Hypertensive Emergency With Cardiac Tamponade Associated With Hypothyroidism

A 46‐year‐old Korean American man came to the hospital complaining of nausea, vomiting, and headaches for 1 week. For the past 3 days he had been dizzy and unsteady. For 3 months, he had experienced shortness of breath on exercise and at rest without paroxysmal nocturnal dyspnea, orthopnea, leg swelling, fever, chills, or cough. Also, during the past 3 months he had been bothered by abdominal bloating and a feeling of distension.

He appeared ill in the emergency department. His blood pressure (BP) was 258/146 mm Hg, with a heart rate of 79 bpm. The thyroid gland was not palpable. Cardiac examination revealed distant heart tones without murmurs or gallops. Neck veins were minimally pulsatile at 20 cm above the right atrium in the sitting position. Chest examination revealed bronchial breath sounds at the right base and diminished breath sounds at the left base. There was no edema. The patient was able to stand up from a sitting position with assistance and could walk with assistance 4 or 5 steps, with a wide‐based gait.

The chest radiograph revealed a gigantic cardiac silhouette filling the left chest and extending halfway into the right hemithorax (Figure 1). Brain computed tomography, magnetic resonance imaging (MRI), and magnetic resonance angiography (MRA) showed bilateral multiple focal hemorrhagic foci, especially involving the right temporal lobe, and small‐vessel ischemic disease with a 1‐cm right cerebellar hemorrhage and extensive cerebellar edema (Figure 2, Figure 3). The electrocardiogram showed only low voltage. An echocardiogram demonstrated late diastolic collapse of both the right atrium and the right ventricle, with a large pericardial effusion. The anterior pericardial clear space measured 6.5 cm, and the posterior clear space was 6.0 cm The patient underwent emergency pericardiocentesis, which removed 4100 mL of straw‐colored fluid, and a pericardial drain was inserted. He was placed on intravenous nitroprusside before changing to a labetalol drip that reduced his BP to 180/120 mm Hg in the first few hours, then 160/100 mm Hg by the next morning. Over the next 3 days, an additional 715 mL of pericardial fluid was drained, and a follow‐up echocardiogram showed resolution of the pericardial effusion but with severe left ventricular hypertrophy.

Figure 1.

Chest radiograph showing massively enlarged cardiomediastinal silhouette filling the entire left lower hemithorax and most of the right hemithorax. Trachea is deviated to the right.

Figure 2.

Computed tomographic scan showing 1‐cm right cerebellar hemorrhage with edema.

Figure 3.

Magnetic resonance imaging on the T2 sequence showing right temporal edema from a subacute hemorrhage.

Laboratory findings are listed in Table I. Negative serologies included antinuclear antibody, human immunodeficiency virus, rheumatoid factor, antineutrophil cytoplasmic antibodies, and anticardiolipin antibodies. On renal sonography, the right kidney measured 11.6 cm × 4.9 cm and the left kidney measured 11.7 cm × 5.2 cm. Renal/adrenal MRI/MRA showed normal kidneys and adrenal glands with nonobstructed renal arteries.

Table I.

Laboratory Parameters

Parameter	Patient	Reference
Pericardial fluid
White cells, × 103/μL	5	na
Polymorphonuclear, %	50	na
Red cells, × 106/μL	32	na
Routine organisms	neg	neg
Acid‐fast organisms	neg	neg
Protein, g/dL	6.9	na
Erythrocyte sedimentation rate, mm/h	9	0–15
Plasma
Total metanephrines, pg/mL	190	61–256
Metanephrines, pg/mL	67	<82
Normetanephrines, pg/mL	123	100–400
Serum renin, ng/mL/h	0.2	0.65–5
Paired aldosterone, ng/mL	4	≤28
Blood urea nitrogen, mg/dL	21–23	<19
Creatinine, mg/dL	1.7–1.8	0.7–1.3
GFR, estimated, mL/min	43	>89
Serum thyrotropin, μU/mL	34.85	0.4–4.0
Serum free L‐thyroxine, ng/dL	0.75	0.70–1.48
Thyroperoxidase antibodies, U/mL	>6500	<60
Urine, 24 h
Aldosterone, μg	2.6	2.3–21.0
Vanillylmandelic acid, mg	4.2	<7
Epinephrine, μg	4	0–25
Norepinephrine, μg	39	0–105
Total catecholamines, μg	43	0–135
Metanephrine, μg	433	44–540
Total metanephrines, μg	545	990–690
na indicates not applicable; neg, negative; and GFR; glomerular filtration rate.

The patient's breathing difficulty and abdominal bloating quickly resolved following pericardiocentesis, but although his ability to ambulate improved, he had continuing dizziness. Predischarge BP was 134/82 mm Hg on a regimen of lisinopril/hydrochlorothiazide 20/25 mg and felodipine 20 mg daily.

Follow‐up echocardiography revealed reaccumulating pericardial fluid though the patient was asymptomatic, leading to a pericardectomy 3 weeks following his hospital discharge. Pathology of the pericardial tissue showed nonspecific reactive changes including mesothelial hyperplasia; both routine and acid‐fast cultures of the tissue returned negative results.

DISCUSSION

This patient presented with a hypertensive emergency with a BP of 258/146 mm Hg associated with symptoms of dizziness and ataxia and MRI findings of cerebellar hemorrhage along with multiple bilateral hemorrhagic foci, as well as cardiac tamponade. The concomitant tamponade and the enormity of the pericardial effusion were striking. Pericardial effusions usually originate posteriorly, and with moderate‐sized effusions there is anterior spread of fluid. ¹ Clear pericardial space indicative of effusion has been considered significant by various authors when it measures >0.5–2.0 cm. ² , ³ , ⁴ Total pericardial clear space for this patient was 12.5 cm, pointing to a very gradual process of accumulation. This patient reported symptoms of exertional dyspnea and abdominal bloating of at least 3 months' duration. These were attributed to his large pericardial effusion; the symptoms resolved quickly following pericardiocentesis. Very large pericardial effusions have been reported to persist as long as 15 years without developing tamponade. ³ , ⁵ Distended neck veins and echocardiographic demonstration of diastolic collapse of the right atrium and right ventricle established the diagnosis of cardiac tamponade.

Is hypertension with cardiac tamponade a frequent occurrence? Beck's original triad of decreasing BP, rising venous pressure, and a small quiet heart was used to describe acute cardiac tamponade; however, his clinical triad of high venous pressure, a small quiet heart, and ascites to describe chronic cardiac compression did not include hypotension. ⁶ Hypertension with tamponade, while infrequent, is not rare and has been described as a tamponade variant due to excessive adrenergic drive and is associated with preceding hypertension. ⁷ Brown et al ⁴ described a group of 6 out of 18 consecutive cardiac tamponade patients with hypertension. Following pericardiocentesis, there was a significant decline in peripheral vascular resistance (PVR) in both the hypertensive and hypotensive patients. PVR is a critical compensatory mechanism, along with increased myocardial contractility, when cardiac output is reduced as a result of pericardial restriction. Relief of this restriction causes an immediate reduction in intracardiac pressure, improved cardiac output, and relaxation of compensatory PVR. PVR fell in the hypertensive group from 2150 dyne • s • cm‐⁵ before pericardiocentesis to 1207 dyne • s • cm‐⁵ after pericardioscentesis. ⁴ Following pericardiocentesis, BPs uniformly decreased in the 6 hypertensive patients, and rose in the hypotensive patients. Hemodynamic data for both groups of patients are shown in Table II.

In the series of cardiac tamponade patients reported by Reddy et al, ⁸ 6 out of 14 had BPs from 140/90 mm Hg to 227/113 mm Hg. Unlike the experience of Brown et al, however, none experienced a significant decrease in BP post‐pericardiocentesis (Table III). All of the Brown et al study patients with hypertensive tamponade had antecedent chronic hypertension, and probably this was also the case for the hypertensive tamponade patients in Reddy et al. In another series of tamponade patients, 36 of 56 (64%) had systolic pressures of at least 100 mm Hg, but BPs were not further characterized into a hypertensive group. ⁹ Hemodynamic data collected during a case of hypertensive cardiac tamponade in a patient with a BP of 208/74 mm Hg showed subclinical deterioration in left ventricular ejection time when he was administered nitroglycerin and nifedipine before pericardiocentesis. ¹⁰ These authors recommended β‐blockade for hypertensive pretamponade to improve stroke volume by reducing heart rate; however, this idea has not been tested. It is also possible that a disturbance of compensatory tachycardia and contractility may induce deterioration of cardiac function.

The cause for this patient's enormous pericardial effusion culminating in cardiac tamponade was not completely certain. How often does idiopathic tamponade occur? Large pericardial effusions in the absence of acute inflammatory signs such as chest pain, friction rub, fever, and generalized ST‐segment elevations are not commonly idiopathic. Fourteen of 79 (18%) patients in a series of patients with large chronic pericardial effusions were considered to have idiopathic effusions ¹¹ (Table IV). Seven out of 57 (12%) large chronic effusion patients in another series were considered idiopathic. ² In a series of 28 patients with large chronic idiopathic pericardial effusions followed for up to 15 years, it was found that tamponade occurred unpredictably in 8 patients (29%), and those with recurrent effusion postpericardiocentesis treated with pericardiectomy did well. ³ Our case discussion patient also required pericardiectomy for this reason, and pathology of the surgical specimen was unrevealing as to etiology.

Table IV.

Causes of Moderate and Severe Pericardial Effusions

Diagnosis, No. (%)	Moderate Effusion Without Tamponade (n=124)	Severe Effusion Without Tamponade (n=79)	Tamponade (n=119)	Total Series (N=322)
Acute idiopathic pericarditis	19 (29)	20 (30)	27 (41)	66 (20)
Iatrogenic effusion	19 (38)	10 (20)	21 (42)	50 (16)
Neoplastic pericardial effusion	11 (26)	6 (14)	26 (60)	43 (13)
Chronic idiopathic pericardial effusion	8 (28)	14 (48)	7 (24)	29 (9)
Acute myocardial infarction	12 (46)	4 (15)	10 (38)	26 (8)
End‐stage renal disease	6 (32)	9 (47)	4 (21)	19 (6)
Heart failure	13 (76)	4 (23)	0	17 (5)
Collagen vascular disease	12 (80)	3 (20)	0	15 (5)
Tuberculosis or purulent	1 (7)	3 (21)	10 (71)	14 (4)
Miscellaneous	23 (53)	6 (14)	14 (33)	43 (13)
Reprinted with permission from Sagrista‐Sauleda et al. 11

Cardiac tamponade and massive pericardial effusions rarely occur with severe hypothyroidism and myxedema ¹² , ¹³ , ¹⁴ , ¹⁵ , ¹⁶ , ¹⁷ and may be associated with severe systemic hypertension. ¹² , ¹⁷ Features of these effusions include large size due to the slow accumulation of up to 6 L of pericardial fluid ¹³ and relative bradycardia. ¹⁵ Hypothyroid status can be associated with diastolic hypertension, but in a patient with hypertensive hypothyroid tamponade presenting with a BP of 210/110 mm Hg, ¹² and another patient with hypertensive hypothyroid massive effusion and a BP of 150/100 mm Hg, ¹⁷ the hypertension persisted following pericardiocentesis and treatment of the hypothyroid condition. While pericardial effusions may occur in 30%–80% of myxedema patients, echocardiographic surveys in patients with simple hypothyroidism show only a 3%‐6% prevalence of pericardial effusions. ¹⁸ Hypothyroid pericardial effusions respond rapidly to thyroid replacement ¹⁹ ; even large effusions can respond. ¹⁵

Large pericardial effusions due to hypothyroidism have been attributed to several mechanisms: (1) extravasation of exudative fluid into the body cavities due to increased capillary permeability, decreased lymphatic drainage, and increased retention of salt and water ¹⁴ ; (2) cholesterol pericarditis where cholesterol crystals in the pericardium incite a cellular reaction ²⁰ ; and (3) hypothyroid related low‐output cardiomyopathy. ²⁰ Our patient had no evidence of pleural effusion or ascites; pericardial tissue pathology did not show evidence of cholesterol crystal‐related inflammation; and echocardiography showed normal cardiac function. Only 20 cases of hypothyroid cardiac tamponade had been reported until 1993, ¹² mostly associated with myxedema or severe hypothyroid status and thyrotropins as high as 247.1 mU/L. ¹⁶ Massive pericardial effusion in a patient with Hashimoto's thyroiditis and severe systolic/diastolic hypertension requiring an 800‐mL pericardiocentesis has been recorded with a thyrotropin of 38.99 mU/L (normal, 0.24–3.70 mU/L) and a thyroxine of 0.8 μg/dL (normal, 4.5–12.3μg/dL), however, close to the values in the present case discussion; the present patient also had Hashimoto's thyroiditis. The extraordinary size of this patient's pericardial effusion, however, along with the lower‐normal range free thyroxine, would make it unique if hypothyroidism were the solitary explanation. Interestingly, the presenting heart rate in the 70s could be interpreted as inappropriate bradycardia, an occasional feature of hypothyroid tamponade. ¹⁵ As described, the spectrum of hypothyroid cardiac tamponade has also been associated with severe systemic hypertension at a BP range similar to the present case, ¹² as well as very large, slowly accumulating pericardial effusions.

This patient underwent a 4100‐mL pericardiocentesis followed by 715 mL of additional drainage via a pericardial catheter over 3 days, and had a 12.5‐cm pericardial clear space on the echocardiogram. Series of large pericardial effusions have reported drainages of 2100 mL, ³ 1050 mL, ⁴ 2000 mL, ⁹ and up to 6000 mL reported in a hypothyroid patient, ¹³ with 9000 mL in a case of hepatic hydro‐pericardium where there was a connection between the peritoneal and pericardial cavities in a cirrhotic patient with ascites. ²¹

In their discussion of possible causes of hypertensive cardiac tamponade, Brown et al ⁴ listed “increased serum catecholamine levels, enhanced nonadrenergic reactivity of the vascular smooth muscle level, and an increase in the binding of alpha 1 adrenergic receptors.” In this case, an extensive workup to rule out etiologies of secondary hypertension included plasma total metanephrines, plasma metanephrines, and plasma normetanephrines; along with 24‐hour urine collections for vanillylmandelic acid, epinephrine, norepinephrine, total catecholamines, metanephrine, normetanephrine, and total metanephrines, all of which were normal. Therefore, increased catecholamines would be an unlikely etiology. Our patient's hypertension improved with thyroid replacement, but still required 3 antihypertensive medications. Hypothyroidism may explain the tamponade. This appears to be the first case description of hypertensive cardiac tamponade associated with a hypertensive emergency and hemorrhagic stroke.