Congestive Heart Failure
(Kozier, “Nursing Management: Heart Failure and Cardiomyopathy,” chp.34)
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Heart Anatomy Preload Contractility Afterload CO
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Congestive Heart Failure Definition • Abnormal condition involving impaired cardiac pumping.
• CHF is not a disease. • Ventricular dysfunction caused by cardiac and non-cardiac dysfunctions. L Del Balso
Definition (Cont’d) • Cardiac diseases: long-standing hypertension coronary artery disease (CAD) • Characteristics: ventricular dysfunction ↓ exercise tolerance ↓ quality of life shortened life expectancy L Del Balso
Definition (Cont’d) • incidence for men = women • High rate of mortality and morbidity • 1 in 100>65yrs
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ETIOLOGY & RISK FACTORS – – – – – –
CAD Age Hypertension Obesity, high cholesterol level Smoking DM
– African American descent
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Manifestation of Ventricular Failure • low BP, • low CO • poor renal perfusion, • poor exercise tolerance, • ventricular arrhythmias
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PATHOPHYSIOLOGY • CO depends on: – Preload – Afterload – Myocardial contractility – Heart rate
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Compensatory Mechanisms 1. Ventricular dilatation 2. Ventricular hypertrophy- in chronic
CHF
3. Sympathetic nervous system stimulation 4. Neurohormonal responses: >Kidneys: angiotensin aldosterone >Brain: antidiuretic hormone (ADH) L Del Balso
Types of CHF • One-sided failure eventually leads to biventricular failure – –
Left sided failure Right sided failure
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Left Sided Failure – Most common form (LV dysfunction) – Blood backs up through the LA into the pulmonary veins Pulmonary congestion and edema – Causes: HTN, CAD, rheumatic heart disease (streptococcus L Del Balso
Lt Sided Failure Symptoms • dyspnea, orthopnea & paroxysmal
nocturnal dyspnea • adventitious sounds: crackles at bases of lungs --- throughout lungs • moist, hacking productive cough w/frothy sputum • restlessness & anxiety, fatigue • Nocturia L Del Balso
Right Sided Failure – Backward flow to the RA and venous circulation – Results from diseased RV – Leads to venous congestion in systemic circulation peripheral edema, etc.. – Causes: Lt sided failure, Cor Pulmonale, Rt ventr. infarction L Del Balso
Rt sided Failure Symptoms • jugular vein distention • ascities: hepatomegaly • Anorexia, nausea, GI bloating • weight gain • Dependant edema • Peripheral edema • fatigue L Del Balso
Acute CHF • Manifestation: Pulmonary edema. • Cause: Lt ventricular failure secondary to CAD • Symptoms: -Pale or cyanotic, Cold, clammy skinsecondary to vasoconstriction from sympathetic nervous system response -Agitation -Severe dyspnea-use of accessory muscles, orthopnea -Tachypnea , wheezing, crackles, coughing -Nocturia L Del Balso L Del Balso
CHRONIC CHF • Fatigue. • Dyspnea, orthopnea (key symptom) • • • • • • •
-Paroxysmal nocturnal dyspnea Dry hacking cough. Tachycardia- (compensatory mechanism) Edema-pitting edema, dependant edema (sacral edema). Sudden weight gain Nocturia (6-7 x/night) Skin changes Behavioral changes L Del Balso
Complications of CHF 1. Pleural effusion: collection of fluid in pleural space. 2. Arrhythmias: alteration normal electrical pathway. 3. Left ventricular thrombus: enlarged LV and decrease CO can increase chance of clot. 4. Hepatomegaly (RV failure) L Del Balso
CLASSIFICATION OF CHF by the NY Heart Association
– Class 1: No limitation of physical activity – Class 2: Slight limitation
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CLASSIFICATION (cont’d) – Class 3: Marked limitation – Class 4: Inability to carry on any physical activity without discomfort
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Diagnostic Studies • Primary goal is to determine
underlying cause – Physical exam – Chest x-ray – ECG – Hemodynamic assessment L Del Balso
Diagnostic studies (cont’d) – Echocardiogram-measures ejection fraction. – Stress testing – Cardiac catheterization – Ejection fraction (EF)
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Collaborative Care • Treat underlying cause • Maximize CO • Alleviate symptoms
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Drug Therapy Goal: improve symptoms, minimize side effects of treatment, prevent morbidity and prolong survival
• ACE inhibitors • Diuretics ∀β-Adrenergic blockers • Inotropics agents • Vasodilators L Del Balso
ACE Inhibitors Enalapril & Capoten
• Action: -Block production of
angiotensin II decrease aldosterone -Dilate arterioles and veins, decrease SVR, afterload and increase CO. • Adverse effects -hypotension - hyperkalemia L Del Balso
DIURETICS • Action: -Reduce blood volume and decrease
preload
-Mobilize edematous fluid -Decrease venous pressure and afterload -Decrease pulmonary edema, peripheral edema, cardiac dilation L Del Balso
Diuretics (cont’d) 3 Types: • Thiazide-Hydrochlorothiazide: tubule
Inhibit Na/H2O resorption of distal
2. Loop Diuretics- Lasix
severe
-Acts on ascending loop of Henle -Na, CL, H2O excretion. -SE: hypokalemia, ototoxicity, hypotension. L Del Balso
DIURETICS (cont’d) 3. K sparing diuretics: Spironolactone (aldactone)
>Improves survival of CHF pts by blocking effects of aldosterone in heart. >Excretion of Na,H2O
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Beta Adrenergic Carvedilol, Metoprolol, Bisoprolol • Action: -Blocks the sympathetic nervous system (high HR) -improve L ventricular ejection fraction, increase exercise tolerance, slow progression of CHF, • Adverse effects: fluid retention from worsening CHF, fatigue, hypotension, bradycardia, MI
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INOTROPIC AGENTS 1.DIGOXIN(LANOXIN) • cardiac glycoside, anti-arrthymic (digitalis) • used CHF & arrthymias • functions in 2 ways: – increases force of myocardial contractility – slows conduction from AV node slows HR ventricular emptying >inhibits K Intracellular levels uptake >increase intracellular Na, Ca--L Del Balso increase contractility .
Digoxin (cont’d) • NRSG: – take AP for full minute – note rate & rhythm (if AP < 60, HOLD) – monitor K+ levels – educate client & family to assess pulse for rhythm & rate – educate & monitor for signs of digoxin toxicity *(sign of toxicity??)*
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Digoxin (cont’d) • SE: -Therapeutic range: 1.54 +/- 0.5 mmol /L -First sign is arrthymia -anorexia, N & V, malaise (mild) -vision disturbances: “yellow” -changes in HR & rhythm through palpation, auscultation or on ECG -monitor K+ levels: hypokalemia may predispose to toxicity L Del Balso
INOTROPIC AGENTS 2.sympathomimetics: • • •
Dopamine Dobutamine Hydralazine (APRESOLINE)
Increases CO and renal blood flow.
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INOTROPIC AGENTS (cont’d) 3.Phosphodiesterase inhibitor • Inamarinone lactate(INOCOR): -increases contractility (increasing ca entry) -Vasodilator, increases CO and decreases afterload (lower BP)
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Vasodilators • Sodium Nitrate: (Nitroprusside) -IV vasodilator for pulmonary edema • Nitrates: -decrease preload -beneficial in MI: increase vasodilatation of arteries L Del Balso
POTENTIAL COMPLICATIONS • Electrolyte imbalances due to use of diuretics & digoxin • Hypokalemia: (low K+)
– weakens cardiac contractions – leads to digoxin toxicity – Signs of hypokalemia: weak pulse, hypotension, muscle flabbiness, generalized weakness & diminished deep tendon reflexes
• K supplements(K-Dur) if not on ACE
inhibitor or K sparing diuretics. Give with meals.
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POTENTIAL COMPLICATIONS (cont’d)
• Hyponatremia: low Na+ – due to prolonged diuretic therapy – signs: apprehension, weakness, fatigue, muscle cramps & twitching, rapid, thready pulse
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Nutritional Therapy for CHF • Fluid restrictions not commonly prescribed only for severe CHF • Na restriction in order to decrease circulating volume and decrease workload of heart – 2 g sodium diet for mild CHF – 500-1000mg for severe CHF • Daily weights L Del Balso
Nursing and Collaborative Management - Goal: Improve LV function by: - Action demands: – Decreasing intravascular volume – Decreasing venous return – Decreasing afterload – Improving gas exchange and oxygenation L Del Balso
Nursing and Collaborative Management (Cont’d) Action demands: – Improving cardiac function – Reducing anxiety – Promote skin integrity – Promote activity tolerance – Provide client & family education: self care at home L Del Balso