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Heart Failure
| Question | Answer |
|---|---|
| Heart Failure (HF) | Impaired pumping (systole) and or filling (diastole) of the heart Heart is unable to produce an adequate CO to meet metabolic needs Characteristics: Ventricular dysfunction Reduced exercise tolerance Diminished quality or length of life |
| Heart Failure risk factors | CAD, Hypertension Diabetes, tobacco, obesity, high serum cholesterol |
| Factors affecting cardiac output (CO) | 1) Preload: Volume of blood in the ventricles at the end of diastole, before the next contraction 2.)Afterload: Peripheral resistance against which the LV must pump 3. Myocardial contractility 4. Heart rate |
| Preload | Volume of blood in the ventricles at the end of diastole, before the next contraction |
| Afterload | Peripheral resistance against which the LV must pump |
| Heart failure with reduced ejection fraction (most common) | LV loses its ability to generate enough pressure to EJECT blood forward through the aorta (systole) EF 40% or lower |
| Causes of HF with reduced EF | • Impaired contractile function (e.g., MI) • Increased afterload (e.g., hypertension) • Cardiomyopathy • Mechanical abnormalities (e.g., valve disease |
| Heart failure with preserved ejection fraction | Impaired ability of the ventricles to relax and FILL during diastole, resulting in decreased stroke volume and CO NORMAL EF |
| Ejection Fraction | Measured as a percentage FINSH THIS FINISH THIS |
| Causes of HF with preserved EF | • Left ventricular hypertrophy from chronic hypertension • Aortic stenosis • Hypertrophic cardiomyopathy |
| Mixed Heart Failure | EF less than 35% Seen in Dilated cardiomyopathy (DCM) High pulmonary pressures Biventricular failure Hypotension, low CO, poor renal perfusion |
| SNS compensatory mechanism | First and LEAST effective Release if catecholamines (epinephrine and norepinephrine) to increase HR and BP |
| Neurohormonal responses (compensatory mechanism) | Kidneys release renin via RAAS (raise BP) Decreased cerebral blood flow causes pituitary to release ADH Endothelin is stimulated by ADH causing VASOCONSTRICTION |
| Dilation (consequence of compensatory mechanism) | ENLARGEMENT OF THE CHAMBERS of the heart that occurs when pressure in the LV is elevated • Initially an adaptive mechanism • Eventually this mechanism becomes inadequate, and CO decreases |
| Hypertrophy (consequence of compensatory mechanism) | INCREASE IN MUSCLE MASS and cardiac wall thickness in response to chronic dilation, resulting in • Poor contractility • Higher O2 needs • Poor coronary artery circulation • Risk for ventricular dysrhythmias |
| Counterregulatory Process | Natriuretic peptides: Atrial natriuretic peptide (ANP), b-type natriuretic peptide (BNP) released in response to increase atrial volume and ventricular pressure ANP: released with minor cardiac muscle stretch BNP: triggered by increased pressure |
| Left-Sided HF | LV dysfunction: backup of blood into the Lt atrium and pulmonary veins causing pulmonary congestion |
| Right-sided HF | From left-sided HF, cor pulmonale, right ventricular MI Backup of blood into the right atrium and venous systemic circulation |
| Effects of the Counterregulatory Process | Promotes venous/arterial VASODILATION (reduce preload/afterload) Released with minor contraction |
| Effects of Left-Sided HF (Backup effects) | Dyspnea and orthopnea- Develops as fluid accumulates in the lungs Cough- Associated with fluid irritating the respiratory passages Paroxysmal nocturnal dyspnea- may present with acute pulmonary edema and can cause to pneumonia Rales |
| Effects of Right-Sided HF (Backup effects) | • Jugular venous distension • Hepatomegaly, splenomegaly • Vascular congestion of GI tract • Peripheral edema, ascites • Headache, flushed face |
| HF Compensations | Tachycardia, pallor, secondary polycythemia (blood cancer), low urinary output in the day (daytime oliguria) |
| Forward effects of HF | Fatigue, weakness, dyspnea, exercise intolerance, cold intolerance |
| Pulmonary Edema | Abnormal, life-threatening accumulation of fluid in the alveoli/interstitial spaces of the lungs Pulmonary venous pressure increases Increased airway resistance Tight alveoli lining disrupted: fluid with RBCs moves in Airway flooded with fluid |
| Pulmonary Edema Manifestations | Skin clammy from vasoconstriction (SNS stimulation) Wheezing and coughing +/- frothy blood-tinged sputum Crackles on auscultation Anxiety Pale and cyanotic Tachypnea, dyspnea, orthopnea, use of accessory muscles Decrease in PaO2/ Increase in PaCO2 |
| Chronic HF Manifestations | 1) Fatigue Dyspnea, orthopnea, paroxysmal nocturnal dyspnea Persistent, dry cough, with no relief Tachycardia Dependent Edema Nocturia Skin changes Restlessness, confusion, decreased memory Angina Weight changes |
| Complications of HF | Pleural effusion Dysrhythmias (risk for thrombus/embolus formation, increasing risk for stroke • Rate control, cardioversion, antidysrhythmics, and/or systemic anticoagulation LV thrombus Hepatomegaly Renal insufficiency or failure |
| HF Diagnostic Studies | • History and physical examination • Chest x-ray • ECG • Lab studies (e.g., cardiac enzymes, BNP) • Hemodynamic assessment • Echocardiogram • Stress testing • Cardiac catheterization • Ejection fraction |
| Ventricular remodeling | Changes in left ventricular (LV) geometry, mass, and volume in response to myocardial injury or alterations in load. |
| Nursing Management HF | Decrease intravascular volume Decrease venous return (PRELOAD) Decrease AFTERLOAD Improve gas exchange and oxygenation Improve cardiac function Reduce anxiety |
| HF Drug management | Loop diuretics (decrease volume) IV nitroglycerin (decrease preload) O2, morphine sulphate, BiPAP (gas exchange and O2 increase) Inotropic therapy (dobutamine, milrinone) for heart contractions Sedatives- morphine sulphate (reduce anxiety) |
| Nutritional therapy HF | Sodium is restricted to 2g per day Daily weighing (morning) **Weight gain of 2 kg (4 lb) over 2 days or a 2.5 kg (5-lb) gain over a week should be reported to health care provider |
Created by:
selenay15
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