Risk factors may include
Direct effect of alcohol on the heart muscle
Altered systemic vascular resistance
Electrical alterations in rate, rhythm, conduction
Possibly evidenced by
(Not applicable; presence of signs and symptoms establishes an actual diagnosis)
Desired Outcomes/Evaluation Criteria—Client Will
Display vital signs within client’s normal range; absence, or reduced frequency, of dysrhythmias.
Demonstrate an increase in activity tolerance.
Nursing intervention with rationale:
1. Monitor vital signs frequently during acute withdrawal.
Rationale: Hypertension frequently occurs in acute withdrawal phase. Extreme hyperexcitability, accompanied by catecholamine release and increased peripheral vascular resistance, raises BP and heart rate; however, BP may become labile and progress to hypotension. Note: Client may have underlying cardiovascular disease, which is compounded by alcohol withdrawal.
2. Monitor cardiac rate and rhythm. Document irregularities and dysrhythmias.
Rationale: Long-term alcohol abuse may result in cardiomyopathy and heart failure (HF). Tachycardia is common because of sympathetic response to increased circulating catecholamines. Dysrhythmias may develop with electrolyte imbalance. All of these may have an adverse effect on cardiac output.
3. Monitor body temperature.
Rationale: Elevation may occur because of sympathetic stimulation, dehydration, and/or infections, causing vasodilation and compromising venous return and cardiac output.
4. Monitor intake and output (I&O). Note 24-hour fluid balance.
Rationale: Preexisting dehydration, vomiting, fever, and diaphoresis may result in decreased circulating volume that can compromise cardiovascular function. Note: Hydration is difficult to assess in the alcoholic client because the usual indicators are not reliable, and overhydration is a risk in the presence of compromised cardiac function.
5. Be prepared for and assist in cardiopulmonary resuscitation.
Rationale: Causes of death during acute withdrawal stages include cardiac dysrhythmias, respiratory depression and arrest, oversedation, excessive psychomotor activity, severe dehydration or overhydration, and massive infections. Mortality of unrecognized or untreated DTs may be as high as 35% (Gossman, 2007).
6. Monitor laboratory studies, such as serum electrolyte levels, RBCs, Hgb and Hct, and platelets.
Rationale: Potassium and magnesium imbalances potentiate risk of cardiac dysrhythmias. Anemia may be present and platelets can be decreased in late stage alcoholism due to liver dysfunction.
7. Administer fluids and electrolytes, as indicated.
Rationale: Severe alcohol withdrawal causes the client to be susceptible to excessive fluid losses associated with fever, diaphoresis, and vomiting; electrolyte imbalances, especially potassium and magnesium; and glucose.
8. Administer medications, as indicated, for example: Clonidine (Catapres) or atenolol (Tenormin)
Rationale: Although the use of benzodiazepines is often sufficient to control hypertension during initial withdrawal from alcohol, some clients may require more specific therapy. Note: Atenolol and other beta-adrenergic blockers may speed up the withdrawal process and eliminate tremors as well as lower the heart rate, BP, and body temperature.