Heart Failure Med Ed Ppt
Transcript of Heart Failure Med Ed Ppt
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Critical Care Nuts & Bolts Acute and Chronic Heart Failure:The Epidemic
P R E S EN T E D B Y :
LISA M. SOLTIS, APRN, MSN, CCRN-CSC, CCNS
Heart Failure2
Clinical syndrome of decreased cardiacfunction
One or both ventricles are unable tomaintain adequate output
Can be systolic or diastolic
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Characteristics
Circulatory disorder characterized by abnormalitiesin the control of sodium balance, cardiac function,and Neurohormonal activation.
Systolic- the syndrome of heart failure occurring because of a difficulty emptying the left ventricle dueto impairment of myocardial contractility
Characteristics
Diastolic- the syndrome of heart failure occurring because the heart if unable to relax, and thereforeunable to fill at normal diastolic pressuressufficiently enough to accommodate an adequate
amount of oxygenated blood returning frompulmonary vasculature. Leads to either a decreased left ventricular (LV) end
diastolic volumes with a fall in cardiac output (CO) or arise in left ventricular filling pressures to maintain CO.
Lead to pulmonary hypertension, leading to pulmonarycongestion.
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Causes of Heart Failure
Coronary Artery Disease-
Myocardial Infarction-
Hypertension
Valvular Disease
Arrhythmias
Substance abuse
Viral Syndromes
Pathophysiology
Norepinepherine- Increases heart rate, contractility, vasoconstriction
Angiotensin
RAAS activation
Aldosterone secretion
Stimulates fibroblast proliferation, myocardial fibrosis
ACE effect on bradykinins
ACE-I block degradation of bradykinins, promotes vasodilation
Vasopressin
ADH fluid reabsorption at distal tubules
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Neuro-Hormonal Response
Low CardiacOutput
SympatheticNS
AdrenalMedulla
EpinephrineNor-
epinephrine
Renin
AT I to ATII
Aldosterone
HPA Axis
PituitaryGland
Vasopressin
AdrenalCortex
Cortisol
Ventricular Remodeling
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Homeostatic Mechanisms
The atria and ventricles secrete hormones, atrialnatriuretic peptide (ANP) and brain natriureticpeptide (BNP) in response to increased EDV and
ventricular stretch
ANP and BNP secretion causes vasodilatation anddiuresis (natriuresis - renal sodium loss) by
inhibiting the release of renin, angiotensin,aldosterone and epinephrine.
Left-Sided Heart Failure/Systolic Dysfunction
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Poor LV function
Decreased ability to pump blood forward
EF < 65%
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Compensation Gone a Wry
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LV Dilation
Increased LVPressure
Increased LA &pulmonary venous
pressure
Pulmonarycongestion &
edema
R heart failure
Systemiccongestion/edema
Patient Symptoms-Chronic
Shortness of breath (SOB)
Dyspnea on exertion (DOE)
Activity intolerance
Fatigue/weakness Lack of appetite
Nocturia
Swelling of feet, ankles, legs, or abdomen
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Patient Symptoms- Acute
Severe/sudden shortnessof breath
Paroxysmal nocturnaldyspnea
Orthopnea
Cough, possiblyproductive with pink,foamy sputum
Chest pain/fullness
Increased fatigue, weakness
Nausea/vomiting
Abdominal distention
Rapid or irregular heart beat
Sudden increase in weight
Increased edema
Physical Findings
Edema (including sacral edema, and ascites) Rales, pulmonary edema, tachypnea Hypotension Third heart sound S3- indicating fluid overload; S4 –
indicating stiff ventricle (as in HTN) Jugular vein distention –JVD indicating fluid overload
and right heart failure Hepatojugular reflux- increase venous congestion
leading to hepatic congestion (due to increased preload) Pale skin color/Cyanosis Resting tachycardia or arrhythmias including
bradycardia
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Pulmonary Edema
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Life-threatening complication of CHF
LV failure
Pressure in pulmonary vessels > 18-25 mmHg
Fluid leaks from pulmonary capillaries into theinterstitial tissue and intra-alveolar spaces
Signs and Symptoms16
Dyspnea
Orthopnea
Hypoxemia
Auscultation:
Crackles/rales
Sputum:
Pink, frothy
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Systolic Dysfunction: Treatment
Treatment is the sameas the treatment forleft-sided heart failure
Oxygen
May need non-invasivepositive-pressure ventilation (NIPPV) ormechanical ventilation
Decrease preload withloop diuretics
(furosemide, etc)
Morphine ornitroglycerinvasodilate, decreasingafterload
Morphine alsodecreases anxiety
Dobutamine ormilrinone to improvecardiac output
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Left-Sided Heart Failure/DiastolicDysfunction
Normal EF
LV stiff, non-compliant
◦ Inadequate LV filling
◦ Increased diastolic filling pressures
Leads to elevated LA, pulmonary venous, & PCWP
Can result in right heart failure & pulmonary HTN ifuntreated
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Left Sided Diastolic Dysfunction19
Diastolic Dysfunction: Treatment
Negative chronotropic medications todecrease heart rate & increase diastolic
filling time & stroke volume
Beta blockers (metoprolol, atenolol, etc)
Calcium channel blockers (verapamil, diltiazem)
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Right Heart Failure21
What Causes Right Heart Failure?
Pulmonary Disease
COPD, Chronic Bronchitis
Essential Pulmonary HTN PE
Isolated Right Coronary Ischemia
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Signs and Symptoms
Hepatic congestion
JVD
Edema
Ascites
Liver engorgement
Increased cardiac pressures, CVP
Treatment- Low Na diet, fluid restrictions
Nesiritide promotes diuresis and vasodilation
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Heart Failure Classification
I: Symptoms with strong exertion
II: Symptoms with normal exertion
III: Symptoms with minimal exertion
IV: Symptoms occur at rest
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Work-up
BNP: Prognostic indicator. Generally increases asHF worsens
BMP, TSH, CBC, LFTs CXR EKG Echo: assess LVEF & side/type of failure—R or L,
systolic or diastolic
Stress test: treadmill or nuclear May need cardiac catheterization
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Goals of Care
Alleviate symptoms
Stabilize hemodynamics
Correct fluid volume overload
Prevent complications, i.e. arrhythmias
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Neurohormonal Influences
HF is a vicious cycle
Flogging of the myocardium by norepinephrine
Vasopressin released, SIADH common
Continuous activation of RAA system
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Pharmacologic Agents
NON-Decompensated Heart Failure
Beta Blocker (metroprolol, Coreg) ACE Inhibitor or ARB
Spironolactone (Class 3 or 4 heart failure)
Aldosterone antagonist
Loop diuretics
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Acute Decompensated Heart Failure
(ADHF)
Signs & symptoms of worsening failure &fluid overload
May see:
JVD, weight gain, oliguria
Peripheral edema
Cool, pale, cyanotic skin
Dyspnea, crackles on auscultation
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ADHF: Treatment
Oxygen
If pulmonary edema, may need NIPPV ormechanical ventilation
Loop diuretics Positive inotropes: dobutamine or milrinone
Increase myocardial contractility
Decrease afterload
No role for -blockers in ADHF
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Cardiomyopathies
Dilated
• Progressive congestive L/R sided heart failure• Increased volume size, impaired EF%• Dysrhythmias, thromboembolism, or sudden cardiac arrest
Hyper-
trophic
• Fatigue, mild dyspnea, progressive LV failure, atrial fibrilaltion• Hypertrophic changes with increased collagen in septum and ventricular wall• Small ventricular cavity, decreased volume, normal EF%
Restrictive
• Right sided HF, tachycardia, periph. edema, ascites, liver enlargement• Restrictive filling, reduced diastolic volume, normal wall motion• Dilated atria from increased LVEDP, mitral & tricuspid regurgitation