1Congestive Heart Failure & Valvular Disease Keith Rischer RN, MA, CENImpaired cardiac pumpingCAD and age are primary risk factors…HTN, DM, smoking, obesity, high cholesterol can contributeHTN most significant contributor along w/DMHF caused by any interference in CO…this can involve preload, afterload, contractility, HRImpacts 5 million Americans550,000 new cases annuallyAffects 10% of all those over 65Most common reason for adm to hospital for the elderlyPrevelance is increasing probably due to increased treatmentTerminal dx-80% will be dead in 8 years if dx after age 65Most often due to dysfunction of the LVOverall patient’s quality of life is ↓ by HF, even when it is mild to moderate. The pt has less energy, a lower fitness level, engages in fewer social activities and has more physical complaints.The cost of HF mgmt has been est. at 38.1 billion-5.4% of the total.MGMT DEPENDANT ON PT COMPLIANCE-NSG…PT EDUCATION ESP MEDS-YOU CAN MAKE A DIFFERENCE!
2Todays Objectives… Review essential cardiac patho concepts Compare and contrast left-sided heart failure to rightDescribe special considerations for older adults with heart failureDiscuss the prevention of complications for patients with heart failurePrioritize nursing care for clients with heart failureIdentify common nursing diagnoses and collaborative problems for patients with heart failureEvaluate the effects of interventions for reducing preload and afterload through pharmacological managementCompare and contrast common valvular disorders
3Introduction Definition of CHF Left sided vs. Right sided EtiologyHTNMILeft sided vs. Right sidedRt sidedCOPDSystolic vs. DiastolicEjection Fraction50-70% normalDefinition of CHF: physiologic state in which the heart is unable to pump enough blood to meet the metabolic needs of the body. The LV is unable to eject a sufficient quantity of bloodLike a car with bad timing, the damaged heart does not function smoothly.HTN causes 75%Left sided vs. Right sidedSystolic vs. DiastolicSystolic refers to ventricular dysfunctionDiastolic-LV unable to relax adequately during diastole-inadequate relaxation or stiffening prevents ventricle from filling-decr SV though EF may be normal-not as common
4CO = Stroke volume x heart rate SV (80cc) x HR (80)= 6400cc (6.4 lpm) Cardiac OutputCO = Stroke volume x heart rateSV (80cc) x HR (80)= 6400cc (6.4 lpm)Daily pumps 1800 gallons657,000 gallons every yearOver 80 year lifetime:52,560,000 gallonsEvery 10 days fills a gallon swimming poolEvery year appx 36 poolsOver lifetime appx 3000 poolsFactors that influence CO are preload, afterload, myocardial contractility, and HR4
5Definitions Pre-load Stroke volume Systole primarily venous blood return to RARight and left side of heart filling pressure (atria>ventricles)Pressure/Stretch in ventricles end diastoleStroke volumeAmount of blood ejected from the ventricle with each contractionSystoleContraction; myocardium are tightening and shorteningPreload Preload is the filling pressure of the RV-LV and is influenced by venous return…higher venous return or blood volume in atria-the higher the SV will be…opposite is also trueWhat cardiac meds will most strongly influence preload???How will volume depletion such as by dehydration or blood loss affect preload???
6Definitions Inotropic state/contractility Afterload: Diastole Force of resistance that the LV must generate to open aortic valveCorrelates w/SBPDiastoleMuscle fibers lengthen, the heart dilates, and cavities fill with bloodContractility-Afterload Arterial vasodilation will decreaseImportant when in AMI we need to decr workload of heart by intentionally lowering afterloadNTG indirectly affects afterload through decreasing preloadWhat meds??? B-blockers….ACE inhibitors calcium channel blockers and arterial vasodilators such as hydralazineEpi will do what to afterload???
7Patho: Starling’s Law of the Heart Maximum efficency of CO achieved when myocardium stretched appx 2 ½ times lengthThink rubber bandCO decreased with lower preload/filling pressures or too highHF occurs when it takes higher filling pressures to accomplish normal contractile forceIncr in preload cause a decrease in SV and higher LVEDPThis causes back pressure into lungs causing leakage of fluid into alveoli causing PE7
8Compensatory Mechanisms in CHF Increased Sympathetic Nervous System StimulationRenin-angiotensin system activationNatriuretic peptidesBNPVentricular hypertrophycompensatory mechanisms- When the heart begins to fail, the body activates several defense mechanisms in an attempt to maintain CO and O2 to vital organs.sympathetic nervous system stimulation is the least effective comp. mechanism triggered by ↓ CO. Produces venous & arteriole vasoconstriction-↑resistance (afterload) and ↑myocardial workload. In addition, Symp. Stim. Reduces renal blood flow, and the kidneys respond by activating the renin-angiotensin system causing Na & H2O retention. The ↑ blood vol. ↑ the myocardial O2 demand on an already compromised heart.Renin-angiotensin-reduced flow to kidneys…RAS…vasoconstriction pronounced…incr …aldosterone secretion causes sodium and water retention…angiotensin II contributes to ventricular remodeling causing myocardial cell contractile dysfunction over timeBNPHormone that promote vasodilation and diuresis through sodium loss to counterbalance the RASVentricular hypertrophy Represents and ↑ in myocardial muscle mass and cardiac thickness in an attempt to ↑ CO. The heart works harder hence ↑ myocardial O2 demand.Cardiac decompensation occurs when the heart, despite these mechanisms are unable to meet the metabolic demands→CHF develops
9Acute Pulmonary Edema: Elevated capillary pressure within the lungs fluid pushed from circulating blood to interstitial tissues then to the alveoli, bronchioles, and bronchi*Results from LV failure in clients with severe decompensation*A medical emergency – can cause death from suffocation if untreated
10Nursing Assessment:Left Failure DyspneaCoughBilateral cracklesOrthopneaPNDPulmonary EdemaS3 (ken-tuck-ee)confusionfatigue and muscular weaknessnocturiaincrease retention of sodium and water due to lowered glomerular filtration edemaS3 occurs at the end of the rapid filling period of the ventricle during the beginning of (ventricular) diastole. An S3, if heard should occur msec after S2. A patient could have a left sided S3 (best heard with the bell of the stethoscope at the apex of heart while the patient is in the left lateral decubitus position), a right sided S3 (best heard with the bell of the stethoscope in the tricuspid region with the patient in the supine position during inspiration) or both. An S3 can either be physiological or pathological.A normal S3 is common in:childrenyoung adults (sometimes up to age 35-40)third trimester of pregnancyAn abnormal S3 (an S3 heard in anyone above 40) (also known as a ventricular gallop) is associated with:decreased myocardial contractionmyocardial failurevolume overload of a ventricle (such as from mitral or tricuspid regurgitation)
11Nursing Assessment: Right Failure Dependent edema –early signsymmetric pitting edemaBedrest-sacral edemaanasarca- late sign of CHFAscitesAnorexia, nausea and bloatingCyanosis of nail bedsAnxious, frightened, depressedWeight gain >2# daily
12Diagnostic Assessment Chest x-rayCardiac Enlargement12 lead EKGEchocardiogramassess ejection fractionLabsBNPLiver enzymes…AST, ALTCreatinine/GFR12 lead EKG cardiac dysrhythmia, PACs or atrial fibIncreased BUN and creatinine levels – sign of decreased renal perfusionBNP ( Brain Natriuretic Peptide): A simple test that could diagnose pts. w/CHF. BNP a hormonal ↑ levels by heart tissue when organ is overloaded w/ pressure & vol. is expanded. ↑ BNP is highly sensitive and specific for the Dx. Of HF-it is also useful for differentiating pulmonary and cardiac causes of dyspnea.
13Acute Left Failure/Pulmonary Edema: Collaborative Management: O2 treatmentDrug TreatmentDiureticsVasodilators-NTGMSDigitalisSemi- Fowler’s positionFrequent Heart and Lung AssessmentDietary RestrictionsPlanned rest periodsWeigh dailyReport to MD immediately:persisting productive cough; dyspnea; pedal edema; restlessness
14Drug therapy: Diuretics ACE Inhibitors Beta Blockers Calcium Channel BlockersNitroglycerinePositive Inotropic agentsDigitalisBeta Adrenergic StimulatorDopamine,Dobutamine.Digitalis: has inotropic effect, increased C.O.different preparations are availablecontra-indicated: cardiac tamponade and constrictive pericarditisuse with caution in acute MI, can cause increase myocardial O2 demandwatch for s/s of toxicity; G.I.; CNS; CV; visual, slow HRDopamine – has dose related effect A naturally occurring catecholamine with alpha-adrenergic, beta adrenergic, and dopaminergic activitycheck apical pulseDobutamine – a synthetic derivative of Dopamine and has strong beta stimulatory effects; increases the heart rateCapable of increasing CO without increasing the myocardial O2 demand or reducing coronary blood flow NTG-Venous dilating, ↓ afterload primarily through decr preload, properties that ↓ LV congestionIsosorbide dinitrate reduces angina by dilating both the veins and the arteries. Isosorbide dinitrate is in the class of drugs called anti-anginal medicationsNitroprusside releases a chemical call nitric oxide (NO). Nitric oxide enters the muscle cells in the walls of the blood vessels and causes them to relax. When the muscles relax, the blood vessels become wider and the blood pressure decreases.
15Pharmacologic: Diuretics Mechanism of Action:Thiazides, Loop, Potassium SparingS/E:fluid and electrolyte imbalancesCNS effectsGI effectsNursing Considerations:Monitor for orthostatic hypotensionHypokalemiaThiazides, Loop, Potassium SparingPatho-block Na+ reabsorption in nephron-Na+ follows water and increases water/urine excretionLoop of henle has highest concentration of Na+ in filtrate from glomerulus therefore they are the most potentRecommended for initial drug therapy of uncomplicated HTN (along with beta-blockerNewly diagnosed HTN preferred durg combo for initial treatment = diuretics and beta blockersThiazides first and most commonly used due to more gentle diuresis
16Angiotensin Converting Enzyme (ACE) Inhibitors Mechanism of ActionS/E:HypotensioncoughHyperkalemia…esp w/CHF, CKD, DMAngioedemaFacial/laryngeal swellingNursing considerations:Do not use with potassium sparing diureticMetabolized by liver-excreted by kidneysCO falls blood flow decreases-kidneys secrete enzyme renin>angiotensin 1> converted to Angiotensin 2 most potent vasoconstrictors kown by converting enzyme in lungsAngiotensin 2 causes adrenal cortex to release hormone Aldosterone incr Na+ reabsorption which causes water retention>salt and water retention…incr blood volume and elevates BP/vasoconstrictionBy blocking angiotensin II decreases BP through lowering peripheral resistence-AFTERLOAD….and decreasing blood volume-PRELOAD
17Adrenergic Inhibitors: Beta Blockers Mechanism of ActionRecommended for initial drug therapy of uncomplicated HTN (along with diuretic)S/E:Orthostatic hypotensionbradycardiabronchospasmNursing considerations:monitor pulse regularlyBy decr HR and contractility reduce CO and lower SBP…also block/inhibit renin secretion and resultant formation of Angiotensin IIFor example a patient receiving Rx for minipress (Prazosin HCL) make sure you tell them to take it at bedtime.
18Calcium Channel Blockers Amlodipine, Diltiazem, NifedipineMechanism of Action:S/E:NauseaH/APeripheral edemaNursing considerations:use with caution in patients with heart failureOrthostatic changescontraindicated in patients with 2nd or 3rd degree heart blockConcurrent use w/b-blockers incr risk of CHFBy blocking channels of Ca++-decr contractility and relax smooth muscle lowering peripheral resistence-AFTERLOADReduces the force of contractionSlows AV node-decreases HRVasodilation of smooth muscle in the blood vessels decreased peripheral resistance reduces BP and dec afterload reduced O2 needs.Dilates coronary arteries provide more O2 to myocardiumACTIONS:Decrease BPDecrease AnginaDecrease Heart Rate/ Dysrhythmias
19Vasodilators Mechanism of Action-NTG Vasodilater-predominant on venous system by relaxing smooth muscles of vesselsDilates coronary arteries/improves collateral flowUp to 20% normal coronaries…30-40% pre/post stenosisDecreases LVEDP…why?Decreases O2 needs myocardiumSide effectsHA, hypotension, tachycardiaHydralazinearterial vasodilatorVasodilator-which aspect of CO are we manipulating???Can be given IV, transdermal or sublingual/spray and po as Isordil/isosorbideIf subl need to keep pills cool-dry place and replace every 6 months-should gently tingle tongueHYDRALAZINE-direct arterial vasodolator-AFTERLOADProduce reflex tachycardia-compensatory response to sudden decr in BP---increases workload of heart-negating effect-bblockers can negate this effect19
20Priority Nursing Diagnosis Impaired Gas exchange r/t ventilation perfusion imbalanceDecreased Cardiac Output r/t altered contractility, preload and afterloadActivity Intolerance r/t imbalance between O2 supply and demandKnowledge DeficitActivity scheduleRecognizing worsening heart failureMedicationsDiet therapy
21Valvular Heart Disease:Mitral Valve Mitral StenosisPathoMitral RegurgitationMitral Valve ProlapseWhy is the tricuspid and pulmonic valve rarely involved in valvular disease and dysfunction???Mitral StenosisPatho- rheumatic fever…valve thickening-stiffening of valve…valve becomes narrow impacting SV to LVLA enlarges-PA pressures rise RV enlarges and can go into RV failureSystolic murmurMitral Regurgitation or insufficiencyFibrotic and calcification on valve prevent complete closure of valve…blood backflows into LA causign enlargement as well as blood leaking through to LV during diastole incr. SV and then LV enlargement…Rheumatic fever-heart disease most commonBegins slowly-heart compensates will see both RV and LV failureSys. murmurMitral Valve Prolapsevalvular leaflets enlarge and prolapse into LA during systole-usually benign but can progress to mitral regurg
22Valvular Heart Disease:Aortic Valve Aortic StenosisPathoCausesCongenitalAtheroclerosisCalcificationAortic Regurgitation (Insufficiency)Aortic StenosisPatho AV narrows/stiffens and obstructs LV outflow during systole. Increased resistence to ejection or afterload causes LV hypertrophy…due to congenital changesEventually causes LV failure and resultant CHF sxSOB, angina, fatigueSystolic murmurAortic Regurgitation (Insufficiency)Patho leaflets do not close during diastole allowing regurgitant blood flow back into LV causing incr SV and LV hypertrophyDIASTOLIC MURMUR…WHY???
23Treatment Valvular Disease Non-surgical ManagementDiureticsBeta blockersDigoxinAntibioticsBefore any invasivesCoumadin-if artificial valveSurgical ManagementBalloon ValvuloplastyOpen heartWhy is AFIB bad with valvular disease….difficult to maintain adequate CO
24Pericarditis Patho Assessment findings Complications Open heart AMI Friction rubCP w/inspCP relieves sitting upGlobal ST elevationComplicationsPericardial effusionCardiac tamponadepericardiocentesisPatho-inflammation of pericardiumMost often seen w/cancer…MI, CABG (10-40% develop)Pericardial effusion-excess can cause tamponade which will decr. Diastolic filling…does what to SV??? Does what to BP???