Arrhythmias and heart rate variability during and after therapeutic hypothermia for cardiac arrest*

Tiainen, Marjaana; Parikka, Hannu; Mäkijärvi, Markku; Takkunen, O.; Sarna, Seppo; Roine, Risto O.

doi:10.1097/ccm.0b013e31819572c4

Cited by 74 publications

(41 citation statements)

References 39 publications

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“…Increased atrial and ventricular arrhythmias, re-entrant arrhythmias and prolonged asystole have also been described [53,54]. However, these effects are more common at temperatures below 32°C, and many recent studies have found that mild induced hypothermia was associated with no clinically significant arrhythmias [29,[54][55][56].…”

Section: Resultsmentioning

confidence: 98%

The effects of mild induced hypothermia on the myocardium: a systematic review

Kelly

Nolan

2010

Anaesthesia

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SummaryMild induced hypothermia improves neurological outcome and reduces mortality among initially comatose survivors of out-of-hospital cardiac arrest. Similar pathological processes occur in the heart and the brain, namely ischaemia followed by reperfusion injury. Animal data indicate that mild induced hypothermia results in improved myocardial salvage, reduced infarct size, reduced left ventricular remodelling and better long-term left ventricular function. Several small human studies suggest that infarct size may be reduced by mild induced hypothermia, although this has not reached significance in any human study to date. There are variable reports of harm to the myocardium caused by mild induced hypothermia, including reduced myocardial contractility and cardiac output, electrocardiographic changes and arrhythmias, especially bradycardia. These harmful effects are reversible with rewarming. Most patients who have a cardiac arrest do not survive, and full neurological recovery occurs in only 6-23% [1]. In order to improve survival and reduce such neurological injury, guidelines have recently been published describing the post-cardiac arrest bundle of care: this includes early coronary reperfusion if appropriate (primary angioplasty or thrombolysis), haemodynamic optimisation, and control of ventilation, blood glucose, temperature and seizures [2,3].Therapeutic hypothermia has become established as a recognised intervention following cardiac arrest [2]. Two randomised controlled trials have shown improved neurological outcome and reduced mortality in adults who were therapeutically cooled following out-ofhospital ventricular fibrillation (VF) cardiac arrest, where the patient was comatose following initial resuscitation, and where cooling was initiated within minutes to hours [4,5]. The International Liaison Committee on Resuscitation has recommended that all unconscious adult patients with spontaneous circulation after out-of-hospital VF cardiac arrest should be cooled to 32-34°C for 12-24 h [6]. Such cooling may also be beneficial for other rhythms or in-hospital cardiac arrest [6].Cardiac arrest is thought to cause neurological injury by several mechanisms, including perfusion failure leading to cerebral ischaemia, and reperfusion leading to re-oxygenation injury [7][8][9][10]. Therapeutic hypothermia is thought to attenuate both these processes. Firstly, hypothermia is thought to protect against many of the processes associated with reperfusion and re-oxygenation [14][15][16][17][18]. Secondly, hypothermia reduces the cerebral metabolic rate for oxygen (CMRO 2 ) [11], and may therefore provide protection from ongoing cerebral ischaemia [12,13].Similar pathological processes occur in the heart following cardiac arrest and ⁄ or acute myocardial infarction (AMI), including perfusion failure followed by reperfusion and re-oxygenation injury [19][20][21][22]. It has been suggested that mild induced hypothermia may also be beneficial to the myocardium in a similar way that it is neuroprotective to the brain [2...

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Section: Resultsmentioning

confidence: 98%

The effects of mild induced hypothermia on the myocardium: a systematic review

Kelly

Nolan

2010

Anaesthesia

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“…Although survival rates following cardiac arrest and cardiopulmonary resuscitation (CA/CPR) remain staggeringly low, advancements in both patient care and public awareness of risk factors have allowed many individuals to survive incidents that would have previously proven fatal (2)(3)(4). Although such developments represent an important advancement, survivors of CA/ CPR are predisposed to suffer from a myriad of chronic physiological and psychiatric conditions as a result of neuronal damage caused by widespread deprivation of blood flow to the brain, otherwise known as global cerebral ischemia (5).…”

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confidence: 99%

Social interaction modulates autonomic, inflammatory, and depressive-like responses to cardiac arrest and cardiopulmonary resuscitation

Norman¹,

Zhang

Morris³

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

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Psychological factors, including depression and social isolation, are important determinants of cardiovascular health. The current study uses a well-validated mouse model of cardiac arrest/cardiopulmonary resuscitation (CA/CPR) to examine the effect of social environment on several pathophysiological and behavioral responses to cerebral ischemia. Male experimental mice were either housed in pairs with an ovariectomized female or socially isolated for the duration of the experiment. Cardiac arrest increased the mRNA expression of the proinflammatory cytokines TNF-α, IL-1β, and IL-6, as well as the microglia marker MAC-1; expression of each of these factors, except IL-6, was further increased among socially isolated mice. Furthermore, socially isolated animals exposed to the CA/CPR procedure displayed significantly higher levels of neuronal cell death and microglia staining within the hippocampus at 7 d following surgery. Social isolation also exacerbated CA/CPR-induced depressive-like behavior and cardiac autonomic dysregulation. In the absence of ischemic damage, social environment had no significant effect on the expression of neuronal cell death, autonomic cardiac control, or behavior. Together, these data suggest that social factors influence the pathophysiological trajectory following cardiac arrest.

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“…Tiainen et al showed in adult patients with out of hospital cardiac arrest (OHCA) treated with hypothermia (33 • C), that preserved HRV was associated with moderately favorable outcomes. 24 Li et al studied the effects of therapeutic hypothermia on HRV in pigs after VF cardiac arrest from 60 to 240 min after ROSC as well as neurological outcome of survivors. These animals had markedly decreased heart rate variability (RMSSD, SDNN) after cardiac arrest but treatment with hypothermia (34 • C) preserved the time domain measures of heart rate variability (RMSSD and SDNN) without changes in frequency domain measures (VLF, LF and HF).…”

Section: Discussionmentioning

confidence: 99%

Whole body periodic acceleration (pGz) preserves heart rate variability after cardiac arrest

et al. 2016

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Arrhythmias and heart rate variability during and after therapeutic hypothermia for cardiac arrest*

Abstract: The use of therapeutic HT of 33 degrees C for 24 hours after CA was not associated with an increase in clinically significant arrhythmias. Preserved 24 to 48-hour HRV may be a predictor of favorable outcome in patients with CA treated with HT.

Cited by 74 publications

References 39 publications

The effects of mild induced hypothermia on the myocardium: a systematic review

The effects of mild induced hypothermia on the myocardium: a systematic review

Social interaction modulates autonomic, inflammatory, and depressive-like responses to cardiac arrest and cardiopulmonary resuscitation

Whole body periodic acceleration (pGz) preserves heart rate variability after cardiac arrest

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