Studies evaluating cardiac output (CO) in acute brain injury patients

Reference	Patient number	Study design	Group	Technique assessment	End-point	Findings	Quality of evidence
Incidence of altered CO
Mutoh et al. [24]	46	P	SAH	TT	To evaluate the time course of cardiac function	High CI on admission which diminished on day 5 Hgher CI in patients with poor neurological status	Low
Trieb et al. [25]	30	P	Stroke	PAC	To evaluate CO after ischemic stroke	Patients with stroke had significantly higher CO than comparable controls	Low
Laurent et al. [26]	165	R	CA	PAC	To evaluate hemodynamics after CA	Low CI is common in the early phase after CA, which normalizes thereafter, except in those dying with cardiogenic shock and MOF	Very low
Rzheutskaya et al. [102]	13	P	TBI	TT	To assess hemodynamic alterations after TBI	Four different hemodynamic response according to CI, SVR, SVV and response to fluid administration	Very low
Schulte Esch et al. [40]	12	P	TBI	PAC	To assess hemodynamic alterations after TBI	Elevated CI with high PAOP and low SVRI were reported	Very low
Role of CO monitoring to explain the mechanisms of brain injury-related cardiopulmonary complications
Sato et al. [37]	49	P	SAH	TT	To assess variables related to the development of PE	Patients with PE had lower CI than others	Low
Deehan et al. [38]	24	R	SAH	PAC	To evaluate hemodynamics in patients with PE To assess effects of dobutamine	Variable hemodynamic variables Increased CI and decreased PAOP in patients with PE	Very low
Vespa et al. [39]	56	R	SAH	PAC	To evaluate the mechanisms of poor oxygenation after SAH	Similar hemodynamics between patients with and without poor oxygenation	Very low
Tamaki et al. [103]	15	P	TBI	PAC	To assess hemodynamic alterations after TBI	All patients had high PAOP and PVR Hypotensive patients had low CI and elevated SVRI Normotensive patients had high SVRI	Very low
Nicholls et al. [104]	60	P	TBI		To assess hemodynamic alterations after TBI	High CI and MAO with reduced tissue oxygenation were found Survivors had higher CI and tissue oxygenation than non-survivors	Low
Bergman et al. [41]	50	P	OHCA	PAC	To evaluate the effects of TH on hemodynamics	TH lowered heart rate, filling pressures, CO and MAP without deleterious effects on SvO2	Low
Zobel et al. [42]	40	P	CA	PAC	To evaluate the effects of TH on hemodynamics during cardiogenic shock	TH improved hemodynamics during cardiogenic shock following CA	Low
Sato et al. [43]	60	P	SAH	PAC	To evaluate the effects of TH on systemic and cerebral hemodynamics during surgery	TH was associated with decreased CI and increased arterio-jugular difference in oxygen	Low
Association between CO and brain perfusion, neurological complications or outcome
Tone et al. [48]	42	P	SAH	PAC	To evaluate the correlation between hemodynamic variables and CBF	CBF was correlated with CI	Very low
Hashimoto et al. [105]	20	P	BS	TT	To evaluate the correlation between hemodynamic variables and CBF	CBF was not correlated with CI after BAVM resection	Very low
Watanabe et al. [34]	34	P	SAH	TT	To evaluate which hemodynamic variable was associated with the occurrence of DCI	DCI was associated with lower CI	Low
Mayer et al. [45]	72	R	SAH	Echography	To evaluate which hemodynamic variable was associated with the occurrence of DCI	DCI was associated with lower CI	Very low
Yousef et al. [47]	149	P	SAH	Echography	To evaluate which hemodynamic variable was associated with the occurrence of DCI	DCI was associated with lower CI	Low
Torgesen et al. [106]	153	R	CA	PAC	To evaluate the impact of hemodynamic variables on outcome during NT	No association of hemodynamic variables with outcome	Very low
Torgesen et al. [107]	134	R	CA	PAC	To evaluate the impact of hemodynamic variables on outcome during TH	Elevated CI was associated with poor outcome	Very low
Yamada et al. [108]	34	P	TBI	Dye Dilution	To evaluate the impact of hemodynamic variables on outcome after severe TBI	Low CI was associated with poor outcome	Very low
Effects of therapies modifying CO on neurological status
Chatterjee et al. [109]	15	P	BS	Echography	To evaluate the effects of mannitol on systemic hemodynamics	Mannitol increased CI during 15 min after administration	Low
Stoll et al. [110]	20	P	Stroke	BioImp	To evaluate the effects of HES on systemic hemodynamics decrease	HES administration avoided nocturnal in CO and MAP No effects on neurological status were reported	Very low
Finn et al. [52]	32	P	SAH	PAC	To evaluate the effects of hemodynamic optimization on neurological status	Maintaining PAOP between 14 and 16 mmHg reversed neurological deficit; all patients had CI > 4.5 L/min m2	Very low
Mori et al. [53]	98	P	SAH	PAC HHH	To evaluate the effects of HHH therapy on CBF and neurological status	HHH increased PAOP and CI Increased MAP and CI was associated with increased CBF	Low
Otsubo et al. [51]	41	P	SAH	PAC NV-HT	To evaluate the effects of NV-HT on neurological status	NV-HT increased also CI and improved neurological status in 71 % of symptomatic vasospasm	Low
Muench et al. [54]	47	P	SAH	PAC HHH (NE)	To evaluate the effects of different component of HHH therapy on brain perfusion and oxygenation	Increased MAP but unchanged CI Increase in rCBF/PbO2 only with HTN	Low
Mutoh et al. [111]	7	P	SAH	TT	To evaluate the effects of hyperdynamic therapy on brain oxygenation during symptomatic vasospasm	TT-guided therapy Increased rSO2 during VSP	Very low
Levy et al. [55]	23	P	SAH	PAC Dobu	To evaluate the effects of dobutamine on neurological status	Increased CI improved neurological status during CV in 78 % of patients who failed to respond to NE	Low
Tanabe et al. [50]	10	R	SAH	PAC	To evaluate the effects of IV albumin on systemic hemodynamics	Increased CI improved neurological status during CV	Very low
Hadeishi et al. [49]	8	R	SAH	PAC Dobu	To evaluate the effects of dobutamine on neurological status	Increased CI improved neurological status during CV	Very low
Kim et al. [112]	16	P	SAH	PAC Dobu/Phenyl	To evaluate the effects of dobutamine and phenylephrine on neurological status	Both drugs increased CBF in patients with vasospasm	Very low
Miller et al. [113]	24	P	SAH	PAC Phenylephr	To evaluate the effects of phenylephrine on neurological status	Increased MAP did not result in CI changes—88 % of patients improved neurological status	Low
Naidech et al. [114]	11	R	SAH	PACDobu/xMilri	To evaluate the effects of different inotropes on systemic hemodynamics	Milrinone was more effective to increase CI but was also associated with lower MAP	Very low
Impact of specific therapies dealing with optimization of CO on outcomes
Tagami et al. [65]	1,482	R (b/a)	OHCA	TT-guided therapy	To assess the impact of TT-guided therapy on outcome of CA patients	Improved good neurological outcome	Low
Kim et al. [67]	453	P (b/a)	SAH	PAC	To evaluate the effects of hemodynamic monitoring on the occurrence of complications	Reduced incidence of sepsis and pulmonary edema Reduced mortality (29 vs. 34 %, p = 0.04)	Moderate
Mutoh et al. [78]	45	P	SAH	TT	To evaluate the effects of hemodynamic monitoring on the occurrence of complications	4/8 DCI in patients with VSP No pulmonary edema or heart failure	Low
Vermeij et al. [115]	348	R (b/a)	SAH	PAC (VSP) HHH	To evaluate the effects of hemodynamic monitoring on the occurrence of complications	Reduced mortality among patients with DCI	Low
Medlock et al. [69]	47	P	SAH	PAC Proph. HHH	To evaluate the effects of hemodynamic monitoring on the occurrence of complications	Proph HHH did not prevent DNID 26 % incidence of PE	Low
Rondeau et al. [66]	41	RCT	SAH	TT	To evaluate the effects of hemodynamic monitoring on the occurrence of complications	Dobu versus NE: similar VSP and DCI but lower MV duration and ICU stay	Moderate
Mutoh et al. [68]	116	RCT	SAH	PAC (late) TT	To evaluate the effects of hemodynamic monitoring on the occurrence of complications	Reduced VSP, DCI, VSP-related infarctions, CV complications—improved mRS	Moderate
Lennihan et al. [116]	82	RCT	SAH	PAC HV versus NV	To evaluate the effects of hemodynamic monitoring on the occurrence of complications	HV did not increase CBF but raised filling pressures No differences in occurrence of VSP and DCI	Moderate

P prospective, R retrospective, SAH subarachnoid haemorrhage, TBI traumatic brain injury, TT transpulmonary thermodilution, PE pulmonary edema, CO cardiac output, PCWA pulse contour wave analysis, LVEF left ventricular ejection fraction, NPE neurogenic pulmonary edema, NR not reported, CV cerebral vasospasm, CI cardiac index, PE pulmonary edema, IABP intra-aortic balloon counterpulsation, LVEF low ventricular ejection fraction, cTnI troponin I, GEDVI global end-diastolic volume index, GEF global ejection fraction, DCI delayed cerebral infarction, BNP brain natriuretic peptide, SV stroke volume, ECG electrocardiogram, VA ventricular arrhythmias