congestive heart failure

Congestive Heart Failure

Disease/Disorder Etiology/Pathogenesis Pathology


*20 million people affected wordlwide*30-40% die w/in 1 year of diagnosis

Restore CV function short term, thus causing pts to be asymptomatic for years

Heart can’t maintain circulator needs of the body (can be inherited or genetic)

2 Major Types/Categories (50/50)1.HF w/ reduced/depressed EF (systolic failure/<40-50%)2.HF w/ preserved EF (diastolic failure)

Considerable Overlap*CAD (60-70%)*HTN (75%)*DM*Idiopathic (20-30% diastolic failure)—post viral, alcohol, genetic defects (mostly autosomal dominant)

Pathogenesis*index event kicks things off: heart’s pumping capacity declines (either muscle damaged b/c myocytes aren’t functioning/force or contraction issues from diseases/ heriditary/EtOH)

Heart Compensates by activating:1.RAAS System (renin-angiontension-aldosterone-system): 2.adrenergic nervous system**RAAS & Adrenergic NS are responsible for maintaining CO by increased retention NA and H2O + increased contractility3. cytokine system (IL-6)**activation of vasodilatory molecules which decrease peripheral vasoconstriction (atrial & brain naturetic peptides, prostaglandins, NO)

*Most asymptomatic for prolonged periods of time (compensatory mechanisms)

*Eventually heart cant compensatesymptomatic HF occurs & is accompanied by increasing activation of neurohormonal, adrenergic, & cytokine systemscause adaptive change in heart muscle (AKA LV remodeling)

**a lot known about how CFH & depressed EF/systolic failure work**little known about CHF & preserved/diastolic failure (increased vascular stiffness, impaired renal function, & diastolic dysfunction-factors)

Biologic Stimuli: neurohormones (Norephinephrine, & angiotensin II, inflammatory cytokines (TNF), & other peptides and growing factors (endothelin) & reactive O2 species (superoxide)overexpressed & contribute to HF by deleterious/harmful effects they have on heart and circulation (important b/c forms clinical rationale for using pharmacologic antagonizing agents (ACE & BB)Systolic Dysfunction:LV remodeling (factors that lead to symptomatic HF) develops in a series of complex events (occur in cellular & molecular levels)1.myocute hypertrophy2.alterations in contractile properties of myoctes3.progressive loss of myocytes (via necrosis, apoptosis, & autophagic cell death)4.B-adrenergic desensitization5. abnormal myocardial energetics & metabolism6. reorg of extracellular matrix (organized collagen structural weave dissolvesreplaced by interstitial/fibrotic collagen that doesn’t provide support)*sustained neurohormonal activation and mechanical overload result in trasnscriptional & posttranscriptional changes in genes & proteins that regulate excitation-contraction coupling & cross bridge interaction (changes include: decreased function of sarcoplasmic reticulum Ca2+ adenosine triphosphatase-SERCA2A, lower Ca2+

uptake in SR, hyperphosphorylation of ryanodine reception causing leakage of Ca2+ from SR)*cross-bridge changes include decreased a-myosin increased b-myosin, myocytolysis, + disruption of cystoskeletal links b/w sarcomeres and extracellular matrix = poor contractility

Diastolic Dysfunction (can occur alone or w/systolic dysfunction): Background: myocardial relaxation/diastole is an adenosine triphosphate dependent process (ATP) that’s regulated by uptake of Ca2+ into SR by SERCA2A and release/exit of Ca2+ by sarcolemmal pumps *reductions in ATP, which occurs in ischemia, impairs relaxation *hypertrophy/fibrosis= reduced compliance= causes filling to be delayedelevated LV pressures at end diastole*HR increases causing shorted diastolic filling time (could lead to elevated LV filling pressures (particularly non-compliant ventricles)leads to increase in pulmonary capillary pressures) ↑HR shortens diastolic fill time ↑ LV filing pressure ↑capillary pressuresdyspnea


NYHA functional class is a predictor of prognosis Class I: asymptomaticClass II: slight limitation in physical activity(5-10% annual mortality)Class III: comfortable at rest, less than ordinary activity causes fatigueClass IV: can’t do any physical activity w/out discomfort (30-70% mortality)

LV Remodeling*changes in LV mass, volume, shape, & composition of heart after cardiac injury or abnormal hemodynamic condition*can contribute independently to progression of HF (mechanical burdens ↑ by changes in shape of heart) -LV wall thinning occurs from LV dilationafterload mismatchfurther decrease in stroke volume -high end-diastolic wall stress may lead to 1. Hypofusion of subendocardium (worsening of LV function) 2. increased oxidative stressactivates genes/families that are sensitive to free radical generation (TNF, IL) 3. Sustained activation of stretch activated genes (angiotensin II, endothelin, and TNF) and/or Activation of hypertrophic signaling pathways↑LV dilation/tethering of papillary muscles Incompetence of mitral valve and mitral regurgitation further hemodynamic overloading


Symptoms Investigation & FindingsCardinal SymptomsFatigue & dyspnea

Fatigue: low CO output + skeletal muscle abnormalities + noncardiac comorbities (anemia)

Dysnpea: progresses as CHF gets worse**most important mechanism is pulmonary congestion w/ accumulation of interstitial or intra-alveolar fluidactivates juxtacapillary J receptorsstimulate rapid, shallow breathing (Stage III)*pulmonary compliance, increased airway resistance, respiratory muscle and/or diaphragm fatigue, and anemia play a role as well **can become less frequent w/ onset of RV failure & tricuspid regurgitation

Orthopnea: trouble breathing lying down*usually later manifestation*fluid redistributes from the splanchnic circulation (gastric, small intestinal, colonic, pancreatic, hepatic, & splenic circulations) & lower extremities into central circulation when lying down/recumbent ↑pulmonary capillary pressure *nocturnal cough *normally indication of HF but can be present with ascites/pulmonary disease = people who favor upright position

Paroxysmal Nocturnal Dyspnea: acture episodes of shortness of breath & coughing (generally occur at night after 1-3 hours of sleep)NOT RELIEVED SITTING UP*increased pressure in bronchial arteriesairway compression + interstitial pulmonary edema*Cardiac asthma closely related to PBDwheezing occurs secondary to bronchospasms

Cheyne Stokes Respiration (aka periodic or cyclic respiration): abnormal pattern of breathing characterized by progressively deeper and sometimes faster breathing, followed by a gradual decrease that results in a temporary stop in breathing (apnea) *caused by decreased sensitivity of respiratory center to arterial PCO2

*present in 40% pts w/ advanced HF

Other Symptoms: *GI, anorexia, nausea, eat minimal have abdominal pain*edema of bowel and/or congestive liverstretching/congestion of liver may lead to RUQ pain*cerebral symptoms: confusion, disorientation, sleep and mood disturbances PM peeing

General Appearance & Vitals*mild to moderate HF-appears in no distress at rest except for uncomfortable when lying flat for more than a fever minutes*severe HF-must sit upright, labored breathing, sometimes cant finish sentence bc breath shortness*Systolic BP- normal or high in early HFlow in late HF (LV dysfunction)

Jugular Veins*examination of JVs provides estimation of atrial pressurebest when lying flat head at 45 degree*normal is 8-10cm*early stages normal at rest may be abnormally elevated w/ sustained pressure on abdomen

Pulmonary Exam *pulmonary crackles (rales or crepitations) result from the transudation of fluid from the intravascular space into alveoli *rales frequently absent in pts with chronic HF because of increased lymphatic drainage of alveolar fluid*pleural effusions result from elevation of elevation of pleural capillaries pressure + transudation of fluid into the pleural cavities*since pleural veins drain into both system & pulmonary veins, pleural effusions occur mostly in biventricular failure

Cardiac Exam*usually doesn’t provide useful info*point of maximal impulse (PMI) usually displaced below 5th intercostal space and/or lateral to midclavicular line if cardiomegaly is presentenlarged and sustained*Severity of LV hypertrophy leads to sustained PMI* S3 (protodiastolic gallop) is audible and palpable at apex ; commonly present in pts w/ volume overload + tachypnea and tachycardia* S4 not specific indicator of HF but present in pts w/ diastolic dysfunction *murmurs of tricuspid and mitral valves frequently present in advanced HF

Abdomen & Extremities*Hepatomegaly important sign in patients with HRfrequently tender may pulsate during systole (ascites-late sign-increased pressure on hepatic veins & drainage, jaundice also late sign *Peripheral Edema: cardinal manifestation but absent w/ diuretic use—prominent in ankles and pretibial regions- in bedridden pts can be found in presacral and scrotal region

Cardiac Cachexia*vomiting due to congestive hepatomegaly & abdominal fullness, nausea, anorexia*elevation of resting metabolic rate*elevation of concentrations of cytokines & TNF*impairment of intestinal absorption due to congestion of intestinal veins *POOR PROGNOSIS WHEN PRESENT

http://en.wikipedia.org/wiki/Breath


Diagnosis*Key to making diagnosis is to have high index of suspicion, particularly w/ high risk patients-

Blood Work*CBC, panel of electrolytes, BUN, SCr, Hepatic Enzymes, & urinalysis (some should have dyslipidemia (cholesterol), fasting serum glucose or oral glucose (DM), and thyroid stimulating hormone levels (thyroid abnormalities)

ECG*assess rate/rhythm to determine presence of LV hypertrophy or prior MI (presence/absence of Q wave)*look at QRS width to see if resynchronization therapy would help

Chest X-Ray*provides useful info about size and shape & state of pulmonary vasculature*acute pts may have interstitial pulmonary edema*chronic usually do not (increased capacity of lymphatics to remove interstitial and/or pulmonary fluid)

Assessment of LV Function*2-D echo/doppler essential for diagnosis, evaluation, and management of HF*provides semiquantitative assessment of LV size & function*assess LV wall motion abnormalities (valvular or regional—both indicative of past MI)*presence of LAE, LVH, and diastolic abnormalities in regards to EF*invaluable in assessing RV size & pulmonary pressures (critical to management of cor pulmonale)MRI assesses LV structure, mass, volume & determining cause of HF (amyloidosis, ischemic cardiomyopathy, hemochromatosis)*EF: most useful index of LV function is EF (stroke volume/end diastolic volume)*isn’t a true measure of contractility since it is influenced by alterations in preload & afterload- but is good* EF normal 50-70%, and systolic usually normal; when EF is low <30-40% contractility usually depressed

Biomarkers in HR*Beta Naturetic Peptide (BNP) & N-terminal pro-BNP are released from failing heart, and are relatively sensitive markers for 1.presence of HR & depressed EF 2. HF pts w/ preserved EF 3. Important to know natriuretic peptide levels increase w/ age and renal impairment (moreso in women) & can be elevated in right HF from any cause **serial measurement not recommended troponin T & I, CrP, TNF, uric acid provide good prognostic data

Exercise Testing*Not advocated for acute HF – MAY BE HELPFUL IN CHRONIC HF TO ASSESS FOR TRANSPLANT

Differential DiagnosisHF should be distinguished from 1. Circulatory congestions secondary to abnormal salt and water retention (renal failure) 2. Non cardiac causes of pulmonary edema (acute respiratory distress syndrome) dyspnea secondary to pulmonary edema may be difficult to differentiate (echo, BNP, pulmonary function testing helpful) 3. Ankle edema may arise secondary to varicose veins, obesity, renal disease, or gravitational effects


TreatmentHF continuum has 4 interrelated stagesStage A: Pts high risk, but do not have HF (DM, HTN)Stage B: Pts have structural heart disease but no symptoms of HF (previous MI, assymptomatic LV dysfunction) Stage 1 NYHA- slow disease progression by blocking neurohormonal systems that lead to cardiac remodeling (treat w/ ACEI & BBs)Stage C: Pts have structural heart disease & symptoms (previous MI, dyspnea, fatigue) Stage 2-4 NYHA Primary goal to alleviate fluid retention, lessen disability, & reduce risk of further disease progression (combo of diuretics & neurohormonal transmitters)Stage D: Pts w/ refractory HF requiring heart transplant (if 85, send to hospice) every effort should be made to treat preventable causes (HTN) and/or w/ drugs (ACEI & BBs)

Management of HF w/ Depressed EF (<40%)Treat comorbidities: HTN, CAD, DM, anemia, limit EtOH, stop smoking, sleep apnea*AVOID NSAIDS, cyclooxygenase 2 inhibitors (risk renal failure & retain fluid), ANABOLIC STERIODS (volume retention), & DIETARY SUPPLMENTS (unproven)*should get influenza & pneumococcal vaccines- influenza & pneumovax (prevent respiratory infection)*Educate families *Activity: nothing strenuous (60% max HR), modest aerobic exercise (stationary bike, walking) beneficial for class 1-IIIimproves HF symptoms, QOL & increases exercise capacity*Diet: Na restriction (2-3 g/day)- further restriction for severe HF, fluid restriction unnecessary unless hypernatremia present (RAAS excessively excreting ADH or loss of salt)- usually class IV *Note: if hyponatremic, and sodium restriction + diuretics not working, vasopressin antagonists helpful*Increase caloric intake for patients with advanced HF or unintentional weight loss

Diuretics (start w/ low dose, titrate up—goal is attempt to obtains pts dry weight--can be administered via IV (beneficial to relieve congestion accurately)*only pharmalogical agent that can control fluid retention in advanced HF & should be used to restore fluid in pts w/ congestive symptoms (dyspnea, orthopnea, edema)*Loop diuretics (furosemide, torsemide, bumetanide) act on Loop of Henle by reversibly inhibiting absorption of Na, K, & Cl in thick ascending limb of Henle’s loop (fractional excretion of NA 20-25%) usually used to restore normal volume status in pts **watch for hypokalemia*Thiasizes & metolazone reduce reabsorption of Na and Cl in 1st ½ of distal convoluted tubule (thiazide fractional excretion of NA 5-10%- tend to lose their effectiveness in pts w/ moderate or severe renal insufficiency- creatinine >2.5 mg/dL) **watch for hypokalemia*Potassium- sparing diuretics are aldosterone antagonists (spironolactone) act at level of collecting duct—use in class III and IV if needed **watch for hyperkalemia*all increase sodium excretion & urinary volume= potency differs*refractoriness (unruly/resistant) to diuretic therapy can be pt nonadherance, if not, use thiazides or metolazone (usually more potent and longer acting in this setting) 1 or 2 times a day w/ loop diureticIF THAT FAILS ULTRAFILTRATION & DIALYSIS ARE USEDAdverse Effects*Electrolyte & volume depletion + worsening azotemia (high levels of N containing compounds urea/creatinine) can lead to worsening HF & more neurohormonal activity* Most important adverse consequences is imbalance of K homeostatsis—can lead to life-threatening arrhythmias

ACE Inhibitors (initiated at low doses, increase dose until dose is similar to those shown to be effective in clinical trials)*stop enzyme responsible for conversion of Angiotensin 1 to 2* also inhibit kinase II, which may lead to further up regulation of bradykinin further enhances effects of angiotensin suppression*stabilizes LV remodeling, improves symptoms, reduces hospitalizations, & prolong life* diuretic can slow effects of ACE, so better to start diuretic before the ACE (may be necessary to reduce dose of diuretic during ACE initiation to prevent HTN) Adverse Effects*majority related to suppression of RAAS system—decrease BP, mild azotemia, hyperkalemia, Angioedema* if hypotension is accompanied w/ dizzy & poor renal function, reduce dose


Treatment Continued

ARB: used in ACE intolerant symptomatic/asymptomatic patients w/ an EF of <40% & who are intolerant for reasons other than hyperkalemia*use for pts intolerant of ACE (cough, skin rash, angioedema)*ARBs block the effects of angiotensin II on the angiotensin type I receptorAdverse Effects*majority related to suppression of RAAS system—decrease BP, hypotensive, & hyperkalemia

B-Adrenergic Receptor Blocker: indicated for PTs w/ symptomatic or asymptomatic HF & a decreased EF of 40%-- start w/ low doses, titrate up (SLOWLY-2 week intervals- bcv more chance of fluid retention) (carvedilol 25-50mg bid or metroprolol 200mg/day) + diuretic*Antagonize B1, B2, and A2 receptors- B1 most potent *when given with an ACE, beta blockers reverse LV remodeling, improve pt symptoms, prevent hospitalization & prolong life*If fluid retention does occur w/in 3-5 days- more HF damage is occurring (may have to reduce dose like ACE)*Comorbid issues (DM, COLD, and PVD) are tolerated well among majority- 10-15% don’t tolerate well Adverse Effects*generally occur bc of concomitant medications taken w/ BBs*not recommended for pts w/ asthma w/ active bronchospasm*bradycardia and heart blocks can be present

Aldosterone Antagonists: recommended w/ class III-IV HR w/ EF less than 35% (spironolactone-25-50mg/day & eplerenon-50 mg/day)*potassium sparing diuretics that block the effects of aldosterone which have beneficial effects on sodium balance*titrate up recommended dose Adverse Effects*life threatening hyperkalemia is the biggest issue (renal insufficient pts most at risk(*not recommended when SCr is >2.5mg/dL or when serum potassium is >5mmol/L*painful gynecomastia (big boobs) can develop- try switching from spironolactone to eplerenone

*for class II-IV African American pts, use hydralazine & isosorbide dinitrate in addition to ACE and BB


PTs Still Symptomatic*Digoxin recommended for pts w/ symptomatic LV systolic dysfunction who have concomitant a-fib – should also be considered for pts resistant to therapy who are in normal sinus rhythm

Anticoagulation (Wafarin) & Antiplatelet Therapy (Aspirin)*depressed LV function is believed to promote relative stasis of blood in dilated cardiac chambers w/ increased risk of thrombus formation*treatement w/ warfarin is recommended for pts w/ HF & chronic or pulmonary emboli, stoke or TIA (INR goal 2-3) *pts w/ recent large anterior MI or recent MI w/ left ventricular thrombus- keep on Wafarin for 2-3 months*aspirin is recommended in HF patients w/ ischemic heart attack disease for prevention of MI & death- lower doses usually preferably (81mg)

Antiarrythmic Therapy: Amiodarone preferred dofetilide backup*A-fib occurs in 15-30% of pts w/ HF- which is worse for heart* amiodarone has few or no negative inotropic and/or proarrythmic effects and is most effective againt supraventricular arrhythmias—increases level of phenytoin & digoxin, which prolongs INR in pts w/ warfarin, maintain/restores sinus rhythm & may improve electrical success for cardioconversion

Implantable Cardiac Device: recommended for pts in sinus rhytm w/ an EF <35% and a QRS >120 ms + symptomatic pts (class III-IV) despite optial drug therapy*1/3 of pts w/ depressed EF and symptomatic HD (class III-IV) manifest a QRS duration >120 ms. * mechanical consequences of ventricular dyssynchronous ventricular contraction include: poor ventricular filling, reduction in LV contractility, prolonged duration of mitral regurg, and paradoxical & septal wall motion *benefits of CRT in PTs w/ a-fib HAVE NOT been established

Implantable Cardiac Defibrillator (ICD): Indicated in PTs at risk for sudden cardiac death w/ ischemic/nonischemic cardiomyopathy*can also be considered for PTs in class II-III w/ EF <35% who have had optimal therapy up to this point and are still resistant

Management of HF w/ Preserved EF (>40-50%)- NONE proven, focus on underlying disease process (HTN, Ischemia, Dyspnea from diuretics/nitrates)

Acute Decomposition HF (ADHF): 2 primary hemodynamic determinants of ADHF 1. Elevated filling pressures 2. Depressed CODesign Appropriate Therapeutic Strategy

1. Stabilize hemodynamic derangements that provoked symptoms2. ID & treat reversible factors that caused decline/decompensation3. Reestablish effective outpatient medical regimen


4 Hemodynamic Profiles- therapeutic approach should be tailored to reflect pts hemodynamic presentation

A- Normal LV filling pressure w/ normal perfusion (not congested (dry) & have normal tissue perfusion(warm)) Sx usually not due to HF, but hepatic disease, PE, or TIA)B- Elevated LV filling pressure w/normal perfusion (congested (wet) and normal tissue perfusion (warm) ) treat w/ vasodilators & diureticsC- Elevated LV filling pressure w/decreased perfusion (congested (wet) and reduced CO and elevated SVR (cold) treat w/ IV inotropes- dobutamine, low-dose dopamine,

milrinoneL- Normal of low filling pressure w/ decreased tissue perfusion (not congested (dry) and reduced CO and elevated SVR (cold) CAREFUL EVAL VIA HEART CATH, IF FILLING PRESSURES LOW (WEDGE PRESSURE <12 mmHG, TRIAL FLUID REPLACEMENT

Intravenous Vasodilator – 2nd most useful med for acute HF (diuretic #1) nitroglycerin, nitroprusside, and nesirtide *Stimulate guanylyl cyclase w/in smooth muscle cellsdilates arteries and veins lowering LV filling pressure (preload), lower mitral regurg, improves CO (afterload) w/ increase HR or causing arrhythmias*Goal:reduce symptoms, reduce LV filling pressure, avoid hypotension

Intravenous Inotropic Agents- improve CO and decrease LV filling pressure- dobutamine, milirone*produce direct hemodynamic effects by stimulating cardiac contractility as well as by producing peripheral vasodilation*dobutamine- most common- stimulates B1 and B2 receptors (little effect on A1 receptors)-vasodilates & increases CO- given as continuous effusion; higher doses needed for hypofusion*milirone- phosphodiesterase III inhibitorincreases cAMP by inhibiting its breakdown- has greater increase on CO & more effective vasodilator than dobutamine but higher risk of hypotension*good short term use + hemodynamic benefits: agents prone to cause tachyarrythmias

Vasoconstrictors: support systemic BP in pts w/ HF (dopamine- 1st choice--epinephrine, & phenylephrine are potent- AVOID long use)*dopamine: endogenous catecholamine stimulates A1 & B1 receptors & dopaminergic receptors (DA1/DA2)- effects dose dependent- low dose increase CO, high dose increase vasoconstrict

Vasopressin Antagonists: Tolvaptan (oral)_& Conivaptan (IV) approved for hyponatremia not for HF


*reduce body weight, edema, & normalize associated improved outcomes

Cor Pulmonale (aka pulmonary heart disease)*dilation and hypertrophy of R ventricle in response to disease of the pulmonary vasculature*Etiology: develops in response to acute/chronic changes in vasculature sufficient to cause pulmonary HTN *prognosis of pts with cor pulmonale + HF worsens prognosis (chronic bronchitis, COLD, cystic fibrosis, chronic hypoventilation-fat, neuromuscular disease, chest wall abnormality-living at high altitude)s*most common mechanisms that lead to pulmonary HTN, including vasoconstriction, activation of clotting cascade, & obliteration of pulmonary arterial vessels


MnemonicsCHF: causes of exacerbation A SMITH PEAR:AnemiaSalt/ Stress/ Stopping medsMIInfection/ IschemiaThyroid (high/low)HTNPericarditisEndocarditis (valve disease)ArrhythmiaRx (beta blocker, etc)

Heart failure: signs TAPED TORCH:TachycardiaAscitesPulsus alternansElevated jugular venous pressureDisplaced apex beatThird heart soundOedemaRight ventricular heaveCrepitations or wheezeHepatomegaly (tender)

CHF: Left-sided systolic failure signs and symptoms "Left Systolic Failure Can Have Dialated Heart Cause Of Pulmpnary Backflow":Loss of hair on legsSkin cold and clammyFatigueCracklesHigh heart rateDyspneaHTNCyanosisOrthopneaPink Sputum

Acute LVF management LMNOP:Lasex (frusemide)Morphine (diamorphine)NitratesOxygen (sit patient up)Pulmonary ventilation (if doing badly)

Heart compensatory mechanisms that 'save' organ blood flow during shock "Heart SAVER":


Symphatoadrenal systemAtrial natriuretic factorVasopressinEndogenous digitalis-like factorRenin-angiotensin-aldosterone system· In all 5, system is activated/factor is released

> Heart failure: causes HEART FAILED:

HypertensionEndocrineAnemiaRheumatic heart diseaseToxinsFailure to take medsArrythmiaInfectionLung (PE, pneumonia)ElectrolytesDiet

congestive heart failure

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