7 Hyperthyroidism Nursing Care Plans

Risk for Decreased Cardiac Output

Hyperthyroidism can cause a hypermetabolic state which leads to an increased demand for oxygen and nutrients by the body, including the heart. This increased demand can lead to an increase in cardiac load and a decrease in cardiac output, which can be further exacerbated by alterations in heart rate, rhythm, and conduction, as well as changes in venous return and vascular resistance. If left uncontrolled, these factors can contribute to a higher risk of decreased cardiac output and potentially even heart failure in patients with hyperthyroidism.

Nursing Diagnosis

• Risk for Decreased Cardiac Output

Risk factors may include

• Uncontrolled hyperthyroidism, hypermetabolic state
• Increasing cardiac workload
• Changes in venous return and systemic vascular resistance
• Alterations in rate, rhythm, conduction

Possibly evidenced by

• Not applicable. A risk diagnosis is not evidenced by signs and symptoms, as the problem has not occurred and nursing interventions are directed at prevention.

Desired Outcomes

• The client will maintain adequate cardiac output for tissue needs as evidenced by stable vital signs, palpable peripheral pulses, good capillary refill, usual mentation, and absence of dysrhythmias.

Nursing Assessment and Rationales

1. Observe signs and symptoms of severe thirst, dry mucous membranes, weak or thready pulse, poor capillary refill, decreased urinary output, and hypotension.
Rapid dehydration can occur, which reduces the circulating volume and compromises cardiac output.

2. Note history of asthma and bronchoconstrictive disease, sinus bradycardia and heart blocks, advanced HF, or current pregnancy.
The presence or potential recurrence of these conditions affects the choice of therapy. For example use of [beta]-adrenergic blocking agents are contraindicated.

3. Observe for adverse side effects of adrenergic antagonists: severe decrease in pulse, BP; signs of vascular congestion/HF; cardiac arrest.
Indicates the need for reduction or discontinuation of therapy.

4. Investigate reports of chest pain or angina.
This may reflect increased myocardial oxygen demands or ischemia.

5. Assess pulse and heart rate while the patient is sleeping.
Provides a more accurate assessment of tachycardia.

6. Auscultate heart sounds, note extra heart sounds, development of gallops, and systolic murmurs.
Prominent S₁ and murmurs are associated with a forceful cardiac output of a hypermetabolic state; the development of S₃ may warn of impending cardiac failure.

7. Auscultate breath sounds. Note adventitious sounds.
An early sign of pulmonary congestion, reflecting developing cardiac failure.

8. Monitor BP lying, sitting, and standing, if able. Note widened pulse pressure.
General or orthostatic hypotension may occur as a result of excessive peripheral vasodilation and decreased circulating volume. Widened pulse pressure reflects a compensatory increase in stroke volume and decreased systemic vascular resistance (SVR).

9. Monitor temperature; provide a cool environment, limit bed linens or clothes, and administer tepid sponge baths.
Fever (may exceed 104°F) may occur as a result of excessive hormone levels and can aggravate diuresis and/or dehydration and cause increased peripheral vasodilation, venous pooling, and hypotension.

10. Record I&O. Note urine specific gravity.
Significant fluid losses through vomiting, diarrhea, diuresis, and diaphoresis can lead to profound dehydration, concentrated urine, and weight loss.

11. Weigh daily. Encourage chair rest or bed rest. Limit unnecessary activities.
Activity increases metabolic and circulatory demands, which may potentiate cardiac failure.

12. Monitor ECG, noting rate and rhythm. Document dysrhythmias.
Tachycardia (greater than normally expected with fever and/or increased circulatory demand) may reflect direct myocardial stimulation by thyroid hormone. Dysrhythmias often occur and may compromise cardiac output.

13. Monitor central venous pressure (CVP), if available.
Provides a more direct measure of circulating volume and cardiac function.

14. Monitor laboratory and diagnostic studies: 

• 14.1. Serum potassium
  Hypokalemia resulting from intestinal losses, altered intake, or diuretic therapy may cause dysrhythmias and compromise cardiac function/output. In the presence of thyrotoxic paralysis (primarily occurring in Asian men), close monitoring and cautious replacement are indicated because rebound hyperkalemia can occur as the condition abates releasing potassium from the cells.

• 14.2. Serum calcium
  Elevation may alter cardiac contractility.

• 14.3. Sputum culture
  Pulmonary infection is the most frequent precipitating factor of crisis.

• 14.4. Serial ECGs
  May demonstrate the effects of electrolyte imbalance or ischemic changes reflecting inadequate myocardial oxygen supply in the presence of increased metabolic demands.

• 14.5. Chest x-rays
  Cardiac enlargement may occur in response to increased circulatory demands. Pulmonary congestion may be noted with cardiac decompensation.

Nursing Interventions and Rationales

1. Provide supplemental O₂ as indicated.
May be necessary to support increased metabolic demands and/or O₂ consumption.

2. Provide a hypothermia blanket as indicated.
Occasionally used to lower uncontrolled hyperthermia (104°F and higher) to reduce metabolic demands/O₂  consumption and cardiac workload.

3. Administer IV fluids as indicated.
Rapid fluid replacement may be necessary to improve circulating volume but must be balanced against signs of cardiac failure and the need for inotropic support.

4. Administer medications as indicated:

• 4.1. Thyroid hormone antagonists: propylthiouracil (PTU), methimazole (Tapazole)
  May be a definitive treatment or used to prepare the patient for surgery, but the effect is slow and so may not relieve thyroid storm. Once PTU therapy is begun, abrupt withdrawal may precipitate a thyroid crisis. Acts to prevent the release of thyroid hormone into circulation by increasing the amount of thyroid hormone stored within the gland. May interfere with RAI treatment and may exacerbate the disease in some people.

• 4.2. [beta]-blockers: propranolol (Inderal), atenolol (Tenormin), nadolol (Corgard), pindolol (Visken)
  Given to control the thyrotoxic effects of tachycardia, tremors, and nervousness, and is the first drug of choice for an acute storm. Decreases heart rate or cardiac work by blocking [beta]-adrenergic receptor sites and blocking the conversion of T₄ to T₃. If severe bradycardia develops, atropine may be required. Blocks thyroid hormone synthesis and inhibits the peripheral conversion of T₄ to T₃.

• 4.3. Strong iodine solution (Lugol’s solution) or supersaturated potassium iodide (SSKI) PO
  May be used as surgical preparation to decrease the size and vascularity of the gland or to treat thyroid storm. Should be started 1–3 hr after initiation of antithyroid drug therapy to minimize hormone formation from the iodine. If iodide is part of the treatment, mix it with milk juice, or water to prevent GI distress and administer it through a straw to prevent tooth discoloration.

• 4.4. RAI (Na¹³¹I or Na¹²⁵I) following NRC regulations for radiopharmaceutical
  Radioactive iodine therapy is the treatment of choice for almost all patients with Graves’ disease because it destroys abnormally functioning gland tissue. Peak results take 6–12 wk (several treatments may be necessary); however, a single dose controls hyperthyroidism in about 90% of patients. This therapy is contraindicated during pregnancy. Also, people preparing or administering the dose must have their own thyroid burden measured, and contaminated supplies and equipment must be monitored and stored until decayed.

• 4.5. Corticosteroids: dexamethasone (Decadron)
  Provides glucocorticoid support. Decreases hyperthermia; relieves relative adrenal insufficiency; inhibits calcium absorption; and reduces the peripheral conversion of T₃ from T₄. May be given before thyroidectomy and discontinued after surgery.

• 4.6. Digoxin (Lanoxin)
  Digitalization may be required in patients with HF before [beta]-adrenergic blocking therapy can be considered or safely initiated.

• 4.7. Potassium (KCl, K-Lyte)
  Increased losses of K⁺ through intestinal and/or renal routes may result in dysrhythmias if not corrected.

• 4.8. Acetaminophen (Tylenol)
  Drug of choice to reduce temperature and associated metabolic demands. Aspirin is contraindicated because it actually increases the level of circulating thyroid hormones by blocking the binding of T₃ and T₄ with thyroid-binding proteins.

• 4.9. Sedative, barbiturates
  Promotes rest, thereby reducing metabolic demands and cardiac workload.

• 4.10. Furosemide (Lasix)
  Diuresis may be necessary if HF occurs. It also may be effective in reducing calcium level if the neuromuscular function is impaired.

• 4.11. Muscle relaxants
  Reduces shivering associated with hyperthermia, which can further increase metabolic demands.

5. Administer transfusions; assist with plasmapheresis, hemoperfusion, and dialysis.
May be done to achieve rapid depletion of the extrathyroidal hormone pool in a desperately ill or comatose patient.

6. Prepare for possible surgery.
Subtotal thyroidectomy (removal of five-sixths of the gland) may be the treatment of choice for hyperthyroidism once a euthyroid state is achieved.