10.2 Thyroid and Adrenal Disorders in the Cardiac Patient

Thyroid Hormone Is a Cardiovascular Drug

Thyroid hormone acts directly on the myocardium and vasculature: it increases beta-adrenergic receptor density and post-receptor signaling, increases the expression of the fast myosin heavy chain and the sarcoplasmic reticulum calcium ATPase (SERCA2a), raises heart rate and contractility, shortens diastolic relaxation time, and relaxes vascular smooth muscle so that systemic vascular resistance (SVR) falls. That combination — high output, low resistance — explains almost every cardiac finding in thyroid disease.

Hyperthyroidism, atrial fibrillation and thyroid storm

Every patient with new-onset atrial fibrillation needs a thyroid-stimulating hormone (TSH) level. The 2023 ACC/AHA/ACCP/HRS atrial fibrillation guideline includes thyroid function in the initial evaluation. Thyrotoxic AF is often refractory to standard rate control until the patient is rendered euthyroid, and a substantial proportion converts spontaneously once thyroid function normalizes. Anticoagulation is decided by CHA2DS2-VASc, not by the presence of hyperthyroidism alone.

Thyroid storm is decompensated thyrotoxicosis with organ dysfunction. Precipitants that a cardiac nurse will actually encounter: surgery, infection, myocardial infarction, iodinated contrast, amiodarone, abrupt withdrawal of antithyroid drugs, DKA, and trauma. The Burch-Wartofsky point scale (fever, central nervous system effects, gastrointestinal-hepatic dysfunction, tachycardia, heart failure, atrial fibrillation, and a precipitant) supports the diagnosis at 45 points or more. Cardiovascular presentation is temperature above 38.5 to 41 degrees Celsius, a heart rate disproportionate to the fever, AF with rapid ventricular response, high-output or frankly decompensated heart failure, agitated delirium, and vomiting or diarrhea driving volume loss. Mortality is 10 to 30 percent.

The management sequence matters and is heavily tested:

1. Beta blockade first for the adrenergic storm. Propranolol 60 to 80 mg orally every 4 to 6 hours, or 0.5 to 1 mg IV slowly, additionally blocks peripheral T4-to-T3 conversion. In the ICU an esmolol infusion is preferable because it is titratable and can be turned off in seconds.
2. Thionamide to stop new hormone synthesis. Propylthiouracil (PTU) 500 to 1,000 mg load then 250 mg every 4 hours is preferred in storm because it also blocks peripheral conversion; methimazole 20 mg every 4 to 6 hours is an alternative.
3. Iodine at least one hour after the thionamide. Saturated solution of potassium iodide 5 drops every 6 hours or Lugol solution blocks hormone release (Wolff-Chaikoff effect). Giving iodine first supplies substrate to an unblocked gland and can worsen thyrotoxicosis (Jod-Basedow phenomenon). This one-hour rule is a classic exam item.
4. Corticosteroid — hydrocortisone 300 mg IV then 100 mg every 8 hours — blocks T4-to-T3 conversion and covers the relative adrenal insufficiency of storm.
5. Cooling with acetaminophen, not aspirin: salicylates displace thyroid hormone from thyroid-binding globulin and raise free hormone levels.

The nursing caution: in storm with high-output or decompensated heart failure, aggressive beta blockade can remove the tachycardia that is sustaining cardiac output and precipitate cardiovascular collapse. Use short-acting esmolol, titrate against blood pressure, mental status, urine output and, when available, cardiac output or mixed venous saturation; be prepared to stop the infusion and support with inotropes.

Hypothyroidism and myxedema coma

Overt hypothyroidism produces bradycardia, reduced contractility, low cardiac output, increased SVR with diastolic hypertension, a narrow pulse pressure, pericardial effusion (usually slowly accumulating and rarely tamponading), atherogenic dyslipidemia, elevated creatine kinase, and QT prolongation with a real risk of torsades de pointes.

Myxedema coma is the decompensated form: hypothermia without shivering, hypoventilation with carbon dioxide retention, hyponatremia, hypoglycemia, bradycardia, hypotension, and depressed mentation, usually precipitated by cold exposure, infection, sedatives, or an acute cardiac event. Management principles for the CMC exam:

• Give hydrocortisone 100 mg IV before thyroid hormone whenever coexisting adrenal insufficiency cannot be excluded. Thyroid replacement accelerates cortisol clearance and can precipitate adrenal crisis in a patient with limited reserve.
• Levothyroxine 200 to 400 mcg IV load, then 50 to 100 mcg daily, with lower loading doses in older patients and those with coronary disease because rapid repletion increases myocardial oxygen demand and can trigger ischemia or arrhythmia. Liothyronine (T3) may be added in refractory cases.
• Passive rewarming with blankets. Active external rewarming causes peripheral vasodilation and can precipitate hypotension in a volume-depleted, low-output patient.
• Treat hyponatremia with free-water restriction, support ventilation, correct hypoglycemia, and monitor continuously for bradyarrhythmia and QT-related ventricular arrhythmia.

Amiodarone and the thyroid

Amiodarone is 37 percent iodine by weight. A single 200 mg tablet liberates roughly 7 mg of free iodine daily against a recommended daily allowance of 150 micrograms — a 40- to 50-fold iodine load. Its half-life of 40 to 58 days means thyroid effects persist for months after the drug is stopped.

• Amiodarone-induced hypothyroidism (AIH) is the more common problem in iodine-sufficient countries such as the United States, occurring in up to 20 percent of patients. It is treated with levothyroxine, and amiodarone can usually be continued if it is controlling a serious arrhythmia.
• Amiodarone-induced thyrotoxicosis (AIT) type 1 occurs in an abnormal gland (nodular goiter or latent Graves disease). The iodine load fuels excess synthesis. Color-flow Doppler shows increased vascularity. Treatment is a thionamide, sometimes with potassium perchlorate.
• AIT type 2 is a destructive thyroiditis in a structurally normal gland releasing preformed hormone. Doppler shows low or absent vascularity. Treatment is a glucocorticoid, typically prednisone 40 to 60 mg daily.
• Mixed and indeterminate forms are common and are treated with both. Thyroidectomy is an option in refractory AIT with hemodynamic compromise.
• Monitoring: TSH and free T4 at baseline, at 3 months, and then every 6 months for the duration of therapy and for up to a year after discontinuation. Amiodarone surveillance also includes liver enzymes, a baseline chest radiograph and pulmonary function with diffusing capacity, and periodic ophthalmologic examination.

Interpretation caveat: amiodarone inhibits deiodinase, so in the first few months a transient TSH rise with a normal or slightly high free T4 and a low T3 is an expected drug effect, not disease. Judge on the trend and the free T4, not on a single TSH.

Euthyroid sick syndrome

Non-thyroidal illness syndrome appears in acute MI, cardiogenic shock, after cardiac surgery, and in advanced heart failure. The pattern is a low T3 first (impaired 5-prime-deiodinase activity), then a falling T4 in severe illness, with a normal or low TSH and an elevated reverse T3. It reflects an adaptive reduction in metabolic rate. Treating it does not improve outcomes and may cause harm. Do not order routine thyroid panels in the acutely ill cardiac patient unless thyroid disease is genuinely suspected; if a panel was drawn and is abnormal, recheck 6 to 8 weeks after recovery. During recovery the TSH may rebound above normal, which is not new hypothyroidism.

Adrenal Disorders in the Cardiac Patient

Primary versus secondary adrenal insufficiency

Adrenal crisis: vasopressor-refractory distributive shock

This is the single highest-yield adrenal item on the CMC exam. Suspect adrenal crisis in any patient with distributive shock that will not respond to fluid and escalating norepinephrine. Supporting features are hyponatremia, hyperkalemia, hypoglycemia, eosinophilia, a mildly elevated urea-to-creatinine ratio, unexplained fever, abdominal pain and vomiting, and a low or low-normal cortisol in a physiologically stressed patient. The at-risk populations in a cardiac unit are patients on chronic corticosteroids (more than 5 mg of prednisone equivalent daily for more than three weeks) whose steroid was abruptly held on admission or omitted while NPO, patients with adrenal hemorrhage on anticoagulation or in HIT, and patients with known hypopituitarism.

Diagnosis: a random cortisol below 5 mcg/dL during shock is strongly suggestive, because an appropriately stressed adrenal axis should produce a value above 18 mcg/dL. Confirmation is the cosyntropin stimulation test — 250 mcg IV with cortisol measured at baseline and 30 and 60 minutes; a peak below 18 mcg/dL indicates insufficiency.

Never delay steroids for the test. Draw a random cortisol and treat. If testing must proceed after treatment has begun, dexamethasone 4 mg IV provides glucocorticoid activity without interfering with the cortisol immunoassay, whereas hydrocortisone cross-reacts.

Treatment: hydrocortisone 100 mg IV bolus, then 50 mg every 6 hours or 200 mg per 24 hours as a continuous infusion, plus aggressive isotonic crystalloid with dextrose for hypoglycemia. At doses of 50 mg per day or more, hydrocortisone provides enough mineralocorticoid effect that fludrocortisone is unnecessary. The clinical response is often dramatic: vasopressor requirements fall within hours, and that response is itself diagnostic support.

Stress dosing around procedures: a patient on chronic replacement usually needs only the usual dose or 25 mg of hydrocortisone for a diagnostic cardiac catheterization, 50 to 75 mg per day for moderate procedures, and 100 to 150 mg per day for 2 to 3 days with a taper for major surgery. The nursing responsibility is to notice the home steroid on the medication reconciliation and ensure it is not silently dropped when the patient is NPO.

Critical-illness-related corticosteroid insufficiency (CIRCI) describes inadequate cortisol activity relative to the severity of illness. Surviving Sepsis Campaign 2021 suggests IV hydrocortisone 200 mg per day for adults with septic shock and an ongoing vasopressor requirement (for example, norepinephrine at 0.25 mcg/kg/min or more for at least 4 hours after initiation). Monitor for hyperglycemia, hypernatremia, and rebound hypotension when it is withdrawn abruptly.

Pheochromocytoma

A catecholamine-secreting tumor presenting with paroxysmal hypertension, headache, palpitations and diaphoresis — the classic triad — plus pallor, anxiety, and orthostatic hypotension between spells. It can mimic ACS with chest pain and troponin elevation, or produce a takotsubo-like catecholamine cardiomyopathy with normal coronary arteries. Screening is plasma free metanephrines or 24-hour urinary fractionated metanephrines.

The absolute rule: alpha blockade must precede beta blockade. Phenoxybenzamine 10 mg twice daily titrated upward, or doxazosin, for 10 to 14 days with liberal salt and fluid intake to re-expand the contracted intravascular volume; a beta blocker is added only afterward for reflex tachycardia. Giving a beta blocker first removes beta-2-mediated vasodilation and leaves unopposed alpha vasoconstriction, producing a hypertensive crisis, pulmonary edema, and possible cardiovascular collapse. During an intraoperative or spontaneous crisis, use phentolamine, nicardipine, clevidipine, or nitroprusside for pressure and esmolol for rate. After tumor resection, expect abrupt hypotension from catecholamine withdrawal and residual alpha blockade — have volume and vasopressors at the bedside.

Cortisol and aldosterone excess as causes of resistant hypertension

Cushing syndrome produces hypertension, hypokalemia, glucose intolerance, central obesity, left ventricular hypertrophy, and a hypercoagulable state with elevated venous thromboembolism risk. Primary hyperaldosteronism is the most common secondary cause of resistant hypertension, found in 5 to 20 percent of resistant hypertensives, and classically presents as hypertension with spontaneous or diuretic-provoked hypokalemia and metabolic alkalosis (though many patients are normokalemic). Screen with an aldosterone-to-renin ratio, holding interfering agents where feasible. Treatment is a mineralocorticoid receptor antagonist — spironolactone or eplerenone — or adrenalectomy for a unilateral adenoma. The cardiac relevance is direct: aldosterone excess drives myocardial and vascular fibrosis, left ventricular hypertrophy, atrial fibrillation, and stroke independently of the blood pressure it causes.