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24 Cards in this Set
- Front
- Back
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Define Heart Failure
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-Failure of heart to pump blood at a rate commensurate with requirements of the body
-Abnormality of neurohormonal regulation |
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Preload
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-Filling P
-P exerted in LV before ventricle contracts -Estimated by PCWP |
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Afterload
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-Load after onset of contraction against which LV contracts secondary to SVR
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Cardiac contractility
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-How well heart contracts for any given HR, preload, & afterload
-Measured with EF -Normal EF = 60% -EF <40-45% = Systolic Dysfunction |
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Factors that influence preload
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-V depletion
-V expansion |
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Factors that influence afterload
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-SVR
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Factors that influence contractility
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-Myocardial damage (MI, HTN)
-Inotropic agents |
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Etiology of Diastolic Dysfunction:
-LVH secondary to HTN |
Etiology of Systolic Dysfunction:
-CAD -HTN -Genetic |
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Management of Diastolic Dysfunction:
-Avoid tachycardia -Tx ischemia -Control BP |
Management of Systolic Dysfunction:
-Diuretics + Na+ restriction -ACEI/ARB -BB -Aldosterone Antagonist/ARB -Hyd/ISDN for AA -CRT -ICD |
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Diastolic Dysfunction:
-Inability of ventricle to relax & adequately fill with blood |
Systolic Dysfunction:
-Inability of ventricle to adequately eject blood |
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Progression of CHF
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Inury-->LVH+Dilation=Remodeling-->CHF-->Death
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What is endothelin
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Peptides released from endothelial cells. Most potent vasoconstricting hormones known
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Potential adverse effects with Spironolactone (Aldosterone Antagonist used in CHF)
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Hyperkalemia -> renal failure. Monitor labs during treatment.
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Natural History of Chronic Heart Failure
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* Normal heart experiences an injury (e.g. MI). Leads to change in size, geometry, and function of heart. Results in cell death, ventricular wall thinning, hypertrophy, spherical instead of eliptical (Mavericks instead of Cowboys), and accumulation of collagen in cardiac interstitium.
* This is known as Cardiac Remodeling. A big reason it occurs is from neurohormonal activation (RAS, SNS, ET) resulting from decreased cardiac output. Positive feedback downward spiral ensues. |
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Right Heart Failure Etiology, Pathophys, CP
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Eti & Pathophys: RV failure. Most commonly results from LV failure. Can be from pulmonary disease (e.g. emphysema which can result in pulmonary hypertension, straining the RV. Results in increased pressure in systemic veins
CP: Edema, Ascites, Pleural effusion, increased JVP, Anorexia, Weight Change, cachexia, poor vitals, hepatomegaly, tricuspid regurg. JVP IS MOST IMPORTANT FINDING |
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Left Heart Failure Etiology, Pathophys, CP
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Eti & Pathophys: LV failure. systolic or diastolic dysfunction. Can be secondary to valvular abnormality. Increased pressure in pulmonary veins leads to pulmonary congestion/edema.
CP: Breathlessness (DOE, Orthop, PND), Fatigue, Cerebral (TIA, CVA, Syncope), Rales, lung effusion, S3 heart sound, triscuspid regurg |
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Heart Failure Diagnostics
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*B-Type Natriuretic Peptide! (Does not work in obese patients) - increased value is positive finding. Very important biomarker. Secreted from LV from myocyte stretch
*Chest X-Ray - Heart Size, pulmonary edema * Labs: Na (hyponatermia), LFT (rise in liver function) *Pulmonary Capillary Wedge Pressure |
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Typical radiographic findings of a HF patient
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Increased heart size, PVR/pulmonary edema.
(PVR - pulmonary vascular resistance?) |
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Pharmacologic agents for treating HF
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#1) ACE Inhibitor & Diuretics - 1st line Tx. Results in diuresis and salt excretion -> lower BP. Not sure how this helps CHF. Use an ARB if ACE-intolerant
#2) Beta Blockers - "Mechanism Unclear", but it's likely that chronic chatecholamines and SNS activity cause myocyte damage. Only 3 work: Bisoprolol, Metoprolol, Carvedilol #3) Aldosterone Antagonist - Spironolactone, Eplerenone. Carries Risk of Hyperkalemia -> renal failure. Monitor! #4) If black, then add Isosorbide Dinitrate/Hydralazine. #5) Add Digoxin if necessary to treat residual symptoms. |
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General management principles of CHF, including nonpharmacologic management
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* Use pharmaceuticals to control neurohormonal activation caused by HF. These neurohormonal chemicals (RAAS, SNS, ET) cause a) myocardial toxicity and b) peripheral vasoconstriction, exacerbating HF.
* In addition to pharmaceuticals, educate patients on SALT RESTRICTION, about implementing a "flexible diuretic regimen". Weigh oneself daily, adjust diuretics to minimize fluctuations in body fluid weight. And of course, EXERCISE * DEVICE THERAPY: CRT +/- ICD. Cardiac Resynchronization Therapy if symptoms persist and if patient has IVCD (interventricular conduction defect) -> poor ventricular coordination. The EKG sign is a WIDE QRS. Can add an ICD if risk of arrythmias. |
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Precipitating causes which may lead to decompensation of chronic heart failure
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* Noncompliance of diet and medication
* HTN * Arrythmia * Iatrogenic * Infection * MI/Ischemia * Endocrine/anemia * Pulmonary Embolism |
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Indicators for hospitalization for patients with chronic CHF
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* Deterioration of symptoms not responsive to oral medications
* Concern for ischemia/MI in ischemic cardiomyopathy * Altered lab results: Cr, K, INR * Syncope * Thromboembolic Event * Arrhythmia: VT/VF, new atrial fib |
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NYHA Classes of CHF
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Class 1 - Asymptomatic
Class 2 - "Mild Limitations". Some symptoms Class 3 - "Moderate Limitation". Walk 1-2 blocks on level or 1 flight of stairs Class 4 - "Severe Limitation". SOB @ rest, dressing, or showering. |
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ACC/AHA Stages of HF
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Stage A - High risk for HF, but no structural hear disease of symptoms
Stage B - Structural heart disease but no symptoms Stage C - Structural heart disease with prior or current HF symptoms Stage D - Refractory HF requiring specialized interventions. Stage A & Stage B = NYHA Class 1 Stage C = NYHA Class 2 & 3 Stage D = NYHA Class 4 |
