Cardiogenic shock in hypothyroidism.

Abstract: A patient with minimal coronary artery disease presented in cardiogenic shock when her previously undiagnosed hypothyroid state was complicated by an episode of AV nodal re-entrant tachycardia. She did not respond to multiple pressors, and recovered dramatically after starting thyroid supplementation. Hypothyroidism caused her lack of responsiveness to pressors and perpetuated her hypotension and increased filling pressures long after she reverted to a sinus rhythm. Our case dramatically demonstrates the severe lack of physiologic reserve that can be associated with hypothyroidism.

Key Words: hypothyroidism, AV nodal re-entrant tachycardia, cardiogenic shock

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Hypothyroidism is well known to be associated with bradycardia, mild hypertension, narrowed pulse pressure and pericardial effusion. (1) We report a patient with hypothyroidism and moderate coronary artery disease who presented to our institution in cardiogenic shock with ischemic changes on electrocardiogram (EKG). Her past medical history was notable, retrospectively, for a barely noticeable heart flutter that represented AV nodal re-entrant tachycardia (AVNRT).

Case Report

A 71-year-old female patient with a history of occasional "heart fluttering" experienced an episode of fluttering followed by weakness, lightheadedness, nausea, and ultimately, chest and back discomfort. Emergency medical services were called after a family member was unable to obtain a blood pressure reading. At the hospital, the patient's systolic blood pressure was 50 to 60 mm Hg by palpation with a pulse of 130 beats per minute (beats/min). She had jugular venous distension, clear lung fields, distant heart sounds and cold extremities. EKG (Fig. 1) showed AVNRT at a rate of 130 beats/min (read as sinus tachycardia), inferior and anterolateral ST segment depression with ST segment elevation in leads V1 and aVR. V4R on a separate strip showed ST segment elevation. Laboratory studies disclosed a hematocrit of 38% (36-46%), potassium 3.9 mmol/L (3.5-5.1), creatine kinase (CK) 250 U/L (0-215) and troponin I < 0.15 ng/mL (<0.15). Chest x-ray revealed clear lung fields. Echocardiogram showed a hyperdynamic left ventricle (LV) with subtle right ventricular (RV) dilation and a reported anterior effusion. The patient was treated with IV saline, dopamine and dobutamine at rates of 20 [micro]g/kg/min and air lifted to our center.

Upon arrival, the patient had a blood pressure of 70/50 mm Hg. The pulse rate of 130 beats/min abruptly slowed during bladder catheterization to 60 beats/min and then rose to 110 beats/min. Jugular venous distension, distant heart sounds, clear lung fields and cold extremities were present. Femoral pulses were palpable but the distal pulses were absent. EKG showed sinus tachycardia at 111 beats/min with persistent ST segment depression in the anterolateral and inferior leads and ST segment elevation in V1 and aVR (Fig. 2). Pulse oximetry revealed saturations of 89% on a 100% nonre-breather. The patient was placed on mechanical ventilation. A transthoracic echocardiogram revealed normal right and left ventricular internal dimensions, and preserved right and left ventricular systolic function and a small pericardial effusion. A transesophageal echocardiogram revealed normal valves and the absence of aortic dissection. She underwent an emergency right and left heart catheterization, which showed pulmonary artery oxygen saturation of 49% and femoral artery saturation of 95% on 0.5 Fi[O.sub.2]. Right atrial pressures were 23/21 (a/v) mm Hg. The right ventricular pressure was 36/22 mm Hg, with a pulmonary artery pressure of 36/22 mm Hg, a mean pulmonary capillary wedge pressure of 24 mm Hg, cardiac index 2.2 L/min/[m.sup.2] and systemic vascular resistance 1,127 dynes/[cm.sup.5]. Coronary angiography was notable only for an 80 to 90% stenosis in the lower branch of the circumflex posterolateral vessel (Fig. 3). The CK peak was 2,818 U/L, with a myoglobin of 468 and troponin I <0.15 ng/mL. Serum thyroid stimulating hormone level was 49.34 mU/L (0.35-5.5) with a free T4 of 0.7 (4-11) and serum cortisol of 38.2 [micro]g/dL (2.5-20.0). After being placed on replacement doses of thyroxine, she diuresed spontaneously and was weaned off mechanical ventilation and vasopressors. She had two recurrent episodes of AVNRT at a rate of 165 beats/min, one of which required adenosine. The patient subsequently underwent ablation of the slow pathway and was discharged on thyroxine. She was asymptomatic at follow-up 3 months later.

Discussion

Triiodothyronine thyroid hormone increases peripheral oxygen consumption directly and secondarily increases cardiac contractility. Triiodothyronine also decreases systemic vascular resistance by dilating the resistance arterioles. (2) The mechanism of action is felt to be direct vascular smooth muscle relaxation along with an increase in endothelial cell production of nitric oxide. (3,4) Although reported, overt heart failure is uncommon in hypothyroidism despite slowed diastolic relaxation and increased vascular resistance, probably due to lowered demand for peripheral oxygen delivery. (2) Our patient presented with an AVNRT followed by profound hypotension and ultimately, cardiogenic shock and diffuse right and left ventricular ST segment changes that persisted even when she was in sinus rhythm. She had an 80 to 90% stenosis in the lower branch of the posterolateral artery that alone could not explain her elevated filling pressure or her hypotension even on pressors, but could theoretically account for (in the setting of hypotension and prior tachycardia) all of the ST segment changes except the V4R ST segment elevation. Her dramatic response to the initiation of thyroid hormone suggests hypothyroidism as a critical ingredient in her development of cardiogenic shock. Our patient had a history of fluttering that was probably the AVNRT which was well tolerated until she became hypothyroid. She may also have had age- and thyroid-related diastolic dysfunction.

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Hypothyroidism is associated with reduced total blood volume. (5) A diminished blood volume, combined with a rapid heart rate and loss of atrial contribution to filling, allowed her to develop hypotension. Delayed diastolic relaxation associated with hypothyroidism and then modest macrovascular, and more importantly, microvascular ischemia made her filling pressures rise rapidly as she received volume.

Reduced capillary blood flow velocities and prolonged times to post occlusion peak flow velocities have been reported with hypothyroidism, and have been shown to revert to normal with euthyroidism. (6) Hypothyroid-mediated lack of reserve, due to endothelial and smooth muscle dysfunction and microcirculatory abnormalities combined with tachycardia and hypotension could have resulted in global RV and LV underperfusion with diffuse ST segment changes. Our patient's persistent hypotension was refractory to adrenergic agents and IV fluids long after her tachycardia resolved. This could be due to the diminished adrenergic sensitivity seen in hypothyroidism. (4,7) Overall, she demonstrated abnormal vascular response in terms of diminished coronary arterial ability to vasodilate, in addition to diminished large vessel lack of response to pressors.

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Conclusion

We speculate that our patient's tachycardia in the setting of modest coronary artery disease and hypothyroid-related volume reduction, diastolic dysfunction and microcirculatory abnormalities triggered hypotension and persistent ST segment change. Her hypothyroidism caused her lack of responsiveness to pressors and perpetuated her hypotension and increased filling pressures long after she reverted to a sinus rhythm. Our case dramatically demonstrates the severe lack of physiologic reserve that can be associated with hypothyroidism.

References

1. Ladenson PW. Recognition and management of cardiovascular disease related to thyroid dysfunction. Am J Med 1990;88:638-641.

2. Klein I, Ojamaa K. Thyroid hormone and the cardiovascular system. N Engl J Med 2001;344:501-509.

3. Taddei S, Caraccio N, Virdis A, et al. Impaired endothelium-dependent vasodilatation in subclinics hypothyroidism: beneficial effect of levothy-roxine therapy. J Clin Endocrinol Metab 2003;88:3731-3737.

4. Gomberg-Maitland M, Frishman WH. Thyroid hormone and cardiovascular disease. Am Heart J 1998;135:187-196.

5. Gibson JG, Harris AW. Clinical studies of the blood volume. V. hyperthyroidism and myxedema. J Clin Invest 1939;18:59-65.

6. Pazos-Moura CC, Moura EG, Breitenbach MM, et al. Nailfold capillaros-copy in hypothyroidism and hyperthyroidism: blood flow velocity during rest and postoocclusive reactive hyperemia. Angiology 1998;49:471-476.

7. Napoli R, Biodi B, Guardasole V, et al. Impact of hyperthyroidism and its correction on vascular reactivity in humans. Circulation 2001; 104:3076-3080.

Mahi Lakshmi Ashwath, MD, Gurjaipal Kang, MD, Mike Cunningham, MD, and Dale S. Adler, MD

From the University Hospitals of Cleveland, Case Western Reserve University, Cleveland, Ohio

Reprint requests to Dr. Mahi Lakshmi Ashwath, UHC, Division of Gen Internal Medicine, HRV 6033, 11100 Euclid Avenue, Cleveland, OH 44106. Email: [e-mail]

Accepted January 24, 2006.

RELATED ARTICLE: Key Points

* AV nodal re-entrant tachycardia may complicate hypothyroidism, causing cardiogenic shock.

* Hypothyroidism may cause a lack of responsiveness to pressors and a lack of physiological reserve.

* Diminished blood volume, combined with rapid heart rate and loss of atrial contribution to filling, may cause hypotension.