WIXLIB

Heart failure

Heart failure Heart Failure is the inability of the heart to pumpsufficient blood to meet the needs of the tissuesfor oxygen and nutrients. It is otherwise known as Congestive CardiacFailure. Heart failure results in intravascular andinterstitial volume overload and poor tissueperfusion.

causes Reduced ventricular contractility Ventricular outflow obstruction (pressureoverload ) Ventricular inflow obstruction Ventricular volume overload Arrhythmia Diastolic dysfunction

Acute causes Acute myocardial infarctionDysrrhythmiasPulmonary emboliThyrotoxicosisHypertensive crisisRupture of papillary muscle( eg: mitral valve)Ventricular septal defectMyocarditis

Chronic causes Coronary artery diseaseHypertensionRheumatic heart diseaseCongenital heart diseaseCor pulmonaleCardiomyopathyAnemiaBacterial endocarditisValvular disorders

RISK FACTORS Advancing ageHypertensionDiabetesObesityHigh serum cholesterolCigarette smoking

PRECIPITATING CAUSES AnemiaInfectionHypothyroidismBacterial endocarditisPaget’s diseaseNutritional deficienciesHypervolemia

PATHO PHYSIOLOGYCompensatory mechanism 1. Hemodynamic alterations2. Neurohormonal responses3. Ventricular dilation4. Ventricular hypertrophy

Alterations in Beta-adrenergic Receptor pathway Increased NE concentration cause down regulation ofbeta-1 adrenergic receptors in the ventricles. Beta- adrenergic receptor kinase(BARK) enzyme levelincreases.

Role of Arginine Vasopressin (AVP) Circulating AVP is elevated. This leads to salt and waterretention and systemic vasoconstriction.

Role of cytokinine They have crucial roles in mediating thechanges in myocardial structure and functionin CHF.

Cellular and Molecular Mechanisms Role of calcium Calcium plays a central role in myocardialcontraction and relaxation. In CHF, there isprolonged elevation of intracellular calciumduring relaxation

Role of free radicals and apoptosis Altered mitochondrial oxygen metabolismresults in formation of free radicals. Free radicals produced by various mechanismshave been shown to result in apoptosis ofcardiac myocytes in CHF.

DECOMPENSATED HEART FAILURE Ventricular remodeling Sustained neurohumoral activation

Counter regulatory mechanism ANP and BNP are hormones produced by the heartmuscle . ANP is released in response to stretch or increasedvolume in the chambers. Levels of circulating ANP can be correlate withfunctional class prognosis and hemodynamic state.

Inhibit renin, aldosterone and ADH secretion and resultsin excretion of sodium and water Promotes venous and arterial vasodilatation. BNP is released in response to an increase in wall stressor triggered by pressure.

TYPES OF HEART FAILURE Left –sided heart failure or left ventriculardysfunction Right sided heart failure or rightventricular failure Biventricular heart failure Diastolic and systolic dysfunction

High output versus low output failureHigh output failure occurs when the heart despitenormal output to high output levels is simplynot able to meet the accelerated needs of thetissuesLow output failure occurs in most forms of heartdisease resulting in hypoperfusion of tissuecells .

Backward versus forward failure Backward failure focuses on the ventriclesinability to eject completely ,which increasesventricular filling pressures ,causing venousand pulmonary congestion . Forward failure is a problem of inadequateperfusion. It results when reduced contractilityproduces a decrease in stroke volume andcardiac output

Acute versus chronic heart failure

CLINICAL MANIFESTATIONS Left Sided HeartFailure Acute LVF presents with a sudden onset ofdyspnoea at rest. progresses to acute respiratory distress,orthopnoea and prostration. appears agitated ,pale and clammy Rapid pulse

Cool peripheryHigh BPElevated JVP if associated with RVF.Auscultaition – crepitations,triple gallop rhythm.Displaced apex beat.

Respiratory system TachypneaCapillary refill 3 secondsOrthopneaDyspnea on exertionNocturnal dyspneaCough with frothy sputum (indicative ofpulmonary edema)

Basilar crackles or rhonchiCyanosisHypoxia (respiratory acidosis)Kussmaul’s signCheyne stokes respiration

Cardiovascular system Diaphoresis Audible S3 and S4 heart tones Murmur or mitral insufficiency Enlarged left ventricle on X-ray Enlarged left atrium on X-ray Narrowing pulse pressure Pulses alternans (alteration of weak and strongbeats)

Basilar crackles or rhonchiCyanosisHypoxia (respiratory acidosis)Kussmaul’s signCheyne stokes respirationElevated pulmonary artery pressuresElevate pulmonary artery occlusive pressures

Central nervous system Mental confusionGeneralized symptoms Weight gain. Fatigue/weakness/lethargy

Right sided heartfailureGastro intestinal system Hepatomegaly Splenomegaly Hepatojugular reflux Ascites

Weight gain Weight loss and emaciation as a result of inadequateintake of food and wasting of tissues. This picture istermed as cardiac cachexia

Cardiovascular system ArrhythmiasElevated CVPElevated right atrial pressureElevated right ventricular pressureNarrowing pulse pressureMurmur or tricuspid insufficiency

Audible S3 and S4 heart tonesEnlarged right atrium on X-rayEnlarged right ventricle on X-rayDependant pitting edemaVenous distention

Urinary system Oliguria Nocturia

Chronic heart failure FatigueDyspneaOrthopneaParoxysmal nocturnal dyspneaTachycardiaEdema

Nocturia Skin changesChronic swelling result in pigment changescausing the skin to appear brown cool and damp to the touch Behavioral changes Chest pain Weight changes

COMPLICATIONS Pleural effusion DysrhythmiasEF less than 35%have a high risk of fataldysrhythmias and sudden cardiac death. Renal failure Impaired liver function & Cardiac cirrhosis ThromboembolismHypokalemia & Hyperkalemia

DIAGNOSTIC STUDIES History Physical Examination

Electrocardiogram Laboratory data(cardiac enzymes, BNP,serum chemistries,liver function studies ,thyroid function studies andcomplete blood count). In severe CHF dilutionalhyponatremia occurs. BUN and creatinine are moderatelyelevated.

BNP levels are used to assess the HF. BNP 100pg/ml- heart failure veryimprobable BNP100-500pg/ml-HF probable BNP 500pg/ml-HF very probabl

Echocardiogram : EF less than 40% accepted as evidenceof systolic dysfunction. Asessment of myocardial viabilityThis can be done by using dobutamine or dipyridamolestress echocardiography, nuclear imaging using thalliumor sestamibi and positron emission tomography

Identify patients who will benefit from long term therapywith drugs such as ACE inhibitors Stress testing,(treadmill test, stress echocardiography andnuclear perfusion studies) Cardiac catheterization and coronary angiography:

Endomyocardial biopsyThis is indicated in patients with clinical indication ofmyocarditis and systemic disease with possible cardiacinvolvement such as hemochromatosis, amyloidosis,sarcoidosis and those who have received adriamycinchemotherapy.

MANAGEMENT OF ACUTE PULMONARY EDEMA Sit the patient up Give oxygen(high flow ,high concentration ).non invasive positive pressure ventilation(CPAP-5-10 mmhg) IV glceryl trinitrate 10-200 microgram/minute until clinical improvement occurs orsystolic blood pressure falls to 110mmHg. loop diuretic such as frusemide 50-100mg IV

continuous monitoring Ionotropic agents Intra aortic balloon pump

Management General measuresPharmacologic therapyDevicesSurgeryNewer evolving therapies

General measures Rest Correction of aggravating factors Salt restriction – sodium intake should belimited to 2g/day Fluid restriction- to 1-2l/day is advisable inpatients with dilutional hyponatremia. Smoking cessation Avoid alcohol Management of co morbidities

Pharmacologic therapyTo Reduce workload Angiotensin converting enzyme inhibitors Angiotensin II receptor blockers Vasodilators Diuretics Beta blockers

ACE inhibitors Interrupts the vicious cycle of neurohumoral activation Prevents salt and water retension ,peripheral arterial andvenous vasoconstriction Also increase the concentrations of the vasodilatorbradykinin. Decreases SVR and improves myocardial performance.

Enalapril: 2.5 mg 12 hrlyLisinopril 2.5 mg dailyRamipril :1.25 mg dailyCaptopril :50 mg tds

Adverse effects Persistant coughHypotensionHyperkalemia\deteriorating renal functionLoss of taste

Angiiotensin II receptor blockers Similar hemodynamic effects to ACE inhibitorsDo not affect bradykinin metabolismLosartan, Valsartan, Irbesartan and EprosartanLosartan :25 mg dailyCandesartan:4 mg dailyValsartan : 40 mg daily

Vasodialators Venous dialationblood is trapped in theveins ,and venous return to the heart isdecreased .This reduces preload eg: nitroglycerin and isosorbide dinitrate Dilation of arterioles: arteriolar vasodilatorsdecreases peripheral vascular resistance andafterload Eg:ACE inhibitors

Combined action on veins and arterioles decrease both preload and afterload sodium nitroprusside relaxes the smooth muscle of bothveins and arterioles.it does not directly affect the heartmuscle or heart rate

Beta blockers Directly block the direct effects of the SNS Cardio selective agents block beta 1 adrenergicreceptors.non selective agents block beta 1 and beta 2adrenergic receptors. Eg: atenolol,metoprolol , bisoprolol, bucindolol,labetalol,carvedilol,esmolol (25-50 mg bd)

Diuretics To mobilize edematous fluid , reduce pulmonary venouspressure ,and reduce preload Thiazide diuretics may be the first choice in chronic HF lazone

Loop diuretics eg.Frusimide ,torsemide Spironolactone is an inexpensive ,potassium sparingdiuretic.

Human b-type natriuretic peptideNesiritide is a synthetic form of human BN

Beta adrenergic agonists short term treatment E.g.:-dopamine, dobutamine

Cardiac glycosides Eg ; Digoxin Slow the ventricular rate, improves cardiac function Optimum therapeutic level os digoxin in serum is 1-1.5ng/ml Toxic level is above 2ng/ml

Calcium channel blockers Vasodilator Anti ischemic effects Eg: Verapamil, diltiazem, amlodipine

Phosphodiesterase inhibitors:Eg: amrinone,milrinone Antidysrhythmic drugse.g.adenosine, digoxin, ibutilide, magnesium

Devices Implantable cardiac defibrillators andresynchronization therapy

Ventricular assist devices

Extracorporeal membrane oxygenator

Surgery Heart transplantationCoronary revascularizationDynamic cardiomyoplastyPartial left ventriculectomy( Batista procedure)AneurysmectomyMitral annuloplasty and mitral valve repair

Newer evolving therapies Gene therapy To increase the myocardial contractility at molecularlevel Genes expressing SERCA2a are increased by usingadenovirus transfection of myocytes

NURSING ASSESSMENT

Nursing diagnosisDecreased cardiac output r/t heart failure,dysrhythmia or both Assess blood pressure for hypotension orhypertension Assess heart rate and rhythm Document rhythm strips q8h Auscultate heart rate q2h Monitor lung sounds

Monitor intake and outputAssess for change in mental statusAdminister prescribed medicationsEncourage physical and mental supportEncourage client to eat small frequent feeds

Excess fluid volume related to cardiac failureas evidenced by edema ,dyspnea on exertion,increased weight gain Monitor intake and output chartAssess for presence of peripheral edemaAssess for jugular vein distentionFollow low sodium or fluid restrictionAuscultate breath soundsAdminister diuretic therapy

Impaired gas exchange related to increased preload,mechanical failure or immobility as evidenced byincreased respiratory rate, shortness of breath, anddyspnea on exertion Auscultate breath sounds q2hAssess respiratory rateAsses for cyanosisMonitor pulse oximetryPosition the client to facilitate breathingAdminister diuretic therapy

Ineffective tissue perfusion related to decreasedcardiac output Note colour and temperature of the skin q4hMonitor peripheral pulsesq4hProvide a warm environmentEncourage active rang of motionMonitor urine output