CHF.txt

• 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
• Inability to maintain adequate cardiac output

• 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
• Previous MI, ischemia, impairment of valves, conduction defects, arrhythmias
• Results in left ventricular hypertrophy due to increased afterload

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

• Hypertension (due to strain of pumping against high SVR; dysfunctional hypertrophy)
• CAD
• Congenital heart disease
• Rheumatic heart disease
• Cardiomyopathy
• Valvular heart disease
• Atrial fibrillation (loss of atrial kick)
• Cor Pulmonale (right sided heart failure that results from lung disease; damage to lung causes increased pressure on right side of heart)
• 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)
• Failure of left ventricle causes back up of fluid into lungs
• Failure of right ventricle causes JVD and peripheral edema

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

• Systolic
• Diastolic
• Mixed Systolic & Diastolic failure
• 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; anemia, hyperthyroidism)

• Most common cause
• LV loses contractile ability to eject blood forward through the high pressure aorta (impaired ventricular emptying)
• Hallmark sign is decrease in ejection fraction (the fraction of total vent. filling volume ejected on each contraction; normal is greater than 50%)
• Causes: impaired contractile function (MI), increased afterload (HTN), or mechanical abnormalities (VHD)

• 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 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)

• Most common initial heart failure, results from LV dysfunction
• Blood to backs 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 (will ultimately worsen heart failure)
• Ventricular dilation (due to back flow of fluid; muscle fibers become overstretched and overstrained)
• Ventricular hypertrophy (increase in muscle mass; poor contractility)
• Increased SNS activity (body senses inadequate cardiac output; vasoconstriction; increases HR, demand, afterload)
• Hormonal response (RAAS, kidneys sense decrease in perfusion so respond by releasing renin; results in fluid retention and vasoconstriction; increases preload and afterload)
• Myocardial Remodeling (compensatory mechanism causes ventricle to remodel; becomes less effective pump)

• Hormones released from heart muscle related to heart being stretched out
• 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 (produced by ventricles; serum level diagnostic marker)

• Indicates severity of heart failure
• 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 (due to low amount of oxygen to brain)
• Course rales
• Wheezes
• Frothy pink sputum (leakage from capillaries)

• Acute Care Admission.
• High flow O2
• Continuous monitoring
• Labs (BNP, ABGs, electrolytes, cardiac enzymes, BUN, Cr, CBC), CXR (shows enlargement of heart, pulmonary congestion), 12 lead EKG (looking for conduction defects, rhythm disturbances)
• IV Lasix (assess for hemodynamic/renal status)
• IV Morphine (decreases afterload)
• IV Nitrogylecrin or Nitroprusside (decreases preload)
• IV Dopamine (risk for hypertension)
• IV Natrecor

• Factors (age, underlying type, extent of heart disease, which ventricle is failing)
• Fatigue (caused by decreased cardiac output, impaired circulation, decreased O2 of tissues)
• Dyspnea (increased pulmonary pressure, poor gas exchange, SOB, rapid shallow breaths, orthopnea, paroxysmal nocturnal dyspnea)
• Tachycardia (due to decreased cardiac output, increase in SNS)
• Peripheral edema (legs, liver, ascites, pitting)
• Nocturia (decreased cardiac output, impaired renal function, decreased urinary output during day, at night fluid moves from interstitial spaces back into circulation)
• Behavioral changes
• Chest pain
• Weight changes
• Arrhythmias

• Daily weights (same time, clothes, scale, empty bladder)
• If gain > 2 to 3lbs per day is a sign of deterioration

• CBC, CMP (anemia, renal function, liver function, electrolytes)
• CXR (pulmonary congestion, cardiomegaly.
• EKG (ischemia, arrhythmias, LVH)
• Echo (ejection fraction, 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
• 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) (decrease in myocardial contractility, morbidity and mortality; control BP and HR; prevent myocardial remodeling; start low and go slow)
• Loop Diuretics (decrease preload; do not prolong survival, just symptom management)
• Digoxin (positive inotropic action; increases contractility; decreases HR and conduction; low therapeutic index; watch for toxicity e.g. headache, nausea, vision changes, arrhythmias, heart block, "green-yellow halos" around eyes; monitor levels and serum electrolytes; no reduction in mortality; benefit to reduce hospitalization and symptoms)
• Spironolactone (K sparing diuretic; helpful in severe CHF; must have adequate renal function; watch K with ACEI)
• Nitrates (decrease preload; vasodilation)
• Statins (to treat any underlying hyperlipidemia)
• BiDil® (Isosorbide and Hydralazine)

Hyperkalemia

• ACEI
• Beta blockers
• ARBs 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; electrolytes; renal function)
• Medication Administration (multiple meds; beware of side effects and interactions)
• Patient Education (how to do daily weights; 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; increases contractility)
• IABP (intra-aortic balloon pump; inflates during diastole; improves coronary perfusion; decreased workload for LV)
• VAD (ventricular assist device; surgically implanted pump; bridge to transplant; “Destination Therapy”.
• Bridge to transplant (heart is in bad shape so are kept alive on VAD until transplant is available)
• Destination therapy (patient is not a candidate for transplant but will try out VAD to help support ventricle and increase survival)

• Group of diseases 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 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 (resembles CHF, but the walls of the ventricles do not hypertrophy)
• Treatment (same as CHF, +/- anticoagulants, +/- antiarrthymics)
• Transplantation (accounts for 50% of heart transplants)

• Idiopathic Hypertrophic Subaortic Stenosis (IHSS)
• Overgrowth of myocardium that obstructs outflow of blood through aorta (impedes systolic outflow and diastolic filling)
• Causes: genetic, congenital, aortic stenosis, HTN
• Very poorly tolerate tachycardia (decreased time in diastole; left ventricular filling) and hypovolemia (don't adequately fill ventricle; need big bolus of blood to push past obstruction)
• Hard to diagnose (ECHO)
• Results in exertional dyspnea, syncope, angina, arrhythmias
• Cause of sudden death in athletes

• 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

• Ventricles stiffen; resistent to diastolic filling; systolic function not affected
• Causes: idiopathic, tumors, radiation, sarcoidosis, amyloidosis
• Symptoms: exercise intolerance, angina, syncope, dyspnea on exertion
• Cannot tolerate increased HR or increased CO to meet demand
• Diagnosed via ECHO
• Treatment: same as CHF; treat arrhythmias, transplant, avoid exertion and dehydration

• Demand exceeds supply (half of candidates die waiting for organ)
• Criteria (age restriction, must be younger than 67 years old; otherwise good health; able to comply with complex medical regimen; no active infection; no active or recent maligancy
• Procedure: evaluated for place on wait list; must be matched; may require vasopressors or IABP
• Life-long immunosuppresants (increases risk of infection and malignancy)

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