By: Darryl JamisonNREMT-PMacon County EMS Training Coordinator

Approximately 30-40% of patients with CHF are hospitalized each year. Leading diagnosis-related group over 65. The 5 year mortality after Dx was reported as 60% in men and 45% in women in 1971. In 1991, data from the Farmington heart study showed the 5 year mortality rate remaining unchanged, with a median survival of 3.2 years for men, and 5.4 years for women, post dx.The most common cause of death is progressive heart failure, but sudden death may account for up to 45% of all deaths.Patients with coexisting IDDM have a significantly higher mortality rate.

Effects an estimated 4.9 million Americans1% of adults 50-6010% adults over 80Over 550,000 new cases annually$28.7 million committed in research dollars each year$132 million for lung cancer, affecting 390,000 Americans Responsible for 5-10% of all hospital admissionsCauses or contributes to approximately 250,000 deaths per year

An imbalance in pump function in which the heart fails to maintain the circulation of blood adequately.

Summarized as an imbalance in Starlings forces or an imbalance in the degree of end-diastolic fiber stretch proportional to the systolic mechanical work expended in the ensuing contraction.Or basically like a rubber band, the more it is stretched, the greater the releasing velocity.

Under normal circumstances, when fluid is transferred into the lung interstitium with increased lymphatic flow, no increase in interstitial volume occurs.However, when the capacity of the lymphatic drainage is exceeded, liquid accumulates in the interstitial spaces surrounding the bronchioles and lung vasculature, this creating CHF.When increased fluid and pressure cause tracking into the interstitial space around the alveoli and disruption of alveolar membrane junctions, fluid floods the alveoli and leads to pulmonary edema

Coronary artery disease--chronicHTN--bothValvular heart disease (especially aorta and mitral disease)--chronicInfections--acuteDysrhythmias--acute

Alcohol--chronicMI--acuteDiabeteschronic

PreloadThe amount of blood the heart must pump with each beatDetermined by:Venous return to heartAccompanying stretch of the muscle fibersIncreasing preload increase stroke volume in normal heartIncreasing preload impaired heart decreased SV. Blood is trapped chamber enlargementAfterloadThe pressure that must be overcome for the heart to pump blood into the arterial system.Dependent on the systemic vascular resistanceWith increased afterload, the heart muscles must work harder to overcome the constricted vascular bed chamber enlargementIncreasing the afterload will eventually decrease the cardiac output.

When cholesterol and fatty deposits build up in the hearts arteries, less blood reaches the heart muscle. This damages the muscle, and the healthy heart tissue that remains has to work harder

Uncontrolled HTN doubles the chances of failureWith HTN, the chambers of the heart enlarge and weaken.

Can result from disease, infection, or be congenitalDont open and/or close completely increased workload failure

Tachycardias decreased diastolic filling time decreased SV.Atrial dysrhythmias as much as 30% reduction in stroke volume

The ischemic tissue is basically taken out of the equation, leaving a portion of the heart to do the work of the entire heart decreased SV CHF.

Tend to be overweightHTNHyperlipidemia

Types of Rhythms Associated with CHF

Left Ventricular Failure with Pulmonary EdemaAkasystolic heart failure

Right Ventricular FailureAkadiastolic heart failure

Occurs when the left ventricle fails as an effective forward pumpback pressure of blood into the pulmonary circulation pulmonary edemaCannot eject all of the blood delivered from the right heart.Left atrial pressure rises increased pressure in the pulmonary veins and capillariesWhen pressure becomes to high, the fluid portion of the blood is forced into the alveoli. decreased oxygenation capacity of the lungs AMI common with LVF, suspect

Severe resp. distress Evidenced by orthopnea, dyspneaHx of paroxysmal nocturnal dyspnea.Severe apprehension, agitation, confusionResulting from hypoxiaFeels like he/she is smotheringCyanosis

DiaphoresisResults from sympathetic stimulationPulmonary congestionOften presentRalesespecially at the bases.Rhonchiassociated with fluid in the larger airways indicative of severe failureWheezesresponse to airway spasm

Jugular Venous Distentionnot directly related to LVF. Comes from back pressure building from right heart into venous circulation Vital SignsSignificant increase in sympathetic discharge to compensate.BPelevatedPulse rateelevated to compensate for decreased stroke volume.Respirationsrapid and labored

LOCmay vary.Depends on the level of hypoxiaChest PainMay in the presence of MICan be masked by the RDS.

REMEMBER LEFT VENTRICULAR FAILURE IS A TRUE LIFE THREATENING EMERGENCY

EtiologyAcute MIInferior MIPulmonary disease COPD, fibrosis, HTNCardiac disease involving the left or both ventriclesResults from LVFPathophysiologyDecreased right-sided cardiac output or increased pulmonary vascular resistance increased right vent. Pressures.As pressures rise, this increased pressure in the right atrium and venous systemHigher right atrium pressures JVP

In the peripheral veins, pressures rise and the capillary pressures increase, hydrostatic pressure exceeds that of interstitial pressureFluid leaks from the capillaries into the surrounding tissues causing peripheral edemaLungs are clear due to left ventricular pressures are normal

Marked JVDClear chestHypotensionMarked peripheral edemaAscites, hepatomegalyPoor exercise tolerance

The first three are for an inferior MI, describe cardiac tamponade.Often will be on Lasix, Digoxin,Have chronic pump failure

Neurohormonal systemRenin-angiotensin-aldosterone systemVentricular hypertrophy

Stimulated by decreased perfusion secretion of hormones

EpiIncreases contractilityIncreases rate and pressureVasoconstriction SVRVasopressinPituitary glandMild vasoconstriction, renal water retention

Decreased renal blood flow secondary to low cardiac output triggers renin secretion by the kidneysAldosterone is released increase in Na+ retention water retentionPreload increasesWorsening failure

Long term compensatory mechanismIncreases in size due to increase in work load ie skeletal muscle

COPDCHFPneumoniaCoughFrequentOccasionalFrequentWheezeFrequentOccasionalFrequentSputumThickThin/whiteThick/yellow/ brownHemoptysisOccasionallyPink frothyoccasionallyPNDSometimes after a few hoursOften within 1 hourRareSmokingCommonLess commonLess commonPedal edemaOccasionalCommon with chronicnone

COPDCHFPneumoniaOnsetOften URI with coughOrthopnea at nightGradual with fever, coughChest PainpleuriticSubsternal, crushingPleuritic, often localizedClubbingOftenRareRareCyanosisOften and severeInitially mild but progressesMay be presentDiaphoresisMay be presentMild to heavyDry to moistPursed LipsOftenRareRare unless COPD

COPDCHFPneumoniaBarrel ChestCommonRareRare unless COPD JVDMay be present with RVFMild to severeRareBPUsually normalOften highNormalDysrhythmiaOccasionalMay precipitate CHFCommonWheezeCommonLess commonCommonCracklesCoarse, diffuseFine to coarse, begin in gravity dependent areasLocalized to diffuse, coarse

Aimed at diminishing the compensatory mechanisms of low cardiac output and also improving contractility

VasodilatorsACE inhibitorsDiuretic agentsInotropic agents

Dilate blood vesselsOften constricted due to activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system.AkaACE inhibitorsCommon ACE inhibitorsCaptoprilLisinoprilVasotecMonoprilAccuprilNitrates

LasixHydrochlorothiazide(HCTZ)Spironolactone

These inhibit reabsorption of Na+ into the kidneys

DigoxinLanoxin

Increases the contractility of the heart increasing the cardiac output

NifedipineDiltiazemVerapamilAmlodipineFelodipine

Used to dilate blood vesselsUsed mostly with CHF in the presence of ischemia

MetoprololAtenololPropanololAmiodaroneUseful by blocking the beta-adrengergic receptors of the sympathetic nervous system, the heart rate and force of contractility are decreased could actually worsen CHF

The prehospital goals for managing CHFPromotion of restRelief of anxietyDecreasing cardiac workloadAttainment of normal tissue perfusion

DO NOT make these patients walkCould start a fluid rush into the alveoliTry to get them to sit still if they appear agitated and hypoxic

Often experiencedLeads to increase in O2 demand and cardiac workloadExplain what you are doingMS 2 mg for treatment of anxiety and for decreasing preload

NTGMSLasixO2High flow O2

ACE InhibitorsDigitalisDiureticsHydralazineNitrates

Prevent the production of the chemicals that causes blood vessels to narrowResulting in blood pressure decreasing and the heart pumping easier

Inotropic effects on the heartNegative chronotropic effects

Decrease the bodys retention of salt and waterReduces blood pressureProbably will be on potassium

Widens the blood vessels, therefore allowing more blood flow

Relaxation of smooth muscle Widens blood vesselsLowers systolic blood pressure

Particularly difficult in elderlyAtypical presentations Predominant symptoms include:AnorexiaGeneralized weaknessFatigueMental disturbances Anxiety

Bubbling RhonchiCoarse CracklesFine CracklesGurgling RhonchiRales