Recent studies show that evaluation of APACHE II and TNF-α in the first day and APACHE II and IL-6 in the third and seventh days of severe septic patients are independent outcome predictors and suggest that IL-6 and APACHE II are useful cytokine and scoring systems respectively in prediction of mortality and clinical evaluation of these patients.
Although reducing heart rate is a therapeutic target to improve outcomes in cardiovascular patients, the question of transferability to critically ill traumatic brain injury patients remains unanswered. Nevertheless as a result of elevated intracranial pressure, heart rate might be even lowered than the therapeutic range for instance in spinal cord injury and neurogenic shock, heart rate could be less than 60 bpm. The same thing is true for sever traumatic brain injury where the Glasgow Coma Score is less than 8 and cerebral perfusion pressure is below 60 mmHg and intracranial pressure is beyond 20 mmHg. The results of our study have indicated that there is a correlation between baseline heart rate and 60th day mortality but mean heart rate was not different between groups of alive and diseased patients. To our knowledge, this was the first study which was evaluated the role of a physiological parameter (heart rate) as a predicting tool for estimating mortality.
There are number of studies which have evaluated the reliability of different scoring systems in predicting morbidity and mortality in ill patients. Chen et al. had shown that there was a good correlation between expected mortality predicted by the APACHE II scoring system and observed mortality and APACHE II was useful for evaluating ICU performance and risk stratification. Rehman has demonstrated that this score did not show any correlation between predicted mortality and observed mortality in critically ill patients but it was useful for substantial reduction in suffering and cost. In our study, use of APACHE II score was useful for predicting prognosis and there was a significant difference in mean APACHE II score between groups of deceased and alive patients. Therefore, this scoring system not only allows a grading of disease severity but also dependably describe patient prognosis.
Vincent’s study had shown that the SOFA score was a simple, but effective method to describe organ dysfunction/failure in critically ill patients and regular, repeated scoring enables patient condition and disease development to be monitored and better understood. Also, it may enable comparison between patients that would benefit clinical trials. In our study, this score was useful for evaluating disease development because of significantly difference in mean SOFA score between diseased and alive patients.
Ferreira’s study had shown that both mean and highest SOFA scores were good indicators of prognosis and have predicted outcome usefully during the first few days of ICU admission. Independent of the initial score, an increase in SOFA during the first 48 hours in the ICU has predicted a mortality rate of at least 50%. In our study a significant correlation between baseline SOFA score and 60 days mortality was observed.
Adverse impact of increased heart rate has different pathophysiological explanations such as increased myocardial oxygen demand and reduced coronary blood flow due to shortened diastole. Also, it has been shown that there is an increased disposition to rupture atherosclerotic plaques at elevated heart rates.
Endotoxin, which is a frequent cause of sepsis and consecutive MODS and increased in heart failure, directly affects the hyperpolarization-activated cyclic nucleotide gated (HCN) channels mediating the pacemaker of human cardiomyocyte. Apart from that, endotoxin sensitizes the HCN (Hyperpolarization-activated Cyclic Nucleotide) channels for sympathetic stimulation and increasing heart rate. Therefore, endotoxin increases heart rate and reduces heart rate variability in chronically instrumented mice and blocking sympathetic and vagal activity induces bradycardia. Totally endotoxin induces inadequately high heart rate and narrowed heart rate variability which causing cardiac and autonomic dysfunction and indicating poor prognosis in patients with MODS.
Elevation of heart rate leads to increasing of intracranial pressure. Increased intracranial pressure reflects the presence of mass effect in the brain and is associated with a poor outcome with acute neurological injury. If sustained, it has a negative effect on cerebral blood flow and cerebral perfusion pressure, can cause direct compression of vital cerebral structures, and can lead to herniation. The management of the patient with increased intracranial pressure involves the maintenance of an adequate cerebral perfusion pressure, prevention of intracranial hypertension, and optimization of oxygen delivery.
If the metabolic demands exceed the supply, cerebral ischemia will ensue, leading to irreversible neurological damage.
In addition, elevated ICP may intensify the processes involved in secondary brain injury, negatively affecting outcomes. It is well established that intracranial hypertension negatively affects morbidity and mortality.
Many complications are commonly associated with TBI, such as deep vein thrombosis (DVT), hyperglycemia, and excessive protein loss. By promoting optimal ICP (Intra Cranial Pressure) and CPP (Cerebral Perfusion Pressure) DVT (Deep Venous Thrombosis) complications, inadequate nutrition, detrimental hyperglycemia, and seizures in adults with severe TBI can be prevented.
In the multifactor primary prevention trial in GÖteborg, a clear correlation between resting heart rate and all-cause-mortality was shown. Compared with individuals with a heart rate <60 bpm, a heart rate >90 bpm in participants was associated with a two- to three-fold elevated mortality. Another trial which followed up patients with coronary heart disease has shown a significant correlation of elevated heart rate with mortality. In GISSI-2 trial, the heart rate of patients with acute myocardial infarction at discharge without atrial fibrillation proved to be an independent predictor of survival and 6-month mortality was higher for heart rate>100 bpm in compared to heart rate<60 bpm. In addition to heart rate at baseline, the mortality rate also depends on the extent of heart rate reduction by using beta-blocker.
In our study, a correlation between elevated baseline heart rate and 60th day mortality was shown; But this was not true about 7th day mortality. Mortality in brain injury is mainly dependent to severity of the injury and elevated baseline heart rate is also a reflection of disease severity.
The relative correlation between baseline Heart Rate and 60th day mortality is not observed in last 7 days. These differences may be a reflection of modifications by medications or other therapeutic measurements during acute phase of treatment.
A fast heart rate on the day of admission was an independent and early predictor of death due to MODS in a prospective, multicenter, observational cohort trial of high-risk patients with noncardiac surgery.
Following cardiac arrest, therapeutic hypothermia by decreasing heart rate and cathecolamine storm may also improve neurological recovery[25, 26].
Based on the results of the BEAUTIFUL-trial, the patients with stable coronary heart disease and heart failure with a heart rate >70 bpm have a worse prognosis. Above a heart rate of 65 bpm, every increase in heart rate of 5 bpm was associated with a higher risk of all-cause-mortality, hospitalization because of worsening heart failure, hospitalization because of myocardial infarction and hospitalization because of coronary revascularization.
Increasing data indicate treatment with beta blockers might improve survival after traumatic brain injury. The optimal heart rate range for these patients is unknown. Admission heart rate in moderate to severe TBI patients was analyzed to determine if a specific range is associated with decreased mortality. After isolated moderate to severe TBI, HR <50, 50–59, 60–69, and > or =110 were independent predictors of increased mortality compared with HR 80–89. HR outside the range 70–109 could serve as a marker for aggressive resuscitation. As mortality increased significantly with HR <50, 50–59, and 60–69, avoiding HR <70 in patients with moderate to severe TBI recommended.