Terms in this set (12)
Left ventricle heaves
Pulsus alternans, (alternating pulses, strong weak), Increased heart rate, PMI displaced inferiorly and posteriorly. (LV hypertrophy),
decreased PaO2, slight increase in PaCO2, (poor O2 exchange),
Crackles, pulmonary edema
s3 and s4 heart sounds
Pleural effusion
Changes in mental status
Restlessness, confusion
Weakness, fatigue, anxiety, depression, dyspnea, shallow respiration up to 32-40 min, Paroxysymal Nocturnal Dyspnea, Orthopnea (SOB in recumbent position, dry hacking cough, nocturia, frothy pink tinged sputum (advanced pulmonary edema) (Patients will often sleep sitting up with pillows and will have difficulty breathing when flat)
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visual disturbances
Digoxin toxicity may cause visual disturbances (e.g., flickering flashes of light, colored or halo vision, photophobia, blurring, diplopia, and scotomata), central nervous system abnormalities (e.g., headache, fatigue, lethargy, depression, irritability and, if profound, seizures, delusions, hallucinations, and memory loss),
and cardiovascular abnormalities (e.g., abnormal heart rate, arrhythmias). Digoxin toxicity doesn't cause taste and smell alterations. Dry mouth and urine retention typically occur with anticholinergic agents, not inotropic agents such as digoxin. Nocturia and sleep disturbances are adverse effects of furosemide — especially if the client takes the second daily dose in the evening, which may cause diuresis at night.
Myocardial ischemia
Myocardial
dysfunction and HF can be caused by a number of conditions, including coronary artery disease, hypertension, cardiomyopathy, valvular disorders, and renal dysfunction with volume overload. Atherosclerosis of the coronary arteries is a primary cause of HF, and coronary artery disease is found in the majority of clients with HF. Ischemia causes myocardial dysfunction because it deprives heart cells of oxygen and causes cellular damage. MI causes focal heart muscle necrosis, myocardial cell death,
and a loss of contractility; the extent of the infarction correlates with the severity of HF. Left-sided heart failure is caused by myocardial ischemia. Ineffective right ventricular contraction, pulmonary embolus, and cystic fibrosis cause right-sided heart failure.
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Left-Sided Heart Failure.
Left-sided heart failure is an abnormal condition characterized by decreased functioning of the left ventricle. If left ventricular failure is significant, the amount of blood ejected from the left ventricle drops greatly, resulting in decreased cardiac output. Signs and symptoms include fatigue, breathlessness,
dizziness, and confusion as a result of tissue hypoxia from the diminished cardiac output. As the left ventricle continues to fail, blood begins to pool in the pulmonary circulation, causing pulmonary congestion. Clinical findings include crackles in the bases of the lungs on auscultation, hypoxia, shortness of breath on exertion, cough, and paroxysmal nocturnal dyspnea.
Right-Sided Heart Failure.
Right-sided heart failureRight-Sided Heart
Failure.
Right-sided heart failure results from impaired functioning of the right ventricle. It more commonly results from pulmonary disease or as a result of long-term left-sided failure. The primary pathological factor in right-sided failure is elevated pulmonary vascular resistance (PVR). As the PVR continues to rise, the right ventricle works harder, and the oxygen demand of the heart increases. As the failure continues, the amount of blood ejected from the right ventricle declines, and
blood begins to "back up" in the systemic circulation. Clinically the patient has weight gain, distended neck veins, hepatomegaly and splenomegaly, and dependent peripheral edema. results from impaired functioning of the right ventricle. It more commonly results from pulmonary disease or as a result of long-term left-sided failure. The primary pathological factor in right-sided failure is elevated pulmonary vascular resistance (PVR). As the PVR continues to rise, the right ventricle works
harder, and the oxygen demand of the heart increases. As the failure continues, the amount of blood ejected from the right ventricle declines, and blood begins to "back up" in the systemic circulation. Clinically the patient has weight gain, distended neck veins, hepatomegaly and splenomegaly, and dependent peripheral edema.