Cardiogenic shock in hypothyroidism.

- Free Online Library

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
**********
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
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.
[FIGURE 1 OMITTED]
Hypothyroidism is associated with reduced total blood volume. (5) A diminished blood volume,
combined with a rapid heart rate and loss cold feet thyroid 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.
[FIGURE 2 OMITTED]
[FIGURE 3 OMITTED]
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;344:501509.
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;88:37313737.

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: mahi.ashwath@case.edu
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.

COPYRIGHT 2006 Southern Medical Association

No portion of this article can be reproduced without the express written permission from the
copyright holder.
Copyright 2006, Gale Group. All rights reserved. Gale Group is a Thomson Corporation Company.