disease (copd, fibrosis, htn)
  • cardiac diseases involving the left or both ventricles
  • results from lvf


  • decreased right sided cardiac output or increasd pulmonary vascular resistance leading to increased right vent. pressures
  • as pressures rise this increased pressure in the right atrium and venous system
  • higher righ atrium pressures


higher right atrium pressure result in:

  • peripheral vein, pressures rise and the capillary pressures increase, hydrostatic pressures exceeds that of interstitial pressure
  • fluid leaks from the capillaries into the surrounding tissues causing peripheral edema
  • lungs are clear due to left ventricular pressures are normal


Clinical presentation of right sided HF

  • Marked JVD
  • clear chest
  • hypotension
  • marked peripheral edema
  • ascites, hepatomegaly
  • poor exercise tolerance
  • often will be on lasix, digoxin
  • have chronic pump failure


copd presentation vs chf vs pneumonia


  • frequent cough
  • frequent wheeze
  • thick sputum
  • hemoptusis ocassionally
  • sometimes PND after a few hours
  • smoking is common
  • pedal edema ocassionally
  • chest pain is pleuritic
  • clubbing
  • cyanosis severe
  • diuresis may be present
  • pursed lips often
  • barrel chest
  • bp usually normal
  • wheezes common
  • crackles coarse and diffuse


  • thin white sputum
  • pink frothy hemoptysis
  • PND within oone hour
  • common pedal edema with chronic
  • orthopnea at night
  • substernal crushing pain
  • progressing cyanosis
  • diaphoresis mild to heavy
  • jvd mild to severe
  • bp high
  • crackles fine to coarse, being in gravity dependent areas


  • prequent cough, wheese, with thick yellow or brown sputum
  • no pedal edema
  • onset gradual with fever cough
  • chest pain pleuritic
  • dysrhytmia is common
  • wheeze is common
  • localized to diffuse coarse crackles


non pharm treatment of HF

  • Sodium intake: limit, 203 g a day over 3 meals, recheck sodium intake when weigth gain experienced
  • Fluid intake: HF patients wiht hyponatremia, high dose diuretics, severe HF.  LImit to 6-8 glasses a day.  Fruit=1/2 cup liquid
  • exercise: hf patients with stable heart and stable voume status.  5-10 minutes a day 2-3 times a day to start
  • monitor wieght gain.  Report gain of 2.5 kg a week.


pharm intervention of HF

  • aimed at diminishing the compensatory mechanisms of low cardiac output and also improving contractility
  • vasodilators: ace inhibitors
  • diuretics
  • inotropic agents


vasodilaters for HF

  • dilate blood vessels
  • ace inhibitors (prils): block production of chemicals that cause bp to narrow, decreasing the heart pumping easier.  Side effects: cough, hyperkalemia (blood tests every 6 weeks), angioedema, orthostasis
  • nitrates (african american patients respond well)


diuretics for HF

  • lasix (can develop tolerance to lasix)
  • hydrochlorothiazide: works as a vasodilator primarliy at low doses
  • spironolactone: for patients with stage 3 or 4 heart failure  Watch for hyperkalemia
  • loop diuretics (furosemide, bumentanide, torsemide) to treat volume overload.  No effect on mortality


inotropic agents

  • digoxin, lanoxin
  • decreased heart rate increases stroke volume, increaseing the CO
  • 10-20% develop toxicity
  • side effects include arrhythmias, cisual changes, gi complaints, altered mental status
  • therapeutic range: 0.8-2.0
  • steady state : 7-10 days
  • toxic: 2.4
  • half life: 33-51 hours
  • obtaining levels: determine serum digoxin levels at least 4 hours after IV 6 hours after oral


calcium channel blockers

  • slow conduction, allows more time for filling pressures, counteracts natural response to increase hr, relaxing of peripheral blood vessels
  • used in pts wiht diastolic bp
  • ex: nifedipine, diltiazem, verapamil, amlodipine, felodipine


beta blockers

  • useful by blocking beta-adrenergic receptors of the sympathetic nercous system,the heart rate and force of conractility are decreasd
  • may worsen HF
  • ex: metoproplol, atenolol, propanolol, amiodarone


basic pharmacotherapy

  • all pts with systolic HF started on ace and beta-blockers unless contraindicated wiht asthma (arbs subsituted)
  • concerns about renal function happen as drugs are titrated upwards



  • short term studies, is the first oral vasopressin antagonist reulted in statistically significant improvement relative to placebo 
  • added to standard meds rapidly lowered body weight and the weight was kept off during therapy
  • did not lower bp or change blood levels of k, bun, or creat
  • greatest benefit is seen in the sickest patients


device therapy in HF

  • cardiac resynchronization therapy (right ant left)
  • implantable cardioverter defibrillators
  • left ventricular assist devices
  • cardiac contractility modulation
  • implatable fluid monitors
  • implatable hemodynamic monitors



  • internal cardiac defibrillator
  • help treat arrhythmia to help prevent sudden cardiac death
  • restores normal orderly beating of heard


vetnricular assist devices

  • temproary life-sustaining device
  • decrease work load of heart and increase contractility
  • been shown to double the one year survival rate
  • bridge therapy to heart transplants, or patients who had an acute injury to the heart to let the heart rest


inpatient vs outpatient managment

  • nesiritide: synthetic BNP that vasodilates vessels and seves as a potent diuretic agent
  • inotropic agents (dobutamine, milrinone): often used inpatient, potent to increase cardiac output, use is controversial in outpatient settings, has increased risk of arrhythmias


nursing managment of HF

  • promote rest: don't walk during exacerbation, getting them to sit still if they appear agitated or hypoxic
  • relief of anxiety: O2 delivery, decrease demand on heart itself (morphine increases vasodilation of coronary arteries decreases pain)
  • decreasing cardiac workload: NTG, Morphine sulfate, lasix, 02 high flow
  • attainment of normal tissue perfusion


challenges with elderly and HF

  • atypical presentation
  • anorexia, generalized weakness, fatigue, mental disturbances, anxiety


end of life care symptoms for chf

  • SOB, dry mouth, nausea, fatigue, pain, restlessness, and apprehension


Congenital heart disease

  • most are structural malformations
  • cyanotic: right to left shunting
  • non-cyanotic: left to right shuntin
  • Ventricular septal defects are most common, followed by atrial septal defect, patent ductus arteriosus



  • atrial septal defects (asd)
  • centricular septal defects
  • patent ductus arteriosus
  • obstruction to blood flow: pulmonic stenosis, aortic stenosis, aortic coarctation


atrial septal defect

  • most commonly asymptomatic
  • essentials for dx: right ventricular heave, s2 widely split and usually fixed, grade 1-4/4 systolic murmer at the pulmonary area, widely ratiading systolic murmuer cardiac enlargement on cxr
  • treated: closure generally recommended when ratio of pulmonary to systemic bf is .2:1.  Operation performed 1-3 years of age
  • previously surgical, no often closed interventionally


3 types of atrial septal defects

  • ostium secundum: most common, in the middle of the septum in the region of the foramen ovale
  • ostium primum: low position, form of av septal defect
  • sinus venosus: least common, positioned high in the atrial septum, frequently associated with papvr


ventricular septal defect

  • single most common congenital malformation
  • can occur both the membranous portion of the septum and the muscular portion
  • 3 types
  • small hemodunamically insignificant: between 80% and 85% of vsds, less than 3mm, all close spontaneously in school years, muscular close sooner than membranous
  • Moderate: 3-5 mm, least common group of children, without evidence of CHF or pulmonary htn, may be followed until spontaneous closure occurs
  • large VSD with normal PVR: 6-10 mm in diameter, usually requires surger, otherwise chf and fft by afe 3-6 months


clinical findings of ventricular septal defects

grade 2-3/4, medium to high pitched, harsh pansystolic murmer heard best at the left sternal border with radiation over the entire precordium


treatment of ventricular septal defect

  • indicated for closure of vsd associated with hf and ftt or pulm htn
  • patients with cardiomegaly, poor growth, poor exercise tolerance, or other clinical abnormalities and .2:1 typically undergo surgical repair at 3-6 months


patient ductus arteriousus

  • persistence of normal fetal vessel joining the pulmonary artery to the aorta
  • closes spontaneously in normal term infants at 3-5 days of age
  • higher incidence at higher altitueds
  • more common in females
  • clinical findings course depend on size of the shunt and the degree associated pulmonary htn
  • pulses bound and pulse pressure widens
  • characteristically has a rough machinery murmer which peaks at s2 and becomes a decreascendo murmur and fades before the s1


treatment of patent ductus arteriosis

  • surgical correction when is larger exept in patient with pulm vascular obstructive disease
  • transcatheter closure of small defects is standard
  • preterm infants: indomethacin is used


tetrology of fallot

cyanosis result of a small number of cardiac malformations well determines, one is much more frequent than the others.  Consissts of stenosis of pulm artery, interventricular communication, deviation of the origin of the aorta to the right, hypertrophy almost always concentric type of the right ventricle.  Fialure of obliteration of the foramen ovale may occasionally be added in whilly accessory manner


typical features of tetralogy of fallot

  • cyanosis after the neonatal period
  • hypoxemic spells during infancy
  • right sided aortic arch in 25% of all patients 
  • systolic ejection murmur at the upper LSB
  • most patients are cyanotic by 4 months
  • hypoxemic spells are one of the hallmarks of severe tetrology


tet spells most commonly start?

  • around 4-6 months of age
  • characterized by sudden onset or deepening cyanosis, sudden onset of dyspnea, alterations of consciousness, decreas in intensity of systolic murmor


consequences of cyanosis late/missed dx

  • mortality
  • ischemic brain injury
  • multiorgan failure
  • higher postop morbidity