Progression of Illness Positive progression of this disease toward increased functioning and discharge from the hospital includes

the following. Improved symptoms of pulmonary congestion evidenced by lack of dyspnea when weaned from ventilator. Improved pulmonary & extremity edema. Transition from IV to PO fluids. No significant alterations in electrolyte values with special attention paid to creatinine and sodium. No auscultation of crackles and rales in lung fields. Chest x-ray displaying improved ventilation and decrease or absent infiltrates. Patient and family education need have been sufficiently addressed. Echocardiogram displays ejection fraction of at least 40%. Blood pressure is within normal parameters. O2 level greater than 95% on RA or patient’s norm. Ability to ambulate without exacerbation of symptoms including dyspnea and orthostatis.

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Nursing Diagnoses Decreased Cardiac Output Risk for ineffective coping PC: Pulmonary Embolism Risk for infection Ineffective tissue perfusion Acute pain Impaired gas exchange Impaired verbal communication

(Ignatavicius &Workman, 2010; Ackley & Ladwig, 2011).

(Ackley & Ladwig, 2011)

Pathophysiology Heart Failure may present acutely as a result of myocardial ischemia secondary to a MI. The weakened cardiac muscle causes the CO to decrease. The decreasing cardiac output then triggers in increased in systemic vascular resistance and afterload, which only further decreases the CO. Eventually the heart is unable to effectively push against the increased afterload and fluid begins to flow back through the pulmonary veins and fills the lungs. In CHF with acute pulmonary edema this will be the terminal event if the systemic vascular resistance is not promptly reversed. (Ignatavicius &Workman, 2010).

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Interventions Continually assess for signs and symptoms of precipitating heart failure. Monitor for signs of bleeding due to anticoagulation and blood thinning therapies. Try to find underlying cause and treat the cause. Monitor ST segment continuously to determine changes in myocardial tissue perfusion. Assess that urine output hourly, alert physician if less than 30 ml/hr. Maintain the patient in the semi-fowlers position to lessen the work of breathing and facilitate venous return. Continuously monitor O2 and assess vital signs.

Congestive Heart Failure and Pulmonary Edema
Medications Loop diuretics such as Lasix should be used to remove excess fluid volume except in the case of severe renal dysfunction. Vasodilators such as nitroglycerin should be used to lower the systemic vascular resistance and therefore decrease the cardiac afterload. Beta-blockers should be used to decrease the preload and afterload placed on the heart. Anticoagulation therapy drugs: coumadin, heparin, lovenox, aspirin. ACE inhibitor regimen should be started because of their effect on slowing even reversing left ventricular remodeling over time. ARDs may be used if ACE inhibitors are not well tolerated.

(Ignatavicius &Workman, 2010; Urden, Stacy, & Lough, 2008)

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Signs and Symptoms Fatigue Weakness SOB Distended neck veins Dizziness Decreased exercise tolerance Anxiety Syncope Palpitations Chest pain or discomfort Hypotension Hypertension Pulmonary and extremity edema

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Risk Factors Coronary artery disease Male gender History of hypertension, diabetes mellitus, valvular disease, and myocardial infarction. Alcohol, cardiac surgery, kidney conditions, pericarditis, myocarditis, viruses. Congenital heart defects, sleep apnea,

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(Ignatavicius &Workman, 2010)

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(Ignatavicius & Workman, 2010; Urden et al., 2008)

Treatments The first priority of treatment is airway management. This is judged by the severity of the presenting symptoms. Could include supplemental oxygen via nasal cannula or mask, noninvasive ventilation or in this patient’s case endotracheal intubation. Urinary catheter should be placed to closely monitor renal function and allow patient to rest. A 12-lead ECG to assess for cardiac abnormalities. IV access to provide prompt medication administration. Frequent vital sign assessments to monitor for a decline in cardiac function.

(Urden et al., 2008)

(Ignatavicius &Workman, 2010; Urden et al., 2008)

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