Sinus bradycardia is defined as a heart rate of less than 60 beats per minute and can occur as an adaptive response but can also be pathologic. Sinus bradycardia can be a normal finding in children, individuals who exercise often, and as a physiologic response during sleep. Pathologic causes of sinus bradycardia include sinus node dysfunction, medications, acute myocardial infarction, heart failure, obstructive sleep apnea, exaggerated vagal activity, increased intracranial hypertension, infection, hypothyroidism, hypothermia, anorexia nervosa, and prolonged hypoxia. When pathologic, addressing the underlying cause will lead to an improvement in heart rate. Here, we present a case of sinus bradycardia in a 61-year-old female with hypothermia. Evaluation for common causes of bradycardia including cardiac evaluation was unremarkable. Treatment of hypothermia led to the resolution of bradycardia. The importance of the case is to help clinicians recognize hypothermia as a cause of bradycardia.

Hypothermia is defined as a significant drop in core body temperature below 35°C (95°F). It is traditionally staged as mild, moderate, severe, and profound at temperatures of 35°C to 32°C (95°F to 89.6°F), 32°C to 28°C (89.6°F to 82.4°F), <28°C (<82.4°F), and <24°C (75.2°F), respectively. It can also be classified into the same stages by clinical presentations. We present a patient that fits into two different stages based on core body temperature and clinical presentation.  A 58-year-old homeless male with a history of seizures and alcohol use presented via emergency medical services after spending the night outside and uncovered with a core body temperature of 25.1°C (77.1°F) via a urinary bladder thermometer, meeting criteria for severe, near profound, hypothermia. However, he was alert and communicating, shivering, with tachycardia, tachypnea, normal oxygen saturation, and elevated blood pressure, suggestive of mild hypothermia clinically. Passive and active external and internal rewarming were utilized to treat, with the removal of wet clothing, forced air patient warming system, warm blankets, and warm lactated ringers given intravenously. He was soon transferred to the intensive care unit and first returned to normothermic levels after approximately 10 hours from presentation. An electrocardiogram was obtained after resolution of shivering and revealed atrial fibrillation without Osborn waves. He remained in the hospital for the following week to treat his atrial fibrillation, hypothermia-induced rhabdomyolysis, and alcohol withdrawal. He was discharged without neurologic deficits and medically stable with appropriate resources.  This case demonstrates a unique presentation of severe hypothermia. To our knowledge, there has not been a reported case of severe hypothermia that does not involve severe central nervous system depression, severe slowing of vitals, and/or comatose status. These clinical symptoms normally begin during moderate hypothermic levels near 32°C (89.6°F), yet our patient presented without any central nervous system depression and with accelerated vitals that are more consistent with mild hypothermia yet had a core temperature of 25.1°C (77.1°F). Treatment was dictated by his core body temperature rather than clinical presentation. Because of this incongruence between symptoms and true severity of disease in hypothermia, we recommend diagnosis and treatment of hypothermia always be confirmed and based on core body temperature via a low-reading thermometer instead of clinical presentation alone.

BACKGROUND: Shapiro syndrome is extremely rare and is characterized by the triad of spontaneous periodic hypothermia, hyperhidrosis and agenesis of the corpus callosum, resulting in neurological and psychological disorders. The exact mechanism of this syndrome is unknown and treatment consists of controlling the periodic attacks. This case report describes a case of Shapiro syndrome presenting with ventricular fibrillation (VF) who was treated with dual chamber implantable cardioverter defibrillator (ICD) therapy.
METHODS: A 45-year-old man, suffering from Shapiro syndrome with frequent hypothermic attacks, was admitted to the emergency department with an out of hospital cardiac arrest caused by VF due to hypothermia. To prevent cardiac death during future hypothermic attacks with VF, the patient was treated with a dual chamber ICD. Within 1 month after ICD implantation the patient had two events of ventricular tachycardia/VF during hypothermia, which were both successfully terminated by an ICD shock. One year after ICD implantation the patient suffered from an uncontrolled urinary tract infection and the patient passed away. Post-mortem interrogation of the ICD did not reveal further episodes of VF and showed a higher supraventricular heartrate in the last days before his death, probably due to a sinus tachycardia driven by the infection. It was concluded that the most likely cause of death was an uncontrolled sepsis.
CONCLUSIONS: The current case showed that ICD therapy can be successful in treating VF episodes in patients with unexpected periods of hypothermia.

Osborn waves are produced when the J-point deviates from baseline. While there are many known causes of Osborne waves, hypothermia remains the most common. Previous studies have been inconsistent about the risk of Osborne waves progressing to a deadly arrhythmia. Commonly, once patients are rewarmed, they no longer exhibit Osborne waves or experience cardiac arrhythmias. This patient presented with hypothermia on a hot, humid August day demonstrating two factors known to cause Osborne waves - hypothermia and hypocalcemia. While replenishing the calcium was beneficial, providing ventilator support and active rewarming remained the mainstays of treatment.

BACKGROUND: A 56-year-old man without known medical history was brought to our ED after he was found next to his bed, agitated and with waxing and waning consciousness. He has been bedbound for 5 days after a long-standing period of malnutrition. Physical examination reveals Kussmaul breathing, heart rate of 62/min and blood pressure of 135/100 mm Hg, normal cardiac, abdominal and a non-focal neurological examination other than confusion and altered level of consciousness. An EKG was performed (figure 1).emermed;36/1/51/F1F1F1Figure 1EKG at presentation in our ED.
OBJECTIVE: What abnormalities are the clues to the severity of his condition? How would you confirm your suspicion?The minimally prolonged QTc time.The subtle horizontal ST segment elevation in V2 and V3.The subtle positive deflection at the J point.Nothing, this EKG is not interpretable because of the movement of baseline.

J waves develop during hypothermia, but the dynamicity of hypothermia-induced J waves is poorly understood.
The purpose of this study was to investigate the mechanism of the rate-dependent change in the amplitude of hypothermia-induced J waves.
Nineteen patients with severe hypothermia were included (mean age 70 ± 12 years; 16 men [84.2%]). The rectal temperature at the time of admission was 27.8° ± 2.5°C. In addition to prolonged PR, QRS complex, and corrected QT intervals, the distribution of prominent J waves was widespread in all 19 patients.
Nine patients showed changes in RR intervals. When the RR interval shortened from 1353 ± 472 to 740 ± 391 ms (P = .0002), the J-wave amplitude increased from 0.50 ± 0.29 to 0.61 ±0.27 mV (P = .0075). The J-wave amplitude increased in 7 patients (77.8%) and decreased in 2 patients (22.2%) after short RR intervals. The augmentation of J waves at short RR intervals was associated with a significant prolongation of ventricular activation time (35 ± 5 ms vs 46 ± 5 ms; P = .0020), suggesting accentuated conduction delay. Increased conduction delay at short RR intervals was suggested to accentuate the phase 1 notch of the action potential and J waves in hypothermia. None developed ventricular fibrillation, and in 2 of 9 patients with atrial fibrillation, atrial fibrillation persisted after rewarming to normothermia.
J waves in severe hypothermia were augmented after short RR intervals in 7 patients as expected for depolarization abnormality, whereas 2 patients showed a bradycardia-dependent augmentation as expected for transient outward current-mediated J waves. Increased conduction delay at short RR intervals can be responsible for the accentuation of the transient outward current and J waves during severe hypothermia.

The Osborn or J-wave, an upright deflection of the J-point on the electrocardiogram (ECG), is often observed during severe hypothermia. A possible relation between Osborn waves (OW) and increased risk of ventricular arrhythmia has been reported. We sought to determine whether the level of targeted temperature management (TTM) following out-of-hospital cardiac arrest (OHCA) affects the prevalence of OW and to assess the associations between OW and risk of ventricular arrhythmia and death.
The present study is part of the TTM-trial ECG-substudy (including OHCA-patients randomized to TTM at 33 °C vs. 36 °C from 24 of 36 sites). Serial 12-lead ECGs from 680 (94%) patients were analysed and stratified by OW at predefined time-points (0, 4, 28, 36, 72-h after admission). On admission, the overall prevalence of OW was 16%, increasing to 32% at target temperature, with higher prevalence in the 33 °C-group (40% vs. 23%, p < 0.0001). No difference in prevalence was found between the 33 °C- and 36 °C-groups on admission (18% vs. 14%, p = .11) or after rewarming (13% vs. 10%, p = .44). OW were not associated with increased risk of ventricular arrhythmia (Odds ratio = 0.78 (0.51-1.20), p = .26), but associated with significantly lower 180-day mortality as compared to no OW (38% vs. 52%, plog-rank = 0.001) in univariable analyses only.
OW are frequent during TTM, particularly in patients treated with 33 °C. OW are not associated with increased risk of ventricular arrhythmia, and may be considered a benign physiological phenomenon, associated with lower mortality in univariable analyses.

Prominent J-waves are observed in several clinical conditions many of which are highly arrhythmogenic and may lead to ventricular fibrillation (VF) and/or sudden cardiac death. We present the case of a 34-year-old male patient with hypothermia. Prominent J-waves (Osborn waves) and prolonged QT interval was evident in nearly every lead. Early recognition of these arrhythmogenic electrocardiogram (ECG) findings and treatment of hypothermia is important to minimize the risk of arrhythmic events.

Organophosphorus poisoning cases are routinely treated across all Intensive Care Units adjoining the rural areas where agriculture is the main source of income. We present a unique case of severe hypothermia seen in a case of organophosphorus poisoning, which led to electrocardiogram disturbances and life-threatening arrhythmias.

Hypothermia occurs when the core body temperature falls below 35°C, which, in severe cases, can lead to electrocardiographic changes. Several conditions that occur in the psychiatric population increase the risk of hypothermia. This risk can be further increased by the use of several classes of medications such as antipsychotics, beta-adrenergic antagonists and benzodiazepines. We report on three psychiatric patients who were admitted for hypothermia and developed electrocardiographic manifestations (sinus bradycardia, QT prolongation and Osborn waves), which completely resolved after treatment.