Cushing reflex (also referred to as vasopressor response , Cushing effect , Cushing reaction , <> Cushing phenomenon , Cushing , or Cushing's Law ) is the response of the physiological nervous system to an increase in intracranial pressure (ICP) that results in Cushing triads increasing blood pressure, irregular breathing, and bradycardia. Usually seen at the terminal stage of acute head injury and may indicate brain herniation. Can also be seen after administration of intravenous epinephrine and similar drugs. It was first described in detail by American neurosurgeon Harvey Cushing in 1901.
Video Cushing reflex
Definisi
Cushing reflexes appear classically as an increase in systolic and pulse pressure, reduced heart rate (bradycardia), and irregular respiration. This is due to increased pressure inside the skull. These symptoms may indicate insufficient blood flow to the brain (ischemia) as well as arteriolar compression.
In response to increased intracranial pressure (ICP), the respiratory cycle changes in regularity and rate. Different patterns show different locations of the brain where injuries occur. Improved ventilation is exhibited as an increase in rate rather than depth of ventilation, so Cushing's reflexes are often associated with slow and irregular breathing. As a result of the now defective heart rate and blood pressure setting, the physiological response is a peripheral blood flow decline, which may be present as a Mayer wave. These are only pathological waves seen in HR searches (ie, arterial pathways, electrocardiographs (ECG, etc.), which reflects decreased intravascular blood flow.14 These declining streams often cause reflexive HTN (increased blood pressure) despite the actual decrease in intravascular volume.
Maps Cushing reflex
Differential diagnosis
Every time a Cushing reflex occurs, there is a high chance of death in seconds to minutes. As a result, Cushing's reflexes indicate the need for immediate treatment. Because of its existence is a good high ICT detector, it is often useful in the medical field, especially during surgery. During neurosurgery performed in the brain, there is always the possibility that an increase in intracranial pressure may occur. This early recognition is very important for the patient's health. Although direct measurements of ICP are possible, it is not always accurate. In the past, doctors and nurses relied on hemodynamic or bradycardic changes, the final phase of the reflex, to identify ICP increases. After the initial stages of Cushing reflex (bradycardia combined with hypertension) is found, it offers a much more reliable and rapid ICP warning sign. It was found that hypertension and bradycardia occurred 93% of the time when cerebral perfusion pressure (CPP) fell below 15 mmHg due to increased ICP. Also, Cushing reflex is known to arise only from acute acute increases in ICP. Thus, it can be used as a tool by physicians to distinguish acute and chronic increases in ICP.
It is also reported that the presence of Cushing reflexes due to increased ICP may allow one to conclude that ischemia has occurred in the posterior cranial fossa. Finally, Cushing's reflex can be one of many ways to identify whether a patient has rejected the transplant organ. Aside from the congenital autoimmune response, ischaemia in the skull region has been detected with transplanted organs rejected. Thus, the presence of Cushing reflexes due to ICP may indicate that ischemia may occur due to rejection of foreign organs.
As first postulated by Harvey Cushing, increased intracranial pressure is a major cause of Cushing's reflexes. Furthermore, an increase in ongoing cranial pressure allows the occurrence of Cushing reflexes. Conversely, rapid and dramatically increased pressure does not allow the mechanism of reflex to sufficiently occur. Increased intracranial pressure can result from various pathways of brain damage, including: subarakhnoid hemorrhage, ischemia, trauma, including concussions, hypoxia, tumors, and stroke. In one study, it was confirmed that increased ICP due to subarachnoid hemorrhaging caused mechanical distortion of the brainstem, particularly the medulla. Because of the Cushing reflex mechanism, brainstem distortion is then rapidly followed by the sympathetic nervous system of activity. In addition, during neurosurgical procedures in patients, especially those involving neuroendoscopy techniques, frequent ventricular washing has been known to cause high intracranial pressure. Cushing reflexes can also be produced from low CPP, especially below 15 mmHg. CPP typically falls between 70-90 mmHg in adult humans, and 60-90 mmHg in children.
Changes in brainwave plates are also associated with Cushing's reflexes. This wave is characterized by an acute increase of ICP, and is accompanied by a decrease in cerebral perfusion pressure. It has been found that if Cushing's reflexes occur, changes in brain plate waves can be removed due to high ICP loss.
Mechanism
Cushing reflexes are complex and seem paradoxical. Reflexes begin when some events cause increased intracranial pressure (ICP). Because the cerebrospinal fluid is located in the region surrounded by the skull, increasing the ICT consequently increases the pressure in the fluid itself. The pressure in the cerebral spinal fluid eventually rises to a point that fills and gradually exceeds the mean arterial blood pressure (MABP or MAP). When ICP exceeds MABP, the arterioles located in the cerebrum brain become compressed. Compression then results in a reduced blood supply to the brain, a condition known as cerebral ischemia.
During ICP upgrading, both the sympathetic nervous system and the parasympathetic nervous system are activated. In the first stage of the reflex, stimulation of the sympathetic nervous system is much greater than for parasympathetic stimulation. The sympathetic response activates alpha-1 adrenergic receptors, causing artery narrowing of the body. This narrowing increases the total resistance of blood flow, lifting blood pressure to high levels, known as hypertension. Body-induced hypertension is an attempt to restore blood flow to the ischemic brain. Sympathetic stimulation also increases the rate of cardiac contraction and cardiac output. An increase in heart rate is also known as tachycardia. This combined with hypertension is the first stage of the Cushing reflex.
Meanwhile, baroreceptors in the aortic arch detect an increase in blood pressure and trigger a parasympathetic response through the vagus nerve. It induces bradycardia, or a slowing heartbeat, and signifies the second stage of the reflex. Bradycardia may also be caused by an increase in ICT due to direct mechanical distortion of the vagus nerve and subsequent parasympathetic response. Moreover, a reflexive increase in parasympathetic activity is thought to contribute to the formation of Cushing's ulcers in the stomach, due to uncontrolled parietal cell activation. Blood pressure can be expected to remain higher than the pressure from the cerebral spinal fluid that is raised to continue allowing blood to flow into the brain. The pressure rises to the point where it overcomes the resistive pressure of the compressed arteries, and the blood is allowed to pass, giving oxygen to the brain hypoxic area. If an increase in blood pressure is not enough to compensate for compression of the arteries, an infarction occurs.
Increased ICP, tachycardia, or other endogenous stimuli can cause distortion and/or increased pressure on the brainstem. Because the brain stem controls unintentional breathing, homeostatic changes often lead to irregular breathing patterns and/or apnea. This is the third and final stage of the reflex.
Generally, in various reflex pressors, central chemoreceptors, which convert chemical signals into action potentials, and baroreceptors, which feel the pressure changes from the carotid sinus, work together to increase or decrease blood pressure. However, chemoreceptors do not play a role in Cushing's reflexes. So even with the sympathetic stimulation of the brain, which usually produces tachycardia, there is actually bradycardia.
Function
Increased intracranial pressure may eventually lead to shifting or destruction of brain tissue, adversely affecting the patient's physiological health. As a result, Cushing's reflex is the last attempt by the body to maintain homeostasis in the brain. It has been widely accepted that Cushing reflexes act as baroreflex, or homeostatic mechanisms for the maintenance of blood pressure, in cranial regions. In particular, the reflex mechanism can maintain normal brain blood flow and pressure under stressful situations such as ischemia or subarachnoid hemorrhage. A case report of a patient undergoing spontaneous subarachnoid hemorrhage shows that Cushing reflexes play a role in maintaining cerebral perfusion pressure (CPP) and cerebral blood flow. Finally, ICP goes down to varying degrees where the induced hypertension state in the form of Cushing reflex is no longer necessary. Cushing reflex is then canceled, and CPP is maintained. It has also been shown that an increase in mean arterial pressure due to hypertension, reflex characteristics, can lead to normalization of CPP. This effect is protective, especially during increased intracranial pressure, leading to a decrease in CPP.
Triad Cushing
Triad Cushing is a clinical triad defined differently as having:
- Irregular, decreased respiration (caused by impaired brainstem function)
- Bradycardia
- Systolic hypertension (dilation of pulse pressure)
History
Cushing reflex is named after Harvey Williams Cushing (1869-1939), an American neurosurgeon. Cushing began his research in Bern, Switzerland studying abroad with Emil Theodor Kocher. One month on its way, Cushing accepted the formal proposition of Emil Theodor Kocher to begin testing how brain compression affects the blood vessels. Cushing also enlisted the help of Hugo Kronecker, a known blood pressure researcher. Utilizing Kroenecker's help and resources, Cushing began his research. Cushing left Bern in 1901 to work in Turin, Italy with Angelo Mosso, a former Kroenecker student. He continues to work on the same research project, while simultaneously improving his method of recording the coincidence of blood pressure and ICP. In June 1901 Cushing published his first paper through the Johns Hopkins Hospital Bulletin entitled "Regarding the exact regulatory mechanism of the vasomotor center that controls blood pressure during brain compression". Between 1901 and 1903, Cushing published five papers related to his research on vasopressor responses. The paper is published in German and English, and one is written by Emil Theodor Kocher.
Settings and experimental results
Cushing started experimenting after he obtained approval from Kocher. His experimental setup was a modified version of the Leonard Hill model to test the effects of brain pressure on sinus pressure, cerebrospinal fluid pressure, arterial and venous blood pressure. Like Hill, Cushing uses dogs for his experiments. To begin, Cushing monitors the caliber and color caliber vessels by placing the glass window into the dog's skull. The intracranial pressure is raised by filling the intracranial, soft, with mercury rubber bags. Cushing notes intracranial pressure along with blood pressure, pulse, and respiratory rate simultaneously. This three-part effect is often referred to as the Cushing triad. In later experiments performed by Mosso, intracranial pressure was induced by injecting physiological salts into subarachnoid space rather than increasing mercury levels from the intracranial sac.
This study clearly shows the cause and effect relationship between intracranial pressure and cerebral compression. Cushing notes this relationship in the next publication. He also notes that there should be a special regulatory mechanism that raises blood pressure to a high enough point so as not to create an anemia condition. The Cushing publication contains its observations and no statistical analysis. The sample sample size is also unknown.
Other researchers
Some important medical figures, including Ernst von Bergmann, Henri Duret, Friedrich Jolly, and others experimented with intracranial pressure similar to Cushing. Some of these researchers published similar findings about the intracranial pressure relationship to arterial blood pressure before Cushing started experimenting. Cushing studied this relationship more carefully and offered a better explanation of the relationship.
Some controversy over plagiarism surrounds several Cushing studies. Bernhard Naunyn, a German and contemporary Cushing pathologist, made a statement claiming that Cushing did not mention it in Cushing's research or expanded on any of the results he found in his original experiment.
Direction of research
Although much progress has been made since 1901 when Harvey Cushing first expanded his knowledge of what is now known as Cushing's reflex, there are still many aspects of research to be seen. The exact pathogenesis of this disease remains undetermined. The possibility that intracranial pressure (ICP) may not be the sole cause of Cushing reflexes per se comes from the Cushing blood pressure response occurring prior to ICP elevation. Several studies have observed Cushing's reflex symptoms, without increased ICP and medullary anemia, suggesting other causes that still require research. Axial brainstem distortion may be a Cushing reflex pathogenesis.
The receptor properties mediating the Cushing response are also unknown. Several studies have demonstrated the presence of intracranial baroreceptor to trigger a specific Cushing baroreceptor reflex. Experiments by Schmidt and his fellow researchers show that Cushing's reflexes are directed by the autonomic nervous system, because their physiological changes are related to the balance of the sympathetic nervous system and the parasympathetic nervous system. However, the specific relationship between the response of the autonomic nervous system and the Cushing reflex and its symptoms has not been identified.
It has been determined that the respiratory rate is influenced by Cushing's reflexes, although induced respiratory alteration is still an area requiring further investigation. Some researchers have reported apnea, while others have reported an increase in respiratory rate. Other researchers have found that the increase in respiratory rate after ICP decreases, while others say it is a response to ICP increase. One should also consider the use of anesthesia in the initial trial. The study was initially performed on animals or patients under anesthesia. The anesthesia used in the experiment has caused respiratory depression, which may have an impact on outcomes. Initial experiments also placed the animal subject under artificial ventilation, allowing only for a limited conclusion about respiration in Cushing's reflexes. The use of anesthesia suggests an idea for future research, as the creation of a Cushing response is difficult to make under basal or no anesthesia.
Some researchers also suggest long-term effects of Cushing's reflexes. So far only observed as acute acute response, but there is some evidence to suggest that the effect can be prolonged, such as an increase in long-term blood pressure. High sensitivity of the neurological response system leading to arterial hypertension is also possible, but has not been examined.
Although Cushing's reflexes are primarily identified as physiological responses when the bloodstream is almost stopped, its activity has also been seen in fetal life. This activity has not been fully investigated, so there is a need for more research in this area.
The mechanisms underlying reflexes at the cellular level have not been discovered, and will likely be the next field of research if scientists and or physicians choose to do so.
See also
- Traumatic brain injury
- Bainbridge reflex
References
Source of the article : Wikipedia
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