Congestive Heart Failure

Congestive Heart FailureDefinitionImpaired cardiac pumping such that heart is unable to pump adequate amount of blood to meet metabolic needsNot a disease but a syndromeAssociated with long-standing HTN and CAD

Factors Affecting Cardiac OutputCardiac OutputPreloadAfterloadContractilityHeart RateStroke Volume=X

Factors Affecting Cardiac OutputHeart RateIn general, the higher the heart rate, the lower the cardiacE.g. HR x SV = CO60/min x 80 ml = 4800 ml/min (4.8 L/min)70/min x 80 ml = 5600 ml/min (5.6 L/min)But only up to a point. With excessively high heart rates, diastolic filling time begins to fall, thus causing stroke volume and thus CO to fall

Factors Affecting Cardiac OutputPreloadThe volume of blood/amount of fiber stretch in the ventricles at the end of diastole (i.e., before the next contraction)

Factors Affecting Cardiac OutputPreload increases with:Fluid volume increasesVasoconstriction (squeezes blood from vascular system into heart)Preload decreases withFluid volume lossesVasodilation (able to hold more blood, therefore less returning toheart)

Factors Affecting Cardiac OutputStarlings Law Describes the relationship between preload and cardiac outputThe greater the heart muscle fibers are stretched (b/c of increases in volume), the greater their subsequentforce of contraction but only up to a point. Beyond that point, fibers get over-stretched and the force of contraction is reducedExcessive preload = excessive stretch reduced contraction reduced SV/CO

Factors Affecting Cardiac OutputAfterload The resistance against which the ventricle must pump. Excessive afterload = difficult to pump blood reduced CO/SVAfterload increased with:HypertensionVasoconstrictionAfterload decreased with:Vasodilation

Factors Affecting Cardiac OutputContractility Ability of the heart muscle to contract; relates to the strength of contraction.

Factors Affecting Cardiac OutputContractility decreased with:infarcted tissue no contractile strengthischemic tissue reduced contractile strength. Electrolyte/acid-base imbalanceNegative inotropes (medications that decrease contractility, such as beta blockers).Contractility increased with:Sympathetic stimulation (effects of epinephrine)Positive inotropes (medications that increase contractility, such as digoxin, sympathomimmetics)

Pathophysiology of CHFPump fails decreased stroke volume /CO. Compensatory mechanisms kick in to increase CO SNS stimulation release of epinephrine/nor-epinephrineIncrease HRIncrease contractility Peripheral vasoconstriction (increases afterload)Myocardial hypertrophy: walls of heart thicken to provide more muscle mass stronger contractions

Pathophysiology of CHFHormonal response: d renal perfusion interpreted by juxtaglomerular apparatus as hypovolemia. Thus:Kidneys release renin, which stimulates conversion of antiotensin I angiotensin II, which causes:Aldosterone release Na retention and water retention (via ADH secretion)Peripheral vasoconstriction

Pathophysiology of CHFCompensatory mechanisms may restore CO to near-normal. But, if excessive the compensatory mechanisms can worsen heart failure because . . .

Pathophysiology of CHFVasoconstriction: s the resistance against which heart has to pump (i.e., s afterload), and may therefore CO

Na and water retention: s fluid volume, which s preload. If too much stretch (d/t too much fluid) strength of contraction and s CO

Excessive tachycardia d diastolic filling time d ventricular filling d SV and CO

Congestive Heart FailureRisk FactorsCADAgeHTNObesityCigarette smokingDiabetes mellitusHigh cholesterolAfrican descent

Congestive Heart FailureEtiologyMay be caused by any interference with normal mechanisms regulating cardiac output (CO)Common causesHTN Myocardial infarction DysrhythmiasValvular disorders

Congestive Heart FailureTypes of Congestive Heart FailureLeft-sided failureMost common form Blood backs up through the left atrium into the pulmonary veinsPulmonary congestion and edemaEventually leads to biventricular failure

Congestive Heart FailureTypes of Congestive Heart FailureLeft-sided failureMost common cause: HTNCardiomyopathyValvular disordersCAD (myocardial infarction)

Congestive Heart FailureTypes of Congestive Heart FailureRight-sided failureResults from diseased right ventricleBlood backs up into right atrium and venous circulationCausesLVFCor pulmonaleRV infarction

Congestive Heart FailureTypes of Congestive Heart FailureRight-sided failureVenous congestionPeripheral edemaHepatomegalySplenomegalyJugular venous distension

Congestive Heart FailureTypes of Congestive Heart FailureRight-sided failurePrimary cause is left-sided failureCor pulmonaleRV dilation and hypertrophy caused by pulmonary pathology

Acute Congestive Heart FailureClinical ManifestationsPulmonary edema (what will you hear?)AgitationPale or cyanoticCold, clammy skinSevere dyspneaTachypneaPink, frothy sputum

Pulmonary EdemaFig. 34-2

Chronic Congestive Heart FailureClinical ManifestationsFatigueDyspneaParoxysmal nocturnal dyspnea (PND)TachycardiaEdema (lung, liver, abdomen, legs)Nocturia

Chronic Congestive Heart FailureClinical ManifestationsBehavioral changesRestlessness, confusion, attention spanChest pain (d/t CO and myocardial work)Weight changes (r/t fluid retention)Skin changesDusky appearance

Congestive Heart FailureClassificationBased on the persons tolerance to physical activityClass 1: No limitation of physical activityClass 2: Slight limitationClass 3: Marked limitationClass 4: Inability to carry on any physical activity without discomfort

Congestive Heart FailureDiagnostic StudiesPrimary goal is to determine underlying causePhysical examChest x-rayECGHemodynamic assessment

Congestive Heart FailureDiagnostic StudiesPrimary goal is to determine underlying causeEchocardiogram (Uses ultrasound to visualize myocardial structures and movement, calculate EF)Cardiac catheterization

Acute Congestive Heart FailureNursing and Collaborative Management

Primary goal is to improve LV function by:Decreasing intravascular volumeDecreasing venous returnDecreasing afterloadImproving gas exchange and oxygenationImproving cardiac functionReducing anxiety

Acute Congestive Heart FailureNursing and Collaborative Management

Decreasing intravascular volumeImproves LV function by reducing venous returnLoop diuretic: drug of choiceReduces preloadHigh Fowlers position

Acute Congestive Heart FailureNursing and Collaborative Management

Decreasing afterloadDrug therapy: vasodilation, ACE inhibitorsDecreases pulmonary congestion

Acute Congestive Heart FailureNursing and Collaborative Management

Improving cardiac functionPositive inotropesImproving gas exchange and oxygenationAdminister oxygen, sometimes intubate and ventilateReducing anxietyMorphine

Chronic Congestive Heart FailureCollaborative CareTreat underlying causeMaximize COAlleviate symptoms

Chronic Congestive Heart FailureCollaborative CareOxygen treatmentRestBiventricular pacingCardiac transplantation

Chronic Congestive Heart FailureDrug TherapyACE inhibitorsDiureticsInotropic drugsVasodilators-Adrenergic blockers

Chronic Congestive Heart FailureNutritional TherapyFluid restrictions not commonly prescribedSodium restriction2 g sodium dietDaily weightsSame time each dayWearing same type of clothing

Chronic Congestive Heart FailureNursing ManagementNursing AssessmentPast health historyMedicationsFunctional health problemsCold, diaphoretic skin

Chronic Congestive Heart FailureNursing ManagementNursing AssessmentTachypneaTachycardiaCracklesAbdominal distensionRestlessness

Chronic Congestive Heart FailureNursing ManagementNursing DiagnosesActivity intoleranceExcess fluid volumeDisturbed sleep patternImpaired gas exchangeAnxiety

Chronic Congestive Heart FailureNursing ManagementPlanningOverall goals: Peripheral edema Shortness of breath Exercise toleranceDrug complianceNo complications

Chronic Congestive Heart FailureNursing ManagementNursing ImplementationAcute interventionEstablishment of quality of life goalsSymptom managementConservation of physical/emotional energySupport systems are essential