CHF

Cardiovascular condition in which the heart is unable to pump an adequate amount of blood to meet the metabolic needs of the body’s tissues. Impaired cardiac pumping. Leads to fluid overload and congestion in lungs or periphery.

• Currently 5 million people in the U.S. with CHF.
• Leading cause of hospitalization for those older than 65.

• Long-standing hypertension, CAD, and DM.
• The risk of CHF increases with the severity of Htn.
• DM predisposes a person to CHF.

High rate of morbidity and mortality. Variable prognosis. Annual health care costs exceed $57 billion.

• Hypertension - Major risk factor is hypertension due to strain of pumping against high SVR. Dysfunctional hypertrophy.
• CAD.
• Congenital Heart Disease.
• Rheumatic Heart Disease.
• Cardiomyopathy.
• Valvular Heart DiseaseAtrial Fibrillation - loss of atrial kick.
• Cor Pulmonale - caused by chronic lung disease.
• Ischemic myocardium or old MI.

Impaired Ventricular function - Inability of Ventricle to adequately pump or fill. Impaired ability to meet metabolic demands leads to fatigue, decreased organ function.

Pulmonary Congestion - LV dysfunction results in excessive fluid backs up into pulmonary system resulting in congestion. Results in cough, rales, dyspnea.

Systemic Congestion - RV dysfunction causes back up of fluid into periphery cause JVD, edema, hepatomegaly.

Preload elevated beyond ventricular capacity. Failure of starlings law. Impaired contractility. Excessive Afterload due to increased systemic vascular resistance.

• Systolic
• Most common cause—LV looses its ability to eject blood forward through the high pressure aorta (impaired ventricular emptying). Hallmark sign is the decrease in EF (the fraction of total vent. filling volume ejected on each contraction. Normal is greater than 50%).
• Results from not able to pump blood to aorta: decreased LVEF, increase in LVEDP, increase in PAWP, pulmonary congestion.
• Caused by: impaired contractile function (MI), increased afterload (HTN)), or mechanical abnormalities (VHD)

• Diastolic
• Not a disorder of contractility but of relaxation and ventricular filling. Impaired ability of the ventricles to fill during diastole. Results in decreased stroke volume. Normal systolic function.
• High filling pressures with resultant ventricular engorgement in both the pulmonary and systemic vascular systems.
• Diagnosis made based on pulmonary congestion and pulmonary hypertension with normal ejection fraction.
• Result from LVH from chronic hypertension or hypertrophic cardiomyopathy (aortic stenosis).

• Mixed Systolic & Diastolic failure:
• Mixed origin, dilated cardiomyopathy (weakened muscle function, dilated LV wall), poor ejection fractions, poor exercise tolerance, pulmonary congestion and edema. Both ventricles are affected with poor emptying and filling capacity.
• Ventricular failure of any type: Low CO, poor renal perfusion, exercise intolerance, ventricular arrythmias.

• Left Sided:
• Left sided will eventually cause right sided failure.

• Right Sided:
• Chronic Lung Disease.

• High output Failure:
• Results when normal CO inadequate to meet hypermetabolic state. E.g. Anemia, hyperthyroidism.

• Left sided: most common initial heart failure, results from LV dysfunction, blood to back up through the left atrium and into pulmonary veins results in pulmonary congestion and edema—causes are coronary arteries, hypertension, cardiomyopathy, and rheumatic heart disease, MI
• 

• Decreased right ventricle causes backflow to right atrium and venous circulation—peripheral edema, hepatomegaly, splenomegaly, vascular congestion of GI tract, and jugular venous distention—primary cause is left sided failure, can be caused by chronic hypertension, Cor pulmonale (right ventricular dilation caused by pulmonary pathology).
• 

• Attempts to increase cardiac output.
• Ventricular dilation.
• Ventricular hypertrophy.
• Increased SNS activity.
• Hormonal response.
• Myocardial Remodeling.

Initially help maintain CO but ultimate worsen heart function.

Enlargement of chambers of heart—pressure in heart is elevated over time (LV)—increase CO, adaptive mechanism to cope with increasing blood volume, becomes inadequate because the elastic elements of muscle fibers are overstretched and overstrained.

An increase in muscle mass and cardiac wall thickness in response to overwork and strain, slowly occurs, increase in CO and maintenance of tissue perfusion, has poor contractility.

First mechanism triggered in low CO states, least effective compensatory mechanism, happens because of inadequate SV and low CO, thus a release of epi and norepi which increases HR, myocardial contractility, and peripheral vasoconstriction. Increases myocardium’s need for O2 and workload of an already failing heart Increases SVR and afterload. Diastolic failure intolerant of increased HR.

CO decreases blood flow to kidney decreases causing decrease in glomerular blood flow—juxtaglomerular apparatus release renin, increase in peripheral vasoconstriction- release of aldosterone causing sodium retention. Increases Preload and afterload. Hypothalamus senses and causes posterior pituitary to secrete ADH causes water retention.

Compensatory mechanism cause ventricle to remodel becomes less effective pump.

• Atrial Natriuretic Peptide
• Produced by atrium when stretched. Promotes vasodilation and diuresis. Decreases preload and afterload.

• Natrecor
• Drug given IV in acute CHF. Chemically similar to ANP.

• B-type Natriuretic Peptide
• Originally brain but actually produced by ventricles. Serum level diagnostic marker.

• Less than 100 no heart failure.
• Between 100-500 possible heart failure.
• Greater than 500 confirms heart failure.
• Greater than 900 severe heart failure.

• Manifests as Pulmonary edema - Acute and life-threatening. Because of the decreased LV function, pulmonary venous pressures rise causing engorgement of the pulmonary vascular system. Fluid moves into the interstitial space causing interstitial edema. Alveoli are disrupted (alveolar edema) as they are flooded with fluid and lungs fill with serosanguineous fluid.
• 

• Acute Dyspnea
• Tachypnea
• Tachycardia
• Hypoxia
• Change in Mental Status
• Course Rales
• Wheezes
• Frothy Pink Sputum

• Acute Care Admission.
• High Flow O2
• Continuous monitoring
• Labs, CXR, 12 lead EKG
• IV Lasix - Assess for hemodynamic/renal status
• IV Morphine
• IV Nitrogylecrin or Nitroprusside
• IV Dopamine
• IV Natrecor

May need CCU or ICE.

May need 100% NRB

Monitor V/S O2 sat telemetry

CXR shows pulmonary congestion, CBC, CMP, BNP, ABG, Cardiac Enzymes

Potent loop diuretic decreases preload. Monitor lytes

Decreases Afterload, pulmonary pressure. Helpful for anxiety. Monitor resp status.

Decreases Preload and afterload

Increases CO. Improves renal blood flow and assist with diuresis.

• Factors
• Fatigue
• Dyspnea
• Tachycardia
• Peripheral Edema
• Nocturia
• Behavioral Changes
• Chest Pain
• Weight Changes
• Arrhythmias

Patient’s age, underlying type, and extent of heart disease, and which ventricle is failing.

• Fatigue caused by decreased CO, impaired circulation, and decreased O2 of tissues “sick fatigue”
• Dyspnea: increased pulmonary pressure, poor gas exchange, SOB, get rapid shallow breaths—orthopnea: patient is in recumbent position---Paroxysmal nocturnal dyspnea (PND) occurs when patient is asleep dry cough. Bibasalar rales.
• Tachycardia due to decreased CO—increase in SNS.

• Edema: legs liver ascites. Pitting.
• Nocturia: decreased CO, impaired renal perfusion, decreased urinary output during day—at night fluid moves from interstitial spaces back into circulation—increases renal blood flow and UO.
• Behavioral changes: restlessness, confusion, and decreased attention span from impaired cerebral circulation due to low oxygen state.
• Chest pain: decreased CO and increased myocardial workload.
• Weight changes: fluid retention, ascites, hepatomegaly. Renal failure contributes to symptoms. Patients are nauseous and anorexic. Best Indicator of fluid status.
• Atrial fib due to dilated LA worsens CHF loss of atrial kick. Increased rate decreases ventricular filling and coronary perfusion. Increased risk of ventricular arrhythmias.

Daily weights.

• CBC, CMP
• Look for anemia, renal function, liver function lytes.

• CXR
• Look for pulmonary congestion, cardiomegaly.

• EKG
• Ischemia, arrhythmias, LVH.

• Echo
• EF, valve function, wall motion, chamber size.

• BNP
• Confirmatory and marker of response to therapy.

• Stress Testing.
• Determine if CAD is a causative factor.

• Cardiac Cath.
• Plan for possible re-vascularization or valve procedure.

• Low sodium diet.
• Improves diuresis and decreases fluid overload/ edema.

• Daily weight.
• Best measure of fluid status. Weight gain of 3 pounds in 2-5 days indicative of a problem.

• O2 if needed.
• Based on ABG or pulse ox.

• Control hypertension.
• Decrease SVR.

• Correct CAD.
• Improve myocardial performance.

• Control or correct arrhythmias
• Cardioversion or medications to control rhythm and rate.

• Correct Valve disorders.
• Improves function.

• Medications.
• Next Slide.

• Bi-ventricular pacing.
• Improves synchronization of ventricles and CO.

• ACEI
• Proven reduction in morbidity and mortality. Decreases preload, afterload and myocardial remodeling.

• ARB
• If ACE not tolerated.

• Beta Blockers: Carvedilol (Coreg), Metoprolol (Toprol XL)
• Counter-intuitive due to decrease in myocardial contractility.Proven to decrease morbidity and mortality. Interrupt sympathetic over stimulation. Control BP and HR. Prevent myocardial remodeling. Start low and go slow.

• Loop Diuretics
• Decrease Preload.

• Digoxin
• Especially for rate control in A-fib. Positive Inotropic action. Negative Chronotropic action. Low therapeutic index. Watch for Toxicity e.g. headache, nausea, vision changes, arrhythmias, heart block. Monitor levels and serum lytes. No reduction in mortality. Benefit to reduce hospitalization and symptoms.

• Spironolactone (Aldactone)
• K sparing diuretic. Helpful in severe CHF. Must have adequate renal function. Watch K with ACEI.

• Nitrates
• Decrease Preload.Statins

BiDil® (Isosorbide and Hydralazine)

Hyperkalemia

• ACEI
• Betablockers

Allison said - ARB and sometimes aldactone

• On-going Assessments
• Vital signs, O2 sat, Heart sounds, lung sounds, cardiac rhythm, weight, urine output, edema, JVD, PND, orthopnea, dyspnea, mental status.

• Lab Monitoring
• BNP levels. Lytes. Renal function.

• Medication Administration
• Multiple meds. Beware of side effects and interactions.

• Patient Education
• How to do daily weights e.g. 1st in AM after void same clothes. Report weight gain of 2 pounds in 1 day or 3 pounds in 2-5 days. Low salt diet. Alternate rest and activity. How to take meds.

• Discharge Planning
• How to avoid future exacerbations. Follow-up appointments, Home health, Medications Need to report changes early.

• Ideal 2 grams or less per day.
• Read labels.
• Do not cook with salt.
• Avoid using salt shaker.
• Try using different spices.
• Limit processed, pickled or cured foods.
• Be cautious with canned soups, vegetables.
• Avoid fast food and salty snacks.

• Inotropes
• Dopamine, Dobutamine, Milrinone

• IABP
• Inflates during diastole.
• Improves coronary perfusion.
• Decreased workload for LV.

• VAD
• Surgically implanted pump.
• Bridge to transplant.
• “Destination Therapy”.

Group of disease resulting in damage to heart muscle structure and function.

• 3 Types
• Dilated, Hypertrophic, and Constrictive.

• Most Common 90%
• Idiopathic

• Primary
• Alcohol, Viral, Doxorubicin (Adriamycin), ischemia, drug abuse

• Secondary
• Cardiomegaly (enlargement of the heart) with ventricular dilatation, impaired systolic function, atrial enlargement, stasis of blood in LV. Increased risk of thrombi and arrhythmias. Patients often younger than CHF patients.

• Pathophysiology
• This disorder resembles CHF, but the walls of the ventricles do not hypertrophy as they do in CHF.

• Difference between dilated cardiomyopathy and CHF.
• Echo and Cardiac Cath

• Diagnosis
• Same as CHF, +/- anticoagulants, +/- antiarrthymics

Treatment

• Transplantation
• Accounts for 50% of heart transplants

• Idiopathic Hypertrophic
• Subaortic Stenosis (IHSS)

Genetic, Aortic Stenosis, HTN

• Enlarged ventricularwall and septum impede systolic
• outflow and diastolic filling. Usuallyyoung healthy people. Results in
• exertional dyspnea, syncope, angina,arrhythmias. Cause of sudden death
• in athletes.

May be none. May have S3 S4 orsystolic murmur.

Echo

• Beta Blockers and Calcium Channel Blockers.
• Decrease contractility, improve outflow and ventricular filling.

ICD or antiarrhythmic if indicated.

Surgery.

Percutaneous transluminal septal myocardial ablation (PTSMA).

Patients must avoid strenuous activity and dehydration.

• Decrease contractility, improve outflow and ventricular filling.
• Implanted cardiac defibrillator.
• Shave down ventricular septum.
• Inject ETOH into septal artery

Idiopathic, tumors, radiation, sarcoidosis, amyloidosis.

• Ventricles stiffen. Resistant to diastolic filling.
• Systolic function unaffected.

• Exercise intolerance, angina, syncope, dyspnea on exertion.
• Cannot tolerate increased HR or increased CO to meet demand.

Echo

Same as CHF, treatarrhythmias, transplant, avoid exertion, dehydration.

• Demand Exceeds Supply
• Half of candidates die waiting for organ.

CriteriaAge restriction > 67, otherwise good health, able to comply with complex medical regimen, no active infection, no active or recent malignancy.ProcedureEvaluated for place on wait list. Must be matched. If condition dteriorates may be hospitalized. May require pressors or IABP.Life Long Immunosuppressants.Increased risk of infection and malignancy

Age restriction > 67, otherwise good health, able to comply with complex medical regimen, no active infection, no active or recent malignancy.

Evaluated for place on wait list. Must be matched. If condition deteriorates may be hospitalized. May require pressors or IABP.

Increased risk of infection and malignancy